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Lecture 18 Feb 24 Shisto.Pdf Digeneans: All life cycles involve a mollusc and a vertebrate All life cycles are similar but different All life cycles are a variation of one theme. Adult-egg-miracidium-[black box of sprorocyst/rediae] Cercariae leave snail (usually): 1) penetrate host (definitive or intermediate) 2) encyst on vegetation Among human parasitic diseases, schistosomiasis (sometimes called bilharziasis) ranks second behind malaria in terms of socio-economic and public health importance in tropical and subtropical areas. The disease is endemic in 74 developing countries, infecting more than 200 million people in rural agricultural and peri-urban areas. Of these, 20 million suffer severe consequences from the disease and 120 million are symptomatic. In many areas, schistosomiasis infects a large proportion of under-14 children. An estimated 500-600 million people worldwide are at risk from the disease Globally, about 120 million of the 200 million infected people are estimated to be symptomatic, and 20 million are thought to suffer severe consequences of the infection. Yearly, 20,000 deaths are estimated to be associated with schistosomiasis. This mortality is mostly due to bladder cancer or renal failure associated with urinary schistosomiasis and to liver fibrosis and portal hypertension associated with intestinal schistosomiasis. Biogeography The major forms of human schistosomiasis are caused by five species of water- borne flatworm, or blood flukes, called schistosomes: Schistosoma mansoni causes intestinal schistosomiasis and is prevalent in 52 countries and territories of Africa, Caribbean, the Eastern Mediterranean and South America Schistosoma japonicum/Schistosoma mekongi cause intestinal schistosomiasis and are prevalent in 7 African countries and the Pacific region Schistosoma intercalatum is found in ten African countries Schistosoma haematobium causes urinary schistosomiasis and affects 54 countries in Africa and the Eastern Mediterranean. In the case schistosomiasis, the adult worms reside in the blood vessels lining the liver, intestine, or bladder . Only about a half of the eggs are excreted in the feces (intestinal schistosomiasis), or in the urine (urinary schistosomiasis). The rest stay in the body, damaging other vital organs. It is the eggs and not the worm itself which cause damage to the intestines, the bladder and other organs. The miracidium swim through the water until they come in contact with a suitable snail host (suitability being determined by the species of both the parasite and the snail). S. mansoni only infect S. haematobium snails of the genus S. japonicum are infect species of Biomphalaria. found in Oncomelania sp. Bulinus. Intermediate hosts The life cycle within the snail is the same for all schistosome species. The miracidium actively searches out its specific snail host, penetrates snail tissue, changes into a mother sporocyst and gives rise to a daughter sporocyst. This sporocyst migrates to the digestive gland or reproductive organ, where further multiplication occurs and a new larva, the cercariae (the stage infective to man), is produced. It takes approximately four weeks at 26-28 OC for the miracidium to produce cercariae within the snail body. After maturing, the cercariae emerge from the snail and enter the surrounding water. One miracidium may end up generating several thousand cercariae. Freshwater snails are considered the intermediate hosts of schistosome infection, rather than vectors, because transferring the infection requires no physical contact between man and snail. The relationship between parasite and snail first intermediate host is very specific Once the cercariae penetrate the skin of their host, they burrow into the peripheral capillary bed of the blood circulatory system or enter the lymphatic system. Worms reach the right side of the heart and then enter the pulmonary capillaries of the lungs During this process, 3 significant morphological changes occur in the cercariae: the tail is lost, the surface coat is lost, and contents of the penetration gland is spent. The transformed cercaria is called a schistosomule After about a week, the schistosomules move through the pulmonary vein to the left side of the heart and then into the systemic circulation About 3 weeks post penetration the worms reach the hepatic portal veins (S. mansoni), veins of the small intestine (S. japonicum), or those of the urinary bladder (S. haematobium) where they reach sexual maturity and mate • S. mansoni and S. japonicum reside within the blood vessels that line the liver/intestine, while S. haematobium live in the vessels of the bladder. Paired male and female adult worms. The female is the darker, curled worm within the male's gynacophoric canal. The females then begin to produce eggs about 25 to 30 days after host infection. Females are able to produce up to 3,000 eggs per day for 3 to 8 years. The mouth of the adult schistosome is surrounded by an oral sucker; a ventral sucker is located immediately posterior to the level of bifurcation of the gut No pharnyx is present; however, here is an esophagus with prominent esophageal glands Life Cycle Female deposits eggs • The egg must penetrate the venuole endothelium and traverse the intervening tissues and the mucosal lining before entering the lumen of the gut or the bladder to escape to the outside •Eggs probably pass through tissues via hydrolytic secretions emitted through the porous shell; only about 1/3-1/2 of the eggs produced reach the exterior, with the remaining eggs being trapped in the urinary bladder, intestinal walls or swept back by the blood flow to become lodged in ectopic sites (liver or spleen) • After reaching the lumen, the egg passes out in either feces or urine •IF THIS WERE THE END OF THE STORY THE LECTURE WOULD BE OVER! •Some eggs are trapped in body tissues. Immune reactions to eggs lodged in tissues are the cause of disease. Pathology 1. The migration phase (from penetration to egg production) There are often no symptoms • Characterized by toxic reactions and pulmonary congestion, fever • This phase may last 4-10 weeks, during which the worms migrate from the lungs to the final destination where they reach sexual maturity and mate 2. The acute phase (begins at egg production) This phase is considerably longer, lasting 2 months to several years • Symptoms such as blood in stools (S. mansoni and S. japonicum) and hematuria (S. hematobium) are caused by passage of eggs through the intestinal and urinary bladder walls 3. The chronic phase Usually there is mild, chronic bloody diarrhea, with mild abdominal pain and lethargy, or with S. haematobium there is pain during urination. Also characterized by severe intestinal, renal, and hepatic pathology, caused by the reaction of the host to schistosome eggs. Enlargement of the liver (=liver fibrosis) and spleen is a common symptom of advanced schistosomiasis. Eggs trapped in the walls of the intestine and urinary bladder as well as ectopic regions, notably the liver and the spleen, elicit inflammatory reactions resulting from leucocystic and fibroblastic infiltration and producing cirrhosis, anemia, etc Pre-patent period skin invasion, maturation and migration of worms- rash, itching, allergic reaction, diarrhea, fever, inflammation of intestinal tissues Egg deposition blood/mucous in feces or urine, fever (immune response to eggs) Tissue proliferation, repair, degenerative effects eggs trapped in tissues, WBC surround eggs, lay down connective tissue to isolate eggs- granuloma. So much tissue may be layed down over time that organs lose elasticity, vessels become blocked, eggs transported to liver, same reaction, liver function affected, progressive damage S. hematobium: eggs can reach 200-800 eggs/ml of urine In urinary schistosomiasis (due to S. haematobium) damage to the urinary tract is revealed by blood in the urine. Urination becomes painful and is accompanied by progressive damage to the bladder, ureters and then the kidneys. Bladder cancer is common in advanced cases. In intestinal schistosomiasis (infection with S. mansoni, S. japonicum, S. mekongi) disease is slower to develop. There is progressive enlargement of the liver and spleen, intestinal damage due to fibrotic lesions around eggs lodged in these tissues, and hypertension of the abdominal blood vessels. Bleeding from these vessels leads to blood in stools, and can be fatal. Sufferers become seriously weakened by the disease and, in some cases, the functioning of organs such as spleen and kidneys becomes impaired. Death is mostly due to bladder cancer associated with urinary schistosomiasis and to bleeding from varicose veins in the oesopahagus associated with intestinal schistosomiasis. Children are especially vulnerable to infection, which develops into chronic disease if not treated. • Eventually, a granuloma forms around each egg or cluster of eggs; the result of leukocyte infiltration and secretion of fibroblast growth factors • Small abscesses, accompanied by occlusion of small blood vessels, lead to necrosis and ulceration Schistosoma egg in the liver : granuloma formation Intestinal schistosomiasis: eggs in the wall of the gut The morbidity associated with schistosomiasis results from the mechanical and toxic irritation caused by eggs lodged in blood vessels and by granulomas, which are localized tissue reactions to eggs. As the immune system recognizes the egg as a foreign body and tries to destroy it, scar tissue develops around the egg, forming a granuloma. There is a direct relationship between the number
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