| dc.description.abstract | Using molecular typing methods like: MLST, capsular serotyping and virulence gene screening on 16 S. agalactiae isolates (6 ST-23 isolates, 5 ST-1 isolates and 5 ST-103 isolates) from bulk tank milk from Danish dairy farms, we tried to find a possible explanation for the re-emergence of S. agalactiae on dairy farms in Denmark. Preliminary data from Denmark showed that bovine isolates may belong to human strains, although it is not known why human strains would have emerged in dairy cattle (Zadoks et al. 2011). Screening for virulence genes we expect that isolates coming from bulk tank milk from dairy farms in Denmark will at least contain the lac operon and possibly also other virulence genes, which may have been acquired through lateral gene transfer (LGT) and enhance their survival and spread in cattle herds.
Results obtained by MLST show that most dairy isolates from Denmark are likely to come from a human strain. Two of the isolates had a slightly different allelic profile. Results from this part of the study suggest that re-emergence of S. agalactiae may be due to a host-species jump of human strains, rather than to re-emergence of strains that were historically associated with cattle. Looking at the isolates capsular type we found that most bovine isolates also had capsular type Ia (which is primarily associated with human strains) but two of them had capsular type III. These isolates were also slightly different compared to the other isolates on the expanded MLST scheme.
Screening for virulence genes we hypothesized that acquisition of virulence genes by human derived strains of S.agalactiae might give them a survival advantage in cattle. None of the bovine isolates of ST1, ST23 or ST103 acquired all virulence genes and most isolates did not have the lac operon. This operon is thought to be essential for survival in the bovine udder. In a subsequent project , those S. agalactiae were shown to grow in lactose broth, proving that they have the ability to ferment lactose even when they did not have the lac operon for which we tested by PCR. One of the possible explanations for the absence of this operon could be that these isolates have a different mechanism to ferment lactose, which could possibly be the same lac operon as S. canis. None of the virulence genes seemed to be essential for the survival in the bovine udder, but it is likely that having one or more of these genes would give the isolates of human origin a survival advantage. | |
