Selection for Vancomycin Resistance in Clinical Isolates of Staphylococcus haemolyticus

Schwalbe, Richard; Ritz, William J.; Verma, Prashant; Barranco, E. A.; Gilligan, Peter H.

doi:10.1093/infdis/161.1.45

Cited by 72 publications

(37 citation statements)

References 34 publications

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“…However, in our screening we also identified two strains of S. haemolyticus which grew abundantly on the BHI agar plates with vancomycin. S. haemolyticus is known for its resistance to vancomycin (9,29). Nosocomial spread of S. haemolyticus in NICUs has been described before (23,26).…”

Section: Discussionmentioning

confidence: 93%

Nosocomial Spread of a Staphylococcus capitis Strain with Heteroresistance to Vancomycin in a Neonatal Intensive Care Unit

Zwet¹,

Debets-Ossenkopp²,

Reinders³

et al. 2002

J Clin Microbiol

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A premature infant in a neonatal intensive care unit (NICU) developed a bloodstream infection caused by coagulase-negative staphylococci (CoNS) sensitive to vancomycin. The infection persisted for 3 weeks, despite therapy with vancomycin and replacement of all intravenous catheters. The neonate died due to necrotizing enterocolitis which developed during the ongoing sepsis. We screened this strain and 216 other strains of CoNS from cultures of blood obtained from neonates between 1997 and 2000 for heteroresistance to vancomycin. Forty-eight isolates, including the strain that caused ongoing sepsis, proved heteroresistant. All isolates were identified as Staphylococcus capitis and were identical, just as their resistant stable subcolonies were, when they were genetically fingerprinted by amplified-fragment length polymorphism analysis. The heteroresistant phenotype of this endemic strain was confirmed by population analysis. We conclude that heteroresistance to vancomycin occurs in S. capitis and might be the cause of therapeutic failures in NICUs. Moreover, heteroresistant strains can become endemic in such units.

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Section: Discussionmentioning

confidence: 93%

Nosocomial Spread of a Staphylococcus capitis Strain with Heteroresistance to Vancomycin in a Neonatal Intensive Care Unit

Zwet¹,

Debets-Ossenkopp²,

Reinders³

et al. 2002

J Clin Microbiol

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“…Under enhanced culture conditions with enriched media and a high inoculum density, the vancomycin MICs for our isolates of CoNS with DVS rose as high as 32 g/ml. The discrepancy in susceptibility to vancomycin under routine and enhanced conditions is perhaps related to the selection of resistant subpopulations, or heteroresistance (9,32,34,42); however, there is no clinical evidence at present to support this concept in vivo. In other reports of CoNS with reduced susceptibilities to vancomycin, resistance appears to develop in a stepwise fashion and is related to the duration of vancomycin administration (13,33).…”

Section: Discussionmentioning

confidence: 99%

Decreased Vancomycin Susceptibility of Coagulase-Negative Staphylococci in a Neonatal Intensive Care Unit: Evidence of Spread of Staphylococcus warneri

Reboli¹,

Hubler

Rodgers

et al. 2003

J Clin Microbiol

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Coagulase-negative staphylococci (CoNS) are important pathogens in premature neonates; decreasing glycopeptide susceptibility has been observed among these isolates. The epidemiology of colonization with CoNS, the organisms' vancomycin susceptibilities, and genetic relatedness were studied over 6 months in a tertiary-care neonatal unit. A total of 321 isolates of CoNS were isolated. Seventy-five percent of the infants were colonized at admission, and virtually all were colonized thereafter. Common species were Staphylococcus epidermidis (69%), S. warneri (12%), S. haemolyticus (9.7%), and S. hominis (5.6%). A total of 3.9% of CoNS isolates had decreased vancomycin susceptibility (DVS) (MICs > 2.0 g/ml); isolate recovery was associated with a stay in a neonatal intensive care unit for >28 days (P ‫؍‬ 0.039), vancomycin exposure (P ‫؍‬ 0.021), and S. warneri colonization (P < 0.0001). Nine of 12 (75%) CoNS with DVS were S. warneri, had enhanceable high-level resistance in vitro, were indistinguishable or closely related by pulsed-field gel electrophoresis, and were different from 29 vancomycin-susceptible S. warneri isolates. Epidemiological analysis suggested unsuspected nosocomial spread. Species determination in certain settings may aid in the understanding of emerging nosocomial problems.

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“…Furthermore, because it certainly differs from ␤-lactams, mersacidin most likely interacts with a target which is not attacked by chemotherapeutic drugs currently in use, particularly against methicillin-resistant S. aureus. The threatening situation with these staphylococci, which eventually become resistant to vancomycin (26), makes it necessary to search for novel targets, and mersacidin has considerable potential in this respect.…”

Section: Discussionmentioning

confidence: 99%

Mode of action of the lantibiotic mersacidin: inhibition of peptidoglycan biosynthesis via a novel mechanism?

Brötz

Bierbaum

Markus

et al. 1995

Antimicrob Agents Chemother

131

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Mersacidin is an antibiotic peptide produced byThe term lantibiotics designates a group of lanthionine (and/or 3-methyllanthionine)-containing peptides with antibiotic activity against gram-positive bacteria (25). In contrast to peptide antibiotics like bacitracin or gramicidin S (10), lantibiotics are ribosomally synthesized and show unique structural properties, which arise from posttranslational modifications (for reviews, see references 3 and 9).With a molecular mass of 1,825 Da, mersacidin is the smallest lantibiotic known so far. Its propeptide template consists of 20 amino acids, 8 of which are modified to yield 4 thioether amino acids: 3 3-methyllanthionines and 1 2-aminovinyl-2-methylcysteine. This leads to the formation of four intramolecular heterocyclic rings. Additionally, the unusual amino acid ␣,␤-didehydroalanine is found. Mersacidin carries no net charge and has overall hydrophobic properties (5). It is produced by Bacillus sp. strain HIL Y-85,54728 and is active against several gram-positive bacteria such as streptococci, bacilli, and staphylococci including methicillin-resistant Staphylococcus aureus strains; enterococci are relatively insusceptible (4, 14). Although in vitro mersacidin is less active than vancomycin, teicoplanin, and daptomycin (17), its activity in vivo is at least comparable to that of vancomycin in the treatment of experimental staphylococcal infections (including those caused by methicillin-resistant S. aureus strains) in mice (4,14).In addition to its potential therapeutical value, mersacidin has been the subject of increased interest because of its position among the lantibiotics described so far, which have been classified into two groups (9). The type A lantibiotics (e.g., Pep5 and nisin) are screw-shaped, positively charged, amphipathic molecules which exert their primary bactericidal action by the formation of pores in the cytoplasmic membrane (20). The type B lantibiotics, as defined so far (e.g., duramycin and cinnamycin), possess a globular shape, carry no net charge or a negative charge, and are described as inhibitors of phospholipase A 2 or the angiotensin-converting enzyme (3). Mersacidin does not completely conform to either group because of atypical structural features (9, 11).Here, we report that it is also different regarding its mode of bactericidal activity. We show that mersacidin inhibits peptidoglycan biosynthesis, probably on the level of transglycosylation. Furthermore, we demonstrate that on the molecular level its mode of action differs from those of glycopeptide antibiotics like vancomycin or teicoplanin. This opens the possibility of using a new target for the antibiotic treatment of methicillinresistant S. aureus strains and makes mersacidin an interesting tool for the investigation of peptidoglycan biosynthesis of gram-positive bacteria. MATERIALS AND METHODSBacterial strains and growth conditions. Staphylococcus simulans 22 (formerly Staphylococcus cohnii 22; Institute for Medical Microbiology and Immunology of the University of Bonn, Bonn, ...

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Selection for Vancomycin Resistance in Clinical Isolates of Staphylococcus haemolyticus

Cited by 72 publications

References 34 publications

Nosocomial Spread of a Staphylococcus capitis Strain with Heteroresistance to Vancomycin in a Neonatal Intensive Care Unit

Nosocomial Spread of a Staphylococcus capitis Strain with Heteroresistance to Vancomycin in a Neonatal Intensive Care Unit

Decreased Vancomycin Susceptibility of Coagulase-Negative Staphylococci in a Neonatal Intensive Care Unit: Evidence of Spread of Staphylococcus warneri

Mode of action of the lantibiotic mersacidin: inhibition of peptidoglycan biosynthesis via a novel mechanism?

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