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Antimicrobial Agents and Chemotherapy, August 1999, p. 1935-1940, Vol. 43, No. 8
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Phenotypes and Genotypes of Erythromycin-Resistant
Streptococcus pyogenes Strains in Italy and Heterogeneity
of Inducibly Resistant Strains
Eleonora
Giovanetti,
Maria
Pia
Montanari,
Marina
Mingoia, and
Pietro Emanuele
Varaldo*
Institute of Microbiology, University of
Ancona Medical School, 60131 Ancona, Italy
Received 2 November 1998/Returned for modification 15 April
1999/Accepted 18 May 1999
 |
ABSTRACT |
A total of 387 clinical strains of erythromycin-resistant (MIC, 
1
µg/ml) Streptococcus pyogenes, all isolated in Italian laboratories from 1995 to 1998, were examined. By the
erythromycin-clindamycin double-disk test, 203 (52.5%) strains were
assigned to the recently described M phenotype, 120 (31.0%) were
assigned to the inducible macrolide, lincosamide, and streptogramin B
resistance (iMLS) phenotype, and 64 (16.5%) were assigned to the
constitutive MLS resistance (cMLS) phenotype. The inducible character
of the resistance of the iMLS strains was confirmed by comparing the
clindamycin MICs determined under normal testing conditions and those
determined after induction by pregrowth in 0.05 µg of erythromycin
per ml. The MICs of erythromycin, clarithromycin, azithromycin,
josamycin, spiramycin, and the ketolide HMR3004 were then determined
and compared. Homogeneous susceptibility patterns were observed for the
isolates of the cMLS phenotype (for all but one of the strains, HMR3004
MICs were 0.5 to 8 µg/ml and the MICs of the other drugs were >128
µg/ml) and those of the M phenotype (resistance only to the 14- and
15-membered macrolides was recorded, with MICs of 2 to 32 µg/ml).
Conversely, heterogeneous susceptibility patterns were observed in the
isolates of the iMLS phenotype, which were subdivided into three
distinct subtypes designated iMLS-A, iMLS-B, and iMLS-C. The iMLS-A
strains (n = 84) were highly resistant to the 14-, 15-, and 16-membered macrolides and demonstrated reduced susceptibility
to low-level resistance to HMR3004. The iMLS-B strains
(n = 12) were highly resistant to the 14- and
15-membered macrolides, susceptible to the 16-membered macrolides (but
highly resistant to josamycin after induction), and susceptible to
HMR3004 (but intermediate or resistant after induction). The iMLS-C
strains (n = 24) had lower levels of resistance to the
14- and 15-membered macrolides (with erythromycin MICs increasing two
to four times after induction), were susceptible to the 16-membered
macrolides (but resistant to josamycin after induction), and remained
susceptible to HMR3004, also after induction. The erythromycin
resistance genes in 100 isolates of the different groups were
investigated by PCR. All cMLS and iMLS-A isolates tested had the
ermAM (ermB) gene, whereas all iMLS-B and
iMLS-C isolates had the ermTR gene (neither methylase gene
was found in isolates of other groups). The M isolates had only the
macrolide efflux (mefA) gene, which was also found in
variable proportions of cMLS, iMLS-A, iMLS-B, and iMLS-C isolates. The
three iMLS subtypes were easily differentiated by a triple-disk test
set up by adding a josamycin disk to the erythromycin and clindamycin
disks of the conventional double-disk test. Tetracycline resistance was
not detected in any isolate of the iMLS-A subtype, whereas it was
observed in over 90% of both iMLS-B and iMLS-C isolates.
| |
INTRODUCTION |
Target site modifications due to
methylase activity, i.e., the most common and most extensively
investigated mechanism of erythromycin resistance, usually result in
coresistance to macrolide, lincosamide, and streptogramin B (MLS)
antibiotics (12, 23, 24). It has been known for a long time
that in gram-positive cocci MLS resistance can be expressed either
constitutively (cMLS phenotype) or inducibly (iMLS phenotype) (8,
12, 22). Unlike staphylococci, in which resistance is dissociated
between 14- and 15-membered macrolides, which are inducers, and
16-membered macrolides and lincosamides, which are not, in streptococci
there is cross-resistance between MLS antibiotics, which are efficient inducers (12). This feature of streptococci may explain
previous data about the diversity of the resistance patterns observed
by agar diffusion (7) and zonal resistance to lincomycin
(6, 13). In Streptococcus pyogenes, MLS
resistance can be mediated by two classes of methylase genes, i.e., the
conventional ermAM (ermB) determinant
(12) and the recently described ermTR determinant (19). By means of an erythromycin-clindamycin double-disk
test, a novel macrolide resistance pattern characterized by
susceptibility to lincosamides, also after induction, and 16-membered
macrolides has been recognized in S. pyogenes isolates
(18). This new resistance pattern (M phenotype) has also
been observed in Streptococcus pneumoniae and has been shown
to be mediated by an efflux system (21). A gene
(mefA) that encodes a membrane protein responsible for this
efflux-mediated resistance has been characterized (3).
A significant increase in the percentage of erythromycin-resistant
S. pyogenes strains was reported in Italy in the mid-1990s (2, 5). The present study describes the distribution of recently isolated Italian strains of S. pyogenes into the
recognized phenotypes and focuses on the phenotypic heterogeneity of
inducibly resistant strains, which were subdivided into three distinct
subtypes. Erythromycin resistance genes ermB,
ermTR, and mefA were investigated by PCR in
several isolates of the different groups. A triple-disk assay
(erythromycin and clindamycin plus josamycin) which easily differentiates, in addition to the known major phenotypes, the different subtypes within the iMLS phenotype is also described.
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MATERIALS AND METHODS |
Bacterial strains.
A total of 387 clinical isolates of
erythromycin-resistant S. pyogenes (the vast majority of
which were from cultures of throat swabs from children) were collected
from several Italian laboratories between October 1995 and June 1998. Multiple isolates from the same patient were avoided. Strain
identification was confirmed in our laboratory with bacitracin disks
(Difco Laboratories, Detroit, Mich.) and by a latex agglutination assay
(Streptex; Wellcome, Dartford, United Kingdom), and erythromycin
resistance (MIC, 1 µg/ml) was confirmed by the broth microdilution
method (see below). The strains were maintained in glycerol at 
70°C
until all isolates were collected and were subcultured twice on blood
agar before susceptibility testing.
Erythromycin-clindamycin double-disk test.
The
erythromycin-clindamycin double-disk test was carried out by a
modification of the assay described by Seppälä et al. (18). Commercial disks (Oxoid Ltd., Basingstoke, United
Kingdom) of erythromycin (30 µg) and clindamycin (10 µg) were used.
Preliminary tests indicated that the results obtained with these disks
were fully comparable to those obtained by Seppälä et al.
(18) with disks with larger amounts of drug. The disks were
placed 15 to 20 mm apart on Mueller-Hinton II agar (BBL Microbiology Systems, Cockeysville, Md.) supplemented with 5% sheep blood, which
had been inoculated with a swab dipped into a bacterial suspension with
a turbidity equivalent to that of a 0.5 McFarland standard. After
18 h of incubation at 37°C, the absence of a significant zone of
inhibition around the two disks was taken to indicate constitutive
resistance (cMLS phenotype), blunting of the clindamycin zone of
inhibition proximal to the erythromycin disk was taken to indicate
inducible resistance (iMLS phenotype), and susceptibility to
clindamycin with no blunting of the zone of inhibition around the
clindamycin disk was taken to indicate the M phenotype.
Antibiotics.
Erythromycin and clindamycin were purchased
from Sigma Chemical Co. (St. Louis, Mo.). The other antibiotics were
obtained as follows: clarithromycin, Abbott Laboratories (Abbott Park, Ill.); azithromycin, Pfizer Inc. (New York, N.Y.); josamycin, ICN
Biomedicals (Costa Mesa, Calif.); spiramycin, Rhône-Poulenc Rorer
(Paris, France); and HMR3004, Hoechst Marion Roussel (Romainville, France).
Susceptibility tests.
MICs were determined by the broth
microdilution method (15) with Mueller-Hinton II broth (BBL
Microbiology Systems) supplemented with 3% lysed horse blood as the
test medium. The inoculum was 5 × 105 CFU/ml. The
antibiotics were tested at final concentrations (prepared from twofold
dilutions) that ranged from 0.015 to 128 µg/ml. S. pneumoniae ATCC 49619 was used for quality control. The MIC
breakpoints suggested by the National Committee for Clinical Laboratory
Standards (17) were considered for erythromycin,
clindamycin, and clarithromycin (susceptible, 
0.25 µg/ml;
intermediate, 0.5 µg/ml; resistant, 1 µg/ml) and for azythromycin
(susceptible, 0.5 µg/ml; intermediate, 1 µg/ml; resistant, 2
µg/ml). The MIC breakpoints suggested by the French Society for
Microbiology (4) were considered for spiramycin and
josamycin (susceptible, 1 µg/ml; intermediate, 2 µg/ml;
resistant, 4 µg/ml). In the absence of established interpretive standards, the MIC breakpoints unofficially proposed for HMR3647, another ketolide (susceptible, 1 µg/ml; intermediate, 2 µg/ml; resistant, 4 µg/ml) (1), were tentatively applied to
HMR3004, too.
Tetracycline and chloramphenicol susceptibilities were determined by a
standard agar diffusion test (16) with commercial disks
(Oxoid) containing 30 µg of either antibiotic. The zone diameter
breakpoints (17) were as follows: for tetracycline, susceptible, 23 mm; intermediate, 19 to 22 mm; and resistant, 18
mm; for chloramphenicol, susceptible, 21 mm; intermediate, 18 to 20 mm; and resistant, 17 mm.
Induction of MLS resistance.
Induction of MLS resistance was
evaluated by pregrowth (3 h at 37°C) in erythromycin at a
subinhibitory concentration (0.05 µg/ml), as described previously
(13). The culture was then washed and the cells were used to
prepare the inoculum for MIC testing by the usual broth microdilution method.
Detection of erythromycin resistance genes.
The
ermB gene was detected by PCR with the oligonucleotide
primer pair reported by Sutcliffe et al. (20) (the expected
PCR product was 639 bp). The ermTR gene was detected with
the primers designated III8 and III10 by
Seppälä et al. (19) (the expected PCR product
was 208 bp). The mefA gene was detected with the primer pair
reported by Sutcliffe et al. (20) (the expected PCR product was 348 bp). DNA preparation and amplification and electrophoresis of
PCR products were carried out by established procedures (9, 19,
20).
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RESULTS |
Identification of macrolide resistance phenotypes.
On the
basis of the erythromycin-clindamycin double-disk test, 203 (52.5%) of
the 387 strains of erythromycin-resistant S. pyogenes tested
were assigned to the M phenotype, 120 (31.0%) were assigned to the
iMLS phenotype, and 64 (16.5%) were assigned to the cMLS phenotype
(Table 1).
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TABLE 1.
Determination of the macrolide resistance phenotype in
387 throat isolates of erythromycin-resistant S. pyogenes by the double-disk test and correlation with
clindamycin susceptibility
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The inducible character of the resistance of the strains assigned to
the iMLS phenotype by the double-disk test was confirmed
by comparing
the clindamycin MICs determined under normal testing
conditions and
those determined after induction by pregrowth in
0.05 µg of
erythromycin per ml. Without induction, clindamycin
MICs were in the
range of susceptibility for all except three
iMLS isolates, for which
the MICs (0.5 µg/ml) were consistent
with intermediate
susceptibility; after induction, the clindamycin
MICs for the iMLS
isolates invariably exceeded 128 µg/ml. By the
same method, all the
isolates previously assigned to the cMLS
phenotype were found to be
highly resistant to clindamycin (MICs,
>128 µg/ml) without
induction, whereas those assigned to the M
phenotype remained
susceptible even after induction (Table
1).
Patterns of susceptibility to MLS antibiotics.
The MICs of two
14-membered (erythromycin and clarithromycin), one 15-membered
(azythromycin), and two 16-membered (josamycin and spiramycin)
macrolides and of the ketolide HMR3004 were determined and compared.
Homogeneous susceptibility patterns were observed among the isolates of
the cMLS phenotype (with one exception) and those
of the M phenotype,
whereas among the isolates of the iMLS phenotype
patterns were
heterogeneous (Table
2). For 63 of the 64 cMLS
strains, the MICs of HMR3004 ranged from 0.5 to 8 µg/ml, while
those of the other drugs tested exceeded 128 µg/ml. The remaining
cMLS strain was highly susceptible to HMR3004 (MIC,
0.015 µg/ml)
and was resistant to the macrolides (MIC range, 2 to 32 µg/ml).
For
the M-phenotype isolates, resistances were recorded only to
the 14- and
15-membered macrolides (MIC range, 2 to 32 µg/ml).
For the isolates
of the iMLS phenotype, the susceptibilities of
the 16-membered
macrolides ranged from susceptibility to high-level
resistance values,
those of HMR3004 ranged from susceptibility
to resistance, and those of
the 14- and 15-membered macrolides
ranged from low-level resistance (or
intermediate susceptibility
to clarithromycin in three isolates) to
high-level resistance.
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TABLE 2.
Susceptibilities of 387 isolates of
erythromycin-resistant S. pyogenes, subdivided into the
three recognized phenotypes of macrolide resistance, to
MLS antibiotics
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With the inducibly resistant strains, the MICs of erythromycin,
josamycin, and HMR3004 were also determined after induction
with
erythromycin, by the same pregrowth procedure used previously
for
clindamycin susceptibility tests. Three distinct patterns
of resistance
to MLS antibiotics were recognized among these isolates
(Table
3). The most frequently observed pattern,
observed for
84 (70%) inducibly resistant strains and designated
iMLS-A, was
characterized by high-level resistance to the 14-, 15-, and
16-membered
macrolides (MICs, >128 µg/ml) and reduced susceptibility
to low-level
resistance to HMR3004 (MICs, 0.5 to 8 µg/ml without
induction
and 1 to 16 µg/ml after induction). The second pattern,
observed
for 12 (10%) inducibly resistant strains and designated
iMLS-B,
was characterized by high-level resistance to the 14- and
15-membered
macrolides (MICs, >128 µg/ml), susceptibility to the
16-membered
macrolides but high-level resistance to josamycin (MICs,
>128
µg/ml) after induction, and susceptibility to HMR3004 without
induction but intermediate susceptibility or resistance (MICs,
2 to 8 µg/ml) after induction. The third pattern, observed for
the remaining
24 (20%) inducibly resistant strains and designated
iMLS-C, was
characterized by resistance to the 14- and 15-membered
macrolides (with
MICs not exceeding 16 µg/ml and erythromycin
MICs increasing two to
four times after induction), susceptibility
to the 16-membered
macrolides but resistance to josamycin after
induction (MICs, 4 to 16 µg/ml), and susceptibility to HMR3004,
also after induction.
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TABLE 3.
Susceptibilities of 120 isolates of S. pyogenes with the iMLS phenotype to MLS antibiotics and their
subdivision into three subtypes
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Erythromycin resistance genes.
The presence of the
erythromycin resistance genes ermB, ermTR, and
mefA in 100 isolates (20 cMLS, 42 iMLS-A, 6 iMLS-B, 12 iMLS-C, and 20 M) was investigated by PCR (Table
4). All cMLS and iMLS-A isolates tested
had the ermB gene, whereas all iMLS-B and iMLS-C isolates
had the ermTR gene (neither methylase determinant was found
in isolates of the other groups). All M-phenotype isolates had the
mefA gene, which was also found in several isolates of the
cMLS (40%) and iMLS (31% iMLS-A, 100% iMLS-B, and 92% iMLS-C) phenotypes.
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TABLE 4.
Distribution of erythromycin resistance genes
ermB, ermTR, and mefA among 100 erythromycin-resistant S. pyogenes isolates of different
phenotypes and subtypes of macrolide resistance
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Susceptibility to tetracycline and chloramphenicol.
The
susceptibilities to two non-MLS antibiotics (tetracycline and
chloramphenicol) were determined by agar diffusion. Chloramphenicol resistance was not encountered in any of the erythromycin-resistant S. pyogenes test strains. Tetracycline resistance (Table
5) was detected in the majority of
isolates of the cMLS (71.9%) and M (69.5%) phenotypes. An overall
incidence of tetracycline resistance of 27.5% recorded in the iMLS
isolates resulted, in fact, from the uniform susceptibility observed
among the iMLS-A strains and the greater than 90% incidence of
resistance observed among both iMLS-B and iMLS-C strains.
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TABLE 5.
Susceptibilities of 387 isolates of
erythromycin-resistant S. pyogenes, subdivided into
phenotypes and iMLS subtypes of macrolide resistance, to tetracycline
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Triple-disk test.
Considering the crucial importance of the
16-membered macrolides in discriminating the three subtypes of
inducibly resistant S. pyogenes strains, a triple-disk test
was set up by adding a josamycin disk (30 µg; Oxoid) to the
erythromycin and clindamycin disks of the conventional double-disk
test. The erythromycin disk was placed at the center of the agar plate,
with the clindamycin and josamycin disks placed 15 to 20 mm apart on
either side. All strains were tested by this triple-disk assay.
While the clindamycin zone of inhibition proximal to the erythromycin
disk was uniformly blunted among the iMLS strains, in
agreement with
the inducible nature of the resistance in these
strains, blunting of
the josamycin zone of inhibition proximal
to the erythromycin disk was
taken to indicate inducible resistance
to the 16-membered macrolides.
As shown in Fig.
1, the iMLS-A
strains
were characterized by the absence of any zone of inhibition
around both
the erythromycin and the josamycin disks (in line
with their high-level
resistance to both drugs). The iMLS-B and
iMLS-C strains were both
characterized by blunting of the josamycin
zone of inhibition proximal
to the erythromycin disk. However,
no zone of inhibition was seen
around the erythromycin disk in
the case of the iMLS-B strains (in
agreement with their high-level
erythromycin resistance), whereas a
restricted zone of inhibition
(not exceeding 15 mm in diameter) was
visible in the case of the
iMLS-C strains (in line with their
lower-level erythromycin resistance).
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FIG. 1.
Phenotypes and iMLS subtypes of erythromycin-resistant
S. pyogenes isolates determined by the triple-disk test. The
erythromycin disk (30 µg) is at the center, with the clindamycin disk
(10 µg) on the right and the josamycin disk (30 µg) on the left.
(A) cMLS phenotype. (B) iMLS phenotype (subtype iMLS-A). (C) iMLS
phenotype (subtype iMLS-B). (D) iMLS phenotype (subtype iMLS-C). (E) M
phenotype.
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|
S. pyogenes strains of both the cMLS phenotype
(characterized by the absence of a zone of inhibition around the
clindamycin
disk) and the M phenotype (characterized by no blunting of
the
clindamycin zone of inhibition) were identified by the triple-disk
test as easily as by the double-disk
test.
The performance of the triple-disk test did not substantially change
when a spiramycin disk (100 µg; Oxoid) was used instead
of the
josamycin
disk.
| |
DISCUSSION |
Our findings indicate that, among the erythromycin-resistant
S. pyogenes strains which have increasingly arisen in Italy
over the last few years (2, 5), the M phenotype is
encountered for over one-half (52.5%) of the strains and the iMLS
phenotype is encountered for almost one-third (31.0%) of the strains,
while the cMLS phenotype is encountered less frequently (16.5%).
Interestingly, the iMLS strains, although easily and sharply
distinguishable from isolates of the cMLS and M phenotypes on the basis
of the inducible character of their resistance, were found to be
homogeneous in their response to clindamycin (with all strains turning
from susceptible or, occasionally, intermediate without induction to highly resistant after induction) but heterogeneous in their
susceptibility to the macrolides and the ketolide. On the basis of this
phenotypic heterogeneity, three distinct subtypes of inducibly
resistant strains (designated iMLS-A, iMLS-B, and iMLS-C) were
distinguished. Susceptibility to the 16-membered macrolides was of
particular importance in discriminating the three subtypes: the iMLS-A
strains were highly resistant to josamycin, and this was also the case without induction; and the iMLS-B and iMLS-C strains were josamycin susceptible but became high-level and low-level resistant,
respectively, after induction. A triple-disk test, which was set up by
adding a josamycin disk to the erythromycin and clindamycin disks of the conventional double-disk test, enabled us to distinguish easily not
only the three known phenotypes of erythromycin-resistant S. pyogenes (cMLS, iMLS, and M) but also the three iMLS subtypes (iMLS-A, iMLS-B, and iMLS-C). As for the non-MLS antibiotics, the
acquisition of resistance to tetracycline and/or chloramphenicol has
been considered a prerequisite for S. pyogenes resistance to
macrolides (14). While chloramphenicol resistance was not detected in our test strains
as among Finnish isolates collected in
1990 (18), whereas resistance was reported in 3% of the
iMLS isolates collected in Finland in 1994 and 1995 (11)variable rates of tetracycline resistance were
associated with the different phenotypes of macrolide resistance. In
particular, among the iMLS strains, tetracycline resistance was not
observed in the isolates of the predominant subtype iMLS-A, whereas it
was recorded in over 90% of both iMLS-B and iMLS-C isolates.
Some particular or atypical resistance patterns have been reported
previously in macrolide-resistant S. pyogenes strains
(10, 18); however, correspondence with our findings appears
to be only partial. In our study the sole cMLS isolate that was highly susceptible to HMR3004 and that had low-level resistance to the macrolides is likely to correspond to a subtype of the cMLS phenotype previously described by Seppälä et al. (18),
which accounted for over half of the cMLS strains among Finnish
isolates. Other atypical subtypes of cMLS strains, characterized by
susceptibility or low-level resistance to clindamycin, described among
Swedish isolates (10) were not encountered in our
experience. The subtypes of the iMLS strains characterized by
high-level resistance to erythromycin and inducible resistance to
clindamycin described by Seppälä et al. (18) and
Jasir and Schalén (10) probably correspond to our
iMLS-A or iMLS-B strains, depending on their susceptibilities to
16-membered macrolides. On the other hand, the prevalence of the
recognized phenotypes of erythromycin-resistant S. pyogenes
may also vary from area to area and over time. Indeed, although the M
phenotype was the most frequent in our study as well as among
erythromycin-resistant S. pyogenes isolates collected in
1994 and 1995 in the United States, Ireland, and Sweden (21) and from 1980 to 1990 in Sweden (10), its frequency was
second to that of the iMLS phenotype among the Finnish isolates
collected in 1990 (18). Even more strikingly, in Sweden
inducibly resistant strains were absent from 1980 to 1990, and
constitutively resistant strains were absent from 1980 to 1985 (10).
It seems that the whole matter of phenotypic diversity in
macrolide-resistant S. pyogenes strains is still far from
being settled and that its comprehension must pass through a careful correlation of phenotypic and genotypic characteristics. However, the
knowledge of erythromycin resistance determinants in S. pyogenes also seems far from complete to date. Only recently have
a gene (mefA) encoding a membrane protein responsible for
efflux-mediated resistance (3) and a methylase gene
(ermTR) other than ermAM (ermB)
(19) been characterized. Among our strains, ermB
was invariably detected in cMLS and iMLS-A isolates, and the same was
true of ermTR for iMLS-B and iMLS-C isolates and of
mefA for M isolates. However, while the two methylase
determinants were not found in isolates of different groups,
mefA was also present in less than half of cMLS and iMLS-A
isolates and in all or the vast majority of iMLS-B and iMLS-C isolates.
It is worth noting that, in a recent survey of erythromycin resistance
genes among Finnish isolates of S. pyogenes, Kataja et al.
(11) detected only ermTR in 24 iMLS isolates.
Most of the Finnish iMLS isolates might, however, fall in our iMLS-B
and iMLS-C subtypes (which possess ermTR), as suggested by
the reported 93% incidence of tetracycline resistance in these strains
(11) (all of our iMLS-A isolates, which all possess
ermB, are susceptible to tetracycline). On the other hand,
the mefA determinant, which has been found in all or the
vast majority of our iMLS-B and iMLS-C isolates, was not detected among
the Finnish isolates of iMLS S. pyogenes tested
(11).
| |
FOOTNOTES |
*
Corresponding author. Mailing address: Institute of
Microbiology, University of Ancona Medical School, Via Ranieri, Monte d'Ago, 60131 Ancona, Italy. Phone: 39 71 2204694. Fax: 39 71 2204693. E-mail: pe.varaldo{at}popcsi.unian.it.
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Abstract
Introduction
