Lecture #2 on Gastrointestinal Parasites PDF

Lecture#2 Gastrointestinal parasites (Protozoa).  Objectives Mention names and the major structural features, life cycle stages, pathogenetic mechanisms, clinical significance of the main parasites that cause GIT infections. Describe the structure, life cycle stages, pathogenesis and clini...

Lecture#2 Gastrointestinal parasites (Protozoa).  Objectives Mention names and the major structural features, life cycle stages, pathogenetic mechanisms, clinical significance of the main parasites that cause GIT infections. Describe the structure, life cycle stages, pathogenesis and clinical significance of the following Gastrointestinal parasites:  Entamoeba histolytica Protozoa  Giardia lamblia  Echinococcus granulosus (Cestode)  Schistosoma mansoni (Fluke) Helminths  Enterobius vermicularis (Nematode)  Ascaris lumbricoides (Nematode) Laboratory diagnosis will be discussed separately in Lab section.....  Lower GIT parasites Lower GIT parasites – diarrhea, abdominal pain or distension. Enterobius vermicularis- Puritis ani Amoebiasis or schistosomiasis- Bleeding per rectum (colonic erosions or ulcerations)  Entamoeba histolytica Morphology; occurs in two forms, 1.Trophozoite (Motile by pseudopods)  Unicellular  Single spherical nucleus  Pseudopodia  Some times red blood cell can be seen ingested in cytoplasm. 2.Cyst (Non motile)  Round in shape  Mature cyst has 4 nuclei Transmission. of Entamoeba histolytica Fecal-oral route, ingestion of cyst contaminated food and water. CYST IS THE INFECTIVE STAGE. Direct contact with infected person Mechanical transmission of cyst by house flies. Life cycle of Entamoeba histolytica Infection by Entamoeba histolytica occurs by ingestion of mature cysts. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts which are passed in the feces. Cysts can survive days to weeks in the external environment and are responsible for transmission.  Life cycle of Entamoeba histolytica.  Pathogenesis  Ingestion of cyst In intestine excystation and trophozoite is released  Trophozoite attach to epithelium of colon Micro ulceration and dysentery  Disintegration of epithelial cells layer invasion of submucosa, (flask-shaped ulcer).  Invasion of portal blood vessel & spread to other organs causing extra intestinal amoebiasis. Clinical importance of E. histolytica Range from asymptomatic cyst passage to amoebic colitis, amoebic dysentery. Amoebic dysentery ( bloody, mucus-containing diarrhea) accompanied by fever, lower abdominal discomfort, flatulence, tenesmus and extra intestinal disease. Extra intestinal disease usually leads to Liver abscess but can include brain abscess, pleuro pulomonary disease. Amoebic Liver abscess Trophozoite of E.histolytica can enter the portal venous system from the colon and is carried to liver where it form abscess. Mostly abscesses are formed in the right lobe of the liver. An amoebic abscess of the liver is usually single space occupying lesion, the center of the abscess contains a viscous chocolate colored fuid consisting of digested liver tissue and trophozoites. Giardia lamblia Protozoan parasite that lives in the upper portion of the small intestine by adhering to brush border of the epithelial cells. Morphology; occurs in two forms, 1.Trophozoite (Motile by fagella) Pear shaped two oval nuclei, four pairs of fagella and a sucking disk for attachment. 2.Cyst (Non motile) Cyst is oval thick walled with four nuclei and several internal fbers.  Life cycle of Giardia lamblia Transmission; Fecal-oral route, ingestion of cyst contaminated food and water. Direct contact with infected person Mechanical transmission of cyst by house fies. Life cycle; Human are infected by ingestion of cysts In the duodenum excystation occurs and trophozoites are released. Trophozoites adhere to the mucosa of duodenum by help of sucking discs Some trophozoites encyst themselves. Cysts are excreted with stool.  Pathogenesis Trophozoite attach to epithelium of duodenum by help of sucking disc but does not invade the mucosa and does not enter the bloodstream. The trophozoite causes infammation of the duodenal mucosa , leading to malabsorption of protein and fat due to interference with digestion & absorption along with atrophy of villi. Clinical features Watery , foul-smelling greasy diarrhea accompanied by nausea, anorexia, fatulence, and abdominal cramps. Weight loss Echinococcus granulosus (Dog tapeworm) Hermaphrodite (segments containing both male. female reproductive organs) and  Life cycle of E. granulosus The definitive hosts are infected through the consumption of viscera of intermediate hosts Transmission; Humans are accidental intermediate dead end hosts. They are infected when they ingest food contaminated with dog feces containing the eggs. Life cycle of E. granulosus.  Pathogenesis & Clinical features Accidently E.granulosa eggs are ingested by humans The embryo emerge in the small intestine and migrate primarily to the liver but also to the lung, bones, and brain The embryo develop into large fluid-filled hydatid cysts The cyst acts as a space occupying lesion, putting pressure on adjacent tissue. If the cyst ruptures spontaneously or during trauma or surgical removal, Life threatening anaphylactic shock can occur. Symptoms vary depending on organ in which cyst is located; Liver cysts may cause hepatic dysfunction. Lungs cysts can erode into a bronchus Cerebral cysts can cause headache and focal neurologic signs. Reference Levinson...