The pathogens are paired flukes Schistosoma spec., which are bisexually differentiated Trematodes of the phylum Parenchymia (Plathelminthes). The female of circular crossection is surrounded by the flat enrolled male forming the canalis gynaecophorus (fig. 2.65, page 132). Life cycle of Schistosoma spec. (fig. 2.64, page 130): In man, the adult flukes are united and live as pairs inside the veins of the ileum (S. japonicum), colon (S. mansoni) or bladder and the internal sexual organs (S. haematobiumi). Their embryonated eggs are excreted in faeces or urine and in sexual products. Their miracidia hatch in fresh water and are already sexually differentiated. They attack the intermediate host (IH), freshwater snails, in which they propagate by a mother sporocyst followed by numerous daughter sporocysts produced parthenogetically. The snails leave cercariae, which attack the definitive host (DH), humans, in which they develop from a schistosomulum to fertile paired flukes, the eggs of which are deposited by the female into the veinoles of the affected tissues. Paired flukes live together for 3-4 years (harmonic mean), whereas the miracidium and cercaria live in fresh water for 1 and 2 days, respectively.
The miracidia orient in the microhabitate to specific IH snails by chemokinesis or chemotaxis, perceiving the pheromones of the snails (probably for dispersion and sex finding) as luring agents. They penetrate the snails skin, while they shed their ectodermal epithelium, replacing it by a mesodermal tegument (Neodermata, see end of next summary 2.10 flukes, tegument). The migrating stages reach the tubuli of the liver of the snail via the haemolymph. The establishment of the daughter sporocysts and the swarming out of the cercariae each cause a mortality wave. The physiology of the surviving snails changes to the starvation metabolism and the further production of cercariae is retarded. The cercariae leave the snail in diurnal batches. Turbulence in the water and the body warmth of DHs stimulate the contact reaction of the cercariae; this consists of turning, remaining stationary, creeping and skin penetration at which they discard their tails and change to a schistosomulum.
Course of the disease called Bilharziasis: During the prodromal stage, the migrating schistosomula induce acute symptoms in the lungs. When the incubation period of 4-7 weeks has passed, fever, headache, pains in the neck and limbs, and epigastric syndrome appear: Manifestation. Eggs appear for the first time 5-7 weeks p.i. in faeces, 10-12 weeks p.i. in urine (onset of patency). The liver and spleen swell after large numbers of eggs are washed into them, causing accumulated granulomas. One pair of flukes of the species S. mansoni is estimated to produce 300-600 eggs/day, S. haematobium 120-200 eggs/day, and in S. japonicum up to 3000 eggs/day. The amount of eggs excreted daily by a patient and its worm load are not strictly related, both being distributed in the several age classes in a negative binomial manner. During patency, there is effectively a premunition against superinfestations; the parasitosis leaves no protective immunity against reinfestation but a delayed type hypersensitivity (DTH) persists a long time even during postpatency.
The long-term course is chronic. Serious health problems appear after exposure for years to an accumulated worm load. Primarily, these problems arise because of vascular injuries and tissue damage by the eggs. In bladder bilharziasis (S. haematobium), ulcers occur in the bladder and, following bleeding from these ulcers, the urine appears reddish (haematuria). Later on, the bladder looses its elasticity and urinary obstruction develops with many secondary consequences. In intestinal bilharziasis (S. mansoni, S. japonicum), the ulcers accompanied by inflammation (colitis) leading to intermittent diarrhoea and impare resorption. Attack of the genital organs affects the hosts fecundity (Box 2.5, page 134).
Pathogenesis: the eggs drifting via the veinous downflow are sieved out by the subsequent capillary networks and therafter produce granulomas. In intestinal bilharziasis, portal damming up (fig. 2.66, page 135) cause varicosities of the oesophagus and multiple embolisms cause death; obstruction of the lungs overtasks the heart (cor pulmonale). In bladder bilharziasis, cancer of the bladder and renal failure are major risks (Box 2.5, page 134).
For diagnosis, the finding of eggs, which are terminally (S. haematobium) or laterally spined (S. mansoni), is essential. The concentration of eggs (after Telemann), the miracidium-hatching experiment (MHE) and, serologically, the cercarial shedding reaction (CSR) are sometimes employed. A circulating anodic antigen establishes the presence of living flukes. A dermal test for DTH activity remains positive over long periods, even after successful treatment. During chemotherapy, Praziquantel® is given orally once. This is suitable for mass treatment (with some restrictions), because of its low toxicity. Some protective immunisation was achieved experimentally in cattle by using UV-radiated cercariae. In experiments with mice, Paramyosin reduces the worm load of S. japonicum by 60-80%.
Intestinal and bladder bilharziasis caused by S. mansoni and S. haematobium are anthroponoses, whereas that attributable to S. japonicum with domesicated water-buffalo and pigs and rats as parasitological reservoirs is an anthropo-zoonosis.
The intermediate hosts (IHs) of S. haematobium and S. mansoni are hermaphroditic limnic pulmonate snails of the genera Bulinus and Biomphalaria, which live on vegetation in standing or slowly flowing, shallow water. Bulinus spec. survives the dry season borrowed in the ground for up to 7 months; Biomphalaria spec. cannot persist in arid regions. The expulsion of cercariae starts in both genera at 25 oC about 4 weeks p.i. The life expectancies are just over 1 year (Box 2.6, page 140).
The IHs of S. japonicum are bisexual prosobranchiate snails of the genus Oncomelania. They live on wet muddy surfaces of river banks and feed on detritus and algae, which they take up together with mud. They colonize areas that experience warm humid summers and dry cold winters. They survive well once they have borrowed into soil. The expulsion of cercariae starts 3-4 months p.i. and the life expectancy is about 3-5 years (Box 2.6, page 140).
In endemic regions, only a small proportion (about 1 %) of the IH-snail population shares the parasite cycle. The immediately reacting internal defence system (IDS) of the snails is primarily directed against microbial pathogens that can spread epidemically during a single season. Snails parasitized by trematodes survive because of the regulatory self control of the daughter sporocysts initiated by the snails starvation metabolic reaction. Experimentally, the production of cercariae is potentially unlimited.
The transmission of human schistosomiasis depends exclusively on the contamination of the breeding waters of the IH-snails and the contact of the DHs with the cercariae, both being determined by human behaviour (fig. 2.63, page 129).
In man, the prevalence of S. mansoni attains a maximum in juveniles of 15 to 24 years of age independent of their exposure (fig. 2.67, page 141). The following decrease is attributable to the increased mortality of flukes and a diminishing natality (number of eggs per individual pair of flukes) because of accumulated worms. The pathological alterations affect the passage of eggs in the tissues. A premunition impairs reinfestations.
An epidemiological study of human bilharziasis (chapter 184.108.40.206) caused by S. japonicum comprising 12,000 people from an urban and a rural population has yielded data for a deterministic mathematical model. Of the total eggs excreted, one third was from man and two thirds were from mostly wild-living rats, dogs and pigs. The egg excretion of infested persons decreased drastically when the worm load increased from 2 to 8 flukes per person; the most evident effect was found in adolescents aged 10-14 years (fig. 2.68, page 144). However, at large worm loads, a high rate of eggs is not vital. The daily effective natality (living eggs per fluke and day) of S. japonicum culminates markedly in adolescents and is optimal even when only 1-2 fertile pairs of flukes are present (fig. 2.69, page 144). The total effective natality (living eggs during the whole lifetime of the flukes) is also highest in juveniles but, in urban areas, it constantly exceeds that of rural regions (fig. 2.70, page 145). Obviously, when 3-5 pairs of flukes are present, a type of crowding effect starts, reducing the fecundity (quantitative propagation) of the flukes. The notable evidence in the group of juveniles at 10-14 years of age indicates, on the one hand, the synchronisation of the parasite and DH in man including the delay attributable to the duration of pregnancy and the transmission in the IHs (fig. 2.71, page 145). On the other hand, irrespective of the control measures taken, we conclude that an extremely lowered worm load will be compensated by a higher fecundity. Thus, even a reduction of up to 90% of the worm load by control measures, as has been achieved, for example, in cattle (see above), is compensated for by an increase in the flukes fecundity.
In Africa and Asia, ruminants (chapter 2.9.3), predominantly cattle, suffer intestinal bilharziasis caused by various Schistosoma spec., as do sheep, goats and wild-living ruminants, but these last-mentioned to a lesser extent. The egg expulsion per gram faeces is not strictly related to the worm load, as determined by perfusion at slaughtering. The maximum egg expulsion coincides with the time point of the first calving and compensates the age drift of the adult parasites. As in man, the propagation of parasite and definitive host is synchronized despite the faster generation time in cattle, i.e. one year.
In Eastern Asia, the water buffalo and domesticated pigs, cattle and dogs are attacked by S. japonicum to high degrees. Rats predominantly constitute the natural reservoir (fig. 2.63 b, page 129). In Eastern Africa, the baboon (Papio deguera) constitutes the natural reservoir for S. mansoni, whereas in Egypt, the semiaquatic nile rat (Arvicanthus niloticus) and other small wild mammals are adequate hosts for S. mansoni. No natural reservoir is known for S. haematobium.
A campaign for control will be succesful only if the life cycle of the parasite is impaired effectively at several points at the same time. In addition to animal hosts, domestic animals and especially rats must be included in Eastern Asia. If transmission is depressed permanently, than the worms will accumulate in the DHs more slowly. At a lower production of eggs, the pathogenic alterations shift to higher age classes. Small wild mammals (rats) have close contacts to snails, so that a low density of snails may sustain the population of the parasite. The worm load distributes in a negative binomial fashion as usual, i.e. small loads are predominant. To lower the prevalence of any parasitosis permanently, the net reproduction rate of the pathogen has to be depressed below the value of 1. This value must be established for the demonstration of effectivity, whatever the chosen strategy, cannot be given up.
Hydraulic engineering of larger dimensions as reservoirs or irrigation constructions support the distribution of bilharziasis. The access of people, particularly children, to shallow waters are generally not to prevent. Mollucicides must be applied regularly during long periods. A biological control is not in sight as less as a vaccine protecting sufficiently.
The advances of a heteroxenous transmission for parasites in the evolutionary term became obvious on the ecological level (synopsis below).