Gastrointestinal Prozozoa
Amebiasis
Transmission: Fecal-oral contamination.
Distribution: Worldwide, but highest incidence in tropical and subtropical developing nations.
Life cycle: The cysts of Entameba histolytica (the most common causative agent) are ingested with contaminated food or water. The passage of the cysts through the stomach with exposure to gastric acid leads to formation of trophozoites in the duodenum, which then inhabit the large intestine. The organisms multiply by binary fission. Cysts may also form, which are passed into the feces. In some cases, the organisms gain access to submucosal vessels and travel to the liver or beyond.
Clinical manifestations: Light infestations are often asymptomatic, or may produce mild diarrhea. Persons may remain infected carriers for years. Increased numbers of trophozoites may produce colonic mucosal necrosis and severe dysentery. The findings may resemble an acute inflammatory bowel disease.
Diagnosis: Examination of the stool for cysts is required for diagnosis. Colonic mucosal biopsies may reveal the organisms. Serologic titers may aid in diagnosis, particularly with disseminated infections.
Giardiasis
Transmission: Fecal-oral contamination.
Distribution: Worldwide.
Life cycle: The cysts of Giardia lamblia are ingested with contaminated water. The organisms multiply by binary fission in the small intestine, forming trophozoites. Cysts may also form, which are passed into the feces.
Clinical manifestations: Perhaps a third of infections are asymptomatic, or there may be mild diarrhea. In some cases there is severe diarrhea and malabsorption.
Diagnosis: Examination of stool or duodenal aspirate for cysts is required for diagnosis. Enzyme immunoassay or immunofluorescent staining methods may be utilized.
Cryptosporidiosis
Transmission: Fecal-oral contamination.
Distribution: Worldwide.
Life cycle: The oocysts of Cryptosporidium parvum are ingested with contaminated food or water. The oocysts release sporozoites that invade the brush border of small intestinal epithelium where they develop into trophozoites. Oocysts may develop and pass into stool.
Clinical manifestations: Many infections are asymptomatic, or there may be a mild watery diarrhea. Immunocompromised hosts (such as persons with AIDS) may be more severely affected, with many loose watery stools per day.
Diagnosis: Examination of stool or duodenal aspirate for oocysts is required for diagnosis. Biopsy may reveal the organisms in the brush border.
Microsporidiosis
Transmission: Fecal-oral contamination.
Distribution: Worldwide. There are two major species:
Enterocytozoon bieneusi
Encephalitozoon cuniculi
Life cycle: The spores of either microsporidial species are ingested with contaminated food or water. The spore injects sporuloplasm into a cell (typically an intestinal epithelial cell) and the organism multiplies there and spreads from cell to cell. Spores are released into the stool.
Clinical manifestations: Many infections are asymptomatic, or there may be a mild watery diarrhea. Immunocompromised hosts (such as persons with AIDS) may be more severely affected, with many loose watery stools per day. The infection may disseminate to other organs in such hosts.
Diagnosis: Examination of stool spores is required for diagnosis. Biopsy with electron microscopy may reveal the organisms in the intestinal cells.
Pulmonary Prozozoa
Pneumocystis carinii (jirovecii)
Transmission: Airborne.
Distribution: Worldwide.
Life cycle: The cysts of Pneumocystis carinii (jirovecii) are inhaled and reach the alveoli, where they release sporozoites that grow within an alveolar exudate, adherent to epithelial cells. These form trophozoites that mature to cysts that release sporozoites. Genetic studies suggest that Pneumocystis is more closely related to fungi, but it looks and acts similar to a protozoan parasite.
Clinical manifestations: Infection is asymptomatic in immunocompetent hosts. In immunocompromised persons, a fulminant pneumonitis with fever, cough, and severe dyspnea may result.
Diagnosis: Examination of induced sputum, bronchoalveolar lavage fluid, or biopsies for the cysts is required. A direct fluorescent antigen (DFA) assay can be done. In cytologic and tissue sections, staining with Gomori methenamine silver (or Giemsa in cytologic smears) can highlight the organisms.
Bloodstream Prozozoa
Malaria
Transmission: Anopheles mosquito bite.
Distribution: Tropical and subtropical regions, primarily in Africa, Asia, and South America.
Forms of malaria: There are four species that affect man, caused by the genus Plasmodium:
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Plasmodium falciparum
Life cycle: The bite of an infected mosquito introduces sporozoites into the capillaries of a human host. The sporozoites then invade hepatocytes and multiply. Infected hepatocytes then rupture, releasing merozoites into the blood stream, where they invade red blood cells. Within RBC's, the parasites become trophozoites that feed on hemoglobin. Trophozoites can mature to schizonts, which rupture to release more merozoites into circulation. A few merozoites diferentiate into gametocytes that, when taken up by a mosquito as a blood meal, can initiate the sexual cycle of development in the mosquito that completes the life cycle. Hemoglobinopathies have become more prevalent in some populations where malaria is more frequent, because the abnormal RBC's resist infection.
Clinical manifestations: Malaria produces an acute febrile illness several weeks following initial infection. Headache, malaise, shaking chills, and diaphoresis can occur. The symptoms may become cyclical in some cases.
Pathologic findings: Infected persons may develop anemia, hepatomegaly, splenomegaly (sometimes massive), and in severe cases cerebral involvement with congestion of cerebral vessels and edema.
Diagnosis: The parasites are identified in a peripheral blood smear. There are slight variations in morphology that determine which Plasmodium species is present.
African Trypanosomiasis
Transmission: Bite of tsetse fly.
Distribution: Across central Africa. There are two species:
Life cycle: The bite of the tsetse fly introduces infective trypomastigotes into the circulation, where they divide and multiply and also spread to lymph nodes and spleen. Eventually they reach the central nervous system and proliferate in cerebrospinal fluid. Infected humans pass the organisms to additional tsetse flies.
Clinical manifestations: The location of the tsetse bite becomes an erythematous nodule that subsides in a couple of weeks. Systemic manifestations of fever, lymphadenopathy, headache, and arthralgias occur at this time. CNS involvement follows and can manifest with convulsions, behavioral changes, and coma (hence the disease may be termed "sleeping sickness"). T. brucei rhodesiense has a more virulent course, typically resulting in death in a year. T. brucei gambiense may be more chronic over several years.
Pathologic findings: A meningoencephalitis may be present in the CNS. Lymphadenopathy may be promient. Renal and myocardial damage may occur with the virulent T. brucei rhodesiense.
Diagnosis: Giemsa-stained blood smears can reveal the trypomastigotes. Examination of CSF may reveal them as well. Serologic methods are helpful.
Tissue Prozozoa
Chagas' Disease
Transmission: From the reduviid bug passing the organisms into its feces that are rubbed into the bite or abrasions of the human host.
Distribution: Tropical and subtropical regions of South and Central America where reduviid bugs are found and people dwell in mud huts where the bugs live.
Life cycle: The reduviid bug passes the trypomastigotes of Trypanosoma cruzi in its feces on the skin of persons it is biting. The organisms are rubbed into the bite or into skin abrasions. In the blood, the trypomastigotes are phagocytized by macrophages and convert to amastigotes that divide by binary fission. Macrophages carry the infection to cells of the mononuclear phagocyte system, to muscle, and to the central nervous system. Amastigotes can transform to trypomastigotes released into blood from cell rupture. Infected persons can pass the infection by being bitten by reduviid bugs.
Clinical manifestations: A local area of erythema and induration at the site of the bite, typically on the face, can be seen and is called a chagoma. Fever, chills, myalgia, and malaise can occur during the acute phase of a few weeks' duration. Chronic disease includes involvement of smooth muscle of the gastrointestinal tract and autonomic nervous system that can lead to motility problems and megacolon. Cardiac involvement can lead to congestive heart failure and arrhythmias. Young children tend to be affected more severely.
Pathologic findings: Myocarditis, cardiomegaly.
Diagnosis: Giemsa-stained blood smears may reveal the trypomastigotes during acute infection. Serologic testing is useful for both acute and chronic infections. Biopsy or needle aspirates of lymph node, liver, or bone marrow may reveal the amastigotes.
Leishmaniasis
Transmission: From bite of the sand fly.
Distribution: there are three major forms of the disease:
Leishmania tropica - seen around the Mediterranean Sea, across the Middle East to Central Asia, China, and India.
Leishmania donovani - seen around the Mediterranean Sea, in Africa, India, China, and also in South America.
Leishmania braziliensis - seen from Mexico down through Central America to South America.
Life cycle: The bite of the sandfly introduces promastigotes that travel via bloodstream to tissues of the mononuclear phagocyte system (lymph nodes, liver, spleen, marrow) where they transform into amastigotes that multiply by binary fission until the infected cells rupture and release amastigotes that infect additional cells. Sand flies biting an infected host are infected through ingested amastigotes.
Clinical manifestations: there are three forms of Leishmaniasis:
Cutaneous leishmaniasis: caused by Leishmania tropica, it results in nodular to ulcerative skin lesions, typically at the site of the sand fly bite, developing over weeks to months, sometimes with local lymphadenopathy. Lesions usually resolve within months, though secondary bacterial infections can complicate the lesions.
Visceral leishmaniasis: caused by Leishmania donovani, there may be marked hepatosplenomegaly and fever developing in months after infection. However, most infections are asymptomatic.
Mucocutaneous leishmaniasis: caused by Leishmania braziliensis, there can be cutaneous ulcers, as well as ulceration of buccal, pharyngeal, and nasal mucosal surfaces in the months following infection. Secondary bacterial infections are common. The lesions heal slowly over months.
Pathologic findings: Amastigotes are often seen in macrophages and free in tissues, along with mixed inflammatory cell infiltrates and variable necrosis.
Diagnosis: Giemsa-stained smears of scrapings from ulcerative lesions can demonstrate the amastigotes, as can smears from bone marrow or liver biopsies, as well as fine needle aspirates of lymph nodes and liver. Serologic testing may be helpful.
Toxoplasmosis
Transmission: Fecal-oral contamination, from poorly cooked meat, or as a congenital infection.
Distribution: Worldwide, where cats are found.
Life cycle: The cat is the definitive host for Toxoplasma gondii and passes infective oocysts into feces that can contaminate soils from which man can become infected. Alternatively, man may ingest poorly cooked meat with trophozoites from mammals serving as intermediate hosts. Mothers infected with T. gondii can pass the trophozoites through placenta to fetuses. Within man, the oocysts
Clinical manifestations: Infections in immunocompetent hosts are typically asymptomatic, though lymphadenopathy with fever, headache, myalgia, and malaise may occur in a few persons. Immunocompromised persons can develop systemic infections, though central nervous system infection is most likely to be life-threatening. Infected fetuses are often stillborn.
Pathologic findings: The trophozoites in tissues are found in two forms: free tachyzoites and bradyzoites within cysts. Toxoplasma cysts are either true cysts formed outside of cells or pseudocysts that develop within cells. Foci of infection within tissues have focal necrosis with mixed inflammatory cell infiltrates. Abscesses may be seen, particularly in the CNS.
Diagnosis: Serologic diagnosis is helpful, though not always positive in immunocompromised hosts. Radiographic findings of multiple ring-enhancing lesions in the brain by CT scan are suggestive of the diagnosis.
Gastrointestinal Helminths
Ascariasis
Transmission: Fecal-oral contamination.
Distribution: Worldwide
Life cycle: The eggs of Ascaris lumbricoides are ingested and hatch in the small intestine. The larvae then penetrate the intestinal mucosa and enter the bloodstream. The larvae are carried to the pulmonary capillary bed, where they mature for several days, then rupture into the alveoli and are coughed up and swallowed, reaching the small intestine where they mature into adult worms up to 15 to 35 cm long. The adult male and female worms mate, and the female begins releasing eggs passed with feces, completing the cycle. Adult worms live less than a year.
Clinical manifestations: Most infections are asymptomatic. Children are affected more often than adults. Heavy and repeated infestations may produce an allergic reaction with asthmatic pulmonary symptoms. Rarely, large numbers of worms may cause intestinal obstruction.
Diagnosis: Examination of the stool can reveal the appearance of the characteristic 35 to 55 micron mammillated eggs.
Trichuriasis
Transmission: Fecal-oral contamination.
Distribution: Worldwide
Life cycle: The eggs of Trichuris trichiuria are ingested and the larvae are released in the small intestine. The larvae then migrate to the cecum where they penetrate the mucosa and mature into adults. Trichuris sp. are known as "whipworms" because of the slender anterior end of this 3 to 5 mm roundworm that remains embedded in the mucosa. The bulbous posterior end remains free in the colonic lumen, where eggs are passed and out with feces.
Clinical manifestations: Most infections are asymptomatic. Heavy infestations may produce diarrhea, mucosal hemorrhage, and anemia.
Diagnosis: Examination of the stool can reveal the appearance of the characteristic 20 x 50 ovoid eggs with bipolar plugs.
Enterobiasis
Transmission: Fecal-oral contamination or inhalation.
Distribution: Worldwide
Life cycle: The eggs of Enterobius vermicularis (pinworm) are ingested and hatch in the small intestine, then travel to the cecum, where they mature into adults. After mating, adult female worms can begin egg production. The female worms characteristically migrate to the perianal region at night to lay eggs. The eggs are passed into feces or picked up on the hands.
Clinical manifestations: Enterobiasis produces anal pruritis, particlarly in children. Secondary infection in excoriated perianal skin from scratching is possible.
Diagnosis: Examination of the perianal region at night may reveal the adult female worms. The thick-shelled 20 x 50 micron eggs appear flattened on one side. Eggs can be obtained for diagnosis with adhesive tape applied to the perianal skin and then placed on a microscope slide.
Strongyloidiasis
Transmission: Through unprotected skin walking on infected soils.
Distribution: Worldwide, in warm and moist soils.
Life cycle: From the infected host, the larvae are passed in stool and develop in soil for about a week, after which time they are capable of penetrating the skin. After crossing the skin, the larvae travel via the lymphatics or the bloodstream, eventually depositing in the lungs, where they rupture into the alveoli, are coughed up, swallowed, and pass down to the intestine, where they take up residence in the mucosa. Male and female larvae mate. Eggs produced by the female worms hatch in the mucosa, and the larvae are passed in the stool.
A self-perpetuating infection can occur in cases where the intestinal passage in the host is slowed, allowing development of larvae that are capable of penetrating the mucosa or anal skin. This leads to extensive infestations, called "superinfections". Such infestations are more likely to involve extraintestinal sites and are more severe in immunocompromised hosts.
An indirect life cycle is possible when larvae passed into the stool and into soil become free living adult worms. The eggs laid by free living female worms can hatch and develop into infective larvae.
Clinical manifestations: Many infections are asymptomatic. Heavier infestations may lead to diarrhea and malabsorption. Only occasionally is there mucosal ulceration. With dissemination, there can be a pneumonitis, a lymphadenitis, and/or hemorrhage in multiple organs.
Diagnosis: Examination of the stool for larvae. Examination of an intestinal biopsy may reveal the 2 mm worms in the mucosa. With disseminated infections, the worms may appear in extraintestinal tissues on biopsy.
Hookworm
Transmission: Through unprotected skin from infected soils.
Distribution: Worldwide, but highest incidence in tropical and subtropical developing nations with warm, moist soils.
Life cycle: The eggs passed in feces from the host hatch in warm, moist soil to become infective larvae in about a week. These larvae can penetrate unprotected skin. Then the larvae migrate via lymphatics, eventually reaching the lungs, where they rupture into the alveoli, are coughed up, and then swallowed. The larvae pass down the gastrointestinal tract and take up residence in the duodenum and jejunum. The larvae attach to the mucosa via hook-like mouth parts, where they feed on the blood that is released from the mucosa traumatized by the mouth parts. The adult worms reach a size of 1 cm and mate. The female worms then release eggs that are passed via stool.
Clinical manifestations: When few worms are present, the infection is asymptomatic. Heavier infestations lead to greater blood loss and iron deficiency anemia. Diarrhea or pneumonitis may also occur when many worms are present.
Diagnosis: Examination of the stool for the 40 x 70 micrometer thin-shelled eggs.
Cysticercosis
Transmission: Ingestion of poorly cooked meat, or fecal-oral contamination.
Distribution: Worldwide. The two major species are:
Life cycle: The ingestion of uncooked or poorly cooked meat containing the larvae results in man becoming a definitive host, with mature tapeworms in the small intestine that release eggs into the stool. However, if the eggs are ingested via fecal-oral contamination, then man becomes an intermediate host, and the ingested eggs hatch to become embryos that, after penetrating the mucosa, are carried by the bloodstream to many organs, where they become a cystic larva.
Clinical manifestations: Presence of adult tapeworms in the intestine is typically asymptomatic. Cysticerci in brain can cause seizures.
Diagnosis: Examination of the stool for eggs. Computed tomographic (CT) scan of the head may reveal cysticerci. Removed cysticerci can be examined histologically.
Echinococcosis
Life cycle: The ingestion of infective eggs by man is followed by hatching of oncospheres in the intestine. The oncospheres penetrate the intestinal wall and migrate to various tissues, often liver or lungs, where hydatid cyst development occurs over many years. The laminated wall of the cyst is lined by a germinal epithelium from which daughter larvae develop by the thousands and float into the clear fluid filling the unilocular cyst of Echinococcus granulosus. These larvae (one of which is seen here with characteristic hooklets of the scolex) settle out and form the so-called "hydatid sand". Ingestion of eggs by sheep, goats, and cattle is followed by development of hydatid cysts in the intestine. When carnivores (typically dogs) feed on the viscera of these intermediate hosts, the hydatids release scolices that develop into adult worms in the intestine that can release eggs into feces.
Clinical manifestations: The hydatids produce mass lesions. Rupture of hydatid cysts may produce anaphylaxis; scolices released from rupture can produce additional cysts.
Diagnosis: Radiographic methods to locate hydatid cysts can be done. Serologic methods may aid in diagnosis as well.
Blood and Tissue Helminths
Schistosomiasis
Transmission: Infective cercaria, found in standing water where snails are located, penetrate unprotected skin.
Distribution: Tropical and subtropical regions, depending upon distribution of the intermediate snail hosts. The three major species are:
Schistosoma mansoni - Found in tropical regions of Africa, the Middle East, South America, Central America, and some islands of the Caribbean.
Schistosoma japonicum - Found in tropical and subtropical regions of East Asia.
Schistosoma hematobium - Found in tropical regions of Africa and the Middle East.
Life cycle: The cilated, free-swimming cercariae are released from the intermediate host, the snail, that lives in standing or slow moving water (such as irrigation canals). These cercariae can penetrate the skin of a human host who is in the water, then they migrate to penetrate the vascular system and are carried to the portal venous system, where they mature to adult male and female worms. These adults worms remain in apposition and migrate to the intestinal venous plexuses (S. mansoni and S. japonicum) or venous plexuses near bladder and rectum (S. hematobium). The female worm releases eggs with sharp spines that cut through tissues into the small intestine or colon (S. mansoni and S. japonicum respectively) or the bladder (S. hematobium). The eggs in stool or urine reach the water and hatch, releasing miracidia that can infect snails, where they develop to cercariae.
Clinical manifestations: The cercariae penetrating skin produce local itching and erythema. The adult worms do not elicit a significant inflammatory response, but the eggs produce considerable tissue destruction with inflammation.
Diagnosis: Examination of the stool for eggs of S. mansoni or S. japonicum; examination of urine for eggs of S. hematobium. Blood may be present in stool or urine.
Filariasis
Transmission: Mosquito bite.
Distribution: Tropical regions with mosquito species capable of harboring the worms.
Life cycle: The microfilaria are taken up via a mosquito bite into the mosquito, where they are then transformed into infective larvae that can be transferred to the next host bitten by the mosquito. The larvae migrate either to lymphatics or to subcutaneous connective tissue, depending upon the species. There they mature into adult worms that mate, and the females can release microfilaria.
Clinical manifestations: There are varying host responses to filarial infections, and repeated infections over years may be necessary for the most severe manifestations to occur. There are two major forms of disease:
Lymphatic filariasis: the worms live in lymphatics and may cause lymphedema of lower extremities, external genitalia, and sometimes upper extremities. Acutely, within months after acquring the infection, there may be fever and lymphadenopathy. Eventually, a chronic form of the disease manifests with pronounced lymphedema that may lead to the condition known as "elephantiasis" because of the marked enlargement. Adult worms can be up to 10 cm long. The two main species are:
Onchocerciasis: the worms live in subcutaneous connective tissues connective tissues of the eye that can lead to an inflammatory response. The inflammation can result in blindness. Skin involvement can result in dermatitis with pruritis, depigmentation or hyperpigmentation, and fibrosis with nodularity. The species responsible is Onchocerca volvulus, which may be found in Central Africa, Central America, and the northern parts of South America. Adult worms can be up to 50 cm long.
Diagnosis: Microfilaria can be seen in smears made from tissue that is infected. The adult worms may be seen in tissue sections of involved areas. A peripheral eosinophilia can be present.
Trichinosis
Transmission: Ingestion of poorly cooked meat.
Distribution: Worldwide.
Life cycle: The definitive host is a carnivore or an omnivore (most often a pig, but wild animals such as bears may also be a definitive host). Adult worms live in the duodenum and jejunal mucosa of the definitive host, where the adult male and female worms mate. The female worm releases larvae that penetrate the mucosa, entering the bloodstream, and are carried to skeletal muscle, where they encyst and remain viable for years. Another carnivore or omnivore (including man) that eats the meat (skeletal muscle) of the definitive host can become infected. Thoroughly cooking the meat destroys the cysts. If viable cysts are ingested, they release larvae in the stomach, which then penetrate the mucosa and are carried via the bloodstream to skeletal muscle.
Clinical manifestations: Fever, weakness, malaise, myalgia, and headache. Onset is typically a couple of weeks after ingestion, with symptoms continuing for several more weeks.
Diagnosis: Clinical suspicion after obtaining history. Peripheral eosinophilia. Serologic titers may aid in diagnosis. Muscle biopsy is not often done.
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