Salmonella interactions with professional phagocytes.

Abstract

Salmonella enterica serotype Typhimurium (S. typhimurium) initiates infection by adhering to and invading the intestinal mucosa. Bacterial multiplication in the gut-associated lymphoid tissue (GALT) is accompanied by spread to the regional lymph nodes where macrophages that line the lymphatic sinuses form a first effective barrier to prevent further spread. In humans, pigs or cattle, this host defense mechanism successfully limits bacterial expansion and the infection remains localized to the intestine and the GALT. This localized disease is termed Salmonella gastroenteritis and the prominent symptom or sign of disease is acute diarrhea (Figure 1). However, if the macrophages located in the draining lymph nodes fail to limit bacterial spread, S. typhimurium can cause a systemic illness. Both the immune status of the host and the innate susceptibility of the host species determine whether infection results in localized or systemic disease. For instance, in children, elderly or immunocompromised patients S. typhimurium infections are more frequently complicated by bacteremia and systemic illness, than in immunocompetent individuals (Miller et al. 1995). In contrast, in immunocompetent, genetically susceptible mice, S. typhimurium causes a systemic disease called murine typhoid (Figure 1). During this infection S. typhimurium spreads from the GALT by way of the efferent lymphatics and the thoracic duct into the vena cava. Open image in new window Figure 1 Course of infection characteristic of the two main disease syndromes caused by S. typhimurium. Murine typhoid (left half) is a systemic illness with signs of disease that differ from those developing in pigs, cattle or man infected with S. typhimurium (right half).