Shigellosis (Bacillary Dysentery) Reporting and Case Investigation
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Shigella Infection - Factsheet
Shigella Infection - Factsheet What is Shigellosis? How common is it? Shigellosis is an infectious disease caused by a group of bacteria (germs) called Shigella. It’s also known as bacillary dysentery. There are four main types of Shigella germ but Shigella sonnei is by far the commonest cause of this illness in the UK. Most cases of the other types are usually brought in from abroad. How is Shigellosis caught? Shigella is not known to be found in animals so it always passes from one infected person to the next, though the route may be indirect. Here are some possible ways in which you can get infected: • Shigella germs are present in the stools of infected persons while they are ill and for a week or two afterwards. Most Shigella infections are the result of germs passing from stools or soiled fingers of one person to the mouth of another person. This happens when basic hygiene and hand washing habits are inadequate, such as in young toddlers who are not yet fully toilet trained. Family members and playmates of such children are at high risk of becoming infected. • Shigellosis can be acquired from someone who is infected but has no symptoms. • Shigellosis may be picked up from eating contaminated food, which may look and smell normal. Food may become contaminated by infected food handlers who do not wash their hands properly after using the toilet. They should report sick and avoid handling food if they are ill but they may not always have symptoms. • Vegetables can become contaminated if they are harvested from a field with sewage in it. -
Purification and Characterization of a Shigella Dysenteriae 1- Like Toxin Produced by Escherichia Coli
CORE Metadata, citation and similar papers at core.ac.uk Provided by UNL | Libraries University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Uniformed Services University of the Health Sciences U.S. Department of Defense 1983 Purification and Characterization of a Shigella dysenteriae 1- Like Toxin Produced by Escherichia coli Alison D. O'Brien Uniformed Services University of the Health Sciences, [email protected] Gerald D. LaVeck Uniformed Services University of the Health Sciences Follow this and additional works at: https://digitalcommons.unl.edu/usuhs Part of the Medicine and Health Sciences Commons O'Brien, Alison D. and LaVeck, Gerald D., "Purification and Characterization of a Shigella dysenteriae 1- Like Toxin Produced by Escherichia coli" (1983). Uniformed Services University of the Health Sciences. 99. https://digitalcommons.unl.edu/usuhs/99 This Article is brought to you for free and open access by the U.S. Department of Defense at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Uniformed Services University of the Health Sciences by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. INFECTION AND IMMUNITY, May 1983, p. 675-683 Vol. 40, No. 2 0019-9567/83/050675-09$02.00/0 Copyright C 1983, American Society for Microbiology Purification and Characterization of a Shigella dysenteriae 1- Like Toxin Produced by Escherichia coli ALISON D. O'BRIEN* AND GERALD D. LAVECKt Department of Microbiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814 Received 10 January 1983/Accepted 18 February 1983 A toxin from an enteropathogenic strain of Escherichia coli (E. coli H30) was purified to apparent homogeneity from cell lysates. -
E. Coli: Serotypes Other Than O157:H7 Prepared by Zuber Mulla, BA, MSPH DOH, Regional Epidemiologist
E. coli: Serotypes other than O157:H7 Prepared by Zuber Mulla, BA, MSPH DOH, Regional Epidemiologist Escherichia coli (E. coli) is the predominant nonpathogenic facultative flora of the human intestine [1]. However, several strains of E. coli have developed the ability to cause disease in humans. Strains of E. coli that cause gastroenteritis in humans can be grouped into six categories: enteroaggregative (EAEC), enterohemorrhagic (EHEC), enteroinvasive (EIEC), enteropathogenic (EPEC), enterotoxigenic (ETEC), and diffuse adherent (DAEC). Pathogenic E. coli are serotyped on the basis of their O (somatic), H (flagellar), and K (capsular) surface antigen profiles [1]. Each of the six categories listed above has a different pathogenesis and comprises a different set of O:H serotypes [2]. In Florida, gastrointestinal illness caused by E. coli is reportable in two categories: E. coli O157:H7 or E. coli, other. In 1997, 52 cases of E. coli O157:H7 and seven cases of E. coli, other (known serotype), were reported to the Florida Department of Health [3]. Enteroaggregative E. coli (EAEC) - EAEC has been associated with persistent diarrhea (>14 days), especially in developing countries [1]. The diarrhea is usually watery, secretory and not accompanied by fever or vomiting [1]. The incubation period has been estimated to be 20 to 48 hours [2]. Enterohemorrhagic E. coli (EHEC) - While the main EHEC serotype is E. coli O157:H7 (see July 24, 1998, issue of the “Epi Update”), other serotypes such as O111:H8 and O104:H21 are diarrheogenic in humans [2]. EHEC excrete potent toxins called verotoxins or Shiga toxins (so called because of their close resemblance to the Shiga toxin of Shigella dysenteriae 1This group of organisms is often referred to as Shiga toxin-producing E. -
Zoonotic Diseases Fact Sheet
ZOONOTIC DISEASES FACT SHEET s e ion ecie s n t n p is ms n e e s tio s g s m to a a o u t Rang s p t tme to e th n s n m c a s a ra y a re ho Di P Ge Ho T S Incub F T P Brucella (B. Infected animals Skin or mucous membrane High and protracted (extended) fever. 1-15 weeks Most commonly Antibiotic melitensis, B. (swine, cattle, goats, contact with infected Infection affects bone, heart, reported U.S. combination: abortus, B. suis, B. sheep, dogs) animals, their blood, tissue, gallbladder, kidney, spleen, and laboratory-associated streptomycina, Brucellosis* Bacteria canis ) and other body fluids causes highly disseminated lesions bacterial infection in tetracycline, and and abscess man sulfonamides Salmonella (S. Domestic (dogs, cats, Direct contact as well as Mild gastroenteritiis (diarrhea) to high 6 hours to 3 Fatality rate of 5-10% Antibiotic cholera-suis, S. monkeys, rodents, indirect consumption fever, severe headache, and spleen days combination: enteriditis, S. labor-atory rodents, (eggs, food vehicles using enlargement. May lead to focal chloramphenicol, typhymurium, S. rep-tiles [especially eggs, etc.). Human to infection in any organ or tissue of the neomycin, ampicillin Salmonellosis Bacteria typhi) turtles], chickens and human transmission also body) fish) and herd animals possible (cattle, chickens, pigs) All Shigella species Captive non-human Oral-fecal route Ranges from asymptomatic carrier to Varies by Highly infective. Low Intravenous fluids primates severe bacillary dysentery with high species. 16 number of organisms and electrolytes, fevers, weakness, severe abdominal hours to 7 capable of causing Antibiotics: ampicillin, cramps, prostration, edema of the days. -
Communicable Diseases Communiqué DECEMBER 2012, Vol
Communicable Diseases Communiqué DECEMBER 2012, Vol. 11(12) CONTENTS Shigellosis outbreak 1 Rabies 2 Trypanosomiasis 3 Influenza 4 Beyond our Borders 5 Shigellosis Outbreak in Nelson Mandela Bay Health District, Eastern Cape Province An NHLS pathologist based in Port Elizabeth (Nelson isolated from both blood culture and stool in a 2- Mandela Bay Health District, Eastern Cape Province) year-old child with severe bloody diarrhoea and noticed a sudden marked increase in the number of fever. There has been one fatal case to date (a 76- shigellosis cases at a provincial public hospital and year-old female who presented with bloody primary health care clinic in the district during the diarrhoea and dehydration). last week of November 2012. This was reported to the National Outbreak Unit (NICD-NHLS and Of the Shigella spp. isolates referred to the Centre National Department of Health) which prompted for Enteric Diseases (NICD-NHLS) for further further investigation. characterisation, 11 have been tested to date and all are Shigella flexneri 1b. Twelve laboratory-confirmed cases of S. flexneri had been reported between 23 and 26 November Humans and other large primates are the only 2012; by 3 December 2012 the number of natural reservoirs of Shigella spp. Person-to-person laboratory-confirmed cases had risen to 24 (21 of spread is the commonest mode of transmission, but whom had severe disease necessitating hospital infection and outbreaks can also be caused by admission). Although cases were identified in both contaminated food or water. Shigellosis is one of public and private healthcare facilities in the district, the most communicable of the bacterial causes of the majority were resident in the Kwazakhele area diarrhoea, since a low dose of organisms readily and shared no other common risk exposures. -
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. -
Amoebic Dysentery
University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1934 Amoebic dysentery H. C. Dix University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Dix, H. C., "Amoebic dysentery" (1934). MD Theses. 320. https://digitalcommons.unmc.edu/mdtheses/320 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. A MOE B leD Y SEN T E R Y By H. c. Dix University of Nebraska College of Medicine Omaha, N~braska April 1934 Preface This paper is presented to the University of Nebraska College of MediCine to fulfill the senior requirements. The subject of amoebic dysentery wa,s chosen due to the interest aroused from the previous epidemic, which started in Chicago la,st summer (1933). This disea,se has previously been considered as a tropical disease, B.nd was rarely seen and recognized in the temperate zone. Except in indl vidu8,ls who had been in the tropics previously. In reviewing the literature, I find that amoebio dysentery may be seen in any part of the world, and from surveys made, the incidence is five in every hun- dred which harbor the Entamoeba histolytlca, it being the only pathogeniC amoeba of the human gastro-intes tinal tract. -
Plesiomonas Shigelloides S000142446 Serratia Plymuthica
0.01 Plesiomonas shigelloides S000142446 Serratia plymuthica S000016955 Serratia ficaria S000010445 Serratia entomophila S000015406 Leads to highlighted edge in Supplemental Phylogeny 1 Xenorhabdus hominickii S000735562 0.904 Xenorhabdus poinarii S000413914 0.998 0.868 Xenorhabdus griffiniae S000735553 Proteus myxofaciens S000728630 0.862 Proteus vulgaris S000004373 Proteus mirabilis S000728627 0.990 0.822 Arsenophonus nasoniae S000404964 OTU from Corby-Harris (Unpublished) #seqs-1 GQ988429 OTU from Corby-Harris et al (2007) #seqs-1 DQ980880 0.838 Providencia stuartii S000001277 Providencia rettgeri S000544654 0.999 Providencia vermicola S000544657 0.980 Isolate from Juneja and Lazzaro (2009)-EU587107 Isolate from Juneja and Lazzaro (2009)-EU587113 0.605 0.928 Isolate from Juneja and Lazzaro (2009)-EU587095 0.588 Isolate from Juneja and Lazzaro (2009)-EU587101 Providencia rustigianii S000544651 0.575 Providencia alcalifaciens S000127327 0.962 OTU XDS 099-#libs(1/0)-#seqs(1/0) OTU XYM 085-#libs(13/4)-#seqs(401/23) 0.620 OTU XDY 021-#libs(1/1)-#seqs(3/1) Providencia heimbachae S000544652 Morganella psychrotolerans S000721631 0.994 Morganella morganii S000721642 OTU ICF 062-#libs(0/1)-#seqs(0/7) Morganella morganii S000129416 0.990 Biostraticola tofi S000901778 0.783 Sodalis glossinidius S000436949 Dickeya dadantii S000570097 0.869 0.907 0.526 Brenneria rubrifaciens S000022162 0.229 Brenneria salicis S000381181 0.806 OTU SEC 066-#libs(0/1)-#seqs(0/1) Brenneria quercina S000005099 0.995 Pragia fontium S000022757 Budvicia aquatica S000020702 -
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. -
Use of the Diagnostic Bacteriology Laboratory: a Practical Review for the Clinician
148 Postgrad Med J 2001;77:148–156 REVIEWS Postgrad Med J: first published as 10.1136/pmj.77.905.148 on 1 March 2001. Downloaded from Use of the diagnostic bacteriology laboratory: a practical review for the clinician W J Steinbach, A K Shetty Lucile Salter Packard Children’s Hospital at EVective utilisation and understanding of the Stanford, Stanford Box 1: Gram stain technique University School of clinical bacteriology laboratory can greatly aid Medicine, 725 Welch in the diagnosis of infectious diseases. Al- (1) Air dry specimen and fix with Road, Palo Alto, though described more than a century ago, the methanol or heat. California, USA 94304, Gram stain remains the most frequently used (2) Add crystal violet stain. USA rapid diagnostic test, and in conjunction with W J Steinbach various biochemical tests is the cornerstone of (3) Rinse with water to wash unbound A K Shetty the clinical laboratory. First described by Dan- dye, add mordant (for example, iodine: 12 potassium iodide). Correspondence to: ish pathologist Christian Gram in 1884 and Dr Steinbach later slightly modified, the Gram stain easily (4) After waiting 30–60 seconds, rinse with [email protected] divides bacteria into two groups, Gram positive water. Submitted 27 March 2000 and Gram negative, on the basis of their cell (5) Add decolorising solvent (ethanol or Accepted 5 June 2000 wall and cell membrane permeability to acetone) to remove unbound dye. Growth on artificial medium Obligate intracellular (6) Counterstain with safranin. Chlamydia Legionella Gram positive bacteria stain blue Coxiella Ehrlichia Rickettsia (retained crystal violet). -
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. -
United States Patent (10) Patent No.: US 7820,184 B2 Stritzker Et Al
USOO782O184B2 (12) United States Patent (10) Patent No.: US 7820,184 B2 Stritzker et al. (45) Date of Patent: Oct. 26, 2010 (54) METHODS AND COMPOSITIONS FOR 5,833,975 A 1 1/1998 Paoletti et al. ............. 424.93.2 DETECTION OF MICROORGANISMS AND 5,976,796. A 1 1/1999 Szalay et al. ................... 435/6 SirNRTREATMENT OF DISEASES AND 6,025,155 A 2/2000 Hadlaczky et al. ......... 435/69.1 6,045,802 A 4/2000 Schlom et al. ........... 424,199.1 (75) Inventors: Jochen Harald Stritzker, Kissing (DE); 6,077,697 A 6/2000 Hadlaczky et al. 435/1723 Phil Hill, West Bridgford (GB); Aladar 6,080,849 A 6/2000 Bermudes et al. .......... 536,23.7 A. Szalay, Highland, CA (US); Yong A. 6,093,700 A 7/2000 Mastrangelo et al. ......... 514,44 Yu, San Diego, CA (US) 6,099,848. A 8/2000 Frankel et al. ........... 424,246.1 6,106,826 A 8/2000 Brandt et al. .............. 424.93.2 (73) Assignee: stylus Corporation, San Diego, CA 6, 190,657 B1 2/2001 Pawelek et al. ............ 424,931 6,217,847 B1 4/2001 Contaget al. ................ 4249.1 (*) Notice: Subject to any disclaimer, the term of this 6,232,523 B1 5/2001 Tan et al. ...................... 800, 10 patent is extended or adjusted under 35 6,235,967 B1 5/2001 Tan et al. ...................... 800, 10 U.S.C. 154(b) by 362 days. 6,235,968 B1 5/2001 Tan et al. ...................... 800, 10 6,251,384 B1 6/2001 Tan et al.