Nematodes

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Nematodes (Roundworms)

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G WHAT R PFTS

Guinea worm (dracunculiasis)

Whipworm (trichuria trichuris)

Hookworm (ancylostoma, necatur)

Ascarias (ascara)

Thread (strongyloides)

Round (toxocara)

Pin (enterobius)

Filaria

Trichinosis (Trichinella)

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Guinea Worm

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Cause: dracunculus medinensis

Vector: cepopods (small crustaceans)

Pathophysiology: drinking unfiltered water containing copepods (small crustaceans) which are infected with larvae of D. medinensis. Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space. After maturation into adults and copulation, the male worms die and the females (length: 70 to 120 cm) migrate in the subcutaneous tissues towards the skin surface. Approximately one year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures.

Presentation: The clinical manifestations are localized but incapacitating. The worm emerges as a whitish filament (duration of emergence: 1 to 3 weeks) in the center of a painful ulcer, accompanied by inflammation and frequently by secondary bacterial infection.

Diagnosis: clinical picture

Treatment: removal of worm

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Whipworm

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Cause: trichuria trichiuris

Vector: none (water)

Pathophysiology: 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.

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

Diagnosis: Microscopic identification of whipworm eggs in feces

Treatment: Albendazole

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Hookworm

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Cause: Ancylostoma duodenale, necatur americanus

Vector: None (water)

Pathophysiology: 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; 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

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

Diagnosis: Microscopic identification of eggs in the stool

Treatment: Albendazole

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Ascariasis

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Cause: Ascaris lumbricoides

Vector: None

Pathophysiology: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

Presentation: 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

Diagnosis: Microscopic identification of eggs in the stool

Treatment: Albendazole

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Threadworm

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Cause: Strongyloides stercoralis

Vector: None (filaria)

Pathophysiology: Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine. 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

Presentation: Frequently asymptomatic. Gastrointestinal symptoms include abdominal pain and diarrhea. Pulmonary symptoms (including Loeffler’s syndrome) can occur during pulmonary migration of the filariform larvae. Dermatologic manifestations include urticarial rashes in the buttocks and waist areas. Disseminated strongyloidiasis occurs in immunosuppressed patients, can present with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal.

Diagnosis: Microscopic identification of larvae (rhabditiform and occasionally filariform) in the stool or duodenal fluid

Treatment: Ivermectin

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Roundworm

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Cause: toxocara canis

Vector: none (dog)

Pathophysiology: Humans are accidental hosts who become infected by ingesting infective eggs in contaminated soil or infected paratenic hosts . After ingestion, the eggs hatch and larvae penetrate the intestinal wall and are carried by the circulation to a wide variety of tissues (liver, heart, lungs, brain, muscle, eyes) . While the larvae do not undergo any further development in these sites, they can cause severe local reactions that are the basis of toxocariasis.

Presentation: Many human infections are asymptomatic, with only eosinophilia and positive serology. The two main clinical presentations of toxocariasis are visceral larva migrans (VLM) and ocular larva migrans (OLM). In VLM, which occurs mostly in preschool children, the larvae invade multiple tissues (liver, heart, lungs, brain, muscle) and cause various symptoms including fever, anorexia, weight loss, cough, wheezing, rashes, hepatosplenomegaly, and hypereosinophilia.

Diagnosis: Serology

Treatment: Albendazole

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Pinworm

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Cause: enterobius

Vector: none

Pathophysiology: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.

Presentation:Enterobiasis is frequently asymptomatic. The most typical symptom is perianal pruritus, especially at night, which may lead to excoriations and bacterial superinfection. Occasionally, invasion of the female genital tract with vulvovaginitis and pelvic or peritoneal granulomas can occur.

Diagnosis: Microscopic identification of eggs collected

Treatment: Albendazole (or mebendazole)

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Filarial Nematodes

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MOWLD

Mansonella

Onchocerciasis

Wuchereria

Loa loa

Dirofilariasis

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Trichinellosis

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Cause: Trichinella

Vector: none

Pathophysiology:Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms. After 1 week, the females release larvae that migrate to striated muscles where they encyst. [Domestic or Sylvatic Cycles]

Presentation:Light infections may be asymptomatic. Intestinal invasion can be accompanied by gastrointestinal symptoms (diarrhea, abdominal pain, vomiting). Larval migration into muscle tissues (one week after infection) can cause periorbital and facial edema, conjunctivitis, fever, myalgias, splinter hemorrhages, rashes, and peripheral eosinophilia.

Diagnosis:The suspicion of trichinellosis (trichinosis), based on history, clinical symptoms, and eosinophilia, can be confirmed by specific diagnostic tests, including antibody detection, muscle biopsy, and microscopy.

Treatment: Albendazole

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Diagnosis for all non-filarial Nematodes (except filarial forms [including strongyloides] and forms where humans are incidental hosts [toxocariasis & trichinella])

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Identification of eggs in stool

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Diagnosis for toxocariasis and trichinellosis

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Serology

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Treatment for all Nematodes (except strongyloides)

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Albendazole

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Treatment for Strongyloides

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Ivermectin

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Filarial Nematodes

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MOWLD

Mansonella

Onchocerciasis

Wuchereria

Loa loa

Dirofilariasis

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Mansonella

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Cause: Mansonella streptocerca (skin), perstans or ozzardi

Vector: Midge (culicoides)

Pathophysiology:During a blood meal, an infected midge (genus Culicoides) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that reside in the dermis. Adults produce unsheathed and non-periodic microfilariae, which reside in the skin but can also reach the peripheral blood.

Presentation: Often asymptomatic, can be associated with angioedema, pruritus, fever, headaches, arthralgias, and neurologic manifestations. M. streptocerca can cause skin manifestations including pruritus, papular eruptions and pigmentation changes. M. ozzardi can cause symptoms that include arthralgias, headaches, fever, pulmonary symptoms, adenopathy, hepatomegaly, and pruritus.

Diagnosis:Mansonella perstans and M. ozzardi are diagnosed by the finding of microfilariae circulating in blood. Mansonella streptocerca is usually diagnosed by finding microfilariae in skin snips. NO PERIODICITY.

Treatment: No great single agent well studied (doxy, albendazole).

There are no bad times to listen to Marilyn Manson (no periodicity)

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Onchocerciasis

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Cause: Onchocerca volvulus

Vector: Blackfly (Simulium)

Pathophysiology:An infected blackfly introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound. In subcutaneous tissues the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues.Adults can live in the nodules for approximately 15 years.

Presentation:Onchocerciasis can cause pruritus, dermatitis, onchocercomata (subcutaneous nodules), and lymphadenopathies. The most serious manifestation consists of ocular lesions that can progress to blindness.

Diagnosis: Finding of microfilariae in skin snips or adults in biopsy specimens of skin nodules.

Treatment: Ivermectin

Water never stops flowing: no periodicity, also skin snip is diagnostic test so periodicity doesn't really matter

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Lymphatic Filiariasis

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Cause: Wuchereria bancrofti

Vector: Many (culex, aedes, anopheles, mansonia)

Pathophysiology: An infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly reside in the lymphatics. Adults produce microfilariae which are sheathed and have nocturnal periodicity.The microfilariae migrate into lymph and blood channels moving actively through lymph and blood.

Presentation: Most commonly asymptomatic. Some patients develop lymphatic dysfunction causing lymphedema and elephantiasis (frequently in the lower extremities) and hydrocele and scrotal elephantiasis. Episodes of febrile lymphangitis and lymphadenitis may occur.

Diagnosis: Identification of microfilaria in peripheral blood smears (thick or thin)

Treatment: Diethylcarbmazine

BANCrofti - BANCs are robbed at night - nocturnal periodicity

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Laoisis

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Cause: Loa loa

Vector: Flies (Chrysops)

Pathophysiology: An infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue. Adults produce microfilariae which are sheathed and have diurnal periodicity. During the day they are found in peripheral blood, but during the non-circulation phase, they are found in the lungs.

Presentation: Most commonly asymptomatic. Episodic angioedema (Calabar swellings) and subconjunctival migration of an adult worm can occur.

Diagnosis: Finding of microfilaria in peripheral blood smears or adults in the subconjunctiva.

Treatment: Diethylcarbamazine

Eye, Cry, Chrysops crying Calabria swelling

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Dirofilariasis

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Cause: Dirofilaria immitis

Vector: Mosquito (Culex, Aedes, Anopheles, Mansonia)

Pathophysiology: During a blood meal, an infected mosquito (Aedes, Culex, Anopheles, Mansonia) introduces third-stage filarial larvae into the skin of the definitive host, which is usually a domestic dog or coyote in the United States (or humans in the case of human disease) where they penetrate into the bite wound. In the definitive host, the L3 larvae turn into adults. Adults reside in pulmonary arteries, and are occasionally found in the right ventricle of the heart . Adults can live for 5 - 10 years. In the heart, the female worms are capable of producing microfilariae over their lifespan. The microfilariae are found in peripheral blood. In humans , D. immitis larvae tend to follow the same migratory pathway as in the canine host, ending up in the lungs, where they often lodge in small-caliber vessels, causing infarcts and typical "coin lesions" visible on radiographs.

Presentation: Dirofilaria immitis

causes pulmonary disease in humans. The parasite cannot develop in the human host and larvae that migrate to the heart usually die. Dead worms produce infarcts when they lodge in pulmonary vessels; these infarcts are usually referred to as "coin lesions". Following embolization, patients may present with chest pain, cough, fever, chill, malaise, and hemoptysis.

Diagnosis: D. immitis is usually diagnosed by the finding of coin lesions on chest roentgenograms. The species that produce subcutaneous nodules are diagnosed by the finding of adult worms in biopsy specimens of the nodules.

Treatment: The definitive treatment of Dirofilaria infection in humans is surgical removal of lung granulomas and subcutaneous nodules; this treatment is also curative. In many cases, no drug treatment is necessary.

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Treatment of all filariform nematodes (except onchocerciasis)

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Diethylcarbamazine

Diethylfilarizime

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Diagnosis of all filariform nematodes (except Dirofilariasis)

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Visualization of the microfilaria or the adult worms in skin snip/subcutaneous nodule biopsies

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Pathophysiology of All Filaria

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An infected vector introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that have a specific are they usually reside and produce microfilariae.

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Treatment of Onchocerciasis

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Ivermectin

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Flatworms (Platyhelminths)

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Tapeworms-Cestodes

Flukes-Trematodes

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Flukes

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Intestinal: Fasciolopsis

Hepatic: Fasciola hepatica

Biliary: Clonorchis Opisthorchis

Pulmonary: Paragonimus

Blood: Schistosomiasis

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Intestinal Fluke

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Cause: Fasciolopsis buski

Vector: Snail - Aquatic Plants

Pathophysiology:Immature eggs are discharged into the intestine and stool. Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host . In the snail the parasites undergo several developmental stages (sporocysts , rediae, and cercariae). The cercariae are released from the snail and encyst as metacercariae on aquatic plants . The mammalian hosts become infected by ingesting metacercariae on the aquatic plants. After ingestion, the metacercariae excyst in the duodenum and attach to the intestinal wall. There they develop into adult flukes

Presentation: Most infections are light and asymptomatic. In heavier infections, symptoms include diarrhea, abdominal pain, fever, ascites, anasarca and intestinal obstruction.

Diagnosis: Microscopic identification of eggs, or more rarely of the adult flukes, in the stool or vomitus (eggs are indistinguishable from those of fasciola hepatica [similar name])

Treatment: Praziquantel

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Liver Fluke

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Cause: Fasciola hepatica

Vector: Snail - Watercress

Pathophysiology:Eggs become embryonated in water, eggs release miracidia , which invade a suitable snail intermediate host. In the snail the parasites undergo several developmental stages (sporocysts , rediae , and cercariae). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress. After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults. The adult flukes reside in the large biliary ducts of the mammalian host.

Presentation: During the acute phase (caused by the migration of the immature fluke through the hepatic parenchyma), manifestations include abdominal pain, hepatomegaly, fever, vomiting, diarrhea, urticaria and eosinophilia, and can last for months. In the chronic phase (caused by the adult fluke within the bile ducts), the symptoms are more discrete and reflect intermittent biliary obstruction and inflammation.

Diagnosis: Microscopic identification of eggs is useful in the chronic (adult) stage. Eggs can be recovered in the stools or in material obtained by duodenal or biliary drainage (eggs are indistinguishable from fasciolopsis buski [similar name])

Treatment: Triclabendazole

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Biliary Fluke

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Cause: Clonorchis sinensis, Opisthorchis viverrini

Vector: Snail - Fish

Pathophysiology: The adult flukes deposit fully developed eggs that are passed in the feces. After ingestion by a suitable snail, the eggs release miracidia, which undergo in the snail several developmental stages (sporocysts, rediae, cercariae). Cercariae are released from the snail and penetrate freshwater fish, encysting as metacercariae in the muscles or under the scales. The mammalian definitive host (including humans) become infected by ingesting undercooked fish containing metacercariae. After ingestion, the metacercariae excyst in the duodenum and ascend through the ampulla of Vater into the biliary ducts, where they attach and develop into adults. The adult flukes reside in the biliary and pancreatic ducts of the mammalian host, where they attach to the mucosa.

Presentation: Most infections are asymptomatic. In mild cases, manifestations include dyspepsia, abdominal pain, diarrhea or constipation. With infections of longer duration, the symptoms can be more severe, and hepatomegaly and malnutrition may be present. In rare cases, cholangitis, cholecystitis, and chlolangiocarcinoma may develop.

Diagnosis: Diagnosis is based on microscopic identification of eggs in stool specimens (indistinguishable between clonorchis and opisthorchis).

Treatment: Praziquantel

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Lung Fluke

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Cause: Paragonimus westermani

Vector: Snail - Crustacean

Pathophysiology:In the external environment, the eggs become embryonated, and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues. Miracidia go through several developmental stages inside the snail: sporocysts, rediae, with the latter giving rise to many cercariae, which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host. Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite. The metacercariae excyst in the duodenum, penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults

Presentation: The acute phase (invasion and migration) may be marked by diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia. During the chronic phase, pulmonary manifestations include cough, expectoration of discolored sputum, hemoptysis, and chest radiographic abnormalities.

Diagnosis: Diagnosis is based on microscopic demonstration of eggs in stool or sputum

Treatment: Praziquantel

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Blood Fluke

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Cause: Schistosoma hematobium, japonicum or mansoni

Vector: Snail - Human (skin)

Pathophysiology: Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia, which swim and penetrate specific snail intermediate hosts. The stages in the snail include 2 generations of sporocysts and the production of cercariae. Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host, and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins. Adult worms in humans reside in the mesenteric venules in various locations. S. japonicum is more frequently found in the superior mesenteric veins draining the small intestine, and S. mansoni occurs more often in the superior mesenteric veins draining the large intestine. S. haematobium most often occurs in the venous plexus of bladder

Presentation: Many infections are asymptomatic. Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by S. mansoni and S. japonicum. Manifestations include fever, cough, abdominal pain, diarrhea, hepatosplenomegaly, and eosinophilia. Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include: colonic polyposis with bloody diarrhea (Schistosoma mansonimostly); portal hypertension with hematemesis and splenomegaly (S. mansoni, S. japonicum, S. mansoni); cystitis and ureteritis (S. haematobium) with hematuria, which can progress to bladder cancer; pulmonary hypertension (S. mansoni, S. japonicum, more rarely S. haematobium); glomerulonephritis; and central nervous system lesions.

Diagnosis: Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected.

Treatment: Praziquantel

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Pathophysiology of all Flukes

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In the external environment, the eggs become embryonated, and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues. Miracidia go through several developmental stages inside the snail: sporocysts, rediae, with the latter giving rise to many cercariae, which emerge from the snail.

The cercariae encyst as metacercariae on secondary host (vegetation, watercress, fish, crustaceans, humans [schistosoma]) and are ingested. They excyst in the duodenum and migrate to their respective locations becoming adults.

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Common Vector in all Flukes

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Snail

But most have a specific secondary host: watercress, crabs/crayfish, fish

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Diagnosis of all Flukes

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Visualization of eggs in stool, urine, vomitus, sputum or biliary drainage (all depending on where adult worm resides)

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Treatment of all Flukes (except fasciola hepatica)

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Praziquantel

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Treatment of Fasciola hepatica

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Triclabendazole

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Two flukes that have direct ingestion of metacercaria from water/vegetation

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Intestinal and Liver (watercress) Flukes

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Tapeworms (Cestodes)

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Pig: Taenia solium

Cow: Taenia saginatum

Fish: Diphylobothrium latum

Dog: Dypilidium caninum

Rat: Hymenolepis diminutum

Dwarf: Hymenolepis nana

Pastoral: Echinococcus

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Pig and Cow Tapeworm

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Cause: Taenia solium, T. saginatum

Vector: Pig

Pathophysiology: Eggs or gravid proglottids are passed with feces. Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or gravid proglottids. In the animal's intestine, the oncospheres hatch, invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat. In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine.

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

Diagnosis: Microscopic identification of eggs and proglottids in feces is diagnostic for taeniasis

Treatment: Praziquantel

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Fish Tapeworm

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Cause: Diphylobothrium latum

Vector: Fish

Pathophysiology: Immature eggs are passed in feces. Under appropriate conditions, the eggs mature (approximately 18 to 20 days) and yield oncospheres which develop into a coracidia. After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae. Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum). The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, e.g., trout, perch, walleyed pike. In this case, the sparganum can migrate to the musculature of the larger predator fish and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked. After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms which will reside in the small intestine. The adults of D. latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex

Presentation: Diphyllobothriasis can be a long-lasting infection (decades). Most infections are asymptomatic. Manifestations may include abdominal discomfort, diarrhea, vomiting, and weight loss. Vitamin B12 deficiency with pernicious anemia may occur. Massive infections may result in intestinal obstruction.

Diagnosis: Microscopic identification of eggs in the stool is the basis of specific diagnosis.

Treatment: Praziquantel

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Dog Tapeworm

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Cause: Dipylidium caninum

Vector: Dog, flea, children

Pathophysiology: Gravid proglottids are passed intact in the feces or emerge from the perianal region of the host. Following ingestion of an egg by the intermediate host (larval stages of the dog or cat flea Ctenocephalides spp.), an oncosphere is released into the flea's intestine. The oncosphere penetrates the intestinal wall, invades the insect's hemocoel (body cavity), and develops into a cysticercoid larva. The larva develops into an adult, and the adult flea harbours the infective cysticercoid. The vertebrate host becomes infected by ingesting the adult flea containing the cysticercoid. The dog is the principal definitive host for Dipylidium caninum. Other potential hosts include cats, foxes, and humans (mostly children). Humans acquire infection by ingesting the cysticercoid contaminated flea. This can be promulgated by close contact between children and their infected pets. In the small intestine of the vertebrate host the cysticercoid develops into the adult tapeworm which reaches maturity about 1 month after infection.

Presentation:Most infections with Dipylidium caninum are asymptomatic. Pets may exhibit behavior to relieve anal pruritis (such as scraping anal region across grass or carpeting). Mild gastrointestinal disturbances may occur. The most striking feature in animals and children consists of the passage of proglottids.

Diagnosis: Demonstrating the typical proglottids or egg packets in the stool or the environment.

Treatment: Praziquantel

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Rat Tapeworm

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Cause: Hymenolepis diminuta

Vector: Rat, arthropods

Pathophysiology:Eggs of Hymenolepis diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host, which develop into cysticercoid larvae. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H. diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (e.g., oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall.

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

Diagnosis: Demonstration of eggs in stool specimens.

Treatment: Praziquantel

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Dwarf Tapeworm

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Cause: Hymenolepis nana

Vector: Rodents, Fleas

Pathophysiology:Eggs of Hymenolepis nana are passed with the stool. When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine.

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

Diagnosis: Demonstration of eggs in stool specimens.

Treatment: Praziquantel

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Pastoral Tapeworm

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Cause: Echinococcus granulosus

Vector: Dogs,

Pathophysiology:The adult Echinococcus granulosus (3 to 6 mm long) resides in the small bowel of the definitive hosts, dogs or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages

Presentation: Echinococcus granulosus infections remain silent for years before the enlarging cysts cause symptoms in the affected organs. Hepatic involvement can result in abdominal pain, a mass in the hepatic area, and biliary duct obstruction. Pulmonary involvement can produce chest pain, cough, and hemoptysis. Rupture of the cysts can produce fever, urticaria, eosinophilia, and anaphylactic shock, as well as cyst dissemination. Echinococcus multilocularis affects the liver as a slow growing, destructive tumor, with abdominal pain, biliary obstruction, and occasionally metastatic lesions into the lungs and brain.

Diagnosis: The diagnosis of echinococcosis relies mainly on findings by ultrasonography and/or other imaging techniques supported by positive serologic tests.

Treatment: Albendazole

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Vector for all Tapeworms

Back 45

Various (Pig, Cow, Fish, Dog/Flea, Rat/Arthropod, Pastoral animals)

Front 46

Pathophysiology for all Tapeworms

Back 46

Eggs or proglottids are passed with feces and are ingested by a suitable host (either intermediate or primary [to be followed by a secondary]) and form cysticerca which, upon ingestion by a human, turns into adult tapeworm and attaches to small intestinal wall

Front 47

Diagnosis for all Tapeworms (except Echinococcus)

Back 47

Visualization of Eggs and/or Proglottids in stool

Front 48

Diagnosis of Echinococcus

Back 48

Imaging (US or otherwise) and serology

Front 49

Treatment for all Tapeworms (except Echinococcus)

Back 49

Praziquantel

Front 50

Treatment for Echinococcus

Back 50

Albendazole