Pathogenicity of foodborne Salmonella.

ABSTRACT

Salmonella remains a leading etiological agent in bacterial foodborne diseases. Although human salmonellosis generally presents as a self-limiting episode of enterocolitis, the disease can degenerate into chronic and debilitating conditions. Antibiotic treatment of uncomplicated salmonellosis is contra-indicated because it tends to prolong the carrier state. Clinical management of systemic infections with newer drugs such as third-generation cephalosporins and quinolones is most promising, particularly in light of the increasing resistance of Salmonella to the traditional ampicillin, chloramphenicol and trimethoprim sulfamethoxazole therapeutic agents. Research into the development of effective vaccines from avirulent auxotrophic or from virulence plasmid-cured strains may ultimately facilitate the control of salmonellosis in human populations and in various agricultural sectors. Human salmonellosis reflects the outcome of a confrontation between humoral and cellular immune responses of the host, and virulence determinants of the invasive pathogen. Following an adhesion-dependent attachment of salmonellae to lumenal epithelial cells, the invasive pathogen is internalized within an epithelial cell by a receptor-mediated endocytotic process. Cytotoxin localized in the bacterial cell wall suggestively may facilitate Salmonella entry into the epithelial layer. Cytoplasmic translocation of the infected endosome to the basal epithelial membrane culminates in the release of salmonellae in the lamina propria. During this invasive process, Salmonella secretes a heat-labile enterotoxin that precipitates a net efflux of water and electrolytes into the intestinal lumen. Although non-typhoid salmonellae generally precipitate a localized inflammatory response in deeper tissues via lymphatics and capillaries, and elicit a major immune response. Current research efforts have focused on the molecular characterization and role of virulence plasmids and chromosomal genes in Salmonella pathogenicity.