Jpn. J. Infect. Dis., 52, 238‑241, 1999

Original Article

Methicillin Resistance among Trinidadian Isolates of Community andHospital Strains of Staphylococcus aureus and Their Pattems ofResistance to Non‑β ‑Lactam Antibiotics
Fitzroy A. 0汀ett*

Department of Pathology and Microbiology, the Universityof West lhdies,
FacultyofMedical Sciences, Eric l砺Iliams Medical Sciences Complex,Champs Fleurs, Trinidad and 7Tobago, West lhdies(Received September 27, 1999. Accepted November 17, 1999)

StJMMARY: The prevalence of methicillin‑resistant Staphylococcus aweus (MRSA) Strains in Trinidad andthe extent of their resistance to other antimicrobial agents in hospital‑acquired and community‑acquired infec‑
tions were evaluated over a 21year Period. A totalof 450 S. aweus strains were isolated from different patients･
The prevalence of methicillin resistance among S. aweus strains was 9.8% (44/450). The proportion of MRSA
isolated from hospital sources and commumity sources was 12.5% (38/305) and 4.1% (6/145), respectively(P < 0.05). The resistant rates of MRSA to the non‑8‑1actam antibiotics were as follows: 93.2% resistance totetracycline, 68.2% to erythromycin, 61.4% to gentamicin, 45.5% to co‑trimoxazole, and 20.5% to cipronoxacin･No MRSA resistant to vancomycln Was Observed in this study. Study results showed significant increases inMRSA in hospital, 2% in 1995 to 12.5% in 1998 (P < 0.05), and commumity, 0% in 1995 to 4.1% in 1998
(P < 0.05). It has become apparent that infection control and surveillance initiatives must be focused now on thecommunity in order to monitor and limit the spread of this new and expanding reseⅣoir of MRSA･to other antibiotics, isolation and treatment of patients andINT RODIJCT ION

camiers, and strict adherence to hand washing practices by

Staphylococcus aureus is the single most frequently encoun‑

medical staff.

The objectives of this study were to detemine the prevalence

tered bacterial species in hospitals (1) andthe most common
etiologiCalagent of hospital‑acquired post‑operative surgicalwound infections (2,3). In the 1960S, methicillin‑resistantof Trinidadian strains of MRSA isolated from hospitalpracticeand community practice and theirantimicrobialresistance

Staphylococcus aweus (MRSA) stmins first emerged as aprofiles.

major hospital‑acquired pathogen, both in Europe (4), North
America (5),and other parts of the world, and the emergence

MATERIALS AND METHODSof this resistance correlates with the development of increaslng

resistance to otherantimicrobialagents (6). Therefore, MRSA

Between January I, 1997 and December 31, 1998, westmins maybe resistant to severalother classes ofantimicrobial

examined stmins of S. aureus from variousclinicalsources inagents, including the qulnOlones, clindamycin, tetracyclines,

hospital and community practices in Trinidad fわr methicillin

erythromycin, trimethopnm‑sulfamethoxazole as well as theresistance. SpeclmenS Were derived from patients on the wards

aminoglycosides (7,8).
Several mechanisms for the methicillin resistance seen in

andfromthose attending outpatient climics atthe Erie Wllliams
Medical Sciences Complex (EWMSC). The EWMSC is a

S･ aureus have been elucidated. The most important is produc‑560‑bed medical facility located in the northwest part of thetion of a umiquepemicillin‑binding protein (PBP)that has a low

country of Trinidad, which is the larger of the twin islandaffinity for 8‑lactam drugs and whose effects are determined

Republic, Trinidad and Tobago, located about I 1 km off theby several structural genes (mecA, mecRJ, mec†) (9, 1 0). Other

known mechanisms of methicillin resistance are the produc‑

northem coast of Venezuela in South America. The popula‑tion of the Republic is about 1.25 million. For purposes oftion of theusualPBPs, but with modified affinities for the B‑

this investigation, We did not differentiate between isolates

lactamdrugs,and the hyperproduction ofpenicillinase enzyme

from Inpatients and outpatients; all isolates were classified(8).

as "hospital‑practice". Specimens received from patients

MRSA stmins canSpread from infected patients to medical

attending health care centers in the communityand from those

staff, who often become transient carriers ( I 1 ). Infections withseen by general practitioners were classified as "community‑

these organi sms are life‑threatening ln immunocompromised

practice" isolates. For purposes of gathering infection control

patients, often difficult to manage,and problematic to eradi‑surveillance data, other organismsand duplicates of clinicallycate. It is therefore of primary Importance tO decrease theslgnificant isolates were excluded from the hospitalspecimens

prevalence of MRSA by measures such as rapid and reliable

that were received.

identification of the organisms along with their sensitivities

S. auTleuS Strains were tested for resistance to methicillin*Corresponding author: Mailing address: P.0. Box 371, Curepe

on Mueller‑Hinton agar (BBL Microbiology Systems,Cockeysville, Md.) viathe disc diffusion method outlined by

Post Office, Curepe, Trinidadand Tobago, West Indies. Fax:

the National Committee for Clinical Laboratory Standards+ 1 ‑868‑663‑9836(NCCLS) (12) using a I LLg OXaCillin disc･ Plates were238

incubated aerobically at 33‑350C for a full 24 h. Strains withrespectively. This difference was statistically slgnificant

zone sizes less than 10 mm were regarded as methicillin(P < 0.05･).

resistant･ By the disc di飢sion method specified by theTable 2 shows the prevalence of resistance of MRSA toNCCLS, MRSA isolates were tested against the followlng

other antibiotics.Levels of resistance tothese non‑B‑lactam

antibiotics and concentrations (in brackets): vancomycin (30antibiotics ranged from 93.2% for tetracycline to 20.5% forLLg), cipmfloxacin (5 LLg), gentZmicin (10 LL g), Cひtrimoxazole

cIPrOnOXaCin.

(trimethoprim‑sulfamethoxazole) (25 LLg), erythromycin ( 15The major sources of MRSA and MSSA (methicillin‑LLg),and tetracycline (30 LLg) (12). The MRSA control strain

sensitive S･ aweus) strains are sho竺n in Table 3･ Among 44was S. aweus (ATCC 49476), obtained from the Caribbean

strains of MRSA, 24 (54.5%) were lSOlated from wounds, 8

Epidemiology Center (CAREC), a branch of the PanAmeriCan(18･2%) from urine, 5 (ll.4%) from lower respiratory tract
specimens, 4 (9.1%) from boils and abscesses,and 3 (6.8%)

Health Organization/Wわrld Health Organization･from bloodstream infections.

REStJLTSDISCUSSION

From也e 1 5,922 speclmenS Submitted to the EWMSC fromclinicalSources for microbiologlCal investigations, a total of450 (2･8%) strains of S･ aweus were isolated during the study

identified in 1995, and the overall rate for the country wasperiod (305 from hosp血l practice and 145 from community

about 2% (13,14). The prevalence of MRSA in this study

practice sources) Crable 1 ). The overall methicillin‑resistant

was found to be 9.8%, With a concomitant increase in theThe first documented case of MRSA at this hospital wasrate in S･ aweus was 9･8% (44/450)･ The p.revalence ofpercentage of isolates resistant to tetracyclines, gentamicin,

co‑trimoxazoleand erythromycin,thoughal1 strains appear tomethicillin resistance among S. aweus strains ISOlated from

hospital and community patients was 12･5% and 4.1%,

have maintained fdl susceptibilityto vancomycin. In this study,
the zone sizes for vancomycln Were 15‑20 mm in diameter,

thoughthe disc diffusion method of susceptibility testing has
Table 1. Distribution of 450 Staphylococcus aureus stmins isolated

been reported to be misleading for detecting intermediate orfrom hospitaland community sources according to methicillineven resistant strains (12). This increase in the rate of resis‑
tance to antibiotics, in particular to methicillin, has become aresistance, 1997‑1998

70%31

worldwide problem.

(90.2)

44(9.8)Asia, and other parts of the world. In Japan, the rate was 60%
nationwide and as high as 90% in individual hospitals (15).

Methcillin "iOs'.Taft:sos(p群"oiso.fl;tOeTT芸)mity

The incidence of MRSA stminsis particular high in Europe,
Sensitive

267

Resistant

TOTAL(87･5)

38(139(12･5)

305 (100･0)

95.9)

6(406

4.I)

145 (loo.0)450 ( loo.0)

In Denmark it was fわund to be 46% (16); it was 46‑67.5% inHospitalMRSA: 1995 vs 1998, X2 =5.48; P < 0.05.
Community MRSA: 1995 vs 1998, X2 =5.39; P < 0.05.

Greek hospitals (17); and in Turkey, 25‑80% (18). In No仙America (19,20) and the Middle East (21), rates of 20‑50%
and 3‑ 18% have been reported, respectively. MRSA rates fromthe Caribbean are scanty but one report from Jamaica showed

rates of isolation to be I ‑2% (22)･ These different rates amo.ng

Table 2. Prevalence of resistance of 44 MRSAI strains to other anti̲

MRSAsfrom different countries may be attributable to vana‑

microbial agents, 1997‑ 1998
Antimicrobialtions in patient populations, the biological characteristics of

Nol 0fstrains tested No. ofstmins resistant(%)

the S･ aulleuS Strains, and/or infection control practices (23).
Vancomycl n

舶舶叫叫舶30

The rate of methicillin resistance among S. aweus strains

Tetracycli ne

41 (93.2)

was low in the community (4.1%) compared to that in theErythromyci n

30 (68.2)

Gentami ci m

hospital (12.5%), but significantly higher than the 1995 rate

27 (61.4)

Co‑ trimoxazol e2

20 (45.5)

of O% in the community (X2 = 5.39; P < 0.05). This increaseof 4. I % is certainly a cause for concem in Trinidad and may

Ci prom oxaci n8 (20.5)

very well represent a trend in the changlng ePidemiology oflMRSA=methicillin‑resistant Staphyk)coccus aureus; 2Co‑trimoxazole=MRSA in the late 1990S. Many factors may be at play in theunexpected prevalence of community‑acquired MRSA. One

trimethoprim‑sulfamethoxazol e.

reason for this increase may be lateral dissemination fromthe hospital to the community, most patients diagnosed withTable 3. ClinicalSources of MRSAl and MSSA2 stmins isolated atMRSA discontinue therapy, once discharged, because of thethe EWMSC3, 1997‑ 1998

cost of prescriptions at local pharmacies.

MRSANo.

Wounds

MS%

SANo.

5

Two reports from Australia suggestthat, after patientdischarge from hospital, MRSA camage continues, and that%long‑ten carriers can ultimately become reseⅣoirs fわr the24

54.

279

68.

7

Uri ne818.2

53

13.

1

organisms in the community. Infected superficial wounds andLower Respiratory Tract

51266.4py∝lermas are commonly seen in health centersandthe oWICeS

1.4of general practitioners (unpublished data). Other factors(sputum)Boils

andabscesses

4BloodTOTAL

9.

3

44

6.8

100.0

11929406

previously identified as contributory to community MRSA

4.7
1

include overcrowding (24)and skin sepsis (25). Another factor

00.0

may be inappropriate prophylactic and therapeutic use of

7.

1lMRSA=methicillin‑resistant Staphylococcus aureus, 2MSSA=antimicrobials in both hospital and community practices. An

methicillin‑sensitive staphylococcus aureus, 3EWMSC=Eric W111iams

earlier report from this country identified over‑the‑counter

Medical Sciences Complex･

sale of antibiotics, without a prescription, as a contributing

239

factor in the emergence of multi‑resistant organisms in theChemother., 34, 1703‑ 1706.

community (26)･ The six MRSA strains from the community
included one each from two diabetic patients,and one isolate

1 1. Cookson, B., Peters, B., Webster, M., Phillips, I., Rahman,
M. and Noble, W. (1989): Staff camiage of epidemic

each from patients with long standing hypertension, skinmethicillin‑resistant Staphylococcus aureus. J. Clin.

sepsIS, Chronic alcoholism and renal dialysIS.

Microbio1., 27, 147ト1476.

The emergence of MRSA in our hospitals re‑emphasizes

12. National Committee for Clinical Laboratory Standards

the need for intensive surveillance and prevalence‑culturing(1997): Pe血mance Standards fわr Antimicrobial Diskof patientsand health care providers (HCP) in order to identify
all infected and colonized persons･ This would requlre theSusceptibility Tests. Approved standard M2‑A6. NCCLS,Villanova, Pa.

establishment of MRSA isolation units to physically separate

13. Adesiyun, A. A., Prabhakar, P., Ali, C. andLewis, M.

the infected patientsand their HCPsfrom the uninfected ones;( 1 995): Characteristics of Staphylococcus aweus strains

treatment protocols for eradicating MRSA from patient and
HCP camiers; stringent environmental disinfection in areas
houslng infected patients;and the application of bamier isola‑

isolated from clinical and non‑clinical human sources inTrimidad: Susceptibility to bacteriophagesand antimicro‑tion precautions, including strictly enforced hand washing,

5 19‑532.

bial agents, and toxigenicity. Zentralbl. Bakteriol. 282,

to interrupt spread pattems･ A previous report from this institu‑

14. Orrett, F. A. (1997): Antimicrobial resistance in Trinidad:

tion revealed that hand washing practices and sanitation

hospital practice strains versus community practicetechniques of HCPs at all levels of seⅣice were not strictly

stmins of Staphylococcus aulleuS. Med. Sci. Res. , 25, 663‑

adhered to (27).

666.

This study has shown that MRSA is not only a problem of15･ Mehtar, S. (1994): The continuing problem of hospital

hospitalized patients, but also a problem of people within thestaphylococci: why? J. Chemother. (Italy), 6 (Suppl. 4),community･ Tb address this expanding reservoir of multト

25‑31.

resistant organisms, infection control initiatives that involve

16･ Emmerson, M. (1994): Nosocomial staphylococcal ouト

and includethe healthcentersand generalpractitioners'otrlCeS

breaks. Scand. J. Infect. Dis., 93 (Suppl. I), 471 54.

should be extended to the community in order to monitor and

17. Kosmidis, ∫., Polychronopoulou‑Karakatsanis, C.,limit the spread of MRSA.

Milano‑Petropoulou, D., MavrogenlS, N., ⅩenakトKondyli, M. and Gargalianos, P. (1988): Staphylococcal
infections in hospital: the Greek experience. J. Hosp.
Infect., I I(Suppl. A), 109‑1 15.

REFERENCES

l･ Emori, T･ G･ and Gayn.es, R･ P･ (1993): An overvie.w of

18･ Erkmen, 0･, Balci, Ⅰ. and Gungor, S. (1996): Staphylo‑

nosocomial infection, Including the role of the mlCrO‑coccal infectionsin a hospital. Turk. J. Med. Sci., 26,biology laboratory. Clin. Microbiol. Rev., 6, 428‑442.

367‑370.

2･ Tumidge, ∫. D., Nimmo, G. 良. and Francis, G. (1996):

19･ Panlilio,A. L., Culver, D. H., Gaynes, R. P., BanerJee, S.,

Evolution of resistance in Staphylococcus aureus inHenderson, T. S., Tolson, J. S. and Martone, W. J. (1992):
Methicillin‑resistant Staphylococcus aureus in U.S.

Australian teaching hospitals. Med. J. Aust., 164, 68171.
3･ Schaberg, D･ R･, Culver, D. H. andGaynes, R. P. (1991):
Major trends in the microbial etiology of nosocomial

hospitals, 1975‑1991. Infect. Control Hosp. Epidemio1.,
13, 582‑586.

infections. Am. J. Med., 91, 72S‑75S.

20. Nath, S. K., Shea, B., Jackson, S.and Rotstein, C. (1995):

Ribotyping of nosocomial methicillin‑resistant Staphylo‑

4･ Jevons, M･ P･ (1961): …Celbemin" ‑resistant Staphyloc∝ci.

coccus aureus isolates from a Canadianhospital. Infect.

Br. Med. ∫., 1, 124‑125.

5･ Barrett, F. F., McGehee, R. F., Jr.andFinland, M. (1968):
Methicillin‑resistant Staphylococcus aweus at Boston
CityHospital. N. Engl. J. Med., 279, 441‑448.

ControI Hosp. Epidemio1., 16, 717‑724.

21. Araj, G. F., Uwaydah, M. M.andAlami, S. Y. (1994):
Antimicrobial susceptibility pattems of bacterial isolates

at the American University Medical Center in Lebanon.
Diagn. Microbiol. Infect. Dis., 20, 151‑158.

6･ E曲torial(198 I): Of gentamicinand staphyl∝o∝i. I｣mcet,
ⅠⅠ, 127‑128.

7. Unal, S., Hoskins, J., Flokowitsch, J. E., Wu, C. Y.,

22･ Bodonaik, N. C.,King, S. D. and Narla, V. R. (1984):

Preston, D. A. and Skatrud, P.L. (1992): Detection of

Antimicrobial resistance in clinical isolates of Staphylo‑

methicillin‑resistant Staphyloco∝i byuslng the polymerase

Coccus aureus at the University Hospital of the Westlndies. West IndianMed. J., 33, 8‑13.
23. Wakefield, D. S., Pfaller, M., Massanori, R. M. andchain reaction ∫. Clin. Microbio1., 30, 1685‑1691.

8. Tomasz,A., Drugeon, H. B., deLencastre, H. M., Jabes,D･, McDougall, L and Rille, ∫. (1989): New mechanism

Hammons, G. T. (1987): Ⅵ山ationsin methicillin‑resistantfor methicillin resistance in Staphylococcus aureus:

Staphylococcus aureus by geographic location andclinical isolates that lack the PBP 2a gene and containhospital characteristics. Infect. Control, 8, 15 I‑ 157.

normalpenicillin‑binding proteinswith modifiedpemici1‑

24. Munoz, E., Powers, ∫. 良., Nienhuyo, T. G. and Mathews,

1in‑binding capacity･ Antimicrob･ Agents Chemother･ , 33 ,J. D. (1992): Socialand environmental factors in 10

1 869‑ 1 874.

Aboriginalcommmities in the northem temitory: relation‑

9･ Murakami, K･ and TomTsz, A･ (1989): Involvement ofmultiple genetic detemlnantS in high‑level methicillin

ship to hospital admissions of children. Med. ∫. Åust.,

156, 529‑533.

25･ Van Buynder, P. G., Gaggin, J. A., Martin, D., nlgSley, D.

resistance in Staphylococcus aweus. J. Bacteri01., 171 ,and Mathews, J. D. (1992): Streptococcal infection and874‑879.

10･ Tesch, W･, Ryffel, C･, Strassle, A･, Kayser, F･ H･ andrural disease markers in Australian Aboriginal children.

Berger‑Bachi, B･ (1990): Evidence of a novel StaphyloIMed. ∫. Åust., 156, 537‑540.

c.occalmec‑encoded element (mecR) controlling expres‑26. Orrett, F. A. and Shurland, S. M. (1996): Production ofsl0n Of penicillin‑binding protein 2'･ Antimicrob･ Agents

8‑lactamase by bacterialpathogens in Trinidad: correla‑240

tion with resistance to B‑lactam antibiotics. Med. Sci.

developlng COuntry･. infection rates by site, service, Cost

Res., 24, 519‑522.

and infection control practices. Infect. Control Hosp.

27. Orrett, F. A., Brooks, P. J. and Richardson, E. G. (1998):
Nosocomial infections in arural reglOnal hospital in a

Epidemio1., 19, 136‑140.

241