Minocycline resistance in an oral Streptococcus infantis isolate is encoded by tet(S) on a novel small, low copy number plasmid. Issue 2 (19th March 2014)

• Record Type: Journal Article
• Authors: Ciric, Lena; Brouwer, Michael S. M.; Mullany, Peter; Roberts, Adam P.
• Is Part Of: FEMS microbiology letters. Volume 353:Issue 2(2014:Apr.)
• Page Start: 106
• Page End: 115
• Publication Date: 2014-03-19
• Subjects: Microbiology -- Periodicals; 579
• DOI: 10.1111/1574-6968.12410
• Languages: English
• ISSNs: 0378-1097

Abstract

<abstract abstract-type="main" id="fml12410-abs-0001"> <title>Abstract</title> <p>We have determined the genetic basis of minocycline resistance in a strain of <italic>Streptococcus infantis</italic> isolated from a healthy human oral cavity. We demonstrate that <italic>tet</italic>(S), identical to <italic>tet</italic>(S) found on the enterococcal conjugative transposon Tn<italic>6000</italic>, is responsible for the observed resistance. The gene is located on a small, low copy number plasmid and is flanked by IS<italic>1216</italic> elements. The <italic>tet</italic>(S) gene is capable of excising from the plasmid together with one of the IS<italic>1216</italic> elements. The plasmid contains a putative toxin/antitoxin system related to <italic>relBE</italic>. Deletion of the toxin, <italic>relE</italic>, did not result in plasmid instability but did increase the fitness of the mutant compared to the wild‐type strain.</p> </abstract>