Protozoa

Protozoa

GI infection Urogenital infection Systemic infection

E. histolytica G. lamblia C. parvum B. coli T. vaginalis T. gondii L. donovani T. cruzi T. brucei P. falciparum, B. microti,
vivax, divergens
ovale,
malariae

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 Protozoa
All protozoa are unicellular eukaryotes. Many can exist in two forms:
(1) as trophozoites (the feeding/reproducing form found in favorable environments)
(2) as cysts (the protective/dormant form found in difficult environments)

Protozoa can also be classified based on how they locomote in their trophozoite form.
AMOEBAS SPOROZOANS FLAGELLATES CILIATES
(MOVE WITH PSEUDOPODIA) (NOT MOTILE) (MOVE WITH FLAGELLA) (MOVE WITH CILIA)
E. histolytica C. parvum G. lamblia Balantidium coli
T. gondii T. vaginalis
P. falciparum L. donovani
P. vivax T. cruzi
P. ovale T. brucei
P. malariae

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 Entamoeba histolytica Amebiasis
Protozoa

A mature E. histolytica
cyst has four nuclei

Pseudopods allow
trophozoite to move GI infection
along intestinal wall
and take up food
Cyst

Ingested RBCs are often

found in trophozoites

Nucleus

E. histolytica G. lamblia B. coli C. parvum

Trophozoite

CLINICAL CASE
After a camping trip to Mexico, a patient visits her doctor complaining of loose stools and abdominal cramps. The patient
describes the stools as having flecks of blood and lots of mucus. The doctor orders a stool specimen in which she finds motile
amoeba with ingested RBCs. She starts the patient on metronidazole and considers a CT scan to detect any liver abscesses.

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 Entamoeba histolytica Amebiasis
CLINICAL PRESENTATION
amebic dysentery (bloody diarrhea)
liver abscess
PATHOBIOLOGY
fecal–oral transmission from contaminated food or water → cyst ingested → in ileum, cyst differentiates to
trophozoite (motile amoeba) → trophozoite can lead to:
• asymptomatic carrier (most common): trophozoite becomes 4-nuclei cyst → cyst released in stools
• intestinal amebiasis: trophozoite invades colonic epithelium → local necrosis → dysentery
• invasive amebiasis: trophozoite invades through colonic epithelium producing raindrop-shaped ulcers →
enters portal circulation → travels to liver and forms abscess → abscess enlarges → RUQ pain, weight loss
(from liver abscess, trophozoite may invade diaphragm and create pulmonary abscess)
DIAGNOSIS
diarrheal specimen (active state): trophozoite with ingested RBC
hard stool specimen (carrier state): 4-nuclei cyst
serology
TREATMENT
metronidazole (for active state)
iodoquinol, diloxamide furoate (for carrier state) Study Tip
in severe cases, drain hepatic abscesses
prevention: killed by boiling, not by chlorination Diarrhea caused by
QUICK FACTS protozoa:
Because cysts survive outside the host, carriers shedding cysts are more contagious than sick patients shedding trophozoites. bloody → Entamoeba
Anal–oral transmission of Entamoeba histolytica also occurs. This type of spread is seen in homosexual male populations. histolytica
Acanthamoeba species and Naegleria fowleri, two other amoebas, can cause meningoencephalitic conditions in fatty → Giardia lamblia
immunosuppressed and immunocompetent patients, respectively. watery →
Acanthamoeba species can cause keratitis in people wearing contact lenses. This may lead to blindness. Cryptosporidium
parvum

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 Giardia lamblia Giardiasis
Protozoa

Note:
• 4 nuclei
• thick wall
• internal fibers
GI infection

Note:
Cyst • 2 nuclei
• 4 pairs of flagella

E. histolytica G. lamblia B. coli C. parvum

Trophozoite

CLINICAL CASE
A student cuts short an extended backpacking trip in Yosemite Park after developing diarrhea. He explains to his doctor that
the diarrhea is nonbloody but smells very bad. On further questioning, the student tells his doctor that he has been drinking
water from a fresh water spring. The patient appears malnourished on physical exam. A diarrhea sample reveals 2-nuclei
motile amoeba with a tear-drop shape and 4 pairs of flagella. The student is given metronidazole.

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 Giardia lamblia Giardiasis
CLINICAL PRESENTATION
non-bloody diarrhea
asymptomatic carrier
PATHOBIOLOGY
fecal–oral transmission from contaminated food or water → cyst ingested → in duodenum, cyst differentiates
into trophozoite → trophozoite attaches to duodenal wall via “suction” disk (no invasion) → damage to microvilli,
inflammation → malabsorption, nonbloody & foul-smelling (fatty) diarrhea, weight loss
DIAGNOSIS
stool ova and parasites examination
diarrheal specimen (active state): tear-shaped trophozoite with 2 nuclei, 4 pairs of “moustache” flagella
hard stool specimen (carrier state): 4-nuclei cyst
ELISA for giardia antigen
“string test” for duodenal pathogens: trophozoites can be detected after attaching to swallowed string
TREATMENT
metronidazole
prevention: killed by boiling or iodine treatment
QUICK FACTS Study Tip
Many infected hosts remain asymptomatic carriers and shed cysts for years.
Giardia is also common in urban centers with poor sanitation and in day care centers with poor hygiene. Diarrhea caused by
protozoa:
bloody → Entamoeba
histolytica
fatty → Giardia lamblia
watery →
Cryptosporidium
parvum

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 Cryptosporidium parvum Cryptosporidiosis
Protozoa
Oocyst with four motile sporozoites

GI infection

E. histolytica G. lamblia B. coli C. parvum

CLINICAL CASE
An HIV patient becomes alarmed after developing a persistent diarrhea. He tells his physician that the diarrhea is watery and
without blood. Upon learning that the patient visited a vacation farm before the diarrhea started, the doctor orders an acid-fast
stain of the patient’s stool sample.

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 Cryptosporidium parvum Cryptosporidiosis
CLINICAL PRESENTATION
watery diarrhea
PATHOBIOLOGY
fecal–oral transmission from animals or humans → oocysts ingested → oocysts release sporozoites in small intestine
→ sporozoites differentiate into trophozoites and attach to intestinal microvilli → watery, non-bloody diarrhea
in immunocompromised patients, prolonged and more severe diarrhea → malnutrition
DIAGNOSIS
stool sample: oocysts seen using acid-fast stain
serology
TREATMENT
supportive
prevention: water purification
QUICK FACTS
In AIDS patients, Cryptosporidium is an important cause of severe watery diarrhea.
Cryptosporidium can cause diarrhea outbreaks due to contaminated city water reservoirs.

Study Tip
Diarrhea caused by
protozoa:
bloody → Entamoeba
histolytica
fatty → Giardia lamblia
watery →
Cryptosporidium
parvum

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 Balantidium coli Balantidiasis
Protozoa

GI infection

E. histolytica G. lamblia B. coli C. parvum

CLINICAL CASE
A medical student traveled to the Philippines for the summer, hoping to integrate into rural life and better understand the
language and culture. His host family herded swine, and shortly after their first dinner together, he developed severe vomiting
and bloody diarrhea. Stool examination showed ciliated, round, single-cell microorganisms.

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 Balantidium coli Balantidiasis
CLINICAL PRESENTATION
acute diarrhea (watery or bloody)
asymptomatic (excrete cysts)
PATHOBIOLOGY
fecal–oral transmission from porcine fecal contamination of food or water → cyst ingested → trophozoite emerges from cyst
in normal pH of small intestine → trophozoites colonize large intestine, leading to:
• Asymptomatic carrier: trophozoite becomes cyst → cysts passed in stool
• Acute colitis: trophozoites invade colonic wall → ⫹/⫺ intestinal perforations → watery or bloody diarrhea

DIAGNOSIS
ciliated cysts or trophozoites on stool examination
TREATMENT
tetracycline or metronidazole
unclear if warranted for asymptomatic carriers
QUICK FACTS
For carriers, symptoms may be precipitated by malnutrition, immunosuppression, or low stomach acidity.
In rare acute cases, intestinal perforation can be life threatening.
Only known ciliated protozoan to cause human disease.

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 Trichomonas vaginalis Trichomoniasis
T. vaginalis is transmitted between humans by sexual contact. Lacking a cyst, Protozoa
it does not survive well in the external environment.

Urogenital infection

T. vaginalis

Trophozoite resides in vagina or orifice of urethra and is spread in vaginal or

prostatic secretions as well as in urine.

CLINICAL CASE
A teenage girl complains of vaginal itching and burning. Sexual history reveals numerous sexual partners. Her gynecologist
performs a pelvic exam and finds a greenish, foul-smelling thin discharge from the vagina. A wet mount of the discharge
reveals motile amoeba, each with 1 nucleus and 5 flagella. The patient is started on metronidazole.
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 Trichomonas vaginalis Trichomoniasis
CLINICAL PRESENTATION
vaginitis
urethritis (mainly in males)
PATHOBIOLOGY
sexual transmission → trophozoite colonizes:
• vagina in females → greenish, watery, & foul-smelling vaginal discharge; itching
• urethra in males → mostly asymptomatic
DIAGNOSIS
wet mount of vaginal or urethral discharge: tear-drop shaped trophozoites; 5 flagella, 1 nucleus
TREATMENT
metronidazole to the patient and patient’s sexual partner(s)
QUICK FACTS
Trichomonas can be distinguished from other flagellate protozoa in that it lacks a cyst form (by sexual transmission,
the organism never leaves a host).

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 Toxoplasma gondii Toxoplasmosis
Protozoa

Systemic infection

T. gondii L. donovani T. cruzi T. brucei P. falciparum, B. microti,

vivax, divergens
ovale,
Crescent-shaped trophozoites within macrophage malariae

CLINICAL CASE
An AIDS patient is brought to the EW after suffering a grand mal seizure. The man informs the EW physician that he has
suffered a persistent headache in the past few weeks but denies any sensory problems or weakness. Fearing a brain tumor,
the EW physician orders a CT scan of the patient. However, the scan, instead, reveals several ring-enhancing masses in the
patient’s brain. The physician confirms his suspicions when he learns the patient has many cats at home. He expects that a
brain biopsy would show crescent-shaped trophozoites.

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 Toxoplasma gondii Toxoplasmosis
CLINICAL PRESENTATION
in immunocompetent patients: asymptomatic, mononucleosis-like illness
in immunocompromised patients: encephalitis, chorioretinitis
congenital infection: mental retardation, chorioretinitis
PATHOBIOLOGY
cysts ingested from undercooked meat or cat feces → in small intestine, cysts release invasive form → penetrate
intestinal wall → phagocytosed and disseminated by macrophages → infects, damages cells at distant sites
→ host response contains infections (with mononucleosis-like symptoms ) → in tissue, invasive forms become
dormant → contained within cyst
if host becomes immunocompromised → cyst ruptures and releases invasive form → encephalitis, chorioretinitis,
other infections
if active infection in pregnant mother → invasive form crosses placenta to fetus → congenital toxoplasmosis →
mental retardation, chorioretinitis, other birth defects → invasive form becomes dormant and may reactivate
later in life
DIAGNOSIS
serology (IgM in infants)
tissue biopsy: trophozoites (active), cysts (dormant)
Study Tip
CT, MRI of head
Organisms that cross
TREATMENT placenta and therefore
sulfonamide ⫹ pyrimethamine allow infection to pass from
QUICK FACTS pregnant mother to fetus
(TORCHES):
Toxoplasma is the most common cause of encephalitis in HIV patients.
Only pregnant mothers with an active primary infection can result in congenital toxoplasmosis; mothers with previous Toxoplasma gondii
infections mount an immune response that protects the fetus. Rubella
Pregnant mothers, especially those without previous exposure, are encouraged to avoid cats to prevent congenital Cytomegalovirus
toxoplasmosis. Herpes, HIV
Syphilis

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 Leishmania donovani Leishmaniasis, “Kala-Azar”
Protozoa

Systemic infection

T. gondii L. donovani T. cruzi T. brucei P. falciparum, B. microti,

vivax, divergens
Nonflagellated protozoa within macrophages ovale,
(flagellated protozoa occur outside macrophages) malariae

CLINICAL CASE
A recent immigrant from a tropical country presents with weight loss and fever. A physical exam reveals massive
hepatosplenomegaly with associated edema, as well as hyperpigmented skin patches. The doctor orders a CBC and spleen
biopsy. CBC reveals thrombocytopenia, anemia, and leukopenia, while spleen biopsy shows macrophages containing
protozoa. The doctor begins the patient on an antimony compound.

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 Leishmania donovani Leishmaniasis, “Kala-Azar”
CLINICAL PRESENTATION
visceral leishmaniasis (kala-azar)
PATHOBIOLOGY
reservoir in dogs and rodents, transmitted by sand fly vector → sand fly bite releases protozoan → protozoan engulfed by
macrophages → divides within and destroys infected cells → over months, spreads through reticuloendothelial
system → damage to spleen, liver, bone marrow → splenomegaly, thrombocytopenia, anemia, leukopenia
weakened immune state → secondary infections → death
DIAGNOSIS
biopsy: nonflagellated protozoan within macrophages
leishmanin skin test: intradermal injection of killed Leishmania causes DTH response
TREATMENT
stibogluconate (an antimony compound)
QUICK FACTS
Kala-azar means “black illness,” named for the hyperpigmented skin lesions found in infected individuals.
Infections by other Leishmania species can result in a spectrum of less severe illnesses, depending on the organism’s
invasiveness and the strength of host response:
local cutaneous leishmaniasis (single skin ulcer)
diffuse cutaneous leishmaniasis (many skin nodules)
mucocutaneous leishmaniasis (nasal/oral mucosal ulcers)
Cutaneous leishmaniasis was a significant illness among U.S. soldiers returning from the Persian Gulf War.

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 Trypanosoma cruzi Chagas’ Disease,
American Trypanosomiasis
Protozoa
Protozoan

RBC

Systemic infection

Flagellated protozoan
in blood

T. gondii L. donovani T. cruzi T. brucei P. falciparum, B. microti,

Nonflagellated protozoa vivax, divergens
in cardiac muscle ovale,
malariae

CLINICAL CASE
A Mexican man complains to his doctor of worsening constipation and stomach pains. On physical exam, the doctor is
surprised to find an enlarged heart on auscultation and moderate arrhythmia. Following an abdominal X-ray revealing
megacolon, the doctor makes his diagnosis. Unfortunately, the treatments she offers are only symptomatic.

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 Trypanosoma cruzi Chagas’ Disease,
American Trypanosomiasis
CLINICAL PRESENTATION
acute: chagoma, Romaña’s sign, congestive heart failure, myocarditis (rare)
chronic: arrhythmias, dilated cardiomyopathy, megacolon, megaesophagus
PATHOBIOLOGY
reservoir in South and Central American animals, transmitted by reduviid bug vector → reduviid bug leaves
protozoan-containing feces at bite site → host scratches protozoan into skin
acute phase: diagnostic chagoma (inflammatory nodule at bite site) → protozoan enters bloodstream and
lymphatics → infects tissue, especially cardiac muscle → usually self-limiting inflammation, may cause congestive
heart failure, myocarditis
chronic phase: may lead to inflammation around cardiac tissue or colonic nerves → cardiac arrhythmias, dilated
cardiomyopathy, megacolon, dysphagia from megaesophagus
DIAGNOSIS
acute:
flagellated protozoa in blood
xenodiagnosis (allow uninfected reduviid bugs to bite patient, then examine bugs for protozoa)
chronic:
serology
nonflagellated protozoa in cells
TREATMENT
acute: nifurtimox, benznidazole
chronic: no treatment
QUICK FACTS
Romaña’s sign (soft tissue and lymphoid swelling around the eyes) occurs when the protozoan enters through the conjunctiva.
In chronic Chagas’ disease, it is unclear if tissue damage results from direct infection by the protozoan or by a slow, chronic
inflammatory response.

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 Trypanosoma brucei gambiense, Sleeping Sickness,
Trypanosoma brucei rhodesiense African Trypanosomiasis
Protozoa

Antigenic variation of
the surface coat allows
protozoan to evade
immune response

Systemic infection

T. gondii L. donovani T. cruzi T. brucei P. falciparum, B. microti,

vivax, divergens
ovale,
Protozoa in blood malariae

CLINICAL CASE
An East African man is asked to leave his job after repeatedly falling asleep. He visits the doctor hoping to cure his
somnolence, as well as accompanying headache and dizziness. During the interview, the patient explains that he had suffered
recurring bouts of fever and enlarged lymph nodes before the sleepiness started. The doctor decides to perform a lumbar
puncture, and after finding a flagellated protozoan in the CSF, he plans to start the patient on melarsoprol.

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 Trypanosoma brucei gambiense, Sleeping Sickness,
Trypanosoma brucei rhodesiense African Trypanosomiasis
CLINICAL PRESENTATION
enlarged lymph nodes, fever (recurring)
somnolence, coma
PATHOBIOLOGY
reservoir in animals or humans, transmitted by tsetse fly vector → tsetse fly bite releases protozoan into
bloodstream →divides in blood → host immune response → hard red ulcer at bite site ⫹ enlarged lymph
nodes, fever
some protozoa change surface coat to escape host antibodies → divide in blood → host immune response → enlarged
lymph nodes, fever (cycle recurs every 2 weeks)
after many cycles, protozoa may escape immune response and infect CNS → encephalitis, meningitis →
somnolence (sleeping sickness), coma
DIAGNOSIS
blood, lymph node, CSF: flagellated protozoan
TREATMENT
T. b. gambiense:
suramin (before CNS infection because does not cross BBB)
eflornithine (with CNS infection)
T. b. rhodesiense:
suramin (before CNS infection because does not cross BBB)
melarsoprol (with CNS infection)
QUICK FACTS
West African Sleeping Sickness is caused by T. b. gambiense and occurs slowly; East African Sleeping Sickness is caused by
T. b. rhodesiense and occurs quickly.
Trypanosoma varies its coat by moving different surface genes into transcriptionally active sites (gene shuffling).

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 Plasmodium falciparum, vivax, ovale, malariae Malaria
Mosquito Protozoa

Sporozoite

Schizonts
in RBC
Systemic infection

Schizonts

Merozoites RBC
T. gondii L. donovani T. cruzi T. brucei P. falciparum, B. microti,
Characteristic trophozoite vivax, divergens
in RBC (“small rings” in P. falciparum) ovale,
malariae

CLINICAL CASE
A student reports to his college clinic complaining of “the flu.” He explains that he has been suffering from intermittent
headaches, fever, and muscle aches. Assuming the flu, the physician sends the student home with acetaminophen. Now, days
later, the student returns to the clinic EW with chills, extreme fever, and debilitating fatigue. Physical exam also reveals yellow
sclera and severe splenomegaly. CBC reveals low hematocrit, and urinalysis shows hemoglobinuria. Alarmed, the EW doctor
questions the student about recent travels and learns that he has just returned from a visit to India. A blood smear showing
ring shapes confirms the diagnosis, and the patient is begun on mefloquine.

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 Plasmodium falciparum, vivax, ovale, malariae Malaria
CLINICAL PRESENTATION
anemia, fever, chills in cycles: P. falciparum: irregular
P. vivax/ovale: every 2 days
P. malariae: every 3 days
P. falciparum complications: cerebral malaria, kidney failure, lung edema
PATHOBIOLOGY
transmitted by Anopheles mosquito → mosquito bite releases sporozoite into bloodstream → carried to liver and infects hepatocytes → in hepatocytes, sporozoite divides into merozoites
→ liver cells burst, releasing merozoites → merozoites invade RBCs → in RBCs, merozoites develop into trophozoites with characteristic shapes → trophozoite divides into many merozoites
→ merozoites burst infected RBCs and spread to other RBCs → with each burst cycle, fever, chills, and anemia are manifested
infected RBCs become less flexible → accumulated and destroyed in spleen → splenomegaly
P. vivax/ovale (relapsing infection): some sporozoites do not immediately divide in hepatocytes → form dormant hypnozoites in liver → relapses possibly months to years later
P. falciparum (most severe infection): knobs formed in infected RBCs → knobs cause RBCs to stick to capillary/venule walls → vessel occlusion and hemorrhage → damage to the brain
(cerebral malaria), kidneys, and lungs
to complete cycle, some merozoites become male and female gametocytes → ingested by mosquito → gametocytes fuse to form diploid zygote → zygote generates haploid sporozoites that are
stored in mosquito salivary glands
DIAGNOSIS
blood smear:
P. falciparum P. vivax/ovale P. malariae
trophozoite shapes small rings large, irregular rings band or rectangular
gametocyte shapes banana-like round round
TREATMENT
prophylaxis and treatment:
chloroquine (North America, Central America, Haiti, Middle East)
mefloquine for chloroquine-resistant P. falciparum (in Africa, South America, South and Southeast Asia)
primaquine for P. vivax/ovale dormant liver infections
QUICK FACTS
Malaria infects between 200 and 300 million people in tropical climates every year. One million infected children, mostly in Africa, die annually.
Several blood disorders overlap with malaria geographically because they may confer resistance: (1) sickle cell trait—protects against P. falciparum because the RBCs are too weak to support parasite;
(2) RBCs are lacking the antigens Duffy a and b—protects against P. vivax because the protozoan binds to these antigens; (3) thalassemia; and (4) glucose-6-phosphate dehydrogenase deficiency.
Some P. falciparum infections are known as “blackwater fever” because of the hemoglobinuria that results from RBC lysis and kidney damage.
P. vivax/ovale infects young RBCs, P. malariae infects old RBCs, and P. falciparum infects all RBCs. Hence, P. falciparum infections are most severe.

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 Babesia microti, divergens Babesiosis
Protozoa
Ixodes
scapularis tick
Merozoites
in RBC
Sporozoite

Merozoites Systemic infection

RBC
No pre-erythrocyte Characteristic trophozoite
hepatic stage in RBC (“pear shaped” T. gondii L. donovani T. cruzi T. brucei P. falciparum, B. microti,
forms or piroplasms) vivax, divergens
ovale,
malariae

CLINICAL CASE
An elderly New England man presents to his physician with high fevers, chills, and weakness. On exam, he appears icteric, and
laboratory results showed severe anemia, low haptoglobin, and high unconjugated bilirubin. His physician, who had graduated
from medical school in south Asia, initially suspected malaria. However, the physician made the correct diagnosis after
eliciting a more detailed history, in which the patient recalled removing a tick from his skin approximately 5 weeks earlier.
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 Babesia microti, divergens Babesiosis
CLINICAL PRESENTATION
hemolytic anemia, fevers, chills
PATHOBIOLOGY
transmitted by Ixodes tick → tick release sporozoites into dermis → sporozoites travel to bloodstream → sporozoites infect
RBCs → sporozoites become trophozoites → trophozoites divide and become merozoites → merozoites lyse RBCs →
released merozoites infect more RBCs
DIAGNOSIS
blood smear: “pear-shaped”
PCR
serology
TREATMENT
atovaquone plus azithromycin
quinine plus clindamycin
QUICK FACTS
Asplenic, immunosuppressed, and HIV⫹ patients are particularly vulnerable to severe babesiosis.
Babesiosis should be suspected in patients with Lyme disease because coinfection by Ixodes is common.
Removing ticks within 48 hours reduces transmission because sporozoites typically move to the host on the third day of
attachment. Study Tip
Babesiosis can also be transmitted via blood transfusion from asymptomatic donors.
B. microti is the predominant species in the U.S., whereas B. divergens is the predominant species in Europe. Some microorganisms
The natural reservoir for B. microti is in mice; humans are accidental hosts. transmitted by the Ixodes
tick:
Borrelia burgdorferi
(Lyme disease)
Babesia microti
(Babesiosis)

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 Helminths
Helminths

transmitted by ingestion transmitted by contact transmitted by bite

intestinal infection tissue infection intestinal infection tissue infection tissue infection

nematodes platyhelminthes nematodes platyhelminthes nematodes platyhelminthes nematodes

(roundworms) (flatworms) (roundworms) (flatworms) (roundworms) (flatworms) (roundworms)

A. lumbricoides E. vermicularis Cestodes T. spiralis Cestodes S. stercoralis N. americanus, Trematodes Filariae

(tapeworms) (tapeworms) A. duodenale (flukes)

T. saginata T. solium E. granulosus Schistosoma species O. volvulus W. bancrofti

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 Helminths
Helminths are multicellular parasites (vs. protozoa, which are unicellular parasites).

Structurally, they are organized as follows:

Helminths

Nematodes Platyhelminthes
(roundworms) (flatworms)

Structure:
adult form: nonsegmented,
with complete digestive Cestodes Trematodes
tube (mouth to anus) (tapeworms) (flukes)
Examples:
A. lumbricoides Structure: Structure:
E. vermicularis adult form: adult form: nonsegmented,
T. spiralis segmented, with incomplete digestive
S. stercoralis scolex and system; in some species,
N. americanus proglottids females reside within
A. duodenale grooves (schists) of males
O. volvulus Examples:
W. bancrofti T. saginata Examples:
T. solium Schistosoma species
E. granulosus

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 Ascaris lumbricoides Ascariasis
Rough surface Helminths

transmitted by ingestion

intestinal infection
30 cm

nematodes
Female and egg (roundworms)

A. lumbricoides E. vermicularis

CLINICAL CASE
A man in Louisiana develops coughing, fever, and abdominal pain. His doctor orders a series of X-rays that show pulmonary
infiltrates characteristic of pneumonia, as well as intestinal images consistent with obstruction. On CBC, the patient has
increased eosinophils. The doctor examines a stool sample from the patient and discovers microscopic oval eggs with rough
surfaces. The doctor makes a diagnosis, administers pyrantel pamoate, and forewarns the patient to expect worms in his stool.

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 Ascaris lumbricoides Ascariasis
CLINICAL PRESENTATION
asymptomatic
ascaris pneumonia
malnutrition
PATHOBIOLOGY
fecal–oral transmission → eggs ingested in contaminated soil → hatch in small intestine → larvae invade intestinal wall
→ enter bloodstream and transported to lungs → enter alveoli and ascend toward trachea → respiratory tract
inflammation → may cause pneumonia
larvae pass from trachea to pharynx → swallowed → larvae mature into adults in small intestine → adults swim freely in
lumen and consume food ingested by host → host malnutrition
adults lay eggs that pass in feces
DIAGNOSIS
stool: detect eggs with rough surface
eosinophilia
TREATMENT
pyrantel pamoate
mebendazole, albendazole
QUICK FACTS
Ascaris is common to tropical climates, causing several hundred million infections annually; in the U.S., infections are found
in the South.
Some complications include intestinal occlusion by a mass of worms (worm ball) or biliary obstruction by a single worm
migrating up the biliary tree. Study Tip
Dog ascaris (Toxocara canis) can also infect humans, but their larvae migrate to many organs instead of entering the respiratory
tract (visceral larva migrans); the effects are diffuse and include hepatosplenomegaly and blindness.
Ascariasis is the most
common helminthic
infection.

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 Enterobius vermicularis Pinworm
Helminths

transmitted by ingestion

intestinal infection

Female and egg

nematodes
(roundworms)

A. lumbricoides E. vermicularis

CLINICAL CASE
A mother brings her child to a developmental specialist. She is concerned because of what she considers “negative” behavior.
When asked to elaborate, she explains that her child scratches his anal region continuously, even in public places. Indeed,
even his kindergarten teacher mentioned it in the last parent–teacher meeting. Before pursuing psychological studies, the
specialist recommends a “Scotch tape” test based on past cases with similar complaints.

137

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 Enterobius vermicularis Pinworm
CLINICAL PRESENTATION
perianal itchiness
PATHOBIOLOGY
fecal–oral transmission → eggs ingested from contaminated surfaces → hatch in duodenum and jejunum → mature into
adults in ileum and large intestine → mate in colon → at night, females migrate out of rectum to perianal skin →
lay eggs → perianal itchiness
scratching contaminates hand → eggs spread
DIAGNOSIS
“Scotch tape” technique: Adhere tape to perianal region, remove tape, and examine for eggs
TREATMENT
mebendazole, albendazole
pyrantel pamoate
QUICK FACTS
Pinworm infections are the most common worm infections in the U.S. that primarily infects children.
Whipworm (Trichuris trichiura) is also a nematode with a similar life cycle; however, it may cause diarrhea (even intestinal
ulceration and hemorrhage in severe cases) but not perianal itching.

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 Taenia saginata Beef Tapeworm
Scolex Gravid proglottids Helminths

Uterus
transmitted by ingestion
Genital
Sucker pore
intestinal infection

Immature proglottids platyhelminthes

(flatworms)
Yolk
Ovary
Genital pore
Testes cestodes
Uterus Gravid (tapeworms)
proglottids
and eggs
Mature proglottids in stool
T. saginata T. solium

CLINICAL CASE
A cow rancher arrives at the EW terrified after discovering a wormlike structure protruding from his anus. After reassuring the
man and taking a proper history and physical, the doctor examines a stool sample. As expected, the doctor finds rectangular
proglottid segments with the naked eye and uses a low-power microscope to detect eggs. The doctor prescribes niclosamide
and a cathartic, confident that the patient will be cured with a single dose. The doctor also instructs the patient to avoid poorly
cooked beef in the future.

138

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 Taenia saginata Beef Tapeworm
CLINICAL PRESENTATION
asymptomatic
malnutrition, abdominal discomfort
PATHOBIOLOGY
larvae found as cystercerci in cow muscle → ingested in poorly cooked beef → in small intestine, larvae mature and grow →
adults consist of scolex (head) and numerous proglottids (autonomous segments) → scolex attaches to intestinal
wall, proglottids containing eggs passed in feces → cows ingest eggs to complete cycle
worm consumes food ingested by host → malnutrition
DIAGNOSIS
stool: proglottids, eggs
TREATMENT
niclosamide ⫹ cathartic
praziquantel
QUICK FACTS
By adding proglottids, the adult worm may extend up to 10 meters long.
Fish tapeworm (Diphyllobothrium latum), acquired from poorly cooked fish, most characteristically leads to vitamin B12
deficiency (megaloblastic anemia).
In contrast to T. solium, T. saginata has no hooks on its scolex.

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 Taenia solium Pork Tapeworm
Scolex Gravid proglottids Helminths

Uterus
Hooks transmitted by ingestion
Genital
Sucker pore
intestinal infection tissue infection

Immature proglottids platyhelminthes platyhelminthes

(flatworms) (flatworms)
Yolk
Ovary
Genital pore Cestodes
Testes Cestodes
Uterus Gravid (tapeworms) (tapeworms)
proglottids
and eggs
Mature proglottids in stool
T. saginata T. solium T. solium E. granulosus

CLINICAL CASE
A Vietnamese immigrant of 10 years presents with severe headaches and seizures. A physical exam reveals several nodules
across her body. Concerned about a neurologic disease, the doctor first orders a head CT scan that shows five calcified cysts.
This observation, along with high eosinophils on a CBC, prompts the doctor to perform a biopsy of a nodule. A diagnosis is
made after the doctor finds cysts in the nodule, and the patient is begun immediately on praziquantel and steroids.

139

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 Taenia solium Pork Tapeworm
CLINICAL PRESENTATION
intestinal infection: asymptomatic; malnutrition, abdominal discomfort
tissue infection: cysticercosis (neurologic defects, blindness)
PATHOBIOLOGY
intestinal infection:
larvae found as cystercerci in pig muscle → ingested in poorly cooked pork → in small intestine, larvae mature and
grow → adults consist of scolex (head) and numerous proglottids (autonomous segments) → scolex attaches
to intestinal wall, proglottids containing eggs passed in feces → worm consumes food ingested by host →
malnutrition
tissue infection:
humans ingest eggs from infected feces (vs. larvae in pork) → eggs hatch into oncospheres in small intestine →
oncospheres penetrate intestinal wall and travel to other tissues → form cysticerci containing larvae, especially
in brain, skeletal muscle, and eye
cysts grow slowly → neurologic defects (seizures, focal symptoms) or blindness → when cysts die after several years,
increased inflammation → aggravated symptoms
DIAGNOSIS
intestinal infection:
proglottids, eggs in stool
tissue infection:
calcified cysticerci in muscle, brain on X-ray, CT
eosinophilia in muscle, brain on X-ray, CT
TREATMENT
intestinal infection: niclosamide ⫹ cathartic; praziquantel
tissue infection: praziquantel or albendazole ⫹ steroids (reduce inflammation from dying cysts)
QUICK FACTS
In cysticercosis, larvae sometimes can be detected swimming in the vitreous humor of the eyes.

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 Trichinella spiralis Trichinosis
Helminths

transmitted by ingestion

tissue infection

nematodes
(roundworms)

Cysts with larvae in skeletal muscle

T. spiralis

CLINICAL CASE
A pig farmer visits his doctor with muscle aches, fever, and periorbital and facial edema. These symptoms were preceded
2 weeks earlier by an upset stomach and diarrhea. Blood labs show eosinophilia, ↑ IgE, and muscle enzymes. Because the
symptoms are not severe, the doctor opts not to perform a muscle biopsy; however, if she had performed the biopsy, she
would have expected to find cysts.

140

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 Trichinella spiralis Trichinosis
CLINICAL PRESENTATION
gastroenteritis, myalgia
PATHOBIOLOGY
reservoir in pigs → encysted larvae ingested from uncooked meat → larvae mature into adults in small intestine → adults
mate and eggs mature to larvae → larvae penetrate intestinal wall into bloodstream → may cause diarrhea, pain
larvae carried by blood to skeletal muscle (often extraoculars, masseters, tongue, diaphragm) → initial inflammation →
myalgia → larvae form fibrous cyst → cysts can last for years, may calcify
if many encysted larvae ingested → severe infection → larvae migrate to heart and brain → myocarditis, encephalitis
DIAGNOSIS
eosinophilia
striated muscle biopsy: cysts with larvae
serology (for chronic infection)
TREATMENT
mebendazole/thiabendazole (against adult worms in small intestine)
no treatment to remove cysts from muscle
steroids for severe myositis, myocarditis
QUICK FACTS
In the U.S., trichinosis infections have decreased following legislation that prohibits feeding pigs uncooked garbage.

Study Tip
Trichinosis is the most
common parasitic cause of
myocarditis.

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 Echinococcus granulosus Dog Tapeworm
Scolex Helminths

Scolex
Hooks
transmitted by ingestion

tissue infection
Sucker
Three
proglottids
platyhelminthes
(flatworms)

Cestodes
(tapeworms)

Adult worm
T. solium E. granulosus

CLINICAL CASE
A woman presents with abdominal discomfort. The discomfort begins as a mild sensation in the RUQ but has become
progressively more painful. Physical exam reveals hepatomegaly. The doctor decides to perform an abdominal CT, which
shows a large circular mass in the liver with multiple daughter cysts encapsulated by “eggshell” calcifications. Serology, but
not stool samples, is used to make a diagnosis. The doctor elects to surgically remove the mass but first neutralizes the cyst
contents by injecting ethanol.

141

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 Echinococcus granulosus Dog Tapeworm
CLINICAL PRESENTATION
echinococcosis or hydatid cyst disease
PATHOBIOLOGY
eggs found in dog feces → humans ingest eggs → eggs hatch into larvae in small intestine → larvae penetrate intestinal wall
and travel to other tissues → form hydatid cysts in liver, lung, or brain
cysts grow and divide → expansion causes organ displacement → organ dysfunction, especially in liver → enlarged
cyst may also rupture:
• release of antigenic cyst contents → severe anaphylaxis
• release of larvae → infection spreads
DIAGNOSIS
X-ray or CT: cysts (presence of daughter cysts within hydatid cyst is pathognomonic)
serology
TREATMENT
surgery to remove cysts (rupture is a major complication)
albendazole
QUICK FACTS
Because rupture may disseminate the infection during surgery, the cyst contents are first killed by injecting larvicidal solutions.
Echinococcosis is common in sheepherders who acquire the tapeworm from sheep dog feces; the sheep dogs become infected
after eating raw sheep meat.
Echinococcus, composed of a scolex and only three proglottids, is very small relative to other tapeworms.

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 Strongyloides stercoralis Strongyloidiasis
Helminths

transmitted by contact

Adult and larvae

intestinal infection

nematodes
(roundworms)

S. stercoralis N. americanus,
A. duodenale

CLINICAL CASE
A South Carolina woman visits her doctor after developing diarrhea. The doctor performs a blood test and finds elevated
eosinophils. Suspecting a parasite infection, the doctor examines a stool specimen. After finding larvae without eggs, the
doctor solidifies a diagnosis upon learning that the patient frequently walks around her house barefoot. The patient is started
on thiabendazole to cure the symptoms as well as to prevent complications such as peritonitis.

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 Strongyloides stercoralis Strongyloidiasis
CLINICAL PRESENTATION
asymptomatic
pneumonia
gastroenteritis
diffuse autoinfection (in immunodeficient)
PATHOBIOLOGY
fecal–cutaneous transmission → infectious (filariform) larvae penetrate skin of feet, causing local itching → enter
bloodstream and transported to lungs → enter alveoli and ascend toward trachea → respiratory tract inflammation
→ may cause pneumonia
larvae pass from trachea to pharynx → swallowed → larvae mature into adults in small intestine → mate → females
invade mucosa and lay eggs → eggs hatch into larvae in intestinal wall → inflammation → pain, diarrhea
larvae may:
• exit with feces → contaminate soil
• penetrate intestinal wall → enter bloodstream and transported to lungs → infectious cycle repeated (autoinfection)
DIAGNOSIS
stool: detect larvae, not eggs (vs. hookworm)
eosinophilia
“string test” for duodenal pathogens: swallow a long string to pull out larvae
TREATMENT
ivermectin, thiabendazole
QUICK FACTS
When Strongyloides larvae tunnel through the intestinal wall, bacteria may follow into the peritoneum and cause peritonitis.
In immunodeficient patients with autoinfection, invasive larvae may infect other organs in addition to the lungs.
Strongyloidiasis is associated with HTLV-1 infection.

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 Necator americanus, Hookworm
Ancylostoma duodenale
Helminths

Suckers used to attach

to intestinal mucosa
transmitted by contact

intestinal infection

nematodes
(roundworms)

Adult

S. stercoralis N. americanus,
A. duodenale

CLINICAL CASE
A child from a small Alabama community presents with severe weakness and pallor. A CBC shows reduced hematocrit with
hypochromic microcytic RBCs as well as increased eosinophils. To investigate the possibility of parasites, the physician orders
a stool sample in which she finds numerous eggs. The physician prescribes mebendazole and iron tablets and explains that
the child may have acquired the illness by walking barefoot.
143

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 Necator americanus, Hookworm
Ancylostoma duodenale
CLINICAL PRESENTATION
pneumonia
gastroenteritis
anemia
PATHOBIOLOGY
fecal–cutaneous transmission → infectious (filariform) larvae penetrate skin of feet, causing local itching → enter
bloodstream and transported to lungs → enter alveoli and ascend toward trachea → respiratory tract inflammation
→ may cause pneumonia
larvae pass from trachea to pharynx → swallowed → larvae mature into adults in small intestine → attach to mucosa
via cutting plates or teeth → may cause gastroenteritis initially → secrete anticoagulant and suck blood from host
→ anemia
in lumen, adults mate → eggs passed in feces → eggs hatch to infectious larvae in soil
DIAGNOSIS
stool: detect eggs, not larvae (vs. Strongyloides stercoralis)
eosinophilia
TREATMENT
mebendazole
pyrantel pamoate
iron and folic acid for anemia
QUICK FACTS
Cat and dog hookworm larvae can also infect humans but cannot invade the bloodstream; as a result, the larvae travel
subcutaneously causing a trail of itchiness until they die (cutaneous larva migrans).

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 Schistosoma species Schistosomiasis, Blood Fluke,
Katayama Fever
Helminths

transmitted by contact

Female tissue infection

Male
platyhelminthes
(flatworms)

Trematodes
(flukes)
Adult male and female paired

Schistosoma species

CLINICAL CASE
An African man comes to the EW after vomiting blood. He also reports that his stools have been dark for the last few years. In
the history, the patient denies alcohol use and states that freshwater fishing is a hobby. Endoscopy shows esophageal varices,
and stool specimens contain eggs. The patient is started on praziquantel.

An African woman visits her doctor after urinating blood. In her history, she states that she worked in freshwater rice fields
before coming to the U.S. Cytoscopic examination of the bladder shows inflammatory lesions, and urinalysis demonstrates
eggs. Imaging reveals hydronephrosis of the right kidney and a mass extending from the right ureter into the bladder. She is
started on praziquantel. 144

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 Schistosoma species Schistosomiasis, Blood Fluke,
Katayama Fever
CLINICAL PRESENTATION
acute:
itchiness at site of infection
fever, chills, lymphadenopathy
chronic:
periportal fibrosis and consequences
intestinal polyps
bladder inflammation, hematuria, carcinoma
PATHOBIOLOGY
larvae (cercariae) released by snails into fresh water → penetrate human flesh and enter bloodstream → travel to portal vein → larvae mature into adults → adult pairs
migrate against portal flow to various venous plexuses:
• in intestinal venous plexus (S. mansoni, S. japonicum) → mate → eggs released → acute inflammatory response (Katayama fever, chills, lymphadenopathy) → eggs
exit to intestinal lumen → passed in feces
some eggs carried to portal circulation → chronic inflammatory response → periportal fibrosis and consequences (portal hypertension, splenomegaly, esophageal varices)
some eggs lodge in intestinal wall → chronic inflammatory response → intestinal inflammation and consequences (polyps)
• in bladder venous plexus (S. haematobium) → mate → eggs released → acute inflammatory response (Katayama fever, chills, lymphadenopathy) → eggs exit to
bladder lumen → passed in urine
some eggs lodge in bladder wall → chronic inflammatory response → bladder inflammation and consequences (hematuria, bladder carcinoma)
excreted eggs hatch in fresh water and infect snails
DIAGNOSIS
feces or urine: detect eggs, eosinophilia
TREATMENT
praziquantel
QUICK FACTS
Whereas schistosomal eggs are highly immunoreactive, the adult forms evade the immune system by coating with host antigens; hence, adult forms survive for years in the venous
plexuses.
Whereas most bladder cancers are transitional cell carcinomas, S. haematobium-associated bladder cancers are more frequently squamous cell carcinomas.

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 Onchocerca volvulus River Blindness, Onchocerciasis
Helminths

transmitted by bite

tissue infection

nematodes
(roundworms)

Filariae
Microfilaria in skin

O. volvulus W. bancrofti

CLINICAL CASE
A traveling physician visits a remote riverside village in a South American country and discovers that most of the older village
inhabitants are blind. On physical exam of some of the members, she notes skin nodules and hyperpigmented rashes. To
prevent other village members from becoming blind, she administers donated ivermectin to many people in the village and
urges mosquito control.

145

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 Onchocerca volvulus River Blindness, Onchocerciasis
CLINICAL PRESENTATION
skin nodules
thick, hyperpigmented pruritic rash
blindness
PATHOBIOLOGY
transmitted by black fly near rivers → black fly bite releases larvae into skin → larvae move through subcutaneous tissue →
mature to adults → fibrosis around adults, creating subcutaneous nodules → adults mate and release microfilariae
into subcutaneous tissue
microfilariae move subcutaneously throughout the body → inflammation → thickened, hyperpigmented pruritic rash
microfilariae may reach eye → inflammation → blindness (river blindness)
microfilariae can be ingested by mosquito → form larvae in mosquito, completing cycle
DIAGNOSIS
skin biopsy: detect microfilariae (adults in nodules)
TREATMENT
ivermectin (only effective against microfilariae, not adults)
surgical removal of nodules
QUICK FACTS
In endemic areas, this disease causes blindness in large numbers of people.

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 Wuchereria bancrofti Filariasis, Elephantiasis
Helminths

transmitted by bite

tissue infection

nematodes
(roundworms)

Microfilaria in blood
Filariae

O. volvulus W. bancrofti

CLINICAL CASE
A patient from a tropical village has an enormously swollen scrotum and lower extremity. The skin around the swelling has
become scaly and thick. The patient remembers feeling enlarged nodes in the groin months before the swelling began, but
because of poor health resources in the area, he never saw a physician. Samples of his blood drawn at night show wormlike
organisms under a microscope. A visiting doctor strongly recommends that the patient and other villagers sleep with a
mosquito net to prevent more infections.

146

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 Wuchereria bancrofti Filariasis, Elephantiasis
CLINICAL PRESENTATION
fever
edema and scaly skin of legs and genitalia
PATHOBIOLOGY
transmitted by mosquito → mosquito bite releases larvae (microfilariae) into bloodstream → larvae carried to lymph nodes of
genitals and lower extremities → larvae mature to adults over the span of a year → adults mate and release larvae
into bloodstream
adult worms trigger inflammation → fever, swelling of lymph nodes
with repeated infections → fibrosis around dead adult worms in lymph nodes → obstruction of lymphatic drainage →
edema and scaly skin in legs, scrotum (elephantiasis)
DIAGNOSIS
blood: detect microfilariae (most common at night)
TREATMENT
diethylcarbamazine (only effective against microfilariae, not adults)
QUICK FACTS
Brugia malayi is a helminth that causes elephantiasis endemic to Malaysia and Southeast Asia.
Larval forms have a nocturnal schedule: They emerge in the blood at night.

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 Prions Mad Cow Disease, Creutzfeldt-Jakob Disease
CLINICAL CASE
A 75-year-old man is brought by his family for evaluation of behavioral changes. The man was previously highly functional
but has developed confusion, inattentiveness, and insomnia that have progressively worsened over a month. The family also
notes his gait is unstable. On exam, he has signs of cerebellar ataxia and myoclonus. Workup including CT, MRI/MRA, and
toxicology screen is unremarkable, and Gram stain, viral PCR, and cytology of CSF are unrevealing. Over the next month, the
patient has worsening myoclonic jerking and cognitive impairment, and on the fourth week, he dies. Autopsy reveals myriad
microscopic holes throughout the cerebral cortex giving a sponge-like appearance.

147

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