Serotypes of serious, sometimes fatal, streptococcal infections in Sweden during 1988-1989 were analyzed. The T1M1 type totally dominated, representing almost 70% of all group A streptococci from serious and uncomplicated infections at the peak of the outbreak. Immunoblots of isolates from various patient groups showed that all isolates produced high amounts of erythrogenic toxin (ET) B and high amounts of ET-C, whereas ET-A was released only in small amounts and from few isolates. ELISAs showed high antibody levels to these toxins and to the M1 antigen in patients with uncomplicated infections. Low antibody levels against M1 were seen in patients with bacteremia and in fatal cases; the latter also had low antibody levels against ET-B. It seems likely that a combination of production of large amounts of toxin and low antibody titers to it and to the M antigen of the infecting isolate are determining factors for the outcome of the infection. No signs of primary immune deficiency were noted.

Streptococcus agalactiae, also designated group B streptococcus (GBS), is an important pathogen in neonates, pregnant women, and nonpregnant adults with predisposing conditions. We used multilocus sequence typing (MLST) to characterize 158 GBS isolates that were associated with neonatal and adult invasive disease and that were collected in northern and western Sweden from 1988 to 1997. Five major genetic lineages (sequence type [ST] 19, ST-17, ST-1, ST-23, and ST-9 complexes) were identified among the isolates, including serotype Ia, Ib, and II to V isolates, indicating a highly clonal population structure among invasive GBS isolates. A number of STs were found to contain isolates of different serotypes, which indicates that capsule switching occurred rather frequently. Two distantly related genetic lineages were identified among isolates of serotype III, namely, clonal complex 19 (CC19), and CC17. CC19 was equally common among isolates from adult and neonatal disease (accounting for 10.3% of GBS isolates from adult disease and 18.7% from neonatal disease), whereas CC17 significantly appeared to be associated with neonatal invasive disease (isolated from 21.9% of neonatal isolates but only 2.6% of adult isolates). The distribution of the mobile elements GBSi1 and IS1548 reveals that they can act as genetic markers for lineages CC17 and CC19, respectively.

Background. The incidence and severity of invasive group A streptococcal infection demonstrate great variability over time, which at least, in part, seems to be related to group A streptococcal type distribution among the human population.Methods. An enhanced surveillance study of invasive group A streptococcal infection (746 isolates) was performed in Sweden from April 2002 through December 2004. Noninvasive isolates from either the throat or skin (773 isolates) were collected in parallel for comparison. Clinical and epidemiological data were obtained from 88% of patients with invasive disease and were related to isolate characteristics, including T type, emm sequence type, and the presence of 9 superantigen genes, as well as pulsed-field gel electrophoresis pattern comparisons of selected isolates.Results. The annual incidence was 3.0 cases per 100,000 population. Among the patients with invasive disease, 11% developed streptococcal toxic shock syndrome, and 9.5% developed necrotizing fasciitis. The overall casefatality rate was 14.5%, and 39% of the patients with streptococcal toxic shock syndrome died ( ). The T3/ P ! .001 13/B3264 cluster accounted for 33% of invasive and 25% of noninvasive isolates. Among this most prevalent type cluster, emm types 89 and 81 dominated. Combined results from pulsed-field gel electrophoresis, emm typing, and superantigen gene profiling identified subgroups within specific emm types that are significantly more prone to cause invasive disease than were other isolates of the same type.Conclusions. This study revealed a changing epidemiology of invasive group A streptococcal infection in Sweden, with emergence of new emm types that were previously not described. The results also suggest that some clones may be particularly prone to cause invasive disease.

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The present study shows that active, self-splicing group II intron GBSi1 is located downstream of the C5a-peptidase gene, scpB, in some group B streptococcus (GBS) isolates that lack insertion sequence IS1548. IS1548 was previously reported to be often present at the scpB locus in GBS isolated in association with endocarditis. Since none of 67 GBS isolates examined, 40 of which were of serotype III, harbored both IS1548 and GBSi1, these two elements are suggested to be markers for different genetic lineages in GBS serotype III. The DNA region downstream of scpB in GBS isolates harboring either GBSi1, IS1548, or none of these mobile elements was found to encode the laminin binding protein, Lmb, which shows sequence similarities to a family of streptococcal adhesins. IS1548 is inserted 9 bp upstream of the putative promoter for lmb, while the insertion site for GBSi1 is located 88 bp further upstream. Sequences highly similar to GBSi1 exist also in Streptococcus pneumoniae. An inverted repeat sequence, with features typical of transcription terminators, was identified immediately upstream of the insertion site for the group II intron both in the GBS and S. pneumoniae sequences. This motif is suggested to constitute a target for the GBS intron as well as for rather closely related introns in Bacillus halodurans, Pseudomonas alcaligenes, and Pseudomonas putida. When transcripts containing the GBSi1 intron were incubated at high concentrations of ammonium and magnesium, a major product with the expected length and sequence for the ligated exons was generated. Unlike, however, all members of group II investigated so far, the excised intron was in linear, rather than in a branched (lariat), form.

A chromosomal DNA fragment which mediates Pap (pili associated with pyelonephritis) pili formation, mannose‐resistant hemagglutination (MRHA) and binding to uroepithelial cells has been isolated from the uropathogenic Escherichia coli clinical isolate J96, and genetically studied. Analysis of polypeptides expressed by the Pap DNA led to detection of a number of polypeptides ranging in mol. wt. from 13 000 to 81 000 daltons. The gene order and transcriptional orientation for four of the corresponding cistrons was: 13 000 (papB) 19 500 (papA, structural gene for the Pap pilus subunit), 81 000 (papC) and 28 500 (papD). Analyses of a lacZ‐ papA gene fusion located a promoter upstream from papA within the cloned DNA. Transposon Tn5 insertions in any of these four cistrons decreased or eliminated Pap pili formation. A number of transposon Tn5 mutations were identified in a region distal to papD that expressed normal levels of the papA protein on the cell surface in the form of recognizable pili structures but did not agglutinate human erythrocytes or adhere to uroepithelial cells. This region expressed polypeptides of 15 000, 24 000, 26 000 and 35 000 daltons. This finding shows that Pap pili formation and binding properties can be genetically dissociated.

Hyaluronidase has been postulated to be a virulence factor in group B streptococci (GBS). No hyaluronidase activity was found in 15 of 50 GBS isolates from adults studied. Most of these hyaluronidase-negative strains belonged to serotype III. In strains lacking hyaluronidase activity, an insertion of 1317 nucleotides was found in the hyaluronidase gene. The fragment was cloned and sequenced and found to have characteristics of a novel insertion sequence, designated IS1548. As well as in GBS serotype III, this sequence was found in 3 of 6 serotype II isolates and in all 10 group A streptococcal strains (GAS) tested. Homologies were found with repeated sequences in Streptococcus pneumoniae and with H repeats in Escherichia coli. All GBS strains harboring IS1548 and some GAS strains had one copy of IS1548 located downstream of the C5a peptidase gene. IS1548 was present in 9 of 13 GBS isolates from blood in endocarditis patients and in 3 of 22 vaginally colonizing strains.

In a retrospective study of invasive infections due to group A Streptococcus (GAS) in Stockholm during 1987 to 1995, the average incidence per 100,000 residents per year was 2.3, varying between 3.7 per 100,000 (in 1988) and 1.3 per 100,000 (in 1993). Incidence was 1.8 in the age group of 0-4 years but otherwise increased by age, from 0.48 in the age group of 5-14 years to 6.1 among those over 65 years of age. A review of 151 invasive episodes occurring in 1983-1995 showed cyclic increases of infections due to T1M1-serotype strains during 1986-1990 and 1993-1995. The T1M1 serotype accounted for 27 (20%) of 135 available GAS strains. Streptococcal toxic shock syndrome (STSS) developed in 19 (13%) of the 151 episodes. The case fatality rate was 11% overall but 47% among patients with STSS. In a multivariate logistic regression model, STSS was associated with a history of alcohol abuse (odds ratio [OR], 6.3; P = .004) and infection with a T1M1 strain (OR, 6.7; P = .007). Case fatality was associated with age (OR, 14.5; P = .08), immunosuppression (OR, 4.7; P = .02), and STSS (OR, 21.5; P < .0001) but not with T1M1 infection. Hypotension was significantly associated with a fatal outcome, regardless of whether STSS developed (P < .0001).