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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
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
4) Epidemiology: fecal-oral transmission, often via streams in
the wilderness as many animals carry Giardia as well, classic
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FIGURE 4.1 Classic Entamoeba Cyst

Classic Entamoeba cyst (light arrow) with an ingested red blood cell (dark arrow).
Boards scenario is a hiker who drinks from a stream and gets

diarrhea, disease is common in patients with IgA deficiency
5) Clinical Diseases: chronic diarrhea, no tissue invasive disease
6) Treatment: metronidazole
7) Resistance: none
8) Prophylaxis: boiling or filtering water, chlorination doesn’t
work
d. Trichomonas
1) Appearance: there is no cyst stage, pear-shaped trophozoite,
with four flagella, highly motile on wet mount
2) Lab assays: wet mount
4) Epidemiology: sexually transmitted, resides in the vagina or,
rarely in male GU tract, can be spread by asymptomatic carriers
5) Clinical Diseases: vaginitis with green, frothy discharge, can
cause urethritis in men, watch out for Boards questions
where both the male and female sex partners have GU symp-
toms, or questions in which the female is diagnosed with
Trichomonas and treated appropriately but comes back
62 | PARASITES
FIGURE 4.2 Giardia Trophozoites

A) Typical appearance of Giardia trophozoites from an intestinal biopsy. B) Close-up
of an individual trophozoite, revealing the presence of two nuclei and four pairs of
flagella.
shortly with a new infection—both sex partners must be

treated simultaneously to eradicate the disease
6) Treatment: metronidazole, treat both sex partners
7) Resistance: none
8) Prophylaxis: condoms
2. Invasive protozoa
a. Babesia
1) Appearance: intracellular ring forms within red cells similar to
malaria
2) Lab assays: blood smear, serology
4) Epidemiology: transmitted via tick bite, typically occurs in the
New England area, specifically along the coast
5) Clinical Diseases: high fevers, shaking chills, myalgias, abdomi-
nal pain, nausea/vomiting, followed by severe hemolytic
anemia particularly dangerous in splenectomized patients
6) Treatment: clindamycin plus quinine
7) Resistance: none
8) Prophylaxis: avoid tick bites
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TABLE 4.1 Summary of GI/GU Protozoa
ORGANISM APPEARANCE DISEASE TREATMENT
Cryptosporidium Cyst stain pink in stool, Watery diarrhea, Immune

nuclei not visible typically in AIDS reconstitution
Entamoeba Thin-walled cyst with Bloody diarrhea, Metronidazole

4 nuclei, trophozoite invasive hepatic and
ingests red blood abscess iodoquinol
cells and is not
flagellated
Giardia Thick-walled cyst with Non-bloody Metronidazole

4 nuclei, trophozoite diarrhea, often
is oval and has in hikers
4 pairs of flagella
Trichomonas No cyst, trophozoite Vaginitis Metronidazole

is oval with 4 single (treat both sex
flagella partners)
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
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
64 | PARASITES
disseminate to multiple mucosal spots, creating granulo-

matous erosions of nose and mouth
6) Treatment: sodium stibogluconate, ketoconazole, liposomal
amphotericin B, miltefosine
7) Resistance: unusual
8) Prophylaxis: long-sleeve shirts, long pants, insect repellents,
pesticides to kill sandflies
c. Plasmodium (malaria): falciparum, vivax, ovale, malariae
1) Appearance: schizonts appear like “signet rings” in red blood
cells, while the gametocyte of P. falciparum appears like a
large crescent attached to a thin ring (see Figure 4.3)
2) Lab assays: thin and thick smear of whole blood to detect
trophozoites
4) Epidemiology: transmitted by bite of Anopheles mosquito,
infects several hundred million people worldwide, particu-
larly affects Africa and all Mediterranean countries, causes
about 1 million deaths per year, life cycle is complicated:
FIGURE 4.3 (A and B) “Signet Ring” Schizonts of Malaria, (C) P. falciparum

A) and B) show typical “signet ring” schizonts of malaria in red blood cells.
C) shows the classic “crescent” shaped gametocyte of P. falciparum found in
peripheral blood.
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sporozoites inoculated into blood from mosquito bite, seed

the liver and transform into merozoites, leave the liver and
infect red blood cells, transform into trophozoite which multi-
plies and then transforms back into merozoites and bursts the
red cell, infects new red cells and then the cycle repeats—note
that P. ovale and P. vivax can lie dormant in the liver, allow-
ing long-term relapse
a) General characteristics: all four species cause a cluster of
symptoms including paroxysmal fevers and shaking rigors,
myalgias, diaphoresis, severe headache, arthralgias, and
signs such as splenomegaly and hepatomegaly, red cell
lysis causes anemia, initially the fever is continuous, but
after several days the red cell bursts become synchronized
in P. vivax, ovale, and malariae infections, note that
falciparum may never become synchronized
b) Tertian fever: synchronous red cell bursts in P. vivax and
ovale cause tertian fevers (q48 hrs = tertian because it
occurs on the 3rd day, it is not q3 days), relapse is common
in tertian fever because vivax and ovale have a latent
phase in the liver
c) Quartan fever: synchronous red cell bursts in P. malariae
causes quartan fevers (q72 hrs because it occurs on the
4th day, it is not q4 days)
d) P. falciparum causes the most severe malaria, can cause
continuous or irregular fevers without patterns, the organ-
ism burden in P. falciparum infections is much higher, and
the red cells become sticky and can clog capillaries and
cause DIC, leading to strokes and renal failure, CNS disease
in a malaria patient is almost always due to P. falciparum,
and carries a very high mortality
6) Treatment:
a) Tertian fever: if P. vivax or ovale proven or suspected, treat
with chloroquine (for merozoites in blood) plus primaquine
(for latent organisms in liver)—beware pts with G6PDH
deficiency, in whom quinine-derivatives cause dangerous
hemolytic anemia
b) P. falciparum and Quartan fever: if P. falciparum or
malariae proven or suspected, treat with chloroquine
alone (primaquine not needed since there is no latent
liver phase)—beware pts with G6PDH deficiency
7) Resistance: an increasingly severe problem, resistance endemic
in South America, Africa, SE Asia, and parts of Middle East
with few proven alternatives to quinine-derivatives, quinine
plus doxycycline may cover some resistant organisms, other
regimens are so unusual they are not likely testable on the
USMLE
66 | PARASITES
TABLE 4.2 Summary of Plasmodium spp.
ORGANISM FEVER TIMING CNS Dz LATENT? TREATMENT*
Falciparum Irregular or q48 hr Yes No CQ
Vivaxlovale q48 hr No Yes CQ + PQ
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
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
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
PARASITES | 67
upstream of the drug-induced block in the biosynthetic path-

way, folinic acid is used because it is downstream of the
block)
7) Resistance: none, but alternative therapies are required in
sulfa-allergic patients
8) Prophylaxis: AIDS patients and pregnant women should avoid
kittens and should not clean kitty litter, cook meats thor-
oughly, AIDS patients with CD4 count <200 per L should be
on trimethoprim-sulfamethoxazole prophylaxis
e. Trypanosoma
1) Appearance: large, crescentic trypomastigotes seen in blood,
smaller, circular amastigotes seen in tissues
2) Lab assays: biopsy and serologies
3) Virulence factors: antigenic shift—the organism can shift its
surface antigens as antibody responses develop, keeping it
one step ahead of the immune response
4) Epidemiology: T. cruzi transmitted via reduviid bug, endemic
to Central and South America, which bites the patient and
then passes organism through the broken skin by defecating
in the bite wound, T. gambiense and T. rhodesiense transmit-
ted by the tsetse fly, endemic to Africa
a) Chagas disease: caused by T. cruzi, reduviid bug often bites
the face near the eyes, so look for Romana’s sign, a
swollen/puffy cheek near the eye, acutely the organism
causes lymphoreticular disease with fever, lymphadenopa-
thy, and hepatosplenomegaly, chronic persistence of the
organism leads to amastigote invasion of the heart and
colon, causing heart block and myocarditis/dilated car-
diomyopathy as well as megacolon, and achalasia
b) African Sleeping Sickness: caused by T. gambiense and
T. rhodesiense, presents with an ulcer at the site of the fly
bite, can lead to either an acute, severe encephalitis with
rapid decline in CNS function leading to coma, or a chronic
course over several years
6) Treatment:
a) Chagas disease: if caught during acute infection, nifur-
timox effective, there is no antimicrobial therapy for
chronic disease; however, pacemakers are crucial if heart
block develops
b) African Sleeping Sickness: suramin or melarsoprol may be
effective prior to onset of CNS disease but they don’t cross
the blood brain barrier well, so useless once CNS disease
sets in
7) Resistance: unusual
8) Prophylaxis: insect netting, insect repellent
68 | PARASITES
TABLE 4.3 Summary of Invasive Protozoa
TRANSMISSION EPIDEMIOLOGY TISSUE TROPISM
Babesia Tick bite • Coastal New England Red blood cells
Leishmania Sandfly bite • Mucocutaneous dz in Macrophages

Central/South America
• Cutaneous dz in
Central/South America
& Asia/Africa
• Visceral dz in
Asia/Africa
Plasmodium Anopheles Africa, Middle East, RBCs (liver for

mosquito Caribbean, Central/ P. vivax/ovale)
South America, SE Asia
Toxoplasma Cat feces or cysts Ubiquitous Brain

in undercooked
meat
Trypanosoma • Reduviid bug • Central/South Heart (cruzi), CNS

(cruzi) America (cruzi) (other spp)
• Tsetse fly • Africa (other spp)
(other spp)
B. Metazoa (Multicellular Animals)

1. Tapeworms (cestodes)
a. Diphyllobothrium latum
1) Appearance: longest tapeworm, up to 30 feet
4) Epidemiology: acquired by consuming raw, freshwater fish
5) Clinical Diseases: weight loss, diarrhea, vitamin B12 deficiency
6) Treatment: praziquantel/niclosamide
7) Resistance: none
8) Prophylaxis: cook fish
b. Echinococcus
1) Appearance: small tapeworm
4) Epidemiology: fecal oral transmission from dog feces, with
sheep an important intermediate host—thus shepherds are
commonly patients
5) Clinical Diseases: hydatid cysts in any organ of the body, if
cysts rupture can cause fatal anaphylaxis
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6) Treatment: careful surgical excystation with or without

albendazole
7) Resistance: none
8) Prophylaxis: good hygiene
c. Hymenolepis nana
1) Appearance: small tapeworm (up to 5 cm long)
4) Epidemiology: fecal oral transmission, with humans as major
host
5) Clinical Diseases: typically asymptomatic
7) Resistance: none
d. Taenia saginata (beef tapeworm)
1) Appearance: tapeworm can be several meters long
4) Epidemiology: ingestion of undercooked beef, transmitted to
cattle via fecal-oral route
5) Clinical Diseases: typically asymptomatic, although some
patients might suffer discomfort (and embarrassment!) due
to the occasional protrusion of the tapeworm tail from the
anus
7) Resistance: none
e. Taenia solium (pork tapeworm)
1) Appearance: tapeworm can be several meters long
4) Epidemiology: can be transmitted either by ingestion of larva
in undercooked pork causing tapeworm infection of gut, or
by ingestion of eggs in food due to fecal contamination, eggs
mature into larva in gut and burrow into tissues, causing
cysticercosis
a) Tapeworm infection: like T. saginata, often asymptomatic
b) Cysticercosis: space-occupying lesions occur in tissues, often
in brain, and death of the larva induces inflammatory re-
sponse which can cause seizures and chemical meningitis—
new onset seizures in an immigrant from Latin America is
neurocysticercosis until proven otherwise
6) Treatment: seizure medications, steroids for edema, with or
without albendazole or praziquantel
70 | PARASITES
TABLE 4.4 Summary of Tapeworms (cestodes)
TRANSMISSION CLINICAL Dz
Diphyllobothrium Raw fish Weight loss, diarrhea, B12

deficiency
Echinococcus Dog feces or ingestion Causes anaphylaxis when cysts

of infected sheep meat rupture often after trauma/
traffic accident
Hymenolepis Human feces Asymptomatic
Taenia saginata Undercooked beef Typically asymptomatic, worm

may protrude from anus
Taenia solium Undercooked pork Asymptomatic tapeworm

or human feces infection, or ingestion of eggs
in feces causes cysticercosis,
which presents with seizures
and chemical meningitis from
ruptured cysts in the brain
7) Resistance: none
2. Flukes (trematodes)
a. Clonorchis sinensis (Asian liver fluke)
1) Appearance: not remarkable
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
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: chronic cough, hemoptysis and dyspnea

6) Treatment: praziquantel
7) Resistance: none
8) Prophylaxis: cook crab meat
c. Schistosoma japonicum, mansoni, and haematobium
1) Appearance: ova are ovoid with sharp protuberance called a
spine at one end, S. haematobium ova have a big spine at the
very terminus of the egg, S. mansoni ovum have big spine off
to the side (about 2 o’clock if the terminus is 12 noon), while
S. japonicum have a less prominent spine (see Figure 4.4)
4) Epidemiology:
a) Infection occurs by direct penetration of human skin by
free-swimming larva, life-cycle requires freshwater envi-
ronment with snails (which are intermediate hosts)
b) S. mansoni occurs in tropical areas around the world,
including Africa, the Middle East, and South America, but
does not occur in Asia
c) S. japonicum occurs in Asia
d) S. haematobium occurs in Africa and the Middle East
FIGURE 4.4 (A) Schistosoma mansoni, (B) Schistosoma haematobium

A) The classic appearance of Schistosoma mansoni, with a terminal spine at
approximately 2 o’clock. B) In contrast, the spine of Schistosoma haematobium
is at the very terminus (12 o’clock).
72 | PARASITES
TABLE 4.5 Summary of Flukes (trematodes)
TRANSMISSION LOCATION CLINICAL Dz
Clonorchis Raw freshwater fish Asia Hepatitis, biliary

obstruction
Paragonimus Raw crab meat Asia Chronic cough,

hemoptysis
Schistosoma Skin penetration by Africa, Hematuria,

haematobium freshwater larvae Middle East transitional
bladder CA
Schistosoma Skin penetration by Asia Granulomatous

japonicum freshwater larvae hepatitis, cirrhosis,
portal hypertension
Schistosoma Skin penetration by Africa, Middle Granulomatous

mansoni freshwater larvae East, South hepatitis, cirrhosis,
America portal hypertension
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)
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
PARASITES | 73
FIGURE 4.5 Ascaris Worms

Appearance of a mass of Ascaris worms.
so that they are swallowed back down into the intestine

where they mature into adults and pass more eggs—this is
the most common parasitic infection in the world, with up to
1 billion people infected
5) Clinical Diseases: although infection can be asymptomatic,
eosinophilic pneumonia occurs during larval migration into the
alveoli, malnutrition can occur due to adult worms scavenging
nutrients in the gut, and bowel obstruction can occur due to
luminal occlusion by large numbers of the large adult worms
6) Treatment: albendazole or mebendazole, pyrantel pamoate as
2nd line
7) Resistance: none
b. Enterobius vermicularis (pinworm)
1) Appearance: small white worms, 1 cm or less
2) Lab assays: scotch tape test = place scotch tape over anus and
examine on a slide, the tape picks up the eggs which are visi-
ble under the microscope, worms can be directly visualized by
stool O&P (but eggs are not present in stool)
4) Epidemiology: most common helminthic infection in the U.S.,
transmission is fecal-oral, at night the female worm migrates
out the anus and lays eggs in the perianal area
5) Clinical Diseases: perianal pruritus
74 | PARASITES

2nd line
7) Resistance: none
c. Hookworm (Ancylostoma duodenale and Necator americanus)
1) Appearance: long, thin worms, Necator has cutting plates to
grab hold of the intestinal wall while Ancylostoma uses teeth
4) Epidemiology: Ancylostoma duodenale is found in most of
the underdeveloped world (Old World hookworm), while
Necator americanus (New World hookworm) is found in the
southeastern U.S., infection occurs via direct penetration of
skin in contact with moist soil containing larvae, like Ascaris
the larvae migrate via blood to the lungs where they are
coughed up and swallowed, allowing mature adults to
develop in the intestines and to pass eggs in the stool
5) Clinical Diseases: a pruritic, erythematous dermatitis occurs
at the site in the skin where the larvae penetrate, and
eosinophilic pneumonia occurs during transmigration of the
larvae through the alveoli, some time after infection iron
deficient anemia develops (hookworm is the #1 cause of iron
deficiency anemia in the world), with all the usual anemia
symptoms (e.g., weakness, fatigue, etc.), eosinophilia is typical
2nd line
7) Resistance: none
8) Prophylaxis: good sanitation, avoid direct skin contact with
contaminated soil (e.g., don’t walk barefoot through the soil)
d. Strongyloides stercoralis
1) Appearance: small round worms (see Figure 4.6)
4) Epidemiology: endemic throughout the tropical world, and also
in the southeastern U.S., direct contact of skin with soil conta-
minated by feces allows larval penetration into the host, the
larva migrates via blood to the lung where they are coughed
up and swallowed, allowing adult maturation in the intestines,
the adult worms lay eggs which either are defecated out to
start the next cycle, or mature into larva within the infected
host, allowing another round of infection within the same
host in a process called autoinfection, autoinfection can lead
to overwhelming infection in immunocompromised patients
5) Clinical Diseases: Cutaneous Larva Migrans = severe local
contact dermatitis occurs at the site of skin penetration, pts
can be asymptomatic, but some develop diarrhea, eosinophilic
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FIGURE 4.6 Strongyloides

Appearance of Strongyloides in the sputum of an infected patient.
pneumonia, or sepsis from bacterial translocation across a

damaged gut wall, peripheral eosinophilia is prominent
6) Treatment: ivermectin or albendazole
7) Resistance: none
8) Prophylaxis: good sanitation, avoid bare skin contact with
contaminated soil (e.g., don’t walk barefoot through the soil)
e. Trichuris trichiura (whipworm)
1) Appearance: long thin worm, with a thread-like tail extending
twice the length of the worm
4) Epidemiology: fecal-oral transmission of eggs, eggs mature
into adults in intestine, which then lay more eggs, there is no
tissue phase
5) Clinical Diseases: often asymptomatic, but may cause invasive
diarrhea, does NOT typically cause iron-deficient anemia, in
patients with heavy worm burden rectal prolapse can occur
6) Treatment: albendazole or mebendazole
7) Resistance: none
8) Prophylaxis: good sanitation and good hygiene
f. Trichinella spiralis
1) Appearance: larvae are oval with ring-like centers, found in
tissue, particularly muscle
2) Lab assays: muscle biopsy, note stool O&P not helpful, look
for marked eosinophilia
76 | PARASITES

4) Epidemiology: typically transmitted via ingestion of under-
cooked pig, bear, or deer meat containing larvae, larvae
mature in the intestine, and lay eggs which penetrate into the
bloodstream, seeding striated muscle throughout the body
5) Clinical Diseases: Trichinosis: an initial diarrhea is followed
within 2 weeks by severe myositis, headache with diffuse
muscle aches, high fever, and extreme eosinophilia (up to
90% of peripheral white blood cells), can also cause CNS and
cardiac damage
6) Treatment: albendazole or mebendazole with or without
corticosteroids
7) Resistance: none
8) Prophylaxis: cook meats thoroughly
4. Tissue Roundworms (nematodes)
a. Dracunculus medinensis
1) Appearance: coiled worm up to a foot or more long can be
seen burrowed beneath the skin, skin typically blisters and
then ulcerates over the worm
TABLE 4.6 Summary of Intestinal Roundworms (nematodes)
Ascaris Fecal oral Eosinophilic pneumonia, bowel

obstruction
Enterobius Fecal oral Perianal pruritius in children
Ancylostoma Skin penetration Pruritic, erythematosus dermatitis

by larvae in moist at site of penetration, iron deficient
soil anemia and eosinophilia, occurs in
Europe and Asia
Necator Skin penetration Pruritic, erythematosus dermatitis

by larvae in moist at site of penetration, iron deficient
soil anemia and eosinophilia, occurs in
the SE U.S.
Strongyloides Skin penetration Local contact dermatitis at site

by larvae in moist of skin penetration, diarrhea,
soil eosinophilic pneumonia, sepsis
Trichuris Fecal oral Invasive diarrhea, rectal

prolapse
Trichinella Undercooked Diarrhea, severe myositis, headache,

pork or game extreme eosinophilia
(bear or deer)
PARASITES | 77
2) Lab assays: none

4) Epidemiology: transmission is via ingestion of fresh-water
crustaceans containing larvae, larvae mature in the intestine
and the adult migrates to skin, the disease is on the decline in
Africa due to WHO efforts to eradicate
5) Clinical Diseases: pruritic and painful welts overlying the sub-
cutaneous worm, with ulceration over the worm’s head
6) Treatment: surgical withdrawal of the worm
7) Resistance: none significant
8) Prophylaxis: boil or filter suspect drinking water, avoid ingestion
b. Loa loa
1) Appearance: can be seen as small (centimeter) subconjunctival
worm burrowing across the eye or skin
2) Lab assays: thick and thin smear to identify parasites in the
blood
4) Epidemiology: endemic to Africa, transmitted by the bite of
the deer fly
5) Clinical Diseases: dermatitis or conjunctivitis caused by hyper-
sensitivity to migrating worm in skin or eye
6) Treatment: diethylcarbamazine, surgical excision may be
required for conjunctival infections
7) Resistance: none
8) Prophylaxis: eradication of deer fly vector
c. Oncocerca volvulus
1) Appearance: worm less than a millimeter long
2) Lab assays: skin biopsy revealing the parasite
4) Epidemiology: endemic to Africa, particularly riverbeds, trans-
mitted by bite of blackfly, the organisms do not travel
through blood, instead migrate subcutaneously
5) Clinical Diseases: causes “river blindness” (that’s right, the
people go blind from worm migration into the eyes, hence
the name)
6) Treatment: ivermectin plus corticosteroids for patients with
eye infection
7) Resistance: none
8) Prophylaxis: eradicate blackfly vector, ivermectin can be taken
prophylactically
d. Toxocara canis
1) Appearance: not significant
2) Lab assays: tissue biopsy
78 | PARASITES
4) Epidemiology: transmitted via dog feces contaminating soil

and foodstuffs, eggs hatch into larvae in the intestine, the
larvae then disseminate to multiple tissues
5) Clinical Diseases: “Visceral Larva Migrans” = diffuse granulo-
matous reactions causing fevers, myalgias, headache, CNS
disease and retinal disease, with a prominent eosinophilia,
typically presents in children playing in soil with dogs
6) Treatment: treat symptoms with corticosteroids and antihista-
mines, ivermectin, albendazole, or diethylcarbamazine for
worms
7) Resistance: none
8) Prophylaxis: good sanitation and hygiene
e. Wuchereria bancrofti and Brugia malayi
1) Appearance: worm less than a millimeter long
2) Lab assays: thick blood smears with blood drawn at night
4) Epidemiology: Wuchereria is endemic to Africa while Brugia is
endemic to Asia (particularly Malaysia hence the species name
malayi), both transmitted by mosquito bites, organisms
mature in lymph nodes and then circulate in the blood, partic-
ularly at night
5) Clinical Diseases: elephantiasis, obstruction of lymphatics
leads to severe lymphedema
6) Treatment: ivermectin effective against larvae but not adult
worms
7) Resistance: none
8) Prophylaxis: prevention of mosquito bites
TABLE 4.7 Summary of Invasive Roundworms (nematodes)
Dracunculus Freshwater Welts overlying the subcutaneous

crustaceans worm
Loa Deerfly bite Hypersensitivity to migrating

worm
Oncocerca Blackfly bite Blindness
Toxocara Dog feces Visceral larva migrans = diffuse

granulomas, retinitis, eosinophilia,
headache, myalgias
Wuchereria Mosquito Elephantiasis

and Brugia
PARASITES | 79
TABLE 4.8 Overall Summary of Parasites
KEY WORD/PHRASE TREATMENT
GI/GU Protozoa
Cryptosporidium • Diarrhea in AIDS patient Immune reconstitution
Entamoeba • Amoebic dysentery Metronidazole plus

iodoquinol
• Amoebic liver abscess
Giardia • Chronic non-bloody diarrhea Metronidazole

in a hiker/camper
Trichomonas • Vaginitis with green, Metronidazole

frothy discharge
• Frequent recurrences
because sexual partner needs
treatment as well
Invasive Protozoa
Leishmania • Sandfly bite in Asia, Africa, Sodium stibogluconate

Latin America
• Cutaneous ulcer
• Lymphadenopathy,
hepatosplenomegaly
Plasmodium • Mosquito bite in Africa, Chloroquine ±

Mediterranean, Latin primaquine
America
• Shaking rigors, severe
headache, myalgias
• Cyclical fevers
Toxoplasma • Exposure to kitten feces or Pyrimethamine +

poorly cooked meat sulfadiazine +
folinic acid
• Typically in AIDS pts with
ring-enhancing brain lesions
Trypanosoma • Reduviid bug bite in Nifurtimox or suramin

Latin America acutely, nothing works
for chronic dz
• Tsetse fly bite in Africa
• Romana’s sign = swelling
near eye where bite occurred
• Heart block in young person
Megacolon
(Continued )
80 | PARASITES
TABLE 4.8 Continued
Tapeworms (cestodes)
Diphyllobothrium • Raw fish consumption Albendazole

• B12 deficiency
Echinococcus • Shepherds, exposure to dogs Albendazole and

and sheep surgery
• Large cysts seen in liver
or lung
Hymenolepis • Dog feces Albendazole
Taenia saginata • Undercooked beef Albendazole

• Tapeworm protrusion
from anus
Taenia solium • Undercooked pork or Albendazole ± seizure

fecal-oral medicine
• Seizures and encephalitis in
a Hispanic person
Flukes (trematodes)
Clonorchis • Asian liver fluke Albendazole

• Raw freshwater fish
Paragonimus • Asian lung fluke Albendazole

• Raw crab meat
Schistosoma • Swimming in freshwater Albendazole

with snails nearby
• Portal hypertension
• Hematuria, bladder cancer
Intestinal Roundworms (nematodes)
Ascaris • Eosinophilic pneumonia Albendazole

• Bowel obstruction
• Iron deficiency
Enterobius • Kid with itchy anus Albendazole

• Small white worms seen
near anus
• Eggs picked up from anus
with scotch-tape
PARASITES | 81
TABLE 4.8 Continued
Intestinal Roundworms (nematodes) (Continued)
Ancylostoma • Dermatitis at site of contact Albendazole

with moist soil
• Iron deficiency anemia
Necator • Dermatitis at site of contact Albendazole

with moist soil
• Iron deficiency anemia
• Southeastern U.S., poor areas
Strongyloides • Local contact dermatitis Ivermectin or

(cutaneous larva migrans) albendazole
at site of contact with
moist soil
• Eosinophilic pneumonia,
auto infection
Trichuris • Rectal prolapse Albendazole
Trichinella • Undercooked pig, bear, or Albendazole

deer meat
• Severe myalgias with
extreme eosinophilia
Invasive Roundworms (nematodes)
Dracunculus • Long worm seen coiled Worm extraction

beneath soil
Loa • Small worm seen Diethylcarbamazine

underneath conjunctiva
Oncocerca • Blackfly bite Ivermectin

• River blindness in Africa
Toxocara • Visceral larva migrans Steroids,

antihistamines,?
• Retinal disease
ivermectin
• Prominent eosinophilia
Wuchereria • Elephantiasis Ivermectin

(Brugia)

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qxd 1/25/05 3:05 PM Page 60

FIGURE 4.1 Classic Entamoeba Cyst

Boards scenario is a hiker who drinks from a stream and gets

FIGURE 4.2 Giardia Trophozoites

shortly with a new infection—both sex partners must be

TABLE 4.1 Summary of GI/GU Protozoa

ORGANISM APPEARANCE DISEASE TREATMENT

Cryptosporidium Cyst stain pink in stool, Watery diarrhea, Immune

Entamoeba Thin-walled cyst with Bloody diarrhea, Metronidazole

Giardia Thick-walled cyst with Non-bloody Metronidazole

Trichomonas No cyst, trophozoite Vaginitis Metronidazole

disseminate to multiple mucosal spots, creating granulo-

FIGURE 4.3 (A and B) “Signet Ring” Schizonts of Malaria, (C) P. falciparum

sporozoites inoculated into blood from mosquito bite, seed

TABLE 4.2 Summary of Plasmodium spp.

ORGANISM FEVER TIMING CNS Dz LATENT? TREATMENT*

Falciparum Irregular or q48 hr Yes No CQ

Vivaxlovale q48 hr No Yes CQ + PQ

upstream of the drug-induced block in the biosynthetic path-

TABLE 4.3 Summary of Invasive Protozoa

TRANSMISSION EPIDEMIOLOGY TISSUE TROPISM

Babesia Tick bite • Coastal New England Red blood cells

Leishmania Sandfly bite • Mucocutaneous dz in Macrophages

Plasmodium Anopheles Africa, Middle East, RBCs (liver for

Toxoplasma Cat feces or cysts Ubiquitous Brain

Trypanosoma • Reduviid bug • Central/South Heart (cruzi), CNS

B. Metazoa (Multicellular Animals)

6) Treatment: careful surgical excystation with or without

TABLE 4.4 Summary of Tapeworms (cestodes)

Diphyllobothrium Raw fish Weight loss, diarrhea, B12

Echinococcus Dog feces or ingestion Causes anaphylaxis when cysts

Hymenolepis Human feces Asymptomatic

Taenia saginata Undercooked beef Typically asymptomatic, worm

Taenia solium Undercooked pork Asymptomatic tapeworm

5) Clinical Diseases: chronic cough, hemoptysis and dyspnea

FIGURE 4.4 (A) Schistosoma mansoni, (B) Schistosoma haematobium

TABLE 4.5 Summary of Flukes (trematodes)

TRANSMISSION LOCATION CLINICAL Dz

Clonorchis Raw freshwater fish Asia Hepatitis, biliary

Paragonimus Raw crab meat Asia Chronic cough,

Schistosoma Skin penetration by Africa, Hematuria,

Schistosoma Skin penetration by Asia Granulomatous

Schistosoma Skin penetration by Africa, Middle Granulomatous

FIGURE 4.5 Ascaris Worms

so that they are swallowed back down into the intestine

6) Treatment: albendazole or mebendazole, pyrantel pamoate as

FIGURE 4.6 Strongyloides

pneumonia, or sepsis from bacterial translocation across a

3) Virulence factors: none significant

TABLE 4.6 Summary of Intestinal Roundworms (nematodes)

Ascaris Fecal oral Eosinophilic pneumonia, bowel

Enterobius Fecal oral Perianal pruritius in children

Ancylostoma Skin penetration Pruritic, erythematosus dermatitis

Necator Skin penetration Pruritic, erythematosus dermatitis

Strongyloides Skin penetration Local contact dermatitis at site

Trichuris Fecal oral Invasive diarrhea, rectal

Trichinella Undercooked Diarrhea, severe myositis, headache,