Infections in Young Elite Athletes: Risks, Impacts and Prevention

Infections are the leading medical issue among adolescent elite athletes, accounting for 30%–70% of all illness-related consultations during a competitive season.1 Studies from Olympic and World Championship events show that nearly 50% of acute illnesses are respiratory, while gastrointestinal (GI), skin and genitourinary infections comprise the remainder.2,3 Infections are a common cause of missed training and competition in young athletes. Upper respiratory tract infections (URTIs) predominate, with an estimated incidence of 4.7 episodes per athlete-year.4 Even a single week of illness-related training disruption can reduce the likelihood of achieving performance goals by up to 25%.5 GI and skin infections are also frequent, especially in team environments. Outbreaks of gastroenteritis (eg, norovirus, Salmonella) have been linked to shared meals and accommodations, while skin infections such as impetigo, tinea and herpes are prevalent in contact sports.6,7 Data on the etiology and outcomes of infections in this population remain limited, often based on retrospective studies lacking microbiological confirmation.8 The absence of high-quality evidence hinders the development of sport-specific guidelines, particularly those addressing the pediatric population. Entry age into professional sports ranges from 13 to 19 years in various disciplines.9 Young athletes frequently under-report symptoms to avoid missing play.10,11 Accordingly, vaccinations, implementation of preventive measures, early detection of infectious diseases and careful medical evaluation are essential to ensure safe and effective athletic development in adolescent elite athletes. PATHOGENS AND ROUTES OF EXPOSURE Pathogen distribution among athletes largely reflects that of the general population. Rhinoviruses, human coronaviruses, influenza, respiratory syncytial virus, adenoviruses and SARS-CoV-2 are the predominant pathogens.1 Norovirus, Salmonella spp. and Giardia cause travel- or catering-related GI outbreaks, while Staphylococcus aureus (including community Methicillin-resistant Staphylococcus aureus (MRSA)), streptococci, dermatophytes and Herpes simplex virus drive contact-sport skin disease.1,12 Blood-borne exposures (hepatitis B) remain exceptional in combat sports.6 Less common but notable infections include leptospirosis or rickettsial diseases in adventure races, meningococcal disease in dormitory-style housing and vaccine-preventable diseases (eg, measles and influenza) associated with travel. RISK FACTORS SPECIFIC TO YOUNG ELITE ATHLETES Several modifiable factors increase the risk of infection in young athletes. Heavy, monotonous training without adequate rest (“non-tapered” load)—especially during winter or at high altitude—has been linked to increased respiratory illness risk.8 Travel and shared housing during international tournaments increase exposure, which predisposes individuals to outbreaks.11 Recent data showed that insufficient calorie intake, particularly in young female athletes, was associated with a four- to eightfold higher rate of URTI.10 Vitamin D deficiency, common in indoor athletes or those training at high latitudes, is also an identifiable risk factor for URTI.8 Contact sports (wrestling, football, rugby and hockey) significantly increase skin infection risk due to skin abrasions and shared gear.7 Anxiety over missing a competition can lead athletes to train or compete while ill, potentially worsening their outcomes.10 IMPACT OF PHYSICAL TRAINING ON IMMUNITY (EXERCISE IMMUNOLOGY) The J-shaped model has traditionally described the relationship between physical activity and URTI risk, suggesting that moderate exercise enhances immunity. At the same time, high-intensity or prolonged training may increase susceptibility to illness.13,14 However, a newer S-shaped model suggests that elite athletes may experience lower infection rates despite heavy training, likely due to exceptional immune conditioning.14 Elite athletes demonstrated a significantly lower incidence of acute respiratory infections (4.2; 95% confidence interval, 3.3–5.3) compared with nonelite athletes (8.7; 95% confidence interval, 6.1–12.5), likely reflecting superior conditioning or preventive strategies.4 The “open window” hypothesis describes a transient immunosuppressive phase (2–72 hours) that occurs after intense exercise, during which the risk of infection may increase.13 This is characterized by alterations in T regulatory cells, cytokines and a decrease in salivary IgA.15,16 Innate immune cells such as neutrophils, monocytes, dendritic cells and natural killer (NK) cells are mobilized during exercise, with changes in their number and function.17 The function of adaptive immune cells can be observed by variations in salivary IgA after periods of intensive training.16 Adaptive immunity is also affected, as evidenced by fluctuations in salivary IgA, a key marker of mucosal defense. Although low salivary IgA often precedes URTI, the correlation is not fully understood.17 Elite athletes may also experience exercise-induced bronchoconstriction, which can mimic respiratory infections.18 Contributing noninfectious factors include allergies, chlorine exposure in swimmers, and air pollution in runners.18 Bronchial hyperresponsiveness is reported in over 40% of athletes and is particularly common in winter sports.19 Vaccine Responsiveness in Athletes Receiving a vaccination during a training cycle is a safe and effective preventive strategy for athletes.20,21 Immediate-postexercise and next-day vaccination do not differ in terms of side effects or training disruption.22 Evidence shows that intense training does not impair vaccine responsiveness. A recent study found that elite athletes developed a more pronounced immune response after influenza vaccination compared with nonathletic controls, with a greater increase in CD4+ T-cells and higher neutralizing antibody titers 1 week after vaccination.23 It was demonstrated that 90 minutes of moderate exercise performed immediately after influenza or COVID-19 vaccination may act as an adjuvant, enhancing antibody production.24 CLINICAL FEATURES AND COMMON PRESENTATIONS The spectrum of infections in young athletes mirrors the general population, but with sport-specific nuances. URTI usually presents with nasal congestion, sore throat or cough, and is often dismissed as minor. Systemic symptoms (fever and myalgias) should prompt rest. Influenza typically presents with the abrupt onset of high fever and muscle aches, which can impair performance. GI infections usually present with symptoms such as vomiting, diarrhea and dehydration, often affecting teammates. Skin infections include impetigo, folliculitis, abscesses, tinea or grouped herpes lesions on exposed skin. Myocarditis (usually caused by Coxsackie B virus, influenza and SARS-CoV-2) is a critical concern due to the risk of sudden cardiac death during exercise (nearly 4 % of deaths in youth sports).6 Symptoms may include chest pain or palpitations, but may also be silent. Infectious mononucleosis causes prolonged fatigue (lasting for weeks or months),25 sore throat, fever and tender lymph nodes, with hepatosplenomegaly in ~50% of adolescents. Persistent fever or unusual symptoms warrant careful assessment. Infection diagnostics in athletes is performed based on the clinical symptoms and follows standard medical practice. Currently, most sporting events lack standardized recommendations for infectious disease screening. Emerging data suggest that asymptomatic respiratory viral carriage is common among athletes and may be epidemiologically relevant. In a 12‑month controlled cohort, cross‑country skiers experienced significantly more virus‑positive asymptomatic episodes than orienteers (P = 0.014); during the prepandemic period, this was the only significant between‑group difference (P = 0.024).26 Community cohort data likewise show that a substantial fraction of Polymerase Chain Reaction (PCR)‑detected respiratory viral episodes can be asymptomatic, underscoring the potential for silent transmission.27 In close‑contact, team‑sport environments, pragmatic screening strategies (eg, targeted multiplex PCR during clusters/outbreaks or before high‑stakes events) merit consideration, implemented alongside isolation and return‑to‑play protocols. TREATMENT STRATEGIES AND RETURN-TO-PLAY Treatment is etiology-specific and must consider antidoping regulations. For example, pseudoephedrine, commonly used in some countries, is prohibited during competition and must be discontinued at least 24 hours before the start. Imidazoline derivatives for dermatological, nasal, ophthalmic or otic use (eg, brimonidine, oxymetazoline and xylometazoline) are permitted but included in the 2025 Monitoring Program.28 Patients with URTI receive supportive care (rest, hydration and analgesics). Influenza warrants early antiviral therapy (oseltamivir) to reduce duration. Antibiotics are indicated only for confirmed bacterial infections. The mean symptom duration of URTI in athletes is 7 days; however, most athletes with URTI do not miss any training or competition.27 Gastroenteritis is managed with rehydration and dietary adjustments; athletes should avoid antimotility agents that may delay recovery. Skin infections require appropriate antimicrobial therapy.7 Notably, team guidelines often mandate exclusion from play until therapy is instituted, and lesions are nondraining or covered. Bacterial skin infections generally require ≥72 hours of effective antibiotic therapy before return, whereas tinea corporis may permit immediate return if all lesions are adequately covered.7 Viral skin infections (HSV) often require antiviral therapy and return only after lesions have crusted, typically after about 5–7 days of treatment.7 Myocarditis Any suspected viral myocarditis requires immediate cessation of exercise. Athletes must rest (often for months) with close cardiology follow-up (echocardiogram, magnetic resonance imaging) before clearance. Return-to-play (RTP) guidelines from sports cardiology consensus recommend 3–6 months of no exercise and normalization of cardiac function.29 Mononucleosis Management is supportive (Nonsteroidal Anti-Inflammatory Drugs (NSAIDs), rest). RTP is individualized; however, contact sports are generally deferred for at least 3–4 weeks after symptom onset and until splenomegaly resolves.25 Laboratory or ultrasound confirmation of spleen status can guide timing, but clinical judgment prevails. Generally, RTP after an infection follows a graduated approach. Athletes should be entirely symptom-free at rest (no fever and no systemic symptoms) and have returned to baseline strength/endurance with light training before resuming whole competition. Many clinicians use the “neck check” for mild URTI: if symptoms are above the neck (runny nose, sore throat) and no fever, light exercise may be attempted; any “below the neck” symptoms (chest congestion, cough and myalgia) or fever require rest.6 For all infections, RTP thresholds remain conservative: trainers ensure 24–48 hours of full recovery after symptom resolution before progression. Psychological support is vital, as athletes may feel eager to return. Key RTP guidelines and prevention strategies are summarized in Table 1. TABLE 1. - Key Infections in Young Athletes, Return-to-Play, and Prevention Common Infections in Adolescent Athletes, Typical Clinical Course, Recommended Return-to-Play Intervals, and Key Prevention Measures Infection Typical Course Return-to-Play Guideline* Prevention URTI(common cold, influenza) Self-limited (7–10 days for cold; influenza often with fever/myalgias).Risk of prolonged fatigue in elite athletes. Mild “above-the-neck” symptoms: light training possible; fever or systemic symptoms: strict rest until ≥24–48 h after fever/symptoms resolve. Gradual return.6 Vaccination (influenza, COVID, etc.)Hand hygieneAvoid sharing bottlesAdequate sleep/nutrition Skin infections(impetigo, abscess, tinea, HSV) Bacterial: warm red lesions, pus.Fungal: scaly rash.HSV: painful clustered vesicles. Bacterial (impetigo/MRSA): off play ≥72 h after antibiotics started.7 Fungal (tinea): may return immediately if lesions are covered.7 HSV/herpes gladiatorum: off until lesions crust (~5–7 days of antivirals).7 All must have wounds covered on return. Avoid skin-to-skin contact with infected athletesShower immediately after practiceDo not share towels or gearVaccination against varicellaTreat underlying atopic skin conditions GI infections(norovirus, salmonella, giardia) Acute onset diarrhea, vomiting (1–5 days). May cause dehydration and systemic symptoms. No sports during acute illness. Resume training only after ≥48 hours symptom-free and rehydrated.30 Hand hygiene (especially after restroom)Safe food preparationAvoid communal food/drink spoutsClean shared facilities promptlyTravel precautions for water/food. Viral myocarditis(Coxsackie, influenza, SARS-CoV-2) Often follows a viral illnessMay cause chest pain, fatigue, arrhythmias or heart failure; sometimes asymptomatic until cardiac decompensation. Strict no exercise if suspected. Full cardiac workup (ECG, echo, MRI). RTP only after 3–6 months rest and normalization of cardiac function. Any chest symptoms warrant evaluation.29 Avoid exertion during any systemic viral infection. No specific vaccine (influenza vaccine may reduce certain viral myocarditis). Recognize warning signs early. Infectious mononucleosis(EBV) Fever, sore throat, fatigue, lymphadenopathy; splenomegaly in 50%–60%. Course is variable; fatigue can last weeks. No contact or collision sports for at least 3–4 weeks after onset (often longer until spleen normal). RTP should be individualized and guided by symptom resolution.25 Some advocate ultrasound clearance of spleen. Hand hygieneAvoid sharing bottlesAdequate sleep/nutrition *All return-to-play (RTP) steps must be individualized and symptom-free at each progression.ECG indicates echocardiogram; MRI, magnetic resonance imaging. PREVENTION STRATEGIES Vaccinations Athletes should follow all routine immunizations. The annual influenza vaccine, updated SARS-CoV-2 boosters, measles, mumps and rubella vaccine (MMR), varicella, Tdap and hepatitis B form the core schedule. Vaccines for measles, mumps, rubella, varicella and pertussis (Tdap) prevent outbreaks in close-contact teams. Hepatitis B vaccination is recommended for athletes participating in contact sports. Travel vaccines (such as typhoid, hepatitis A, meningococcal and yellow fever) should be updated before international travel. Notably, vaccinated training partners and staff create herd immunity that protects athletes. Scheduling of vaccines should consider training cycles to avoid side effects during competition.11 Hygiene and Exposure Control Rigorous hand hygiene and respiratory etiquette (cover coughs and avoid sharing water bottles) reduce respiratory and GI spread. Athletes with any contagious infection (eg, conjunctivitis and open skin lesions) should be kept from team activities. Shared equipment and facilities must be disinfected regularly. Showering with antiseptic (eg, chlorhexidine) can reduce staph colonization. In outbreaks of GI illness or skin infections, temporary cohorting or exclusion policies may be needed.27 Nutrition and Supplements Maintaining adequate energy intake and a balanced diet supports immunity. Vitamin D supplementation should be considered in athletes with a deficiency.8 Some evidence suggests probiotics or zinc may modestly reduce URTI risk in athletes.10 Load Management and Nutrition Periodized programs, avoiding monotony, ≥1 rest day per week, preserve immune competence.31 Outbreak Response Early case detection, cohorting and ring vaccination or antiviral prophylaxis limit the spread during tours or camps. Preventive strategies for particular infectious diseases in athletes are presented in Table 1. PRACTICAL RECOMMENDATIONS Ensure all athletes’ vaccinations are up to date and screen for health risks (eg, splenomegaly). Educate athletes and coaches on recognizing and reporting symptoms. Enforce strict hygiene practices, including regular hand washing, disinfection of shared gear and postpractice showering. At the first sign of fever or systemic symptoms, recommend immediate rest and evaluation. Adjust training load during seasons of high infection risk, ensure adequate recovery, nutrition and vitamin D levels. Collaborate with sports medicine providers to develop clear RTP criteria for different infections. Maintain communication with athletic trainers who can observe healing progress. Provide mental health support. Isolate sick individuals, review infection control (eg, food sources and locker room ventilation) and consider prophylaxis/vaccination of teammates. CONCLUSION Young elite athletes balance the immune benefits of regular exercise against the risks imposed by heavy training, close contact and travel. While moderate, periodized activity enhances immunity, prolonged heavy loads without adequate recovery can increase the risk of infection. Infections in athletes may lead to significant time loss from sports and can precipitate serious complications if not properly managed. Early recognition, appropriate evaluation (including cardiac screening) and conservative RTP protocols are crucial. Moreover, preventive strategies—especially vaccinations and strict hygiene—are critical. Multidisciplinary coordination between physicians, coaches and trainers is essential to ensure sick athletes rest adequately without pressure to return prematurely. By combining awareness of sport-specific risk factors with evidence-based infection control measures (such as hand washing, decontamination, immunization and nutrition), the burden of infections in young athletes can be minimized, thereby preserving both their health and performance. ACKNOWLEDGMENT The English language and grammar of this manuscript were refined using ChatGPT (OpenAI, San Francisco, CA).