An R Plasmid of &lt;i&gt;Serratia&lt;/i&gt; &lt;i&gt;marcescens&lt;/i&gt; Transferable to &lt;i&gt;Pseudomonas aeruginosa&lt;/i&gt;

Olexy, Vera M.; Mucha, D K; Bird, Thomas J.; Grieble, Hans G.; Farrand, Stephen K.

doi:10.1159/000238054

Cited by 5 publications

(7 citation statements)

References 10 publications

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“…R factors are transferred very efficiently among pseudomonads, with a transfer rate that approaches 0.1 event per CFU (214), and the transduction of drug resistance genes between P. aeruginosa strains has been demonstrated to occur under environmental conditions (198,268). Additionally, pseudomonads can acquire plasmid-borne antibiotic resistance from nonpseudomonads, as evidenced in the case of Serratia marcescens resistance plasmids (213). The concatamerization of multiple drug resistance genes on a single episomal element is thought to occur through a stepwise fusion of multiple resistance plasmids.…”

Section: Mechanisms Of Antibiotic Resistancementioning

confidence: 99%

Lung Infections Associated with Cystic Fibrosis

2002

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While originally characterized as a collection of related syndromes, cystic fibrosis (CF) is now recognized as a single disease whose diverse symptoms stem from the wide tissue distribution of the gene product that is defective in CF, the ion channel and regulator, cystic fibrosis transmembrane conductance regulator (CFTR). Defective CFTR protein impacts the function of the pancreas and alters the consistency of mucosal secretions. The latter of these effects probably plays an important role in the defective resistance of CF patients to many pathogens. As the modalities of CF research have changed over the decades from empirical histological studies to include biophysical measurements of CFTR function, the clinical management of this disease has similarly evolved to effectively address the ever-changing spectrum of CF-related infectious diseases. These factors have led to the successful management of many CF-related infections with the notable exception of chronic lung infection with the gram-negative bacterium Pseudomonas aeruginosa. The virulence of P. aeruginosa stems from multiple bacterial attributes, including antibiotic resistance, the ability to utilize quorum-sensing signals to form biofilms, the destructive potential of a multitude of its microbial toxins, and the ability to acquire a mucoid phenotype, which renders this microbe resistant to both the innate and acquired immunologic defenses of the host

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Section: Mechanisms Of Antibiotic Resistancementioning

confidence: 99%

Lung Infections Associated with Cystic Fibrosis

2002

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“…We previously showed the resistant S. marcescens isolates at HVAH to be of two types. The group 1 isolates, including Sm608, Sm1835, and Sm612 in this study, harbor two R plasmids, pFMH1010 and pFMH2010 (Table 1), and the group 2 isolates harbor only pFMH1010 (24). The two other S. marcescens strains in this study, Sm645 and Sm1047, also exhibit all the resistances of the group 1 isolates (all those encoded by pFMH1010 and pFMH2010).…”

Section: Methodsmentioning

confidence: 63%

“…We also showed that pFMH1010 is conjugally transmissible from nosocomial Serratia marcescens isolates to the P. aeruginosa laboratory strain, PA038-1 (23,24). The resulting transconjugants gain resistance to carbenicillin, gentamicin, tobramycin, kanamycin, streptomycin, and sisomicin (23,24).…”

mentioning

confidence: 78%

“…We previously described an 89-megadalton (MDa) plasmid, pFMH1010, which encodes resistance to beta-lactams, five aminoglycosides, and sulfonamide (24,33). This plasmid was found to be endemic among members of the family Enterobacteriaceae isolated at Hines Veterans Administration Hospital (HVAH) (33).…”

mentioning

confidence: 99%

“…Several of the nosocomial Serratia strains harboring pFMH1010 (24) were isolated from patients from whom Cb, Gm, and Tm P. aeruginosa strains were also obtained. We undertook this investigation to determine whether pFMH1010 is also responsible for linked Cb, Gm, and Tm in the nosocomial P. aeruginosa isolates from HVAH.…”

mentioning

confidence: 99%

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Diversity of determinants encoding carbenicillin, gentamicin, and tobramycin resistance in nosocomial Pseudomonas aeruginosa

Mucha¹,

Farrand²

1986

Antimicrob Agents Chemother

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Plasmid pFMH1010, an 89-megadalton R plasmid, is endemic among members of the family Enterobacteriaceae at Hines Veterans Administration Hospital, Hines, Ill. It encodes resistance to nine antibiotics, including resistance to carbenicillin (Cb), gentamicin (Gm), and tobramycin (Tm). Pseudomonas aeruginosa strains resistant to carbenicillin, gentamicin, and tobramycin were isolated from five patients at Hines Veterans Administration Hospital from whom Serratia marcescens strains harboring pFMH1010 were also obtained. The P. aeruginosa strains were investigated to determine whether their Cb, Gm, and Tm characteristics derived from pFMH1010. One of the isolates, Ps559, was shown by Southern hybridization to contain approximately 76% of pFMH1010. Several lines of evidence suggested that the pFMH1010 sequences in Ps559 are integrated in the chromosome. Southern hybridization also demonstrated that the beta-lactam resistance of pFMH1010 is most probably due to the presence of sequences homologous with Tn3 and that these sequences are retained in Ps559. In two other Pseudomonas isolates, resistance to carbenicillin, gentamicin, tobramycin, and kanamycin was encoded by R plasmids unrelated to pFMH1010. In the last two isolates, resistance to gentamicin and tobramycin and several other antibiotics appeared to be chromosomally encoded, and it was rescuable from one of these strains by RP4-mediated mobilization.

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