Athletic activities and the competitive sports environment present the athlete with unique exposures and risks for infectious diseases. Infections in athletes pose a significant public health concern because of a high frequency of close social and physical contact with teammates, coaches, support staff, and spectators, especially in organized sports at the high school, college, and professional levels. In most cases, the morbidity associated with infectious diseases is mild in this generally healthy population. However, in some rare cases, significant morbidity or even death may occur. Moreover, infectious diseases can disrupt the performance of an individual athlete or a team in competition.
Epidemiology
In sports, the three general modes of transmission of infection are (1) direct person-to-person contact, that is, through skin; (2) indirect contact (which may be respiratory, blood-borne, or fecal-oral); and (3) a common source, such as shared water coolers, athletic equipment, locker rooms, whirlpools, swimming pools, and contaminated freshwater venues. Athletes may be more susceptible to infection than the general population for several reasons. Athletes come into close physical contact with each other and may share personal items and equipment. Athletes often live in dormitories or hotel rooms while traveling and come into close contact with one another in these settings. Several studies suggest that athletes may be more likely than the general population to engage in risky behaviors. For example, fewer athletes practice safe sex, and athletes are more likely to use illicit drugs, alcohol, and injectable substances such as steroids and hormones, placing them at higher risk for intravenous needle exposures. Lastly, the growing popularity of adventure sports and eco-tourism places participants at risk for exotic illnesses.
Turbeville and colleagues performed a systematic review of the literature characterizing infectious disease outbreaks among athletes that occurred between 1966 and 2005. The skin was the most common site of infection, representing 56% of reported infectious disease outbreaks. Direct, person-to-person (skin-to-skin) contact was the most common mode of transmission. As might be expected, the majority of outbreaks occurred in high-contact sports such as football (34%), wrestling (32%), and rugby (17%). Outbreaks were also reported in soccer, adventure races, swimming, triathlon, track and field, gymnastics, basketball, and fencing. The most common pathogens are as follows: herpes simplex virus (HSV) (22%), Staphylococcus aureus (22%), enteroviruses (19%), tinea (14%), Streptococcus pyogenes (7%), hepatitis A and B viruses (7%), measles virus (5%), leptospira (3%), and Neisseria meningitides (3%). Norwalk virus, rickettsia, chlamydia, and pseudomonas infections were also reported. It is important to note that nonoutbreak infections also occur and that infections common in the general population are also common in athletes.
Exercise and the Immune System
Physical exercise is known to have important effects on the human immune system that may affect an athlete’s risk of infection. The human immune system consists of the innate immune system and the adaptive or acquired immune system. The innate immune system is set up to fight infection regardless of whether a person has been previously exposed. The innate system includes physical and functional barriers including the skin, mucous membranes, nasal hairs, areas of extreme temperature and pH, and debris removal systems such as the gastrointestinal tract and the mucociliary elevator. The innate immune system also fights infection through natural killer (NK) cells, phagocytes, and proteins such as tumor necrosis factor, cytokines, and the complement system. The acquired immune system is activated by exposure to specific antigens and provides long-lasting protection against anything it has previously encountered, but it does not immediately begin to fight new pathogens. It comprises T and B lymphocytes and their products, immunoglobulins (Ig), and cytokines. The acquired immune system produces IgM about 7 days after exposure to a new pathogen and IgG about 7 days later. Secretory IgA resides in mucous membranes and acts as a first line of defense against infection.
The relationship between the intensity and duration of exercise and the incidence of upper respiratory tract infections (URTIs) tends to follow a J-shaped curve, as illustrated in Figure 20-1 . It is thought that other infectious diseases may follow a similar pattern. Persons who exercise at moderate intensity have the lowest incidence of URTIs. Sedentary persons have a higher incidence of URTIs, whereas extreme exercisers have the highest risk. Moderate exercise, defined as exercise for 5 to 60 minutes within a range of 40% to 60% of the maximum heart rate, enhances the immune system by increasing neutrophil and NK counts, as well as salivary IgA concentrations. On the other hand, intense exercise, defined as 5 to 60 minutes of exercise at 70% to 80% of maximal heart rate, and prolonged exercise, that is, more than 60 minutes, has detrimental effects on the immune system. An increased requirement for oxygen necessitates transition from nose breathing to mouth breathing during intense exercise. In addition to bypassing the nasal hairs and turbulent flow that normally protects the lungs from exposure to pathogens, inhaling larger volumes of colder and drier hair also thickens mucus and disrupts the mucociliary elevator. Thus greater quantities of foreign particles reach the lungs, and the body’s natural defenses are impaired in their ability to clear them. With intense exercise, NK cell, lymphocyte, and neutrophil cell numbers fall, B-cell function decreases, and secretory IgA and serum IgG1, IgG2, and IgE concentrations decline. Levels of cortisol, prolactin, adrenaline, and growth hormone increase, thereby impairing cell immunity. A decrease in salivary lactoferrin and lysozyme concentrations impairs mucosal immunity. All of these factors contribute to a relative immunosuppression that may increase the risk of infection after intense exercise.
Prevention
Preventive efforts should focus on primary prevention—that is, avoiding infection before it occurs. Primary prevention includes immunization and good personal hygiene. Secondary prevention consists of infection control measures aimed at preventing the spread of disease to others or recurrence in the source patient, which may include isolation of infected persons or, in some cases, postexposure prophylaxis.
Immunization
Active immunization stimulates an immune response to protect against future exposure to an infectious organism by administering all or part of a microorganism, or a modified product of the microorganism, such as antigens or proteins. Most vaccines are more than 90% effective, but they are not guaranteed to provide immune protection. Before participation in organized sports, a physician should verify that the athlete has received appropriate immunizations and administer “catch-up immunization” if necessary. Athletes traveling abroad should consider the diseases endemic in the geographic area to which they are traveling. Ideally, immunizations should be planned at least 4 months in advance to ensure adequate time for administration.
Hygiene
Good personal hygiene can help reduce the transmission of infectious agents among athletes. The following general measures are advisable :
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Use universal body fluid precautions; wash hands frequently and always use disposable gloves when coming into contact with bodily fluids, the oral cavity, or wounds.
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Avoid sharing personal items (e.g., soap, towels, and water bottles), food, and water.
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Routinely clean shared equipment; bleach diluted with tap water in a 1 : 10 ratio is an effective cleanser.
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Any athlete with skin lesions that are weeping or leaking blood or serous fluid should be excluded from play until the area has dried and can be securely covered with occlusive bandages or dressings.
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Athletes should be instructed to report all illnesses or skin lesions promptly.
Return-to-Play Guidelines
Appropriate and timely guidelines are pivotal for prevention. The decision about whether an athlete may return to play after experiencing an infectious illness is based on a number of factors, including the judgment of physicians, coaches, and individual athletes. The first consideration is the effect of athletic activity on the health and safety of the individual athlete. Another important consideration is preventing the transmission of infectious diseases to teammates, support staff, coaches, and spectators. Frequent close contact during practice, in locker rooms, and in shared living spaces, as well as sharing of equipment and facilities, create abundant opportunities for spreading and acquiring illness.
Exercise may prolong or intensify the disease course or cause dangerous complications. Fever inhibits fluid and temperature regulation while also impairing coordination, concentration, muscle strength, aerobic power, and endurance. Viral illnesses contribute to tissue wasting, muscle catabolism, and negative nitrogen balance. Drugs used to treat infectious diseases may also have considerable effects on the athlete. For example, quinolone antibiotics carry a risk of tendon rupture. The use of compounds that contain ephedrine, which is banned by many sports organizations, may lead to disqualification of an athlete. Finally, illness may limit an athlete’s performance in competitive sports. Pain, discomfort, and other symptoms of infection can be distracting during play.
A good rule of thumb traditionally used in sports medicine is Eichner’s “neck check.” Athletes should not work out while experiencing systemic symptoms (e.g., fever or myalgias) or symptoms below the neck (such as a hacking cough, vomiting, or diarrhea). If symptoms are limited to above the neck, such as a runny nose, watery eyes, or sore throat, the athlete can attempt a “test drive.” The athlete exercises at “half speed,” and if he or she feels better after 10 minutes, it should be safe to complete the workout at a tolerated intensity. Where specific return-to-play guidelines exist, they will be discussed in their corresponding sections.
Skin and Soft Tissue Infections
Skin and soft tissue infections comprise most common infectious disease outbreaks in athletes, representing 56% of outbreaks. Participants in contact sports such as wrestling, football, and rugby are at highest risk of acquiring such an infection. Frequent skin trauma, moist environments, and direct contact with equipment and other players are all factors that make athletes particularly vulnerable to these infections. The most common causative agents are S. aureus and HSV, each constituting 22% of reported infectious disease outbreaks. During the past decade, methicillin-resistant S. aureus (MRSA) has emerged as a common cause of superficial skin infections in the community and has been known to affect a significant number of athletes at the high school and collegiate level. Although most skin infections resolve without complication, they are highly contagious and can result in significant loss of playing time and thus warrant prompt recognition and treatment. The Centers for Disease Control and Prevention and the American College of Sports Medicine recommend the following preventive measures:
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Practice good personal hygiene: minimize contact, wash hands frequently, shower with hot soap and hot water after all practices and competitions, and wear sandals in public showering facilities.
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Avoid sharing items that come in contact with skin (e.g., razors, clothing, linens, and towels).
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Discourage body shaving, which increases the risk of trauma and predisposes to infection.
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Cover wounds (including abrasions, blisters, and lacerations) until they have healed. When wounds cannot be properly covered (by a securely attached bandage that will contain all drainage and remain intact throughout the activity), athletes should be excluded from play.
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Immediately inform coaches of any skin lesions.
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Athletes with active infections or open wounds should avoid common-use water facilities such as swimming pools.
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Clean high-touch surfaces (i.e., surfaces that come in frequent contact with people’s bare skin each day), including counters, doorknobs, bathtubs, and toilet seats.
When an athlete is diagnosed with a skin infection, care should be taken to appropriately document the diagnosis and treatment to ensure adequate treatment and guarantee meeting return-to-play guidelines. Documentation should include the diagnosis, culture results, date and time of initiation of therapy, and exact names of medications used.
Bacterial Skin Infections
Definition
Superficial bacterial skin infections are most often caused by Streptococcus or Staphylococcus species. The prevalence of MRSA has risen dramatically in the community during the past decade. MRSA is a type of staphylococcal bacteria that is resistant to traditional penicillin-based antibiotics and has historically affected patients in health care settings.
Epidemiology
Open or broken skin is the biggest risk factor for bacterial skin infection. Close skin-to-skin contact, contact with contaminated items and surfaces, crowded living conditions, and poor hygiene also place a person at risk for bacterial skin infection. Whereas 25% to 30% of people are colonized in the nose with Staphylococcus, fewer than 2% are colonized with MRSA. S. aureus and HSV are the most common causes of infectious disease outbreaks in athletes, with each responsible for 22% of outbreaks.
Pathobiology
Bacterial skin infections have a variety of clinical presentations. S. aureus and MRSA commonly present as folliculitis, furuncles or “boils” (abscessed hair follicles), carbuncles (coalesced masses of furuncles), and abscesses. Impetigo describes a weepy skin lesion with a honey-colored crust. Erysipelas (a superficial infection of the skin with well-demarcated borders) and cellulitis (subcutaneous involvement with possible systemic symptoms) are most commonly caused by group A Streptococcus and Staphylococcus species in the athletic population. More virulent strains of Staphylococcus , including MRSA, can cause osteomyelitis, sepsis, toxic shock syndrome, and necrotizing pneumonia.
Diagnosis
The hallmarks of a bacterial skin and soft tissue infection include redness, swelling, warmth, and pain/tenderness. MRSA should be considered in the differential diagnosis of any such skin lesions. Cellulitis and abscesses are both considered to be types of superficial wound infections. Cellulitis demonstrates features of both skin erythema and increased warmth and can be more diffuse in nature ( Fig. 20-2 ). An abscess, on the other hand, involves a localized collection of purulent material ( Fig. 20-3 ). MRSA infections are commonly mistaken for spider bites. On physical examination, lesions suspicious for MRSA are purulent, exhibiting fluctuance (i.e., a palpable, movable, compressible fluid-filled cavity), a yellow or white center, and a central point or head ( Fig. 20-4, A and B ). They are commonly found at sites of visible skin trauma and areas of the body covered by hair. Nonpurulent cellulitis or erysipelas strongly suggests Streptococcus as the causative agent. Bacterial skin infections may resemble insect bites, trauma, superficial burns, contact dermatitis, acne, tinea, dermatophytes, or herpes simplex virus. A gram stain may elucidate the diagnosis in uncertain cases. A culture of the skin lesion may be useful in cases of recurrent or persistent infection, antibiotic failure, or advanced or aggressive infections.
Treatment and Prevention
In 2011, the Infectious Diseases Society of America released evidence-based guidelines for the empiric treatment of bacterial skin infections based on clinical features. Simple infections presenting as impetigo, simple abscesses, furuncles, and carbuncles may resolve by applying moist heat and/or applying mupirocin topically, twice daily for 10 days. Incision and drainage is the mainstay therapy for simple infections that do not resolve when treated with moist heat and mupirocin. Drainage fluid should be sent for culture and susceptibility testing to direct antibiotic therapy. In addition to incision and drainage, empiric antimicrobial therapy with coverage for MRSA should be considered if the lesion is severe or extensive (e.g., involving multiple sites, associated with cellulitis, or having signs and symptoms of systemic illness), located in an area that is difficult to drain (such as the face, hand, and genitalia), or fails to respond to incision and drainage alone after 48 hours, or if the patient is immunosuppressed or at the extremes of ages. Five to 10 days of therapy is recommended. If cellulitis is present without evidence of purulence or abscess, the causative organism is more likely to be Streptococcus and can be treated with a β-lactam antibiotic (e.g., first-generation cephalosporin). If it fails to improve or the patient experiences systemic symptoms, treating physicians should strongly consider the possibility of community-associated MRSA. The treatment of purulent cellulitis warrants empiric treatment for MRSA with trimethoprim-sulfamethoxazole, doxycycline, clindamycin, linezolid, or minocycline.
No clear evidence exists for the effectiveness of decolonization therapy for recurrent MRSA skin and soft tissue infections. However, decolonization may be considered if (1) the patient experiences recurrent skin and soft tissue infections despite optimizing hygiene and wound care or (2) ongoing transmission is occurring among close contacts despite optimization of hygiene and wound care. Decolonization methods include use of nasal mupirocin, skin antiseptic solution (e.g., chlorhexidine), or dilute bleach baths. Oral antimicrobial therapy is recommended only for the treatment of active infection. An oral agent in combination with rifampin may be considered for decolonization if infections recur despite use of the aforementioned methods.
Return-to-Play Guidelines
Return-to-play guidelines for all bacterial skin infections (e.g., furuncles, carbuncles, folliculitis, impetigo, cellulitis, erysipelas, staphylococcal disease, and community-acquired MRSA) are grouped together. As published in the National Collegiate Athletic Association (NCAA) guidelines for wrestling, the following criteria apply before returning to play :
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The athlete must have no new skin lesions for 48 hours before participating in a tournament or practice.
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The athlete must have completed 72 hours of oral antibiotic therapy (the National Federation of High Schools requires oral antibiotic therapy for 48 hours).
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The athlete must have no moist, exudative, or draining lesions while participating in a tournament or practice.
Although no specific guidelines are outlined for other sports, the guidelines for wrestling should be followed for other contact sports (such as football and rugby), sports with shared equipment or facility use (such as gymnastics or aquatic sports), and noncontact sports on a case-by-case basis. All dry lesions should be covered during play.
Herpes Simplex Virus
Definition
HSV can cause primary or recurrent infections and is highly contagious. HSV infections are exceedingly common in the general population and sufficiently prevalent in the athletic population that special terms were coined to describe outbreaks in sports medicine: “Herpes gladiatorum” originally was used to describe HSV infection in wrestlers, and “scrumpox” was used to describe HSV in rugby players.
Epidemiology
HSV is responsible for 22% of infectious disease outbreaks in athletes, making it the most common pathogen encountered, along with MRSA. One survey reported that the annual incidence of HSV lesions was 7.6% among college wrestlers and 2.6% among high school wrestlers. Transmission can occur by direct skin-to-skin contact or bodily fluids including saliva, semen, and vaginal secretions. It is estimated that the likelihood of contracting herpes when sparring with an infected partner during an active outbreak is 32.7%.
Pathobiology
HSV-1 is the most common cause of herpes labialis (affecting the lips), and HSV-2 is the most common cause of urogenital herpes. Primary infection occurs after an incubation period of 2 to 20 days and may be accompanied by systemic symptoms including fever, adenopathy, malaise, myalgias, and headache. HSV remains latent in the neural ganglia, and reactivation may occur in the setting of reexposure, autoinoculation, physical or emotional stress, poor nutrition, ultraviolet radiation, fever, coexisting infection, or immunosuppression. Reactivation skin lesions are typically preceded by a prodromal phase of neuralgia, tingling, or burning sensations. Systemic symptoms are typically absent in reactivation. Lesions most commonly present on the lips, head, extremities, and trunk but can also affect the eyes.
Diagnosis
Diagnosis is typically made on the basis of the characteristic clinical appearance of the lesions. Herpetic lesions form a cluster of vesicles on an erythematous base. Vesicles may ulcerate and leave a shallow painful ulcer with surrounding erythema. Lesions subsequently crust or scab while healing, and complete resolution may take up to 2 to 3 weeks. Laboratory testing can be performed to confirm questionable diagnoses but is not required. Viral isolation from tissue culture is the test of choice. A Tzanck test of fluid from a vesicle reveals characteristic multinucleated giant cells.
Treatment
Oral systemic antiviral medication for 5 days is the standard treatment for HSV outbreaks to reduce the duration of the outbreak and time to complete lesion healing. Medications are effective if taken within the first 48 hours of the appearance of any lesion. Acyclovir, valacyclovir, and famciclovir are commonly used. Athletes with a history of recurrent herpes labialis or herpes gladiatorum should be considered for season-long suppressive therapy. Ocular herpes requires an urgent ophthalmologic referral.
Return-to-Play Guidelines
Athletes engaged in contact sports should refrain from playing until all lesions are dry with a firm adherent crust and until the athletes have been taking an appropriate dose of systemic antiviral therapy for at least 120 hours. The NCAA guidelines for return to play for wrestlers after HSV infection are summarized in Table 20-1 . Although no official guidelines are available for other sports, these same guidelines can be used to guide return to play for all other contact sports.
| Nature of Infection | Guidelines |
|---|---|
| Primary | Free of systemic symptoms (e.g., fever and malaise) |
| No new blisters for 72 hours before practice or tournament | |
| No moist lesions; must be dried and surrounded by a firm adherent crust | |
| Must have been taking an appropriate dose of a systemic antiviral therapy for at least 120 hours before and at the time of practice or play in a tournament | |
| Recurrent | No moist lesions; must be dried and surrounded by a firm adherent crust |
| Must have been taking an appropriate dose of systemic antiviral therapy for at least 120 hours before and at the time of practice or play in a tournament | |
| Questionable cases | Tzanck preparation and/or herpes simplex virus antigen assay |
Fungal Skin Infections
Definition
Superficial fungal skin infections are caused by dermatophytes, and nomenclature is based on the location of lesions on the body. Tinea capitis refers to infection of the skin and hair on the scalp. Tinea corporis, also known as ringworm, refers to infections on the body. Tinea cruris, or jock itch, is the term used to describe groin infections. Foot infections are called tinea pedis or athlete’s foot. Tinea gladiatorum describes fungal infections of the skin or scalp in athletes.
Epidemiology
Fungal infections affect between 10% and 20% of the population worldwide, with tinea pedis being the most common clinical manifestation; 70% of adults experience tinea pedis in their lifetime. Tinea pedis is common in athletes, with an infection rate of about 35%, and it is especially common in swimming pool users and marathon runners.
Pathobiology
The causative agents of fungal skin infections are dermatophytes. The major genera of dermatophytes are Trichophyton, Microsporum, and Epidermophyton . Dermatophytes are transmitted by direct person-to-person contact, animal-to-human contact, contact with fomites, or directly from the soil. Dermatophytes infect the stratum corneum layer of the skin. The host responds by increasing proliferation of the basal cell layer, resulting in epidermal thickening and scale formation. The characteristic tinea corporis lesion is singular, well-defined, erythematous plaque with an expanding red, raised ring and a central clearing, often accompanied by flaking and pruritus. Tinea corporis in athletes most commonly affects the head, neck, trunk, and upper extremities. Tinea capitis is characterized by an annular patch of hair loss and a gray hyperkeratotic plaque. Tinea cruris affects the pubic area, inguinal folds, and medial thighs. Tinea pedis can present as the interdigital type, with red, weeping, macerated skin and fissures in the web space between toes; the moccasin type, with plaques on the sole and sides of the foot; or the bullous type, with vesicles or bullae filled with clear fluid.
Diagnosis
Dermatophyte infection may be diagnosed clinically based on the characteristic appearance of the skin lesions. Questionable cases may be confirmed by direct microscopy of a potassium hydroxide (KOH) preparation demonstrating septated hyphae. A fungal culture using Sabouraud dextrose agar may be performed if lesions are suspicious but the KOH preparation is negative. Tinea capitis can be distinguished from other causes of localized alopecia by its characteristic gray hyperkeratotic plaque. Tinea corporis and tinea cruris may be distinguished from impetigo, psoriasis, lichen planus, seborrheic dermatitis, pityriasis rosea, and secondary or tertiary syphilis with use of a KOH preparation or fungal culture. Erythrasma, a Corynebacterium infection, may resemble tinea cruris, but examination under a Wood’s light reveals a coral-red color.
Treatment and Prevention
Topical or oral medications may be used to treat cutaneous fungal infections. For the general population, topical therapy is the first-line treatment for tinea corporis and tinea cruris. Oral medications can have significant adverse effects and are thus reserved for extensive or disabling disease, patients for whom topical therapy has failed, and patients who are immunosuppressed. However, tinea capitis requires treatment with an oral agent. When possible, wrestlers and participants in contact sports should also be treated with oral fungicidal medications. Topical agents include imidazoles, allylamines, and napthiomates. Standard duration of treatment is 2 to 4 weeks, and common regimens include terbinafine 1% cream one to two times daily, ketoconazole 2% cream once daily, or clomitrazole cream, lotion, or solution once daily. Oral agents include fungicidal drugs such as allylamines and fungistatic drugs such as imidazoles and griseofulvin. Fungicidal drugs are often preferred because they require shorter courses of therapy. Showering daily after practice or play, drying thoroughly, and wearing cotton socks and underwear can help reduce the incidence of fungal rashes.
Return-to-Play Guidelines
As with other skin infections, athletes with active tinea lesions should refrain from participating in contact sports until the infection has cleared and been adequately treated to avoid transmission to other athletes. The affected athlete should have completed a minimum of 72 hours of topical therapy for skin lesions and a minimum of 2 weeks of systemic antifungal therapy for scalp lesions. Resolution of treated lesions can be evaluated by KOH preparation or review of the therapeutic regimen. All lesions should be covered with a gas-permeable dressing. If lesions are extensive and cannot be adequately covered, the athlete should refrain from play.
Upper Respiratory Tract Infections
Epidemiology
A URTI, or the common cold, is the most common acute illness in the general population. It affects every healthy adult one to six times each year, especially during the fall and winter seasons, and thus it is also the most common infection seen among athletes. Transmission occurs through (1) direct contact, when secretions are transferred from hand to hand, then from hand to mucus membranes of the nose or eyes, or (2) respiratory transmission via small-particle aerosols and large-particle droplets. Athletes have an elevated risk of exposure because of a high frequency of close contact while practicing and traveling together.
Pathobiology
The vast majority of URTIs have a viral etiology: rhinoviruses (40%), coronaviruses (20%), respiratory syncytial virus (10%), influenza virus, parainfluenza virus, and adenovirus. Two to 3 days after exposure, a patient typically experiences rhinorrhea, cough, and fever. URTIs are generally self-limiting and last 5 to 14 days. Complications may include acute sinusitis, lower respiratory tract infection, otitis media, and asthma exacerbation. URTIs are a common trigger for asthma attacks and are estimated to be responsible for 40% of asthma attacks.
Inflammation of the paranasal sinuses, especially maxillary and frontal sinuses, are caused by the same viruses that cause URTIs, and approximately 2.5% of adult patients experience acute bacterial sinusitis as a complication after a URTI. Acute bacterial sinusitis is most commonly caused by Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, S. aureus, and anaerobes. Athletes who participate in swimming, diving, water polo, and surfing seem to have a higher incidence of sinusitis.
Diagnosis
Laboratory testing is not routinely needed for URTIs; the diagnosis is clinical and treatment is based on symptoms. Acute bacterial sinusitis should be suspected in patients whose URTI symptoms are accompanied by purulent nasal discharge and maxillary or facial pain and who demonstrate poor response to decongestants or abnormal transillumination. Sinus aspirate culture is the gold standard for diagnosing sinusitis, but it is rarely performed because of its invasive nature. Imaging studies such as a computed tomography (CT) scan or magnetic resonance imaging (MRI) may be used if disease persists despite optimal therapy.
Treatment and Prevention
URTIs are treated symptomatically with oral decongestants and antihistamines or nasal decongestant sprays, analgesics, and antipyretic agents. The use of compounds that contain ephedrine, including many oral decongestants, is banned by many sports organizations and may lead to disqualification of an athlete. Athletes should take care to remain adequately hydrated. If the URTI is caused by an influenza virus, a neuraminidase inhibitor such as zanamivir or oseltamivir may decrease the severity and duration of symptoms if it is initiated within 48 hours of exposure. Antibiotics are not beneficial for simple URTIs but may be useful for acute bacterial sinusitis if symptoms worsen over 5 to 7 days or fail to improve after 10 days. Empiric treatment for acute bacterial sinusitis is amoxicillin for 10 to 14 days. Influenza vaccine has an efficacy of 70% to 90%, and thus athletes without contraindications should be vaccinated annually.
Return-to-Play Guidelines
In the case of a simple URTI, return to play generally depends on the athlete. It can be expected that athletic performance may be adversely affected during illness, but exercise does not seem to alter the course of the illness. Sedentary subjects who exercised after getting a URTI did not experience an effect on symptoms or duration of illness. The “neck check” principle applies; as long as the patient is afebrile and symptoms described are “above the neck,” an athlete may continue physical activity as tolerated.
Infectious Mononucleosis
Definition
Infectious mononucleosis (IM), a common medical condition caused by Epstein-Barr virus (EBV), warrants special mention for two reasons: (1) epidemiologically, it is most clinically significant in the adolescent and young adult age group, which is the primary age group engaged in athletic activity, and (2) the most feared complication of IM, splenic rupture, raises important questions for sports medicine physicians making decisions for suitability of an athlete to return to play.
Epidemiology
The prevalence of IM in the general population is 45 cases for every 100,000 people. Antibodies to EBV eventually develop in approximately 95% of adults, indicating prior infection. The peak incidence of IM occurs in 15- to 25-year-olds, and this age group is also most likely to experience acute symptomatic infection. Symptoms rarely develop in adults older than 35 years and in children younger than 15 years.
Pathobiology
EBV is a DNA herpesvirus that is transmitted via oropharyngeal secretions, and it is thus referred to as the “kissing disease.” It may be acquired through sharing drinks or eating utensils and through aerosolized secretions from sneezing and coughing. EBV enters squamous epithelial cells of the oropharynx and has also been isolated from epithelial cells of the cervix and semen. It is often difficult to identify the source because EBV has a very long incubation period of 30 to 50 days before the onset of symptoms. The classic triad of IM is fever, sore throat, and lymphadenopathy. Patients often experience a prodrome of malaise, headache, and high fever that can last up to 3 weeks. Splenomegaly occurs in 50% to 100% of patients. A rash on the trunk and upper arms occurs in 10% to 40% of patients and is more common in persons treated with ampicillin or amoxicillin.
Whereas most cases of IM are moderate in severity and resolve without complication, complications have the potential to be severe. Reported but rare complications include Guillain-Barré syndrome, meningitis, neuritis, hemolytic uremic syndrome, disseminated intravascular coagulation, and aplastic anemia. In the athletic population, three complications are of particular concern:
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Severe tonsillar enlargement leading to acute respiratory compromise
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Prolonged fatigue limiting return to pre-illness level of activity for up to 3 months
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Splenic rupture, which, although extremely rare, usually occurs within the first 3 weeks of symptomatic illness
It is thought that lymphocytic infiltration of the spleen disrupts its normal anatomy, weakening supporting structures and increasing splenic fragility. Rupture can be caused by trauma in the setting of a sudden increase in portal venous pressure from a Valsalva maneuver or compression from external trauma. The occurrence of spontaneous rupture in the absence of trauma has been reported in only a handful of cases.
Diagnosis
Clinical assessment remains the predominant method of diagnosing IM. The differential diagnosis should include viral or bacterial pharyngitis, Streptococcus, Gonococcus, human immunodeficiency virus (HIV), and cytomegalovirus. It is particularly important to test for Streptococcus , with which an estimated 30% of patients with IM are coinfected. Untreated group A, β-hemolytic streptococcal infections may result in glomerulonephritis or rheumatic fever.
On physical examination, fever is often high and can be greater than 104 ° F. Exudative tonsillar pharyngitis is present and may be accompanied by palatal petechiae. Lymphadenopathy is typically painful and most commonly affects the posterior cervical chain. Axillary and inguinal involvement may help to differentiate IM from other forms of viral or bacterial pharyngitis. Laboratory findings of leukocytosis in the range of 12,000 to 18,000 white blood cells with greater than 50% lymphocytes and at least 10% atypical lymphocytes on a peripheral blood smear are highly suggestive of IM. The monospot test for heterophile antibodies is specific but not sensitive, especially early on in the disease course. The false-negative rate is 25% in the first week but drops to 5% in the third week. In children younger than 10 years, the monospot test detects fewer than 50% of EBV infections. In a small minority of patients, a seropositivity for heterophile antibodies will never develop. When the monospot test is negative, and IM is strongly suspected, EBV titers can be obtained. Specific antibody tests for EBV include viral capsid antigen (VCA), immunoglobulin G (IgG), and immunoglobulin M (IgM) antibodies, along with antibody to Epstein-Barr nuclear antigen. VCA IgM appears early in infection and disappears after 4 to 6 weeks. VCA IgG peaks at 2 to 4 weeks after onset and then declines slightly and persists for life. Epstein-Barr nuclear antigen antibody appears after 2 to 4 months and persists for life.
Splenomegaly is almost universal, but no gold standard exists for its diagnosis. The utility of bedside examination to detect splenomegaly is limited. Both palpation and percussion are recommended, but they have a sensitivity of 46% and a specificity of 97%. Physical examination may further be limited by the rigid abdominal musculature of athletes. Few data exist to support the use of diagnostic imaging to evaluate for splenic size. When evaluating for splenomegaly, serial measurement by ultrasound is preferred rather than CT because of its lower cost and the avoidance of radiation exposure. Although the spleen can be accurately sized, spleen size varies greatly between persons, and no normative data are available. Without knowing a baseline spleen size, one cannot determine whether a patient has splenomegaly, but serial studies may be helpful. If splenic injury is suspected, CT or MRI is preferable compared with ultrasound to acquire higher resolution images.
Treatment and Prevention
IM is generally self-resolving, and thus the mainstay of treatment is symptomatic relief and supportive care: fever control, analgesia for pharyngitis, rest, and hydration. Antiviral medications have not been shown to diminish the severity or duration of symptoms. All patients should be evaluated for coexisting streptococcal pharyngitis. If present, it should be treated with antibiotics other than amoxicillin and ampicillin, which may provoke rashes in patients with IM. Oral corticosteroids may be helpful if the course is complicated by hepatitis, myocarditis, hemolytic uremic syndrome, neurologic complications, or airway obstruction. Patients should be advised to avoid consumption of excessive alcohol, acetaminophen, and other liver toxins. Athletes should be advised that EBV is present in oropharyngeal secretions. Avoiding contact with secretions through the sharing of food, eating utensils, water bottles, and kissing may decrease risk of transmission.
Return-to-Play Guidelines
The decision about when an athlete can return to play after an IM infection is difficult because the risk of splenic rupture is not well characterized. The consensus statement by the American College of Sports Medicine states that light, noncontact activity may be gradually introduced as tolerated 3 weeks after illness onset, provided that the patient is afebrile, has good energy levels, and has no other complications. Although splenic rupture can occur with trauma, most ruptures are atraumatic and occur in the first 3 weeks of illness. During this time, athletes should be advised to avoid chest or abdominal trauma, significant exertion, or Valsalva activities including weightlifting and rowing.
The American College of Sports Medicine recommends avoiding contact or collision sports until 4 weeks after the onset of illness. However, it is important to remember that splenic rupture has been reported to occur up to 7 weeks after the onset of illness. Athletes should be aware that the risk of splenic rupture decreases with time but is never zero. Many persons advocate that the athlete should have a “normal”-sized spleen before returning to play, with the thought that risk of rupture may be highest when the spleen is enlarging. In reality, the relationship between splenomegaly and rupture is unclear. Because of the limitations previously discussed, it is not standard practice to determine splenic size using diagnostic imaging. Serial ultrasonography may be useful in cases in which the patient becomes clinically asymptomatic early and is considering early return to play. Prolonged fatigue may limit full performance status for as long as 3 months.
Measles
Definition and Epidemiology
Measles, or rubeola, is an acute, highly contagious viral illness. Airborne measles outbreaks have been known to occur in indoor sports among gymnasts, wrestlers, basketball players, and spectators in crowded and humid gymnasiums and sports domes. Measles is still endemic in many countries worldwide and results in an estimated 800,000 deaths per year. In the United States, between 1996 and 2000, the incidence of measles was less than 1 case per million. Approximately 62% of cases were internationally imported, but a number of cases had an unknown source. The majority of infections occur in unvaccinated patients (46%) and in patients in whom vaccination status was unknown (27%), but 27% of cases in the year 2000 occurred in patients with a documented history of measles vaccination.
Pathobiology
Measles is primarily transmitted directly via respiratory droplets traveling over short distances and less commonly via small-particle aerosols that persist in the air for a long time. During the incubation period of 10 to 14 days, the measles virus replicates initially in the epithelial cells of the upper respiratory tract and then spreads to local lymphatic tissue, the blood, and many organs including the lymph nodes, skin, kidney, gastrointestinal tract, and liver. The host cellular immune response at the sites of replication produces signs and symptoms. Persons with impaired cellular immunity may have absent or delayed presentation of symptoms. The prodromal phase of measles presents with fever, cough, coryza, and conjunctivitis. Koplik spots, which are small white lesions on the buccal mucosa during the prodromal phase, are diagnostic for measles. Several days before the onset of rash, prodromal symptoms intensify. The characteristic rash is an erythematous macropapular eruption beginning on the face and then spreading to the trunk and extremities, which lasts for 3 to 5 days. Patients are infectious for several days before and after the onset of the rash.
In uncomplicated cases of measles, resolution begins shortly after the appearance of the rash. However, after infection with measles, persons have depressed immunity as a result of delayed-type hypersensitivity and are thus more susceptible to secondary bacterial or viral infection. Consequently, approximately 40% of cases are followed by complications, including pneumonia, laryngotracheobronchitis, keratoconjunctivitis, stomatitis, and diarrhea. Rare but serious central nervous system (CNS) complications may occur 2 weeks to several years after infection, including postmeasles encephalomyelitis, measles inclusion body encephalitis, and subacute sclerosing panencephalitis.
Diagnosis
Measles should be suspected in any patient who presents with fever and a generalized rash. The differential diagnosis includes other viral exanthems such as rubella. Koplik spots are diagnostic of measles prior to the appearance of a rash. A physical examination should include investigation for secondary viral or bacterial infections. The diagnosis of acute measles can be confirmed with serology. The most common test is detection of measles virus–specific IgM in serum or oral secretions, but it may not be detectable for 4 days after rash onset and disappears within 4 to 8 weeks of infection. Levels of measles virus–specific IgG four times greater than convalescent levels may also be diagnostic of an acute infection.
Treatment
The World Health Organization recommends administration of vitamin A, 200,000 international units daily for 2 consecutive days, for all patients older than 12 months to treat measles and reduce morbidity and mortality. No specific antiviral agents are indicated for treatment of measles, but ribavirin, interferon-β, and other antiviral drugs are used in persons with severe infections. Antibiotics may be required if the patient is coinfected with bacteria. S. pneumoniae and H. influenzae b are common pathogens. An attenuated vaccine is available and is the best available method of primary prevention.
Return-to-Play Guidelines
Athletes with suspected measles should be isolated from other players expediently. All cases of measles should be reported to public health authorities to administer appropriate infection control measures.
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