The parasitic flatworm Schistosoma haematobium causes urogenital schistosomiasis, historically known as bilharzia. This blood fluke is a public health concern, particularly in tropical and subtropical regions where it is classified as a neglected tropical disease. The infection affects millions globally, leading to chronic illness and significant long-term health complications. Understanding the parasite’s biology and complex life cycle is important for controlling its spread.
Defining the Parasite and Its Habitat
Schistosoma haematobium is a digenetic trematode, or blood fluke, distinct from other flukes because it has separate male and female sexes. The male worm is 10 to 18 millimeters long and holds the longer, thinner female worm permanently paired for reproduction within its gynaecophoric canal. Adult worms reside in the human host’s venous plexus, specifically the small blood vessels surrounding the urinary bladder.
The disease’s pathology is caused not by the adult worms, but by the eggs they produce. These oval-shaped eggs measure 110 to 170 micrometers long and possess a unique, conspicuous terminal spine positioned at one end. This morphology helps distinguish S. haematobium from other schistosome species. The parasite’s endemic geographical range is concentrated primarily in Africa and the Middle East, where it causes the majority of schistosomiasis cases.
The Transmission Cycle
The life cycle of S. haematobium requires both a human host and a specific freshwater snail intermediate host. The cycle begins when an infected human urinates into fresh water, releasing the parasite’s eggs. Upon contact with water, the eggs hatch, releasing a ciliated larval stage called a miracidium.
The free-swimming miracidium then seeks out and penetrates a freshwater snail of the genus Bulinus, the required intermediate host. Inside the snail, the parasite undergoes asexual reproduction, developing through successive sporocyst stages. This process amplifies the number of parasites, leading to the release of thousands of fork-tailed larvae called cercariae back into the fresh water.
The cercariae are the infective stage for humans and swim freely until they encounter a host. Upon contact with human skin, the cercariae actively penetrate the skin barrier, shedding their tails. Once inside, the larvae transform into schistosomulae, which migrate through the circulatory system. They eventually reach the venous plexuses around the bladder to mature into adult worms, completing the cycle.
Health Impacts of Infection
Health concerns stem from the immune response to the parasite’s eggs trapped within urinary tract tissues. Adult female worms lay hundreds of eggs daily in the blood vessels surrounding the bladder. While some are excreted, many lodge in the bladder wall and other pelvic organs, triggering a chronic inflammatory reaction and the formation of granulomas, which causes the disease’s pathology.
The most recognizable initial sign is hematuria, or blood in the urine, which appears within two to three months after initial exposure. Chronic inflammation eventually leads to the hardening and thickening of the bladder wall, known as fibrosis. Severe, long-term infection can result in obstructive uropathy, where fibrotic changes block the ureters. This causes a backup of urine that damages the kidneys, a condition called hydronephrosis.
A severe long-term consequence of chronic urogenital schistosomiasis is its association with squamous cell carcinoma of the bladder. The International Agency for Research on Cancer (IARC) classified chronic infection with S. haematobium as a Group 1 carcinogen, definitively linked to cancer in humans. Furthermore, in women, eggs lodged in the genital tract cause female genital schistosomiasis, which can increase the risk of HIV transmission.
Medical Management and Prevention
Diagnosis is typically achieved through microscopic identification of the parasite’s distinctive terminally-spined eggs in a urine sample. Because egg excretion fluctuates, samples are often collected around midday to maximize detection. Serological tests, which detect antibodies, are also used, particularly when infection is light or in travelers.
The standard and effective treatment for all major Schistosoma species, including S. haematobium, is the drug Praziquantel. The recommended dosage is 40 milligrams per kilogram of body weight, administered orally in two divided doses over a single day. This medication causes rapid muscle paralysis in the adult worms, allowing the host’s immune system to clear them.
Prevention strategies focus on interrupting the parasite’s life cycle and reducing human exposure to contaminated water sources. Public health programs often employ mass drug administration (MDA), periodically treating entire at-risk populations with Praziquantel to reduce the community parasite load. Improving sanitation infrastructure to prevent egg-containing urine from reaching fresh water is a long-term control goal. Education about avoiding contact with fresh water in endemic areas and controlling the Bulinus intermediate host snail population are also important.

