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Journal of Clinical Microbiology, April 2001, p. 1669-1671, Vol. 39, No. 4
0095-1137/01/$04.00+0 DOI: 10.1128/JCM.39.4.1669-1671.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Low Prevalence of Community-Acquired
Methicillin-Resistant Staphylococcus aureus in Adults at a
University Hospital in the Central United States
Nila
Suntharam,1
Donna
Hacek,2,3 and
Lance R.
Peterson1,2,3,4,*
Northwestern Prevention
EpiCenter2 and Clinical Microbiology
Division,3 Northwestern Memorial Hospital, and
Infectious Disease Division1 and
Department of Pathology,4 Northwestern
University Medical School, Chicago, Illinois 60611
Received 18 September 2000/Returned for modification 12 December
2000/Accepted 29 January 2001
 |
ABSTRACT |
Community-acquired MRSA (CA-MRSA) is potentially a new emerging
pathogen with most strains susceptible to many antimicrobials except
for
-lactam antibiotics. We retrospectively reviewed MRSA isolates
during a 20-month study period (January 1998 through August 1999) and
investigated those that were clindamycin susceptible. Patients were not
considered to harbor CA-MRSA if they had been admitted to a hospital
within the preceding 2 years or if their isolate had been obtained more
than 72 h after admission. There were 2,817 S. aureus
isolates, with 1,071 (38%) being MRSA. Of these 1,071 isolates, 161 were clindamycin susceptible; these were recovered from 81 patients. Of
these 81 patients, 20 appeared to have community-acquired strains, but
only 2 could be confirmed as having CA-MRSA.
 |
TEXT |
Community-acquired
methicillin-resistant Staphylococcus aureus (CA-MRSA)
appears to be a new emerging pathogen, with recent reports coming from
various areas in the United States (1, 4-7, 10),
Australia (9, 12), and Canada (3). S. aureus is an important human pathogen that has been recognized for
decades; however, the percentage of S. aureus isolates that
are methicillin resistant has increased from 2% in 1974 to nearly 50%
in 1997 in some areas (8). The emergence of CA-MRSA is a
recent occurrence, raising considerable concern since this type of
S. aureus would cause infections difficult to treat in the
outpatient setting and would markedly increase the need for vancomycin
therapy. O'Brien and colleagues related the incidence of CA-MRSA to be
as high as 42% in certain rural communities in Western Australia
(12). The published studies from Chicago have been based
mostly in pediatric populations (5, 7), as was the recent
report of the Centers for Disease Control and Prevention of four deaths
due to CA-MRSA (4). The actual prevalence of CA-MRSA in
communities in the United States is unknown. Interestingly, CA-MRSA
isolates appear to uniquely differ from the nosocomial MRSA isolates in
that they are generally more susceptible to multiple antimicrobial
agents other than
-lactam antibiotics. Given their different
antimicrobial susceptibility patterns, the CA-MRSA isolates may not
simply be hospital strains that have been transferred into the
community. Clindamycin susceptibility has been shown to have a very
significant correlation with CA-MRSA (5). Our study
examined whether clindamycin susceptibility could be a specific
surrogate marker for CA-MRSA in patients served by our institution.
Using this marker, we also assessed the number of CA-MRSA infections
that may occur in our adult population cared for in the large urban
area of Chicago, Ill.
Study setting.
Northwestern Memorial Hospital (NMH) is a
688-bed tertiary-care teaching facility serving an adult population.
During the study period, no MRSA isolates were recovered from children.
Study design and case definition.
We retrospectively reviewed
the MRSA isolates during a 20-month period (January 1998 through August
1999) and selected those that were clindamycin susceptible for further
investigation. The MRSA recovered were obtained from the Sunquest
laboratory information system, with duplicates removed by the
computer's search function. Patients were eliminated from
consideration of harboring CA-MRSA if they had been admitted to NMH
within the preceding 2 years or if their isolate had been obtained more
than 72 h after admission, based on information retrieved from the
hospital information system. For those remaining patients with
potential CA-MRSA, the medical record was reviewed to determine if
there had been an admission to an outside facility or other healthcare
contact within 2 years. If, after the record was reviewed, a
determination could not be made, the attending physician or the patient
was contacted and questioned in order to obtain that information. The
Institutional Review Board of Northwestern University approved these inquiries.
Microbiology procedures.
All cultures were evaluated in the
NMH microbiology laboratory. Staphylococci were identified by colonial
morphology, catalase testing, tube coagulase testing, DNase reaction,
mannitol fermentation, tellurite reduction, and an
oxidation-fermentation test. All isolates were tested for
susceptibility by the agar dilution MIC method according to the methods
approved by the National Committee for Clinical Laboratory Standards
(11). An MIC of
4 µg/ml for oxacillin determined the
S. aureus isolates to be methicillin resistant.
Detection of CA-MRSA.
In reviewing these patients, we were
unable to access only one chart. In 1998, there were a total of 1,658 S. aureus isolates recovered, with 616 being MRSA. Of these
616 isolates, the 80 (13%) that were clindamycin susceptible were
recovered from 47 patients. Strains from 15 of these patients appeared
potentially community acquired based on chart review. Through the first
8 months of 1999 there were 1,159 S. aureus isolates
cultured, with 455 being MRSA. Of the 455 isolates, 81 (18%) were
clindamycin susceptible and were recovered from 34 patients; isolates
from 5 of these 34 patients appeared to be community acquired. Figure 1 shows the various proportions of
S. aureus we identified by our investigation. The majority
of the cases that were of potential community origin had skin or soft
tissue infections.

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FIG. 1.
Isolates and patients representing S. aureus
in the adult population at NMH during 1998 and the first 8 months of
1999. ClindaS, MRSA isolates susceptible to clindamycin.
|
|
Of the presumed community-acquired isolates from 20 patients, all were
susceptible to gentamicin, isolates from 19 were susceptible
to
tetracycline, and isolates from 16 were susceptible to ciprofloxacin.
Despite multiple attempts, we were only able to contact 4 of the
20 patients suspected of being infected with CA-MRSA in order
to confirm
that there had been no admission to a healthcare facility
within the
prior 2 years. We found in these four cases that there
had been no
recent hospital admission; however, two of these four
individuals were
healthcare workers. Thus, only 2 of the 1,071
MRSA strains could be
confirmed as CA-MRSA.
Concluding comments.
During this era of antimicrobial overuse
and increasing reports of multidrug-resistant organisms, CA-MRSA has
appeared as a newly emerging problem. The isolates considered as
representing CA-MRSA differ from nosocomial isolates in both
antimicrobial susceptibility and molecular typing patterns
(4). Interestingly, two prospective studies carefully
looking for patient contact with the healthcare system failed to detect
significant numbers of true community-acquired MRSA in New York (United
States), and London (Canada) (14, 15). Our results from
Chicago, Ill., support these latest reports.
We selected clindamycin susceptibility as a surrogate to screen for
CA-MRSA since this has been found as a unique marker in
the published
reports of CA-MRSA (
5) and can be useful by narrowing
the
number of MRSA isolates from patients whose infection may
need to be
considered as community acquired. This approach should
exclude the vast
majority of nosocomial isolates that are typically
resistant to
clindamycin. While clindamycin susceptibility eliminated
a large number
of MRSA strains from patients that needed medical
record review, it was
not highly specific in that we found very
few CA-MRSA in our adult
population despite a fairly high number
of clindamycin-susceptible
isolates. The accepted mechanism for
methicillin resistance is the
acquisition of the
mecA gene cluster,
which codes for the
penicillin-binding protein PBP2a. However,
some CA-MRSA isolates may
only have borderline resistance to methicillin
and may not contain the
mecA gene (
2) and thus not be truly
MRSA. We
did not test for the
mecA gene in our study, although
most
of our isolates were highly resistant to oxacillin (77% with
an MIC of
>8 µg/ml; 23% with an MIC of 8 µg/ml), strongly suggesting
the
presence of
mecA in these
strains.
A limitation to this study is its retrospective design and the fact
that we were not able to speak with the majority of patients
that
potentially had CA-MRSA in order to confirm their lack of
risk factors
associated with the acquisition of MRSA. Two of the
four contacted had
ongoing contact with the healthcare system,
thus only confirming two
adults as CA-MRSA. If a patient had been
admitted to a hospital within
the prior 2 years, we did not include
that patient since MRSA
colonization has been shown to persist
a long time after
hospitalization: even up to 40 months in one
report (
13).
Interestingly, if this 2-year criterion for hospital
contact had been
used in the Canadian study, only 2 of 331 (0.6%)
newly identified
patients with MRSA would have been considered
as CA-MRSA
(
15).
Routinely reviewing patient risk factors from whom
clindamycin-susceptible MRSA is recovered may be a useful tool for
detecting
CA-MRSA infection. However, even though using multidrug
susceptibility
as a surrogate for suspecting a community-acquired MRSA
was a
sensitive screen, it was not specific since the vast majority
of
even these isolates (>98%) came from patients with a demonstrated
risk factor for MRSA carriage. Our data indicate that the prevalence
of
this unique
S. aureus (CA-MRSA) is extremely low in adults
served by our hospital, as opposed to what appears to be the case
for
children, in Chicago, but is similar to the low levels of
community-acquired MRSA detected in New York and Canada (
14,
15).
 |
ACKNOWLEDGMENTS |
U.S. Public Health Service grant no. UR8/CCU515081, the Excellence
in Academic Medicine program from the State of Illinois, Northwestern
Memorial Hospital, and Northwestern University supported this work.
 |
FOOTNOTES |
*
Corresponding author. Mailing address: Northwestern
Prevention EpiCenter, Galter Carriage House, Room 701, Northwestern
Memorial Hospital, 251 E. Huron St., Chicago, IL 60611. Phone: (312)
926-2885. Fax: (312) 926-4139. E-mail:
lancer{at}northwestern.edu.
 |
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Journal of Clinical Microbiology, April 2001, p. 1669-1671, Vol. 39, No. 4
0095-1137/01/$04.00+0 DOI: 10.1128/JCM.39.4.1669-1671.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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