Of these, mba30bp was found attached to the conserved domain of the MBA and is the equivalent of the active TRU in UUR4. The same TRU was also present in the mba loci of UUR12 and UUR13. Isolate 2608 contained 3 Selleckchem AG-881 identifiable TRUs (mba24bp.1, mba267bp, and mba330bp). The conserved domain was found attached to mba24bp.1, as in UUR5; this TRU was also present in UUR2 and UUR8. Clinical isolate 4318 selleck compound had 3 identifiable TRUs (mba24bp.1, mba276bp, and mba333bp). The conserved

domain was attached to mba24bp.1. Isolate 4155 had 5 identifiable TRUs (mba24bp.1, mba45bp, mba213bp.2, mba252bp.1, and mba276bp). The conserved domain was attached to mba276bp; this TRU had not been previously seen attached to a conserved domain in any of the 14 ATCC type strains, including the clinical UPA3 described by Glass et al. [25]. This is a further confirmation that the TRUs found in the mba locus are part of this phase variable system, which trough recombination should be capable to present on the surface of the ureaplasma cell different TRUs at different times. It would be interesting to investigate whether some TRUs

are more immunogenic selleckchem than others and therefore may contribute to differential pathogenicity. As mentioned earlier the mba variable domain has been used as one of the determinants of serovar classification. It is interesting to note that serovars 4 and 12, which have an identical set of MBA genes, have a percent difference at the nucleotide level in a whole genome comparison (Table 

3) of only 0.06 or 0.07% (value depends on which genome is used as reference sequence), making these serovars almost identical, with the exception of some minor rearrangements and small insertion/deletion events (see Additional file 2: Figure S5). In addition, we observed two chimeric U. parvum strains in a clinical isolate that had exchanged through horizontal gene transfer their mba genes [26]. Taken together, these observation suggest that the mba locus is dynamic and can comprise of a different set of variable domains at different times, therefore making this gene an unsuitable target for serovar differentiation. Conclusions Ureaplasmas have been associated with many different clinical outcomes; however, they have been detected also in healthy individuals. Due to their differential pathogenicity, effort Vildagliptin has gone into assignment of patient isolates into serovars and attempting to correlate specific serovars with specific clinical outcomes. Analysis of ureaplasma samples obtained from patients in the 1970s identified 14 different serovars based on patient and animal antiserum reactions. The expanded serotyping scheme developed by Robertson and Stemke in 1979 is based on antiserum generated by injecting rabbits with emulsified preparations of cell suspensions of each strain separately [59]. Studies were not done at this time to determine the antigen that the sera antibodies were recognizing. In a later study, Watson et al.