Virulence System of <i>Salmonella</i> with Special Reference to <i>Salmonella enterica</i>

Abstract

Virulence system of Salmonella is very complex as many genes are involved in contributing the virulence of Salmonella. Some of the genes are involved in enhancing the invasion of organism in host defense system; some are playing their role in survival and replication of organism inside the host, while some genes are involved in the production of molecules that produce the clinical symptoms of the disease. Broadly, we can classify virulence genes into two categories: genes that are located on the virulence contributing plasmid like spvc gene and genes that are chromosomal in nature like stn. On chromosome, virulence genes are located in various clusters, which are known as Salmonella pathogenicity islands and till today seventeen pathogenicity islands have been identified. The genes located on these pathogenicity islands produce several effector molecules, which assist in invasion, replication and survival of Salmonella inside the host. The role of plasmid is still not very clear, but it is presumed that the genes located on virulence plasmids affect the intracellular growth of Salmonella in macrophages. Though lot of research work has been carried out to understand the virulence regulation system of Salmonella, still many questions are to be answered to decode the virulence regulation of Salmonella.

Detection of Salmonella pathogenicity island and Salmonella plasmid virulence genes in Salmonella Enteritidis originated from layer and broiler farms in Java Island

“…There are a total of 17 SPI described in Salmonella [22]. SPI-1 to SPI-5 have been widely characterized and can be found in most S. enterica .…”

“…While the genes that make up each SPI are not known whether all serovars have the same SPI constituent gene. In S. Typhimurium [23] and S. Typhi [22], the SPI-1 to SPI-5 genes have been wholly identified. Amavisit et al [24] reported that there were genetic variations between SPI-1, SPI-3, and SPI-5, while the genetic variation of SPI-4 and SPI-2 was not easily changed among 13 Salmonella serovars isolated from cattle, pigs, poultry, horses, environment, and humans [24].…”

“…Salmonella contained in the feed will enter the digestive tract, after passing gastric acid will go to the small intestine, large intestine, and cecum which has a low pH, and Salmonella can survive in a low pH environment. In the small intestine, Salmonella will attach to host epithelial cells, then SPI-1 will express the first Type 3 Secretion Systems (T3SS) or T3SS-1 which are multiprotein complexes that facilitate bacteria in the process of invasion and absorption through endothelial [22]. The T3SS-1 acts as a syringe molecule in the form of a channel to connect the bacterial cytoplasm with the membrane of the host cell.…”

Thymol and Carvacrol Downregulate the Expression of Salmonella typhimurium Virulence Genes during an In Vitro Infection on Caco-2 Cells

“…Structural proteins are responsible for the assembly of the T3SS apparatus, formed by two rings crossing the inner and outer bacterial membrane, linked to a needle-like system that pierces the host cellular membrane [10,11]. The latter structure is crucial for the transport of the effector proteins, delivered by translocators from the bacterial cell into the host: here, effectors manage fundamental changes enabling key steps for Salmonella pathogenesis [12]. During the bacterial infection, Salmonella invade the enterocyte and survive into the host cytoplasm surrounded by large vesicles, called Salmonella-containing vacuoles (SCV) [13].…”

<p>Molecular Mechanisms of <em>Salmonella</em> Effector Proteins: A Comprehensive Review</p>

“…125,126 Another effector that mediates apoptosis in epithelial cells is SrfT, which is encoded in SPI-2. 127 Moreover, SrfH mediates actin remodeling and is located in prophage. SrfD, SrfE, SdrI, SrfK, SrfL, and SrfM also are encoded by Phage.…”