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The genetic diversity of 123 Streptococcus suis strains of capsular types 2, 1/2, 3, 7, and 9, isolated from pigs in France and from humans in different countries, was evaluated by pulsed-field gel electrophoresis (PFGE) of DNA restricted with SmaI. The method was highly discriminative (D = 0.98), results were reproducible, and the PFGE analysis was easy to interpret. Among all S. suis strains, 74 PFGE patterns were shown. At 60% homology, three groups (A, B, and C) were identified, and at 69% homology, eight subgroups (a to h) were observed. Strains isolated from diseased pigs or from humans were statistically clustered in group B, especially in subgroup d. By contrast, S. suis strains isolated from clinically healthy pigs were preferentially included in subgroup b of group A. Relationships could be established between capsular types 1/2, 3, and 9 and groups A, e, and B, respectively. S. suis strains isolated from humans were homogeneous, and a very high level of association between these strains and four DNA patterns was observed. The PFGE used in this study is a very useful tool for evaluating the genetic diversity of S. suis strains, and it would be used for epidemiological investigations.

A collection of 114 independent Streptococcus agalactiae strains, including 54 strains isolated from the cerebrospinal fluid (CSF) samples of neonates and 60 strains from asymptomatic patients, was characterized by pulsed-field gel electrophoresis (PFGE) of DNA restricted with SmaI and by PCR analysis of the hylB gene. All strains were previously studied by multilocus enzyme electrophoresis (MLEE) (R. Quentin, H. Huet, F.-S. Wang, P. Geslin, A. Goudeau, and R. K. Selander, J. Clin. Microbiol. 33:2576-2581, 1995). Among these 114 strains, there were 92 PFGE patterns. Eleven genetic groups (A to K) were identified with 38% divergence. A more homogeneous group (PFGE group A) was defined, consisting of 73% of the strains previously identified as belonging to a particular MLEE phylogenetic group. A 162-kb fragment was identified as a marker of strains that invaded the central nervous system of neonates. It was detected in 69% of the PFGE patterns obtained with CSF isolates and in only 1.8% of the PFGE patterns obtained with carrier strains. The hylB gene encoding hyaluronate lyase was amplified for all strains in our collection. Ten of 15 isolates belonging to an MLEE subgroup, previously described as being likely to cause invasive infection, had an insertion in the hylB gene (IS1548).