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Antimicrobial Agents and Chemotherapy, September 1999, p. 2335-2336, Vol. 43, No. 9
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
LETTERS TO THE EDITOR
Incidence of mefA and mefE Genes in
Viridans Group Streptococci
 |
LETTER |
Viridans group streptococci form the major part of the commensal
flora of the human upper respiratory tract. However, these organisms
are also the leading cause of infective endocarditis and an increasing
source of bacteremia in neutropenic patients (1).
Beta-lactam agents are the treatment of choice for these infections,
but macrolides and related drugs are recommended for prophylaxis and
alternative treatment in allergic patients (1). The two
presently recognized mechanisms of resistance to macrolide antibiotics
in streptococci are (i) target site modification mediated by
erythromycin resistance methylases (Erm), which confer cross-resistance to macrolides, lincosamides, and streptogramin B components
(MLS phenotype), and (ii) active-drug efflux pumps, encoded either by
the mefAE genes or by the mreA gene (3, 4,
11). The efflux systems encoded by the mef genes cause
resistance to 14- and 15-membered macrolide compounds only, and this
phenotype is designated M (10). Phenotype M is widespread
among beta-hemolytic streptococci and Streptococcus
pneumoniae in a number of countries (6, 7, 10). During
a survey of antimicrobial resistance in viridans streptococci, strains
with the M phenotype were investigated.
A total of 90 consecutive strains of viridans group streptococci were
isolated from 90 patients hospitalized in a French hospital (Haut-Lévêque, Pessac), between 1988 and 1995. These
strains were identified with two commercial kits, API20 STREP and Rapid ID32 (Biomérieux): 57 isolates belonged to the
Streptococcus mitis group, 24 to the Streptococcus
milleri group, and 9 to the Streptococcus salivarius
group. By the disk diffusion method, the strains were classified in
three categories with regard to their MLS behavior: (i) 55 strains
(61.1%) were susceptible, 27 (30%) had the MLS phenotype, and 8 (8.9%) had the M phenotype. The latter strains (five S. mitis strains, two Streptococcus oralis strains, and
one S. salivarius strain) were susceptible to all other
antibiotics, except for three which were additionally penicillin resistant. MICs of MLS antibiotics were determined by the agar dilution
method on Mueller-Hinton medium supplemented with 5% horse blood.
The eight isolates with the M phenotype exhibited low-level resistance
to erythromycin and other 14- and 15-membered macrolides, although the
intrinsically more active new ketolide HMR 3647 retained significant
activity; in contrast, they remained fully susceptible to
16-membered macrolides, lincosamides, and streptogramins (Table
1). The DNAs of the eight isolates were amplified with primers specific to the mefAE genes
(2). The PCR protocol consisted of a 5-min melt at 94°C,
followed by 35 cycles (1-min melt at 94°C, 1-min primer-annealing
step at 50°C, and 1-min extension step at 72°C), with a final
extension step of 10 min at 72°C. All strains except for one
(S. mitis 4) yielded a PCR product of the expected size (1.2 kb), whether no amplification was obtained with the DNAs of
negative-control strains (sensitive or MLS phenotype strains). The
amplicons were analyzed by restriction using four endonucleases
designed to differentiate mefA and mefE (ClaI, HindIII, AccI, and
HhaI) (2). The results showed that six strains
carried a mefE gene, while the remaining one (S. oralis 6) possessed a mefA gene (Table 1). Thus,
mefE appears to be predominant in viridans streptococci with
the M phenotype, as previously observed for S. pneumoniae
(6) and Streptococcus agalactiae (2).
With specific primers for ermA, -B, -C
(9), ermTR (8), and mreA
(4), no PCR amplification was obtained with S. mitis 4 under the above conditions (Table 1). These results suggest the existence of a novel erythromycin resistance gene or
mechanism in these species.
The erythromycin resistance rate in viridans group streptococci was
similar to those reported recently (around 40%) (1, 5), but
the incidence of the M phenotype was lower than that reported elsewhere
(about 20%) (1, 12). This is consistent with a lower
incidence of beta-hemolytic streptococci and pneumococci with
mef genes in France (<1%) (2). Commercially
available 14- and 15-membered macrolides appear to be of limited value
for chemoprophylaxis and therapy in viridans streptococcal infections.
 |
FOOTNOTES |
*
Phone: (33) 5-57-57-10-75
Fax: (33) 5-56-90-90-72
E-mail: corinne.arpin{at}bacterio.u-bordeaux2.fr
 |
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| | | | |
Corinne Arpin*
Marie-Hélène Canron
Jeannette Maugein
|
| | | | |
Claudine Quentin
Laboratoire de Microbiologie Université Victor Segalen Bordeaux 2 146 rue Léo Saignat 33076 Bordeaux, France
|
Antimicrobial Agents and Chemotherapy, September 1999, p. 2335-2336, Vol. 43, No. 9
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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