Three major species of schistosomes produce human disease. These have marked differences in geographical distribution. Prevalence is dependent on the presence of a susceptible intermediate snail host and faecal contamination of water supplies. The size of snail populations varies with the season and availability of freshwater breeding grounds. An increase in the world prevalence of schistosomiasis is partly due to dam construction and irrigation programmes.
LIFE-CYCLE AND PATHOGENESIS
Human infection occurs after penetration of the skin ormucous membranes by cercariae, the infective form of the parasite that is liberated into fresh water by the specific intermediate snail host. Cercariae penetrate unbroken skin and migrate as schistosomules through the venous circulation to the liver, where the adult worms mature. Eventually pairs of male and female worms migrate upstream along the portal vein to the mesenteric venules, until the calibre of the vessels halts their progress. They remain in this location for many years copulating continuously and producing enormous numbers of eggs. To complete the life-cycle, eggs must leave the body, either by penetrating the intestinal wall (Schistosoma mansoni and S. japonicum) or the bladder wall (5. haematobium) and returning to the environment via faeces or urine, respectively. The larvae (miracidia) develop inside the eggs but do not hatch until they arrive in fresh water, when they search actively for the specific snail host to invade. Once inside the snail, multiplication occurs-a single miracidium produces up to 100 000 cercariae, released at the rate of 5000 per day. Eggs retained in host tissues, particularly the liver, urinary bladder and intestine, are responsible for the clinical manifestations of schistosomiasis. Egg antigens initiate both immediate and delayed-type hypersensitivity reactions with granuloma formation. Humoral substances such as lymphokines, macrophage migration inhibitory factor and fibroblast stimulating factors are found at the site of these granulomas and presumably support the cellular inflammatory response. Healing eventually occurs by fibrosis.
The first clinical sign of an acute infection is a local inflammatory response at the site of the invading cercariae known as ‘swimmer’s itch’. Within a week or more there is a generalized allergic response characterized by fever, urticaria, eosinophilia, myalgia and malaise. Nausea, vomiting and profuse diarrhoea are common, as are respiratory symptoms, particularly cough. Clinical findings at this time include generalized lymphadenopathy, hepatosplenomegaly and signs of patchy pneumonia. In ia the acute disease is called Katayama fever. It is most pronounced in infection with S. japonicum and S. manSOnt.
Chronic schistosomiasis varies in its clinical presentation depending on the type of schistosome involved.
Chronic schistosomiasis varies in its clinical presentation depending on the type of schistosome involved. Schistosoma mansoni and Schistosoma japonicum S. mansoni is found predominantly in Africa, South America and the West Indies, whereas S. japonicum is common in China and other specific sites in South East Asia. S. mansoni predominantly affects the colon, where the presence of ova produces macroscopic lesions such as mucosal granularity, erythema and superficial ulceration. However, a particularly severe form of colonic disease is seen in Egyptians, with gross ulceration and polyp formation, particularly in the rectosigmoid; extensive polyposis results in significant blood and protein loss from the colon. Progressive fibrosis in the intestinal wall leads to rigidity and stricture formation, although intestinal obstruction is rare. A localized granulomatous reaction in the intestine (pseudotumour or bilharzioma) may be mistaken for a colonic cancer. The development of granulomatous hepatitis, followed by progressive periportal fibrosis and portal hypertension, is signified by marked hepatosplenomegaly, often associated with osophageal varices. In advanced cases death is due to the complications of portal hypertension, as hepatocellular function remains remarkably good. S. japonicum affects the small intestine and proximal colon in addition to causing fibrotic liver disease. S. japonicum produces larger numbers of eggs than S. mansoni, which accounts for the more extensive pattern of disease and the frequency of ectopic deposition of ova, particularly in the lungs, spinal cord and brain. The latter may result in fits or hemiplegia. Epithelial dysplasia in the colon has been reported in patients with chronic S. japonicum colitis, and it is nowclear that this condition has premalignant potential in endemic areas.
This is mainly a urinary tract schistosome found predominantly in Egypt, East Africa and the Middle East. Chronic inflammation is found in the bladder, ureters and urethra, causing urinary frequency, dysuria and haematuria. Chronic infection leads to obstructive uropathy, chronic pyelonephritis and renal failure, and contraction of the bladder. Epidemiological studies confirm an association between bladder carcinoma and this infection. The internal genitalia may be involved and rectal inflammation and ulceration may be found in up to 70% of patients.
In endemic areas a confident diagnosis can often be obtained on clinical grounds. Confirmation is achieved by detecting the characteristic eggs in the stools, the urine or in a rectal biopsy. Different species of Schistosoma can be distinguished not only by the clinical pattern but also by egg morphology.
A plain abdominal radiograph may reveal intramural calcification in the wall of the bladder or the colon. Barium contrast studies of the colon show spiculating mucosal ulceration, polyposis, strictures, and possibly a mass lesion that could either be a bilharzioma or, in the case of S. japonicum infection, a carcinoma. Intravenous urography may confirm an obstructive uropathy and demonstrate bladder contraction. Immunodiagnostic tests are available, the most sensitive of which detect antibodies against a gut-associated polysaccharide antigen by either ELISA or indirect immunofluorescence.
The two major objectives of treatment of schistosorruasis are:
1 Reduction in egg production
2 Prevention or reduction of tissue damage by eggs already in situ
In endemic and hyperendemic areas, curative therapy is usually inappropriate, since reinfection occurs rapidly, whereas infected individuals who are no longer exposed to the parasite can be effectively treated. Suppressive noncurative chemotherapeutic approaches have been used in mass treatment programmes in Egypt with good clinical improvement following a reduction in the ‘worm burden’. All antischistosomal drugs have the same effect: they cause worms to leave the mesenteric and vesical veins and to enter the liver and lungs where they are eventually destroyed by host tissue responses. Praziquantel is active against all species of schistosome and is probably the drug of choice as it is well tolerated and relatively free from serious side-effects. A single dose (40 mg kg”) cures more than 90% of patients with S. haematobium, with slightly lower rates against S. mansoni. S. japonicum is best treated with a total dose of 60 mg kg'” given in divided doses over 1 or 2 days. Oxamniquine is active against S. mansoni and rnetriphonate against S. haematobium.
Colonscopic polypectomy can control the number of colonic polyps, but surgery may be required to relieve obstructive uropathy and for inflammatory masses in the eNS.
Personal protection is to avoid infected water. General control is difficult but depends on the provision of good sanitation, which is largely an economic problem