Group B Streptococcal Toxic Shock Syndrome and covR/S Mutations Revisited.

Gene mutations in the virulence regulator CovR/S of group A Streptococcus play a substantial role in the pathogenesis of streptococcal toxic shock syndrome. We screened 25 group B Streptococcus (GBS) isolates obtained from patients with streptococcal toxic shock syndrome and found only 1 GBS clone harboring this kind of mutation.

Human infections due to Streptococcus dysgalactiae subspecies equisimilis.

Human streptococci that belong to Streptococcus dysgalactiae subspecies equisimilis (SDSE) have long been known under the name of beta-hemolytic groups C and G streptococci. Extensive taxonomic studies during the past years have distinguished most of the veterinary pathogens belonging to Lancefield groups C and G from those of human origin. After being considered nonpathogenic for many years, SDSE is now recognized as an important bacterial pathogen. The clinical spectrum of diseases caused by this species closely resembles Streptococcus pyogenes infections, including the occurrence of poststreptococcal sequelae. In accordance with these observations, many of the virulence factors present in S. pyogenes can also be found in SDSE strains. High nucleotide-sequence identities in virulence genes and the association of these genes with mobile genetic elements support the hypothesis of extensive horizontal gene-transfer events among streptococcal species of the pyogenic group. Recent epidemiological studies have shown increasing numbers of invasive SDSE infections, often among immunocompromised patients, and suggest that this species will probably gain even more clinical importance in the near future. For a better understanding of the changing epidemiology and pathogenicity of SDSE, an increased awareness of these microorganisms as human pathogens and proper identification are mandatory.

Lack of mitogenic activity of speG- and speG(dys)-positive Streptococcus dysgalactiae subspecies equisimilis isolates from patients with invasive infections.

In recent years, Streptococcus dysgalactiae subspecies equisimilis has been isolated with an increasing frequency as the cause of invasive streptococcal diseases. For 46 S. dysgalactiae subspecies equisimilis isolates from invasive infections and four isolates from superficial infections, the presence of emm/emmL genes and of genes encoding various different streptococcal superantigens was determined by polymerase chain reaction (PCR). Subsequently, PCR products were identified by DNA sequencing, and the expression of mRNA from superantigen genes was assessed by reverse transcriptase-PCR. The mitogenic activity of S. dysgalactiae subspecies equisimilis was assessed by [3H]thymidine incorporation into human lymphocytes and compared with that of Streptococcus agalactiae and Streptococcus pyogenes. All S. dysgalactiae subspecies equisimilis isolates studied harbored an emm/emmL gene. Only in six of the S. dysgalactiae subspecies equisimilis isolates from invasive infections, speG was detected by PCR, two of which were further identified as speGdys by sequencing of the PCR product. None of the S. dysgalactiae subspecies equisimilis isolates harbored any of the genes speA, speB, speC, speF, speH, speI, speJ, speK, speL, speM, smeZ, or ssa of S. pyogenes. In contrast to S. pyogenes, no expression of speG or speGdys mRNA, respectively, was detected in the reverse transcriptase-PCR assay for any of the speG- or speGdys-positive S. dysgalactiae subspecies equisimilis isolates. Moreover, S. dysgalactiae subspecies equisimilis and S. agalactiae revealed no or very low mitogenic activity, while S. pyogenes was a very powerful inducer of proliferative responses. These findings support the hypothesis that the pathogenicity of S. dysgalactiae subspecies equisimilis may be associated in part with the presence of emm/emmL genes, and suggest that the severity of S. dysgalactiae subspecies equisimilis invasive infections is not mediated by superantigen-induced mitogenicity.

Streptococcus pyogenes meningitis complicating varicella in a 3-month-old child.

Varicella is a common, usually self-limited infectious disease, and complications are believed to be rare. Despite the dramatic increase in invasive Streptococcus pyogenes infections associated with varicella zoster virus infections in recent years, post-varicella S. pyogenes meningitis occurs very rarely. The third case in the literature is described here.

drs (Distantly related sic) gene polymorphisms among emm12-type Streptococcus pyogenes isolates.

Twenty-eight emm12-type Streptococcus pyogenes isolates from patients with invasive and noninvasive infections or from asymptomatic carriers were genetically typed. Sequencing of drs (distantly related sic [streptococcal inhibitor of complement]) genes identified two novel alleles and revealed a polymorphism for drs similar to that of sic. No association was observed between the five different drs alleles and the five restriction patterns of the vir regulon for the isolates studied. These data suggest that drs sequencing may be useful for further differentiation of S. pyogenes isolates with emm12 and identical vir regulon restriction patterns.

Intrahost sequence variation in the streptococcal inhibitor of complement gene in patients with human pharyngitis.

Selection of new variants of the streptococcal inhibitor of complement protein has been implicated in the perpetuation of epidemics caused by serotype M1 strains of group A Streptococcus (GAS). The frequency at which new streptococcal inhibitor of complement (Sic) variants arise in an infected individual is not known. To study this issue, the sic gene was sequenced in 100 isolates cultured from throat swabs of each of 20 patients with acute pharyngitis caused by serotype M1 GAS. Five patients were infected with GAS populations expressing 2 Sic variants characterized by deletion of a region of the protein. In contrast, no intrahost variation was detected in the number of a pentanucleotide repeat (CAAAA) that controls production of a bacterial cell-surface collagen-like protein by slipped-strand mispairing. Sic variation occurs at a sufficient frequency in vivo to result in mixed infections on the mucosal surface of human hosts, potentially contributing to pathogen survival.