Schistosoma mansoni

Structure

Schistosomes are long, cylindrical worms that are sexually dimorphic, unlike other trematodes. The male S. mansoni is about 1 cm long and 0.1 cm wide, white in color, with a funnel-shaped oral sucker and a pediculated ventral sucker. Its body is covered by a double bilayer called the membranocalyx, which is continuously shed, and the tegument bears small tubercles. The male has six to nine testicular masses and a seminal vesicle located at the beginning of the gynaecophoric canal.

The female is longer and thinner, measuring 1.2 to 1.6 cm in length and 0.016 cm in width, and appears gray due to hemozoin pigment from digested blood. Her ovary is elongated and lobulated, located in the anterior half, and the genital pore opens ventrally. The digestive tube begins at the oral sucker, consists of an esophagus that splits into two branches, and ends blindly with no anus.

Life cycle

Eggs released in human feces hatch into miracidia when they reach water, triggered by temperature, light, and dilution. The miracidium seeks a freshwater snail of the genus Biomphalaria and penetrates its soft tissue. Inside the snail, it develops into a mother sporocyst, which produces daughter sporocysts through asexual reproduction. These daughter sporocysts move to the snail's liver and gonads, and within 2–4 weeks, they transform into fork-tailed cercariae.

Cercariae emerge from the snail during daylight and can survive in water up to 12 hours, with peak infectivity between 1 and 9 hours. They attach to human skin, creep to a suitable site such as a hair follicle, and penetrate using secretions from glands. The head transforms into a schistosomule, which spends days in the skin before entering the circulation. It migrates to the lungs and then to the hepatoportal circulation, where it matures into an adult if it pairs with a partner of the opposite sex.

Pathology

The eggs of S. mansoni are the primary cause of pathology, as they become lodged in host tissues. Eggs that do not exit the body through the intestinal wall are carried to the liver, causing periportal fibrosis. Acute schistosomiasis, known as Katayama fever, may occur when egg laying begins, but chronic forms are more significant. Intestinal and hepatic schistosomiasis result from granulomas forming around eggs trapped in the intestinal wall or liver.

Hepatic disease is more severe, leading to fibrosis, hepatosplenomegaly, and portal hypertension. Granuloma formation is triggered by antigens from the miracidium, and the immune response to these granulomas causes symptoms. Over time, collateral circulation develops, and eggs spread to the lungs, causing pulmonary arteritis and cor pulmonale. Symmers' fibrosis around portal veins contributes to portal hypertension.

Granuloma size is linked to levels of IL-13, and the IL-13 receptor α2 can block IL-13 effects, preventing progression to chronic disease.

Did You Know?

• Developing S. mansoni worms lyse host red blood cells to obtain nutrients, and they discard iron waste via regurgitation.
• The parasite's genome is approximately 270 MB with eight pairs of chromosomes; females are heterogametic (ZW) and males are homogametic (ZZ).
• S. mansoni is most effective at destroying red blood cells at a pH of 5.1 and a temperature of 37 °C.