Trematodes, or flatworms, are a group of morphologically and biologically heterogeneous organisms that belong to the phylum Platyhelminthes. Human infection with trematodes occurs in many geographic areas and can cause considerable morbidity and mortality. The dependence on one drug—praziquantel—for treatment of most infections caused by helminths, including trematodes, raises the specter of developing resistance in these worms; several instances of reduced drug efficacy have already been reported.
For clinical purposes, significant trematode infections of humans may be divided according to tissues invaded by adult flukes: blood, biliary tree, intestines, and lungs (Table 219-1). Trematodes share some common morphologic features, including macroscopic size (from one to several centimeters); dorsoventral, flattened, bilaterally symmetric bodies (adult worms); and the prominence of two suckers. Except for schistosomes, all human parasitic trematodes are hermaphroditic. Their life cycles involve a definitive host (mammalian/human), in which adult worms initiate sexual reproduction, and an intermediate host (snails), in which asexual multiplication of larvae occurs. More than one intermediate host may be necessary for some species of trematodes. Human infection is initiated either by direct penetration of intact skin or by ingestion. Upon maturation within humans, adult flukes initiate sexual reproduction and egg production. Helminth ova leave the definitive host in excreta or sputum and, upon reaching suitable environmental conditions, they hatch, releasing free-living miracidia that seek specific snail intermediate hosts. After asexual reproduction, cercariae are released from infected snails. In certain species, these organisms infect humans; in others, they find a second intermediate host to allow encystment into metacercariae—the infective stage.
Table 219-1 Major Human Trematode Infections
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Table 219-1 Major Human Trematode Infections
|Schistosoma mansoni||Skin penetration by cercariae released from snails||Africa, South America, Middle East|
|S. japonicum||Skin penetration by cercariae released from snails||China, Philippines, Indonesia|
|S. intercalatum||Skin penetration by cercariae released from snails||West Africa|
|S. mekongi||Skin penetration by cercariae released from snails||Southeast Asia|
|S. haematobium||Skin penetration by cercariae released from snails||Africa, Middle East|
|Biliary (Hepatic) Flukes|
|Clonorchis sinensis||Ingestion of metacercariae in freshwater fish||Far East|
|Opisthorchis viverrini||Ingestion of metacercariae in freshwater fish||Far East, Thailand|
|O. felineus||Ingestion of metacercariae in freshwater fish||Far East, Europe|
|Fasciola hepatica||Ingestion of metacercariae on aquatic plants or in water||Worldwide|
|F. gigantica||Ingestion of metacercariae on aquatic plants or in water||Sporadic, Africa|
|Fasciolopsis buski||Ingestion of metacercariae on aquatic plants||Southeast Asia|
|Heterophyes heterophyes||Ingestion of metacercariae in freshwater or brackish-water fish||Far East, North Africa|
|Paragonimus westermani||Ingestion of metacercariae in crayfish or crabs||Global except North America and Europe|
The host-parasite relationship in trematode infections is a product of certain biologic features of these organisms: they are multicellular, undergo several developmental changes within the host, and usually result in chronic infections. In general, the distribution of worm infections in human populations is overdispersed; i.e., it follows a negative binomial mathematical relationship in which most infected individuals harbor low worm burdens while a small percentage are heavily infected. It is the heavily infected minority who are particularly prone to disease sequelae and who constitute an epidemiologically significant reservoir of infection in endemic areas. Equally important is an appreciation that worms do not multiply within the definitive host and that they have a relatively long life span, ranging from a few months to a few years. Morbidity and death due to trematode infections reflect a multifactorial process that results from the tipping of a delicate balance between intensity of infection and host reactions, which initiate and modulate immunologic and pathologic outcome. Furthermore, the genetics of the parasite and of the human host contribute to the outcome of infection and disease. Infections with trematodes that migrate through or reside in host tissues are associated with a moderate to high degree of peripheral-blood eosinophilia; this association is of significance in protective and immunopathologic sequelae and is a useful clinical indicator of infection.
Approach to the Patient: Trematode Infection
The approach to individuals with suspected trematode infection begins with a question: Where have you been? Details of geographic history, exposure to freshwater bodies, and indulgence in local eating habits without ensuring safety of food and drink are all essential elements eliciting the history of present illness. The workup plan must include a detailed physical examination and tests appropriate for suspected infection. Diagnosis is based either on detection of the relevant stage of the parasite in excreta, sputum, or (rarely) tissue samples or on sensitive and specific serologic tests. Consultation with physicians familiar with these infections or with the U.S. Centers for Disease Control and Prevention (CDC) is helpful in guiding diagnosis and selecting therapy.
Human schistosomiasis is caused by five species of the parasitic trematode genus Schistosoma: the intestinal species S. mansoni, S. japonicum, S. mekongi, and S. intercalatum and the urinary species S. haematobium. Infection may cause considerable morbidity in the intestines, liver, and urinary tract, and a proportion of affected individuals die. Other schistosomes (e.g., avian species) may invade human skin but then die in subcutaneous tissue, producing only self-limiting cutaneous manifestations.
Human infection is initiated by penetration of intact skin with infective cercariae. These organisms, which are released from infected snails in freshwater bodies, measure ∼2 mm in length and possess an anterior and a ventral sucker that attach to the skin and facilitate penetration. Once in subcutaneous tissue, cercariae transform into schistosomula, with morphologic, membrane, and immunologic changes. The cercarial outer membrane changes from a trilaminar to a heptalaminar structure that is then maintained throughout the organism's life span in humans. This transformation is thought to be the schistosome's main adaptive mechanism for survival in humans. Schistosomula begin their migration within 2–4 days via venous or lymphatic vessels, ...