Antimicrobial Activity of the Circular Bacteriocin AS-48 against Clinical Multidrug-Resistant Staphylococcus aureus
Metadatos
Mostrar el registro completo del ítemAutor
Velázquez Suárez, Cristina; Sorlozano Puerto, Antonio; Gutiérrez Fernández, José; Martínez Bueno, Manuel; Maqueda Abreu, Mercedes; Valdivia Martínez, Dolores EvaEditorial
MDPI
Materia
Staphylococcus aureus MRSA Enterocin AS-48 Antibiotic resistance Biofilms
Fecha
2021-07-30Referencia bibliográfica
Velázquez-Suárez, C... [et al.]. Antimicrobial Activity of the Circular Bacteriocin AS-48 against Clinical Multidrug-Resistant Staphylococcus aureus. Antibiotics 2021, 10, 925. [https://doi.org/10.3390/antibiotics10080925]
Patrocinador
Spanish Ministry of Economy and Competitiveness SAF2013-48971-C2-1-R BIO160Resumen
The treatment and hospital-spread-control of methicillin-resistant Staphylococcus aureus
(MRSA) is an important challenge since these bacteria are involved in a considerable number of
nosocomial infections that are difficult to treat and produce prolonged hospitalization, thus also
increasing the risk of death. In fact, MRSA strains are frequently resistant to all -lactam antibiotics,
and co-resistances with other drugs such as macrolides, aminoglycosides, and lincosamides are
usually reported, limiting the therapeutical options. To this must be added that the ability of these
bacteria to form biofilms on hospital surfaces and devices confer high antibiotic resistance and
favors horizontal gene transfer of genetic-resistant mobile elements, the spreading of infections, and
relapses. Here, we genotypically and phenotypically characterized 100 clinically isolated S. aureus
for their resistance to 18 antibiotics (33% of them were OXA resistant MRSA) and ability to form
biofilms. From them, we selected 48 strains on the basis on genotype group, antimicrobial-resistance
profile, and existing OXA resistance to be assayed against bacteriocin AS-48. The results showed
that AS-48 was active against all strains, regardless of their clinical source, genotype, antimicrobial
resistance profile, or biofilm formation capacity, and this activity was enhanced in the presence of the
antimicrobial peptide lysozyme. Finally, we explored the effect of AS-48 on formed S. aureus biofilms,
observing a reduction in S. aureus S-33 viability. Changes in the matrix structure of the biofilms as
well as in the cell division process were observed with scanning electron microscopy in both S-33
and S-48 S. aureus strains.