Ability of clinical isolates of group A streptococci to adhere to and invade HEp-2 epithelial cells.

Individual strains of group A streptococci (GAS) differ in virulence, but the reasons for these differences are incompletely understood. To determine if the ability of GAS to cause invasive disease corresponded with their capacity to adhere to or invade epithelial cells, 63 clinical isolates of GAS (40 from patients with systemic infection and 23 from superficial disease) were examined in quantitative assays of bacterial adhesion to and invasion of HEp-2 cells, a continuous line of human pharyngeal epithelial cells. The results showed that individual isolates of GAS varied considerably in their ability to adhere to and penetrate HEp-2 cells. However, on the whole, strains from patients with invasive disease adhered to cells in numbers c.1.5 greater than those from superficial infection. Paradoxically, strains from patients with invasive disease invaded HEp-2 cells to a significantly lesser extent than those from superficial sites, with a two-fold difference in invasion index (defined as the percentage of cell-associated bacteria located intracellularly). To determine if these differences were caused by differences in the production of hyaluronic acid capsule or M protein by the two groups of bacteria, the adherence and invasive capacities of bacteria carrying defined mutations in the genes for these factors were examined. Although M6-protein-deficient [corrected] bacteria were less adherent to HEp-2 cells than the wild-type, neither the hyaluronic acid capsule nor the M protein had a significant influence on the ability of GAS to adhere to or invade HEp-2 cells. The results of this study demonstrate that there are biological differences between GAS isolates associated with invasive and superficial diseases and that these differences can be demonstrated by an assay of bacterial adherence to and invasion of HEp-2 epithelial cells.

Transfer of attaching and effacing from a strain of enteropathogenic Escherichia coli to E. coli K-12.

The ability to cause attaching and effacing (AE) lesions in intestinal epithelial cells is an essential virulence trait of enteropathogenic E. coli (EPEC) that requires several chromosomal genes acting in concert with one another. In this study, we show that the ability to cause AE lesions can be transferred by conjugal mating from a high frequency recombinant (Hfr) derivative of a rabbit EPEC strain, E. coli RDEC-1, to a strain of E. coli K-12. Although the recipient acquired a considerable amount of donor DNA during the transfer process, it expressed the AE phenotype phenotype only weakly. The findings suggest the AE is a multigene phenomenon, the genes for which may not reside on a single region of the bacterial chromosome.