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Parasitic diarrhoea
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    Parasitic diarrhoea Parasitic diarrhoea Presentation Transcript

    • Parasitic DiarrhoeaDr. Devika IddawelaDept. of ParasitologyY3S2
    • Epidemic of Infective Diarrhoea in a Refugee Camp
    • • Refugeecamps in SL
    • 1. List the common intestinal parasites causingdiarrhoea.2. Recall the pathological consequences ofamoebiasis, giardiasis & cryptosporidosis.2. Describe clinical consequences ofamoebiasis, giardiasis & cryptosporidosis.3. State the principles underlying the preventionand the control of parasitic diarrhoeas.4.Name the drugs used against these protozoaOBJECTIVES
    • Diarrhoeaincrease in frequency and/or volume andchange in form (loose, watery, bloody) offaecesAcute - watery diarrhoea, dysenteryChronic- >2 weeks (watery, +blood)fatty diarrhoea (steatorrhoea)
    • Parasitic DiarrhoeaBLOOD & MUCOUS DIARRHOEA= DYSENTERY• Entamoeba histolytica – amoebiasis[Entamoeba dispar – NON PATHOGENIC butidentical morpholgy to E.histolytica]• Trichiuris trichiura – Trichiuris dysenterysyndrome• Balantidium coli - balantidiosis
    • WATERY DIARRHOEA• Commonest protozoan – Giardia intestinalis –giardiasis• COCCIDIA- Cryptosporidium spp. – C.parvum, C.hominis- Cyclospora cayetanensis- Isospora belli• Microsporidia - microsporidiosis- Enterocytozoon bieneusi- E. intestinalis• Strongyloides stercoralis (intestinal nematode) –
    • Epidemiology :•Has world wide distribution• Endemic in most countries with lowsocioeconomic condition• Transmission – faeco – oral routeRecognized high risk groupsTravelers, immigrants, individuals in mentalinstitution, prisons and children in day carecentersAmoebiasis
    • PathogenesisMost remain asymptomaticTrophozoites advance laterally and downwardinto the submucosa producing a flask-shapedulcer.Amoebiasis
    • Flask shaped ulcers -Base in submucosa and smallopening on the mucosal surface
    • The mucosal surfaceof the colon fromfulminatingamebiasis caseshowing severalulcers.
    • Trophozoites penetrate themuscle and serous layersintestinal perforation ,peritonitisAmoeboma - inflammatory thickening of theintestinal wallpainful palpable mass - DD : Ca Coloncommon sites - ascending colon & caecumExtra intestinal amoebiasis-haematogenous spread to other organs
    • Liver is the most commonlyaffected organ causing liverabscessLiver abscess complicatedbyPulmonary infectionsgenerally result from adirect extension of thehepatic lesion across thediaphragm and into thepleura and lungsPericarditis & peritonitis
    • Hepatic abscess ( common site is right lobe)
    • Amoebiasis - Clinical featuresAmoebic colitisMost common presentation - gradual onsetof bloody diarrhoea, abdominal pain, andtenderness spanning several weeks’duration.Rectal bleeding without diarrhoeacan occur, especially in children.
    • • Only 10 – 30 % develop fever• Weight loss and anorexia may occurFulminant or necrotizing colitissevere bloody diarrhoea and widespreadabdominal pain with evidence of peritonitisand fever.Predisposing factors for fulminant colitispoor nutritionpregnancycorticosteroid usevery young age
    • amoeboma (amoebic granuloma)- painfulabdominal massperianal ulceration & fistulas
    • Extraintestinal Amoebiasis ( in <1%)1.Commonest - liver abscessadults > than childrenhepatomegaly, liver tenderness, pain in theupper abdomen, fever and anorexia,weight loss, vomiting, fatigue2. Local spread - pleuropulmonary amebiasis-cough, chest pain, dyspnea and fever.3. Systemic spread - brain and other organs
    • Diagnosis: Intestinal Amoebiasis•Demonstration of E.histolytia trophozoites in faeces•Examination of 3 stool samples over no more than 10 days canimprove the detection rate to 85-95%.•Sigmoidoscopy- characteristic ulcers• antigen detection in faecescan differentiate E. histolytica from E. disparCulture – faeces, rectal biopsy specimens
    • IngestedRed Blood Cellsin E.histolyticatrophozoitedifferentiate itfrom E.dispar
    • •WBC/DC –leucocytosis >10,000/mm3•serology - Ab•Ag detection•imaging - X –ray, CT, MRI, ultrasound•abscess aspiration - reddish brown liquidtrophozoites at abscess wallDiagnosis of Extraintestinal - Hepatic
    • Amoebiasis TreatmentLuminal amoebicides ( drugs that act onorganisms in lumen)– Diloxanide furoate ,iodoquinol,paromomycin,•Two classes of drugs are usedTissue amoebicides – Metronidazole,tinidazole, dihydroemetine andchloroquine
    • Asymptomatic amebiasis should be treated with aluminal agent to eradicate infection.This recommendation is based on,Invasive disease may developshedding of E histolytica cysts in the environmentis a public health concern.Asymptomatic E dispar infections shouldnot be treated, but education should bepursued since it is a marker of fecal-oralcontamination.
    • Acute amoebic dysentery / liver abcessMetronidazole – 750 mg tds for 10 daysfollowed by diloxanide furoate 500mg tds -10daysto eradicate the colanisationFollow-up stool examination after therapycompletion is recommended to ensure intestinaleradication.
    • How do you differentiate amoebic dysenteryfrom bacillary dysentery?Amoebic BacillaryIP Long shortInsidious acuteFever absent presentBlood &mucous with bulky stools blood& mucoushardly any stoolsLaboratory diagnosisFew WBC WBC +++Trophozoites +++ absentCharcot-leyden crystals present absent
    • Amebiasis is prevented byeradicating faecal contamination of food andwater through improved sanitation, hygiene, andwater treatment.Prevention and controlAmebic cysts are not killed by soapor low concentrations of chlorine oriodine;water in endemic areas should be boiledAvoiding sexual practices that involve faecal-oral contact may reduce the risk of sexualtransmission of infective cysts.Screen family members or close contacts of anindex case, since re-infection is possible.
    • GiardiasisEpidemiologyIn endemic areas childrenmost commonly affectedcause traveler’s diarrhoeaCysts are infective when ingested directly orthrough contaminated water or foodMan is the most important reservoir host butcross infection of Giardia species in otheranimals has been recorded. ZOONOSIS
    • PathogenicityDuodenum & upper jejunumTrophozoites attached NOT invasive
    • Pathogenicity disrupts mucosal structure & function luminal factors- contribute to diarrhoea, malabsorption
    • Cross section of Giardia trophozoiteon microvilli of intestinal epithelial cell
    • Intestinal section showing Giardia intestinalis.
    • Attachment to the mucosa•
    • Giardiasis - Clinical features Children exhibit clinical symptoms morefrequently than adults Acute self resolving diarrhoea- sudden onsetof watery, foul smelling diarrhoea with out bloodand mucus associated with anorexia , nausea andvomitingChronic illness – repeated brief episodes ofloose foul-smelling faeces, nutritional disorders,weight loss, steatorrhoea, lethargyfailure to thrive is an important symptom ofchronic infection in children
    • GiardiasisDiagnosisDemonstration of cystor trophozoites in faecesExamination of duodenal fluidfor trophozoites-Endoscopy or- Enterotest (string test)ImmunodetectionELISA- detection of Giardia antigen in faeces
    • Giardiasis TreatmentMetronidazole 2g daily for 3 daysorTinidazole-2g single doseAll cases of proven giardiasis should be treatedALL WATERY DIARRHOEASPREVENT DEHYDRATIONWITHORAL REHYDRATION SALTS
    • Cryptosporidium parvum: an emerging pathogenWATERBOURNE OUTBREAKSsix major outbreaks in the United States- contamination of drinking waterhighly environmentally resistant cyst ofC. parvum survives drinking water filtrations chlorinationoocysts do not survive cookingFeco-oraltransmission
    • Cryptosporidiuminfecting enterocytesSEMParasite of man &vertebratesComplete LC onepithelial cells(intestinal/respiratory) ofONE host
    • Lack of tissue specificityInfects biliary tract and respiratory system(1) Sporozoites released from the oocystadhere to the epithelial mucosal surface(2). Release cytokines intestinal secretion ofwater and chlorideand inhibit absorption(3). villus atrophy and crypt hyperplasiaPATHOGENESIS
    • Immunocompetent - IP – 7 days (2-10 days)AsymptomaticWatery dairrhoea associated withdehydration, weight loss, abdominal pain, fever,nausea and vomiting.self limiting (1-2 weeks)Common in children - age peak between 1 -5 yearsTraveler’s diarrhoeaCryptosporidium parvumCLINICAL FEATURES & TREATMENT
    • Immunocompromised – fatal diarrhoea Chronic diarrhoea in AIDS patients severe cholera like watery diarrhoea(can lose 20L/day) associated withsevere abdominal cramps, malaise , low-grade fever,weight loss , anorexiaCD4+ count <100/mm2 -life threateningAntiviral treatment improvesPost – organ transplant – immunosuppressivesCryptosporidium parvumCLINICAL FEATURES & TREATMENTTREATMENT – only in immunesuppressed.Drug of Choice = NITAZOXANIDE
    • SLIM diseaseChronic cryptosporidialdiarrhoea is acase defining diagnosisfor AIDS
    • Diagnosis1. Modified acid-fast stain +/- stool concentration–most labs2. METHOD OF CHOICE – most sensitive & specificImmunofluorescence microscopy3. ELISA – Ag in stoolsRESEARCH - genetictechniques using PCR / DNAbased antigen detection
    • Diagnosisoocystsin faecesfaecal smearsstained withacid-fast stainsother intestinal coccidia with larger oocyst>8-10µm Cyclospora cayetanensisCryptosporidium spp. oocyst
    • Parasitic diarrhoea in immuno-suppressedCoccidia and microsporidia – causes severe andprolonged diarrhoea in immuno- suppressed patientsas defined by the CD4 levelsCD4+ count < 150 ( normal – 700) associated withincrease duration and severity of diarrhoeaCoccidians important in HIV/AIDsCryptosporidium spp.Cyclospora cayetanensisIsospora beli
    • MicrosporidiaObligatory intracellular spore forming protozoaRarely found in immunocompetantCause 10 – 40% of chronic diarrhoea inimmunosupressedAlbendazole has some effect against somespeciesNormal stool Examination does not show theorganismNeed special staining technique.
    • Cyclospora cayetanensisSource : water, rasberriesOocysts are not infective when pass in thefaeces.Needs 5 days for sporulation.Direct person to person transmission does notoccurClinical features: watery diarrhoea, relapsingor persisting for 3 months, anorexia, nausea,weight lossLaboratory diagnosis:stool microscopyNeeds modified acid fast stainingTreatment: trimethoprim- sulfamethoxazole
    • Trichuris trichiura- Whip wormAnterior part threaded in the mucosaCause damage- bleedingaccess to other pathogens
    • PathologyFew worms – little damageHeavy infection- spread throughoutthe colon to the rectum causing• Haemorrhages• Muco-purulent stools, dysenteryand rectal prolapseTreatment:Mebendazole is the drug of choice, withalbendazole as an alternative.
    • Strongyloides stercoralisThe females embedded in the epithelium of the smallintestineRhabditiform larvae passé out in faecesWorldwide but more common in warm climates. Majoropportunistic infection among immunocompromisedpersons.Frequently asymptomatic.Gastrointestinal symptoms include abdominalpain and watery diarrhoea.Clinical features
    • Disseminated strongyloidiasis occurs inimmunosuppressed patients, severe watery diarrhoea,often with malabsorption,Diagnosis•Demonstration of 1st stage rhab.larvae in stools1. Ivermectin is the treatment of choice in theimmunosuppressed patient, especially HIVinfection2. Albendazole (child <=10 kg: 200 mg) 400 mg orally, daily for 3days (repeat after 7 days in complicated or disseminatedinfections)  Note: Albendazole should be avoided in pregnancy and inchildren under 6 months of age.Treatment
    • Prevention and control ofparasitic diarrhoeas Provision of safe water Provision of proper toilets Proper food handling and preparationmethods Good personal hygiene – proper handwashing (using soap and water before handlingfood, after using toilet, before each meal)
    • Prevention of Diarrhoea – Safe Drinking Water!Displaced Sri Lankans access clean water