Risk factors for Salmonella Typhimurium DT104 and non-DT104 infection: a Canadian multi-provincial case-control study

Doré, Kathryn; Buxton, Jane A.; Henry, Brandon V.; Pollari, Frank; Middleton, Dean; Fyfe, Murray; Ahmed, Rafiq; Michel, Pascal; King, Alejandra; Tinga, Carol; Wilson, Jeffrey B.

doi:10.1017/s0950268803001924

Cited by 47 publications

(35 citation statements)

References 18 publications

(20 reference statements)

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“…Interestingly, while prior antimicrobial use has been shown in multiple epidemiological studies to increase the risk of infection with both antibioticresistant and drug-sensitive serotypes of S. Typhi [14,16,17], two recent case-control studies in Turkey and Bangladesh failed to show such a link [12,13]. It is postulated that, in addition to providing a selective advantage to resistant S. Typhi strains, antimicrobial exposure can lead to prolonged alterations in gastro-intestinal flora and a decreased barrier to bacterial colonisation, lowering the dose of Salmonella necessary to cause infection [18,19].…”

Section: Transmission and Risk Factorsmentioning

confidence: 99%

The Burden of Enteric Fever

Kothari

Pruthi

Chugh

2008

J Infect Dev Ctries

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Enteric fever is a disease of developing countries associated with poor public health and low socio-economic indices. Cases of enteric fever occurring in travelers returning to the United States and the UK suggest that it is present across the developing world but that the Indian subcontinent represents a hotspot of disease activity. The best figures available for the global burden of enteric fever support this and suggest that Africa (50/ 100,000) has a far lower burden of disease than Asia (274/100,000). However these figures are based mainly on data for typhoid fever in Asia and the data for returning travelers is biased by preferred travel destinations. Given that most socio-economic indices, including known risk factors for enteric fever, such as provision of safe drinking water and sanitation, are much lower in most parts of Africa than in South-East and South-Central Asia it seems remarkable that Africa has such a low burden of disease. In such a scenario, rather than comparing whole continents, it may be more relevant to estimate region-specific burden of disease. It is clear is that there is an urgent need for more population-based studies of typhoid fever incidence in different parts of Africa to clarify the typhoid fever situation for the continent and so guide public health intervention.

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Section: Transmission and Risk Factorsmentioning

confidence: 99%

The Burden of Enteric Fever

Kothari

Pruthi

Chugh

2008

J Infect Dev Ctries

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“…This model has been utilized to demonstrate that Salmonella-induced intestinal inflammation requires bacterial activity dependent on the SPI1 effector sipA, as well as functional flagella and chemotaxis (1,11,24). Antibiotic treatment is a risk factor for acquiring S. enterica serovar Typhimurium colitis (6), and the dependence of inflammation on streptomycin treatment is inferred to be due to alterations in the host microflora, resulting in environmental changes and decreased colonization resistance (20,21).…”

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confidence: 99%

Salmonella entericaSerovar Typhimurium Pathogenicity Island 2 Is Necessary for Complete Virulence in a Mouse Model of Infectious Enterocolitis

2005

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Salmonella species cause a wide range of disease in multiple hosts. Salmonella enterica serovar Typhimurium causes self-limited intestinal disease in humans and systemic typhoid-like illness in susceptible mice. The prevailing dogma in murine S. enterica serovar Typhimurium pathogenesis is that distinct virulence mechanisms-Salmonella pathogenicity islands 1 and 2 (SPI1 and SPI2)-perform distinct roles in pathogenesis, the former being important for invasion and intestinal disease and the latter important for intracellular survival and systemic persistence and disease. Although evidence from bovine infections has suggested that SPI2 has a role in ileal disease, there is no evidence that SPI2 is important for inflammation in a disease that more closely recapitulates human colitis. Using S. enterica serovar Typhimurium strains that lack functional type III secretion systems, we demonstrate that SPI2 is essential for complete virulence in murine infectious enterocolitis. , we demonstrate that SPI1 mutants are unable to cause intestinal disease 48 h after infection and that SPI2-deficient bacteria also cause significantly attenuated typhlitis. We show that at the peak of inflammation in the cecum, SPI2 mutants induce diminished intercellular adhesion molecule 1 expression and neutrophil recruitment but that wild-type and mutant Salmonella are similarly distributed in the lumen of the infected organ. Finally, we demonstrate that attenuation of intestinal inflammation is accompanied by resolution of typhlitis in the mutant, but not wild-type, infections. Collectively, these results indicate that SPI2 is needed for enterocolitis, as well as for systemic disease.

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“…The presence of S. enterica serovar Typhimurium in worker hands and contact surface areas eventually causes illness to consumers. Infections and outbreaks with S. enterica serovar Typhimurium have been linked to consumption of contaminated food such as vegetable salads (Doré et al, 2004;Wasyl et al, 2006).…”

Section: Resultsmentioning

confidence: 99%