Claudia Barberis1, Mabel Budia2, Susana Palombarani2, Carlos Hernán Rodriguez2, María Soledad Ramírez3, Barbara Arias4, Laura Bonofiglio4, Angela Famiglietti2, Marta Mollerach4, Marisa Almuzara2, Carlos Vay2. 1. Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Bioquímica Clínica, Hospital de Clínicas José de San Martín, Ciudad Autónoma de Buenos Aires, Argentina. Electronic address: claudiabar07@gmail.com. 2. Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Bioquímica Clínica, Hospital de Clínicas José de San Martín, Ciudad Autónoma de Buenos Aires, Argentina. 3. Universidad de Buenos Aires, Facultad de Medicina, Instituto de Microbiología y Parasitología Médica (IMPaM, UBA-CONICET), Ciudad Autónoma de Buenos Aires, Argentina. 4. Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Microbiología, Inmunología y Biotecnología, Cátedra de Microbiología, Ciudad Autónoma de Buenos Aires, Argentina.
Abstract
OBJECTIVES: Patterns of antimicrobial susceptibility in Actinomyces and related genera are very limited in the literature. Data of predominant susceptibility profiles could contribute to the establishment of an accurate empirical treatment. METHODS: A total of 113 isolates from clinical samples were included in this study. Each isolate was identified using phenotypic methods and MALDI-TOF/MS. When discrepancies were observed, 16S rRNA gene sequencing was performed. The minimum inhibitory concentrations (MICs) of nine antimicrobial agents (penicillin, ceftriaxone, linezolid, tetracycline, clindamycin, erythromycin, ciprofloxacin, levofloxacin and vancomycin) were tested against the species Actinotignum schaalii (n=23), Actinomyces turicensis (n=18), Actinomyces europaeus (n=13), Actinomyces naeslundii/Actinomyces viscosus group (n=12), Actinomyces urogenitalis (n=11), Actinomyces radingae (n=11), Actinomyces neuii (n=9), Actinomyces odontolyticus (n=8), Bifidobacterium scardovii (n=3), Actinomyces graevenitzii (n=2), Alloscardovia omnicolens (n=2) and Varibaculum cambriense (n=1). RESULTS: All of the isolates were susceptible to penicillin, ceftriaxone, vancomycin and linezolid. Almost all of the A. urogenitalis isolates (8/11) were resistant to clindamycin and showed susceptibility to erythromycin, suggesting an L-phenotype, however no determinants of clindamycin resistance (lnu and lsa genes) were detected by PCR. High MIC values to quinolones were observed in 54/113 isolates (47.8%). All of the A. urogenitalis isolates were highly resistant to ciprofloxacin and levofloxacin. CONCLUSIONS: These data highlight the importance of ongoing surveillance to provide relevant information for empirical management of infections caused by these organisms.
OBJECTIVES: Patterns of antimicrobial susceptibility in Actinomyces and related genera are very limited in the literature. Data of predominant susceptibility profiles could contribute to the establishment of an accurate empirical treatment. METHODS: A total of 113 isolates from clinical samples were included in this study. Each isolate was identified using phenotypic methods and MALDI-TOF/MS. When discrepancies were observed, 16S rRNA gene sequencing was performed. The minimum inhibitory concentrations (MICs) of nine antimicrobial agents (penicillin, ceftriaxone, linezolid, tetracycline, clindamycin, erythromycin, ciprofloxacin, levofloxacin and vancomycin) were tested against the species Actinotignum schaalii (n=23), Actinomyces turicensis (n=18), Actinomyces europaeus (n=13), Actinomyces naeslundii/Actinomyces viscosus group (n=12), Actinomyces urogenitalis (n=11), Actinomyces radingae (n=11), Actinomyces neuii (n=9), Actinomyces odontolyticus (n=8), Bifidobacterium scardovii (n=3), Actinomyces graevenitzii (n=2), Alloscardovia omnicolens (n=2) and Varibaculum cambriense (n=1). RESULTS: All of the isolates were susceptible to penicillin, ceftriaxone, vancomycin and linezolid. Almost all of the A. urogenitalis isolates (8/11) were resistant to clindamycin and showed susceptibility to erythromycin, suggesting an L-phenotype, however no determinants of clindamycin resistance (lnu and lsa genes) were detected by PCR. High MIC values to quinolones were observed in 54/113 isolates (47.8%). All of the A. urogenitalis isolates were highly resistant to ciprofloxacin and levofloxacin. CONCLUSIONS: These data highlight the importance of ongoing surveillance to provide relevant information for empirical management of infections caused by these organisms.
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