Schistosomiasis There are five species of the genus Schistosoma which commonly cause disease in humans: S. haematobium, S. mansoni, S. japonicum, S. mekongi and S. intercalatum. S. haematobium was discovered by Theodor Bilharz in Cairo in 1861 and the disease is sometimes called bilharzia or bilharziasis. Habitat Adult worms live in the mesenteric veins (S. mansoni, S. japonicum, S. mekongi, and S. intercalatum) or in the venous plexus around the lower ends of the ureters and the urinary bladder (S. haematobium). In these sites, they start their sexual reproduction by releasing eggs. Once deposited in the host, eggs may stay in the mesenteric vein, be trapped in the intestines, escape to the intestinal lumen, and migrate by portal blood to the liver (S. mansoni, S. japonicum). Eggs of S. haematobium may be trapped in the intestines and bladder and may escape to the intestinal or bladder lumen. Life cycle After the egg being excreted with feces or urine into fresh water, the eggs hatch and release ciliated motile miracidia that penetrate into the snail intermediate host. Following asexual multiplication in the snail, the development of cercariae, the infective forms for humans, takes 4 to 7 weeks. After leaving the snails, the cercariae can survive in fresh water for almost 72 hours. When penetration of the skin in the human host occurs, the cercariae lose their tails and change into schistosomula. Schistosomula migrate to the lungs and, in about 6 weeks, mature to adult worms and descend to their final habitat. pathology This depends on the species and the stage of infection. Most disease is due to: 1- The passage of eggs through mucosa . 2- Granulomatous reaction to eggs deposited in tissues. The eggs of S. haematobium pass mainly through the wall of the bladder, but may also involve rectum, seminal vesicles, vagina, cervix and uterine tubes. Eggs of S. haematobium may leave the vesical plexus and be carried directly to the lung S. mansoni and S. japonicum eggs pass mainly through the wall of the lower bowel or are carried to the liver and then reach the lungs after the development of portal hypertension and consequent portasystemic collateral circulation. In both circumstances egg deposition in the pulmonary vasculature, and the resultant host response, can lead to the development of pulmonary hypertension. Clinical features 1- During the early stages of infection there may be itching lasting 1– 2 days at the site of cercarial penetration (swimmers itch). 2- Acute schistosomiasis (Katayama syndrome) develops after a symptom-free period of 3–5 weeks, may present with allergic manifestations such as urticaria, fever, muscle aches, abdominal pain, headaches, cough and sweating. On examination hepatomegaly, splenomegaly, lymphadenopathy and pneumonia may be present. These allergic phenomena may be severe in infections with S. mansoni and S. japonicum, but are rare with S. haematobium. The features subside after 1–2 weeks. Chronic schistosomiasis is due to egg deposition and occurs months to years after infection. The symptoms and signs depend upon the intensity of infection and the species of infecting schistosome. Schistosoma haematobium As adult worms can live for 20 years or more. It is highly endemic in Egypt and East Africa, and occurs throughout Africa and the Middle East 1- Painless terminal haematuria is usually the first and most common symptom. 2- Frequency of micturition due to bladder neck obstruction. 3- Later the disease may be complicated by frequent urinary tract infections, bladder or ureteric stone formation, hydronephrosis, and ultimately renal failure with a contracted calcified bladder. 4- Pain is often felt in the iliac fossa or in the loin, and radiates to the groin. 5- In several endemic areas there is a strong epidemiological association of S. haematobium infection with squamous cell carcinoma of the bladder. 6- Intestinal symptoms may follow involvement of the bowel wall. Schistosoma mansoni S. mansoni is endemic throughout Africa, the Middle East, Venezuela, Brazil and the Caribbean. Characteristic symptoms begin 2 months or more after infection. They may be slight, no more than malaise, or consist of abdominal pain and frequent stools which contain blood-stained mucus. With severe advanced disease,increased discomfort from rectal polyps may be experienced. The early hepatomegaly is reversible, but portal hypertension may cause massive splenomegaly, fatal haematemesis from oesophageal varices, or progressive ascites. Liver function is initially preserved because the pathology is fibrotic rather than cirrhotic. Schistosoma japonicum, S. mekongi and S. intercalatum The clinical features resemble those of severe infection with S. mansoni, with added neurological features. The small and large bowel may be affected, and hepatic fibrosis with splenic enlargement is usual. Deposition of eggs or worms in the CNS, especially in the brain or spinal cord, causes symptoms in about 5% of infections, notably epilepsy, blindness, hemiplegia or paraplegia. Investigations 1- There is marked eosinophilia. 2- Serological tests (ELISA) are useful as screening tests but remain positive after chemotherapeutic cure. 3- In S. haematobium infection, dipstick urine testing shows blood and albumin. 4- The eggs can be found by microscopic examination of the centrifuged deposit of terminal stream urine . Ultrasound is useful for assessing the urinary tract; bladder wall thickening, hydronephrosis and bladder calcification can be detected. 5- Cystoscopy reveals ‘sandy’ patches, bleeding mucosa and later distortion. 6- Sigmoidoscopy may show inflammation or bleeding. Biopsies should be examined for ova. Management 1- The object of specific treatment is to kill the adult schistosomes and so stop egg-laying. 2- Praziquantel is the drug of choice for all forms of schistosomiasis. 3- Surgery may be required to deal with residual lesions such as ureteric stricture, small fibrotic urinary bladders, or granulomatous masses in the brain or spinal cord
