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Common Bacterial Dermatoses

Protecting Competitive Athletes

CPT (P) Jeffrey A. Levy, DO

Sports Dermatology Series Editor:
William Dexter, MD


In Brief: Athletes competing in a wide variety of sports are at risk of contracting and spreading bacterial skin infections. Bacteria proliferate in environments of wet, macerated skin that is repeatedly abraded against competing athletes, equipment, clothing, or objects in the field of play. Common infections include impetigo, folliculitis, furunculosis, pitted keratolysis, and otitis externa. Diagnosis and treatment are often straightforward and vary little from care for nonathletes. However, knowledge of preventive strategies and return-to-play criteria, as outlined by the National Collegiate Athletic Association, are paramount for clinicians who care for competitive athletes.

Participation in sports requires athletes to come in close contact with each other and with clothing, equipment, and environmental hazards, such as water. Normal flora of the skin or environment can become pathologic when athletes inadvertently provide an appropriate environment in the course of training or competing. Water, perspiration, and abraded skin can weaken the stratum corneum (the protective outer layer of the epidermis), providing an excellent medium for bacteria to proliferate.

Certain infections can be found in epidemic numbers in athletes. Vigilant surveillance and early treatment can help teams avoid disease outbreaks. Clinicians knowledgeable in cause, diagnosis, treatment, and return-to-play criteria can spare the athlete from a more significant infection and protect other participants from contracting these diseases.

Impetigo Contagiosa

As its name suggests, impetigo contagiosa is easily spread from person to person. A superficial skin infection caused by either staphylococci or streptococci bacteria,1 impetigo is particularly common in sports with close skin-to-skin contact, such as wrestling, football, and rugby.2

Impetigo has two different presentations: bullous and nonbullous. The bullous form typically begins as multiple fluid-filled vesicles that either coalesce or individually enlarge, forming blisterlike lesions that eventually collapse centrally. The center has the classic honey-crusted lesion that, when removed, reveals erythematous plaques draining serous fluid. Nonbullous impetigo originates as small vesicles or pustules with erythematous bases and honey-colored crusts, which also drain fluid (figure 1). Breaks in the skin provide an avenue for bacterial invasion. Some evidence suggests that initial colonization of the nares with staphylococcus spreads to normal skin before infection.3,4 Patients are typically afebrile; however, regional lymphadenopathy can be seen with both types of impetigo.1

Diagnosis and treatment. In most cases, the diagnosis is made clinically and confirmed with bacterial cultures when necessary.

Impetigo may progress, become chronic, or resolve spontaneously. When the disorder is widespread, oral therapy may be warranted.1 The topical antibiotic mupirocin treats both staphylococci, including methicillin-resistant strains, and streptococci.1 Local debridement of the crusts with soap and water helps to allow full penetration of the topical antibiotic.5 Topical mupirocin is as effective as systemic antibiotics and has fewer side effects.6 The ointment should be applied three times a day until all lesions have resolved. Washing the entire body with an antibacterial soap may also help prevent spread to distal sites.1 Oral dicloxacillin sodium, cloxacillin sodium, cephalexin hydrochloride, and macrolides (for patients who have penicillin allergy) are all effective systemic therapies.1

Patients who have recurrent impetigo should be treated as Staphylococcus aureus carriers. The nares are the most common site of colonization. Treatment consists of mupirocin calcium cream applied to the nares twice a day for 5 days.1

Return-to-play criteria. According to the National Collegiate Athletic Association (NCAA) wrestling guidelines, any patient who has impetigo must take oral antibiotics for at least 72 hours and be free from any new skin lesions for 48 hours before competition.7 Additionally, all lesions must be covered with a nonpermeable bandage that will not dislodge during the event.

Folliculitis and Furunculosis

Folliculitis is a superficial infection of the upper portion of the hair follicle and surrounding areas characterized by mildly tender papules or pustules surrounded by erythema (figure 2). Furunculosis is an infection of the deeper hair follicle cavity, and the lesions usually contain pus.2 Furuncles, commonly called abscesses or boils, are large, well-defined, erythematous, and fluctuant nodules that commonly occur in areas of increased sweating and friction, such as the buttock, belt line, anterior thigh, and axilla.

Both folliculitis and furunculosis are caused by S aureus. One study8 of wrestlers showed that 22% of furuncles contained methicillin-resistant strains.

A study9 at one high school found that 20% of basketball players and 25% of football players were affected by these remarkably common infections. Contact with lesions and a prior skin injury are significant predisposing factors.4

Hot tubs, whirlpools, and swimming pools used during rehabilitation may be colonized with Pseudomonas aeruginosa, leading to hot tub folliculitis.4,10 Although not absolute, open skin wounds are common predisposing factors.2,4,10 Approximately 6 hours to 2 days after exposure, the submerged skin will develop multiple, pruritic, follicular, and often green pustules.2,10 Systemic manifestations of fever, nausea, vomiting, and malaise are also possible.

Diagnosis. Both folliculitis and furuncles can be diagnosed by history and physical examination. For folliculitis, a bacterial culture may be done by removing an entire lesion with a #15 scalpel and placing it on a cotton swab of the transport media.1 Merely swabbing the area does not provide enough of the causative bacteria to ensure an accurate diagnosis. A bacterial culture of furuncles will be of little value in an immunocompetent host, because the infecting organism will typically be S aureus or a mix of normal flora bacteria from the infected body region.1

Treatment. Infectious folliculitis that is limited to a few lesions may be treated with mupirocin ointment.2 In more widespread infection, antistaphylococcal antibiotics (eg, dicloxacillin, cephalexin) are required at 500 mg, three times a day for 10 to 14 days.1

Furuncles and abscesses typically require incision and drainage. Warm compresses produce a point on the abscess to allow for easier drainage and help reduce symptoms. Under local anesthetic, the center of the lesion is incised with a #11 blade. The material is expressed and, in larger abscesses, a wick is inserted to prevent early closure or recurrence. The wound is left to close by secondary intention. Antibiotics, although often prescribed by practitioners, are not required.1

For hot tub folliculitis, treatment is supportive, because the infection is self limited over 7 to 14 days.2,4,10 Some studies2,4,10 have shown that antibiotic use increases the recurrence rate. If the infection is severe or unremitting, a fluoroquinolone antibiotic should be used.2,4 Because of the colonization, the hot tub or pool should be sanitized before any further use.

Return-to-play criteria. Similar to criteria for impetigo, the NCAA return-to-play criteria for both folliculitis and furunculosis consist of ensuring that each affected athlete has no new skin lesions for 48 hours and is taking oral antibiotics for at least 72 hours before competition.7 Lesions must be securely covered by nonpermeable bandages.

Pitted Keratolysis

The foot malady called pitted keratolysis typically occurs in active people who wear socks that retain moisture. Athletes are particularly susceptible, because their feet are often chronically in perspiration-soaked socks and shoes.

Numerous bacteria have been implicated, including different members of the Corynebacterium, Dermatophilus, and Kytococcus genera.2,11 Corynebacterium species, which are gram-positive rods, are normal skin microorganisms that are not typically pathologic unless certain predisposing factors are present, such as prolonged wet feet or immunosuppression.2,11

Callus formation is another factor contributing to pitted keratolysis in athletes. Corynebacterium organisms produce enzymes that degrade calluses and thrive in environments with high amounts of keratin.12 Histolopathologically, the calluses of the stratum corneum stain dark pink to purple. Areas of deep scalloped depressions appear where the proteolytic enzymes have eroded through the callus.

On exam, the bottoms of the feet have multiple craterlike pits that are often yellow-brown.11 The pits coalesce and form plaques along high-pressure areas, such as the heels (figure 3), balls of the feet, and plantar aspects of the toes.11 The feet are often wet with perspiration and are malodorous. Although the patient is usually asymptomatic, a bacterial or fungal superinfection can become painful.

Diagnosis. The differential diagnosis of pitted keratolysis includes plantar warts and tinea pedis, but, because pitted keratolysis has a classic appearance, the diagnosis is clinical, and culture is not needed.11 If further proof is needed, illuminating the foot with a Wood's lamp may reveal the classic coral red fluorescence of pitted keratolysis.11

Treatment. The first step in successful treatment includes removal of the moist environment to inhibit continued and future bacterial growth.2,4,11 Socks that are made of either cotton or a synthetic material designed for absorption are essential. Bathing the feet with antibacterial soap followed by drying with a blow dryer is beneficial.11 Going barefoot or wearing sandals, when possible, will allow more air to keep feet dry.11 Pharmacologic treatments include drying solutions, such as 20% aluminum chloride twice a day, and antibiotics, such as 2% erythromycin gel twice a day.2,11 Pharmacologic therapies are not usually needed but may be necessary, particularly with patients who have hyperhidrosis.

Return-to-play criteria. Although often concerning to the patient, the primary infection is not a reason for disqualification. Athletes who have pitted keratolysis may be cleared for full participation. Clinical judgment is needed if an athlete has a superinfection.

Otitis Externa

Swimmer's ear, or otitis externa, is a common infection of the external auditory canal in aquatic athletes. It is most often caused by either P aeruginosa or S aureus.5 The external auditory canal contains cerumen, which is a natural defense against infection. Cerumen is hydrophobic to repel water from the walls of the canal and acidic to create an inhospitable environment for bacterial growth.5,13 If the cerumen is washed out of the external auditory canal, the skin lining can become macerated by moisture, and the pH level can increase, creating conditions for bacterial overgrowth. Other factors that contribute to infection include excessive cleaning of the external auditory canal (which can either cause trauma or remove the protective cerumen), narrow ear canals, and, possibly, eustachian tube dysfunction.5

Diagnosis. In the early stages, symptoms of mild pain and itching will lead to the clinical diagnosis. If untreated, otitis externa may progress to moderate or severe otalgia and otorrhea.5 The external ear canal is often filled with macerated skin debris. Acute tenderness to palpation or movement of the pinna, erythema, edema of the external auditory canal and pinna, severe pain when chewing, fever, and lymphadenopathy may also be present.

Treatment. Cleaning the external auditory canal is of utmost importance to ensure delivery of antibiotics and drying agents to the infection.5,13 The cleaning should be done with a cotton swab under otoscopic visualization. It is important to make sure flushing of the external auditory canal is not performed, if at all, until the tympanic membrane is visualized and confirmed to be intact.5

To avoid continued manipulation of the auricle in a patient who has severe pain or excessive discharge, a wick to facilitate delivery of antibiotics may be inserted into the external auditory canal.5 The best and most cost-effective treatment is three drops of 2% acetic acid solution in the affected ear three to four times a day.5 This will restore the environment to an acidic pH level and will inhibit pseudomonad growth.14 Other otic antibiotics are efficacious, although the newer fluoroquinolone antibiotics are significantly more expensive. Treatment should continue approximately 48 hours after all the patient's symptoms related to otitis extrerna have resolved.5

Measures should be taken to prevent future otitis externa. Swimming caps, drying drops before and after swimming, water-impermeable earplugs, and blow drying the external auditory canal after swimming are all appropriate steps.5

Return-to-play criteria. The NCAA does not have any guidelines for athletes competing with otitis externa, but resolution of symptoms should be achieved prior to swimming. This can usually be accomplished in 2 to 3 days.

Transmission and Protection

Bacterial skin infections can keep athletes out of practice, disqualify them from competition, and prevent teams from performing to their expectations because of an absent team member. Some infections can also spread to other team members, preventing multiple athletes from participating. If a team outbreak occurs, each player's carrier status can be determined through cultures of the nares and inguinal regions. Proper follow-up treatment is in order.4,15 Immediate care for infected patients and adherence to the NCAA guidelines for disqualification will limit the overall impact of the outbreak.

Athletic infections are spread primarily through skin-to-skin contact. Other modes of transmission are fomites, such as wrestling mats and other equipment that contacts the skin.15 The equipment should be sanitized regularly, particularly after an outbreak.

NCAA guidelines specify that open wounds or skin infections must be adequately protected before athletes can be cleared for competition7 (table 1). If not, the athlete is disqualified. "Adequately protected" means the area is deemed noninfectious (no new lesions), the athlete is taking an appropriate medication, if required, and the area is covered by a nonpermeable bandage that will not fall off or dislodge and allow the area to become exposed during competition.7

TABLE 1. Return-to-Play Criteria for Athletes Who Have Common Dermatoses
DiseaseNCAA GuidelinesTreatment Notes

Impetigo, folliculitis, or furunculosisNo new lesions for 48 hr
before competition

Use of oral antibiotics for
72 hr before competition

Lesions covered with
nonpermeable bandage that
will not dislodge with activity
Treat nares with mupirocin ointment if
outbreaks are recurrent or carrier
status is determined

Use antibacterial soap on entire body
Pitted keratolysisNo disqualification unless athlete
has a superinfection
Wear moisture-wicking socks or sandals

Use blow dryer on feet after bathing

Use antibacterial soap to bathe feet

Patients who have hyperhidrosis may
need to apply aluminum chloride solution
or erythromycin solution twice a day
Otitis externaNo disqualificationClean the external auditory canal and
apply 3 drops of 2% acetic acid solution
3 or 4 times a day, continue for 48 hr
after symptoms abate

Wear swimming cap and earplugs

NCAA = National Collegiate Athletic Association

Keeping Athletes' Skin Safe

Athletes are susceptible to a wide variety of skin disorders, and bacterial dermatoses are of particular concern, because many are communicable. Often, with antibiotic treatment and barrier coverage of the infection site, athletes can continue competing safely. When an infection is recognized, prevention of transmission is key. Strict adherence to return-to-play criteria and infection management education for athletes, coaches, and athletic trainers is essential.

Special thanks to LTC Keith Salzman, Deputy Commander of Outlying Clinics at Heidelberg Medical Activity, for his help and editing of this paper.

The views and statements contained in this article are the authors' and do not reflect those of the United States Army, the Department of Defense, or the United States government.


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Dr Levy is Commander of the US Army Health Clinic in Friedberg, Germany, a Captain in the US Army Medical Corp, and a family practice physician. Address correspondence to Jeffrey A. Levy, DO, CPT(P), MC, CMR 453 Box 3324, APO, AE 09074.

Disclosure information: Dr Levy discloses no significant relationship with any manufacturer of any commercial product mentioned in this article. Aluminum chloride and erythromycin gel are mentioned in this article for an unlabeled use.