ANATOMY AND PHYSIOLOGY 2

ACTIVITY 2

COMMON INFECTIOUS DISEASES

MEASLES

What is the MOST COMMON causative agent of this disease? What kind of organism is it?

 RNA paramyxoviruses are the cause of measles. During the prodromal phase or the initial stages of rash, the
illness is spread through infected secretions of the nose, throat, and respiratory system. (Rubeola Virus).

 Measles is a kind of a highly contagious virus.

 Also, a single-stranded, enveloped RNA virus with one serotype is what causes measles. It is categorized as a
member of the family Paramyxoviridae's genus Morbillivirus. The measles virus only naturally inhabits humans.
In fact, nine of ten unvaccinated persons would get the disease if a person with the disease was in a room with ten
others. You can spread measles by coughing, sneezing, or talking, which releases contaminated droplets into the
air.

Discuss the pathophysiology of the disease, including the virulence factors of the organism.

PATHOPHYSIOLOGY OF THE DISEASE

The lymphocytes, dendritic cells, and alveolar macrophages of the respiratory tract are initially infected by the
virus that is inhaled from the exposed droplets. After then, it disseminates throughout the circulation, causing
viremia, before migrating to distant organs and neighboring lymphoid tissue. When a person coughs or sneezes,
the virus that lives in their dendritic cells and lymphocytes spreads to their respiratory tract epithelial cells,
which are shed and discharged as respiratory droplets, infecting others and continuing the cycle. The early
inflammation causes cough, conjunctivitis, and coryza symptoms. The onset of fever and the growth of viremia
are related. After spread, perivascular and lymphocytic infiltrates cause a cutaneous rash.
The nonstructural proteins V and C of the measles virus inhibit the generation of interferon during the
prodromal phase, which lowers host immunity. The escalating viral replication subsequently causes immune
reactions at the cellular and humoral levels. IgM antibody production makes up the first humoral reaction,
which is noticeable 3 to 4 days after the rash first occurs and can last for 6 to 8 weeks. The subsequent
production of IgG antibodies is predominantly directed against the viral nucleoprotein. Elevated plasma
interferon-gamma levels dependent on Th1 during the acute phase, and afterwards higher levels of Th2
dependent interleukin 4, interleukin 10, and interleukin 13 levels, show that cellular immune responses are
crucial for recovery.
The typical Warthin-Finkeldey large cells (fused lymphocytes) in lymph node biopsy will be seen against a
paracortical hyperplasia background.

Immunosuppression brought on by the measles virus has been reported to endure for weeks, months, or even
years. Due to this, people are more vulnerable to bacterial and other secondary illnesses. Despite the lack of
clear mechanisms underlying this phenomenon, it is hypothesized that measles infection leads to proliferation of
measles-specific lymphocytes that displace the pre-existing memory cells, resulting in "immune amnesia,"
which increases the host's susceptibility to secondary infections and accounts for the majority of the morbidity
and mortality related to measles. Lifelong protection is provided by the neutralizing IgG antibodies against
hemagglutinin, which prevent host cell receptors from attaching to the virus.

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 VIRULENCE FACTORS

 It consists of a helical nucleocapsid, 100-300 nm in

diameter, surrounded by an envelope. The envelope is lined
by matrix proteins and carries transmembrane
hemagglutinin and fusion glycoproteins which are the
virulence factors.

SIGN AND SYMPTOMS OF MEASLES

 Dry Cough and Runny Nose

 Sore Throat

 Body Pains and Headache

 Watering and swelling in Eyes

 Discomfort and Fatigue

 Loss of Appetite

 Diarrhea

 Light Sensitivity

 Inflammation in Lymph Nodes

 Koplik’s Spots (blue and red spots in the
mouth)
 Fever

DIAGNOSTIC TESTS FOR MEASLES

 The diagnosis is usually apparent from the characteristic clinical picture; laboratory confirmation is
rarely needed.
 Testing for measles IgM antibodies is recommended in some situations.
 Measles IgM is detectable for 1 mo after illness, but sensitivity of IgM assays may be limited in the first
72 hr of the rash illness.
 Isolation of measles virus from clinical samples is also useful in identifying the genotype of the strain to
track transmission patterns.
 All suspected measles cases should be reported immediately to local or health departments.
 During the prodromal stage multinucleated giant cells can be demonstrated in smears of the nasal
mucosa.
 Antibodies become detectable when the rash appears;
 Testing of acute and convalescent sera demonstrates the diagnostic seroconversion or fourfold increase
in titer.
 Measles virus can be isolated by tissue culture in human embryonic or rhesus monkey kidney cells.
 Cytopathic changes, visible in 5-10 days, consist of multinucleated giant cells with intranuclear
inclusions.

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  The white blood cell count tends to be low with a relative lymphocytosis.
 Cerebrospinal fluid in patients with measles encephalitis usually shows an increase in protein and a
small increase in lymphocytes.The glucose level is normal.

PREVENTION AND TREATMENT FOR MEASLES

There is no particular antiviral medicine for measles; instead, supportive care is the mainstay of treatment. The
cornerstones of therapy are the management of fever, the avoidance and correction of dehydration, and efforts
to prevent and control infection, including proper isolation.

For malnourished children, the WHO advises giving daily vitamin A dosages for at least two days. Early
detection of measles complications is essential, as is the beginning of proper treatment.

To help manage symptoms:

 Give plenty of fluids

 Encourage extra rest
 Give a non-aspirin fever medicine, such as acetaminophen or ibuprofen if a fever makes your child
uncomfortable. Never give aspirin to a child who has a viral illness, as such use is linked to Reye
syndrome.

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