Antimicrobial Susceptibilities of Group B Streptococci in New Zealand

Increasing resistance of group B Streptococcus (GBS) to clindamycin and erythromycin has been noted in many parts of the world (1-4, 6, 8-10, 12, 13, 16). Recent studies from North America have documented clindamycin and erythromycin resistance rates of 2.1 to 15% and 7.4 to 32%, respectively (1, 4, 8-10, 12, 13), and rates of 43 and 46%, respectively, have been reported in Taiwan (6).

A recent study from New Zealand noted that 15 and 7.5% of a small number of invasive GBS isolates were resistant to clindamycin and erythromycin, respectively (5). This resistance rate is surprisingly high, given that New Zealand generally has lower antimicrobial resistance rates than most of the world, and given that a recent study from Australia demonstrated an erythromycin resistance rate of only 2.8% (15).

To further evaluate GBS resistance in New Zealand, we determined the antimicrobial susceptibilities of 177 consecutive GBS strains isolated in our laboratory. The GBS strains were isolated from both invasive and mucocutaneous sites; 7 were from neonates, 10 were from children, 28 were from pregnant women, and 132 were from nonpregnant adults. Antimicrobial susceptibilities were determined by the broth microdilution method (MicroScan MICroSTREP plus; Dade Behring Inc., West Sacramento, Calif.) following guidelines recommended by the National Committee for Clinical Laboratory Standards (11). Precise MICs for resistant isolates were determined with the E test (AB Biodisk, Dalvägen, Sweden). Streptococcus agalactiae ATCC 12386 was used as a control for all antimicrobial susceptibility testing.

A summary of the antimicrobial susceptibilities of the 177 isolates tested is given in Table 1. A total of 29 isolates (16%) were resistant to clindamycin (MIC, ≥1 μg/ml) and/or erythromycin (MIC, ≥1 μg/ml). Of these 29 isolates, 19 (11%) demonstrated an unusual resistance phenotype, with low-level resistance to clindamycin (MIC, 1 to 4 μg/ml) and susceptibility to erythromycin (MIC, <0.25 μg/ml), 2 (1%) were resistant to erythromycin alone, and 8 (4%) were resistant to both clindamycin and erythromycin. No predominant serotype was seen among the isolates showing resistance to clindamycin and/or erythromycin: III-R (seven isolates), III (eight), Ia/c (two), Ia (one), Ib (two), I a/b (one), V-R (two), V (one), IV (one), R (one), and nontypeable (three).

TABLE 1.

Antimicrobial susceptibilities of 177 GBS isolates

Antibiotic	MIC (μg/ml)a			% Resistance
	Range	50%	90%
Ampicillin	0.12-0.25	0.25	0.25	0
Penicillin	0.12-0.25	0.12	0.12	0
Ceftriaxone	0.06-0.25	0.12	0.12	0
Tetracycline	≤1->4	>4	>4	84
Meropenem	≤0.06-0.12	0.12	0.12	0
Erythromycin	≤0.125->256	≤0.25	≤0.25	6
Vancomycin	≤0.5-1	≤0.5	≤0.5	0
Clindamycin	0.094->256	≤0.25	2	15
Chloramphenicol	≤1->8	2	4	1

^a50% and 90%, MICs at which 50% and 90% of isolates are inhibited, respectively.

The findings of this study indicate that there is a clinically significant level of macrolide and lincosamide resistance in GBS isolates from New Zealand and confirm the findings of the smaller New Zealand study (5). The most widely documented resistance patterns are the macrolide-lincosamide-streptogramin B phenotype, conferring coresistance to erythromycin and clindamycin, and the M phenotype, conferring resistance to only erythromycin (7). In contrast to other studies, our most common resistance phenotype demonstrated resistance to only clindamycin. We performed double disk diffusion testing (14) of the isolates with this phenotype and did not demonstrate inducible resistance to erythromycin. The underlying mechanism responsible for this phenotype is unclear and is the subject of ongoing investigation.

In conclusion, GBS isolates from New Zealand exhibit rates of macrolide and lincosamide resistance similar to those in other parts of the world but differ in the distribution of resistance phenotypes. Erythromycin and clindamycin cannot be viewed as reliable alternatives for treating GBS infections in patients with penicillin allergy.