Abstract
Non-typhoidal Salmonellae (NTS) belong to Salmonella enterica subspecies enterica and are common causes of foodborne illnesses in humans. Diarrhea is a common symptom but infection occasionally results in life-threatening systemic involvement. One member of the group, S. enterica subspecies enterica serovar Typhimurium has been extensively studied in live animal models particularly mice and cattle, leading to a better understanding of the pathogenesis of NTS and the development of diarrhea, respectively. This comprehensive review provides an insight into the genetic regulation of over 200 virulence determinants and their involvement in the four steps of Salmonella pathogenesis, namely: attachment, invasion, macrophage survival and replication, and systemic dissemination. There is, however, a paucity of information on the functions of some virulence factors present on the Salmonella pathogenicity islands (SPIs). The emergence of next generation sequencing (NGS) technology and the availability of more bacterial genomes should provide further insights into the biology of virulence determinants, mechanisms of NTS pathogenesis and host adaptation of Salmonella. The new knowledge should translate into improvement and innovations in food safety, and control of salmonellosis as well as better understanding of zoonotic infections in the context of One Health capturing the risks to humans, animals and the environment.
Highlights
Non-typhoidal Salmonella (NTS), a major cause of diarrheal disease globally, is estimated to cause 93 million enteric infections and 155,000 diarrheal deaths each year and is a leading cause of foodborne infections worldwide [1]
This review provides an outline of over 200 identified virulence determinants and details of their involvement in the four steps of Salmonella pathogenesis, namely: attachment, invasion, intramacrophage survival/replication and systemic dissemination
The genetic regulation of only some of the virulence determinants have been elucidated in live animal models such as mice and cattle, and this has enriched our understanding of the pathogenesis and mechanism of diarrhea and systemic disease
Summary
Non-typhoidal Salmonella (NTS), a major cause of diarrheal disease globally, is estimated to cause 93 million enteric infections and 155,000 diarrheal deaths each year and is a leading cause of foodborne infections worldwide [1]. Examples of host-restricted Salmonella are serovars Typhi, Gallinarum, and Abortusovis, and they predictably cause systemic infection in their hosts namely, humans, fowls and ovines, respectively [7]. Another group of serovars are host-adapted including Dublin and Choleraesuis and primarily cause. The most common non-adapted Salmonella are serovars Typhimurium and Enteritidis and they have been studied in live animal models such as mice and cattle, leading to a better understanding of the pathogenesis of NTS and the development of diarrhea [7]. Many virulence factors have distinct and unique functions but cooperative crosstalk has been documented at the different steps of infection, e.g., protein products of genes encoded on two Salmonella pathogenicity islands (SPI), SPI-2 and SPI-4
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