12..trematodes full


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12..trematodes full

  1. 1. Trematodes
  2. 2. 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.
  3. 3.       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.
  4. 4.  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. 
  5. 5.   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.
  6. 6.   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.
  7. 7.  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.  
  8. 8.  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.    
  9. 9.  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.     
  10. 10.  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.       
  11. 11.  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.     
  12. 12.     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.
  13. 13.       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.
  14. 14.     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.
  15. 15.  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. 
  16. 16.  Treatment and prevention:  Praziquantel is the treatment of choice. Prevention proper disposal of human waste, eradication of intermediate host, the snail species and education. 
  17. 17.  Flukes of genera Clonorchis, and Fasciola infect the human biliary tract and at times produce manifestations of ductal obstruction.  Clonorchis sinensis, the chinese liver fluke is the most important. Causes Clonorchiasis. 
  18. 18.   Is a long and narrow bodied fluke with a cone-shaped anterior pole. The mature egg is yellowish-brown and its operculum is small and fits into the broad rim of the eggshell. The eggs urn-shaped and have a discernible shoulder at their operculum ring and a tiny knob on the broader posterior pole.
  19. 19.    C.sinensis has a typical life cycle: Human flukes mature in the bile-ducts of the definitive host – eggs discharged and pass down the bile duct into the fecal stream. The egg contain a well developed Miracidium – reach fresh water – ingested by the intermediate host ( snail) – the miracidium hatch in the snail – transforms into a sporocyst – number of embryos develop asexually to become Rediae.
  20. 20.   Additional embryos develop within the redia – transforms into Cercariae. Each redia produces 5-50 cercariae. Cercariae emerge from the snail and contact the second intermediate host, the fresh-water fish. It attaches to the fish epithelium with its sucker, cast off its tail and penetrates the tissue of the fish in which it encysts to form a Metacercariae. Thousands of metacercariae can accumulate in the fish.
  21. 21.    The definitive host infected on eating the raw or undercooked fish containing the encysted metacercariae (larvae). The larvae are released in the duodenum, ascend the common bile-duct – migrate to the liver and mature around 30 days. The hermaphrodite adult can now produce eggs.
  22. 22.  Pathogenesis and clinical symptoms:  Pathological consequences of C.sinensis infection is mainly in the intra-hepatic secondary bile-ducts and its neighboring tissue. The basic pathogenesis is the erosion of the epithelial lining of the bile ducts. The adult worm induces proliferation of epithelial cells, desquamation of the biliary epithelium, epithelial hyperplasia, adenoma formation, bile-duct hyperplasia, periductal fibrosis, inflammation and gradual thickening and occlusion of the ducts. Infiltrating eggs become surrounded by granulomas, thereby interfering with the liver function. Can lead to obstructive jaundice, cholangitis, cholelithiasis, and epithelial cancer.   
  23. 23.  Clinical symptoms:  Acute stage: Migration of larvae from the duodenum to bile ducts may produce fever, chills, gastrointestinal discomfort, nild jaundice and hepatomegaly. Leucocytosis, eosinophilia and elevation of Alkaline phosphatase levels usuall seen.     Chronic stage: Numerous reinfections may produce worm loads of 500-1000, resulting in the formation of bile stones. Bile-duct carcinoma in long-standing severe infections. Occasionally, adult worms in the pancreatic duct may result in duct obstruction or acute pancreatitis.
  24. 24.      Laboratory diagnosis: Typical eggs of C.sinensis demonstrated in the stool specimen. Treatment and Prevention: Treatment of choice : Praziquantel. Prevention is adequate cooking of fish and proper human waste disposal.
  25. 25.    Fasciola hepatica is the sheep-liver fluke. Definitive host : sheep, Humans. Humans infected when eat contaminated ( with metacercaria) aquatic plants or raw sheep liver – excyst in the duodenum – penetrate the gut wall, reach liver – mature into adults – adults in the bile-ducts produce eggs – excreted – hatch in fresh water – miracidia enters snail – cercariae – cercariae encyst on aquatic plants.
  26. 26.  Pathogenesis and clinical symptoms:  Adult worms in the biliary ducts cause the symptoms – right-upper-quadrant pain, fever- hepatomegaly. Chronic cases may develop obstructive jaundice. Adult flukes on the posterior pharyngeal wall, acquired by eating raw-sheep liver may cause a painful pharyngitis, typically called Halzoun.  
  27. 27.    Treatment of choice: Triclabendazole. Surgical removal of adult flukes in the pharynx and larynx. Prevention: Avoid raw liver and contaminated aquatic vegetation.
  28. 28.  Fasciolopsis Buski:  Causes: Fasiolopsiasis. Scientifically known as the largest intestinal fluke in humans. Also named as Giant Asian intestinal fluke. Definitive hosts: Humans, pigs.  
  29. 29.     F.buski is an elongated-oval shaped adult fluke. It has a visible cone-shaped acetabulum, larger than the oral sucker and located close to it. The eggs are ellipsoidal, with a small but distinct operculum having a fertilized ovum inside and many vitelline cells. Eggs passed through feces – enter fresh-water and hatch into miracidia – Miracidia penetrate snails, the intermediate host – sporocyst – rediae – cercariae. Cercariae released from the snail and encyst as metacercariae on various aquatic plants like water chestnut, lotus, water bamboo etc…
  30. 30.  Humans infected on ingestion of these raw vegetables – metacercaria excyst in the duodenum – and attach to the intestinal walls and develop into adult worms.
  31. 31.  Pathogenesis and clinical manifestations:  Pathogenesis due to the damage of the intestinal mucosa by the adult fluke. No noticeable symptom during the developmental period of the fluke ( 3 months). The condition resulting after, is traumatic, obstructive and toxic. Irritation at the site of attachment provokes inflammation, ulceration, hemorrhage and abscess of the intestinal wall with excess mucous secretion accompanied by chronic diarrhea are the typical symptoms. Profound toxemia caused by absorption of the allerginic metabolite of the fluke may also lead to prostration and death, particularly in children.   
  32. 32.  Lab diagnosis based on the typical egg findings in the stool specimen.  Treatment usually effective in early or light infected cases. Praziquantel, the drug of choice. Prevention: proper disposal of human waste and avoid undercooked, raw aquatic vegetation and elimination of the intermediate host. 
  33. 33.  Pargonimus spp:  More than 50 different species known to be human parasites. P.westermani is the most frequently involved. Also known as Lung Fluke causes Pargonimiasis. 
  34. 34.    The adult fluke is reddish-brown, thick with a flat ventral and protuberant back, like a semi-peanut. The oral and ventral suckers are almost equal in size. Adult flukes are characteristically found encapsulated in the lung parenchyma. The eggs are yellowish-brown, oval, a fertilized ovum inside with 10 vitelline cells and surrounded by a thick shell. Definitive host: Humans and also pigs, dogs and other mammals.
  35. 35.  Life cycle:  The eggs are often trapped in the surrounding tissues and cannot leave the lungs – the capsule erodes into a bronchiole – eggs are coughed up – spat out or swallowed and passed in the stool. The eggs reach the fresh water – hatch into miracidia – enter snails (first intermediate host) – develop into sporocyst, rediae, cercariae - leave the snail – invade the gills, musculature and viscera of certain cray-fish or fresh-water crabs – the larval forms transform into metacercariae – eaten raw or undercooked by humans get infected. 
  36. 36.    The metacercariae excyst in the duodenum burrow through the gut wall into the peritoneal cavity – majority continue migration through the diaphragm and reach maturity in the lungs after 5-6 weeks. Some retained in the intestinal wall wander to other foci such as liver, pancreas, kidney, skeletal muscle or subcutaneous tissue. Some young worms migrating through the neck and the jugular foramen may encyst in the brain.
  37. 37.  Pathogenesis and clinical manifestations:  The presence of adult worms in the lungs elicits an eosinophillic inflammatory reaction and eventually the formation of fibrous capsule that surrounds and encloses one or more parasites. The infected patient may harbour as many as 25 lesions. With the onset of oviposition, the capsule swells and erodes into a bronchiole, resulting in expectoration of the brownish eggs, blood and an inflammatory exudate. Secondary bacterial infection of the evacuated cysts is common, producing a clinical picture of chronic bronchitis or bronchiectasis. If cysts rupture into the pleural cavity, chest pain and effusion can result. Eventually, cystic rings, fibrosis and calcification occur, closely resembling a clinical picture of pulmonary tuberculosis (these two diseases often coexist).   
  38. 38.  Adult flukes in the intestines produce pain, bloody diarrhea and on occasion, palpable, abdominal or cutaneous masses.  Parasites lodged in the brain may produce, a variety of neurological manifestations like epilepsy, paralysis, optic atrophy etc…
  39. 39.       Lab diagnosis: Typical operculated eggs in sputum or feces. Treatment of choice: Praziquantel Prevention: Avoid undercooked crabs.
  40. 40.  Heterophyes heterophyes:  Intestinal parasite. Endemic in Africa and middle-east. Definitive host: humans. Intermediate hosts: Primary: snail Secondary: Fish.   
  41. 41.   Life cycle: Eggs from the adult pass into feces –reach brackish water – ingested by snails – sporocyst, rediae, cercariae – cercariae leave snail and encyst under scales of fishes as metacercariae – raw fish containing cysts eaten – larvae excyst in the small intestine – attach to the mucosa – develop into adults – lay eggs – passes out in the feces.
  42. 42.  Pathogenesis and clinical symptoms:  Presence of the adult fluke causes inflammation of the intestinal epithelium. Most infections are asymptomatic, but abdominal pain and diarrhea may be manifested. 
  43. 43.  Lab diagnosis: Demonstration of typical eggs in the feces.  Treatment of choice : Praziquantel.  Prevention: proper disposal of human sewage, elimination of the primary host and to avoid undercooked or raw fish. 