Salmonellosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

The pathogenesis of salmonellosis varies between different Salmonella serovars and depends on the interaction of multiple virulence programs with host defense mechanisms. These interactions occur in different tissues and at various stages of infection leading to variable host morbidity and mortality. Salmonella enterica serovar Typhi (S. Typhi) and Salmonella Paratyphi A both cause bacteremia. Non-typhoidal Salmonella (NTS) usually cause self-limiting diarrhea although NTS may lead to secondary bacteremia. Immunocompromised individuals and infants in sub-Saharan Africa may develop primary NTS bacteremia.

Typhoidal and nontyphoidal Salmonella (NTS) serovars elicit different immune responses in humans. NTS serovars induce a greater inflammatory interaction with human gut mucosa compared to typhoidal serovars. In animal models, S. enterica colonizes the intestine and localizes to the apical epithelium, inducing inflammatory changes. These changes include PMN infiltration, necrosis of the epithelium, crypt abscesses, and edema. The recruitment of neutrophils to the intestinal epithelium is the histopathological hallmark of intestinal disease. The various S. enterica serovars that are able to cause intestinal disease do so by attracting PMNs, specifically by inducing interleukin-8. With serovar Typhimurium, this recruitment occurs within the first few hours of infection. Massive migration of neutrophils and exudate secretion into the intestinal lumen then occurs approximately 8-10 hours after infection. The onset of diarrhea begins between 8-72 hours after colonization. Salmonella serovar Typhimurium enterocolitis is the most severe in the caudal ileum, cecum, and proximal colon.

In typhoid infection, ''S''. Typhi bacteria is first ingested, usually through contaminated water or animal products. The bacteria is able to withstand the highly acidic environment of the stomach and proceeds to colonize the ileum and cecum. Upon colonization, the bacteria can gain entry into host circulation by either invading phagocytic M-cells or through dendritic cell uptake. Dissemination via the reticuloendothelial system (RES)occurs once extraintestinal infection is achieved. The bacteria can then take up residence in splenocytes, mostly within macrophages, dendritic cells, and polymorphonuclear leukocytes. Hepatocytes and other hepatic non-professional phagocytes may also serve as targets for infection and replication. Once Salmonella is internalized in the host cells, it resides in the Salmonella containing vacuole(SCV). In phagocytes, this specific vacuole formation evades fusion with the phagocyte oxidase complex. The ability of Salmonella to survive phagocytic killing is a central component of the bacteria's virulence.

Transmission

Salmonella bacteria are widely distributed in domestic and wild animals. They are prevalent in food animals such as poultry, pigs, cattle; and in pets, including cats and dogs, birds and reptiles such as turtles. Salmonella can pass through the entire food chain from animal feed, primary production, and all the way to households or food-service establishments and institutions. Salmonellosis in humans is generally contracted through the consumption of contaminated food of animal origin (mainly eggs, meat, poultry and milk), although other foods, including green vegetables contaminated by manure, have been implicated in its transmission. Person-to-person transmission through the faecal-oral route can also occur. Human cases also occur where individuals have contact with infected animals, including pets. These infected animals often do not show signs of disease.

Human typhoid usually occurs after ingesting water or animal products contaminated with S. Typhi. Close contact with carriers or infected individuals may also cause typhoid.

References

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