Schistosomiaza

The main forms of human schistosomiasis are caused by five species of the flatworms, or blood flukes, known as schistosomes: Schistosoma haematobium, S. mansoni, S. japonicum, S. mekongi, S. intercalatum.

This disease, also called bilharzias, is transmitted by a sweet water snail. The larvae, called cercariae will penetrate through pores of skin, enter the blood stream and develop into adult schistosoms. Adult worms, pair, mate and females lay hundreds of eggs each day for many years in humans. Eggs are excreted in the faeces or urine and the parasite lifecycle is completed when these hatch into miracidiae (upon contact with water), which then infect the intermediate snail host. Disease is often caused when, rather than being excreted, eggs become lodged in host tissues such as the intestine, liver or bladder, where they stimulate an inflammatory granulomatous response

Schistosoma mansoni eggs in a patient from Egypt Schistosoma mansoni eggs in a patient from Egypt.  These eggs are large (length 114 to 180 µm) and have a characteristic shape, with a prominent lateral spine near the posterior end.  The anterior end is tapered and slightly curved.  When the eggs are excreted, they contain a mature miracidium (especially visible in A).

Schistosoma mansoni eggs

Schistosomiasis. Eggs of S Schistosomiasis. Eggs of S. mansoni in faeces showing characteristic lateral spine.

Schistosoma mansoni eggs in intestinal wall.

Schistosoma japonicum eggs

Schistosoma japonicum eggs in liver

Schistosoma japonicum eggs in colon

Schistosoma haematobium eggs

Urinary schistosomiasis. Egg of S. haematobium in the urinary sediment Urinary schistosomiasis. Egg of S. haematobium in the urinary sediment. Note the terminal spine.

Schistosoma cercaria The fork-tailed larval stage of Schistosoma mansoni, known as a cercaria, emerges from an infected aquatic snail and swims about seeking contact with the skin of a potential host.

When contact is made, the cercaria initiates infection by penetrating the epidermis, at which time it sheds its tail, and heading deeper into the dermis.

Schistosomiasis. The slender female worm lies in a groove (the gynecophoral canal) in the lateral edge of the body of the male. Scaning electron micrograph.

Skin vesicles created by the penetration of Schistosoma

Cercarial dermatitis of schistosomiasis Cercarial dermatitis of schistosomiasis. Each lesion represents a cercarial invasion site.

A boy with swollen abdomen due to schistosomiasis (bilharziasis) with hepatosplenomegaly.

Schistosomiasis (Bilharziasis). Uninary infection.

Hepatosplenic schistosomiasis These two boys have end-stage hepatosplenic schistosomiasis. The child on the right shows massive ascites, with tremendous engorgement of the enlarged collateral venous structures. He died soon after the photograph was taken.

School children in Niger with gross haematuria (blood in urine) caused by schistosomiasis.

Schistosomiasis. Barium study of oesophagus showing oesophageal varices secondary to portal hypertension in S. mansoni infection.

Schistosomiasis. Eggs of S Schistosomiasis. Eggs of S. mansoni in mucosa of colon with surrounding granulomatous reaction (G).

Higher magnification showing the caracteristic lateral spine on one of the eggs.

Schistosomiasis. Eggs of S Schistosomiasis. Eggs of S. mansoni in liver with surrounding granulomatous reaction.

Schistosomiasis. The ova of Schistosoma mansoni are seen in the portal-periportal area with a foreign-body type reaction. Eggs can also be seen in the lower right corner of the section, and there is increased fibrous tissue in the portal area. Of the five species of Schistosoma (trematode, blood flukes) that infect humans, two species—S. mansoni and S. japonicum —account for most cases of hepatobiliary involvement. Tissue damage is essentially a consequence of the deposition of the schistosomal eggs, especially in the smaller intrahepatic portal vessels.

Eggs of Schistosoma mansoni with a granulomatous response and eosinophilia. Schistosome eggs evoke a granulomatous reaction. Advanced schistosomiasis results in portal and septal fibrosis, eventually giving rise to Symmers’ portal fibrosis. Note also the accumulation of brown-black pigment (“schistosomal pigment”) in portal macrophages and scattered Kupffer cells. Schistosomal pigment is indistinguishable from malarial pigment and is a breakdown product of hemoglobin. Schistosomal pigment may be seen even in the absence of ova.

Schistosomal pigment stains negative for iron.

Liver sections revealing ova of Schistosoma japonicum. A, Marked infestation by ova of S. japonicum with a prominent granulomatous response and fibrous expansion of portal areas. Whereas the eggs of S. mansoni usually measure 114 to 175 mm Ч 45 to 68 mm and have a prominent lateral spine, the eggs of S. japonicum are smaller, ranging from 70 to 100 mm Ч 50 to 65 mm, with a minute spine on one side.

note the prominent subcapsular as well as portal involvement. B. In another section, Schistosoma japonicum, note the prominent subcapsular as well as portal involvement.

Schistosomiasis. Section of mesentery showing adult Schistosoma mansoni worm lodged in mesenteric vein.

Schistosomiasis. Eggs of S Schistosomiasis. Eggs of S. haemoatobium in bladder wall with surrounding chronic inflammatory reaction and fibrosis.

Urinary schistosomiasis. High power view showing eggs of S Urinary schistosomiasis. High power view showing eggs of S. haematobium surrounded by granulomatous reaction within bladder wall.

Severe periportal fibrosis from schistosomiasis Severe periportal fibrosis from schistosomiasis. Ultrasound and computed tomography (CT) scans of the liver demonstrate severe periportal fibrosis. A.The ultrasound scan demonstrates intense echogenicity in the periportal region, which causes considerable sonic dropout (shadowing).

B. In the CT scan, the periportal fibrosis is manifested as the low-density thickening of soft tissues around the portal vein (arrows). Both patients developed periportal fibrosis due to infection with Schistosoma mansoni.

Schistosomiasis of the urinary tract Schistosomiasis of the urinary tract. Plain film of the pelvis shows dense calcification in the distal ureter and bladder (arrows) typical of urinary tract infection by Schistosoma haematobium.

Schistosoma mansoni, S. japonicum, and S. haematobium THE SCHISTOSOMES: Schistosoma mansoni, S. japonicum, and S. haematobium   A. Epidemiology: Over 200 million people worldwide are infected, mostly in Asia (S. japonicum), Africa (S. mansoni and S. haematobium) and Latin America (S. mansoni). Endemic range depends upon the snail intermediate hosts. S. japonicum is the only schistosome for which domestic animals serve as a reservoir. B. Mode of transmission: Fresh water contaminated with human feces or urine carries eggs to the snail intermediate host where cercariae develop. Humans become infected by wading in water containing the cercariae. C. Clinical manifestations: A pruritic papular skin rash develops at the site of cercarial penetration of the skin. Symptoms are due to immediate and delayed hypersensitivity to parasite antigens. A more severe form of Schistosomiasis coincides with the onset of egg-laying by the mature adults   (4-8 weeks after initial infection). Symptoms include fever, chills, headache, lymphadenopathy, hepatomegaly, splenomegaly, and eosinophilia. A syndrome like serum sickness sometimes occurs that may be due to circulating immune complexes. Chronic phase disease is associated with GI hemorrhage, massive hepatosplenomegaly, and hematuria. Death is commonly caused by internal bleeding from rupture esophageal varices. NOTE: In the U.S., especially the Great Lakes region, a form of Schistosomiasis is seen in the summer months that is described as “Swimmer’s Itch”. This is caused by a variety of Schistosome endemic in the freshwater snails in that area. The cercariae do not survive within the human body (humans are an aberrant host). The itch is caused by the host inflammatory response to the parasite antigens. D. Pathology:Humans are infected when the free-living fork-tailed cercariae penetrate the skin, differentiate to metacercariae, enter the blood and are carried to the portal circulation. Mature flukes develop in the liver; females live within a groove in the male fluke (the schist). S. mansoni and S. japonicum adults migrate to the mesenteric venules. S. haematobium adults migrate to the bladder veins (increased incidence of squamous cell carcinoma of the bladder is associated with S. haematobium). Once at the venous site, the female lays fertilized eggs that penetrate the vascular endothelium and enter the gut or bladder lumen to be released in either urine or stool. Eggs hatch to ciliated larvae in fresh water, where they must find the snail intermediate host to complete the life cycle. Pathology is mostly due host inflammatory response to the presence of eggs in the liver, spleen, or gut/bladder walls. Additional damage is caused by proteolytic enzymes released by the eggs. Granuloma formation is common. Obstruction of circulation leads to organ enlargement. E. Laboratory diagnosis:Examination of urine or fecal samples for the presence of eggs. Large terminal or lateral spines are unique to Schistosome eggs. No serology.   F. Treatment:Praziquantel.