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Thymidine‐auxotrophic Staphylococcus aureus small‐colony variant bacteremia in a patient with cystic fibrosis
Author(s) -
Souza Dilair C.,
Cogo Laura L.,
Palmeiro Jussara K.,
DallaCosta Libera M.,
Oliveira Tomaz Ana P.,
Riedi Carlos A.,
Rosario Filho Nelson A.
Publication year - 2020
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.24730
Subject(s) - staphylococcus aureus , microbiology and biotechnology , menadione , hemin , auxotrophy , biology , medicine , gene , mutant , genetics , biochemistry , bacteria , heme , enzyme
Background Small‐colony variants (SCVs) are a morphologic subtype of Staphylococcus aureus that may occur through several mechanisms including auxotrophism for thymidine, hemin, or menadione. Auxotrophic SCV for thymidine fail to synthesize DNA specifically because of mutations in the thymidylate synthase gene. We isolated S. aureus thymidine‐dependent SCVs (TD‐SCV) from blood and respiratory samples of a pediatric patient with cystic fibrosis and pulmonary exacerbation. Methods Nutritional dependence of SCVs on hemin, menadione, and thymidine was evaluated. Antimicrobial susceptibility testing was performed through broth microdilution. Polymerase chain reaction was carried out for mec A, erm A, erm B, erm C, msr A, and msr B resistance genes. DNA sequencing was used to determine mutations in thyA and the multilocus sequence typing to identify genetic relatedness. Results Methicillin‐sensitive S. aureus with normal and TD‐SCV phenotypes were isolated from respiratory samples and a TD‐SCV phenotype was isolated from blood culture. Macrolides resistance was attributed to ermC and msr B genes. All isolates belonged to ST398. The thy A gene in S. aureus is 957 nucleotides in length and encodes a protein of 318 amino acids. The TD‐SCV isolates carried a −2 nt frameshift mutation (delta 667GC668) in thy A, creating a stop codon at residue 222 close to the predicted binding site for deoxyuridine monophosphate. Conclusions The pathogenesis of SCVs is complex and not fully elucidated. Factors inherent to the patient such as physiological conditions, recurrent infections, or coinfection should be considered. Although SCVs are considered less virulent, they showed the ability to invade and cause bacteremia in the patient.