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Biomedical subjects

L B Rice

Publications and source records attributed to L B Rice.

At least 37 records · Page 2Linked to original sources
PubMed1999

A polyclonal outbreak of predominantly VanB vancomycin-resistant enterococci in northeast Ohio. Northeast Ohio Vancomycin-Resistant Enterococcus Surveillance Program.

We studied the molecular epidemiology of vancomycin-resistant enterococci (VRE) isolated in northeast Ohio during 1996 and examined the association between isolation of VRE from samples other than stool and antimicrobial purchases for five Cleveland hospitals. Susceptibility testing and pulsed-field gel electrophoresis were used to analyze 363 isolates from individual patients from 13 hospitals. Susceptibility testing indicated that 287 strains (79%) expressed the VanB phenotype and 76 (21%) expressed the VanA phenotype. The outbreak was polyclonal, with 30 total genotypes. Both VanA and VanB VRE demonstrated multiple genotypes. One genotype was present in all hospitals, suggesting spread between hospitals. For five teaching hospitals, rates of isolation from non-stool sources and from blood correlated positively with purchases of ticarcillin/clavulanic acid (P = .005). In summary, this outbreak demonstrates transmission of VRE between several hospitals in a geographic region and suggests that use of certain beta-lactam antibiotics may be associated with an increased prevalence of VRE.

Disease Outbreaks↗
PubMed1999

Emerging issues in antibiotic resistant infections in long-term care facilities.

Managing patients infected with antibiotic resistant bacteria is becoming one of the major clinical obstacles facing physicians who treat patients in long-term care facilities (LTCFs). Penicillin-resistant pneumococci (PRP), vancomycin-resistant enterococci (VRE), gram-negative bacteria that produce extended-spectrum and ampC-type beta-lactamase enzymes, and quinolone-resistant gram-positive and gram-negative bacteria are the major resistant pathogens that are emerging in these settings. The mechanisms responsible for the evolution of these antibiotic resistant organisms (molecular rearrangement of penicillin binding protein genes, acquisition of a mobile genetic element, and point mutation that alter the active site) are reviewed. Vancomycin intermediate Staphylococcus aureus (VISA) and multidrug efflux pumps in gram-negative bacteria are also threatening our most potent antimicrobials. Aggressive screening, education, antibiotic-control measures, and immunization are advocated as important preventive measures. The combined efforts of the medical directors, infection-control personnel, and administrators are needed to stem this problem.

Aged↗
PubMed1999

Antifungal agents: mode of action, mechanisms of resistance, and correlation of these mechanisms with bacterial resistance.

The increased use of antibacterial and antifungal agents in recent years has resulted in the development of resistance to these drugs. The significant clinical implication of resistance has led to heightened interest in the study of antimicrobial resistance from different angles. Areas addressed include mechanisms underlying this resistance, improved methods to detect resistance when it occurs, alternate options for the treatment of infections caused by resistant organisms, and strategies to prevent and control the emergence and spread of resistance. In this review, the mode of action of antifungals and their mechanisms of resistance are discussed. Additionally, an attempt is made to discuss the correlation between fungal and bacterial resistance. Antifungals can be grouped into three classes based on their site of action: azoles, which inhibit the synthesis of ergosterol (the main fungal sterol); polyenes, which interact with fungal membrane sterols physicochemically; and 5-fluorocytosine, which inhibits macromolecular synthesis. Many different types of mechanisms contribute to the development of resistance to antifungals. These mechanisms include alteration in drug target, alteration in sterol biosynthesis, reduction in the intercellular concentration of target enzyme, and overexpression of the antifungal drug target. Although the comparison between the mechanisms of resistance to antifungals and antibacterials is necessarily limited by several factors defined in the review, a correlation between the two exists. For example, modification of enzymes which serve as targets for antimicrobial action and the involvement of membrane pumps in the extrusion of drugs are well characterized in both the eukaryotic and prokaryotic cells.

Amphotericin B↗
PubMed1999

Factors that predict preexisting colonization with antibiotic-resistant gram-negative bacilli in patients admitted to a pediatric intensive care unit.

OBJECTIVE: To predict which patients hospitalized in a pediatric intensive care unit (ICU) are colonized with antibiotic-resistant gram-negative rods on admission. METHODS: Consecutive children admitted to a pediatric ICU over a 6-month period were entered into the study. A questionnaire soliciting information regarding the child's medical history and home environment was completed by the parent or guardian. Nasopharyngeal and rectal cultures were obtained on each of the first 3 days of ICU admission, and organisms resistant to ceftazidime or tobramycin were identified. Only clonally distinct organisms, as confirmed by pulsed field gel electrophoresis, were analyzed. The association between identification of colonization with an antibiotic-resistant gram-negative rod within 3 days of ICU admission and factors included in the questionnaire was tested by chi2 or t test. RESULTS. In 64 (8.8%) of 727 admissions, an antibiotic-resistant gram-negative bacillus was isolated within the first 3 ICU days. More than half were identified on the day of admission. Colonization was associated with two factors related to the patient's medical history, namely, number of past ICU admissions (1.98 vs.87) and administration of intravenous antibiotics within the past 12 months (67.9% vs 28.2%). No association was found between colonization and exposure to oral antibiotics. In addition, factors related to the child's environment were also associated with presumed importation of an antibiotic-resistant gram-negative rod into the ICU. Specifically, residence in a chronic care facility was strongly associated with colonization (28.3% vs 2.6%); exposure to a household contact who had been hospitalized in the past 12 months also predicted colonization (41.7% vs 18.5%). CONCLUSIONS: These data suggest that a profile can be established characterizing children colonized with resistant gram-negative bacilli before admission to a pediatric ICU. Infection control measures may help to contain these potentially dangerous bacteria once they have been introduced into the unit.

Anti-Bacterial Agents↗
PubMed1999

Successful interventions for gram-negative resistance to extended-spectrum beta-lactam antiobiotics.

Antibiotic resistance among nosocomial pathogens in this country's hospitals adds significantly to patient morbidity and mortality, and the cost of health care. Optimism for identifying antimicrobial agents that would "solve the problem" of resistance has been replaced by a much more guarded and realistic view of the battle between humans and pathogenic microorganisms. Efforts now are more appropriately directed toward limiting, rather than completely eliminating, resistance, generally by either infection control or antibiotic control measures, and sometime combinations of the two. Methicillin-oxacillin resistance in Staphylococcus aureus (MRSA) results from the expression of an acquired penicillin-binding protein (PBP 2a) that is not transferable in vitro. In most hospitals, even those with high percentages of MRSA, relatively few resistant clones are identified, suggesting transmission of individual strains throughout the hospital population. Because person-to-person spread is so important in transmission of MRSA, strategies aimed at preventing transmission of the resistant strains are remarkably effective when strictly enforced. Ceftazidime resistance in Enterobacteriaceae results from point mutations within genes that encode widely prevalent and often transferable plasmid-mediated enzymes. In addition, mutations of these genes that allow hydrolysis of cephalosporins usually result in decreased activity against other drugs, including the penicillins and beta-lactamase inhibitors. Effective measures to control ceftazidime-resistant Enterobacteriaceae have as their cornerstone limiting administration of antibiotics that select for the emergence and spread of these mutations, especially ceftazidime. The importance of infection-control techniques in limiting the prevalence of ceftazidime-resistant Enterobacteriaceae is less well established. Methods that are informed by a detailed understanding of the molecular mechanisms of resistance and resistance spread offer the best hope for limiting dissemination of antibiotic-resistant bacteria in a cost-effective manner.

Anti-Bacterial Agents↗
PubMed1998

Transferable, plasmid-mediated vanB-type glycopeptide resistance in Enterococcus faecium.

An approximately 60-kb transferable, vanB-carrying plasmid has been identified in a clinical Enterococcus faecium strain. A similar plasmid has been observed in an unrelated E. faecium strain, suggesting that plasmid transfer of vanB operons occurs in nature and plays a role in the dissemination of VanB-type resistance among strains of E. faecium.

Anti-Bacterial Agents↗
PubMed1998

Genetic linkage and cotransfer of a novel, vanB-containing transposon (Tn5382) and a low-affinity penicillin-binding protein 5 gene in a clinical vancomycin-resistant Enterococcus faecium isolate.

Mechanisms for the intercellular transfer of VanB-type vancomycin resistance determinants and for the almost universal association of these determinants with those for high-level ampicillin resistance remain poorly defined. We report the discovery of Tn5382, a ca. 27-kb putative transposon encoding VanB-type glycopeptide resistance in Enterococcus faecium. Open reading frames internal to the right end of Tn5382 and downstream of the vanXB dipeptidase gene exhibit significant homology to genes encoding the excisase and integrase of conjugative transposon Tn916. The ends of Tn5382 are also homologous to the ends of Tn916, especially in regions bound by the integrase enzyme. PCR amplification experiments indicate that Tn5382 excises to form a circular intermediate in E. faecium. Integration of Tn5382 in the chromosome of E. faecium C68 has occurred 113 bp downstream of the stop codon for the pbp5 gene, which encodes high-level ampicillin resistance in this clinical isolate. Transfer of vancomycin, ampicillin, and tetracycline resistance from C68 to an E. faecium recipient strain occurs at low frequency in vitro and is associated with acquisition of a 130- to 160-kb segment of DNA that contains Tn5382, the pbp5 gene, and its putative repressor gene, psr. The interenterococcal transfer of this large chromosomal element appears to be the primary mechanism for vanB operon spread in northeast Ohio. These results expand the known family of Tn916-related transposons, suggest a mechanism for vanB operon entry into and dissemination among enterococci, and provide an explanation for the nearly universal association of vancomycin and high-level ampicillin resistance in clinical E. faecium strains.

Anti-Bacterial Agents↗
PubMed1998

Transfer of Tn5385, a composite, multiresistance chromosomal element from Enterococcus faecalis.

Tn5385 is a ca. 65-kb element integrated into the chromosomes of clinical Enterococcus faecalis strains CH19 and CH116. It confers resistance to erythromycin, gentamicin, mercuric chloride, streptomycin, tetracycline-minocycline, and penicillin via beta-lactamase production. Tn5385 is a composite structure containing regions previously found in staphylococcal and enterococcal plasmids. Several transposons and transposon-like elements within Tn5385 have been identified, including conjugative transposon Tn5381, composite transposon Tn5384, and elements indistinguishable from staphylococcal transposons Tn4001 and Tn552. The divergent regions of Tn5385 are linked by a series of insertion sequence (IS) elements (IS256, IS257, and IS1216) of staphylococcal and enterococcal origin. The ends of Tn5385 consist of directly repeated copies of enterococcal IS1216. Within the chromosomes of strains CH19 and CH116, Tn5385 has interrupted an open reading frame with substantial homology to previously described alkyl hydrogen peroxide reductase genes. Segments of this open reading frame in both CH19 and CH116 have been deleted, but the amount of deleted DNA differs for the two insertions. Transfer of Tn5385 from both donors into E. faecalis recipients occurs at a low frequency. Two types of transconjugants have been identified. In one type, the target alkyl hydrogen peroxide reductase open reading frame has been deleted, and sequences flanking Tn5385 in the respective donors are carried over to the transconjugants. These data suggest that the mechanism of Tn5385 insertion into the recipient chromosome in these transconjugants was recombination across flanking regions in the donors and homologous sequences in the recipients. The second type of transconjugant appears to have resulted from excision of Tn5385 from the CH19 chromosome by recombination across the terminal IS1216 elements and insertion into the recipient chromosome by recombination across Tn5381 (within Tn5385) and a previously transferred Tn5381 copy in the recipient chromosome. These data confirm that Tn5385 is a composite structure with genetic material from diverse genera and suggest that it is a functional transposon. They also suggest that chromosomal recombination is a mechanism of genetic exchange in enterococci.

Base Sequence↗
PubMed1997

Enterococcal transposon Tn5384: evolution of a composite transposon through cointegration of enterococcal and staphylococcal plasmids.

Mechanisms for the possible transfer of antimicrobial resistance genes between staphylococci and enterococci remain poorly defined. We have previously reported the transfer between Enterococcus faecalis strains of a multiresistance chromosomal element (beta-lactamase positive and resistance to erythromycin, gentamicin, mercuric chloride, streptomycin, and tetracycline) which we have tentatively designated Tn5385. Tn5385 is a composite of several smaller transposable elements, including Tn5384, a 26-kb composite transposon conferring resistance to erythromycin, gentamicin, and mercuric chloride. Analyses of 7 kb within Tn5384 and flanking sequences within the larger element revealed sequences characteristic of staphylococcal beta-lactamase and small, mobilizable plasmids flanking a region with a sequence identical to those of the replication genes previously described for enterococcal and streptococcal broad-host-range plasmids. These diverse regions are linked by insertion sequences IS256 and IS257 in a manner which suggests a series of cointegration events as the genesis of the current relationship. Taken together, these data suggest that Tn5384 and the larger element within which it is incorporated (Tn5385) evolved at least in part as a result of cointegration between an enterococcal broad-host-range plasmid and staphylococcal beta-lactamase and small mobilizable plasmids. These results implicate broad-host-range plasmids in the transfer of resistance determinants from staphylococci to enterococci.

Base Sequence↗
PubMed1996

Sequences found on staphylococcal beta-lactamase plasmids integrated into the chromosome of Enterococcus faecalis CH116.

We have previously reported the presence of the staphylococcal beta-lactamase gene in chromosomes of Enterococcus faecalis strains CH19 and CH116. CH116 also harbors a 26-kb mobile element, designated Tn5384, which confers resistance to erythromycin and gentamicin. Sequence analysis of the rightmost 9 kb of Tn5384 indicates that this element lies immediately upstream of the beta-lactamase determinant in E. faecalis CH116. This 9-kb region consists of sequences highly homologous to those previously described in staphylococcal beta-lactamase plasmids, including a beta-lactamase transposon indistinguishable from Tn552, an open reading frame encoding a deduced amino acid sequence 94% identical to a previously described potential staphylococcal invertase, an intact copy of staphylococcal insertion-like element IS257, and the major portion of the staphylococcal organomercurial lyase (merB) gene. These data are consistent with the hypothesis that several of the resistance genes encoded within the large transferable region of the CH116 chromosome were originally components of a staphylococcal beta-lactamase plasmid.

Base Sequence↗
PubMed1996

Ceftazidime-resistant Klebsiella pneumoniae isolates recovered at the Cleveland Department of Veterans Affairs Medical Center.

The rate of ceftazidime resistance among Klebsiella pneumoniae isolates recovered from patients at the Cleveland Department of Veterans Affairs Medical Center increased from 6% in the first quarter of 1993 to 28% in the first quarter of 1994. The outbreak was hospitalwide, with the highest rates of resistance occurring on wards where ceftazidime was administered most frequently. Although many plasmid patterns were observed in the clinical isolates, molecular epidemiological analysis with use of pulsed field gel electrophoresis revealed substantial similarities between the strains; this finding suggested that most of the strains-if not all of them-were derived from the original clone. The addition of piperacillin/tazobactam to the hospital formulary and educational efforts focused on minimizing the administration of ceftazidime were associated with a marked decrease in the drug's use and a concomitant decrease in the percentage of ceftazidime-resistant isolates. We have not yet observed a significant rise in the rate of resistance to piperacillin/tazobactam among clinical isolates of K. pneumoniae.

Ceftazidime↗
PubMed1996

Molecular genetics of resistance to both ceftazidime and beta-lactam-beta-lactamase inhibitor combinations in Klebsiella pneumoniae and in vivo response to beta-lactam therapy.

The molecular basis of ceftazidime resistance in 2 isolates of Klebsiella pneumoniae was studied. The first (21300) expressed resistance to ceftazidime and piperacillin-tazobactam. The second (26139) expressed resistance to ceftazidime but remained susceptible to piperacillin-tazobactam. The 2 strains harbored similar large plasmids that hybridized to TEM- and SHV-related beta-lactamase genes. An Escherichia coli strain harboring the plasmid conferring resistance to both compounds (pLRM7) produced beta-lactamases of pI 5.9 (TEM-6) and pI 7.6 (SHV-1). E. coli harboring the other plasmid (pLRM8) expressed only the TEM enzyme because of insertion of IS15 within blaSHV-1. In vivo studies suggested that resistance to beta-lactam-beta-lactamase inhibitor combinations conferred by pLRM7 will be clinically important. Clinical resistance to both extended-spectrum cephalosporins and beta-lactam-beta-lactamase inhibitor combinations is achievable via the production of two enzymes, with only one possessing an extended spectrum of activity.

Abdominal Abscess↗
PubMed1995

Vancomycin resistance in the enterococcus. Relevance in pediatrics.

Enterococci are nosocomial pathogens intrinsically resistant to a variety of commonly used antimicrobial agents. The frequent use of antimicrobial agents such as cephalosporins has been associated with the increased isolation of enterococci in pediatric hospitals. In addition to their intrinsic resistance traits, the enterococci have rapidly accumulated a variety of acquired resistance determinants. Strains that are resistant to all currently available antibiotics are now being isolated from infected children. The threat of untreatable enterococcal infection and the possibility that vancomycin resistance may spread from the enterococci to the more virulent pneumococci or staphylococci argue for vigilant surveillance for resistant strains, isolation and barrier precautions for infected patients, increased research into the mechanisms of resistance, and a reinvigorated effort to identify new classes of antimicrobial agents.

Child↗
PubMed1995

Controlling vancomycin-resistant enterococci.

After controlling an epidemic of vanB-type vancomycin-resistant Enterococcus faecium (VRE), we contained a subsequent vanA E faecium outbreak by using prospective laboratory-based surveillance, placing patients with VRE in private rooms, requiring the use of both gowns and gloves by all personnel entering the patients' rooms, and conducting prevalence surveys of patients on affected wards.

Anti-Bacterial Agents↗
PubMed1995

Tn5384, a composite enterococcal mobile element conferring resistance to erythromycin and gentamicin whose ends are directly repeated copies of IS256.

We have identified a 26-kb mobile element from Enterococcus faecalis CH116, designated Tn5384, which confers resistance to erythromycin and to high levels of gentamicin. Tn5384 is a composite element containing three copies of insertion element IS256. Two of the IS256 copies flank the aac6'-aph2" bifunctional aminoglycoside-modifying-enzyme gene in the inverted orientation, forming a structure similar to staphylococcal gentamicin resistance transposon Tn4001. One of the IS256 elements involved in the Tn4001-like structure also forms the left end of Tn5384, the right end of which is a directly repeated insertion of IS256 approximately 23 kb downstream of the leftmost insertion. Insertions of Tn5384 into enterococcal plasmid pLRM1 have been found associated with 8- and 9-bp duplications of the target sequence.

Base Sequence↗