Frequent acquisition of multiple strains of methicillin-resistant Staphylococcus aureus by healthcare workers in an endemic hospital environment.

Methicillin-resistant Staphylococcus aureus (MRSA) has been an endemic nosocomial pathogen at the VA medical center (VAMC) in Providence, Rhode Island since 1981. From 1985 to 1987, more than 30% of all unique S aureus isolates were methicillin resistant. To evaluate the frequency of acquisition of MRSA isolates by healthcare workers, we compared the antimicrobial susceptibility patterns, multilocus enzyme genotypes and plasmid profiles of isolates recovered from nasal and hand cultures from VAMC nurses and house staff on rotation at the VAMC with those of clinical isolates from patients at the VAMC and four other affiliated hospitals. Fifty-six percent of ward nurses cultured (n = 112) were colonized with S aureus, of which 65% was methicillin resistant. Six isolates of MRSA were identified on the initial culturing of house staff (n = 65); 16 MRSA isolates were recovered at the end of a four-week rotation (p less than .02). Phenotypic and genotypic analyses demonstrated that numerous distinct MRSA strains were recovered in the study period. The incidence of MRSA among clinical isolates at the VAMC and affiliated institutions was remarkably constant throughout the three-year study period. Moreover, despite regularly sharing resident physicians, interns and medical students, MRSA isolates were commonly recovered at the other university-affiliated hospitals. Our study failed to reveal evidence of significant interhospital transmission of MRSA isolates by healthcare workers. While healthcare workers may contribute to the dissemination of MRSA within institutions, they appear to be less important in spreading MRSA between institutions.

Survey of purported virulence factors of Escherichia coli isolated from blood, urine and stool.

One hundred randomly selected urinary and blood isolates and 50 stool isolates of Escherichia coli were analyzed for phenotypic characteristics which may contribute to their virulence potential. Bacteremic isolates were more likely to have K1 capsules and express mannose-sensitive hemagglutination compared to stool isolates. Blood-stream isolates more frequently contained complete 0 side-chains in their lipopolysaccharide layer and less frequently exhibited mannose-resistant hemagglutination when compared to urinary isolates. Total plasmid content, hemolysin, total colicin and colicin V production were not significantly increased in Escherichia coli from blood or urine when compared to those recovered from stool.

Analysis of an outbreak of penicillinase-producing Neisseria gonorrhoeae in Rhode Island, 1987.

In June of 1987, an outbreak of penicillinase-producing Neisseria gonorrhoeae (PPNG) occurred in Rhode Island. PPNG persists as an endemic pathogen despite a concerted statewide effort to eradicate the organism. Detailed analysis of PPNG isolates demonstrated that multiple strains are circulating concurrently, complicating control measures.

Aerobactin and alpha-hemolysin as virulence determinants in Escherichia coli isolated from human blood, urine, and stool.

Because iron acquisition is essential to the survival of invasive strains of Escherichia coli, the frequency of two potential iron acquisition systems, aerobactin and hemolysin production, were compared in E. coli isolated from human blood (n = 95), urine (n = 100), and stool (n = 50). By phenotypic and genotypic methods, the prevalence of hemolysin production was 22% in bacteremic, 38% in urinary, and 22% in fecal isolates of E. coli. Aerobactin production was detected in 76% of blood and in 73% of urinary isolates but in only 52% of fecal isolates (P less than .01). A reciprocal relationship was found in blood isolates between aerobactin and hemolysin; the majority of blood isolates (55%) that lacked aerobactin were hemolytic, whereas only 14% of blood isolates that expressed aerobactin were hemolytic (P less than .0001). Aerobactin may be the principal mechanism of iron acquisition in extraintestinal isolates of E. coli, and hemolysin may serve as an alternative mechanism in the absence of aerobactin genes.

Modification of homogeneous resistance in a methicillin-resistant strain of Staphylococcus aureus by acquisition of a beta-lactamase encoding plasmid.

Nearly all clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA) are heterogeneously resistant and produce beta-lactamases which generally are plasmid mediated. In order to study the role of beta-lactamase plasmids in the expression of methicillin resistance, a beta-lactamase plasmid from Enterococcus faecalis HH22 (pBEM10) was transferred into a homogeneously resistant, beta-lactamase-negative strain of MRSA (MUSC284). By single disc diffusion testing at 42 degrees C, beta-lactamase producing transconjugants (SA-MM1) were found to be more susceptible than the parent strain to methicillin, imipenem, SCH 34343 and cloxacillin, but more resistant to piperacillin. The heterogeneity observed in transconjugants was not affected by the addition of clavulanic acid, indicating that beta-lactamase itself was not responsible for this effect. By population analysis over 50% of MUSC284 colonies and less than 1% of SA-MM1 colonies remained viable after incubation at 42 degrees C in agar plates containing 25 mg/l of cloxacillin. Cured derivatives of SA-MM1 reverted to homogeneous resistance to beta-lactam antibiotics as observed in the initial parenteral strain MUSC284. Thus, the introduction of a beta-lactamase coding plasmid into a homogeneously resistant MRSA yielded transconjugants which resembled heterogeneously resistant strains of MRSA. These results suggest that regulatory genes, capable of altering the expression of methicillin resistance, may be located on beta-lactamase plasmids commonly found in these organisms.