Amebiasis

[Entamoeba histolytica]

Cyst of E. histolytica/E. dispar stained with trichrome. Note the chromatoid body with blunt
ends (red arrow).

Trophozoites of E. histolytica with ingested erythrocytes stained with trichrome. The ingested
erythrocytes appear as dark inclusions. The parasite above show nuclei that have the typical
small, centrally located karyosome, and thin, uniform peripheral chromatin.
Entamoeba histolytica trophozoites in colon tissue stained with H&E.

Causal Agents

Several protozoan species in the genus Entamoeba colonize humans, but not all of them are
associated with disease. Entamoeba histolytica is well recognized as a pathogenic ameba,
associated with intestinal and extraintestinal infections. The other species are important because
they may be confused with E. histolytica in diagnostic investigations.

Life Cycle
Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas
trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by
ingestion of mature cysts in fecally contaminated food, water, or hands.  Excystation occurs
in the small intestine and trophozoites are released, which migrate to the large intestine. The
trophozoites multiply by binary fission and produce cysts , and both stages are passed in the
feces . Because of the protection conferred by their walls, the cysts can survive days to weeks
in the external environment and are responsible for transmission. Trophozoites passed in the
stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to
the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen
( : noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their
stool.  In some patients the trophozoites invade the intestinal mucosa ( : intestinal disease), or,
through the bloodstream, extraintestinal sites such as the liver, brain, and lungs ( :
extraintestinal disease), with resultant pathologic manifestations. It has been established that the
invasive and noninvasive forms represent two separate species, respectively E. histolytica and E.
dispar. These two species are morphologically indistinguishable unless E. histolytica is observed
with ingested red blood cells (erythrophagocystosis).  Transmission can also occur through
exposure to fecal matter during sexual contact (in which case not only cysts, but also
trophozoites could prove infective).

Geographic Distribution

Worldwide, with higher incidence of amebiasis in developing countries. In industrialized

countries, risk groups include male homosexuals, travelers and recent immigrants, and
institutionalized populations.

Clinical Presentation

A wide spectrum, from asymptomatic infection ("luminal amebiasis"), to invasive intestinal

amebiasis (dysentery, colitis, appendicitis, toxic megacolon, amebomas), to invasive
extraintestinal amebiasis (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and
genital amebic lesions).

Trypanosomiasis, African
[Trypanosoma brucei gambiense] [Trypanosoma brucei rhodesiense]

Trypansoma brucei ssp. in a thick blood smear stained with Giemsa.

Trypanosoma brucei ssp. in a thin blood smear stained with Giemsa.

Causal Agents

Protozoan hemoflagellates belonging to the complex Trypanosoma brucei. Two subspecies that
are morphologically indistinguishable cause distinct disease patterns in humans: T. b. gambiense
causes West African sleeping sickness and T. b. rhodesiense causes East African sleeping
sickness. (A third member of the complex, T. b. brucei, under normal conditions does not infect
humans.

Life Cycle
During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects
metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass
into the bloodstream . Inside the host, they transform into bloodstream trypomastigotes , are
carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and
continue the replication by binary fission . The entire life cycle of African trypanosomes is
represented by extracellular stages. The tsetse fly becomes infected with bloodstream
trypomastigotes when taking a blood meal on an infected mammalian host , ). In the fly’s
midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission ,
leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary
glands and continue multiplication by binary fission . The cycle in the fly takes approximately
3 weeks. Humans are the main reservoir for Trypanosoma brucei gambiense, but this species can
also be found in animals. Wild game animals are the main reservoir of T. b. rhodesiense.

Geographic Distribution

T. b. gambiense is found in foci in large areas of West and Central Africa. The distribution of T.
b. rhodesiense is much more limited, with the species found in East and Southeast Africa.

Clinical Presentation
Infection occurs in 3 stages. A trypanosomal chancre can develop on the site of inoculation. This
is followed by a hemolymphatic stage with symptoms that include fever, lymphadenopathy, and
pruritus. In the meningoencephalitic stage, invasion of the central nervous system can cause
headaches, somnolence, abnormal behavior, and lead to loss of consciousness and coma. The
course of infection is much more acute with T. b. rhodesiense than T. b. gambiens.

Hookworm
[Ancylostoma braziliense] [Ancylostoma caninum] [Ancylostoma duodenale] [Necator
americanus]

Hookworm egg in an unstained wet mount.

Anterior end of an adult of Ancylostoma caninum, a dog parasite that has been found to produce
a rare human infection known as eosinophilic enteritis.

Causal Agent

The human hookworms include the nematode species, Ancylostoma duodenale and Necator
americanus. A larger group of hookworms infecting animals can invade and parasitize humans
(A. ceylanicum) or can penetrate the human skin (causing cutaneous larva migrans), but do not
develop any further (A. braziliense, A. caninum, Uncinaria stenocephala). Occasionally A.
caninum larvae may migrate to the human intestine, causing eosinophilic enteritis. Ancylostoma
caninum larvae have also been implicated as a cause of diffuse unilateral subacute neuroretinitis.

Life Cycle

Intestinal Hookworm Infection

Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae
hatch in 1 to 2 days. The released rhabditiform larvae grow in the feces and/or the soil , and
after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective
. These infective larvae can survive 3 to 4 weeks in favorable environmental conditions. On
contact with the human host, the larvae penetrate the skin and are carried through the blood
vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the
bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where
they reside and mature into adults. Adult worms live in the lumen of the small intestine, where
they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are
eliminated in 1 to 2 years, but the longevity may reach several years.

Some A. duodenale larvae, following penetration of the host skin, can become dormant (in the
intestine or muscle). In addition, infection by A. duodenale may probably also occur by the oral
and transmammary route. N. americanus, however, requires a transpulmonary migration phase.

Cutaneous Larval Migrans

Cutaneous larval migrans (also known as creeping eruption) is a zoonotic infection with
hookworm species that do not use humans as a definitive host, the most common being A.
braziliense and A. caninum. The normal definitive hosts for these species are dogs and cats. The
cycle in the definitive host is very similar to the cycle for the human species. Eggs are passed in
the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2
days. The released rhabditiform larvae grow in the feces and/or the soil , and after 5 to 10 days
(and two molts) they become filariform (third-stage) larvae that are infective . These infective
larvae can survive 3 to 4 weeks in favorable environmental conditions. On contact with the
animal host , the larvae penetrate the skin and are carried through the blood vessels to the heart
and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the
pharynx, and are swallowed. The larvae reach the small intestine, where they reside and mature
into adults. Adult worms live in the lumen of the small intestine, where they attach to the
intestinal wall. Some larvae become arrested in the tissues, and serve as source of infection for
pups via transmammary (and possibly transplacental) routes . Humans may also become
infected when filariform larvae penetrate the skin . With most species, the larvae cannot
mature further in the human host, and migrate aimlessly within the epidermis, sometimes as
much as several centimeters a day. Some larvae may persist in deeper tissue after finishing their
skin migration.

Geographic Distribution
Hookworm is the second most common human helminthic infection (after ascariasis).
Hookworm species are worldwide in distribution, mostly in areas with moist, warm climate.
Both N. americanus and A. duodenale are found in Africa, Asia and the Americas. Necator
americanus predominates in the Americas and Australia, while only A. duodenale is found in the
Middle East, North Africa and southern Europe.

Clinical Presentation

Iron deficiency anemia (caused by blood loss at the site of intestinal attachment of the adult
worms) is the most common symptom of hookworm infection, and can be accompanied by
cardiac complications. Gastrointestinal and nutritional/metabolic symptoms can also occur. In
addition, local skin manifestations ('ground itch') can occur during penetration by the filariform
(L3) larvae, and respiratory symptoms can be observed during pulmonary migration of the
larvae.

The most common manifestation of zoonotic infection with animal hookworm species is
cutaneous larva migrans, also known as ground itch, where migrating larvae cause an intensely
pruritic serpiginous track in the upper dermis. Less commonly, larvae may migrate to the bowel
lumen and cause an eosinophilic enteritis. In some cases of diffuse unilateral subacute retinitis,
single larvae compatible in size to A. caninum have been visualized in the affected eye.

Ascariasis
[Ascaris lumbricoides]

Adult female A. lumbricoides.

Unfertilized egg of A. lumbricoides in an unstained wet mount, 200x magnification.

Fertilized egg of A. lumbricoides in unstained wet mounts of stool, with embryos in the early
stage of development.

Causal Agents

Ascaris lumbricoides is the largest nematode (roundworm) parasitizing the human intestine.
(Adult females: 20 to 35 cm; adult male: 15 to 30 cm.)
Life Cycle:

Adult worms . live in the lumen of the small intestine. A female may produce approximately
200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but
are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks
, depending on the environmental conditions (optimum: moist, warm, shaded soil). After
infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried
via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs
(10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are
swallowed . Upon reaching the small intestine, they develop into adult worms . Between 2 and
3 months are required from ingestion of the infective eggs to oviposition by the adult female.
Adult worms can live 1 to 2 years.

Geographic Distribution:

The most common human helminthic infection. Worldwide distribution. Highest prevalence in
tropical and subtropical regions, and areas with inadequate sanitation. Occurs in rural areas of the
southeastern United States.
Clinical Presentation

Although infections may cause stunted growth, adult worms usually cause no acute symptoms.
High worm burdens may cause abdominal pain and intestinal obstruction. Migrating adult worms
may cause symptomatic occlusion of the biliary tract or oral expulsion. During the lung phase of
larval migration, pulmonary symptoms can occur (cough, dyspnea, hemoptysis, eosinophilic
pneumonitis - Loeffler's syndrome).

Balantidiasis
[Balantidium coli]

B. coli cysts in a wet mount, unstained.

B. coli trophozoite in a wet mount, 500× magnification. Note the visible cilia on the cell surface.

Balantidium coli trophozoites in colon tissue stained with hematoxylin and eosin (H&E) at 400x
magnification.

Causal Agents

Balantidium coli, a large ciliated protozoan parasite.

Life Cycle

Cysts are the parasite stage responsible for transmission of balantidiasis . The host most often
acquires the cyst through ingestion of contaminated food or water . Following ingestion,
excystation occurs in the small intestine, and the trophozoites colonize the large intestine . The
trophozoites reside in the lumen of the large intestine of humans and animals, where they
replicate by binary fission, during which conjugation may occur . Trophozoites undergo
encystation to produce infective cysts . Some trophozoites invade the wall of the colon and
multiply. Some return to the lumen and disintegrate. Mature cysts are passed with feces.

Geographic Distribution
Worldwide. Because pigs are an animal reservoir, human infections occur more frequently in
areas where pigs are raised. Other potential animal reservoirs include rodents and nonhuman
primates.

Clinical Presentation

Most cases are asymptomatic. Clinical manifestations, when present, include persistent diarrhea,
occasionally dysentery, abdominal pain, and weight loss. Symptoms can be severe in debilitated
persons.

Lymphatic Filariasis
[Brugia malayi] [Brugia timori] [Wuchereria bancrofti]

Microfilaria of W. bancrofti in a thick blood smear stained with Giemsa. Image courtesy of the
Oregon State Public Health Laboratory.
Adults of W. bancrofti. The male worm is on the left; the female is on the right.

Microfilaria of B. malayi in a thin blood smear, stained with Giemsa.

Causal Agent

The filarid nematodes Wuchereria bancrofti, Brugia malayi, and (less-commonly) B. timori.
Humans can also be infected with several zoonotic Brugia species.

Life Cycles
Brugia Malayi

Wuchereria bancrofti

Geographic Distribution

Among the agents of lymphatic filariasis, Wuchereria bancrofti is encountered in tropical areas
worldwide; Brugia malayi is limited to Asia; and Brugia timori is restricted to some islands of
Indonesia.

Clinical Presentation

Lymphatic filariasis most often consists of asymptomatic microfilaremia. Some patients develop
lymphatic dysfunction causing lymphedema and elephantiasis (frequently in the lower
extremities) and, with Wuchereria bancrofti, hydrocele and scrotal elephantiasis. Episodes of
febrile lymphangitis and lymphadenitis may occur. Persons who have newly arrived in disease-
endemic areas can develop afebrile episodes of lymphangitis and lymphadenitis. An additional
manifestation of filarial infection, mostly in Asia, is pulmonary tropical eosinophilia syndrome,
with nocturnal cough and wheezing, fever, and eosinophilia.

Bed Bugs
[Cimex hemipterus] [Cimex lectularius]

Close up of Cimex lectularius, collected in a hotel in urban Georgia.

Nymph of C. lectularius. The blue marks represent 1 mm.

Causal Agents

The two species of bed bugs (Insecta: Hemiptera: Cimicidae) usually implicated in human
infestations are Cimex lectularius and C. hemipterus. Although rare, humans may become
incidental hosts of Cimex species of bats and birds.

Life Cycle
Adults and all nymphal stages of Cimex spp. need to take blood meals from warm-blooded hosts,
which are typically humans for C. lectularius and C. hemipterus, although other mammals and
birds can be utilized in the absence of a human host. Female bed bugs lay about five eggs daily
throughout their adult lives in a sheltered location (mattress seams, crevices in box springs,
spaces under baseboards, etc). Eggs hatch in about 4-12 days into first instar nymphs which
must take a blood meal before molting to the next stage. The bugs will undergo five nymphal
stages ( , , , , ), each one requiring a blood meal before molting to the next stage, with
the fifth stage molting into an adult . Nymphs, although lacking wing buds, resemble smaller
versions of the adults. Nymphs and adults take about 5-10 minutes to obtain a full blood meal.
The adults may take several blood meals over several weeks, assuming a warm-blooded host is
available. Mating occurs off the host and involves a unique form of copulation called ‘traumatic
insemination’ whereby the male penetrates the female’s abdominal wall with his external
genitalia and inseminates into her body cavity. Adults live 6-12 months and may survive for long
periods of time without feeding.

Geographic Distribution

Cimex lectularius is cosmopolitan in distribution; C. hemipterus is distributed in the tropics and

sub-tropics

Clinical Presentation
Although bed bugs have been found naturally-infected with blood-borne pathogens, they are not
effective vectors of disease. The primary medical importance is inflammation associated with
their bites (due to allergic reactions to components in their saliva)

Schistosomiasis Infection
[Schistosoma haematobium] [Schistosoma intercalatum] [Schistosoma japonicum]
[Schistosoma mansoni] [Schistosoma mekongi]

Egg of S. mansoni in unstained wet mounts.

Egg of S. haematobium in a wet mount of a urine concentrate.

Egg of S. japonicum in an unstained wet mount of stool.

Causal Agents

Schistosomiasis is caused by digenetic blood trematodes. The three main species infecting
humans are Schistosoma haematobium, S. japonicum, and S. mansoni. Two other species, more
localized geographically, are S. mekongi and S. intercalatum. In addition, other species of
schistosomes, which parasitize birds and mammals, can cause cercarial dermatitis in humans.

Life Cycle

Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release
miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the
snail include 2 generations of sporocysts . and the production of cercariae . Upon release
from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed
their forked tail, becoming schistosomulae . The schistosomulae migrate through several
tissues and stages to their residence in the veins ( , ). Adult worms in humans reside in the
mesenteric venules in various locations, which at times seem to be specific for each species .
For instance, S. japonicum is more frequently found in the superior mesenteric veins draining the
small intestine , and S. mansoni occurs more often in the superior mesenteric veins draining
the large intestine . However, both species can occupy either location, and they are capable of
moving between sites, so it is not possible to state unequivocally that one species only occurs in
one location. S. haematobium most often occurs in the venous plexus of bladder , but it can
also be found in the rectal venules. The females (size 7 to 20 mm; males slightly smaller) deposit
eggs in the small venules of the portal and perivesical systems. The eggs are moved
progressively toward the lumen of the intestine (S. mansoni and S. japonicum) and of the bladder
and ureters (S. haematobium), and are eliminated with feces or urine, respectively . Pathology
of S. mansoni and S. japonicum schistosomiasis includes: Katayama fever, hepatic perisinusoidal
egg granulomas, Symmers’ pipe stem periportal fibrosis, portal hypertension, and occasional
embolic egg granulomas in brain or spinal cord. Pathology of S. haematobium schistosomiasis
includes: hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic
egg granulomas in brain or spinal cord.

Human contact with water is thus necessary for infection by schistosomes. Various animals, such
as dogs, cats, rodents, pigs, hourse and goats, serve as reservoirs for S. japonicum, and dogs for
S. mekongi.

Geographic Distribution

Schistosoma mansoni is found in parts of South America and the Caribbean, Africa, and the
Middle East; S. haematobium in Africa and the Middle East; and S. japonicum in the Far East.
Schistosoma mekongi and S. intercalatum are found focally in Southeast Asia and central West
Africa, respectively.

Clinical Presentation

Many infections are asymptomatic. Acute schistosomiasis (Katayama's fever) may occur weeks
after the initial infection, especially by S. mansoni and S. japonicum. Manifestations include
fever, cough, abdominal pain, diarrhea, hepatosplenomegaly, and eosinophilia. Occasionally
central nervous system lesions occur: cerebral granulomatous disease may be caused by ectopic
S. japonicum eggs in the brain, and granulomatous lesions around ectopic eggs in the spinal cord
from S. mansoni and S. haematobium infections may result in a transverse myelitis with flaccid
paraplegia. Continuing infection may cause granulomatous reactions and fibrosis in the affected
organs, which may result in manifestations that include: colonic polyposis with bloody diarrhea
(Schistosoma mansoni mostly); portal hypertension with hematemesis and splenomegaly (S.
mansoni, S. japonicum, S. mansoni); cystitis and ureteritis (S. haematobium) with hematuria,
which can progress to bladder cancer; pulmonary hypertension (S. mansoni, S. japonicum, more
rarely S. haematobium); glomerulonephritis; and central nervous system lesions.

Cryptosporidiosis
[Cryptosporidium spp.]


Cryptosporidium sp. oocysts stained with modified acid-fast.

Cryptosporidium sp. oocysts stained with safranin.

Cryptosporidium sp. oocysts labeled with immunofluorescent antibodies. Image contributed by
the Kansas Department of Health and Environment.

Causal Agents

Many species of Cryptosporidium exist that infect humans and a wide range of animals.
Although Cryptosporidium parvum and Cryptosporidium hominis (formerly known as C.
parvum anthroponotic genotype or genotype 1) are the most prevalent species causing disease in
humans, infections by C. felis, C. meleagridis, C. canis, and C. muris have also been reported.

Life Cycle:
Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces and
possibly other routes such as respiratory secretions . Transmission of Cryptosporidium parvum
and C. hominis occurs mainly through contact with contaminated water (e.g., drinking or
recreational water). Occasionally food sources, such as chicken salad, may serve as vehicles for
transmission. Many outbreaks in the United States have occurred in waterparks, community
swimming pools, and day care centers. Zoonotic and anthroponotic transmission of C. parvum
and anthroponotic transmission of C. hominis occur through exposure to infected animals or
exposure to water contaminated by feces of infected animals . Following ingestion (and
possibly inhalation) by a suitable host , excystation occurs. The sporozoites are released and
parasitize epithelial cells ( , ) of the gastrointestinal tract or other tissues such as the
respiratory tract. In these cells, the parasites undergo asexual multiplication (schizogony or
merogony) ( , , ) and then sexual multiplication (gametogony) producing microgamonts
(male) and macrogamonts (female) . Upon fertilization of the macrogamonts by the
microgametes ( ), oocysts ( , ) develop that sporulate in the infected host. Two different
types of oocysts are produced, the thick-walled, which is commonly excreted from the host ,
and the thin-walled oocyst , which is primarily involved in autoinfection. Oocysts are infective
upon excretion, thus permitting direct and immediate fecal-oral transmission.

Note that oocysts of Cyclospora cayetanensis, another important coccidian parasite, are
unsporulated at the time of excretion and do not become infective until sporulation is completed.
Refer to the life cycle of Cyclospora cayentanensis for further details.

Geographic Distribution:

Worldwide. Outbreaks of cryptosporidiosis have been reported in several countries, the most
remarkable being a waterborne outbreak in Milwaukee (Wisconsin) in 1993, that affected more
than 400,000 people.

Clinical Presentation

Infection with Cryptosporidium sp. results in a wide range of manifestations, from asymptomatic
infections to severe, life-threatening illness; incubation period is an average of 7 days (but can
range from 2 to 10 days). Watery diarrhea is the most frequent symptom, and can be
accompanied by dehydration, weight loss, abdominal pain, fever, nausea and vomiting. In
immunocompetent persons, symptoms are usually short lived (1 to 2 weeks); they can be chronic
and more severe in immunocompromised patients, especially those with CD4 counts < 200/µl.
While the small intestine is the site most commonly affected, symptomatic Cryptosporidium
infections have also been found in other organs including other digestive tract organs, the lungs,
and possibly conjunctiva.

Cysticercosis
[Taenia solium]


Larval Taenia solium cyst in a section of a lesion found in the right frontal lobe of a patient
stained with hematoxylin and eosin (H&E), magnification 40×.

Cross-sections of cysticerci stained with H&E, at 40x magnification

Causal Agents

The larval form (cysticercus) of the pork tapeworm, Taenia solium.

Life Cycle

Cysticercosis is an infection of both humans and pigs with the larval stages of the parasitic
cestode, Taenia solium. This infection is caused by ingestion of eggs shed in the feces of a
human tapeworm carrier . Pigs and humans become infected by ingesting eggs or gravid
proglottids , . Humans are infected either by ingestion of food contaminated with feces, or by
autoinfection. In the latter case, a human infected with adult T. solium can ingest eggs produced
by that tapeworm, either through fecal contamination or, possibly, from proglottids carried into
the stomach by reverse peristalsis. Once eggs are ingested, oncospheres hatch in the intestine ,
invade the intestinal wall, and migrate to striated muscles, as well as the brain, liver, and other
tissues, where they develop into cysticerci . In humans, cysts can cause serious sequellae if they
localize in the brain, resulting in neurocysticercosis. The parasite life cycle is completed,
resulting in human tapeworm infection, when humans ingest undercooked pork containing
cysticerci . Cysts evaginate and attach to the small intestine by their scolex . Adult
tapeworms develop, (up to 2 to 7 m in length and produce less than 1000 proglottids, each with
approximately 50,000 eggs) and reside in the small intestine for years .

Geographic Distribution:

Taenia solium is found worldwide. Because pigs are intermediate hosts of the parasite,
completion of the life cycle occurs in regions where humans live in close contact with pigs and
eat undercooked pork. Taeniasis and cysticercosis are very rare in Muslim countries. It is
important to note that human cysticercosis is acquired by ingesting T. solium eggs shed in the
feces of a human T. solium tapeworm carrier, and thus can occur in populations that neither eat
pork nor share environments with pigs.

Clinical Presentation

The symptoms of cysticercosis are caused by the development of cysticerci in various sites. Of
greatest concern is cerebral cysticercosis (or neurocysticercosis), which can cause diverse
manifestations including seizures, mental disturbances, focal neurologic deficits, and signs of
space-occupying intracerebral lesions. Death can occur suddenly. Extracerebral cysticercosis can
cause ocular, cardiac, or spinal lesions with associated symptoms. Asymptomatic subcutaneous
nodules and calcified intramuscular nodules can be encountered.

Echinococcosis
[Echinococcus granulosus] [Echinococcus multilocularis] [Echinococcus oligarthrus]
[Echinococcus vogeli]


Protoscoleces in a hydatid cyst removed from lung tissue, stained with hematoxylin and eosin
(H&E). Image taken at 200x magnification. Image courtesy of Phoenix Children's Hospital,
Phoenix, AZ.

Protoscolex of Echinococcus granulosus in an unstained wet mount made from a liver aspirate.
Protoscolex of Echinococcus from a liver aspirate stained with Papanicolaou (PAP) stain.

Causal Agent

Human echinococcosis (hydatidosis, or hydatid disease) is caused by the larval stages of cestodes
(tapeworms) of the genus Echinococcus. Echinococcus granulosus causes cystic echinococcosis,
the form most frequently encountered; E. multilocularis causes alveolar echinococcosis; E.
vogeli causes polycystic echinococcosis; and E. oligarthrus is an extremely rare cause of human
echinococcosis.

Life Cycle
The adult Echinococcus granulosus (3 to 6 mm long) resides in the small bowel of the
definitive hosts, dogs or other canids. Gravid proglottids release eggs that are passed in the
feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat,
swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere
that penetrates the intestinal wall and migrates through the circulatory system into various
organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst  that
enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The
definitive host becomes infected by ingesting the cyst-containing organs of the infected
intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa
, and develop into adult stages in 32 to 80 days. The same life cycle occurs with E.
multilocularis (1.2 to 3.7 mm), with the following differences: the definitive hosts are foxes, and
to a lesser extent dogs, cats, coyotes and wolves; the intermediate host are small rodents; and
larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of
the surrounding tissues. With E. vogeli (up to 5.6 mm long), the definitive hosts are bush dogs
and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other
organs) develops both externally and internally, resulting in multiple vesicles. E. oligarthrus (up
to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as
intermediate hosts. Humans become infected by ingesting eggs , with resulting release of
oncospheres in the intestine and the development of cysts , , , , , in various
organs.

Geographic Distribution
Echinococcus granulosus occurs practically worldwide, and more frequently in rural, grazing
areas where dogs ingest organs from infected animals. Echinococcus multilocularis occurs in the
northern hemisphere, including central Europe and the northern parts of Europe, Asia, and North
America. Echinococcus vogeli and Echinococcus oligarthrus occur in Central and South
America.

Clinical Presentation

Echinococcus granulosus infections remain silent for years before the enlarging cysts cause
symptoms in the affected organs. Hepatic involvement can result in abdominal pain, a mass in
the hepatic area, and biliary duct obstruction. Pulmonary involvement can produce chest pain,
cough, and hemoptysis. Rupture of the cysts can produce fever, urticaria, eosinophilia, and
anaphylactic shock, as well as cyst dissemination. In addition to the liver and lungs, other organs
(brain, bone, heart) can also be involved, with resulting symptoms. Echinococcus multilocularis
affects the liver as a slow growing, destructive tumor, with abdominal pain, biliary obstruction,
and occasionally metastatic lesions into the lungs and brain. Echinococcus vogeli affects mainly
the liver, where it acts as a slow growing tumor; secondary cystic development is common.

Intestinal Amebae
[Endolimax nana] [Entamoeba coli] [Entamoeba gingivalis] [Entamoeba hartmanni]
[Entamoeba polecki] [Iodamoeba buetschlii]

Cyst of Entamoeba coli in an unstained wet mount. Note the presence of more than four nuclei.
Trophozoite of Endolimax nana stained with trichrome.

Cyst of Iodamoeba buetschlii stained with trichrome. Note the glycogen vacuole (arrow).

Causal Agent

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are
generally considered nonpathogenic and reside in the large intestine of the human host.
Entamoeba gingivalis is also considered nonpathogenic and resides in the oral cavity of the
human host, in the gingival pockets at the base of the teeth.
Life Cycles

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii

Entamoeba gingivalis

Geographic Distribution

All six species are distributed worldwide. Entamoeba polecki in nature is primarily a parasite of
pigs and monkeys, and human infection is more prevalent in areas where the people have animal
contact.

Clinical Presentation

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are
generally considered nonpathogenic, although they have been found in the stool of patients
presenting with diarrhea where no known pathogens were identified. Their presence in stool can
be an indicator of fecal contamination of a food or water source, and does not rule-out the
presence of other parasites. Entamoeba gingivalis is also considered nonpathogenic, but is found
in about 95% of patients with gum disease and about 50% of patients with healthy gums.

Enterobiasis
[Enterobius vermicularis]
Cross-section of a male E. vermicularis from tissue, stained with H&E. Notice the presence of
the alae (blue arrow), intestine (red arrow) and testis (black arrow).

Adult male of E. vermicularis from a formalin-ethyl acetate (FEA) concentrated stool smear. The
worm measured 1.4 mm in length. Image contributed by the Centre for Tropical Medicine and
Imported Infectious Diseases, Bergen, Norway.

Eggs of E. vermicularis in a wet mount.

Causal Agents
The nematode (roundworm) Enterobius vermicularis (previously Oxyuris vermicularis) also
called human pinworm. (Adult females: 8 to 13 mm, adult male: 2 to 5 mm.) Humans are
considered to be the only hosts of E. vermicularis. A second species, Enterobius gregorii, has
been described and reported from Europe, Africa, and Asia. For all practical purposes, the
morphology, life cycle, clinical presentation, and treatment of E. gregorii is identical to E.
vermicularis.

Life Cycle

Eggs are deposited on perianal folds . Self-infection occurs by transferring infective eggs to the
mouth with hands that have scratched the perianal area . Person-to-person transmission can also
occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired
through surfaces in the environment that are contaminated with pinworm eggs (e.g., curtains,
carpeting). Some small number of eggs may become airborne and inhaled. These would be
swallowed and follow the same development as ingested eggs. Following ingestion of infective
eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon .
The time interval from ingestion of infective eggs to oviposition by the adult females is about
one month. The life span of the adults is about two months. Gravid females migrate nocturnally
outside the anus and oviposit while crawling on the skin of the perianal area . The larvae
contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal
conditions . Retroinfection, or the migration of newly hatched larvae from the anal skin back
into the rectum, may occur but the frequency with which this happens is unknown.

Geographic Distribution

Worldwide, with infections more frequent in school- or preschool-children and in crowded

conditions. Enterobiasis appears to be more common in temperate than tropical countries. The
most common helminthic infection in the United States (an estimated 40 million persons
infected).

Clinical Presentation

Enterobiasis is frequently asymptomatic. The most typical symptom is perianal pruritus,

especially at night, which may lead to excoriations and bacterial superinfection. Occasionally,
invasion of the female genital tract with vulvovaginitis and pelvic or peritoneal granulomas can
occur. Other symptoms include anorexia, irritability, and abdominal pain.

Fascioliasis
[Fasciola gigantica] [Fasciola hepatica]


Egg of F. hepatica in an unstained wet mount, taken at 400x magnification.

Adult of F. hepatica stained with carmine.

Causal Agent

The trematodes Fasciola hepatica (the sheep liver fluke) and Fasciola gigantica, parasites of
herbivores that can infect humans accidentally.

Life Cycle
Immature eggs are discharged in the biliary ducts and in the stool . Eggs become embryonated
in water , eggs release miracidia , which invade a suitable snail intermediate host ,
including the genera Galba, Fossaria and Pseudosuccinea. In the snail the parasites undergo
several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are
released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces.
Mammals acquire the infection by eating vegetation containing metacercariae. Humans can
become infected by ingesting metacercariae-containing freshwater plants, especially watercress
. After ingestion, the metacercariae excyst in the duodenum and migrate through the
intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they
develop into adults . In humans, maturation from metacercariae into adult flukes takes
approximately 3 to 4 months. The adult flukes (Fasciola hepatica: up to 30 mm by 13 mm; F.
gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. Fasciola
hepatica infect various animal species, mostly herbivores.

Geographic Distribution

Fascioliasis occurs worldwide. Human infections with F. hepatica are found in areas where
sheep and cattle are raised, and where humans consume raw watercress, including Europe, the
Middle East, and Asia. Infections with F. gigantica have been reported, more rarely, in Asia,
Africa, and Hawaii.

Clinical Presentation
During the acute phase (caused by the migration of the immature fluke through the hepatic
parenchyma), manifestations include abdominal pain, hepatomegaly, fever, vomiting, diarrhea,
urticaria and eosinophilia, and can last for months. In the chronic phase (caused by the adult
fluke within the bile ducts), the symptoms are more discrete and reflect intermittent biliary
obstruction and inflammation. Occasionally, ectopic locations of infection (such as intestinal
wall, lungs, subcutaneous tissue, and pharyngeal mucosa) can occur.

Fleas
[Ctenocephalides canis] [Ctenocephalides felis] [Pulex irritans] [Xenopsylla cheopis]

The Oriental rat flea, Xenopsylla cheopis.

Causal Agents

Many species of fleas can feed on humans. The human flea, Pulex irritans, is less-commonly
seen these in industrialized areas. This species is not an effective vector of disease but can serve
as an intermediate host for the cestodes Dipylidium caninum and Hymenolepis nana. The cat and
dog fleas (Ctenocephalides canis and C. felis) may also feed on humans. In addition to being
intermediate hosts for cestodes, C. felis can serve as a vector of Bartonella henselae (cat-scratch
disease) and Rickettsia felis (feline rickettsiae). The Oriental rat flea (Xenopsylla cheopis) is the
primary vector for Yersinia pestis (plague). Humans with close contact with birds may also be
fed upon by the sticktight flea (Echidnophaga gallinacea). The chigo flea (Tunga penetrans) is
discussed separately here.

General Flea Life Cycle

Fleas, like other holometabolous insects, have a four-part life cycle consisting of eggs, larvae,
pupae, and adults. Eggs are shed by the female in the enviroment . Eggs hatch into larvae in
about 3-4 days and feed on organic debris in the environment. The number of larval instars
varies among the species. Larvae eventually form pupae , which are in cocoons that are often
covered with debris from the environment (sand, pebbles, etc). The larval and pupal stages take
about 3-4 weeks to complete. Afterwards, adults hatch from pupae and seek out a warm-
blooded host for blood meals. The primary hosts for Ctenocephalides felis and C. canis are cats
and dogs, respectively, although other mammals, including humans, may be fed upon. The
primary hosts for Xenopsylla cheopis are rodents, especially rats. In North America, plague
(Yersinia pestis) is cycled between X. cheopis and prairie dogs. Humans are the primary host for
Pulex irritans.

The chigoe flea (Tunga penetrans) has different life cycle and is discussed in more detail here.

Geographic Distribution

Worldwide.

Giardiasis
[Giardia duodenalis (syn. G. lamblia, G. intestinalis)]
 

Giardia duodenalis cyst in a wet mount stained with iodine.

G. duodenalis cyst stained with trichrome.

G. duodenalis trophozoite stained with trichrome.

Causal Agents

Giardia duodenalis is a protozoan flagellate (Diplomonadida).

Life Cycle:
Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and
trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive
several months in cold water. Infection occurs by the ingestion of cysts in contaminated water,
food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases
trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal
binary fission, remaining in the lumen of the proximal small bowel where they can be free or
attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit
toward the colon. The cyst is the stage found most commonly in nondiarrheal feces .  Because
the cysts are infectious when passed in the stool or shortly afterward, person-to-person
transmission is possible. While animals are infected with Giardia, their importance as a reservoir
is unclear.

Geographic Distribution:

Worldwide, more prevalent in warm climates, and in children.

Clinical Presentation

The spectrum varies from asymptomatic carriage to severe diarrhea and malabsorption. Acute
giardiasis develops after an incubation period of 1 to 14 days (average of 7 days) and usually
lasts 1 to 3 weeks. Symptoms include diarrhea, abdominal pain, bloating, nausea, and vomiting.
In chronic giardiasis the symptoms are recurrent and malabsorption and debilitation may occur.

Hymenolepiasis
[Hymenolepis diminuta] [Hymenolepis nana]

Egg of H. diminuta in an unstained wet mount. Four hooks are clearly visible at this level of
focus.
H. nana egg in an unstained wet mount. Note the presence of hooks in the oncosphere and polar
filaments within the space between the oncosphere and outer shell.

Scolex of H. nana in an unstained wet mount of stool. Image courtesy of Dr. David Bruckner.

Causal Agents

Hymenolepiasis is caused by two cestodes (tapeworm) species, Hymenolepis nana (the dwarf
tapeworm, adults measuring 15 to 40 mm in length) and Hymenolepis diminuta (rat tapeworm,
adults measuring 20 to 60 cm in length). Hymenolepis diminuta is a cestode of rodents
infrequently seen in humans and frequently found in rodents.

Life Cycles

Hymenolepis nana

Hymenolepis diminuta

Geographic Distribution

Hymenolepis nana is the most common cause of all cestode infections, and is encountered
worldwide. In temperate areas its incidence is higher in children and institutionalized groups.
Hymenolepis diminuta, while less frequent, has been reported from various areas of the world.

Clinical Presentation

Hymenolepis nana and H. diminuta infections are most often asymptomatic. Heavy infections
with H. nana can cause weakness, headaches, anorexia, abdominal pain, and diarrhea.

Leishmaniasis
[Leishmania spp.]

Leishmania sp. amastigotes in a Giemsa-stained tissue scraping.

Leishmania sp. amastigotes; touch-prep stained with Giemsa.

Causal Agent

Leishmaniasis is a vector-borne disease that is transmitted by sandflies and caused by obligate

intracellular protozoa of the genus Leishmania. Human infection is caused by about 21 of 30
species that infect mammals. These include the L. donovani complex with 3 species (L.
donovani, L. infantum, and L. chagasi); the L. mexicana complex with 3 main species (L.
mexicana, L. amazonensis, and L. venezuelensis); L. tropica; L. major; L. aethiopica; and the
subgenus Viannia with 4 main species (L. (V.) braziliensis, L. (V.) guyanensis, L. (V.)
panamensis, and L. (V.) peruviana). The different species are morphologically indistinguishable,
but they can be differentiated by isoenzyme analysis, molecular methods, or monoclonal
antibodies.

Life Cycle
Leishmaniasis is transmitted by the bite of infected female phlebotomine sandflies. The sandflies
inject the infective stage (i.e., promastigotes) from their proboscis during blood meals .
Promastigotes that reach the puncture wound are phagocytized by macrophages and other
types of mononuclear phagocytic cells. Progmastigotes transform in these cells into the tissue
stage of the parasite (i.e., amastigotes) , which multiply by simple division and proceed to
infect other mononuclear phagocytic cells . Parasite, host, and other factors affect whether the
infection becomes symptomatic and whether cutaneous or visceral leishmaniasis results.
Sandflies become infected by ingesting infected cells during blood meals ( , ). In sandflies,
amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial
organisms in the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus),
and migrate to the proboscis .

Geographic Distribution

Leishmaniasis is found in parts of about 88 countries. Approximately 350 million people live in
these areas.  Most of the affected countries are in the tropics and subtropics. The settings in
which leishmaniasis is found range from rain forests in Central and South America to deserts in
West Asia. More than 90 percent of the world's cases of visceral leishmaniasis are in India,
Bangladesh, Nepal, Sudan, and Brazil.

Leishmaniasis is found in Mexico, Central America, and South America—from northern

Argentina to Texas (not in Uruguay, Chile, or Canada), southern Europe (leishmaniasis is not
common in travelers to southern Europe), Asia (not Southeast Asia), the Middle East, and Africa
(particularly East and North Africa, with some cases elsewhere).

Clinical Presentation

Human Leishmaniasis encompasses multiple clinical syndromes, most notably visceral,

cutaneous, and mucosal forms. Infections can result in two main forms of disease, cutaneous
leishmaniasis and visceral leishmaniasis (kala-azar). Different species can be associated with
diverse clinical manifestations and sequelae. Species identification can facilitate clinical
management, such as decisions regarding whether/which treatment is indicated. species,
geographic location, and immune response of the host. Cutaneous leishmaniasis is characterized
by one or more cutaneous lesions on areas where sandflies have fed. Persons who have
cutaneous leishmaniasis have one or more sores on their skin. The sores can change in size and
appearance over time. They often end up looking somewhat like a volcano, with a raised edge
and central crater. A scab covers some sores. The sores can be painless or painful. Some people
have swollen glands near the sores (for example, in the armpit if the sores are on the arm or
hand).

Persons who have visceral leishmaniasis usually have fever, weight loss, and an enlarged spleen
and liver (usually the spleen is bigger than the liver). Some patients have swollen glands. Certain
blood tests are abnormal. For example, patients usually have low blood counts, including a low
red blood cell count (anemia), low white blood cell count, and low platelet count. Some patients
develop post kala-azar dermal leishmaniasis. Visceral leishmaniasis is becoming an important
opportunistic infection in areas where it coexists with HIV.

Malaria
[Plasmodium falciparum] [Plasmodium knowlesi] [Plasmodium malariae] [Plasmodium ovale]
[Plasmodium vivax]


Gametocyte of P. falciparum in a thin blood smear. Also seen in this image are ring-form
trophozoites and an RBC exhibiting basophilic stippling (upper left).

Trophozoite of P. ovale in a thin blood smear. Note the fimbriation and Schüffner's dots.
Adult of Anopheles freeborni.

Causal Agent

Blood parasites of the genus Plasmodium. There are approximately 156 named species of
Plasmodium which infect various species of vertebrates. Four species are considered true
parasites of humans, as they utilize humans almost exclusively as a natural intermediate host: P.
falciparum, P. vivax, P. ovale and P. malariae. However, there are periodic reports of simian
malaria parasites being found in humans, most reports implicating P. knowlesi. At the time of
this writing, it has not been determined if P. knowlesi is being naturally transmitted from human
to human via the mosquito, without the natural intermediate host (macaque monkeys, genus
Macaca). Therefore, P. knowlesi is still considered a zoonotic malaria.

Life Cycle
The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected
female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect
liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in
P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by
invading the bloodstream weeks, or even years later.) After this initial replication in the liver
(exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the
erythrocytes (erythrocytic schizogony ). Merozoites infect red blood cells . The ring stage
trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites
differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are
responsible for the clinical manifestations of the disease.

The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an

Anopheles mosquito during a blood meal . The parasites' multiplication in the mosquito is
known as the sporogonic cycle . While in the mosquito's stomach, the microgametes penetrate
the macrogametes generating zygotes . The zygotes in turn become motile and elongated
(ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts .
The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito's
salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life
cycle .

Geographic Distribution
Malaria generally occurs in areas where environmental conditions allow parasite multiplication
in the vector.  Malaria today is usually restricted to tropical and subtropical areas and altitudes
below 1,500 m., although in the past malaria was endemic in much of North America, Europe
and even parts of northern Asia, and today is still present on the Korean peninsula. However, this
present distribution could be affected by climatic changes and population movements.
Plasmodium falciparum is the predominant species in the world. P. vivax and P. ovale are
traditionally thought to occupy complementary niches, with P. ovale predominating in Sub-
Saharan Africa and P. vivax in the other areas; but their geographical ranges do overlap. These
two species are not always distinguishable on the basis of morphologic characteristics alone, and
the use of molecular tools will help clarify their diagnosis and exact distribution. P. malariae has
wide global distribution, being found in South America, Asia, and Africa, but it is less frequent
than P. falciparum in terms of association with cases of infection. P. knowlesi is found in
southeast Asia.

More on: Malaria Risk Information and Prophylaxis by Country

Clinical Presentation

The symptoms of uncomplicated malaria can be rather non-specific and the diagnosis can be
missed if health providers are not alert to the possibility of this disease. Since untreated malaria
can progress to severe forms that may be rapidly (<24 hours) fatal, malaria should always be
considered in patients who have a history of exposure (mostly: past travel or residence in
disease-endemic areas). The most frequent symptoms include fever and chills, which can be
accompanied by headache, myalgias, arthralgias, weakness, vomiting, and diarrhea. Other
clinical features include splenomegaly, anemia, thrombocytopenia, hypoglycemia, pulmonary or
renal dysfunction, and neurologic changes. The clinical presentation can vary substantially
depending on the infecting species, the level of parasitemia, and the immune status of the patient.
Infections caused by P. falciparum are the most likely to progress to severe, potentially fatal
forms with central nervous system involvement (cerebral malaria), acute renal failure, severe
anemia, or acute respiratory distress syndrome. Other species can also have severe
manifestations. Complications of P. vivax malaria include splenomegaly (with, rarely, splenic
rupture), and those of P. malariae include nephrotic syndrome.

Pediculosis
[Pediculus humanus capitis] [Pediculus humanus humanus]


Adult of P. humanus.

Causal Agent

Pediculosis is infestation with the human head-and-body louse, Pediculus humanus. There are
two subspecies, the head louse (P. h. capitis) and the body louse (P. h. humanus). They are
ectoparasites whose only known hosts are humans. Recent molecular data suggest that the two
subspecies are ecotypes of the same species and that evolution between the two populations take
place continually.

Reference: Veracz A, Raoult D. 2012. Biology and genetics of human head and body lice.
Trends in Parasitology. 28: 563-571.

Life Cycle
The life cycle of the head louse has three stages: egg, nymph, and adult.

Eggs: Nits are head lice eggs. They are hard to see and are often confused for dandruff or hair
spray droplets. Nits are laid by the adult female and are cemented at the base of the hair shaft
nearest the scalp . They are 0.8 mm by 0.3 mm, oval and usually yellow to white. Nits take
about 1 week to hatch (range 6 to 9 days). Viable eggs are usually located within 6 mm of the
scalp.

Nymphs: The egg hatches to release a nymph . The nit shell then becomes a more visible dull
yellow and remains attached to the hair shaft. The nymph looks like an adult head louse, but is
about the size of a pinhead. Nymphs mature after three molts ( , ) and become adults about 7
days after hatching.
Adults: The adult louse is about the size of a sesame seed, has 6 legs (each with claws), and is
tan to grayish-white . In persons with dark hair, the adult louse will appear darker. Females are
usually larger than males and can lay up to 8 nits per day. Adult lice can live up to 30 days on a
person's head. To live, adult lice need to feed on blood several times daily. Without blood meals,
the louse will die within 1 to 2 days off the host.

Body lice: Body lice are morphologically similar to head lice. They have a different life cycle,
whereas body lice reside on and lay their eggs on the clothing and fomites of infected individuals
and migrate to the human body to feed.

Geographic Distribution

Head lice infestation is very common and is distributed worldwide. Preschool and elementary-
age children, 3 to 11 years of age are infested most often. Females are infested more often than
males, probably due to more frequent head to head contact. Body lice are also cosmopolitan but
are less common and usually seen in settings of poverty, war, and homelessness.

Clinical Presentation

 The majority of head lice infestations are asymptomatic. When symptoms are noted they may
include a tickling feeling of something moving in the hair, itching, caused by an allergic reaction
to louse saliva, and irritability. Secondary bacterial infection may be a complication. Body lice
can serve as vectors for Rickettsia prowazekii (epidemic typhus), Bartonella quintana (trench
fever), and Borrelia recurrentis (louse-borne relapsing fever).

Modes of Transmission:

The main mode of transmission of head lice is contact with a person who is already infested (i.e.,
head-to-head contact). Contact is common during play (sports activities, playgrounds, at camp,
and slumber parties) at school and at home.

Less commonly, transmission via fomites may occur with regards to head lice (more common
with body lice). Wearing clothing, such as hats, scarves, coats, sports uniforms, or hair ribbons
worn by an infested person; using infested combs, brushes or towels; or lying on a bed, couch,
pillow, carpet, or stuffed animal that has recently been in contact with an infested person may
result in transmission. Of note, both nymph and adult lice forms need to feed on blood to live. If
an adult louse does not have a blood meal, it can die in 2 days.

Pneumocystis
[Pneumocystis jirovecii]


Cysts of P. jirovecii in lung tissue, stained with methenamine silver and hematoxylin and eosin
(H&E). The walls of the cysts are stained black; the intracystic bodies are not visible with this
stain.

Causal Agents

Pneumocystis jirovecii (previously classified as Pneumocystis carinii) was previously classified

as a protozoa. Currently, it is considered a fungus based on nucleic acid and biochemical
analysis.

Life Cycle
Pneumocystis stages were reproduced from a drawing by Dr. John J. Ruffolo, South Dakota State
University, USA published in Cushion M. Pneumocystis carinii. In: Collier L, Balows A,
Sussman M, editors. Topley and Wilson's Microbiology and Microbial Infections: Volume 4
Medical Mycology, 9th ed. New York: Arnold Publishing; 1998. p. 674. Copyright held by
Arnold Publishing and reproduced here by permission of Arnold and Dr. Ruffolo.
Our thanks to Dr. Melanie T. Cushion for her comments on the life cycle text.

This is a generalized life cycle proposed by John J. Ruffolo, Ph.D. (Cushion, MT, 1988) for the
various species of Pneumocystis. These fungi are found in the lungs of mammals where they
reside without causing overt infection until the host's immune system becomes debilitated. Then,
an oftentimes lethal pneumonia can result. Asexual phase: trophic forms replicate by mitosis
to . Sexual phase: haploid trophic forms conjugate and produce a zygote or sporocyte
(early cyst) . The zygote undergoes meiosis and subsequent mitosis to produce eight haploid
nuclei (late phase cyst) . Spores exhibit different shapes (such as, spherical and elongated
forms). It is postulated that elongation of the spores precedes release from the spore case. It is
believed that the release occurs through a rent in the cell wall. After release, the empty spore
case usually collapses, but retains some residual cytoplasm . A trophic stage, where the
organisms probably multiply by binary fission is also recognized to exist. The organism causes
disease in immunosuppressed individuals.

Geographic Distribution
Worldwide, in humans and animals. Serologic evidence indicates that most healthy children have
been exposed by age 3 to 4. Pneumocystis pneumonia (PCP) occurs in immunosuppressed
individuals and in premature, malnourished infants.

Clinical Presentation

The symptoms of Pneumocystis pneumonia (PCP) include dyspnea, nonproductive cough, and
fever. Chest radiography demonstrates bilateral infiltrates. Extrapulmonary lesions occur in a
minority (<3%) of patients, involving most frequently the lymph nodes, spleen, liver, and bone
marrow. Typically, in untreated PCP increasing pulmonary involvement leads to death.

Strongyloidiasis
[Strongyloides stercoralis]

Filariform (L3) larva of S. stercoralis in a sputum specimen, stained with Giemsa. Image taken at
200x magnification.
’Rhabditiform (L1) larva of S. stercoralis.

Causal Agents

The nematode (roundworm) Strongyloides stercoralis. Other Strongyloides include S. fülleborni,

which infects chimpanzees and baboons and may produce limited infections in humans.

Life Cycle
The Strongyloides life cycle is more complex than that of most nematodes with its alternation
between free-living and parasitic cycles, and its potential for autoinfection and multiplication
within the host. Two types of cycles exist: Free-living cycle: The rhabditiform larvae passed in
the stool (see "Parasitic cycle" below) can either molt twice and become infective filariform
larvae (direct development) or molt four times and become free living adult males and females
that mate and produce eggs from which rhabditiform larvae hatch . The latter in turn can
either develop into a new generation of free-living adults (as represented in ), or into
infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the
parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate
the human skin , and are transported to the lungs where they penetrate the alveolar spaces; they
are carried through the bronchial tree to the pharynx, are swallowed and then reach the small
intestine . In the small intestine they molt twice and become adult female worms . The
females live threaded in the epithelium of the small intestine and by parthenogenesis produce
eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the
stool (see "Free-living cycle" above), or can cause autoinfection . In autoinfection, the
rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal
mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either
case, the filariform larvae may follow the previously described route, being carried successively
to the lungs, the bronchial tree, the pharynx, and the small intestine where they mature into
adults; or they may disseminate widely in the body. To date, occurrence of autoinfection in
humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria
philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility
of persistent infections for many years in persons who have not been in an endemic area and of
hyperinfections in immunodepressed individuals.

Geographic Distribution

Tropical and subtropical areas, but cases also occur in temperate areas (including the South of
the United States). More frequently found in rural areas, institutional settings, and lower
socioeconomic groups.

Clinical Presentation

Frequently asymptomatic. Gastrointestinal symptoms include abdominal pain and diarrhea.

Pulmonary symptoms (including Loeffler’s syndrome) can occur during pulmonary migration of
the filariform larvae. Dermatologic manifestations include urticarial rashes in the buttocks and
waist areas. Disseminated strongyloidiasis occurs in immunosuppressed patients, can present
with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia,
and is potentially fatal. Blood eosinophilia is generally present during the acute and chronic
stages, but may be absent with dissemination.

Taeniasis
[Taenia asiatica] [Taenia saginata] [Taenia solium]

Taenia sp. egg in unstained wet mounts.

Proglottid of T. saginata injected with India Ink. Image courtesy of the Orange County Public
Health Laboratory, Santa Ana, CA.

Eggs of Taenia sp. in a gravid proglottids, stained with hematoxylin and eosin (H&E). Note the
characteristic striations, typical for the taeniids. Not visible in these images are the hooks
commonly seen in cestode eggs. Hooks do not stain with H&E but are refractile.

Causal Agents
The cestodes Taenia saginata (beef tapeworm), T. solium (pork tapeworm) and T. asiatica
(Asian tapeworm). Taenia solium can also cause cysticercosis.

Life Cycle

Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata, T. solium or T.
asiatica. Humans are the only definitive hosts for these three species. Eggs or gravid proglottids
are passed with feces ; the eggs can survive for days to months in the environment. Cattle (T.
saginata) and pigs (T. solium and T. asiatica) become infected by ingesting vegetation
contaminated with eggs or gravid proglottids . In the animal's intestine, the oncospheres hatch
, invade the intestinal wall, and migrate to the striated muscles, where they develop into
cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by
ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops
over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach
to the small intestine by their scolex and reside in the small intestine . Length of adult worms
is usually 5 m or less for T. saginata (however it may reach up to 25 m) and 2 to 7 m for T.
solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm,
and migrate to the anus or are passed in the stool (approximately 6 per day). T. saginata adults
usually have 1,000 to 2,000 proglottids, while T. solium adults have an average of 1,000
proglottids. The eggs contained in the gravid proglottids are released after the proglottids are
passed with the feces. T. saginata may produce up to 100,000 and T. solium may produce 50,000
eggs per proglottid respectively.

Geographic Distribution

Taenia saginata and T. solium are worldwide in distribution. Taenia solium is more prevalent in
poorer communities where humans live in close contact with pigs and eat undercooked pork.
Taenia asiatica is limited to Asia and is seen mostly in the Republic of Korea, China, Taiwan,
Indonesia, and Thailand.

Clinical Presentation

Taenia saginata taeniasis produces only mild abdominal symptoms. The most striking feature
consists of the passage (active and passive) of proglottids. Occasionally, appendicitis or
cholangitis can result from migrating proglottids. Taenia solium taeniasis is less frequently
symptomatic than Taenia saginata taeniasis. The main symptom is often the passage (passive) of
proglottids. The most important feature of Taenia solium taeniasis is the risk of development of
cysticercosis.

Ticks
[Amblyomma spp.] [Dermacentor spp.] [Ixodes spp.] [Ornithodoros spp.] [Rhipicephalus spp.]

Female Dermacentor variabilis. Image courtesy of Tom Murray, Massachusetts.

Ventral view of a nymph of Ixodes sp.  Image courtesy of the Washington State Public Health
Laboratories.

Causal Agent

There are many genera and species of ticks in the families Ixodidae (hard ticks) and Argasidae
(soft ticks) that are of public health importance. Some representative genera, and diseases they
are known vectors for, include:  Amblyomma (tularemia, ehrlichiosis, Rocky Mountain spotted
fever (RMSF), and boutonneuse fever); Dermacentor (RMSF, Colorado tick fever, tularemia,
Siberian tick typhus, and Central European tick-borne encephalitis, as well as being an agent of
tick paralysis); Hyalomma (Siberian tick typhus, Crimean-Congo hemorrhagic fever); Ixodes
(Lyme disease, babesiosis, human granulocytic ehrlichiosis, and Russian spring-summer
encephalitis); Rhipicephalus (RMSF and boutonneuse fever); Ornithodoros (tick-borne relapsing
fever); Carios (tick-borne relapsing fever).

Life Cycles

Most tick species undergo one of four different life cycles. Members of the family Ixodidae
undergo either one-host, two-host or three-host life cycles. During the one-host life cycle, ticks
remain on the same host for the larval, nymphal and adult stages, only leaving the host prior to
laying eggs. During the two-host life cycle, the tick molts from larva to nymph on the first host,
but will leave the host between the nymphal and adult stages. The second host may be the same
individual as the first host, the same species, or even a second species. Most ticks of public
health importance undergo the three-host life cycle, whereby the tick leaves the host after the
larval and nymphal stages. The three hosts are not always the same species, but may be the same
species, or even the same individual, depending on host availability for the tick. Members of the
family Argasidae undergo what is called a multihost life cycle. Argasid ticks have two or more
nymphal stages, each requiring a blood meal from a host. Unlike the ixodid ticks, which stay
attached to their hosts for up to several days while feeding, argasid ticks are adapted to feeding
rapidly (about an hour) and then promptly leaving the host.

One-Host Ixodid Tick Life Cycle

Two-Host Ixodid Tick Life Cycle

Three-Host Ixodid Tick Life Cycle

Multihost Argasid Tick Life Cycle

Geographic Distribution

While ticks as a whole are worldwide in distribution, most species are restricted to various
regions. All major biogeographic regions (except Antarctica) have tick species of public health
importance.

Clinical Presentation

Most ticks do not elicit any response from their host while feeding. Ticks in the genera
Dermacentor and Ixodes have been implicated in tick paralysis, a condition characterized by an
acute, ascending, flaccid motor paralysis that can result in death if the tick is not removed. The
condition is believed to be caused by toxins in the ticks' saliva.

Toxocariasis
[Toxocara canis] [Toxocara cati]


Side view of T. cati, showing the characteristic broad, arrow-shaped alae with striations.

Cross-section of Toxocara sp. larvae in liver tissue stained with hematoxylin and eosin (H&E)

Causal Agents

Toxocariasis is caused by larvae of Toxocara canis (dog roundworm) and less frequently of T.
cati (cat roundworm), two nematode parasites of animals.
Life Cycle

Toxocara canis accomplishes its life cycle in dogs, with humans acquiring the infection as
accidental hosts. Unembryonated eggs are shed in the feces of the definitive host . Eggs
embryonate and become infective in the environment . Following ingestion by dogs , the
infective eggs hatch and larvae penetrate the gut wall. In younger dogs, the larvae migrate
through the lungs, bronchial tree, and esophagus; adult worms develop and oviposit in the small
intestine . In older dogs, patent infections can also occur, but larval encystment in tissues is
more common. Encysted stages are reactivated in female dogs during late pregnancy and infect
by the transplacental and transmammary routes the puppies , in whose small intestine adult
worms become established . Puppies are a major source of environmental egg contamination.
Toxocara canis can also be transmitted through ingestion of paratenic hosts: eggs ingested by
small mammals (e.g. rabbits) hatch and larvae penetrate the gut wall and migrate into various
tissues where they encyst . The life cycle is completed when dogs eat these hosts and the
larvae develop into egg-laying adult worms in the small intestine. Humans are accidental hosts
who become infected by ingesting infective eggs in contaminated soil or infected paratenic
hosts . After ingestion, the eggs hatch and larvae penetrate the intestinal wall and are carried
by the circulation to a wide variety of tissues (liver, heart, lungs, brain, muscle, eyes) . While
the larvae do not undergo any further development in these sites, they can cause severe local
reactions that are the basis of toxocariasis. The two main clinical presentations of toxocariasis
are visceral larva migrans and ocular larva migrans. Diagnosis is usually made by serology or the
finding of larvae in biopsy or autopsy specimens.
Geographic Distribution

Worldwide.

Clinical Presentation

Many human infections are asymptomatic, with only eosinophilia and positive serology. The two
main clinical presentations of toxocariasis are visceral larva migrans (VLM) and ocular larva
migrans (OLM). In VLM, which occurs mostly in preschool children, the larvae invade multiple
tissues (liver, heart, lungs, brain, muscle) and cause various symptoms including fever, anorexia,
weight loss, cough, wheezing, rashes, hepatosplenomegaly, and hypereosinophilia. Death can
occur rarely, by severe cardiac, pulmonary or neurologic involvement. In OLM, the larvae
produce various ophthalmologic lesions, which in some cases have been misdiagnosed as
retinoblastoma, resulting in surgical enucleation. OLM often occurs in older children or young
adults, with only rare eosinophilia or visceral manifestations.

Toxoplasmosis
[Toxoplasma gondii]

Toxoplasma gondii tachyzoites, stained with Giemsa, from a smear of peritoneal fluid obtained
from a laboratory-inoculated mouse.
Toxoplasma gondii cyst stained with hematoxylin and eosin.

Causal Agent

Toxoplasma gondii is a protozoan parasite that infects most species of warm blooded animals,
including humans, and can cause the disease toxoplasmosis.

Life Cycle
The only known definitive hosts for Toxoplasma gondii are members of family Felidae
(domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces . Although
oocysts are usually only shed for 1-2 weeks, large numbers may be shed. Oocysts take 1-5 days
to sporulate in the environment and become infective. Intermediate hosts in nature (including
birds and rodents) become infected after ingesting soil, water or plant material contaminated with
oocysts . Oocysts transform into tachyzoites shortly after ingestion. These tachyzoites localize
in neural and muscle tissue and develop into tissue cyst bradyzoites . Cats become infected
after consuming intermediate hosts harboring tissue cysts . Cats may also become infected
directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game
may also become infected with tissue cysts after ingestion of sporulated oocysts in the
environment . Humans can become infected by any of several routes:

 eating undercooked meat of animals harboring tissue cysts .

 consuming food or water contaminated with cat feces or by contaminated environmental
samples (such as fecal-contaminated soil or changing the litter box of a pet cat) .
 blood transfusion or organ transplantation .
 transplacentally from mother to fetus .

In the human host, the parasites form tissue cysts, most commonly in skeletal muscle,
myocardium, brain, and eyes; these cysts may remain throughout the life of the host. Diagnosis is
usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens
 . Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic
fluid using molecular methods such as PCR .

Geographic Distribution

Serologic prevalence data indicate that toxoplasmosis is one of the most common of humans
infections throughout the world. A high prevalence of infection in France has been related to a
preference for eating raw or undercooked meat, while a high prevalence in Central America has
been related to the frequency of stray cats in a climate favoring survival of oocysts and soil
exposure. The overall seroprevalence in the United States among adolescents and adults, as
determined with specimens collected by the third National Health and Nutrition Examination
Survey (NHANES III) between 1988 and 1994, was found to be 22.5%, with a seroprevalence
among women of childbearing age (15 to 44 years) of 15%.

Clinical Presentation

The diagnosis of toxoplasmosis may be documented by:

 Observation of parasites in patient specimens, such as bronchoalveolar lavage material

from immunocompromised patients, or lymph node biopsy.
 Isolation of parasites from blood or other body fluids, by intraperitoneal inoculation into
mice or tissue culture. The mice should be tested for the presence of Toxoplasma
organisms in the peritoneal fluid 6 to 10 days post inoculation; if no organisms are found,
serology can be performed on the animals 4 to 6 weeks post inoculation.
 Detection of parasite genetic material by PCR, especially in detecting congenital
infections in utero.
 Serologic testing is the routine method of diagnosis.

Trichomoniasis
[Trichomonas vaginalis]


Two trophozoites of T. vaginalis obtained from in vitro culture, stained with Giemsa.

Causal Agent

Trichomonas vaginalis, a flagellate, is the most common pathogenic protozoan of humans in

industrialized countries.

Life Cycle
Trichomonas vaginalis resides in the female lower genital tract and the male urethra and prostate
, where it replicates by binary fission . The parasite does not appear to have a cyst form, and
does not survive well in the external environment. Trichomonas vaginalis is transmitted among
humans, its only known host, primarily by sexual intercourse .

Geographic Distribution

Worldwide. Higher prevalence among persons with multiple sexual partners or other venereal
diseases.

Clinical Presentation

Trichomonas vaginalis infection in women is frequently symptomatic. Vaginitis with a purulent

discharge is the prominent symptom, and can be accompanied by vulvar and cervical lesions,
abdominal pain, dysuria and dyspareunia. The incubation period is 5 to 28 days. In men, the
infection is frequently asymptomatic; occasionally, urethritis, epididymitis, and prostatitis can
occur.
Trichuriasis
[Trichuris trichiura]

Egg of T. trichiura in an unstained wet mount.

Adult male T. trichiura removed during a colonoscopy.

Causal Agent

The nematode (roundworm) Trichuris trichiura, also called the human whipworm.

Life Cycle

The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell
stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in
15 to 30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small
intestine, and release larvae that mature and establish themselves as adults in the colon . The
adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult
worms are fixed in that location, with the anterior portions threaded into the mucosa. The
females begin to oviposit 60 to 70 days after infection. Female worms in the cecum shed
between 3,000 and 20,000 eggs per day. The life span of the adults is about 1 year.

Geographic Distribution
The third most common round worm of humans. Worldwide, with infections more frequent in
areas with tropical weather and poor sanitation practices, and among children. It is estimated that
800 million people are infected worldwide. Trichuriasis occurs in the southern United States.

Clinical Presentation

Most frequently asymptomatic. Heavy infections, especially in small children, can cause
gastrointestinal problems (abdominal pain, diarrhea, rectal prolapse) and possibly growth
retardation.