Amoebic Dysentery
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The Intestinal Protozoa
The Intestinal Protozoa A. Introduction 1. The Phylum Protozoa is classified into four major subdivisions according to the methods of locomotion and reproduction. a. The amoebae (Superclass Sarcodina, Class Rhizopodea move by means of pseudopodia and reproduce exclusively by asexual binary division. b. The flagellates (Superclass Mastigophora, Class Zoomasitgophorea) typically move by long, whiplike flagella and reproduce by binary fission. c. The ciliates (Subphylum Ciliophora, Class Ciliata) are propelled by rows of cilia that beat with a synchronized wavelike motion. d. The sporozoans (Subphylum Sporozoa) lack specialized organelles of motility but have a unique type of life cycle, alternating between sexual and asexual reproductive cycles (alternation of generations). e. Number of species - there are about 45,000 protozoan species; around 8000 are parasitic, and around 25 species are important to humans. 2. Diagnosis - must learn to differentiate between the harmless and the medically important. This is most often based upon the morphology of respective organisms. 3. Transmission - mostly person-to-person, via fecal-oral route; fecally contaminated food or water important (organisms remain viable for around 30 days in cool moist environment with few bacteria; other means of transmission include sexual, insects, animals (zoonoses). B. Structures 1. trophozoite - the motile vegetative stage; multiplies via binary fission; colonizes host. 2. cyst - the inactive, non-motile, infective stage; survives the environment due to the presence of a cyst wall. 3. nuclear structure - important in the identification of organisms and species differentiation. 4. diagnostic features a. size - helpful in identifying organisms; must have calibrated objectives on the microscope in order to measure accurately. -
6.5 X 11 Double Line.P65
Cambridge University Press 978-0-521-53026-2 - The Cambridge Historical Dictionary of Disease Edited by Kenneth F. Kiple Index More information Name Index A Baillie, Matthew, 80, 113–14, 278 Abercrombie, John, 32, 178 Baillou, Guillaume de, 83, 224, 361 Abreu, Aleixo de, 336 Baker, Brenda, 333 Adams, Joseph, 140–41 Baker, George, 187 Adams, Robert, 157 Balardini, Lodovico, 243 Addison, Thomas, 22, 350 Balfour, Francis, 152 Aesculapius, 246 Balmis, Francisco Xavier, 303 Aetius of Amida, 82, 232, 248 Bancroft, Edward, 364 Afzelius, Arvid, 203 Bancroft, Joseph, 128 Ainsworth, Geoffrey C., 128–32, 132–34 Bancroft, Thomas, 87, 128 Albert, Jose, 48 Bang, Bernhard, 60 Alexander of Tralles, 135 Bannwarth, A., 203 Alibert, Jean Louis, 147, 162, 359 Bard, Samuel, 83 Ali ibn Isa, 232 Barensprung,¨ F. von, 360 Allchin, W. H., 177 Bargen, J. A., 177 Allison, A. C., 25, 300 Barker, William H., 57–58 Allison, Marvin J., 70–71, 191–92 Barthelemy,´ Eloy, 31 Alpert, S., 178 Bartlett, Elisha, 351 Altman, Roy D., 238–40 Bartoletti, Fabrizio, 103 Alzheimer, Alois, 14, 17 Barton, Alberto, 69 Ammonios, 358 Bartram, M., 328 Amos, H. L., 162 Bassereau, Leon,´ 317 Andersen, Dorothy, 84 Bateman, Thomas, 145, 162 Anderson, John, 353 Bateson, William, 141 Andral, Gabriel, 80 Battistine, T., 69 Annesley, James, 21 Baumann, Eugen, 149 Arad-Nana, 246 Beard, George, 106 Archibald, R. G., 131 Beet, E. A., 24, 25 Aretaeus the Cappadocian, 80, 82, 88, 177, 257, 324 Behring, Emil, 95–96, 325 Aristotle, 135, 248, 272, 328 Bell, Benjamin, 152 Armelagos, George, 333 Bell, J., 31 Armstrong, B. -
Traveler's Diarrhea
Traveler’s Diarrhea JOHNNIE YATES, M.D., CIWEC Clinic Travel Medicine Center, Kathmandu, Nepal Acute diarrhea affects millions of persons who travel to developing countries each year. Food and water contaminated with fecal matter are the main sources of infection. Bacteria such as enterotoxigenic Escherichia coli, enteroaggregative E. coli, Campylobacter, Salmonella, and Shigella are common causes of traveler’s diarrhea. Parasites and viruses are less common etiologies. Travel destination is the most significant risk factor for traveler’s diarrhea. The efficacy of pretravel counseling and dietary precautions in reducing the incidence of diarrhea is unproven. Empiric treatment of traveler’s diarrhea with antibiotics and loperamide is effective and often limits symptoms to one day. Rifaximin, a recently approved antibiotic, can be used for the treatment of traveler’s diarrhea in regions where noninvasive E. coli is the predominant pathogen. In areas where invasive organisms such as Campylobacter and Shigella are common, fluoroquinolones remain the drug of choice. Azithromycin is recommended in areas with qui- nolone-resistant Campylobacter and for the treatment of children and pregnant women. (Am Fam Physician 2005;71:2095-100, 2107-8. Copyright© 2005 American Academy of Family Physicians.) ILLUSTRATION BY SCOTT BODELL ▲ Patient Information: cute diarrhea is the most com- mised and those with lowered gastric acidity A handout on traveler’s mon illness among travelers. Up (e.g., patients taking histamine H block- diarrhea, written by the 2 author of this article, is to 55 percent of persons who ers or proton pump inhibitors) are more provided on page 2107. travel from developed countries susceptible to traveler’s diarrhea. -
Enteric Protozoa in the Developed World: a Public Health Perspective
Enteric Protozoa in the Developed World: a Public Health Perspective Stephanie M. Fletcher,a Damien Stark,b,c John Harkness,b,c and John Ellisa,b The ithree Institute, University of Technology Sydney, Sydney, NSW, Australiaa; School of Medical and Molecular Biosciences, University of Technology Sydney, Sydney, NSW, Australiab; and St. Vincent’s Hospital, Sydney, Division of Microbiology, SydPath, Darlinghurst, NSW, Australiac INTRODUCTION ............................................................................................................................................420 Distribution in Developed Countries .....................................................................................................................421 EPIDEMIOLOGY, DIAGNOSIS, AND TREATMENT ..........................................................................................................421 Cryptosporidium Species..................................................................................................................................421 Dientamoeba fragilis ......................................................................................................................................427 Entamoeba Species.......................................................................................................................................427 Giardia intestinalis.........................................................................................................................................429 Cyclospora cayetanensis...................................................................................................................................430 -
Ulcerative Post-Dysenteric Colitis
Gut: first published as 10.1136/gut.7.5.438 on 1 October 1966. Downloaded from Gut, 1966, 7, 438 Ulcerative post-dysenteric colitis S. J. POWELL AND A. J. WILMOT From the Amoebiasis Research Unit' and the Department ofMedicine, University ofNatal, Durban, South Africa EDITORIAL COMMENT Better treatment is resulting in more severe cases of amoebic colitis surviving and these patients may have severe residual damage to the bowel resulting in ulcerative post-dysenteric colitis. This is considered to be a distinct entity. The term 'post-dysenteric colonic irritability' was thousand patients who attend this hospital annually introduced by Sir Arthur Hurst (1943) to describe with acute amoebic dysentery complications are persistent irritability of the bowel following an acute common and we have had the opportunity to study attack of bacillary or amoebic dysentery. The early them (Wilmot, 1962). It is from this material that we symptoms were attributed to a non-specific chronic have based the following report of ulcerative post- colitis occurring after the specific infection had died dysenteric colitis in 33 African patients observed in out, but in the later stages were thought to be due to recent years. 'functional irritability' of the colon. Stewart (1950) found that post-dysenteric colitis was more common- CLINICAL FINDINGS ly a sequel to acute amoebic dysentery and was able All patients presented initially with severe amoebic to recognize two forms in his patients: 1 Those with dysentery, sigmoidoscopic examination showing a mild symptoms and no colonic ulceration, which he congested, oedematous mucosa with extensive rectal named 'functional post-dysenteric colitis', and (2) ulcers the surfaces of which were covered by sloughs http://gut.bmj.com/ Those with colonic ulceration and more severe and exudate. -
Entamoeba Histolytica?
Amebas Friend and foe Facultative Pathogenicity of Entamoeba histolytica? Confusing History 1875 Lösch correlated dysentery with amebic trophozoites 1925 Brumpt proposed two species: E. dysenteriae and E. dispar 1970's biochemical differences noted between invasive and non-invasive isolates 80's/90's several antigenic and DNA differences demonstrated • rRNA 2.2% sequence difference 1993 Diamond and Clark proposed a new species (E. dispar) to describe non-invasive strains 1997 WHO accepted two species 1 Family Entamoebidae Family includes parasites • Entamoeba histolytica and commensals • Entamoeba dispar • Entamoeba coli Species are differentiated • Entamoeba hartmanni based on size, nuclear • Endolimax nana substructures • Iodamoeba bütschlii Entamoeba histolytica one of the most potent killers in nature Entamoeba histolytica • worldwide distribution (cosmopolitan) • higher prevalence in tropical or developing countries (20%) • 1-6% in temperate countries • Possible animal reservoirs • Amebiasis - Amebic dysentery • aka: Montezuma’s revenge Taxonomy • One parasitic species? • E. histolytica • E. dispar • E. hartmanni 2 Entamoeba Life Cycle - Direct Fecal/Oral transmission Cyst - Infective stage Resistant form Trophozoite - feeding, binary fission Different stages of cyst development Precysts - rich in glycogen Young cyst - 2, then 4 nuclei with chromotoid bodies Metacysts - infective stage Metacystic trophozoite - 8 8 Excystation Metacyst Cyst wall disruption Ameba emerges Nuclear division 48 Cytokinesis Nuclear division -
38 Entamoeba Histolytica and Other Rhizophodia
MODULE Entamoeba Histolytica and Other Rhizophodia Microbiology 38 Notes ENTAMOEBA HISTOLYTICA AND OTHER RHIZOPHODIA 38.1 INTRODUCTION Amoebae can be pathogenic called Entamoeba histolytica and non pathogenic called Entamoeba coli (large intestines), Entamoeba gingivalis (oral cavity). These parasites are motile with pseudopodia. The pseudopodia are cytoplasmic processes which are thrown out. OBJECTIVES After reading this lesson you will be able to: z describe morphology, its life cycle, pathogenecity of Entameba Histolytica, other amoebae and free living amoeba z differentiate between amoebic and Bacillary dysentery z differentiate between Entamoeba Histolytica and Entamoeba Coli z demonstrate Laboratory diagnosis of Entameba 38.2 ENTAMOEBA HISTOLYTICA It belongs to the class Rhizopoda and family Entamoebidae. It is the causative agent of amoebiasis. Amoebiasis can be intestinal and extra intestinal like amoebic hepatitis, amoebic liver abscess. 38.3 MORPHOLOGY The Entamoeba is seen in three stages 344 MICROBIOLOGY Entamoeba Histolytica and Other Rhizophodia MODULE (a) Trophozoite: The trophozoite is 18-40 µm in size. The trophozoite is Microbiology actively motile. The cytoplasm is demarcated into endoplasm and ectoplasm. Ingested food particles and red blood cells are seen in the cytoplasm No bacteria are seen in the cytoplasm. The nucleus is 6-15 µm and has a central rounded karyosome. Nuclear membrane has chromatin granules and spoke like radial arrangement of chromatin fibrils. Notes Fig. 38.1 (b) Precyst: Smaller in size. 10-20 µm in diameter. It is round to oval in shape with blunt pseudopodium. The nuclei is similar to the trophozoite. (c) Cyst: These are round 10-15 µm in diameter. It is surrounded by a refractile membrane called as the cyst wall. -
Remarks on Pelvic Peritonitis and Pelvic Cellulitis, with Illustrative Cases
Article IV.- Remarks on Pelvic Peritonitis and Pelvic Cellulitis, with Illustrative Cases. By Lauchlan Aitken, M.D. Rather moie than a year ago there appeared from the pen of a well- known of this a gynecologist city very able monograph on the two forms of pelvic inflammation whose names head this article; and it cannot have escaped the recollection of the reader that Dr M. Dun- can, adopting the nomenclature first proposed by Yirchow, has used on his different terms title-page1 than those older appellations I still to retain. Under these propose ^ circumstances I feel at to compelled least to attempt justify my preference for the original names: and I trust to be able to show that are they preferable to, and less con- others that fusing than, any have as yet been proposed, even though we cannot consider them absolutely perfect. 1 Treatise on A Practical Perimetritis and Parametritis (Edin. 1869). 1870.] DR LAUCI1LAN AITKEN ON PELVIC FERITONITIS, ETC. 889 Passing over, then, such terms as 'periuterine cellulitis or phleg- mons periuterins as bad compounds ; others, as inflammation of the broad ligaments, as too limited in meaning ; and others, again, as engorgement periutdrin, as only indicating one of the stages of the affection,?I shall endeavour as succinctly as possible to state my reasons for preferring the older names to those proposed by Virchow. ls?. The two Greek prepositions, peri and para, are employed somewhat arbitrarily to indicate inflammatory processes which are essentially distinct. I say arbitrarily, because I am not aware that para has been generally employed in the form of a compound to ex- press inflammation of the cellular tissue elsewhere.1 By those who remember that the cellular tissue not only separates the serous membrane from the uterus at that part where the cervix and body of the organ meet, but is even abundant there,2 perimetritis might readily be taken to indicate one of the varieties, though indeed not a in for which very common one, of pelvic cellulitis?a variety, fact, the term perimetric cellulitis has been proposed. -
Molecular Characterization of Enterotoxigenic Escherichia Coli
iolog ter y & c P a a B r f a o s i l t o a l n o r Yameen et al., J Bacteriol Parasitol 2018, 9:3 g u y o J Bacteriology and Parasitology DOI: 10.4172/2155-9597.1000339 ISSN: 2155-9597 Research Article Open Access Molecular Characterization of Enterotoxigenic Escherichia coli: Effect on Intestinal Nitric Oxide in Diarrheal Disease Muhammad Arfat Yameen1, Ebuka Elijah David2*, Humphrey Chukwuemeka Nzelibe3, Muhammad Nasir Shuaibu3, Rabiu Abdussalam Magaji4, Amakaeze Jude Odugu5 and Ogamdi Sunday Onwe6 1Department of Pharmacy, COMSATS Institute of Information Technology, Abbottabad, Pakistan 2Department of Biochemistry, Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria 3Department of Biochemistry, Ahmadu Bello University, Zaria, Kaduna State, Nigeria 4Department of Human Physiology, Ahmadu Bello University, Zaria, Kaduna State, Nigeria 5Medical Laboratory, Ahmadu Bello University, Teaching Hospital, Zaria, Kaduna State, Nigeria 6Laboratory Service Unit, Federal Teaching Hospital, Abakiliki, Ebonyi State, Nigeria *Corresponding author: Ebuka Elijah David, Department of Biochemistry, Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria, Tel: +2348033188823; E-mail: [email protected] Received date: May 01, 2018; Accepted date: May 25, 2018; Published date: May 30, 2018 Copyright: ©2018 Yameen MA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract This study was aimed to investigate the effect of enterotoxigenic E. coli (ETEC)-induced diarrhea on fecal nitric oxide (NO) and intestinal inducible nitric oxide synthase (iNOS) expression in rats. -
The Global View of Campylobacteriosis
FOOD SAFETY THE GLOBAL VIEW OF CAMPYLOBACTERIOSIS REPORT OF AN EXPERT CONSULTATION UTRECHT, NETHERLANDS, 9-11 JULY 2012 THE GLOBAL VIEW OF CAMPYLOBACTERIOSIS IN COLLABORATION WITH Food and Agriculture of the United Nations THE GLOBAL VIEW OF CAMPYLOBACTERIOSIS REPORT OF EXPERT CONSULTATION UTRECHT, NETHERLANDS, 9-11 JULY 2012 IN COLLABORATION WITH Food and Agriculture of the United Nations The global view of campylobacteriosis: report of an expert consultation, Utrecht, Netherlands, 9-11 July 2012. 1. Campylobacter. 2. Campylobacter infections – epidemiology. 3. Campylobacter infections – prevention and control. 4. Cost of illness I.World Health Organization. II.Food and Agriculture Organization of the United Nations. III.World Organisation for Animal Health. ISBN 978 92 4 156460 1 _____________________________________________________ (NLM classification: WF 220) © World Health Organization 2013 All rights reserved. Publications of the World Health Organization are available on the WHO web site (www.who.int) or can be purchased from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: [email protected]). Requests for permission to reproduce or translate WHO publications –whether for sale or for non-commercial distribution– should be addressed to WHO Press through the WHO web site (www.who.int/about/licensing/copyright_form/en/index. html). The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. -
Unusual Presentation of Shigellosis: Acute Perforated Appendicitis And
Case Report 45 Unusual Presentation of Shigellosis: Acute Perforated Appendicitis and Peritonitis Gülsüm İclal Bayhan1, Gönül Tanır1, Haşim Ata Maden2, Şengül Özkan3 1Pediatric Infection Clinic, Dr. Sami Ulus Gynecology, Child Care and Treatment Training and Research Hospital, Ankara, Turkey 2Department of Pediatric Surgery, Dr. Sami Ulus Gynecology, Child Care and Treatment Training and Research Hospital, Ankara, Turkey 3Microbiology Clinic. Dr. Sami Ulus Gynecology, Child Care and Treatment Training and Research Hospital, Ankara, Turkey Abstract Shigella spp. is one of the most common agents that cause bacterial diarrhea and dysentery in developing coun- tries. Clinical presentation of shigellosis may vary over a wide spectrum from mild diarrhea to severe dysentery. We report the case of 5.5-year-old previously healthy boy, who presented to our clinic with abdominal pain, vomiting, and constipation. On examination, we noticed abdominal tenderness with guarding at the right lower quadrant. With the diagnosis of acute appendicitis, open appendectomy was performed. Exploration of the abdominal cavity revealed perforated appendicitis and generalized peritonitis. Shigella sonnei was isolated from the peritoneal fluid culture. The patient completely recovered without any complications. Surgical complications, including appendicitis, could have developed during shigellosis. There are few reported cases of perforated appendicitis associated with Shigella. Prompt surgical intervention can be beneficial to prevent morbidity and mortality if it is performed early in the course of the disease. (J Pediatr Inf 2015; 9: 45-8) Keywords: Shigella spp., acute appendicitis, peritonitis, surgical complication Introduction intestinal and extra-intestinal complications. There are few reported cases of perforated Shigella spp., a group of Gram-negative, appendicitis complicated with peritonitis due to Received: 04.10.2013 Accepted: 03.02.2014 small, non-motile, non-spore forming, and rod- Shigella spp. -
Bacillary Dysentery
Bacillary dysentery by Sudhir Chandra Pal uring the first half of 1984, a infectious dose. It requires only 10 to drome and leukaemoid reactions were severe epidemic of bacillary 100 shigella bacteria to produce dys also reported. dysentery swept through the entery, whereas one million to ten Similar epidemics due to the districts of West Bengal and a few million germs may need to be swal multiple-drug-resistant S. shigae have other eastern Indian States, affecting lowed to cause cholera. also occurred in Somalia (1976), three over 350,000 people and leaving By 1920, dysentery due to the most villages in South India (1976), Sri about 3,500, mostly children, dead. It virulent variety, the Shiga bacillus, Lanka (1978-80), Central Africa was like a nightmare as the disease had almost disappeared from Europe (1980-82), Eastern India, Nepal, Bhu stubbornly refused to respond to con and North America. However, it con tan and the Maldives (1984) and Bur ventional treatment, and its galloping tinued to be reported from the de ma (1984-85). The pattern was more spread could not be contained by all veloping countries in the form of local or less the same everywhere. The available public health measures. ised outbreaks. During the late sixties, disease spread with terrific speed in People became confused and panicky, Shiga's bacillus reappeared with a big spite of all available public health not knowing what to do. bang as the main culprit of a series of measures, attacking over 10 per cent Bacillary dysentery, characterised devastating epidemics of dysentery of the population and killing between by frequent passage of blood and in a number of countries in Latin two and 10 per cent even of the mucus in the stools accompanied by America, Asia and Africa.