Salmonella, the host and disease: a brief review

Abstract

Salmonella species cause substantial morbidity, mortality and burden of disease globally. Infections with Salmonella species cause multiple clinical syndromes. Central to the pathophysiology of all human salmonelloses is the induction of a strong host innate immune/inflammatory response. Whether this ultimately reflects an adaptive advantage to the host or pathogen is not clear. However, it is evident that both the host and pathogen have evolved mechanisms of triggering host responses that are detrimental to the other. In this review, we explore some of the host and pathogenic mechanisms mobilized in the two predominant clinical syndromes associated with infection with Salmonella enterica species: enterocolitis and typhoid.

Salmonella Typhi: from a Human Pathogen to a Vaccine Vector

“…Both macrophages and T cells may be involved in cell-mediated immunity to Salmonella infection, while antibody also plays a role. Central to the pathophysiology of all human salmonellosis is the induction of a strong host innate immune/inflammatory response (52). Both the host and pathogen have evolved mechanisms of triggering host responses.…”

First case report of blood and urine cultures positive bacteraemia by Salmonella enterica serotype Choleraesuis from India

“…It primarily has four different clinical manifestations: enteric fever, gastroenteritis, bacteraemia and an asymptomatic carrier state (Coburn et al, 2007). Although systemic infections such as enteric fever caused by serovars Typhi and Paratyphi are common in developing countries such as India (Ochiai et al, 2008), invasive salmonellosis caused by non-typhoidal Salmonella (NTS) species has been more frequently reported from sub-Saharan African countries (Gordon et al, 2008;Mtove et al, 2010) and south-eastern Asian countries such as Taiwan (Chen et al, 2007;Chiu et al, 2004;Jean et al, 2006).While a longer duration of fever and younger age (school age) are associated with typhoid fever, invasive NTS infections are more common in patients with malaria, anaemia, jaundice, hypoglycaemia, malnutrition, HIV infection and other immunosuppressive conditions (Chen et al, 2007;Chiu et al, 2004;Gordon et al, 2008;Mtove et al, 2010).…”

Protective Role of Akt2 in Salmonella enterica Serovar Typhimurium-Induced Gastroenterocolitis

“…Salmonella enterica is a Gram-negative facultative intracellular bacterial pathogen capable of infecting a number of hosts and causing significant morbidity and mortality globally (12). S. enterica serovar Typhimurium infection in humans is typically acquired by ingestion of contaminated food or water, leading to acute gastroenteritis with clinical manifestations of diarrhea, abdominal pain, nausea, and vomiting (12,49).…”

“…S. enterica serovar Typhimurium infection in humans is typically acquired by ingestion of contaminated food or water, leading to acute gastroenteritis with clinical manifestations of diarrhea, abdominal pain, nausea, and vomiting (12,49). After ingestion, Salmonella reaches the small intestine, where it invades the mucosa by penetrating the epithelial barrier through microfold (M) cells, which subsequently transport it to lymphoid cells in the underlying Peyer's patches (29,34), where the bacteria multiply and disseminate throughout the body.…”

“…Such bacterial cell-epithelial cell interactions result in the secretion of chemoattractant molecules such as cytokines and chemokines that recruit neutrophils, monocytes, dendritic cells, and lymphocytes from the circulation to the site of infection (53). While the recruited phagocytes engulf and destroy the invading bacteria to help control the infection (40), infiltration of polymorphonuclear lymphocytes (PMNs) also causes the erosion of the intestinal mucosa, giving rise to the histopathological characteristics of intestinal inflammation (12,16). Studies of the cellular and molecular mechanisms involved in Salmonellainduced intestinal inflammation have been greatly facilitated by the development of an acute gastroenteritis model in mice in response to oral S. Typhimurium infection (2).…”