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Journal Article IELTS: global implications of curriculum and materials design Get access Craig Wallace Craig Wallace Currently Director of the ELS Language Centre at Charles Sturt University in Sydney, Australia. In addition to TESOL qualifications he has an MA in Educational Administration specializing in ELT. He has worked extensively in tertiary education in the Arabian Gulf, Australia, New Zealand, and Europe. His current research interests include the effect of first language instruction methods on Middle Eastern students' literacy performance, and the implications of quality processes in the management of ELT contexts. Search for other works by this author on: Oxford Academic Google Scholar ELT Journal, Volume 51, Issue 4, October 1997, Pages 370–373, https://doi.org/10.1093/elt/51.4.370 Published: 01 October 1997 Article history Received: 01 September 1996 Published: 01 October 1997

The effects of culture filtrates of Escherichia coli were studied in perfused canine jejunal Thiry-Vella loops and in ligated segments of rabbit small bowel.The enterotoxigenic E. coli strain employed was isolated from the jejunum of a man with acute cholera-like diarrhea in Calcutta.A culture filtrate of this strain demonstrated enterotoxic activity which was partially heat-stable.A control E. coli strain yielded no enterotoxic activity.A dose-response curve of the effect of the enterotoxin on canine jejunal absorption or secretion was obtained.The maximum secretory rates obtained were about 25 % of those produced by cholera enterotoxin.The effect upon jejunal absorption was maximally developed within the first 90 min of exposure and disappeared equally rapidly, except at the highest doses studied, after removal of the enterotoxin.The E. coli enterotoxin did not increase jejunal clearance of serum albumin or diminish the magnitude of enhanced sodium absorption when the jejunal perfusion solution contained glucose.The electrolyte content of rabbit small bowel fluids induced by E. coli and cholera enterotoxins were similar.Perfusion of E. coli enterotoxin during maximal jejunal secretion induced by cholera enterotoxin did not further increase the secretory rate, suggesting that the two enterotoxins may act upon the same secretory mechanism.Repeated jejunal challenge with E. coli enterotoxin over a period of 8 weeks led to no decrease in jejunal responsiveness to the enterotoxin.The time course and dose response of E. coli enterotoxin upon jejunal function may explain differences in the clinical course of human diarrhea due to enterotoxigenic E. coli and Vibrio cholerae.There is increasing evidence that some strains of Escherichia coli are enterotoxigenic and that these strains cause a portion of the previously unexplained acute diar-

Journal Article Stimulation of Intestinal Secretion In Vitro by Culture Filtrates of Escherichia coli Get access Qais Al-Awqati, Qais Al-Awqati From the Department of Medicine, The Johns Hopkins Hospital, Baltimore, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Craig K. Wallace, Craig K. Wallace From the Department of Medicine, The Johns Hopkins Hospital, Baltimore, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar William B. Greenough, III William B. Greenough, III From the Department of Medicine, The Johns Hopkins Hospital, Baltimore, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 125, Issue 3, March 1972, Pages 300–303, https://doi.org/10.1093/infdis/125.3.300 Published: 01 March 1972 Article history Received: 21 May 1971 Revision received: 29 October 1971 Published: 01 March 1972

Complete recovery balance studies on six infants with severe cholera are reported. Supporting data from a larger group of children with cholera, with particular reference to stool and small intestinal fluid composition, are also reported. The mean and range (in parentheses) for net retention at the end of the balance studies were: water, 96 gm (47—119); sodium, 10.5 mM (5.3—16.7); chloride, 8.9 mM (5.8—12.5); and potassium, 6.5 mM (4.3—9.7); all values are per kilogram of final body weight. Mean values for average evaporative water losses over day and night ranged from 31 gm to 63 gm/kg/24 hours. Stool output requiring parenteral replacement continued for 24 to 60 hours in five of six patients, and 48-hour stool output equaled 1:3 to 22% of final body weight. Stool composition in pediatric cholera is compared to that in infantile diarrhea and adult cholera. Significant differences from each of the latter two are described in this paper.

Intravenous replacement of the diarrhoeal fluid and electrolyte losses to restore a physiological state of hydration is well established as the basis for successful management of cholera patients. The use of oral tetracycline as an adjunct in reducing the volume and duration of diarrhoea, as well as eradicating the vibrio from the gastrointestinal tract, has been proven beneficial. An optimal dose schedule has not been established previously, and clinical or bacteriological relapses have been generally reported. Chloramphenicol and sulfaguanidine have also been mentioned as adjuncts. The present report shows that 3 g or 4 g of tetracycline in one of 3 dose schedules were predictably efficacious. Chloramphenicol, while of benefit, was not as effective and sulfaguanidine was of little benefit compared with the tetracycline regimens.

Editorial Notes1 July 1968Antibiotic Drugs in CholeraCRAIG K. WALLACE, M.D., EUGENE J. GANGAROSA, M.D.CRAIG K. WALLACE, M.D.Search for more papers by this author, EUGENE J. GANGAROSA, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-69-1-166 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA cholera pandemic, caused by Vibrio cholerae biotype El Tor, has spread from its endemic focus in Indonesia since 1960. Southeast and South Asia have been affected, and even now the Middle East is threatened. There is great concern about further extension by means of rapid ground and air travel from multiple-infected foci and a totally unpredictable pattern of geographic spread. Cholera terrorizes a population. It strikes swiftly. Mortality may exceed 60%, especially where medical facilities are inundated and practitioners are unfamiliar with treatment.Therapy has been simple and dramatically successful since Watten and coworkers (1) introduced the concept that...References1. WATTENMORGANSONGKHLAVANIKIATIPHILLIPS RHFMYBRA: Water and electrolyte studies in cholera. J. Clin. Invest. 38: 1879, 1959. CrossrefMedlineGoogle Scholar2. WALLACEFABIEMANGUBATVELASCOJUINIOPHILLIPS CKAEOECRA: The 1961 cholera epidemic in Manila, Republic of the Philippines. Bull. WHO 30: 795, 1964. MedlineGoogle Scholar3. CARPENTERSACKMONDALMITRA CCRBAPP: Tetracycline therapy in cholera. J. Indian Med. Ass. 43: 309, 1964. MedlineGoogle Scholar4. GREENOUGHGORDONROSENBERGBENENSONDAVIES WBRSISASBJ: Tetracycline in the treatment of cholera. Lancet 1: 355, 1964. CrossrefMedlineGoogle Scholar5. LINDENBAUMGREENOUGHISLAM JWBMR: Antibiotic therapy of cholera. Bull. WHO 36: 871, 1967. MedlineGoogle Scholar6. LINDENBAUMGREENOUGHISLAM JWBMR: Antibiotic therapy of cholera in children. Bull. WHO 37: 529, 1967. MedlineGoogle Scholar7. WALLACECARPENTERMITRASACKKHANRAWERNERDUFFYOLEINICKLEWIS CKCCPPRBSRASTPAGW: Oral tetracycline therapy in cholera. Trans. Roy. Soc. Trop. Med. Hyg. 59: 621, 1965. CrossrefGoogle Scholar8. GANGAROSASAGHARIEMILESIADAT EJHJH: Detection of Vibrio cholerae biotype El Tor by purging. Bull. WHO 34: 363, 1966. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAntimicrobial drugs for treating cholera 1 July 1968Volume 69, Issue 1Page: 166-167KeywordsAntibioticsCholeraDrugsMortalityVibrio cholerae ePublished: 1 December 2008 Issue Published: 1 July 1968 PDF downloadLoading ...

Forty-three cholera patients have been investigated during convalescence as possible asymptomatic vibrio carriers, thirty-four in the immediate postinfection period, eight approximately 1 year later, and one on both occasions. Duodenal intubation and purging were performed in twenty-eight cases, intubation alone in four studies, and purging alone in twelve studies. Two asymptomatic vibrio carriers were found. One patient had positive stool cultures for Vibrio cholerœ after purging with magnesium sulphate on seven occasions over a 23-week period, starting 9 days after his last routine positive rectal swab culture. During the entire 23 weeks he had negative stool cultures except after purging. The second patient was first intubated on the 4th day after his last positive stool culture and on two occasions over a 2-week convalescent period had V. cholerœcultured from the resultant duodenal aspirate only after being given intravenous cholecystokinin. After both duodenal aspirations, purges by magnesium sulphate also yielded vibrio-positive stools. All subsequent specimens following intubation and purging were negative for vibrios. These two patients, neither of whom received antibiotic therapy, are too few to confirm the efficacy of antibiotics in eradicating vibrios from the cholera patient. The observations do indicate that the gallbladder may harbour vibrios in convalescent cholera patients. The existence of such carriers may well explain recurrence and transmission of cholera.

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Abstract : Tracer studies of fluid compartment changes were made possible during the 1961 cholera outbreak in Manila, Philippine Islands. TBW, Nae, ECF and intracellular fluid shifts were measured during rehydration therapy and durring controlled periods of diarrheal dehydration. When fecal, urine and estimated insensible losses are replaced by equivalent volumes of isotonic NaCL at a plasma specific gravity of 1.024, some degree of sodium loading occurs. For otherwise normal patients, this would lie within reasonable range of renal compensation. At high fecal outputs, the tracer sodium initially excreted into the gut appears not to be reabsorbed, and it is delayed several hours in appearing in stool. Cholera dehydration causes marked depletion of extracellular water with comparatively small losses from intracellular water. (Author)