Molecular Characterization ofSalmonella entericaSerotype Enteritidis Isolates from Humans by Antimicrobial Resistance, Virulence Genes, and Pulsed-Field Gel Electrophoresis

Abstract

Salmonella enterica serovar Enteritidis (S. Enteritidis) is a major serovar associated with human salmonellosis. A total of 425 clinical S. Enteritidis isolates of human origin were collected between June 2009 and September 2010 from North Carolina. The isolates were further characterized for antimicrobial susceptibility, antimicrobial resistance coding determinants, virulence genes, and fingerprint profiles to determine whether they were similar or different to the S. Enteritidis strain responsible for the human outbreak due to consumption of contaminated eggs. Ten different antimicrobial resistance phenotypes were observed with the highest frequency of resistance exhibited to ampicillin (n = 10; 2.35%). The isolates were predominantly pansusceptible (n = 409; 96.23%); however, seven isolates were multidrug resistant (MDR; i.e., resistant to three or more antimicrobials). Extended spectrum b-lactamase (ESBL) coding genes (bla TEM and bla PSE) were detected in the ampicillin-resistant isolates, whereas a single MDR isolate tested positive for class 1 integron (1 kb). The majority of the isolates (n = 422; 99.3%) carried the invA, mgtC, stn, sopB, sopE1, and sefA virulence genes. However, 37 (8.7%) and 46 (10.82%) S. Enteritidis isolates tested negative for the plasmid encoded genes spvC and rck, respectively. Pulsed-field gel electrophoresis (PFGE) typing of 118 S. Enteritidis isolates by restriction enzymes XbaI and BlnI resulted in seven clusters, each with a discriminatory index (DI) of 0.715 and 0.785, respectively. The combination of XbaI-BlnI patterns generated a dendrogram with 14 clusters and a higher DI of 0.914. The PFGE profile of 80 isolates matched 100% with the S. Enteritidis strain that has been cited for the recent outbreak in the United States due to consumption of contaminated eggs. In conclusion, we identified a genotypic similar S. Enteritidis population in our study based on antimicrobial susceptibility, virulence gene, and PFGE fingerprint profiles.

Prevalence of Salmonella species from poultry eggs of local stores in Duhok

“…15 In USA (2010), Salmonellosis outbreak associated with contaminated eggshells with Salmonella showed the importance of shell contamination, which this outbreak caused illness in 1939 persons. 16 The ability of Salmonella enteritidis to persist on the surface of the egg shell and contaminate the content of egg when eggs are broken for preparation of food, which could pose a potential health risk to the society. Therefore, removal of the quails wastes and disinfection can greatly reduce Salmonella contamination on the shell and the content.…”

Genotypic diversity, pathogenic potential and the resistance profile of Salmonella Typhimurium strains isolated from humans and food from 1983 to 2013 in Brazil

“…The SPI-1-associated proteins include the following: Sop (SopA-E), effector proteins; SipA and InvA, associated with invasion; SipD, a translocon assembly protein; and FlgK, FljB and FlgL proteins, associated with flagella. The SPI-2-associated proteins, such as SsaR and SifA, are associated with survival and replication within the host cells (Giacomodonato et al, 2007;Hur et al, 2011;Shah et al, 2011;Zou et al, 2012). Moreover, there are virulence-associated plasmids that have the spv operon, which consists of five genes (spvRABCD) associated with Salmonella survival and growth in macrophages (Rychlik et al, 2006).…”

Molecular Detection of InvA, OmpA and Stn Genes in Salmonella Serovars from Broilers in Egypt

“…In accordance, (Murugkar et al 2003 andShalaby, 2012) reported that stn gene was detected in all the isolated Salmonella strains. Moreover, (Zou et al, 2012) identified stn gene in all 425 isolates (100%) of poultry origin. Regarding to ompA gene, this gene have a significant role in adaptation of Salmonella to environmental stresses, as well as adhesion, invasion and damage of host tissue or evasion of host defense resulting in clinical disease or death (Krishnan and Prasadarao,2012).…”