A Nosocomial Outbreak of Fluoroquinolone-Resistant Salmonella Infection

Olsen, Sonja J.; DeBess, Emilio; McGivern, Teresa; Marano, Nina; Eby, Tom; Mauvais, Steve; Balan, V.; Zirnstein, Gerald; Cieslak, Paul R.; Angulo, Frederick J.

doi:10.1056/nejm200105243442102

Cited by 138 publications

(72 citation statements)

References 17 publications

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“…Among 16 neonates, 10 had received cefotaxime and 2 had received ceftazidime. As previously reported (24,30,42), the emergence of highly resistant Salmonella in an environment characterized by a heavy use of antimicrobial agents may provide a setting that is conducive to nosocomial transmission. In our study, the emergence of the CTX-M-27 ESBL in the neonatal ward could be correlated with heavy use of extended-spectrum cephalosporins by the physicians.…”

Section: Discussionmentioning

confidence: 54%

Nosocomial Outbreak Caused by Salmonella enterica Serotype Livingstone Producing CTX-M-27 Extended-Spectrum β-Lactamase in a Neonatal Unit in Sousse, Tunisia

Bouallègue-Godet¹,

Salem²,

Fabre

et al. 2005

J Clin Microbiol

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In this study, we report an outbreak of Salmonella enterica serotype Livingstone resistant to extendedspectrum cephalosporins that occurred in a neonatal ward of the maternity department of Farhat Hached Hospital, Sousse, Tunisia, in 2002. A total of 16 isolates were recovered from 16 babies hospitalized in the ward during the period 1 to 16 July. All these babies developed diarrhea, and three of them developed septicemia. All the isolates demonstrated resistance to ceftriaxone and ceftazidime due to the production of an extendedspectrum ␤-lactamase (ESBL). The isolates were also resistant to aminoglycosides (kanamycin, tobramycin, netilmicin, gentamicin, and amikacin) and sulfamethoxazole-trimethoprim. DNA profiles were determined by pulsed-field gel electrophoresis using the XbaI and SpeI endonucleases and by ribotyping with PstI digestion. They yielded the same patterns, showing that the outbreak was caused by a single clone. The ESBL was identified as CTX-M-27 by sequencing of PCR products and by isoelectric focusing. The ESBL resistance was transferred by a 40-kb conjugative plasmid. The mobile insertion sequence ISEcp1 was found to be located upstream of bla CTX-M-27 in the same position as that known for a bla CTX-M-14 sequence. A new gene named dfrA21, encoding resistance to trimethoprim and carried by a 90-kb plasmid, was characterized. The dfrA21 gene was inserted as a single resistance cassette in a class I integron. The babies were treated with colistin, and all except two recovered. The outbreak came to an end when appropriate actions were taken: patient isolation, hand washing, and disinfection of the ward.Salmonellosis in humans is usually a self-limited gastroenteritis that does not warrant antimicrobial therapy. However, these infections can occasionally lead to life-threatening systemic infections that require effective chemotherapy. With the emergence of ampicillin-resistant Salmonella enterica serotype Typhimurium DT104 isolates, extended-spectrum cephalosporins (ESC) are currently the agents of choice for such chemotherapy, especially for children, for whom the use of fluroquinolones is not yet approved. The selective pressure created by the use of ESC has been described as one of the most important factors in the appearance of extended-spectrum

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Section: Discussionmentioning

confidence: 54%

Nosocomial Outbreak Caused by Salmonella enterica Serotype Livingstone Producing CTX-M-27 Extended-Spectrum β-Lactamase in a Neonatal Unit in Sousse, Tunisia

Bouallègue-Godet¹,

Salem²,

Fabre

et al. 2005

J Clin Microbiol

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“…These observations could be part of the explanation for the high rates of nosocomial infections, where antibiotics are abundantly used. In fact, nosocomial Salmonella enterica infections, particularly with multidrug-resistant strains, are a concern in developing countries (22,42) and occasionally even happen in developed countries (18,33). Although our findings cannot be indiscriminately extrapolated to all diseases where microbiota imbalance has been implicated in the etiology, they show that, at least in infectious colitis, microbial imbalance precedes the onset of pathology rather than being the result of it.…”

Section: Discussionmentioning

confidence: 58%

Antibiotic-Induced Perturbations of the Intestinal Microbiota Alter Host Susceptibility to Enteric Infection

et al. 2008

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Intestinal microbiota comprises microbial communities that reside in the gastrointestinal tract and are critical to normal host physiology. Understanding the microbiota's role in host response to invading pathogens will further advance our knowledge of host-microbe interactions. Salmonella enterica serovar Typhimurium was used as a model enteric pathogen to investigate the effect of intestinal microbiota perturbation on host susceptibility to infection. Antibiotics were used to perturb the intestinal microbiota. C57BL/6 mice were treated with clinically relevant doses of streptomycin and vancomycin in drinking water for 2 days, followed by oral infection with Salmonella enterica serovar Typhimurium. Alterations in microbiota composition and numbers were evaluated by fluorescent in situ hybridization, differential plating, and Sybr green staining. Antibiotics had a dose-dependent effect on intestinal microbiota composition. The chosen antibiotic regimen did not significantly alter the total numbers of intestinal bacteria but altered the microbiota composition. Greater preinfection perturbations in the microbiota resulted in increased mouse susceptibility to Salmonella serovar Typhimurium intestinal colonization, greater postinfection alterations in the microbiota, and more severe intestinal pathology. These results suggest that antibiotic treatment alters the balance of the microbial community, which predisposes the host to Salmonella serovar Typhimurium infection, demonstrating the importance of a healthy microbiota in host response to enteric pathogens.

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“…These mutations are known to mediate quinolone resistance in S. enterica and E. coli (44,47). S. enterica strains of serotype Schwarzengrund were responsible for the first recognized outbreak of fluoroquinolone-resistant salmonellosis in the United States (55). The parC Ser80Arg mutation, found in Schwarzengrund but not in any other S. enterica genome examined in the present study, is thought to occur rarely among S. enterica serovars (34).…”

Section: ) (33)mentioning

confidence: 53%

Comparative Genomics of 28 Salmonella enterica Isolates: Evidence for CRISPR-Mediated Adaptive Sublineage Evolution

et al. 2011

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Despite extensive surveillance, food-borne Salmonella enterica infections continue to be a significant burden on public health systems worldwide. As the S. enterica species comprises sublineages that differ greatly in antigenic representation, virulence, and antimicrobial resistance phenotypes, a better understanding of the species' evolution is critical for the prediction and prevention of future outbreaks. The roles that virulence and resistance phenotype acquisition, exchange, and loss play in the evolution of S. enterica sublineages, which to a certain extent are represented by serotypes, remains mostly uncharacterized. Here, we compare 17 newly sequenced and phenotypically characterized nontyphoidal S. enterica strains to 11 previously sequenced S. enterica genomes to carry out the most comprehensive comparative analysis of this species so far. These phenotypic and genotypic data comparisons in the phylogenetic species context suggest that the evolution of known S. enterica sublineages is mediated mostly by two mechanisms, (i) the loss of coding sequences with known metabolic functions, which leads to functional reduction, and (ii) the acquisition of horizontally transferred phage and plasmid DNA, which provides virulence and resistance functions and leads to increasing specialization. Matches between S. enterica clustered regularly interspaced short palindromic repeats (CRISPR), part of a defense mechanism against invading plasmid and phage DNA, and plasmid and prophage regions suggest that CRISPR-mediated immunity could control short-term phenotype changes and mediate long-term sublineage evolution. CRISPR analysis could therefore be critical in assessing the evolutionary potential of S. enterica sublineages and aid in the prediction and prevention of future S. enterica outbreaks.

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A Nosocomial Outbreak of Fluoroquinolone-Resistant Salmonella Infection

Abstract: We describe a prolonged nosocomial outbreak of infection with fluoroquinolone-resistant S. enterica serotype Schwarzengrund. More such outbreaks are likely in institutional settings, particularly those in which there is heavy use of antimicrobial agents.

Cited by 138 publications

References 17 publications

Nosocomial Outbreak Caused by Salmonella enterica Serotype Livingstone Producing CTX-M-27 Extended-Spectrum β-Lactamase in a Neonatal Unit in Sousse, Tunisia

Nosocomial Outbreak Caused by Salmonella enterica Serotype Livingstone Producing CTX-M-27 Extended-Spectrum β-Lactamase in a Neonatal Unit in Sousse, Tunisia

Antibiotic-Induced Perturbations of the Intestinal Microbiota Alter Host Susceptibility to Enteric Infection

Comparative Genomics of 28 Salmonella enterica Isolates: Evidence for CRISPR-Mediated Adaptive Sublineage Evolution

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