Contact Sports and Skin Infections

6 02 2012

(Welcome to guest blogger Rebecca Kreston, MSPH and thanks, Rebecca, for sharing this post from your blog: bodyhorrors!)

In honor of one of the most lucrative American events that happened just yesterday, I thought I’d explore sports and infectious diseases. Specifically, contact sports and skin infections!

Since starting this blog, I’ve gathered that readers just love reading about transmissible skin infections, so what could be better than watching the Super Bowl and knowing just exactly what kind of diseases could possibly be smeared between the players of the Patriots and Giants?

There is a glut of infectious diseases that one can acquire from dabbling in combat or contact sports such as American or Aussie-style football, rugby, wrestling, and sumo. In fact, skin infections are the most common injury associated with all sports (1). All that body bashing and face-to-face smearing in contact sports does wonders for spreading skin or cutaneous infections. A number of these ailments are common to us non-athletic mortals—athlete’s foot, jock rash and ringworm (or tinea corporis). Two diseases in particular, with the marvelous potential to initiate larger epidemics within and beyond the locker room, form the focus of this article.

Herpes gladiatorum is a wonderfully evocative name used to describe an athlete’s infection with herpes simplex virus 1 (HVS-1), a terribly contagious virus that many have the misfortune of being acquainted with; it’s estimated that 65% of people will become infected with the virus by the time they reach their 40s (2). Symptoms can include painful, blistery cold sores on the face and neck, along with a sore throat, infected lymph nodes and malaise.

It’s a tricky little bugger of a virus. It can remain dormant, hiding away in nerve cells known as sensory ganglia, only to spring out on one’s face or genitals during periods of physical or emotional stress or, say, when you’re sunbathing in tropical locales on vacation. It has an uncanny sense of knowing when to erupt at the most inappropriate of times, though I’ve been unable to track down any research examining the molecular basis of how it goes about conducting this remarkable mechanism.

Most people rightfully assume that HSV-1 infection is a rather personal, intimate matter: we hear about transmission between a mother and her child, between romancing couples and so on. This makes sense considering that it’s spread by respiratory droplets or direct contact with infected lesions; you’ve really got to get up close and personal in someone’s face if you want to get a sense of what HSV-1 infection feels like (2). But given social situations with a generous amount of skin-to-skin contact with many individuals—sports, for instance—the virus will happily engage in a bit of unplanned host-hopping. As such, it has a frustrating tendency to erupt into outbreaks in sports team and during competitions.

Many athletes may sport micro-abrasions and skin breaks stemming from turf burns, powerful body-to-body collisions, facial stubble or beard burn, and shaving. Depending upon the level of protective clothing and gear, these athletes can experience substantial exposure with their opponent’s infected HSV-1 lesions, not to mention the respiratory droplets, spit and mucus that may transmit other types of infections. Charming! Among teammates, a grab-bag of infections can also be spread by sharing towels, water bottles, clothing, equipment, and hygiene and cosmetic products.

HSV-1 is considered to be particularly endemic in rugby players due to the style of the sport and the lack of protective gear (3). Its rampant presence in rugby leagues has earned it the moniker “herpes rugbiorum” or “scrum pox” (“scrum strep”, caused by the bacterium Streptococcus pyogenes, can also plague rugby players).

In rugby, the “scrum” is a type of huddle maneuver used to return the ball into play. It is a sensational way to spread HSV-1: players in the forward position interlock their heads with their opponents in facing rows before the ball is launched between them. These forwards are the most likely of their teammates to contract scrum pox due to their prominent role in scrums and the increased prospect of serious face-to-face contact. The fact that rugby players do not use protective gear, including helmets, exposes a greater part of their body to physical contact and further increases their risk.

HSV-1 regularly rears its ulcerous face on wrestlers as well. A research group checking serum samples from wrestlers to determine previous HSV 1 exposure found that 29.8% of college wrestlers had reported previous HSV infection (4).

The level of intimacy required in grappling almost makes it inevitable that something is going to be transmitted between two athletes, whether that be sweat, saliva or HSV-1. Indeed, in a 1989 outbreak in high-school wrestling camp for boys, 34% of participants were diagnosed with HSV-1 (5). Lesions commonly appeared on regions of the body most likely to encounter direct skin-to-skin contact with their opponents – 73% on the head, 42% on the extremities and 28% on the trunk of the body.

How do you tell if a wrestler is right or left-handed? Check which side of their face, head, neck and arms has the greatest amount of lesions. Athletes will tend to prominently use the most powerful sides of their body, regardless of which sport, and it will be this side that can receive the greatest amount of skin-to-skin contact with opponents.

Getting a touch of HSV-1 and sharing it with your teammates may be the least of an athlete’s problems. In 2003, a ghastly outbreak of methicillin-resistant Staphylococcus aureus (MRSA) emerged during a college football camp in Connecticut (6). Ten players were infected, of whom two required hospitalization. The infection was discovered to have spread due to the combination of body shaving and turf burns from the artificial grass. Infections were most commonly located at the elbow, thigh, hip, chin, forearm and knee, parts of the body most likely to incur abrasions on the turf. Those players with turf burns had a seven-fold risk of acquiring MRSA infection than those who emerged from scrimmage and active play unscathed (6). Cornerbacks and wide receivers were particularly susceptible due to their frequent body contact during drills and scrimmage play.

A quick browse through the research literature pulls up dozens of MRSA outbreaks like this. In 2002, two college football players in Los Angeles were hospitalized due to MRSA infection (7). A one-year surveillance of a football team at an unnamed major university in the southeastern United States found that 19% of the players showed evidence of nasal colonization of the bacteria at the end of the football season; though the high prevalence of MRSA among these men did not yield any active skin and soft tissue infections, it goes to show how endemic of a problem this really is (8). In 2007, six football players on a Brooklyn high school football team showed evidence of MRSA skin and soft tissue infection; the players had just recently returned from a preseason training camp (9). The infections were serious enough that they generated abscesses requiring surgical incision and drainage.

MRSA colonization of football players is apparently becoming so commonplace that some researchers have suggested using them as human sentinels for public health surveillance of outbreaks within the surrounding community (10). It is regrettably becoming a rather conventional type of emerging infection in athletes.

These infections aren’t just unseemly looking but can be disfiguring, have long-lasting effects within the body and can temporarily disqualify an athlete from practice and competition to prevent localized outbreaks. Hell, some of them can kill ya! These outbreaks can ruin seasons for the team while for salaried athletes, these kinds of infections have serious economic, professional and personal repercussions. Medical professionals recommend that players abstain from play until they’ve started antiviral medications or antibiotics, they are free of systemic symptoms – fever, malaise and lymph node swelling – and until any moist lesions have subsided. Seems reasonable, no?

Infectious diseases are always context specific and spread through particular practices. In the case of contact sports, there are several variables at play that help to spread some nasty infections. While there isn’t a lot we can do about changing how a sport is played (or can we?), coaches and referees can keep an eye out for athletes who seem ill or are showing visible evidence of infection. Fighting against poor hygiene practices and ensuring that wounds are cleaned and dressed immediately can also keep these kinds of sticky situations in line. Game on!

RESOURCES
A mission statement and guidelines on how to deal with herpes gladiatorum from the Sports Medicine Advisory Committee at the National Federation of State High School Associations.
Wrestlers filed a “herpes lawsuit” in 2008 against their coach and trainer holding them responsible for a localized HSV-1 outbreak.
In 2008, researchers discovered a unique herpes strain that only affects sumo wrestlers.

REFERENCES
1. BB Adams. (2010) Skin Infections in Athletes. Expert Rev Dermatol. 5(5): 567-577
2. R Sharma et al. (2011) Herpes Simplex in Emergency Medicine. Accessed online on Feb 2, 2012. Link.
3. BB Adams. (2000) Transmission of cutaneous infections in athletes. Br J Sports Med. 34(6): 413–414
4. B.J. Anderson (2008) Managing Herpes Gladiatorum Outbreaks in Competitive Wrestling: The 2007 Minnesota Experience. Curr Sports Med Rep. 7(6): 323-7
5. Belongia EA, Goodman JL, Holland EJ, et al. (1991) An outbreak of herpes gladiatorum at a high-school wrestling camp. N Engl J Med. 325(13): 906-10
6. EM Begier et al. (2004) A High-Morbidity Outbreak of Methicillin-Resistant Staphylococcus aureus among Players on a College Football Team, Facilitated by Cosmetic Body Shaving and Turf Burns. Clin Infect Dis. 39(10): 1446-1453
7. DM Nguyen et al. (2005) Recurring Methicillin-resistant Staphylococcus aureus Infections in a Football Team Emerg Infect Dis. 11(4): 526-32
8. CB Creech (2010) One-year surveillance of methicillin-resistant Staphylococcus aureus nasal colonization and skin and soft tissue infections in collegiate athletes. Arch Pediatr Adolesc Med. 164(7): 615-20
9. Centers for Disease Control & Prevention (CDC). (2009) Methicillin-resistant Staphylococcus aureus among players on a high school football team–New York City, 2007. MMWR Morb Mortal Wkly Rep. 58(3): 52-5
10. B Barr, M Felkner & PM Diamond. (2006) High school athletic departments as sentinel surveillance sites for community-associated methicillin-resistant staphylococcal infections. Tex Med. 102(4):56-61





Move Over MRSA, C. difficile is Here

30 04 2010

Clostridium difficile, or C. difficile, is a tough bacterium that’s been around a long time and has always been more prevalent in hospitals and healthcare facilities than MRSA.

It plagues those who are older, or immunocompromised, or have a serious illness. However, those on simple antibiotics can also be at risk.

A new strain of C. difficile has been detected and it is more drug-resistant, more virulent, and more deadly than other, older strains.

C. difficile can be transmitted in feces, so anything that comes into contact with feces in or out of a healthcare setting can readily spread the bacterium. This includes any surface, or standard objects such as rectal thermometers, commodes, bathing tubs, or table tops. It also includes healthcare professionals with contaminated hands or clothing.

C. difficile can be recurring. The germ creates spores which remain dormant on surfaces for weeks or months at a time. If we touch the contaminated surface and eat something without washing our hands, we might just “eat” C. difficile.

Testing procedures include various kinds of stool testing, an examination of the colon, or a CT scan.

There’s no specific test that differentiates between the various C. difficile strains, including the more virulent, drug-resistant strain.

Common symptoms include watery diarrhea, fever, nausea, abdominal pain and lack of appetite.

Complications from C. difficile may result in a torn colon or perforated bowel, PMC colitis, sepsis, and death.

Treatment might be as simple as stopping an antibiotic, or changing to a different one, but sometimes the infection is so bad that patients will try a fecal transplant. And you have to read about this, even if just for the “eeeewww” factor.

Alcohol-based hand sanitizers are effective in cutting back MRSA infections, but for C. difficile, good old fashioned handwashing with soap and water works better.

MRSA and C. difficile are in our communities as well as in our hospitals, and they’re not the only superbugs defeating the antibiotics we have.

Scientists are trying to stay a step ahead by developing more and better drugs to defeat these stubborn and drug-resistant microbes.

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MRSA

5 09 2008

Nurse Mary Beth provides tips on protection against MRSA.

Listen now!

Right-click here to download podcast (6MB,13min)





MRSA

25 02 2008

MRSA is in the news these days and it can be scary.  MRSA (Methicillin-resistant Staphylococcus aureus) is a bacterium that causes infections in and on the body.

It’s considered the super bug of staph (Staphylococcus aureus) infections because this strain is resistant to some of our antibiotics.  This resistance makes it harder to treat.

A MRSA infection on the skin may cause boils or pimples or it may cause an infection that runs so deep it has to be drained.  Treatment for such an infection may or may not include antibiotics. 

MRSA may also infect wounds or get into the lungs, the bloodstream or the urinary tract.

About 25 percent of us walk around with staph bacteria on our bodies or maybe up our noses, but we don’t become infected.  Of the 25 percent, about one percent carries MRSA. 

Should the staph get into the body through, say, a cut, we could get an infection.  Usually these infections aren’t serious, although it’s possible for them to become dangerous.  They may even cause pneumonia.

The good news is, staph is usually treated with antibiotics.  The bad news is, there are strains of staph, like MRSA, that have developed resistance to some of our antibiotics.  This super bug keeps changing and adapting, making it necessary for us to develop new antibiotics in a hurry.

To the disgrace of everyone involved, MRSA infections are exploding in healthcare settings, with MRSA now causing up to 40 to 50 percent of the staph infections in U.S. hospitals.

MRSA has also expanded from hospitals and other healthcare settings out into the community, where it is referred to as Community-Associated MRSA (CA-MRSA).

CDC tells us that in 2003, 12 percent of MRSA infections were acquired in the community.

Prevention is key to remaining MRSA-free and CDC recommends the following:

  • Wash your hands thoroughly for at least 15 seconds. Use soap and water or an alcohol-base hand sanitizer.
  • Cover your cuts and scrapes with a clean bandage to prevent bacteria from entering the wound.  If you have to touch another person’s wounds or bandages, put a barrier between your hands and the soiled materials or open skin.
  • Don’t share personal care items like nail clippers or scissors, razors, towels and so on. 
  • Wipe down shared gym equipment before and after use.
  • Using the dryer rather than line drying helps kill bacteria.

MRSA is identified with lab tests.  Should your provider determine you have a MRSA infection, there are plenty of antibiotics that do work, although you may not even need to be on antibiotics.





MRSA

1 06 2007

There’s an old enemy in town, the microbe called MRSA (frequently pronounced MURsah). MRSA stands for methicillin-resistant staphylococcus aureus. It’s a bacterium that used to be picked up during hospital stays and was easily knocked out by a dose of penicillin.

Not anymore. It’s resistant to many common antibiotics, making it harder to treat.

This bug is now found in gyms and other places where people get together. It’s a problem for everyone. It usually looks like a skin infection, but it can get in the bloodstream and urinary tract and cause multiple symptoms.

Time was, it would take a couple of days to get the labs back identifying MRSA in a patient, but now it’s just a couple of hours. Technology is a wonderful thing.

And then there is the anti-tech treatment – maggots.

Doctors at the University of Manchester in Britain have successfully treated foot ulcers in diabetics with maggots. Yes, maggots. They put the little larvae on the ulcers several times a day and watched them dine on damaged tissue. Reports are that the patients healed much faster than with normal treatment.

Hard to get over the willies with that bit of news.

The best prevention is to keep your hands clean, wash and cover your wounds, avoid touching other people’s wounds or bandages, and don’t share personal items (towels, razors and so on).

There are more conventional treatments for MRSA, but if you’re not careful, you, too, may find yourself at the business end of a maggot.