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Infection
Locker Room Acquired Methicillin-resistant Staphylococcus
Aureus
By Amar Patel, MD; Staci Fischer, MD; Ryan Calfee, MD; Matthew Plante, MD; Paul Fadale, MD
ORTHOPEDICS 2007; 30:532
July 2007
Community-acquired MRSA infections are highly communicable and require a high degree of
clinical suspicion in both the diagnosis and treatment.
Staphylococcus aureus has proven to be one of the most adaptable human pathogens. This
bacteria has reacted to selection pressures, both natural and those imposed by humans, to evolve
into new strains capable of causing a variety of infections. One adaptation that caused alarm in
the 1960s was the development of resistance to the semi-synthetic penicillins, including
methicillin, creating a strain known as methicillin-resistant Staphylococcus aureus (MRSA).
While traditionally a bacterial strain acquired in the hospital or other health care settings, MRSA
has become prevalent in many communities, demonstrating a unique pattern of virulence,
antibiotic resistance, and clinical presentation. Consequently, MRSA strains either are referred
to as health-care or community-acquired (MRSA), a distinction that has important treatment
implications. Surprisingly, several large outbreaks of community-acquired MRSA have been
described in sports settings, affecting otherwise healthy, active adolescents and adults. Hence,
the distinction between these two MRSA patterns is of particular importance to orthopedic
sports physicians who treat patients in both the hospital and community settings.
Unfortunately, due to the rapid evolution of MRSA and the relative paucity of information on
this topic in the orthopedic literature, it has been difficult to remain current on this topic. This
article defines the current state of community-acquired MRSA as it relates to the athletic
environment and provides a structural framework that the team physician can use in preventing,
diagnosing, and treating these infections.
The Evolution of Community Acquired MRSA
In the pre-antibiotic era, Staphylococcus bacteremia had an 80% mortality. The development of
penicillin, which binds specific proteins required for bacterial cell wall synthesis, improved
survival dramatically. Soon penicillin resistance, imparted by a gene that encodes an enzyme
capable of cleaving the basic beta lactam ring of penicillin (ie, beta lactamases), was noted in
staphylococci.
The semi-synthetic penicillins, manufactured via the alteration of side chains off of the beta
lactam, were introduced in the 1960s. This class was more resistant to bacterial enzymatic
cleavage than the native penicillins and became the antibiotic of choice for penicillin-resistant
strains.
Methicillin resistance, in turn, emerged shortly after methicillin’s release. The mechanism of
resistance is through the expression of altered proteins integral in cell wall production that do
not have any affinity for the beta-lactam antibiotics. In this manner, all penicillins and
cephalosporins are rendered ineffective. These altered proteins, referred to as PBP2a, are
encoded on the mecA gene. This gene, in turn, is carried on the highly mobile staphylococcal
cassette chromosome.1 Approximately five types of the staphylococcal cassette chromosome
gene complex exist, each conferring a different antimicrobial resistance profile.
Selection pressure within varied environments has likely driven the divergence of MRSA into
two distinct clinical strains. Hospital-acquired MRSA, an increasingly common pathogen in the
orthopedic setting, has emerged in a population that typically is older and more susceptible to
infections than the average outpatient. Advancing age, immune senescence, respiratory and
urinary tract infections requiring frequent antibiotic therapy, and underlying conditions such as
rheumatoid arthritis or diabetes mellitus serve to increase the risk of MRSA infection. Hospitalacquired MRSA strains generally are resistant to multiple antimicrobials, including all beta
lactams and clindamycin.
Community-acquired MRSA is thought to have resulted from the acquisition of the mecA gene
by a ubiquitous strain of S aureus with low pathogenetic capacity. Many community-acquired
MRSA strains also express the Panton Valetine leukocidin gene that encodes a protein that
opsonizes neutrophils, and predisposes the bacteria to soft-tissue and lung infections.2,3
Furthermore, community-acquired MRSA has evolved in a generally healthy, young population
that typically is not on long-term antibiotic therapy. Thus, community-acquired MRSA, due to
the lack of chronic antibiotic exposure, typically is sensitive to a broader array of antimicrobials.
When discussing MRSA infections, it is important to identify which strain is the most likely
causative organism. The Table demonstrates the primary differences between the two strains.
Due to the limited number of population based studies, the reported community-acquired MRSA
carrier rate varies widely. A recent meta analysis, however, has placed the carrier rate of
community-acquired MRSA in the community at approximately 1%.4 In addition, transmission
most likely occurs from direct person-to-person contact, placing athletes involved in high-
contact sports at particular risk.
Community-acquired MRSA & Athletes
Athletes at all levels of competition, including high school, collegiate, and professional, have
been the subject of an increasing number of reported MRSA soft-tissue infections. Because of
the cost to both the individual athlete as well as to the team as a whole, it is incumbent on the
team physician and athletic training staff to be proficient in the recognition of potential
infections, treatment of documented infections, as well as prophylactic measures for the entire
staff.
Staphylococcus aureus infections were first described in healthy athletic team members in the
1960s. The initial report was from the Dartmouth College football team during the 1964 season
in which 24 of 74 players sustained infections. The majority presented with folliculitis and
cellulitis on the forearms and lower extremities.5 In subsequent years, there were interspersed
reports of staphylococcal infections in several athletic settings, however, these primarily
involved high school football teams.6
One of the first documented outbreaks of community-acquired MRSA occurred in a Vermont
high school wrestling team in 1993. Six of the 32 wrestlers developed cutaneous lesions
described as fluctuant abscesses on the forearms or lower extremities; cultures grew MRSA. The
spread of these lesions was thought to be through direct skin-to-skin contact as well as from the
infection of abrasions produced from the wrestling mat.7
Three years later, an outbreak was reported in an English rugby team. Five of the 20 team
members were affected with cutaneous abscesses on the face, neck, and back. All of the players
were forwards participating in a recent tournament.8
In the 2002 football season, three documented outbreaks of community-acquired MRSA
infections were reported at the high school and college level in Indiana, Los Angeles, and
Pennsylvania. In Pennsylvania, 7 of 10 affected members of a college football team required
hospitalization. Risk factors for infection identified in this outbreak included skin abrasions
from artificial turf, shaving of skin, and the sharing of unwashed towels. In all of the players
who were tested, the MRSA strain was genetically similar by pulsed field gel electrophoresis.9
In the same year, an outbreak of community-acquired MRSA infection was reported in a
Colorado fencing club in which shared equipment may have contributed to the infection to 5 of
the 70 club members.
The most visible community-acquired MRSA infection in athletes involved the St Louis Rams
professional football team. In the 2003 season, 5 of 58 players developed MRSA soft-tissue
infections at turf abrasion sites. These infections were associated with a high body mass index
and the linebacker position. Methicillin-resistant S aureus was cultured from the team
whirlpools, taping gels, and from 42% of staff nasal swabs. Pulsed field gel electrophoresis
confirmed a single community-acquired MRSA strain that carried the Panton Valetine
leukocidin gene. All of the infections progressed into abscesses that required surgical drainage
and recurrent infections developed in 3 of the 5 players.10 Since this report, a number of
professional athletes have required treatment for community-acquired MRSA soft-tissue
infections. Many sports publications as well as local and national news media have documented
high-profile athletes who have had community-acquired MRSA infections and have
subsequently brought attention to this topic.
One important aspect of community-acquired MRSA is that untreated or mistreated infections
can lead to morbidity. The pathogenetic capacity of community-acquired MRSA was
documented in four children who contracted community-acquired MRSA bacteremia and
subsequently died from sepsis.11 None of these children had traditional risk factors for infection.
The most serious case of a MRSA soft-tissue infection in an athlete occurred in a Division 3
football receiver who contracted a community-acquired MRSA soft-tissue infection that
progressed rapidly to bacteremia, sepsis, and death. Sports physicians and trainers must keep
this catastrophic result in mind when evaluating athletes with soft-tissue infections, especially
those in high contact sports.
Prevention
All athletic institutions should have basic prophylactic measures instituted to prevent infections.
Teams should limit equipment sharing and routinely clean all equipment with an Environmental
Protection Agency approved disinfectant detergent. Trainers and physicians as well as team
members should aggressively monitor wounds. This would ideally include training on both how
to adequately dress wounds and identify wound infections. All open wounds should be
occlusively dressed during practices and competitions. Athletes should prescrub prior to
whirlpool use with chlorhexidine soaps. Towels, razors, and other personal hygiene equipment
should not be shared.12
Identification & Treatment
First and foremost, physicians and trainers must approach soft-tissue infections in athletes with a
high degree of clinical suspicion for community-acquired MRSA. Community-acquired MRSA
soft-tissue infections may present as cellulitis, pustules, and abscesses.13 Many athletes may
present with what they feel are bug or spider bites. Suspicion should be heightened when these
findings are in the context of pre-existing soft-tissue abrasions from athletic turf or mats.
Once a soft-tissue infection has been identified, the wounds must be carefully dressed to prevent
the spread to other team members and staff. Oral antibiotic treatment should be prescribed and
be based on the team physician’s suspicion for community-acquired MRSA. Any drainable
collections should first be evacuated and cultured for sensitivities. Empiric and then targeted
antibiotic treatment can then be initiated.
In cases of cellulitis that do not have any culturable fluid or while awaiting fluid culture results,
treatment should begin with trimethoprim-sulfamethoxazole (two double-strength tablets twice
daily) or, in those with sulfa allergy, doxycycline (100 mg twice daily). These patients should be
monitored closely for a clinical response. If there is no response to treatment after 48 hours, any
drainable focus should be incised and the drainage cultured, with consideration given for the
addition of rifampin.
Patients who demonstrate rapid infection progression should be admitted to the hospital for
intravenous antibiotic therapy or further wound irrigation and debridement.14 The Figure
provides the basic structural framework that can be used to approach these infections.
In cases of documented community-acquired MRSA infection, a protocol for the athletic
facility, staff, and team decontamination should be initiated. This protocol should include daily
chlorhexidine (2% or 4%) washes and intranasal mupirocin ointment application twice daily for
5 days for all staff and team members. In addition, the facilities, including all shared weight
training equipment, shared sport specific equipment, ie, whirlpools should be rigorously cleaned
with a disinfectant detergent.
Figure: Approach for community-acquired methicillin-resistant
Staphylococcus aureus soft-tissue infections in athletes. Abbreviations:
IV=intravenous and MRSA=methicillin-resistant Staphylococcus aureus.
Conclusion
Community-acquired MRSA is becoming a frequent cause of soft-tissue infections in previously
healthy athletic participants. These infections are highly communicable and require a high
degree of clinical suspicion in both the diagnosis and treatment. All members of the athletic
staff–athletes, trainers, and team physicians–should be involved in the monitoring and treatment
of community-acquired MRSA infections.
References
1. Rice L. Antimicrobial resistance in gram positive bacteria. Am J Med. 2006; 119(6 Suppl
1): S11-S19.
2. Vandenesch F, Naimi T, Enright MC, et al. Community acquired methicillin resistant
Staphylococcus aureus carrying the Panton-Valentine leukocidin genes: worldwide
emergence. Emerg Infect Dis. 2003; 9:978-984.
3. Zetola N, Francis JS, Nuermberger EL, Bishai WR. Community-acquired methicillin
resistant Staphylococcus aureus: an emerging threat. Lancet InfecDis. 2005; 5:275-286.
4. Salgado CD, Farr BM, Calfee DP. Community-acquired methicillin-resistant
Staphylococcus aureus: a meta analysis of prevalence and risk factors. Clin Infect Dis.
2003; 36:131-139.
5. Pollard JG. The Staphylococcus plagues a football team. College Health. 1966; 234-238.
6. Bartlett PC, Martin RJ, Cahill BR. Furunculosis in a high school football team. Am J
Sports Med. 1982; 10: 371-374.
7. Lindenmayer J, Schoenfeld S, O’Grady R, Carney J. Methicillin resistant
Staphylococcus aureus in a high school wrestling team and the surrounding community.
Arch Int Med. 1998; 158:895-899.
8. Stacey AR, Endersby KE, Chan PC, Marples RR. An outbreak of methicillin resistant
Staphylococcus aureus infection in a rugby football team. Br J Sports Med. 1998;
32:153-154.
9. Centers for Disease Control and Prevention (CDC). Methicillin resistant Staphylococcus
aureus infections among competitive sports participant-Colorado, Indiana, Pennsylvania
and Los Angeles county, 2000-2003. MMWR Morb Mortal Wkly Rep. 2003; 53:793-795.
10. Kazakova S, Hageman J, Matava M, et al. A clone of methicillin-resistant
Staphylococcus aureus among professional football players. N Engl J Med. 2005;
352:468-475.
11. From the Centers for Disease Control and Prevention. Four pediatric deaths from
community-acquired methicillin-resistant Staphylococcus aureus—Minnesota and North
Dakota, 1997-1999. JAMA. 1999; 282:1123-1125.
12. Cohen P. Cutaneous community-acquired methicillin-resistant Staphylococcus aureus
infection in participant of athletic activities. South Med J. 2005; 98:596-602.
13. Cohen P, Kurzrock R. Community acquired methicillin-resistant Staphylococcus aureus
skin infection: an emerging clinical problem. J Am Acad Dermatol. 2004; 50:277-280.
14. Cohen P, Grossman M. Management of cutaneous lesions associated with an emerging
epidemic: community-acquired methicillin-resistant Staphylococcus aureus skin
infections. J Am Acad Dermatol. 2004; 51:132-135.
Authors
Drs Patel, Calfee, Plante, and Fadale are from the Department of Orthopedic Surgery and Dr
Fischer is from the Department of Medicine, Brown University, Providence, RI.
Correspondence should be addressed to: Amar Patel, MD, Dept of Orthopedic Surgery, Brown
University, 593 Eddy St, COOP 1, Providence, RI 02903.
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