to complete the life-cycle by urine and fecal contamination of fresh water (World Health Organization, 1993). Once inside the snails, the miracidium sheds its ciliated glycocalyx and reforms into a primary sporocyst (Webbe, 1982a; Jourdane and Theron, 1987). The primary sporocyst migrates into the snail's digestive gland or matures in its foot process. Germinal cells of the sporocyst replicate (asexual multiplication, increasing parasite numbers by several logs). These replicating cells mature and bud off as secondary sporocysts, then migrate to the snail's liver and mature. This process is repeated multiple times until the snail contains many maturing sporocysts. The germinal cells mature into motile, forked-tailed, infective 0.4-0.6 mm larval forms called cercariae.
Cercariae are infective to the definitive host (man). Infected snails continue to shed cercariae for many weeks. The cercariae leave the snail from the edge of the snail's mantle and enter the surrounding water. The cercariae have a discrete head and a bifurcated tail that allows locomotion. The head carries small oral and ventral suckers, flame cells and a non-functional gut. Unicellular glands near the ventral suckers secrete mucilage, which assists the parasite in attachment, while other glands (penetration glands) secrete digestive enzymes, which aid in skin penetration. The parasite is able to migrate
Fig. 16.1 The various stages of schistosomes
S. mamoni S. haematobium S. japonicum S. intercalatum mekongi
Fig. 16.1 The various stages of schistosomes through human epidermis in 5-10 minutes. The total lifespan of a shed cercarium in fresh water is about 48 hours, but infectivity decreases dramatically after about 4 hours. Death occurs due to exhaustion of the glycogen stores (Wilson, 1987).
During penetration, the cercaria leaves its tail on the dermis, and the cercarial head penetrates into deeper structures (Figure 16.2). The parasite glycocalyx is transformed into a heptalaminate
double lipid bilayer as part of its rapid adaptation to the definitive host (Wiest et al., 1988). This transformed cercaria is then called a schistosomula. Schistosomulae take up host antigens and attach them to their surface membranes, thus preventing host immune attack.
Other mechanisms of immune evasion are described in greater detail in the section on Immunology (see below). In the first 48 hours, the schistosomula penetrates into subcutaneous tissues and migrates through the dermis to gain access into the veins and/or lymphatics (Wilson,
1987). The host range for any specific schistoso-mula species is often very narrow. Cercariae can penetrate a wide range of animals and even plants but rapidly die in the dermis of the wrong host. During the next 5-7 days, successful schistosomulae are transported via the heart to the lungs (Miller and Wilson, 1980).
10-20 days. Each schistosomula is either male or female. After migration to the appropriate peripheral venous plexus, maturation takes place. Adult worms pair with the opposite sex and live out their lifespan together. Migration in the veins is aided by the worm's ventral and oral suckers, which are used to attach to the endothelial wall. The worm pair migrates against the mesenteric or vesical blood flow to lay their eggs. Different species tend to prefer different anatomical locations for optimal growth and survival. Thus, S. haematobium prefers the vesical veins, while adult S. mansoni, S. japoni-cum, S. mekongi and S. intercalatum worms prefer the portal circulation (Elliott, 1996b). Throughout infection, the adult worm pair migrates up and down these veins, laying eggs. S. mansoni prefers the colonic vasculature, while S. japonicum can deposit eggs throughout the length of the small and large intestine. Overlap of sites of preference for adult worms occurs, so that S. haematobium eggs can occasionally be found in the stool, while S. intercalatum and S. mansoni eggs have been described in the urine (Elliott, 1996b; Zwingenberger, 1990).
During migration, when the diameter of the venule becomes small enough to restrict further movement, the female often leaves the male and continues to migrate to the farthest point permitted by the worm's diameter. This minimizes backflow of ova. Adult worms induce little direct damage to the host unless they die and embolize to the liver or lungs (S. haematobium). The eggs, however, are capable of boring through tissue planes and generally cause microperforations in the colon and urinary bladder (von Lichtenberg, 1987).
The schistosomulae migrate via the pulmonary capillaries to enter the left side of the heart and systemic circulation (Wilson, 1987; Miller and Wilson, 1980). Schistosomulae are carried with the arterial blood flow to the mesenteric arteries, splanchnic arteries and portal veins and eventually reach the appropriate venous plexus and mature. Repeated cycles through the systemic circulation may be required. This process takes
The lifespan of the schistosome adult worms averages 3-10 years, but survival for more than 30 years has been reported (Arnon, 1990; Christopherson, 1924). Pathology results primarily from the eggs, either through microperforation of tissue or from an exuberant host immune response to the ova (Doenhoff and Bain, 1978; Elliott, 1996b). The maximum number of eggs that can be laid daily by each worm pair depends on the schistosome species (500 for S. mansoni to 5000 for S. japonicum). Eggs of S. mansoni and S. haematobium are released singly, while the smaller eggs of S. japonicum are released as aggregates of 8-10 (World Health Organization, 1985).
The eggs release histolytic enzymes and a variety of antigenic macromolecules (mostly glycoproteins). Nearly half the eggs fail to reach the lumen of the bladder (with S. haematobium) or intestine (with all other species) and instead get trapped permanently in host tissues. All eggs in tissues induce a T lymphocyte-dependent granu-lomatous response (Cheever and Powers, 1971). Subsequent tissue damage occurs as an indirect result of this inflammatory reaction. The pathologic sequelae of this process are discussed in later sections. The eggshell is composed of glycine-rich protein that is highly cross-linked by tyrosine residues (Cordingley, 1987). This structure makes the eggs resistant to host protease activity and can therefore allow the maturing egg to survive aggressive host inflammatory responses for several weeks. Granuloma formation is, in fact, required for successful migration of the ova across tissue planes and into the environment with the urine or stool (Doenhoffand Bain, 1978;Doenhoff et al, 1986). Animals unable to form egg granulomas around schistosome eggs (T cell-deficient animals) do not successfully secrete eggs in their stool and the ova collect in tissues, inducing only a foreign-body reaction from the host. Thus, some host inflammatory response appears to be a necessity for successful completion of the life-cycle.
Eggs gain access to the environment by urination, defecation, laundering of soiled clothing or bathing after recent defecation. The hypotonic environment of fresh water allows the eggs to hatch. When this occurs in proximity to the intermediate host (snails), the life-cycle is completed.
As a result of this complex life-cycle, schisto-somiasis is not acquired by person-to-person contact. Adult schistome worms do not multiply in the human host, which has important epide-
miologic implications. It also implies that less than 100% curative drugs or vaccines should still be highly useful in the control of the infection.
Human schistosomiasis infects a very narrow range of snail hosts (Wright, 1973). S. haematobium and S. intercalatum infect snails of the Bulinus spp. while S. mansoni infects Biompha-laria spp. Both snails are aquatic and therefore direct water contact is required for transmission (Brown, 1980). Only a few species are capable of prolonged survival without immersion in water. Thus, most transmission occurs in areas of persistent moisture, such as rivers and lakes.
Bulinus and Biomphalaria snails do not breed well outside the tropical environment and thus limit the potential geographic range of S. mansoni and S. haematobium. In the New World, a narrow spectrum of the genus Biom-phalaria can successfully transmit infection, and these are restricted to specific Caribbean Islands, Venezuela, Surinam, French Guyana and Brazil (Malek, 1988). This, to a large extent, explains the current endemic foci in the New World.
S. japonicum is transmitted by Oncomelania snails (Webbe, 1982b). These are amphibious snails and can survive out of water. Thus, transmission can also occur through contact with moist vegetation such as grass and reeds and on muddy surfaces. Some Oncomelania snails can survive harsh climatic changes, enduring prolonged dry spells and freezing winters. As a result, schistosomiasis can be found in a wide variety of habitats in China. In The Philippines, the endemic genus Oncomelania requires continuous moisture and thus infection is restricted to the eastern islands, where continuous rainfall occurs (Figure 16.3). The intermediate hosts of S. mekongi are fully aquatic and have a range restricted to the Mekong River Basin in southeast Asia.
Cercarial production also varies between the schistosome species and specific snail hosts (Meulemann, 1972). Large South American Biophilia snails can shed 2000-4000 cercariae/ day, while many Oncomelania, infected with S. japonicum, shed less than 20 cercariae/day.
Light is the major stimulus for cercarial shedding for all species. Most species maximally shed cercariae in mid- to late morning, which results in optimal human transmission (Pesigan et al., 1958). Some S. japonicum species shed cercariae maximally late in the afternoon and occasionally at night, perhaps as an adaptation to maintenance in rodent definitive hosts (Webbe, 1982a; Rollinson et al., 1986).
South America and the Caribbean by the slave trade. S. haematobium is confined to Africa and the Middle East, while S. japonicum and S. mekongi are found only in Asia (Doumenge et al., 1987). A map of the geographic distribution of schistosomiasis is shown in Figure 16.4 and Table 16.2 lists specific endemic countries (World Health Organization, 1987, 1993).
S. mansoni and S. haematobium are restricted in nature to humans. Some epidemiological evidence suggests that baboons can transmit S. haematobium infection in the wild (Fenwick, 1969). Rats, mice and a variety of other mammals can be infected experimentally, but under natural conditions appear not to be an important reservoir in transmission to humans (Cheng, 1971; Rollinson et al., 1986). Infection of young dogs may play a minor role in the transmission of S. mansonii in Africa (Bruce et al., 1980). In Brazil, the Nectomys species of rodent appears to maintain infection in some areas (Rollinson and Southgate, 1987).
S. japonicum has a broad host range. Wild rodents appear to maintain infection in some endemic areas. A variety of domestic animals are also important to transmission, including dogs, pigs and, most importantly, cattle and cariboo (Pesigan et al., 1958). In The Philippines and China, the latter two animals are critical reservoirs of infection, particularly in rice-growing areas, where cariboo are involved extensively in agriculture (Cheng, 1971).
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