Gentamicin- and silver-resistant pseudomonas in a burns unit.

Bridges, Kim; Kidson, A.; Lowbury, E. J. L.; Wilkins, M. D.

doi:10.1136/bmj.1.6161.446

Cited by 117 publications

(53 citation statements)

References 8 publications

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“…Resistance of clinical P. aeruginosa isolates to SSD was also detected (23) and was assumed to be plasmid related. From 1977 to 1998 some gentamicin-resistant P. aeruginosa strains were found to be resistant to silver nitrate, but this resistance was revealed to be unstable and disappeared upon repeated subculture (8). The resistance of the AFLP8 strain to SSD also diminished upon subculture and subsequent cryopreservation.…”

Section: Downloaded Frommentioning

confidence: 96%

Molecular Epidemiology of Pseudomonas aeruginosa Colonization in a Burn Unit: Persistence of a Multidrug-Resistant Clone and a Silver Sulfadiazine-Resistant Clone

et al. 2003

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To study the epidemiology of Pseudomonas aeruginosa colonization in a 32-bed burn wound center (BWC), 321 clinical and 45 environmental P. aeruginosa isolates were collected by prospective surveillance culture over a 1-year period and analyzed by serotyping, drug susceptibility testing, and amplified fragment length polymorphism (AFLP) analysis. Among 441 patients treated at the center, 70 (16%) were colonized with P. aeruginosa, including 12 (17%) patients who were colonized on admission and 58 (83%) patients who acquired the organism during their stay. Of the 48 distinct AFLP genotypes found, 21 were found exclusively in the environment, 15 were isolated from individual patients only, and 12 were responsible for the colonization of 57 patients, of which 2 were also isolated from the environment, but secondary to patient carriage. Polyclonal P. aeruginosa colonization with strains of two to four genotypes, often with different antibiotic susceptibility patterns, was observed in 19 patients (27%). Two predominant genotypes were responsible for recurrent outbreaks and the colonization of 42 patients (60% of all colonized patients). The strain with one of those genotypes appeared to be endemic to the BWC and developed multidrug resistance (MDR) at the end of the study period, whereas the strain with the other genotype was antibiotic susceptible but resistant to silver sulfadiazine (SSD r ). The MDR strain was found at a higher frequency in sputum samples than the SSD r strain, which showed a higher prevalence in burn wound samples, suggesting that anatomic habitat selection was associated with adaptive resistance to antimicrobial drugs. Repeated and thorough surveys of the hospital environment failed to detect a primary reservoir for any of those genotypes. Cross-acquisition, resulting from insufficient compliance with infection control measures, was the major route of colonization in our BWC. In addition to the AFLP pattern and serotype, analysis of the nucleotide sequences of three (lipo)protein genes (oprI, oprL, and oprD) and the pyoverdine type revealed that all predominant strains except the SSD r strain belonged to recently identified clonal complexes. These successful clones are widespread in nature and therefore predominate in the patient population, in whom variants accumulate drug resistance mechanisms that allow their transmission and persistence in the BWC.

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Section: Downloaded Frommentioning

confidence: 96%

Molecular Epidemiology of Pseudomonas aeruginosa Colonization in a Burn Unit: Persistence of a Multidrug-Resistant Clone and a Silver Sulfadiazine-Resistant Clone

et al. 2003

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“…These resistances are selected frequently when metal salts are used as antiseptics. Ag + -resistant bacteria have been reported periodically from sources such as hospitals and burn wounds where silver toxicity might be expected to select for resistance (Annear et al, 1976 ;Bridges et al, 1979 ;Hendry & Stewart, 1979 ;McHugh et al, 1975 ;Pruitt et al, 1998). The physiological, biochemical and molecular basis of bacterial Ag + resistance were not described prior to our studies .…”

Section: Some Metal Cations (Zn#mentioning

confidence: 99%

Diversity of silver resistance genes in IncH incompatibility group plasmids

et al. 2001

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Silver compounds are used as antimicrobial agents in medicine and bacteria that develop resistance to silver cations (Ag M ) pose problems similar to those of antibiotic-resistant bacteria. The first set of Ag M resistance genes (sil) was from plasmid pMG101, now assigned to the IncHI incompatibility group. Questions of whether sil genes are unique to pMG101 or are more widely found, and whether they are associated with a specific incompatibility group or occur in many plasmid groups and on bacterial chromosomes were addressed. sil genes were identified in five IncH plasmids, but not in plasmids of the IncP incompatibility group. Three sil genes (silP, silR and silE) from these plasmids were PCR-amplified, cloned, sequenced and compared to those of pMG101. Differences of 0-50 nt per kb of sequence were found. Predicted gene products were 0-6 % different in amino acid sequence, but the differences did not alter residues thought to be involved in protein function (see supplementary data at http ://mic.sgmjournals.org or http ://www.uic.edu/depts/mcmi/individual/gupta/index.htm). For representative IncH plasmid R476b and pMG101 the effects of Ag M exposure on resistance levels were measured by growth. The inducibility of silC, silR and silE gene expression after Ag M exposure was studied by reverse transcriptase (RT)-PCR. Silver resistance increased after Ag M exposure for strains carrying plasmid R476b. silC and silE expression from R476b was inducible after Ag M exposure and was constitutive and high from pMG101. The mRNA levels for the regulatory gene silR was constitutive for both pMG101 and R476b. Close homologues for silABC(ORF96)RS from pMG101 are clustered on the chromosomes of Escherichia coli strains K-12 and O157 :H7, without contiguous silP and silE homologues. Insertion deletions of the E. coli K-12 chromosomal homologues for silA and silP gave Ag M hypersensitivity for growth. The silA homologue knockout was complemented back to wild-type resistance by the same gene cloned on a plasmid. Homologues of sil genes have also been identified on other enterobacterial genomes.

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“…Since the late 1960s, when silver compounds were routinely applied to burn wounds (e.g., silver sulfadiazine in Flamazine), mortality rates rapidly reduced to about 1/4 (35). A decade later, a series of studies reported silver resistance in Enterobacteriaceae and nonfermenters (3,6,20,33). Since that time, an increasing number of outbreaks due to silver-resistant strains of Enterobacteriaceae have been reported.…”

Section: Discussionmentioning

confidence: 99%

Subtractive Hybridization Yields a Silver Resistance Determinant Unique to Nosocomial Pathogens in the Enterobacter cloacae Complex

Kremer¹,

Hoffmann

2012

J Clin Microbiol

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The heterogeneity and the increasing clinical importance of the Enterobacter cloacae complex have often been discussed. However, little is known about molecular factors causing pathogenicity within this nomenspecies. Here, we analyzed the genetic differences between an avirulent plant isolate and a pathogenic strain causing an outbreak with septicemia in three patients. We identified an IncHI-2 plasmid as a major difference between these two strains. Besides resistance to several antibiotics, this plasmid encoded a silver resistance determinant. We further showed that this sil determinant was present not only in the analyzed outbreak strain but also in the vast majority of clinical isolates of the E. cloacae complex, predominantly in (sub)species that frequently cause nosocomial infections. The identified sil determinant was highly conserved within the E. cloacae complex and mediated resistance to up to 600 μM silver nitrate. As silver is often used as a disinfectant and treatment for burn wounds, we present here an important fitness factor within the clinically most prevalent subspecies of the E. cloacae complex. This provides a possible explanation for their unequal involvement in nosocomial and especially burn wound infections.

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Gentamicin- and silver-resistant pseudomonas in a burns unit.

Cited by 117 publications

References 8 publications

Molecular Epidemiology of Pseudomonas aeruginosa Colonization in a Burn Unit: Persistence of a Multidrug-Resistant Clone and a Silver Sulfadiazine-Resistant Clone

Molecular Epidemiology of Pseudomonas aeruginosa Colonization in a Burn Unit: Persistence of a Multidrug-Resistant Clone and a Silver Sulfadiazine-Resistant Clone

Diversity of silver resistance genes in IncH incompatibility group plasmids

Subtractive Hybridization Yields a Silver Resistance Determinant Unique to Nosocomial Pathogens in the Enterobacter cloacae Complex

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