Community-Acquired Methicillin-Resistant Staphylococcus aureus

Abstract & Commentary

Synopsis: Staphylococcus aureus is a versatile enemy. It is spreading in the community, as well as in the hospital, with increasing resistance to antibiotics. Its armamentarium now includes not only resistance to methicillin and vancomycin but also means of spread and pathogenic mechanisms we clearly need to know more about—and soon.

Source: Infect Control Hosp Epidemiol. 2003;24:397-458, 460.

The June 2003 issue of Infection Control and Hospital Epidemiology contains a series of articles on community-onset infections due to methicillin-resistant Staphylococcus aureus (MRSA). Although most of the studies are several years old, there are some important points to be made and ideas for future research. It is important to recognize that there has already been a lot of work done with 20,000 articles on MRSA referenced in Medline. It should also be noted that even the NNIS study indicates more than half of the nosocomial S aureus infections acquired in the hospital are due to methicillin strains.

The Baggett1 study describes an outbreak of community MRSA (COMRSA) in rural southwest Alaska, where 240 cases are reported from 1999 to 2000. Eighty percent of the S aureus infections were reported as resistant, which was a dramatic increase from several years before. The infections caused were almost all skin and soft-tissue and were more likely in men. Only 19% of patients were hospitalized. Of the strains, it was remarkable that so many were susceptible to non-beta-lactam antibiotics. Virtually all strain were susceptible to tetracycline, rifampin, trimethoprim-sulfa, and ciprofloxacin. Seventy percent were reported as susceptible to clindamycin, although only 30% were susceptible to erythromycin.

Seal2 reported an increase in MRSA from 13% in 1986 to 28% in 2000 of the S aureus strains isolated at the University of Chicago medical complex. This was accompanied by a comparable rate of increase in the resistance to macrolides, as well as ciprofloxacin, but not to gentamicin or trimethoprim-sulfa. The study also found the methicillin-resistant strains to be more resistant to other antibiotics than the methicillin-susceptible one.

Jernigan3 cultured patients admitted to Grady Hospital in Atlanta and found essentially all could be traced to prior hospitalizations, but his study was done in 1998.

Fishbain4 looked for acquisition of MRSA among patients hospitalized at Tripler Army Medial center in Honolulu and found only 1.7%, but the study period was short and the percent of admissions sampled low. Acquisition seemed to correlate with time in the hospital as well as the intensive care unit.

Calfee5 sampled family members of patients with MRSA who returned home after being hospitalized in Charlottesville, Va. They found about 15% at least colonized, but the follow-up times were variable, and it was unclear whether the hospitalized patients were the source or not.

Campbell6 sampled 62 children in Louisville, Ky, and found the hospital and community-onset strains the same by antibiogram testing.

Johnson7 studied 26 COMRSA strains in Detroit and found there to be at least 3 clones by pulse-field electrophoresis.

Tambyah8 found virtually all strains of MRSA isolated within 48 hours of admission in a large teaching hospital in Singapore in 1998 were health care-associated and resistant to clindamycin, gentamicin, and trimethoprim-sulfa.

Kenner9 cultured 404 patients seen in the outpatient clinics at Tripler Army Medical Center and found 38% colonized with S aureus and 2% with MRSA. Risk factors for MRSA included male gender and recent hospital care. COMRSA strains were more likely to be susceptible to oral antibiotics.

Jernigan10 also studied 494 patients in an outpatient clinic in Atlanta and found 24.7% colonized with S aureus and 3% with MRSA, but the survey was done in 1997-98. The MRSA strains were associated with prior hospitalization and chronic diseases.

Said-Salim11 reviewed the available literature on COMRSA stains and found evidence of at least 30 geographically distinct strains.

Scarnato12 found up to 3.3% of staff in a geriatric facility in France were at least colonized with MRSA and virtually all of them were nurses or nursing assistants.

Eckhardt13 found evidence of spread of MRSA in a neonatal intensive care unit in Atlanta.

Comment by Alan D. Tice, MD, FACP

It is clear from the reports in this issue that S aureus is a formidable and versatile microbe. It has successfully eluded many of our best antimicrobials and can carry a tool kit that makes it a deadly pathogen in many respects.14

The concept of community-acquired or community-onset strains is a difficult yet important one as it has been thought that most strains are bred in the hospital and may not survive long in the community. It would be nice if we could control the acquisition and spread of these strains in the hospital, but such is not the case. It is clear from the articles that strains can be carried home to set up a focus there—and then be brought back into the hospital—as was the case a few years ago.

What is also apparent is that there are distinct strains, or more likely sets of strains, of MRSA in the community that are not hospital acquired but may cause serious infections as well. They seem to be replacing the methicillin-susceptible strains and possibly some of the hospital-acquired strains as well, but it is not clear why. The origin of these strains is also uncertain, although there is talk of a Samoan strain.15 Many also appear surprisingly susceptible to oral antibiotics, although their clinical value has not been adequately demonstrated. They produce primarily skin and soft-tissue infections that are eventually self-limited, although the sores and boils may be extensive and painful at times. It is interesting to see how many patients survive and even recover even though they have been on antibiotics that appear completely inactive by in vitro testing.

The definition of which MRSA strains are "health-care associated" and which are not is also problematic. A 48-hour window after admission does not help in many instances, as health care is so pervasive in our society. Most people are exposed to the medical care industry on a frequent basis—either through their own care or by employment or through other people close to them who are.

The classification of a strain of S aureus as MRSA vs MSSA is also limited, as it is only one component of this complex organism. Toxin production, survival factors, growth factors, and other pathogenic mechanisms may be more important in many instances. This may be even more important with the advent of vancomycin resistance.

It is obvious that S aureus is a major threat and that it is growing. We need a variety of means to respond. Means of more rapid identification and infection control are critical. Clinical trials of the older oral antibiotics are also urgently needed, although there are few pharmaceutical companies interested in supporting them. Understanding of how it causes disease and how to combat the processes would also be helpful. A vaccine would be great, but it is not on the near horizon.16

Dr. Tice of Infectious Limited, PS Tacoma, WA; Infectious Disease Consultant, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI Section Editor, Managed Care.

References

1. Baggett HC, et al. Infect Control Hosp Epidemiol. 2003;24:397-402.

2. Seal JB, et al. Infect Control Hosp Epidemiol. 2003;24:403-408.

3. Jernigan JA, et al. Infect Control Hosp Epidemiol. 2003;24:409-414.

4. Fishbain JT, et al. Infect Control Hosp Epidemiol. 2003;24:415-421.

5. Calfee DP, et al. Infect Control Hosp Epidemiol. 2003;24:421-426.

6. Campbell AL, et al. Infect Control Hosp Epidemiol. 2003;24:427-430.

7. Johnson LB, et al. Infect Control Hosp Epidemiol. 2003;24:431-435.

8. Tambyah PA, et al. Infect Control Hosp Epidemiol. 2003;24:436-438.

9. Kenner J, et al. Infect Control Hosp Epidemiol. 2003;24:439-444.

10. Jernigan JA, et al. Infect Control Hosp Epidemiol. 2003;24:445-450.

11. Said-Salim B, et al. Infect Control Hosp Epidemiol. 2003;24:451-455.

12. Scarnato F, et al. Infect Control Hosp Epidemiol. 2003;24:456-458.

13. Eckhardt C, et al. Infect Control Hosp Epidemiol. 2003;24:460.

14. Baba T, et al. Lancet. 2002;359(9320):1819-1827.

15. Adhikari RP, et al. J Antimicrob Chemother. 2002; 50(6):825-831.

16. Shinefield H, et al. N Engl J Med. 2002;346(7): 491-496.