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Any Word 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. · TJA patients with persistent wound drainage respond best with irrigation, debridement within 7 days postop · New variables leading to periprosthetic infections found for TKA, THA patients · Laminar air flow and ultraviolet light can combat operating room contamination