Pediatric Annals

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SPORTS MEDICINE 

Common Infections in the Young Athlete

Mark E Halstead, MD; David T Bernhardt, MD

Infection in the young athlete can create a significant dilemma for players, coaches, and physicians. Illnesses may affect the athlete's ability to compete or result in medical disqualification. This article reviews common infections that significantly impact the ability of the athlete to perform or compete, and looks briefly at the effects of exercise on the athlete's immune system.

INFECTIOUS MONONUCLEOSIS

Infectious mononucleosis is caused by the Epstein-Barr virus (EBV), a member of the herpes virus family. EBV infections can occur at any age, but infectious mononucleosis typically affects adolescents and young adults. B-lymphocytes are preferentially infected by EBV, resulting in a lymphoproliferative response. The virus is transmitted primarily through saliva.1 The incidence of the symptomatic form of EBV infection typically peaks between 15 and 24 years of age.

Presenting complaints vary but often include the classic triad of fever, pharyngitis, and cervical lymphadenopathy. The pharyngitis is usually exudative and can be severe. A 3- to 5-day prodrome of malaise, fatigue, anorexia, and lowgrade headache often precedes the triad.2 The general course consists of the prodrome followed by the triad of fever, pharyngitis, and fatigue for roughly 5 to 15 days.2 The course of recovery varies. Most patients are well by 6 to 8 weeks after the onset of symptoms.

The spleen is palpable by the second week of the illness in only approximately 50% of patients. Jaundice is infrequent. Cytomegalovirus infections can present a similar clinical picture. Group A beta-hemolytic streptococcal infection may occur concurrently in up to 30% of patients with infectious mononucleosis.1

Diagnosis is typically based on clinical symptoms and the results of the heterophil antibody test. Infectious mononucleosis leads to the production of IgM antibodies that react with antigens completely unrelated to those that helped to induce them.2 In the first week of illness, this test is relatively unreliable. By the third week, 85% to 90% of infected patients will have positive results on the heterophil antibody test (monospot). The test has a specificity of 85% and a sensitivity of 97%.1 Approximately 15% of patients lack positive results on the heterophil test and will need specific EBV antibody studies to confirm infection. Serologie testing can also be useful when an early diagnosis may affect decisions regarding return to play.

Table

TABLEInterpretation of EBV Antibody Serology

TABLE

Interpretation of EBV Antibody Serology

An EBV infection can be confirmed by serologie testing of antibody levels. Four components are evaluated: IgG and IgM antibodies to the viral capsid antigen (IgG-VCA and IgM-VCA), EBV nuclear antigen antibodies, and EBV early antigen antibodies.1 In an acute infection, IgG and IgM directed to the capsid antigen rise, with a rise in the antibodies to the early antigen occurring later. Antibodies to nuclear antigen typically do not increase until months after the initial illness. The earlier presence of EBV nuclear antigen antibodies should suggest a secondary or reactivated infection (Table).

Other confirmatory laboratory findings include leukocytosis with significant lymphocytosis. Atypical lymphocytes are often present and commonly comprise 10% to 20% of all leukocytes.2 Patients may have a striking atypical Iymphocytosis of 40% or greater of all leukocytes. In such cases, a diagnosis of infectious mononucleosis is nearly certain and confirmation with the heterophil test may be unnecessary.3 Transient neutropenia and a mild decrease in platelet count may also be seen.2 Up to 90% of patients with infectious mononucleosis have transient abnormalities of liver function tests, suggesting a mild hepatitis. Most laboratory values return to normal by the fourth or fifth week of illness.2

The most serious complication is splenic rupture. Most authors estimate that 0.1% to 0.2% of cases of infectious mononucleosis will result in splenic rupture, but this has been as high as 0.5%.4 Spontaneous splenic rupture not associated with trauma has been reported. Indications of a splenic rupture include hypovolemia, left upper quadrant abdominal pain, and Kehr 's sign (left shoulder pain referred from diaphragmatic irritation).4 Patients may also have referred pain to the back or the right shoulder. One review of splenic ruptures in infectious mononucleosis found that all patients had spleens that were 2 to 3 times larger than normal (250 to 500 g) and palpable in fewer than 50% of the cases. Most ruptures occurred between the 4th and the 21st day of the illness, and a large proportion had "spontaneous rupture" (ie, with no associated traumatic event).2

Imaging for a suspected rupture can be performed by ultrasound or computed tomography. Although splenectomy had been the treatment of choice, nonsurgical management with intensive monitoring of hemodynamically stable patients has become an acceptable treatment strategy. Criteria for nonoperative management include hemodynamic stability, absence of other intraabdominal injuries on computed tomography scan requiring celiotomy, and limited need for splenic-related transfusion (s£ 2 units).5

Other complications include cranial nerve palsies, encephalitis, Guillain-Barré syndrome, pneumonitis, subclinical hepatitis, and airway obstruction.1'2 Death has been reported in 1 per 3,000 cases, usually due to hepatic failure.1

Treatment is symptomatic in most cases. Acetaminophen, ibuprofen, or acetaminophen with codeine is usually adequate for pain control.

Reye's syndrome has been reported in association with aspirin use and EBV infection, so aspirin should be avoided.6 Bed rest is also recommended. Stool softeners may be considered to minimize straining with bowel movements because this could theoretically increase the risk of splenic rupture. Corticosteroids are generally not recommended for the acute illness unless there is concern over airway obstruction or neurologic impairment.2 Oral acydovir has not reduced the duration of symptoms.7 If streptococcal pharyngitis is also posent, treatment with amoxicillin should be avoided because rash is nearly always associated with this. The presence of a rash while taking an antibiotic may give a false impression that there is an allergy to that antibiotic, when, in fact, the rash is more likely to be immune mediated.

Unfortunately, concrete guidelines for when to allow an athlete to return to athletic activity and competition are lacking. Most authors believe that athletes should refrain from physical activity for at least 3 to 4 weeks after the onset of symptoms.2-8 Rutkow advocates withholding athletes from sports for 6 months following the onset of infectious mononucleosis.9 Ii splenomegaly is still present at 3 to 4 weeks, it would be reasonable to continue to have the athlete avoid sports and reassess weekly, perhaps with imaging of the spleen until the spleen has returned to normal. Because most ruptures occur within the first 3 weeks after the onset of symptoms, some sports medicine physicians advocate a minimum of 3 weeks prior to returning to contact or collision sports.2-8

OTITIS EXTERNA (SWIMMER'S EAR)

Acute otitis externa, or "swimmer's ear," is inflammation and infection of the external auditory canal. The external canal uses cerumen as a natural defense against infection. Cerumen creates an acidic environment mat is inhospitable to pathogenic organisms. It is also hydrophobic, preventing water from causing damage to the thin, easily macerated skin of the auditory canal.10'11 Water can wash out the cerumen. This facilitates trauma and maceration of the skin in the canal and increases the pH, thus improving the environment for pathogenic organisms. The most common causes are Pseudomonas aeruginosa and Staphylococcus aureus.

Patients may present with a variety of symptoms. The two most common are otalgia and otorrhea. Initially, there may be minimal pain and pruritis. This may progress to a sensation of ear fullness, otorrhea, tenderness with manipulation of the ear, and erythema and edema of the ear canal. When symptoms are severe, pain with chewing and localized lymphadenopathy may occur.12

The gold standard for treatment is suction of the purulent discharge by an experienced health care professional via direct microscopic visualization. Gentle debridement can also be completed using a cotton swab that has had the cotton "fluffed out" to gently sweep out the discharge.11 The canal is only 2.5 cm deep. Irrigation with a syringe should not be attempted unless one can confirm there is no perforation of the tympanic membrane.

The use of a wick may be helpful when significant discharge or severe pain prevents adequate cleansing of the canal. The wick will facilitate delivery of topical antibiotics to the canal and allow for increased drainage.

Most infections respond to application of a topical solution of 2% acetic acid.11 The solution helps to create an acidic environment, rendering the ear canal less hospitable to the pathogens. This is, by far, the most cost-effective treatment.

Many topical antibiotic choices exist, including neomycin, polymyxin B, gentamicin, tobramycin, ciprofloxacin, and ofloxacin.11 The otic preparations tend to be more acidic than the ophthalmic preparations, which may justify switching to the latter if the acidity is too irritating. Dosing is generally 3 to 4 drops into the affected ear 4 times daily. The fluoroquinolones are more convenient because of twice daily dosing, but, in general, are more expensive than other choices. Recommendations for treatment duration vary, but treatment is usually continued for 2 to 3 days after the symptoms have resolved. Many mild infections will respond to these topical antibiotics without aggressive suctioning.

There are no agreed upon published guidelines concerning when to allow the athlete to return to water sports following otitis externa. Most authors recommend avoiding water sports for 2 or 3 days, but some advocate up to 10 days.10,11,13 Current recommendations focus on prevention, primarily through advocating using water-impermeable earplugs, blow drying the ear when getting out of the water, or using 70% ethyl alcohol drops as a preventive. Counseling must occur to avoid further trauma to the canal. The use of swim caps may also help prevent otitis externa.13

Figure 1. Wrestler with characteristic vesicular lesions of herpes giadiatorum at various stages of healing (new vesicles and crusting). Lesions are typically located on the forehead.

Figure 1. Wrestler with characteristic vesicular lesions of herpes giadiatorum at various stages of healing (new vesicles and crusting). Lesions are typically located on the forehead.

Figure 2. The same wrestler as in Figure 1 with herpes giadiatorum lesions on the neck and the upper trunk resembling the distribution of skin left exposed by the uniform.

Figure 2. The same wrestler as in Figure 1 with herpes giadiatorum lesions on the neck and the upper trunk resembling the distribution of skin left exposed by the uniform.

SKIN INFECTIONS

Herpes Giadiatorum

Herpetic skin lesions are not uncommon in die young athlete, particularly the wrestler. Herpes giadiatorum, so named because of the population it commonly affects, is an infection by herpes simplex virus type 1. It is estimated to affect 2.6% of high school and 7.6% of college wrestlers during a season.14 Infection occurs by direct skin contact with another individual's skin lesions. These lesions are primarily confined to the areas of greatest exposure in the wrestler (the head, the face, the upper extremities, and the trunk). In several outbreaks, more than 70% of the lesions were found on the head, 22% to 42% on the extremities, and 11% to 28% on the trunk.15,16

Individuals may have a burning or tingling sensation in the area of skin where lesions will subsequently arise, as is the case in other herpetic skin infections. Concurrent symptoms may include fever, chills, headache, sore throat, fatigue, and cervical lymphadenopathy. Lesions typically develop on the forehead (Fig. 1) and may initially appear as a raised erythematous rash rather than the more common vesicular lesions clustered around an erythematous base. As lesions progress to the healing phase, they will crust over. Many appear on the right side of the head and neck (Fig. 2) because of the position wrestlers assume during competition. Diagnosis can be made using a Tzanck stain for multinucleate giant cells of scrapings of the lesions. A complication of lesions on the face, particularly those near the eye, is herpes conjunctivitis or herpes blepharitis, which have been reported in outbreaks.16 Herpetic conjunctivitis can be diagnosed with fluorescein dye examination by noting the classic dendritic corneal ulcer seen during a Wood's lamp examination. Suspicion of this complication warrants early referral to an ophthalmologist for confirmation and treatment.

Current recommendations are to keep wrestlers from competition and practice until their lesions have fully healed. Most outbreaks resolve completely within 10 to 14 days. Treatment options include 200 mg of oral acyclovir 5 times per day for 7 days or 400 mg given 3 times per day for 7 days.17 One small study examined the use of valacyclovir for prevention of herpes giadiatorum.14 A significant reduction in outbreaks was observed in wrestlers who took 500 to 1,000 mg of valacyclovir orally once a day during the wrestling season. Prevention is an area that requires more research.

Figure 3. Tinea gladiatorum. This lesion has the characteristic scaly appearance, particularly of the leading edge of the rash, which is also seen with papular and pustular lesions.

Figure 3. Tinea gladiatorum. This lesion has the characteristic scaly appearance, particularly of the leading edge of the rash, which is also seen with papular and pustular lesions.

The physician should be aware of various methods wrestlers use to hide lesions. Makeup to hide the lesions, sandpaper to abrade them/ and methanol or household bleach to dry the lesions have been used.14 These methods are not believed to reduce the transmission of the virus, but are meant to fool an inexperienced examiner so that the wrestler may continue to compete.

Tinea Gladiatorum

Tinea gladiatorum is a "subset" of tinea corporis or ringworm (infection of the trunk and extremities). It is so named because of its uniqueness to the wrestler. Infection is caused by the dermatophyte Trichophyton tonsurans, which is also commonly seen in tinea capitis infections. Given the significant contact involving the head in "locked" positions in wrestling, it is not surprising that this dermatophyte also causes tinea gladiatorum infections. The wrestling environment is hospitable for dermatophytes. Occlusive clothing for weight loss, significant person-toperson contact/ and frequent mat burns contribute warm, moist environments and traumatized skin for the dermatophyte to thrive in.18 Although head gear and mats have been implicated as possible fomite reservoirs for G. tonsurane, no dermatophytes have been isolated from them.18

Lesions appear as a scaly, pruritic, erythematous rash on the trunk or extremities. The classic lesion has central clearing with surrounding erythematous and scaly elevated borders (Fig. 3). However, the physician must be aware that early lesions may not have the "classic" appearance. They may be mildly erythematous and scaly and not have central clearing or elevated borders.

Diagnosis can be confirmed with a potassium hydroxide preparation on a microscope slide using scrapings of the leading edge of the lesion and 10% or 20% potassium hydroxide. Under the microscope, hyphae appear as long, branching filaments of equal width.18 A culture can be performed using dermatophyte test media or Sabouraud's dextrose agar. Dermatophytes are notoriously slow growing organisms, limiting the clinical usefulness of cultures for guiding initiation of treatment.

Treatment of tinea gladiatorum is primarily by topical therapy. Options include over-the-counter clotrimazole 1% or miconazole 2% applied to the lesion twice daily for 2 to 4 weeks. Prescription options include econazole 1%, ketoconazole 2%, oxiconazole 1%, and sulconazole 1% also applied twice daily for 2 to 4 weeks.19 Agents in the allylamine group, including terbinafine 1% (over the counter) and naftifine 1%, can be used once or twice daily for 2 to 4 weeks. Terbinafine has been shown to persist in the skin at fungicidal concentrations for up to 7 days after the discontinuation of therapy.18

For cases that do not improve with topical therapy alone, oral therapy may include 500 mg of griseofulvin twice daily for 4 weeks, 100 mg of itraconazole daily for 15 days, 150 mg of fluconazole once per week for 3 to 4 weeks, or 250 mg of terbinafine daily for 2 to 4 weeks.18 A recent study examined the use of fluconazole for the prevention of tinea gladiatorum during a wrestling season.20 The use of 100 mg of fluconazole orally once per week reduced the infection rate to only 6% of wrestlers compared with 22% of the placebo group. The cost-effectiveness of fluconazole needs to be examined more thoroughly before further recommendations can be made regarding its use.

Several measures have been recommended to prevent tinea gladiatorum. These include removing sweaty or wet gear as soon as possible after practice or competitions, laundering practice gear daily, and showering immediately after practice.18 Wrestlers should be withheld from practice and competition until cleared by a physician or until they are being actively treated.18

Other Tinea Infections

Tinea pedís, also known as athlete's foot, is the most common dermatophyte infection in the athlete. A warm and moist environment, coupled with occlusive athletic footwear (socks and shoes), allows the dermatophyte to thrive. Trichophyton rubrum is the more common causative agent.

Lesions commonly present as macerated, white areas between the fourth and the fifth toe webs. They may also have a "moccasin type" distribution as hyperkeratosis of the soles and heels or acute pustular lesions on the midsole. These lesions are often pruritic.

Topical therapy similar to that used for tinea corporis is the usual treatment. Drying powders may help when used with the topical imidazoles and allylamines described for treating tinea gladiatorum. Oral therapy may be more effective in treating hyperkeratotic tinea pedis.19

Molluscum Contagiosum

Molluscum contagiosum is caused by a member of the poxvirus family. It is spread through direct contact with another individual via fomite transmission or autoinnoculation. Among athletes, swimmers and wrestlers are most commonly affected and swimming pools has been implicated as a method of spread.21 Lesions may occur on the face, the trunk, the extremities, and, occasionally, the genitals. Individual lesions are flesh-colored, domed papules with the characteristic central umbilication. They are generally 1 to 5 mm in diameter.21 Distribution may be in a small group or along a linear pattern described as Koebner lines.

Most patients have fewer than 20 to 30 lesions, although several hundred may be seen. Most lesions spontaneously regress in 6 to 9 months, but treatment may be necessary to allow return to play. The most common treatment regimens are curettage and cryosurgery. Many topical agents have been tried, including podophyllin, adhesive tape occlusion, salicylic acid, tretinoin, trichloroacetic acid, and silver nitrate, with varying success. Most authors advocate keeping athletes out of practice and competition until the lesions have resolved.17,22

Impetigo

Impetigo is the most common bacterial infection of the skin in children and can also be seen in contact sports such as wrestling, football, and hockey. The most common organisms cultured from lesions include group A beta-hemolytic streptococci (Streptococcus pyogenes) and S. aureus.

The two forms of impetigo are nonbullous and bullous. Nonbullous is most common, accounting for 70% of cases. However, lesions may vary from small vesicles to large bullae.17 There is often a history of preceding trauma to the skin, such as lacerations, abrasions, insect bites, or burns. Infection can rapidly develop, classically appearing as a "honey-colored" crusted plaque or serous fluid.23 Lesions may regress slowly during 2 weeks without scarring. Bullous impetigo, caused by coagulase-positive S. aureus, is not discussed here.

Topical or oral antibiotics may be used to treat impetigo. For smaller, more isolated lesions, topical therapy is preferred and may include neomydn, bacitracin, badtracin-polymyxin, gentamiun, and mupirocin.23 In more extensive lesions, cephalexin (40 to 50 mg/kg/d 3 times daily) would be a reasonable choice, as would erythromycin estolate (30 mg/kg/d 3 times daily) or ethylsuccinate (40 mg/ kg/d 3 times daily). Dicloxacillin (30 mg/kg/d 4 times daily) and clindamycin (15 mg/kg/d 3 times daily) are other alternatives.23 Duration of treatment is usually between 7 and 10 days. Topical mupirocin has been found to be as effective as most oral regimens for treating impetigo.23

Athletes with impetigo should be held from sports until lesions are cleared. These lesions are contagious, so athletes should be counseled to avoid sharing towels and equipment.

EFFECTS OF EXERCISE ON THE IMMUNE SYSTEM

A few studies have examined the effect of exercise on the immune system and infection rates in the adolescent population. Several have found no differences in the incidence of infection between those who participate in mildly strenuous exercise and those who are less active.24 Adult runners, who are considered to be in the strenuous exercise category, have been shown to have an increased incidence of upper respiratory tract infection (related to increased mileage) during the week after the race and compared with nonrunners.24

Some evidence exists that strenuous exercise in times of infection has negative effects on the course of the illness. The most recent American Academy of Pediatrics policy statement on medical conditions affecting sports participation recommends not allowing a young athlete to participate in sporting events if he or she has a fever.25 Reasons include the increase in cardiopulmonary effort, reduction in maximum exercise capacity, increased likelihood of heat illness, and increase in orthostatic hypotension during exercise. It is also believed that fever may rarely accompany myocarditis or other infections that make exercise dangerous. More research needs to be undertaken in this area to better comprehend the effect that infection has on exercise and vice versa.

REFERENCES

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2. Maki DG, Reich RM. Infectious mononudeosis in the athlete: diagnosis, complications, and management. Am J Sports Med. 1982;10:162-173.

3. Haines JD. When to resume sports after infectious mononucleosis: how soon is safe. Postgrad Med. 1987; 81:331-333.

4. Asgan MM, Begos DG. Spontaneous splenic rupture in infectious mononucleosis: a review. Yale J Biol Med. 1997; 70:175-182.

5. Pachter HL, Guth AA, Hofstetter SR, Spencer FC. Changing patterns in die management of splenic trauma: the impact of nonoperative management. Ann Surg. 1998;27:708-717.

6. Bailey RE. Diagnosis and treatment of infectious mononucleosis. Am Fam Physician. 1994;49:879-885.

7. Andersson J, Britton S, Emberg I, et al. Effect of acyclovir on infectious mononucleosis: a double-blind, placebocontrolled study. J Infect Dis. 1986;153:283-290.

8. Burroughs KE. Athletes resuming activity after infectious mononucleosis. Arch Fam Med. 2000;9: 1122-1123.

9. Rutkow IM. Rupture of the spleen in infectious mononucleosis: a critical review. Arch Surg. 1978;113:71 8-720.

10. Bojrab DI, Bruderly T, Abdulrazzak V. Otitis externa. Otolaryngol Clin North Am. 1996;29:761-782.

11. Sander R. Otitis externa: a practical guide to treatment and prevention. Am Fam Physician. 2001;63:927-936.

12. Boustred N. Practical guide to otitis externa. Ausi Fam Physician. 1999;8:217-221.

13. Nichols AW. Nonorthopaedic problems in the aquatic athlete. Clin Sports Med. 1999;18:395-411.

14. Anderson BJ. The effectiveness of valacyclovir in preventing reactivation of herpes gladiatorum in wrestlers. Clin J Sport Med. 1999;9:86-90.

15. Belongia EL, Goodman JL, Holland EJ, et al. An outbreak of herpes gladiatorum at a high-school wrestling camp. N Engl J Med. 1991325:906-910.

16. Becker TM, Kodsi R, Bailey P, Lee F, Levandowski R, Nahmias AJ. Grappling with herpes: herpes gladiatorum. Am J Sports Med. 1988;16:665-669.

17. Sevier TL. Infectious disease in athletes. Med Clin North Am. 1994;78:389-412.

18. Kohl TD, Lisney M. Tinea gladiatorum: wrestling's emerging foe. Sports Med. 2000;29:439-447.

19. Noble SL, Forbes RC. Diagnosis and management of common tinea infections. Am Fam Physician. 1998;58:1 63-174.

20. Kohl TD, Martin DC, Nemeth R, Hill T, Evans D. Fluconazole for the prevention and treatment of tinea gladiatorum. Pediatr Infect Dis J. 2000;19:717-722.

21. Lewis EJ, Lam M, Crutchfield CE 3rd. An update on molluscum contagiosum. Cutis. 1997;60:29-34.

22. Mellman MF, Podestà L. Common medical problems in sports. CKn Sports Med. 1997;16:635-662.

23. Darmstadt GL, Lane AT. Impetigo: an overview. Pediatr Dermatol. 1994;11:293-303.

24. Hughes WT. The athlete: an immunocompromised host. Ado Pediatr Infect Dis. 1998;13:79-99.

25. American Academy of Pediatrics. Committee on Sports Medicine and Fitness. Medical conditions affecting sports participation. Pediatrics. 2001;107:1205-1209.

TABLE

Interpretation of EBV Antibody Serology

10.3928/0090-4481-20020101-10

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