Distribution of 141 <i>S. agalactiae</i> isolates from adult (ACSF and AB) and neonatal (NCFS and NB) patients with invasive disease between prophage DNA groups, on the basis of PCR evaluations of the prophage content of isolates.

<p>Jaccard analysis generated a dendrogram of similarity values for the 10 prophage sequences described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0020256#pone-0020256-t001" target="_blank">table 1</a> (SYSTAT 12 software). Five major prophage DNA groups were defined (groups A to E). The mean number of prophage DNA fragments amplified from strains by PCR and the mean number of absolute deviations (Avedev) were calculated for each prophage DNA group. ^a anatomic origin of isolates; ^b serotype of isolates; ST, sequence-type; CC, clonal complex; NT, nontypeable.</p

Distribution of the SLVs of the major clonal complexes as a function of difference in the number of nucleotides (one or more) with respect to the sequence of the founder sequence type.

<p>Distribution of the SLVs of the major clonal complexes as a function of difference in the number of nucleotides (one or more) with respect to the sequence of the founder sequence type.</p

Distribution of the <i>S. agalactiae</i> isolates of various origins, serotypes, sequence types, and clonal complexes between prophage DNA groups, as displayed by SYSTAT 12 software^a.

a<p>NP no prophage amplification; NT, nontypable.</p

CC, ST of <i>S. agalactiae</i> isolates from adult and neonatal invasive infections.

<p>CC, ST of <i>S. agalactiae</i> isolates from adult and neonatal invasive infections.</p

Genetic diversity and sequence type (ST) distribution, determined by MLST [<b>10</b>], of 142 <i>S. agalactiae</i> isolates from cases of adult (AI) and neonatal (NI) invasive disease.

<p>We show the phylogenetic network applied to 43 parsimonious-informative sites from a total of 3,456 nucleotides generated with the neighbour-net algorithm for the 142 strains studied (<a href="http://splitstree.org/" target="_blank">http://splitstree.org/</a>) <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0020256#pone.0020256-Huson1" target="_blank">[29]</a>. Strains were grouped into clonal complexes (CCs) with eBURST software (<a href="http://eburst.mlst.net/" target="_blank">http://eburst.mlst.net/</a>). Columns indicate the percentages of AI and NI strains in each CC. Recombination (R) and mutation (M) rates, based on MLST data, were evaluated as described by Feil <i>et al. </i><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0020256#pone.0020256-Feil1" target="_blank">[31]</a>. The estimated recombination-mutation ratio (R/M) varied as a function of the CC to which the strain belonged.</p

PCR primers and amplicon sizes for prophage screening.

<p>PCR primers and amplicon sizes for prophage screening.</p

Serotype of <i>S. agalactiae</i> isolates from the various STs and CCs implicated in adult and neonatal invasive infections.

a<p>NT, nontypable.</p

Oligonucleotide primers.

<p>Oligonucleotide primers.</p

Binding ability to immobilized human fibrinogen of the wild type (WT) L1 strain, and of isogenic mutant and complemented strains for <i>rgfAC</i>, <i>fbsA</i>, and <i>fbsB</i> genes.

<p>Flat bottomed 96-well polystyrene plates were coated with 21 nM human fibrinogen and 5×10⁶ to 5×10⁸ CFU per ml were added for 90 min at 37°C. Binding ability was calculated from the ratio between the number of bound bacteria and the number of bacteria present in the inoculum. Each experiment was performed at least three times. Boxes are means and bars are standard deviation of the means. The binding values of the mutant strains were significantly lower, at a <i>P</i> value of <0.001, than the values of the L1WT strain and of the corresponding complemented strains carrying <i>rgfAC</i>, <i>fbsA</i>, and <i>fbsB</i> genes on the pP1 plasmid.</p

Prevalence of the <i>fbs</i> genes and of their regulator genes in a collection of 134 isolates belonging to the GBS major clonal complexes.

<p>Prevalence of the <i>fbs</i> genes and of their regulator genes in a collection of 134 isolates belonging to the GBS major clonal complexes.</p