Abstract
Salmonella enterica is one of the most common causes of foodborne illness in the United States. Although salmonellosis is usually self-limiting, severe infections typically require antimicrobial treatment, and ceftriaxone, an extended-spectrum cephalosporin (ESC), is commonly used in both adults and children. Surveillance conducted by the National Antimicrobial Resistance Monitoring System (NARMS) has shown a recent increase in ESC resistance among Salmonella Heidelberg isolated from food animals at slaughter, retail meat, and humans. ESC resistance among Salmonella in the United States is usually mediated by a plasmid-encoded bla(CMY) β-lactamase. In 2009, we identified 47 ESC-resistant bla(CMY)-positive Heidelberg isolates from humans (n=18), food animals at slaughter (n=16), and retail meats (n=13) associated with a spike in the prevalence of this serovar. Almost 90% (26/29) of the animal and meat isolates were isolated from chicken carcasses or retail chicken meat. We screened NARMS isolates for the presence of bla(CMY), determined whether the gene was plasmid-encoded, examined pulsed-field gel electrophoresis patterns to assess the genetic diversities of the isolates, and categorized the bla(CMY) plasmids by plasmid incompatibility groups and plasmid multi-locus sequence typing (pMLST). All 47 bla(CMY) genes were found to be plasmid encoded. Incompatibility/replicon typing demonstrated that 41 were Incl1 plasmids, 40 of which only conferred bla(CMY)-associated resistance. Six were IncA/C plasmids that carried additional resistance genes. pMLST of the Incl1-bla(CMY) plasmids showed that 27 (65.8%) were sequence type (ST) 12, the most common ST among bla(CMY)-Incl1 plasmids from Heidelberg isolated from humans. Ten plasmids had a new ST profile, ST66, a type very similar to ST12. This work showed that the 2009 increase in ESC resistance among Salmonella Heidelberg was caused mainly by the dissemination of bla(CMY) on Incl1 and IncA/C plasmids in a variety of genetic backgrounds, and is likely not the result of clonal expansion.
Generated Summary
This study, published in the journal Foodborne Pathogens and Disease in 2012, investigates the characterization of extended-spectrum cephalosporin-resistant Salmonella enterica serovar Heidelberg isolates. The research, conducted in the United States in 2009, aimed to understand the increase in resistance to extended-spectrum cephalosporins (ESCs) among Salmonella Heidelberg strains. The study examined isolates from food animals at slaughter, retail meat, and humans. The methodology involved identifying the presence of bla(CMY) genes (which confer resistance), determining whether the genes were plasmid-encoded, and analyzing pulsed-field gel electrophoresis patterns to assess genetic diversity. The study also categorized bla(CMY) plasmids based on plasmid incompatibility groups and plasmid multi-locus sequence typing (pMLST) to understand the mechanisms of resistance spread.
Key Findings & Statistics
- The study identified 47 ESC-resistant bla(CMY)-positive Heidelberg isolates.
- 18 isolates were from humans.
- 16 isolates were from food animals at slaughter.
- 13 isolates were from retail meats.
- Almost 90% (26/29) of the animal and meat isolates were from chicken carcasses or retail chicken meat.
- All 47 bla(CMY) genes were plasmid encoded.
- 41 isolates were Incl1 plasmids.
- 40 of which only conferred bla(CMY)-associated resistance.
- 6 were IncA/C plasmids that carried additional resistance genes.
- 27 (65.8%) of Incl1-bla(CMY) plasmids were sequence type (ST) 12.
- Ten plasmids had a new ST profile, ST66.
Other Important Findings
- The study found a recent increase in ESC resistance among Salmonella Heidelberg, particularly in isolates from food animals, retail meat, and humans.
- ESC resistance was mediated by plasmid-encoded bla(CMY) β-lactamase.
- The study demonstrated that the increase in ESC resistance was mainly due to the dissemination of bla(CMY) on Incl1 and IncA/C plasmids.
- The study showed that the 2009 increase in ESC resistance was not the result of clonal expansion.
Limitations Noted in the Document
The study does not explicitly mention any limitations or constraints. However, potential limitations could include the scope of the study, which is limited to a specific timeframe (2009) and geographic location (United States). Also, since the research focuses on genetic analysis, it may not fully address the environmental or behavioral factors contributing to the spread of antibiotic resistance. The study is also limited by the types of samples it examined, not including other potential sources of Salmonella Heidelberg. Finally, it’s also possible that the study had limitations associated with sample collection and representativeness of the wider population.
Conclusion
The research successfully identified the mechanisms behind the increase in extended-spectrum cephalosporin resistance among Salmonella Heidelberg strains in the United States in 2009. The key finding was the dissemination of bla(CMY) genes on Incl1 and IncA/C plasmids, which were not due to clonal expansion. This shows the importance of surveillance and monitoring for antibiotic resistance. Further research can focus on how these plasmids spread within different populations, and how to decrease the spread. It’s important to note that the widespread use of ESCs in both human and animal medicine could promote the selection and spread of resistant bacteria. The findings highlight the significance of a One Health approach in addressing antibiotic resistance. This includes the need for improved antimicrobial stewardship practices in both human and animal medicine. Also, the research supports the need for ongoing surveillance programs to monitor changes in antimicrobial resistance patterns in foodborne pathogens. This helps to identify emerging threats and to inform public health interventions.