Schistosomiasis Mansoni NINU GIT 2025 PDF

‫هللا مسب‬ ‫رلبللمللا‬  Parasites Causing Dysentery (A) Schistosomiasis mansoni Year: two Semester: one Module: GIT SCHISTOSOMIASIS mansoni Name: Prof. Dr. Ola Ali Ismail Department: Medical Parasitology Faculty: Medicine University: Suez Canal University By the end of...

‫هللا مسب‬ ‫رلبللمللا‬  Parasites Causing Dysentery (A) Schistosomiasis mansoni Year: two Semester: one Module: GIT SCHISTOSOMIASIS mansoni Name: Prof. Dr. Ola Ali Ismail Department: Medical Parasitology Faculty: Medicine University: Suez Canal University By the end of this lecture, students will be able to: 1. Enumerate parasites causing dysentery. 2. List the differences between Schistosoma spp. and other trematodes. 3. Describe with illustration the main morphological features of different stages of Schistosoma mansoni. 4. Describe the life cycle of Schistosoma mansoni in steps. 5. Relate the pathological changes with the clinical manifestations in schistosomiasis mansoni. 6. Define the main complications of Schistosoma mansoni. 7. Identify the diagnostic methods in Schistosoma mansoni. 8. Explore from the life cycle the strategy for prevention and control of schistosomiasis mansoni.  Dysentery means: infection of the intestines resuling in severe diarrhoea with the presence of blood and mucus in the faeces.  Parasites causing dysentery Schistosoma mansoni. Balantidium coli. Trichuris trichura. Leishmania donovani. Entamoeba histolytica. Plasmodium falciparum. Dientamoeba fragilis. Human Parasitology  Round Flat worms worms Trematoda Nematoda Cestoda  Trematodes – Flukes Hepatic flukes------- Fasciola spp. blood fluke------- Schistosoma spp. Intestinal fluke------- Heterophyes hetrophyes. Lung fluke--------- Paragonimus westermani.  Class: Trematoda (Flukes): General Characters of Trematodes: 1- Flattened, Leaf-like & non-segmented (one segment). 2- Suckers are organs of fixation; oral, ventral & genital. 3- Hermaphrodite (separate sex) except Schistosoma spp. 4- Reproduction; sexual and asexual. 5- Cuticle; spines & tubercles. 6- Life cycle is passed in two hosts; definitive host (man) and intermediate host (snail). 7- Eggs should reach water to complete the life cycle. 8- Development inside the snail; sporocyst, redia to cercaria. 2. General Characters of Schistosomes: 1. Adults in blood vessels. 2. Cylindrical. 3. Sex is separate. 4. Suckers are organs of fixation. 5. Eggs are colorless & have spines. 6. Life cycle is passed in two hosts; definitive host (man) and intermediate host (snail). 7. Development inside the snail; sporocyst, daughter sporocyst, to cercaria (furcocercus); no redia stage. Schistosoma spp. picture & story 14  Schistosoma mansoni CLASS  Trematoda ORDER  Digenea FAMÍLY  Schistosomatidae GÊNERA  Schistosoma  Schistosoma mansoni  Schistosoma haematobium  Schistosoma japonicum  Schistosoma intercalatum  Schistosoma mekongi  Adult Male & Female Schistosoma mansoni 1. Male: 2. Female: -Size: 8-10 mm x l mm. - Size: 15 mm x0.2 mm. -Cuticle: coarsely - Cuticle: coarsely tuberculated. tuberculated. - Suckers: Oral sucker & - Suckers: the same. ventral sucker. - Digestive system: as male - Digestive system: intestinal - Ovary: in front of intest.S. caeca unite at ant.1\3 with mansoni. post 2\3. -Testes: 6-9 as a mass.  Inside the human host: Schistosome adult worm: § Male & female pair copulate throughout life-produce eggs. § Females resides in canal---important for maturation. § Worm pairs can live for more than 10 years in a host. § Pair migrate back against the blood flow to the mesenteries around the intestine.  Egg of Schistosoma mansoni 3. Egg: Size: 140 x 70 µ. Shape: oval. Shell: thin with lateral spine. Colour: translucent. Contents: mature miracidium. - Eggs sweep out with feces and rarely in urine.  Cercaria characteristics Cercaria: Furcocercus. Body: - 5 pairs of penetration glands. - Oral & ventral suckers. Tail: Forcked & divided part is less than half of the tail length. Schistosoma mansoni intermediate host Biomphalaria alexandrina l Habitat: mansoni - Veins draining the rectum & pelvic colon→Inferior mesenteric & haemorhoidal venous plexus. - Portal vessels. - Some times urogenital vessels.  Mode of infection: Life cycle: 1. Definitive host. → contact with fresh water and penetration of 2. Reservoir host. skin by furcocercous 3. Infective stage. cercaria 4. Mode of infection. 5. Habitat. 6. Diagnostic stage. 7. Intermediate host. Life Cycle Schistosoma spp. Schistosoma mansoni pathology Pathogenesis Progression of the disease caused by all three species is commonly divided into three stages: 1- Stage of invasion (1-4 days): Skin penetration by cercaria--- dermatitis Swimmers itch or cercarial dermatitis. immediate hypersensitivity (type 1). 2- Stage of migration: (4-6 weeks) Due to migration of young immature worms. acute febrile reaction - - with hypereosinophilia - - -” o Lung: verminous pneumonitis. o Liver/spleen: hyperplasia. o Metabolic by products: toxic & allergic manifestations.  Acute schistosomiasis (also known as Katayama fever Systemic hypersensitivity reaction that may occur 2-8 weeks after infection. Fever, myalgia, nonproductive cough, fatigue, abdominal pain, eosinophilia and occasionally bloody stools. Liver, spleen and lymph nodes are often enlarged. In severe cases, death can occur with heavy infections. Eggs may not be seen in stools until late in the illness. 3- Stage of Egg deposition & Extrusion (10 -12 weeks): - Excess egg production without being passed. - The schistosomes eggs secrete SEA --- provoke a granulomatous reaction (schistosome granuloma) - - - cell mediated delayed hypersensitivity  Cont. stage 3 Egg extrusion “Trauma & Haemorrhage—Chronic disease” The female parasite lays its eggs in venules draining the pelvic colon & rectum. Eggs escape from venules to perivascular tissue to lumen of the large intestine are voided with stool aided by contraction of the segmoid colon—tissue damage/haemorrhage--- “Early phase of Chronic SCHISTOSOMIASIS”  Note Eggs are either: o Voided with stool. o Trapped in the wall of colon & rectum. o Swept into portal tributaries to the liver. o Embolise via Porto-caval by pass to the lung, kidneys, C.N.S and skin.  Cont. stage 3 This will lead to the following clinical picture: - Diarrhea // Dysentry (diarrhoeic stool with blood & mucus together with strain & tenesmus. - Liver enlarged & tendr (mild hepatomegaly) - Splenomegaly. - Abdominal pain. - Allergic manifestations. - Blood: hypereisinophilia leucocytosis Fe dificiency anaemia  Note Early hepatomegaly: (due to development of egg granulomas in the portal triad of the liver- portal tracts become blocked by granulomas---diffuse inflammatory lesions. Massive splenomegaly “hypersplenism”: (due to congestive splenomegaly secondary to portal hypertension. Pancytopenia: due to hyperplasia of RBC & Atrophy of lymphoid follicles of the spleen. 4- Stage of Tissue Proliferation & Fibrosis: (months- years): Tissue Proliferation: “ delayed type hypersensitivity” - --- Bilharzial granulomas in perivascular tiussues”--- diffuse inflamatory lesions---reverse obstructive lesions (chemotherapy effective). Tissue fibrosis: “immune suppresion---fibroblastic proliferation”---irreversible obstructive lesions (chemotherapy is ineffective).  This may lead to the following clinical picture: Trapped in the wall of * chronic diarrhea with colon & rectum: tenesmus. will give rise to the * protein losing enteropathy. following: * malabsorption syndrome. Ø Focal granulomas * significant blood loss Ø Polyps leading to anaemia Ø papillomata More advanced lesions will give Ø abscess rise to: stricture, sinus, ulcer, abscess, fistula and rectal prolapse. Ø sandy patches  Extraintestinal Schistosomiasis Hepatosplenic disease Egg emboli swept via the portal vein to portal tributaries in the liver provoke a delayed type hypersensitivity. Perivascular infiltration around trapped eggs– Granulomatous nodules—diffuse inflammatory lesions—Periportal fibrosis— Obstruction of the portal blood flow– Portal Hypertension. ↓ This will lead to the following complications:  Complications of Portal hypertension Portal Hypertension Collaterals Portocaval Hepatospleenomegaly Corpulmonale Oesophageal varieces Glomerulonephritis Bleeding varices/Ascitis Piles/bleeding piles  Corpulmonale: (due to development of collateral portocaval by-pass 2ry to increased portal hypertension. Massive egg embolism—granulomatous pulmonary arteritis— pulmonary arterial pressure—pulmonary hypertension—right ventricular failure. Glomerulonephropathy: (due to devlopment of collateral portocaval by-pass- circulating immune complexes are deposited in the kidney glomeruli instead of being cleared up by the liver kupffer cells).  Chronic Phase prolonged infection (up to 10 years) symptoms: - enlargement of liver and spleen - cirrhosis of the liver - bleeding of upper bowel  Diagnosis: intestinal schistosomiasis 1. History of freshwater exposure. 2. Stool for O&P (egg counts and viability). 3. Serology-- Elisa and Western Blot. 4. Antigen capture. 5. Eosinophilia. 6. Rectal snips or biopsies. 7. Liver biopsy. 8. Ultrasound or CT of abdomen.  Treatment Praziquantel: effective against all species S. haematobium: single dose (40 mg/kg) S. mansoni, S. japonicum: 2-3 doses of 30mg/kg  Control of schistosomiasis Health education. Environmental sanitation. Mass treatment. Personal prophylaxis. Snail control.  The morbidity spectrum of schistosomiasis mansoni The 2 faces of schistosomiasis ‘Intestinal’ asymptomatic schistosomiasis at the Egyptian village level Egyptian boy with hepatosplenomegaly, ascites fluid build-up and superficial collateral circulation (NAMRU-3 clinical ward in Cairo) Members of Phylum Platyhelminthes are: a) Dorsoventrally flattened. b) Laterally Compressed. c) Round. d) None. Schistosoma SPP. IS: 1) Intestinsl flucke. 2) Liver flucke. 3) Blood flucke. 4) Pulmonary flucke. Snail intermediate host of Schistosoma mansoni is: a) Biomphalaria alexandrina b) Pirenella conica. c) Bulinus truncates. d) Lymnaea.