I may never go to the gym again!
In the January 2017 issue of JBJS Reviews, Mitchell et al. report on sport-related skin and soft tissue infections (SSTIs) as an ongoing problem across a diverse range of recreational, collegiate, and professional athletes. They note that these infections often occur during training for competitive sports or during the competition and that the majority are bacterial or fungal in origin. The review describes the mechanisms by which SSTIs occur in healthy athletes and the prevalence among players in various sports, including the effect of player position. The authors discuss the mechanisms by which SSTIs are spread and the hygiene measures that are recommended to prevent their spread. They extrapolate these lessons to the general population of so-called weekend warriors or fitness enthusiasts. This is what worries people like me, as studies have shown that these infections easily occur during regular visits to fitness centers and gymnasiums, which are sources of large quantities of bacteria that could cause SSTIs!
Studies have shown that billions of bacteria, fungi, and other microbes inhabit the skin and that the types of organisms vary between individuals and between different sites of the skin. In fact, they may vary in relation to each region of the body. Indeed, factors such as skin characteristics, sebaceous gland concentration, moisture content, temperature, and genetics as well as exogenous environmental factors can influence each so-called community of organisms. The authors hypothesize that sports in which participants have substantial skin-to-skin collisions might disrupt these ecosystems on the skin and allow microbes to be shared among players, noting that contact athletes have been shown to be potential carriers of methicillin-resistant Staphylococcus aureus (MRSA) more than twice as frequently as athletes who participate in noncontact sports. Other mechanisms by which SSTIs occur in healthy athletes include maceration of the skin due to sweating as well as strenuous training. Of particular interest is the observation that extended periods of intense exercise may temporarily depress certain aspects of the immune system, including natural killer cells, neutrophils, lymphocytes, immunoglobulin levels, and interleukin-2 levels and thus facilitate and promote infection and its potential host transfer.
The article goes on to explain how SSTIs are spread, the prevalence of SSTIs among players in various sports, the importance of personal and environmental hygiene, and specific forms of treatment of SSTIs in athletes.
When you do go to the gym or fitness center, just remember to clean off any equipment both before and after use and to change out of your workout clothes and shower as soon as possible after the workout. Be sure to cover benches with a towel, and if you practice yoga, bring your own mat.
I definitely will continue to use the gym but will pay more attention to the issues raised in this review.
Thomas A. Einhorn, MD
Editor, JBJS Reviews
Despite the relative rarity of necrotizing fasciitis (NF), orthopaedists can expect to see at least 1 case of NF in their career. This month’s “Case Connections” springboards from a recent case report about necrotizing fasciitis in which the infectious source was highly unusual, followed by three additional case reports related to NF from the JBJS Case Connector archives
- In the June 8, 2016, edition ofJBJS Case Connector, Connor et al. reported on the case of a 70-year-old man who developed necrotizing fasciitis of the thigh and calf through a colon perforation caused by sigmoid diverticulitis.
- Zani and Babigian described a case of NF in the shoulder of a 53-year-old woman following acromioplasty and open rotator cuff repair.
- The bacteriumAeromonas hydrophila caused NF in a 58-year-old non-immunocompromised man, as described in a case report by Borger van der Burg et al.
- Cheng et al. described 3 fatal cases of necrotizing fasciitis caused by methicillin-resistant Staphylococcus aureus(MRSA).
Time and teamwork are of the essence in the management of necrotizing fasciitis. To hasten diagnosis, clinicians are advised to submit blood and tissue samples for pathological analysis as soon as possible. A multidisciplinary team that includes an infectious-disease specialist should be assembled in cases of suspected NF.
The treatment of periprosthetic infection remains one of the most difficult and challenging problems in orthopaedic surgery. Conventional approaches such as the use of tissue and/or fluid cultures to identify and treat organisms are not nearly as successful as they need to be in order to address these conditions. The limitations of treatment, including the inaccessibility of microorganisms at the time of irrigation and debridement, the development of resistant strains of microorganisms, and the elaboration by microorganisms of protective biofilms, have led to unsuccessful outcomes in a large number of cases.
In this issue of JBJS Reviews, Chen and Parvizi provide an update on some of the new methods that may possibly advance this field. Molecular methods such as polymerase chain reaction to amplify bacteria can improve the likelihood of identifying the pathogen in a patient with a periprosthetic joint infection. Synovial markers such as C-reactive protein, leukocyte esterase, α-defensin, human β-defensin-2 (HBD-2) and HBD-3, and cathelicidin LL-37 are known to be elevated in patients with periprosthetic joint infection and may be used as markers for diagnosing infection at the time of operative management. Serum markers such as interleukin-4 (IL-4) and IL-6, and others such as soluble intracellular adhesion molecule-1 (sICAM-1) and procalcitonin (PCT), have been shown to be elevated in patients with periprosthetic joint infection.
Molecular detection methods probably have received the most attention and interest as an advancement that may improve our ability to diagnose periprosthetic infections. The limitations of these methods, however, include their high sensitivity and an increased rate of false-positive results. Methods to reduce the number of false-positive results are currently in development and include, among other things, the measurement of 16S ribosomal RNA in the belief that targeting RNA will result in amplification of only the genetic material of live bacteria. In addition, use of the mecA gene for identifying methicillin-resistant Staphylococcus aureus (MRSA) can reduce this rate.
Although this article does not provide definitive new approaches to the problem, the review of recent advances with the development of promising biomarkers and molecular techniques provides optimism that this field is evolving in a positive way.