Medication Summary
Chemotherapy objectives in trematode infections are to cure the disease, to reduce morbidity, and to prevent transmission of parasitic infection in endemic areas.
Anthelmintics
Class Summary
Parasite biochemical pathways are different enough from the human host to allow selective interference by relatively small doses of chemotherapeutic agents.
Praziquantel (Biltricide)
Praziquantel is drug of choice in most trematode infections except fascioliasis.
Praziquantel increases cell membrane permeability in susceptible worms, resulting in loss of intracellular calcium, massive contractions, and paralysis of musculature. In addition, it produces vacuolization and disintegration of the schistosome tegument. This is followed by attachment of phagocytes to the parasite and death.
Swallow tablet whole with some liquid during meals. Keeping the tablet in the mouth may reveal bitter taste, which can produce nausea or vomiting.
Triclabendazole (Egaten)
Triclabendazole is an anthelmintic agent. The mechanism by which triclabendazole exhibits its effect against Fasciola species is not fully elucidated. Studies in vitro and/or in infected animals suggest that triclabendazole and its active metabolites (sulfoxide and sulfone) are absorbed by the tegument of the immature and mature worms, leading to a decrease of the resting membrane potential and inhibition of tubulin function, as well as protein and enzyme synthesis. It is indicated for the treatment of fascioliasis in patients aged 6 years or older.
Nitazoxanide (Alinia)
Limited data suggest nitazoxanide might be effective therapy in some patients with fascioliasis. Interferes with pyruvate:ferredoxin oxidoreductase (PFOR), essential to anaerobic energy metabolism.
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Adult worms in humans reside in the veins in various locations: Schistosoma mansoni in the inferior mesenteric veins, Schistosoma japonicum in the superior mesenteric veins, and Schistosoma haematobium in the vesical veins (these locations are not absolute). The females (size 7-20 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 they are eliminated with feces or urine, respectively. 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 migrate through several tissues and stages to their residence in the veins. Human contact with water is thus necessary for infection by schistosomes. Various animals serve as reservoirs for S japonicum and Schistosoma mekongi. Image courtesy of the US Centers for Disease Control and Prevention.
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These are small operculated eggs. Size is 27-35 μm X 11-20 μm. The operculum, at the smaller end of the egg, is convex and rests on a visible "shoulder." At the opposite (larger, abopercular) end, a small knob or hooklike protrusion is often visible (as here). The miracidium is visible inside the egg. Image courtesy of the US Centers for Disease Control and Prevention.
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Wet mounts with iodine. The eggs are ellipsoidal. They have a small, barely distinct operculum (upper end of the eggs in panel A). The operculum can be opened (egg in panel B), for example, when slight pressure is applied to the coverslip. The eggs have a thin shell that is slightly thicker at the abopercular end. They are passed unembryonated. Size range is 120-150 μm X 63-90 μm. Image courtesy of the US Centers for Disease Control and Prevention.
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Adult flukes size range is 20-75 mm by 8-20 mm. Image courtesy of the US Centers for Disease Control and Prevention.
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Eggs are excreted unembryonated in the sputum, or, alternately, they are swallowed and passed with stool (1). In the external environment, the eggs become embryonated (2), and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues (3). Miracidia go through several developmental stages inside the snail (4): sporocysts (4a), rediae (4b), with the latter giving rise to many cercariae (4c), which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, in which they encyst and become metacercariae. This is the infective stage for the mammalian host (5). Human infection with Paragonimus westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite (6). The metacercariae excyst in the duodenum (7), penetrate through the intestinal wall into the peritoneal cavity, and then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (8) (7.5-12 mm X 4-6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this occurs, completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65-90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. Image courtesy of the US Centers for Disease Control and Prevention.
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The average egg size is 85 μm by 53 μm (range, 68-118 μm X 39-67 μm). They are yellow-brown, ovoidal or elongate, have a thick shell, and are often asymmetrical with one end slightly flattened. At the large end, the operculum is clearly visible. The opposite (abopercular) end is thickened. The eggs of P westermani are excreted unembryonated. Image courtesy of the US Centers for Disease Control and Prevention.