Experimental Infection of Mice with Yersinia enterocolitica Serotype O9 by Oral and Parenteral Routes: Spreading and Enterotropism of Virulent Yersiniae

Abstract

An isogenic pair of Yersinia enterocolitica serotype O9 strains, with and without virulence plasmid, was used to study the plasmid role in the infection of BALB/c mice by oral, intraperitoneal, and intravenous routes. The plasmid-bearing strain, but not its plasmid-less derivative, caused enteric infection after challenge by all three routes. The virulence plasmid did not influence the peritoneal clearance of yersiniae, but only the plasmid-bearing yersiniae were able to move from the peritoneal cavity to the bloodstream, and thus they spread to spleen and liver. Moreover, plasmid-bearing yersiniae were able to move from the liver to the gallbladder, and they shed in bile into the intestine. Western blot analysis of antibody responses to chromosomally encoded outer membrane proteins revealed similar patterns with sera from mice challenged with each one of two strains by intraperitoneal route. In contrast, only the plasmid-bearing strain elicited an antibody response to these antigens in mice challenged by oral route. Although mice experimentally infected with plasmid-bearing O9 yersiniae developed an enteric infection, irrespective of the inoculation route, differences between the first steps in infection by oral and parenteral routes may be important, especially when the infection model is used as an approach to study the yersinia-host interactions.

Intestinal infection of BALB/c mice with Yersinia enterocolitica O9 causes major modifications in phenotype and functions of spleen cells

“…Therefore, an inflammatory reaction to bacterial components may be involved in splenomegaly development. However, in our assays, spleens from 10-d-infected mice were sterile, although recovery of yersiniae from faeces was always demonstrated (data not shown) ; this is in agreement with our previous description of the experimental infection of BALB\c mice with Y. enterocolitica O9 (Ruiz-Bravo et al, 1999).…”

“…Therefore, an inflammatory reaction to bacterial components may be involved in splenomegaly development. However, in our assays, spleens from 10-d-infected mice were sterile, although recovery of yersiniae from faeces was always demonstrated (data not shown) ; this is in agreement with our previous description of the experimental infection of BALB\c mice with Y. enterocolitica O9 (Ruiz-Bravo et al, 1999).Flow cytometry analysis of spleen cells revealed that the absolute numbers of CD3 + total T cells, CD4 + helper T cells, CD8 + cytotoxic T cells and CD11b + phagocytic cells were significantly increased (1n7-fold, P 0n05 ; 1n4-fold, P 0n025 ; 1n7-fold, P 0n04 ; and 5n6-fold, P 0n04, respectively) in 10-d-infected animals (Fig. 1).…”

“…In humans, enteric colonization with low-virulence serotypes may persist for periods of up to 14 weeks without symptoms (Morris et al, 1991) ; however, there is no information available about the possible effects of the intestinal carriage of these strains on the immune condition of the hosts. In this study, we used a murine intestinal infection model (Ruiz-Bravo et al, 1999) to examine the immune status as outlined above. Lymphocyte proliferation was measured as described by Mosmann (1983).…”

“…Bacteria were grown on Tryptic soy agar (Difco) at 25 mC for 24 h, harvested, washed and resuspended in sterile water to obtain 10* bacteria ml − ". Mice were infected via the oral route, as described previously (Ruiz-Bravo et al, 1999). Phenotypic analysis of spleen cells.…”

Enhancement of Mice Susceptibility to Infection with Listeria monocytogenes by the Treatment of Morphine

“…Dissemination of L. monocytogenes after morphine administration in BALB/c mice. Mice were infected with 6.1ϫ10while others, including diarrheagenic E. coli, S. flexneri, Y. enterocolitica, are not capable of establishing systemic infection in the mice model via intraperitoneal infection and are immediately excreted from the mice when infected via oral or intraperitoneal routes (22). However, it was reported that morphine caused the systemic dissemination of other extracellular bacteria such as Klebsiella pneumoniae, and Streptococcus pneumoniae when these pathogens were intranasally inoculated to cause lethal infection even in the untreated mice (25,27).…”