YERSINIA-ENTEROCOLITICA INVASIN - A PRIMARY ROLE IN THE INITIATION OFINFECTION

The ability to invade the intestinal epithelium of mammals is an essen tial virulence determinant of Yersinia enterocolitica. The chromosomal ly encoded Y. enterocolitica 8081v invasion gene, inv, was disrupted t o assess its role in pathogenesis. The inv mutant (JP273v) was almost- equal-to 80-fold less invasive than wild type for cultured epithelial cells. When mice were infected intragastrically, up to 10(7) fewer JP2 73v were recovered from Peyer's patches early (6-18 hr) after infectio n compared with wild type. Analysis of the course of infection reveale d that the inv mutant had distinct differences relative to wild type i n the distribution of visible infectious foci and in tissue colonizati on; however, the mutant and wild-type strains had similar LD50 values for both orally and intraperitoneally infected mice. The invasion defe ct of the inv mutant was fully complemented in vitro and in vivo by in troduction of the wild-type inv gene in trans. The inv gene product, i nvasin, appears to play a vital role in promoting entry during the ini tial stage of infection. During the subsequent establishment of a syst emic infection, invasin may be of secondary importance, since the Y. e nterocolitica inv mutant was as proficient as wild type at causing a f atal infection in mice. Based on these data, we discuss the role of in vasin in a naturally occurring Y. enterocolitica infection.