Antibiotic Resistance and Presence of Persister Cells in the Biofilm-like Environments in <i>Streptococcus agalactiae</i>
Pamella Silva Lannes-Costa,
Isabelle Rodrigues Fernandes,
João Matheus Sobral Pena,
Brunno Renato Farias Verçoza Costa,
Marcel Menezes Lyra da Cunha,
Bernadete Teixeira Ferreira-Carvalho,
Prescilla Emy Nagao
Affiliations
Pamella Silva Lannes-Costa
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University—UERJ, Rio de Janeiro 20550-013, RJ, Brazil
Isabelle Rodrigues Fernandes
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University—UERJ, Rio de Janeiro 20550-013, RJ, Brazil
João Matheus Sobral Pena
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University—UERJ, Rio de Janeiro 20550-013, RJ, Brazil
Brunno Renato Farias Verçoza Costa
Núcleo Multidisciplinar de Pesquisa UFRJ—Xerém em Biologia, Campus UFRJ—Duque de Caxias Professor Geraldo Cidade, Universidade Federal do Rio de Janeiro, Rio de Janeiro 25240-005, RJ, Brazil
Marcel Menezes Lyra da Cunha
Núcleo Multidisciplinar de Pesquisa UFRJ—Xerém em Biologia, Campus UFRJ—Duque de Caxias Professor Geraldo Cidade, Universidade Federal do Rio de Janeiro, Rio de Janeiro 25240-005, RJ, Brazil
Bernadete Teixeira Ferreira-Carvalho
Departamento de Microbiologia Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-902, RJ, Brazil
Prescilla Emy Nagao
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University—UERJ, Rio de Janeiro 20550-013, RJ, Brazil
Objectives: This study investigated antibiotic resistance and presence of persister cells in Streptococcus agalactiae strains belonging to capsular types Ia/ST-103, III/ST-17, and V/ST-26 in biofilm-like environments. Results: S. agalactiae strains were susceptible to penicillin, clindamycin, and erythromycin. Resistance genes were associated with tetM (80%), tetO (20%), ermB (80%), and linB (40%). Persister cells were detected in bacterial strains exposed to high concentrations of penicillin, clindamycin, and erythromycin. S. agalactiae capsular type III/ST-17 exhibited the highest percentage of persister cells in response to penicillin and clindamycin, while type Ia/ST-103 presented the lowest percentages of persister cells for all antimicrobials tested. Additionally, persister cells were also detected at lower levels for erythromycin, regardless of capsular type or sequence type. Further, all S. agalactiae isolates presented efflux pump activity in ethidium bromide-refractory cell assays. LIVE/DEAD fluorescence microscopy confirmed the presence of >85% viable persister cells after antibiotic treatment. Conclusions: These findings suggest that persister cells play a key role in the persistence of S. agalactiae during antibiotic therapy, interfering with the treatment of invasive infections. Monitoring persister formation is crucial for developing strategies to combat recurrent infections caused by this pathogen.
