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1103IMPLICATION OF CLOSTRIDIUM SORDELLII ANTITOXINDepartment Ann U.S.A 1103IMPLICATION OF CLOSTRIDIUM SORDELLII ANTITOXINDepartment Ann U.S.A

1103IMPLICATION OF CLOSTRIDIUM SORDELLII ANTITOXINDepartment Ann U.S.A - PDF document

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1103IMPLICATION OF CLOSTRIDIUM SORDELLII ANTITOXINDepartment Ann U.S.A - PPT Presentation

1104were intradermally blue 2 diameters of oedema ofand dye hours according of Evans Each solution tested in at leastand was giving mean least 5 mmfor of tissue diploid Inc with filtrate or solu ID: 414057

1104were intradermally blue (2%) diameters

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1103IMPLICATION OF CLOSTRIDIUM SORDELLII ANTITOXINDepartment Ann U.S.A.R. Department City and Hopkins Baltimore, A toxin(s) been demonstrated in patients antibiotic-toxin(s) was lethal hamsters, vascular skin, was cytotoxic for It neutralised prepared ichia coli, Vibrio the ætiologyantibiotic-induced the 1104were intradermally blue (2%) diameters of oedema, ofand dye hours according of Evans Each solution tested in at leastand was giving mean least 5 mmfor of tissue diploid Inc., with filtrate or solutions and 48 Reactions were gradedno change in positive cells 75-100% disrupted.from in Y-1 Toxicity for hamsters.-All filtrate case within loss, 10 days animals case I. Necropsieshamsters in caecum and and fat, distension, pleural clots the of those 10 Microscopic and of When 100 case incubated P.C.A. before injection, longer (table In-a toxic similar that filtrate noted. observations injected with lil from n (before van-therapy) was hamsters. injection animals 200 filtratequantity from was further could out.Stool specimens case 11 2 and dayswere not in ten hamsters). often hamsters injected with control in well.permeability factor in When were either hours and their by 18-24 factorboth filtrate from case II) that induced oedemaTABLE ANTISERA MORTALITY HAMSTERS INTRAPERITONEALLYfaeces saline or at before intraperitoneal TABLE OF SKIN CULTURESmm average and disrupted; $1 human immune 1105TABLE PROPERTIES OF STOOL FILTRATES IN CULTURESaverage of bluing; Weakly Neg.=normal least mm and of increased permea-mean diameters least 8 mm. were (zero mm the with P.C.A., and sordellii were not altered by with normal horse or produced against Cl. septicum, and Vascular permeability in theseby heat, 10to pH 5 Bluing presentat 6. Trypsinisation not factor but produced by by filtrate from prepared the stool n shereceiving vancomycin did per-meability factor. filtrates, antitoxins,and solutions active. ’Tissue culture assay.-The fromtwo patients diploid corresponded to activity the rab-III). antitoxinwas only produced In thisfrom n as cytotoxicity ofits were pH although ofthis from but did its toxicity.with hamster and skin filtratesprepared mycin solutions, trypsin were out be serially.a those seen city and P.C.A., to coli dilution) not neutralise of from investigation the et heat-labile toxin(s) present inthe patients with colitis and oedema, and increased cytotoxic Toxic properties were in-vitro incubation filtrates clostridial, effect of hamsters, on permeability in and at effective,all resemble properties cause either hæmorrhage.10 tests used might or toxins in the In addition, toxinF.D.A., bit skin, iden-tical those of cases i and (unpublishedpathogenic been has Cl. with a colitis man demonstrated that col-itis be by stool hamsters protected byvancomycin afterthe onset of hours. same disappeared from stool be effective in pseudomembranous colitis.13 review has questioned aetiological Staphylo-coccus colitis ;2 isolate staphylococci from stools do not believe staphylo-the re-sponse to reported previously, hamsters, and of warrants controlled this ofcolitis.report siimulate microbiologi-and toxicological of 1106branous colitis in define clearly Cl. sordellii, organisms, this study was Frederick Infectious the Upjohn reprints should R., Infectious Arbor, Michigan 1. L., G. M. 1952, intern. 1977, 22, 455.R., Devine, B. J., L., Suppl., S111.4. Larson, H. B., R., Tyrrell,i, 1246.Rifkin, Gastroenterology. B. Infect. Evans, G., 9. R. Arseculeratine, N., S. Floyd, Cohn, 1964, 5, 233.R. Silva, J., D. I., Work, O., Abrams,M. Intern. CLOFIBRATE INCREASESHOLDSWORTHD. Bartholomew’s LondonSummary of in were hypertriglyceridæmic before a therapy (2 Plasma-triglycerides significantly triglyceride increased from 1·3±0·2 creases nmol fatty inextractable to nmol fattyconcluded an importantof may the levels treatment mechanism understood. may lipoprotein by demon-of protein-lipase treatment this drug.1-3step for the blood.therapy has beenWe studiedthe effect therapy on and in six patients.years, kg, blood-5-4+0-8 were investigated. admission theocca-sions men were Secondary excess diseaseexcluded. were classified W.H.O. hos-admission. None of the drugtherapy, they diets andof the of day after samples taken by subcutaneous needle biopsy wall lignocaine a to deter-fasting plasma-triglyceride concentration. An (Vitrum) tolerance then with a From test rate constant (k2)clearance of the this shown turnover rate of triglyceride.6 remained clofibrate g twicedaily repeated.vitro was inEarle’s bicarbonate buffer 2.5% serum and (2 U/ml) ath. The assayed for bythe method Krauss substrate emulsion together with fLCi 25lysolecithin for at mum by of an MSE ultrasonic titanium a solution of ml 0.16 pH containing crystalline serum albumin. 250 µ1 substratewas in assay with µ1 normal human37°C 1 and then extracted in Vaughan of upper in Packard liquid was determined by homo-8.6, and homogenate assayed for as Adipose-cell size enabling enzyme as fatty means±S.E.M., significance ferences paired Mean fromthe in-creased on clofi-brate This with an (table).lipase all