Salmonella challenges: prevalence in swine and poultry and potential pathogenicity of such isolates.

Salmonellosis is the second leading cause of bacterial foodborne illness in the United States, and the great majority of these infections are associated with the consumption of products such as meat, poultry, eggs, milk, seafood, and fresh produce contaminated with Salmonella. The per capita consumption of meat and poultry in United States has increased significantly over the past century. This increase is especially evident with poultry products, where there has been a nearly 6-fold increase in chicken consumption and 17-fold increase in turkey consumption since 1909. The per capita consumption of pork has also increased over this time from 18.7 to 21.7 kg/yr. With this increase in meat and poultry consumption, the dynamics of animal production and consumer exposure have changed leading to new challenges in limiting salmonellosis. To meet the demands of consumers, more intensive agricultural practices have been adopted, which has likely changed the population characteristics of Salmonella present among poultry flocks and swine populations. In Salmonella isolated from swine in the United States, S. Typhimurium has replaced S. Choleraesuis as the predominant serovar in recent years. Among isolates from turkeys collected in 2004, serovars S. Senftenberg and S. Hadar were most common overall; however, S. Heidelberg was most common from clinical diagnostic sources, potentially indicating increased virulence. Salmonella Heidelberg was also the most commonly detected serovar among chicken isolates from clinically ill birds and Salmonella surveillance samples. Overall among the 10 serovars most commonly associated with human infections, 6 are also found in the top serovars of swine and poultry. These include S. Typhimurium, S. Enteritidis, S. Heidelberg, S. Montevideo, S. Saintpaul, and S. I 4,[5],12:i:-.

Food animal-associated Salmonella challenges: pathogenicity and antimicrobial resistance.

Salmonellosis is a worldwide health problem; Salmonella infections are the second leading cause of bacterial foodborne illness in the United States. Approximately 95% of cases of human salmonellosis are associated with the consumption of contaminated products such as meat, poultry, eggs, milk, seafood, and fresh produce. Salmonella can cause a number of different disease syndromes including gastroenteritis, bacteremia, and typhoid fever, with the most common being gastroenteritis, which is often characterized by abdominal pain, nausea, vomiting, diarrhea, and headache. Typically the disease is self-limiting; however, with more severe manifestations such as bacteremia, antimicrobial therapy is often administered to treat the infection. Currently, there are over 2,500 identified serotypes of Salmonella. A smaller number of these serotypes are significantly associated with animal and human disease including Typhimurium, Enteritidis, Newport, Heidelberg, and Montevideo. Increasingly, isolates from these serotypes are being detected that demonstrate resistance to multiple antimicrobial agents, including third-generation cephalosporins, which are recommended for the treatment of severe infections. Many of the genes that encode resistance are located on transmissible elements such as plasmids that allow for potential transfer of resistance among strains. Plasmids are also known to harbor virulence factors that contribute to Salmonella pathogenicity. Several serotypes of medical importance, including Typhimurium, Enteritidis, Newport, Dublin, and Choleraesuis, are known to harbor virulence plasmids containing genes that code for fimbriae, serum resistance, and other factors. Additionally, many Salmonella contain pathogenicity islands scattered throughout their genomes that encode factors essential for bacterial adhesion, invasion, and infection. Salmonella have evolved several virulence and antimicrobial resistance mechanisms that allow for continued challenges to our public health infrastructure.

Detection of Iss and Bor on the surface of Escherichia coli.

AIMS: To confirm the presence of Iss and Bor on the outer membrane of Escherichia coli using Western blots of outer membrane protein (OMP) preparations and fluorescence microscopy, and explore the use of fluorescence microscopy for the detection of avian pathogenic E. coli (APEC) and diagnosis of avian colibacillosis. METHODS AND RESULTS: Knockout mutants of iss and bor were created using a one-step recombination of target genes with PCR-generated antibiotic resistance cassettes. Anti-Iss monoclonal antibodies (Mabs) that cross-react with Bor protein were used to study the mutants relative to the wild-type organism. These Mabs were used as reagents to study OMP preparations of the mutants with Western blotting and intact E. coli cells with fluorescence microscopy. Iss and Bor were detected in Western blots of OMP preparations of the wild type. Also, Iss was detected on Deltabor mutants, and Bor was detected on Deltaiss mutants. Iss and Bor were also detected on the surface of the intact, wild-type cells and mutants using fluorescence microscopy. CONCLUSIONS: These results demonstrate that Bor and Iss are exposed on E. coli's outer membrane where they may be recognized by the host's immune system. SIGNIFICANCE AND IMPACT OF THE STUDY: To our knowledge, this is the first report confirming Iss' location in the outer membrane of an E. coli isolate. Such surface exposure has implications for the use of these Mabs for APEC detection and colibacillosis control.

Resistance to serum complement, iss, and virulence of avian Escherichia coli.

Control of avian colibacillosis is hampered by lack of easily identifiable markers for virulent Escherichia coli. Resistance to serum complement appears to be a widespread trait of virulent avian E. coil, suggesting that bacterial factors promoting survival in serum may be useful in discriminating between virulent and avirulent isolates. Such distinguishing factors may prove useful in diagnostic protocols or as targets in future colibacillosis control protocols. Interestingly, the factors responsible for resistance to complement differ in the E. coli isolated from mammalian and avian hosts, which may reflect differences in the nature of avian and mammalian colibacillosis. In some cases, genetic determinants for serum complement resistance in avian E. coli are found on aerobactin- or Colicin V-encoding plasmids. One such gene, iss, first described for its role in the serum resistance associated with a ColV plasmid from a human E. coli isolate, occurs much more frequently in isolates from birds with colibacillosis than in faecal isolates from healthy birds. Efforts to identify the genomic location of iss in a single, virulent avian E. coli isolate have revealed that it occurs in association with several purported virulence genes, all linked to a large conjugative R plasmid. At this time, it is not known whether iss merely marks the presence of a larger pathogenicity unit or is itself a contributor to virulence. Nevertheless, the presence of the complement-resistance determinant, iss, may be a marker of virulent avian E. coli exploitable in controlling avian colibacillosis.

Virulence factors of Escherichia cofi from cellulitis or colisepticemia lesions in chickens.

This study was designed to compare virulence factors of cellulitis-derived Escherichia coli to colisepticemic E. coli in order to clarify whether E. coli associated with cellulitis comprise a unique subset of pathogenic E. coli. Isolates were tested for serotype, capsule, aerobactin production, colicin production, the presence of the iss gene, and serum resistance. Untypable isolates made up the greatest percentage of each group. Serotypes O2 and O78 were the most commonly identified among both groups of isolates. No statistical differences in the distribution of aerobactin or colicin production, capsule, or iss gene were observed between groups. Cluster analysis showed that 90% of the E. coli isolates had greater than 42% livability in serum-resistance tests. No separation of colisepticemic vs. cellulitis E. coli isolates was observed on the basis of SR. Colicin production by E. coli was highly correlated with serum resistance (P = 0.0029). These data suggest that cellulitis E. coli have virulence traits similar to those of colisepticemic E. coli.