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Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
Amebiasis
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Amebiasis

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  • 1. AMEBIASIS AND INFECTION WITH FREE LIVING AMEBAS Dr R L Khare Assistant Professor Department of Medicine Pt JNM Medical College Raipur
  • 2. DEFINITION  Amebiasis is infection with intestinal pathogen Entameba histolytica (tissue lysing ameba)  Most Infection are asymptomatic  Can cause disease ranging from Dysentry to extaintestinal infectons like liver absess  Most of asymptomatic infection is due to E.dispar  Endemic area Mexico,India & tropical regions of Africa,South and Central America
  • 3. LIFE CYCLE AND TRANSMISSION  E. histolytica exists in two stages multinucleate cyst Motile Trophozoite
  • 4. TRANSMISSION E. histolytica are most common in areas where poor sanitation and crowding compromise the barrier to contamination of food and drinking water  Infection is acquired by ingestion of cysts in faecally contaminated water or food or rarely,through oralanal sexual contact  Cysts are resistant to the acid in the stomach 
  • 5. LIFE CYCLE
  • 6. PATHOGENESIS AND PATHOLOGY  E. histolytica posses a potent repertoire of  adhesins, proeinases and pore forming proteins and other molecules that enable them to lyse cells and tissue These mol. Induce cellular necrosis and apoptosis  Resist both innate and adaptive immunity  E. histolytica trophozoites adhere to the colonic mucosal epithelial cells leads to disruption  Adherence is mediated by a family of surface lectin molecules capable of binding to galactose and Nacetylgalactosamine residues 
  • 7. PATHOGENESIS AND PATHOLOGY E.histolytica can lyse host cells upon contact through a family of amphipathic peptides called amoebopores  E.histolytica posses a large family of cysteine proteinases that are capable of lysing the extracellular matrix between the cells and cleaving host defense molecules (complement and antibodies)  The ultimate effect of all these amebic virulance factors on the human colon is the production of small ulcers that have heaped borders and contains focal areas of epithelial cell loss 
  • 8. PATHOGENESIS AND PATHOLOGY  The interveining mucosa is normal  E.histolytica trophozoites can then invade laterally through the submucosal layer, creating the classic flask shaped ulcers that appear on pathologic examination as narrow-necked lesions broadin the submucosal region  E.histolytica trophozoites found at the margin between dead and the live tissues
  • 9. FLASK SHAPED ULCER
  • 10. CLINICAL MANIFESTATIONS Two types- Intestinal and Extra Intestinal  Most patients harboring Entamoeba species are asymptomatic,but individuals with E.histolytica can develop disease  Amebic colitis generally appear 2-6 weeks after ingestion of the cyst of parasite  Heme positive diarrhea and abdominal pain are the most common complaints  Malaise and wt.loss may be found later  Fever is present in 40% cases  Severe dysentry with 10-12 small volume, blood and mucus containing stools may develop 
  • 11. CLINICAL MANIFESTATIONS Fulminant amebic colitis with even profuse diarrhea,severe abdominal pain,fever,and pronounced leukocytosis are rare  It affects young children,pragnant women, indivisuals treated with steroids and pts. With diabetes and alcoholism  Intestinal perforation occus in >75% of pts.with fulminant disease  Complications includes  Toxic Megacolon in .5% with severe bowel dilatation and intraluminal air  Ameboma-presents as abd. mass 
  • 12. AMEBIC LIVER ABSCESS Most cmmon extraintestinal complication  Disease begins when trophozoites penetrate through the colonic mucosa, travel through the portal circulation and reach the liver  The classical presentation of ALA are right upper – quadrant pain,fever and liver tenderness  Its acute in nature lasting < 10 days  With chronic presentation wt. loss and anorexia are prominent  Jaundice is uncommon 
  • 13. OTHER MANIFESTATIONS AND COMPLICATIONS Rt-sided pleural effusion and atelectesis are common in cases of ALA  In 10% rupture of abscess through diaphragm may cause pleuro-pulmonary amebiasis  Sudden onset cough,pleuritic chest pain and shortness of breath are suggestive symptom  Hepatobronchial fistula is dramatic complication in which pt has complaint of cough with content of liver abscess  Liver abscess may rupture into pericardial cavity and can cause pericarditis with 30% mortality due to cardiac temponade 
  • 14. DIAGNOSTIC TESTS Demonstration of E.histolytica or cyst in the stool or colonic mucosa of pts with diarrhea  Antigen detection based ELISAs that can specifically identify E.histolytica in the stool probably represent the best choice in the endemic areast  PCR assay for DNA in the stool samples is currently the most sensitive and specific method for identification but used as research and epidemiological tool 
  • 15. DIAGNOSTIC TESTS Diagnosis of amebic liver abscess is based on the detection of one or more space occupying lesions in the liver by Ultrasound and CT scan and a positive serology  Amebic liver abscess are classically described as single, large and located in right lobe of liver  When a pt. with space ahs a occupying lesion in the liver, a positive serology is highly sensitive(>94% ) and highly specific(>95%) for the diagnosis of the liver abscess 
  • 16. CT SCAN LIVER WITH ALA IN RT LOBE
  • 17. TREATMENT The nitroimidazole compounds are the drug of choice  To date E.histolytica has not demonstrated resistance to any of the compound metronidazole and tinidazole  Tinidazole appears to be better tolerated  Whenever possible fulminant amebic colitis should be managed conservatively 
  • 18. TREATMENT  Aspiration of liver abscess reserved for      the indivisual in whom pyogenic abscess a bacterial superinfection is suspected but diagnosis is uncertain, for pts failing to respond to tinidazole or metronidazole ( those who have fever or abdominal pain after 4 days of treatment), for indivisuals with large liver abscesses in the left lobe large abscsee with risk of rupture
  • 19. TREATMENT In contrast, aspiration and percutaneous catheter drainage improves outcome in pleuropulmonary amebiasis and empyema  Percutneous drainage or surgical drainage is absolutely indicated in amebic pericarditis  Rupture of an amebic liver abscess in peritoneum is managed conservatively with medical therapy and percutaneous catheter drainage 
  • 20. TREATMENT Neither metronidazole nor tinidazole reaches high levels in the gut lumen therefore, patients with amebic colitis or ALA should also receive treatment with luminal agents (Paramomycin or iodoquinol) to ensure eradication of infection  Paramomycin is preferred agent  Nitazoxanide, abroad spectrum antiparasitic drug,is efficacious against E.histolytica trophozoitesin the both tissue and gut 
  • 21. TREATMENT Drug Dosage Duration Tinidazole 2g/day with food 3 Metronidazole 750mgtid PO or IV 5-10 Paramomycin 30mg/kg qd PO in 3 divided dose 5-10 Iodoquinol 650 mg PO tid 20 Amebic Colitis Or ALA Luminal Infection
  • 22. PREVENTION Avoidance of ingestion of food and water contaminated with humen feces is the only way of prevention  No prophylaxis  No vaccine 

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