Schistosomiasis

Schistosomiasis

Schistosomiasis, AKA Bilharzia
Parasitic disease caused by several species of flatwormAffects many in developing countries Can contract it by wading or swimming in lakes, ponds and other bodies of water infested with the parasite’s snail host.

Distribution Map

A Brief History...
First described by German pathologist Theodore Maximilian BilharzBilharz performed autopsies on Egyptian patients who had died from the disease: found male & female parasite eggs in the liver portal system, bladder.Later seen in Japan, called Katayama feverSymptoms: rash on legs, fever, diarrhoea, bloody stools  emaciation, edema  death.

Classification

Genus: Schistosoma Species: S. mansoni  S. japonicum S. haematobium S. indicum

Life Cycle (Basic)

Life Cycle (Eggs  larvae  into snail) Parasite eggs released into freshwater (from human urine, feces)Eggs hatch  ciliated miracidia, free swimmingMiracidia find & infect snail host (different species prefer diff’t snail sp.)Each miracidia transforms into many fork-tailed, free swimming forms called cercariae within 4-6 weeks of entering snail.Cercariae leave snail and move into water at a rate of 1500/day for up to 18 days. Miracidia larva with cilia


6. Cercariae find a human host, penetrate skin, and differentiate into larval forms called schistosomulae.7. Migrate through the host’s skin, gain access to the lymphatic system.8. Travel to the lungs (stay 3-8 days and ~70% are eliminated)9. Migrate to liver portal system, mature into male & female adults Cercariae with forked tail
Life Cycle (Into human  lymphatics  lungs  liver)

10. In liver, m & f pair up  female inserts herself into the gynecophoral canal of male  they are now ‘paired’.11. Migrate to favoured sites:S. mansoni – mesenteric venules of large bowel & rectumS. japonicum – mesenteric veins of the small intestineS. haematobium – perivesical venous plexus surrounding the bladder Life Cycle (maturation  movement to target organs  egg production) Paired male & female


12. Females release eggs.Egg characteristics- Covered in microbarbs  cling to vascular endothelium- Pores, which allow the release of1) Antigens2) Enzymes (aid in passage of eggs through host tissues)12. Eggs enter lumen of excretory organs50%  passed out of body50%  trapped in tissues, carried away by blood circulation, lymph. Life Cycle (Egg release)


Cercariae penetrate skin  rash- called schistosome or swimmer’s itch.Eggs laid in target organs release antigens  cause Katayama fever- fever- urticaria- malaise- diarrhea Acute Infection(Early)


Symptoms of chronic infection caused by eggs that travel to various parts of bodyEggs remain trapped in host tissues  secrete Ags  granulomatous inflammatory immune responseGranulomas: macrophages surrounded by lymphocytes (CD4, CD8 Tcells), which aggregate at site of infection. Fibroblast cells also at site of infection.During late stage of chronic infection, they replace the granulomas. Their prolif. is stim. by factors produced by the schistosome egg, & by cytokines from macrophages & CD4 Tcells. Fibroblasts mediate collagen deposition in the granuloma, leading to fibrosis (=fibrous connective tissues development Chronic Infection(Late)

Granuloma

In S. mansoni infectionsWall of colon is damaged as eggs pass throughInflamm. response  ulcers, inflammatory polypsCan lead to fibrosisClinically: diarrhea, abdominal painEggs can also accumulate in the appendixCan lead to appendicitis (inflammation of the appendix) Chronic Infection(When eggs meet the GI tract)


Hepatosplenic schistosomiasisEggs carried by portal circulation  liverGranulomatous responseGranulomas are walled off with fibrous tissue  fibrosis obstructs portal veins  portal hypertensionEsophageal varices (dilated esophageal veins bursting can cause bleeding to death. Caused directly by portal hypertension.)Splenomegaly (enlarged spleen) Chronic Infection(When eggs meet the meet the liver/spleen)


In those with severe hepatosplenic schistosomiasisBlood gets shunted directly back to the heart (doesn’t pass through liver).Eggs accumulate in heart, sometimes lodged in pulmonary arterioles.Form granulomas  block pulmonary circulation  pulmonary hypertension.Can lead to right ventricular strain, and eventually cardiovascular collapse. Chronic Infection(When eggs meet the meet the heart)


Genitourinary complicationsEggs lodge themselves in wall of bladder & can develop into polypsPolyps can erode, ulcerate & cause hematuria (blood cells in urine)Eggs lodge in ureters and urethra, cause lumps and lesions  kidney failureEggs lodge into ovaries, the uterus, cervix, fallopian tubes  lumps  complications incl. infertility (For the men: eggs can also lodge into the testes and the prostate )CNS complicationsS. haematobium and S. mansoni can migrate to the spine S. japonicum found in the brain and causes encephalopathy (general brain dysfunction) Chronic Infection(When eggs meet the meet the genitourinary areas & CNS)

Diagnosis

Microscopic Detection Take stool or urine sample to detect eggs S. haematobium eggs are oval and have a spike at the tip S. japonicum eggs small and almost spherical with tiny spine S. mansoni eggs have a spike on the side (spine)

S. mansoni

S. japonicum
S. haematobium

Diagnosis

Antibody testsAn earlier and more sensitive form of detectionSome complicationsCross-reactivity with other helminthic infections (other flatworm parasites)Can’t tell the difference between current and old infections as antibodies stay long after infection is over. Can’t tell you anything about overall worm burden so we can’t tell how serious the infection is


Diagnosis
Antigen tests: Detect antigens in blood with immunoelectrophoresis 2 types are detected though share similar complications with antibody testsMolecular detection:20-25% of schistosomiasis genome has been sequenced  can use 2 probes to detect S. mansoni DNA in human bloodGenome sequencing has the potential to yield DNA vaccines