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PRACTICE ESSENTIALS

Herpes and Tinea in Wrestling

Managing Outbreaks, Knowing When to Disqualify

Gregory L. Landry, MD; Cindy J. Chang, MD

Practice Essentials Series Editors:
Kimberly G. Harmon, MD; Aaron Rubin, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 32 - NO. 10 - OCTOBER 2004


In Brief: The two most troublesome skin infections in wrestlers are herpes gladiatorum and tinea gladiatorum. Determining whether athletes should or should not be disqualified from practice or competition because of these infections requires some expertise. Recommendations are presented to assist the practitioner in the care of these conditions in wrestlers and other athletes who have frequent skin-to-skin contact.

The management of skin infections in wrestlers and other athletes in sports involving skin-to-skin contact is challenging, from making an accurate diagnosis to determining eligibility for play. The two most common skin infections in wrestlers are tinea and herpes simplex, although the same issues are relevant to rugby, football, and other sports that require skin-to-skin contact. Based on the National Collegiate Athletic Association (NCAA) injury surveillance system, of the skin infections reported from 1991 to 2003, herpes accounted for 39% and tinea represented 23% (figure 1).1

Herpes Gladiatorum

Herpes infections in athletes have been described in the medical literature for many years. The first report2 appeared in 1964, and the term herpes gladiatorum was coined by the authors to describe a cutaneous herpes simplex virus infection acquired via direct skin-to-skin contact during participation in sports such as wrestling. Three more reports appeared in one issue of the Journal of the American Medical Association in 1965. Outbreaks were reported in 6 of 30 wrestlers at the University of Georgia3 and in 7 of 19 wrestlers at Dartmouth College.4 The third report5 discussed the importance of early recognition of an infected athlete and isolation of athletes to prevent transmission to other athletes.

Transmission. Although early reports expressed concern that herpes could be transmitted by infected mats, most infections are acquired by skin-to-skin contact between an infected and noninfected wrestler. Herpes viruses do not survive long outside the body and would not survive long on a wrestling mat. Some of these infections probably occur from contact with individuals who have a history of herpes labialis. Coaches may also play a role in the spread of herpes infections since they, by the nature of the sport, teach wrestling techniques on the mat. In an outbreak in Washington, three coaches and nine athletes were affected.6

Abrasive clothing may also play a role in transmission. Shirts made of 50/50 cotton-polyester blend were worn by Ohio State wrestlers. Friction with the material may have caused tiny breaks in the skin, and during the first season that the new shirts were worn, the number of cases of herpes infections increased significantly.7 In the following season, return to wearing 100% cotton shirts was associated with a fall in the number of herpes infections.

Epidemiology. Herpes gladiatorum appears to be increasing in frequency, but the prevalence varies in published studies. A 1988 study by Becker et al8 reported that 2.6% of high school wrestlers and 7.6% of collegiate wrestlers had herpes. The high frequency of infections during outbreaks demonstrates the high contagion associated with herpes infections. During a summer Minnesota wrestling camp, 60 of 175 (34%) wrestlers were diagnosed with herpes infections, and 58 of the 60 were primary infections.9 In 1999, Anderson10 reported that 20% to 40% of NCAA Division 1 wrestlers were infected.

The only potential longitudinal data are from the NCAA injury surveillance system.11 Unfortunately, all skin infections, regardless of the infective organism, are reported together and are only reported if time is lost from practice or competition. The number of infections causing time loss from participation is reported per school each year (figure 2). The average number of infections per school per year in the 6 years from 1986 to 1992 was 1.76, and this nearly doubled to 2.96 in the 6 years from 1992 to 1998. It is not clear how much of this increase is from herpes gladiatorum. From 1998 to 2003, the average number of infections per school per year fell to 2.1, possibly because of more widespread use of prophylactic antiviral medication, although other factors could have contributed to this change.

Diagnosis. Several elements can make diagnosing herpes gladiatorum challenging. The incubation period is 2 to 20 days, but the outbreak usually occurs 2 to 5 days following exposure. The athlete may develop constitutional symptoms such as fever, chills, malaise, myalgia, pharyngitis, headache, anorexia, or regional lymphadenopathy. The rash begins with tingling, burning, stinging, or itching at the infected site. Scattered clusters of vesicles on an erythematous base develop with a variable appearance. The vesicles are usually 1 to 2 mm in diameter and have clear fluid. In wrestlers, the vesicles may be absent and the lesions look like ulcers, because they have been traumatized by contact with the mat or a fellow wrestler.12 Furthermore, with a large inoculum, the vesicles may be larger and appear pustular. This rash can easily be confused with impetigo or contact dermatitis, especially in a primary infection.

Wrestlers may have widespread lesions (figure 3) on many different areas of the body that were inoculated during the encounter with an infected wrestler. It is always important to ask a wrestler if the rash has been present before in the same area. This is one of the few clues that the rash may be herpetic. The tingling or stinging pain is also a clue that the rash is caused by herpes, because impetigo or contact dermatitis usually do not cause pain or any neurologic symptoms. When available, Tzanck test, culture, or immunofluorescent studies may confirm the diagnosis.

Complications. Because herpes infections in wrestlers often involve the face, ocular herpes is a special risk. During one outbreak involving 60 wrestlers, 5 cases of ocular herpes were reported.13 Usually caused by autoinoculation, the initial infection may involve only the conjunctiva or the eyelid, but it can spread to the cornea. Herpes keratoconjunctivitis is a major cause of blindness in the United States. In an athlete who has corneal involvement, the most important symptom is pain, especially with blinking (similar to a corneal abrasion). An athlete who has a herpetic rash and any eye symptoms should be evaluated by an ophthalmologist. Other complications from spread of the virus include encephalitis, meningitis, and Bell's palsy, but these are rare in otherwise healthy athletes.

Treatment. Herpes lesions will dry up and heal without treatment. The median time between onset of lesions and complete eschar formation was 6 days in the Minnesota outbreak.9 The range for healing was 2 to 21 days. Early treatment with antiviral medication may shorten the course and may reduce contagion.

Treatment of herpes gladiatorum is identical to the treatment for genital herpes.14 For a primary infection, treatment with an antiviral medication is usually longer than with recurrent infections, because the primary infections are usually more severe. Acyclovir may be given as 400 mg tid or 200 mg five times a day for 7 to 10 days. Valacyclovir hydrochloride at 1,000 mg bid for 10 days is a more convenient regimen, but it is considerably more expensive. Famciclovir at 250 mg tid for 10 days is also acceptable. No evidence suggests that one antiviral is more effective than another. Oral valacyclovir is slowly metabolized into acyclovir and produces higher and more persistent acyclovir blood levels than oral acyclovir, but no difference was found between patients treated with acyclovir versus valacyclovir for herpes genitalis when comparing days for resolution of symptoms and days to negative viral cultures.15,16

For recurrent infections, the doses can be reduced for valacyclovir and famciclovir and are used for a 5-day course (table 1). Five-day dosing of famciclovir is 125 mg bid. Valacyclovir at 500 mg bid for 3 days may be as effective in treating recurrences as a 5-day regimen. Athletes need to know that the earlier the antiviral is taken in the course, the more effective it is. It is best to start the medication at the first symptom of tingling or itch at the site of a previous infection. For wrestlers with recurrent herpes, most team physicians provide prescriptions before outbreaks to allow the athletes to start the medication without delay for a call to the physician's office. Local treatment of lesions with benzoyl peroxide and use of a hair dryer may help the lesions dry and crust more quickly. When the diagnosis is unclear between herpes simplex and impetigo, it is reasonable to treat the athlete with an antiviral medication and an antibiotic simultaneously.

   TABLE 1. Dosage and Cost* of Antiviral Medications Used to Treat or Prevent Herpes Gladiatorum
Recurrent Outbreaks (5 dy)
  Prophylaxis (1 mo)
Medication    StrengthFrequencyCostFrequencyCost
Acyclovir400 mgTID$8.98BID$35.90
Famciclovir125 mgBID$38.98BID$233.90
Valacyclovir500 mgBID$40.98Daily$122.95

*Purchased from an online pharmacy.
BID = twice a day; TID = three times a day

Return to Play With Herpes

The issue of playability is controversial. Herpes transmission is more serious than other skin infections, because it is incurable and lifetime recurrences are possible.

Viral shedding during treatment has not been studied in herpes gladiatorum. The only data are from extensive studies of herpes genitalis, and the data may have relevance to herpes gladiatorum. In one multicenter trial17 of acyclovir versus placebo, the duration of virus shedding was 2.1 ± 0.2 days in the treatment group with all patients culture-negative by day 7 of treatment, and 95% of the patients were culture-negative by day 4 of treatment. In the placebo group, the duration of virus shedding was 3.9 ± 0.3 days with all patients culture negative by day 12 (P<0.001). No significant difference with treatment using acyclovir, valacyclovir, or famciclovir is known.15 Most everyone agrees that any wrestler who has herpes gladiatorum should be treated with an appropriate antiviral to speed healing, but also to reduce viral shedding.

No wrestler should compete until the scabs have dried and there are no further vesicles, ulcers, or drainage.12 Herpes is highly contagious, and no one should rely on any kind of dressing to allow a wrestler to compete with herpes. Dressings often do not stay affixed to sweaty skin with the trauma that occurs on the mat.

The National Federation of State High School Associations (NFHS) Sports Medicine Handbook18 recommends that the wrestler be withheld from competition until there are "no new lesions in 48 hours and all lesions must be scabbed over." The NCAA wrestling rules are more strict and state that the wrestler must be free of systemic symptoms of viral infection (fever, malaise, etc) and must have developed no new blisters for 72 hours before the examination.19 Furthermore, the NCAA states that a wrestler must have no moist lesions and they must all be dried and surmounted by a firm, adherent crust. The wrestler must take an appropriate dosage of systemic antiviral therapy for at least 120 hours (5 days) before and at the time of the meet or tournament. Finally, the NCAA states, "active herpetic infections shall not be covered to allow participation."

None of these recommendations on herpes gladiatorum is evidence-based. Anderson10 recommends that a wrestler could return to play 4 to 7 days after a recurrent outbreak, based on the herpes genitalis virus shedding studies. Further studies are needed to examine viral shedding and contagion in wrestlers.

Preventing Herpes Outbreaks

An important aspect of prevention is early recognition of the disease to prevent further spread. Wrestlers should be screened with skin checks before any competition—especially tournaments—in which infections can become widespread. Wrestlers must be educated about the high contagion of herpes gladiatorum and informed that prompt treatment can minimize time off the mat.

Pharmaceutical prophylaxis has become an important part of prevention. Many college and high school teams have their wrestlers use antiviral agents for a good share of the season because of their safety and effectiveness. One study10 used 500 mg of valacyclovir per day for wrestlers who had herpes gladiatorum for more than 2 years and 1,000 mg per day for wrestlers who had the disease for less than 2 years. The study showed a dramatic decrease in outbreaks in both groups.

Acyclovir (400 mg bid) has been used for many years as prophylaxis for genital herpes. In a study16 in the prevention of genital herpes outbreaks, patients were randomized to receive acyclovir at 400 mg bid, or valacyclovir at 250 mg, 500 mg, or 1,000 mg once a day, valacyclovir at 250 mg bid, or a placebo. The twice-daily doses of acyclovir and valacyclovir were similar in effectiveness, and a dose-response relationship was found across the once-daily valacyclovir regimens. Because acyclovir is considerably less expensive, it should be the first-line therapy for prophylaxis in most cases.

The role of hygiene in preventing transmission of the herpes simplex virus is uncertain. Spread by fomites is not a major cause of infection, because the viral membrane is quite fragile and incapable of survival for prolonged periods. A virus with a lipid envelope that has been damaged by drying is not infectious. The lipid envelope is also sensitive to acids, detergents, and organic solvents. Therefore, it is recommended to take additional precautionary measures by cleaning wrestling mats with bleach or another disinfectant at least once a day and laundering practice gear in hot water daily.

Tinea Gladiatorum

Tinea corporis, also known as ringworm, is extremely common in wrestling and other sports with close skin-to-skin contact during practice and competition. Because herpes infections in wrestlers became known as herpes gladiatorum, tinea corporis in wrestlers became known as tinea gladiatorum. Some have used the name tinea corporis gladiatorum or trichophytosis gladiatorum, reflecting the genus of the most common causative organism.20

Transmission. Wrestlers acquire this infection from skin-to-skin contact, thus the predilection for the head, neck, and upper extremities. Wrestlers spend much time in practice and competition in the upright, "lock-up" position. With the wrestler's heads adjacent to each other, the cheeks are in contact with the competitor's, and their heads contact each other's shoulders and necks.

Fungal organisms have been difficult to culture from wrestling mats. It is not clear if viable organisms are not present or the culture techniques are insufficient. In one study,21 a group was able to isolate Trichophyton tonsurans from wrestling mats in Sweden. Asymptomatic carriers may be an important source of fungal organisms.22 Risk factors for becoming carriers were active infection during the season, history of head and neck tinea, failure to wear headgear, and failure to wash practice clothes at least once weekly.22 Kohl et al23 studied 107 high school and college wrestlers in Pennsylvania. Monitoring of scalp fungal cultures showed that none were carriers preseason, but 22 (20.6%) became carriers by midseason. Postseason cultures revealed that 11 (10%) of the wrestlers were still carriers.

Epidemiology. Most studies that examined the prevalence of tinea corporis were associated with an outbreak, such as in an Alaskan high school team in 1992 to 1993 when 75% of the wrestlers had tinea corporis gladiatorum.24 A Cincinnati high school team without a known epidemic had a prevalence of 24%.25 The school's indoor track team served as a control, and no identifiable lesions were found in those individuals. Ten studies from around the world report prevalence rates for tinea corporis gladiatorum.26 They range from 20% in a Hungarian wrestling team27 to 44.1% in a recent report from Lanzarote in the Canary Islands.28 None of these topped the 75% prevalence reported in the Alaska outbreak.

Diagnosis. Patients who have tinea gladiatorum present with well-defined annular plaques with mild erythema and raised borders (figure 4). Lesions in wrestlers are usually found on the head, neck, and upper extremities, less often on the trunk, and occasionally on the legs. Early lesions are indistinguishable from atopic dermatitis. Some lesions are more papular and are difficult to distinguish from acne, impetigo, or early herpes simplex lesions. If the lesions are cultured, about 40% grow T tonsurans, and 40% grow T rubrum.29 Microsporum canis occurs in about 14% of cases. It is not clear why wrestlers tend to be infected by T tonsurans and T rubrum, but several authors have suggested that some wrestlers may be asymptomatic carriers.

Treatment. With superficial fungal infections, the practitioner has a choice between topical and oral antifungal agents. Most practitioners treat a single lesion with a topical agent, and if there are two or more lesions they use an oral agent. Beller and Gessner24 recommend use of griseofulvin for 1 month for wrestlers with two or more lesions or any facial lesions and a topical agent for 1 month for one lesion. They suggested disqualification for 10 days for wrestlers using topical treatment and 15 days for those using oral medication.

Another study30 compared topical and oral treatments for tinea gladiatorum. One group of wrestlers used topical clotrimazole twice daily, and the other group took oral fluconazole (200 mg weekly) for 3 weeks. In the topical group, 50% of the athletes had negative cultures after 22.7 days; in the oral group, 50% had negative cultures at 11.1 days. The authors concluded that weekly doses of fluconazole should be the first line therapy for tinea gladiatorum. A follow-up study31 treated wrestlers with fluconazole (200 mg weekly for 4 wk) and found more than 60% had negative cultures after 7 days. All wrestlers had negative cultures at the end of the 4-week therapy. It is not known exactly how long an athlete has to be treated to become noninfectious or which antifungal agent is best to use in wrestlers, but several regimens have been tried (table 2). To our knowledge, a study has not been done in wrestlers comparing the effectiveness of new topical agents (eg, terbinafine hydrochloride) with the azole topical agents, such as miconazole nitrate, clotrimazole, and ketoconazole. The topical azole antifungals are still the first-line treatment, but no evidence suggests superiority of one over another.32

 TABLE 2. Dosage and Cost* of Antifungal Medications Used to Treat Tinea Gladiatorum

MedicationStrengthFrequencyDurationCost
Fluconazole150 mg1X/wk3 wk$42.98
200 mg1X/wk3 wk$46.25
Griseofulvin500 mgBID4 wk$109.20
Itraconazole100 mgDaily15 dy$127.75
Terbinafine250 mgDaily2 wk$133.00

*Purchased from an online pharmacy.
BID = twice a day

Tinea Return-to-Play Issues

One group recommended that a wrestler be held off the mat for 5 days if tinea lesions cannot be covered.12 Adams26 suggested that an athlete treated topically or orally should stay off the mat for 1 week unless a lesion could be adequately covered. The NFHS Sports Medicine Handbook18 recommends that the wrestler can return to play after 72 hours or more of antifungal therapy with no active lesions.

The NCAA wrestling rules19 state, "A minimum of 72 hours of topical therapy is required for skin lesions. A minimum of 2 weeks of systemic therapy is required for scalp lesions. Wrestlers with extensive and active lesions will be disqualified." Activity of treated lesions can be judged by either use of a potassium hydroxide (KOH) preparation or review of the therapeutic regimen. Unlike requirements for herpes, the NCAA rules state, solitary lesions may be covered. The NCAA specifically recommends washing the lesion with selenium sulfide or ketoconazole shampoo, followed by the application of naftifine hydrochloride or terbinafine hydrochloride cream, then covering with a gas permeable dressing, followed by ProWrap (Fabrifoam, Exton, Pennsylvania) and stretch tape. The NCAA rules state, "The disposition of tinea cases will be decided on an individual basis as determined by the examining physician and/or certified athlete trainer."

Disagreement on the feasibility of covering lesions arises because the NFHS guidelines state that "covering a communicable condition shall not be considered acceptable." Traditionally, medical personnel have not been as strict about tinea infections, because, unlike with herpes, they are all potentially curable and are associated with minimal discomfort.

Preventing Tinea Infections

Little research has been done on prophylaxis of tinea in wrestlers. One study33 used oral itraconazole twice daily for 1 day every 2 weeks. During the first half of the season, 27% of the wrestlers were infected, and during the last half of the season, using the every-other-week regimen, none of the wrestlers developed tinea gladiatorum. In a double-blind, placebo study31 of wrestlers, the effectiveness of 100 mg of once-weekly fluconazole was examined. In the placebo group, 13 of 58 (22%) wrestlers were infected, but only 3 of 46 (6%) in the treatment group were infected. Although these results look promising, the high cost of these agents and the potential serious side effects such as hepatitis make prophylaxis for entire teams less desirable.34 Prophylaxis for susceptible individuals, especially late in the season when the most important meets occur, may be reasonable.

Pinning Down Contagion

Herpes gladiatorum recurrences can be lifelong. Aggressive treatment and disqualification should occur until the athlete has no new lesions for a minimum of 48 hours and has no active lesions. Active herpes lesions cannot be adequately covered to allow participation in contact sports. Antiviral prophylaxis is inexpensive and safe for herpes gladiatorum and should be used liberally.

Tinea gladiatorum is a more benign infection that can be cured. Although it is not clear how long athletes are contagious, liberal return-to-play guidelines are more feasible with tinea, and athletes should be allowed to securely cover solitary lesions. An oral antifungal agent should be used if two or more fungal lesions are present. Antifungal prophylaxis is expensive and potentially dangerous and should be used only in selected cases.

Wrestlers should undergo skin checks at all competitions and tournaments to help prevent the spread of these common infections. Further studies are needed to help determine when athletes are no longer contagious after beginning treatment. Patient education on prevention is also important (see the Patient Adviser, "Treating and Avoiding Herpes and Tinea Infections in Contact Sports").

References

  1. National Collegiate Athletic Association: NCAA committee heightens awareness of skin infection issue. NCAA News 2003;40(22):8. Available at https://www.ncaa.org/news/2003/20031027/awide/4022n16.html. Accessed September 7, 2004
  2. Selling B, Kibrick S: An outbreak of herpes simplex among wrestlers (herpes gladiatorum). N Engl J Med 1964;270:979-982
  3. Wheeler CE Jr, Cabaniss WH Jr: Epidemic cutaneous herpes simplex in wrestlers (herpes gladiatorum). JAMA 1965;194(9):993-997
  4. Porter PS, Baughman RD: Epidemiology of herpes simplex among wrestlers. JAMA 1965;194(9):998-1000
  5. Dyke LM, Merikangas UR, Bruton OC, et al: Skin infection in wrestlers due to herpes simplex virus. JAMA 1965;194(9):1001-1002
  6. Dworkin MS, Shoemaker PC, Spitters C, et al: Endemic spread of herpes simplex virus type 1 among adolescent wrestlers and their coaches. Pediatr Infect Dis J 1999;18(12):1108-1109
  7. Strauss RH, Leizman DJ, Lanese RR, et al: Abrasive shirts may contribute to herpes gladiatorum among wrestlers. N Engl J Med 1989;320(9):598-599
  8. Becker TM, Kodsi R, Bailey P, et al: Grappling with herpes: herpes gladiatorum. Am J Sports Med 1988;16(6):665-669
  9. Belongia EA, Goodman JL, Holland EJ, et al: An outbreak of herpes gladiatorum at a high-school wrestling camp. N Engl J Med 1991;325(13):906-910
  10. Anderson BJ: The effectiveness of valacyclovir in preventing reactivation of herpes gladiatorum in wrestlers. Clin J Sport Med 1999;9(2):86-90
  11. National Collegiate Athletic Association Injury Surveillance Data Notebook. Available at https://www2.ncaa.org/media_and_events/ncaa_publications/health_and_safety/index.html. Accessed October 6, 2004
  12. Dienst WL Jr, Dightman L, Dworkin MS, et al: Pinning down skin infections: diagnosis, treatment, and prevention in wrestlers. Phys Sportsmed 1997;25(12):45-56
  13. Holland EJ, Mahanti RL, Belongia EA, et al: Ocular involvement in an outbreak of herpes gladiatorum. Am J Ophthalmol 1992;114(6):680-684
  14. Geers TA, Isada CM: Update on antiviral therapy for genital herpes infection. Cleve Clin J Med 2000;67(8):567-573
  15. Engel JP: Long-term suppression of genital herpes. JAMA 1998;280(10):928-929
  16. Reitano M, Tyring S, Lang W, et al: Valacyclovir for the suppression of recurrent genital herpes simplex virus infection: a large-scale dose range-finding study. International Valacyclovir HSV Study Group. J Infect Dis 1998;178(3):603-610
  17. Reichman RC, Badger GJ, Mertz GJ, et al: Treatment of recurrent genital herpes simplex infections with oral acyclovir: a controlled trial. JAMA 1984;251(16):2103-2107
  18. National Federation of State High School Associations Sports Medicine Handbook, ed 2. NFHS Sports Medicine Advisory Committee, Indianapolis, 2002, pp 50-51
  19. National Collegiate Athletic Association: 2003-2004 Wrestling Rules, Appendix D Skin Infections. Indianapolis, 2004. Available at https://www2.ncaa.org/media_and_events/ncaa_publications/playing_rules/. Accessed October 6, 2004
  20. Stiller MJ, Klein WP, Dorman RI, et al: Tinea corporis gladiatorum: an epidemic of Trichophyton tonsurans in student wrestlers. J Am Acad Dermatol 1992;27(4):632-633
  21. Hradil E, Hersle K, Nordin P, et al: An epidemic of tinea corporis caused by Trichophyton tonsurans among wrestlers in Sweden. Acta Derm Venereol 1995;75(4):305-306
  22. Kohl TD: Are there carriers of ringworm among competitive wrestlers? Abstract presented at the National Athletic Trainers, Association National Symposia, Dallas, June 2002
  23. Kohl TD, Giesen DP, Moyer J Jr, et al: Tinea gladiatorum: Pennsylvania's experience. Clin J Sport Med 2002;12(3):165-171
  24. Beller M, Gessner BD: An outbreak of tinea corporis gladiatorum on a high school wrestling team. J Am Acad Dermatol 1994;31(2 pt 1):197-201
  25. Adams BB: Tinea corporis gladiatorum: a cross-sectional study. J Am Acad Dermatol 2000;43(6):1039-1041
  26. Adams BB: Tinea corporis gladiatorum. J Am Acad Dermatol 2002;47(2):286-290
  27. Eros N, Karolyi Z, Molnar E: Trichophyton equinum infections among young wrestlers in Hungary. Acta Dermato-Venereologica (Alpina) 1999;8(2):63-66
  28. Piqu E, Copado R, Cabrera A, et al: An outbreak of tinea gladiatorum in Lanzarote. Clin Exp Dermatol 1999;24(1):7-9
  29. Kemna ME, Elewski BE: A US epidemiologic survey of superficial fungal diseases. J Am Acad Dermatol 1996;35(4):539-542
  30. Kohl TD, Martin DC, Berger MS: Comparison of topical and oral treatments for tinea gladiatorum. Clin J Sport Med 1999;9(3):161-166
  31. Kohl TD, Martin DC, Nemeth R, et al: Fluconazole for the prevention and treatment of tinea gladiatorum. Pediatr Infect Dis J 2000;19(8):717-722
  32. Hart R, Bell-Syer SE, Crawford F, et al: Systematic review of topical treatments for fungal infections of the skin and nails of the feet. BMJ 1999;319(7202):79-82
  33. Hazen PG,Weil ML: Itraconazole in the prevention and management of dermatophytosis in competitive wrestlers. J Am Acad Dermatol 1997;36(3 pt 1):481-482
  34. Kohl TD, Lisney M: Tinea gladiatorum: wrestling's emerging foe. Sports Med 2000;29(6):439-447


Dr Landry is a professor of pediatrics and sports medicine at the University of Wisconsin Medical School in Madison, Wisconsin. Dr Chang is an assistant clinical professor in the departments of family and community medicine at the University of California, Davis and the University of California, San Francisco. Address correspondence to: Gregory L. Landry, MD, 2880 University Ave, Madison, WI 53705; e-mail to [email protected].

Disclosure information: Drs Landry and Chang disclose no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.


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