Schistosoma haematobium

Schistosoma haematobium
Schistosoma haematobium
Histopathology of bladder shows eggs of Schistosoma haematobium surrounded by intense infiltrates of eosinophils.
Scientific classification
Kingdom: Animalia
Phylum: Platyhelminthes
Class: Trematoda
Subclass: Digenea
Order: Strigeidida
Family: Schistosomatidae
Genus: Schistosoma
Species: S. haematobium
Binomial name
Schistosoma haematobium
(Bilharz, 1852)

Schistosoma haematobium is an important digenetic trematode, and is found in the Middle East, India, Portugal and Africa. It is a major agent of schistosomiasis; more specifically, it is associated with urinary schistosomiasis.

Adults are found in the Venous plexuses around the urinary bladder and the released eggs traverse the wall of the bladder causing haematuria and fibrosis of the bladder. The bladder becomes calcified, and there is increased pressure on ureters and kidneys otherwise known as hydronephrosis. Inflammation of the genitals due to S. haematobium may contribute to the propagation of HIV.[1] Studies have shown the relationship between S. haematobium infection and the development of squamous cell carcinoma of the bladder.[2]


Life cycle

The free swimming infective larval cercariae burrow into human skin when it comes into contact with contaminated water. The cercariae enter the blood stream of the host where they travel to the liver to mature into adult flukes. In order to avoid detection by the immune system inside the host, the adults have the ability to coat themselves with host antigens.[3] After a period of about three weeks the young flukes migrate to the bladder to copulate. The female fluke lays as many as 3,000 eggs per day eggs which migrate to the lumen of the urinary bladder and ureters. The eggs are eliminated from the host into the water supply with micturition. In fresh water, the eggs hatch forming free swimming miracidiae which penetrate into the intermediate snail host[3] (Bulinus spp., e.g. B. globosus, B. forskalii, B. nyassanus and B. truncatus). Inside the snail, the miracidium sheds it epithelium and develops into a mother sporocyst. After two weeks the mother begins forming daughter sporocysts. Four weeks after the initial penetration of the miracardium into the snail furcocercous cercariae begin to be released. The cercariae cycle from the top of the water to the bottom for three days in the search of a human host. Within half an hour the cercariae enter the host epithelium.[4]


The majority of diagnoses are made by examination of the urine for eggs. In chronic infections, or if eggs are difficult to find, an intradermal injection of schistosome antigen to form a wheal is effective in determining infection. Alternate diagnosis can be made by complement fixation tests.[3]


The main cause of schistomiasis is the dumping of human waste into water supplies. Hygienic disposal of waste would be sufficient to eliminate the disease.[3]


The immune system responds to eggs in liver causing hypersensitivity; an immune response is necessary to prevent damage to hepatocytes. The hosts' antibodies which bind to the tegument of the Schistosome don't bind for long since the tegument is shed every few hours. The schistosome can also take on host proteins. Schistomiasis can be divided into three phases: (1) the migratory phase lasting from penetration to maturity,(2) the acute phase which occurs when the schistosomes begin producing eggs, and (3) the chronic phase which occurs mainly in endemic areas.[3]


The ova are initially deposited in the muscularis propria which leads to ulceration of the overlaying tissue. Infections are characterized by pronounced acute inflammation, squamous metaplasia, blood and reactive epithelial changes. Granulomas and multinucleated giant cells may be seen.


The drug of choice is praziquantel, a quinolone derivative.


  1. ^ Leutscher PD, Pedersen M, Raharisolo C, et al. (2005). "Increased prevalence of leukocytes and elevated cytokine levels in semen from Schistosoma haematobium-infected individuals". J Infect Dis 191 (10): 1639–47. doi:10.1086/429334. PMID 15838790. 
  2. ^ Khurana S, Dubey ML, Malla N (April 2005). "Association of parasitic infections and cancers". Indian J Med Microbiololgy 23 (2): 74–79. doi:10.1016/S0300-483X(01)00357-2. 
  3. ^ a b c d e Black, J. (2005). Microbiology: Principles and Explorations. Wiley, New York. 
  4. ^ Roberts, L., Janovy, J. (1996). Foundations of Parasitology, 5th edition. Wm. C. Brown Publishers, Dubuque, Iowa. 

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