The Route of Enteric Infection in Normal Mice

Abstract

The inability of Salmonella typhi to induce a progressive fatal infection in most laboratory animals, analogous to that seen in man, dictated that most experimental studies of typhoid immunity had to be performed in the mouse typhoid model. ~Drskov and Moltke (1) carried out a classical study into the early distribution of Salmonella in the mouse gut after the ingestion of bread soaked in an S. typhimurium broth culture. However, these workers were unable to precisely delineate the primary site of bacterial invasion in these animals. Until relatively recently, surprisingly little more has been published which contributes to our understanding of the primary site of enteric infection in the mouse. Earlier studies from this laboratory indicated that although the majority of orally introduced S. enteritidis had a rapid transit time through the normal mouse intestine, a small proportion of the inoculum established itself within the walls of the small intestine and in the cecum several days before a systemic infection could be demonstrated (5, 6). However, the primary site of the infection, and particularly, the route taken by the organisms to reach the liver and spleen, was unclear. Studies in opium-treated guinea pigs or in streptomycintreated prestarved mice indicated a heavy early involvement of the lamina propria of the small intestine (7, 8). However, it was possible that the highly artificial experimental conditions used by these investigators may have contributed to this localization (5), so it was decided to follow the early distribution of an intragastric inoculum of virulent S. enteritidis in sequential sections of the normal undisturbed mouse intestinal tract. The fate of the inoculum was followed quantitatively throughout the gastrointestinal tract and the primary site of muscosal penetration was determined. Materials and MethodsAnimals.--6-to 8-wk old specific pathogen-free CD-1 (Charles River Breeding Laboratories, Inc., Wilmington, Mass.) and B6D2 (C57B1/6 X DBA/2 F1) mice of either sex were

Lack of flagella disadvantages Salmonella enterica serovar Enteritidis during the early stages of infection in the rat

“…Thus, there was rapid distribution throughout the gastrointestinal tract, translocation to the mesenteric lymph nodes and spread to the liver and spleen of the rats. Significant numbers of viable salmonella were detected in the mesenteric lymph nodes even within 1 h of oral infection and in the liver and spleen by 24 h. This systemic appearance of pathogen, particularly in liver and spleen, occurred much sooner than reported previously for conventional rats or mice (Islam et al, 2000;Baumler et al, 1996Baumler et al, , 1997Carter & Collins, 1974;Garcia-Del Portillo et al, 1999). This may be linked to the rat strain used (Hooded-Lister), which has been kept as a closed colony for over 50 years, or perhaps to reduced levels of commensal bacteria in the small intestine (Grant, 1996).…”

Intestinal inflammation abrogates the tolerogenic properties of MLN CD103+ dendritic cells

“…T-cell transfer colitis is characterised by severe inflammation in the colon as well as a milder inflammation in the SI [11] (our unpublished observation). As MLN have been shown to drain both the large and the SI [12], we analysed DC number and subset composition in both tissues. The large accumulation of DC within the MLN of colitic mice correlated with more than a fivefold increase in the numbers of DC in the inflamed colon and SI (Fig.…”

Intracellular replication ofSalmonella typhimuriumstrains in specific subsets of splenic macrophagesin vivo

“…In susceptible (Ity s ) host strains, less than 10 wild-type bacteria administered by the subcutaneous, intravenous or intraperitoneal route are sufficient to cause a fatal infection (Plant and Glynne, 1974;Shea et al, 1999). After oral inoculation, translocation of S. typhimurium across the gut epithelium into the bloodstream occurs by invasion of M cells in ileal Peyer's patches (Carter and Collins, 1974;Jones et al, 1994), and also via transmigrating CD18-expressing phagocytes (Vazquez-Torres et al, 1999). Regardless of the route of inoculation, a transient bacteraemia is followed over the course of several days by the accumulation of large numbers of bacteria within the spleen and liver, leading to a second, fatal bacteraemia (Carter and Collins, 1974;Shea et al, 1999).…”