Life Cycle of Wuchereria bancrofti:



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[Schistosoma haematobium] [Schistosoma intercalatum] [Schistosoma japonicum]

[Schistosoma mansoni] [Schistosoma mekongi]

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:

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Eggs are eliminated with feces or urine [pic].  Under optimal conditions the eggs hatch and release miracidia [pic], which swim and penetrate specific snail intermediate hosts [pic].  The stages in the snail include 2 generations of sporocysts [pic]and the production of cercariae [pic].  Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host [pic], and shed their forked tail, becoming schistosomulae [pic].  The schistosomulae migrate through several tissues and stages to their residence in the veins ([pic], [pic]).  Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species [pic].  For instance, S. japonicum is more frequently found in the superior mesenteric veins draining the small intestine [pic], and S. mansoni occurs more often in the superior mesenteric veins draining the large intestine [pic].  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 [pic], 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 [pic].  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.

 

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[Entamoeba histolytica]

Causal Agent:

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:

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Cysts and trophozoites are passed in feces [pic].  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 [pic]in fecally contaminated food, water, or hands.  Excystation [pic]occurs in the small intestine and trophozoites [pic]are released, which migrate to the large intestine.  The trophozoites multiply by binary fission and produce cysts [pic], and both stages are passed in the feces [pic].  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 ([pic]: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool.  In some patients the trophozoites invade the intestinal mucosa ([pic]: intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs ([pic]: 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.

 

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

Causal Agents:

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):

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Eggs are passed in the stool [pic], 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 [pic], and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective [pic].  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 [pic].  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 [pic].  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.

Life Cycle (cutaneous larval migrans):

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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 [pic], 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 [pic], and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective [pic].  These infective larvae can survive 3 to 4 weeks in favorable environmental conditions.  On contact with the animal host [pic], 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 [pic].  Humans may also become infected when filariform larvae penetrate the skin [pic].  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.

 

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[Capillaria (=Eucoleus) aerophila] [Capillaria (=Calodium) hepatica] [Capillaria (=Paracapillaria) philippinensis]

Causal Agents:

The nematode (roundworm) Capillaria philippinensis causes human intestinal capillariasis.  Two other Capillaria species parasitize animals, with rare reported instances of human infections.  They are C. hepatica, which causes in humans hepatic capillariasis, and C. aerophila, which causes in humans pulmonary capillariasis.

Life Cycle:

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Typically, unembryonated eggs are passed in the human stool [pic]and become embryonated in the external environment [pic]; after ingestion by freshwater fish, larvae hatch, penetrate the intestine, and migrate to the tissues [pic].  Ingestion of raw or undercooked fish results in infection of the human host [pic].  The adults of Capillaria philippinensis (males: 2.3 to 3.2 mm; females: 2.5 to 4.3 mm) reside in the human small intestine, where they burrow in the mucosa [pic].  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) [pic].  Capillaria philippinesis is currently considered a parasite of fish eating birds, which seem to be the natural definitive host [pic].

 

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Capillaria hepatica has a direct life cycle that requires only one host.  Adult worms invade the liver of the host (usually rodents, but may also be pigs, carnivores and primates, including humans), and lay hundreds of eggs in the surrounding parenchyma [pic].  The eggs are not passed in the feces of the host, and remain in the liver until the animal dies and decomposes [pic], or is eaten by a predator or scavenger [pic].  Eggs ingested by such an animal are unembryonated, are not infectious, and are passed in the feces, providing an efficient mechanism to release eggs into the environment [pic].  Cannibalism has been reported as an important role in transmission among rodent populations.  Eggs embryonate in the environment [pic], where they require air and damp soil to become infective.  Under optimal conditions, this takes about 30 days.  The cycle continues when embryonated eggs are eaten by a suitable mammalian host [pic].  Infective eggs hatch in the intestine, releasing larvae.  The larvae migrate via the portal vein to the liver.  Larvae take about four weeks to mature into adults and mate.  Humans are usually infected after ingesting embryonated eggs in fecal-contaminated food, water, or soil [pic].  Occasionally in humans, larvae will migrate to the lungs, kidneys, or other organs.  The presence of C. hepatica eggs in human stool during routine ova-and-parasite (O&P) examinations indicates spurious passage of ingested eggs, and not a true infection.  Diagnosis in humans is usually achieved by finding adults and eggs in biopsy or autopsy specimens.

Geographic Distribution:

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.  Rare cases of human infections with C. hepatica and C. aerophila have been reported worldwide.

 

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[Ascaris lumbricoides]

Causal Agent:

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:

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Adult worms [pic]live in the lumen of the small intestine.  A female may produce approximately 200,000 eggs per day, which are passed with the feces [pic].  Unfertilized eggs may be ingested but are not infective.  Fertile eggs embryonate and become infective after 18 days to several weeks [pic], depending on the environmental conditions (optimum: moist, warm, shaded soil).  After infective eggs are swallowed [pic], the larvae hatch [pic], invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs [pic].  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 [pic].  Upon reaching the small intestine, they develop into adult worms [pic].  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.

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[Brugia malayi] [Brugia timori] [Dirofilaria spp.] [Loa loa] [Mansonella ozzardi] [Mansonella perstans]

[Mansonella streptocerca] [Onchocerca volvulus] [Wuchereria bancrofti]  

Causal Agents:

Filariasis is caused by nematodes (roundworms) that inhabit the lymphatics and subcutaneous tissues.  Eight main species infect humans.  Three of these are responsible for most of the morbidity due to filariasis: Wuchereria bancrofti and Brugia malayi cause lymphatic filariasis, and Onchocerca volvulus causes onchocerciasis (river blindness).  The other five species are Loa loa, Mansonella perstans, M. streptocerca, M. ozzardi, and Brugia timori.  (The last species also causes lymphatic filariasis.)

Life Cycles:

Infective larvae are transmitted by infected biting arthropods during a blood meal.  The larvae migrate to the appropriate site of the host's body, where they develop into microfilariae-producing adults.  The adults dwell in various human tissues where they can live for several years.  The agents of lymphatic filariasis reside in lymphatic vessels and lymph nodes; Onchocerca volvulus in nodules in subcutaneous tissues; Loa loa in subcutaneous tissues, where it migrates actively; Brugia malayi in lymphatics, as with Wuchereria bancrofti; Mansonella streptocerca in the dermis and subcutaneous tissue; Mansonella ozzardi apparently in the subcutaneous tissues; and M. perstans in body cavities and the surrounding tissues.  The female worms produce microfilariae which circulate in the blood, except for those of Onchocerca volvulus and Mansonella streptocerca, which are found in the skin, and O. volvulus which invade the eye.  The microfilariae infect biting arthropods (mosquitoes for the agents of lymphatic filariasis; blackflies [Simulium] for Onchocerca volvulus; midges for Mansonella perstans and M. streptocerca; and both midges and blackflies for Mansonella ozzardi; and deerflies [Chrysops] for Loa loa).  Inside the arthropod, the microfilariae develop in 1 to 2 weeks into infective filariform (third-stage) larvae.  During a subsequent blood meal by the insect, the larvae infect the vertebrate host.  They migrate to the appropriate site of the host's body, where they develop into adults, a slow process than can require up to 18 months in the case of Onchocerca.

Brugia malayi Mansonella streptocerca

Loa loa Onchocerca vovulus

Mansonella ozzardi Wuchereria bancrofti

Mansonella perstans

Click on genus and species name above to see specific life cycles of each parasite.

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.  The agent of river blindness, Onchocerca volvulus, occurs mainly in Africa, with additional foci in Latin America and the Middle East.  Among the other species, Loa loa and Mansonella streptocerca are found in Africa; Mansonella perstans occurs in both Africa and South America; and Mansonella ozzardi occurs only in the American continent.

 

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[Brugia malayi] [Brugia timori] [Dirofilaria spp.] [Loa loa] [Mansonella ozzardi] [Mansonella perstans]

[Mansonella streptocerca] [Onchocerca volvulus] [Wuchereria bancrofti]

Life Cycle of Wuchereria bancrofti:

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Different species of the following genera of mosquitoes are vectors of W. bancrofti filariasis depending on geographical distribution.  Among them are: Culex (C. annulirostris, C. bitaeniorhynchus, C. quinquefasciatus, and C. pipiens); Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas, A. merus, A. punctulatus and A. wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A. darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, A. rotumae, A. scapularis, and A. vigilax); Mansonia (M. pseudotitillans, M. uniformis); Coquillettidia (C. juxtamansonia).  During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound [pic].  They develop in adults that commonly reside in the lymphatics [pic].  The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while the males measure about 40 mm by .1 mm.  Adults produce microfilariae measuring 244 to 296 μm by 7.5 to 10 μm, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity.  The microfilariae migrate into lymph and blood channels moving actively through lymph and blood [pic].  A mosquito ingests the microfilariae during a blood meal [pic].  After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles [pic].  There the microfilariae develop into first-stage larvae [pic]and subsequently into third-stage infective larvae [pic].  The third-stage infective larvae migrate through the hemocoel to the mosquito's prosbocis [pic]and can infect another human when the mosquito takes a blood meal [pic].

 

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[Giardia intestinalis (syn. Giardia lamblia)]

Causal Agent:

Giardia intestinalis is a protozoan flagellate (Diplomonadida).  This protozoan was initially named Cercomonas intestinalis by Lambl in 1859 and renamed Giardia lamblia by Stiles in 1915, in honor of Professor A. Giard of Paris and Dr. F. Lambl of Prague.  However, many consider the name, Giardia intestinalis, to be the correct name for this protozoan.  The International Commission on Zoological Nomenclature is reviewing this issue.

Life Cycle:

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Cysts are resistant forms and are responsible for transmission of giardiasis.  Both cysts and trophozoites can be found in the feces (diagnostic stages) [pic].  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) [pic].  In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) [pic].  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 [pic].  Encystation occurs as the parasites transit toward the colon.  The cyst is the stage found most commonly in nondiarrheal feces [pic].  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.

 

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[Pediculus humanus capitis] [Pediculus humanus humanus]

Causal Agent:

Pediculus humanus capitis, the head louse, is an insect of the order Psocodea and is an ectoparasite whose only host are humans.  The louse feeds on blood several times daily and resides close to the scalp to maintain its body temperature.

Life Cycle:

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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 [pic].  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 [pic].  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 ([pic], [pic]) 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 [pic].  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.

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.  In the United States, African-Americans are rarely infested with head lice.  This is believed to be due to the American louse’s preference for the shape and width of the hair shaft of other races.

 

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[Sarcoptes scabiei]

Causal Agent:

Sarcoptes scabiei var. hominis, the human itch mite, is in the arthropod class Arachnida, subclass Acari, family Sarcoptidae.  The mites burrow into the upper layer of the skin but never below the stratum corneum.  The burrows appear as tiny raised serpentine lines that are grayish or skin-colored and can be a centimeter or more in length.  Other races of scabies mites may cause infestations in other mammals, such as domestic cats, dogs, pigs, and horses.  It should be noted that races of mites found on other animals may cause a self-limited infestation in humans with temporary itching due to dermatitis; however they do not multiply on the human host.

Life Cycle:

[pic]

Sarcoptes scabiei undergoes four stages in its life cycle:  egg, larva, nymph and adult.  Females deposit 2-3 eggs per day as they burrow under the skin [pic].  Eggs are oval and 0.10 to 0.15 mm in length [pic]and hatch in 3 to 4 days.  After the eggs hatch, the larvae migrate to the skin surface and burrow into the intact stratum corneum to construct almost invisible, short burrows called molting pouches.  The larval stage, which emerges from the eggs, has only 3 pairs of legs [pic]and lasts about 3 to 4 days.  After the larvae molt, the resulting nymphs have 4 pairs of legs [pic].  This form molts into slightly larger nymphs before molting into adults.  Larvae and nymphs may often be found in molting pouches or in hair follicles and look similar to adults, only smaller.  Adults are round, sac-like eyeless mites.  Females are 0.30 to 0.45 mm long and 0.25 to 0.35 mm wide, and males are slightly more than half that size.  Mating occurs after the active male penetrates the molting pouch of the adult female [pic].  Mating takes place only once and leaves the female fertile for the rest of her life.  Impregnated females leave their molting pouches and wander on the surface of the skin until they find a suitable site for a permanent burrow.  While on the skin’s surface, mites hold onto the skin using sucker-like pulvilli attached to the two most anterior pairs of legs.  When the impregnated female mite finds a suitable location, it begins to make its characteristic serpentine burrow, laying eggs in the process.  After the impregnated female burrows into the skin, she remains there and continues to lengthen her burrow and lay eggs for the rest of her life (1-2 months).  Under the most favorable of conditions, about 10% of her eggs eventually give rise to adult mites.  Males are rarely seen; they make temporary shallow pits in the skin to feed until they locate a female’s burrow and mate.

Transmission occurs primarily by the transfer of the impregnated females during person-to-person, skin-to-skin contact.  Occasionally transmission may occur via fomites (e.g., bedding or clothing).  Human scabies mites often are found between the fingers and on the wrists.

Geographic Distribution:

Scabies mites are distributed worldwide, affecting all races and socioeconomic classes in all climates.

 

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[Trichuris trichiura]

Causal Agent:

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

Life Cycle:

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The unembryonated eggs are passed with the stool [pic].  In the soil, the eggs develop into a 2-cell stage [pic], an advanced cleavage stage [pic], and then they embryonate [pic]; 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 [pic]that mature and establish themselves as adults in the colon [pic].  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.

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[Strongyloides stercoralis]

Causal Agent:

The nematode (roundworm) Strongyloides stercoralis.  Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.

Life Cycle:

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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 [pic](see "Parasitic cycle" below) can either molt twice and become infective filariform larvae (direct development) [pic]or molt four times and become free living adult males and females [pic]that mate and produce eggs [pic]from which rhabditiform larvae hatch [pic].  The latter in turn can either develop [pic]into a new generation of free-living adults (as represented in [pic]), or into infective filariform larvae [pic].  The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) [pic].

Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin [pic], 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 [pic].  In the small intestine they molt twice and become adult female worms [pic].  The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs [pic], which yield rhabditiform larvae.  The rhabditiform larvae can either be passed in the stool [pic](see "Free-living cycle" above), or can cause autoinfection [pic].  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 Features:

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.

Laboratory Diagnosis:

Diagnosis rests on the microscopic identification of larvae (rhabditiform and occasionally filariform) in the stool or duodenal fluid.  Examination of serial samples may be necessary, and not always sufficient, because stool examination is relatively insensitive.

The stool can be examined in wet mounts:

▪ directly

▪ after concentration (formalin-ethyl acetate)

▪ after recovery of the larvae by the Baermann funnel technique

▪ after culture by the Harada-Mori filter paper technique

▪ after culture in agar plates

The duodenal fluid can be examined using techniques such as the Enterotest string or duodenal aspiration.  Larvae may be detected in sputum from patients with disseminated strongyloidiasis.

Diagnostic findings

▪ Microscopy

▪ Antibody detection

▪ Morphologic comparison with other intestinal parasites

Treatment:

The drug of choice for the treatment of uncomplicated strongyloidiasis is ivermectin with albendazole* as the alternative.  All patients who are at risk of disseminated strongyloidiasis should be treated.  For additional information, see the recommendations in The Medical Letter (Drugs for Parasitic Infections).

*This drug is approved by the FDA, but considered investigational for this purpose.

[pic]

[Enterobius vermicularis]

Causal Agent:

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:

[pic]

Eggs are deposited on perianal folds [pic].  Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area [pic].  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 [pic]and the adults establish themselves in the colon [pic].  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 [pic].  The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions [pic].  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 Features:

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.

Laboratory Diagnosis:

Microscopic identification of eggs collected in the perianal area is the method of choice for diagnosing enterobiasis.  This must be done in the morning, before defecation and washing, by pressing transparent adhesive tape ("Scotch test", cellulose-tape slide test) on the perianal skin and then examining the tape placed on a slide.  Alternatively, anal swabs or "Swube tubes" (a paddle coated with adhesive material) can also be used.  Eggs can also be found, but less frequently, in the stool, and occasionally are encountered in the urine or vaginal smears.  Adult worms are also diagnostic, when found in the perianal area, or during ano-rectal or vaginal examinations.

Diagnostic findings

▪ Microscopy

▪ Morphologic comparison with other intestinal parasites

Treatment:

The drug of choice is pyrantel pamoate.  Measures to prevent reinfection, such as personal hygiene and laundering of bedding, should be discussed and implemented in cases where infection affects other household members.  For additional information, see the recommendations in The Medical Letter (Drugs for Parasitic Infections).

 

[pic] Hookworm ova (Ancylostoma duodenale) [pic]Adult hookworm head [pic]Ascaris ova

[pic]Microfilaria of W. Bancrofti

[pic]Capillaria philippinensis egg

[pic] [pic]

Giardia intestinalis cysts and trophozoites

[pic][pic]

A B

A:  Eggs of E. vermicularis in a cellulose-tape preparation.

B:  Eggs of E. vermicularis in a wet mount.

[pic]

[Enterobius vermicularis]

Adult males of Enterobius vermicularis measure up to 2.5 mm long by 0.1-0.2 mm wide; adult females measure 8-13 mm long by 0.3-0.5 mm wide.  Adult males have a blunt posterior end with a single spicule; females possess a long pointed tail.  In both sexes, there are cephalic expansions.

[pic]

A

A:  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.

[pic] [pic]

B C

B:  Close-up of the anterior end of the worm in Figure A.  The esophagus, divided into muscular and bulbous portions and separated by a short, narrow isthmus, is visible in the image, as are the cephalic expansions.

C:  Close-up of the posterior end of the worm in Figure A.  Note the blunt end.  The spicule is withdrawn into the worm in this specimen.

[pic] [pic]

D E

D:  Anterior end of an adult female of E. vermicularis, recovered from a colonscopy.  Image contributed by the South Carolina Department of Health and Environmental Control, Bureau of Laboratories.

E:  Posterior end of the worm in Figure D. Note the long, slender pointed tail.

 

[pic]

[Strongyloides stercoralis]

Adults of Strongyloides stercoralis may be found in the human host or soil.  In the human host there are no parasitic males, and parasitic females are long, slender and measure 2.0-3.0 mm in length.  In the environment, rhabditoid larvae may develop into infective filariform (L3) larvae (direct cycle) or free-living adults that contain both males and females (indirect cycle).  Free-living adult males measure up to 750 µm long; free-living females measure up to 1.0 mm long.

[pic] [pic]

A B

A: Free-living adult male S. stercoralis. Notice the presence of the spicule (red arrow).

B: Free living adult male S. stercoralis, showing a spicule (red arrow).  A smaller, rhabditiform larva lies adjacent to the adult male.

[pic] [pic]

C D

C: Adult free-living female S. stercoralis alongside a smaller rhabditoid larva.  Notice the developing eggs in the adult female.

D: Adult free-living female S. stercoralis.  Notice the row of eggs within the female’s body.

[Strongyloides stercoralis]

The first-stage rhabditoid larvae (L1) of Strongyloides stercoralis are 180-380 µm long, with a short buccal canal, a rhabditoid esophagus and a prominent genital primordium.  These L1 larvae are usually found in stool, as the eggs embryonate and hatch in the mucosa of the small intestine of the host.  They may also be found in soil and cultured feces.

[pic] [pic]

A B

A, B: Rhabdititoid larvae of S. stercoralis in unstained wet mounts of stool.  Notice the short buccal canal and the genital primordium (red arrows).

[pic] [pic]

C D

C: Close-up of the anterior end of a rhabditoid larva of S. stercoralis, showing the short buccal canal (red arrow) and the rhabditoid esophagus (blue arrow).  Image taken at 1000x oil magnification.

D: Rhabditoid larva of S. stercoralis in an unstained wet mount of stool.  Notice the short buccal canal and the genital primordium (red arrow).

[pic] [pic]

E F

E: Rhabditoid larva of S. stercoralis in an unstained wet mount of stool.  Notice the rhabditoid esophagus (blue arrow) and prominent genital primordium (red arrow).

F: Rhabditoid larva of S. stercoralis in an unstained wet mount of stool.  Notice the prominent genital primordium (blue arrow), rhabditoid esophagus (red arrow) and short buccal canal (green arrow).

 

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