ABSTRACT Animal contact is an established risk factor for nontyphoidal Salmonella infections and outbreaks. During 2015–2018, the U.S. Centers for Disease Control and Prevention (CDC) and other U.S. public health laboratories began implementing whole-genome sequencing (WGS) of Salmonella isolates. WGS was used to supplement the traditional methods of pulsed-field gel electrophoresis for isolate subtyping, outbreak detection, and antimicrobial susceptibility testing (AST) for the detection of resistance. We characterized the epidemiology and antimicrobial resistance (AMR) of multistate salmonellosis outbreaks linked to animal contact during this time period. An isolate was considered resistant if AST yielded a resistant (or intermediate, for ciprofloxacin) interpretation to any antimicrobial tested by the CDC or if WGS showed a resistance determinant in its genome for one of these agents. We identified 31 outbreaks linked to contact with poultry ( n = 23), reptiles ( n = 6), dairy calves ( n = 1), and guinea pigs ( n = 1). Of the 26 outbreaks with resistance data available, we identified antimicrobial resistance in at least one isolate from 20 outbreaks (77%). Of 1,309 isolates with resistance information, 247 (19%) were resistant to ≥1 antimicrobial, and 134 (10%) were multidrug-resistant to antimicrobials from ≥3 antimicrobial classes. The use of resistance data predicted from WGS increased the number of isolates with resistance information available fivefold compared with AST, and 28 of 43 total resistance patterns were identified exclusively by WGS; concordance was high (>99%) for resistance determined by AST and WGS. The use of predicted resistance from WGS enhanced the characterization of the resistance profiles of outbreaks linked to animal contact by providing resistance information for more isolates.

After more than 3 years without a documented cholera case, the Republic of Haiti reported its first resurgent case on 30 September 2022 (1–3). As of 18 February 2023, more than 27,000 cholera cases have been hospitalized and 594 deaths confirmed from all 10 departments (4). Here, we describe Vibrio cholerae isolates first characterized by the Laboratoire National de Santé Publique (LNSP) and include both genotypic and phenotypic antimicrobial resistance profiles. Whole-genome sequencing (WGS) analysis was compared with recently circulating cholera toxin-producing V. cholerae O1 in a maximum likelihood phylogeny.

Objectives: Our objectives were to identify Shigella isolates in the United States with decreased susceptibility to azithromycin (DSA) and characterize the genetic mechanisms responsible for this resistance. Methods: The National Antimicrobial Resistance Monitoring System (NARMS) at the US Centers for Disease Control and Prevention (CDC) collects and conducts broth microdilution antimicrobial susceptibility testing on Shigella to determine minimum inhibitory concentrations (MICs) for up to 15 drugs, including azithromycin. Isolates with decreased susceptibility to azithromycin were subjected to molecular methods (e.g., polymerase chain reaction [PCR], whole-genome sequencing, and plasmid typing/transformation) to identify the genetic mechanisms of resistance. Results: A total of 118 isolates with decreased susceptibility to azithromycin were tested—65 (55%) isolates contained only mphA, 1 (<1%) isolate contained only ermB, and 51 (43%) isolates contained both mechanisms. Seven isolates contained IncFII plasmids with mphA, ermB, or mphA and ermB, whereas one isolate contained an IncB/O plasmid with mphA. One (<1%) isolate that contained neither mphA nor ermB contained mutations in rrlH, rplD, and rplV genes and an insertion in rplV, the functions of which are not yet known. Conclusion: Additional studies are needed to understand the effect on treatment outcomes, epidemiology and possible additional mechanisms responsible for the decreased susceptibility of azithromycin in Shigella.

Gastrointestinal illnesses are the most frequently diagnosed conditions among returning U.S. travelers. Although most episodes of travelers' diarrhea do not require antibiotic therapy, fluoroquinolones (a type of quinolone antibiotic) are recommended for treatment of moderate and severe travelers' diarrhea as well as many other types of severe infection. To assess associations between quinolone susceptibility and international travel, we linked data about isolate susceptibility in NARMS to cases of enteric infections reported to FoodNet. We categorized isolates as quinolone-nonsusceptible (QNS) if they were resistant or had intermediate susceptibility to ≥1 quinolone. Among 1,726 travel-associated infections reported to FoodNet with antimicrobial susceptibility data in NARMS during 2004-2014, 56% of isolates were quinolone-nonsusceptible, of which most (904/960) were Campylobacter. International travel was associated with >10-fold increased odds of infection with quinolone-nonsusceptible bacteria. Most QNS infections were associated with travel to Latin America and the Caribbean (390/743; 52%); however, the greatest risk of QNS infection was associated with travel to Africa (120 per 1,000,000 passenger journeys). Preventing acquisition and onward transmission of antimicrobial-resistant enteric infections among travelers is critical.

Nontyphoidal Salmonella (NTS) causes an estimated 1.2 million illnesses, 23,000 hospitalizations, and 450 deaths each year in the United States. Decreased susceptibility to ciprofloxacin (DSC) has historically been associated with chromosomal mutations of the quinolone resistance determining region (QRDR), but plasmid-mediated quinolone resistance (PMQR) genes are increasing. To investigate DSC among Salmonella enterica serotype Newport strains, we examined 40 isolates from 1996 to 2016 with DSC. Thirty isolates (71%) contained the PMQR gene qnrB and eight isolates (19%) contained a QRDR.

Enterotoxigenic Escherichia coli (ETEC) are an important cause of diarrhea globally, particularly among children under the age of five in developing countries. ETEC O6 is the most common ETEC serogroup, yet the genome wide population structure of isolates of this serogroup is yet to be determined. In this study, we have characterized 40 ETEC O6 isolates collected between 1975-2016 by whole genome sequencing (WGS) and by phenotypic antimicrobial susceptibility testing. To determine the relatedness of isolates, we evaluated two methods-whole genome high-quality single nucleotide polymorphism (whole genome-hqSNP) and core genome SNP analyses using Lyve-SET and Parsnp respectively. All isolates were tested for antimicrobial susceptibility using a panel of 14 antibiotics. ResFinder 2.1 and a custom quinolone resistance determinants workflow were used for resistance determinant detection. VirulenceFinder 1.5 was used for prediction of the virulence genes. Thirty-seven isolates clustered into three major clades (I, II, III) by whole genome-hqSNP and core genome SNP analyses, while three isolates included in the whole genome-hqSNP analysis only did not cluster with clades I-III by both analyses and formed a distantly related outgroup, designated clade IV. Median number of pairwise whole genome-hqSNPs in clonal ETEC O6 outbreaks ranged from 0 to 5. Of the 40 isolates tested for antimicrobial susceptibility, 18 isolates were pansusceptible. Twenty-two isolates were resistant to at least one antibiotic, nine of which were multidrug resistant. Phenotypic antimicrobial resistance (AR) correlated with AR determinants in 22 isolates. Thirty-two isolates harbored both enterotoxin virulence genes while the remaining 8 isolates had only one of the two virulence genes. In summary, whole genome-hqSNP and core genome SNP analyses from this study revealed similar evolutionary relationships and an overall diversity of ETEC O6 isolates independent of time of isolation. Less than 5 pairwise hqSNPs between ETEC O6 isolates is circumstantially indicative of an outbreak cluster. Findings from this study will be a basis for quicker outbreak detection and control by efficient subtyping by WGS.

We tested a diverse set of 500 isolates of nontyphoidal Salmonella enterica subsp. enterica from various animal, food, and human clinical sources for susceptibility to antimicrobials currently lacking epidemiological cutoff values (ECOFFs) set by the European Committee on Antimicrobial Susceptibility Testing. A consortium of five different laboratories each tested 100 isolates, using broth microdilution panels containing twofold dilutions of ceftriaxone, cefepime, and colistin to determine the minimum inhibitory concentrations of each drug when tested against the Salmonella isolates. Based on the resulting data, new ECOFFs of 0.25g/mL for ceftriaxone, 0.12g/mL for cefepime, and 2g/mL for colistin have been proposed. These thresholds will aid in the identification of Salmonella that have phenotypically detectable resistance mechanisms to these important antimicrobials.

Newport is the third most common Salmonella enterica serotype identified among the estimated 1.2 million human salmonellosis infections occurring annually in the United States. Risk factors for infection and food items implicated in outbreaks vary by antimicrobial resistance pattern. We conducted a descriptive analysis of data from four enteric disease surveillance systems capturing information on incidence, demographics, seasonality, geographic distribution, outbreaks, and antimicrobial resistance of Newport infections over a 10-year period from 2004 through 2013. Incidence increased through 2010, then declined to rates similar to those in the early years of the study. Incidence was highest in the South and among children <5 years old. Among isolates submitted for antimicrobial susceptibility testing, 88% were susceptible to all antimicrobials tested (pansusceptible) and 8% were resistant to at least seven agents, including ceftriaxone. Rates of pansusceptible isolates were also highest in the South and among young children, particularly in 2010. Pansusceptible strains of Newport have been associated with produce items and environmental sources, such as creek water and sediment. However, the role of environmental transmission of Newport in human illness is unclear. Efforts to reduce produce contamination through targeted legislation, as well as collaborative efforts to identify sources of contamination in agricultural regions, are underway.

BACKGROUND Enteric fever in the United States has been primarily associated with travel and with worrisome changes in global patterns of antimicrobial resistance. We present the first comprehensive report of National Typhoid and Paratyphoid Fever Surveillance System (NTPFS) data for a 5-year period (2008-2012). METHODS We reviewed data on laboratory-confirmed cases reported to NTPFS, and related antimicrobial susceptibility results of Salmonella Typhi and Paratyphi A isolates sent for testing by participating public health laboratories to the Centers for Disease Control and Prevention's National Antimicrobial Resistance Monitoring System laboratory. RESULTS During 2008-2012, 2341 enteric fever cases were reported, 80% typhoid and 20% paratyphoid A. The proportion caused by paratyphoid A increased from 16% (2008) to 22% (2012). Foreign travel within 30 days preceding illness onset was reported by 1961 (86%) patients (86% typhoid and 92% paratyphoid A). Travel to southern Asia was common (82% for typhoid, 97% for paratyphoid A). Among 1091 (58%) typhoid and 262 (56%) paratyphoid A isolates tested for antimicrobial susceptibility, the proportion resistant to nalidixic acid (NAL-R) increased from 2008 to 2012 (Typhi, 60% to 68%; Paratyphi A, 91% to 94%). Almost all NAL-R isolates were resistant or showed decreased susceptibility to ciprofloxacin. Resistance to at least ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole (multidrug resistant [MDR]) was limited to Typhi isolates, primarily acquired in southern Asia (13%). Most MDR isolates were also NAL-R. CONCLUSIONS Enteric fever in the United States is primarily associated with travel to southern Asia, and increasing resistance is adding to treatment challenges. A bivalent typhoid and paratyphoid vaccine is needed.

To the Editor: The agents of epidemic cholera are Vibrio cholerae toxigenic serogroups O1 and O139. Cholera symptoms include watery diarrhea and severe dehydration, which can rapidly result in death unless rehydration therapy is prompt (1). Antimicrobial agents may reduce the severity and duration of disease (1); commonly used are tetracyclines, fluoroquinolones, macrolides, and trimethoprim/sulfamethoxazole (1). However, V. cholerae resistance to antimicrobial drugs is increasing because of the accumulation of genetic mutations and the acquisition of resistance genes, which are usually transferred on mobile genetic elements such as integrating conjugative elements (ICEs) (1). As of March 12, 2014, the ongoing cholera outbreak that began in Haiti in October 2010 had caused 700,796 cases and 8,548 deaths (2). To characterize infections, the National Public Health Laboratory in Haiti and the US Centers for Disease Control and Prevention (CDC) collaborated to perform standard microbiological and antimicrobial-drug susceptibility testing on isolates from case-patients. Since October 2010, the National Public Health Laboratory has identified 465 isolates, which were then forwarded to CDC for determination of MICs for 15 antimicrobial agents by broth microdilution (Sensititer; Trek Diagnostics Systems, Cleveland, OH, USA) according to manufacturer’s recommendations (Table). Resistance was defined by the Clinical and Laboratory Standards Institute interpretive standards, when available (3). The typical outbreak strain (2010EL-1786) displayed resistance to streptomycin, sulfisoxazole, trimethoprim/sulfamethoxazole, and nalidixic acid, and decreased susceptibility to ciprofloxacin and chloramphenicol (4). Resistance was caused by mutations in the QRDR regions of the gyrA and parC genes and presence of ICEVchHai1 containing the dfrA1, floR, strAB, and sul2 resistance genes (4). Table Susceptibility, resistance genes, and plasmids associated with Haiti Vibrio cholerae outbreak isolates In April of 2012, the 2 agencies began sentinel laboratory-based surveillance for acute diarrheal disease at 4 hospitals in Haiti (5). As part of this surveillance, fecal specimens were sent to the National Public Health Laboratory for organism isolation, identification, antimicrobial-drug testing, and subsequently to CDC for expanded antimicrobial-drug testing and molecular characterization. One isolate, 2012EL-2176, showed the typical resistance phenotype of the outbreak strain but additional resistance to ampicillin, amoxicillin/clavulanic acid, cefoxitin, ceftriaxone, ceftiofur; the tetracycline MIC was intermediate (Table). Analysis of this isolate by serotype, pulsed-field gel electrophoresis, multilocus variable number–tandem repeat analysis, and whole-genome sequencing confirmed that the isolate was similar to outbreak isolates (data not shown) (6). PCR and whole-genome sequencing analysis by use of ResFinder (http://www.genomicepidemiology.org/) identified the original outbreak resistance determinants and additional determinants (aac(3)-IIa, blaCMY-2, blaCTX-M-2, blaTEM-1, dfrA15, mphA, sul1, and tetA) (7). Plasmid transfer by electroporation into Escherichia coli (DH10B) confirmed that the resistance determinants were plasmid encoded. PCR-based replicon testing identified an IncA/C2 plasmid, and PCR and whole-genome sequencing confirmed that the plasmid encoded a unique set of resistance determinants (aac(3)-IIa, blaCMY-2, blaCTX-M-2, blaTEM-1, dfrA15, mphA, sul1, and tetA) and a second copy of the resistance genes floR, strAB, and sul2 identical to those located in ICEVchHai1 (8). Antimicrobial-drug susceptibility testing of the transformant demonstrated transfer of the resistance profile and additional resistance to chloramphenicol, tetracycline, and decreased susceptibility to azithromycin (Table). The lack of association between the presence of the resistance determinants floR and tetA and the lack of resistance in V. cholerae has been observed previously, possibly because of lower gene expression (9). The plasmid was mobilizable by conjugation (conjugation efficiency = 1.3–1.4 × 10−2) when E. coli J53 was used as the recipient. IncA/C plasmids are widespread in Enterobacteriaceae and commonly confer multidrug resistance. BLASTn (http://blast.ncbi.nlm.nih.gov/Blast.cgi) comparison of the completed plasmid p2012EL-2176 sequence with the National Center for Biotechnology Information nucleotide collection showed similarities to other IncA/C-blaCMY plasmids; most similarity (total score = 3.009 × 105) was to pAR060302, found in an E. coli isolate from a dairy calf (10). Most IncA/C-blaCMY plasmids have 3 resistance regions: sul2 region (floR-tetA-strAB-sul2), cmy-2 insertion region, and Tn21-like region (aad-aac). Plasmid p2012EL-2176 contains the sul2 and cmy-2 insertion regions and a putative arr3-drfA27-aadA16-sul1 resistance gene cassette at the Tn-21 location. This plasmid has additional resistance gene insertions: a putative cassette containing a blaTEM-1 and aac(3)-IIa gene upstream of the sul2 region and insertions of blaCTX-M-2, sul1, and mphA genes downstream of the arr3-drfA27-aadA16-sul1 cassette (Technical Appendix). Since discovery of isolate 2012EL-2176, sentinel surveillance has not detected increased antimicrobial-drug resistance among V. cholerae in Haiti. The ability of IncA/C plasmids to acquire novel resistance cassettes from multiple sources makes it difficult to hypothesize as to the origins of plasmid p2012EL-2176. Although this plasmid was most closely related to a plasmid found in E. coli, it was also closely related to plasmids in Salmonella, Klebsiella, and Providencia. Enterobacteriaceae are found in the environment and/or in the host gut; therefore, the isolate could have acquired the plasmid in the environment or within the host. The latter scenario would limit the possible spread of this plasmid and could explain its rarity. The original Haiti outbreak isolate has been shown to be poorly naturally transformable, accounting for the lack of acquired chromosomal genes and nearly homologous genomic content among outbreak isolates (6). Therefore, the acquisition of plasmids, and their resistance genes, may represent the major source of future variability among V. cholerae involved in the Haiti outbreak. Technical Appendix: Additional methods and comparison of plasmid p2012EL-2176 and plasmid pAR060302. Click here to view.(121K, pdf)

To the Editor: The agents of epidemic cholera are Vibrio cholerae toxigenic serogroups O1 and O139. Cholera symptoms include watery diarrhea and severe dehydration, which can rapidly result in death unless rehydration therapy is prompt (1). Antimicrobial agents may reduce the severity and duration of disease (1); commonly used are tetracyclines, fluoroquinolones, macrolides, and trimethoprim/sulfamethoxazole (1). However, V. cholerae resistance to antimicrobial drugs is increasing because of the accumulation of genetic mutations and the acquisition of resistance genes, which are usually transferred on mobile genetic elements such as integrating conjugative elements (ICEs) (1). As of March 12, 2014, the ongoing cholera outbreak that began in Haiti in October 2010 had caused 700,796 cases and 8,548 deaths (2). To characterize infections, the National Public Health Laboratory in Haiti and the US Centers for Disease Control and Prevention (CDC) collaborated to perform standard microbiological and antimicrobial-drug susceptibility testing on isolates from case-patients. Since October 2010, the National Public Health Laboratory has identified 465 isolates, which were then forwarded to CDC for determination of MICs for 15 antimicrobial agents by broth microdilution (Sensititer; Trek Diagnostics Systems, Cleveland, OH, USA) according to manufacturer’s recommendations (Table). Resistance was defined by the Clinical and Laboratory Standards Institute interpretive standards, when available (3). The typical outbreak strain (2010EL-1786) displayed resistance to streptomycin, sulfisoxazole, trimethoprim/sulfamethoxazole, and nalidixic acid, and decreased susceptibility to ciprofloxacin and chloramphenicol (4). Resistance was caused by mutations in the QRDR regions of the gyrA and parC genes and presence of ICEVchHai1 containing the dfrA1, floR, strAB, and sul2 resistance genes (4). Table Susceptibility, resistance genes, and plasmids associated with Haiti Vibrio cholerae outbreak isolates In April of 2012, the 2 agencies began sentinel laboratory-based surveillance for acute diarrheal disease at 4 hospitals in Haiti (5). As part of this surveillance, fecal specimens were sent to the National Public Health Laboratory for organism isolation, identification, antimicrobial-drug testing, and subsequently to CDC for expanded antimicrobial-drug testing and molecular characterization. One isolate, 2012EL-2176, showed the typical resistance phenotype of the outbreak strain but additional resistance to ampicillin, amoxicillin/clavulanic acid, cefoxitin, ceftriaxone, ceftiofur; the tetracycline MIC was intermediate (Table). Analysis of this isolate by serotype, pulsed-field gel electrophoresis, multilocus variable number–tandem repeat analysis, and whole-genome sequencing confirmed that the isolate was similar to outbreak isolates (data not shown) (6). PCR and whole-genome sequencing analysis by use of ResFinder (http://www.genomicepidemiology.org/) identified the original outbreak resistance determinants and additional determinants (aac(3)-IIa, blaCMY-2, blaCTX-M-2, blaTEM-1, dfrA15, mphA, sul1, and tetA) (7). Plasmid transfer by electroporation into Escherichia coli (DH10B) confirmed that the resistance determinants were plasmid encoded. PCR-based replicon testing identified an IncA/C2 plasmid, and PCR and whole-genome sequencing confirmed that the plasmid encoded a unique set of resistance determinants (aac(3)-IIa, blaCMY-2, blaCTX-M-2, blaTEM-1, dfrA15, mphA, sul1, and tetA) and a second copy of the resistance genes floR, strAB, and sul2 identical to those located in ICEVchHai1 (8). Antimicrobial-drug susceptibility testing of the transformant demonstrated transfer of the resistance profile and additional resistance to chloramphenicol, tetracycline, and decreased susceptibility to azithromycin (Table). The lack of association between the presence of the resistance determinants floR and tetA and the lack of resistance in V. cholerae has been observed previously, possibly because of lower gene expression (9). The plasmid was mobilizable by conjugation (conjugation efficiency = 1.3–1.4 × 10−2) when E. coli J53 was used as the recipient. IncA/C plasmids are widespread in Enterobacteriaceae and commonly confer multidrug resistance. BLASTn (http://blast.ncbi.nlm.nih.gov/Blast.cgi) comparison of the completed plasmid p2012EL-2176 sequence with the National Center for Biotechnology Information nucleotide collection showed similarities to other IncA/C-blaCMY plasmids; most similarity (total score = 3.009 × 105) was to pAR060302, found in an E. coli isolate from a dairy calf (10). Most IncA/C-blaCMY plasmids have 3 resistance regions: sul2 region (floR-tetA-strAB-sul2), cmy-2 insertion region, and Tn21-like region (aad-aac). Plasmid p2012EL-2176 contains the sul2 and cmy-2 insertion regions and a putative arr3-drfA27-aadA16-sul1 resistance gene cassette at the Tn-21 location. This plasmid has additional resistance gene insertions: a putative cassette containing a blaTEM-1 and aac(3)-IIa gene upstream of the sul2 region and insertions of blaCTX-M-2, sul1, and mphA genes downstream of the arr3-drfA27-aadA16-sul1 cassette (Technical Appendix). Since discovery of isolate 2012EL-2176, sentinel surveillance has not detected increased antimicrobial-drug resistance among V. cholerae in Haiti. The ability of IncA/C plasmids to acquire novel resistance cassettes from multiple sources makes it difficult to hypothesize as to the origins of plasmid p2012EL-2176. Although this plasmid was most closely related to a plasmid found in E. coli, it was also closely related to plasmids in Salmonella, Klebsiella, and Providencia. Enterobacteriaceae are found in the environment and/or in the host gut; therefore, the isolate could have acquired the plasmid in the environment or within the host. The latter scenario would limit the possible spread of this plasmid and could explain its rarity. The original Haiti outbreak isolate has been shown to be poorly naturally transformable, accounting for the lack of acquired chromosomal genes and nearly homologous genomic content among outbreak isolates (6). Therefore, the acquisition of plasmids, and their resistance genes, may represent the major source of future variability among V. cholerae involved in the Haiti outbreak. Technical Appendix: Additional methods and comparison of plasmid p2012EL-2176 and plasmid pAR060302. Click here to view.(121K, pdf)

Salmonella enterica is one of the most common bacterial causes of foodborne illness, and nontyphoidal Salmonella is estimated to cause ∼1.2 million illnesses in the United States each year. Plasmids are mobile genetic elements that play a critical role in the dissemination of antimicrobial resistance determinants. AmpC-type CMY β-lactamases (bla(CMY)) confer resistance to extended-spectrum cephalosporins and β-lactam/β-lactamase inhibitor combinations and are commonly plasmid-encoded. A variety of plasmids have been shown to encode CMY β-lactamases and certain plasmids may be associated with particular Salmonella serotypes or environmental sources. In this study, we characterized bla(CMY) β-lactamase-encoding plasmids among Salmonella isolates. Isolates of Salmonella from specimens collected from humans in 2007 were submitted to the Centers for Disease Control and Prevention National Antimicrobial Resistance Monitoring System laboratory for susceptibility testing. Three percent (65/2161) of Salmonella isolates displayed resistance to ceftriaxone (minimum inhibitory concentration [MIC] ≥4 mg/L) and amoxicillin/clavulanic acid (MIC ≥32 mg/L), a combination associated with the presence of a bla(CMY) mechanism of resistance. Sixty-four (98.5%) isolates were polymerase chain reaction-positive for bla(CMY) genes. Transformation and conjugation studies showed that 95% (61/64) of the bla(CMY) genes were plasmid-encoded. Most of the bla(CMY)-positive isolates were serotype Typhimurium, Newport, Heidelberg, and Agona. Forty-three plasmids were replicon type IncA/C, 15 IncI1, 2 contained multiple replicon loci, and 1 was untypeable. IncI1 plasmids conferred only the bla(CMY)-associated resistance phenotype, whereas IncA/C plasmids conferred additional multi-drug resistance (MDR) phenotypes to drugs such as chloramphenicol, sulfisoxazole, and tetracycline. Most of the IncI1 plasmids (12/15) were sequence type 12 by plasmid multi-locus sequence typing. CMY β-lactamase-encoding plasmids among human isolates of Salmonella in the United States tended to be large MDR IncA/C plasmids or single resistance determinant IncI1 plasmids. In general, IncI1 plasmids were identified among serotypes commonly associated with poultry, whereas IncA/C plasmids were more likely to be identified among cattle/beef-associated serotypes.