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MRSA Skin Infection in Athletes

Overview

Nosocomial infections of methicillin-resistant Staphylococcus aureus (MRSA) (ie, hospital-acquired MRSA [HA-MRSA]) have been reported since 1963.[1] Community-acquired MRSA (CA-MRSA) infections are a more recent variant and are becoming more common in athletes[2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14] and active individuals since the first reported cases in a high school wrestling team in 1993[15] and a British rugby club in 1998.[16] CA-MRSA differs from HA-MRSA in its genetic makeup, increased pathogenicity, and susceptibility to antibiotic treatment.[17, 18, 19]

The resistance of MRSA to beta-lactam antibiotics is due to the presence of the mecA gene sequence. The mecA gene produces transpeptidase PBP2a (penicillin-binding peptide) that decreases the bacterial affinity of the beta-lactam antibiotics. The mecA gene is a subset of a larger SCCmec gene that is responsible for the differences seen in HA-MRSA and CA-MRSA bacteria.[18, 20]

Several variations of the SCCmec gene have been sequenced; SCCmec gene types I, II, and III are found in HA-MRSA, whereas CA-MRSA bacteria have the SCCmec type IV gene.[21] The SCCmec gene types I-III are larger genes, and other portions of the gene provide resistance factors against other antibiotic classes. The type IV SCCmec gene is a small gene that has fewer of these additional resistance factors. This difference may explain the continued susceptibility of CA-MRSA compared with HA-MRSA to some oral antibiotics such as trimethoprim-sulfamethoxazole.

For excellent patient education resources, visit eMedicineHealth's Infections Center. Also, see eMedicineHealth's patient education articles MRSA Infection, Sepsis (Blood Infection), Life-Threatening Skin Rashes, and Antibiotics.

NextVirulence

CA-MRSA has been found in some cases to be a more virulent form compared with HA-MRSA. Up to 70% of CA-MRSA strains contain the Panton-Valentine leukocidin (PVL) virulence factor, including the most common form of CA-MRSA isolated from outbreaks in the United States.[22]

PreviousNextPrevalenceMRSA colonization

Studies have shown that approximately 25-30% of the population is colonized with methicillin-sensitive S aureus bacteria. Colonization is usually on the skin or in the nasal passages. One study demonstrated a 3% rate of MRSA nasal colonization in adult patients visiting an outpatient clinic for unrelated medical appointments.[23] A similar study in an outpatient pediatric population detected MRSA colonization rates slightly above 1%.[24]

CA-MRSA infections in the general population

A prospective study in an Oakland, California, emergency department found that 51% of patients with a skin infection who presented for evaluation and treatment had positive culture results for MRSA; 99% of the MRSA infections contained the type IV SCCmec gene that is associated with the CA-MRSA strain, and 94% of MRSA isolates also contained the PVL gene.[25]

CA-MRSA outbreaks in athletes and other populations

Most publicized reports of CA-MRSA infection have been in college or professional football teams.[2, 3, 4, 5, 6, 7] However, outbreaks have also been reported in other sports, such as wrestling, rugby, and fencing. In a study of all Nebraska high schools between 2006 and 2008, Buss et al determined that among the schools that responded, MRSA infections rose from 4.4% in school year 2006-2007 to 14.4% in 2007-2008; the incidence per 10,000 wrestlers rose 3-fold from 19.6 to 60.1 and that per 10,000 football players increased 5-fold from 5.0 to 25.1.[10]

Other populations at risk for CA-MRSA outbreaks include military recruits, children in day care, prison inmates, homosexual men, injection drug users, and veterinarians, particularly those who have contact with farm animals, notably pigs.[5, 26, 27]

PreviousNextClinical Presentation

Most CA-MRSA infections initially manifest as folliculitis or a similar soft-tissue or skin infection. Typically, the athlete may describe his or her presentation as an "infected pimple" or "insect bite." Some CA-MRSA infections may have progressed to abscess formation. In other cases, the infection may manifest as a life-threatening illness, such as a rapidly progressing sepsis or pneumonia.

The initial clinical examination usually reveals a limited area of redness, warmth, and swelling that is consistent with folliculitis. Occasionally, the patient may have swelling and pain in a joint. In more advanced cases, moderate to severe pain at the site of the infection may be reported; the pain may be due to soft-tissue necrosis from PVL activity.

Transmission

In severe cases of CA-MRSA infection, endocarditis, septicemia, necrotizing fasciitis, osteomyelitis, and multisystem organ failure, or death due to overwhelming sepsis may occur. Severe cases may progress extremely rapidly from the initial manifestation of an abscess.

The most common route of transmission of CA-MRSA is though an open wound, such as a superficial abrasion, or from contact with a CA-MRSA carrier. Other methods of transmission include poor hand washing, poor personal hygiene (eg, not showering after workouts), sharing personal items (eg, razors, towels, clothing), or a failure to properly clean and disinfect exercise and training equipment.

PreviousNextTreatment & ManagementOutpatient treatment

The primary method of treatment for CA-MRSA skin and soft-tissue infections includes incision and drainage (I&D) of the abscess and therapy with appropriate antibiotics when indicated. Wound exudates should be cultured to accurately determine the causative organism and appropriate antibiotics for therapy.

The susceptibility of CA-MRSA is dependent on local resistance rates (US Centers for Disease Control and Prevention guidelines [see Antibiotic/Antimicrobial Resistance: Clinical Guidelines and CDC Surveillance Systems and Published Data, as well as Diseases Connected to Antibiotic Resistance: Methicillin-Resistant Staphylococcus aureus (MRSA)]). Typical treatment choices include oral antibiotics.

Oral antibiotics Trimethoprim-sulfamethoxazole (Bactrim DS; available as generic) twice daily, with or without rifampin, at 600 mg/d. Note: Rifampin is not a first-line drug for CA-MRSA, but this agent may be used in conjunction with other antibiotics for infections that do not respond to the initial treatment or for patients who experience recurrent infections. Doxycycline at 100 mg twice dailyClindamycin at 450 mg 3 times a day (96% sensitive): Resistance to clindamycin is increasing because of the inducible macrolide-lincosamide-streptogramin B (iMLSb) phenotype, which may result in cross-resistance to clindamycin. TetracyclineMinocyclineNot recommended due to resistance Ciprofloxacin: This drug has a 33% sensitivity in some areas. Ciprofloxacin is not a good choice in pediatric patients because of concerns about its effect on growth plates. Cephalexin (Keflex; MiddleBrook Pharmaceuticals, Inc, Germantown, Md)Not recommended due to poor oral absorption Oral vancomycinLength of treatment

There are no well-controlled studies that demonstrate an optimal length of antibiotic treatment for CA-MRSA.

Inpatient treatment

Treatment of moderate to severe CA-MRSA infections may require surgical debridement of the abscess, intravenous antibiotics, and hospitalization. The need for hospitalization should be made on a case-by-case basis.

Intravenous antibiotics Vancomycin: Note that reports have described some intermediate vancomycin susceptibility in Japan, Texas, and New York.Some studies also indicate vancomycin treatment failure with MRSA bacteremia is associated with high mortality rates (1) when this agent is initiated after an inappropriate empiric antibiotic was used and (2) when vancomycin itself is the empiric agent in cases when the infective strain had a high vancomycin minimum inhibitory concentration (MIC).[28, 29] Another study demonstrated previous antibiotic exposure is itself a risk for MRSA isolation.[30] Linezolid at 600 mg twice daily: The FDA warns against the concurrent use of linezolid with serotonergic psychiatric drugs, unless indicated for life-threatening or urgent conditions. Linezolid may increase serotonin CNS levels as a result of MAO-A inhibition, increasing the risk of serotonin syndrome.[31] Daptomycin at 4 mg/kg/dQuinupristin-dalfopristin at 7.5 mg/kg every 8-12 hoursInvestigational antibiotics

There are 2 anti-CA-MRSA beta-lactams, ceftaroline (cephalosporin) and ME1036 (carbapenem), that are under investigation. A preliminary study of susceptibility testing indicated that ceftaroline was 64-fold more potent than ceftriaxone, whereas ME1036 was >128-fold more potent than ceftriaxone.[32] All isolates had the PVL genes and type IV SCCmec, and 67.8% showed the USA300-0114 strain, cloned via pulsed field gel electrophoresis (PFGE).

Another agent that is under study and that may hold potential for the prevention of catheter-associated infections, particularly against MRSA, is omiganan pentahydrochloride, a novel topical cationic peptide.[33]

Recurrent infections

If an athlete has recurrent MRSA infections, suspect resistance to the previous antibiotic or nasal colonization, and send a nasal swab for culture. A different antibiotic may also be prescribed if the practitioner is concerned about a poor response to treatment. If the nasal swab culture is positive for CA-MRSA, then treat with mupirocin antibiotic ointment (Bactroban; GlaxoSmithKline, Research Triangle Park, NC) twice a day applied to the nares and oral rifampin at 300 mg twice daily for 7 days.

PreviousNextPrevention

Several key methods can be used for prevention of the spread of CA-MRSA infections.[34] Because the most common source of infection is from close contact or from an open wound, preventive measures should focus on proper hygiene. Hand washing, using soap and water or antibacterial hand gels, should be encouraged by the infected patient and by individuals who come in direct contact with the patient. Additionally, open wounds and abrasions should be covered and protected.

Athletes should be educated and instructed to not share personal hygiene products such as razors or towels. Medical and training staff should continue to practice universal infectious disease protection measures. These personnel should ensure the proper disposal of bandages after dressing changes and the routine cleaning of equipment such as training tables, whirlpools, and exercise mats.

PreviousNextReturn to Play

Athletes with mild cases of CA-MRSA infections may be allowed to return to athletic participation once an appropriate antibiotic treatment has commenced and the risk of transmission to other athletes has been significantly reduced or eliminated. Abrasions should be covered with a protective covering, and the athlete should be reevaluated daily for signs or symptoms of recurrence or worsening of the infection. The athlete and teammates should also be counseled about the need to avoid sharing towels, razors, or other personal items. Training staff should ensure proper disinfection of equipment and surfaces with which the infected athlete may come in contact, such as training tables, protective equipment, or wrestling mats, among other items.

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Myofascial Pain in Athletes

Background

Voluntary, or skeletal, muscle is the largest single organ of the human body and accounts for nearly 50% of the body's weight. The number of muscles in the body depends on the degree of subdivision that is considered and on the number of variable muscles that are included. Not counting heads, bellies, and other divisions of muscles, the Nomina Anatomica reported by the International Anatomical Nomenclature Committee under the Berne Convention lists 200 paired muscles, or a total of 400 muscles. Any one of these muscles can develop myofascial trigger points (MTrPs).[1] MTrPs are hyperirritable tender spots in palpable tense bands of skeletal muscle that refer pain and motor dysfunction, often to another location.[2, 3]

The myofascial pain syndromes (MPS) owe their ever-widening acceptance to the pioneering work of Travell and her later collaboration with Simons.[2, 3] In 1983, they combined their clinical experience in a detailed description of the multiple pain syndromes attributed to this disorder. In doing so, they further defined the major clinical components that are characteristic of myofascial pain, the most important being the TrP, the taut band, and the local twitch response. See the image below.

Myofascial pain in athletes. Cross-sectional drawing shows flat palpation of a taut band and its trigger point.Left: Skin pushed to one side to begin palpation (A). The fingertip slides across muscle fibers to feel the cord-line texture of the taut band rolling beneath it (B). The skin is pushed to other side at completion of movement. This same movement performed vigorously is snapping palpation (C).Right: Muscle fibers surrounded by the thumb and fingers in a pincer grip (A). The hardness of the taut band is felt clearly as it is rolled between the digits (B). The palpable edge of the taut band is sharply defined as it escapes from between the fingertips, often with a local twitch response (C). NextEpidemiologyFrequencyUnited States

MTrPs are extremely common and become a painful part of nearly everyone's life at one time or another. Latent TrPs, which often cause motor dysfunction (eg, stiffness, restricted range of motion) without pain, are far more common than active TrPs that cause pain.

Active TrPs are commonly found in postural muscles of the neck, shoulder, and pelvic girdles and in the masticatory muscles. In addition, the upper trapezius, scalene, sternocleidomastoid, levator scapulae, and quadratus lumborum muscles are commonly involved.

Reports of the prevalence of MTrPs in specific patient populations are available. The data indicate a high prevalence of this condition among individuals with a regional pain complaint, as shown in Table 1.

Table 1. Prevalence of Myofascial Pain (Open Table in a new window)

RegionPracticeNumber StudiedPrevalence of Myofascial Pain, %GeneralMedical17230GeneralPain medical center9693GeneralComprehensive pain center28385CraniofacialHead and neck pain clinic16455LumboglutealOrthopedic clinic9721

The wide range in the prevalences of myofascial pain caused by TrPs is likely due to differences in the patient populations examined and in the degree of chronicity, at least in part. Probably even more important are differences in the criteria used to diagnose MTrPs and, most important, differences in the training and skill of the examiners.

PreviousNextFunctional Anatomy

Some isolated large round muscle fibers and some groups of these darkly staining, enlarged, round muscle fibers appear in cross-sections. In longitudinal sections, the corresponding feature is a number of contraction knots. An individual knot appears as a segment of muscle fiber with extremely contracted sarcomeres. This contractured segment has a corresponding increase in diameter of the muscle fiber.

The structural features of contraction knots presents a likely explanation for the palpable nodules and the taut bands associated with TrPs. Three single contraction knots can be seen scattered among normal muscle fibers. Beyond the thickened segment of the contractured muscle fiber at the contraction knot, the muscle fiber becomes markedly thinned and consists of stretched sarcomeres to compensate for the contractured ones in the knot segment. In addition, a pair of contraction knots separated by empty sarcolemma may represent one of the first irreversible complications that result from the continued presence of the contraction knot.

PreviousNextSport Specific Biomechanics

The activation of a TrP is usually associated with some degree of mechanical abuse of the muscle in the form of muscle overload, which may be acute, sustained, and/or repetitive. In addition, leaving the muscle in a shortened position can convert a latent TrP to an active TrP; this process is greatly aggravated if the muscle is contracted while in the shortened position.

In paraspinal muscles (and likely other muscles, too), a degree of nerve compression that causes identifiable neuropathic electromyographic (EMG) changes is associated with an increase in the numbers of active TrPs. These TrPs may be activated by disturbed microtubular communication between the neuron and the endplate because the motor endplate is involved in the pathophysiologic process of the peripheral core TrP.

The histopathologic complications that could contribute to the chronicity of the condition and make treatment more difficult include the following:

Distortion of the striations (sarcomere arrangement) in adjacent muscle fibers for some distance beyond the contraction knot (see the image below). This produces unnatural shear forces between fibers that could seriously and chronically stress the sarcolemma of the adjacent muscle fibers. If the membrane were stressed to the point at which it became pervious to the relatively high concentration of calcium in the extracellular space, it could induce massive contracture that could compound the shear forces. Myofascial pain in athletes. Schematic of a trigger point complex of a muscle in longitudinal section.A: The central trigger point (CTrP) in the endplate zone contains numerous electrically active loci and numerous contraction knots. A taut band of muscle fibers extends from the trigger point to the attachment at each end of the involved fibers. The sustained tension that the taut band exerts on the attachment tissues can induce a localized enthesopathy that is identified as an attachment trigger point (ATrP).B: Enlarged view of part of the CTrP shows the distribution of 5 contraction knots. The vertical lines in each muscle fiber identify the relative spacing of its striations. The space between 2 striations corresponds to the length of one sarcomere. The sarcomeres within one of these enlarged segments (ie, contraction knot) of a muscle fiber are markedly shorter and wider than the sarcomeres in the neighboring normal muscle fibers, which are free of contraction knots. The occasional finding of a segment of an empty sarcolemmal tube between 2 contractions knots may represent an additional irreversible complication of a contraction knot.

Latent TrPs can produce other effects characteristic of a TrP, including increased muscle tension and muscle shortening; but these do not produce spontaneous pain. Both active and latent TrPs can cause significant motor dysfunction. The same factors that are responsible for the development of an active TrP can, to a lesser extent, cause a latent TrP. An active key TrP in one muscle can induce an active satellite TrP in another. Inactivation of the key TrP often inactivates its satellite TrP without treatment of the satellite TrP itself.

The intensity and extent of the pattern of referred pain depends on the degree of irritability in the TrP, not on the size of the muscle. MTrPs in small, obscure, or variable muscles can be as troublesome to the patient as TrPs in large familiar muscles.

TrPs are activated directly by acute overload, overwork fatigue, direct impact trauma, and radiculopathy. TrPs can be activated indirectly by other existing TrPs, visceral disease, arthritic joints, joint dysfunctions, and emotional distress. Satellite TrPs are prone to develop in muscles that lie within the pain reference zone of key MTrPs or within the zone of pain referred from a diseased viscus, such as the pain due to myocardial infarction, gastric ulcer, cholelithiasis, or renal colic. A perpetuating factor increases the likelihood of overload stress that can convert a latent TrP to an active TrP.

With adequate rest and in the absence of perpetuating factors, an active TrP may spontaneously revert to a latent state. Pain symptoms disappear; however, occasional reactivation of the TrP by exceeding that muscle’s stress tolerance can account for a history of recurrent episodes of the same pain over a period of years.

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