Parasitology - Trematodes

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Schistosoma mansoni

Infection

Back 1

Humans acquire S. mansoni by coming in contact with the cercaria which have been released from the snail vector into fresh water. Teh cercaria enters the host by penetrating the unbroken skin where it transforms into the schistosomula before eventually migrating to the liver where it matures into an adult male or female

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Schistosoma mansoni

Adult worm

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Adult worms are harbored in the venous system surrounding the small intestine. The male worm encompasses the male and live as a pair in the small intestines in the vessels. The rough surface of the worm helps in absorption of nutrients. The adult has a blind guy with no exit so it absorbs and regurgitates what it doesn't want through the mouth.

Schistosome adults remain in copula during their life span, and live attached by their sucker disks to the endothelium of the veins. S. masoni lives in the inferior mesenteric veins that drain the intestines. S. japonicum and S. mekongi live in the superior mesenteric veins. S. japonicum adult worms can also find their way to the choroid plexus and other ectopic locations. S. haematobium is found almost exclusively in the venus plexus that drain the urinary bladder. Schisotosomes are facultative anaerobes, deriving energy primarily from through the degradation of glucose and glycogen, Adults ustilize hemoglobin as a primary source of AA, which is ingested into their blind bifurcated gut. They employ hemoglobinase, digesting the globin portion of the molecule, and detoxifying the heme moiety into a pigment before it is regurgitated back into the blood stream. The female lies within the gynecophoral canal of the male.

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Schistosoma mansoni

Pathology

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The pathologic effects fo the schistosomes are due to the damage done by their eggs to the various organs and tissues in which they lodge. Note eggs in lung. Dead eggs in lung capillaries elicit pseudo-tubercles. Obstruction of pulmonary blood flow may result in a condition known as cor pulmonale.

Front 4

Schistosoma mansoni

Diagnosis

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Some patients have striking signs and symptoms, but light infections often produce no clinical evidence for many years, hence diagnosis is made by stool examination for eggs. If no eggs are found and schisosomiasis is still suspected, a rectal snip often reveals the eggs in positive cases.

Front 5

Schistosoma mansoni

Evades immune system

Back 5

Avoids immune attack by employing a unique set of
molecular mechanisms. One scheme involves incorporating host serum proteins onto the tegumental surface as camouflage, mimicking the strategy of the decorated crab. The other employs a mimic
surface molecule similar to beta -2-microgloblulin, a macrophage recognition factor.
Possible application: transplant heterologous

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Schistosomes

Embryonated egg

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Miracidium - larvae
Schistosoma mansoni has a lateral spine
Schistosoma japonicum has inapparent spine.
Schisosoma mekongi has no spine
Schistosoma haematobium has a terminal spine

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Schistosomes

Lifecycle

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Eggs hatch in fresh water and the miracidium (larvae) penetrate the snail. They grow to become cercaria and when the sun is shining secaria get free of the snail and go to the surface of the water looking for a human host. The cercaria (infectious stage for humans) enter the skin, and then circulation, and encounters the lungs and then somehow finds the liver. Male and females accumulate in the liver and have to find each other (by secreting phermones) to mate and then travel together to go against the blood circulation to the mesenteric venule (S. haematobium goes to venous plexus of the bladder). The worms then follow the chemical signals given off by organs. The female produces eggs that pass through the birth pore located above the posterior sucker. When the worm applies the sucker to the endothelial surface, the embryonated eggs secrete lytic enzymes (metalloproteases), enabling them to enter the surrounding connective tissue. Eggs collect in the sub-mucosa before entering the lumen of the small intestine (or for S. haematobium the urinary bladder). The eggs are released into fresh water either through feces or urine (S. haematobium).

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Schistosoma masoni
Schistosoma japonicum

Pathology

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1. Miracidium inside egg in small intestine releases proteases, dissolves tissues, induces bleeding and diarrhea.
2. Eggs (50% of those produced) wash back into liver, lodge in presinusoida capillaries, eventually block flow of blood.
3. Blockage of portal circulation results in portal hypertension. Get eosphageal varices.
4. Portal hypertension leads to induction of embryonic circulatory paths, eggs then by-pass liver. Toxic brain syndrome may ensue.
5. Adults avoid immune detection by:
a. camouflage strategy, incorporating host serum proteins on tegumental surface.
b. synthesizing β-2 microglobulin-like molecule on tegumental surface.

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Schistosoma masoni
Schistosoma japonicum

Clinical disease

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Acute Phase
1.“Katayama Fever” - acute fever
2. Paralysis
3. CNS involvement
Chronic Phase
1. GI bleeding and diarrhea
2. Portal hypertension due to blockage of presinusoidal
capillaries
3. Esophageal varices
4. Ascites
5. Rupture of varices, bleeding, death
6. Cor pulmonale, right side heart failure, death
7. Toxic brain syndrome

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Schistosoma masoni
Schistosoma japonicum

Diagnosis

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1. Microscopic examination of feces, urine, rectal “snip” for eggs.
2. Capture ELISA for detecting circulating antigens (experimental).
3. Serological tests (e.g., ELISA): indirect measure of exposure, not active disease.

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Schistosoma masoni
Schistosoma japonicum

Treatment

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Praziquantel

MOA: Interferes with Ca2+ ion channels, leads to disrupted tegument. This drug is more effective if the patient has already developed antibodies against tegumental antigens.

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Schistosoma haematobium

Pathogenesis

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Instead of migrating to mesenteric venules, migrates to venous plexus of the bladder. The eggs of S. haematobium lodge in the bladder wall, inducing cellular changes associated wtih granuloma formation. Causes calcifications of the dome of the bladder. Causes the bladder to fill up and back up to the kidney, causing hydronephrosis and because of back up, toxin from foods and liquids can build up and cause squamous cell epithelioma.

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Schistosoma haematobium

Treatment

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Praziquantel

MOA: Interferes with Ca2+ ion channels, leads to disrupted tegument. This drug is more effective if the patient has already developed antibodies against tegumental antigens.

Front 14

Swimmer's itch

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Hypersensitivity reaction due to contact with avian schistosomes. Body temperature of bird is similar to human skin and so can get infected, but the schistosomes will die because of the different internal temperature. The 2nd time this is encountered, a hypersensitivity reaction occurs.

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Schistosomes

Immune reaction

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TH2 protective mechanism: eosinophils and specific IgE antibodies combine to kill the parasite.

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Schistosomes

Transmission encouraged by

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1. Dam building, irrigation projects (e.g., 3 Gorges Dam, China).
2. Reservoir hosts (primates, oxen).
3. Indiscriminate dispersal of feces and urine into environ

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Schistosomes

Prevention and control

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1. Sanitary disposal of feces
2. Public health education.
3. Snail control.
4. Community-based drug programs (praziquantel).
5. Vaccine development for reservoir hosts (e.g., water buffalo and oxen).