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

Autor: Gabrielle Limeira Genteluci, Ana Maria de Amorim Ferreira, Mariana Masello Maia, Victor Lima Santos, José Nelson Couceiro, Caroline Lopes Martini, Bernadete Teixeira Ferreira-Carvalho, Viviane Sant’Anna, Agnes Marie Sá Figueiredo, Ligia Guedes Silva, Isis Hazelman V. Anjos
Rok vydání: 2020
Předmět:
Zdroj: Journal of Medical Microbiology. 69:576-586
ISSN: 1473-5644
0022-2615
Popis: Introduction. 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 Streptococcus remain poorly understood. In Brazil, a previous study revealed the predominance of two main lineages of Streptococcus dysgalactiae subsp. equisimilis (SDSE). Aim. 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. Methodology. emm 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 Caenorhabditis elegans models and competitive fitness was analysed in murine models. Results. The predominant lineages A and B were mostly typed as emm stC839 and stC6979, 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 C. elegans. In the competitive fitness assays, they also showed increased adaptability. Consistent with the increased virulence observed in the ex vivo and in vivo models, the predominant lineages A and B showed a higher number of virulence-associated genes and a superior ability to accumulate biofilm. Conclusion. 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.
Databáze: OpenAIRE