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Group B Streptococcus highly resistant to gentamicin.

Sir, Antibiotic resistance in the group B Streptococcus (GBS) is not widely appreciated and many clinical laboratories do not undertake full antibiotic susceptibility tests of clinical isolates. However, antibiotic combinations such as a penicillin plus gentamicin are often used to manage severe GBS infection, exposing patients to enhanced risk of antibiotic-related toxicity whilst attempting to improve clinical response. We report the isolation of a strain of GBS that was highly resistant to gentamicin (MIC > 500 mg/L). Appropriate surveillance is required to control the spread of antibiotic resistance in GBS that now threatens effective therapy. Streptococcus agalactiae, the GBS, is the most frequent cause of severe neonatal sepsis. Significant infection is also seen in adult women as a complication of pregnancy and among immunocompromised patients.1 Surveillance has shown that GBS remains universally susceptible to penicillins and glycopeptides such as vancomycin.2 However, in vitro studies indicate that the rate of killing of GBS by these antibiotics is relatively slow compared with other streptococcal pathogens and have led some authors to recommend dual therapy using a penicillin plus gentamicin for severe GBSassociated infection.1,3 This approach attempts to achieve synergic antibiotic activity against the GBS and requires the pathogen to be susceptible to both penicillins and aminoglycoside antibiotics. We report the isolation of a strain of GBS showing high-level resistance to gentamicin. A 49-year-old woman with no significant past medical history presented to her general practitioner complaining of dysuria. A clinical diagnosis of urinary tract infection was formed and the patient made an uneventful recovery following empirical ampicillin therapy. Microscopy of a mid-stream urine sample found leucocytes (90/μL) but no red blood cells. Culture showed GBS (107–108/L) that was sensitive to ampicillin and nitrofurantoin but resistant to trimethoprim and gentamicin (disc testing/BSAC methodology). In view of these findings, detailed investigations were carried out. The identity of the isolate was confirmed as S. agalactiae (GBS) by biochemical and 16S ribosomal RNA gene sequence analysis, but was found to be non-typeable by the UK national reference laboratory at Colindale, North London. Results of MIC estimation by microdilution methodology carried out in our laboratory are shown in Table 1. Notably, the isolate was highly resistant to gentamicin. We were able to find only one previous report of highly gentamicin-resistant GBS by interrogation of the MEDLINE database. Strain B128 of GBS was isolated from the infected leg wound of a French patient in 1987. B128 was shown to be highly resistant to all aminoglycosides, including gentamicin. The isolate was also resistant to tetracycline, fucidin and rifampicin, but remained susceptible to penicillin and vancomycin. In vitro testing confirmed a lack of synergy between gentamicin plus either penicillin or vancomycin. B128 was found to be type II. This strain was resistant to gentamicin due to production ofaminoglycoside-modifying enzymes6′ acetyltransferase and 2′ phosphotransferase.1 B128 carries the chromosomal resistance transposon TN 3706, which is indistinguishable from TN 4001 found in Staphylococcus aureus and TN 5281 found in Enterococcus faecalis. 4 Comparative studies of B128 and the present isolate are in progress. These results emphasize the need to undertake continuous surveillance for antibiotic resistance among significant pathogens. In the case of GBS, resistance to antibiotics such as erythromycin varies between geographical regions but may be as high as 25% and is associated with specific serotypes.2 However, GBS surveillance schemes may not include gentamicin susceptibility testing and this investigation is often omitted in clinical laboratories. Table 1. Antimicrobial susceptibility of group B Streptococcus