ASCARIS LUMBRICOIDES
INFECTIVE
DIAGNOSTIC
Ascaris lumbricoides is the largest nematode (roundworm) parasitizing the human intestine. (Adult females:
20 to 35 cm; adult male: 15 to 30 cm.)
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.
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.
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).
TRICHURIS THICHIURA
INFECTIVE
DIAGNOSTIC
The nematode (roundworm) Trichuris trichiura, also called the human whipworm.
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.
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.
Most frequently asymptomatic. Heavy infections, especially in small children, can cause gastrointestinal
problems (abdominal pain, diarrhea, rectal prolapse) and possibly growth retardation.
HOOKWORM
INFECTIVE
DIAGNOSTIC
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.
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 LARVA 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.
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.
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.
STRONGYLOIDES STERCORALIS
INFECTIVE Filariform larva
DIAGNOSTIC Rhabditiform larva
The nematode (roundworm) Strongyloides stercoralis. Other Strongyloides include S. fülleborni, which infects
chimpanzees and baboons and may produce limited infections in humans.
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 become infective filariform larvae (direct development) , or free-living adult males and females that
mate and produce eggs from which rhabditiform larvae hatch and eventually become 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 by various, often
random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the
bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also
evidence that L3 larvae can migrate directly to the intestine via connective tissues. 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 disseminate throughout 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.
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.
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.
ENTEROBIUS VERMICULARIS
INFECTIVE Fully embryonated egg
DIAGNOSTIC Unembryonated egg
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.
gregoriiis identical to E. vermicularis.
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.
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).
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.
CAPILLARIA PHILIPPINENSIS
INFECTIVE Infective larvae
DIAGNOSTIC Unembryonated egg
The nematode (roundworm) Capillaria philippinensis causes human intestinal capillariasis.
Typically, unembryonated eggs are passed in the human stool and become embryonated in the external
environment ; after ingestion by freshwater fish, larvae hatch, penetrate the intestine, and migrate to the
tissues . Ingestion of raw or undercooked fish results in infection of the human host. Humans are the only
demonstrated hosts . The adults of Capillaria philippinensis (males: 2.3 to 3.2mm; females: 2.5 to 4.3 mm)
reside in the human small intestine, where they burrow in the mucosa . The females deposit
unembryonated eggs. Some of these become embryonated in the intestine, and release larvae that can cause
autoinfection. This leads to hyperinfection (a massive number of adult worms). Capillaria philippinesis is
currently considered a parasite of fish eating birds, which seem to be the natural definitive host .
Capillaria philippinensis is endemic in the Philippines and also occurs in Thailand. Rare cases have been
reported from other Asian countries, the Middle East, and Colombia.
Intestinal capillariasis (caused by C. philippinensis) manifests as abdominal pain and diarrhea, which, if
untreated, may become severe because of autoinfection. A protein-losing enteropathy can develop which may
result in cachexia and death.
CRYPSTOSPORIDIUM HOMINIS
INFECTIVE Thick-walled oocyst with 4 sporozoites
DIAGNOSTIC Thick-walled oocyst with 4 sporozoites
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.
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.
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.
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.
CYCLOSPORA CAYETANENSIS
INFECTIVE Sporulated oocyst (2 sporocysts each with 2 sporozoites)
DIAGNOSTIC Unsporulated oocyst
When freshly passed in stools, the oocyst is not infective (thus, direct fecal-oral transmission cannot occur; this
differentiates Cyclospora from another important coccidian parasite, Cryptosporidium). In the environment,
sporulation occurs after days or weeks at temperatures between 22°C to 32°C, resulting in division of the sporont
into two sporocysts, each containing two elongate sporozoites . Fresh produce and water can serve as vehicles
for transmission and the sporulated oocysts are ingested (in contaminated food or water) . The oocysts excyst
in the gastrointestinal tract, freeing the sporozoites which invade the epithelial cells of the small intestine. Inside the
cells they undergo asexual multiplication and sexual development to mature into oocysts, which will be shed in
stools . The potential mechanisms of contamination of food and water are still under investigation.
Cyclosporiasis has been reported in many countries, but is most common in tropical and subtropical areas. Since
1990, at least 11 foodborne outbreaks of cyclosporiasis, affecting approximately 3600 persons, have been
documented in the United States and Canada.
After an average incubation period of 1 week, symptomatic infections typically manifest as watery diarrhea, which
can be severe. Other symptoms include anorexia, weight loss, abdominal pain, nausea and vomiting, myalgias, low-
grade fever, and fatigue. Untreated infections typically last for 10-12 weeks and may follow a relapsing course.
Infections, especially in disease-endemic settings can be asymptomatic.
CYTOISOSPORA BELLI
INFECTIVE Mature oocyst (with 2 sporocyst each with 4 sporozoites)
DIAGNOSTIC Immature/unsporulated oocyst (with one sporoblast)
The coccidian parasite, Cystoisospora belli, infects the epithelial cells of the small intestine, and is the least common
of the three intestinal coccidia that infect humans.
At time of excretion, the immature oocyst contains usually one sporoblast (more rarely two). In further maturation
after excretion, the sporoblast divides in two (the oocyst now contains two sporoblasts); the sporoblasts secrete a
cyst wall, thus becoming sporocysts; and the sporocysts divide twice to produce four sporozoites each. Infection
occurs by ingestion of sporocysts-containing oocysts: the sporocysts excyst in the small intestine and release their
sporozoites, which invade the epithelial cells and initiate schizogony. Upon rupture of the schizonts, the merozoites
are released, invade new epithelial cells, and continue the cycle of asexual multiplication . Trophozoites develop
into schizonts which contain multiple merozoites. After a minimum of one week, the sexual stage begins with the
development of male and female gametocytes . Fertilization results in the development of oocysts that are
excreted in the stool.
Worldwide, especially in tropical and subtropical areas. Infection occurs in immunodepressed individuals, and
outbreaks have been reported in institutionalized groups in the United States.
Infection causes acute, nonbloody diarrhea with crampy abdominal pain, which can last for weeks and result in
malabsorption and weight loss. In immunodepressed patients, and in infants and children, the diarrhea can be
severe. Eosinophilia may be present (differently from other protozoan infections).
TOXOPLASMA GONDII
INFECTIVE Mature oocyst (2 sporocysts each with 4 sporozoites)
DIAGNOSTIC
Toxoplasma gondii is a protozoan parasite that infects most species of warm blooded animals, including humans,
and can cause the disease toxoplasmosis.
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 .
Serologic prevalence data indicate that toxoplasmosis is one of the most common human 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%. In a more recent evaluation using data from NHANES 2009-2010, the
overall age-adjusted T. gondii antibody seroprevalence among persons > 6 years of age was 12.4%, and among
women 15–44 years of age was 9.1%.
Acquired infection with Toxoplasma in immunocompetent persons is generally an asymptomatic infection. However,
10% to 20% of patients with acute infection may develop cervical lymphadenopathy and/or a flu-like illness. The
clinical course is usually benign and self-limited; symptoms usually resolve within a few weeks to months. In rare
cases ocular infection with visual loss can occur. Immunodeficient patients often have central nervous system
(CNS) disease but may have retinochoroiditis, pneumonitis, or other systemic disease. In patients with AIDS,
toxoplasmic encephalitis is the most common cause of intracerebral mass lesions and is thought to usually be
caused by reactivation of chronic infection. Toxoplasmosis in patients being treated with immunosuppressive drugs
may be due to either newly acquired or reactivated latent infection.
Congenital toxoplasmosis results from an acute primary infection acquired by the mother during pregnancy. The
incidence and severity of congenital toxoplasmosis vary with the trimester during which infection was
acquired. Because treatment of the mother may reduce the incidence of congenital infection and reduce sequelae
in the infant, prompt and accurate diagnosis is important. Many infants with subclinical infection at birth will
subsequently develop signs or symptoms of congenital toxoplasmosis. Ocular Toxoplasma infection, an important
cause of retinochoroiditis in the United States, can be the result of congenital infection, or infection after birth. In
congenital infection, patients are often asymptomatic until the second or third decade of life, when lesions develop in
the eye.
SARCOCYSTIS SPP.
INFECTIVE Sarcocysts with bradyzoites
DIAGNOSTIC
Sarcocystis hominis and S. suihominis use humans as definitive hosts and are responsible for intestinal
sarcocystosis in the human host. Humans may also become dead-end hosts for non-human Sarcocystis spp. after
the accidental ingestion of oocysts.
Both sporulated oocysts (containing two sporocysts) and individual sporocysts can be passed in stool. Sporocysts
contain four sporozoites and a refractile residual body. Sporocysts ingested by the intermediate host (cattle for S.
hominis and pigs for S. suihominis) rupture, releasing sporozoites. Sporozoites enter endothelial cells of blood
vessels and undergo schizogony, resulting in first-generation schizonts. Merozoites derived from the first-generation
invade small capillaries and blood vessels, becoming second-generation schizonts. The second generation
merozoites invade muscle cells and develop into sarcocysts containing bradyzoites, which are the infective stage for
the definitive host. Humans become infected when they eat undercooked meat containing these sarcocysts.
Bradyzoites are released from ruptured cysts in the small intestine and invade the lamina propria of the intestinal
epithelium . There, they differentiate into macro- and microgametocytes. Fusion of male and female
gametes results in the formation of oocysts. Oocysts sporulate in the intestinal epithelium and are shed from the
host in feces . Due to the fragile nature of the oocyst wall, individual sporocysts may also be detected in feces.
Worldwide, but more common in areas where livestock is raised.
In cases of intestinal sarcocystosis, when humans serve as the definitive hosts, infections are often asymptomatic
and clear spontaneously. Occasionally, mild fever, diarrhea, chills, vomiting and respiratory problems may occur.
When humans become infected with sarcocysts of non-human species, the infections are not intestinal but rather
result in muscle cysts; symptoms such as myalgia, muscle weakness and transitory edema may occur. In these
cases, humans are dead-end intermediate hosts.
