Trematodes PDF

Warith Al-Anbiyaa University College of Medicine Department Microbiology- Parasitology Trematodes INTRODUCTION Trematodes are leaf-shaped unsegmented, flat and broad helminths (hence the name fluke,...

Warith Al-Anbiyaa University College of Medicine Department Microbiology- Parasitology Trematodes INTRODUCTION Trematodes are leaf-shaped unsegmented, flat and broad helminths (hence the name fluke, from the Anglo-Saxon word floe meaning flatfish). The name trematode comes from their having large prominent suckers with a hole in the middle. (Greek trema: hole, eidos: appearance).  Classification Systemic: Trematodes belong to: – Phylum: Platyhelminthes – Class: Trematoda Classification Based on Habitat: Trematodes can be classified as: – Blood flukes – Tissue flukes: Liver flukes Intestinal flukes Lung flukes.  BLOOD FLUKES GENERAL CHARACTERISTICS They vary in size from 1 mm to several centimeters. Males are shorter and stouter than females. The unique feature of flukes is the presence of two suckers: oral sucker surrounding the mouth at the anterior end and the ventral sucker BLOOD FLUKES GENERAL CHARACTERISTICS All Schistosomes live in venous plexuses in the body of the definitive host, the location varying with the species: Urinary bladder in S. haematobium, Sigmoidorectal region in S. mansoni Ileocecal region in S. japonicum.  Schistosoma Haematobium This vesical blood fluke, formerly known as bilharzia haematobium, has been endemic in the Nile valley in Egypt. The adult worms live in the vesical and pelvic plexuses of veins. Mechanism of egg expulsion The eggs are laid usually in the small venules of the vesical and pelvic plexuses, though sometimes they are laid in the mesenteric portal system, pulmonary arterioles and other ectopic sites. The eggs are laid one behind the other with the spine pointing posteriorly.  From the venules, the eggs make their way through the vesical wall by the piercing action of the spine, assisted by the mounting pressure within the venules and a lytic substance released by the eggs. The eggs pass into the lumen of the urinary bladder together with some extravasated blood. They are discharged in the urine, particularly towards the end of micturition. The eggs laid in ectopic sites generally die and evoke local tissue reactions. They may be found, for instance in rectal biopsies, but are seldom passed live in feces. Life Cycle S. haematobium passes its life cycle in two hosts: 1. Definitive host: Humans are the only natural definitive hosts. No animal reservoir is known. 2. Intermediate host: Freshwater snails (snail of the genus Bulinus). Infective form: Cercaria larva. Development in man: After penetrating the skin, the cercariae loss their tails and become schistosomulae which travel via peripheral venules to systemic circulation. They then start a long migration, through the vena cava into the right heart, the pulmonary circulation, the left heart and the systemic circulation, ultimately reaching the liver. In the intrahepatic portal veins, the schistosomulae grow and become sexually differentiated adolescents about 20 days after skin penetration. They then start migrating against the bloodstream into the inferior mesenteric veins, ultimately reaching the vesical and pelvic venous plexuses, where they mature, mate and begin laying eggs. Eggs start appearing in urine usually 10-12 weeks after cercarial penetration. The adult worms may live for 20- 30 years.  Pathogenicity Clinical illness caused by schistosomes can be classified as: Acute and Chronic based on the stages in the evolution of the parasite. Acute Schistosomiasis During skin penetration of cercariae, intense irritation and skin rash may develop at the side of cercarial penetration (swimmer's itch). It is particularly severe when infection occurs with cercariae of nonhuman schistosomes. Anaphylactic or toxic symptoms may develop during incubation period due to liberation of toxic metabolites by schistosomules. Migration of schistosomulae into lungs may cause cough and mild fever.  Chronic Schistosomiasis Egg deposition in urinary bladder causes mucosal damages leading to painless hematuria, dysuria and proteinuria, particularly in children in endemic areas. There is inflammation of the urinary bladder due to release of soluble antigens from the eggs causing pseudoabscesses in the surrounding tissues. The whole mucosa is inflamed, ulcerated and thickened. There is heavy infiltration of macrophages, lymphocytes, eosinophils and fibroblasts. Chronic Schistosomiasis Many of the eggs die and become calcified eventually producing fibrosis of vesical mucosa and formation of egg granulomas (sandy patches). Fibrosis may cause obstructive uropathies like hydronephrosis and hydroureter. Chronic schistosomiasis has been associated with urinary bladder carcinoma. Chronic cystitis may develop due to secondary bacterial infection. Chronic infection may result in calculus formation.  Treatment Prazjquantel: is the drug of choice. Metriphonate is the alternative drug of choice in schistosomiasis due to S. haematobium Prophylaxis Eradication of the intermediate molluscan hosts by using molluscicides. Prevention of environmental pollution with human urine and feces. Effective treatment of infected persons. Avoid swimming, bathing and washing in infected water.  Schistosoma mansoni It is widely distributed in Africa, South America. Adult worm lives in the inferior mesenteric vein. Definitive host: Humans are the only natural definitive hosts, though in endemic areas monkeys and baboons have also been found infected. Intermediate host: freshwater snails of the genus Biomphalaria. Infective form: Fork-tailed cercaria. Pathogenicity Cercarial dermatitis: Katayama Fever: - After 4-8 weeks of cercarial invasion a serum sickness like illness may happened during production of eggs. - It results from high worm load and egg antigen stimuli which leads to formation of immune complexes. Sign and symptoms include high fever, rash, arthralgia, hepatosplenomegaly, lymphadenopathy and eosinophilia.  Pathogenicity Intestinal bilharziasis: During the stage of egg deposition in small intestine, patients may develop pain in abdomen and bloody dysentery, which may go on intermittently for many years. The eggs deposited in the intestinal wall may cause microabscesses, granulomas and eventual fibrosis. Egg granulomas are found in the distal part of the colon and rectum. Ectopic lesions include hepatosplenomegaly and periportal fibrosis. Pathogenicity Portal hypertension may cause gastrointestinal hemorrhage. Portal hypertension, as some of the eggs are carried through portal circulation into liver. Portal Hypertension Portal Hypertension  Laboratory Diagnosis Stool microscopy: Eggs with lateral spines may be demonstrated microscopically in stools. Kato-Katz thick smear. Rectal biopsy Serological diagnosis Imaging Blood examination Schistosoma Japonicum Common Name: Oriental blood fluke. Distribution: S. japonicum is found in the Far East, Japan, China, Taiwan, Philippines.  Schistosoma Japonicum Definitive host: Man is the definitive host but in endemic areas, natural infection occurs widely in several domestic animals and rodents, which act as reservoirs of infection. lntermediate host: Amphibian snails of the genus Oncomelania. Infective form for humans: Fork-tailed cercaria. Schistosoma Japonicum Eggs deposited in the superior mesenteric venules penetrate the gut wall and are passed in feces. They hatch in water and the miracidia. infect the intermediate hosts, amphibian snails of the genus Oncomelania. The fork-tailed cercaria, which escapes from the snails is the infective form for men and other definitive hosts.  Schistosoma Japonicum Pathogenicity Disease caused by S. japonicum is also known as Oriental Schistosomiasis or Katayama disease. Pathogenesis is almost similar to that of S. mansoni. But the disease is more severe due to higher egg production. During the acute phase of the disease, Katayama Fever is similar to that seen in S. mansoni. Schistosoma Japonicum Pathogenicity Chronic illness is characterized by intestinal mucosal hyperplasia, hepatosplenomegaly and portal hypertension. Liver is hard and shows periportal fibrosis (clay pipestem fibrosis). Portal hypertension leads to esophageal varices and gastrointestinal bleeding.  Schistosoma Japonicum Laboratory Diagnosis Similar to that of S. mansoni. Treatment S. japonicum infection is more resistant to treatment than other schistosomiasis. Praziquantel is the drug of choice. Prophylaxis Same as S. haematobium Paniker s Textbook of Medical Parasitology 8th- e-2018