11..trematodes
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11..trematodes

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11..trematodes 11..trematodes Presentation Transcript

  • Trematodes
  • Schistosoma       Schistosomes are a group of closely related flukes that inhabit the portal vascular system. Schistosomes are therefore known as Blood flukes. Of the seven species known to infect humans, S.haematobium, S.mansoni and S.japonicum are of primary importance. S.mansoni and S.japonicum usually affect the gastrointestinal tract. S.haematobium affects the urinary tract. Schistosomiasis is a major cause of debilitating illness in the world with about 10% having a chronic disease with significant impaired liver function. The deposition of schistosome eggs within the host is the principal pathological vause of chronic schistosomiasis.
  •       Characteristic features: In contrast to other Trematodes, Schistosomes are not hermaphrodites. They exist as separate sexes with the female residing in the groove of the male known as the “schist” and hence the name. The three species can be distinguished by the morphological features of their eggs. S.mansoni eggs have a prominent lateral spine, S.japonicum have a small lateral spine, and S.haematobium eggs are with a terminal spine. Schistosomes have evolved a remarkable process to avoid host defences by absorbing host molecules, including immunoglobulins, blood group glycolipids, and HLA antigens. These limit the ability of the immune system to recognize them as foreign.
  •  Life Cycle:  Includes and requires one intermediate host (specific species of snail for the different S.species). Humans are the definitive host harboring the adult flukes that lay eggs  passes out in the stool eggs have miracidia Miracidia hatch in fresh water and penetrate a specific species of snail sheds its epithelium and develops into a mother sporocyst that give rise to daughter sporocysts  the cercaria larva (forked tailed) emerge from the daughter sporocysts and exit the snail. 
  •   The cercariae are the infectious stage and have a strong attraction for skin secretions especially arginine  penetrate the skin  transform into schistosomules (little schistosomes) within 24 hours enter the peripheral circulation  enter the heart  exit the heart through the pulmonary capillaries  enter the left side and thereby into the systemic circulation. A small number leave the mesenteric arteries , traverse the intestinal capillary bed and reach the liver by the hepatic portal system.
  •   After about three weeks of development in the liver sinusoids, the young parasites use their suckers to ascend the superior mesenteric vessels against the blood flow and migrate to the walls of the gut  copulate and produce eggs. The eggs are release via stools.
  •  Pathogenesis:  The pathogenesis is almost entirely due to the eggs and not the adult worm. The eggs located in the liver, spleen or the walls of the gut or the bladder liberate antigens over a considerable period of time that ultimately induce granulomas leading to fibrosis, hepatomegaly and portal hypertension. The primary lesion however, begins with a delayed type Hypersensitivity (DTH) around the egg.  
  •  Pathogenesis divided into 3 stages:  I) Early stage: A large number of schistosomules usually die within 24 hours of the cercariae entering the skin. Immediate and DTH to the parasitic antigens results in an intensely pruritic papular skin rash reulting in characteristic itching and local edema that resolves within around 4 days. This is called Cercarial dermatitis. Fever, abdominal pain and headache indicate the migration of the schistosomula to the liver. Fever may be due to the secretion and excretion materials of the migrating schistosomules  allergic reaction not as severe as with their egg antigens.    
  •  II) The Intermediate stage:  After about 1-2 months of primary exposure, the patient may experience the onset of acute febrile illness bearing a striking resemblance to serum sickness. This may be due to the egg antigens, now in excess results in soluble immune complexes being deposited in the tissues. Antigen-antibody complexes do correlate with the severity of the illness and may induce glomerulonephritis. Besides, fever, chills, arthralgia, lymphadenopathy, splenomegaly, abdominal pain, diarrhea with inflamed colonic mucosa and petechial hemorrhages. Typically, leucocytosis,marked peripheral eosinophilia and elevated levels of IgG, IgM and IgE antibodies are present. This symptom complex is termed as Katayama syndrome.     
  •  III) The chronic stage:  The eggs retained in the intestines, liver and the bladder initiate the final and the most morbid stage of Schistosomiasis. They induce inflammation and scarring and finally fibrosis. Soluble antigens excreted by the eggs stimulate the formation of T-lymphocyte mediated eosinophilic granulomas often marked by the inflammatory signals or lymphokines from the T cells bringing about a host of cell types like macrophages, eosinophils, meutophils, fibroblasts etc… As the granuloma around each egg or cluster of eggs contain large number of eosinophils and macrophages that get degenerated or die, these are termed as eosinophilic abscesses. These eosinophilic abscesses involving many cell types around the eggs in the granuloma is called the Hoeppli phenomenon. Fibroblasts stimulated by factors released by both the retained eggs and the granulomas now lay down scar tissue and the earlier granuloma induced vascular obstruction is permanent. This inflammatory reaction leads finally to the development of periportal fibrosis and hepatic enlargement. Splenomegaly also is the resultant manifestation. The circulating immune-complexes may cause nephropathy. The severity of the tissue damage is directly related to the number of eggs retained.       
  •  Clinical Manifestations:  Acute Schistosomiasis: Papules and erythema on the skin. Cercarial dermatitis. Fever, peaking in the late evenings and recedes by midnight or early morning. Rigors, sweating, headache, cough, muscular pain and gastrointestinal disturbances like diarrhea, nausea, mucous and bloody stools etc… usually associated. Liver and spleen slightly enlarged. Leucocytosis, eosinophilia, urticaria etc.. Can be the additional symptoms.     
  •     Chronic schistosomiasis: Acute can become chronic if not treated adequately or on time. Generally the symptoms are not pronounced except with a slightly large liver and spleen and intermittent chronic diarrhea or dysentry that is significant especially after tiredness or other mild infections. Mild anemia is common with an increase in eosinophil levels.
  •       Advanced Schistosomiasis: A portal hypertension syndrome after hepatic fibrosis, severe growth retardation or granulomatous disease of the colon usually defines Advanced schistosomiasis. This is usually after untreated cases for 3-5 years. Hepatosplenomegaly, ascites, portal hypertension, abdominal collateral vein dilation and esophagogastric varices are the clinical symptoms. Severe cases include upper gastrointestinal bleeding, hepatic coma may lead to death. S.haematobium infections can also lead to the carcinoma of the bladder.
  •     Ectopic schistosomiasis: Eggs carried around the liver may get lodged in the small pulmonary arterioles where they produce interstitial scarring, pulmonary hypertension, fibrosis of the pulmonary bed and right ventricular failure. Pulmonary involvement often seen with heavy worm burdens. If the underlying schistosome infection is not treateed , Salmonella infections will continue to recur and this association is most frequently seen in males between 15-30 years of age.
  •  Lab diagnosis:  Characteristic eggs in the feces or urine. Serological tests, detecting the circulating Ag-Ab complexes, Antigens and antibodies, do not differentiate between active and inactive infection and hence not useful. These are however, very sensitive and can be a useful and economic epidemiological tool. 
  •  Treatment and prevention:  Praziquantel is the treatment of choice. Prevention proper disposal of human waste, eradication of intermediate host, the snail species and education. 