Abstract
Human infections with Salmonella enterica results in two major groups of diseases: gastroenteritis and typhoid fever. Clinical observations suggest that gastroenteritis, caused by non-typhoidal Salmonella serovars, is characterized by a massive neutrophil influx, which keeps the infection localized to the intestinal mucosa. In contrast, the absence of neutrophilic intestinal infiltrates in the acute phase of typhoid fever suggests a propensity for typhoidal Salmonella serovars (S. Typhi, S. Paratyphi A, S. Paratyphi B and S. Paratyphi C) to evade aspects of the innate immune response and cause a systemic infection. The fact that there are no virulence genes shared by typhoidal Salmonella serovars that are absent from non-typhoidal Salmonella serovars, suggests that this innate immune evasion is mediated by different mechanisms in different typhoidal serovars. This review discusses what is known about the clinical pathogenesis of typhoid fever.
Highlights
Typhoid fever, one of the major bacterial infections worldwide, is caused by the humanadapted S. enterica serovar Typhi [1]
Invasion of the intestinal mucosa by nontyphoidal Salmonella serovars (NTS) is detected by the innate immune system of the host, which responds by recruiting neutrophils to the site of infection [24]
Typhi expresses virulence mechanisms allowing it to down-regulate a pathogen recognition receptors (PRRs)-mediated host response in the intestinal mucosa that results in the absence of neutrophil infiltration and inflammatory diarrhoea
Summary
One of the major bacterial infections worldwide, is caused by the humanadapted S. enterica serovar Typhi [1]. Raffatellu et al – Clinical pathogenesis of typhoid fever of time, indicating that the organism has a greater propensity to evade immune responses than nontyphoidal Salmonella serovars. Typhi does not require an immunodeficient host to cause a systemic infection, as shown by its ability to cause typhoid fever in both healthy individuals and AIDS patients with similar efficiency.
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