Ceftriaxone-Resistant<i>Salmonella enterica</i>Serotype Newport, France

Sa, Egorova; Timinouni, Mohammed; Demartin, Marie; Granier, Sophie A.; Whichard, Jean M.; Sangal, Vartul; Fabre, Laëtitia; Delaune, Aurélia; Pardos, Maria; Millemann, Yves; Espié, Emmanuelle; Achtman, Mark; Grimont, Patrick A. D.; Weill, François‐Xavier

doi:10.3201/eid1406.071168

Cited by 50 publications

(45 citation statements)

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“…Further selection for a lineage containing this plasmid may reflect the common prophylactic use of tetracycline, because tetracycline resistance is also encoded on the same plasmid. It has been suggested that all MDR-AmpC strains have a recent global origin (2,25,39), and our assignment of all MDR-AmpC S. Newport isolates to two closely related STs within Newport-II is consistent with the recent clonal expansion from a single S. Newport strain. pSN254 is not conjugative, unlike other IncA/C plasmids (34), which might explain why the MDR-AmpC phenotype has apparently not spread to other STs of S. Newport.…”

Section: Ssupporting

confidence: 70%

“…Salmonella enterica subspecies enterica (referred to herein as S. enterica) has been subdivided serologically into Ͼ1,500 serovars (35), but we focus on S. enterica serovar Newport (S. Newport) here because over the last decade it has been a very common cause of human salmonellosis in both the United States and Europe (13,16,27). Furthermore, multidrug-resistant S. Newport isolates that are also resistant to extended-spectrum cephalosporins (MDR-AmpC) have now been reported from several countries (3,24,36) and are a serious problem among both food animals and humans (17,25,36,48,67). MDR-AmpC isolates are resistant to ␤-lactams, including third-generation cephalosporins, aminoglycosides, tetracyclines, sulfonamides and chloramphenicol (12,36).…”

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confidence: 99%

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Evolution and Population Structure of Salmonella enterica Serovar Newport

et al. 2010

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Salmonellosis caused by Salmonella enterica serovar Newport is a major global public health concern, particularly because S. Newport isolates that are resistant to multiple drugs (MDR), including thirdgeneration cephalosporins (MDR-AmpC phenotype), have been commonly isolated from food animals. We analyzed 384 S. Newport isolates from various sources by a multilocus sequence typing (MLST) scheme to study the evolution and population structure of the serovar. These were compared to the population structure of S. enterica serovars Enteritidis, Kentucky, Paratyphi B, and Typhimurium. Our S. Newport collection fell into three lineages, Newport-I, Newport-II, and Newport-III, each of which contained multiple sequence types (STs). Newport-I has only a few STs, unlike Newport-II or Newport-III, and has possibly emerged recently. Newport-I is more prevalent among humans in Europe than in North America, whereas Newport-II is preferentially associated with animals. Two STs of Newport-II encompassed all MDR-AmpC isolates, suggesting recent global spread after the acquisition of the bla CMY-2 gene. In contrast, most Newport-III isolates were from humans in North America and were pansusceptible to antibiotics. Newport was intermediate in population structure to the other serovars, which varied from a single monophyletic lineage in S. Enteritidis or S. Typhimurium to four discrete lineages within S. Paratyphi B. Both mutation and homologous recombination are responsible for diversification within each of these lineages, but the relative frequencies differed with the lineage. We conclude that serovars of S. enterica provide a variety of different population structures.Salmonellosis is a major global cause of diarrheal and extraintestinal disease in humans and animals (66). Salmonella enterica subspecies enterica (referred to herein as S. enterica) has been subdivided serologically into Ͼ1,500 serovars (35), but we focus on S. enterica serovar Newport (S. Newport) here because over the last decade it has been a very common cause of human salmonellosis in both the United States and Europe (13,16,27). Furthermore, multidrug-resistant S. Newport isolates that are also resistant to extended-spectrum cephalosporins (MDR-AmpC) have now been reported from several countries (3,24,36) and are a serious problem among both food animals and humans (17,25,36,48,67). MDR-AmpC isolates are resistant to ␤-lactams, including third-generation cephalosporins, aminoglycosides, tetracyclines, sulfonamides and chloramphenicol (12, 36). Resistance to ␤-lactams is caused by plasmids carrying the ampC gene bla CMY-2 , which encodes the CMY-2 ␤-lactamase (11,65).Most of our current understanding of the population structure of S. enterica relies on a series of seminal publications from R. K. Selander's group in the 1990s. These publications showed that some serovars consisted of monophyletic groups-so-called clonal groupings-but many other serovars confounded isolates from multiple lineages and were therefore polyphyletic (5,51,55,56). More recent studie...

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Section: Ssupporting

confidence: 70%

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confidence: 99%

Evolution and Population Structure of Salmonella enterica Serovar Newport

et al. 2010

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“…The bla CMY-2 genes have also been detected in E. coli and Salmonella isolates from ground meat (54). The presence of bla CMY-2 plasmid-bearing Salmonella enterica serovars Newport and Typhimurium presumptively of animal origin has been reported in human clinical cases (17,18).…”

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confidence: 83%

“…140-to 160-kb) IncA/C plasmids (bla CMY-2 plasmids) from a diverse range of bacterial hosts, including Escherichia, Salmonella, Shigella, Klebsiella, Edwardsiella, and Aeromonas (31,35,50). These bla CMY-2 plasmid-bearing bacteria have been detected in mammals and fish without a documented or consistent pattern of antibiotic selection pressure (2,17,26,31,37,(50)(51)(52). There is a high prevalence (up to 100%) of bla CMY-2 plasmids reported in commensal and pathogenic bacteria such as Escherichia coli and Salmonella enterica in cattle herds across the United States (1,15,30,42,51).…”

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confidence: 99%

Selection Pressure Required for Long-Term Persistence of bla _CMY-2 -Positive IncA/C Plasmids

Subbiah

Top

Shah

et al. 2011

Appl Environ Microbiol

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Multidrug resistance bla CMY-2 plasmids that confer resistance to expanded-spectrum cephalosporins have been found in multiple bacterial species collected from different hosts worldwide. The widespread distribution of bla CMY-2 plasmids may be driven by antibiotic use that selects for the dissemination and persistence of these plasmids. Alternatively, these plasmids may persist and spread in bacterial populations in the absence of selection pressure if a balance exists among conjugative transfer, segregation loss during cell division, and fitness cost to the host. We conducted a series of experiments (both in vivo and in vitro) to study these mechanisms for three bla CMY-2 plasmids, peH4H, pAR060302, and pAM04528. Results of filter mating experiments showed that the conjugation efficiency of bla CMY-2 plasmids is variable, from <10؊7 for pAM04528 and peH4H to ϳ10 ؊3 for pAR060302. Neither peH4H nor pAM04528 was transferred from Escherichia coli strain DH10B, but peH4H was apparently mobilized by the coresident trimethoprim resistance-encoding plasmid pTmpR. Competition studies showed that carriage of bla CMY-2 plasmids imposed a measurable fitness cost on the host bacteria both in vitro (0.095 to 0.25) and in vivo (dairy calf model). Long-term passage experiments in the absence of antibiotics demonstrated that plasmids with limited antibiotic resistance phenotypes arose, but eventually drug-sensitive, plasmid-free clones dominated the populations. Given that plasmid decay or loss is inevitable, we infer that some level of selection is required for the long-term persistence of bla CMY-2 plasmids in bacterial populations.

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“…There have been several reports of IncA/C plasmids from various Salmonella and E. coli strains that harbor the bla CMY-2 gene and more recent reports of IncA/C plasmids harboring both bla CMY-2 and floR in human clinical isolates of Salmonella serovar Newport (7,14) and in an isolate of the fish pathogen Aeromonas salmonicida subsp. salmonicida from Atlantic salmon in Canada (10).…”

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confidence: 99%

IncA/C Plasmid-Mediated Florfenicol Resistance in the Catfish Pathogen Edwardsiella ictaluri

Welch

Evenhuis

White

et al. 2009

Antimicrob Agents Chemother

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ᰔFlorfenicol (FFC) has recently been approved by the Food and Drug Administration for the treatment of several bacterial diseases of cultured fish species in the United States, including enteric septicemia of catfish (ESC) caused by Edwardsiella ictaluri. The FFC-resistant E. ictaluri strain (M07-1) described herein was isolated from a moribund catfish obtained from the Thad Cochran National Warmwater Aquaculture Research Center (Stoneville, MS) in May of 2007 and was confirmed to be E. ictaluri by 16S rRNA gene sequencing (6). Fish showing signs of ESC were examined for FFC-resistant E. ictaluri because losses due to ESC persisted in this population despite FFC treatment. To characterize the resistance properties of this strain, conjugative transfer experiments were performed as described previously (14) using FFC (30 g/ml) for selection. The antimicrobial susceptibilities of M07-1, the corresponding FFCresistant transconjugant, and the isogenic parent strain (Table 1) were quantified using standard microdilution assays (3, 4, 11), demonstrating that the resistance phenotype observed in strain M07-1 was self-transmissible, conferring resistance to FFC, chloramphenicol, tetracycline, streptomycin, ampicillin, amoxicillin-clavulanic acid, ceftiofur, and cefoxitin, as well as decreased susceptibility to trimethoprim-sulfamethoxazole and ceftriaxone. Resistance transfer correlated to a 150-kb plasmid (referred to hereinafter as pM07-1), suggesting the presence of a multidrug resistance plasmid in this isolate (data not shown). PCR analysis (15) followed by sequencing confirmed that E. ictaluri M07-1 and its multidrugresistant (MDR) transconjugant harbored the floR gene.E. ictaluri plasmid pM07-1 also conferred resistance to ceftiofur and concomitant decreased susceptibility to ceftriaxone, implying the presence of the bla CMY-2 beta-lactamase gene. Recent data indicate a rapid increase in the dissemination of cephalosporin resistance linked to self-transmissible MDR plasmids harboring bla 16). Plasmid-borne bla CMY-2 genes in bacteria isolated from food animals, retail meats, and humans in the United States have been identified previously (1, 2, 5, 8, 16) but have not been detected before in bacteria associated with U.S. aquaculture and were not expected, as there are currently no cephalosporin antimicrobials approved for use in U.S. aquaculture. Therefore, PCR analysis using previously described primers specific to bla CMY-2 was performed to verify the presence of this gene in E. ictaluri

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Ceftriaxone-ResistantSalmonella entericaSerotype Newport, France

Cited by 50 publications

References 15 publications

Evolution and Population Structure of Salmonella enterica Serovar Newport

Evolution and Population Structure of Salmonella enterica Serovar Newport

Selection Pressure Required for Long-Term Persistence of bla _CMY-2 -Positive IncA/C Plasmids

IncA/C Plasmid-Mediated Florfenicol Resistance in the Catfish Pathogen Edwardsiella ictaluri

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Ceftriaxone-ResistantSalmonella entericaSerotype Newport, France

Cited by 50 publications

References 15 publications

Evolution and Population Structure of Salmonella enterica Serovar Newport

Evolution and Population Structure of Salmonella enterica Serovar Newport

Selection Pressure Required for Long-Term Persistence of bla CMY-2 -Positive IncA/C Plasmids

IncA/C Plasmid-Mediated Florfenicol Resistance in the Catfish Pathogen Edwardsiella ictaluri

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Selection Pressure Required for Long-Term Persistence of bla _CMY-2 -Positive IncA/C Plasmids