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Biomedical subjects

B E Murray

Publications and source records attributed to B E Murray.

At least 163 records · Page 9Linked to original sources
PubMed1984

Evidence for an epidemic trimethoprim-resistance plasmid in fecal isolates of Escherichia coli from citizens of the United States studying in Mexico.

A previous study revealed the emergence of high-level resistance to trimethoprim-sulfamethoxazole in strains of Escherichia coli isolated from 95% of students from the United States who were taking either trimethoprim alone or trimethoprim-sulfamethoxazole for prophylaxis of travelers' diarrhea while in Guadalajara, Mexico. Many of these strains were subsequently demonstrated to cotransfer resistance to trimethoprim along with that to streptomycin and ampicillin. The present study demonstrated that at least 12 (60%) of 20 transferable (tra+) trimethoprim-resistance plasmids studied possessed both an identical Hind III restriction pattern and type I dihydrofolate reductase genes. Donor strains were shown to be distinct; this finding suggested that a common tra+ trimethoprim-resistance plasmid was widely disseminated among E. coli strains in Guadalajara. These results may explain in part the surprising degree of resistance encountered in trimethoprim-consuming persons in that region.

Conjugation, Genetic↗
PubMed1984

Ribosomal resistance of clinical enterococcal to streptomycin isolates.

The mechanism of high-level resistance to streptomycin was studied in 12 clinical isolates of Streptococcus faecalis. Six strains produced streptomycin-modifying enzymes. Each of three enzyme-negative strains tested demonstrated ribosomal resistance to streptomycin. Lack of ribosomal susceptibility is a significant cause of high-level streptomycin resistance among clinical enterococcal isolates.

Drug Resistance, Microbial↗
PubMed1983

Transfer of trimethoprim resistance from fecal Escherichia coli isolated during a prophylaxis study in Mexico.

Forty-one of 100 trimethoprim-resistant fecal isolates of Escherichia coli isolated during a diarrhea prophylaxis study transferred trimethoprim resistance to an E. coli K12 derivative at frequencies ranging from 1 x 10(-7) to 2 x 10(-2). Analysis of these transconjugants, after attempting to select those that had received only one plasmid, revealed that 34 (83%) were resistant to trimethoprim plus only one or two of seven other antimicrobial agents tested, most often ampicillin and/or streptomycin. In contrast, 91% of the donor strains were resistant to four or more antimicrobial agents. Plasmid analysis demonstrated that a 35-megadalton plasmid was present in 35 transconjugants and was usually associated with resistance to trimethoprim, streptomycin, and ampicillin; 19 transconjugants had only a 35-megadalton plasmid and were resistant to only these three antimicrobial agents, raising the possibility that a common plasmid was present in many strains. Although resistance to multiple antimicrobial agents could be transferred to the K12 recipient, resistance to more than three agents was seldom mediated by a single plasmid. The high degree of transferability of trimethoprim resistance from these fecal isolates of E. coli emphasizes the potential for the dissemination of genes carrying trimethoprim resistance.

Anti-Bacterial Agents↗
PubMed1983

High-level resistance to gentamicin in clinical isolates of enterococci.

Nine clinical isolates of Streptococcus faecalis from a university hospital were found to be resistant to high levels (minimal inhibitory concentration, greater than 2,000 micrograms/ml) of gentamicin, tobramycin, amikacin, streptomycin, and kanamycin. The high-level resistance to these aminoglycosides and resistance to penicillin-aminoglycoside synergism were transferable by conjugation to a susceptible recipient strain. In three strains tested, the aminoglycoside resistance was mediated by four aminoglycoside-modifying enzymes: a 3'-phosphotransferase transferred from two strains, a 2"-phosphotransferase and a 6'-acetyltransferase transferred from all three strains, and a streptomycin adenylyltransferase transferred from two strains. This is the first report of the occurrence of high-level gentamicin resistance in enterococcal isolates from the United States.

Aminoglycosides↗
PubMed1983

Bacteriological studies of the enteric flora of patients treated with bicozamycin (CGP 3543/E) for acute nonparasitic diarrhea.

During a therapeutic trial of bicozamycin (BI) for traveler's diarrhea, aerobically grown, gram-negative bacteria, predominantly Escherichia coli, were decreased by 2 to 3 logs per g of stool; the number of BI-resistant gram-negative bacteria did not increase. Resistant species were most often Citrobacter freundii, Klebsiella pneumoniae, and Morganella morganii, and few BI-resistant E. coli strains were isolated. Cross-resistance between BI and other antimicrobial agents was not found. Resistance to BI could not be transferred or mobilized to an E. coli K-12 recipient.

Acute Disease↗
PubMed1983

Enterococci from Bangkok, Thailand, with high-level resistance to currently available aminoglycosides.

Enterococcal endocarditis is usually treated with a combination of a penicillin and an aminoglycoside. Recent reports have documented the emergence of enterococci in France with high-level resistance to gentamicin, tobramycin, and kanamycin and the emergence of strains in Houston, Tex. with high-level resistance to all of these drugs and streptomycin. In this study, we examined strains from a geographic area where newer aminoglycosides have been less commonly used. Of 125 distinct patient isolates, 18 (14%) were resistant to greater than 2,000 micrograms of gentamicin and most other aminoglycosides per ml. Four of these strains transferred gentamicin resistance to a laboratory recipient. One strain, chosen for further study, was resistant to synergism between penicillin and gentamicin, tobramycin, kanamycin, streptomycin, and amikacin and demonstrated the following enzymatic activities: 3'- and 2"-aminoglycoside phosphotransferases, 6'-aminoglycoside acetyltransferase, and adenylylation of streptomycin. Optimal therapy for endocarditis caused by such highly resistant strains is currently unknown.

Aminoglycosides↗
PubMed1983

CFA/I-ST plasmids: comparison of enterotoxigenic Escherichia coli (ETEC) of serogroups O25, O63, O78, and O128 and mobilization from an R factor-containing epidemic ETEC isolate.

Colonization factor antigen I (CFA/I) plays an important role in the pathogenesis of diarrhea due to enterotoxigenic Escherichia coli. In this study, we examined 11 CFA/I+ enterotoxigenic E. coli from serogroups O25, O63, O78, and O128 and found that with all strains, spontaneous loss of CFA/I was associated with the loss of heat-stable toxin (ST) and with the loss of a single plasmid ranging in size from 54 to 60 megadaltons; when heat-labile toxin was lost, this was associated with the loss of another plasmid. The R factor of one strain, TX432 (O78:H12:CFA/I+; ST+), was found to mobilize the CFA/I-ST plasmid into E. coli K-12 at a frequency of 20%. These studies provide further evidence that CFA/I production is plasmid mediated in enterotoxigenic E. coli belonging to serogroups O25, O63, O78, and O128.

Antigens, Bacterial↗
PubMed1983

ST:LT:CFA/II plasmids in enterotoxigenic Escherichia coli belonging to serogroups O6, O8, O80, O85, and O139.

Colonization factor antigen II-producing enterotoxigenic Escherichia coli serotypes possessed at least one large plasmid. Loss of colonization factor antigen II correlated with either complete or partial loss of the large plasmid. Complete loss of the plasmid always correlated with complete loss of enterotoxin production. Three of five deletion events also correlated with the loss of toxin production.

Antigens, Bacterial↗
PubMed1983

Transferable beta-lactamase. A new mechanism for in vitro penicillin resistance in Streptococcus faecalis.

Although enterococci are relatively resistant to penicillin, the mechanism of resistance is largely unknown and enzymatic inactivation does not play a role. In this study, an isolate of Streptococcus faecalis was found to have beta lactamase activity resulting in complete inactivation of penicillin. With a high inoculum, this strain was resistant to greater than 1,000 micrograms/ml of penicillin. Penicillin resistance and beta lactamase activity were transferred by conjugation at a high frequency to an enterococcal laboratory recipient strain together with two plasmids of molecular size 34 X 10(6) and 56 X 10(6), thus demonstrating the emergence of plasmid-mediated penicillin resistance in the genus Streptococcus.

Enterococcus faecalis↗
PubMed1982

Emergence of high-level trimethoprim resistance in fecal Escherichia coli during oral administration of trimethoprim or trimethoprim--sulfamethoxazole.

The effect of daily administration of trimethoprim (TMP), trimethoprim--sulfamethoxazole (TMP--SMX), or placebo on aerobically grown fecal gram-negative bacteria was monitored in 136 students from the United States during a two-week diarrhea-prevention study in Mexico. Unlike patients in other studies with these agents, who had urinary-tract infection or granulocytopenia, most persons in this study had no change in total fecal Enterobacteriaceae and had high-level TMP and SMX resistance in virtually all these strains. Escherichia coli was the predominant TMP-resistant organism isolated; 96 per cent of 165 TMP-resistant Esch. coli isolates were resistant to at least four antimicrobial agents, and 25 per cent were resistant to seven. TMP resistance was transferable in 40 ot 100 strains tested. Despite the lack of TMP resistance in other studies of prophylaxis, our results clearly demonstrate the remarkable capacity for emergence and dissemination of resistance to this agent.

Anti-Bacterial Agents↗