Para Outline PDF
Para Outline PDF
Para Outline PDF
60 | PARASITES
IV. PARASITES
A. Protozoa
1. GI/GU
a. Cryptosporidium
1) Appearance: cysts are small, stain pink in stool specimens
2) Lab assays: stool O&P
3) Virulence factors: none significant
4) Epidemiology: ubiquitous but typically causes disease in AIDS
patients
5) Clinical Diseases: watery diarrhea, causes severe malabsorption
in AIDS patients
6) Treatment: supportive and immune reconstitution—
nitazoxanide may have a role
7) Resistance: none
8) Prophylaxis: boil or filter water, chlorination does not work
b. Entamoeba histolytica
1) Appearance: two phases of life-cycle: cyst has four nuclei,
trophozoite has one nucleus and is not flagellated and often
contains ingested red blood cells (see Figure 4.1)
2) Lab assays: stool O&P should reveal cyst or trophozoite,
anti-amoeba antibody titers are diagnostically useful
3) Virulence factors: none significant
4) Epidemiology: fecal-oral transmission
5) Clinical Diseases: amoebic dysentery and amoebic liver abscess
6) Treatment: metronidazole followed by iodoquinol or
paromomycin—the latter are necessary to kill encysted organ-
isms in the bowel lumen that are not killed by metronidazole
7) Resistance: none
8) Prophylaxis: boil or filter water, chlorination has no effect,
careful hand-washing and separation of human wastes from
crop fields (don’t fertilize crops with human feces)
c. Giardia lamblia
1) Appearance: two phases of life cycle: cyst has four nuclei and
has a thicker wall than Entamoeba, trophozoite is oval with
two nuclei and has four pairs of flagella (see Figure 4.2)
2) Lab assays: stool O&P, string test = patient swallows a string
down into the duodenum while the physician holds onto the
far end and then pulls the string back up out of the mouth,
revealing the trophozoites stuck onto the string
3) Virulence factors: none significant
4) Epidemiology: fecal-oral transmission, often via streams in
the wilderness as many animals carry Giardia as well, classic
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b. Leishmania spp.
1) Appearance: amastigotes are small intracellular organisms
seen within macrophages
2) Lab assays: blood smear or tissue biopsy reveal organisms
within macrophages, serologies often positive
3) Virulence factors: none significant
4) Epidemiology: transmitted via sandfly bite, visceral disease
seen in Asia and Africa, cutaneous disease seen in Central and
South America as well as Asia and Africa, mucocutaneous dis-
ease seen only in Central and South America
5) Clinical Diseases:
a) Kala azar = visceral leishmaniasis: caused by L. donovani,
organism is concentrated in the reticuloendothelial system
(liver, spleen, lymph nodes, bone marrow), causing massive
hepatosplenomegaly, pancytopenia, hemorrhage, and sus-
ceptibility to secondary infections, patients also get hyper-
pigmented skin
b) Cutaneous leishmaniasis: caused by L. tropica (Old World
disease in Asia and Africa) and L. mexicana (New World
disease in Central/South America), disease starts with ery-
thematous papule at site of sandfly bite, can either heal
spontaneously or progress to large, granulomatous ulcera-
tions which often is secondarily infected by bacteria
c) Mucocutaneous leishmaniasis: caused by L. braziliensis,
also starts as papule at site of sandfly bite, but can
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Malariae q72 hr No No CQ
*
Assumes not resistant.
CQ, chloroquine; PQ, primaquine.
8) Prophylaxis:
a) Mosquito netting and DEET insect repellent are keys to
avoid inoculation—it is much more effective to prevent bites
than to treat infection due to increasing drug resistance
b) Chemoprophylaxis depends on if travel is to area with
resistant organism
i) Non-resistant area (Central America north of the
Panama Canal, some parts of the Middle East and
some parts of the Caribbean): chloroquine for several
weeks before the trip, during the trip, and for several
weeks after the trip
ii) Resistant area: mefloquine, atovaquone-proguanil, or
doxycycline before, during the trip, and after the trip
d. Toxoplasma gondii
1) Appearance: biopsy of infected tissue reveals crescent-shaped
organisms
2) Lab assays: IgM serologies to detect acute infection
3) Virulence factors: none significant
4) Epidemiology: transmitted via the feces of kittens (older cats
less likely), or via ingestion of poorly cooked meat containing
cysts, can also be transmitted vertically if the mother is newly
infected during pregnancy
5) Clinical Diseases:
a) Immunocompetent people either get asymptomatically ex-
posed or develop mild heterophile negative mononucleosis
b) AIDS patients: clinical disease primarily seen in HIV
patients, immunosuppression allows reactivation of the
organism, classically causing severe encephalitis with multi-
ple ring-enhancing lesions in the brain
c) Congenital: causes multi-organ disease and can lead to
spontaneous abortion or severe congenital retardation
6) Treatment: pyrimethamine plus sulfadiazine plus folinic acid
(folinic acid is used to prevent folate deficiency caused by the
drugs—note that folate cannot be used because folate is
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TRANSMISSION CLINICAL Dz
7) Resistance: none
8) Prophylaxis: good hygiene
2. Flukes (trematodes)
a. Clonorchis sinensis (Asian liver fluke)
1) Appearance: not remarkable
2) Lab assays: stool O&P
3) Virulence factors: none significant
4) Epidemiology: transmitted by ingestion of raw freshwater
fish, endemic to Asia
5) Clinical Diseases: may be asymptomatic, however, the flukes
lodge in the liver and can cause hepatitis and biliary
obstruction ultimately leading to cirrhosis or hepatocellular
carcinoma
6) Treatment: praziquantel/albendazole
7) Resistance: none
8) Prophylaxis: cook fish
b. Paragonimus westermani (Asian lung fluke)
1) Appearance: not remarkable
2) Lab assays: stool O&P
3) Virulence factors: none significant
4) Epidemiology: transmitted by ingestion of raw crab meat,
endemic to Asia, organism penetrates intestinal wall, migrates
through the diaphragm to the lung and can thus be transmit-
ted either by feces or sputum
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5) Clinical Diseases:
a) S. japonicum & mansoni: acute infection causes pruritis and
erythematous eruption at the site of skin penetration,
after several weeks fevers and lymphadenopathy begin,
tissue penetration causes marked eosinophilia, adult schis-
tosomes reside in the liver venules and their eggs cause
granulomatous reaction in the liver, leading to portal
hypertension and hepatosplenomegaly, can induce cirrho-
sis leading to all the usual sequelae
b) S. hematobium: adult worms reside in the bladder venous
plexus, and their eggs cause granulomas and fibrosis in the
bladder, leading to hematuria, can also induce transitional
cell carcinoma of the bladder
6) Treatment: praziquantel
7) Resistance: starting to be seen for S. mansoni
8) Prophylaxis: avoid swimming in waters with host snails
3. Intestinal Roundworms (nematodes)
a. Ascaris lumbricoides
1) Appearance: large roundworms, can be a foot long, and can
form mass-like conglomerations in the intestines (see Figure 4.5)
2) Lab assays: stool O&P
3) Virulence factors: none significant
4) Epidemiology: fecal-oral transmission of eggs, after ingestion,
eggs hatch in the intestine, the larva penetrate the intestinal
wall and enter the bloodstream, then the larva escape into the
lungs, penetrate the alveoli and are coughed up the trachea
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GI/GU Protozoa
Cryptosporidium • Diarrhea in AIDS patient Immune reconstitution
Invasive Protozoa
(Continued )
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Tapeworms (cestodes)
Flukes (trematodes)
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