[Genetic mechanisms of cell differentiation].
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OBJECTIVE--To compare the accuracy of clinical epidemiologic findings with results of molecular epidemiologic analysis in identifying the source of recurrent epidemics of erythromycin-resistant Staphylococcus aureus (ERSA) infections in a well-baby nursery. DESIGN--Epidemic investigations with retrospective and prospective microbiological surveillance. Staphylococcus aureus isolates were evaluated by plasmid analysis and genotyping. SETTING--A well-baby nursery in a 700-bed university teaching hospital with approximately 250 deliveries per month. PATIENTS--Newborn infants who developed ERSA infections during 1990 and 1991. INTERVENTION--Traditional infection control measures, including cohorting of infected infants and hand washing, were implemented. Personnel were cultured for nasal carriage of S aureus during both epidemics. Employees carrying ERSA were removed from the nursery and treated with mupirocin. RESULTS--In the first epidemic, 15 infants were infected with ERSA. A nursing assistant who cared for most of the infants was found to be a carrier of ERSA. She was removed from the nursery and the epidemic resolved. Fifteen months after the first epidemic ended, an epidemic that involved 11 infants began. The attending physician had a facial furuncle and was found to be a carrier of ERSA. The physician was treated and the epidemic resolved. Plasmid and genotyping showed the ERSA organisms from both epidemics were the same. The employee implicated in the first epidemic did not have the epidemic strain, but the physician who attended during both epidemics did. CONCLUSIONS--Traditional epidemic investigations may lead to false conclusions that can only be recognized with molecular epidemiologic techniques. For these techniques to be useful in the control of outbreaks, plasmid analysis and/or genotyping must be readily available.
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Some R factors, like some colicin factors, confer partial protection against the bactericidal effect of ultraviolet (UV) irradiation. Of 31 plasmids (17 R, 3 col, and 11 R-col factors) tested in Escherichia coli K-12, 15 protected, 11 had little or no effect, and 5 caused increased UV susceptibility. The effect of representative plasmids was qualitatively the same in K-12 of wild-type UV sensitivity, lambda-lysogenic or non-lysogenic, and in UV-sensitive mutants of classes uvrA, uvrB, uvrC, and recA (except that a sensitizing factor did not increase the sensitivity of two recA hosts). It is inferred that the UV-protecting effect of some plasmids does not result from their specifying enzymes similar to those deficient in such mutants. UV killing of multiply auxotrophic K-12, of wild-type sensitivity or recA or uvrC, was reduced by deprivation of required amino acids for 2 hr before irradiation, and further reduced if "starvation" was continued for 2 hr after irradiation. The plasmids tested in these conditions produced qualitatively the same effects as in nonstarved cells-except that in K-12 of wild-type UV sensitivity the effect of protecting plasmids was reversed (i.e. they caused decreased survival) when the cells were starved after irradiation. Two UV-protecting R factors reduced the ability of HCR(+) K-12 to support growth of irradiated phage T1.
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