Table 4.
Overview of known markers to potentially identify the invasive subgroup, comparing the results of our study with those of previous works
| Ref. | Origin of the strains | Subgroups (n) | Method | Marker -a or +b | P-valuec |
|---|---|---|---|---|---|
| Neonatal invasive (EOD and LOD) and vaginal and rectal colonizing GBS from The Netherlands and Taiwan | NL invasive (44) NL colonizing (92) |
PCR and serotyping | {ST (II-, III+), gbs1987-, gbs227-, gbs1073+, gbs1125-, gbs1313- } | <0.05 | |
| TW invasive (43) TW colonizing (58) |
{ST (III+, V-), gbs1987-, gbs227-, gbs1135-, sag915+ } | <0.05 | |||
| 22d | Invasive strains from neonates, elderly and pregnant women | Invasive (269) | Selection of known and putative virulence genes, PCR | spb1 + | 0.23 |
| Anal, vaginal, throat, and urine from healthy individuals | Colonizing (152) | bac | ns | ||
| Rib | ns | ||||
| Brp | ns | ||||
| pag - | <0.01 | ||||
| psp | ns | ||||
| 23d | Neonatal meningitis isolates, EOD | Invasive (100) | Selection of known virulence genes, PCR | bca - | 0.002 |
| Colonizing isolates from cervix, vagina, anus | Colonizing (360) | bac | ns | ||
| rib + | 0.09 | ||||
| ST Ia | bca - | 0.03 | |||
| ST | bca + | 0.002 | |||
| 24e | GBS from neonatal CSF (EOD and LOD), vagina pregnant women, and neonatal gastric fluid (colonizing) | Invasive phylogenetic subgroups I, II-ET11, II-ET12 (MLEE) (62) | RAPD, followed by PCR of a tRNA gene cluster | 1,2 kb fragment + | <0.0001 |
| Non-invasive phylogenetic subgroup II (MLEE) (52 | +IS1548 + | <0.0001 | |||
| 25e | CSF neonates 1986–1990 | Invasive phylogenetic subgroups (MLEE) (63) | RAPD, followed by differential display of DNA and PCR of prophagic DNA | DNA fragment F5 + | 0.017 |
| Vagina and gastric fluid neonates (colonizing) | Non-invasive phylogenetic subgroups (MLEE) (46) | DNA fragment F7 + | 0.007 | ||
| DNA fragment F10 + | <0.001 | ||||
| At least one fragment + | 0.002 | ||||
| 26e | GBS from neonatal CSF (EOD and LOD), vagina pregnant women, and neonatal gastric fluid (colonizing) | RAPD group A (virulent clone family) (38) | RAPD, primer A4 | 0.64 kbp fragment | <0.001 |
| Not RAPD gr.A (76) | RAPD, primer AP42 | 1.2 kbp fragment - | <0.001 | ||
| RAPD, primer OPS16 | 2.4 kbp fragment + | <0.001 | |||
| 27f | GBS from neonatal CSF (EOD and LOD), vagina pregnant women, and neonatal gastric fluid (colonizing) | Invasive (54) | PFGE, SmaI restriction | 183 kb fragment + | ns |
| Colonizing (59) | 162 kb fragment + | <0.0001 | |||
| Quadruplet + | 0.009 | ||||
| 28f | Neonatal meningitis isolates, EOD and LOD, all ST III | Invasive (92) | PFGE, SmaI digestion probes of potential virulence genes, and mobile genetic elements | cpsA | ns |
| Ears and gastric fluid healthy neonates | Colonizing (37) | neuA (15kb fragment) + | <0.0001 | ||
| scpB | ns | ||||
| hylB | ns | ||||
| IS1548 | ns | ||||
| GBSi1 + | <0.0001 |
aAbsence of the marker(s) is associated with the specific virulent subgroup. The significance level of this association is expressed by the P-value
bPresence of the marker(s) is associated with the specific virulent subgroup. The significance level of this association is expressed by the P-value
cns means not significant (P > 0.05)
dDistribution of virulence genes among invasive and colonizing GBS. Smith et al. examined the distribution of eight known and putative virulence genes as a function of type of isolate on a heterogeneous collection of strains. With the exception of the pag (phage-associated) gene, appearing more often in colonizing isolates, and the spb1 gene, appearing slightly more often in invasive isolates, no difference was found in the distribution of the selected genes [22]. Manning et al. studied the presence of the rib and the bca and bac genes among colonizing and invasive isolates and found only marginally significant differences in frequency. The calculated sensitivity and specificity of these markers to identify virulent strains is generally low, except for some limited serotype–gene combinations [23]
eDistribution of RAPD fragments among virulent phylogenetically related lineages. With RAPD, Rolland et al. identified a fragment corresponding to a tRNA gene cluster [24]. van der Mee-Marquet et al. identified several prophagic DNA fragments that were significantly more prevalent in strains belonging to invasive MLEE-related subgroups of GBS [25]. Chatellier et al. demonstrated that, with four primers, neonatal invasive strains can be grouped into three predominant RAPD groups, corresponding to the same virulent MLEE lineages as found by van der Mee-Marquet et al. [26]
fPFGE fragments and virulence gene probes, distribution among virulent vs. colonizing (ST III) GBS. Rolland et al., using PFGE, revealed that isolates recovered from meningitis were clustered within three PFGE groups [27]. Bidet et al. found a significant association of a mobile genetic element (GBSi1) and a 15 kb fragment bearing the neuA virulence gene with meningitis isolates [28]