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- 1. GIARDIASIS M.Moghadami Internist, subspecialist of infectious disease 1
- 2. INTRODUCTION van Leeuwenhoek 1600 Giardia lamblia (intestinalis and duodenalis ) 1900s intestinal flagellates in the division Protozoa Human but other such as dog, cat, cow, beaver, and sheep 2
- 3. A common cause of epidemic and endemic diarrhea in world 3
- 4. SPECIES Giardia lambelia in human Giardia muris ,G agilis, G microti, G psittaci 4
- 5. LIFE CYCLE: TROPHOZOITE freely living stage 9 to 21 亮m long and 5 to 15 亮m wide Morphology Growth : biliary lipids, a high concentration of cysteine, and low oxygen tension 5
- 6. LIFE CYCLE: CYST smooth, oval, thin-walled cysts 8 to 12 亮m long and 7 to 10 亮m wide Encystation: cholesterol starvation ,alkaline pH Excystation :gastric acid and pancreatic enzymes 6
- 7. Cyst resistance to cholorization 3 month stay alive Production in terminal illeum 7
- 8. EPIDEMIOLOGY Giardia is distributed throughout the world. In US G. lamblia has been demonstrated in 4% to 7% of stool specimens, making it the most commonly identified intestinal parasite. In resource-poor regions of the world, Giardia is one of the first enteric pathogens to infect infants, with peak prevalence rates of 15% to 30% occurring in children younger than 10 years. 8
- 9. 擧悋 擧惆 3 惡慍惘擯愕悋悋 惡惘悋惡惘 悽悋 惠 惆悋惘愕 悋 擧惆擧 惆 慍惘 擧惆擧悋 惡悋惘惆悋惘 惆惘 慍悋 5 愕悋 悋愕悋 惆惘 惠悋 悽惘 9
- 10. 愆惘 悛悵惘惡悋悴悋 惆惘 ( : 慍悋惆 愆惘惺惠 惆擧惠惘 愀悋惺 ) 6609 惠惘 愆悋惺 悋惘惆悋 惘 15/2 % 悋惘 惆惘 43/8 % 惆 惆惘 10
- 11. 110 惘愕惠悋 惆悋愆悴 ( 慍悋惆 悋惡 惆擧惠惘 愀悋惺 ) 8/4 % 悋擯 惡 悛惆擯 3.9 % 惘惆悋 悋 惡 悛惆擯 悋慍惆惘悋 惘愕惠悋 : 10.2 % 悛惆擯 11
- 12. ROUTES OF INFECTION contaminated water : Recreational water ,Backpackers , water treated by a faulty purification system, food borne transmissions person-to-person :young children in daycare centers (30-50% cyst passer) 12
- 13. PATHOGENESIS Infection ingestion of as few as 10 to 25 cysts After excystation, colonize and multiply in the upper small bowel. Adherence in gut is via the ventral disk, with attachment at the brush border of enterocytes . 13
- 14. Avoidance of peristalsis Disruption of brush border cells Disacharidse defeciency Rarely invasion,enterotoxin,.. 14
- 15. GI INVOLVMENT Duodenum: 82.5% Jejunum: 2,1% Stomach: 8.7% Ileum: 12.1% Colon: 0.4% 15
- 16. IMMUNE RESPONSE Important in clearing of infection Prevalence in developing countries is higher in younger ages Humoral immunity Cellular immunity Inflammatory response enterocytes damage Human milk 16
- 17. PREDISPOSITION common variable immunodeficiency and in children with X-linked agammaglobulinemia gastric surgery and reduced gastric acidity Role of HIV Infection 17
- 18. 18
- 19. CLINICAL MANIFESTATIONS 19 asymptomatic cyst passage acute self-limited diarrhea chronic syndrome of diarrhea, malabsorption, and weight loss
- 20. 100 ingesting cysts, an 5% to 15% asymptomatic cyst passers, 25% to 50% symptomatic with an acute diarrheal syndrome, and the remaining 35% to 70% have no trace of infection. 20
- 21. ACUTE DIARRHEA acute onset of diarrhea, abdominal cramps, bloating, and flatulence symptomatic for more than 1 week to 10 days severe illness 21
- 22. CHRONIC DIARRHEA profound malaise diffuse abdominal and epigastric discomfort Small volume ,greasy stool Weight loss Periodic diarrhea Malabsorption post-Giardia lactose intolerance As cause for growth retardation? 22
- 23. DIAGNOSIS should be considered in all patients with prolonged diarrhea, particularly that which is associated with malabsorption or weight loss OB & OP Examination: Giardia should be identified 60% to 80% of the time after one stool, and some report over 90% identification after three stools 23
- 24. ANTIGEN ASSAYS 85% to 98% sensitive and 90% to 100% specific CWP-1 by ELISA, fluorescein-tagged monoclonal antibodies ,. 24
- 25. SAMPLING OF THE DUODENAL CONTENTS the string test or Entero-Test (HDC Corporation, Milpitas, CA), duodenal aspiration duodenal biopsy 25
- 26. TREATMENT Indication Drugs Pregnant ladies 26
- 27. PREVENTION proper handling and treatment of water used for communities good personal hygiene on an individual basis 27
- 28. AMEBIASIS
- 29. ENTAMOEBA HISTOLYTICA Entamoeba species (histolytica and dispar) close to lowest branch of eukaryotic tree Although the organism was originally thought to lack mitochondria, nuclear-encoded mitochondrial genes and a remnant organelle have now been identified. E. histolytica and E. dispar trophozoites are morphologically indistinguishable, ranging in size from 10 to 60 亮m, with an average of 25 亮m
- 30. Pseudopod-forming, non-flagellated protzoa Replicate by binary fission Most invasive parasite of the Entamoeba group Only member that causes: Amebic colitis & liver abscess
- 31. AMEBAS INTESTINALES Entamoeba _E.histolytica (patogena) _E.coli _E.hartmani _E.gingivalis(oral)
- 33. Trophozoites of Entamoeba histolytica (Trichrome stain). Two diagnostic characteristics: Two of the trophozoites have ingested erythrocytes, and the nuclei have typically a small, centrally located karyosome, as well as thin, uniform peripheral chromatin.
- 34. Free-living E. histolytica with Ingested RBCs
- 35. EPIDEMIOLOGY worldwide incidence = 0.2-10% estimated that 10% of worlds population may be infected 50 million cases of invasive amebiasis/yr 100,000 deaths/yr
- 36. Region Infection Disease Death Africa 85 million 10 million 10-30 thousand Asia 300 million 20-30 million 25-50 thousand Europe 20 million 100 million minimum America 95 million 10 million 10-30 thousand total 650 million 150-200 million 40-110 thousand
- 37. EPIDEMIOLOGIC RISK FACTORS Persons with lower socioeconomic status in endemic area, including those with Crowding Immigrants from endemic area Institutionalized populations, especially developmentally and cognitively impaired Promiscuous male homosexuals malnourished individuals at any age acquired immunodeficiency syndrome??
- 38. TRANSMISSION Faeces- mouth Contaminated water Contaminated meals Street vendors of meals
- 39. LIFE CYCLE A cyst that is excreted into the environment is ingested by a human host though a fecally contaminated product. The cyst then undergoes excystation in the small bowel, becoming a trophozoite. The trophozoite, attaches to the colonic mucin and then reproduces by clonal expansion, most commonly in the cecum. Encystment cysts may survive for as long as 48 hours at 20属 to 25属 C on foods and have been found to remain viable in sewage and natural surface water, at 4属 C, for 1 month.
- 40. PATHOGENESIS Adhesion (The trophozoite possesses a surface protein (lectin) that recognizes the sugars galactose and N-acetylgalactosamine on the host cell surface) Colitis results when the trophozoite penetrates the intestinal mucous layer, which otherwise acts as a barrier to invasion by inhibiting amebic adherence to the underlying epithelium and by slowing trophozoite motility. killing of epithelial cells, neutrophils, and lymphocytes amoebapore, caspase 3,host inflammatory response
- 41. PATHOLOGY A spectrum of colonic lesions ranging from nonspecific thickening of the mucosa to the classic flask-shaped ulcer may be associated with amebic infection Liver abnormality :necrotic abscess or periportal fibrosis, ascending the portal venous system , proteinaceous debris rather than white cells and is surrounded by a rim of amebic trophozoites invading tissue
- 44. HOST IMMUNITY IgA and IgG response to the lectin protein. Serum IgA antibody responses are found in subjects with asymptomatic E. histolytica infection, but not during infection with E. dispar. Cell-mediated immune defense mechanisms probably have a role in limiting invasive disease and resisting a recurrence after pharmacologic cure Cell-mediated responses have been described in patients with amebic liver abscess.
- 45. CLINICAL MANIFESTATIONS Intestinal Disease Extraintestinal Disease Asymptomatic infection Liver abscess Symptomatic noninvasive infection Liver abscess complicated by Acute rectocolitis (dysentery) Peritonitis Fulminant colitis with perforation Empyema Toxic megacolon Pericarditis Chronic nondysenteric colitis Lung abscess Ameboma Brain abscess Perianal ulceration Genitourinary disease
- 46. ASYMPTOMATIC INTESTINAL INFECTION Noninvasive intestinal infection may be established by confirmation of E. histolytica in the stool in association with Hemoccult-negative stools, and normal mucosa on colonoscopy In contrast to infection with E. dispar, asymptomatic infection with E. histolytica is associated with a serum anti-amebic antibody response, and frequently a stool antigen test will be positive . approximately 10% of patients will go on to manifest invasive disease and most individuals will clear their infection within 18 months. Asymptomatic infection should be treated because of its potential to progress to invasive disease.
- 47. INVASIVE INTESTINAL DISEASE Patients with amebic colitis typically present with a several-week history of cramping abdominal pain, weight loss, and watery or bloody diarrhea. The insidious onset and variable signs and symptoms make diagnosis difficult, with fever and grossly bloody stool absent in most cases. Fulminant colitis : predisposition for occurring in malnourished, pregnant women, recipients of corticosteroids, or very young patients. Such patients are severely ill with fever, leukocytosis, profuse bloody mucoid diarrhea, and widespread abdominal pain. Toxic megacolon : occurs in 0.5% of cases, and is a definite complication of inappropriate corticosteroid therapy. Recognition is important because these patients do not respond to drug therapy and require colectomy
- 49. HISTOPATHOLOGY OF A TYPICAL FLASK- SHAPED ULCER OF INTESTINAL AMEBIASIS
- 50. AMEBOMA: Segmented mass of granulation tissue in the cecum or ascending colon Occurs in 0.5% to 1.5% of patients with intestinal amebiasis Tender palpable abdominal mass Concurrent amebic dysentery present in 2/3 of patients Apple-core lesions on barium enema study Lesions resolve with anti-amebic chemotherapy Intestinal constriction occurs in the colon in <1% of patients
- 52. LIVER ABSCESS can appear concurrently with colitis, but more frequently there is no evidence or history of recent intestinal infection by E. histolytica. Liver abscess can manifest with an acute onset (less than 10 days) with abdominal pain and fever or subacutely , with weight loss being prominent and less than half the patients having fever or abdominal pain.
- 53. LABORATORY FINDINGS IN LIVER ABSCESS leukocytosis in 80% mild anemia > 50% elevated alkaline phosphatase 80% Elevated transaminase levels in more aggressive disease, and a Elevation erythrocyte sedimentation rate
- 54. LIVER ABSCESS COMPLICATION Complications of amebic liver abscess may arise from rupture of the abscess with extension into the peritoneum, pleural cavity, or pericardium. Extrahepatic amebic abscesses have occasionally been described in the lung, brain, and skin and presumably result from hematogenous spread.
- 56. GROSS PATHOLOGY OF LIVER CONTAINING AMEBIC ABSCESS
- 58. GROSS PATHOLOGY OF AMEBIC ABSCESS OF LIVER. TUBE OF "CHOCOLATE" PUS FROM ABSCESS.
- 59. DIAGNOSIS OF INTESTINAL AMEBIASIS In developing countries, intestinal amebiasis is most commonly diagnosed by identifying cysts or motile trophozoites on a saline wet mount of a stool specimen. The drawbacks of this method include its low sensitivity and false positive results owing to the presence of E. dispar or E. moshkovskii infection. The diagnosis should ideally be based on the detection in stool of E. histolytica specific antigen or DNA and by the presence of antiamebic antibodies in serum. the trophozoites have ingested red blood cells, they may be assumed to be E. histolytica and the patient should be treated. If, however, there is no such distinguishing microscopic feature, a serum antibody test, stool antigen test, or both should be utilized to confirm the diagnosis of E. histolytica and not E. dispar infection, prior to initiation of treatment
- 61. THERAPY OF CYST PASSER Type Efficacy (%) Paromomycin, 30 mg/kg/day in 3 divided doses for 510 days 8590 Tetracycline, 250 mg qid for 10 days then iodoquinol (Yodoxin), 650 mg tid for 20 days 95 Iodoquinol (diiodohydroxyquin, Yodoxin), 650 mg three times daily for 20 days
- 63. Therapeutic aspiration of an amebic liver abscess is occasionally required as an adjunct to antiparasitic therapy. Drainage of the abscess should be considered in patients who have no clinical response to drug therapy within five to seven days or those with a high risk of abscess rupture, as defined by a cavity with a diameter of more than 5 cm or by the presence of lesions in the left lobe.