Presentation on theme: "Amebiasis Paul R. Earl Facultad de Ciencias Biológicas Universidad Autónoma de Nuevo León San Nicolas, NL, Mexico email@example.com."— Presentation transcript:
1Amebiasis Paul R. Earl Facultad de Ciencias Biológicas Universidad Autónoma de Nuevo León San Nicolas, NL, Mexico
2Amebiasis or amebic dysentary is caused by the protozoan Entamoeba histolytica. Improved sanitation and clean water supply decrease the incidence of amebiasis. The amount of chlorine normally used to control pathogens is inadequate in killing the cysts. Drinking water can be rendered safe by boiling or iodination with tetraglycine hydroperiodide. Nevertheless, drinking water is usually not much of the problem.Perhaps vegetables grown in untreated drainage (aguas negras) should be iodinized or treated with caution. Amebiasis, famous by transmission by foodhandlers, can be also transmitted on the surface of foods.The larger problem is water supply & drainage, particularly in agricultural countries as in much of Latin America. Recycling scarce water is one very large civic task, and safely fertilizing crops with drainage is another. At the same time, the demand for sanitary services is increasing, because of the population explosion. Then the question can be: What is the role of E. histolytica in current and future water management problems?
3Generalities Amebiasis is an intestinal infection in which cysts are passed in the feces. Symptoms can include fever, chills and diarrhea, sometimes bloody or with mucus and often with cramps. Some people may have only mild abdominal discomfort or no symptoms at all. Symptoms can start 2 or more weeks after infection. Rarely, trophozoites (the mobile amebas) may invade the liver, lung or brain, or perforate the colon causing septicemia.Cerebral amebiasis is fatal. Cysts are spread from one person to another directly or via contaminated objects or in food or water. People are infectious as long as the cysts are being shed in their feces. When others touch the objects or eat contaminated food, they get the cysts on their hands and into their mouths. When they swallow the cysts, they get infected. Diagnosis is made by examining fecal samples under the microscope for the presence of trophozoites and cysts of Entamoeba histolytica..
4E. dispar is a nonpathogenic protozoon morphologically identical to E histolytica. Previously reported asymptomatic infections due to the so-called nonpathogenic strains of E histolytica now are recognized to be due to E. dispar. These 2 species of Entameba can be distinguished by monoclonal antibodies. Other morphologically distinct organisms, such as Entamoeba coli ( E. coli ! ! ) and Entamoeba hartmanni are also nonpathogenic.
5Amebiasis is the third leading parasitic cause of death worldwide, surpassed only by malaria and schistosomiasis. On a global basis, amebiasis affects approximately 50 million persons each year, resulting in nearly 100,000 deaths.In 1875 in St. Petersburg, Russia, Losch first described amebiasis, proving the ameba’s pathogenicity by infecting a dog with fecal cysts from a hospital patient. Councilman & Lafleur at Johns Hopkins University Hospital, Baltimore, Md, USA distinguished between bacillary and amebic dysentery in 1891.
6Laboratory diagnosis An iodine-stained cyst of the pathogen Entamoeba hystolytica with 4 nuclei is illustrated. The harmless commensal Entamoeba coli has larger cyts with 8 nuclei. Furthermore, recall that E. histolytica has a lookalike E. dispars that is harmless.
8Many other amebas and flagellates inhabit the human intestine, mostly harmless. Regardless, they should be recognized by anyone diagnosing fecal samples. Illustrations are through the courtesy of Chiang Mai University, Thailand: dept/parasite/image.htm.
9The cyst of E histolytica averages 12 m, ranging from 5-20 m The cyst of E histolytica averages 12 m, ranging from 5-20 m. It has 1-4 nuclei that are morphologically similar to the nuclei of the trophozoite. The cyst may have iodine-stainable glycogen clumps and chromatoid bodies with smooth rounded edges. The ending –oid means LIKE so chromatoid bodies are like chromatin in that they stain with hematoxylin.
10Trophozoites Entamoeba coli Trophozoites Entamoeba coli Entamoeba histolytica 15 mm - 40 mm in size 10 mm - 35 mm size Nondirectional motility Unidirectional motility Multiple pseudopodia Single pseudopodia No ingested erythrocytes Ingested erythrocytes Cytoplasm rough looking Finely granular cytoplasm Large, eccentric karyosome Small, central karyosome Clumped nuclear chromatin Finely beaded chromatin
11Cysts Entamoeba coli. Entamoeba histolytica 10 mm - 35 mm in size Cysts Entamoeba coli Entamoeba histolytica 10 mm - 35 mm in size 10 mm - 20 mm in size May have 8 nuclei Never more than 4 nuclei Karyosomes eccentric Karyosomes small, central Nuclear chromatin clumped Chromatin finely beaded Splintered chromatoidal bars Rounded chromatoidal bars
12Leukocytosis and mild anemia can occur Leukocytosis and mild anemia can occur. Erythrocyte sedimentation rate generally is elevated. Liver function tests reveal elevated alkaline phosphatase in 80% of patients, elevated transaminases and reduced albumin. Urinalysis may reveal proteinuria. Rectosigmoidoscopy and colonoscopy may show small mucosal ulcers covered with yellowish exudates. The intervening mucosa appears normal. Biopsy results and scrapings of ulcer edge may locate trophozoites.Indications for endoscopy in suspected intestinal amebiasis include the following: a) serum antibody positive, yet feces negative, b) immediate diagnosis required and feces negative, c) high suspicion without evidence, and d) evaluation of lesions.
13Symptoms and pathology Symptoms and pathology. Primary intestinal flask-shaped (button hole) necrotic ulcers occur in the submucosa of the large intestine, most commonly the cecal and sigmoidorectal regions.Ulcers contain necrotic debris, actively feeding trophozoites with ingested erythrocytes, cytolyzed cells and mucous; polymorphonuclear leukocytes and round inflammatory cells.Patients can have chronic protracted diarrhea, dysentery (minority), cramping abdominal pain and tenderness. Fever may result from bacterial superinfections. red blood cells, neutrophils, mucus and shreds of necrotic mucosa may be seen in stool specimens.Complications include appendicitis, perforation, hemorrhage, stricture and pseudopolyposis. Chronic irritable colon or postdysenteric colitis may be experienced.
14Extraintestinal features Extraintestinal features. Hematogenous spread may result in abscesses of the liver, spleen, lung or brain. Hepatic amebiasis (abscess, hepatitis) is the most common and grave complication: Enlarged, tender liver and upper abdominal pain that may radiate to the right shoulder. Mild jaundice may be evident, transaminases and alkaline phosphatase elevations may be seen.Most infections lead to uneventful recoveries. However. fulminant amebic colitis has a mortality rate of more than 50%, whereas pleuropulmonary amebiasis has a mortality rate of 15-20%, amebic pericarditis has a case fatality rate of 40%.
15Drugs for treatment. Five pharmaceuticals are briefly noted Drugs for treatment. Five pharmaceuticals are briefly noted. Asymptomatic intestinal infection may be treated with iodoquinol, paromomycin or diloxanide furoate. Recommended drugs for treatment of symptomatic intestinal disease and for hepatic abscess are metronidazole and tinidazole. Since these drugs may not eliminate the cysts of the intestine, immediately follow metronidazole and tinidazole with iodoquinol, paromomycin or diloxanide furoate.
161/ Metronidazole (Flagyl, Protostat). Kills trophozoites of E 1/ Metronidazole (Flagyl, Protostat). Kills trophozoites of E. histolytica in intestine and tissue. Does not eradicate cysts from intestines. Adult oral dose: mg 3 times per day for 10 day. Elimination is accelerated by simultaneous use of phenytoin and phenobarbital; clearance is decreased by cimetidine.
172/Tinidazole (Fasigyn) 2/Tinidazole (Fasigyn). 5-nitroimidazole derivative with selective antimicrobial activity against anaerobic bacteria and protozoa. Not available in United States. Adult oral dose: 600 mg bid or 800 mg 2 times a day for 5 days. Pediatric dose mg/kg for 5 days, not to exceed 2 g/day.
183/Paromomycin (Humatin) 3/Paromomycin (Humatin). Amebicidal aminoglycoside antibiotic that is poorly absorbed. Active only against intestinal form of amebiasis. Used to eradicate cysts of E. histolytica following treatment with metronidazole or tinidazole for an invasive disease. Adult oral dose: mg/kg/day divided 3 times for 7 days. Pediatric dose: Administer as in adults.
194/Diloxanide furoate (Furamid, Entamizole, Furamide) 4/Diloxanide furoate (Furamid, Entamizole, Furamide). Luminal amebicide; acts primarily in bowel lumen since it is poorly absorbed. Used to eradicate cysts of E. histolytica after treatment of invasive disease. Available through US CDC Drug Service ( ). Adult oral dose 500 mg 2 times a day for 10 days. Pediatric dose 20 mg/kg/ divided twice a day for 10 days, not to exceed 1500 mg/day.
205/Iodoquinol (Yodoxin). Halogenated hydroxyquinoline 5/Iodoquinol (Yodoxin). Halogenated hydroxyquinoline. Luminal amebicide; acts primarily in bowel lumen since it is poorly absorbed. Best tolerated when given with meals. Since active only against intraluminal form of amebiasis, used to eradicate cysts of E. histolytica after treatment of invasive disease. Adult oral dose 650 mg 2 times a day for 20 days. Pediatric dose: mg/kg/day divided 2 times for 20 days; not to exceed 2 g/day.Have these and other drugs including the antimitotic type been adequately tested in in vitro, i. e., in trophozoite and cyst cultures? They have not. Is simple mitosis understood? It is not.
21The control of infection The control of infection. The epidemiology of amebiasis is folkloric, beginning with infected foodhandlers. While elements of truth are scattered through this neglected syndrome, much more can be done. Frankly, the ecology is unknown. Are there reservoir animals?
22What civic water treatments kill and which ones tolerate E. histolytica? What part does chronic malnutrition play in susceptibility to infection? What part does exposure then the rise of natural antibodies play in defense? What are the water-borne pathogens intimately associated with E. histolytica? Has radioactivity been used to trace ecological dispersion of an element like phosphorus in a parasite? If ever, how is E. histolytica considered in civic water management?Is patient data well anaylzed by locality, income, age, sex, etc. Would questionaires help? Are these patients rural, migrant or urban? How does amebiasis relate to rural poverty? Where did certain travelers become infected? Is amebiasis a medical, a water-and-drainage or a social problem? Is underfinancing of research a problem? What distinguishes persons with antibodies against E. histolytica from others without?
23The main point of this lecture is to sketch E The main point of this lecture is to sketch E. histolytica as a distinct pathogen differing from E. coli and E. dispar. More, decades pass without fruitful reseach results. Perhaps you find this a challenge.