Low lineage diversity and increased virulence of group C Streptococcus dysgalactiae subsp. equisimilis

• Published in: Journal of medical microbiology Vol. 69; no. 4; pp. 576 - 586
• Main Authors: Santos, Victor Lima, Silva, Ligia Guedes, Martini, Caroline Lopes, Anjos, Isis Hazelman V, Maia, Mariana Masello, Genteluci, Gabrielle L, Sant'Anna, Viviane, Ferreira, Ana Maria A, Couceiro, José Nelson S S, Figueiredo, Agnes Marie Sá, Ferreira-Carvalho, Bernadete Teixeira
• Format: Journal Article
• Language: English
• Published: England 01.04.2020
• Subjects: Caenorhabditis elegans; adhesion; Streptococcus dysgalactiae subsp. equisimilis; invasion; fitness
• ISSN: 0022-2615; 1473-5644
• DOI: 10.1099/jmm.0.001165

In some species, the population structure of pathogenic bacteria is clonal. However, the mechanisms that determine the predominance and persistence of specific bacterial lineages of group C remain poorly understood. In Brazil, a previous study revealed the predominance of two main lineages of subsp. (SDSE). The aim of this study was to assess the virulence and fitness advantages that might explain the predominance of these SDSE lineages for a long period of time. typing was determined by DNA sequencing. Adhesion and invasion tests were performed using human bronchial epithelial cells (16HBE14o-). Biofilm formation was tested on glass surfaces and the presence of virulence genes was assessed by PCR. Additionally, virulence was studied using models and competitive fitness was analysed in murine models. The predominant lineages A and B were mostly typed as 839 and 6979, respectively. Notably, these lineages exhibited a superior ability to adhere and invade airway cells. Furthermore, the dominant lineages were more prone to induce aversive olfactory learning and more likely to kill . In the competitive fitness assays, they also showed increased adaptability. Consistent with the increased virulence observed in the and models, the predominant lineages A and B showed a higher number of virulence-associated genes and a superior ability to accumulate biofilm. These results suggest strongly that this predominance did not occur randomly but rather was due to adaptive mechanisms that culminated in increased colonization and other bacterial properties that might confer increased bacteria-host adaptability to cause disease.