Multiple antimicrobial resistance in pneumococci was detected in Johannesburg in July, 1977, and prompted an investigation of the prevalence of resistant strains in two hospitals. Carriers of Types 6A and 19A penicillin-resistant pneumococci, resistant to antibiotic concentrations ranging between 0.12 and 4 microgram per milliliter were found in 29 per cent of 543 pediatric patients and 2 per cent of 434 hospital staff members. Multiply resistant Type 19A strains, resistant to beta-lactam antibiotics, erythromycin, clindamycin, tetracycline and chloramphenicol, were isolated from 128 carriers, and were responsible for bacteremia in four patients. Isolates from 40 other carriers were resistant to penicillin alone or to penicillin and chloramphenicol or to penicillin, chloramphenicol and tetracycline. Pneumococci can be screened for penicillin resistance with a modified Kirby--Bauer technic; the strains with zones of less than 35 mm around 6-microgram penicillin disks or less than 25 mm around 5-microgram methicillin disks should be tested for sensitivity to penicillin by measurements of minimum inhibitory concentration.
SUMMARY The pathogenicity of classical enteropathogenic Escherichia coli strains of human origin was investigated in gnotobiotic piglets. One to two day old piglets in groups of four were infected perorally with approximately 10 colony forming units of one of eight enteropathogenic E coli strains or a non-pathogenic control strain. Animals were necropsied 24 or 48 hours after infection and their intestines were subjected to histological examination, quantitative bacterial culture and estimation of lactase activity. Four enteropathogenic E coli strains caused mild to moderate diarrhoea in nine of the 16 piglets inoculated with them. Piglets given two of these strains later became moribund. One enteropathogenic E coli strain caused a severe illness unaccompanied by diarrhoea. Inflammation of the intestinal mucosa occurred with all eight enteropathogenic E coli strains, but not with the control strain. Pathological changes were most pronounced in the distal ileum and colon and adherent bacteria were seen on the surface of the inflamed mucosa. The extent of the inflammatory response in infected piglets for the most part paralleled the severity of the clinical signs, the degree of bacterial colonisation and the reduction in lactase activity. Electron microscopic examination of tissue from piglets infected with three different strains showed that bacterial adherence to the apical plasma membrane of epithelial cells was accompanied by distinctive ultrastructural changes. These included degeneration of the microvillous brush border, together with cupping and pedestal formation of the plasma membrane at sites of bacterial attachment. The same changes have been seen in naturally occuring enteropathogenic E coli diarrhoea in humans and rabbits. The combined clinical and pathological findings indicate that the neonatal gnotobiotic piglet is a suitable model of infection with enteropathogenic E coli.Escherichia coli is both the predominant member of the normal aerobic colonic flora and a prominent cause of gastroenteritis.
Summary. Nine strains of Escherichia coli isolated from infants with diarrhoea between 1947 and 1960 and designated " enteropathogenic " were examined for phenotypic and genetic characters associated with virulence. Each strain belonged to a different serotype. All the isolates were historically significant in that they were amongst the first strains of E. coli reported to be causally associated with infantile diarrhoea. Five strains possessed the virulence properties of class I enteropathogenic E. coli (EPEC). All these strains were isolated originally from symptomatic children during outbreaks of diarrhoea. Two isolates from sporadic cases of diarrhoea fulfilled the criteria for classification as class I1 EPEC. One strain was identified as enteroaggregative E. coli and the other carried no known virulenceassociated properties. These findings indicate that most early isolates of E. coli which were designated "enteropathogenic " were indeed EPEC, as currently defined.
Twelve strains of Escherichia coli previously reported to cause diarrhea in rabbits were examined for properties associated with virulence. Ten strains met the criteria for classification as enteropathogenic E. coli in that they were diarrheagenic strains that evoked attaching-effacing lesions in the small intestine and did not produce detectable enterotoxins or cytotoxins. These bacteria exhibited a variety of patterns when investigated for adherence to HEp-2 epithelial cells. Although several strains displayed localized and/or diffuse adherence to epithelial cells, they did not hybridize with DNA probes that recognize the genes responsible for these phenotypes in diarrheagenic E. coli from humans. The bacteria also varied in their ability to bind to erythrocytes and intestinal brush borders from various animal species. Six strains adhered to rabbit brush borders; two of these also adhered to brush borders from other animals. Two strains that did not adhere to rabbit brush borders adhered to those from guinea pigs or sheep. Only one of the strains investigated carried AF/Ri fimbriae, which are believed to govern the host specificity of this category of diarrheagenic E. coli. This strain was E. coli RDEC-1, which remains the only E. coli strain to date that is known to carry fimbriae of this type. The results indicate that although diarrheagenic E. coli strains from rabbits may have common properties associated with the ability to produce attaching-effacing lesions, they differ from each other and from enteropathogenic E. coli of humans in terms of some of the adhesins that mediate binding to eukaryotic cells.
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