Etiology and Epidemiology Schistosomiasis

Blood Flukes: Schistosomiasis 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. Etiology 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, reaching the lungs and finally the liver parenchyma. Sexually mature worms descend into the venous system at specific anatomic locations: intestinal veins (S. mansoni, S. japonicum, S. mekongi, and S. intercalatum) and vesical veins (S. haematobium). After mating, adult gravid females travel against venous blood flow to small tributaries, where they deposit their ova intravascularly. Schistosome ova (Fig. 212-1) have specific morphologic features that vary with the species. Aided by enzymatic secretions through minipores in eggshells, ova move through the venous wall, traversing host tissues to reach the lumen of the intestinal or urinary tract, and are voided with stools or urine. Approximately 50% of ova are retained in host tissues locally (intestines or urinary tract) or are carried by venous blood flow to the liver and other organs. Schistosome ova that reach freshwater bodies hatch, releasing free-living miracidia that seek the snail intermediate host and undergo several asexual multiplication cycles. Finally, infective cercariae are shed from snails.

Adult schistosomes are ~1–2 cm long. Males are slightly shorter than females, with flattened bodies and anteriorly curved edges forming the gynecophoral canal, in which mature adult females are usually held. Females are longer, slender, and rounded in cross-section. The precise nature of biochemical and reproductive exchanges between the two sexes is unknown, as are the regulatory mechanisms for pairing. Adult schistosomes parasitize specific sites in the host venous system. What guides adult intestinal schistosomes to branches of the superior or inferior mesenteric veins or adult S. haematobium worms to the vesical plexus is unknown. In addition, adult worms inhibit the coagulation cascade and evade the effector arms of the host immune responses by still-undetermined mechanisms. The genome of schistosomes is relatively large (~270 Mb) and is arrayed on seven pairs of autosomes and one pair of sex chromosomes. For S. mansoni, a total of ~14,000 genes have been estimated; some are species-conserved. The complete sequence of the schistosome genome should be available soon.

Epidemiology

The global distribution of schistosome infection in human populations. Information on prevalence and global distribution is inexact. The five Schistosoma species are estimated to infect 200–300 million individuals in South America, the Caribbean, Africa, the Middle East, and Southeast Asia. The total population living under conditions favoring transmission approximates double or triple that number—a fact reflecting the public health significance of schistosomiasis

In endemic areas, the rate of yearly onset of new infection, or incidence, is generally low. Prevalence, on the other hand, starts to be appreciable by the age of 3–4 years and builds to a maximum that varies by endemic region (up to 100%) in the 15- to 20-year age group. Prevalence then stabilizes or decreases slightly in older age groups (>40 years). Intensity of infection (as measured by fecal or urinary egg counts, which correlate with adult worm burdens in most circumstances) follows the increase in prevalence up to the age of 15–20 years and then declines markedly in older age groups. This decline may reflect acquisition of resistance or may be due to changes in water contact patterns, since older people have less exposure. Furthermore, the overdispersed distribution of schistosomes in human populations may be due to the heterogeneity of worm populations, with some more invasive than others; alternatively, it may be due to the demonstrated differences in genetic susceptibility of host populations.

Disease due to schistosome infection is the outcome of parasitologic, host, and additional infectious, nutritional, and environmental factors. Most disease syndromes relate to the presence of one or more of the parasite stages in humans. Disease manifestations in the populations of endemic areas correlate, in general, with the intensity and duration of infection as well as with the age and genetic susceptibility of the host. Overall, disease manifestations are clinically relevant in only a small proportion of persons infected with any of the intestinal schistosomes. In contrast, urinary schistosomiasis manifests clinically in most infected individuals. Recent estimates of total morbidity due to chronic schistosomiasis indicate a significantly greater burden than was previously appreciated.

Patients with both HIV infection and schistosomiasis excrete far fewer eggs in their stools than those infected with S. mansoni alone; the mechanism underlying this difference is unknown. Treatment with praziquantel may result in reduced HIV replication and increased CD4+ T lymphocyte counts.

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Harrison's Internal Medicine > Chapter 212. Schistosomiasis and Other Trematode Infections