UNIT I: INTRODUCTION TO VIROLOGY

GENERALITIES VIRION
● Structure - Different Structures of the Viruses ● Complete viral particle, the unit of a virus
● Replication - Manner of Replication ● Composed of 2 or 3 parts (depending on the type of
● Taxonomy - Manner of Classification of the Medically the virus; basically, all viruses must have at least two
Important Viruses components - nucleic acid core and capsid)
VIRUS ○ Nucleic acid core (Genome)
● The word virus is a Latin term for “poison” ■ Genome - would either be a DNA or an
● Obligate intracellular organisms RNA genetic material
○ Viruses would always require a host for survival; ○ Capsid - Protein coat of the viral particle
thus, they will only survive inside the host ■ Protects the genome / genetic material
○ Viruses are inactive outside the host inside the viral particle
● No metabolic systems of their own; highly dependent ○ Envelope - Some viruses have this third
on its host cell component
○ Viruses will not survive in the absence of the host ■ Host cell-derived
■ Host is either human (or even plants & ● Meaning, during the release of the viral
animals) or bacteria particle from the host, a portion of the
■ The virus can use different types of host in cell membrane or even nuclear
its life cycle membrane of the virus is attached onto
● Filterable organisms the released viral particle
○ Meaning, viruses are very small organisms ● A part of host cell which is composed
(smaller than bacteria) to as it is being released from the host
■ Thus, when a typical filter for filtering out / cell
removing bacteria is used, viruses can also ■ A lipid-rich component of the virion;
be removed Primarily composed of lipid
● Submicroscopic infectious particles ■ Once the virus possesses an envelope, the
● Host cell specific organisms virus becomes an enveloped virus
○ Viruses only infect certain cells if these cells ● Enveloped virus - Ether labile
have receptors ● Picture A is an enveloped virus
■ If the viruses DO NOT possess an
envelope, it is now called a naked virus
● Naked virus - Ether stable / Ether
resistant
○ Meaning, they are not destroyed
by an organic solvent such as
ether
DEFINITION OF TERMS
● Defective virus
○ Viral particle that is functionally deficient
○ Can be deficient in an aspect in its viral
replication (deficiency in the manner of
replication)
an illustration of a smallpox viral particle
○ Example: Hepatitis B Virus
● Capsomere
○ Morphologic unit of the capsid
○ Repeating units that are chemically composed of
polypeptides

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● Nucleocapsid ● Viruses are strands of nucleic acids that are enclosed
○ Composed of the genome surrounded by a within a protein coat. They possess either DNA or
capsid RNA but not both
○ Also described as the packaged form of the ○ A virus that has both DNA and RNA is not yet
genome identified
○ Usually encountered when dealing RNA viruses ● Diameters of viruses range from 20-300 nm
since capsids are closely interconnected with the ○ Very small organism
genome of RNA viruses
■ Note: Don’t be confused with virion and ESSENTIAL CHARACTERISTICS
nucleocapsid ● SIZE: Ranges from 25nm to 25x350 nm
● Protomers ● Comparative Sizes of Viruses and Bacteria
○ Found in protein coat (capsid); thus, are
composed of proteins
● Peplomers
○ Protein spikes that are present on the surface of
the envelope
○ Used for attachment to the target host cell
■ Used by the virus to interact with the
receptors found in the host cell
■ Thus, peplomers are important in the
attachment process of viral replication Different virus species are shown here
● Matrix protein to scale inside an E. coli bacterium
○ Can be found in certain types of viruses (e.g.
HIV, some types of Herpes viruses) ○ Escherichia coli - Type of bacteria
○ Found in between the envelope and the capsid ■ Many viruses can fit in one bacterium since
○ Also important during the replication process of they are smaller than a typical bacterium
the virus

Another picture showing the relative size of a virus

compared to red blood cell (erythrocyte) and bacteria

VIRAL PARTICLE
● GENOME
SUMMARY ○ Genetic material composed of DNA or RNA but not
● Composed of genetic material enclosed in a protein both
coat ○ Viruses contain only one copy of genome except
● Have the genome Retrovirus such as HIV
■ HIV - Has two copies of the genome; thus,
called a diploid virus)

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 Can be single stranded or double stranded RNA VIRUSES
○ Can have linear or circular genetic material ■ Usually single stranded and some are
■ Some can have a segmented genetic segmented
material ● Advantage of a segmented genome
● Genome is fragmented or in pieces ○ There is an enhanced potential
● As a general rule, segmented viruses for genetic reassortment; thus,
there is a possibility of forming a
are encountered in RNA viruses
new type or strain of the
● Segmented genome has not been particular virus
identified in DNA viruses ● Exceptions: Reoviridae and
Picobirnaviridae
DNA VIRUSES ○ These are double stranded RNA
■ Usually (most are) double stranded, and viruses
linear or circular ■ Sense of Plus Strand RNA Virus
● Exceptions: Parvoviridae, Circoviridae ● Viruses that function already as mRNA
○ These are single stranded DNA ○ There’s no need for transcription
viruses to process since the genome itself
of the virus functions already as
mRNA and goes straight to
translation
■ Anti-sense or Minus Strand Virus
● Polarity opposite of mRNA; it must be
transcribed first
○ The genome would have to
undergo transcription before
becoming an mRNA; thus, protein
translation can now occur if it has
Important DNA viruses been transcribed
(details are more elaborated in Unit II) ○ RNA dependent RNA
polymerase - needed for the
transcription to happen

Short background on DNA viruses

During the replication process of the virus (e.g. DNA
virus), only the positive strand is used during the
replication process, particularly in the transcription
process to produce mRNA. The negative strand is ignored
and not used in the replication process. The mRNA will
undergo translation to produce enzymes and proteins of
the viruses.

Examples of RNA viruses

(more diverse as compared to DNA viruses)

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 CAPSID - “shell” or protein coat
○ Composed of Capsomeres, the repeating subunits
○ Encloses the nucleic acid
○ Determines specific viral antigenecity
■ These antigens serve as identification
markers of the virus
○ Important for the attachment to the target cell
especially if the virus is naked
■ Naked virus - The capsid would have the
antigens (serves as an identifying marker
for the virus) to be used as an attachment
Illustration showing positive and to the host cell
negative sense RNA viruses ○ For protection of genetic material and to prevent
• + goes straight to translation denaturation
• - needs RNA dependent RNA polymerase to
convert it to mRNA NUCLEOCAPSID
• Note: There are certain RNA viruses that would ○ Function - Protection of the genetic material from
have a different manner of replication denaturation
o Retroviruses - Viruses that need an enzyme
called reverse transcriptase
▪ Reverse transcriptase functions to be
used by the viruses to turn its RNA
genome to become a DNA genome
■ Note: Retroviruses (e.g. HIV)
have this enzyme to convert RNA
to DNA.

Why does it need to become a DNA?

The retroviruses would happen in the nucleus. In order
to gain access to the nucleus, the genome should be a
DNA. Once it becomes a DNA, it would then undergo the
usual process of transcription to form the mRNA; then
the mRNA would go out of the nucleus to undergo
translation for the production of proteins and enzymes

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 ENVELOPE
○ Surrounds the capsid of certain viruses
○ Lipoprotein membrane - Composed of lipoprotein
○ It is acquired during viral maturation (and release of
the virus inside the host cell) by a budding process
through the host’s membrane
■ As the viral particle is being released from
the host cell, it gets a portion of the
membrane of the host cell
■ Eventually, that portion of the membrane
would become the envelope
○ Other structures present on the envelope
■ Peplomers (spike-like structures) - for
attachment
■ Matrix protein - important during replication
● Can also be important for certain
inhibition (e.g. processes in viral
replication)
■ Enzymes

○ ENVELOPED VIRUSES
■ Either labile / ether sensitive
● Destroyed by organic solvents
■ More sensitive and easily destroyed as
compared to naked viruses

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 ■ Usually transmitted by contact (close
contact, direct contact, sexual contact) and HELICAL VIRUSES
rarely transmitted via oral fecal route
o Shaped like hollow protein cylinders, which
○ FACTORS THAT CAN DAMAGE ENVELOPE: may be either rigid or flexible
o Most are flexible, except Rhabdovirus (an
■ High and very low temperatures
example is rabies, which is rigid)
■ pH of less than 6 or pH above 8 o Nucleic acid and protein are closely associated
■ Disinfectants such as (Hydrogen peroxide, o Example:
phenol) ▪ Tobacco Mosaic Virus(not medically
○ Capsids that are helical are enveloped important)
○ Is there a correlation between mode of transmission ▪ Ebola Virus
of Enveloped and Naked viruses? o If helical structure = always a RNA virus
■ MOT of enveloped virus: close contact, o Helical viruses are enveloped
sexual contact
■ MOT of naked virus: usually oral fecal route
via ingestion
■ Enveloped virus is easily destroyed and has
helical capsids

OTHER COMPONENTS OF THE VIRAL PARTICLE

○ Enzymes such as neuraminidase, RNA
polymerase, DNA polymerases and reverse
transcriptase
○ Hemagglutinin
○ Tegument - located between the nucleocapsid and
envelope (HSV, CMV)

TYPES OF STRUCTURAL PATTERNS

▪ Helical ICOSAHEDRAL VIRUS
▪ Icosahedral o Polyhedrons/geometric shape with:
▪ Complex ▪ 20 triangular sides
▪ 12 vertices
▪ 60 identical subunits
o Assemble in a cubic manner
o These capsids appear spherical when viewed
at low power in the electron microscope
o Can be crystallized and viewed using
radiocrystallography
o Example: Adenovirus
o Can be enveloped or naked

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 COMPLEX VIRUSES VIRAL REPLICATION
• Capsid symmetry but not purely icosahedral Could be described in 2 ways:
nor helical • Viral Growth Curve
• Complex Coat – primarily Ether Resistant • Viral Growth Cycle
• They may possess tails and other structures
(e.g. many bacteriophages) or have complex, VIRAL GROWTH CURVE
multi-layered walls surrounding the nucleic Virion Entering the Cell (Attachment)
acid (e.g. poxviruses such as vaccinia) • Once the virus find its specific host, it would attach
to the host cell. The antigen will interact with the
corresponding receptor. Take note that the receptor
is present in the host cell. If the antigens of the virus
fix the receptor in the host cell, it would allow
attachment of the virus. Once the virus would
already interact with the specific host cell receptor,
it would now then allow entry of the viral particle.
• Once it enters, you would observe that the number
of viral particles go down because it coincides with
the eclipse period.

Latent Period
• Time between time of infection (virus entry) and
appearance of virus outside the host or
extracellularly
• Once the virus enters and once the virus is released
• Patient might be asymptomatic

Eclipse Period
• No detectable viral particle inside the host cell
because during this period, the virus is uncoating.
Meaning, it is removing its capsid (protein coat) to
release the genome.

Extracellular Release of Viruses

• Viral release- last part when viral components are
already assembled
• Some virus, when released, destroys the cell.
Others do not. It depends on the virus.
During the whole duration of the eclipse period and the first
half of the latent period, replication process occurs (either
REACTION OF VIRUSES TO
happen in nucleus [for DNA viruses] or cytoplasm [for RNA
PHYSICAL AND CHEMICAL AGENT
viruses])
• Heat and Cold
▪ H Heat Labile – enveloped viruses
The Replication Process:
▪ Heat Stable – icosahedral viruses
Transcription > Production of mRNA > Translation
▪ Generally, infectivity is destroyed at
50-60 C for 30 mins (except HBV,
Translation - happens in cytoplasm of host cell) where
polyomavirus)
there would be production of proteins and enzymes of the
• Stable with 1mol/L of salts virus.
• pH: generally stable (5-9)
• Either Susceptibility and Detergents: At the end of the eclipse period and the second half the
Enveloped Viruses latent period
• Formalin: inactivated (esp. single stranded As the virus is already producing the proteins and
viruses) enzymes, Maturation of the viral particles takes place.
• Penetrable by vital dyes That’s why the graph is slowly increasing because there is
• Radiation: inactivate viruses already the assembly of the virus.

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 Host Cell Receptors

One-Step Virus Growth Curve

VIRAL GROWTH CYCLE (STEP-WISE) ACE2 (Angiotensin converting enzyme-2) is the

o Infectious Cycle SARS-CoV-2 host receptor
o Adsorption (Attachment)
o Penetration PENETRATION
o Uncoating o Viral Entry
o Macromolecular Synthesis (Transcription and o Varied mechanisms for entry through:
Translation) ▪ Fusion with the cell membrane (e.g.
o Assembly and Release enveloped viruses)
▪ Syncytia formation
Mnemonic for Viral Growth Cycle from ▪ Endocytosis – entry through cytoplasmic
Sir Greg AKA Daddy Marts (from Lab) vacuole
▪ Translocation – direct penetration of host cell
APUSAR (e.g. naked viruses)
A – attachment ▪ Injection of Viral Material - use of several tail
P – penetration ( °͡ ʖ
͜ °͡ ) fibers and lysozyme (e.g. bacteriophages)
U – uncoating
S – synthesis
A – assembly
R – release

ADSORPTION / ATTACHMENT
o First Step
o “attachment”
o Recognition of a suitable host cell
o Specific binding with capsid proteins and
carbohydrate receptor of host cell
▪ Receptors – each are specific for a virus
▪ Tropism – affinity of the virus to a particular
host cell (due to presence of specific receptor)

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 UNCOATING ASSEMBLY AND RELEASE
o Disassembly • Viral Maturation/Morphogenesis
o Loss of the protein coat o Assembly of produced viral capsid proteins and
o Exposes the nucleic acid genomes
▪ Free Genome (as in picornaviruses) o Production of different components of the
▪ Nucleocapsid (as in reoviruses) virus
*DNA virus – released in the nucleus o Assembled to new infectious virions
*RNA virus – released in the cytoplasm

• Release of the new infectious virions

o Ways of Release:
Attachment, Penetration, and Uncoating ▪ Lysis of the Infected Cell – host cell
dies; usually seen in naked viruses
MACROMOLECULAR SYNTHESIS ▪ Exocytosis of viral particles –
o Transcription and Translation packaged in the Golgi apparatus then
o Replication and expression of genetic material relased
and protein polymers ▪ Budding off – usually in enveloped
o Production of different components of the virus viruses
o Formation of inclusion bodies ▪ Cell-to-cell transport – fusion of two
▪ Nuclear inclusion bodies – found in the adjacent cells (Syncytia)
nucleus, generally indicative of DNA virus
▪ Cytoplasmic inclusion bodies – found in the
cytoplasm, generally indicative of RNA virus
o Coincides with the Eclipse Stage

Transcription and Translation

o DNA Viruses usually replicate in the nucleus
▪ Positive (+) strand of DNA virus is the one
used for transcription
▪ Uses host cell DNA-dependent RNA
polymerase to synthesize mRNA

o RNA Viruses replicate in the cytoplasm

▪ (+) sense RNA viruses = use host cell RNA
polymerase; no need for transcription
▪ (-) sense RNA viruses = uses its own RNA- Enveloped viruses – not infective without its
dependent RNA polymerase; has to be envelope
converted to (+) sense first before transcription
happens. PATHOGENESIS AND LIFE CYCLE
▪ Double stranded RNA = carries its own 1. Incubation Period
polymerase to convert it to mRNA o Period between time of infection and appearance
▪ Retroviruses = has (+) ssRNA that is of signs and symptoms
transcribed into dsDNA by reverse transcriptase o Patients are usually symptomatic
(RNA-dependent DNA polymerase, a.k.a. 2. Spread
reverse transcriptase). o infects nearby cells, migratory cells, disseminate
▪ This DNA copy is then turned to mRNA by host via blood (viremia), neuronal, via lymph
RNA polymerase o Viruses usually replicate at the primary site of
entry and may not spread to distant sites; but
some spread to distant sites

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3. Prodromal
o early nonspecific symptoms (fever, aches, pain and Pseudolysogenic or Episomal Virus
nausea) o viral persistence w/o integration
Episomes
4. Active Disease o non-integrated, persistent viral genomes
o either causing immediate (acute) or long-lived o genetic material persists but can be diluted
(chronic) infection when replicating
o Subsequent viremia (secondary viremia)
▪ Certain viruses, after initially spreading from
the blood, goes back to blood and spread
again (eg. Varicella, measles)

*Provirus
o genetic material persists and cannot be diluted
when replicating (unlike episomes)

ACTIVE DISEASE
o Lytic Viruses – destroy host cell after replication
▪ Manifestation of acute infection
▪ Usually a naked virus
o Lysogenic Virus – causes long-lived, latent
infection (e.g. Herpes viridae) ▪ Autoimmune pathogenesis
▪ Integrates into host genome • immune reaction allow cross-reaction with host
o Provirus* tissue antigens
▪ Subclinical Infection • certain viruses can cause “the body to fight
▪ Latency of viruses in host tissues itself”
o Can reactivate silently allowing viral ▪ Promotion of transformation or immortalization of host
shedding with no symptoms or cells
reactivate actively causing • Could trigger malignancies that lead to cancer
symptomatic disease (e.g. reactivation ▪ Oncogenesis – transformative viruses;
of chickenpox virus as Shingles or • stimulate uncontrolled growth of host cells
Zoster) • Could also promote tumour formation (e.g.
o Exit of viruses certain retroviruses, papillomaviruses)

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5. Resolution of Disease
o Innate IR – non-specific response of the body
against viral infection
o Adaptive IR – more specific; involves antibody
production, cytokine production
o Host Recovery
• Mechanisms: Innate and Adaptive IR
• Acute Infections: recovery is associated with
viral clearance Cytoplasmic
• But Persistent Infections can also occur Vacuoles
o Viral Shedding
• Shedding (release) of virion into the
environment
• Occurs at different stages of disease
• Patient: Infectious (Contagious)
• Shedding does not always occur in all viral
infections
o Frequency of Virus Colonization/ Infection
• Seasons: Winter vs Spring
• Age Group: Infants vs Adults These inclusion bodies
in particular are called
Negri bodies
EFFECTS OF VIRAL INFECTION ON THE HOST CELL
• Cytopathology: AKA Cytopathic Effects
• Structural changes leading to necrosis Inclusion
• Seen in virally infected cell cultures (diagnostic Bodies
purposes) (e.g. Negri
• Can be seen as: Bodies**)
o Plaque Formation
o Formation of multinuclear giant cells
o Cytoplasmic Vacuoles
o Inclusion bodies Cell degeneration and
necrosis

**Negri bodies
o cytoplasmic inclusion in neurons which is
associated with Rabies infection
• Apoptosis: programmed cell death
o Defense Mechanism of Host cell
• Noncytocidal Infection
o No extensive restructuring of host cell
o Virions are released by budding
• Appearance of new antigenic determinants on the cell
Plaque surface
• Cell fusion
o Formation of giant syncytia

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 MODES OF TRANSMISSION
• Direct Transmission from Person-Person by • Indirect Transmission
Contact o Fecal-Oral Route
• Droplet/Aerosols o Fomites
o Sexual Contact • Animal to Animal
o Hand-Mouth o Humans – accidental host
o Hand-Eye o Droplet or Aerosol infection of rodent urine or
o Mouth-Mouth feces
o Exchange of Contaminated Blood • Via Arthropod Vectors

CLASSIFICATION AND TAXONOMY OF VIRUSES

Basis Subfamily names Subspecies

• Morphology • end in –virinae • designated by a number
• Physicochemical Properties • capitalized first letter
• Genome Genera usually have the word virus
• Macromolecules Genus
• ends in –virus Sample Families
• Antigenic Properties
• o Poxviridae
• Biological Properties capitalized first letter
o Parvoviridae
Viral Species: o Retroviridae
Taxonomy
International Committee on • group of viruses sharing
In the Family Picornaviridae there are
Taxonomy of Viruses same genetic information 5 genera:
and host. Common names 1. Enterovirus
Family names of virus are used 2. Cardiovirus
• end in –viridae • common names of the 3. Rhinovirus
• capitalized first letter virus 4. Apthovirus
• written in small letters 5. Hepatovirus

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 BALTIMORE CLASSIFICATION
Based on genome, strandedness, sense and method of replication

Group I dsDNA viruses

Group II ssDNA viruses
Group III dsRNA viruses (ambisense)

Group IV positive sense ssRNA viruses

Group V negative sense ssRNA viruses

Group VI reverse transcribing RNA viruses

Group VII reverse transcribing DNA viruses

PREVENTION, TREATMENT AND CONTROL

• Immunization (Vaccination)
• Antiviral Agents

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 POST TEST
1. The protein coat of a virus is termed as? capsid
2. Members of Togaviridae are classified under
which Baltimore Classification? IV
3. True or False: Members of Family Reoviridae
possess dsRNA and are naked. True
4. Which DNA Virus Family is well known for
causing Latent infections? Herpesviridae
5. These are glycoprotein spikes present on the
envelope surface of certain viruses? Peplomers

For numbers 6-8, Classify the following as Ether labile or

Ether sensitive

6. Influenza A ether labile

7. SARS-COV 2 ether labile
8. Hepatitis A Virus ether stable
9. True or False; Helical viruses are always
enveloped and possess RNA. True
10. True or False: Replication of RNA viruses such
as Polio occur in the nucleus. False

You’re halfway through, yayy!!

Start strong and finish stronger

…. wait that sounds wrong but we know u get

what we mean… or do u??? (;

Wishing you all the luck u need this shift <3

On to the next unit

Or take a break, we don’t really mind.

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 UNIT 2: DNA VIRUSES

PRE-TEST • SV40 is an abv. for simian vacuolating virus 40

1. True for False: Adenoviruses are naked icosahedral or simian virus 40, a polyomavirus that is found
viruses with dsDNA. TRUE
in both monkeys and humans. Like other
2. True for False: All herpesviruses share the property of
polyomaviruses, SV40 is a DNA virus that has
producing latency and lifelong persistence in their
hosts. TRUE the potential to cause tumors in animals, but
3. Varicella –Zoster Virus spreads by _________or direct most often persists as a latent infection.
contact with infectious lesions. DROPLET • We will be dealing more on DNA viruses here.
INHALATION What is a DNA virus? A DNA virus is a virus that
4. Variola virus causes ____________. SMALL POX has DNA as its genetic material and replicates
5. The smallest of the DNA viruses are using a DNA dependent DNA polymerase. The
the_____________. PAROVIRIDAE nucleic acid is usually double-stranded DNA
(dsDNA) but may also be single
GENERALITIES
stranded DNA (ssDNA). DNA viruses belong to
• All are linear except Papillomaviridae,
either Group I or Group II of the Baltimore
Polyomaviridae and Hepadnaviridae
• All are doublestranded except Parvoviridae
classification of viruses.
• Smallest DNA Virus = Family Parvoviridae
• All are naked except Herpesviridae,
Hepadnaviridae and Poxviridae • Largest DNA Virus = Family Poxviridae
• All are icosahedral except Poxviridae
• All replicate in the nucleus except Poxviridae
• DNA Tumor Viruses: Ex. Human Papillomavirus,
EBV, HBV, HHV8, Polyomavirus, SV40 virus.
• The Viral genomes consist of DNA or RNA only, but
never both.
• These molecules can be double stranded or single
stranded, linear or circular, segmented or non-
segmented.
• We have the ff generalities for DNA viruses:
o PPH because these three viruses have circular
genomes Parvoviridae
o Parvoviridae is a ssDNA virus
o Herpesviridae, hepadnaviridae and poxviridaeso
these three viruses are all enveloped viruses.
o Poxviridae is brick or oval shaped.
o Poxviridae replicates in the cytoplasm
• The ff are the Viruses that are associated with DNA
tumors
o Human Papillomavirus
o EBV
o HBV
o HHV8
o Polyomavirus
o SV40 virus. Poxviridae

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 HERPESVIRIDAE ▪ The capsid is surrounded by an
• Herpesviridae is a large family of DNA viruses that amorphous protein coat called the
cause infections and certain diseases in animals, tegument.
including humans. The members of this family are ▪ It is encased in a glycoprotein-
also known as herpesviruses. The family name is bearing lipid bilayer envelope.
derived from the Greek word herpein ("to creep"), • Eight species of human herpesvirus (HHV)
referring to spreading cutaneous lesions, usually o HHV-1 or HSV-1 (Herpex simplexvirus 1)
involving blisters, seen in flares of herpes simplex 1, o HHV-2 or HSV-2 (Herpex simplexvirus 2)
herpes simplex 2 and herpes zoster (shingles). In o HHV-3 or VZV (Varicella-Zoster virus)
1971, the International Committee on the Taxonomy o HHV-4 or EBV (Epstein Barr virus)
of Viruses (ICTV) established Herpesvirus as a genus o HHV-5 or CMV (Cytomegalovirus)
with 23 viruses among four groups. Currently, 107 o HHV-6 (Roseolovirus)
species are recognized, all but one of which are in o HHV-7
one of the three subfamilies. o HHV-8 or KS (Kaposi sarcoma) herpesvirus
• An example of this is chickenpox or bulutong. I • General Biology of Human Herpesviruses
Guess you guys have experienced this during your o Of the more than 100 known herpesviruses, 8
childhood. Makati siya diba and there were fluid filled routinely infect only humans: herpes simplex
blisters on your skin that’s why it was called virus types 1 and 2, varicella-zoster virus,
bulutong tubig in Filipino. cytomegalovirus, Epstein-Barr virus, human
herpesvirus 6 (variants A and B), human
GENERAL CHARACTERISTICS herpesvirus 7, and Kaposi's sarcoma virus or
• Herpesviruses belong to the family Herpesviridae human herpesvirus 8. A simian virus, called B
• Genome of linear dsDNA virus, occasionally infects humans. All
• Icosahedral capsid herpesviruses can establish latent infection
• Amorphous integument surrounding the capsid within specific tissues, which are characteristic
for each virus. When you say latent this means
that the virus is present but dormant and is
capable of emerging or developing again when
one becomes immunocompromised.
o Cancer causing: HHV4, HHV8
o Manifestations
o HHV 1, HHV 2 and HHV3 = there’s the presence
of Vesicular Rashes
o HHV 1-3 and HHV 5 = formation of
multinucleated giant cells

HERPES SIMPLEX VIRUS

• STRUCTURE
o Herpesviruses have a unique four-layered
structure:
▪ a core containing the large, double-
stranded DNA genome is enclosed
by an icosahedral capsid which is
composed of capsomers.

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 found on genitalia and HSV-2 being found in the
mouth.
MODE OF TRANSMISSION
• HSV-1
o generally, transmitted orally, direct contact
o Can infect and reside in trigeminal ganglion
and become latent (Lysogenic phase);
• HSV-2
o transmitted by sexual contact
• Generally infections are spread by contact with
contaminated secretions.
• Herpes simplex virus 1 transmission is primarily oral,
and herpes simplex virus 2 primarily genital.
• The herpes simplex virus is categorized into 2 types: Transmission requires intimate contact. This occurs
herpes simplex virus type 1 (HSV-1) and herpes when a person comes in contact with infected lesions
simplex virus type 2 (HSV-2). The difference like oral, genital and mucosal lesions. Transmission
between the two is that: can occur from older lesions as well as from
• HSV-1 asymptomatic patients or those people who present
o mainly transmitted by oral-to-oral contact to no symptoms of the disease. Vertical transmission
cause oral herpes (which can include which occurs from infected mothers to neonates.
symptoms known as “cold sores”) • Contact with contaminated secretions
o Can also cause genital herpes. • Infected individuals are infectious during primary
• HSV-2 infection
o is a sexually transmitted infection that causes • Can be transmitted from older lesions as well as
genital herpes. asymptomatic patients
• Both HSV-1 and HSV-2 infections are lifelong WHICH • Direct contact with the infected tissue lesions (oral,
MEANS THESE VIRUSES LAST OR CONTINUE genital, mucosal), vertical transmission
THROUGH LIFE. • Causes direct cytopathology

GENERAL CHARACTERISTICS
• HSV-1 and HSV-2 belong to the genus Simplex virus
• Primary and recurrent infection
• HSV-1 and HSV-2 belong to the genus Simplex virus.
• Herpes simplex virus is divided into two categories
the primary which is the first or initial infection and the
recurrent or the reactivation of the latent virus.
• HSV-1 and HSV-2 can reside in the ganglion and
establish their latency there.
• Both can recur when, for instance, exposed to UV
light, stress, or immune system is weakened
• HSV-1 usually occurs in the upper area of the body
such as mouth/lips (Herpes labialis), fingers (Herpes
digitorum), cheeks; while HSV-2 usually resides in the TYPES OF INFECTION
lower half of the body such as the genitalia, labia, and • Oral Herpes
scrotum o Thought to have been caused by HSV-1
• But because of various sexual practices and o Incubation period is 2 days to 2 weeks
promiscuous relationships, HSV-1 has also been o Primary infections are asymptomatic

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 o Manifest as mucosal vesicles inside the mouth o Urethra is involved in men and women
or ulcerations o Double the risk of sexual transmission of HIV
o But nowadays there are a Number of cases that
are caused by HSV-2. Primary infections are
usually asymptomatic but when they manifest,
they appear as mucosal vesicles inside the
mouth which is shown on the picture above while
Recurrent or reactivation involves the border of
the lips with vesicles, ulcers and crusted lesions
which are the typical pattern of oral herpes
shown on the picture below.
o Involves the posterior pharynx in young adults
o Recurrent or reactivation involves the border of
the lips
o Burning or pain, vesicles, ulcers and crusted
lesions are the typical pattern

• Neonatal Herpes
o Risk of mother-to-infant transmission is 10 times
higher
o Mortality in treated neonates is 60%, exceeds
70% in untreated neonates
o Infection acquired in utero, intranatally or
postnatally
o Neonatal herpes Infection can be acquired in
utero meaning inside the uterus or before birth,
it can also be acquired itranatally (During birth)
or postnatally or after birth. This is Usually
transmitted during vaginal delivery and is more
severe when HSV-2 is involved. When a mother
• Genital Herpes has a recurrent herpes infection, the risk of
o Usually caused by HSV-2 transmission is very low. There are ways to
o HSV-1 cause one third of infections reduce the risk of transmission: this is thru
o Manifestations in females as vesicles on the Caesarian delivery or the use of suppressive
mucosa of the labia, vagina or both antiviral therapy at delivery. So in the hospitals
o In males, the shaft, glans and prepuce of the or maternity clinics, it is very important that
penis are affected sites pregnant women be screened during their
o Genital herpes infections are usually caused by prenatal checkup to prevent infections can be
HSV-2, although one third of the infections were transmitted to their newborns. These mothers
caused by HSV-1. In females, infection appears are tested for HIV and other sexually transmitted
as vesicles on the mucosa of the labia, vagina or diseases.
both. This is shown on the picture above. In
males, the shaft, glans, and prepuce of the penis
are the sites affected which is shown on the
picture below.

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 • Ocular Herpes
o Infection of the conjunctiva
o Swelling of the eyelids associated with vesicles
o Blindness
o HSV is the common cause of corneal infection in
the United States
o HSV is the common cause of corneal infection in
the united states. A herpes simplex infection of
the conjunctiva is seen as swelling of the eyelids
associated with vesicles which is shown on the
picture above. Ocular herpes may cause also
blindness due to destructive ulceration and
• Herpes Simplex Virus Encephalitis perforation of the cornea. Shown on the picture
o Leading cause of fatal sporadic encephalitis in below.
the United States.
o Usually caused by HSV-2 in neonates and HSV-
1 in older children and adult.
o Herpes simplex virus is the leading cause of fatal
sporadic encephalitis in the united states. In
neonates, encephalitis is caused by HSV-2, and
in older children and adult it is caused by HSV-
1. Neonatal HSV can cause encephalitis which
may then cause brain damage and cerebral
palsy. So, it is important that HSV be monitored
and managed appropriately to prevent severe
consequences.
o Improved by IV antiviral treatment
o FilmArray, Biofire, Salt Lake City, UT (detection
of HSV-1 and HSV-2)

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 CYTOMEGALOVIRUS MODE OF TRANSMISSION
• Cytomegalovirus (CMV) (from the Greekcyto-, "cell," • Close contact with an infected person
and megalo-, "large") is a genus of viruses in the • Shed in saliva, tears, urine, stool and breastmilk
order Herpesvirales, in the family Herpesviridae, in • Sexually transmitted via semen, cervical and vaginal
the subfamily Betaherpesvirinae. Humans and secretions
monkeys serve as natural hosts. The eight species in • Blood and blood products
this genus include the type species, Human • CMV is typically spread by close contact with an
betaherpesvirus 5 (HCMV, human cytomegalovirus, infected person. Cytomegalovirus replicates mainly
HHV-5), which is the species that infects humans. in the salivary glands and kidneys and is shed in
Diseases associated with HHV-5 saliva, tears, urine stool and breastmilk. CMV can
include mononucleosis, and pneumonia. In also be transmitted sexually via semen, cervical and
the medical literature, most mentions of CMV without vaginal secretions and through blood and blood
further specification refer implicitly to human CMV. products.
Human CMV is the most studied of all • Transmission is via intimate contact with infected
cytomegaloviruses. secretions.
• HHV 5 • Cytomegalovirus infections are among the most
• It has the largest genetic content of all human herpes prevalent viral infections worldwide.
virus
• Named because of the cytopathic effect it causes on PATHOLOGY
its host cell • Asymptomatic in immunocompetent host
• CMV – is the most common cause of congenital • Life threatening to transplant recipients and patients
abnormalities in the US with HIV.
• Cytomegalic Inclusion Disease – presence of • Cytomegalovirus causes three clinical syndromes.
multinucleated giant cells with prominent intranuclear o (1) Congenital cytomegalovirus infection seen in
inclusions; affects many organs leading to congenital neonates(when symptomatic) causes
defects hepatosplenomegaly, retinitis, rash, and central
nervous system involvement.
▪ Occurs when pregnant patients become
infected with Cytomegalovirus
▪ Most newborns with congenital CMV are
asymptomatic, but 15% will develop
progressive hearing loss
▪ 10% of congenitally infected newborns
will have the symptoms at birth such as:
➢ Chorioretinitis
➢ Small size for gestational age
➢ Microcephaly
GENERAL CHARACTERISTICS ➢ Purpura
• genus Cytomegalovirus ➢ Petichiae
➢ Jaundice
• Enveloped
➢ Hepatosplenomegaly
• icosahedral
▪ Testing for Cytomegalovirus infection is
• Viruses in Cytomegalovirus are enveloped, with
routine in pregnant patients; part of
icosahedral, spherical to pleomorphic, and round
T.O.R.C.H. (TOxoplasma, Rubella,
geometries, and T=16 symmetry.
Cytomegalovirus, Herpes)
• The diameter is around 150–200 nm.
o (2) In about 10 per cent of older children and
• Genomes are linear and non-segmented, around 200 adults, primary cytomegalovirus infection causes
kb in length.

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 a mononucleosis syndrome with fever, malaise, PREVENTION AND CONTROL
atypical lymphocytosis, and pharyngitis. • No Vaccine
o (3) Immunocompromised hosts (transplant • Antiviral Drugs for AIDS patients
recipients and human immunodeficiency virus • Refrain from sexual contact
[HIV]-infected individuals) may develop life- • Screening blood and organ donors
threatening disseminated disease involving the • Currently there is no available vaccine for the
lungs, gastrointestinal tract, liver, retina, and prevention cmv infection.
central nervous system. • For patients with aids, antiviral drugs are given to
• Pic: cmv congenital infection with purpuric papules them.
and nodules. • Refrain from doing sexual activities if you are
• Symptomatic congenital infection characterized by: suspecting that a person or your partner is infected.
o Petechiae Blood and organ donors are screened to prevent
o Hepatosplenomegaly transfusion transmitted CMV.
o Microcephaly
o chorioretinitis TREATMENT
• Reduced birth weight, CNS involvement, mental • Ganciclovir
impairment, deafness and death • Ganciclovir is an antiviral medication used to treat
• Most are asymptomatic Infections cytomegalovirus infections.
• 80% of adults are infected; no apparent symptoms
• Cytomegalic Inclusion Disease EPSTEIN-BARR VIRUS
• CMV can cross the placenta. • The Epstein–Barr virus (EBV), formally called Human
• Causes petechiae, hepatosplenomegaly, mental gammaherpesvirus 4, is one of the nine
retardation, microcephaly, deafness, seizures and known human herpesvirus types in the herpes family,
other birth defects and is one of the most common viruses in humans.
• Can occur if the pregnant mother becomes infected • It is best known as the cause of infectious
• Picture: Congenital cytomegalovirus(CMV)infection. mononucleosis ("mono" or "glandular fever"). It is
• Seen congenital CMV also associated with various non-
• infections. malignant, premalignant, and malignant Epstein–
• Skin findings include Barr virus-associated lymphoproliferative
• purpuric papules and nodules. diseases such as Burkitt lymphoma, hemophagocytic
lymphohistiocytosis, and Hodgkin's lymphoma; non-
lymphoid malignancies such as gastric
cancer and nasopharyngeal carcinoma; and
conditions associated with human immunodeficiency
virus such as hairy leukoplakia and central nervous
system lymphomas. The virus is also associated with
the childhood disorders of Alice in Wonderland
syndrome and acute cerebellar ataxiaand, based on
some evidence, higher risks of developing
certain autoimmune
diseases, especially dermatomyositis, systemic
lupus erythematosus, rheumatoid arthritis, Sjögren's
syndrome, and multiple sclerosis. About 200,000
cancer cases per year are thought to be attributable
to EBV.
• It is a type of Herpes virus that infects the B-cells.
• It can have a primary infection and persistent
infection.

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 GENERAL CHARACTERISTICS MODE OF TRANSMISSION
• subfamily Gammaherpesvirinae • Transmitted via infected saliva (salivary transmission)
• genus Lymphocryptovirus and genital secretions
• Epstein Barr virus is transmitted by intimate contact,
particularly via the exchange of saliva.
• Example of this is by close oral contact or kissing and
another example is the sharing of personal items
such as toothbrush
• Recovered from oropharynx of symptomatic and
healthy persons
• Mode of Transmission: Close Oral Contact (Kissing),
sharing of personal items such as toothbrush etc.

PATHOLOGY
• Causes Infectious Mononucleosis
o also known as Kissing disease
• The virus is composed of a double • Signs and symptoms include sore throat, fever,
helix of deoxyribonucleic acid .The DNA is lymphadenopathy, hepatomegaly, splenomegaly and
surrounded by a protein nucleocapsid, which is general malaise
surrounded by a tegument made of protein, which in • Epstein-Barr virus causes classic mononucleosis. In
turn is surrounded by an envelope containing immunocompromised hosts, the virus causes a
both lipids and surface projections of glycoproteins, lymphoproliferative syndrome. In some families,
which are essential to infection of the host cell Epstein Barr virus causes Duncan's syndrome.
• The virus is about 122–180 nm in diameter and is • Complications include splenic hemorrhage and
composed of a double helix of deoxyribonucleic rupture, hepatitis, thrombocytopenia purpura with
acid (DNA) which contains about 172,000 base hemolytic anemia, Reye syndrome, encephalitis, and
pairs and 85 genes.The DNA is surrounded by a other neurologic syndrome
protein nucleocapsid, which is surrounded by • When we conduct a CBC from an infected patient, we
a tegument made of protein, which in turn is will see atypical lymphocytes
surrounded by an envelope containing • 2 Main Strains:
both lipids and surface projections of glycoproteins, o EBV1 and EBV2
which are essential to infection of the host cell. In July
• Disease: Infectious Mononucleosis
2020, a team of researchers reported the first
• AKA: Mono, Kissing Disease, Pfeiffer’s Disease,
complete atomic model of the nucleocapsid of the
Glandular Fever
virus. This "first complete atomic model [includes] the
• Infectious Mononucleosis
icosahedral capsid, the capsid-associated tegument
• Highly Affected: Young Adults (infected through
complex (CATC) and the dodecameric portal--the
social contact); Children may be asymptomatic or
viral genome translocation apparatus."
have mild symptoms
• Signs and Symptoms:
o Fever,
o Chills.
o Sweats,
o Headache
o Very Painful Pharyngitis
o Lympadenopathy will also occur

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 • VZV multiplies in the lungs, and causes a wide variety
of symptoms. After the primary infection
(chickenpox), the virus goes dormant in the nerves,
including the cranial nerve ganglia, dorsal root
TREATMENT ganglia, and autonomic ganglia.
• Supportive treatment • Many years after the person has recovered from
o Kung malakas naman yung patient, we’d chickenpox, VZV can reactivate to cause neurological
just give hydration, fever medication and conditions.
they will heal spontaneously. • Occurs in epidemics
• 90% of the general adult population had contracted
VARICELLA-ZOSTER VIRUS VZV in childhood
GENERAL CHARACTERISTICS • Site of Infection: Respiratory Tract
• subfamily Alphaherpesvirinae
• genus Varicellovirus • Lymph nodes (to infect T cells) > Infected T cells
• Also known as Human alphaherpesvirus 3 (HHV-3) enter the blood > liver, spleen, other organs >
• One of nine herpesvirus known to infect humans secondary viremia > skin
• Morphologically and Structurally similar to other
Herpes viruses but differs in antigenecity

MODE OF TRANSMISSION
• Drop Inhalation of droplets • Clinical Manifestations of Chickenpox
• Direct contact with infectious lesions o Incubation period: 2-3 weeks
• Saliva, mucus o Fever, Malaise, pruritic rash and vesicular
lesions
PATHOLOGY o Lesions appear on the head and trunk and
• Varicella (Chickenpox) spreads to limbs
o a disease most commonly affecting children, o Centripetal distribution - trunk has more lesions
teens, and young adults than the extremities (centrifugal is vice-versa)
• Zoster (Shingles) o Rash: papules > vesicles > pustules and crusts
o A disease caused by HHV-3 (Herpes zoster) o Lesions dry crust over and heal in 1-2 weeks.
in adults

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 o Typical lesion (encircled red in picture above) is
characterized as “dew drop on a rose petal”.
▪ Vesicle has clear fluid and is PREVENTION
erythematous sa ilalim • Vaccination
• Shingles – reactivated form of VZV infection • A live attenuated VZV Oka/Merck strain vaccine is
o Presentation of Shingles: available and is marketed in the United States under
▪ Even if chickenpox “disappears”, the the trade name Varivax. It was developed by Merck,
virus will remain latent and sleeping in Sharp & Dohme in the 1980s from the Oka strain virus
(usually thoracic and lumbar) dorsal root isolated and attenuated by Michiaki Takahashi and
ganglion. colleagues in the 1970s. It was submitted to the
▪ If it reactivates, it occurs in dermatome US Food and Drug Administration for approval in
level (occurring in one nerve part) as 1990 and was approved in 1995. Since then, it has
Shingles. been added to the recommended vaccination
▪ Rash followed by vesicular lesions in a schedules for children in Australia, the United States,
UNILATERAL (one side) DERMATOME and many other countries.
PATTERN
TREATMENT
• Acyclovir for chickenpox
• Famciclovir, valaciclovir for shingles
• Within the human body it can be treated by a number
of drugs and therapeutic agents
including acyclovir for the chicken
pox, famciclovir, valaciclovir for the shingles, zoster-
immune globulin (ZIG), and vidarabine. VZV immune
globulin is also a treatment. Acyclovir is frequently
▪ Compared to Chicken pox lesions which used as the drug of choice in primary VZV infections,
are itchy, Shingles lesions are painful and beginning its administration early can
▪ Sometimes, it occurs in the face, significantly shorten the duration of any symptoms.
specifically in the ophthalmic branch of However, reaching an effective serum concentration
trigeminal nerve. This is called Herpes of acyclovir typically requires intravenous
Zoster Opthalmicus. administration, making its use more difficult outside of
▪ Prolonged disabling pain that can a hospital.
remain for months occurs even the • Pain relievers can help ease the sores
lesions disappear. (Postzoster neuralgia
or postherpetic neuralgia) HUMAN HERPESVIRUS 6
▪ Postherpetic neuralgia is the pain kahit • Human herpesvirus 6 (HHV-6) is the common
na nawala na yung lesions minsan collective name for Human betaherpesvirus
meron pa rin pain. This is the most 6A (HHV-6A) and Human betaherpesvirus 6B (HHV-
common complication of Herpes Zoster 6B). These closely related viruses are two of the nine
Opthalmicus. herpesviruses known to have humans as their
primary host.
• Also known as the 6th Disease
o Called as such because in the old times
that merong sequence ng mga disease
yung mga babies, so this the sixth rash
na usually lumalabas sa babies (Roseola
infantum)

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• HHV-6A and HHV-6B are double stranded DNA MODE OF TRANSMISSION
viruses within the Betaherpesvirinaesubfamily and of • Inhalation of respiratory droplets
the genus Roseolovirus. HHV-6A and HHV-6B infect • Close contact with infected individuals
almost all of the human populations that have been • Transmission is believed to occur most frequently
tested. through the shedding of viral particles into saliva.
• HHV-6A has been described as Both HHV-6B and HHV-7 are found in human saliva,
more neurovirulent, and as such is more frequently the former being at a lower frequency. Studies report
found in patients with neuroinflammatory diseases varying rates of prevalence of HHV-6 in saliva
such as multiple sclerosis. HHV-6 (and HHV-7) levels (between 3–90%), and have also described the
in the brain are also elevated in people salivary glands as an in vivo reservoir for HHV-6. The
with Alzheimer's disease. virus infects the salivary glands, establishes latency,
• HHV-6B primary infection is the cause of the common and periodically reactivates to spread infection to
childhood illness exanthema subitum (also known as other hosts.
roseola infantum or sixth disease). It is passed on • Vertical transmission has also been described, and
from child to child. It is uncommon for adults to occurs in approximately 1% of births in the United
contract this disease as most everyone has had it by States.
kindergarten, and once contracted, an antibody is o This form is easily identifiable as the viral
formed help to prevent becoming reinfected in the genome is contained within every cell of an
future. Additionally, HHV-6B reactivation is common infected individual.
in transplant recipients, which can cause several • Mode of Transmission: Inhalation of aerosols, close
clinical manifestations such as encephalitis, bone contact
marrow suppression, and pneumonitis. • Viral Shedding in Saliva
• A variety of tests are used in the detection HHV-6,
some of which do not differentiate the two species.[ PATHOLOGY
• Associated with roseola
• Causes Roseola infantum or exanthem subitum or
GENERAL CHARACTERISTICS Duke’s Disease or 6th disease
• genus Roseolovirus • 2 Variants of HHV6:
• Common pathogen o Variant A causes the disease in
immunocompromised
o Variant B causes the disease (roseola infantum,
exanthem subitum, sixth disease)
• Common among children 6 months to 2 years
• Roseola infantum or exanthem subitum, is a common
exanthem of childhood caused by infection with
human herpesvirus 6.
• It is characterized by a febrile illness with mild
constitutional symptoms lasting 3-5 days. After rapid
• The diameter of an HHV-6 virion is about 2000 defervescence, a pink macular or maculopapular rash
Angstroms. The virion's outer portion consists of a appears, primarily on the trunk and lasting hours to
lipid bilayer membrane that contains days.
viral glycoproteins and is derived from that of the • Virus has been also associated with the development
host. Below this membrane envelope is of progressive multifocal
a tegument which surrounds an icosahedral capsid, leukoencephalopathy multiple sclerosis.
composed of 162 capsomeres. The protective capsid
of HHV-6 contains double stranded linear DNA.

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 GENERAL CHARACTERISTICS
• Genus Roseolovirus

TREATMENT • A mature virus particle measures about 170

• Valganciclovir nanometres (1,700 Å) in diameter.
• Ganciclovir • The genome of HHV-7 is very similar to that of HHV-
• Cidofovir 6, although it is about 10% smaller, with a DNA
• Foscarnet genome of about 145,000 base pairs. There are a
• There are no drugs approved specifically for treating number of key differences between the genome of
HHV-6 infection, so right now the drug of choice HHV-7 and that of HHV-6, but the importance of them
would be the ones used for the treatment of CMV. for viral DNA replication is not yet known
• Although the usage of Cytomegalovirus treatments MODE OF TRANSMISSION
(valganciclovir, ganciclovir,cidofovir, and foscarnet) • Shed in saliva
have shown some success. These drugs are given o Same as that in HHV-6
with the intent of inhibiting proper DNA polymerization
by competing with deoxy triphosphate nucleotides or PATHOLOGY
specifically inactivating viral DNA polymerases. • Causes roseola
• Finding a treatment can be difficult when HHV-6
reactivation occurs following transplant surgery
because transplant medications include
immunosuppressants.

HUMAN HERPESVIRUS 7
• Human betaherpesvirus 7 (HHV-7) is one of nine
known members of the Herpesviridae family that
infects humans. HHV-7 is a member
of Betaherpesvirinae, a subfamily of
the Herpesviridae that also includes HHV-
6 and Cytomegalovirus (HHV-5 or HCMV).
• HHV-7 often acts together with HHV-6, and the • Causes roseola like your HHV6. A reddish papular
viruses together are sometimes referred to by rash in an adult is shown in the picture
their genus, Roseolovirus. • Can also cause exanthem subitum but less common
• HHV-7 was first isolated in 1990 from CD4+ T cells • Quite similar to HHV6
taken from peripheral blood lymphocytes. • Human herpes viruses 6 and 7 are associated with
• Similar to HHV-6 but HHV-7 is not yet well-studied. exanthem subitum (roseola) and with rejection of
• It lives on T lymphocytes transplanted kidneys.
• Antibodies to this virus are present in almost
everyone by age of 5.

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 TREATMENT then surrounded by an amorphous protein layer
• No treatment for HHV-7 infection exists called the tegument, and finally enclosed in a lipid
envelope derived in part from the cell membrane.
HUMAN HERPESVIRUS 8 KSHV has a genome which is approximately 165,000
• Kaposi's sarcoma-associated nucleic acid bases in length. KSHV is a rhadinovirus,
herpesvirus (KSHV) is the ninth known a Herpes genus remarkable since it has stolen
human herpesvirus; its formal name according to numerous genes from host cells including in the case
the International Committee on Taxonomy of of KSHV genes that encode for complement-binding
Viruses (ICTV) is Human gammaherpesvirus 8, protein, IL-6, BCL-2, cyclin-D, a G protein-coupled
or HHV-8 in short. Like other herpesviruses, its receptor, interferon regulatory factor and Flice
informal names are used interchangeably with its inhibitory protein (FLIP), as well as DNA synthesis
formal ICTV name. This virus causes Kaposi's proteins including dihydrofolate reductase, thymidine
sarcoma, a cancer commonly occurring kinase, thymidylate synthetase,
in AIDS patients, as well as primary effusion DNA polymerase and many others. While no other
lymphoma, HHV-8-associated multicentric human tumor virus possesses these same genes,
Castleman's disease and KSHV inflammatory other tumor viruses target the same cellular pathways
cytokine syndrome. It is one of seven currently known illustrating that at a basic level, all tumor viruses
human cancer viruses, or oncoviruses. Even after so appear to attack the same cellular control pathways,
many years of discovery of KSHV/HHV8, there is no so-called tumor suppressor pathways.
known cure for KSHV associated tumorigenesis. • AKA KAPOSI SARCOMA ASSOCIATED
• Also infects B cells like HHV-6 HERPESVIRUS
• Causes malignancy or cancer, specifically Kaposi’s
sarcoma MODE OF TRANSMISSION
o Kaposi’s sarcoma is a cancer of endothelium • Sexual contact
of blood vessels • Blood products (via blood transfusion)
o Nasisira yung endothelium that’s why the • Salivary shedding
capillaries necrotize • Organ transplantation
o Patients have dark nodules • Sexual Contact; Transplantation; Vertical
• Usually seen in HIV patients as they are particularly PATHOLOGY
prone to developing Kaposi’s sarcoma • Role in the development of primary effusion
lymphomas and multicentric Castleman disease
GENERAL CHARACTERSITICS • Human herpesvirus 8 has been found associated with
• genus Rhadinovirus Kaposi's sarcoma in AIDS patients as well as intra-
• Kaposi sarcoma-associated herpesvirus abdominal solid tumors.
• Seen among HIV infected patients
• MSMs are more prone to infection
• As you can see in the picture those are patches or
lesions which are usually red purple. Those are made
up of cancer cells , blood vessels and blood cells.
• Virus is able to cause malignant transformation by
inactivating the retinoblastoma tumor suppressor
protein using the nuclear antigen
• Primary infection is usually asymptomatic or mild
• Disease: Kaposi’s Sarcoma – malignancy common
among AIDS patients
• KSHV is a herpesvirus, and is a large double- • Affects the vascular endothelium
stranded DNA virus with a protein covering that • Systemic disease with cutaneous lesions (patches)
packages its nucleic acids, called the capsid, which is seen in the lining of the nose, mouth, throat

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• Other diseases (AIDS patients): Primary Effusion herpesviruses such as KSHV have been used to
Lymphoma, Multicentric Castleman’s Disease successfully prevent development of Kaposi's
• Picture: sarcoma, although once the tumor develops these
drugs are of little or no use. For patients with AIDS-
KS, the most effective therapy is highly active
antiretroviral therapy to reduce HIV infection. AIDS
patients receiving adequate anti-HIV treatment may
have up to a 90% reduction in Kaposi's sarcoma
occurrence.

PREVENTION AND CONTROL OF HERPESVIRUS

INFECTIONS
• Vaccine for varicella
• Vaccine against HSV-2 and cytomegalovirus (trial)
• A vaccine to prevent varicella-zoster virus infections
was recently licensed in the United States. Vaccines
against herpes simplex virus 2, and cytomegalovirus
are undergoing extensive evaluations in field trials.
• Passive immunization with immunoglobulin or
hyperimmune globulin is used either to prevent
infection or as an adjunct to antiviral therapy.
• Systemic disease with cutaneous lesions (patches)
seen in the lining of the nose, mouth, throat. TREATEMENT FOR HERPESVIRUS INFECTIONS
• HSV-1, HSV-2 and VZV- acyclovir, valaciclovir,
PREVENTION famciclovir
• Use condoms • Cytomegalovirus retinitis- ganciclovir
• Avoid deep kissing • No treatment yet for EBV, HHV 6,7,8
• Blood tests to detect antibodies • Infections with herpes simplex virus 1 and 2 and
• Since persons infected with KSHV will varicella-zoster virus are currently the most amenable
asymptomatically give the virus, caution should be to therapy; acyclovir, valaciclovir and famciclovir are
used by sex partners in having unprotected sex and all licensed therapeutics.
activities where saliva might be shared during sexual • Ganciclovir is used to treat cytomegalovirus retinitis.
activity. Prudent advice is to use condoms when • B virus appears to respond to either of these drugs.
needed and avoid deep kissing with partners with • There is as no treatment for Epstein-Barr virus and
KSHV and HIV infections or whose status is human herpesvirus 6,7 and 8 infections. Although a
unknown. There are Blood tests to detect antibodies number of antivirals were proven to inhibit EBV
to the virus. replication in vitro, they had limited success in the
clinic and to date no antiviral drug has been approved
TREATMENT for treatment of of EBV infections.
• Chemotherapy • At present only experimental data in vitro and limited
• Ganciclovir clinical data have been reported. No antiviral drugs
• for AIDS-KS highly active antiretroviral therapy that inhibit the growth of hhv8.
• Kaposi's sarcoma is usually a localized tumor that can • Right now there is no definitive protocol or regimen
be treated either surgically or through local irradiation. for antiviral therapy of hhv-8 associated diseases.
Chemotherapy with drugs such as
liposomal anthracyclines or paclitaxel may be used,
particularly for invasive disease. Antiviral drugs, such
as ganciclovir, that target the replication of

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 HEPADNAVIRIDAE o The outer capsule contains the antigen called
• Hepadnaviridae[a] is a family of viruses. Humans, the hepatitis B surface antigen
apes, and birds serve as natural hosts. There are o Other common antigens that is detected in the
currently 18 species in this family, divided among 5 lab:
genera. o HBs- Antigen is also called as Australia antigen
• Its best-known member is hepatitis B virus. Diseases (HBsAg).
associated with this family include: liver infections, ➢ Hallmark of active hepatitis B infection
such as hepatitis, hepatocellular carcinomas (chronic o Other hepatitis B antigen:
infections), and cirrhosis. It is the sole family in the ▪ HBe – hepatitis B envelope antigen
order Blubervirales. ▪ HBc – hepatitis B core antigen
• Hepadnaviridae (Hepa = liver; dna o The inner core contains HBV core antigen one is
= deoxyribonucleic acid) includes one virus that is called HBc Ag
pathogenic to man: Hepatitis B virus (HBV). As their o Incorporated into the Core antigen is called
names imply, all of the known hepadnaviruses are HBeAg (envelope antigen); this antigen cannot
hepatotropic, infecting liver cells, and all can cause be seen kasi nasa core nakatago (though the
hepatitis in their known host. Hepatitis is the a antibody can be detected)
syndrome characterized by inflammation of the liver. o The HBcAg is a very small amount so not
It can be caused by hepatitis viruses (not necessarily detectable but its Antibody is found in circulation.
in the Hepadnavirus family), other viruses, amebas,
and non-infectious agents such as alcohol and MODE OF TRANSMISSION
acetaminophen. • Infectious hepatitis- person to person via fecal-oral
• Only DNA virus that causes hepatitis, specifically route
hepatitis B • Serum hepatitis- transfusion of infected blood and
blood products
GENERAL CHARATERISTICS • HAV, HBV, HCV, HDV, HEV, HGV, SEN virus, TTV
• Hepatitis viruses share the same tissue tropism (liver) • HAV and HEV-fecal-oral route
• HBV, TTV and SEN virus have DNA genomes, others
have RNA genome

• Hepatitis viruses are grouped together because they

share the same tissue tropism, which is the liver.
• HBV, TTV and SEN virus have DNA genomes • There are at least 8 different hepatitis viruses. These
whereas the others have RNA genome. are HAV, HBV, HCV, HDV, HEV, HGV, SEN virus,
• Structure of HBV TTV (transfusion-transmitted virus)
o It is an enveloped virus • HAV and HEV-fecal-oral route
o This is a DNA virus and called a Dane particle. • HBV, HCV, HDV, HGV, SEN virus, TTV- transfusion
o It has an inner core surrounded by an outer • In developing countries with the highest prevalence of
capsule. HBV, it becomes clear that parenteral
transmission is the leading cause of HBV spread.

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 The surface antigen as well as the DNA of the virus is transmission. Contact with contaminated blood is
thought to be transmitted through contact of the another major way. IV drug abusers, health care
infected mother's blood with her child during birth workers, renal dialysis patients and blood transfusion
(transplacental transmission is more difficult). recipients are at risk of contracting the disease. Right
• Postnatal transmission through breast milk and now There are ongoing Research studies that show
maternal saliva is also possible. Approximately 50% the possibility of insect transmission in mosquitoes
of the children in countries where HBV is highly and their eggs where Hbsag was discovered
prevalent contract the disease from one member of including bedbugs of the beds of carriers of HbsAg,
the family that is shedding virus through cuts, sores, although this has not been corroborated yet.
or saliva. • In developing countries with the highest prevalence of
• In teens and adults, sexual intercourse becomes a HBV, it becomes clear that parenteral
significant method of viral transmission. In developing transmission is the leading cause of HBV spread.
countries, hetero and homosexual transmission plays The surface antigen as well as the DNA of the virus
an even greater role in HBV transmission and are thought to be transmitted through contact of the
perinatal much less. infected mother's blood with her child during birth
• Contact with contaminated blood is another major (transplacental transmission is more difficult).
way. IV drug abusers, health care workers, renal • Postnatal transmission through breast milk and
dialysis patients and to a lesser extent blood maternal saliva is also possible. Approximately 50%
transfusion recipients are at risk of contracting the of the children in countries where HBV is highly
disease. Thus, in developed countries, adults are the prevalent contract the disease from one member of
target population whereas in developing nations, the family that is shedding virus through cuts, sores,
infants are primarily infected. It is estimated that 1 or saliva.
milliliter of blood from an Hepatitis B positive carrier • In teens and adults, sexual intercourse becomes a
contains 10 billion particles and that the virus can significant method of viral transmission. In developing
withstand drying on a surface for over a week. countries, hetero and homosexual transmission plays
• There have been cases of acute HBV infection that an even greater role in HBV transmission and
occur sporadically in which the method of acquisition perinatal much less.
is unknown. Dr. Baruch Blumberg, Nobel Prize winner • Contact with contaminated blood is another major
for the discovery of the first HBV vaccine, researched way. IV drug abusers, health care workers, renal
the possibility of insect transmission by collecting dialysis patients and to a lesser extent blood
mosquitoes in Uganda and Ethiopia. HBsAg was transfusion recipients are at risk of contracting the
discovered in both the individual mosquitoes and their disease. Thus, in developed countries, adults are the
eggs. Other studies have shown that the North target population whereas in developing nations,
American bedbug also carries the antigen and that infants are primarily infected. It is estimated that 1
the bedbugs of the beds of carriers of HBsAg actually milliliter of blood from an Hepatitis B positive carrier
had a higher infection rate than the bedbugs of non- contains 10 billion particles and that the virus can
carriers. This method of transmission has not been withstand drying on a surface for over a week.
further corroborated, however, could help explain the • There have been cases of acute HBV infection that
cause of HBV infection in many patients. occur sporadically in which the method of acquisition
• HBV,HCV, HDV, HGV, SEN virus, TTV- transfusion is unknown. Dr. Baruch Blumberg, Nobel Prize winner
• In developing countries with the highest prevalence of for the discovery of the first HBV vaccine, researched
HBV, it becomes clear that parenteral the possibility of insect transmission by collecting
transmission is the leading cause of HBV spread. It mosquitoes in Uganda and Ethiopia. HBsAg was
is thought to be transmitted through contact of discovered in both the individual mosquitoes and their
the infected mother's blood with her child during eggs. Other studies have shown that the North
birth . Postnatal transmission through breast milk American bedbug also carries the antigen and that
and maternal saliva is also possible. Sexual the bedbugs of the beds of carriers of HBsAg actually
intercourse becomes a significant method of viral had a higher infection rate than the bedbugs of non-

DE BORJA, DE GUZMAN, DE LOS SANTO, DIMAIWAT, DOLINA, HALILI, OBISPO;3L-MT 31

 carriers. This method of transmission has not been • acute-short course which requires a short term
further corroborated, however, could help explain the medical care
cause of HBV infection in many patients. • Chronic –long time
o Chronic hepatitis is commonly caused by
acute hepatitis B at birth
o When babies are born with hepatitis B, which
came from the mother, there is a very high
chance that they will develop chronic
hepatitis when they get old kasi mas matagal
na nasa liver nila
o Those that are acquired at birth will usually
develop into cirrhosis, and later on, cancer
(hepatocellular carcinoma).
o In adult-acquired hepatitis B, only a little
portion (of the liver) will convert into chronic
and eventually into cancer.
o Majority of all liver cancer due to hepatitis B
PATHOLOGY are cases of birth-acquired hepatitis B.
• All hepadnaviruses cause hepatitis
o Acute Hepatitis PREVENTION
o Fulminant Hepatitis – Severe Acute • Hepatitis B
Hepatitis with rapid destruction of liver o Vaccine
o Chronic Hepatitis ➢ Ano ang mag popositive kapag
o Primary Hepatocellular Carcinoma vinaccinate ka? It is anti-HBs.

o Screening prenatal infants

• All of the known hepadnaviruses are hepatotropic,
o Screening for Hb antigen in blood banks
infecting liver cells, and all can cause hepatitis in their
known host. Hepatitis is a syndrome characterized by
inflammation of the liver. It can be caused by hepatitis
viruses (not necessarily in the Hepadnavirus family),
other viruses, amebas, and non-infectious agents
such as alcohol and acetaminophen.
• The most common symptoms are fatigue, headache,
anorexia, nausea, vomiting, abdominal pain (right
upper quadrant or diffuse), jaundice, itchy skin, and
dark colored urine.

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 ➢ How will we know if the anti-HBs is due address but can be decreased by monogamy,
to vaccine or from real infection? We screening of positive sexual partners, vaccination of
test for anti-HBc partners of known carriers, avoiding use of carrier's
➢ Natural hepa B infection will yield fomites (toothbrush, razor, eating utensils). Perinatal
positive result in anti-HBc; while in transmission can be curtailed by postnatal
vaccination, negative result. vaccination and administration of HBVIG. Those high
• Prophylaxis or protection from the virus causing risk individuals in constant contact with blood or
infection induces both passive and active immunity. serum of carriers should wear gloves and take special
For passive immunity, Hepatitis B Immunoglobulin is precautions when using needles.
given. The screening for Hb antigen in blood banks • Treatment
has greatly reduced transfusion hepatitis. IV drug o After infection with hepatitis B, patients have
users should also be educated about the risk of various options for treatment, the most effective
transmission through needle sharing. Transmission of which being post-prophylaxis immunization.
via sexual contact is more difficult to address but can Those exposed receive Hepatitis B immune
be decreased by monogamy, screening of positive globulin isolated from the blood of individuals
sexual partners, vaccination of partners of known who have anti-Hepatitis B antibodies. This
carriers, avoiding use of carrier's fomites (toothbrush, method is even more effective in preventing the
razor, eating utensils). Perinatal transmission can be negative ramifications associated with infection
curtailed by postnatal vaccination and administration when both antibodies and the active vaccination
of HBVIG. Those high risk individuals in constant are administered to the individual.
contact with blood or serum of carriers should wear • Post-transfusion HBV infection has been markedly
gloves and take special precautions when using reduced by routine screening of donors by
needles. immunoassay or radio immunoassay. Not much can
• This allows the individual to neutralize as much virus be done to treat acute viral hepatitis and restrictions
in the serum as possible. If the virus is reduced to on diet and activity are without scientific basis.
significantly low levels, active immune responses • Chemotherapy is the main source of treatment for
including T cell responses could control or prevent chronic carriers of the virus that develop chronic
latent and persistent infection. Vaccination with either (aggressive) hepatitis. The principle benefit of these
purified or recombinant antigen induces the drugs is to ameliorate and manage the complications
individuals own antibody and T cell response. associated with the disease, not to cure it. The
However, 3-4% of vaccines do not mount a reverse transcriptase and the DNA polymerase
successful immune response to the vaccine and are inhibitors, AZT and acyclovir respectively, have not
not protected from infection. The failure of the vaccine been shown to have much promise in the inhibition of
may be due to adjuvants, the chemicals given with the HBV replication. Ganciclovir in combination
vaccine, and genetic polymorphisms. Just as some with foscarnethas been shown to be the most
individuals are more likely to develop acute hepatitis effective treatment for those afflicted with chronic
rather than asymptomatic infection or more likely to hepatitis, since studies show that a significant amount
have infection progress to Hepatocellular carcinoma of viral replication is halted. Nucleoside analogs such
than remain persistent, some of those vaccinated are as penciclovir, that exploit the nonspecific
protected and others are not. Other factors that polymerase of the virus have been shown to inhibit
influence the immune response to the vaccine are HBV replication in the lab. Nalidixic acid is being
age and weight of the host, smoking, and strength of studied as a DNA gyrase inhibitor that could
immune system. interefere with the initiation of viral transcription by
• The screening for Hb antigen in blood banks has changing the DNA structure. Interferon is also being
greatly reduced transfusion hepatitis. This should used as treatment but has many negative aspects;
continue. IV drug users should also be educated i.e. it must be administered subcutaneously (5-10
about the risk of transmission through needle sharing. million units injected three times a week), is
Needle exchange programs have been successful. expensive, and produces flu-like side effects.
Transmission via sexual contact is more difficult to However, it has been proven to reduce inflammation

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 and aminotransferase levels after a 4-6 month to the host cell via the receptor on the surface of
treatment in a very select group of chronic hepatitis the host cell.
patients (those in which the virus is in the low to high
replicative transition phase). This improvement have
only been seen in 50% of the patients and the benefits
disappear right after treatment is curtailed.

TREATMENT
• Lamivudine
• Entecavir
• Tenofovir
• A few nucleoside analogs (NUC), such
as lamivudine, entecavir, and tenofovir, are available
for antiviral therapy. Although these nucleoside
analogs are quite effective in suppressing viral
genome replication, long-term administration (>5
years) is essential for a clinic benefit .
• Chemotherapy is the main source of treatment for
chronic carriers of the virus that develop chronic
(aggressive) hepatitis. Ganciclovir in combination MODE OF TRANSMISSION
with foscarnethas been shown to be the most • Shed in secretions from the eyes and respiratory tract
effective treatment for those afflicted with chronic • Viral shedding in feces and urine
hepatitis, since studies show that a significant amount • Spread by aerosols, fomites, oral-fecal route and
of viral replication is halted personal contact
• Adenoviruses are unusually stable to chemical or
ADENOVIRIDAE physical agents and adverse pH conditions, allowing
GENERAL CHARACTERISTICS for prolonged survival outside of the body and water.
• Was first isolated from adenoid tissue Adenoviruses are spread primarily via respiratory
• Belong to the family Adenoviridae, genus droplets, however they can also be spread
Mastadenovirus by fecal routes
• Naked icosahedral viruses with dsDNA
• Has 51 distinct serotypes PATHOLOGY
• Most common serotypes are 1 to 8, 11, 21, 35, 37 and • Half of all adenovirus infections are asymptomatic
40 • Pharyngitis, conjunctivitis, sore throat and sore eyes
• Adenoviruses (members of the family Adenoviridae) are signs of infection.
are nonenveloped (without an outer lipid • In addition to these signs, the hallmark of adenovirus
bilayer) viruses with infection is palpable lymph nodes
an icosahedralnucleocapsid containing a double o In front of the ear, may lymph node na
stranded DNA genome. The name was derived from nakakapa
their initial isolation which is from human adenoids in • Respiratory tract, eye and gastrointestinal tract
1953. • Lesser involvement of urinary tract, heart, central
• Adenoviruses represent the largest known nervous system, liver, pancreas and genital tract
nonenveloped viruses. They are able to be • Adenoviruses causes respiratory, gastrointestinal
transported through the endosome (i.e., envelope and genitourinary infections
fusion is not necessary). The virion also has a unique • Adenio is responsible for 10% of all cases of
"spike" or fiber associated with each penton base of pneumonia
the capsid (see picture below) that aids in attachment • And 5% to 15% of all cases of gastroenteritis in
children

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• Cause epidemic keratoconjunctivitis, acute and nose with unwashed hands, and avoiding close
hemorrhagic cystitis and pharyngoconjunctival fever contact with people with symptomatic adenovirus
• Adenovirus serotype 14 causes severe and fatal infection. Those with symptomatic adenovirus
acute respiratory disease infection are additionally advised to cough or sneeze
• Serotypes 3, 4 and 7 are associated with ARD into the arm or elbow instead of the hand, to avoid
• Serotypes 40 and 41 are called enteric adenoviruses sharing cups and eating utensils, and to refrain from
kissing others. Chlorination of swimming pools can
prevent outbreaks of conjunctivitis caused by
adenovirus.
• There was an oral vaccine which was available in
1981-1999 for types 4 and 7 but this was for military
personnel only because they may be at a higher risk
of infection.
• Oral vaccination from 1981-1999 for types 4 and 7
• Development of new vaccine and became available
in October 2011
• Currently, there is a vaccine for adenovirus type 4 and
7 for military personnel only. Military personnel are
the recipients of this vaccine because they may be at
a higher risk of infection. The vaccine contains a live
virus, which may be shed in stool and lead to
• The picture shows a patient with transmission. There is currently no adenovirus
keratoconjunctivitis. vaccine for the general public. The vaccine is not
o It is the inflammation of the cornea and approved for use outside of the military, as it has not
conjunctiva. been tested in studied in the general population or on
• There are Adenovirus Associated Diseases that are people with weakened immune systems.
caused by the ff serotypes • In the past, US military recruits were vaccinated
o Respiratory tract infections against two serotypes of adenovirus, with a
(pneumonia)(1,2,3,5,7) corresponding decrease in illnesses caused by those
o Epidemic keratoconjunctivitis (8,19,37) serotypes. That vaccine is no longer manufactured.
o Swimming pool conjunctivitis (3,7) The U.S. Army Medical Research and Materiel
o Acute hemorrhagic cystitis (children-boys) Command announced on 31 October 2011 that a new
o Pharyngoconjunctival fever adenovirus vaccine, which replaces the older version
o Latency occurs in the lymphoid system (tonsils, that has been out of production for over a decade,
adenoids, Peyer’s patches) was shipped to basic training sites Oct. 18, 2011.
PREVENTION AND CONTROL More information is available here.
• Adequate chlorination of swimming pools to prevent • Prevention of adenovirus, as well as other respiratory
adenovirus-associated conjunctivitis illnesses, involves frequent hand washing for more
• Hand washing for more than 20 seconds than 20 seconds, avoiding touching the eyes, face,
• Avoiding touching the eyes, face, and nose with and nose with unwashed hands, and avoiding close
unwashed hands contact with people with symptomatic adenovirus
• Avoiding close contact with people with symptomatic infection. Those with symptomatic adenovirus
adenovirus infection infection are additionally advised to cough or sneeze
• Cough or sneeze into the arm or elbow into the arm or elbow instead of the hand, to avoid
• Avoid sharing cups and eating utensils, sharing cups and eating utensils, and to refrain from
• Prevention of adenovirus, as well as other respiratory kissing others. Chlorination of swimming pools can
illnesses, involves frequent hand washing for more prevent outbreaks of conjunctivitis caused by
than 20 seconds, avoiding touching the eyes, face, adenovirus.

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 TREATMENT
• Acetaminophen for fever
• Cidofovir
• There are no proven antiviral drugs to treat adenoviral
infections, so treatment is largely directed at the
symptoms (such as acetaminophen for fever). The
antiviral drug cidofovir has helped those patients who
had severe cases of illness; A doctor may give
antibiotic eyedrops for conjunctivitis, while awaiting
results of bacterial cultures, and to help prevent • Papillomaviruses are non-enveloped, meaning that
secondary bacterial infections. Currently, there is no the outer shell or capsid of the virus is not covered by
adenovirus vaccine available to the general public. a lipid membrane. this has a single viral protein,
• the number helped and to what degree, and the called the L1, Like most non-enveloped viruses, the
particular complications or symptoms it helped with, capsid is geometrically regular and
and when and where this happened, were not given presents icosahedral symmetry. This has a double
in the source. A doctor may give antibiotic eyedrops stranded circular DNA molecule.
for conjunctivitis, while awaiting results of bacterial • is necessary and sufficient for formation of a 55–60
cultures, and to help prevent secondary bacterial nanometer capsid composed of 72 star-shaped
infections. Currently, there is no adenovirus vaccine capsomers (see figure). Like most non-enveloped
available to the general public, but a vaccine is viruses, the capsid is geometrically regular and
available for the United States military for Types 4 and presents icosahedral symmetry. Self-
7. assembled virus-like particles composed of L1 are
• Usually self-limiting – patients will heal on their own the basis of a successful group of prophylactic HPV
as long as their immune system is strong vaccines designed to elicit virus-
neutralizing antibodies that protect against initial HPV
PAPILLOMAVIRIDAE infection. As such, papillomaviridæ are stable in
• Papillomaviridae is an ancient taxonomic family of the environment.
non-enveloped DNA viruses, collectively known as • The papillomavirus capsid also contains a viral
papillomaviruses. protein known as L2, which is less abundant.
• Infection by most papillomavirus types, depending on Although not clear how L2 is arranged within the
the type, is either asymptomatic (e.g. most Beta-PVs) virion, it is known to perform several important
or causes small benign tumors, known functions, including facilitating the packaging of the
as papillomas or warts (e.g. human papillomavirus 1, viral genome into nascent virions as well as the
HPV6 or HPV11). Papillomas caused by some types, infectious entry of the virus into new host cells. L2 is
however, such as human papillomaviruses 16 and 18, of interest as a possible target for more broadly
carry a risk of becoming cancerous. protective HPV vaccines.
• Generalities
GENERAL CHARACTERISTICS o Naked, circular icosahesdral dsDNA Virus
• Non-enveloped o Can integrate its genes and persist in infected
• Icosahedral cells episomally
• Double stranded circular DNA molecule o Genus Papillomavirus
o Species: Human Papilloma Virus
o More than 100 serotypes
o Some serotypes are oncogenic

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 MODE OF TRANSMISSION o Butcher’s Warts – occupational hazard to
• More than 40 types are sexually transmitted (genital butchers. Warts are seen in the hands Serotype
types) 7
• skin-to-skin contact often through a cut, abrasion or o Genital Warts – “Venereal Warts” or Condyloma
small tear in your skin. Acuminata May appear as flat or keratotic warts
• Primarily the mode of transmission is by sexual , this is Easily transmitted to sexual partners
contact. More than 40 types are sexually transmitted
(these are the genital types)
• This can also be transmitted by the use of shared
objects or by direct cutaneous contact skin-to-skin
contact often through a cut, abrasion or small tear
(tare) in your skin.
• Use of Shared Objects, direct cutaneous contact

PATHOLOGY
• HPV causes continuous growth of the keratinizing
layer of skin
• Associated with the common wart
• Some HPV types are linked to cancer
• There are several strains of HPV, yung iba tutubo sa
*”Small black dots” (see image above) – refer to the
fingers or sa paa.
capillaries underneath.
• Warts have cauliflower-like appearance

• Common Serotypes causing Genital Warts are 6

and 11
• Carcinomas of Cervix, Penis, Anus and Oropharynx
Serotypes 16 and 18
• Certain serotypes can pose a high risk of association
to malignancy
• Serotypes 16 and 18
o Mechanism of carcinogenesis
o Causes cervical cancer
• E6 and E7 genes
o Encode proteins that inactivate the p53 and
retinoblastoma proteins respectively
• Immunosuppressed patients and with AIDS, HIV(+)
women are at higher risk of developing cervical
cancer
• Cutaneous Warts Found in the Skin is Mostly Caused • Primarily Affects Epithelial Cells either Cutaneous or
by HPV 1-4 Mucosal Types
• Types of Cutaneous Warts • Site of Latency: Epithelial Cells
o Verrucae Vulgaris – common wart seen in • Diseases
Hands, feet, knees Serotype: 2,4 o WARTS (Verrucae or Papillomas) – caused by
▪ Verruca = wart HPV
o Plantar Warts – found on the hands, soles of o Cutaneous, Anogenital (Condyloma), Oral
feet; Inward growth of warts. Painful. Serotype 1 Papilloma
o Flat Warts – “Verrucae Planae” Found on skin, o Epidermodysplasia verruciformis (tree man
forehead, arms, face disease)

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• Cutaneous Warts lesions, women should be referred for further
o Found in the Skin investigations and adequate management.
o Mostly Caused by HPV 1-4 • Cervical cancer screening involves testing for pre-
• Types of Cutaneous Warts cancer and cancer among women who have no
o Verrucae Vulgaris – common wart symptoms and may feel perfectly healthy. When
▪ Seen in Hands, feet, knees screening detects pre-cancerous lesions, these can
▪ Serotype: 2,4 easily be treated, and cancer can be avoided.
o Plantar Warts – found on the hands, soles of Screening can also detect cancer at an early stage
feet; Inward growth of warts. Painful. and treatment has a high potential for cure.
▪ Serotype 1 • Because pre-cancerous lesions take many years to
o Flat Warts – “Verrucae Planae” develop, screening is recommended for every woman
▪ Found on skin, forehead, arms, face from aged 30 and regularly afterwards (frequency
o Butcher’s Warts – occupational hazard to depends on the screening test used). For women
butchers. Warts are seen in the hands living with HIV who are sexually active, screening
▪ Serotype 7 should be done earlier, as soon as they know their
o Genital Warts – “Venereal Warts” or Condyloma HIV status.
Acuminata • Screening has to be linked to access to treatment and
▪ May appear as flat or keratotic warts management of positive screening tests. Screening
▪ Easily transmitted to sexual partners without proper management is not ethical.
• There are 3 different types of screening tests that are
PREVENTION currently recommended by WHO:
• Vaccination • HPV testing for high-risk HPV types.
o “Gardasil” Quadrivalent Vaccine against • visual inspection with Acetic Acid (VIA)
Serotypes 6,11, 16 and 18 • conventional (Pap) test and liquid-based cytology
o Indication: Females 9-26 years old (LBC)
• Vaccines are available to prevent certain types of • For treatment of pre-cancer lesions, WHO
HPV that can cause cancers and warts. These are recommends the use of cryotherapy and Loop
often offered to adolescent girls, men who have sex Electrosurgical Excision Procedure (LEEP). For
with men and people living with HIV. It’s best to have advanced lesions, women should be referred for
the vaccine before you start having sex, although it’s further investigations and adequate management.
sometimes possible to get the vaccine later in life.
POXVIRIDAE
TREATMENT • Poxviridae is a family of viruses. Humans,
• Cryotherapy vertebrates, and arthropods serve as natural hosts.
• Loop Electrosurgical Excision Procedure (LEEP) There are currently 83 species in this family, divided
• For treatment of pre-cancer lesions, WHO among 22 genera, which are divided into two
recommends the use of cryotherapy. Cryotherapy is subfamilies. Diseases associated with this family
a pain treatment that uses a method of localized include smallpox.
freezing temperatures to deaden an irritated • Four genera of poxviruses may infect
nerve. Cryotherapy is also used as a method of humans: orthopoxvirus, parapoxvirus, yatapoxvir
treating localized areas of some cancers. us, molluscipoxvirus.
LEEP stands for Loop Electrosurgical Excision o Orthopox: smallpox virus
Procedure. It's a treatment that prevents cervical (variola), vaccinia virus, cowpox virus, monkeyp
cancer. A small electrical wire loop is used to remove ox virus
abnormal cells from your cervix. LEEP surgery may o Parapox: orf virus, pseudocowpox, bovine
be performed after abnormal cells are found during a papular stomatitis virus
Pap test, colposcopy, or biopsy. For advanced o Yatapox: tanapox virus, yaba monkey tumor
virus

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 o Molluscipox: molluscum contagiosum o vaccinia virus
virus (MCV). o monkeypox virus
▪ causes skin-colored bumps (papules) o cowpox virus
which have a central umbilication. o other poxviruses
▪ A benign lesion; can be removed by • Largest and Most Complex Viruses
curettage • Linear double stranded DNA
• Brick-shaped complex virus with a disk/dumb bell
shaped core
• Multilayered and possess a lipoprotein envelope
• Replicates in the host cell cytoplasm
• Possess DNA-dependent RNA polymerase

MODE OF TRANSMISSION
• Inhalation (respiratory infection) of aerosol droplets,
face to face contact and spread mainly in the
lymphatics; direct contact through fomites
The most common are vaccinia (seen on Indian
• In general, the MOT of poxviruses is the same these
subcontinent) and molluscum contagiosum, but
are by inhalation (respiratory infection) of aerosol
monkeypox infections are rising (seen in west and
droplets, face to face contact and spread mainly in the
central African rainforest countries). The similarly
lymphatics; direct contact through fomites
named disease chickenpox is not a true poxvirus
and is actually caused by the herpesvirus varicella
VARIOLA VIRUS
zoster.
• Smallpox was an infectious disease caused by one of
• Viruses of Medical Importance
two virus variants, Variola majorand Variola
o Smallpox Virus
minor. The last naturally occurring case was
o Vaccinia Virus
diagnosed in October 1977, and the World Health
o Molluscum Contagiosum Virus
Organization (WHO) certified the global
o Other members include: monkeypox, orf virus
eradication of the disease in 1980. The risk of death
following contracting the disease was about 30%,
GENERAL CHARACTERISTICS
with higher rates among babies. Often those who
• family Poxviridae survived had extensive scarring of their skin, and
• subfamily Chordopoxvirinae some were left blind.
• Largest of all viruses • After 1980s, wala ng binakunahan ng small pox
• Brick shape because it has been declared eradicated
• Contain a dsDNA genome • However, they say that some countries are
hiding strain of small pox that can be used for
biological warfare.
GENERAL CHARACTERISTICS
• Causes smallpox
• Synchronous progressive rash
• fever
• Smallpox was an infectious disease caused by one of
two virus variants, Variola major and Variola
minor. The last naturally occurring case was
diagnosed in October 1977, and the World Health
Organization (WHO) certified the global
• Variola virus belongs to genus Orthopoxvirus eradication of the disease in 1980. The risk of death
• Other members of the genus include: following contracting the disease was about 30%,

DE BORJA, DE GUZMAN, DE LOS SANTO, DIMAIWAT, DOLINA, HALILI, OBISPO;3L-MT 39

 with higher rates among babies. Often those who PATHOLOGY
survived had extensive scarringof their skin, and • Variola , smallpox or red plague
some were left blind o Acute contagious disease of the
• Efficacy of vaccination in 1796 reitculoendothelial, vascular endothelial and
• Last reported case in US was in 1949 epithelial cells
• Last case of smallpox worldwide was in Somalia in
1977
• WHO- world free of smallpox was in May1980

MODE OF TRANSMISSION
• Inhalation of airborne Variola virus
• face to face contact with an infected person
• Direct contact with infected body fluids or fomites
• Transmission occurs through inhalation
of airborne Variola virus, usually droplets expressed
from the oral, nasal, or pharyngealmucosa of an
infected person.it can be transmitted from one person • Variola , smallpox or red plague Acute contagious
to another disease of the reitculoendothelial, vascular
• primarily through prolonged face-to-face contact with endothelial and epithelial cells
an infected person but could also be spread through • The initial symptoms of the disease include fever and
direct contact with infected bodily fluids or vomiting. This is followed by formation of sores in the
contaminated objects (fomites) such as bedding or mouth and a skin rash. Over a number of days the
clothing. skin rash turns into characteristic fluid-
• Transmission occurs through inhalation filled bumps with a dent in the center. The picture
of airborne Variola virus, usually droplets expressed shows a child having these fluid filled bumps.
from the oral, nasal, or pharyngealmucosa of an • The bumps then scabbed over and fell off,
infected person. It was transmitted from one person leaving scars. The disease was spread between
to another primarily through prolonged face-to-face people or via contaminated objects. Prevention was
contact with an infected person, usually within a primarily by the smallpox vaccine.Once the disease
distance of 1.8 m (6 feet), but could also be spread had developed, certain antiviral medication may have
through direct contact with infected bodily fluids or helped.
contaminated objects (fomites) such as bedding or • Synchronous Progressive Rash with Fever
clothing. Rarely, smallpox was spread by virus carried o Result of Viral Replication in the skin, followed
in the air in enclosed settings such as buildings, by damage caused by T cytotoxic cells attacking
buses, and trains. The virus can cross the placenta, the infected cells
but the incidence of congenital smallpox was • Now Eradicated/Extinct
relatively low. Smallpox was not notably infectious in
the prodromal period and viral shedding was usually
delayed until the appearance of the rash, which was
often accompanied by lesions in the mouth and
pharynx. The virus can be transmitted throughout the
course of the illness, but this happened most
frequently during the first week of the rash, when most
of the skin lesions were intact. Infectivity waned in 7
to 10 days when scabs formed over the lesions, but
the infected person was contagious until the last
smallpox scab fell off.

DE BORJA, DE GUZMAN, DE LOS SANTO, DIMAIWAT, DOLINA, HALILI, OBISPO;3L-MT 40

• This is to show you the difference between the • 1st Reservoir Host: Rabbits
lesions of smallpox and chickenpox. • Clinical: Lesions are larger than small pox with
• Lesions of small pox are seen on the head and limbs necrotic centers
(centrifugal distribution) while lesions of chickenpox
are concentrated on the chest and back. TREATMENT
• Tecovirimat
Differences between chickenpox and smallpox • Cidofovir
• In July 2018, the Food and Drug
Administration approved tecovirimat, the first drug
CHICKENPOX SMALLPOX
approved for treatment of
[62]
smallpox. Antiviraltreatments have improved
Lesions from stage since the last large smallpox epidemics, and studies
Mode of Lesions appear
to stage suggest that the antiviral drug cidofovir might be
progress in crops
synchronously useful as a therapeutic agent.
• Smallpox vaccination within three days of exposure
Time of will prevent or significantly lessen the severity of
Rapid Relatively low
Evolution smallpox symptoms in the vast majority of people.
• Superficial Deep set Vaccination four to seven days after exposure can
• Oval or totally Tend to be circular offer some protection from disease or may modify
Lesions the severity of disease.[56] Other than vaccination,
irregular and regular
treatment of smallpox is primarily supportive, such
Unilocular Multilocular as wound care and infection control, fluid therapy,
Vesicles Scarring slight Scarring sever and and possible ventilator assistance. Flat and
and superficial deep (pock marks) hemorrhagic types of smallpox are treated with the
same therapies used to treat shock, such as fluid
resuscitation. People with semi-confluent and
• 2 Categories confluent types of smallpox may have therapeutic
o Variola major – severe form, more deadly, issues similar to patients with extensive
causes more disfigurement skin burns.[61]
o Variola minor – “Alastrim”; milder form of
• In July 2018, the Food and Drug
variola
Administration approved tecovirimat, the first drug
• VM – 30% case fatality rate; seen more in asia approved for treatment of
• Alastrim – 1% CFR [62]
smallpox. Antiviraltreatments have improved
since the last large smallpox epidemics, and studies
PREVENTION suggest that the antiviral drug cidofovir might be
• Prevention was primarily by the smallpox vaccine useful as a therapeutic agent. The drug must be
• Eradicated by the Use of Live Attenuated Vaccine administered intravenously, and may cause
(Vaccinia) administered intradermally serious kidney toxicity.[63]
• Prevention was primarily by the smallpox vaccine • ACAM2000 is a smallpox vaccine developed by
which uses Live Attenuated Vaccine which contains Acambis. It was approved for use in the United
the (Vaccinia virus) administered intradermally States by the U.S. FDA on August 31, 2007. It
• Eradicated by the Use of Live Attenuated Vaccine contains live vaccinia virus, cloned from the same
(Vaccinia) administered intradermally strain used in an earlier vaccine, Dryvax. While the
• Vaccinia Virus – used to vaccinate against Dryvax virus was cultured in the skin of calves and
smallpox freeze-dried, ACAM2000s virus is cultured in kidney
• Causes a localized exanthem through epithelial cell epithelial cells (Vero cells) from an African green
infection monkey. Efficacy and adverse reaction incidence
• MOT: sexually transmitted; skin contact are similar to Dryvax.[60] The vaccine is not routinely

DE BORJA, DE GUZMAN, DE LOS SANTO, DIMAIWAT, DOLINA, HALILI, OBISPO;3L-MT 41

 available to the US public; it is, however, used in the virus. The virus enters the body through broken skin
military and maintained in the Strategic National (even if not visible), respiratory tract, or the mucous
Stockpile.[64] membranes (eyes, nose, or mouth). Animal-to-
human transmission may occur by bite or
MONKEYPOX VIRUS scratch, bush meat preparation, direct contact
• Monkeypox is an infectious disease caused by with body fluids or lesion material, or indirect
the monkeypox virus that can occur in certain contact with lesion material, such as through
animals including humans. Symptoms begin contaminated bedding. Human-to-human
with fever, headache, muscle pains, swollen lymph transmission is thought to occur primarily through
nodes, and feeling tired. This is followed by a rash large respiratory droplets. Other human-to-human
that forms blisters and crusts over. The time from methods of transmission include direct contact
exposure to onset of symptoms is around 10 with body fluids or lesion material, and indirect
days. The duration of symptoms is typically 2 to 5 contact with lesion material, such as through
weeks. contaminated clothing or linens,
• Animal-to-human transmission may occur by bite
GENERAL CHARACTERISTICS or scratch, bush meat preparation, direct contact
• First described in primates with body fluids or lesion material, or indirect contact
• First human monkeypox in 1970 with lesion material, such as through contaminated
• Less severe in humans bedding. Human-to-human transmission is thought
to occur primarily through large respiratory droplets.
Respiratory droplets generally cannot travel more
than a few feet, so prolonged face-to-face contact is
required. Other human-to-human methods of
transmission include direct contact with body fluids
or lesion material, and indirect contact with lesion
material, such as through contaminated clothing or
linens.
• The reservoir host (main disease carrier) of
monkeypox is still unknown although African
rodents are suspected to play a part in transmission.
The virus that causes monkeypox has only been
recovered (isolated) twice from an animal in nature.
In the first instance (1985), the virus was recovered
from an apparently ill African rodent (rope squirrel)
in the Equateur Region of the Democratic Republic
• Monkeypox is an infectious disease caused by of Congo. In the second (2012), the virus was
the monkeypox virus that can occur in certain recovered from a dead infant mangabey found in the
animals including humans. Tai National Park, Cote d’Ivoire.
• First described in primates
• First human monkeypox in the year 1970.
• Infections were Less severe in humans.

MODE OF TRANSMISSION
• Contact with the virus from an animal, human or
materials contaminated with the virus
• Transmission of monkeypox virus occurs when a
person comes into contact with the virus from an
animal, human, or materials contaminated with the

DE BORJA, DE GUZMAN, DE LOS SANTO, DIMAIWAT, DOLINA, HALILI, OBISPO;3L-MT 42

 PATHOLOGY PREVENTION
• Vesicular, pustular, febrile illness similar to smallpox • Avoid contact with animals that could harbor the
virus
• Avoid contact with any materials, such as bedding,
that has been in contact with a sick animal.
• Isolate infected patients from others who could be
at risk for infection.
• Practice good hand hygiene after contact with
infected animals or humans. For example, washing
your hands with soap and water or using an alcohol-
based hand sanitizer.
• Use personal protective equipment (PPE) when
caring for patients.
• There are number of measures that can be taken to
prevent infection with monkeypox virus:
• In humans, the symptoms of monkeypox are similar • Avoid contact with animals that could harbor the
to but milder than the symptoms of smallpox. virus (including animals that are sick or that have
Monkeypox begins with fever, headache, muscle been found dead in areas where monkeypox
aches, and exhaustion. The main difference occurs).
between symptoms of smallpox and monkeypox is • Avoid contact with any materials, such as bedding,
that monkeypox causes lymph nodes to swell that has been in contact with a sick animal.
(lymphadenopathy) while smallpox does not. The • Isolate infected patients from others who could be
incubation period (time from infection to symptoms) at risk for infection.
for monkeypox is usually 7−14 days but can range
• Practice good hand hygiene after contact with
from 5−21 days.
infected animals or humans. For example, washing
• The illness begins with: your hands with soap and water or using an alcohol-
o Fever based hand sanitizer.
o Headache
• Use personal protective equipment (PPE) when
o Muscle aches
caring for patients.
o Backache
• Imvamune or imvanex vaccine
o Swollen lymph nodes
o JYNNEOSTM (also known as Imvamune or
o Chills
Imvanex) is an attenuated live virus vaccine
o Exhaustion
which has been approved by the U.S. Food
• Within 1 to 3 days (sometimes longer) after the
and Drug Administration for the prevention of
appearance of fever, the patient develops a rash,
monkeypox. The Advisory Committee on
often beginning on the face then spreading to other
Immunization Practices (ACIP) is currently
parts of the body.
evaluating JYNNEOSTM for the protection of
• Lesions progress through the following stages people at risk of occupational exposure to
before falling off: orthopoxviruses such as smallpox and
o Macules monkeypox in a pre-event setting.
o Papules
o Vesicles TREATMENT
o Pustules
• Currently, there is no proven, safe treatment for
o Scabs
monkeypox virus infection.
• The illness typically lasts for 2−4 weeks. In Africa,
• For purposes of controlling a monkeypox
monkeypox has been shown to cause death in as
outbreak in the United States, smallpox vaccine,
many as 1 in 10 persons who contract the disease.
antivirals, and vaccinia immune globulin (VIG)
can be used.

DE BORJA, DE GUZMAN, DE LOS SANTO, DIMAIWAT, DOLINA, HALILI, OBISPO;3L-MT 43

 • Currently, there is no proven, safe treatment for • The figure above shows the left eye and right ear of
monkeypox virus infection. a man with laboratory acquired vaccinia virus
• Just for the purpose of controlling a monkeypox infection from Virginia in 2008. The man worked for
outbreak in the United States, the following can a laboratory at an academic institution in Virginia.
be used like the smallpox vaccine, antivirals, and He went to a local urgent care clinic reporting
vaccinia immune globulin (VIG). swelling of cervical lymph nodes and pain and
o Reference: CDC inflammation of his right earlobe associated with
purulent discharge beginning July 2, followed on
OTHER POXVIRUSES July 3 by a feverish feeling and swelling of his left
VACCINIA VIRUS eye with no change in his vision. The patient was
• Vaccinia Virus – used to vaccinate against prescribed cephalexin for presumed bacterial
smallpox infection and prednisone for swelling However, on
o Causes a localized exanthem through July 6, his symptoms worsened, and he went to a
epithelial cell infection hospital emergency department. The patient was
o MOT: sexually transmitted; skin contact given bacitracin for his eye and discharged. That
o 1st Reservoir Host: Rabbits night, he noted pustular lesions at similar stages of
o Clinical: Lesions are larger than small pox development on his right ear and left eye.
with necrotic centers
• The initial clinical signs of the infection are focal MOLLUSCUM CONTAGIOSUM VIRUS
red skin areas, fever, and general symptoms similar • Disease of children and young adults
to those of a cold. Then, pustules and ulcerated • Disease: Molluscum Contagiosum/ Water warts
lesions surrounded by edema and erythema follow, • MOT: Direct Skin Contact, intimate contact, indirect
as well as local lymphadenopathy that can last for contact
weeks. The picture shows the left eye and right ear • Molluscum contagiosum (MC), sometimes
of a man with laboratory acquired vaccinia virus called water warts, is a viral infection of
infection from the skin that results in small raised pink lesionswith
• The history of the vaccinia virus is that of smallpox, a dimple in the center. They may become itchy or
a serious illness characterized by the eruption of sore, and occur singularly or in groups. Any area of
small pocklike lesions throughout the skin and the skin may be affected, with abdomen, leg s,
internal organs. This is distinct from the great pox of arms, neck, genital area, and face being the most
syphilis. The variola virus causes smallpox and common.
may have begun infecting humans approximately
10,000 years ago.Oct 1, 2019 POLYOMAVIRIDAE
• The term "polyoma" refers to the viruses' ability to
produce multiple (poly-) tumors (-oma) under
certain conditions.
• Polyomaviridae is a family of viruses whose
natural hosts are primarily mammals and birds. As
of 2019, there are four recognized genera and 102
species, nine of which are unassigned to a
genus. 14 species are known to infect humans,
while others, such as Simian Virus 40, have been
identified in humans to a lesser extent. Most of
these viruses are very common and typically
asymptomatic in most human populations
studied. BK virus is associated
with nephropathy in renal transplant and non-renal
solid organ transplant patients, JC virus

DE BORJA, DE GUZMAN, DE LOS SANTO, DIMAIWAT, DOLINA, HALILI, OBISPO;3L-MT 44

 with progressive multifocal o Seen in BM transplant patients
leukoencephalopathy, and Merkel cell o seen in immunocompromised renal
virus with Merkel cell cancer. transplant patient
• MC Virus – causes Merkel Cell Carcinoma
GENERAL CHARACTERISTICS • Simian Virus 40, have been identified in humans to
• Small, Circular dsDNA Viruses a lesser extent. Most of these viruses are very
• Icosahedral, Naked common and typically asymptomatic in most human
populations studied. BK virus is associated
with nephropathy in renal transplant and non-renal
solid organ transplant patients, JC virus
with progressive multifocal
leukoencephalopathy, and Merkel cell
virus with Merkel cell cancer.
• The term "polyoma" refers to the viruses' ability to
produce multiple (poly-) tumors (-oma) under
certain conditions.
• Polyomaviridae is a family of viruses whose
natural hosts are primarily mammals and birds. As
of 2019, there are four recognized genera and 102
• Viral protein 1,2,3 from the viral capsid species, nine of which are unassigned to a
• Polyomaviruses are unenveloped double- genus. 14 species are known to infect humans,
stranded DNA viruses with circular genomes of while others, such as Simian Virus 40, have been
around 5000 base pairs. The genome is identified in humans to a lesser extent. Most of
packaged in a viral capsid of about 40- these viruses are very common and typically
50 nanometers in diameter, which asymptomatic in most human populations
is icosahedral in shape (T=7 symmetry). The studied. BK virus is associated
capsid is composed of 72 with nephropathy in renal transplant and non-renal
pentameric capsomeres of a protein called VP1, solid organ transplant patients, JC virus
which is capable of self-assembly into a closed with progressive multifocal
icosahedron; each pentamer of VP1 is leukoencephalopathy, and Merkel cell
associated with one molecule of one of the other virus with Merkel cell cancer.
two capsid proteins, VP2 or VP3.[ • Other Viruses
o MC Virus – causes Merkel Cell Carcinoma
MODE OF TRANSMISSION o SV40 (Simian Polyomavirus 40) – can
• Direct Contact with Respiratory Secretions induce tumors in animals and associated
• Urine (BK virus) with human tumors
• Transplacental o Polyoma – refers to the ability of this
organism to produce tumors
PATHOLOGY o JC Virus – disease of CNS affecting
• JC Virus immunocompromised such as AIDS
o Disease: Infect respiratory system, kidneys patient; destroying the oligodendrocytes
or brain PML or Progressive Multifocal which produce myelin; it also affects
Leukoencephalopathy in AIDS & transplant astrocytes
patients ▪ Seen in severely
o demyelinating disease immunocompromised
• BK Virus
o Disease: Hemorrhagic Cystitis; BK virus
associated nephropathy

DE BORJA, DE GUZMAN, DE LOS SANTO, DIMAIWAT, DOLINA, HALILI, OBISPO;3L-MT 45

 randomized clinical trials involving large numbers
of patients.
• Currently, treatment is largely supportive and
involves reduction in the doses of
immunosuppressive agents. However, this
approach requires close follow-up because it may
lead to subsequent graft failure resulting from
acute cellular rejection. A variety of antiviral
agents have been studied in vitro for their effects
against polyomaviruses. These include cidofovir,
• JC and BK – first persons who had the disease retinoic acid, topoisomerase inhibitors, 5′-bromo
(John Cunningham) 2′-deoxyuridine, cytosine arabinoside (AraC), and
• Risk Factor for SV40 – patients who were IFN. The most promising drug is cidofovir, an
vaccinated with a contaminated Salk polio vaccine acyclic nucleoside phosphonate analogue
that is known to have in vitro activity against
the 3 polyomavirus that are able to infect
humans (JCV, BKV, and SV40).There are a few
case reports of hemorrhagic cystitis in BMT
recipients for which cidofovir was used with some
success [56, 57]. In addition, a few renal
transplant recipients have been treated with
cidofovir for BKV nephropathy [58]. However,
cidofovir has yet to be tested for the treatment of
polyomavirus nephropathy in randomized clinical
trials involving large numbers of patients.

SINGLE-STRANDED DNA VIRUS

• MC Virus – causes Merkel Cell Carcinoma PARVOVIRIDAE
• (left) Clinical appearance of Merkel cell • The Parvoviridae are a family of small, rugged,
carcinoma (MCC) lesion. Red, raised, nodular genetically-compact DNA viruses, known
MCC lesion on the arm of a patient. (right) collectively as parvoviruses. There are currently
Genomic organization of Merkel cell more than 100 species in the family, divided among
polyomavirus. NCRR (noncoding regulatory 23 genera in three subfamilies. Parvoviridae is the
region) contains a bidirectional promoter and sole taxon in the order Quintoviricetes.
the origin of replication. LT (large T-antigen), sT • Parvovirus B 19 was the first pathogenic human
(small T-antigen), and 57-kT antigen constitute parvovirus to be discovered and is best known for
the early gene products. causing a childhood exanthem called "fifth disease"
(erythema infectiosum), although it is also
TREATMENT associated with other diseases including arthritis.
• No specific antiviral therapy
• Cidofovir GENERAL CHARACTERISTICS
• There is no specific antiviral therapy for • Smallest of the DNA viruses
polyomaviruses. The most promising drug is • The only DNA virus that is single stranded
cidofovir, which is known to have in vitro • Parvovirus B19 (principal pathogen)
activity against the 3 polyomavirus that are • genus Erythrovirus
able to infect humans (JCV, BKV, and SV40) • Human bocavirus (HBoV)
However, cidofovir has yet to be tested for the
treatment of polyomavirus nephropathy in

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 PATHOLOGY
• Erythema infectiosum (fifth disease)
• Parvovirus B19 cause aplastic crisis
• Hydrops fetalis
• Parvovirus B 19 was the first pathogenic human
parvovirus to be discovered and is best known
for causing a childhood exanthem called "fifth
• Parvoviruses are linear, nonsegmented, single- disease" (erythema infectiosum),
stranded DNA viruses, with an average genome • Clinical Manifestations of 5th
size of 5-6 kilo base pairs (kbp). They are Disease/Erythema Infectiosum
classified as group II viruses in the Baltimore o Causes a Biphasic Illness among Humans
classification of viruses. Parvoviruses are among o Initial Phase: marked fever, malaise,
the smallest viruses (hence the name, myalgia and chills
from Latin parvus meaning small) and are 23– o Second Phase: maculopapular rash,
28 nm in diameter. arthralgia, arthritis
• Currently, viruses that infect humans are o May lead to complications such as
recognized in 5 genera: Bocaparvovirus (human arthritis/arthralgia, apalastic anemia (most
bocavirus 1–4, HboV1– serious), and hydrops fetalis (in babies).
4), Dependoparvovirus (adeno-associated virus
1–5, AAV1–5), Erythroparvovirus (parvovirus
B19, B19V), Protoparvovirus (bufavirus 1–3,
BuV1–3; cutavirus, CuV)
and Tetraparvovirus (human parvovirus 4 G1–3,
PARV4 G1–3).
• HBoV detected by rtPCR assays
• Genera
• Dependovirus – dependent virus upon helper
viruses such as Herpesviruses and Adenoviruses
for replication *Normal bone marrow vs bone marrow of Parvovirus patient with Aplastic anemia

• Erythrovirus – does not require helper cells to

replicate o Rash – “slapped cheek appearance”
▪ Due to immune complex deposition in
• Parvovirus B19
skin capillaries
o Only Medically important
▪ Rashes can also be seen along the
• Parvovirus B19 – only human pathogen
arms or in the body and lace-like and
o Viral Host Receptor: P antigen
reticulated pattern.
o Clinical Presentations
▪ It’s NOT a vesicle, hindi siya matubig,
▪ 5th Disease
hindi rin siya raised, sometimes it’s just
▪ Aplastic Crisis
a patch
▪ Hydrops Fetalis
▪ Arthritis
▪ Chronic B19 Infection

MODE OF TRANSMISSION
• Respiratory and Oral Secretions such as Saliva,
Sputum or Nasal Mucus
• The virus is transmitted via Respiratory and Oral
Secretions such as Saliva, Sputum or Nasal
Mucus

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• Parvovirus b19 causes papular purpuric gloves and TREATMENT
sock syndrome – this is characterized by a painful • Antivirals
red rash; w/ sharp demarcation at the ankles and • Human immunoglobulin-sourced treatments
wrists. • Antivirals and human immunoglobulin-sourced
• Parvovirus b19 also causes slapped cheek treatments are usually for relief of symptoms. Using
syndrome which looks like a – “slapped cheek immunoglobulins is a logical solution for treatment
appearance” due to immune complex deposition in as neutralizing antibodies because a majority of
skin capillaries adults have been in danger from the parvoviruses,
especially B19 virus.

VIDEOS
• Mnemonics of DNA viruses
o https://youtu.be/Df_qAFF58Ec
• RNA and DNA viruses
o https://youtu.be/SMOO2WaMTiI
• DNA VIRUSES
o https://youtu.be/f3M0lPBeFjQ

POST TEST
• True or False: Genital herpes infections are usually
PATHOLOGY caused by HSV-1. FALSE - IT IS USUALLY
• The picture below shows a Papular purpuric Gloves CAUSED BY HSV-2.
and socks syndrome characterized by a red rash; w/ • These viruses have a characteristic brick shape and
sharp demarcation at the ankles and wrists. contain a dsDNA genome. POXVIRUSES
• The majority of clinically significant HPVs are found
in the genus_____________.
ALPHAPAPILLOMAVIRUS
• It is thought that this virus was introduced in the
United States by rodents imported from Africa.
MONKEYPOX VIRUS
• Erythema infectiosum is commonly referred to
as_______. FIFTH DISEASE

PREVENTION
• No vaccine exists
• Currently, no vaccine exists to prevent infection by
all parvoviruses, but recently, the virus's capsid
proteins, which are noninfectious molecules, have
been suggested acting as antigens for improving of
vaccines.

DE BORJA, DE GUZMAN, DE LOS SANTO, DIMAIWAT, DOLINA, HALILI, OBISPO;3L-MT 48

year 03
term 01

MT
SHIFTING
SECOND

63
22
 UNIT III: RNA VIRUSES: POSITIVE STRAND OR SENSE STRAND ssRNA
 Smallest ang picrona but other
Pre-test: reference says polio is smallest
1. Replication of +ssRNA genomes occurs in the which is under the picornaviridae
Cytoplasm family
2. Positive-sense single-stranded RNA (+ssRNA):
can be translated directly to form proteins using
host ribosome. True
3. The most common cause of gastroenteritis in
the US. Norovirus
4. Coronavirus is an envelope virus. True
5. SARS-CoV-2 belong to gamma coronavirus.
False
RECAP

GENERALITIES
 All are ss-RNA except
o Reovirus
 All are helical except
o Calicivirus
o Picornavirus
o Flavivirus
o Togavirus
o Reovirus
o Retrovirus
o They are not helical because they are
icosahedral
 All are enveloped except PCR:
o Picornaviridae
o Caliciviridae FROM PPT NOTES:
o Reoviridae
o They are not enveloped because they are My focus is only on the positive sense RNS
naked viruses plus:
 All replicate inside the CYTOPLASM except  HEPEVIRIDAE
o Orthomyxoviridae  ASTROVIRIDAE
o Retroviridae
o They do not replicate in the cytoplasm What does positive sense RNA virus mean?
because they replicate in the nucleus  Positive-strand RNA virus:
 Arthropodborne: Arbovirus: o AKA sense-strand RNA virus, a
o Bunyaviridae virus whose genetic information
o Flaviviridae consists of a single strand of RNA
o Togaviridae that is the positive (or sense)
 Size strand which encodes mRNA
o Largest: Paramyxoviridae (messenger RNA) and protein.
o Smallest:Picornaviridae Replication in positive-strand RNA
 Other reference: specifically viruses is via a negative-strand
Poliovirus intermediate.

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 The focus is only on the positive strand RNA FROM PPT NOTES:
virus aka sense strand single stranded RNA  Positive-strand RNA virus genomes are
virus, which are: templates for both translation and
 Coronaviridae replication, leading to interactions
 Flaviviridae between hOst translation factors and RNA
 Togaviridae replication at multiple levels. All known
 And all naked icosahedral viruses positive-strand RNA viruses carry genes
o Picornaviridae for an RNA-dependent RNA polymerase
o Caliciviridae (RdRp) used in genome replication.
o Hepeviridae
o Astroviridae  Replication of +ssRNA genomes occurs in
the cytoplasm of the host cell and often
occurs in tandem with the assembly of the
nucleocapsid into which the genetic
material is packaged.

 In many cases, the replication of +ssRNA

viruses occurs spontaneously, without
ATP and thus no energetic cost. In vitro
experiments have also shown that
+ssRNA viral assembly depends on
interactions between proteins and
between proteins and RNA. The genomes
are the templates for translation and
replication, which is what fosters
interactions between the host‘s replication
factors and RNA replication at several
levels.

 Arenaviridae: Rodent borne virus

NOT INCLUDED
 Arbovirus: Bunya, Toga and Flavi
 Positive-sense single-stranded RNA
(+ssRNA): can be translated directly to
form proteins using host ribosome
 Do not have the reverse transcriptase:
HOW DO POSITIVE SENSE RNA VIRUSES
viral genome codes for RNA polymerase
REPLICATE?
→ forms -ssRNA → template for progeny
+ssRNA
 With reverse transcriptase: retroviruses
(e.g., HIV, HTLV)
 Reverse transcriptase transcribes viral
ssRNA to dsDNA
 Negative DNA strand serves as template
for mRNA → viral proteins and progeny
+ssRNA are synthesized
 Negative-sense single-stranded RNA (-
ssRNA): viral genome codes for viral
polymerase → mRNA → new viral
proteins and progeny -ssRNA
 Double-stranded RNA (dsRNA):
Reoviridae

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 IMPORTANCE OF +ssRNA VIRUSES  DSE AND TRANSMISSION
o Transmission: Fecal-oral route
 Positive-sense RNA viruses make up more than o Disease: Hepatitis E
one-third of all known virus genera.
 This includes important pathogens, potential  Dse is self –limiting, supportive care
bioterrorism agents.
 Use host factors in all steps of viral infection, HEPATITIS E
such as entry and replication.  Pathogen: hepatitis E virus (HEV)
 +ssRNA viruses can modulate the gene o The hepatitis E virus, which belongs to
expression and defenses of the host by co- the family of Hepeviridae and the genus
opting host factors. Orthohepeviridae, is a small (34nm in
diameter), non- enveloped virus with
OUTLINE: VIRUSES IN FOCUS single-stranded,positive-sense RNA.
 Epidemiology: HEV is not common in the US.
 UNIT IV RNA VIRUSES (positive sense ssRNA)  Route of transmission: fecal-oral
1. Generalities  Pathophysiology:the degree of hepatic injury is
2. Positive sense ssRNA Viruses of Medical usually mild and the patient may present with
Importance clinical features of acute hepatitis
a. Hepeviridae  Clinicl features:
b. Caliciviridae o Incubation period: 2-8 weeks
c. Astroviridae o Clinical features are similar to those of
d. Coronaviridae hepatitis A
e. Flaviridae o In the majority of cases, the disease is
f. Togaviridae self-limiting with complete recovery
g. Picornaviridae o Fulminant hepatitis among pregnant
 Morphology women
 Mode of Transmission  Fulminant hepatits due to HEV
 Pathophysiology and symptomatology is relatively common among
 Prevention and Control pregnant women (occuring in up
to 20% of cases) and is life-
HEPEVIRIDAE threatening for both the mother
 MORPHOPLOGY and fetus
o Genetic Structure: +ssRNA, Linear o Patients do not become carriers nor
o Capsid: Icosahedral develop chronic hepatitis (unlike in
 IMPORTANT VIRUS hepatitis B and C)
o Hepatitis E virus (HEV)  Diagnostics:
o Laboratory findings are the same as in
hepatitis A
o Confirmatory test
 Anti-HEV IgM: active infection
 Anti-HEV IgG: past infection
 HEV RNA can be detected by
PCR in stool and serum
samples.
 Treatment: supportive care
 Prevention: no vaccine available

FROM MAHON ADDITIONAL INFO:

 Transmitted by fecal oral route particularly in
contaminated drinking water

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 Cause of epidemics of enterically transmitted FROM PPT NOTES:
hepatitis in developing countries in Asia, Africam  Calicivirus virions are non-enveloped
and Central America approximately 35–40 nm in diameter with
 Signs and symptoms include an icosahedral symmetry. This is linear
o Fever and ofcourse positive or senses ssRNA.
o Malaise  The capsid is composed of 90 dimers of
o Nausea the major structural protein VP1 arranged
o Vomiting on a T=3 icosahedral lattice.
o Jaundice  Figure 1:Figure 1 The structure of the
o Dark urine calicivirus capsid exemplified by cryo-
 Viral shedding in feces shown to persist for image reconstruction of recombinant
several weeks Norwalk virus (NV)-like particles (rNV
VLPs) (Left). X-ray structure of the
CALICIVIRIDAE Norwalk virus capsid (Right) with the
 MORPHOLOGY Shell, Protruding 1, and Protruding 2
o Genetic structure: +ssRNA, Linear non domains colored in blue, red and yellow,
enveloped, icosahedral respectively.
o The capsid is composed of major  Characteristically, calicivirus capsid
structural protein VP1 arranged on a architecture has 32 cup-shaped
T=3 icosahedral lattice depressions at each of the icosahedral
o Have distinct virion morphology with five-fold and three-fold axes. In
cup-shaped depressions on a spherical negatively-stained virus preparations,
capsid surface. With a ―STAR OF some cup-shaped depressions appear
DAVID PATTERN‖ distinct and well defined, while in others
o Calici is derived from the Latin word for these depressions are less prominent.
calyx which means cup  Caliciviridae show the following features:
o (1) 5-fold axis, a central dark
patch surrounded by a lighter ring
of virion material which seems to
bear a fringe of ten evenly-spaced
‗spikes‘ formed by the tips of the
cups seen in profile.
o (2) 3-fold axis, a central dark
patch surrounded by 6 others.
This ‗star of David‘ pattern is
unique to this group of viruses.
o (3) 2-fold axis, 4 patches in a
rhomboid or diamond shape,
often separated by a prominent
light area in the shape of an H.

 IMPORTANT VIRUS
o NoVs- Norovirus- most common cause
of gastroenteritis in the US
 Most ofen sa matanda, pero
pwede rin sa bata and sa cruise
siya madalas
 According kay sir, most
common cause of viral
gastroenteritis in pediatrics or

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 children – Reovirus or rotavirus FROM PPT NOTES:
from Reoviridae
o SaVs- Sapoviruses- small with cup-  Caliciviruses have been detected from a
shaped morphology broad range of mammals as well as from
 DSE AND TRANSMISSION birds and fish.
o Transmission: fecal-oral route & o NoVs have been found in drinking
aerosols; highly contagious water, swimming areas,and
o Disease: Both NoVs and SaVs causes contaminated food.
AGE  MOT: most commonly
 NoVs- cause outbreaks of AGE foodborne, although
(Acute gastroenteritis) in waterborne
schools, nursing homes, (fecal-oral route)
families, cruise ships and in and person-to-
resort areas person transmission can
 SaVs- causes diarrhea and be significant.
vomiting in infants, young o SaVs are small (30–35 nm in
children, and older patients diameter) diarrheagenic viruses
distinguished by a cup-shaped
morphology. They usually cause
diarrhea and vomiting in infants,
young children, and older
patients. Originally discovered in
Sapporo, Japan, in 1977,.

 Transmission: of caliciviruses is via direct

contact with an infected host or indirectly
via contact with faecal material, vomitus or
respiratory secretions, contaminated food,
water and fomites. In general, no biologic
vectors appear to be involved in
transmission, however, mechanical,
arthropod vector transmission of RHDV
and VESV has been described.

FROM MAHON ADDITIONAL INFO:

 The family Caliciviridae contains four genera
o Sapovirus
o Norovirus
o Lagovirus
o Vesivirus
 The four genera include Sapporo virus, Norwalk
virus, rabbit hemorrhagic disease virus and
feline calicivirus.
 Sapoviruses (SaVs) and noroviruses (NoVs) are
causative agents of human gastroenteritis.
 NoVs
o 23 million cases annually
o 27-30 nm in diameter
o Incubation period: 24-48 hours
o Onset of severe nausea, vomiting,
diarrhea, and low grade fever is abrupt

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 o Illness usually subsides within 72 hours CORONAVIRIDAE
o Immunity may be short lived  MORPHOLOGY
o Diagnosis o Genetic structure: +ssRNA, Linear
 Electron microscopy o Capsid:helical
 Immune electron microscopy o Protein spikes: club or petal shaped,
 RT PCR (most commonly used crown like
diagnostic assay for detecting o Virulence factor: The S glycoprotein
NoV. may cause fusion of the viral envelope
o Stool is the best sample to detect NoV with the cell membrane
 Collected during acute illness  IMPT. VIRUS
(48 to 72 hours after onset of o Coronavirus
symptoms) o Subtypes: SARS-CoV, MERS-
 In some cases, can be collected CoV,SARS-Cov2
2 weeks after recovery  DSE AND TRANSMISSION
 SaVs o Transmission: respiratory droplet, direct
o Small (30-35 nm in diameter) contact, air-borne
o Distinguishable through cup shaped o Disease cold-like infection, diarrhea and
morphology acute respiratory syndrome
o Detection by  The hemagglutinin as well, the hemagglutinin-
 Electron microscopy esterase and the envelope small membrane
 Molecular (e.g., RT-PCR) protein, actually the spike , ACE2 most
 Immunlogic methods (e.g., especially, these are actually the target of some
ELISA) vaccine, they targeted the spike, specially those
that are protein based vaccine. It is an
enveloped virus and also-airborne in some
ASTROVIRIDAE studies.
 MORPHOLOGY
o Genetic structure: +ssRNA, Linear
o Capsid: Icosahedral
 IMPT. VIRUS
o Astrovirus
 Only occurs in human
 DSE AND TRANSMISSION
o Transmission: fecal-oral route
o Disease: Diarrheal illness
 It is not common, only few important details
about this virus.

 SUBFAMILIES
o Coronavirinae
 1.1 Alphacoronavirus- common
colds among adults
 Human coronaviruses
are: 229E and NL63
 1.2 Betacoronavirus
 OC43, HKU1 –
seasonal coronaviruses
 SARS-CoV: receptor -
angiotensin-converting
enzyme

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 o 2002 - FROM PPT NOTES:
Outbreak in
China  The gammacoronavirus genus contains
 MERS-CoV: receptor - primarily avian coronaviruses, the most
dipeptyl peptidase 4 aka prominent of which is avian infectious
CD26 bronchitis virus (AIBV), an important
o 2012 – veterinary pathogen causing respiratory
Outbreak in and reproductive tract disease in
Middle East chickens.
 SARS-CoV2: receptor -  The deltacoronavirus genus contains
angiotensin-converting recently discovered avian coronaviruses
enzyme found in several species of songbirds.
o 2019 – Displays viral tropism for EPC of the RT
Outbreak in and GIT. Take note of the widely spaced
China on the outer surface of the envelope,
o D614 - for this suggestive of a solar corona.
variation to G  G versus D
variation o Original samples of the novel
o G614 mutation– coronavirus out of Wuhan, China,
Currently the were a variation that scientists
more infectious now call the "D" clade. Before
o Sabi ni sir na March 1, more than 90% of viral
ang receptor samples taken from patients were
daw ng SARS from this D variation. Over the
COV 2 is ACE 2 course of March, G began to
 1.3 Gamma and Delta corona predominate. This mutation is
virus caused by the swapping of an
o Torovirinae adenine (A) nucleotide to a
 Associated with diarrheal guanine (G) nucleotide at a
diseases particular spot in the coronavirus
 It has two subfamilies which are the genome. It always appears
Coronavirinae and Torovirinae alongside three other mutations
 The cause of COVID 19 disease is the SARS that similarly swap one building
COV 2 block of RNA for another. (The
letters in RNA help code for the
proteins the virus makes once
inside a cell.)
o G variant tho more infectious or
some kind of transmissibility
advantage over other strains of
the virus,, The good news is that
so far, there is no evidence that
the G variant causes more severe
disease than any other version of
the coronavirus, nor does the
mutation appear likely to affect
the process of vaccine
development, researchers
agreed.

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FROM MAHON ADDITIONAL INFO:
 First identified by electron microscopy and were
named for the distinctive club-shaped
projections on their surfaces
 Infect a number of different animals; however,
most individual strains of virus typically only
infect a single animal species. Some are able to
infect more than one related species.
 Extremely fragile and difficult to culture
 RT PCR greater sensitivity and specificity
 Researchers in the United States tested bats
from the Rocky Mountain region in 2006 and
detected coronavirus RNA in two species of bats
o Eptesicus fuscus
o Myotis occultus.
 The horseshoe bat are the most likely reservoir
for the SARS-CoV
 SARS CoV targets the epithelial cells of the GI
tract
 Virus can also be isolated from urine and feces,
suggesting other potential routes of transmission
 Detection methods
o Electron microscopy
o ELISA (EUROIMMUN, Lubeck,
Germany)
o RT PCR  Emphasis on betacoronavirus type
o Antibody can be detected by Western  Angiotensin converting enzyme 2 receptor-
blot popular for researchers for vaccine. It is the
ETIOLOGY: THE PATHOGEN receptor binding protein
 MERS- Middle East Respiratory Syndrome
 Coronavirus are zoonotic, meaning they are
NAMING THE 2019- CORONAVIRUS
transmitted between animals and people.
 SARS-CoV-1 virus - originated in a nonhuman
host, most likely bats, was amplified in palm
civets, and was transmitted to humans in live
animal markets
 MERS-CoV- likely originated in bats and
became widespread in camels. It is likely that
contact with either bats or camels leads to initial
human infections, which can then be transmitted
from person to person
 SARS-CoV 2 (2019 coronavirus -, there is some
evidence it went from a bat to a pangolin before
infecting a human in Huanan Market, Wuhan,
China

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FROM PPT NOTES:  Mas mataas mortality ng SARS COV 1 and
 The virus causing the current outbreak of MERS COV kaysa SARS COV 2. But the thing
coronavirus disease has been named is, na prevent kasi yung SARS COV 1 and
"severe acute respiratory syndrome MERS COV. How come most of countries are
coronavirus 2" (SARS-CoV-2). having a hard time with SARS COV 2? One
 The International Committee on thing we can blame is the late information about
Taxonomy of Viruses (ICTV) is concerned the virus.
with the designation and naming of virus CORONAVIRIDAE
taxa (i.e. species, genus, family, etc.)
rather than the designation of virus  Diseases
common names or disease names. o Mild upper respiratory (cause by
 For an outbreak of a new viral disease, seasonal coronaviruses)
there are three names to be decided: and gastrointestinal tract infection
o the disease o SARS-Cov: Severe Acute Respiratory
o the virus Syndrome (SARS; outbreak 2002)
o the species. o MERS-CoV: Middle East Respiratory
syndrome (MERS; outbreak 2012)
 The World Health Organization (WHO) is
o SARS-CoV2: Coronavirus Disease 2019
responsible for the first, expert virologists
(COVID-19; outbreak 2019)
for the second, the ICTV for the third.
 Watch these videos
o Vox.com;
https://www.youtube.com/watch?v=T
PpoJGYlW54
CORONAVIRUS o https://www.weforum.org/agenda/202
 Resembles crown 0/03/a-visual-history-of-pandemics
 TRANSMISSION:  Alpha coronavirus- only mild respiratory
o Respiratory Droplets through sneezing diseases, causative agent of common colds
or coughing, but can also be by direct  Beta coronavirus- worse, causes severe acute
contact with mucus- or droplet- respiratory syndrome for SARS COV 1, Middle
contaminated surfaces (fomites) East respiratory syndrome for MERS COV and
 Most common mode of coronavirus diseases for SARS COV 2.
transmission of coronavirus
o Airborne transmission can also occur
from smaller particles derived from
dried-out droplets that become
aerosolized. The results of aerosols of
particles are more likely from medical
procedures such as manual ventilation,
suction, and bronchoscopy
 Airborne transmission is
possible in hospital setting
 INCUBATION PERIOD:
o SARS-CoV - 1: average of 6 days
o MERS CoV: 2 – 13 days
o COVID-19 (SARS-CoV-2): 14 days
 MORTALITY RATE:
o SARS-CoV-1: 10%
o MERS CoV: 30%
o COVID-19 (SARS-CoV-2): 3.6%
 Incubation period- from moment you become
infected with the pathogen to very first
appearance of symptoms

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FROM PPT NOTES: FROM MAAM: observe the picture as you read
 Common signs of infection include early this portion
symptoms of:  Fever
o respiratory symptoms o Survivors- Day 1-12
o fever o Non survivors- Day 1-13
o malaise  Cough
o chills o Survivors- Day 1-19
o headache o Non survivors- Day 1-16
o dry cough  Dyspnea
o followed a few days later by o Survivors- Day 7-19
shortness of breath and breathing o Non survivors-Day 6-19 (ang
difficulties. sinabi pero parang day 7-19
 Many patients have abnormal chest yata?)
radiographs. Some cases progress rapidly  ICU admission
to acute respiratory distress, requiring o Survivors- Day 12-18
ventilatory support. o Non surviros- Day 11-19 then die
 In more severe cases, infection can (ang sinabi pero parang day 12-
cause: 19 yata?)
o pneumonia,  Systematic corticosteroid
o severe acute respiratory o Survivors- Day 11-19 (ang sinabi,
syndrome, pero parang day 12-19 yata?)
o kidney failure and death . o Non survivors- Day 12-19 and
 Clinical features of coronavirus-associated they die (ang sinabi, pero parang
enteritis have not been clearly described . day 13- 19 yata?)
 AT RISK: elderly >65, individuals with  Detection
chronic medical conditions, individuals o Survivors- Day 1-20
with immunosuppressive conditions, and o Non survivors- Day 1-19
health-care workers  Sa non survivors, andaming organ
failures. For example, sa day 15, may
acute kidney injury and acute cardiac
injury. Meron din secondary infection.
These causes lead to death.

CLINICAL COURSE OF MAJOR SYMPTOMS

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PREVENTION AND CONTROL

FROM PPT NOTES:

 Avoid close contact with people who are
sick
 Avoid touching your eyes, nose, and
mouth
 Stay home when you are sick
 Cover your cough or sneeze with a tissue,
then throw the tissue in the trash
 Clean and disinfect frequently touched
objects and surfaces using a regular
household cleaning spray or wipe
 Wash your hands often with soap and
water
 Limiting travel
 Avoiding crowds
 Social distancing: 6 feet / 2 meters
 Currently, there is no vaccine yet.

TREATMENT
 Treatment is mostly supportive, and precautions are
taken to isolate and/or quarantine infected
individuals.
 Vaccine = on clinical trial

FLAVIVIRIDAE

 MORPHOLOGY
o Genetic structure: +ssRNA, Linear
o Capsid: Icosahedral
 IMPT. VIRUSES
o Hepacivirus- Hepatitis C virus
o Flavivirus: ARBOvirus(Arthropod Borne)
 Japanese encephalitis virus
 Yellow fever virus
 Dengue virus
 West Nile virus
 St. Louis encephalitis virus
 Zika virus

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  Cirrhosis is a major risk factor for
hepatocellular carcinoma.

FROM MAHON ADDITIONAL INFO:

Hepatitis C
 Genus Hepacivirus
 Family Flaviviridae
 Accounts 90% of all previous cases of
NANB (non-A,non-B) hepatitis
 Long incubation period
 Although perinatal and sexual transmission
of infection occur, and parenteral
transmission has been identified as a major
route for infection, HCV antibody has been
detected in patients in whom the routes of
transmission are poorly understood or who
have no evidence of identifiable risk factors.
 50% of patients become chronic carriers
 FLAVIVIRIDAE belong to the ARBOvirus.  20% and 30% develop cirrhosis
EXCEPT FOR HEPACIVIRUS o Cirrhosis is a major risk factor for
 ARBOvirus is an acronym for ARthropod BOrne hepatocellular carcinoma
virus. The mature virions accumulate inside the  HCV is the one with the highest mortality
cisternae of the ER. Most are transmitted by rate among the three hepatitis viruses
mosquito bite except for HEP C virus has NO (HAV,HBV,HCV)
known vector.  HCV is less immunogenic than HBV
 CHIKUNGUNYA belongs to TOGAVIRIDAE  Antibodies appear:
 Most familiar tayo with dengue and zika and o In about 6 weeks in 80% of patients
most of the time the vector is mosquito o Within 12 weeks in 90% of patients
 Very common na di kasama sa flavi is  Infection does not produce lifelong levels of
chikungunya which belongs to Togaviridae antibody, rather, it is because of replicating
HCV
 Screening test used is EIAs although have
GENUS HEPACIVIRUS high false positive rate\
 MORPHOLOGY  HCV infection can be treated with interferon,
o Genetic structure: +ssRNA, Linear with or without ribavirin
o Capsid: Icosahedral  Second generation immunoblot assays use
 DSE AND TRANSMISSION recombinant and/or synthetic proteins to
o MOT: Parenteral transmission detect anti-HCV anti-bodies
o Diseases:  Confirmation currently relies on nucleic acid
 Hepatitis C amplification testing
 Chronicity: only RNA virus that
can persist despite absence of
reverse transcriptase
 Oncogenic potential: liver
cirrhosis → hepatocellular
o Treatment: interferon
 IT IS NOT AN ARBOVIRUS. Naked virus.
 Patients with chronic HCV infection had been
previously treated with interferon,
 Among the three hepatitis viruses— HAV, HBV ,
and HCV—the one with the highest mortality
rate is HCV .

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 Genus Flavivirus
 Contains a number of important human pathogens, many of which are zoonotic arboviruses
 Includes the following: Japanese encephalitis virus, dengue virus, yellow fever virus, St. Louis encephalitis (SLE)
virus, Zika virus, Kyasanur Forest disease virus, Langat virus, Löuping ill virus, Murray Valley encephalitis virus,
Omsk hemorrhagic fever virus, Powassan virus, tickborne encephalitis virus, Wesselsbron virus, and WNV

Summary of Important Flavivirus:

Virus Reservoir Vector Diseases Prevention
Japanese Animals (e.g. birds, Culex mosquito  Major cause of Vaccination
encephalitis virus pigs) encephalitis in Asia
 Most common cause
of arboviral
encephalitis in the
world
Yellow Fever virus Primary monkeys Mosquito (Aedes  Yellow fever Vaccination of
aegypti) persons at risks
 After inoculation, (travelers)
the virus
replicates in
dendritic cells
st
West Nile Virus 1 reservoir – wild Culex, Aedes, West Nile encephalitis No vaccine, prevent
birds; horses, and Anopheles mosquito bites
dogs mosquitoes
St. Louis Primarily wild birds & Mosquitoes (Culex  St. Louis encephalitis Arthropod control
encephalitic virus domestic fowl spp.)  Fever to
meningoencephalitis
Dengue virus humans Mosquitoes  Classic dengue fever Vaccination
Zika Virus Unknown Mosquitoes  Possible Treatment:
(Aedes) complications:  related to
o Congenital symptom control
effects:
microencephaly Prevention and
and mental control:
retardation  No vaccine
o Autoimmune  Prevent
disease mosquito bite
Guillain Barre Syndrome:
demyelination of
peripheral nerves

Japanese encephalitis virus Compre:

Ma’am Tesalona notes:  Vector: Culex tritaeniorhynchus
 leading vaccine preventable cause of encephalitis o prefer breeding in rice paddies
in the Asia and Western Pacific region o usually bites during the night
 incubation period: 5-15 days after the bite of a
mosquito Yellow Fever virus
 more common during rainy season Ma’am Tesalona notes:
 fever, chills, headache, fatigue, nausea, and  Three different transmission cycles:
vomiting o Sylvatic cycle
Book (Mahon):  Yellow fever virus maintained in monkey
 most patient are asymptomatic populations
 disease ranges from flulike illness to acute  Transmitted by mosquitoes
encephalitis  Exists in the jungle
 children are mostly affected by this infection (as o Urban cycle
high as 30%)  Occurs in larger towns and cities
 mortality in adults is much lower  Transmitted by infected A. aegypti
mosquitoes to humans

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 o Intermediate cycle rash on the trunk, swollen lymph glands,
 Occurs in smaller villages in Africa and/or eye pain
 Reservoirs: humans and monkeys  Serious Neuroinvasive disease
 Reservoir and vectors in high-morbidity, o For ages greater than 50 years
low mortality outbreaks: mosquitoes o Typically manifests as meningitis or
 Mosquitoes can transmit yellow fever encephalitis
virus from monkeys to humans, and vice  Treatment:
versa o Supportive care for severe cases requiring
 Outbreak can be triggered when patients from hospitalization
intermediate cycle travel to larger cities and are  IV fluids, respiratory support, and
bitten by mosquitoes prevention of secondary infection
Book (Mahon):
 Considered an emerging infection St. Louis encephalitic virus
 still epidemic in parts of Africa and South America Ma’am Tesalona notes:
o The emergence results from increased  most common flavivirus infection in the US
spread of the mosquito vectors, deforestation (Eastern and Central States)
of Africa and South America, and increased  patients with SLE are most likely to be
travel to endemic regions asymptomatic
 Patients bitten by mosquitoes carrying yellow  Prodrome: fever, malaise, sore throat, and cough
fever virus can develop an asymptomatic or acute  Progresses to aseptic meningitis and/or
infection involving fever, myalgia, backache, encephalitis
headache, anorexia, nausea, and vomiting  milder in children than in adults
o Most recover after about 4 days
 older patients have the greatest risk of serious
o 15% enter a systemic toxic phase in which
illness and death
fever reappears
o Neuroinvasive disease: encephalitis in adults
 The kidneys may fail, and about 50% of
 Most infections occur in the summer months
patients in the toxic phase die.
 The other 50% recover without serious
sequelae Dengue virus
Compre: Ma’am Tesalona notes:
 Reservoir  Dengue virus has four serotypes: DENV1,
o Urban areas: humans are the reservoir hosts DENV2, DENV3, and DENV4
o Jungle: monkeys are the reservoir hosts o DENV3 (DEN-3) is the most prevalent
serotype in the Philippines
West Nile virus  Patient develops fever, headache, myalgia, and
bone pain
Ma’am Tesalona notes:
 Sometimes, there is petechiae
 virus replicates actively inside the avian host
 Classic Dengue fever is also called “breakbone
 Humans at the dead-end host of infection
fever”
o Virus does not replicate well in humans
o Develop fever, headache, myalgia, and
 Signs of viral meningitis:
bone/joint pain (resulting in the nickname
o Fever, headache, meningeal signs (e.g. neck
―breakbone fever‖)
rigidity)
o Some develop a rash
 Signs of Encephalitis o Mild disease
o Altered mental status o Occurs when patients bitten by mosquitoes
o Extrapyramidal symptoms carrying the virus
o Flaccid paralysis o Disease is self-limiting and often resolves in
 More common in summer months (possibility of 1 to 2 weeks
outbreaks)  Dengue Hemorrhagic Fever (DHF)
 fever, chills, headache, fatigue, nausea, and o Occurs when patients have already been
vomiting exposed to one serotype of dengue virus and
Book (Mahon): are then exposed to one of the other three
 First isolated and identified in 1937 from a febrile More severe and sometimes fatal
patient in the West Nile district of Uganda o Patients develop the symptoms of classic
 an ssRNA virus and member of the Japanese DF, along with thrombocytopenia, shock and
encephalitis antigenic complex, similar to SLE sometimes death.
 Most individuals infected with WNV are o Shock: sudden decrease in blood pressure
asymptomatic o Recovery from 1 serotype provides lifelong
 Some cases develop West Nile fever, immunity against that serotype but not to
o includes fever, headache, fatigue, occasional other serotypes.

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 o Severe dengue is potentially deadly due to:  White rash, reddish skin
 Thrombocytopenia  Usually appears on the legs and is very itchy
 Severe hemorrhage
 Plasma leakage Book (Mahon):
 Elevated hematocrit  two distinct diseases—classic dengue fever (DF)
 Hypoproteinemia/ hypoalbuminemia and dengue hemorrhagic fever (DHF)
 Decline in Hct (after volume  average mortality associated with DHF is 5%,
replacement)  Most deaths occur in children younger than 15
 Organ impairment years
 Treatment/Prevention: Compre:
o Combat vector mosquito  Vector:
o Classic DF: No specific treatment  Aedes aegypti
o Severe dengue/DHF: Maintenance of the o primary vectors,
patient‘s body fluid volume is critical to o tiger mosquitoes because of
severe dengue care characteristic alternating black and white
o Immunization: Dengvaxia (late 2015 and stripes
early 2016)  Aedes albopictus
 first dengue vaccine by Sanofi Pasteur o secondary vector
 given to people between 9 – 45 years old o both aegypti and albopictus prefer
breeding in clean stagnant water
 Most rapid spreading mosquito borne disease in
the world
o Spreading because of climate change

Zika virus
Ma’am Tesalona notes:
 MOT: can be passed from pregnant woman to her
fetus, vector bite, sexual contact vertical
transmission
 First isolated from rhesus monkey in Uganda
(1947)
 Common in South Africa and Brazil
 Typically endemic to parts of Africa and Asia
 Signs and symptoms similar to those of infections
with other arboviruses, such as chikungunya virus
(fever, headache, and fatigue, primarily)
 Fever, skin rashes, conjunctivitis, muscle and joint
 Febrile phase: fever pain, malaise, headaches
 Critical Phase: Platelets will only go down pag  Symptoms usually mild and last for 2-7 days
nawala na yung fever
 Incubation period is 12 days after the bite of
infected mosquito
Book (Mahon):
 an insect vector–borne disease
 most commonly transmitted through Aedes (A.
aegypti and A. albopictus) mosquitoes.
 Recent epidemic in Brazil has been marked by
the detection of the disease in fetal amniotic fluid
and an increased reporting of cases of
microcephaly (small head size) in newborns
o FDA give fast approval for a PCR-based
assay
o More rapid testing in pregnant women,
coupled with serology testing for both IgG
and IgM antibodies

Herman’s rash
 Good sign – sign of recovery from dengue

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 Togaviridae
 Genetic structure: +ssRNA, Linear
 Capsid: icosahedral
 contains the genera Alphavirus, Rubivirus, and Arterivirus
o No member of the genus Arterivirus is known to infect humans.
 Important virus:
o Group A: Alpha/Arbo virus: Mosquito-borne
 Western Equine Encephalitis virus (WEE)
 Eastern Equine Encephalitis virus (EEE)
 Venezuelan Equine Encephalitis virus (VEE)
 Chikungunya virus
o Group B: Rubivirus: Air droplets, inhalation
 Rubella virus – has no arthropod vector

Summary of important Togaviridae

Virus Description Diseases Prevention
Western Equine  Occurs on the west coast of the United  Western Equine  Arthropod
Encephalitis virus States Encephalitis control
(WEE)  Reservoir: Horses, birds  Nonspecific febrile  Avoid mosquito
 Vectors: Mosquitoes (Aedes aegypti illness bites
and Aedes albopictus)  No vaccine yet
Eastern Equine  Occurs primarily in the east of the  Eastern Equine for humans
Encephalitis virus Mississippi River (e.g., New York, New Encephalitis
(EEE) Jersey, Michigan)  Nonspecific febrile
 Reservoir: Horses, birds illness
 Vectors: Mosquitoes (Aedes aegypti
and Aedes albopictus)
 Dead end hosts: horses and humans
Chikungunya virus  Mainly occurs in Sub-Saharan Africa,  Chikungunya fever
Southeast Asia, and the Indian (co-infection with
subcontinent dengue possible)
o Derived from ―KIMAKONDE‖
language – to become contorted
 Reservoir: monkeys
 Vector: mosquito (Aedes aegypti)

Western Equine Encephalitis virus (WEE) Venezuelan Equine Encephalitis virus (EEE)
Ma’am Tesalona: Ma’am Tesalona:
 Also causes disease in humans and horses  Arthropod-borne, single-stranded, message-
 Causes a milder disease compared with EEE sense RNA virus
virus  Has caused large outbreaks of human and equine
 Patients develop an asymptomatic or mild encephalitis in the Americas.
infection  Death is much less common in patients than in
o Fever, headache, nausea, and mental status patients with WEE or EEE.
changes
Chikungunya virus
Eastern Equine Encephalitis virus (EEE) Ma’am Tesalona:
Ma’am Tesalona:  First describes in southern Tanzania in 1952
 Birds are the natural reservoir of the virus, which  Patients suffering from joint pain (arthralgia
is spread to humans and horses via bites of  MOT: mosquito bite – Aedes aegypti and Aedes
mosquitoes albopictus
 EEE in horses can be a predictor of human EEE  Also transmit dengue, yellow fever and zika
cases.  Outbreak in Africa, Asia, and Indian subcontinent.

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 Rubella Virus
 Is an enveloped virus belonging to the genus Rubivirus
 Rubella is a contagious viral infection best known by its distinctive red rash
 It is also called German measles or three-day measles
o a mild febrile illness accompanied by an erythematous, maculopapular, discrete rash with postauricular and
suboccipital lymphadenopathy
 Rubella can cause a miscarriage or serious birth defects in a developing baby if a woman is infected while she is
pregnant.
o The syndrome can cause effects ranging from birth of a normal infant to birth of a severely impaired infant, fetal
death, or spontaneous abortion
o rubella virus halts or slows cell growth
 The virus is present in the nasopharyngeal specimens or any secretion or tissue of infected infants, who shed the
virus in large amounts for long periods.
 A rash starts on the face and spreads to the trunk and limbs. No rash appears on the palms and soles
 Like measles, rubella occurs most frequently in winter and spring

RubeOla Rubella
 MOrbillivirus  Rash begins on the face and spreads
(Paramyxoviridae) cephalocaudally
 Rash appears at the o more on lymph node involvement.
hairline and spreads Usually, posterior auricular.
cephalocaudally over 3  More common form
days  Headache, low grade fever, sore throat and
 3C‘s: Conjunctivitis, (dry) coryza
cough, coryza, and fever o Coryza: runny nose or congested nose
 Koplik spots on buccal
mucosa Prominent:
 Lymphadenopathy
 Forchheimer spots on soft palate
o blue-violet spots (parang petechiae) on
soft palate

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 Ma’am Tesalona notes:
 May cause mild symptoms or even no symptoms in most people
 It can cause serious problems for unborn babies whose mothers become infected during
pregnancy
 Rubella spreads when an infected person coughs or sneezes.
 May spread the disease to others up to one week before the rash appears and remain
contagious up to 7 days after.
 25% to 50% of people infected with rubella do not develop a rash or have any symptoms
Prevention and control
 MMR (measles-mumps-rubella) vaccine:
o best protection against rubella
o protects against three diseases: measles, mumps, and rubella
o CDC recommends children get two doses of MMR vaccine
 first dose at 12 through 15 months of age
 second dose at 4 through 6 years of age
o Teens and adults also should be up to date on their MMR vaccination
o Very safe and effective
 One dose of the MMR vaccine is about 97% effective at preventing rubella.
Ma’am Tesalona notes:
 There is no specific medicine to treat rubella or make the disease go away faster.
 In many cases, symptoms are mild

QUESTIONS:
1. A 5 year old unvaccinated girl living in Tondo Manila was exposed to her classmate with fever and rash. Five
days later, she developed fever, dry cough, and redness of the eye, and on the seventh day had rashes on her
face. What is the most likely viral etiology?
A. Rubella virus
B. Rubeola virus

Important Virus Description Diseases Prevention

Rubi virus -  Only affects humans Congenital rubella Attenuated vaccine
Rubella virus  Transmission: air droplets and direct syndrome; German
contact measles
 Special features in virus transmission:
o Early viral shedding by the
infected individual
o Can cross the placenta
Ma’am Tesalona:
 Diseases:
o May lead to fetal death and spontaneous abortion
 Prevention:
o Live virus vaccine uses the weakened (attenuated) form of the virus
o Killed (inactivated) vaccines are made from a protein or other small pieced taken from a virus or bacteria
o The whooping cough (pertussis) vaccine is an example
o Toxoid vaccines contain a toxin or chemical made by the bacteria or virus
 Direct examination of specimens with IF or EIA is recommended
o Serologic procedures are effective because any rubella antibody is presumed to be protective.
o The most sensitive serologic assays are the solid-phase and passive hemagglutination tests.
o Latex agglutination and antigen-coated RBC tests are useful but less sensitive
o RT-PCR and end-point RT-PCR to detect rubella RNA - used by CDC but not FDA approved

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 Picornaviridae o Hepatovirus (Hepa A)
o Rhinovirus
 From the prefix ―pico‖ which designates a very o Parechovirus
small unit of measurement (equivalent to 10-12)
and RNA Ma’am Tesalona:
o describing very small RNA viruses  tropism to intestinal epithelial cells and
 Genetic structure: +ssRNA, Linear lymphoid cells of the gastrointestinal tract
 Capsid: icosahedral and neurons
 One of the largest families of viruses, with more  Infection is generally cytolytic, but persistent
than 280 members infections are common with some species
PICORNa: an acronym and reported with others
 P: poliovirus  Picornaviridae has four genera with human
 I: insensitivity to ether clinical significance belong to the family:
Enterovirus, Hepatovirus, Rhinovirus and
 C: coxsackievirus
Parechovirus
 O: orphan virus
 Enterovirus:
 R: rhinovirus
o Transient inhabitants of the
 Na: ribonucleic acid gastrointestinal tract and are stable at
acid pH
Ma’am Tesalona: o resistant/stable to pH 3 – 9, detergents,
 Picornaviruses are small, with RNA mild sewage treatment and heat
genome o transmitted primarily via aerosols, oral-
 Is a naked virus fecal, and fomites
 It contains many important human and o portal of entry is the alimentary canal
animal pathogens via the mouth
 Most picornaviruses for which the natural o prevalent in areas with overcrowding
hosts have been identified are specific for and poor sanitation
one, or a very few host species o no vaccines available
o Exceptions: foot-and-mouth disease o good personal hygiene and proper
virus (FMDV) and sanitation can reduce the incidence of
encephalomyocarditis virus (EMCV) enterovirus infections
 Members of some species can be grown in  ECHO
cell culture o Entero Cytopathogenic Human Orphan
 Resistant host cells (e.g., mouse cells in o Are being group together because they
the case of the primate-specific infect the human enteric tract
polioviruses) can often replicate virus RNA
(for a single round) by transfection with
naked, infectious RNA. Summary of Enteroviruses:
 Transmission is horizontal, mainly by fecal- Coxsackieviruses ECHOvirus Poliovirus
oral, fomite or airborne routes Coxsackie A Wide spectrum of  Neurotropic
o Transmission by arthropod vectors is  Herpangina diseases virus
not known  Hand, foot,  Conjunctivitis  Considered
o Mechanical transmission is possible and mouth  Myocarditis almost
 EMCV has been isolated from mosquitoes disease  Hepatitis eradicated -
and ticks, and poliovirus from flies  Pericarditis  Severe 2000
 Aseptic neonatal  Poliomyelitis
meningitis diarrhea  Flaccid
 MOT: fecal-oral route, Aerosol inhalation fomites
Paralysis lead
 Viral Genus: Coxsackie B  Along with to the
o Entero virus (Coxsackie A and B, ECHO  Myocarditis Coxsackie, destruction of
virus, Polio virus, HEV E, B, C and D)  Bornholm ECHOvirus is motor neurons
 Enteroviruses are transient inhabitants of disease considered in the spinal
the gastrointestinal tract, and are stable at  Pericarditis the leading cord
acid pH  Aseptic cause of

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 meningitis aseptic Prevention:  Serotypes are classified, depending on genus, by
 Pleurodynia meningitis  OPV is cross-protection, neutralization of infectivity,
 Herpangina preferred
 Treatment:  Inactivated by
complement-fixation, specific ELISA using a capture
no specific heat (55C) for format or immunodiffusion.
treatment 20 mins and  Most common type of poliovirus infection is
 Prevention: by a chlorine
inapparent or asymptomatic Infections
No vaccine  Not affected by
available ether or
sodium
deoxycholate Polioviruses: Types
Ma’am Tesalona:  Inapparent (sub-clinical) Infections:
 Poliomyelitis: is a disease of infancy
o Occurs approximately in 95% of poliovirus
and early childhood (infantile paralysis).
 Pleurodynia: a respiratory illness infection
characterized by severe lower thoracic o There are no presenting symptoms
pain o Recognition by isolation
 Herpangina: a mild self-limiting illness  Abortive Polio or Minor Illness:
characterized by fever, sore throat, and o Occurs approximately in 4-8% of the infection
small red vesicles at the back of the o Causes only a mild or self limiting illness due to
throat
viraemia
o Patient recovers quickly
Polioviruses

 Non paralytic polio

o Occurs approximately in 1% of all infections
o Presenting features are stiffness and pain in
neck and back
o Disease lasts for two to ten days
o Recovery is rapid
 Paralytic polio
o Occurs in less than 1% of infections
o Virus enters the brain and causes varying
degree of disability

Polioviruses: Causes Poliomyelitis

 The poliovirus is rapidly inactivated by heat,

formaldehyde chlorine, and ultraviolet light
 There are three poliovirus serotypes (P1, P2 and
P3)
 There is minimal heterotypic immunity between the
three serotypes
o immunity to one serotype does not produce
significant immunity to the other serotypes.
 Incubation period is 7 to 14 days
 Tend to infect the CNS and can cause paralysis in a
small percentage of infected individuals
 The viruses destroy their host cells
 In the intestines, damage is temporary because the
cells lining the gut are rapidly replaced
 In contrast, neurons are not replaced, which results
in neuron death and permanent paralysis.

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 Poliomyelitis Pathogenesis:  Severe muscle aches
o Entry into mouth  Spasms in the limbs or back
o Replication in pharynx, GI tract  Generally, no further paralysis occurs after
o Hematologic spread to lymphatics and central the temperature returns to normal
nervous system  Prodrome may be biphasic, especially in
o Viral spread along nerve fibers children, with initial minor symptoms
 Destruction of motor neurons separated by a 1-to-7-day period from more
o Humans are the only known reservoir of major symptoms.
infection  The illness progresses to flaccid paralysis
 Clinical Features: with diminished deep tendon reflexes,
o Response to poliovirus infection is highly reaches a plateau without change for days
variable and has been categorized on the basis to weeks, ang is usually asymmetrical.
of severity of clinical presentation Strength then begins to return.
o Incubation period for nonparalytic poliomyelitis  Patients do not experience sensory losses
is 3-6 days. or changes in cognition
o For the onset of paralysis in paralytic o Paralytic polio
poliomyelitis, the incubation period is 7 to 21  Many persons with paralytic poliomyelitis
days recover completely and, in most, muscle
o Nonparalytic aseptic meningitis function returns to some degree.
 Symptoms: stiffness of the neck, back,  Weakness or paralysis still present 12
and/or legs months after onset is usually permanent.
 Usually following several days after a  Paralytic polio is classified into three types,
prodrome similar o that of minor illness depending on the level of involvement
 Occurs in 1%-5% of polio infections in  Spinal polio
children o Most common
 Increased abnormal sensations can also o 1969-1979, accounted for 79% of
occur paralytic cases
 Symptoms will last from 2 to 10 days, o Characterized by asymmetric
followed by compete recovery paralysis that most often involved
o up to 72% of all polio infections in children are the legs
asymptomatic  Bulbar polio
o Infected persons without symptoms shed virus o leads to weakness of muscles
in the stool and are able to transmit the virus to innervated by cranial nerves
others. o accounted for 2% of cases during
o Abortive poliomyelitis this period
 Approximately 24% of polio infections in  Bulbospinal polio
children consist of a minor, nonspecific o A combination of bulbar and
illness without clinical or laboratory evidence spinal paralysis
of CNS invasion. o Accounted for 19% of cases
 Characterized by complete recovery in less o Death-to-case ration is generally
than a week and a low grade fever and sore 2%-5% among children and up to
throat. 15%-30% for adults (depending
o Flaccid paralysis: on age). Increases to 25%-75%
 Fewer than 1% of all polio infections in will bulbar involvement.
children Polioviruses: Prevention and Control
 Paralytic symptoms begin 1 to 18 days after o Inactivated Polio Vaccine (IPV)
prodromal symptoms and progress for 2 to 3  Contains 3 serotypes of vaccine virus
days  Grown in monkey kidney (vero) cells
 Additional prodromal signs and symptoms  Inactivated with formaldehyde
can include:  Contains 2-phenoxyethanol, neomycin,
 Loss of superficial reflexes streptomycin, polymyxin B
 Initially increases deep tendon reflexes o Oral Polio Vaccine (OPV)

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 contains 3 serotypes of vaccine virus  Paralytic poliomyelitis (OPV)
grown in monkey kidney (vero) cells o Polio Vaccinations of Unvaccinated adults
contains neomycin and streptomycin  use standard IPV schedule if possible (0, 1-2
shed in stool for up to 6 weeks following months, 6-12 months)
vaccination  May separate first and second doses by 4 weeks
 for mass immunization if accelerated schedule needed
 for the WHO poliovirus eradication campaign  The minimum interval between the second and
 normal response rate to OPV is close to 100% third dose is 6 months
o IPV Efficacy o Polio Vaccinations of Previously vaccinated
 Highly effective in producing immunity to adults
poliovirus  Previously complete primary series of three or
 90% or more immune after 2 doses more doses
 At least 99% immune after 3 doses  Administer 1 dose of IPV
 Duration of immunity not known with certainty  Incomplete series
o OPV Efficacy  Administer remaining doses in series
 Highly effective in producing immunity to  No need to restart series
poliovirus o Vaccine-Associated Paralytic Poliomyelitis
 Approximately 50% immune after 1 dose  More likely in persons, 18 years of age and older
 More than 95% immune after 3 doses  Much more likely in persons with
 Immunity probably lifelong immunodeficiency
o Polio Vaccination Recommendation, 1996-1999  No procedure available for identifying persons at
 1996: Increased use of IPV (sequential IPV-OPV risk of paralytic disease
schedule) o Polio Eradication
 Intended to reduce the risk of vaccine-associated  Last case in United States in 1979
paralytic polio (VAPP)  Western hemisphere certified polio free in 1994
 Continued risk of VAPP for contacts of OPV  Last isolated of type 2 poliovirus in India in
recipients. October 1999
 Schedules that include both IPV and OPV  Global eradication goal by the year 2000
 Only IPV is available in the US  Adopted by the WHO assembly (1988)
 Schedule begun with OPV should be  Goal not achieved, but substantial progress
completed with IPV has been made
 Any combination of 4 doses of IPV and OPV  Post-Polio syndrome
by 4-6 years of age constitutes a complete o After an interval of 15-40 years, 25%-40% of
series persons who contracted paralytic poliomyelitis
in childhood experience new muscle pain and
Polio Vaccination Schedule exacerbation of existing weakness, or develop
Age Vaccine Minimum Interval new weakness or paralysis
2 months IPV --- o Factors that increase the risk of post-polio
4 months IPV 4 weeks
syndrome include:
6-18 IPV 4 weeks
months  Increasing length of time since acute
4-6 years IPV 6 months poliovirus infection
 Presence of permanent residual impairment
o Combination Vaccines that contain IPV after recovery from the acute illness
 Pediarix: DtaP, Hepatitis B and IPV  Female sex
 Kinrix: DtaP and IPV o The pathogenesis of post-polio syndrome:
 Pentacel: DtaP, Hib and IPV involve the failure of oversized motor units
o Polio vaccine contraindications and Precautions: created during the recovery process of paralytic
 Severe allergic reaction to a vaccine component poliomyelitis
or following a prior dose of vaccine o Post-polio syndrome is not an infectious
 Moderate or severe acute illness process, and persons experiencing the
o Polio Vaccine Adverse Reactions syndrome do not shed poliovirus.
 Local reactions (IPV)

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 Polio-like virus: Enterovirus D68 o Prevention: inactivated vaccine for persons at
 First identified in California 1962 risk and travelers to endemic regions
 Is one of more than 100 non-polio enteroviruses o Disease: Hepatitis A
 Beginning in 1987, small numbers of EV-D68 had o Risk factors for HAV infection include:
been reported to CDC regularly  Sexual or household contact with an
 Outbreaks have been detected between August and infected person, daycare contacts,
November 2014, 2016, and 2018 foodborne or waterborne outbreaks, IV drug
 Can cause mild to severe respiratory illness, or no use, and international travel
symptoms at all o Incubation period: approximately 1 month
o Mild symptoms: runny nose, sneezing, cough,
body aches, and muscle aches Rhinovirus: Viral Genus of Picornaviridae
o Severe symptoms: wheezing and difficulty in  Rhinovirus
breathing o more than 110 serotypes
 MOT: respiratory/ air droplets o very high incidence
o Found in infected person‘s respiratory o MOT: airborne, secretions and fomites
secretions, such as saliva, nasal mucus, or o Proliferation is limited to local portals of entry
sputum (nasopharyngeal epithelium)
o Spreads from person to person o Attaches to ICAM-1 receptors (CD54) on
 In general, infants, children and teenagers are most respiratory epithelial cells
likely to het infected with enteroviruses and become o Acid labile, grows at 33C, pH (<6), resistant to
ill detergents, lipid solvent and extreme
o No immunity (protection) from previous temperature
exposures to these viruses o Diseases:
o Children with asthma may have higher risk for  Complications of rhinovirus infection include
severe respiratory illness caused by EV-D68 otitis media, sinusitis, chronic bronchitis, and
infection exacerbations of reactive disease in children
 Adults can get infected but are more likely to have and adults
no symptoms or mild symptoms.  Major cause of acute respiratory disease in
both children and adults
Ma’am Tesalona:  Clinical spectrum can range from
 No specific viral therapy asymptomatic to more severe lower
 Passive immunity transferred from mother to respiratory tract illness such as obliterative
offspring but gradually disappear after 6 months bronchiolitis and pneumonia
 Serologic studies have shown that seroconversion  Rhinitis and common colds among children
following three doses of either IPV or OPV is o Treatment: self-limiting, supportive treatment
nearly 100% to all three vaccine viruses
 Seroconversion rates after three doses of a Parechovirus: Viral Genus of Picornaviridae
combination of IPV and OPV are lower,
 Parechovirus
particularly to type 3 vaccine virus (as low as
85%) o Contains 16 types, designated human
 A fourth dose (most studies used OPV) usually parechoviruses (HpeV) 1-16
produces seroconversion rates similar to three o HPeV3 is associated with neonatal sepsis and
doses of either IPV or OPV meningitis
o Highly divergent from enteroviruses
o Diseases:
Hepatovirus: Viral Genus of Picornaviridae  Often acquired in early childhood
 Hepatitis A virus (HAV)  Disease similar to enteroviruses
o High infection rate from infected water and  Mild gastrointestinal and respiratory
food, particularly in subtropical and tropical illness
regions  Meningitis
o Transmission: fecal-oral, close personal
 Neonatal sepsis
contact or contaminated food
o Lab diagnosis: PCR
o No chronicity
o Specimens: similar to enteroviruses
o Treatment: supportive treatment

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Post-test:
1. Coronavirus displays a viral tropism for
epithelial cells of the RT and GIT
2. The confirmatory test for SARS-CoV-2. RT-
PCR
3. Incubation period of SARS-CoV-2. 14 days
4. Chikungunya virus belongs to what family of
viruses? Togaviridae
5. Also known as ―break bone‖ fever. Dengue
fever

REEFERENCES:
Unit 3: RNA Viruses: Positive Strand or Sense Strand ssRNA
Department –Sanctioned PPT
Recorded Lecture by Prof. Sherill D. Tesalona, RMT, MSMT

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 UNIT IV: Negative Sense Single-Stranded RNA Viruses

Pre-Test o A (-) RNA template is used for replication, For

1. (T/F) Clinically significant Arenaviruses are Togaviruses, Coronaviruses and Caliciviruses,
recommended to be detected using viral early proteins are translated from the genome
culture methods. ________ and late proteins from smaller mRNAs
2. Members of the bunyaviridae have ________ transcribed from replate.
segments in their genome. • Orthomyxoviruses, Paramyxoviruses,
Rhabdoviruses, Filoviruses and Bunyaviruses
3. The rabies virus attaches to the
o (-) RNA genome is a template for individual
______________ receptor.
mRNAs, but full-length (+) RNA template is
4. The most common way to get infected by the required for replication. Orthomyxoviruses
filoviruses is through _____________. replicate and transcribe in the nucleus, and each
5. Minor changes in the antigenic structure of segment of the genome encodes one mRNA and
influenza viruses are called an antigenic is a template.
____________. • Reoviruses
o (+/-) Segmented RNA genome is a template for
(-) ssRNA = Negative Sense single stranded RNA virus
mRNA (+ RNA) may also be encapsidated to
generate the (+/-) RNA and then more mRNA.
Properties of RNA Viruses
• Retroviruses
From: Medical Microbiology by Murray – 8th edition
o (+) Retrivirus RNA genome is converted into
• RNA is labile and transient
DNA which is integrated into the host chromatin
o When the virus uncoats, the RNA is very much
and transcribed as a cellular gene.
labile, madali siya madedegrade unlike DNA
viruses that are stable which contribute to their Doc Miguel Cajipe – Asynchronous Lec
ability to produce latent infections while RNA
viruses do not produce latent infections. Remember:
• Most RNA viruses replicate in the cytoplasm. All (-) sense RNA viruses are enveloped viruses.
• Cells cannot replicate RNA. RNA viruses must
encode an RNA-dependent RNA polymerase. Tips:
o RNA viruses, except for the (+) strand, must Master the generalities of every virus or the viruses that are
carry polymerases. known to infect humans. You have to be familiar with the
o These (-) stranded RNA don’t look like mRNA how they infect humans. Most of them follow the same
pattern with a few exceptions. When studying individual
so they are required to have polymerases to
viruses, you have to apply these generalities to these
replicate.
individual virus families and take know if it applies to them or
• The genome structure determines the mechanism of not. Also take note the differences per family of the virus.
transcription and replication
• RNA viruses are prone to mutation. Viral Protein Synthesis
o Because they are labile, transient and unstable
which makes them prone to mutations.
o Especially seen in Orthomyxoviruses
• The genome structure & polarity determines how
viral mRNA is generated and proteins are processed
• Piconaviruses, Togaviruses, Flaviviruses,
Caliciviruses and Coronaviruses
o (+) RNA genome resembles mRNA and is
translated into a polyprotein, which is
proteolyzed. ARENAVIRUS
Doc Miguel Cajipe – Asynchronous Lecture Mode of Transmission
• Inhalation of aerosols of infected rodent excrement
• Focus on the rhabdo until filo part o Urine
• Visual representation of some the generalities you o Feces
will encounter in this unit: viral genome o Saliva
reproduction and viral protein synthesis. o nasal secretions
• Remember (-) sense RNA cannot be translated • Direct contact with the rodents
into proteins RNA directly as compared to (+) o Getting bitten by a rat infected and its saliva
sense RNA. enters your bloodstream and that’s how you
become infected with this virus.
• (-) sense RNA should be first translated into a
template that looks like mRNA to be able to
translate it.
• All of the viruses we will describe here has this
particular characteristic.

Basic Characteristics

• Animal reservoir: rodents (rats)

• Clue on prevention: Control rodents in your area

Pathogenesis
• Infects macrophages
• Induces cytokine and interferon release
o This is the time where you will experience the
usual symptoms of any viral infection like
• Spherical headache, fever and joint pain which are the
• Enveloped primary inflammatory response of your body.
• ssRNA o When there is release of the cytokine and
• Have T-shaped glycoprotein spikes interferon, it would cause your body’s
• Clinically significant environment to become unfriendly or
o There are many members of this family but we unfavorable to the virus.
will only focus on these 2: o Again, RNA viruses are labile so if the virus had
▪ Lymphocytic Choriomeningitis Virus (LCM) already released the genome, and the body’s
▪ Lassa Virus condition makes it unfavorable for the virus, that
• Virions contain two single-stranded RNA circles may lead to the degradation of the RNA. That’s
o L-strand – negative sense RNA that encodes the one way our bodies protect us from viral
polymerase infections.
o S-strand – ambisense RNA which encodes • Promotes cell and vascular damage
glycoprotein and nucleoprotein o Because our immune system is not perfect, there
Ambisense means that it can be a positive or a are times that the body’s environment is still
negative sense strand. There are certain conditions favorable for the virus then the usual viral
that will allow it to translate into protein right away replication will proceed and once the cycle is
but there are also conditions where it will not done, cell and vascular damage occurs.
behave like a positive sense RNA virus. • Incubation period: 10-14 days
• Replicates in the cytoplasm o Day 7-9 - experience some of the symptoms
• Acquire their envelope by budding from the host cell o Day 10 – symptoms will be more prominent
membrane o Almost similar to SARS-Cov-2
o Host cell membrane derived enveloped
• Can cause persistent infections due to ineffective
transcription of glycoproteins which result to poor
virion assembly

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 Additional notes from Trans team yayy

Viral hemorrhagic fevers (VHFs) are a group of illnesses

caused by four families of viruses. These include the
Ebola and Marburg, Lassa fever, and yellow fever
viruses. VHFs have common features: they affect many
organs, they damage the blood vessels, and they affect
the body's ability to regulate itself.

Pathophysiology
• Broad range of symptoms Clinically Significant Groups
o Asymptomatic • Lymphocytic Choriomeningitis Virus (LCM)
▪ Patients with good immune system can o Contributed to a proportion of the cases of
remain asymptomatic meningitis in Europe
o Non-specific symptoms • Lassa Virus
▪ Fever, headache, vomiting o Originated from Lassa, Africa
▪ Effect of cytokine and interferon release o Causes a clinical syndrome of hemorrhagic fever
▪ Looks like other viral symptomatology
(similar as to how flu and HIV induces the E.g. you have data that arenavirus is common in an area
same symptoms) and a patient has hemorrhagic fever, most probably the
▪ It’s hard to differentiate if you rely only on patient has Lassa virus. But if meningitis, headaches and
clinical symptoms because all of them mahirap galawin yung neck, most probably it is LCM.
would produce a non-specific symptom
• Severe cases exhibit a clinical syndrome of Treatment
hemorrhagic fever • Ribavirin
o Other viruses will also produce hemorrhagic o Limited activity
fever o (Doc Miguel kwento) Usually we give antivirals
o When you say syndrome, it is a collection of when severe and nakikita naming mamamatay
signs and symptoms that the patient might na yung patient. It’s usually the last-ditch effort
experience. (fancy term for a desperate final attempt) to save
o Usually in hemorrhagic fever, of course you have the patient’s life. But pag wala pa naman siya sa
fever (lol) and then you will have hemorrhage bingit ng kamatayan, super supportive
(didn’t see that one comin did ya). Blood vessels will treatments are given.
somewhat weaken and that will allow the Supportive treatments – ‘pag nilalagayan na ng
extravasation (fancy word for leakage of a fluid swero, blood transfusion is given because of blood
out of its container into the surrounding area) of loss, antibiotics given when there is concomitant
blood. bacterial infection (usually in meningitis, there is
o Like in Dengue fever, you will have bruises, nose bacterial infection also)
bleed, vomiting of blood. • Pest control
o You will also have headaches, joint pain and o Because there is no definitive treatment, pest
abdominal pain. control nalang, diba?
o You don’t need to complete the symptoms for it o Rats and cockroaches, they usually go to areas
to be called a syndrome. where there is food so practice proper food
▪ E.g. we become critical when the patient storage, clean your houses so you will not attract
has fever and nose bleeds but has no these rodents.
abdominal pain yet, we say, “ay hindi pa yan o You need prevention. Mortality rate is high (from
hemorrhagic fever (syndrome)” – it doesn’t what doc miguel has read, from Mahon it’s 15%)
work that way
▪ You only need 2-3 symptoms to say that it Mahon additional notes
is a hemorrhagic syndrome • arena – Latin for sand - appear sandy & granular
▪ Buttt, there are symptoms that must always under electron microscope
be present: fever and hemorrhage (hence the
name lmao)

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 Mahon additional notes • Envelope – Has two glycoproteins.
• The first arenavirus found to cause hemorrhagic Both enclose 3 unique (-) ssRNA
fever was the Junin virus, which causes Argentine o G1
hemorrhagic fever. o G2
• Pet hamsters are also reservoirs. Humans • Doesn’t have a matrix
become infected when they inhale the aerosolized • L-protein – Nucleocapsid
virus or come into contact with fomites.
Doc Miguel
• LCM virus causes an influenza-like illness; about
These characteristics may have implications in the
25% of infected patients develop meningitis
laboratory diagnosis because these parts of the
• Lassa virus is mostly community-acquired,
virions can be antigenic targets for your lab tests that
primarily by contact with excretions from the
would be more emphasized in MycoViro Lab
multimammate rat Mastomys natalensis, which
sheds the virus throughout its life once infected. General Pathophysiology
• Lassa virus is present in throat secretions, can be • G1 protein interacts with the Beta-integrins on the cell
transmitted from person to person, and can also o No particular cell mentioned so any cell with
be transmitted through sexual contact and beta-integrin will be a potential target.
nosocomially. • Virus is endocytosed
• If therapy begins within the first 6 days of • Virions are assembled by budding into the Golgi
exposure, Lassa virus can be effectively treated apparatus and are released via cell lysis or exocytosis
with the antiviral drug ribavirin. o Either sisirain niya yung cell or ilalabas siya nung
• Diagnosis of Lassa virus is typically by ELISA to cell mismo
detect IgM and IgG antibodies. • Therefore, Bunyaviruses are lytic viruses
o Sinisira niya yung cell but not all the time
because exocytosis may also occur
BUNYAVIRIDAE
Clinically Significant Groups
ARBOVIRUSES
• California Encephalitis Virus
• Lacrosse Virus
• Cache Valley Virus
• Jamestown Canyon Virus
• Rift Valley Virus
• Snowshoe Hare Virus
Pathology
• Arthropod-borne (mosquitoes)
• Replicates initially in the gut of the arthropod vector
Basic Characteristics and eventually appears in the saliva.
• Has three single-stranded RNA segments o Similar to dengue
• Genome enclosed in a helical nucleocapsid • Transmission is through the bite of the arthropod
surrounded by a lipid envelope vector via the bite
• Has 300 total members. 12 are known human
Mahon additional notes
pathogens largely under the family of Arboviruses
• The arthropod transmits the virus when feeding on
o Human pathogens = clinically significant
the blood of vertebrate hosts (ex. humans)
• Can be reclassified into 2:
• After a few days, the infected host usually
o Arthropod-borne (Arboviruses):
develops an asymptomatic viremia; however,
Orthobunyavirus, Phlebovirus, Nairovirus
some hosts become febrile, which is far less
o Rodent-borne: Hantavirus
common.
• Roughly spherical
• 90-120 nm in diameter
• Once pumasok na siya, it will integrate in cells that
have B-integrins (medyo marami rami). Once andyan
na siya, pag nagkaroon na ng cell lysis, and there is

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 a significant amount of virus inside the body, it will Mahon additional notes
produce cytokines and interferons which will produce
the clinical manifestations. Lacrosse Virus
• Clinical Manifestations • Incidence is underestimated because the
o Febrile Illness disease manifests as a nonspecific fever,
▪ Not really that specific, some viruses also headache, nausea, vomiting, and lethargy.
induce febrile illness • Commonly found in children and usually
o Hemorrhagic Fever develops in the summer, frequently referred to
▪ A little bit similar to arenaviruses and medyo as the summer flu or summer cold
mahirap i-differentiate from dengue.
o Encephalitis
▪ Goes to the brain parenchyma, in the
Laboratory Testing
cerebrum, cerebellum as compared to
• PCR Testing
meningitis that goes to meninges
▪ Doc Miguel chika: Ang hinahanap ko dyan • Serologic Testing
ay yung decreased sensorium, para bang These tests will be emphasized during laboratory class.
hindi na matino kausap yung patient or
tututlog tulog HANTAVIRUS
▪ They make their way to the brain through • Rodent-borne family of Bunyaviridae
our blood stream • Halos parehas ng arenaviruses
• Rift Valley Virus Transmission
o Brain and Liver are the primary targets causing • Rodents (Urine and Feces)
encephalitis and hepatitis. • Risk factor: contact with deer mouse droppings
• Lacrosse (LACV) & California Encephalitis Virus
o Also causes encephalitis and Crimean-Congo
Hemorrhagic Fever (CCHF)
o CCHF is a clinical syndrome
▪ When you have data that talamak yung
arboviruses and madaming lamok tapos
nangkaroon ng hemorrhagic fever, most
probably ang kalaban natin ay itong
Lacrosse and California Encephalitis
▪ Hindi rin malayong mangyari na magkaroon
ng encephalitis and hemorrhagic fever yung
patient Pathology
• Hemorrhagic Fever with Renal Syndrome (HFRS)
Mahon additional notes o Evidence of kidney damage
o Renal syndrome: umiihi ng dugo, nagmamanas
Crimean-Congo Hemorrhagic Fever (CCHF) o Caused by the following members:
• infects the vascular endothelium and liver and ▪ Hantaan virus
cause high-morality infection in humans ▪ Seoul virus
• begins with fever, myalgia, arthralgia, and ▪ Puumala virus
photophobia ▪ Dobrava virus
• patients develop mental status changes, ranging • Hantavirus Pulmonary Syndrome (HPS)
from confusion and agitation to depression and o Symptoms: coughing of blood, nahihirapan
drowsiness huminga
• petechiae and ecchymoses can form on o Sin Nombre Virus
mucosal surfaces and on skin. The ▪ Sin Nombre (Spanish or more Mexican daw
• patient may bleed from the bowel, nose & gums sabi ni doc) means “no name” bc history:
• About 30% of the patients die. Others begin wala daw sila matawag kaya no name nlng
recovering after about 10 days of illness.

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 HANTAVIRUSES THAT CAUSE HPS (Table 29-6, Mahon) Mahon additional notes

Hantavirus Host Location • Hantaviruses typically affect the peritoneal

Peromyscus cavity, kidneys, thoracic cavity, or lungs.
United States,
Sin Nombre maniculatis
(deer mouse)
Western Canada • Hantaviruses endemic to Europe and Asia are
Sigmodon called Old World hantaviruses
Black Creek United States,
Canal
hispidus
South America • Puumala hantavirus is the most common
(cotton rat)
member of this genus in Europe and causes a
Oryzomys palustris Southeastern mild form of HFRS: nephropathia epidemica
Bayou
(rice rat) United States
• The mortality rate for HFRS is 1% to 15%
Peromyscus
Monongahela maniculatis
Eastern United • Sin Nombre virus is transmitted by inhaling
States
(deer mouse) contaminated aerosolized mouse urine, saliva,
Peromyscus and feces.
leucopus
New York
(white-footed
New York • Generally, person to person transmission does
deer mouse) not occur with hantavirus.
Oligoryzomys • Patients with HPS have a 3- to 5-day febrile
Oran Argentina
longicaudatus prodrome, with fever, chills, and myalgia.
Oligoryzomys • Patients then enter a phase of hypotensive
Andes Argentina, Chile shock and pulmonary edema. The patient
longicaudatus
develops tachycardia, hypoxia, and hypotension.
Oligoryzomys
Lechiguanas
flavescens
Argentina • Severe cases: patient can develop disseminated
intravascular coagulation.
Calomys laucha
Laguna Negra
(vesper mouse)
Paraguay, Bolivia • Mortality rate for HPS is about 50%.
• Treatment: Primarily supportive
Laboratory Testing
RHABDOVIRIDAE (cont.)
• PCR
• Proteins
• Enzyme Immunoassays
o L and NS – RNA-dependent RNA
o Mahon: detect anti-SNV IgM and IgG antibodies,
Polymerase
which may provide some useful information on
o N protein – Main structural protein
infection
o M protein (Matrix)
• Immunohistochemistry G protein – attachment protein
o Tissue samples from lungs
o Mahon: sensitive method used to detect
hantavirus antigens in capillary endothelium.
A high concentration of antigens is found in
capillary tissue from the lung.
Again, will further discussed in lab class. 😊

RHABDOVIRIDAE

General Characteristics
• Known to infect fishes, plants, and arthropods.
• Family: Vesiculovirus, Lyssavirus
• Virion
o (-)ssRNA Pathogenesis
o Helical nucleocapsid surrounded by a • G protein attaches to the acetylcholine receptors
lipid bilayer envelope (AcHR) (found in neurons), neural cell adhesion
o Have spike-like projections on the molecule (NCAM) or other molecule in the neurons.
surface. o Predominantly, Rhabdoviridae loves to attach
o Bullet-shaped/cone appearance (in
electron micrographs)

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• Viral envelopefuses with the membrane on the on the o Rabies Immunoglobulin for Category 2
endosome on acidification of the vesicle. or higher wounds.
• Endosomal vescles then transport virions along o Ideally, it should be administered few
the axon to the neuronal cell bodies. hours (or earlier) after the bite
o Retrograde movement (from axon o Post-exposure or pre-exposure
towards the cell body) prophylaxis are both effective

Rabies Virus
• Neurotropic (loves neurons 3>)
• Found in the saliva of the infected individual
(whether dogs, cats, humans, or bats)
• Can also be transmitted via aerosols

FROM DOC MIGUEL

Because rabies can be transmitted via aerosols, in
hospital setting, di pwedeng tubuhan yung
pasyente kasi kapag nilagyan ng tube yung
trachea niya, and binomba natin using ventilator,
magkakaroon ng aerosols.

• Initially infects the skeletal muscle and peripheral

nerves.
• Retrograde transport in the nerves until it reaches
the central nervous system FILOVIRIDAE
• The virus then multiplies in the CNS neurons then
General Characteristics
spread in the peripheral nerves and some non-
nervous tissues (e.g. salivary glands) • Considered the most pathogenic of the
hemorrhagic fever viruses
• Incubation Phase –60-365 days (2 months to 1
o Fast disease progression
year) after exposure
o Because of fast disease progression,
• Prodrome Phase –2-10 days
doctors have little time to react to cure
• Neurologic Phase –“Hydrophobia” –2-7 days
the patient
• Coma
• Virion
• Death
o Pleomorphic
FROM DOC MIGUEL ▪ It varies in shape; unusual
• “Hydrophobia” – unusual reaction of the larynx shape
of the patient to water; magsasara (spasm) o Enveloped
yung lalamunan (larynx) kapag nakatouch ng o Negative sense ssRNAnon-segmented
tubig so mahihirapang uminom yung patient o Filamentous morphology (hence the
• The disease progression varies extremely term “filo”-virus)
• Prevention is better because there is no cure • RNA genome encodes 7 proteins
• Nucleocapsid is helical and enclosed in an
envelope containing one glycoprotein (GP)
Laboratory Diagnosis
• The GP is cleaved into 2 components
• Postmortem
• Members that are clinically significant:
o Direct immunofluorescence assay
o Marburg Virus
o Negri bodies in the brain tissue –
o Ebola Virus
Hippocampal area
• Post-exposure prophylaxis is a must
• Pre-exposure prophylaxis for veterinary clinic
workers
• Prophylaxis:
o Anti-Rabies Vaccine

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 FROM DOC MIGUEL
• To make matters worse, the
glycoprotein (of the virus) can inhibit
neutrophil activation. So pag walang
neutrophil, walang papatay sa virus.
• The interferons will make harsh
environment for the virus. So pag
walang interferons (due to inhibition by
the viral proteins), magbblunt (hihina)
yung immune system, so di kaagad
makakareact yung immune system to
Pathogenesis fight the virus.
• Virus binds to Niemann Pick C1, a cholesterol
transfer protein and T-cell immunoglobulin and Marburg Virus
mucin domain 1 (TIM-1) • Reservoir is unknown but believed to be native
o Niemann Pick C1 – love ng Filoviridae in Africa
• The virus enters the cell and replicates in the • Monkeys are believed to be the reservoir
cytoplasm like the Rhabdoviruses • Transmission: Nosocomial (hospital-acquired)
o However, ang pinagkaiba is HINDI transmission, casual contact, sexual contact
LOVE ng Rhabdovirus si Niemann Pick • Clinical features: Hemorrhagic fever syndrome
C1 </3 (di kasi siya yung receptor niya) Laboratory Diagnosis
• Virus replicates in the endothelial cells, • Polymerase Chain Reaction
*monocytes, *macrophages, *dendritic cells and • Immunohistochemistry
other cells (*cells involved in Innate Immune • IgM-capture ELISA
System)
• Replication in monocytes triggers a cytokine Ebola Virus
storm (thus producing non-specific symptoms) • Species: EBO-Z (most virulent), EBO-S and
• Cytopathogenesis –Extensive tissue necrosis in EBO-R. EBO-Z is the more virulent species.
the parenchymal cells of the liver, lungs, spleen • No definite reservoir although the first
and lymph nodes. documented reservoir is a human.
• Vascular injury ensues and the virus prevents • Virus is mainly transmitted nosocomially.
production of cell adhesion proteins • Clinical Features: Hemorrhagic fever syndrome
• The glycoproteins can inhibit neutrophil with prominent bleeding from the injection sites
activation and gastrointestinal organs.
• Viral proteins can also inhibit interferon
production and action Laboratory Diagnosis
• PCR
FROM DOC MIGUEL
• Immunofluorescence
• Because nagrereplicate rin siya sa
• Viral Culture
endothelium, magkakaroon ka ng
vascular injury (yung part ng tunica
media). So masisira yung tunica media,
masisira yung blood vessel, and it will
also prevent the production of cell
adhesion proteins so talagang sisirain
niya yung endothelial layer ng tunica
media.
• Kapag nasira yung tunica media,
definitely, blood will extravasate
(tatagas). So, magkakaroon ka talaga
ng hemorrhagic fever.

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 ORTHOMYXOVIRIDAE • Attacks mainly the URT of very young and old, patients
GENERAL CHARACTERISTICS with comorbidities, debilitated individuals
• Major human respiratory tract pathogen (flu) –
FROM SIR BENJIE
worldwide epidemics.
Ididiscuss ulit natin Hemagglutinin however there are
• 3 genera within the family: Influenza A, B, and C
some differences kasi meron tayong different variants
• Pleomorphic
of hemagglutinin unlike paramyxoviridae usually isa
• Spherical lang. Dito umaabot siya ng 16 variants or 16
• Icosahedral capsid subtypes, which will also be used as a marker to
• Enveloped determine the type of influenza virus.
• Segmented (-)ssRNAgenome
• A major human respiratory tract pathogen

FROM SIR BENJIE

• Tagalog ng influenza is trangkaso
• Approximately, 20% of the world population gets
infected with the Influenza virus each year
• 3-5 million cases of severe illness worldwide
• 250,000-500,000 deaths worldwide
• Usually affected are the very old and very young
people Surface Glycoproteins
Hemagglutinin (HA)
•
Hindi lang masyadong focused ang mundo sa
influenzapero kung titignan mo nakakatakot din • Major surface glycoprotein (80%)
kasi marami din namamatay. Usually and • “Rod-shaped glycoprotein/peplomer
naapektuhan ay mga very old and very young • Ability to agglutinate RBCs under certain conditions
people. • Involved in viral neutralization
• ssRNA, (-) sense genome, Enveloped, Icosahedral o Viral entry of the virus into the host cell
capsid • Cellular Receptor binding site – attachment to the
o 8 separate segments – Influenza A and B “sialic acid receptor”
o 7 separate segments – Influenza C (not considered o It has a high viral tropism to the sialic acid
as pathogenic as the A and B) receptors.
• Compared with the paramyxoviridae that are non- • Stalk
segmented, the Orthomyxoviridae are segmented. • 16 subtypes: H1-H16
• Internal Structural Proteins: found in the viral o H1-H3 – most common human
envelope and stabilizes the HA and NA glycoproteins infections
• Yung internal structural proteins medyo may • All influenza subtypes contains HA
similarities siya sa paramyxoviridae.
o Nucleocapsid protein (NP) – forms the viral
nucleocapsid
o Matrix (M) protein – 2 matrix proteins
▪ M1 Protein – important in viral assembly;
major component of virion
▪ M2 Protein – essential in virus uncoating;
ion-channel
• Surface glycoproteins: Hemagglutinin (HA) &
Neuraminidase (NA)
• MOT: Airborne droplets (aerosol inhalation); Fomites
• Influenza peaks during the winter
Rod-shaped Glycoprotein/Peplomer
• For the PH, mas common ang trangkaso kapang
January and February kasi yun yung time na malamig.

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 FROM SIR CHING
• The base of the stalk anchors to the viral
membrane.
• The HA molecule is folded into a complex
structure.
• The binding of the receptor site and sialic acid
activates fusion of the host cell membrane with
the virion membrane resulting in the damping of
the viral genome into the host cell.
• The HA is needed for adsorption
• If there is the presence of antibodies against HA,
there is resistance or merong immunity ang
patient. • Same lang to sa pinakita ko kanina class, where in yung
neuraminidase and HA act as tag-team wrestling
partners. Wrestling down the host defenses yun nga
NEURAMINIDASE yung ating mucin and sialic acid receptors.
• Minor surface glycoprotein (20%) • The neuraminic acid clears the mucin barrier, while the
• Tetramer composed of four identical monomers HA fuses to the cell sialic acid residues, enabling viral
o Parang box-shaped na umbrella type adsorption and penetration
• Slender stalk topped with a box-shaped head. • The use of neuraminidase inhibitors are protective. They
• Destroys neuraminic acid using “neuraminidase” are good to remove the infection of trangkaso or
enzyme. influenza in the body. Yan yung ating mga oseltamivir,
• Facilitates release of virus particles from infected peramivir, and etc.
cell surfaces during the budding process •
• Removal of mucin layer in the RT to reach the target MODE OF TRANSMISSION
epithelial cells. • Airborne droplets (aerosol inhalation)
• From there, the HA will bind to the sialic acid • Fomites
receptors, which are also present in the RT epithelial CLASSIFICATIONS
cells, causing viral entry or viral fusion into the host • Three types: A, B and C
cell. • Influenza A and B – has 8 separate segments
• 11 subtypes known: N1-N11 • Influenza C – has 7 separate segments
o N1 and N2 – most common human influenza o Usually not considered as pathogenic
• Influenza Type A
o the most common type affecting humans
o Flu pandemics, tendency to cause pandemics
lies in its ability to undergo “antigenic shift
and drift
o It can perform both drift and shift = mechanism
to produce new viral strains.
• Influenza Type B
o Outbreaks/epidemics
o Infects humans only (no animal reservoir);
Mushroom-like Glycoprotein/Peplomer antigenic drift only
• Influenza Type C
o Can infect humans but produces only mild
symptoms (mild respiratory illness)
o Does not cause significant human disease
o Lacks the glycoprotein neuraminidase
o Antigenic drift only
• Antigens present:
o Group specific antigens: Viral Nucleoprotein
(NP) & Matrix (M) Protein
o Type specific antigens: HA & NA

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• Other animals, especially pigs and birds, can be • So non-human flu virus is passed from one type of
reservoirs of a mix of any of the 3 types. animal through an intermediate host. From the avian
napunta sa pigs and then napunta sa humans.
A – SHIFT & DRIFT • Associated with Influenza A only
B & C – DRIFT DRIFT • Results in pandemics

ANTIGENIC VARIABILITY
ANTIGENIC DRIFT
• Minor antigenic changes in HA or NA
• Parang sa kotse nagdrift lang siya. May slight
movement lang yung body.
• There are minor antigenic changes in the HA or NA.
• Caused by the accumulation of point mutations in
the gene, resulting in amino acid changes in the
proteins
• Alam naman natin yung central dogma of molecular
biology yung mga nucleotides structures. There are
minimal changes in the structure of nucleotides.
• Minor sequence changes causes:
o Alteration of the antigenic sites
o Ability of the virion to escape recognition by
the host’s immune system
• Slower occurrence leading to new viral strains
• Medyo mabagal yung progress niya para mag evolve
into a new viral strain.
• Associated with Influenza A, B, and C
• This would be a picture to help you visualize the
difference between drift and shift.
ANTIGENIC SHIFT
• For drift class, there is just a minor change. So parang
• Major movement sa current lang onti lang yung current, yung boat
• Major antigenic changes in HA or NA umandar lang ng konti
• Drastic changes in the sequence of a viral surface • For the shift, talagang nag bago yung kanyang
protein antigenic sites, talagang nag transform yung kanyang
• Gene swapping or reassortment between 2 nucleotide structure. Yung bangka napunta na sa
influenza viruses volcano.
• Usually nagcocombine yung human influenza vs the • Kapag may drastic changes sa antigenic sites, yung
avian influenza, which causes pandemic. Usually body natin mahihirapan gumawa ng dedicated
diba yung Hong kong flu galling siya sa avian na antibodies dun sa virus na yun or sa new viral strain
nagcombine sa human which causes ng pandemic sa na nagawa ng orthomyxoviridae
hong kong and sa china area. • So usually for antigenic drift, it will take years to
produce a new viral strain.

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• For antigenic shift, it would only take 1 year to ASIAN FLU
produce a new viral strain. It is quite a concern. • Year: 1957; Origin: China
• Usually ang mga scientists lagi sila nagreresearch • Reassortment of viral genes with avian virus
kung ano ang mga bagong strain na nagtransform or • Mortality: >1 million worldwide; >70 thousand in US
nag formulate. Para makagawa agad sila ng vaccine.
Ang validity ng mga vaccine for trangkaso is usually
for one year lang kasi mabilis nga siya mag palit ng
antigenic structure.

FROM DOC MIGUEL

• Kapag konti lang ang changes (sa NA at HA), Drift
ang tawag dun. Pero kapag ibang-iba na yung
itsura niya, Antigenic Shift ang tawag dun.
• Dahil madaling magbago, kapag nagbago yang HA
at NA meron kang panibagong Influenza na di
kilala ng immune system ng karamihan, kaya HONGKONG FLU (H3N2)
meron siyang pandemic potential. • Year: 1968; Country of origin: China
• It’s also because of these Antigenic Shifts • Reassortment of viral genes with avian virus
nagkakaroon ng mga bagong strains of the virus • Mortality: >1 million worldwide; >34 thousand in
that is actually problematic in terms of making a US
vaccine.
RUSSIAN FLU (H1N1)
• Year: 1977; Country of origin: China, Russia
Human Influenza Pandemics in the 20th Century • Reappearance of viral genes in 1950s (Spanish Flu)
SPANISH FLU (H1N1) • Mortality: low mortality worldwide and in the US
• Year: 1918-1919; highly pathogenic strain • Probably there is the presence of immunity during
• Viral genes contains mammalian and avian genes the 1977 since medyo luma na ang Spanish flu. So
• Mortality: 25-50 million worldwide; 500 thousand in people acquired the immunity with Spanish flu kaya
US hindi na masyado mataas yung mortality.
• The Spanish flu is compared with the pandemic
happening right now, SARS-CoV-2. Recent Influenza Pandemics (21ST CENTURY)
• Time ng war yan tapos hindi maganda yung BIRD/AVIAN FLUE – A(H5N1)
sanitation kaya mabilis magkahawaan. At the same • Year: 1998; Country of Origin: Hongkong
time, yung healthcare system hindi naman ganon • Sporadic human infections are far more severe with
kaganda during that era. high mortality; longer incubation period
• The scientist had traced that the origin of the • Great risk for human pandemic
Spanish flu is sa china din pero naging common
name nalang din yung Spanish flu that time kaya SWINE FLU – A(H1N1)
hindi na rin siya nabago. • Year: 2009
• Similar to seasonal flu

PATHOLOGY
• The viral structure has two main glycoproteins:
Hemagglutinin (HA) and Neuraminidase (NA).
• These glycoproteins are important in how the virus
infects the host cells.
• HA –Attaches to the sialic acid receptors in the host
cell.
• NA –Facilitates the release of mature virions from
the infected cell
• A person is infected through aerosol droplets.

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• Once infected, non-specific symptoms like fever, • Virions attack the ciliated epithelial cells lining the
cough, colds and generalized body weakness respiratory tract causing necrosis and sloughing
ensues. So medyo mabilis yung pagproduce ng of the cells
interferons and cytokines. • Viral glycoproteins lowers the viscosity of the
• Infections in previously healthy individuals resolve mucous films in the RT, laying bare the cellular
spontaneously without any complications. surface receptors
• However infection in people with co-morbidities (e.g. • IP: 2-4 days
ongoing pneumonia, diabetes, asthma) can make the • Progeny virions are soon produced and spread to
current illness complicated. adjacent cells, where the replicative cycle is
• People infected with the influenza virus are more repeated
susceptible to develop bacterial pneumonia • Brief prodrome and malaise and headache lasting a
(Staphylococcus aureus). few hours
• Influenza virus also complicates the overall clinical • S/S: chills, headache, dry cough followed closely by
condition of patients with COVID-19 high fever, generalized muscular aches, malaise,
and anorexia
FROM DOC MIGUEL • Acute illness usually last for 1 week but malaise and
• HA (Hemagglutinin) is sometimes just referred to as H cough may persist for 2 weeks
only; while Neuraminidase is sometimes just referred
to as N only. FROM SIR CHING’S PPT
• I think you’re familiar with that because meron nang • Complications of Influenza Virus Infection:
Influenza H1N1, H5N1 diba. SO yung H is yung o Primary viral pneumonia
Hemagglutinin and N is Neuraminidase. o Croup and Otitis media (children)
• These two are the glycoproteins that contribute to its o Secondary bacterial pneumonia
viral infectivity. o Myositis and cardiac involvement
o Neurological syndromes: Guillain-Barre
syndrome, Encephalopathy, Encephalitis, Reye’s
FROM SIR CHING syndrome
• Factors associated with the increased risk of acquiring
the influenza virus:
o Immune status of the patient
o The presence or absence of underlying disease of
the infected patient
o If the weather condition is cold, it could also
increase the risk in acquring the infection.
• One thing to consider is that the clinical symptoms of
influenza in children are similar to those in adults.

FROM DOC MIGUEL

• This is because the Influenza virus makes changes to
the ciliate epithelium. The cilia is important in ejecting
bacteria/viruses out, thus it has its protective
mechanism. Kasi yun (ciliated epithelium) yung target
ng Influenza virus; sinisira niya yung respiratory
epithelium. PREVENTION
• Once nasira yun, it will be replaced by squamous • Vaccination (live attenuated or inactivated
epithelium which has no ability to fend off itong mga forms) – best way; administered every year
viral infections na’to, making the patient more • The downside: must be administered yearly.
vulnerable to bacterial pneumonia. • Both vaccines are continually being rendered
obsolete as new antigenic variants of influenza
viruses arise.
• Due to their capability to shift and drift

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 TREATMENT • Influenza Virus are mainly classified based on
• Amantadine & Rimantadine their HA and NA component.
o Usually used for Influenza A virus • Strains of Influenza A commonly found in the
o M2-ion channel inhibitors for systemic use in human population are: H1N1, H3N2 and H1N2
the treatment and prophylaxis of Influenza A • Influenza peaks during winter
o Classified as part of Adamantane drugs • For the Philippines, mas common ang trangkaso
• Zanamivir, Oseltamivir (Tamiflu) & Peramivir kapag January and February kasi yun yung time
o Neuraminidase inhibitors na malamig.
o Useful for the treatment of both influenza A • Attacks mainly the URT of very young and old,
and B patients comorbidities, debilitated individuals
o More expensive
• Influenza viruses are one of the few viruses LABORATORY DIAGNOSIS
that has an antiviral treatment • Viral Culture
• Oseltamivir • Polymerase Chain Reaction (PCR)
o Neuraminidase inhibitor o Preferred method
o Basically inhibits the release of mature o Specimen: nasopharyngeal specimens
virions • Antigen Serology
o Improves the survival rate of people
• Tissue Culture
infected with the virus
o Primary Monkey Kidney Media
o Also included in the medical regimens of o For the detection of cytopathic effects
patients with COVID-19 o Some stains do not produce the cytopathic
o Brand: Tamiflu effects which will require confirmation

FROM PPT NOTES ADDITIONAL VIDEOS:

• Oseltamivir • Flu Attack! How A Virus Invades Your Body
o To prevent further proliferation of influenza o https://www.youtube.com/watch?v=Rpj0emEGShQ
virus • Why do you need to get a flu shot every year?
o https://www.youtube.com/watch?v=FZ_jNGKCIWs&
o If there is proliferation of both influenza
t=199s
viruses and SARS-CoV 2 in a patient, it will
• BP: DOH: Kaso ng mga nagkaka-trangkaso, dumarami
only make things worse. kapag Enero at Pebrero.
o If a patient is COVID-19 free and does not o https://www.youtube.com/watch?v=SzNN9QbVIqA
have any comorbidities (physically healthy)
before getting infected with influenza virus,
Hi guys trans team here hihi
they are not given Oseltamivir because the
For Paramyxo, we wont combine the separate ppts (discussed by
body has the capability of fighting them off.
different profs but same topic theyre so labo) muna pero we’ll
o However, if a patient has concomitant arrange it one after the other lang so we won’t leave out info that
bacterial pneumonia prior to influenza virus might be present in one but absent in the other so sorry na
infection, this is the time that Oseltamivir is agad if may mga naulit
administered.

EPIDEMIOLOGY First Paramyxo discussion is from Doc Miguel and Doc Arvin then
• Influenza Virus is known to have a high pandemic yung second one is from Sir Jerry Ching
potential
Pansin niyo ba parang halos lahat ng prof naten nabanggit si
• This is due to the nature of the genome of the virus.
dean nalang ata kulang ng discussion
• Genetic rearrangements occur in animals that can
be reservoirs of multiple types of influenza virus.
• The genetic rearrangements occur during infection
which results in the changes in the viral structure,
most importantly in the glycoproteins HA and NA
• Shifts also make it hard to make an effective
vaccine.

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 PARAMYXOVIRIDAE
General Characteristics
• Spherical
• Enveloped
• Single stranded RNA (ssRNA) viruses
o Negative sense
• ALL members can cause respiratory diseases
• DOES NOT have a segmented genome

Members
• Measles
• Parainfluenza
From sync with Doc Arvin
• Respiratory Syncytial Virus (RSV)
• Croup is a virus that affects the larynx, the
• Nipah
trachea and the bronchioles…kaya siya
• Human Metapneumovirus
LTB… LaryngoTracheoBronchitis
• If you notice ang mga viruses kapag
Parainfluenza Virus
nakakainfect yan class, maraming organs ang
• Common virus affecting children
tinatamaan kesa sa mga bacteria, they’re
• Has four (4) subtypes:
specific
o Parainfluenza—1
• There is the swelling of the larynx, the trache
- most common cause of croup
and the vocal chords and actually a rarely is
o Parainfluenza—2 actually a rarely… medyo delikado siyang
- also cause serious illnesses in children case.. common in children under 2 years old
because pwedeng magbara ang airway….
o Parainfluenza—3 Because of airway obstruction with croup
- second most common virus affecting • And the classic description is that they have
children (RSV is 1st most common) barking cough
- associated with severe diseases and
fatalities Laboratory Diagnosis
• Cell culture
o Parainfluenza—4 • Immunofluorescence Assay
- Little is known about them • Antigen detection (serologic)
- Does not cause much diseases • Polymerase Chain Reaction (PCR)
compared to Parainfluenza 1 and • Specimen: Nasopharyngeal washes and
3(according too Papa Mahon) aspirated secretions
• Parainfluenza Virus 1 and 3 are diabolical o Specimen samples should be kept cold
• Media: Primary Monkey Kidney and LLC-MK2 cells
From sync with Doc Arvin • Identified using:
• The most common cause of croup is? o Hemadsorption
o Parainfluenza Virus 1 o Immunofluroescence (most rapid)
o Enzyme immunoassays
Mode of transmission
• Droplet infection (like SARS-CoV 2)
Respiratory Syncytial Virus (RSV)
• Inoculation of the droplets in the mucous
membranes • Genus: Pneumovirus
• Can be transmitted through fomites • Most significant cause of acute lower respiratory
o Viruses can live up to 10 hours on varying tract infection in children younger than 5 years old
• Ang pinagkaiba nito is croup ay sa upper and RSV
surfaces
ay sa lower..
Doc Miguel • Causes viral pneumonia and bronchiolitis
• These MOTs tell us that prevention of • AOM- common complication
acquiring these viruses can be through: o Acute Otitis Media
✓ Hygiene (like frequent linis or laba as much as • Also a common cause of morbidity and mortality in
possible and taking a bath) people aged 65 years and above
✓ Proper coughing etiquette

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 • Extremes- targets the most youngest and the oldest Measles (Morbillivirus)
populations • Causes Rubeola
• Targets the most vulnerable populations (oldest and • One of the most common viruses affecting
youngest) children
• Some adults get infected but their immune system • Causes a classic viral exanthem
can singlehandedly fight off RSV o Reddish rashes na nag-uumpisa sa trunk
o That’s why they target the most vulnerable
populations because their immune systems are
either still developing or degrading
o RSV is more common in infants than in old
aged people
o RSV is more of a disease of childhood
o Bacterial pneumonia is often encountered in
older populations
• Contains a Fusion Protein (F-protein)
• Direct viral invasion of the respiratory epithelium • What is the common name of Rubella virus?
(almost like influenza virus)
o German measles
• Cell injury is immunologically mediated
o Yung RSV nandun lang siya sa loob ng cell o REMEMBER: Belle (rubella) is wearing a toga
pero hindi niya talaga sinisira yung cell.Yung (from Togaviridae family) from Germany
immune response na ine-elicit ni RSV is THE (German measles) and nagkaroon siya ng
ONE killing or injuring the cells rashes (one of the symptoms)
• The subsequent necrosis leads to formation of • Rubeola vs. Rubella
mucous, fibrin, and debris that can cause formation o Rubella is german measles, rubeola naman..
of plugs.
eto yung measles lang
o Kapag nagkaroon ng plugs, usually sa mga
babies na sobrang narrow pa ng tracheas, that o Most of them present with rash and fever and
will cause respiratory distress the rash appears during the height of the
o Sa older children, mas malalaki na yung mga fever…pag mataas na mataas yung lagnat dun
trachea nila, pero still kelangan parin ma- lang nagkakarashes ang pasyente
prevent kasi baka magkaron ng plug and o Ang pinaka prominent difference nila is Rubella
magkaron ng respiratory distress yung patient. is more on lymph node involvement.. usually
posterior auricular… sa likod ng tenga…
merong kulani dyan eh.. minsan prominent,
mamamaga talaga
o Pag rubeola or ordinary measles prominent
ang dry cough, coryza at tsaka sore eyes,
conjunctivitis… so the 3Cs are related to
rubeola..
o RubeOla comes from mOrbillivirus
Laboratory Diagnosis (Paramyxoviridae) while Rubelle comes from
• Polymerase Chain Reaction(PCR) Togaviridae
• Hard to grow in cell culture o Rubeola (ordinary measles)
• Viral antigen through Immunofluorescence and - Conjunctivitis
EIA - Cough
- Coryza
Treatment - Fever
• Ribavirin - Koplik spots on buccal mucosa
o known MOA: prevents capping of the viral RNA
- Rash appears at the hairline and
o only given in severe cases
o If nasa bingit na ng kamatayan spreads cephalocaudally over 3 days
o Pero most of the time, kapag hindi pa naman (cephalocaudally meaning, the rash
ganun ka-severe, di pa naman binibigyan ng starts from the head down to the feet…
Ribavirin… Supportive treatment lang ang pababa.. pareho sila ng rubella)
binibigay natin - Sore throat
- Coryza(Runny nose or congested nose)

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 - Forchheimer spots on soft palate(These are • Diarrhea(most common)
blue violet spots parang petechiae doon sa o Ominous for babies and smaller children
ngala ngala) o Ang diarrhea sa adults ay hindi naman
o Rubella (German measles) ganun ka-ominous pero sa bata, ominous
ang diarrhea… Ominous, meaning,
- More common form
nakamamatay… Because konti lang naman
- Headache ang fluids ng isang baby or a small child…
- Low grade fever Pag nagtatae sila, mawawala ang
- Sore throat extracellular fluids nila so madedehydrate…
- Coryza(Runny nose or congested nose) and ang bata, lalo na yung mga talagang
- Forchheimer spots on soft palate(These are young, yung mga babies, when they lose
the fluid, ikamamatay nila yun unlike, us,
blue violet spots parang petechiae doon sa
adults.
ngala ngala)
- Lymphadenopathy (and what is more • Encephalitis
prominent in rubella is the presence of o Common for acquisition of measles at a
lymphadenopathy…. Sa rubella mas later age
marami ang lymphadenopathy) o Usually ang encephalitis common yan sam
- Rash begins on the face and spreads ga nagkaron na ng measles at a later age,
cephalocaudally usually kapag nasa teenage years na nung
nagkaron ng measles..
Mode of Transmission o Avoid getting measles especially in teenage
• Through respiratory droplets years as it can cause SSPE or Subacute
Sclerosing panencephalitis
Pathogenesis o Yun yung pine-prevent natin na
• Replication of the virus mainly occurs in the complication din, yung tinatawag nating
respiratory epithelium
SSPE or your Subacute sclerosing
• Monocytes and lymphocytes are also affected
causing viremia panencephalitis that’s a long-term
o Yung virus ay nasa bloodstream complication ng mga taong nagkaron ng
• The immunologic response causes the measles.. ahh I will get back to you on
characteristic rashes o that, alam ko hindi siya latent infection
o So kapag nandun na sila sa skin, okay?.. It’s a complication that is caused by
because of viremia, the virus in the your measles virus which is uniformly
blood vessels will be detected by our fatal… Most of the people na nagkakaron
immunse system and that subsequent
immune response will be causing the ng SSPE ay namamatay, wala pang
rashes…. So magkakaron ka ng nabubuhay…. That’s why we have to
subsequent—somewhat tissue injury.. prevent the measles infection during the
yun yung rashes natin teenage years
• Patients have lifelong immunity after recovery o Acute disseminated encephalomyeitis
o So pag nakahawa ka ng measles you (ADEM)
will lifelong immunity however may o Subacute sclerosing Panencephalitis
complications…
(SSPE)
Complications
• Pneumonia(most common cause of mortality) Laboratory Diagnosis
o Habang may measles ang bata, you • Mainly diagnosed clinically
have to watch out… usually bata o rashes
naiinfect dyan eh. Kase, kapag hindi mo • Specimen: Nasopharynx and urine (early
binantayan yung complications, stage of the infection)
• Culture Media: Primary Monkey Kidney media
pwedeng magkaroon ng concomittant
• Immunofluorescence Assay, Enzyme
pneumonia yung bata
Immunoassay
o Of course, minsan, yung pneumonia • Serology: IgM antibody detection
ang papatay dun sa pasyente

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 Treatment - pamamaga ng panga or yung
• Prevention strategies side nung face
o Vaccination (MMR at 6 months of age) o Epididymoorchitis (Testis), Oophoritis
o Ang measles pwede mo makuha ng solong (Ovaries)
vaccine pero most of the time, hindi na siya - -inflammation of the testis and
solo, kasama niya ang Mumps and Rubella…. ovaries
At 6 months of age binibigay yan para di na o Inflammation of the other organs
magkaron ng measles during the teenage affected by the viremia
o Can also affect the central nervous
years kase they found out na most of those na
system (encephalitis)
nagkakaron ng SSPE, that dreaded o Knowing na may viremia, pwedeng
complication, is na-infect ng measles during siyang pumunta sa bloodstream, mismo
their teenage years so kelangan, ma-prevent sa brain… Encephalitis and pinaka
natin yun.. and what’s a good way to prevent dreaded na complications.
it? By having your vaccination o Since it can cause viremia, it can go up
the brain… ang encephalitis, mahirap
MUMPS yan, magiging 50-50 ang patients
• Rubula nyan… for the other viruses that actually
• Has the H, N, and F surface antigens cause encephalitis, ganun din ang
• Causes parotitis
prognosis nun medyo masama depende
• Only has one serotype(unlike influenza)
o Somewhat etong virus na ito is stable. sa immune system ng patient.. so
So lahat ng mumps na nakikita natin kawawa ang mga patients na
dito sa Pilipinas ay pare-parehas lang nagkakaroon ng encephalitis
ang itsura…. So since meron lang
siyang 1 serotype, pag nahawa ka ng Sync from Doc Arvin
mumps or rubula, most probably hindi Orchitis, which may cause sterility, is a possible
ka na maiinfect ulit… So that will manifestation of Mumps.
somewhat give you a lifelong o Orchitis is the swelling of the testicles
immunity… and better yet, magpa- o Causative agent of mumps is Rubulavirus
vaccine.
o REMEMBER: rubUlavirus & mUmps
• Infection is through droplet infection
• Infects the respiratory tract then invades the
parotid gland via viremia (via the bloodstream)
or the Stensen duct Laboratory Diagnosis
o Parotid Gland: near our ear, sa may jaw, • Specimen: Saliva, urine, pharynx,
has a duct near the buccal cavity Cerebrospinal fluid (CSF)
o Stensen Duct: drainage of the parotid • Presence of virus in specimens:
gland o Urine: 2 weeks
• Reaches the testes, ovaries, thyroid, and other o Saliva: 5 days after the onset of
organs through viremia symptoms
• Clinical Syndromes • Cell culture
o Parotitis: Unilateral or bilateral o Mumps grow well in Primary Monkey
- inflammation of the parotid Kidney Media
gland o CPE: Multinucleated Giant Cells
o Hemadsorption
- unilateral: “isang side lang”
• Serologic Testing- IgM antibody detection.
- bilateral: “parehong sides”

Treatment
• Mainly preventive- Vaccination (MMR at 6
months)
o Mas maganda if napprevent natin to
kasi, well if you have mumps, ayaw
nating mangyari yung encephalitis”
• Self-limiting disease
o Wala namang gamot, kusa nalang
gumagaling

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 o Supportive, needs to rest improperly Pre-Test (NO ANSWERS YET)
during the infection para hindi naman
sobrang ma-depress… pero syempre, 5. The filiviridae is a newly recognized family of
ang trend ng medicine ngayon is negative-sense,ssRNA viruses. Which of the
prevention so kelangan parin magpa- following viruses belongs to this family and
vaccinate.
causes hemorrhagic fever?
Doc Miguel A. Ebola virus C. Dengue virus
Mas okay daw magka-mumps if bata palang dahil B. Yellow fever virus D. Lassa fever virus
nakakabaog?
o Not true. Di naman nagiging sterile
PARAMYXOVIRIDAE
o Di naman sure fire na mababaog
o Yung mga naririnig niyong nababaog most
probably may fertility problems na hindi naman
si mumps ang talagang nag cause.

SIR CHING ASYNCH AND PPT

Pre-Test (NO ANSWERS YET)

1. Influenza and Parainfluenza virus are
differentiated by:
A. Type of nucleic acid
B. Lipid envelope
C. Segmented RNA genome
D. Helical symmetry
2. Respiratory syncytial virus is best isolated
using
A. Cough plate
B. Nasopharyngeal aspirate
C. Throat swab
D. Expectorated sputum
3. Orchitis, which may cause sterility, is a
possible manifestation of which of the
following?
A. Rabies C. Cytomegalovirus
B. Rhinovirus D. Mumps
4. While playing in the forest, a 13-year old boy
was bitten in the lower left leg by a raccoon.
What finding would suggest a serious
neurologic disease could result from the
bite? NOTES FROM SIR CHING:
A. Negri bodies in skin scrapings
• The reason why they are group together is due
B. Presence of Downey cells in the boy’s
to a lot of similarities
blood 2 weeks following the bite
o Mode of transmission: Most of the family
C. Cowdry type A inclusion bodies in skin
infects the patient through inhalation of
scrapings
infectious aerosol.
D. Molluscum bodies on epithelial cells
shed from raccoon’s saliva

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 NOTES FROM SIR CHING: ▪ F glycoprotein- responsible for
o Structure: Both have hemagglutinin and membrane fusion and hemolysis
Neuraminidase spikes which adds to its activity
virulence to infect the potential host cell. • Hemagglutinin +/ Neuraminidase – viral attachment
o Clinical manifestation: Most of the patient ▪ Causative agent for pathogenicity
consists of the symptoms in both Upper and • Six genera: Parainfluenza, RSV, Metapneumovirus,
lower respiratory infection tract infection. Measles, Mumps, Hendra and Nipah viruses
• Viruses induces cell-cell fusion, causing
multinucleated giant cells
GENERAL CHARACTERISTICS • CPE in cell culture: multinucleated giant cells
• Largest RNA virus with a large family
• Enveloped, ssRNA negative-sense, non-
segmented genome
• Non-segmented genome
▪ Isa sa mga marker para madifferentiate sa
orthomyxoviridae since orthomyxoviridae
has a segmented genome
• All are antigenically stable
▪ Some can cause antigenic drift while
orthomyxoviridae can cause antigenic drift or
shift
• Antigenically stable - Do not undergo genetic
reassortment
• MOT: Transmitted by contact or large droplets and
initiate infections through the respiratory tract
• Six structural proteins present
▪ Affinity to viral RNA – N protein, P protein, L- Large Polymerase
L protein N- Nucleocapsid
• Usually present inside the virus P- Phosphoprotein
• N protein- Nucleocapsid protein HN- Hemagglutinin-neuraminidase
▪ Forms the helical nucleocapsid M- Matrix protein; present in the membrane
▪ Other term: Major internal protein
▪ P protein and L Protein –
Synonymous in function: Helps in the
transcription, RNA replication and
viral polymerase activity
▪ Formation of viral envelope – M protein,
HN/H/G glycoprotein, F glycoprotein
▪ Associated for the formation of viral
envelope
▪ Usually responsible for viral
attachment and cell membrane
formation
▪ M protein
• Matrix protein HEMAGGLUTININ
• Important in the virion • One of the important components of virus to induce
assembly disease to potential host.
▪ HN/H/G protein • Usually attaches to sialic acid receptors
• Some genus/genera meron • Sialic acid receptors- Most commonly present in the
syang H or hemagglutinin RBCs however it can also be seen in upper
glycoprotein lang depende respiratory tract epithelial cells
sa genus.

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• As seen in the picture, hemagglutinin injects its PARAINFLUENZA VIRUS
certain compounds or enzyme to hemagglutinate the • Primary cause of respiratory disease in young
RBCs. children
• Neuraminidase: Removes the presence of • Serotypes
neuraminic acid o PIV 1 – primary cause of croup in children
o Neuraminidase: Removes the presence o PIV 3 – bronchiolitis and pneumonia (infants)
of neuraminic acid Neuraminic acid- o PIV 4 – mild upper respiratory tract disease
Important component of the Mucin • There are actually 4 serotypes present in
o Mucin- Part of the upper respiratory tract parainfluenza but the three are the most
epithelial cell which acts as a barrier to pathogenic or infectious. MOT: respiratory
any foreign invader secretions, aerosol inhalation, and direct contact
• So, if the neuraminidase removes the mucin barrier in
the respiratory tract epithelial cells, it now then CLINICAL MANIFESTATIONS
exposes the sialic acid beneath it which would then • Infection appears to be limited to respiratory
give the hemagglutinin the chance to enter the sialic epithelia
acid o Meaning they are non-systemic they usually
• If the virion has entered the sialic acid receptor, it reside to respiratory epithelia
would then give a chance to activate its fusion to the • Nose and throat – “common cold syndrome “
host cell membrane • Croup (laryngotracheobronchitis); barking sound
• Things that you should consider are the presence of (seal-like)
hemagglutinin and neuraminidase in each genus • Bronchiolitis
• Respirovirus, rubulavirus, and morbillivirus • Otitis media – most common complication
o Consists of the hemagglutinin glycoprotein associated with Parainfluenza
• Hernipavirus does not contain hemagglutinin • Secondary bacterial infection – pneumonia
• Respirovirus and Rubulavirus o When immune system is depressed, there
o Contains neuraminidase component could be high risk of secondary bacterial
infection.
o Maternal antibody
▪ Does not protect the infant from
infection.
▪ 2-4 months of age
▪ Increase of viral secretory IgE due to
presence of bronchiolitis in patients
▪ Does not cause viremia or systemic
spread in the body.

IMMUNITY
• Infection induces protective immunity of short
duration
o That is why reinfection can also happen
• IgA antibody – resistance to reinfections

EPIDEMIOLOGY
• IP (Incubation period): 5-6 days
• Parainfluenza Virus 3 – most infectious, prevalent
and endemic
• Common in semi-closed population/spaces – family
houses, nursery
TREATMENT
• Ribavirin – drug of choice
• No vaccine is available
• Control – contact isolation precaution

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 RESPIRATORY SYNCITIAL VIRUS o Male: Testes
PNEUMOVIRUS o Female: Ovaries
o Testes and ovaries are severely
CLINICAL MANIFESTATIONS affected due to lack of elasticity of tunica
• Most common cause of LRT illness in infants and albuginea
young children • Contagion period precedes symptoms and may
• 2 serotypes: A and B cause asymptomatic shedding
• Spreads into the LRT and causes bronchiolitis and o Viral shedding occurs in saliva 3 days
viral pneumonia among children 5 years and below before up to 9 days after the onset of
or infants salivary gland swelling
• Adult: Reinfection with milder symptoms • Primary Replication – nasal or upper respiratory
• Higher chance of mortality in patients with tract (epithelial cells)
preexisting conditions (e.g CHD) • IP: 2-4 weeks (14-18 days)
• Viral pneumonia results from cytopathic effect of virus • Only one serotype: infection or vaccination (MMR)
(syncytial formation) provides lifelong immunity
• Natural infection does not confer lifelong immunity • Propensity to replicate in epithelial cells in various
o So there could be a possibility of reinfection visceral organs
• Otitis media – common complication of RSV
• MOT: Direct contact of respiratory droplets NOTES FORM SIR CHING:
• Aside from Parotid gland, testes, ovaries,
LABORATORY DIAGNOSIS peripheral nerve, eye, inner ear, and CNS
• Detection of viral RNA (RT-PCR) - is the test of choice could also be affected
for respiratory secretions • Pancreas may also be affected wherein if not
• NAT – preferred method for adult specimens treated immediately, it could cause juvenile
• Nasopharyngeal swabs and washes- Preferred diabetes.
method for children
• infects the kidneys and can be detected in the urine
• Freezing of clinical specimens may result in complete
of most patients
loss of infectivity
• Systemic infection, especially of parotid gland,
testes, pancreas, ovaries and CNS (aseptic
TREATMENT
meningitis)
• Ribavirin, Palivizumab – treatment for LRT infection
• Testes – Orchitis (men who are beyond puberty; may
o Ribavirin is usually administered in an
lead to sterility)
aerosol for 3-6 days
• Principal symptom: swelling of parotid glands
because of inflammation
CONTROL
o That is why nauso yung term na “beke”
• Contact isolation
o Mot: Direct contact (highly contagious);
• Proper handwashing
Airborne droplets, Fomites contaminated with
• Restriction of visitors in order to prevent the
saliva or urine
transmission

RUBULAVIRUS (MUMPS VIRUS)

CLINICAL MANIFESTATIONS
• Acute contagious disease characterized by non-
suppurative enlargement of one or both salivary
glands (parotitis)
o Parotitis is the inflammation of parotid
gland
o The inflammation may confine in one
area and is usually enlarged several days
• Mild childhood disease – aseptic meningitis,
parotitis and orchitis are common.

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NOTES FORM SIR CHING: NOTES FORM SIR CHING:
• Incubation phase • This slide pertains to the flowchart how mumps
o First phase virus induces disease and at the same time how
o Virus is adjusting to the potential host cell it affects the other organs
o Mumps virus is highly infectious since the • Inoculation of mumps virus in the respiratory
virus has a high viral replication in the tract epithelial cell
parotid/salivary glands. o Highly contagious and infectious
• Notable symptoms • Local replication- it would start to replicate and
o Orchitis infect another potential host cell
o Parotitis • Viremia- Large presence of virus inside the
o Recovery of virus from mouth to urine systemic circulation which could then cause
through viral diagnostic method systemic infection
• Virus Specific antibody is present when the o When virus enters a Systemic
immune system is starting to react to counteract circulation, it can now go to other
the presence of mumps virus visceral organs such as a parotid gland
o During this time, approximately 29-32 wherein virus multiplies in the ductal
days we could recover the virus from the epithelial cells and there would be
CSF. If the body does not produce the marked swelling due to inflammation
right amount of antibody, it could lead to
meningoencephalitis which is fatal

• Appearance of patient with mumps Infection

o Swelling of the parotid gland
o Swelling of testes and ovary
o “I GOT BUMPS CAUSED BY MUMPS”

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 MORBILLIVIRUS
• Rubeolavirus (Measles)

CLINICAL MANIFESTATION
• One of the six classical childhood exanthems
(eruptive diseases)
• Highly contagious disease of children (high fever,
respiratory disease, maculopapular rash)
• Humans are the only natural hosts
• Infects hosts via the respiratory tract where it
multiplies locally
• Prodromal phase: fever, sneezing, coughing, runny
nose (coryza), redness of eyes, lymphopenia
• “Koplik’s spots” – pathognomonic for measles
o Small-bluish white ulcerations on the buccal
mucosa opposite the lower molar
o A day or two before the rash, the patient
develops small bluish-red or small bluish-white
lesions in the mouth.
o Think of a cop licking a red/white/blue lollipop • If not treated, there could be severe complications
(refer to image below). since the body cannot fight the infection well. There
• “Conjunctivitis” – photophobia can be a downregulation of the immune response,
o Conjunctivitis – inflammation in the eye area. giving the opportunistic bacteria to gain entry to our
o Photophobia – classical manifestation body.
▪ Sensitivity of infected patient to light. • Worse, the patient can develop encephalitis.
• Cough or rhinitis, and high fever is also present. • LONG TERM COMPLICATION:
• Rash starts on the head and then spreads • SUBACUTE SCLEROSING PANENCEPHALITIS
progressively to the chest, trunk, and down the limbs (SSPE)
o Marker for measles virus infection o Occurs 7-10 years after acquiring the
• Otitis media – common complication infection
o Usually it is seen in people infected with
• IP: 8-15 days from exposure to the onset of rash
measles before they were 2 years old.
• Severe Complications:
Parang nagrereactivate nalang yung virus sa
o Secondary bacterial infections –
brain. Latent sila dun for a long time then
Bronchopneumonia (Giant Cell Pneumonia)
nagrereactivate nalang sila.
o Encephalitis
o Central nervous system manifestations
(e.g. personality, behavior, memory changes,
myoclonic jerks, spasticity, and blindness
o Defective measles virus persists in the brain
and acts as a slow virus
o Measles in pregnant women – risk for
stillbirth
• Deadlier than Rubella
• High-risk pop for severe measles:
o Children: Malnourishment, Vitamin A
deficiency
Pregnant, Immunocompromised

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 • CCC – Cough, Conjunctivitis, Coryza and
Photophopbia
• SSPE – SUBACUTE SCLEOSING
PANENCEPHALITIS

Pathogenesis of Measles Virus within the Body

NOTES FORM SIR CHING:

• There will be the inoculation of the virus in the

respiratory tract.
• Replication of the virus in the respiratory tract.
• If there are sufficient amount, they will have access
to the lymphatic system or lymphatic circulation
• If they are numerous in the lymphatic circulation, it
would then proceed to systemic circulation which will
then cause viremia.
• From the viremia, it will enter different organs of the
body via respiratory tract, urinary tract, small blood
vessel, central nervous system, and conjunctiva.
• The virus infected endothelial cells plus immune T-
cells causes rashes.
• Rashes = high chance of recovery or immunity.
• The best way to treat this is through supportive
therapy.
• Complications:
o Post infectious encephalitis
o SSPE
o In case of immunocompromised (organ
transplants, PLHIV): fatal
NOTES FORM SIR CHING:
• This will be the common symptoms associated with
measles virus infection.
• Eto yung itsura nung kolpik spots yung mga bluish-
white lesions. Usually nasa ilalim yan ng buccal
mucosa natin.
• Next is yung rashes natin: nagstastart yan sa head,
sa trunk and then sa lower extremities.

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 o LRTI – bronchiolitis in early childhood;
Tachypnea, fever, cough, hypoxia
• Lower RT infections is most common in infants and
young children.
• Second to RSV as a cause of bronchiolitis in early
childhood.
• The clinical manifestation of Metapneumovirus is
• Eto yung itsura ng patient with SSPE. relatable to RSV infection.
• Disease is only limited to the respiratory tract. There
EPIDEMIOLOGY is no chance that it will go to the systemic circulation.
• Highly contagious; single serotype; no animal • Triggers asthma and wheezing
reservoir • Symptoms are similar to RSV, influenza, and PIV
• The virus is highly contagious that is why there’s a • No specific therapy for human metapneumovirus
need for vaccination. • There are ongoing trials na tinatry nila yung HMPVF
• The vaccine is effective against the virus since it only gene that induces HMPV-specific antibiodies in the
has a single serotype. humans pero hindi pa siya widely used sa ngayon.
• No animal reservoir since humans are the known • No vaccine is available
natural hosts.
• If all the patients are vaccinated, there is a chance
that the virus will be eradicated.
• MOT: Respiratory route (inhalation of large droplets
of infected secretions)

TREATMENT
• Vitamin A treatment
• MMR or AMV (Attenuated Measles Vaccine)
• For vaccination, it is better if prophylaxis. MMR or
AMV is the best prevention. HENDRA AND NIPAH VIRUS
• 2 doses: 15 months, 4-6 years subcutaneously • Zoonotic paramyxoviruses
• Booster is recommended • High mortality rate (>35%-40%)
• Kailangan ng booster kasi nawawala din yung • That is why these two viruses must be performed in a
antibodies natin sa katawan. Lalo if pupunta kayo sa BSL-4 laboratory. As you can see in the picture, they
hospital mag iinternship kayo for the next two are wearing PPEs because there is a high risk of
semesters, need niyo ng booster para di kayo being infected.
mahawa during internship. • Hendra virus
o Equine virus, fruit bats
METAPNEUMOVIRUS o Many horse fatalities
• Other name: turkey rhinotracheitis virus • Nipah virus
• Infects only humans and is related to avian o Fruit bats (flying foxes)
metapneumovirus that causes rhinotracheitis in o From fruit bats naiinfect yung pig, then may
chickens. possibility na mainfect yung humans lalo na
• IP: 4-9 days yung mga caretakers sa poultry. From
• All three of these: metapneumovirus, Hendra and humans infected with Nipah Virus pwedeng
Nipah virus = ZOONOTIC VIRUSES – wherein we mainfect other humans through direct contact
usually acquire the infection through infected animals. or inhalation of the infectious material or
aerosol.
CLINICAL MANIFESTATION • Cause encephalitis and severe interstitial
• Wide range of respiratory illness from mild upper RT pneumonia
symptoms to severe lower RT disease
o URI – coryza, conjunctivitis, pharyngitis, otitis
media, or stomatitis

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 EXPLANATION FROM THE INTERNET

1. Fruit bats acts as natural reservoir of Nipah viruses.

Fruit bats with NiV feeds on date palm sap. Virus
can survive in solutions that are rich in sugar, viz.,
fruit pulp.
2. Virus transmitted to human through the
consumption of date palm sap.
3. Fruit bats of Pteropus spp. which are NiV reservoirs
visited such fruit trees and got opportunity to
naturally spill the drop containing virus in the farm to
contaminate the farm soil and fruits.
4. Contaminated fruits are consumed by pigs and
other animals. Pigs act as intermediate as well as
amplifying host. Combination of close surroundings
of fruiting trees, fruits-like date palm, fruit bats, pigs
and human altogether form the basis of emergence
and spread of new deadly zoonotic virus infection
like Nipah.
5. Pork meat infected with NiV are exported to other
parts.
6. Consumption of infected pork can act as a source of
infection to human.
7. Close contact with NiV affected human can lead to
spread of NiV to other persons.

NOTES FORM SIR CHING:

• So, this figure pertains sa ability ng nipah virus na

matransmit sa potential hosts niya.
• Of course, the reservoir would be the fruit bats
infected with the nipah virus. So, fruit bats the love
to eat fruits or palm saps na pwedeng maconsume
ng tao. Magkakaroon ng infection yung tao.
• Other way: yung mga bats they love to eat fruits,
• NIPAH VIRUS yung mga baboy kinakain nila yung contaminated
fruit na galing sa fruit bat.
• Possibility niyan is yung mga nag aalaga ng baboy
pwede mahawa nung infected pig
• There is also a tendency yung infected prok, when
not properly cooked, pwedeng makahawa.
• Man to man tranmission pwede rin through direct
contact.
•

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 POST-TEST
ADDITIONAL VIDEOS:

1. Which of the following is NOT true of

• TV Patrol: Tigdas outbreak idineklara sa NCR,
Influenza virus?
Central Luzon
a. Some animals can be reservoirs for
o https://www.youtube.com/watch?v=ZY
certain strain
FWHgKdfY8
b. Previous exposure ensures protection
• Measles explained – Kurzgesagt
from subsequent exposure and infection
o https://www.youtube.com/watch?v=y0o
c. It has segmented genome
pgc1WoS4&t=271s
d. Its hemmaglutinin and neuraminidase
•
proteins undergo genetic variation.

2. The following viruses are associated with

gastroenteritis, EXCEPT:
a. Picornaviruses
b. Astroviruses
c. Adenoviruses
d. Norwalk-like viruses

3. The finding of large, multinucleated or

spindle-shaped cells in the bronchial
secretions of a 2-year old girl with acute
• RNA VIRUSES bronchopneumonia suggests that this
o ssRNA infection is caused by
▪ (+) Stranded a. RSV
• Naked b. EBV
o Picornaviridae c. HPV
o Caliciviridae d. HSV
• Enveloped
o Togaviridae
4. Rhabdovirus is most noted for causing
o Flaviviridae
infections of the
o Coronaviridae
o Retroviridae a. Lower respiratory tract
▪ (-) Stranded b. Upper respiratory tract
• Bunyaviridae c. Central nervous system
• Orthomyxoviridae d. Gastrointestinal tract
• Paramyxoviridae
• Rhabdoviridae 5. Which among the following choices is not
• Arenaviridae a characteristic of Orthomyxoviridae
• Filoviridae a. Transmission is primarily through
o dsRNA airborne droplets and fomites
▪ Naked b. Hemagglutinin aids in the entry of the
• Icosahedral viral RNA into the respiratory epithelial
o Reoviridae
cell
c. Influenza C lacks the glycoprotein
neuraminidase
d. M2-ion channel protein is essential in
viral replication and assembly

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 UNIT 5: ARBOVIRUSES
o They usually severe and fatal
DISCUSSION OUTLINE  Arboviruses may be associated with more than one
 Flaviviridae syndrome.
 Bunyaviridae
 Togaviridae

PRE-TEST (NO ANSWERS YET)

TRUE OR FALSE

1. Rubella virus is a non-arthropod-borne virus. TRUE

2. Bunyaviruses can be transmitted by an arthropod
vector or by contact with rodents. TRUE
3. Arboviruses are named after the arthropod vector FLAVIVIRIDAE
involved in the virus or after the geographic area  Initially these viruses, the flaviviruses were included
where the virus was first isolated. FALSE in the togavirus family but they were separated
4. Encephalitis and hemorrhagic fevers are common in because of some differences in their viral genome
arboviruses. TRUE organization.
5. Yellow fever virus was named because of the  These viruses are distributed worldwide
development of jaundice in the patients. TRUE  All flaviviruses are related in terms of their antigen.
 There is this one virus, the Hepatitis C virus,
classified in a separate genus, but also in the
ARBOVIRUSES Flaviviridae family.
 Also known as arthropod-borne viruses o This has no arthropod vector
 Transmitted by bloodsucking arthropods o Not classified as an arbovirus but is under
 Vector acquires a lifelong infection this family.
o That is through ingesting the blood from a
viremic vertebrae. IMPORTANT PATHOGENS
o Viremic – presence of the virus in the blood.  Japanese encephalitis virus
o The viruses multiply in the tissues of the  Dengue virus
arthropod even without evidence of disease  Yellow fever virus
or damage.  St. Louis encephalitis (SLE) virus
 Found in all temperate and tropical zones
 West Nile virus (WNV)
o Most prevalent in the tropics with its
 Zika virus
abundance of animals and arthropods.
 Named after a disease or after geographic area CHARACTERISTICS
o Ex: yellow fever – because of yellow
 Small and (+) ssRNA
discoloration or jaundice
 Enveloped and icosahedral capsid
o West Nile fever
 “flavus” means yellow
 Mode of transmission:
CLINICAL SYNDROMES
o Bite of an infected arthropod
 Fevers of an undifferentiated type
o With or without a maculopapular rash
o They are usually benign
 Encephalitis
o There is inflammation of the brain
o This is often with a high case fatality rate
 Hemorrhagic fevers
 PATHOGENESIS
 Primary viral multiplication DENGUE VIRUS: FLAVIVIRIDAE
o Myeloid and lymphoid cells or vascular Epidemiology
endothelium  Endemic in
 Multiplication in CNS o Latin America
o Blood-brain barrier o Puerto Rico
o Depend on the ability of the virus to pass o Mexico
through the blood-brain barrier so that it can  Cases reported in the US are travel related
infect the nerve cells or the neurons.  Normally affects adults and older children
 Viremia  Most prevalent Arbovirus in the world
o Vectors acquire the virus during this period o More than 100 million people who are infected
o This is time where the arthropod vectors can annually
now acquire the virus by sucking the blood.  Leading cause of illness and death in some tropics
o This is the first step in it its dissemination to Overview
its other hosts.
 Distinct Diseases
o The prevention of this virus in general is to
o Classic Dengue Fever (DF)
avoid contact with the vector or having vector
o Dengue Hemorrhagic Fever (DHF)
control programs.
 Deaths occur mostly in children <15 years
 Has 4 serotypes and can cause a variety of clinical
JAPANESE ENCEPHALITIS VIRUS
manifestations
 Major cause of encephalitis in Asia
o Rashes, arteritis or fever
o China, Japan, Korea, India
o An infection with 1 serotype, confers immunity
 Most common cause of arboviral encephalitis in the
but only to that infecting serotype
world
 Human are considered the main reservoir
 Transmission can be from person to person through
CHARACTERISTICS
a mosquito vector
 Most patients are asymptomatic
 Transmitted by Aedes mosquitoes
 Flulike illness to acute encephalitis
o A. aegypti and A. albopictus
 Most affected are children
o With mortality as high as 30%
 50% with neurologic and psychiatric sequelae
 1st and 2nd trimesters of pregnancy: death
 No treatment available
o There are several effective Japanese
encephalitis vaccines available in Asia these
includes skilled and live attenuated that are
being used in several Asian countries. Classic Dengue Fever
 2009, Vero-cell culture derived vaccine  Relatively mild infection
o Licensed in the United States o Begins with a sudden onset of fever, headache,
o The vaccine is available in the US if travelling chills, myalgia, and bone pain (“breakbone
to endemic countries. fever”)

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 o Some may develop rash visible on the trunk and FROM DOC ARVIN ♥ – SYNCHRONOUS
spreads to the face and extremities
 Self-limiting Out of the 4 serotypes of Dengue, which is the most
o Resolves in 1-2 weeks prevalent in the Philippines? DEN-3
(Dengue Serotype 3)

Dengue Hemorrhagic Fever

 Develops when exposed to two different serotypes
 Described as an immune enhanced disease
 Also known as Dengue Shock Syndrome
 Symptoms of classic dengue fever
o With thrombocytopenia, hemorrhage, shock  Fever sa umpisa, under the Febrile phase
o Sometimes death  The platelets will only go down once the fever is
gone
o Critical phase
o Useless [na makita mo] sa CBC, [pag]
hinahanap mo mataas na platelets habang
may fever, no, you will not see that
 During the recovery period, tataas din yung
platelets
 Infection from 1 serotype will not give you
protection from the others
o So kung nagkadengue-3 na ako, di pa
ko ligtas, meron pang 1,2 and 4
Treatment and Control
 No antiviral drug therapies
 Fluid replacement therapy
 Vaccine is difficult
o Because you must provide protection against all
4 serotypes
 Anti-mosquito measures

 Of course, meron ding rashes, minsan para

siyang measles na rashes kasi isang
exanthem—
‘pag sinabi nating viral exanthem, these are
fevers and rashes cause by viruses
 It’s not typical na it would start from head-
down


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FROM DOC ARVIN ♥ – SYNCHRONOUS
YELLOW FEVER VIRUS: FLAVIVIRIDAE
 Sometimes you will see Petechiae which are flat
Overview
rashes compared to macular ones
o When we say maculopapular, nakaumbok at  One of the great plagues in history
tska mga flat  1900, Panama Canal (construction)
o Dr. Walter Reed discovered the source of
infection
o Monkeys in the jungle serve as the reservoir
o Mosquito as the vector
o 1st virus clearly associated with transmission by
a mosquito
o 1st disease identified in the group Flaviviridae
o Thousands of individuals died during the
construction of this canal
 This is what we call Herman’s rash
Pathogenesis
(whose man? Herman *snorts TAWA KAYO SMH)
 Virus enters through mosquito bite
 You will see the rashes are white, the skin is red
 Spreads to lymph nodes, liver, spleen, kidney, bone
 This is a good sign, a sign of recovery for dengue
marrow, and myocardium
patients usually found in the lower extremities and
 Present in blood during infection
are very itchy
 Primarily infects the liver cells resulting to fever,
jaundice and hemorrhage
Summary of terms from ✨google✨
 Presence of lesions which are caused by localization
 Viral Exanthem - eruptive skin rash that is often
and propagation of the virus in that particular organ
related to a viral infection
o Necrotic lesions present in the liver and kidney
 Petechiae - pinpoint, round spots that appear on the
 At the same time there would be degenerative
skin, usually flat to the touch, don't lose color when
changes in the spleen, lymph nodes and the heart
you press on them
 Maculopapular rash - made of both flat and raised Clinical Symptoms
skin lesions
 Asymptomatic or acute infection
 Herman’s rash - appears as a maculopapular o Fever, myalgia, backache, headache, anorexia,
erythematous rash with islands of normal skin nausea, and vomiting
sparing or scarlatiniform, it blanches upon pressure, o Recovery after 4 days
described as "Islands of white in a sea of red”
 Systemic toxic phase
o 15% of the patients can enter this phase
o Fever reappears
o Jaundice, renal failure, and bleeding
 Bleeding in mouth, nose, eyes and other
areas
o 50% of the patients can die in this phase
o Other 50% can recover
 Hemorrhage and circulatory collapse
 In this viral infection, there can be presence of:
o Vomitus – described as black or with altered
blood bc of hemorrhagic tendencies
o Melena – black tarry feces
o Ecchymosis – bruises
o Encephalitis is rare
o Severe cases: renal dysfunction and
hemorrhage
Regardless of the severity of infection, patients may die
or recover completely.

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 o Increased travel into endemic regions

ST. LOUIS ENCEPHALITIS (SLE): FLAVIVIRIDAE

Overview
 Most common flavivirus infection in U.S.
 Milder in children than adults
 Older patients have risk of serious illness and death
Transmission Cycles  Mostly occur during summer months
 Sylvatic cycle  First recognized in 1933
o Maintained in monkey populations
 Urban cycle Characteristics
o Occurs in larger towns and cities  Most likely asymptomatic
o Mosquitoes transmit infection to people  Symptomatic patients develop fever
o Infected humans can continue the transmission  May develop meningoencephalitis
when they are bitten by uninfected mosquitoes  Transmitted by bird-biting Culex mosquitoes
which can lead to large outbreaks which can
occur in a single case of yellow fever WEST NILE VIRUS
 Intermediate cycle OVERVIEW
o Occurs in smaller villages in Africa only  First isolated and identified in 1937
o Humans and monkeys are the reservoirs o From a febrile patient in West Nile
o Mosquitoes can act as reservoirs and vectors in district of Uganda
high morbidity, low mortality outbreaks  Endemic in Africa, Israel, Europe, and United
o Mosquitoes transmit virus from monkeys to States
humans and vice versa o May occur in Europe, Middle East,
Africa, Southwest Asia, and recently in
the US
When patients acquire the virus from the Intermediate o Considered as the leading cause of
cycle and travel to larger cities where they are bitten by Arboviral encephalitis in the United
mosquitoes, this can trigger an outbreak of Urban YF. States
 Member of Japanese encephalitis antigenic
complex

Prevention
 st
1 flavivirus for which an effective vaccine has been
developed
CHARACTERISTICS
o Vaccine is available
 Transmitted by mosquito vector between birds
 Has greatly reduced and eliminated the
and humans
transmission of the yellow fever in some o It is maintained in a bird-mosquito cycle
countries but still considered as an Epidemic o Birds are the natural reservoir of the
in some parts of Africa and South America virus
o No antiviral drug therapies  Virus replicates actively inside the avian host
 But emergence may result from o Humans
o Increased spread of mosquito vectors  Virus can be present in tissues, blood, serum,
o Deforestation in Africa and South America CSF
o Infected humans or animals

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 - Includes mosquito control and
protection against mosquito bites

WNV EPIDEMIC
 2002, 1st documented case of person-to-person
transmission
o Organ transplantation
o Blood transfusion
o In utero
o Breastfeeding
TRANSMISSION
 Can also be transmitted through person-to- ZIKA VIRUS
person OVERVIEW
o Blood transfusions  1947, Uganda (monkeys)
o Tissue transplantation o
o Human breast milk  1952, Uganda and Tanzania (humans)
 Infection is often accompanied by o Where Zika Virus was first seen in
o Fever, Leuokopenia, and Malaise humans
o May progress to Encephalitis  st
2015, 1 confirmed infection in Brazil
 Endemic to parts of Africa and Asia
 Here are the places where there are high cases
of the Zika virus (pertaining to pic)

CLINICAL FINDINGS
 80% are asymptomatic
 20% are symptomatic
o The symptoms include fever, headache,
fatigue, skin rash, swollen lymph glands,
eye pain
 There can also be a development of
Neuroinvasive disease
o If age is greater than 50 years old (>50)
o Manifests meningitis, encephalitis, or
paralysis

CHARACTERISTICS
 Transmitted by Aedes
o Aedes aegypti and Aedes albopictus
 Mode of transmission
o Exposure to infected blood
o Sexual contact
o Mother to child (less common)
- Can pass through the placenta and
may infect the fetal tissue
TREATMENT
- Zika Virus has now become a major
 No specific treatment cause of birth defects in those
 But in 2003, West Nile Virus Vaccine for horses regions where transmission occurs
became available *naols* CLINICAL SYMPTOMS
 For severe cases  Similar to infections of other arboviruses
o Hospitalization o Fever
o Supportive care (IV Fluids or respiratory o Skin rashes
support) o Conjunctivitis
o Prevention of secondary infection o Muscle and joint pain

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 o Malaise BUNYAVIRIDAE
o Headache OVERVIEW
o Fatigue  First detected in Bunyamwera, Uganda
 Symptoms are usually mild and may last for 2-7
 Triple segmented, enveloped, helical, (-) ssRNA
days
 Incubation period is yet unclear but it’s likely to  Most members cause
be 2 days o Febrile illness
o Hemorrhagic fever
o Encephalitis
 RNA virus consisting of Three single stranded RNA
segments
 Unique feature of this family is that it is described as
tripartite, meaning there is presence of three RNA
segments in the genome
 These viruses are large and a diverse group,
COMPLICATIONS proximately there is about 300 total members of the
 Congenital brain abnormalities viruses with 12 human pathogens and they are
o Disease detected by amniotic fluid mostly transmitted by mosquitoes
o Microcephaly
 The transmission is through mosquito, tick, and
- Small head size
sandfly vectors except for hantaviruses which are
- Smaller circumference of the head
compared to its normal size zoonoses transmitted by contact with rodent host
o Triggers Guillian-Barre Syndrome and/or their excretions
- Outbreak in brazil which was
reported on Guillian-Barre PATHOGENESIS
Syndrome  Arthropod vector
- Pregnant women gave birth to
o Initial replication in the gut then appear
babies with birth defects
- A rare disease but is considered as in saliva
a serious autoimmune disorder o Transmits to host after feeding on blood
(where the immune system attacks  Vertebrate hosts
the healthy nerve cells in the o Develop asymptomatic viremia
peripheral nervous system)  Some hosts become febrile
- May lead to weakness of the
muscles, numbness, and tingling
- May also lead to paralysis GENERA
 Orthobunyavirus
o La Crosse (LACV): encephalitis
 Phlebovirus
o Rift valley fever: encephalitis and
hepatitis
o Sandfly fever
 Nairovirus
o Crimean Congo Hemorrhagic Fever:
vascular endothelium and liver
 Hantavirus
TREATMENT
o Also belong to Bunyaviridae
 No specific treatment o Rodent – borne viruses
o This virus is usually mild.. and people
with Zika Virus should get plenty of rest o Affect the peritoneal cavity, kidneys,
and drink enough fluids and should treat thoracic cavity, lungs
pain and fever with medicines
 No vaccine is available LA CROSSE VIRUS
 BUNYAVIRIDAE- ORTHOBUNYAVIRUS
OVERVIEW
 Member of California encephalitis virus complex

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 Major cause of encephalitis and aseptic animals. Namely the cattle, sheep, goats, the
meningitis in children buffalo and even camels.
 This direct contact can occur through butchering
or slaughtering or while caring for sick animals or
when you are doing veterinary procedures like
assisting the animal in giving birth or if you’re
going to consume raw or undercooked animal
products.

CLINICAL MANIFESTATIONS CLINICAL MANIFESTATIONS

 California encephalitis viral infection  Mild febrile illness
o Severe headache  Complications
o Nonspecific fever o Retinitis
o Vomiting  Primarily the ocular disease or
o Convulsions disease of the eye
o Seizures o Encephalitis
 Common in children  Inflammation of the brain that
o “Summer flu” or “summer cold” may lead to headaches, coma
 Caused by vector woodland mosquitoes. Also the or seizures
Aedes, primarily the Aedes triseriatus o Hemorrhagic fever
 The host usually are squirrels, chipmunks, and  There would be bleeding in the
rabbits gums, or from the nose, skin or
from injection sites.
o Permanent loss of vision may occur

RIFT VALLEY FEVER

 BUNYAVIRIDAE- PHLEBOVIRUS EPIDEMIOLOGY
CHARACTERISTICS  Sub-Saharan Africa
 Targets domestic livestock (zoonotic)  Outbreaks
 Mosquitos: Aedes species o 1977, Egypt
 Transmission to humans o 1987, West Africa
o Contact with infected animal blood o 1997, East Africa
o Body fluids o 2000, Yemen and Saudi Arabia
o Mosquito bites
 Although they target domestic livestock, they can
also be transmitted to humans through contact
with blood, body fluids or tissues of these infected

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 o Abdominal pain
o Leukopenia

TREATMENT AND CONTROL

 No specific treatment
 Use of insect repellents and insecticides
o Small size of sandflies: can pass through
ordinary mosquito nets

Crimean-Congo Hemorrhagic Fever

SANDFLY FEVER Characteristics
 BUNYAVIRIDAE- PHLEBOVIRUS  Bunyaviridae - Nairovirus
 Causes high mortality infection in humans
EPIDEMIOLOGY  Reported nosocomial transmission
 Transmitted through ticks
 Phlebotomus fever or Pappataci fever
 Female sandfly: Phlebotomus papatasii Clinical Manifestations
 Common in childhood  Begins with fever, myalgia, arthralgia,
 Large outbreaks can occur photophobia
 Mistaken for malaria  Mental status changes
o Confusion, agitation, depression, or
drowsiness
 Petechiae and ecchymoses (bruises)
o On the mucosal surfaces and on the
skin
 Bleeding from bowel, nose, and gums
o In general, 30% of patients may die

CLINICAL MANIFESTATIONS
 Small itching skin papules
 Symptoms
o Headache
o Malaise Genus Hantavirus
o Nausea Overview
o Fever  Bunyaviridae – Rodent-borne
o Photophobia
o Stiffness of the neck and back

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 Transmission occurs by inhaling aerosols coming
from rodent excreta (urine, feces, and saliva of Clinical Manifestations
rodents)  Hemorrhagic Fever with Renal Syndrome
 Rodents may also develop infection, that’s why (HFRS)
the virus can shed in their saliva feces and urine o Hantaan virus, Seoul virus, Puumala
virus, Dobrava virus
Classifications o Targets kidney
 Old World Hantaviruses  There could also be renal failure
o Endemic to Europe and Asia or acute renal insufficiency
o Hantaan and Dobrava viruses o Febrile prodrome, fever and shock,
 Cause the severe disease oliguria
o Puumala hantavirus  Hantavirus Pulmonary Syndrome (HPS)
o Fever, chills, myalgia, headache
o Hypotensive shock and pulmonary
 Mild form of HFRS called edema
nephropathia epidemica o Tachycardia, hypoxia, hypotension
(nephritis) o No signs of hemorrhage
- Can generally resolve o Severe cases: DIC (Disseminated
without hemorrhagic Intravascular Coagulation)
complications, because o Therapy: Ribavirin
it’s milder form of  Other Hantaviruses causing HPS:
HRMS o New York virus, Black Creek Canal virus,
o Rodent: Apodemus agarius Bayou virus (US)
o Andes virus (Argentina and Chile)
o Choclo virus (Panama)
o Oran virus
o Monongahela virus
o Lechiguanas virus
o Laguna Negra virus

TOGAVIRIDAE
Overview
 Envelope and icosahedral, ssRNA
 New World Hantaviruses  Mode of transmission
o Sin Nombre Virus (SNV) o Arthropod vector
 Causes Hantavirus Pulmonary o Respiratory and transplacental
Syndrome (HPS)
 “Sin nombre” means “no name” Genera
 First Hantavirus recognized to  Alphavirus
cause disease in North america o Eastern Equine Encephalitis (EEE)
 First to cause primarily an adult o Western Equine Encephalitis (WEE)
respiratory distress syndrome o Venezuelan Equine Encephalitis (VEE)
o Deer mouse: Peromyscus maniculatus o Chikungunya
 Primary host
o Mode of Transmission FROM MA’AM MARIJIEM:
 Inhaling contaminated  Alphaviruses are also distributed worldwide
aerosolized mouse urine, saliva, and are antigenically related
and feces  The viruses can be inactivated by acid pH,
 Rodent-to-human heat, lipid solvents, detergents, bleach
 In general, it does not cause phenols 70% alcohol, and formaldehyde
person-to-person transmission
does not occur

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  Rubivirus Chikungunya
o Rubella virus (non arthropod borne) Overview
 Arterivirus: No member known to infect humans
FROM MA’AM MARIJIEM:
 When we talk about Arbovirus infection, the
mosquito will infect the vertebrate host (e.g.
birds, rodents) and that virus will now multiply
in that host, and it can be picked up and
passed along in subsequent mosquito bites.
 But take note that here, humans are incidental
hosts, and they (we) are just infected
incidentally and are not amplifiers of the virus.
 So, they (we) are incidental host and they are
 Mosquito-borne
dead end host.
 “Chikungunya” means “to become contorted”
o They cannot able to pass on the virus
o Came from Kimakonde language, meaning
either to another human or animal
“to become contorted”, and describes the
stooped appearance with joint pain
Eastern Equine Encephalitis (EEE) (arthralgia)
Overview  1952, 1st outbreak in southern Tanzania
 Togaviridae – Alphavirus  2015, major outbreak in the Region of Americas
 Eastern half of US
 Mild influenza like symptoms to encephalitis Clinical Manifestations
 Permanent damage to CNS (50%)
 Birds natural reservoir
 Horses and humans dead end hosts

 Abrupt onset of fever and joint pain

 Muscle pain, headache, nausea, fatigue, rash
 Occasional cases of eye, CNS, and heart
complications
Western Equine Encephalitis (WEE) Transmission
Overview  Bites of infected female mosquitoes
 Milder than EEE virus o Aedes aegypti and Aedes albopictus
o Comparing to EEE, Western Equine  Biting throughout daylight hours
Encephalitis is milder Treatment
 Asymptomatic or mild infection ̶ Fever, headache,  No specific antiviral drug treatment
nausea, mental status changes o The treatment is directed primarily in relieving
 Permanent CNS damage (30%) the symptoms including the joint pain
Venezuelan Equine Encephalitis (VEE)  No commercial vaccine
Overview
 Large outbreaks
 Influenza-like illness in adults
 Encephalitis in children
 Mortality is less common

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 Rubella Virus POST-TEST
Overview
TRUE OR FALSE
1. German measles can be acquired from
inhalation of contaminated aerosols from the
rodent excreta. FALSE
2. Humans are considered as primary hosts of
Alphaviruses. FALSE
3. Dengue hemorrhagic fever may occur in the
person if exposed to two different dengue
serotypes. TRUE
 Enveloped 4. Zika virus can pass through the placenta
 Causes Rubella or German measles and may cause birth defects. TRUE
o “BELL is wearing TOGA from GERMANY” 5. The urban transmission cycle of yellow fever
o Erythematous, maculopapular, discrete rash virus occurs primarily in the monkey
o Postauricular and suboccipital populations FALSE
Lymphadenopathy
o Transient polyarthralgia and polyarthritis
Transmission by droplets
 Can cross placenta- Congenital rubella syndrome
 Available vaccine
o Children and young women before they
become sexually active

Notes from Ma’am LEE

 This rashes will start on the face and they
will spread to the trunk and the limbs.
There are no rashes that will appear on
the palms and sole.
 Found only in the human population
 Transmitted through direct contact with
the secretions (nasopharyngeal or
congenital) or droplets
 German measles is a benign disease, in
general, it is characterized by having
fever and rashes
 Included in trivalent vaccine which is
known as the MMR (Measles, Mumps
and Rubella)
 Since this a congenital syndrome, that
means the virus can cross the placenta
and the syndrome can range from birth of
a normal infant to the birth of impaired
infant/ Spontaneous abortion.
 Rubella is more on lymph node
involvement with headache, sore throat,
coryza and forchheimer spots on soft
palate

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 DOUBLE STRANDED RNA VIRUSES

REOVIRIDAE
• Classified under the group III of the Baltimore • σ1 protein
classification of viruses o Hemagglutinin (HA) responsible for cell
• Classified into two subfamilies attachment of the virus
o Spinareovirinae o Located in the outer capsid of the virus
▪ Contain large spikes in the 12 vertices of • REO – “Respiratory Enteric Orphan virus”
the particle o Orphan – no association to any disease
▪ Would appear rough
o Sedoreovirinae ROTAVIRUS
▪ Lacks the large surface projections
▪ Would appear smooth
• Four genera of reoviridae:
o Orthoreovirus
o Orbivirus
o Coltivirus
o Rotavirus (A, B, and C)

Genus Species
Rotavirus Rotaviruses A, B,
and C
Orbivirus Changuinola virus,
Sedoreovirinae Corriparta virus,
Great Island virus,
Lebombo virus,
Orungo virus
Coltivirus Colorado tick fever
virus
Spinareovirinae
Orthoreovirus Mammalian
orthoreovirus
• Latin word, Rota – “wheel”
• Replicates in the cytoplasm • sharp-edged double shelled capsids
• Naked virus: • has the Incomplete and complete particles
o transmitted through fecal-oral route o Incomplete:
o After infecting a cell, it would undergo cell lysis ▪ single shelled virus
• Icosahedral symmetry ▪ smaller than the complete particles
▪ already lost the outer shell
• Linear, segmented genome
o Genetic reassortments could occur readily in • rougher surface
cells coinfected with different viruses of the o Complete:
same subgroup ▪ infective
▪ Harboring different viruses would give rise ▪ double shelled virus
to viral particles containing RNA segments ▪ smooth surface
from different parental strains • Seven species (A-G) – VP6
o Number of segments in each of the genus o One Tentative species: (H)
would differ ▪ Based on antigenic epitopes on the
• Two to three protein shells (capsid) presence of internal structural protein VP6
• Not enveloped
• Short spikes
• Three groups o Diarrhea
Strain ▪ Due to impaired sodium and glucose
Group A Majority of human infections/most absorption
common cause o Abdominal pain
Group B Chinese Adult Diarrhea Rotavirus o Respiratory infections (may occur with fever)
(ADRV)
• Stools are yellow or pale, without blood or mucus
Group C Occasional and sporadic outbreaks
• Self-limiting
ROTAVIRUS: Pathogenesis o Recovery within 5-10 days
• Replication at small intestine
ROTAVIRUS: Treatment and control
o In the epithelial cells in the tips of the microvilli
of the small intestine • Replacement of fluids and restoration of electrolytes
o For vomiting and diarrhea
• Causing damage in enterocytes
o Once the virus attaches itself through the • Wastewater treatment and sanitation
presence of the σ1 protein, it would penetrate o For control
the enterocytes and multiply in the cytoplasm of • Vaccines given orally (3 or 2 doses) starting at 2
enterocytes and damage their transport months:
mechanisms o oral live attenuated rhesus-based rotavirus
• NSP4 enterotoxin vaccine (1998)
o NSP – nonstructural protein ▪ withdrawn a year later because of reports
o Cause secretion with intussusception (bowel blockages) as
o Virus would cause stunting of the microvilli a serious side effect
o Adsorption is reduced o oral live attenuated pentavalent human bovine
rotavirus (2006)
• Shed at the lumen of intestine → stool
▪ RV5; RotaTeq, Merck
• can cause nosocomial outbreaks in the absence of
▪ a delay in the onset of the rotavirus season
good hygiene
from mid-November to late February was
seen
ROTAVIRUS: Epidemiology
▪ RotaTeq is a series of three oral vaccines
• Can infect different hosts (e.g. Swine rotavirus)
administered beginning at age 6 to 12
o Swine rotavirus – infecting both infants and
weeks
weanling piglets
o oral live attenuated monovalent human
• Worldwide gastroenteritis in infants and children
rotavirus (2008)
(<5yo)
▪ Rotarix (RV1; GlaxoSmithKline, Brentford,
o Public health concern
UK)
o Major cause of infant mortality
o most common cause of viral gastroenteritis
ORBIVIRUS
• Epidemic diarrhea of infant mice (EDIM)
• 10 segments of dsRNA
• Nebraska calf diarrhea
• Sensitive to low pH
• Simian virus SAII
o Easily degraded when exposed to low pH
• Infection is common during winter seasons in
• Animal and human infection
temperate areas and year-round in subtropical and
• Transmission through an arthropod vector
tropical regions
• Most common in developing countries
Arthropod
vector
ROTAVIRUS: Clinical Features African horse Culicoides Infections in horses
• Fecal-oral transmission sickness virus and mule in India
• 1-4 days incubation Bluetongue virus Culicoides Infects sheep
• Common Signs and symptoms occur suddenly: Palyam (Kasba) Culex *Prevalent in India
and Vellore Infection in sheep,
o Vomiting
viruses calves
▪ Causing rapid loss of fluid and fatal
dehydration which can cause death of the
patient

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 COLTIVIRUS ORTHOREOVIRUS
• an 80-nm spherical particle with two outer shells • Wide range of hosts
containing 12 RNA segments • Asymptomatic infections in humans
• vector: Dermacentor andersoni • Minor febrile illness
o has many hosts in nature, including deer, o Enteritis
squirrels, and rabbits o Mild respiratory disease
• Hemagglutinin for human O or bovine erythrocytes
• Important model system for study of pathogenesis of
viral infections at a molecular level

REFERENCES:
Double Stranded RNA Viruses
Department – Sanctioned PPT
Recorded Lecture by Prof. Rothessa
Mary G. Caringal, RMT

• Colorado tick fever/Mountain fever

o Dengue like infection in western US and SW
Canada
▪ one of the most common diseases
transmitted by ticks in the United States
o Signs and symptoms:
▪ Fever, photophobia, myalgia, arthralgia,
and chills
▪ Biphasic fever with a rash can also occur
▪ Children can experience hemorrhagic fever
o Self-limiting
o Avoid tick-infested areas, using repellent
chemicals and protective clothing

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 UNIT VI & VIII: RETROVIRIDAE AND PRIONS

Pre-test:
1. This virus has ssRNA which is enveloped . Has
reverse transcriptase and the etiologic agent of
Acquired Immunodeficiency Syndrome (AIDS).
Retroviridae
2. Retroviridae is transmitted through sweat,
saliva, tears, urine, milk. FALSE
3. The transient course of HIV is characterized as RETROVIRUSES
Transient febrile disease with • Require RNA-dependent DNA polymerase
lymphadenopathy, pharyngitis, or a diffuse • Oncovirinae
rash. TRUE o Human T-lymphotropic virus 1, 2, 5
4. Destruction of large numbers of CD4 cause (HTLV-1, HTLV-2, HTLV-5)
symptoms of HIV to appear with increased ▪ Cause leukemias (malignant),
susceptibility to opportunistic infections, sarcomas, and lymphomas
disease and malignancy. TRUE • Lentivirinae
5. This is the outer shell of Retrovirus. Viral o HIV-1
envelope o HIV-2

GENERAL CHARACTERISTICS INTRODUCTION

• Etiologic agent of Acquired Immunodeficiency
• Enveloped Syndrome (AIDS).
• ssRNA • Discovered independently by Luc Montagnier of
• Has reverse transcriptase France and Robert Gallo of the US in 1983-84.
• The outer nucleocapsid and matrix protein is derived • Former names of the virus include:
from the lipid envelope of the host cell. o Human T cell lymphotrophic virus
• Three genes (HTLV-III)
o Gag – capsid, matrix and nucleic acid o Lymphadenopathy associated virus
binding proteins (LAV)
o Env – envelope, glycoproteins o AIDS associated retrovirus (ARV)
o Pol – polymerase, protease and integrase
CHARACTERISTICS OF THE VIRUS
• Icosahedral (20 sided), enveloped virus of the
RETROVIRIDAE lentivirus subfamily of retroviruses.
HUMAN IMMUNODEFICIENCY VIRUS • Retroviruses transcribe RNA to DNA.
• HIV can be transmitted through • Two viral strands of RNA found in core
o Sexual contact surrounded by protein outer coat.
o Injection drug use o Outer envelope contains a lipid matrix
o Pregnancy, childbirth and breast feeding within which specific viral glycoproteins
o Occupational exposure are imbedded.
o Blood transfusion/ organ transplant o These knob-like structures responsible
▪ That’s why we have the HIV test for binding to target cell.
for the patients and for the
donor, to check for the presence
of the virus

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 • New cases in 2011
o Associated with:
▪ Heterosexual contact : 27%
▪ Men who have sex with men:
61%
▪ Intravenous (IV)-drug use: 9%
▪ Heterosexual contact and IV-
drug use: 2%
▪ Transfusions of mother to infant
:1%

STRUCTURAL GENES
• Three main structural genes:
o Group Specific Antigen (Gag)
o Envelope (Env)
o Polymerase (Pol)
HIV
• The outer shell of the virus is known as the Viral
GROUP SPECIFIC ANTIGEN (Gag)
envelope
• Located in nucelocapsid of virus.
• Embedded in the viral envelope is a complex
• Icosahedryl capsid surrounds the internal nucleic
protein known as env which consists of an outer
acids made up of p24 and p15.
protruding cap glycoprotein (gp) 120, and a stem
• p17 lies between protein core and envelope and
gp41.
is embedded in the internal portion of the
• Within the viral envelope is an HIV protein called
envelope.
p17 (matrix), and within this is the viral core or
• Two additional p55 products, p7 and p9, are
capsid, which is made of another viral protein p24
nucleic acid binding proteins closely associated
(core antigen)
with the RNA.

ENVELOPE (Env)
• Envelope (Env) gene codes for envelope proteins
gp160, gp120 and gp41.
o These polyproteins will eventually be
cleaved by proteases to become HIV
envelope glycoproteins gp120 and gp41.
o gp160 cleaved to form gp120 and gp41.
o gp120 forms the 72 knobs which protrude
from outer envelope.
o gp41 is a transmembrane glycoprotein
antigen that spans the inner and outer
membranes and attaches to gp120.
RETROVIRUSES o gp120 and gp41 both involved with fusion
• Transmission and attachment of HIV to CD4 antigen on
o Blood or exchange of body fluids (sexual host cells.
contact) or congenital infection
▪ There are some patients that the POLYMERASE (Pol)
mother is HIV positive and the • Polymerase (Pol) codes for p66 and p51 subunits
baby is also HIV positive but of reverse transcriptase and p31 an
there are also cases wherein the endonuclease.
mother is HIV positive but the o Located in the core, close to nucleic
baby is HIV negative acids.
o Not transmitted by sweat, saliva, tears, o Responsible for conversion of viral RNA
urine, milk into DNA, integration of DNA into host

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 cell DNA and cleavage of protein Meaning, there are HIV patients that are not
precursors. experiencing any signs and symptoms. That is the
period of latency.
Disease course • CD4 cell may be destroyed in the process, body
• Initial infection attempts to replace lost CD4 cells, but over the course
o Transient febrile disease with of many years body is unable to keep the count at a
lymphadenopathy, pharyngitis, or a diffuse safe level.
rash. • Destruction of large numbers of CD4 cause
o When we say febrile, it pertains to on and off symptoms of HIV to appear with increased
fever. Fever is 37.8 and above. susceptibility to opportunistic infections, disease and
o Lymphadenopathy- Lymph nodes in the malignancy. So, after years of latency, pag bumalik
neck or mga kulani. siya ulet (naol), mas progressive or mas poor ang
o High levels of circulating virus with absence prognosis.
of specific antibody • Methods of transmission:
o Antibody develops in several weeks to o Sexual transmission, presence of STD
months increases likelihood of transmission.
• Subclinical phase o Exposure to infected blood or blood products.
o Antibody, circulating p24 antigen, low levels o Use of contaminated clotting factors by
of circulating virus. So eto na yung na-iinfect hemophiliacs.
yung immune system of the patient. o Sharing contaminated needles (IV drug users).
Bumababa yung immune system ng patient o Transplantation of infected tissues or organs.
that is why individual with HIV, mas madali o Mother to fetus, perinatal transmission variable,
sila kapitan ng infection, when we say that, dependent on viral load and mother’s CD 4
usually when they are admitted in the count.
hospital, reverse isolation sila. when we say Early Phase HIV Infection
reverse isolation, bawal silang dalawin since
pwede mahawa yung patients.
o Virus continues to mutate to avoid immune
cells and infects immune cells.
Viral Replication
• First step, HIV attaches to susceptible host cell.
o Site of attachment is the CD4 antigen found on
a variety of cells
▪ helper T cells
▪ macrophages
▪ monocytes
▪ B cells
▪ microglial brain cells • In early phase HIV infection, initial viruses are M-
▪ intestinal cells tropic. Their envelope glycoprotein gp120 is able to
▪ T cells infected later on when the disease bind to CD4 molecules and chemokine receptors
becomes progressive called CCR5 found on macrophages
• The gp120 protein on virus binds specifically to CD4
receptor on host cell with high affinity.
• Gp41 causes fusion of the virus to the cell membrane.
o After fusion virus particle enters cell.
o Viral genome exposed by uncoating particle.
• Reverse transcriptase produces viral DNA from RNA.
o Becomes a provirus which integrates into host
DNA.
o Period of latency occurs.
• After a period of latency lasting up to 10 years viral
replication is triggered and occurs at high rate.

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• In late phase HIV infection, most of the viruses are
T-tropic, having gp120 capable of binding to CD4 and • Being that HIV reduces immunologic activity, the
CXCR4 found on T4- lymphocytes intraoral environment is a prime target for
• It is called T-tropic because this is in T4- chronic secondary infections and inflammatory
lymphocytes. In the early phase, we call it M-tropic processes, including OHL, which is due to the
because the location is in the macrophages Epstein-Barr virus under immunosuppressed
conditions or vulnerable patients
Primary HIV Syndrome • OHL- Oral Hairy leukoplakia
• Mononucleosis-like, cold or flu-like symptoms may Kaposi’s Sarcoma (KS)
occur 6 to 12 weeks after infection.
o Lymphadenopathy
o Fever- On and off; low to moderate grade fever
o Rash- Diffused rashes
o headache
o Fatigue
o Diarrhea
o Sore throat
o Neurologic manifestations.
o No symptoms may be present
o Symptoms are relatively nonspecific. • Kaposi’s sarcoma is a rare cancer of the blood
o HIV antibody test often negative but becomes vessels that is associated with HIV. It manifests as
positive within 3 to 6 months, this process is bluish-red oval-shaped patches that may
known as seroconversion. eventually become thickened. Lesions may appear
o Large amount of HIV in the peripheral blood. singly or in clusters.
o Primary HIV can be diagnosed using viral load • Usually this becomes swollen, then parang elevated
titer assay or other tests. tas pag hinawakan parang makapal. So they appear
o Primary HIV syndrome resolves itself and HIV in single hindi kumpol-kumpol in one place.
infected person remains asymptomatic for a AIDS
prolonged period, often years. That is why yung • CD4 count drops below 200, people is considered
iba, hindi nila alam na may HIV sila tapos pag to have advanced HIV disease
bumalik, mas malala na. • If preventative medications did not start, the HIV
Clinical Latency Period infected person is now at risk for:
• HIV continues to reproduce, CD4 count gradually o Pneumocystis carinii pneumonia (PCP)
declines from its normal value of 500-1200. o cryptococcal meningitis
• Once CD4 count drops below 500, HIV infected o toxoplasmosis
person at risk for opportunistic infections. • If CD4 count drops below 50:
• The following diseases are predictive of the o Mycobacterium avium
progression to AIDS: o Cytomegalovirus infections
o Persistent herpes-zoster infection (shingles) o Lymphoma- Rare cancer involving the
o Oral candidiasis (thrush) lymph nodes
o Oral hairy leukoplakia o Dementia- Loss of memory
o Kaposi’s sarcoma (KS) o Most deaths occur with CD4 counts
Oral Hairy Leukoplakia below 50

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Common Opportunistic Infections and Cancers in o Failure to thrive
Patients with AIDS o The patient (baby) is irritable (ayaw
• Candidiasis of the respiratory tract dumede, iyak nang iyak kahit busog and
• Coccidiomycosis kahit hawak naman ni mommy iritable pa
• Cryptococcal meningitis rin)
• Cryptosporidiosis with persistent diarrhea o Persistent oral candidiasis
• Cytomegalovirus infections of organs other ▪ May mga sore in the mouth
than the liver, spleen, or lymph nodes
(mouth sores)
• Histoplasmosis
• Persistent herpes simplex virus infections o Hepatosplenomegaly (enlargement of
• Kaposi sarcoma or lymphoma of the brain in the spleen)
patients <60 years o Lymphadenopathy
• Oral hairy leukoplakia o Recurrent diarrhea
• Lymphoid interstitial pneumonia, pulmonary o Recurrent bacterial infections
lymphoid hyperplasia, or both in children <13 o Abnormal neurologic findings.
years
• Mycobacterium avium complex,
Immunological Manifestations
Mycobacterium kansasii, or Pneumocystic
jirovecii pneumonia
• Progressive multifocal leukoencephalopathy • Early stage slight depression of CD4 count, few
• Recurrent pneumonia symptoms, temporary.
• Toxoplasmosis of the brain in infants >1 month o Many of the patients are asymptomatic if
• Wasting disease the CD4 count is within the normal level
• Window of up to 6 weeks before antibody is
FROM DOC PAGUD (<-mood, pero magiging doc ka detected, by 6 months 95% positive.
rin ☺): o Minsan kasi initially negative. Then after
• These are some of the opportunistic infections
a while dun palang lumalabas yung
that can occur after the period of latency in
patients with HIV antibody/nadedect yung antibody.
• So when the CD4 count below 200 • During window p24 antigen present, acute
nagkakaroon na ng iba’t ibang opportunistic viremia and antigenemia.
infections ang patients. One of the most • Antibodies produced to all major antigens.
common is pneumonia o First antibodies detected produced
Other Opportunistic Infections against gag proteins p24 and p55.
• Respiratory system o Followed by antibody to p51, p120 and
o Pneumocystis Carinii Pneumonia gp41
(PCP) o As disease progresses (or as the disease
o Tuberculosis (TB) worsens) antibody levels decrease.
o Kaposi's Sarcoma (KS) • Immune abnormalities associated with increased
• Gastro-intestinal system viral replication.
o Cryptosporidiosis
o Candida • Decrease in CD4 cells due to virus budding from
o Cytomegolavirus (CMV) cells, fusion of uninfected cells with virally
o Isosporiasis infected cells and apoptosis.
o Kaposi's Sarcoma • B cells have decreased response to antigens
• Central/peripheral Nervous system possibly due to blockage of T cell/B cell
o Cytomegolavirus interaction by binding of viral proteins to CD4 site.
o Toxoplasmosis
• CD8 cells initially increase and may remain
o Cryptococcosis
o Non Hodgkin's lymphoma elevated.
o Varicella Zoster • As HIV infection progresses, CD4 T cells drop
o Herpes simplex resulting in immunosuppression and
• Skin susceptibility of patient to opportunistic infections.
o Herpes simple
o Kaposi's sarcoma
o Varicella Zoster
• Infants with HIV
o Congenital (mother-to-fetus)

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 o So as the HIV worsens, bumabagsak make more copies of itself. This may
talaga ang CD4. This can result to slow down HIV disease
immunocomprised patient and
susceptibility to opportunistic infections.
• Death comes due to immuno-incompetence.
o Many of the patients whohave CD4 count
<50 ito yung worsened na talaga and pag
nag <20 yan, this can cause the death of
the patient due to immunocompetence (I
think ang ibig sabihin ni Ma’am dito is due
to “immunosupression”).

Treatment
• Sustiva + Truvada Treatment
o Sustiva + Truvada (FTC + tenofovor) is
one of the most popular and effective
starting HIV regimens. Important Immunologic Marker for AIDS
o Many patients will have
• Steady decline in number of CD4+ T cells
dream/sleep/central nervous system
• Depression of the CD4+-to-CD8+ cell ratio to
effects particularly in the first month (due
<0.9 (reference value, ≥1.5)
to the Sustiva). • Functional impairment of monocytes and
o Upset stomach/bloating/gas/loose stools macrophages
are also fairly common during the first • Decreased natural killer cell activity (so wala
month and for most patients are fairly nang lumalaban sa infections kasi
mild. nagdedecrease ang NK cells)
o HIV levels in the blood will often drop by • Anergy to recall antigens in skin tests
> 99% in the first month and the CD4
count (marker of immune system • Reverse transcriptase inhibitors
function) will often increase providing o Nucleoside analogs
protection against AIDS related diseases ▪ Azidothymidine,
within weeks/months of starting the dideoxyinosine, d4T (stavudine),
medication. 3TC (lamivudine), and tenofovir
o Non-nucleoside analogs
FROM DOC PAGUD:
▪ Delavirdine, nevirapine, and
• So pag bumabagsak ang CD4,
efavirenz
bumabagsak din ang immune
• Viral protease inhibitors
system ng pasyente na may AIDS.
o Ritonavir, saquinavir, indinavir, and
• So ang ating main goal for the
amprenavir
treatment is to at least normalize the
• Fusion inhibitors
CD4 count to prevent the patient
o T-20, Enfuvirtide
from having immunosupression and
prone to have opportunistic
Immunologic Markers
infections
• Immunologic Markers:
o Decline in CD4+ T Cells from <200,
• Truvada
<100, <50, hanggang sa maging <20
o Truvada is made up of HIV drugs from a
which can cause the death of the patient
class called nucleoside/nucleotide
because of immunosuppression
reverse transcriptase inhibitors
o <0.9 = CD4+ : CD8+ ratio
(NRTIs), also known as “nukes.”
o Impaired monocytes/macrophages
o The NRTIs (nukes) block reverse
o ↓ NK cell activity
transcriptase, a protein that HIV needs to
o Anergy to recall Ag’s in skin test

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 Oncoviruses • Transmissible spongiform encephalopathies
(TSE)
Human Lymphotropic Virus (HTLV) o Normal cellular protein (PrPc) misfolded
when a portion of its α-helical coil
• Originally called RNA tumor viruses
structure refolds to a β-sheet, producing
• Oncogenic Viruses a mutant (PrPsc, a cellular protein)
• Can cause leukemias (a malignancy of the blood) - May be secreted in the urine
• HTLV-1 – has definite association with disease • Animal infection only
• HTLV-2, HTLV-5 – isolated in some hematologic o Scrapie
malignancies (e.g. leukemia) but has no definite - Sheep
o Chronic wasting disease
association
- Mule, deer, and elk
o Transmissible mink encephalopathy
Pathogenesis - Mink
• Mode of Transmission: • Human infection
o Blood transfusion o Very rare to happen unless you have
▪ That’s why we are very careful encountered or you got exposed to
of the donor, so ini-iscreen ng cattle
o Bovine spongiform encephalopathy
mabuti ang donor for HIV
(BSE)
together with hepatitis, - Cattle
malignancies, and contact with - Development of variant Creutzfeldt-
other diseases. Jakob disease (vCJD) from infected
o Sexual intercourse meat of cows with BSE
o Breastfeeding o Kuru
- Aborigines in New Guinea
• Infects T-helper Lymphocytes
o Creutzfeldt-Jakob disease (CJD)
• Once inside the target cell it replicates o Fatal insomnia
competently - All human as natural host
• Aside from replicating the three key genes (gag, Symptoms
env, pol) the Tax protein transactivates the • Dementia, memory loss, behavioral problems
cellular genes for the T-cell growth factor IL-2 • Cerebellar ataxia and shivering-like tremor
and its receptor. This promotes cellular growth. • Complete loss of motor and speech function
o These are the ones the promote the • These are uncontrollable movements and
growth of the virus slurred speech
• HBZ protein limits the activity of Tax thus • Death can occur in 1 month to 1 year
promoting cell survival. o So mas poor ang prognosis nitong
• The virus might remain latent and replicate prions  And this is very rare… also in
slowly for years but may induce clonal outgrowth the philippines this is very rare.
of particular T-cell clones. Transmission
o The same with HIV
• Neural tissue
• Long latency period (30 years on average)
o So matagal ang latency nito unless • Although there might be cases of other tissue
immunosuppressed ang patient noong transmission
nagkaroon siya ng sakit o Can also occur in the brain
o But if the patient is normal, matagal ang o This is usually common in animals
latency period ng oncovirus Other problems
• Antibodies against the gp46 protein are • Survive formalin fixation
produced by the body. o Kahit na finix mo na siya… pwede ka
Clinical Syndrome paring ma-infect so be very careful
• Adult Acute T-Cell Lymphocytic Leukemia • Very resistant to sterilization
(cancer of the blood) o Recommend exposure to 20,000 ppm
chlorine or 1 M sodium hydroxide to
• HTLV-1 myelopathy
inactivate prions
Laboratory Diagnosis
• ELISA
• RT-PCR

PRIONS

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POST TEST

1. These are originally called RNA tumor viruses.

Human Lymphotropic Virus (HTLV) / Oncovirus
2. This is a rare cancer of the blood vessels that is
associated with HIV.
Kaposi’s Sarcoma
T/F 3. Primary HIV syndrome resolves itself and HIV
infected person remains symptomatic for a prolonged
period of time, often years.
FALSE
4. Most deaths occur in AIDS with CD4 counts below 50.
TRUE
T/F 5. Once CD4 count drops below 500, HIV infected
person at risk for opportunistic infections.
TRUE

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 UNIT 7: HEPATITIS
o Yellow Fever Virus (YFV)
PRE-TEST
1. TRUE OR FALSE: Jaundice is often HEPATITIS CLASSIFICATION
initially seen as scleral icterus when the
patient has total serum bilirubin
concentrations above 10 mg/dL.
2. TRUE OR FALSE: HAV only multiplies in
hepatocytes.
3. IDENTIFY: In hepatitis B infection, which
one is undetectable in serum but detected
in BIOPSY of infected hepatocytes.
4. IDENTIFY: RNA virus that can replicate
only in the presence of HBsAg
5. IDENTIFY: Single-stranded non-enveloped
DNA virus belonging to the genus
Annellovirus Infectious Hepatitis
OVERVIEW OF HEPATITIS • Viral Hepatitis
• Hepatitis is an inflammation of the liver. The • Bacterial Hepatitis
condition can be self-limiting or can progress to o Leptospirosis, Syphilis
fibrosis (scarring), cirrhosis or liver cancer. • Parasitic Hepatitis
o Hepatitis comes from the Greek word “Hepar” o Amebiasis, Fascioliasis, Toxoplasmosis,
which means liver and” Itis” which means Opistorchiasis
inflammation
Toxic Hepatitis
o Hepatitis is caused by a virus or a toxin and
characterized by jaundice, liver enlargement • Alcoholic Hepatitis
and fever • Medicinal Hepatitis
o Basically, hepatitis is self-limiting means it can • Clinical Hepatitis
aggravate into a more serious liver cirrhosis o In case of poisoning with various substances
• Hepatitis viruses are the most common cause of
hepatitis in the world but other infections, toxic
substances (e.g. alcohol, certain drugs), and OVERVIEW OF HEPATITIS
autoimmune diseases can also cause hepatitis. Henry’s Clinical Diagnosis
• According to the World Health Organization • Most viral-induced liver pathology is caused by five
viruses that are known to cause hepatocyte injury and
VIRAL HEPATITIS are termed hepatitis viruses, namely, hepatitis A, B,
• Hepato-tropic viruses C, D, and E.
o These viruses are responsible for more than • However, hepatitis A, B, C, D, and E virus infections
80% of the cases of viral hepatitis
characteristically lead to lytic hepatocyte injury and
o Hepatitis A Virus (HAV)
o Hepatitis B Virus (HBV) account for most clinical cases of infectious hepatitis.
o Hepatitis C Virus (HCV) • In actuality, viruses are the cause of 80%–90% of
o Hepatitis D Virus (HDV) acute (< 6 months) and chronic (persist longer)
o Hepatitis E Virus (HEV) hepatitis.
• Newly identified hepatitis G causes only a self-limited
• Other viruses form of hepatitis.
o There are also other viruses that are
implicated to bring about hepatitis.
SIGNS AND SYMPTOMS
o Adenovirus
o Cytomegalovirus (CMV) • Liver is known as the Uncomplaining Organ
o Epstein Barr Virus (EBV) o Much of the liver can be damaged without any
o Herpes Simplex Virus (HSV) symptoms
 Sir Greg – Asynchronous
• Possible Symptoms are easy to miss
o Flu-like symptoms
Hepatitis A & E
▪ Fever, chills, fatigue, loss of appetite,
Both transmitted via fecal-oral route
nausea, vomiting, diarrhea, muscle aches,
(pwede niyo remember as tAE HAHA)
dehydration
o Pain or tenderness under lower right rib
Hepatis B, C & D
o Weight loss, lack of appetite
Parenterally transmitted or via injection
o Extreme Fatigue
• Classical Signs of liver problems
Hepatitis B & C
o Jaundice
Used in screening blood donors (Blood sCreening
▪ Yellowing of the skin pigment and whites
#medyopilit)
(sclera) of eyes
▪ Jaundice is often initially seen as scleral
Hepatitis B
icterus when the patient has total serum
The only DNA virus (Group 7)
bilirubin concentrations above 2 mg/dL
Hepatitis D
Resides inside Hepatitis B and causes the greatest
risk of liver failure

o Dark urine, light stools FOR RECALL LANG DAW ULET THX DAD
o Distended abdomen
▪ Fluid buildup in the stomach area

FOR RECALL DAW AWWE THX LOVE U DAD GREG

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 Sir Greg – Asynchronous

July 28 is considered as World Hepatitis Day

because it’s the birthday of the birthday of Nobel-
prize winning scientist Dr Baruch Blumberg, who
discovered hepatitis B virus (HBV) and developed a
diagnostic test and vaccine for the virus.
#salamatBaruch

DIFFERENT TYPES OF HEPATITIS

HEPATITIS A

Take Note:
• Hepatitis A has a vaccine, but is a self-limited disease
most people resolve the infection within a short period
of time
• Hepatitis B has a treatment that can help to limit liver
damage, but no cure. GENERALITIES
• Hepatitis C has a Cure, but no vaccine • Agent – Hepatitis A Virus, an enterovirus of the
Picornaviridae (yie ano nga ulet meron kay Picorna? yass
she smol). It multiplies only in hepatocytes (liver cells,
but u already knew that hehe)

• Structure
o Picorna virus
o ssRNA virus
o Measures 27-28 nm
o Icosahedral shape
o Non-enveloped – Naked
o Not easily affected by environmental treatments
o Has one serotype and more than 3 genotypes

• VPg (viral protein genome-linked) is a protein that

Sir Greg – Asynchronous is covalently attached to the 5′ end of positive strand
viral RNA and acts as a primer during RNA synthesis
This slide highlights vaccination as an option for • Most common
prevention of Hepatitis. However, some viruses may • Clinical Manifestations and Pathology Symptoms
not have an ultimate cure. If you would remember on o appear abruptly and last fewer than 2 months but
our discussion in our last shifting period (shempre may persist for as long as 6 months in some
naalala mo yan, magaleng ka eh), Interferon was individuals
mentioned and may be helpful for both Hepatitis B o nausea, vomiting, anorexia, fatigue, fever,
and C infection. jaundice, dark urine, and abdominal discomfort
o rarely fatal

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 o symptoms usually resolve within 3 weeks and persons who may be at risk. The vaccine is produced
are generally self-limiting from inactivated HAV.
• It is believed that the risk is low for pregnant women
• HAV infection is also called infectious hepatitis or and that no special precautions should be taken for
short incubation hepatitis immunocompromised persons
• Among the 5 types, HAV has an average of 28 days • Improvement in water purification, good hygiene, and
(4 weeks) incubation period improved sanitation.
• Immune globulin can be used pre-exposure to protect
EPIDEMIOLOGY AND TRANSMISSION those traveling to high HAV–endemic areas or
• Fecal-oral route: spread through water, food, and postexposure to prevent infection in those exposed
person-to-person contact within a family, after an outbreak at a day-care center,
• Poor hygiene and poor sanitation or from a common source of exposure such as a
o Because young children are generally restaurant.
asymptomatic, the disease is predominantly • Immune globulin should be used postexposure within
spread from person to person within the 2 weeks for maximum protection.
household. • Vaccination of Immune globulin provides prophylactic
o Other individuals at risk are those who are remedy and protection as well
exposed in day-care centers, neonatal intensive
care units, and institutions for the mentally Internalize ka muna. U go girl/boy/whatever u identify as, we
handicapped or who have sexual contact with accept u here, no judgement. 😊
infected individuals or illegal-drug users
It’s not the destination, it’s the journey and everything will be
• Incubation period for HAV is 28 days on average, and
alright in the end, if it’s not alright, it’s not the end. sHE beLIEved
the peak viremic period occurs 2 weeks before the
</3 Always remember when life gives you lemons, request ka
onset of the elevation of liver enzymes or the na rin ng Cuervo tas invite mo kami (post-covid)
appearance of jaundice
• Transmission of HAV by clotting factor concentrates HEPATITIS B
treated with solvent or detergent pathogen process
has been reported.
o In blood product replacement therapy and
through unusual sexual practices.
• Certain sex practices can also spread HAV.

GROUPS FOR WHOM HEPATITIS A

VACCINATION IS RECOMMENDED
• Persons at increased risk for infection
o Travelers to countries with high endemicity for
hepatitis A virus infection
o Men who have sex with men (MSM)
o Users of injection and noninjecting il legal drugs
o Persons who receive blood product replacement • Hepatitis B is a life-threatening liver infection caused
therapy for clotting factor disorders by HBV
o Children and adolescents living in states with • It is a major global health problem
historically elevated rates of hepatitis A. • It can cause chronic infection and puts people at high
• Persons at Increased Risk for adverse consequences risk of death from cirrhosis and liver cancer.
of Hepatitis A • Hepatitis B Virus, also referred to as the Dane Particle
o Persons with chronic liver disease of any is a member of the Hepadnaviridae family
etiology
STRUCTURE & ANTIGEN
PREVENTIVE MEASURE • The virion consists of an outer lipid envelope
• Health professionals now routinely vaccinate o Virions are about 42 nm in diameter
children, travelers to certain countries, and other • Icosahedral nucleocapsid composed of a core protein

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• Nucleocapsid encloses the viral DNA and a DNA
Polymerase that has a reverse transcriptase activity
• The virus is divided into 4 major
serotypes/phenotypes based on its antigenic
epitopes presented on its envelope proteins
• Divided into 8 major genotypes from A – H

o Have distinct geographical distribution used in

tracing the evolution and transmission of the
virus

HbsAg – surface (coat) protein, 4 phenotypes (adw, adr,

ayw, ayr)
HbcAg – inner core protein (singe serotype
HbeAg – secreted protein; function unknown

In hepatitis B infection, HBcAg is not a serological marker

because it is undetectable in serum but detected in
BIOPSY of infected hepatocytes.

Doc Arvin – Synchronous

Antigen – S E C (Surface, Envelope Core)

(outside going inside, papasok)
Kapag ang virus, pumasok, when it infects a patient,
ofc the antigens will go in, ganyan ang order of
appearance nya, SEC. So, if you are asked what is the
first antigen to appear in the blood after being infected
with HBV? HbsAg (oh ang galeng oh).
What is the second? HbeAg (perfect na!!). • HBV is one of the few known non-retroviral viruses
What is the third? WALA. (trick question ehhehe) which use reverse transcription as part of its
because the HbcAg cannot be detected by blood test replication process
because it is inside the virion. Diba? Can you recall
• The virus specifically infects human hepatocytes by
that? (di galet si sir swear) binding the cell surface receptor called sodium
taurocholate co-transporting polypeptide (NTCP)
Antibodies – C E S (opposite nemern)
(inside, going outside, palabas)
HEPATITIS B
The first antibody to be produced in acute hepatitis B
MODE OF TRANSMISSION
infection is actually Anti-Hbc followed by Anti-Hbe
and then Anti-Hbs. That’s why Anti-Hbc can also
serve as a marker during the window period.
Sometimes, it’s too early to test. Negative pa sa iba
pero ang positive lang sa Anti-Hbc

• Blood – direct blood to blood contact

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• Sexual transmission – there is a risk during any type • DANE particle: found in all body fluids and
of sexual contact. secretions (blood, saliva, semen, urine, sweat,
• Mother to child – during birth colostrum)
• Household Contact – sharing hygiene equipment
(razors, toothbrushes, earrings, etc.) STAGES OF HBV INFECTION
• Unsterile health practices
• Sharing needles An HBV carrier is one who
• Hepatitis B is present in blood, semen, or other body Carrier State has HBs ag in blood for 6
months with normal liver
fluids from a person infected with the virus enters the
function test results.
body of someone who is not infected. The patient has abnormal
Chronic Persistent liver function test results
CHARACTERISTICS OF HBV INFECTION Hepatitis with a normal liver biopsy
• WHO estimates that in 2015, 257 million people were specimen.
living with chronic hepatitis B infection (defined as The patient has
hepatitis B surface antigen positive). In 2015, Chronic Active abnormal liver function
Hepatitis test results and abnormal
hepatitis B resulted in an estimated 887 000 deaths, liver biopsy.
mostly from cirrhosis and hepatocellular carcinoma • To establish the stage of Hepatitis B Infection, one
(i.e. primary liver cancer). may compare the results of a liver function test and a
• As of 2016, 27 million people (10.5% of all people liver biopsy.
estimated to be living with hepatitis B) were aware of • Chronic hepatitis is differentiated by a liver biopsy.
their infection, while 4.5 million (16.7%) of the people
diagnosed were on treatment. According to latest
WHO estimates, the proportion of children under five
years of age chronically infected with HBV dropped to
just under 1% in 2019 down from around 5% in the
pre-vaccine era ranging from the 1980s to the early
2000s.
• The hepatitis B vaccine is the mainstay of hepatitis B
prevention. WHO recommends that all infants receive
the hepatitis B vaccine as soon as possible after birth,
preferably within 24 hours – followed by two or three
doses of hepatitis B vaccine at least four weeks apart
HbsAg Anti-HBs Anti-HBC
to complete the series.
• There is no specific treatment for acute hepatitis B. Susceptible (-) (-) (-)
• Chronic hepatitis B infection can be treated with Vaccinated (-) (+) (-)
medicines, including oral antiviral agents. Past (-) (+) (+)
• Tenofovir or entecavir - as the most potent drugs to Infection
suppress hepatitis B virus. Acute (+) (-) IgM
Infection Positive
• Liver transplantation is sometimes used in people
with cirrhosis. Chronic (+) (-) IgG
Infection Positive
• AKA: Serum hepatitis, post transfusion hepatitis,
long incubation hepatitis
HEPATITIS C
• Acute infection is frequently symptomatic, with much
STRUCTURE OF HEPATITIS C VIRUS (HCV)
of the liver damage inflicted by CD8+ cytotoxic T
• Enveloped, (+) ssRNA, genus Hepacivirus, family
lymphocytes
Flaviviridae.
• 1% develop fulminant fatal massive hepatocellular
• In this same family: Yellow fever virus, West Nile
necrosis
virus, and Dengue virus.
• May progress to chronic hepatitis and higher risk of
• Particles are spherical and heterogenous in size
cirrhosis and hepatic carcinoma
typically ranging from 14-18 nm in diameter.
• The lipid envelope contains glycoproteins 1 & 2.
• Flavivirus

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• Icosahedral viral protein coat, embedded in cellular therefore represent ideal targets for the development
lipid and surrounding RNA. of small molecules anti-HCV compounds.
• viral RNA encodes a single protein with more than • The HCV is a single stranded positive-sense RNA.
3000 amino acids That is approximately 9600 nucleotide bases in
• The capsid which consists of entire HCV core proteins length.
forms a cell that encapsidates and protects the HCV • There are different proteins encoded by HCV
RNA. genome.
• The polyprotein is co and post-translationally • HCV is formed by an enveloped particle harboring a
processed by cellular and virally encoded proteases (+) strand RNA of 9.6 kilobase.
to produce the mature structural and non-structural • The genome tells (di maintindihan word sorry  ) a
proteins. long open reading frame or ORF coding a polyprotein
precursor of 3010 amino acids.
• Translation of the HCV ORF is directed via 340
nucleotide long 5’ non-translated region or NTR
functioning as an internal ribosome entry site –
permits the direct binding of ribosomes in close
proximity to the start codon of the ORF.
• The HCV polyprotein is prieved (di maintindihan) co
and post-translationally by cellular and viral proteases
into 10 different products. With the structural proteins
coresid (di maintindihan) E1 and E2 located in the N-
terminal thirds and the non-structural NS2-5
replicative proteins in the remainder.
• Series of proteins labeled as NS1–5.
o NS2 is a transmembrane protein
o NS3 contains protease and RNA helicase
activities
o NS4A and B proteins are known cofactors
o NS5A is an interferon resisting protein
o NS5B is RNA polymerase

• HCV virus is enveloped spherical shaped enveloped,

liver RNA virus.
• Single-stranded RNA as genetic material
• Exists in 7 genotypes (1-7) or genetic structures.
• It has a with a lipid envelope € containing
glycoproteins (E1 and E2) and a core of capsid
proteins.

OTHER INFORMATION
• Among the NS proteins, the NS3 serine-like proteins
and the RNA-dependent RNA polymerase (RDRP)
are essential for viral maturation and replication and

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 o Genotype 2 is less frequently represented than
type 1.
o Genotype 3 is endemic in South East Asia.
o Genotype 4 is consequently found in the Middle
East, Egypt, and Africa.
o Genotype 5 is almost exclusively found in South
Africa.
o The most common genotypes found in the UK
are 1 and 3.
o Most people are infected by single, dominant
genotype but it is possible to have more than 1
at the same time, which we call a Mixed
Infection.
o These different genotypes would have
therapeutic implications and they provide
explanation to interferon resistance in therapy
sessions.
o Enters via specific receptors, including CD 81
• In this slide (pic above), I want you to remember the
protein.
different non-structural proteins or NSP associated
o Once inside the hepatocyte, HCV initiates the
with Hepatitis C Virus.
lytic cycle utilizing the intracellular translational
• NS2 protein is a 21-23 kilodaltons transmembrane
machinery required for its replication.
protein.
o Replication using NS5B RNA polymerase
• NS2 protein is a central for completion of the viral
produces a negative strand RNA intermediate,
replication cycle both in vitro and in vivo.
which then serves as a template for the
• NS3 is a 67 kilodalton protein with multifunctionality.
production of new positive strand viral genomes.
NS3 N-terminal has a serine protease activity and a
o Because viral replication does not involve
C-terminal as your NTPase-Helicase activity.
proofreading, the mutation rate for HCV is
• NS4A is a 54 amino acid protein, which act as a co- high.
factor to NS3 protein.
• On the basis of sequencing studies, six genotypes,
• NS4B is a small hydrophobic 27 kilodalton protein, labeled 1–6, that have been further divided into
which play an important role for the recruitment of subgroups (e.g., 1a, 1b, 2a, 2b) have been
other viral proteins. recognized.
• NS5A hydrophilic phosphoprotein, which plays an • Genotype 1a predominates in North America, and 1b
important role in viral replication, modulation of cell- predominates in Europe. Genotypes 4 and 5 are
signaling pathways, and interferon response. NS5A unique to Africa.
has initially attracted consurable (di maintindihan)
• It is important to note that genotypes 1 and 4 are more
interest because of its potential role in modulating the
resistant to interferon therapy than are the other
interferon response.
genotypes, resulting in longer treatment times (48 vs.
• NS5B is an anchor protein which is about 65 24 weeks). Thus, genotyping has therapeutic
kilodalton in size. It acts as an RNA-dependent RNA implications.
polymerase and plays an important role in the
synthesis of new RNA genome. MODE OF TRANSMISSION
• Tropism for hepatocytes
• The hepatitis C virus is a bloodborne virus: the most
o The different genotypes are often but not
common modes of infection are through exposure to
exclusively related to different parts of the world.
small quantities of blood.
o Genotypes 1-3 have a worldwide distribution.
o Types 1A and 1B are the most common
• This may happen through injection drug use, unsafe
injection practices, unsafe health care, transfusion of
accounting for the 60& of global infections. They
unscreened blood and blood products, and sexual
predominate in northern Europe and North
practices that lead to exposure to blood.
America, southern and eastern Europe, and
Japan.

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• Formerly known as nonA, nonB hepatitis, is the
primary etiologic agent, transmitted via blood
transfusions and transplantation before 1990.

• HCV is transmitted primarily through blood-to-blood

contact:
o Injection drug use • Hepatitis D Virus is a dissecting (di maintindihan)
o Needle stick injury RNA Virus which requires the help of Hepatitis B Virus
o Blood Transfusion for its replication and assembly of new virions.
o Unsanitary Tattooing or piercing
• HDV is coated with HBsAg, which is necessary for
o High risk sexual contacts entry and release from hepatocytes.
• 90% of post-transfusion hepatitis are due to HCV. • Usual symptoms are also observed in HDV infections:
• HCV is a more serious problem than HBV o Joint Pain
• For the prevention and treatment, antiviral medicines o Abdominal Pain
can cure more than 95% of persons with hepatitis C o Vomiting
infection, thereby reducing the risk of death from o Loss of Appetite
cirrhosis and liver cancer, but access to diagnosis o Dark Urine
and treatment is low. • Delta agent
• WHO’s updated 2018 guidelines recommend therapy • HDV is a small, spherical virus with a diameter of
with pan-genotypic direct-acting antivirals (DAAs). about 36 nm.
DAAs can cure most persons with HCV infection, and • On the basis of its unique biological and molecular
treatment duration is short (usually 12 to 24 weeks),
properties, the virus has been accorded distinct
depending on the absence or presence of cirrhosis.
taxonomic status of the family Deltaviridae.
• There is no effective vaccine against hepatitis C;
• The viral genome is a circular, (-)ssRNA molecule
prevention of HCV infection depends upon reducing with an internal core Delta Antigen, surrounding by an
the risk of exposure to the virus envelope derived from HBV surface protein.
• The envelope surrounds the genome and the HDAg
HEPATITIS D
composed of all three HBV envelope proteins: small
HBsAg, medium HBsAg, and large HBsAg.
• There are two isoforms of Hepatitis Delta Antigen,
SH-DAg, which is required for the initiation of viral
genome replication, where as your LH-DAg, serves
as a principal inhibitor of replication and is essential
for the assembly of new virion particles.
• RNA virus that can replicate only in the presence of
HBsAg
• Circulating viral particles have viral RNA inside a shell
of HBsAg
• Occurring primarily in injecting drug users and
hemophiliacs

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 NOTE: As HDV cannot exist without HBV, testing
for HBV will eliminate any infections with HDV. • Hepatitis D virus (HDV) affects globally nearly 5% of
people who have a chronic infection with hepatitis B
• In patients with HBV infection, HDV may occur in two virus (HBV).
forms: • Populations that are more likely to have HBV and
o Coinfection HDV co-infection include people who inject drugs,
▪ Infection with both viruses occurs at indigenous populations and recipients of
about the same time hemodialysis.
▪ Course of infection is more severe • Worldwide, the overall number of HDV infection has
▪ Follows an atypical course decreased since 1980s. This trend is mainly due to a
▪ Acute fulminant hepatic failure successful global HBV vaccination programme.
▪ Results to a more sever from of acute • Currently, no vaccination exists specifically for HDV.
hepatitis than infections with HBV alone. One is unlikely to be developed given that vaccination
▪ higher fatality rate than HBV infection against HBV provides protection against HDV.
alone. • Interferent therapy for 12 months has been approved
o Superinfection for Chronic Hepatitis D infection.
▪ If HDV infection occurs in the presence
of persistent HBV infection, progression HEPATITIS E
of disease may be faster.
▪ Superinfection may accelerate to
chronic liver disease in about 70-90% of
the cases.
▪ Given that HBV infection is a requisite
for HDV infection, HBV infections plays
a major role in the clinical manifestation
and diagnosis of HDV. Therefore,
HBsAg must be detectable first to
consider HDV.

Hepatitis D can be contracted 2 ways:

Coinfection Superinfection
Getting Being
Hepatitis B and chronically
Contracted D infected with
by: simultaneously. hepatitis B and
contracting
Hepatitis D.
Likelihood of 5% 70-90%
becoming (Unlikely) (Likely)
chronic:

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• Hepatitis E virus or HEV is a small non-enveloped • HEV is now an emerging disease and is considered
RNA virus in the family Hepeviridae and is associated an autochthonous, possibly zoonotic, disease
with endemic and epidemic acute viral hepatitis in (predominantly genotype 3)
developing countries.
• The virus has an icosahedral symmetry measuring to
about 27-30 nm diameter.
• Hepatitis E is an important public health concern and
an estimated 1/3 of the world population has been
infected with HEV.
• In recent years, autochthonous Hepatitis E is
recognized as a clinical problem in industrialized
• Is an important public health concern, an estimated
countries.
1/3 of the world population has been infected.
• Several animal species especially domestic swine,
• Human infections:
wild boar, and will bear are reservoirs of genotype
o Eating of uncooked or undercooked meat of the
HEV 3 and HEV 4.
infected animals, pig livers, or sausages
• Human infections occur through intake of uncooked
or undercooked meat of the infected animals and pig
livers or sausages made from these livers and sold in
supermarkets.
• Is a small, nonenveloped icosahedral RNA virus
o Measures to 27-39 nanodiameter
• Associated with endemic and epidemic acute viral
hepatitis in developing countries
• RNA virus, now classified as a Hepevirus
• Related to caliciviruses because of its structural
similarity to other caliciviruses
o However, it is now the sole member of the
Hepeviridae family
• Clinical course similar to that of HAV infection
• MOT: fecal–oral route.
• Evidence suggests that humans can contract this
virus from animal reservoirs (e.g., from uncooked
boar and deer meat), but this route of transmission
has not been fully verified
• When infection occurs in pregnancy, there is an
increased fatality rate
• Five genotypes:
o Genotypes 1 and 2
▪ from humans only
▪ occur in younger populations
o Genotypes 3 and 4
▪ from humans and swine
▪ occur in older age groups that may be
immunocompromised
▪ domestic swine, wild boar, and wild deer
are reservoirs for Genotype 4
o Genotype 5
▪ is an avian HEV found in chickens that
represents a branch distinct from human
and swine HEVs.

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 HEPATITIS E
Genotype
Characteristics 1 2 3 4
Geographic Developing countries Mexico, Nigeria, and Developed countries China and Taiwan
Location of Africa and Asia Chad worldwide
Viral Discovery 1983 1986 1995 2003
Subtypes 5 2 10 7
Transmission Water-borne Water-borne Food-borne Food-borne
route Fecal-oral
Person to person Fecal-oral

Groups at high Young adults (15-30) Young adults (15-30) Adults aged over 50 and Young adults
risk for male immuno-
infection compromised persons
Zoonotic no no yes Yes
transmission
Chronic No no yes no
infection
Outbreaks Common, can involve Smaller scale uncommon un
thousands of cases outbreaks
Transfusion yes yes yes yes
related
infection

HEPATITIS E: PREVENTIVE MEASURE

• Prophylaxis and treatment water supplies must be
cleaned and sewage disposal handled properly
to prevent the spread of HEV.
o If HEV transmission is fecal-oral route,
prevention relies on good sanitation and
availability of clean drinking water
o Complete particles of HEV are vulnerable to
boiling or frying, and become inactivated after 5
minutes at temperatures above 90 degrees
Celsius
o To completely inactivate HEV in food, an internal
temperature of 71 degrees Celsius for 20
minutes is necessary HEPATITIS E PREVENTION
- Use bottle water for brushing your teeth in high-
o HEV is also susceptible to chlorine disinfection
risk areas
in fomites and water supplies - Use purified water for washing vegetables or
o Travelers in developing countries can reduce when cooking
infection by not drinking unpurified drinking - Avoid raw meat, particularly pork and game
water. meat
• Currently, no commercially available vaccines - Boil water to purify it
- Wash your hands frequently
exist for the prevention of hepatitis E
o The only vaccine available is the HEV 239,
Hecolin (Xiamen Innovax Biotex) made by
China since 2011 but is not yet approved in
other countries
 HEPATITIS VIRUSES • GBV-C does not appear to be hepatotropic, does
not replicate efficiently in hepatocytes, and does
• Hepatitis A (HAV) Picornaviridae (1973) not cause acute or chronic hepatitis
• Hepatitis B (HBV) Hepadnaviridae (1970) • Self-limiting infection
• Hepatitis C (HCV) Flaviviridae (1973
• MOT: blood borne route, perinatal route, and
• Hepatitis D (HDV)? (1977)
• Hepatitis E (HEV) Caliciviridae (1983), Hepeviridae possibly through sexual contact
• Hepatitis F Not separate entity, Mutant of B virus
• Hepatitis G (HGV) Flaviviridae (1995)

• TTV: First identified in the serum of a Japanese

patient in 1997
• Role of TTV in human disease is unknown but
may be associated with some cases of
posttransfusion hepatitis.
• SENV: Discovered in 1999 in Italy, distantly
related to transfusion transmitted virus (Infect
TTV
Dis 2001;183:359) • AKA: torquetenovirus (TTV, also known as
transfusion transmitted virus)
VIRUSES WITH UNCERTAIN
• single-stranded non-enveloped DNA virus
ASSOCIATION WITH HEPATITIS
belonging to the genus Annellovirus
• Hepatitis F virus (HFV), hepatitis G virus
• Related to animal circoviruses
(HGV), and transfusion-transmitted virus
• Associated with acute and chronic hepatitis
(TTV)
cases and may produce liver damage under
o Newly discovered hepatides
specific circumstances
o Little known about them
• First reported in a Japanese patient in 1997 by
o Hepatitis F – fulminant, posttransfusion
the research scientist Nishizawa
hepatitis
• MOT:
o Hepatitis G – syncytial, giant cell hepatitis
o Parental transmission of the virus through
Historical note:
• During the 1990s, researchers discovered contaminated blood;
two additional viruses in the sera of o presence of the virus in stool, bile, and
patients with hepatitis who were not saliva, suggest transmission by the fecal-
infected with any of the well-characterized oral and respiratory routes
hepatitis viruses as previously described • Laboratory Test:
o Molecular: PCR
HGV
▪ primers for the PCR is especially
• AKA: GB virus type C or GBV-C
important in influencing the test results,
• Enveloped, single-stranded RNA virus in the
since the virus has a tremendous
Flaviviridae family
amount of genetic diversity, with over
• Its genome consists of a positive sense stranded
30 different genotypes discovered
RNA, encoding a single polyprotein of
o Serological:
approximately 3000 amino acids
▪ To date, there are no validated
• First described in the serum of the patient with
serological tests to detect antibody to
non-a non-b non-c hepatitis
TTV.
• GB virus-C (GBV-C), a flavivirus related to
HCV, has been identified in post-transfusion
hepatitis.

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 SEN VIRUS
• Single stranded Non-enveloped Circular DNA
virus
• Bloodborne
• Not been definitively linked to any human
disease
• Patients undergoing hemodialysis
• MOT: blood transfusions
• About 30% of patients with HIV infection have
antibodies to SEN virus.
• SENV consists of 8 strains, A - H
• Strains D and H appear to be associated with
non A - E hepatitis
• Cryptogenic hepatitis (SEN-V NANE)

SUMMARY OR MUST KNOW TABLES

VIRUS HEPATITIS A HEPATITIS B HEPATITIS C HEPATITIS D HEPATITIS E

TYPE OF VIRUS ssRNA Partially dsRNA ssRNA Circular ssRNA
defective ssRNA
VIRAL FAMILY Related to hepadnavirus flaviviridae deltaviridae Calicivirus
picornavirus
ROUTE OF Fecal-oral Parental, sexual Parental, parental Fecal-oral
TRANSMISSION (contaminated contact, intranasal
food or water) perinatal cocaine use is a
risk factor
MEAN 2-4 weeks 1-4 months 7-8 weeks Same as HBV 4-5 weeks
INCUBATION (1-4 months)
PERIOD
FREQUENCY never 10% -80% 5% Never
OF CHRONIC (coninfection);
LIVER DISEASE ≥70% for
superinfection
DIAGNOSIS Detection of Detection of PCR for HCV Detection of IgM PCR for HEV
serum IgM Abs HbsAg or RNA; 3rd and IgG Abs; RNA; detection
antibody to generation HDV RNA serum; of serum IgM
HBcAg ELISA for Ab HDAg in liver and IgG Abs
detection

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NAME OF VIRUS Hepatitis A Virus Hepatitis B Hepatitis C Hepatitis D Hepatitis E Virus
(HAV) Virus (HBV) Virus (HCV) Virus (HDV) (HEV)
CLASSIFICATION picornavirus hepadnavirus flavivirus deltavirus Hepevirus
VIRAL GENOME ssRNA dsRNA ssRNA -ssRNA (-ve) ssRNA
TRANSMISSION enteric parental parental parental enteric
INCUBATION 15-45 days 45-160 days 45-150 days 30-60 days 15-60 days
PERIOD
CHRONIC No Yes Yes Yes No
HEPATITIS 10% chance >50% chance <5% of
coinfectious
>80% of
superinfectious
CURE? No cure. No cure. No cure. No cure. No cure.
Treatments Treatments Treatments Treatments: Treatments
usually tackle the usually tackle usually tackle Alpha interferon usually tackle
symptoms the symptoms the symptoms for 12 months the symptoms

POST – TEST
1. TRUE OR FALSE: Hepatitis G causes only
a self-limited form of hepatitis.
2. TRUE OR FALSE: Dane particle is
associated with Hepatitis D virus.
3. IDENTIFY: 2 Hepatitis viruses that are
transmitted via fecal-oral route.
4. IDENTIFY: NS1 – NS5 are non-structural
proteins associated with________.
5. IDENTIFY: 2 Hepatitis viruses that are
transmitted via fecal-oral route.

REFERENCES:
• Mahon, C and Lehman D. (2018). Textbook of
Diagnostic Microbiology 6 th Edition, Saunders
• McPherson, R. and Pincus, M.R. Henry's
Clinical Diagnosis and Management by
Laboratory Methods 23rd Edition
• Stevens, C.D. Clinical Immunology and
Serology: A Laboratory Perspective, 3rd Edition

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 UNIT I PART 1 INTRODUCTION TO MYCOLOGY

PRE-TEST (No answer) MYCOLOGY

1. Organisms that obtain their energy source through • Study of Fungi
intake and digestion of organic materials o A discipline of Biology that deals with, describes
A. Autotroph an enormous group of organisms denominated
B. Heterotrophs FUNGI
C. Saprotrophs o Branch of Biology, subdiscipline of Microbiology
D. Parasite • Fungi is considered as a vast or an enormous group
2. Masses of hyphae which comprise a fungal colony of organisms
A. Sporangium • Good Mycology
B. Basidium o Highlights the productive or beneficial effects
C. Mycelium and applications of this field of science
D. Ascus particularly in areas of agriculture,
3. They are contained within fruiting bodies of fungi biotechnology, and environmental biology
which are involved in reproduction • Bad Mycology
A. Sporangiophore o “Dark side” of Mycology; Fungi are implicated as
B. Conidiophore a cause of multiple phenomena that have
C. Spores deleterious effect on environment and health
D. thallus
4. Long strands of fungal cell that lack septa or cross GOOD MYCOLOGY
walls Fungi is all around us; it has been a part of nature; it is a
A. fertile hypha major part of our ecosystem.
B. septate hypha • Transformation and recycling of dead material
C. coenocytic hypha • Recycling of carbon and other minerals
D. sterile hypha o Capacity to recycle carbon and other minerals
5. All of the following are benefits we can get from • Provide nutrients to the plants
fungi, except o There is an association between a fungus and
A. Source of antibiotics and the root part of a plant, there is a symbiotic
immunosuppressive drugs relationship or an association between them
B. For production of food, beverage, • Important Biotechnological tool e.g. yeast
spirits recycling of carbon and minerals o Biotechnology involves production of food, as
C. Production of soap and cosmetics well as certain types of spirits like alcohol or wine
D. All are correct also bread, preparation of cheese
• Source of secondary metabolites for production of
antibiotics (ex. Penicillium) and immunosuppressive
drugs (Ex. Cyclosporin A)

Miss mo na? Me din eh. Aral nalang tau BAD MYCOLOGY

• There are significant phytopathogens
o Meaning they cause disease in plants
o We attribute to fungi the occurrence of food
spoilage or rotting of stored crops
o Example: Claviceps purpura which causes
diseases in cereals (cereal as in the type of crop
used in cereals as in Kellogg’s ganon)
 o Even the harvested nuts and grains can be Ma’am Domingo – Asynchronous
tainted with the aflatoxin that is produced by a History would tell us that Fungi was once part of the Plant
different fungus called Aspergillus Kingdom however with further study, they have
o Fungi also cause severe plant diseases discovered that fungi are a totally different organism
▪ Rice Blast because they do not have chlorophyll which plants have.
▪ Coffee Rust
• Cause life threatening disease in patients with risk There are only minimal fungi found in sea and
factors or the immunocompromised freshwater.

BIOLOGICAL RESEARCH Fungi as organisms:

• Saccharomyces cerevisiae Heterotrophs – no capacity to produce on food; energy
o main eukaryotic models in genetics, molecular source would depend on the intake or digestion of
biology, cell biology, biochemistry, and organic molecules using extracellular enzymes that the
metabolism produce to breakdown these molecules
• Schizosaccharomyces pombe Saprotrophs – organism that get their food from dead or
o key organism in understanding the mechanism decaying organic matter (ex. wood, spoiled bread, cow
of regulation of the cell cycle of somatic cells dung aka tae ng baka pinacute lng)
Parasitic – dependent on host for food and survival
FUNGI
• NON-MOTILE, EUKARYOTIC ORGANISMS which Fungi are chemotrophic pertaining to the ability to
can be single celled or usually are the very complex secrete extracellular enzymes that would degrade or
multicellular organisms destroy a wide range of organic substrates bc they are
• A diverse group made up of the classic pathogens, usually feeding on organic materials that they convert
environmental saprobes and parasitic spore into nutrients which will then be transported to their cells
producing eukaryotic organisms that lack chlorophyll. through processes known as passive absorption or
i.e. Achlorophyllous active transport.
• Reside in nature, found in any habitat - on the land,
in soil or on plant material rather than in sea or fresh
water LAYMAN’S DESCRIPTION OF FUNGI
• Are obligate or facultative aerobes
• Fungi may live as heterotrophs, saprotrophs, and
parasitic organisms
• Are chemotrophic secretes enzymes that degrade a MOLD
wide range of organic substrates into soluble
“amag” in
nutrients which are then transported into the cell bread
through passive absorption or active transport
• Historically, they are compared to plants and have
also been compared with bacteria
• Fungi are subdivided based on their life cycles, the
presence or structure of their fruiting body and the MILDEW
arrangement of and type of spores (reproductive or Plant leaf
distributional cells) they produce. with dif spots
of color, also
Ma’am Domingo – Asynchronous found in
bathroom
According to Instituto de Salud Carlos III (2017), they
have estimated more than a million fungi specie all over
the world but those causing disease are very low, less
than a hundred. These have been classified as
belonging to the classic pathogens, environmental
saprobes, parasitic spore producing eukaryotic MUSHROOM
organism which lacks chlorophyll which is why fungi is
considered as an Achlorophyllous organism.

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 BRACKET PLANT CELL
FUNGI

PUFFBALLS

FUNGI

TRUFFLES

PROKARYOTES VS. EUKARYOTES

SIMILARITIES BETWEEN PLANTS & FUNGI PROKARYOTES EUKARYOTES

• Both are EUKARYOTIC organisms 1. µm -2 µm in
10 µm -100 µm
• Numerous organelles diameter
Typical Size in diameter >10
• Possess cell walls 2. µm -5 µm in
µm in length
length
• Mostly are anchored on soil or other substrates
No nuclear
• Reproduction can be asexual or sexual or both Classic
membrane,
• Stationary Nucleus membrane
nucleoid region
bound nucleus
of the cytosol
DIFFERENCES BETWEEN PLANTS & FUNGI
Circular DNA
complexed with
Linear DNA
FUNGI PLANTS RNA at
Genome complexed with
mesosome
Multinucleated One nucleus per cell • Chromosomal basic histones
within nucleoid
DNA & and proteins in
Plasmid – each
Location the nucleus
Autotrophs • Extrachromos carries gene for its
Heterotroph
omal DNA own replication;
In mitochondria
can confer
Importance of the and chloroplasts
Achlorophyllus presence of chlorophyll resistance to
used in photosynthesis antibiotics
Glycogen is the Starch is main Asexual Sexual and
Reproduction
main storage product storage product (binary fission) asexual
Present (e.g.
No stem, Higher plants have stem,
Membrane- mitochondria,
roots and leaves roots and leaves
bound Absent in all lysosome, ER.
Have chitin in organelles Golgi complex,
Cellulose in
their cell wall
their cell wall nucleus)
makes it rigid
Ribosome Present in all Present in all
Lacks chlorophyll With chlorophyll
Chloroplast for Present in algae
No reproduction Some reproduce Photosynthesis
Absent in all
and plants
by seed by seed

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 In the inner
Electron
In the cell membrane of
transport for
membrane mitochondria
energy
and chloroplasts
Sterols in
Absent except in
cytoplasmic Present
Mycoplasmataceae
membrane
Also contains
Plasma Lacks
glycolipids and
membrane carbohydrates
glycoproteins
Cellulose,
phenolic polymers,
Cell wall if Peptidoglycan in
lignin (plants),
present most bacteria
chitin (fungi), other
glycans (algae)
Present in most as
an organized
Present; some
Glycocalyx capsule or
animal cell
unorganized slime
layer

Cilia Absent Present

Complex cilia or
Simple flagella;
flagella; composed
composed of
of MTs and
polymers of
polymers of
Flagella if flagellin; movement
tubulin with dynein
present by rotary action at
connecting MTs;
the base;
movement by
spirochetes have
coordinated sliding
MTs
microtubules
Pili and
Present Absent
Fimbriae

FUNGAL STRUCTURE
Ma’am Domingo – Asynchronous

SPORE PRODUCING STRUCTURES

These are the representations of different forms of fingi.
Fungi can also exist as tubular, filamentous structures,
hyphal structures, complex structure of the fungi (the
mushroom thingy). You can see the fruiting bodies
which are the spore-producing structures.

FRUITING
BODIES

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 MORPHOLOGICAL FORMS • Acting as the site of various extracellular enzymes
Fungi exists in two morphologic forms: engaged in the exchange of nutrients and products of
metabolism and hydrolysis of cell wall components.
YEAST • Acting as a reservoir of carbohydrates
• single vegetative cell • Skeletal Components of CW
in culture, shows All components contribute to CW rigidity
smooth creamy,
o Chitin
bacteria like colony
without aerial hypha o ß Glucan
• buttery consistency o Mannan
and does not produce • Cell Wall Matrix
filamentous o consists of water-soluble polysaccharide
structures or hypha ▪ α glucan and glycoprotein
• reproduce by budding • Miscellaneous Cell Wall Components
or fission can be
o Melanin
identified using
Biochemical test and ▪ production of this pigment contributes to
Molecular Diagnostic fungal virulence
methods ▪ improves resistance to environmental
MOLDS damage such as extreme temperature, UV
• grows in multicellular light and toxins
filaments called ▪ important for invasion and dissemination
hyphae / hyphal ▪ Important in maintaining the viability and
structures integrity of the cell wall
• are made up of
tubular branches
having multiple,
genetically identical
nuclei, yet form a
single organism,
known as a colony.

CYTOLOGICAL FEATURES
When talking about, the Fungal cell,
we are referring to a Yeast Cell

DEFINITE, RIGID CELL WALL

• Exhibits plasticity
• Has turgor pressure
Confers shape to the hypha
• Protects the protoplast against environmental
hazards, osmotic stress
o Protoplast is similar to the protoplasm found in
cell, refers to the living material in the fungal cell
• Cell wall acts as a protective shield against
environmental hazard as well as stresses, particularly
osmotic stress
• Acting as a carrier of specific antigen characteristics Ma’am Domingo – Asynchronous
of the cell and playing an important role in cell
recognition in various cell interactions. 2 layers of mannoprotein in hyphal cell wall, yeast cell
• Acts as a filter controlling to some extent materials wall has 1. B-1,3-glucan in the yeast cell wall are
that enter the fungal protoplast doubled or more expanded that the hyphal cell wall but
o Regulate and control both would have the chitin components.

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 MEMBRANE BOUND ORGANELLES o are edible some are poisonous
• Membrane bound organelles – nucleus, • THALLUS
mitochondrion, E.R. Golgi bodies, microbodies o Refer to the entire vegetative body of the
▪ These microbodies are your hypha
peroxisomes • Septum – partitions or crosswall in hyphal
• Ribosomes structure
• Spindle Polar bodies (SPBs) are plaque-like o Hyphal structures may or may not
structures embedded in the nuclear envelope for present partitions or cross walls
the entire cell cycle in budding yeast and most of o Septate – where hyphal structures are
the cell cycle in fission yeast. It plays the role of interrupted at some points (at regular
the centrosome by initiating organization of interval) by partitions or cross walls
microtubule, particularly during mitosis. o Non septate or Aseptate or coenocytic
▪ These are parts that are unique to – when portions of hyphae grow
fungal cells but have similar actions and vigorously resulting in lack of regularly
functions in organelles found in animal spaced septa.
cells • Several hypha tangled together into a thick mass
▪ Comparable to the microtubule ▪ When these tubular structures occur in
organizing center which is found in masses, then we can call them as
animal cells MYCELIUM
▪ They are important especially for the ▪ A mycelium are thick masses made up
centrosomal part of the cell that is the of several hypha that are tangled
site of mitosis together
▪ They serve as microtubule organizing ▪ On the right side of the pic, you can see
centers. They are very crucial when it a portion of the tubular structure which
comes to the cell cycle of the budding has organelles just like a fungal cell
yeast as well as the fission yeast.
• Lipid bodies, Glycogen storage particles,
vacuoles
▪ There are also what we call as cytosolic
deposits or inclusions
• Filasomes - vesicles associated with
filamentous material, found numerous at the tip
of actively growing hypha
▪ These are present in hyphal structures
▪ From the name itself, they are
associated with filamentous structure of
fungi
FUNGAL STRUCTURE- MOLD
• MOLDS
o A non-motile thallus constructed of apically
elongating walled filaments.
o When we talk about the thallus, that would
refer to the entire vegetative body of a hypha ELEMENTS WITHIN THE HYPHA
o A web of filaments or hypha constitutes a • There are hyphal elements which cannot be
MYCELIUM observed in fungal cells
o The filamentous form of a fungi is known as • Spitzenkorper
a mold o an organizing center necessary for long
• HYPHA range transport of vesicles, via
o filamentous tubular structures that grow by cytoskeleton. Described as nuggets of
elongation (like thread) at the tip of the fungi vesicles in the hyphal tip that is important
o or by branching that contain numerous nuclei in the growth process
distributed throughout.

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 o These are nugget vesicles you find at the • Hyphal elements may be:
tip of your hyphal structures o REPRODUCTIVE HYPHA
o These microtubules (refer to last pic) - portion of the aerial hypha that
constitute the fungal cytoskeleton. bears the reproductive spores or
conidia
o AERIAL HYPHA
- hypha that projects above the
medium and produce reproductive
spores
o VEGETATIVE HYPHA
- portions of the hypha the
penetrates the supporting medium
and absorbs nutrient
o So what you see in this picture is a
growth of a hyphal structure
o So the surface substrate serves as the
medium for the propagation of the hyphal
structure and the one that is submerged
in the substrate are your vegetative
hypha
o So the vegetative hypha penetrate the
supporting medium (substrate) for them
to be able to absorb the nutrients
o Above the substrate is your aerial hypha
o At the tip of the aerial hypha, there may
or may not be reproductive hypha in the
form of conidia or spores
o The part of the hypha which bears these
spores or conidia is the reproductive
hypha

• Fungal cytoskeleton
o In filamentous fungi, these are important
in the regulation of fungal cell
morphogenesis;
o for the delivery of cell membrane and cell
wall components to the growing hyphal
tip and to the septum.
o These are important in regulating the
morphogenesis of fungal cells as wells as
long range transport of vesicles and other
cell wall components
o Engaged in transport of vesicles going to
the growing tip as well as to the septum
o These vesicles will have cellular
elements that would comprise the cell
membrane and the cell wall

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• Types of hyphal elements
o According to the presence or absence
of crosswall
- Septate
- Non Septate/ coenocytic

• Referring to this picture above

o According to the presence of ▪ Hyphal elements can also come in
Pigmentation or the production of different morphologies or forms.
melanin ▪ They can look like an antler of a
- Hyaline (Moniliaceous ) non reindeer, so we call them, antler
pigmented or lightly pigmented hyphae. Normally, they are compared
▪ In the picture (left), they to a favic chandelier. Once example is
are transparent due to the Trichophyton schoenleinii
absence of melanin ▪ There are also ones that look like tennis
- Phaeoid ( Dematiaceous) darkly rackets, hence, the racquet hyphae
pigmented because of the and are observed in Epidermophyton
presence of melanin in the cell wall floccosum which is, like the
▪ So the dark pigmentation trichophyton, a dermatophyte
in their tubular structures ▪ These hyphal elements are evident
is attributed to the among dermatophytes or those which
presence of melanin are causing cutaneous mycotic
▪ Melanin is a minor element infections.
of your cell wall ▪ So the third one, we have a spiral
▪ In the picture (right), they hyphae which we can find among the
are brown due to the Trichophyton mentagrophytes.
presence of melanin

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 ▪ The nodular form is among the production,
Microsporum canis probiotics, and food
▪ There are also hyphal structures that addictive or flavors.
look like combs or suklay, which are Health Can cause Can cause
Hazard infection in allergic reactions
called the pectinate body and we
individuals with and respiratory
observe these in microsporum audouinii compromised problems.
immune systems.
Difference between yeasts and molds
• MONOMORPHISM
Yeasts Molds o having only one growth phase, yeast
form
Habitat Can be found on Found in damp, o Example : yeast and yeast-like
fruit and berries, in dark or organism
the stomach of Steam Typically
mammals and on f-filled areas.
skin, among other • DIMORPHISM
places. Very o ability of fungi to exist in two forms(e.g.
common compared yeast or mold) depending on the growth
to molds because condition/environmental condition
molds only grow in o Example : Systemic fungi (e.g.
dark and steam- Blastomyces, Coccidioides)
filled areas
▪ For blastomycoses, a
Cell Unicellular Multicellular
temperature of about 37
Shape Round or oval in Filamentous degrees C, this will transform
shape fungi, Threadlike into yeast form but at a lower
Growth White and Fuzzy temperature, they can transform
appearance butterlike appearance and into molds.
CONSISTENCY can be an • POLYMORPHISM
orange, green, o have both yeast and mold form in the
black, brown. same culture.
They can also
appear as o Example : Exophiala spp.
cottony, or
grainy. FUNGAL REPRODUCTION
Hyphae Do not have true have • LIFE CYCLE (ONTOGENY ) OF FUNGI consists
hyphae. Instead microscopic of:
they form filaments called o Somatic Phase – feeding stage
structures called hyphae.
▪ It is also called as the feeding
pseudo-hyphae.
Reproduction They reproduce Sexually and stage because in this stage, the
mostly asexually asexually life cycle is characterized by
(budding). reproduce into occurrence of tropic activites
multicellular which means that they are
• Asexual Blastospores None form. producing extracellular enzymes
• Sexual which they will be using to be
Yeasts do not Sporangiospores
able to digest nutrients from the
produce sexual and Conidia
spores because Zygospores, supporting medium or the
they only Ascospores, and substrate
reproduce Basidiospores ▪ This is the time where the fungi
asexually will have to use its enzyme to
Beneficial Making of alcoholic Useful in digest nutrients from the
use beverages which biodegradation, substrate and thereby absorb
contain ethanol, food
this into their cellular structure
used in baking, production
bioremediation, (cheese) o Reproductive phase
industrial ethanol

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• FUNGI REPRODUCE - sexually and / or break happens and therefore each
asexually fragment of the structure is separated
o Fungi that reproduce sexually and / or into pieces
asexually are termed as PERFECT o (right figure) another by fragmentation,
FUNGI. although I consider this as a true
o Fungi that reproduce only by asexual fragmentation but still, it happens in a
means are termed as FUNGI septated hypha wherein there is only a
IMPERFECTI portion that becomes fertile and starts to
o In both sexual and asexual reproduction, produce spores within that fertile portion
fungi produce spores that disperse from and here.. what we have is the
the parent organisms chalmydospores
▪ As the dispersal of spores
happen, each spore will will
undergo germination.
o The only difference between sexual and
asexual reproduction is that in asexual
repro, there is no fusion of nuclei or
gametes which happens in the sexual
reproductive phase
• Vegetative reproduction
o involves the body of a fungal thallus.
o No production of seeds or spores by
meiosis or syngamy • Budding
o This does not require a reproductive o the pinching off of an offspring from the
propagule parent cell.
▪ A reproductive propagule is any o The offspring cell is genetically identical
material that functions in to the parent
propagating organism into its o In budding, the cell division that happens
next stage in its life cycle is mitosis and this is considered as a
o This only happens ONLY among the form of cytokinesis
molds. o Looking at the illustration, what we have
here is the parent cell and, the nucleus
ASEXUAL REPRODUCTION divides mitotically and the daughter cells
• TYPES of ASEXUAL Reproduction: produced then moves on one side of its
o Fragmentation cell wall or membrane and as the
o Fission daughter cell push against the cell wall,
o Budding there will be a protrusion which
o Spore formation eventually becomes enlarged and in that
enlarged part, the daughter cell will
• Fragmentation migrate into that enlarged portion until its
o occurs when a fungal mycelium pinches off from its parent cell.
separates into pieces with each
component growing into a separate
mycelium.
o This normally happens among fungi with
crosswalls or what we call septated
hyphal structure
o So what happens is the hyphal structure
breaks, and each component separates
from each other.
o In figure 5 (left figure) you see a septated
hyphal structure and at its crosswall, the

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• Fission o CONIDIA
o simple splitting of a cell into two daughter - Asexual spores usually produced
cells at the tip or side of hyphae or on
o (referring to the pic) we have a parent cell stalk or special spore-producing
and in this parent cell, first we have the structures called conidiophores.
appearance of a constriction, and this ▪ The conidiophore is actually the
constriction deepens until the parent cell counterpart of the
separates into two daughter cells sporangiophore. In
conidiophore, it is the one that
holds the spore producing
structure or the spore itself
- The process of conidium formation
is called conidiogenesis.

• Spore Formation
o SPORE- a reproductive structure of fungi
and some other organisms (bacteria),
containing one or more cells
o small unit of propagule capable of giving
rise to a new individual.
o they are readily dispersed and are
capable of germination when growth Methods of conidiogenesis
conditions are favorable • Generally, the process of conidiogenesis occur
o more resistant to adverse condition either in a blastic manner or a thallic manner
o Can be derived from both asexual and • BLASTIC
sexual reproduction o Conidia differentiate via expansion from
• Asexual spores- produced after mitosis without the conidiogenous cell.
involvement of meiosis ▪ A conidiogenous cell is a part in
o Genetically identical a hyphal structure that becomes
o The simplest mechanism of spore fertile and are capable of
formation involves the differentiation of producing spores
preformed mycelium. Spores generated o The cell wall of this cell is locally
are termed as thallospores. weakened and the developing conidium
bulges out and is delineated by a septum.
• Major types of asexual spores ▪ TAKE NOTE: in a blastic conidia,
o SPORANGIOSPORES normally it will take place in the
- are spores that are produced in an cell wall of the hyphal structure
enclosed, sac-like structure, called and the hyphal structure is a
a sporangium, at the end of the septated hypha. And the portion
sporangiophores. that becomes fertile is usually
▪ The sporangiophore is a stoke weakened and from there, the
that will hold the sac like developing conidium will emerge
structure which we call as the and will be delineated by the
sporangium and inside the septum
sporangium, we have the
multiple sporangiophores

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 o Holoblastic expansion of a cell includes this will normally happen under the process of
the complete cell wall (inner and outer fragmentation.
wall) of the conidiogenous cell.
o Enteroblastic- the cell wall of the
conidiogenous cell is disrupted and the
conidium appears through an opening in
the cell wall
o So the difference between the two is in
holoblastic, expansion of the cell
involves BOTH the inner and outer cell
wall of the conidiogenous cell. Whereas
in enteroblastic, what matters only is the
inner cell wall of the conidiogenous cell.
• THALLIC
o A preexisting cell differentiates into a
conidium.
o Holothallic involves the entire cell wall • Here, we have the methods but this time, we have
(inner and outer wall) of the hypha. the type of conidia that emerges from holoblastic
o Thallic–arthric- conidia produced in and enterblastic
succession along the entire length of • For the blastic conidiogenesis, a perfect example
the hypha that are formed holoblastically are your
• In blastic, what is involved is only a portion of blastoconidia and your poroconidia
the fertile hypha and but in thallic, the entire • In your blastoconidia the conidiospores are
hyphal structure is involved in the formed by buds through the budding process and
conidiogenesis product again, this would involve inner and outer cell wall
of the fertile part of the hypha
• Whereas in the poroconidia, the conidia will
emerge from an opening or a hole on the
conidiogenous cell.
• Now as for the enteroblastic we have two types,
the phialoconidia and the aneloconidia
• In both your phialo and aneloconidia, there is the
presence of a phialophore and anelophore
respectively, which are special spore bearing
structures that would hold the conidia
• They are called phialoconidia because the
shape of the slope(?) like structure is similar to
that of a vase so it has a vase-like structure and
• In enteroblastic, it only involves from the inner here since it is enteroblastic, it is only the inner
cell wall but if the development of the conidium wall of the fertile hyphal structure that will be
would involve both inner and the outer cell wall producing the conidia. And as it continually
of that fertile hypha, then that is holoblastic produce the spore, this conidia can come as a
• As for thallic, it’s the entire portion of the hyphal chain like structure from the hyaline
structure that develops into a conidia, so both
inner and outer cell wall of the entire hyphal • For aneloconidia, here, the conidia emergers
structure produces the conidia from the inner wall of a fertile hypha. The outer
• Whereas in thallic-arthic, there is a sort of wall that is left out then form a ring beneath the
segmentation process that will happen at areas conidia and this ring is what we call as the
but the entire length is considered fertile and annelation(?)
that hyphal structures will involve cross walls
then it will fragment and separate into pieces. So

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 • So this time, we’re talking of the thallic so we’re • Blastoconidium- asexual spore produced
talking about the entire body becomes fertile. blastically either singly or synchronously in chain
Unlike in the blasic, we have only a portion of from the parent cell
the hyphal structure that becomes fertile. • Chlamydospores- swollen thick walled vesicles
that do not reproduce
• Chlamydoconidium– asexual spore produced
directly from the hyphae , have thickened walls and
is larger than the surrounding hyphal cells
• Endospore- spore formed within a spherule by
cleavage of the cytoplasm
• Fertile hyphae- mycelia from which the
reproductive structures form
• Macroconidium – the larger of the two types of
conidia produced through holothallic mode of
• In holothallic it will entail both productionof the conidiogenesis
conidia bearing the inner and outer cell wall. • Phialoconidia – conidium borne from a phialide
Examples include microconidia and • Poroconidium – Holoblastic conidium produced
macroconidia or macroconidia coming from a through pores in the cell wall of the conidiogenous
dermatophyte organism and we also consider cell or conidiophore
the chlamydospores through a holothallic • Sporongiospore – primary asexual reproductive
process. structures formed in a sac called sporangium
• And remember that chlamydospores is also one • Zygospore – Round thick walled spore formed in
classic example of a spore that is produced a zygosporangium by fusion of the tips of two
asexually by means of fragmentation compatible hypha.
• Now for the thallic-arhic, so we have the thalic
conidiogenesis comparing the holothallic, SEXUAL REPRODUCTION
holoarthic, and the enteroarthic • Meiosis in fungi occurs at a different point in
• For holoarthic, the septated hyphal structure the reproductive lifecycle than in other
that becomes fertile then are broke into pieces higher eukaryotes.
on its crosswall thereby forming fragments • THREE STAGES OF SEXUAL
• In enteroarthic, the entire hyphal structure REPRODUCTION OF FUNGI
becomes fertile but it will only be the inner wall. o Plasmogamy – union or fusion of
There will only be portions of the inner wall that haploid cells of compatible mating types
becomes fertile and in the process, this will be ▪ They may involve 2 different hyphal
notedas an enlargement on the fertile hypha. structure but there should be
And since, the outer cell wall does not portions of that hyphal structures
participate in the conidiogenesis process, it is that are compatible with each other
possible that there will be portions in the hyphal that there will be a possible reunion
structures that will be left as an empty shelllike or fusion of the haploid cells
this one. The dark colored structure is the fertile o Karyogamy - fusion of the two haploid
portion while the spaces in between are the nuclei
empty shells o Meiosis - newly-produced diploid cell
can undergo meiosis to regenerate
TERMINOLOGIES haploid cells, and this often is as a
• Annelloconidium – conidium produced from an response to nutrient limitation
annelide
• Aplanospores – non motile sporangiospores
• Arthroconidia- asexual conidium produced
directly from the hyphae and released from this
structure through fragmentation
• Basidiospore – sexual spore formed on a
basidium following karyogamy and meiosis

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This is a diagram that shows you the different phases of • Karyogamy
sexual reproduction. o Fusion of the nuclei will happen during
• Parent Mycelia – could be two different hyphal karyogamy
structure o Haploid nuclei of these compatible mates will
o For plasmogamy to happen, these two hyphal fuse and produce the zygote.
structures must be first compatible that they • Meiosis
will be attracted to one another. o Haploid spores will be disseminated
o The attraction of these different hypha or o These spores in the environment can undergo
mating types is made possible by the release germination to form either a mycelium to
of a pheromone coming from usually the repeat the sexual reproduction again or some
female parent mycelia. of them will enter the asexual reproduction
o After their attraction, comes their fusion of their stage
cytoplasm. (Plasmogamy)
• Heterokaryotic stage
o Take note that the haploid nuclei are not used
right away but first they will co-exist in the
mycelium.
o Happens between the plasmogamy and the
karyogamy stage
o Prelude to karyogamy
o Unfused nuclei coming from the parent
mycelium, they will be attracted to one another
but not necessarily going into fusion.

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• Perfect fungi - fungi that undergo both sexual and • right side – Basidiomycota
asexual reproduction o Note: NO asexual reproduction stage
o All three phases happen o Can produce sexual spore in a similar way as
• left side – Ascomycota the Ascomycota – plasmogamy, karyogamy,
o Ascogonium and Antheridium and meiosis
▪ Represents the mating strain ▪ Requirement prior to plasmogamy – two
• Antheridium – male strain that mating strains, coming from different
carries the male gamete hyphal structure but are compatible to
• Ascogonium – female strain that one another
carries the female gamete o Difference: spores are contained in a club-
▪ These two will be attracted to each other shaped structure called basidium
but will not immediately undergo fusion ▪ Inside the basidium are the haploid
▪ Ascocarp nuclei.
• represents the fruiting body ▪ These haploid nuclei will undergo meiotic
• will generate the ascospores division to become basidiospores.
o Once the ascogonium and antheridium fuse ▪ These basidiospores will be
together, they will form the dikaryotic hyphae disseminated, germinated and become a
o Dikaryotic hyphae will become a fruiting body mycelium.
and produce zygote
o The zygote will undergo meiosis and produce
four haploid nuclei.
▪ These haploid nuclei can undergo
mitosis to double the number of
ascospores in the ascocarp
▪ These ascospores will be released in the
environment, they will either undergo:
• germination to develop into a hyphal
structure or mycelia
• enter the asexual reproduction
stage.
• Another group of perfect fungi belonging to the TAXONOMY OF FUNGI
family of Glomeromycota, a group of mycorrhizal • Over 100,000 named fungal species
fungi, derived from the Zygomycota. o Only a few are known to be pathogenic
• Plasmogamy→Karyogamy→Meiosis o Estimated 1- 10 million undiscovered
• Requirement: two mating hyphal structures, one is • Basis of Taxonomic Classification:
negative and the other is positive to be attracted to o Species may be recognized and defined on
one another the basis of its asexual state (Anamorph)
• As they are attracted, they grow side by side, ▪ but, its sexual identity (Telemorph),
producing branches. As they grow toward each may have a different name.
other, the tip of these branches will develop into o It is based on the mechanism and spores that
gametangium. result from sexual reproduction
o Gametangium o Taxonomic classification depends on
▪ structure that will contain the pigmentation, growth temperatures, the
gametocytes pattern of conidiogeny and / or sporogeny,
▪ gametes in here will fuse to form a zygote appearance of microscopic structures
▪ resulting zygote will undergo meiosis to
produce zygospores that are enclosed in
a zygosporangium.

GROUP CHARACTERISTICS EXAMPLES

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Glomeromycota • Order Mucorales: Profuse to gray to Mucoromycotina
Subphyla: white, aerial mycelia; hyaline Genera:
Mucoromycotina, sparsely septate hypha Actinomucor,
Entomophthoromycotina, • Asexual Reproduction: Apophysomyces,
Kickxellomycotina, Sporangiospores and Cokemyces,
Zoopagomycotina sporangiosphores. Cunninghamella,
• Sexual Reproduction: Zygospores Lichtheimia, Mucor,
Rhizomucor, Rhizopus,
Saksenaea,
Syncephalastrum
Ascomycota • Molds have septate hyphae Microsporum spp.
Class Ascomycetes • Sexual reproduction involves a Trichphyton spp.
sac or ascus in which karyogamy Scedosprium boydii
and meiosis occur producing
ascospores
• Asexual Reproduction: conidia
Basidiomycota • Sterile mold Filobasidiella neoformans
• Sexual reproduction results in (teleomorph)
four progeny basidiospores
supported by club shaped (anamorph-Cryptococcus
basidium neoformans)
• Hypha have complex septa.
Clamp connections occur at the Mushroom
septation in the vegetative
hypha.
Fungi Imperfecta • Artificial grouping of the Coccidiodes immitis,
(Deuteromycetes) imperfect fungi for which the Paracoccidiodes brasiliensis
teleomorph or sexual Candida albican
reproduction has not been
discovered.
• Anamorphic state is
characterized by asexual conidia

MEDICALLY IMPORTANT GROUPS OF FUNGI

Phylum Typical Examples Key Characteristics Approximate Number
of Living Species
Ascomycota Yeasts, truffles, Develop by sexual means; 32,000
morels ascospores are formed inside a
sac called an ascus; asexual
reproduction is also common

Imperfecta fungi Aspergillus, Sexual reproduction has not 17,000

penicillium been observed; most are thought
to be ascomycetes that have lost
the ability to reproduce sexually

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Basidiomycota Mushrooms, Develop by sexual means; 22,000
toadstools, rusts basidiospores are born on club-
shaped-structures called basidia;
the terminal hyphal cell that
produces spores is called a
basidium; asexual reproduction
occurs occasionally
Zygomycota Rhizopus (black Develop sexually and asexually; 1,050
bread mold) multinucleate hyphae lack septa,
except for reproductive
structures; fusion of hyphae
leads directly to formation of a
zygote, in which meiosis occurs
just before it germinates

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 UNIT I PART 2 INTRODUCTION TO MYCOLOGY

REPRODUCTION OF FUNGI Sir Alvin Flores – Asynchronous

SEXUAL REPRODUCTION Meiosis involves reduction: from diploid, it will now

• Fusion of nuclei of 2 Opposing Matching Strains become haploid again. This would give rise to your
o Exchange of genetic material haploid nucleus after meiosis, reduction of the diploid of
• Gives ride to the TELEMORPH or TELOMORPH or the cell: diploid to haploid and would give rise to the
PERFECT STATE production of spores. The spores produced here are
sexual spores.
Three Distinct Phases of SEXUAL REPRODUCTION
• Plasmogamy – Haploid Donor Cell (+) penetrates the These sexual spores would undergo germination to
cytoplasm of Recipient (-) form mycelium which will then become fungi possessing
• Karyogamy – fusion of two haploid nuclei to form a hyphal components and other elements and then they
zygote would now have production of spores again, this time,
• Meiosis – gives rise to haploid nucleus (sexual asexual spores.
spores)
Take note that the telemorph can eventually proceed to
asexual reproduction which would give rise to an
anamorph.

ASEXUAL REPRODUCTION
• Gives rise to ANAMORPH or IMPERFECT STATE
o No exchange of genetic material, this will be
primarily cell division or mitosis
• Synanomorphs – if a single fungus is able to produce
multiple distinct anamorphs
• Involves
o Vegetative Reproduction – reproduction of
hyphal elements
o Aerial Reproduction – production of asexual
spores
Sir Alvin Flores – Asynchronous
Fungi Can Be
Plasmogamy is the first phase wherein you have a donor • Holomorph – whole fungus
cell and a recipient cell. The donor cell will penetrate the o Composed of / combination of the sexual and
cytoplasm of the recipient cell; the penetration would allow asexual phase
the fusion of the two cytoplasms of these cells. Eventually, • Fungi Imperfecti (Deuteromycota)
after plasmogamy, once their cytoplasms have been fused o There are fungi that do not possess a Sexual
together, the next phase would be Karyogamy. Take note state (imperfect funfi)
that both the donor and recipient cell are both haploid. In ▪ Ex. Candida, Torulopsis, Epidermophytom
Karyogamy, there will now be the fusion of the nuclei. The o In most references, the scientific names are
end result here would be your zygote. Since zygote is the based on the anamorph
fusion of 2 haploid cells or 2 haploid nuclei, this zygote will
now be diploid. After the formation of the zygote, the cell will
now undergo meiosis.
 SEXUAL SPORES TYPES OF ASCOCARPS
o Apothecium- cup-shaped asci are
Sir Alvin Flores – Asynchronous produced inside a cup
▪ The asci contains the ascospores
Acronym for the 4 types of sexual spores: BAZO ▪ In between each asci here, you will
Basidiospore, Ascospore, Zoospore, Oospore see structures in between the ascus
and we call them as paraphyses
• Ascospores
▪ Paraphyses packing hypha found in
o Spores enclose in an ASCUS following
between each ascus in the
karyogamy
apothecium
o Fruiting body: ASCOCARP (carps, bro lol o Cleistothecium – ascocarp is enclosed (no
nobody actually says that in taft) opening)
▪ The combination of multiple ascus / asci ▪ Enclosed protein body
(plural) will form a fruiting body o Gymnothecium – similar to cleistothecium
o Usually there are 8 ascospores inside the ascus except the outer wall of the ascocarp are
loosely organized; asci are released through
the wall opening.
▪ Like a cleistothecium but there are
spaces in between the walls
o Ascostroma – asci are produced in locules
(cavities) in hard masses of supporting
hypha called stroma.
o Perithecium – flask-shaped with an opening
where ascospores are released
▪ So notice that there is a small
opening on top where the
ascospores can be released

• Legend of the pic above:

o A – gymnothecium
Sir Alvin Flores – Asynchronous o B – Cleistothecium
o C- Apothecium
On top of your ascus is your apical pore where your o D- Perithecium
ascospores will be released. o E- Ascostroma
• Basidiospores
B and C (in the photo) are both types of Ascocarps

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 o Spores are formed inside a basidium ▪ Blastoconidia will form from the
(club-shaped reproductive structure mother cell
from which basidiosphore emerges) ▪ In budding, the division is unequal or
• Zygospores
o thick walled spores formed by fusion of
2 hyphal strands (homothallic)
o Keyword for this will be fusion of 2
homothallic hyphal strands
o If it’s homothallic then the hyphal
strands are coming from the same
hyphal elements.
o Zygospores can be seen through the
members of your Zygomycetes (?)
asymmetric.
o Fission
▪ The division is symmetrical
▪ One example of fungus that can
undergo fission is your
Schizosaccharomyces
o We can encounter budding and fission in
yeasts such as in candida
• AERIAL REPRODUCTION
▪ Involves the production of the asexual
• Oospores
spores
o Fusion of cells from 2 separate non-
• SPORE PRODUCTION
identical hypha
o Carried out by fruiting bodies
o In here there is also a fusion of 2 hyphal
- Conidiogenous cells
cells but this time, there are two
(fertile cells that produce
separate non-identical hypha
asexual spores or conidia)
(heterothallic)
- Ex. Phialides (flasked-
shaped conidiogenous
cells that will give rise to
phialoconidia) and
Annellides(conidiogenou
s cells that will give rise to
anneloconidia)
- Production of Conidia
o Carried out by Sporangium (fruiting
bodies with closed sacs)
- Production of
Sporangiospores
ASEXUAL REPRODUCTION
• VEGETATIVE REPRODUCTION – this will
involve the hyphal element
o Fragmentation
▪ So during the fragmentation, this will
eventually form your arthroconidia
(rectangular or barrel-shaped
spores)
o Budding- formation of blastocondia (in
yeasts)

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 FRAGMENTATION

Arthroconidia, another form of asexual reproduction, are

formed by fragmentation of fertile hyphae
This would be an illustration showing how
fragmentation occurs.

Fertile hypha will breakdown or disintegrate to

form arthroconidia. Your arthroconidia are BLASTIC FORMS
barrel-shaped spores. • Blastoconidia
o simplest form and produced by budding
BUDDING AND FISSION o Pseudohypha forms as in cases of Candida

(malabo talaga sorry)

Budding
• asymmetric
• seen in Candida
Fission
• symmetric Pseudohypha:
• seen in Schizosaccharomyces blastoconidia fail
Daughter cell or
blastoconidia to detach from the
CONIDIOGENESIS
mother cell
Can occur in two forms
1. Blastic
o Protoplasm of the conidiogenous cell is blown
out or blasted to form a conidium • Poroconidia
o Ex. Seen in Candida o Formed by the daughter cell by pushing
2. Thallic through a minute pore in the parent cell
o No development of conidium until a septum is o Type of asexual spore that arises from a very
formed between the conidium and the parent minute pore in the conidiogenous cell
cell o So pag galing sa maliit na butas, we call it
o aporoconidium
o The conidium originates from the whole of the
parent cell
o Ex. Dermatophytes and Coccidioides

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 ASEXUAL REPRODUCTION
• Conidium
o Produced in a manner that does not involve
cleavage
o Produced singly or in long chains or clusters by
conidiophores

• Phialoconidia
o Conidia emerges from a phialide
▪ Phialide – flask-shaped conidiogenous
cell
o Ex. As seen in Aspergillus and Phialophora;
Penicillium

• Conidia can be born in:

o Singly (yellow in pic)
o Long Chains (Catenulate) (red in pic)
o In Clusters (blue in pic)

• Annelloconidia
o Conidia formed from an annellide
o As the conidia are released, a distinct ring of
cellular material is left leaving behind a distinct
saw toothed (scar or rings) appearance at the
side of the parent cell
o Ex. Scopulariopsis; Exophiala

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• So, this is just a picture class showing you the fruiting THALLIC FORMS
body or the reproductive structure of your penicillium. • Macroconidia (Fuseaux) - large, septate (cross-
So, under the microscope, the reproductive structure walls or divisions), oval-shaped, spindle-shaped or
of your penicillium would look like a brush, club-shaped.
paintbrush appearance. o The macroconidium would have a wide variety
• So, notice here you have here your conidia, these of appearances, so they can be oval-shape,
conidia are coming from or arising from the phialides spindle, or club-shaped.
(pic) so take note, below the phialides, there is a
structure supporting the phialides, we call this the
metulae.
• So, the metula are sterile cells. So sterile, meaning
they are not fertile, they would not produce spores.
• Below the metula, these are then supported by your
conidiophores (red circle in pic above).
• So, compare that class to the reproductive structure
of your aspergillus (next pic). Red – macroconidia
Blue – spikes or echinulate
o May be thick or thin walled, spiny (echinulate)
or smooth wall surface; may appear as a
dictyospore/muriform; can be an aleurispore.
▪ If it is a dictyospore, it would look
like a mosaic. Mosaic
appearance.

• This is the reproductive structure of your aspergillus.

• So, notice here class, there is no presence of the
metula.
• So, what you see here class are the phialides, the
phialides are attached to the vesicle.
• This vesicle is further supported by the
conidiophore.
• There would be no metula or row of sterile cells that
you would see here in the reproductive structure of Dictyospore/muriform – mosaic appearance
your aspergillus.
• Microconidia – smaller, unicellular; borne on the
sides of the hypha
o Simpler, small asexual spore, and is only
unicellular
o Can be born on the sides of the hypha
o So, the microconidia, would often appear as
tear-shaped of pyriform.

CHLAMYDOCONIDIA

• Thick walled, resistant resting spores

• Produced by rounding up and enlargement of the
terminal hyphal cells
• Also asexual spores
• Can be of three types

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 o Terminal- on the tip or end • Sporangiophore-elongated structure that
o Intercalary- found inbetween the hyphal supports the sporangium
element • Columella -sa dulo ng sporangiophore, may
o Sessile- on the sides swollen part, siya yun, also known as the
• Usually encountered in Candida, particularly extension of the apex of the sporangiophore
Candida albicans • Also take note of the collarette
• Stolon- horizontal hyphal elements that connects
one sporangiophore to another sporangiophore
• Rhizoids- root like processes, very typical of the
members of Rhizopus, for support and anchoring
the hypha
• There are only 4 sexual spores and beyond these
4 are all asexual spores na
• All conidia are all asexual spores

ARTHROCONIDIA

• Rectangular/barrel shaped conidia; derived from

the fragmentation of the mycelium at the septum
o Presence of dysjunctor (disjunctor) cells
giving a checkered appearance
• Asexual spores
• Notice that there are empty cells inbetween TAXONOMY
• The empty cells are the dysjunctor cells which are
inbetween the arthroconidia Most Causative Agents of Infections are found in 4
• Can be seen in Coccidioides and Geotrichum Groups of Fungi
• Order Mucorales
o Phylum Glomeromycota (Zygomycetes)
• Phylum Ascomycota
• Phylum Basidiomycota
• Fungi Imperfecti (Deuteromycota)

Just focus on the scientific names of the asexual phase

SPORANGIOSPORES

• Asexual spores of Zygomycetes

• Borne in a sporangium
• Sporangium is a sac like strucuture
• Examples of Zygomycetes are the Rhizopus and
Mucor

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 Group Characteristics Example

• Rapidly growing usually found in soil

• Mycelia: profuse, gray-white; aseptate
or sparsely septate
• Asexual Rep’n: Sporangiospore
• Sexual Rep’n: Zygospores
• Rhizopus
• Saprophytic
Zygomycota • Absidia or Lichtheimia
• Usually just contaminants and usually
• Mucor
they cause opportunistic fungal
• Rhizomucor
infections
• Their hyphal elements are coenocytic
or aseptate
• Updated term for aseptate is
pauciseptate

• Production of Sexual Spores called

• Aspergillus
ascospores
• Pseudallescheria boydii
Ascomycota • Asexual reproduction is via conidia
• Trichophyton
(arthroconidia, blastosconidia)
• Penicillium
• Molds have septate hyphae

• Sexual reproduction results in four

progeny basidiospores supported by a • Crytococcus neoformans
Basidiomycota
club-shaped basidium (Filobasidiella neoformans)
• Hyphae have complex septa

• Imperfect Fungi • Coccidioides immitis

Deuteromycota • Most causes of mycoses belong to this • Paracoccidioides brasiliensis
group • Candida albicans

WHY ARE FUNGI PATHOGENIC TO HUMANS? oThey are fungi that are able to cause
Determinants of Pathogenicity: disease
• Thermotolerance o This include coccidioides, histoplasma,
o There are certain fungi that prefer blastomyces, sporothrix
growing in body temperature which make o What happens is, you get the infection by
them cause disease in humans inhalation of the mold form. Once inhaled
o Some are yeast at body temp and mold or some cases, directly inoculated to the
in room temp human person, once in the body the mold
• Adaptation to a parasitic lifestyle form becomes the yeast. The yeast then
• Adhesins causes the pathology or disease. The
• Use of enzymes to attach host tissues yeast form is also the one recovered from
• Dimorphism the tissue specimens.
o Fungi can be yeast or mold form. At body • Evasion of immune response
temp (37C), it becomes yeast. It o There are some fungi that are able to
transform to mold at room temperature survive intracellularly. There are certain
yeast cells that are capable of surviving
inside monocytes and macrophages. We

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 can see this in the yeast cells of o Opportunistic Mycoses
Histoplasma ▪ Affects immunocompromised patients
• Presence of cell wall molecules that are barriers ▪ Fungi associated are just usually
that resist lysis by phagocytes and antifungal saprophytic. Healthy patients are not
agents affected.
o Cell wall is composed of complex ▪ If patients have AIDS or has chronic
carbohydrates including chitin, glucans illnesses, they are susceptible to this
and mannans type of infection.
o These complex carbohydrates are • Generally, we call mycotic infection or fungal
effective barriers to prevent phagocytosis infection as Mycoses
and also to prevent anti-fungal agents. • In our study of mycology in this course, we will not
• Toxin Production classify different fungi based on its morphology.
o Fungi are also able to cause disease in • A more practical way of classifying fungi would be
humans because they produce exotoxins based on the affected part of the body
o Exotoxins cause different disease
manifestations or effects in the body. Mycotoxicoses
Some can cause hemorrhage or • Ingestion of mycotoxins
bleeding, some cause neurologic effects. o Ingestion or even inhalation of the toxins.
Some can also cause allergic reactions. These toxins are exotoxins which are
produced by fungi
Diseases Attributed to Fungi • Toxins coming from Amanita Mushroom
Mycoses o Amanitin and Phalloidin: Psychoactive
• Mycotic infections effects (neurological damage) and
• Practical Classification of Fungi Hepatotoxins
o Superficial or Cutaneous Mycoses o Not all mushrooms are edible some are
▪ Superficial: Fungal infection targeting poisonous
the dead, non-living portion of skin/hair
▪ Superficial: Would not cause any
immune response that would only
inhabit the dead/non-living part of the
skin
▪ Cutaneous: This involves the skin, hair
and nails usually caused by
dermatophytes. This is usually
ringworm or tinea infection
o Subcutaneous Mycoses AMANITA MUSHROOM
▪ Fungal infections affecting the deeper • Ergot Alkaloids
layer of the skin like connective tissue o These are metabolic products of Fungi
▪ Primarily affected by traumatic o Causes Ergotism or St. Anthony’s Fire
puncture unlike superficial and o Derived from Claviceps purpura
cutaneous which are both affected via o Claviceps purpura: Fungi that infects grains
direct contact such as Rye (Used in making flour/bread)
o Systemic Mycoses o If Rye is infected by fungi, this can lead to
▪ Also known as primary mycoses ergotism or St. Anthony’s fire.
▪ Fungal infections that would affect o Alkaloids: Ergotamine and Lysergic Acid
different or multiple organs Diethylamide
▪ Initially it would affect the lungs/ Initial ▪ Effect: Vascular and Neurologic effects
respiratory phase ▪ Development of Gangrene and
▪ Initial respiratory phase: Transmitted via Convulsions
inhalation of the spores
▪ After targeting the respiratory tract, it
can spread or disseminate

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 Hypersensitivity Reactions
• Allergies
o Hypersensitivity reactions
▪ Overreaction of the body against
antigens
o Manifested by: asthma reaction
(mediated by IgE)
▪ Eosinophilia and “wheal and
flare” skin test reaction
• Aflatoxins ▪ Can lead to inflammation,
o Important mycotoxicosis since it has economic redness, difficulty in breathing
impact that infects both humans and animals. o Due to immediate hypersensitivity
o Toxins (coumarin derivatives) produced by response to spores
Aspergillus flavus o One good example associated with
o The proliferation of Aspergillus flavus is usually allergic reactions is Aspergillus
associated if there is improper storage of grains
and even peanuts. Kung hindi dry yung peanuts Antifungal Susceptibility Testing and Therapy
and grains, that would promote the growth of • Designed to give information in aiding the
fungi. clinician in selecting the antifungal agent to treat
o Fungi grows if staple commodities are a specific fungal disease.
improperly stored
o Aflatoxins can enter the food chain infecting Antifungal Agents
livestock
▪ Humans are infected when spoiled grains Polyene Macrolide Antifungals
and peanuts are ingested • Amphotericin B
▪ If Aflatoxins are inhaled or ingested, it can o Source: Streptomyces nodosus
cause hepatic carcinoma or liver damage o For: deep seated fungal infections
▪ Not only humans are affected but even (Candida, Cryptococcus, Mucorales)
livestock such as cattle. o Binds ergosterol (a component of the cell
o Can lead to: Hepatic Carcinoma and Liver membrane of fungi) to disrupt or alter
Damage selective permeability of the cell
o Aflatoxin B1 membrane
• Aflatoxins poison is very well known which is o Toxic to: Kidney (nephrotoxic)
caused by eating improperly stored peanuts
• This would affect the food chain and food security • Nystatin
since it can cause disease in livestock and o Source: Streptomyces noursei
humans. o Local antifungal to treat oral or
vulvovaginal candidiasis
• Griseofulvin
o Source: Penicillium spp.

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 o Oral agents for dermatophytosis that are
not responsive to azoles
o Binds microtubular proteins
▪ Microtubular proteins are very
important or necessary for cell
division or mitosis of fungi
• Fluorocytosine
o Acts synergistically with amphotericin B
to treat Candida and Cryptococcus
o Inhibits protein synthesis

Azole Antifungal Agents

• Disrupts cell membrane by interfering with
synthesis of ergosterol
• Common for the treatment of dermatophyte
infections
• Key word is “-azole”
• Clotrimazole and Miconazole
o Mild cases of dermatophytosis
• Fluconazole
o Oral or IV administration
o For Candida or Cryptococcus
• Ketoconazole
o Oral or topical
o For mild cases of
paracoccidioidomycosis
• Itraconazole
o Similar to ketoconazole; effective in
aspergillosis, sporitrichosis,
crytococcosis and onchomycosis

Echinocandins
• Semisynthetic lipopeptides that target fungal cell
wall
o Targets synthesis of the cell wall,
particularly the glucan component of the
cell wall
• Inhibit glucan synthesis (1, 3-beta-D-glucan
synthesis
• For Candida

Allylamines
• Terbinafine and Naftifine
o Lipophilic; interfere cell wall synthesis
o Topical treatments for skin, nail fungal
infections
• Selenium sulfide
o For tinea versicolor
• Potassium iodide
o For cutaneous / lymphatic sporitrichosis

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 SUPERFICIAL MYCOSES

PRE-TEST
1. Superficial mycoses are confined to the
________ of the skin.
a. Stratum corneum
b. Stratum spinosum
c. Stratum basale
d. Stratum lucidum Believed to be caused by burrowing worms
2. Superficial mycoses may cause tissue
response and inflammatory reaction
a. True
b. False
3. Fungal infection of the hair shaft is known as
______.
a. Tinea
b. Conidia
c. Piedra
d. Nigra
Tinea pedis
4. Tinea nigra is characterized as _____.
(tinea + Latin term of the body site)
a. Red patches
Pedis – foot
b. Dark patch on the palm
c. Scaly lesion
d. White pigmentation on the palm
5. Tinea is a fungal infection of the ____.
a. Hair
b. Nail
c. Face
d. Skin
OVERVIEW
• Superficial Mycoses Form ring-shaped pattern in the skin
o Infections confined to the outermost layer of
skin or hair (stratum corneum) AGENTS OF SUPERFICIAL MYCOSES
o Tineas: skin infections MALASSEZIA FURFUR
o Piedras: hair infections CLINICAL MANIFESTATIONS
o Do not show overt symptoms • Tinea versicolor
o A highly prevalent chronic superficial infection
of our stratum corneum
o Can be isolated from normal skin and scalp
o Folliculitis – less common manifestation
▪ Common skin condition where your hair
follicles become inflamed
o AKA pityriasis versicolor
o Patchy lesions or scaling of varied
• “Tinea” pigmentation
o Latin, meaning “worm”
 o Thought to be cause of dandruff
o Affects all ages (5-8%)
o May involve any area of the body
▪ Face, chest, trunk, and abdomen (or Pityriasis versicolor showing hypopigmented lesions
smooth surfaces of the body; upper back,
arms, or even in the shoulders) CAUSATIVE AGENT
o Common endogenous skin colonizer
o Lipophilic
o Epidemiology
o Found worldwide
o Prevalent in hot, humid, and tropical locations

RISK FACTORS
o Pale patches in darkly pigmented skin
• Receiving corticosteroid therapy
o Fawn-colored liver spots in fair skin • Genetic influence
o Evident in warm months • Poor nourishment
• Excessive sweating
• It will also include the immune status of the patient
and also if there is an elevated temperature or
humidity.

TREATMENT
• Antifungal therapy is not typically indicated
• Left: light skinned – darker patches o Antidandruff shampoos
• Removal of indwelling feeding lines
• Right: dark skinned – lighter patches
o Because rarely this M. furfur can cause an
opportunistic fungal infection in patients or
opportunistic fungemia in patients and
particularly these are infants because when
they receive parenteral nutrition, there is
sometimes contamination of lipids.
o M. furfur is lipophilic
o This fungemia is not permanent, this is just a
transient infection and they can also be
eliminated.
o Those receiving lipid replacement therapy
o Particularly infants
• Daily applications of selenium sulfide
• Topical or oral azoles
• The goal of the treatment here is not really to
remove or eradicate the Malassezia form the skin,
but just to reduce the cutaneous population to
Pityriasis versicolor showing hyperpigmented lesions commensal levels.
• There are also species of Malassezia that can cause
seborrheic dermatitis which we are referring to as
dandruff.

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• Sometimes these cases they can also be treated • If there is misdiagnosis, sometimes it can result to
with ketoconazole. unnecessary surgical procedures.
• Melanoma or cancer because this is also how
HORTAEA WERNICKII melanoma looks like, so there could be
CLINICAL MANIFESTATIONS misdiagnosis.
• Tinea nigra • For this superficial mycosis or fungal infection, the
o AKA tinea nigra palmaris disease involves no inflammation, no inflammatory
o This one is a superficial chronic asymptomatic or tissue reaction to this infecting fungus.
skin infection and also affecting our stratum
corneum. CAUSATIVE AGENT
o Brown to black non-scaly macules • Hortaea werneckii
▪ Dark brown to black patch o Formerly known as
o Occur most often on palms and soles ▪ Phaeoannellomyces werneckii
o Misdiagnosis could occur ▪ Exophiala werneckii
▪ These lesions can be compared with • Dematiaceous fungus
silver nitrate staining of the skin, that is • Grows very slowly on common fungal media
why misdiagnosis can occur.
• Epidemiology TREATMENT
o This condition is more prevalent in warm, • Keratolytic solutions
coastal regions and among young women.
• Salicylic acid
o Tropical areas of Central and South Americas,
• Azole antifungal drugs
Africa, and Asia
PIEDRAIA HORTAE
CLINICAL MANIFESTATIONS
• This is the fungal infection affecting the hair and the
scalp and occasionally this can affect the axillary
and the pubic hair.
• Black piedra
o Infection of the hairs of the scalp
o Hard, dark brown to black gritty nodules
▪ Firmly attached to hair shaft
• Epidemiology
o Tropical areas of Africa, Asia, and Latin
As compared to your M. furfur, this one is non-scaly America.

WHICH OF THE FOLOWING IS TINEA NIGRA?

• So, remember, the lesion usually is a dark patch on CAUSATIVE AGENT

the palm of one hand and usually this is well-defined • Piedraia hortae
and there is an irregular margin. No redness or
erythema, but there is this characteristic stained
appearance that is we thought sometimes this is
silver nitrate stains.
• There are occasionally peritus or itchiness and
scaling.
• I mentioned a while ago, that there is sometimes
misdiagnosis that can occur, because sometimes
the clinical presentation of this infection is similar to
other conditions and most of the time it is confused
with malignant melanoma or cancer.

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 o Isolated from animals and soil
o Recognized as opportunistic systemic
pathogens
▪ Frequently fatal
▪ Occur most often in
immunocompromised host
• Especially if they have infections in
the blood, CSF, and in their
organs.
▪ Hematologic disorders or malignancies
▪ Undergoing chemotherapy

TREATMENT
• Removal of infected hair
• Application of topical antifungal agent.
TREATMENT
• Removal of infected hair POST-TEST (Red sure, green not sure)
• Application of a topical antifungal agent
1. Which of the following best describes tinea
TRICHOSPORON SPP. versicolor?
CLINICAL MANIFESTATIONS a. Scaly and pruritic
• White Piedra b. Dark, patchy, inflammatory lesions
o Occurs on hair shaft c. Non-scaly and pruritic
o Soft mycelial mat surrounding hair of the d. Dark lesions commonly seen on the
scalp, face, and pubic region. palmar surface of the hand
o In other references, they can also be 2. The appearance of white macular lesions
described as soft, yellow or pale brown hypopigmentation occur on dark skinned
aggregations around the hair shaft. patients.
• Epidemiology a. True
o Tropical areas of South America, Africa, and
b. False
parts of Asia
3. The fungi causing superficial mycoses do not
interfere with the normal pigmentation of the
skin.
a. True
b. False (not sure)
4. Which organism causes tinea nigra?
a. Piedraia werneckii
b. Malassezia furfur
c. Piedraia hortae
d. Hortaea werneckii
5. Which of the following is recognized as an
opportunistic systemic pathogen?
CAUSATIVE AGENT a. Malassezia furfur
• Trichosporon beigelii b. Trichosporon spp.
o No longer a valid species infecting humans c. Piedraia hortae
• Implicated in most cases of superficial mycoses ̶ d. Trichophyton spp.
o T. ovoides, T. asteroids, T. cutaneum, T.
inkin
• T. asahii
o Severe and frequently fatal disease in
immunocompromised hosts
• T. mucoides
o Causes meningitis
• Trichosporon spp.
o Occasionally found as part of normal skin
biota

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 CUTANEOUS MYCOSES
▪ Epidermophyton
Pre-test: • Dermatophytes are keratinophilic, so they use
TRUE OR FALSE the keratin as the substrate
1. Ringworm of the scalp is most common in • The common term for this dermatophytosis is the
toddlers and school-age children. ringworm or tinea
2. Trichophyton rubrum is the causative agent of
Tinea favus.
3. Tinea corporis is a superficial fungal infection of
the arms and legs, especially on glabrous skin.
4. Tinea barbae is a superficial dermatophyte
infection that is limited to the bearded areas of the
face and neck and occurs almost exclusively in
older adolescent and adult males.
5. Endothrix is the formation of arthroconidia on
the outside of hair shaft.

ECOLOGICAL GROUPS OF DERMATOPHYTES

CUTANEOUS MYCOSES GEOPHILIC
• No living tissue • “earth-loving”
• Host Rxn to fungus • inhabit soil where they decompose
• The cutaneous mycoses are fungal keratinaceous debris
infections of the integument and its • Dead animals
appendages, the superficial infection of the • Free-living soil saprophytes
skin, the hair and the nails
• The fungus localizes in the cornified layer
stratum corneum.

ZOOPHILIC
• Parasitic on animals
• Animal loving
• Causes more severe inflammatory infections
DERMATOPHYTOSIS in human
• Disease
o Dermatophytosis
• Causative organisms
o Dermatophytes
▪ Microsporum
▪ Trichophyton

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 Trichophyton
• Macroconidia Smooth walled
• Microconidia present

ANTHROPOPHILIC FUNGI
• primarily parasitic to man
• man as exclusive host
• for maintenance & dissemination of species
• Examples:
o Microsporum audouinii Epidermophyton
o Trichophyton rubrum
• Macroconidia Smooth walled
o Trichophyton schoenleinii
• Chlamydoconidia
o Trichophyton tonsurans
• Microconidia none
o Trichophyton violaceum
• People loving
• Infects man only
• Causes chronic infections, eliciting relatively
mild response by the host

CLINICAL MANIFESTATIONS OF
DERMATOPHYTES
INFECTIONS INVOLVING HAIR
• Trichophyton schoenleinii
CLASSIFICATION OF DERMATOPHYTES
Microsporum • Microsporum audouinii
• Macroconidia Rough walled • Microsporum ferrugineum
• Microconida present • Trichophyton tonsurans
• Trichophyton violaceum

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 PATTERN OF HAIR INVASION
ECTOTHRIX
• formation of arthroconidia on the outside of
hair shaft
• cuticle of hair is destroyed

Two distinct forms

• Gray patch ringworm
o a common childhood disease that is
easily spread among children.
o colonizes primarily the outer portion of
hair shafts, the so-called ectothrix hair
involvement.
• Hair invasion by a dermatophyte o The lesions are seldom inflamed, but
o Microsporum canis luster and color of the hair shaft may be
o M. gypseum lost.
o Trichophyton equinum o Microsporum audouinii and Microsporum
o T. verrucosum ferrugineum
• Black dot ringworm
ENDOTHRIX o consists of endothrix hair involvement.
• formation of arthroconidia within hair shaft o The hair follicle is the initial site of
• cuticle of hair remains intact infection, and fungal growth continues
• do not fluoresce under Wood’ s UV light within the hair shaft, causing it to
weaken.
o The brittle, infected hair shafts break off
at the scalp, leaving the black dot stubs,
that’s why it is also called as the black dot
ringworm
o Trichophyton tonsurans and
Trichophyton violaceum causes the
• ALL AGENTS ARE ANTHROPOPHILIC black dot ringworm
o Trichophyton tonsurans,
o T. violaceum Risk factors for ringworm of the scalp include:
• Age
TINEA CAPITIS o Ringworm of the scalp is most common in
• Scalp, eyebrow, eyelashes toddlers and school-age children.
• Microsporum & Trichophyton • Exposure to other children
o Outbreaks of ringworm are common in
schools and child care centers where the
infection easily spreads through close
physical contact.
o It is because it is a highly contagious
infection
• Exposure to pets
o A pet, such as a cat or dog, can have the
infection without showing any signs.
Children can get the infection by touching
or petting the animal.

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 • An infection of the hair follicle that can
Note: The signs and symptoms of ringworm of the progresses to a crusty lesion made up of dead
scalp may vary, but it usually appears as itchy, scaly, epithelial cells and fungal mycelia.
bald patches on the head. • Crusty, cup-shaped flakes, called scutula, are
formed.
Ringworm of the scalp, a highly contagious infection, • Hair loss and scar tissue formation commonly
is most common in toddlers and school-age children. follow.
INFECTIONS INVOLVING THE BODY
Treatment: TINEA CORPORIS
• 2% ketoconazole shampoo • Non-hairy skin
• 1% or 2.5% selenium sulfide shampoo • Rings with scaly centers
• Rxn vs fungus
TINEA FAVOSA • Epidermophyton floccosum, Trichophyton,
Microsporum
• A superficial fungal infection (dermatophytosis)
of the arms and legs, especially on glabrous
skin (it may occur on any part of the body)
• A scaly ring-shaped area, typically on the
buttocks, trunk, arms and legs
• Dermatophyte infection of glabrous skin most
caused by species of Epidermophyton
floccosum, Trichophyton, Microsporu.
• Lesions may vary from simple scaly to formation
of erythema and vesicles or can be a deep
• Scutulum
• Mass of mycelia & epithelial debris
• Cup shaped Cutaneous crusts
• This refers to the similarity of scutula which
appears to be a yellow…
• This develops at the hair follicle within the hair
shaft at the center of the raised lesion
TRICHOPHYTON SCHOENLEINII
granuloma.
• Usually restricted to the stratum corneum of
epidermis
CAUSES
• Human to human. Ringworm often spreads by
direct; skin-to-skin contact with an infected
person.
• Animal to human. You can contract ringworm
by touching an animal with ringworm. Ringworm
can spread while petting or grooming dogs or
cats. It's also common in cows.
• Causative agent of Tinea favosa
• Object to human. It's possible for ringworm to
• Anthropophilic
spread by contact with objects or surfaces that
• Cause favus
an infected person or animal has recently
• Chronic scarring form of tinea capitis
touched or rubbed against, such as clothing,
towels, bedding and linens, combs, and
brushes.

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• Soil to human. In rare cases, ringworm can be • Concentric rings
spread to humans by contact with infected soil. • Trichophyton concentricum
Infection would most likely occur only from • Tinea imbricata is a chronic superficial mycosis
prolonged contact with highly infected soil. This caused mainly by Trichophyton concentricum.
occurs in gardener or farmer with prolonged • The condition mainly affects individuals living in
contact on a highly infected soil. primitive and isolated environment in
RISK FACTORS developing countries and is rarely seen in
• You're at higher risk of ringworm of the body if developed countries.
you: TINEA BARBAE
o Live in a warm climate
o Have close contact with an infected person
or animal
o Share clothing, bedding or towels with
someone who has a fungal infection
o Participate in sports that feature skin-to-skin
contact, such as wrestling
o Wear tight or restrictive clothing • Bearded areas of face & neck
o Weak immune system • Tinea barbae is a superficial dermatophyte
TREATMENT infection that is limited to the bearded areas of
• Topical therapy should be applied to the lesion the face and neck and occurs almost exclusively
and at least 2 cm beyond this area once or twice in older adolescent and adult males.
a day depending on the severity for at least 2 • The clinical presentation of tinea barbae includes
weeks. inflammatory, deep, kerion like plaques and
• Topical azoles noninflammatory superficial patches resembling
TINEA IMBRICATA tinea corporis or bacterial folliculitis.
• It may be viewed as an occupational disease
among cattle farmers
• Exclusive for men/adult male that is a
dermatophyte infection of bearded areas of face
and neck
TREATMENT
• Shaving or hair depilation is recommended with
warm compresses to remove crusts and debris.
• Topicals such as griseofulvin
TINEA CRURIS

• This is geographically restricted form of Tinea

corporis caused by Trichophyton
concentricum.
• Characterized by polycyclic concentrically • Also known as Jock itch which is a
arranged rings squamous patches of scales dermatophyte infection pf the groin, perineum,
scattered over and often covering most of the and perianal region which is acute or chronic
body and generally pruritic.

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• The lesion is sharply demarcated with raised • The disease may progress around the sides of
erythematous margin with thin and dry the foot from the sole called moccasin foot.
epidermal scaling. This tends to occur usually in • Infections of the glabrous skin range from mild,
high humid areas involving the lower with only minimal scaling and erythema, to
extremities. severely inflamed lesions.
• More common in men TREATMENT
• Jock itch • Tinea pedis can be treated with topical or oral
• Moist groin area antifungals or a combination of both.
• E. floccosum, T. rubrum • Topical agents are used for 1-6 weeks
• Tinea cruris, a pruritic superficial fungal • Imidazole topical cream - applied once daily for
infection of the groin and adjacent skin. 2 weeks.
• Jock itch is most common in men and • A patient with chronic hyperkeratotic
adolescent boys. The infection causes a rash (moccasin) tinea pedis should be instructed to
that often itches or burns. The affected areas apply medication to the bottoms and sides of his
can also be red, flaky, or scaly. or her feet.
TREATMENT • For interdigital tinea pedis, even though
• Topical terbinafine symptoms may not be present, a patient should
• Itraconazole apply the topical agent to the interdigital areas
INFECTIONS INVOLVING HANDS AND FEET and to the soles because of the likelihood of
• Trichophyton rubrum plantar-surface infection.
• Trichophyton mentagrophytes • Naftifine gel or cream 2% is indicated for
• Trichophyton tonsurans interdigital tinea pedis in adults and
• Epidermophyton floccosum adolescents.
TINEA PEDIS TINEA MANUUM

• This is the dermatophyte infection of hand

particularly the Interdigital areas & palmar
• This is a dermatophyte infection of the feet surfaces
involving particularly the toe webs and the • Interdigital areas & palmar surfaces
soles. • Tinea manuum is an itchy rash that may affect
• The lesions are of several types varying from one or both hands. It often starts on the palm
mild, chronic, scaling, acute, exfoliative, and and may spread to the fingers or back of the
lesions. hand.
• Athlete’s foot • A red raised border with a patch of skin that
• Toe webs & soles, even nails looks like it has healed in the center, giving the
• Infection arises from infected skin scales appearance of a ring, which is what gives
coming into contact with exposed skin via a ringworm its name. This symptom is most likely
carpet, shower floors, or other shared walking/ to appear when the rash is caused by animal or
standing surfaces where shoes are not always soil fungi
worn. • Dry, peeling, or scaly skin: A patch of skin that
is dry, peeling, or scaly with a mild itch may

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 appear and gradually spread. This symptom is o Women of any age who wear artificial nails
most common when the tinea is caused by a (acrylic or "wraps").
human fungus. TREATMENT
• Tiny blisters: A cluster of tiny blisters may • Oral terbinafine
appear on the sides of fingers or on the palm • Itraconazole
that may ooze a sticky, clear fluid. EPIDERMOPHYTON FLOCCOSUM
• Itching or burning: The rash may be mild to
moderately itchy, causing some discomfort.
• Skin discoloration: If the rash is there for a
long time the skin may become discolored. This
change in color can also occur as the tinea
heals.
RISK FACTORS
• Touching the skin of someone else who has a
fungal infection, for example, while playing
sports or having sex • Microscopic:
• Using a well-used public shower, such as in a ▪ Smooth thin-walled macroconidia often
gym in clusters growing directly from hyphae
▪ No microconidia
• Sweating excessively or having another skin
▪ Numerous chlamydoconidia
condition
• Regularly touching pets with bare hands
• Handling livestock or soil such as gardener
• Working as a gardener, handling soil or tools
that have been covered in soil Treatment
TOPICAL ANTIFUNGALS
• Fluconazole
• Itraconazole
TINEA UNGUINUM

• Culture:
• Greenish-brown or “khaki” colored
• Suede-like surface

Species Microconidia Macroconidia

Sparse: Spindle shape,

• Invasion of nail plate by dermatophytes M. canis calavate, spiny surfaces,
• Thickened, discolored & brittle sessile curved tip
• Onychomycosis- Non dermatophyte infection
• Raised & folded center, with flat periphery
• Risk factors for developing onychomycosis
• Yellowish brown reverse pigment
include:
o People with diabetes
o People with disease of the small blood
vessels (peripheral vascular disease); and
o Older women (perhaps because estrogen
deficiency increases the risk of infection);
and

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 Species Microconidia Macroconidia • Microscopic:
Smooth, thin- o Symmetrical ellipsoidal
E. floccosum None
walled o Thin-walled verrucose macroconidia
o Distal end slightly rounded, proximal
MICROSPORUM CANIS (point of attachment) is blunt
o 4 to 6 cells

• Zoophilic MICROSPORUM AUDOUINII

o Cats and dogs • A slow-growing anthropomorphic dermatophyte
• Invades: • Responsible for most of the gray patch Tinea
o Hair capitis of children.
o Skin
o Nails (rarely) TRICHOPHYTON MENTAGROPHYTES
• Distribution • Zoophilic: mice, cats, horses, sheep, rabbits
o Worldwide • Inflammatory skin or scalp lesions in humans
• Microscopic:
• Ectothrix
o Spindle shaped, one end pointed, other
• Distribution: Worldwide
end blunt
• Microscopic:
o Thick walled verrucose macroconidia
o Spherical microconidia
o 6 to 12 cells
o Forming dense clusters (“en grappe” –
grapelike clusters)
o Spiral hyphae
o Smooth thin-walled claviate multiseptate
macroconidia

Species Microconidia Macroconidia

Globose Rare: Cigar-
T.
Grapelike shaped; Coiled
mentagrophytes
clusters spiral hyphae

MICROSPORUM GYPSEUM
• Geophilic
• Usually produces a single inflammatory skin or
scalp lesion
• Distribution: Worldwide

Species Microconidia Macroconidia

Cigar-shaped,
Sparse: claviate, with spiny
M. gypseum
sessile surfaces &
rounded tips

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 • Culture
o Variation in texture & color
o Suede-like to powdery
o Flat with raised center or folded, with
radial grooves
o Pale buff to yellow

TRICHOPHYTON RUBRUM
• Anthropophilic TRICHOPHYTON CONCENTRICUM
• Chronic infections of the skin, nails, scalp (rare) • Anthropophilic
• Ectothrix or endothrix hair infection • Chronic non-inflammatory Tinea corporis
• Distribution: Worldwide • Tinea imbricata – concentric scaling of skin
• Does not invade hair
Species Microconidia Macroconidia
POST-TEST
Clavate- peg-
Pencil-shaped
T. rubrum tear-shaped
Cylindrical 1.) Trichophyton mentagrophytes causes in
Sessile
flammatory skin or scalp lesions in
humans.

2.) Tinea manuum is an itchy rash that may

affect one or both hands.

3.) Epidermphyton floccosum smooth thin-

walled macroconidia often in clusters
TRICHOPHYTON TONSURANS growing directly from hyphae with
microconidia.

4.) Tinea cruris is more common in women.

5.) Tinea imbricata is a chronic superficial

mycosis caused mainly by Trichophyton
• Anthropophhilic
concentricum.
• Causing inflammatory or chronic non-
inflammatory finely scaling lesions of skin, nails
and scalp
• Distribution: Worldwide

Species Microconidia Macroconidia

Abundant tear-
T. tonsurans club- peg- Cylindrical
balloon-shaped

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 SUBCUTANEOUS MYCOSES
 Lesions are progressive; Cutaneous to
General Properties subcutaneous with tissue involvement. There is
also the presence of abscess and this could cause
 Subcutaneous tissue
the presence of the sclerotic cells which is
 Traumatic implantation of foreign objects
important in diagnosing disease.
 Common in soil or on decaying vegetation

Common Clinical Features

 Progressive, nonhealing ulcers
 Draining sinus traits

Notes from Maam:

 Diseases are usually confined in
subcutaneous tissue however in some cases
they can become systemic and they can be
life threating disease.
Agents
 Usual mode of infection is through the
traumatic implantation of foreign objects. It is
introduced to subcutaneous tissue by trauma.
 The fungal agents are common in soil or on
decaying vegetation They are common
disease among agricultural workers that is
why most of them are considered to be as
an occupation hazard
 Ulcers are progressive unless we make use
of antifungal medications.  Fonsecaea compacta
 Fonsecaea pedrosoi
 Phiaophora verrucose
Chromoblastomycosis
 Cladophialophora carrionii
General Information
 Rhinocladiella aquaspersa
 Aka verrucous dermatitis /chromomycosis
 These agents can only be differentiated through
 Barefoot
microscopic testing through the appearance of
 Common in males colony in fungal culture.
 May be mistaken as squamous cell carcinoma Epidemiology
 “Chromo” means a color so that would imply that  Tropical and subtropical regions of America &
the causative organism has a pigment. It is Africa
considered dematiaceous.  Agents reoccur in vegetation and soil, so it is
 If the disease is not being examined, it can be common in the barefoot agrarian community, but
mistaken as squamous cell carcinoma. it is non-communicable
 The pictures below show the different severity
grade of chromoblastomycosis.
 Upper and Lower Left: Mild forms of lesions
 Upper Middle and Lower Middle: Moderate forms
of lesions
 Upper Right and Lower Right: Severe form of the
lesions

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 Clinical Manifestation  Mycetoma means a chronic subcutaneous
infection caused by traumatic inoculation of
fungi.
Clinical aspect of the symptomatic triad
 Tumefaction
 Sinuses
 Grains
o Helps to identify the agent through its
texture, size and color
Agents
 Chronic infection  Scedosporium boydii
o It will take months to years for the primary  Acremonium falciforme
lesion to become verrucous.  Madurella mycetomatis (most common)
 Extremities  Madurella grisea
 Verrucous nodules  Exophiala spp.
 Cauliflower-like surface  Through microscopic testing and its granules,
 Black dots agents can be differentiated
 As seen in the picture the one that is being Epidemiology
pointed by the arrow are black dots or  Tropical and subtropical regions
hemopurulent material that are present in  India, Africa and South America
lesions of chromoblastomycosis. Treatment
Treatment  Itraconazole/ Ketoconazole/ Amphotericin B
 Itraconazole  Topical nystatin or miconazole (P. boydii)
 Surgical excision  Surgical debridement or excision or
 For wide margins of infection, surgical excision is chemotherapy if necessary
an option Phaeohyphomycosis
Mycetoma Subcutaneous Phaeohyphomycosis
Actinomycetoma and Eumycetoma
 2 types of mycetoma is based on the causative
agent
 Actinomycetoma is caused a bacterial agent
such as actinomyces, streptomyces, and
nocardia
 Actinomycetoma can be differentiated with
mycetoma through laboratory testing. For
actinomycetoma, there is no presence of hyphal
elements. However, in eumycetoma there are
hyphal elements
Eumycotic Mycetomas  Caused by darkly pigmented fungi
 AKA Maduramycosis/ Madura foot  Agents: Exophiala dermatitidis
 Mudara foot because it was first isolated in  Treatment: Itraconazole or flucytosine
madurai, India  Mycotic infection is possible both in humans and
Clinical Manifestation animals.
 Chronic, granulomatous infection  Can be differentiated through microscopic testing
 Purplish discoloration  Mode of infection: Traumatic implantation of
 Draining sinuses containing granule fungal element.
 Exudates  Present in soil and decaying vegetation
 May involve bone, muscle and tissues  Aside from cutaneous and subcutaneous
phaeohyphomycosis, it can cause paranasal
phaeohyphomycosis wherein patients would

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 sinusitis which is common to patients with history  Extracutaneous / pulmonary / disseminated
of allergic rhinitis. o Disseminated could only occur in HIV
 Lastly, agents can also cause cerebral patients with very low CD4 cell count
phaeohyphomycosis which is rare and common  Agent: Sporothrix schenckii species complex
only in immunosuppressed patients. o Introduced by traumatic implantation of rose
thorns and splinters
o Seen in grasses and trees
o Agent can be inhaled that could lead to
primary or secondary pulmonary
sporotrichosis.
 This disease is usually associated with
gardening, so it is an occupational hazard
Treatment
 Itraconazole
 Saturated solution of potassium iodide
Cutaneous Phaeohyphomycosis  Amphotericin B
Control
 Minimize accidental inoculation
o Gardeners could wear gloves
 Treating wood or use of fungicides

SPOROTHRIX SPP.
General Information
 usually recovered from soil and decaying
vegetation
o This is common among all subcutaneous
mycoses
 occupational hazard
Subcutaneous phaeohyphomycosis o A common infection among farmers,
nursery workers, gardeners, flourists, and
Sporotrichosis miners
o Kaya siya tinawag na Gardener’s disease
kase common yan sa mga mahilig mag
gardening o sa mga horticulturate
 Epidemiology: Brazil, Mexico, Uruguay, South
Africa, France, Canada
o The agent is usually seen in warm and arid
areas, humid, and temperate areas as well
 Sporothrix is a dimorphic fungi and it has two forms,
the mold form and yeast form
 Therefore, we can grow this agent in 22 degrees
Celsius or in 37 degrees Celsius
 Rose handler’s disease/ Rose gardener’s o This is a diagnostic way for us to identify
disease and isolate Sporothrix species.
 Rose thorns and splinters Agents
 Nodular and ulcerative lesions  Sporothrix schenckii
 Fixed cutaneous sporotrichosis  Sporothrix brasiliensis
o Lesion would only be present at the site of o This can be transmitted through bites or
inoculation scratches of stray cats
 Mucocutaneous sporotrichosis  Sporothrix globosa
o Common among the infections  Sporothrix luriei

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 Remember that aside from inhalation ng fungal POST QUESTIONS
agent, there’s infl ammation from rose thorns, 1. The most common form of sporotrichosis
splinters. is:
Sporothrix schenckii A. Skeletal
 MOT: trauma, rarely inhalation B. Mucosal
o A common mode of transmission can be C. Lymphocutaneous
traumatic implantation D. Disseminated
o However, it can also be inhaled causing
the pulmonary sporotrichosis Answer: C. The most common form of sporotrichosis
 antigenic structure: is Lymphocutaneous sporotrichosis.
o Sporotrichin: carbohydrate fraction
from killed suspensions of the organism 2. The sclerotic bodies are useful for
 dimorphic (can be cultured at 22 ° C and 37° C) diagnosis of:
o infectious form (22 ° C) –conidia/hyphae A. Sporotrichosis
o clinical form (37 ° C) - yeast B. Mycetoma
C. Chromoblastomycosis
 can cause pulmonary infections, D. Phaeohyphomycosis
lymphocutaneous infection, sinusitis, arthritis,
osteomyelitis, meningitis, external otomycosis, Answer: C. Chromoblastomycosis
conjunctivitis, disseminated infections
o Disseminated infections in HIV Explanation from Ma’am
individuals which has low CD4 cell count  When we say sporotrichosis, they are
dimorphic, its ability to grow in its mold and
yeast forms is the diagnostic means for the
detection of the disease.
 For mycetoma naman, this is diagnosed
through the presence of the granules or
grains. So yung grains, meron yang size,
color, and texture that will be discussed fully in
the lab part.
 The granules is the way to diagnose
mycetoma
 Chromoblastomycosis, we have the miriform
or the sclerotic bodies
 And for the phaeohyphomycosis we can be
able to differentiate these by the absence of
sclerotic bodies, the absence of granules sa
ating lesions, and it will only have the
presence of distorted hyphal elements.
 And to differentiate it (phaeohyphomycosis)
with sporotrichosis, hindi po dimorphic ang
agents ng phaeohyphomycosis

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 SYSTEMIC MYCOSES

o So you will notice class, in systemic mycoses, it

Discussion outline
is caused by dimorphic fungi
1. Overview
o Kapag sinabi mong dimorphic, they have two
2. Agents of Systemic mycoses
forms, may mold form, and may yeast form.
a. Characteristics
o Ang mold form ng systemic fungi are usually
b. Clinical features/findings
found in the environment.
c. Pathogenesis
o Nagcchange lang yung morphology ng fungus
d. Risk and Prevention (FAQs)
kapag na-inhale na ng suceptible host
e. Treatment
o From mold form, it will convert in the yeast form.
• Infection occurs by inhalation of air- borne conidia
PRE-TEST (TRUE OR FALSE) o As I have mentioned, inhalation is the primary
1. Any fungus, in an immunocompromised mode of transmission
host, has the potential to become invasive • Fungal infection of internal organs
and disseminate to sites far removed from o Take note that the primary site of infection is
the portal of entry. usually pulmonary following the inhalation of
2. The teleomorph of H. capsulatum is named the air-born conidia
Ajellomyces dermatitidis. Agents of Systemic Mycoses
3. Histoplasmosis is also known as Spelunker's • Blastomyces dermatitidis
Disease • Coccidioides spp.
4. People get paracoccidioidomycosis after o C. immitis
breathing in the fungus Paracoccidioides o C. posadasii
from the environment in certain parts of • Histoplasma capsulatum
Central and South America.
• Paracoccidioides brasiliensis
5. Vaccine is already available for Valley fever. Blastomyces dermatitidis
• Causes BLASTOMYCOSIS
SYSTEMIC MYCOSES o AKA Gilchrist disease, North American
General Information Blastomycosis, and Chicago disease
• AKA endemic mycoses/ disseminated mycoses o A chronic infection with granulomatous and
o Why endemic? Because they are geographically suppurative lesions that is initiated in the lungs
restricted to specific areas of endemicity. And as - And this is frequently followed by the
you will notice in the preceding slides, iddiscuss dissemination to other sites, primarily the
natin yung iba’t ibang organisms and as you will skin and the bones
notice may iba silang terms - Although the diseases was long thought to
o Say for example Blastomycosis, the other term be restricted in the north american
for it is North American Blastomycosis or Chicago continent, in recent years autotonous(?)
Disease okay…depende siya kung san naging cases have been diagnosed in Africa,
endemic yung infection or disease. Asia, and Europe
• fungal infections of the which can overcome the Notes from Ma’am:
physiological and cellular defenses of the normal o These are variable and is not used
human host as a diagnostic tool for detecting
o How do they overcome the physiological and pulmonary blastomycosis
cellular defenses of our system? By changing
their morphological form - And all available clinical and
epidemiological evidence indicates that
humans and lower animals contract

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 blastomycoses from some sources in lesions with irregular borders or yung
nature tinatawag nating ulcers
- Approximately, half of the people infected • Usually ang tinatamaan nito is the upper limbs,
with the fungus of the blastomyces will specifically the neck and the scalp. Those are
the most frequent sites involved in cutaneous
show symptoms
blastomycosis
- The symptoms of this infections usually • This is the most common clinical manifestation
appear between 3 weeks to 3 months of this infection
after a person inhaled the fungal spores • On the right pic, this is the cutaneous
o Most prevalent in middle-aged men blastomycosis
o The symptoms are often similar to the • As I have mentioned a while ago, the
symptoms of flu cutaneous type is the most common form.
- Fever, cough, night sweats, muscle aches, Hence, kaya siya tinawag na blastomycoses
dermatitidis is because the primary
weight loss, chest pain, and fatigue.
manifestation of cutaneous blastomycosis is
dermatitidis and it is usually seen, over
exposed parts like the face, neck, and also the
hands.

3. Disseminated Blastomycosis
Note from Ma’am:
• In disseminated blastomycosis, this is the
form where there are multiple abscesses in
different parts like the bone, the genito-urinary
system, and also pwedeng tamaan ang
breast.
https://www.cdc.gov/fungal/diseases/blastomycosis/symptoms.html
• This picture (left side) pertains to the
ulcerated granuloma
Clinical Types of Blastomycosis
1. Pulmonary Blastomycosis
Notes from Ma’am:
• Here class in most individuals, yung pulmonary
lesions are mostly asymptomatic and they are
not detected until the infection has spread to
the organs.
• From the name itself, disseminated mycoses,
because it can disseminate to the other organs
• And others, they develop symptoms after an
incubation period of 3-15 weeks
• In most cases, the blastomycosis is evident in
patients with chronic symptoms such as the
cough, fever, weight loss.
• The lesions become more extensive with Jawetz Melnick&Adelbergs Medical Microbiology
continuous suppuration, eventual necrosis,
and caveration Notes from Ma’am:
• Since this is pulmonary, a very common • In other sources we also have the Osteoarticular
disease is the Chest Radiographic findings blastomycosis
• These are variable and is not used as a o This occurs in about 30% of patients with the
diagnostic tool for detecting pulmonary spine, pelvis, cranial bones, ribs, and long
blastomycosis bones… those are the most commonly
involved
2. Cutaneous Blastomycosis o Here class yung pasyente, they often remain
asymptomatic until the infection spreads into
Notes from Ma’am:
the contiguous joints or in the adjacent soft
• In cutaneous blastomycosis, there is a
tissue causing subcutaneous abscesses
hematogenous spread which gives rise to
cutaneous lesions in over 70% of the patients
• Actually, cutaneous blastomycosis is painless
and present either as raised verrucous
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 PATHOGENESIS: Biology of Blastomycosis o Symptoms in dogs are similar to the symptoms
of humans.
• How can I prevent blastomycosis?
o There is no vaccine to prevent and it may not be
possible to be exposed to the fungus, lalo na pag
mahilig kang magtravel and hike. People who
have weakened immune systems may want to
consider avoiding activities that involve
disrupting soil in these areas.
• TREATMENT: Amphotericin B (severe cases),
Itraconazole (confined lesions, 6-month course of
Itraconazole is very effective)

Ms. Canlas – Asynchronous

There are 2 species of Blastomyces. The Blastomyces

dermatitidis and Blastomyces gilchristii. They are
Ms. Canlas – Asynchronous morphologically indistinguishable. B. gilchristii can be
identified through sequences of nuclear RNA gene.
In the environment, the systemic fungus exists as a When it comes to the teleomorph, B. dermatitidis has
mold. It has a septate, aerial hyphae. Hyphae can it. Recall, the teleomorph is the sexual form; that is the
produce spores. Spores are either inhaled or Ajellomyces dermatitidis. Teleomorph does not not
inoculated into the skin of the susceptible host. The occur (?) in routine laboratory because the specie is
warmer the temperature of the host, it will signal heterothallic which means it requires 2 mating strains
transformation. Mold usually grows at 22 C and yeast to reproduce sexual forms
can grow in 37 C. It will transform into a broad budding
yeast (red square). The yeast may continue to colonize COCCIDIODES SPP.
the lungs or it can disseminate in the blood stream or
to the other parts of the body such as the skin, the • Probably the most virulent of all human mycotic
bones, joints, organs and also the central nervous agents but not contagious
system (CNS) and causes meningitis. • There are 2 Coccidiodes spp.
o C. immitis
RISK AND PREVENTION o C. posadasis
• Who gets blastomycosis? o Morphologically identical so molecular
o Anyone if they have been in an area (bc it is evaluation is required to differentiate. The
endemic) or people who participate in outdoor species can be traced to specific geogrpahic
activities that expose the to wooden areas such locations, ibig sabihin may specific areas where
as forestry work, hunting & camping. you can encounter a specie. For example, C.
o People who have weakened immune system are immitis, it can be encountered in San Joaquin
more likely to develop sever blastomycosis than Valley of California while C. posadasi, it is found
people who are healthy on the desert areas of the Southwest United
o IMPORTANT: Systemic mycoses, generally States, Mexico and also in South America
refers to the organisms described here, it must • They reside in a narrow ecologic niche known as the
be understood that any fungus in an lower Sonoran Life Zone characterized by low rainfall
immunocompromised host, has the potential to and semi-arid conditions. Highly endemic areas
become invasive and disseminate to sites far include San Joaquin Valley of California, Arizona and
(removed?) from the portal of entry. Southwestern Texas. Outside the United States,
• Is blastomycosis contagious? endemic states are found in Northern Mexico,
o No, it can spread between people or between Guatemala, Honduras, Venezuela, Paraguay,
people and animals Argentina and Columbia.
• Causes: Coccidioidomycosis
• Can my pets get blastomycosis? o Asymptomatic pulmonary disease and allergic
o Yes, particularly the dogs but it is not contagious manifestations
between animals and humans.

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 ▪ Allergies can manifest themselves as toxic PATHOGENESIS
erythema, erythema nodosum (desert
bumps), erythema multiform (valley fever)
also arthritis (desert rheumatism)
o Infection occurs by inhalation
▪ Inhalation of conidia specifically the
Arthroconidia
▪ Reactivation can occur or latent infection in
immunocompromised patients.
o Primary diseases usually resolve without
therapy and confers a strong, specific immunity
to reinfection which can happen only to
immunocompromised patients.
• (#1) In the environment, the coccidioides species
CLIINICAL FEATURES OF COCCIDIODOMYCOSIS
exist as a mold with septate hyphae, and that
• Many develop influenza like fever hyphae it fragments to arthroconidia, which
• Allergic manifestations measures only 2-4 um in diameter and are easily
• 60% of infected individuals are asymptomatic aerosolized when disturbed (#2). That
• Only evidence of infection is the development of arthroconidia are inhaled by a susceptible host
serum precipitins (will be discussed in lab) and (#3).
conversion to a positive skin test within 2-4 weeks. • It will then settle in the lungs. Since, it is a
The precipitins will decline but the skin test will remain dimorphic fungus, the new environment it will
positive for a lifetime signal a new morphologic change do from mold
• The other 40% develop a self-limited Influenza-like → yeast. The arthroconidia become spherules.
illness • The spherules divide internally until they are
o Valley Fever or San Joaquin Valley Fever:
filled with endospores (#7).
Fever, cough, arthralgia, and headache
• Kapag ang spherule, nag rupture, those
o Flu-like illness would start from 7-28 days
(average of 10-16 days) and most patients would endospores are released. Once released, it will
recover completely. disseminate to the surrounding tissues and aside
• < 1% develop chronic progression disseminated from that, those endospores are then able to
disease develop into a new spherule. Kaya pansin niyo
o skin: granuloma, cold abscess sa figure, it could repeat the cycle from spherule,
▪ most common clinical feature division, release of endospores, and develop into
o osteomyelitis & synovitis a new spherule. Yan yung cycle.
o CNS (meningitis)
RISK AND PREVENTION
• FREQUENTLY ASKED QUESTIONS:
1. Who gets Valley fever?
o Anyone who lives in or travels into the
Southwestern US yung namention ko sa
inyong locations: Arizona, California,
Nevada, New Mexico, Texas, Utah, or parts
of Mexico, Central or South America can get
the Valley fever.
o Take note, the Valley Fever can affect people
of any age but it is most common in adults
age 60 and older.
o Certain groups of people may have higher
risks in developing the severe forms of Valley
Fever such as:

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 ▪ People who have weakened immune TREATMENT
systems (PHIV) • Amphotericin B
▪ People who have had an organ • Itraconazole
transplant. • In most persons, symptomatic primary infection is
▪ Taking medications such as self-limited and requires only a supportive treatment.
corticosteroids or Tumor Necroting Although Itraconazole, may reduce the symptoms
Factors (TNF)-Inhibitors. however, patients who have severe diseases require
▪ Pregnant women are also higher risk. treatment with Amphotericin B.
▪ People who have diabetes. • Amphotericin B in coccidioidomycosis is administered
▪ People who are Black or Filipino. intravenously or IV.
2. Is Valley fever contagious?
o NO, the fungus that can cause Valley Fever HISTOPLASMA CAPSULATUM
of Coccidioides cannot spread from the • Histoplasma capsulatum (“histio”; “plasma”)
lungs, between people and animals. o Is dimorphic swell saprophyte (not sure kung
HOWEVER, in extremely rare instances, a tama pagkakarinig ko)
wound infection with Coccidioides can spread o Histio – it is within the histiocytes
Valley Fever to someone else. o Plasma – because it resembles plasmodium,
3. I’ve had it before, could I get it again? the causative agent of Malaria.
o USUALLY NO, if you already had Valley • Causes: Histoplasmosis
Fever, your immune system will most likely o Histoplasmosis is also known as the Darling’s
protect you from getting it again. Some Disease, Reticuloendothelial Cytomycosis,
people can have the infection come back Spelunker’s Disease, and Cave Disease.
again, it is called RELAPSE, after getting o The Histoplasma capsulatum is named from
better the first time, but this is very rare. the appearance of the yeast cells in
4. Can my pets get Valley fever? histopathologic sections. However, it is neither
o YES, pets specifically the dogs can get the a protozoan, neither does it have a capsule.
Valley Fever, but it is not contagious between o In addition to that, the Histoplasma capsulatum
animals and people same with the like the Blastomyces dermatitidis is a
blastomycosis. Pareho din ng symptoms heterothallic ascomycete that produces a
yung sa humans and animals. teleomorphic state. You have the
5. How can I prevent Valley fever? Ajellomyces capsulatus that is the
o It is very difficult to avoid breathing in the teleomorphic form or the teleomorphic state of
fungus coccidioides in areas where it is Histoplasma capsulatum.
common in the environment. People who live o Intracellular infection of the reticuloendothelial
in those areas can try to avoid spending time system caused by the inhalation of the fungus
in the dusty places as much as possible. o Present in soil, rotting areas, and in feces of
6. Is there a vaccine for Valley fever? chicken, bats, and other birds. (High N2
o NONE. Currently there is no vaccine to content).
prevent the Valley Fever. The scientists have o Endemic in parts of the USA
been trying to make one since the 1960s o Actually, the histoplasmosis or that disease
because people who have had Valley Fever has a worldwide distribution. However, the
are usually protected from getting it again. A Mississippi-Ohio River Valley in the USA,
vaccine could make the body’s immune that is recognized as a major endemic region.
system think that it already had the Valley o Africa, Australia, and parts of East Asia, and in
Fever which would likely prevent a person particular India and Malaysia are also endemic
form being able to get the infection. regions.
o 1st described by Samuel Darling.
LINK FROM CDC: o The environmental isolation of the fungus has
been made from again, the soil with high
https://www.cdc.gov/fungal/diseases/coccidioido nitrogen content.
mycosis/risk-prevention.html/

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 o There are three varieties of Histoplasma Blastomyces dermatitidis, Coccidioides spp, and
capsulatum depending on the clinical disease. Histoplasmosis.
▪ Var. capsulatum – most common cause • The hyphae, aerial hyphae (#1), produces
of histoplasmosis. macroconidia and a microconidia. Those spores that
▪ Var. duboisii – the African type. are aerosolized and dispersed (#2). The
▪ Var. farciminosum – causes macroconidia are inhaled into the lungs by a
lymphangitis in horses. susceptible host (#3). The warmer the temperature it
signals a transformation into an oval budding yeast.
• The yeasts are phagocytized by immune cells (#4).
And transported to regional lymph nodes (#5), from
there they travel through the blood (#6) and to the
other parts of the body.
• I will discuss the tissue form or the yeast form of
Histoplasma capsulatum.
o Tissue form – the yeast form of the
dimorphic fungus.
▪ Intracellular to macrophage.
▪ As you can see in the pathogenesis
CLINICAL FINDINGS OF HISTOPLASMOSIS of histoplasmosis, the yeast in the
• The infection is usually limited and asymptomatic. lungs is phagocytized by the immune
1. Acute Pulmonary disease cells specifically the macrophage.
o With heavy exposure, acute pulmonary
disease can occur. RISK AND PREVENTION
2. Reactivation occurs
o In the mild form of the disease, the viable • FREQUENTLY ASKED QUESTIONS:
organisms remain in the host. Quiescent for 1. Who gets histoplasmosis?
years and are the presumed reactivation in o ANYONE can get histoplasmosis if they
individuals with abrogated immune have been in an area where histoplasma
systems. lives in the environment. Histoplasmosis is
o Approximately 95% of cases of this often associated with the activities that
infection are inapparent, subclinical, or
disturb soil. Particularly, those soil contains
benign. So, 5% ng mga cases, can progress
to Chronic Lung Disease or #3. bird or bat droppings.
3. Chronic pulmonary histoplasmosis in 2. Is histoplasmosis contagious?
patients with COPD. o NO. Same with the Blastomycosis and
4. Cutaneous and Mucocutaneous coccidioidomycosis. Certain groups of
people are at high risk for developing the
PATHOGENESIS
severe forms of histoplasmosis
▪ People who have weakened immune
systems (PHIV)
▪ People who have had an organ
transplant.
▪ Taking medications such as
corticosteroids.
3. If I’ve already head histoplasmosis, could I get
it again?
o Please refer to the link below
4. Can my pets get histoplasmosis?
o YES, particularly cats, but it is not
• The pathogenesis of Histoplasmosis in the contagious between animals and people.
environment. You have the Histoplasma capsulatum, The histoplasmosis in cats and dogs is
it exists as a mold. Lahat naman sila from similar to histoplasmosis in humans.

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 o The major symptoms: all stages of that • Clinical Findings of Paracoccidioidomycosis
disease can mimic TUBERCULOSIS. o Usually unaparrent and asymptomatic
o 95% cases are again, inapparent or o Acute of chronic, granulomatous infection
subclinical or mild lang. ▪ Primarily of lungs
5. How can I prevent histoplasmosis? • Pulmonary paracoccidioidomycosis
o You should avoid doing activities that are ▪ Disseminates to skin, mucosa, Lymph
known to be associated with getting nodes and other internal organs
histoplasmosis such as digging in soil, • Mucocutaneous
chopping wood, kasi dun usually yung mga paracoccidioidomycosis
bat and bird droppings. Cleaning chicken • Mouth and nose – most usual sites of
poop, exploring caves (kaya Cave mucosal infection
disease), cleaning, remodeling, or tearing • Painful ulceration develops on the
down old buildings. gums, the tongue, the lips, or the
o Large amount of bird or bat droppings palette. It can progress within weeks or
should be cleaned up by professional months.
companies that are specialized in removing • Swollen lymph nodes:
hazardous waste. o Lymphonodular
paracoccidioidomycosis
LINK FROM CDC: o Lymphadenitis (common in
children)
https://www.cdc.gov/fungal/diseases/histoplasmo
o Cervical and submandibular
sis/risk-prevention.html
changes are the most obvious
TREATMENT manifestation
o Lymph nodes may progress to
• Itraconazole
form abscesses when draining
• In disseminated disease, the systemic treatment with
the sinuses
Amphotericin B is often curative. Though patients
▪ Chronic paracoccidioidomycosis
may need prolong treatment and monitoring for
• More than one organ is involved
relapses. Patients with HIV/AIDS typically relapse
despite therapy that would be curative in other • Vast manifestation of the infection
patients. o Symptoms: lesions in the mouth and throat,
weight loss, swollen lymph nodes, cough, fever,
• Therefore, patients with AIDS require some
night sweats, shortness of breath, fatigue,
maintenance therapy with Itraconazole.
enlarged liver and spleen
▪ In adults, it usually affects the lungs and
AGENTS OF SYSTEMIC MYCOSES
causes lesions in the mouth and throat
• Blastomyces dermatitidis
▪ In children, swollen lymph nodes and skin
• Coccidioides spp. (C. immitis, C. posadasil)
lesions.
• Histoplasma capsulatum
o X-ray is not used as diagnostic tool for
• Paracoccidioides brasiliensis
Pulmonary paracoccidioidomycosis

Paracoccidioides brasiliensis
• Causes: Paracoccidioidomycosis
o a chronic, progressive fungal disease endemic
to Central and South America
o Geographic areas of highest incidence are
typically humid, high-rainfall areas, with
acidic soil conditions
o Aka South American blastomycosis, Brazilian
blastomycosis, Lutz-splendore-de Almeida
disease, paracoccidioidal granuloma

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• Risk and Prevention
o Who gets paracoccidioidomycosis?
▪ Anyone who lives in or visits areas where
Paracoccidioidomycosis is prevalent
▪ But it often affects men who work outdoors,
in rural areas of Central and South America
▪ In children, boys and girls are equally likely
to get this infection
▪ Most cases occur in Brazil, Venezuela,
Columbia, and Argentina
o How can I prevent paracoccidioidomycosis?
▪ Avoid working outdoors
o Sources
▪ Habitat: unknown
▪ It has been found in the soil near armadillo
burrows.
o Treatment:
▪ Itraconazole – most effective
▪ Amphotericin B – for severe cases of all
systemic mycoses
▪ SXT – also effective
▪ Ketoconazole – also effective

POST TEST
1. This mycotic agent is usually recovered from soil
that contains bird or bat droppings Histoplasma
capsulatum
2. North America Blastomycosis is also known as:
Blastomyces dermatitidis
3. Teleomorphic state of H. capsulatum
Ajellomyces capsulatus
4. This mycotic agent resides in a narrow ecologic
niche known as the Lower Sonoran life zone
Paracoccidioides brasiliensis
5. This mycotic infection is usually acquired by
inhalation of arthroconidia Coccidioidomycosis

REFERENCES:
1. Recorded PPT prepared by Canellie P.
Canlas
2. Textbook of Diagnostic Microbiology by
Connie R. Mahon, Donald C. Lehman, and
George Manuselis
3. Jawetz, Melnick, & Adelberg’s Medical
Microbiology
4. https://www.cdc.gov/
5. https://www.sciencefdirect.com

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 OPPORTUNISTIC MYCOSES
 Taxonomic classification of the fungi
PRE-TEST  Phylum: Zygomycota
TRUE OR FALSE  Class: Zygomycetes
1. True pathogens are organisms which are normal
 Order: Mucorales
biota that causes infections in immunosuppressed
and immunocompromised individuals when they o Common mycoses which are of clinical
have opportunity. FALSE significance
2. The most prevalent agent under the order Mucorales  Leading pathogens are in:
is Rhizopus oryzae.TRUE  Family Mucoracea
3. Parenteral is the most common mode of o Genera: Mucor, Rhizomucor,
transmission for Pneumocytis spp.FALSE
Rhizopus, Lichtheimia
4. Pneumocystis jirovecii causes Interstitial Plasma
Cell Pneumonia TRUE  Family: Cunninghamellaceae
5. Talaromyces is formerly known as Penillin. FALSE o Genera: C. bertholletiae

GENERALITIES
TRUE PATHOGENS VS OPPORTUNISTIC
 Ubiquitous thermotolerant saprobes
PATHOGENS
o Present everywhere
o Able to tolerate high temperature
TRUE PATHOGENS OPPORTUNISTIC
o Free-living microorganisms that are present in
PATHOGENS
Organisms recognized to Organisms which are the environment but are not typically of concern
cause disease in healthy normal biota that causes with regards to human disease
Immunocompetent infections in  Common environmental isolates – soil and plants
individuals. immunosuppressed and  Common contaminants – mycology laboratory
Immunocompromised
individuals when they have
RISK FACTORS
an opportunity.
 Diabetes – DKA (Diabetic Ketoacidosis)
MUCORALES o High risk of developing Rhino-orbital-cerebral
mucormycosis
 Defect in phagocytic action
o eg. Neutropenia or Glucocorticoid use
 Elevated levels of Free Iron
o Which supports fungal growth in serum and
tissues
 Deferoxamine use
o Deferoxamine is an iron chelator which serves
as fungal siderophore which directly delivers
iron to the mucorales
o In the past, iron overloaded patients with end
stage renal failure who are treated with
deferoxamine had higher risk of developing
fatal disseminated mucormycosis
 Stem cell or Solid organ transplantation
 Infant prematurity
 Malignancy: Leukemia, Lymphoma
 Severe Burns
 MODE OF TRANSMISSION
 Respiratory route – most common route
 External implantation
 Hematogenous dissemination
 Nosocomial settings
o Can be acquired through the hospital

MUCORMYCOSIS/ZYGOMYCOSIS
 Group of life-threatening infections caused by fungi
in the order Mucorales
 Highly invasive, progressive resulting in higher rates
of morbidity and mortality than any other infections
 Leading pathogens
o Genera Rhizopus, Rhizomucor, Lichtheimia,
Cunninghamella, and Mucor
o Rhizopus oryzae – most prevalent PULMONARY MUCORMYCOSIS
 Second most common manifestation
6 CLINICAL SYNDROMES OF MUCORMYCOSIS  Symptoms: dyspnea, cough, and chest pain ± fever
1. Rhino – Orbital – Cerebral Disease  Infection usually begins as Undifferentiated
2. Pulmonary Disease Pneumonia which may be complicated with
3. Cutaneous Disease hemoptysis and cavitation
4. Gastrointestinal Disease o Hemoptysis: coughing up of blood or bloody
5. Disseminated sputum from the lungs or airway
6. Miscellaneous Forms of Disease
CUTANEOUS MUCORMYCOSIS
RHINO-ORBITAL-CEREBRAL MUCORMYCOSIS  External implantation of the fungus or
 Most common form of disease – Diabetes hematogenous dissemination
o Most cases occur in patients with diabetes. o soil exposure from trauma
Although such cases are increasingly  eg. MVA (Motor Vehicular Accident),
prescribed in the transplantation setting, often natural disaster, or combat related injuries
along with glucocorticoid-induced diabetes o penetrating injury with plant material
mellitus  eg. thorn
 Initial symptoms (Non Specific): o injection of medication
o Eye or facial pain, facial numbness,  eg. Insulin
conjunctival suffusion, blurry vision, ± fever o catheter insertion, contamination of surgical
 If untreated, infection usually spreads from Ethmoid dressings
sinus to Orbit (EOM compromise, proptosis)  or even the use to tape
o From the orbit, it spreads to Frontal Lobe of the  Necrotizing fasciitis – Surgical Debridement
brain (cavernus sinus thrombosis) o Can be highly invasive
 Often through hematogenous route o Can penetrate the muscle, fascia, and even the
 or venous drainage through the cavernous bones
sinus leading to the formation of o Mortality rate approaching up to 80%
cavernous sinus thrombosis o Need prompt and aggressive Surgical
 Onsets of signs and symptoms of Debridement to prevent mortality and have a
cavernous sinus thrombosis: bilateral good prognosis for the patient
proptosis, chemosis, vision loss, and
ophthalmoplegia

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 o Trachea
o Kidneys
o Peritoneum (dialysis)
o Teeth

TREATMENT
 First-line Antifungal Therapy
o Amphotericin B deoxycholate (AmB) -
nephrotoxic, poor CNS penetration,
inexpensive
o Liposomal Amphotericin B (LAmB) –
less nephrotoxic than AmB, better CNS
penetration, expensive
GASTROINTESTINAL MUCORMYCOSIS o Amphotericin B Lipid Complex (ABLC)
– less nephrotoxic than AmB, less
 Premature neonates – Disseminated disease, efficacious than LAmB for CNS
Necrotizing Enterocolitis infection, expensive
o In the past, the gastrointestinal  There are different types of amphotericin B
mucormycosis occurred primarily in pre based on their nephrotoxicity and nervous
mature neonates system penetration
 Adult – Neutropenia, Glucocorticoid use,
Immuncompromised conditions PNEUMOCYSTIS
o However, there has been a marked
increase in case reports describing adult
with neutropenia, glucocorticoid use, or
other immunocompromising conditions
 Nosocomial
o Meaning it can be acquired in the
hospital, following administration of
medications mixed with contaminated
wooden applicator sticks
 Most common symptoms: nonspecific abdominal
pain, distention, nausea, vomiting
 GI bleeding is common and fungating masses
GENERALITIES
may be seen in the stomach when you do the
Pneumocystis carinii (old)
gastroscopy or the endoscopy, and the disease
Pneumocystis jirovecii (new)
may progress into Visceral perforation which has
o The species infecting humans has been
really high mortality rates
renamed into Pneumocystis jirovecii
DISSEMINATED MUCORMYCOSIS  Protozoan (before) – Fungus (present): nucleic
acid and biochemical analysis
 Hematogenously disseminated mucormycosis  Non filamentous fungus
o Which may originate from any primary  Pneumocystis was discovered in rodents in
site of infection 1906 and was initially believed to be a protozoan
 Brain – most common site of dissemination  Because Pneumocystis cannot be cultured by
o But metastatic lesion may be found in then, our understanding of its biology has been
any other organ limited but due to some molecular techniques
that have been demonstrated that the organism
MISCELLANEOUS MUCORMYCOSIS is actually a fungus
 ANY BODY SITE:
o Bone
o Mediastinum

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 RISK FACTORS PNEUMOCYSTIS JIROVECII PNEUMONIA (PCP)/
 Malnourished infants INTERSTITIAL PLASMA CELL PNEUMONIA
 Immunosuppressed patients
o Corticosteroid therapy  The disease associated with your Pneumocystis
o Antineoplastic therapy or your jirovecii is what you call the PCP wherein it is
chemodrugs from the previous name Pneumocystis carinii
o Transplant patients pneumonia and now it is known to be the
 HIV/AIDS Pneumocystis jirovecii pneumonia or it can be
 This organism was first recognized in outbreaks associated to what you call the interstitial
of pulmonary disease among malnourished plasma cell pneumonia wherein you can see this
infants in Eastern Europe during and after the plasma cell when you look into it under the
World War II microscope
 More recently, it has been a major cause of a life  The Pneumocystis jirovecii Pneumonia presents
threatening pneumonia in about 60-80% in HIV an acute or subacute pneumonia that may
infected patients and is subsequently known as initially be characterized by a vague sense of
one of the AIDS defining illness dyspnea alone may but may subsequently
manifest as fever and then non productive
MODE OF TRANSMISSION cough with progressive shortness of breath,
 Life Cycle: 3 Stages ultimately resulting to respiratory failure and
1. Trophozoite – 1-5 µm; irregular shaped death
2. Precyst – 5-8 µm  Clinical Manifestations:
3. Cyst - 8 µm; thick-walled sphere o Dyspnea
containing 8 intracystic bodies o Fever
 Respiratory route o Non-productive cough with progressive
 The cyst is the infective stage shortness of breath –
 The spores or intracystic bodies are released Respiratory failure – Death
from the cyst in the lung and these trophic forms
multiply asexually by binary fission on the TREATMENT
surface of the epithelial cell also known as your  Trimethoprim –Sulfamethoxazole (TMP-SMX) –
pneumocyte, which is the lining of your lung. treatment of choice
 And then the sexual reproduction of trophozoite  Which can be given either intravascular or per
will occur and then it will first produce your pre orem for 14 days for those who have for patients
cyst and then your cyst which contains the who are known to be non HIV infected patients
spores or the intracystic bodies with mild disease but you need to give this
medication for 21 days to all other patients

TALAROMYCES (PENICILLIUM)

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 GENERALITIES o Cough
o Fever
 Penicillium marneffei (old) o Fatigue
 Talaromyces marneffei (new) o Weight loss
It is known to be unique among the talaromyces species o Lymphadenopathy
because:
 Dimorphic TREATMENT
o Means that it can exist in both yeast and  Defined course of Amphotecin B ; followed by
mold forms Itraconazole
 Endemic – Southeast Asia  If you left the patient untreated, the mortality can
o Known to be endemic, opportunistic be exceeded up to 90%
pathogen in several regions of south
east asia including south eastern China,
Thailand, Vietnam, Indonesia, Hong
Kong, Taiwan and Manipur state of India REFERENCES:
 Reservoir – bamboo rat Opportunistic Mycoses
o It has been isolated from soil and Department –Sanctioned PPT
especially soil that is associated with Recorded Lecture by Prof. Cserina V. Gadil,
bamboo rats and in their habitats M.D., R.M.T.
making the bamboo rats as their
reservoir

RISK FACTORS
Major risk of infection is immunodeficiency which may be
due to:
 HIV/AIDS
 Tuberculosis
 Corticosteroid treatment
 Hematologic malignancies - Lymphoproliferative
disease
 Autoimmune disease
 Organ transplantation

MODE OF TRANSMISSION
 Respiratory route

MULTIPLE ORGAN INVOLVEMENT

 Clinical Manifestations:
o Fungemia
o Skin lesions
 Which develop in 70% of the
patients with or without HIV or
AIDS. It can be cutaneous or
subcutaneous papules,
pustules, or rashes which are
often located in the face
o Systemic involvement of multiple organs
– especially in the RES
(Reticuloendothelial system)
 Early signs and Symptoms are non specific
which include:

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DE BORJA, DE GUZMAN, DE LOS SANTOS, DIMAIWAT, DOLINA, HALILI, OBISPO | 3L-MT 6
 OPPORTUNISTIC MYCOSES (CANDIDA SPP, CRYPTOCOCCUS SPP, ASPERGILLUS SPP)
 Infects any or all organs of the body
AGENTS OF MYCOSES o Most especially the Candida
1. Superficial Mycoses albicans or candida species wherein
2. Cutaneous Mycoses they are usually present in mucosal
3. Subcutaneous Mycoses
surfaces and in skin infections
4. Systemic Mycoses
 Medically significant opportunistic fungi
5. Opportunistic Mycoses
o Cryptococcus neoformans,
OPPORTUNISTIC MYCOSES o Candida albicans,
 When we say opportunistic, may exclusively o Pneumocystic pneumonia,
cause fungal infections in debilitated patients o Aspergillus spp,
whose normal defense mechanisms are o Zygomycosis,
impaired. o Talaromycosis
 Candida albicans- most common and most
prevalent among the opportunistic mycoses CANDIDIASIS (Candida spp.)
o Also present in hospital setting and even  The Candida species colonizes the mucosal
in the environment surfaces of all humans soon after birth
 Cyrptococcus species- includes:  There is a risk of endogenous infection and they
o Cryptococcus neoformans (most are usually ever present
common and usually present in AIDS  Diseases:
patients, also has tropism to central o Candidiasis,
nervous system causing Cryptococcal
o moniliasis,
meningitis)
o oral thrush,
o Cryptococcus gattii
o mycotic vulvovaginitis,
 Aspergillus species- ubiquitous or commonly
found in the soil, that is why this fungi has a high o candida perionychia,
prevalence with agricultural workers or farmers. o candida endocarditis
They are also known as “Farmer’s lung  Most notorious agent of yeast infection and
disease”. Particularly, the farmer’s lung disease common cause of fungemia
is correlated or associated with Aspergillus o Even in the hospital setting, in the
fumigatus. laboratory, ito yung usually na
GENERAL CHARACTERISTICS naiidentify if suspected yung patient
 Fungi that do not usually induce disease for fungal infection., pinaka common
o They do not induce disease to ang Candida albicans. If the patient
immunocompetent persons or is suspected for candida infection or
persons who have good immune Candida albicans infection, the
system disease is termed as Candidiasis,
 Cause disease in persons who have altered pwede ring moniliasis, oral thrush,
host defense mechanism mycotic vulvovaginitis, candida
o Immunocompromised (AIDS, perionychia, candida endocarditis
Chemotherapy) o Usually the candida species are
o Debilitated patients (Chronic aggressive with patients with
diseases) multiple comorbidities and they may
o Chronic disease like: Cancer, be difficult to treat with traditional
leukemia and major genetic antifungal therapy
disorders

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 o It causes disease in any site when
host conditions are altered
 Normal Flora: skin, mucous membranes
and GI tract

Species
C. albicans C. glabrata
C. parapsilosis C. krusei
C. tropicalis C. lusitianiae
C. dubliniensis

 Candida albicans- which is the premier cause of

yeast infection in the world
 Candida glabrata- second most common

CANDIDA ALBICANS
 Most common cause of fungal infection in
CLINICAL MANIFESTATION
immunocompromised or debilitated patients
 Major cause of candidiasis
 Cutaneous candidiasis
 It has a wide range of tropism in the body
o Most prevalent fungal infection
 Normal Flora: skin, mucous membranes
among immunocompromised
and GI tract
patients
CLINICAL MANIFESTATION o Intertriginous candidiasis
Cutaneous Vulvovaginal
 Warm parts of the body such
Oropharyngeal Conjunctivitis
Gastrointestinal UTIs as the axillae, groin,
Systemic candidiasis intergluteal or inframammary
folds
 For the clinical manifestation, we have different  Common in obese and
terms used if the Candida albicans is present in diabetic individuals
that particular body site o Diaper candidiasis
o If present in cutaneous area, the  Also known as nappy rash,
disease is termed as cutaneous which are common in infants
candidiasis
who don’t frequently change
o If in vagina area, termed as vulvovaginal
diapers
candidiasis
o Oropharyngeal candidiasis or also o Candidial invasion of the nails and
known as thrush, which is an infection of around the nail plate causes:
the oral mucosa  Onychomycosis
o If the Candida albicans reached the  Complete destruction
systemic circulation, so may fungemia of nails or total
na may present na sa katawan ng detachment of nails,
patient, it is serious and kailangan in tagalog, natuklap
maitreat na agad yan yung kuko
 Paronychia
 Painful and swelling
of the nail
 Onychomycosis and
Paronychia usually develop
in persons whose hands are
subject to continuous

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 wetting. So pag lagi mong
binabasa yung kamay mo,  Vulvovaginal candidiasis (Vaginal
without no reason, so it Thrush)
increases the risk for o High-risk: Sexually active, diabetic
onychomycosis and patients, pregnancy, taking
paronychia antibacterial drugs
 Aside from that, the sugars  yung antibacterial drugs
or solutions that softens the nakaka affect sa proliferation
nails and cuticle could also ng vaginal thrush since it
increase the risk for the alters the microbial flora,
development of local acidity as well as other
onychomycosis and secretions
paronychia o Irritation, pruritus and vaginal
discharge, dysuria
o Balanitis
 Inflammation of the penis

Creamy or curd like appearance

There is complete destruction of the nails

Presence of cutaneous and skin infection  Oropharyngeal Candidiasis (Oral Thrush)

o In tagalog, it is called as, “singaw”
o Patchy to confluent, whitish
pseudomembranous lesion

Presence of cutaneous and skin infection

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 o Composed of epithelial cells, yeasts,
and pseudohyphae when viewed
under microscope
o Common with:
 AIDS patients
 Treatment with
corticosteroids and
antibacterial drugs
 High levels of glucose in the
mouth
- High risk of oral thrush
(singaw) for those who
don’t brush their teeth
 Cellular immunodeficiency
TREATMENT

 Azoles
 Amphotericin B
 Nystatin
White plaques or milk curd appearance

 Conjunctivitis Candidiasis
o People using eyedrops containing
steroids are at high-risk
 Steroids are considered as
immunosupressants
 Gastrointestinal Candidiasis
 Systemic Candidiasis
o Caused by indwelling catheters,
surgery, intravenous drug abuse, CRYPTOCOCCUS (Cryptococcus spp.)
aspiration or major damage to the
skin.  D: Cryptococcosis, torulosis, European
 Use of corticosteroids or blastomycosis, Busse-Buschke disease
immunosuppressive agents can  Important cause of meningitis, pulmonary
increase the risk of systemic disease, and septicemia
candidiasis  Causes systemic infection in both
o Candidial endocarditis immunocompetent (C. gattii) and
immunocompromised (C. neoformans)
patients

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 o Typical signs of meningitis are ABSENT
Etiolo Reserv which could lead to diagnosis of this
Serotypes Cell wall
gy oir disease. The absent signs are:
Opportun Encapsul  Kernig’s sign (knee pain)*
C. istic - A ated  Bruzinski’s sign (neck pain/stiff
World Pigeon (contribut
neoform and D wide es to
neck)*
guano
ans Primary – virulence
B and C ) *Note: These signs are usually present in other meningitis
but absent in cryptococcal meningitis caused by C.
Eucaly neoformans and C. gattii
Tropics ptus
N/A
and trees
C. gattii (only single N/A
subtro (Red
serotype)
pics Gum
Tree)

CLINICAL MANIFESTATION

TREATMENT
 Amphtericin B & Fluorocytosine
o Ideal for CNS involvement
o Taken for 6-10 weeks

ASPERGILLUS SPP.

 MOT: Inhalation of basidiospores

o Basidiospores are usually found in soil
 Ubiquitous saprobes in nature, occurs
or contaminated with pigeon droppings
worldwide.
 So kapag sa soil, it is usually C.
 Usually present in soil that’s why agricultural
gattii or C. neoformans
workers are at risk for aspergillosis
 Kapag pigeon guano or pigeon
 Second most commonly isolated fungus after
droppings, it is usually
Candida spp.
suspected to be C. neoformans
 Produces abundant small conidia that are easily
 Common areas affected: Primarily affects the
aerosolized.
lungs and CNS but lesions in the skin, bones or
o Conidia can be inhaled by potential host
other internal organs can also be seen.
 However, this is generally
 Cryptococcal meningitis
cleared in healthy
o Most common clinical manifestation
immunocompetent individuals
o May resemble as brain tumor, brain
 Mycotoxicosis and Allergic
abscess, or degenerative CNS disease
bronchopulmonary aspergillosis

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 Species: Aspergillus fumigatus (most SIR CHING (referring to the illustration
common), A. flavus, A. niger, A. terreus, A. above):
lentulus  Conidia is released into the
o Can be differentiated using laboratory environment where it is inhaled by
tests the alveolar spaces of the
 Immunocompromised – conidia germinates to
susceptible host
produce hyphae that invade the lungs and
other tissues.
 Inside the lung airspaces, the
conidia germinate into hyphae in the
CLINICAL MANIFESTATION absence of sufficient pulmonary
defenses
 Afterwards, the conidia invades to
the (pulmonary) blood vessels
 The infection spreads
hematogenously and it is not
uncommon to find multi-organ
system involvemement
 So pag nag-proliferate na ang
Aspergillus spp. sa circulation there
 Aspergillosis would be neutropenia
 MOT: inhalation, inoculation or ingestion of o Due to excessive hyphal
conidia or particularly the sporangiospores growth and dissemination.
 Sinusitis – initial infection
o Usually caused by A. fumigatus, which
resides to sinusistis and eventually to
the lungs
 Allergies
o Induces Asthma & Allergic
bronchopulmonary aspergillosis
(ABPA)
 ABPA mimics the symptoms of
allergies and asthma
o “Farmer’s lung disease” –
hypersensitivity reaction leading to
pneumonitis SIR CHING (referring to the illustration
 Called as such because they above):
are prevalent in agricultural  In the soil, the conidia of the
workers
Aspergillus spp. are released into
the environment through aerial
propagation.
 The conidia are easily aerosolized,
which enhances chance of being
inhaled by the potential host
 Subsequently, the conidia resides
into the alveolar spaces of the lungs
and germinates into hyphae
 The photo shown on the right is a
biopsy of the alveolar tissue infected
with Aspergillus spp.

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 Aspergilloma – fungus balls within cavity of old TREATMENT
tuberculosis lesions  Allergic Aspergillosis (Sinusitis & ABPA)
o Seen in patients with chronic lung o Itraconazole, Corticosteroids
disease  Invasive Aspergillosis (Cutaneous & Chronic
 Chronic pulmonary aspergillosis Pulmonary)
o Occur in patients with structural damage o Voriconazole
to their lungs caused by other diseases o Other options: Lipid amphotericin,
such as tuberculosis and sarcoidosis posaconazole , isavuconazole,
 Mycotoxicosis itraconazole, caspofungin , micafungin
o Occurs if patients ingest contaminated  Aspergilloma
grains due to moisture or improper o Surgery and antifungal medications
storage
o Produces aflatoxin
 Potent carcinogen and mutagen
 Toxic to the liver
 Emitted by A. flavus POST-TEST
 Keratomycosis
o Inoculation of Aspergillus spp. to the 1. Birdseed agar is useful in the
eyes identification of which of the following?
 Pain and blurring of vision, may lead to a. Candida albicans
blindness b. Candida glabrata
 OticInfections (A. niger, A. fumigatus)
c. Saccharomyces cerevisiae
o Fluffy growth or discharge in the ear
d. Cryptococcus neoformans
canal
 Green discharge – caused by A. 2. The recovery of some Cryptococcus
flavus species may be compromised if the
 Black discharge – caused by A. isolation media contains
niger a. Cycloheximide
b. Gentamicin
c. Chloramphenicol
d. Penicillin
3. The morphological characteristics of a
yeast grown in rabbit plasma are shown
in the image:

The most likely identification of this yeast

is:
a. Candida tropicalis
b. Candida krusei
c. Candida albicans
d. Candida glabrata

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 4. A 50-year old male agricultural
worker comes to his physician
because he has been experiencing
persistent fever, fatigue, and allergy.
It was also noticed that the patient is
also producing green fluffy discharge
in the ear canal. This organism is
most likely:
a. Candida albicans
b. Talaromyces marneffei
c. Pneumocystis pneumonia
d. Aspergillus fumigatus

5. A 45-year old female tourist went to her

physician and complained of persistent
cough and difficulty in breathing.
Unusual bumps on her face and neck
was also noticed. Her recent travel
history is she went to Fujian, China, a
province in Southern China, wherein
she went hiking in areas prevalent with
bamboo rats. This organism is most
likely:
a. Candida albicans
b. Talaromyces marneffei
c. Pneumocystis pneumonia
d. Aspergillus fumigatus

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