PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES

INTESTINAL PROTOZOA
Entamoeba î Pseudopod-forming Fecal-oral Mature Cysts Trophozoite î Lectin: mediates adherence ASYMPTOMATIC CYST CARRIER STATE ASYMPTOMATIC CYST
nonflagellated protozoa - found in diarrheal stools î Amebapores: for penetration CARRIER STATE
histolytica AMEBIC COLITIS
à Brownian movement and within the intestinal î Cysteine proteases: for cytopathic î Diloxanide furoate
and extraintestinal lesions î Dysentery without fever (DOC)
effect
î Most invasive parasite î Flask-shaped colon ulcer î Iodoquinol
- characteristically contain
among Entamoeba î Paromomycin
ingested red blood cells
î Eukaryotic organism that (erythrophagocytosis) à Ingestion of cysts AMEBOMA
lack membrane-bound hematophagous Ü î granulomatous lesion that may form in AMEBIC COLITIS Trophozoites (with
organelles cyst produces trophozoites in the the cecal or rectosigmoid areas î Metronidazole engulfed RBCs in the
- nucleus has a small central
intestine î associated with dystentery cytoplasm)
nucleolus and fine Ü
î Tinidazole
chromatin granules along amebic dystentery in the colon AMEBIC LIVER ABSCESS î Diloxanide furoate
the border of the nuclear Ü î Paromomycin
î Most common extraintestinal form
membrane spread to the liver (MC), lung, brain
î Usually in the posterosuperior aspect
AMEBIC LIVER ABSCESS
Cyst of the right lobe
- This is according to majority of î Metronidazole
- predominates in non-
references. But according to Schwartz, î Tinidazole
diarrheal stools
- smaller than E. coli it is the superior-anterior aspect. î Percutaneous drainage
- has four nuclei (E. coli has 8) î Anchovy paste-like aspirate (thick for nonresponders
chocolate brown in color)

Giardia lamblia î Flagellate that lives in the Fecal-oral Cysts Trophozoite î Adhesive disc and lectin facilitate ACUTE INFECTION î Metronidazole
duodenum, jejunum, and - found only in diarrheal attachment to avoid peristalsis î abdominal pain
upper ileum stools î Villous flattening, crypt î watery, foul-smelling diarrhea
- pear-shaped with two hypertrophy and disruption of î excessive flatus, smelling like rotten
î Falling leaf motility nuclei, four pairs of flagella, cytoskeleton eggs
î Simple asexual life cycle and a suction disk with î Ultimately leads to enterocyte î No fever and non-bloody (does not
which it attaches to the apoptosis invade the mucosa and does not enter the
î Covered with variant intestinal wall î trophozoite causes inflammation of
bloodstream)
Multinucleated
surface proteins the duodenal mucosa à trophozoites
CHRONIC INFECTION
Cyst malabsorption of protein and fat. î constipation, weight loss, and STRING TEST: swallowing
- found in diarrheal and a weighted piece of string
steatorrhea
formed stools à trophozoites adhere to
the string and can be
visualized after
withdrawal
Cryptosporidium î Opportunistic infection Fecal-oral Thick-walled Thick-walled oocysts î The oocysts excyst in the small î Self-limited nonbloody diarrhea in î Nitazoxanide:
oocysts - using a modified Kinyoun intestine, where the trophozoites immunocompetent patients DOC for immuno-
hominis / parvum î Undergoes schizogony and
acid-fast stain (and other forms) attach to the gut î Severely debilitating prolonged diarrhea if competent patients
gametogony wall. CD4 <200 (due to autoinfection)
î Invasion does not occur. î NO effective drug
î Autoinfection in
î The jejunum is the site most heavily therapy for severely
immunocompromised
infested. immunocompromised
patients
patients, but Oocysts on acid-fast
î Acid-fast organism paromomycin may be stain
useful in reducing
diarrhea.

î HAART for HIV patients

 PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
INTESTINAL PROTOZOA (continued)
Balantidium coli î only ciliated protozoan Fecal-oral Cysts Diagnosis is made by finding BALANTIDIASIS / î Tetracycline:
that causes human large ciliated BALANTIDIAL DYSENTERY treatment of choice
disease (i.e., diarrhea) trophozoites or large î B. coli is locally invasive, causing
î Largest protozoan cysts with a characteristic V- colonic ulcers (round-based, wide- î Metronidazole
parasite of humans shaped nucleus in the stool necked intestinal ulcers)
î extraintestinal lesions do not occur
î Pigs are the main reservoir
(unlike the case with E. histolytica)
à diarrhea among
slaughter house workers

UROGENITAL PROTOZOA
Trichomonas î Exists only as Sexual intercourse Trophozoites Trophozoite TRICHOMONIASIS î Metronidazole 2g
vaginalis trophozoite (“ping-pong” (seen in wet mount of î Watery, foul-smelling, greenish single dose
î Pear-shaped flagellated transmission) vaginal fluid) discharge accompanied by itching and - Treat both the
trophozoite with jerky burning patient and the
motion î Strawberry cervix partner
î cannot exist outside human
because it cannot form cysts
Motile Trophozoites

THE COMMENSAL AMOEBA

- non-invasive and do not cause disease
- reproduce by binary fission
- cysts pass through the acidic stomach unscathed, protected by their cyst wall
- excystation occur in the small intestine

Entamoeba dispar morphologically similar to E. histolytica but their DNA and ribosomal RNA are
different
Entamoeba hartmanni similar to E. histolytica but is much smaller and does not ingest RBC, sluggish
Entamoeba coli cosmopolitan in distribution, harmless inhabitant of colon, has a larger cyst and
greater number of nuclei than E. histolytica
Entamoeba polecki parasite of pigs and monkey, cyst is uninucleated
Entamoeba gingivalis has no cyst stage and does not inhabit the intestines, found in the mouth,
moves quickly and has numerous blunt pseudopodia, transmission is via kissing
or droplet spray
Endolimax nana small size, sluggish movement
Iodamoeba butschlii no peripheral chromatin granules on the nuclear membrane
 PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
BLOOD AND TISSUE PROTOZOA
Plasmodium î Most important parasitic Bite of infected Sporozoites Trophozoite (ring forms) î Most of the pathologic findings of î Paroxysmal fever with malaise and bone PREVENTION BUZZ WORDS
disease in man female mosquito malaria result from the destruction pains î Chemoprophylaxis
species Infected RBC with 1-2
(Anopheles of RBCs. î Hemolytic anemia, jaundice, î Insecticide-treated nets
splenomegaly î Insect repellants with small chromatin dots
î ASEXUAL life cycle consists minimus DIAGNOSTIC TESTS FOR MALARIA - enlarged spleen characteristic
î Parasitic pneumonitis DEET à P. falciparum
of schizogony and flavirostris) î Thick and thin smears with Giemsa stain of malaria is due to congestion of
gametogony sinusoids with erythrocytes, î Cerebral malaria î Biological modification
- Thick smear: to screen for the presence of
coupled with hyperplasia of - Malarial or Durck granulomas à cultivation of snails infected RBC
transmission organism
lymphocytes and macrophages î Acute Renal Failure (Blackwater fever) that eat up mosquito with presence of ring
î SEXUAL life cycle involves across the - Thin smear: for species identification
placenta, in blood î Septic shock (algid malaria) larvae form stage only à P.
sporogony - HIGHEST YIELD WHEN BLOOD SAMPLES
falciparum
transfusions, and TAKEN DURING FEVER OR 2-3 HOURS AFTER î People with RBC defects (G6PD
by intravenous PEAK deficiency, sickle cell) are SPECIAL CLINCAL OUTCOMES
Areas of High Areas of Chloroquine î RECRUDESCENCE infected RBC
drug use also protected against the severe effects
Endemicity Resistance occurs - Recurrence of symptoms after a with presence of
of falciparum malaria
î Palawan î Palawan temporary abatement (2-4 weeks) band form stages à
î Kalinga- Apayao î Davao del Norte - Seen in P. falciparum and P. P. malariae
î Partial immunity based on humoral
î Ifugao î Campostela Valley malariae
antibodies that block merozoites
î Agusan del Sur from invading the red cells occurs in
infected individuals (premunition) î RELAPSE
- Results to low level of - Return of disease after its apparent
COMPARISON OF SPECIES
parasitemia and low-grade cessation (1-6 months) due to
P. falciparum P. malariae P. vivax P. ovale
symptoms reactivation of hypnozoites
Asexual cycle 48 hours 72 hours 48 hours 48 hours
- Seen in P. ovale and P. vivax
Periodicity Malignant Benign Benign Benign
tertian quartan tertian tertian
RBC preference All ages Old RBC Young RBC Young RBC
Parasitemia Highest Lowest Low Low Clinical Setting Drug Therapy Alternative Drug
Merozoites 0 6-12 12-24 8 Chloroquine-sensitive P.
Gametocytes Banana- Large Small falciparum and P. Chloroquine
Compact malariae infections PROPHYLAXIS
shaped round round Drug Prophylactic Use
P. vivax and P. ovale
Cerebral Chloroquine + Primaquine
Yes No No No infections Chloroquine Areas WITHOUT resistant P. falciparum
Malaria
Recrudescence Yes Yes No No Malarone (Atovaquone- Malarone
Uncomplicated Areas WITH chloroquine-resistant P. falciparum
Relapse No No Yes Yes Proguanil)
Infections with Quinine + Doxycycline/ Mefloquine
Drug Resistance Many Few Few Few OR Mefloquine
chloroquine-resistant P. Clindamycin
Malarial Dots Maurer Ziemann Schuffner Schuffner OR Co-Artemether + Doxycycline Areas with MULTIDRUG-resistant P. falciparum
falciparum
Lumefrantine
Terminal prophylaxis of P. vivax and P. ovale
MALARIAL DOTS PRESENT IN INFECTED RBCs: Primaquine
Artesunate + Doxycycline/ infection; alternative for primary prevention
SCHUFFNER MAURER ZIEMANN Severe or complicated Clindamycin Artemether +
Punctate Coarse
infections with P. OR Mefloquine/Malarone Doxycycline/Clindamycin
Fine dots falciparum OR Mefloquine/Malarone
granulations granulations OR Quinidine gluconate
P. vivax SPECIAL SITUATIONS
P. falciparum P. malariae
P. ovale Chloroquine-resistance Mefloquine + Doxycycline
Eradication of hypnozoites Primaquine
Severe cases or pregnant Quinidine or Quinine
 PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
BLOOD AND TISSUE PROTOZOA (continued)
Toxoplasma î Tissue protozoan Ingestion of cysts Fecal oocysts Trophozoites (Bradyzoites) Two Types of Trophozoites: î IMMUNOCOMPETENT: Treatment of Choice: MONONUCLEOSIS
in raw meat, TACHYZOITES - Usually asymptomatic Sulfadiazine + Heterophil-Positive:
gondii
î Domestic cat is the contaminated - rapidly multiplying - some resemble infectious Pyrimethamine î Epstein-Barr Virus
definitive host food - cell-mediated immunity usually mononucleosis, except that the
limits the spread of tachyzoites heterophil antibody test is negative For patients who cannot Heterophil-Negative:
î Humans and other Transplacentally î Cytomegalovirus
LABORATORY DIAGNOSIS: - seen in body fluids in early, receive sulfa drugs,
mammals are î For the diagnosis of acute acute infections î IMMUNOCOMPROMISED: clindamycin can be î Toxopasma
intermediate hosts and congenital infections, - encephalitis
added to
BRADYZOITES - brain abscesses usually seen as
an immunofluorescence pyrimethamine.
- slowly multiplying multiple ring-enhancing lesions on CALCIFICATIONS in
assay for IgM antibody is - contained in cysts in muscle and MRI TORCH INFECTIONS
used.
brain tissue and in the eye Intracranial:
î Microscopic examination of
Giemsa-stained î CONGENITAL TOXOPLASMOSIS î Toxoplasmosis
preparations shows - Can result in abortion, stillbirth or
Periventricular:
neonatal disease with
crescent-shaped î Cytomegalovirus
trophozoites during acute hydrocephalus, encephalitis,
infections. chorioretinitis, and
î Cysts may be seen in the hepatosplenomegaly
tissue. - Fever, jaundice, and intracranial
calcifications are also seen

Leishmania î Flagellate protozoa Bite of the female Promastigotes Amastigote LEISHMANIASIS Conventional Therapy:
species sandfly of the CUTANEOUS MUCOCUTANEOUS VISCERAL Sodium
genus Causative L. tropica stibogluconate
Phlebotomus or Agent L. braziliensis L. donovani (Pentavalent antimonial)
LABORATORY DIAGNOSIS
L. mexicana
Lutzomyia Local Name Oriental Sore Espundia Kala-azar
Examination of Giemsa- Second-line agents:
Presentation ulcerating single or parasite attacks infects macrophages
stained tissue and fluid Amphotericin B
multiple skin sores tissue at the à migrate to the
samples for the Pentamidine
mucosal-dermal spleen, liver, and
nonflagellated form junctions of the bone marrow à
(amastigote), which is the nose and mouth à parasite rapidly
Macrophages containing only form that occurs in multiple lesions multiplies à
L. donovani amastigotes humans and other mammals. hepatosplenomegaly

Babesia microti î Sporozoan Bite Ixodes tick Giemsa-stained blood smears î Babesia infects RBCs, causing them BABESIOSIS Mild to moderate
(same as Borrelia reveal intraerythrocytic to lyse, but unlike plasmodia, it has î Influenza-like symptoms begin gradually disease:
burgdorferi of ring-shaped trophozoites no exoerythrocytic phase. and may last for several weeks Atovaquone +
Lyme disease) are often in tetrads in the î Hepatosplenomegaly and anemia occur Azithromycin
î Asplenic patients are affected
form of a Maltese cross
more severely. Severe disease:
Quinidine +
Clindamycin “Maltese cross”

Cyclospora î Coccidial sporozoa Fecal–oral Spherical oocysts in a causes watery diarrhea in both Trimethoprim-
(contaminated modified acid-fast stain of a immunocompetent and Sulfamethoxazole
cayetanensis
water supplies) stool sample immunocompromised individuals

Isospora belli î Coccidial sporozoa Fecal–oral Oocyst typical oocysts in fecal The oocysts excyst in the upper small The disease in immunocompromised Trimethoprim-
transmission of specimens intestine and invade the mucosa, patients presents as a chronic, profuse, Sulfamethoxazole
oocysts causing destruction of the brush watery diarrhea
border
 PROTOZOA PARASITE BIOLOGY TRANSMISSION INFECTIVE STAGE DIAGNOSTIC STAGE PATHOGENESIS/VIRULENCE FACTORS SPECTRUM OF DISEASE TREATMENT NOTES
BLOOD AND TISSUE PROTOZOA (continued)
Trypanosoma î Blood and tissue protozoan Feces of Reduviid Metacyclic Trypomastigote in blood î Many cells can be affected, but CHAGAS’ DISEASE / AMERICAN Drug of choice for the
î All four forms: bug (“kissing trypomastigote smear myocardial, glial, and TRYPANOSOMIASIS acute phase:
cruzii
- Amastigote bug,” triatoma, reticuloendothelial cells are the î ACUTE PHASE: Nifurtimox
- Promastigote most frequent sites. - facial edema
or cone-nose)
- Epimastigote deposited in a - nodule (chagoma) near the bite Alternative Drug:
LABORATORY DIAGNOSIS: î Cardiac muscle is the most - fever, lymphadenopathy,
- Trypomastigote painless bite Benznidazole
î a stained preparation of a frequently and severely affected hepatosplenomegaly
(Kiss is supposedly
bone marrow aspirate tissue - unilateral palpebral swelling
painless)
or muscle biopsy î neuronal damage leads to cardiac (Romaña’s sign) There is no effective
specimen (which may arrhythmias and loss of tone in the - resolves in about 2 months drug against the
reveal amastigotes) colon (megacolon) and esophagus chronic form.
(megaesophagus) î CHRONIC FORM:
î culture of the organism on
- myocarditis, dilated cardiomyopathy
Trypomastigote in special medium
with apical atrophy
blood smear î Xenodiagnosis: allowing - megacolon, megaesophagus
an uninfected, laboratory- (secondary achalasia)
raised reduviid bug to feed - Death is usually due to cardiac
on the patient and, after arrhythmias or congestive heart
several weeks, examining failure
the intestinal contents of
- leading cause of CHF in Latin
the bug for the organism
America
Trypanosoma î Blood and tissue protozoan Tsetse fly Metacyclic Trypomastigote in blood î Trypomastigotes spread from the skin à blood à lymph nodes à brain Suramin for
î Only two forms: (Glossina), a trypomastigote î The typical somnolence (sleeping sickness) progresses to coma as a result of a bloodborne disease
brucei
- Epimastigote painful bite demyelinating encephalitis (ARAS, brainstem)
- Trypomastigote î In the acute form, a cyclical fever spike (approx. every 2 weeks) occurs that is Melarsoprol for
î exhibit remarkable related to antigenic variation. CNS penetration
antigenic variation of
their surface glycoproteins AFRICAN TRYPANOSOMIASIS / AFRICAN SLEEPING SICKNESS Morula cells of Mott
î initial lesion: indurated skin ulcer (“trypanosomal chancre”) at the site of the
Trypanosoma brucei gambiense Trypanosoma brucei rhodesiense fly bite
î causes the disease along water courses î found in the arid regions of east Africa î intermittent weekly fever and lymphadenopathy
in west Africa î enlargement of the posterior cervical lymph nodes (Winterbottom’s sign) MELlow music will
Trypomastigote in î deep hyperaesthesia (Kerandel's sign) SURely put you to
î runs a low-grade chronic course î causes a more acute, rapidly SLEEP.
blood smear î Encephalitis à excessive somnolence
over a few years progressive disease that, if untreated, is
• Morula cells of Mott: plasma cells with cytoplasmic immunoglobulin
usually fatal within several months MELarsoprol and
globules
î Transmitted by Glossina î Transmitted by Glossina SURamin for African
î Untreated disease is usually fatal as a result of pneumonia.
palpalis (or riverine tsetse) morsitans (or savannah tsetse) SLEEPing sickness
î Treatment: î Treatment:
Stage 1 Stage 2 • Suramin (to clear parasitemia)
Pentamidine Eflornithine followed by Melarsoprol
Suramin Melarsoprol

Acanthamoeba î free-living amebas carried into the Trophozoites Occur primarily in î KERATITIS: most common disease Pentamidine, î MC parasite that
î Most common protist in soil skin or eyes immunocompromised individuals associated with Acanthamoeba infection ketoconazole, or contaminates
castellani
during trauma î GRANULOMATOUS AMEBIC flucytosine contact lenses
ENCEPHALITIS

Naegleria fowleri î free-living amebas Swimming in Trophozoites occur in otherwise healthy persons î PRIMARY AMEBIC Amphotericin-B
freshwater Trophozoites can penetrate the nasal MENINGOENCEPHALITIS
lakes mucosa and cribriform plate