First published report of a sports-related infectious disease outbreak was of Chlamydia trachomatis in professional wrestlers in 1922.

Barriers to recovery for athletes include some of the same reasons athletes are more susceptible to illness in the first place:

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  Difficulty taking time off from training to adequately recover

  
  
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  Often have inadequate caloric intake

  
  
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  Often sleep deprived

In 1994, Nieman demonstrated a relationship between exercise and susceptibility to infections in the form of a J -shaped curve.

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  The model suggested that while engaging in moderate activity enhances immune function above sedentary levels, excessive amounts of prolonged high-intensity exercise have detrimental effects on immune functions (for additional details, refer to the J curve diagram in Chapter 18 , “Aerobic Training”).

A majority of elite athletes suffer from upper respiratory tract infections (URTIs) at a rate similar to those in the general population, but the incidence of infections in such athletes is higher around competitions, with no seasonal variations.

Faster marathon runners and those who train for longer distances per week experience more URTI symptoms.

Tests have been performed on concentration of secretory immunoglobulin A (s-IgA), which is a major effector function of the mucosal immune system, providing a first line of defense against pathogens:

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  s-IgA binds to and opsonizes foreign organisms, including respiratory viruses.

  
  
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  Exercise studies have used salivary s-IgA as a marker of mucosal immunity.

  
  
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  Long-duration and high-intensity exercise , both acutely and chronically, decreases salivary s-IgA and is associated with increased incidence of URTIs.

  
  
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  Acute and chronic moderate-intensity exercise increases s-IgA levels and reportedly lowers the incidence of reported URTIs.

Overall, the negative effects of intense exercise on the immune system are as follows:

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  Immune cell function: decreased effectiveness and number of white blood cells and increased production of free radicals

  
  
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  Stress hormone production: increased adrenaline, cortisol, growth hormone, and prolactin; in addition, such increases in these hormones depress immune cell function

  
  
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  Glutamine function: Glutamine assists in control of the rates of T- and B-lymphocyte proliferation and antibody synthesis. Intense exercise causes glutamine levels to decrease by about 20%. Castell found that oral glutamine supplementation after exercise improves immune function by increasing plasma glutamine levels.

Gleeson found that postexercise immune function depression was most pronounced when exercise is moderate-to-high intensity, continuous, and prolonged.

Leukocyte function may continue to remain depressed at 24 hours after the last exercise bout.

If the recovery time between consecutive bouts of intense exercise is insufficient, chronic immunosuppression can occur, which is often observed in overtrained athletes.

Fever is a normal physiologic response typically to infection with the intent to increase host survival and decrease the length of illness.

The Centers for Disease Control and Prevention (CDC) defines fever as an internal temperature of >38°C.

Fever can cause undesirable effects in the body; these may include increased insensible fluid losses, dehydration, increased metabolic demands, and dysregulation of body temperature.

The combination of hyperthermia and dehydration leads to reduction in both cardiac output and blood pressure, which can be particularly concerning in athletes.

A combination of these factors leads to reduced exercise tolerance, endurance, and muscle strength and an increase in perceived fatigue through cytokine-induced catabolism of muscles, which has been shown to potentially last for months after an illness.

Continuing to exercise during a febrile illness can further potentiate negative effects from the disease process and can evolve into myocarditis, which could be potentially lethal.

Athletes should be withheld from physical activity at least until their fever has resolved, and return to participation should be gradual.

To prevent the spread of febrile illnesses, the most common and effective tool is hand washing. It may be necessary to separate an athlete for a certain period of time from their teammates to prevent spread of infection to other members of the team.

Etiology : In general, URTI and common cold are used interchangeably. They are caused by respiratory viruses, typically rhinoviruses . Transmission is through nasal secretions by sneezing, coughing, and nose blowing.

Epidemiology : Leading reason for physician visits; cough is the 3 ^rd whereas nasal congestion is the 15th most common presenting symptom in all office visits, and URTIs are the third most common primary care diagnosis

Symptoms : Common symptoms include fever, cough, rhinorrhea, nasal congestion, sore throat, headache, and myalgias. Most are self-limited, typically lasting up to 10 days.

Examination and Diagnosis: Fever, rhinorrhea, erythema, cobble stoning or swelling of the posterior oropharynx, fluid level behind the tympanic membrane, and cervical lymphadenopathy; diagnostic testing is not typically necessary unless there is suspicion for Group A streptococcal or mononucleosis infections

Treatment : Treatment is symptomatic and supportive. Effective modalities include antipyretic and anti-inflammatory medications, decongestants, nasal saline irrigation, intranasal ipratropium, and zinc. Antibiotics are not effective.

Return to Play : The “neck check” can be a helpful tool when considering whether physical activity is appropriate. Basically, an athlete with URTI symptoms “above the neck,” with no systemic signs and symptoms, including no fever, should undergo 10–15 minutes of mild to moderate exercise and, if tolerated, may continue participation.

Prevention : Hand washing should be encouraged, and teammates should not share water bottles. Prophylactic vitamin C has been shown to modestly reduce the duration of cold symptoms but not the incidence.

Etiology : Infectious mononucleosis (IM) or “mono” is the result of an infection with the Epstein–Barr virus (EBV). EBV is the primary cause in 90% of cases, but cytomegalovirus and toxoplasmosis can cause a similar syndrome as well. Transmission of the virus is through oral secretions; thus, the disease has been nicknamed as the “kissing disease.” EBV has an incubation period of 30–50 days, and it causes a cell-mediated immune response, which leads to T lymphocyte proliferation. This results in lymphoid hyperplasia, lymphocytosis, and atypical lymphocytes on a peripheral blood smear.

Epidemiology : EBV is very common; 90%–95% of adults display immunity to EBV, indicating prior infection. There are approximately 500 cases per 100,000 persons per year in the United States, with the highest incidence in adults aged 15–24 years. Athletes are at no higher risk to contract the virus than nonathletes.

Symptoms : An infection with EBV can be clinically insignificant in children but results in a symptomatic illness in adolescent and adult patients. Typically, there is a 3–5-day prodrome consisting of malaise, fatigue, and anorexia, which then progresses to the classic “triad” of IM with pharyngitis, fever, and lymphadenopathy . Rarely, laryngeal edema can occur, potentially leading to airway obstruction.

Examination and Diagnosis : The reactive lymphadenopathy classically leads to enlargement of posterior cervical lymph nodes , but axillary and inguinal nodes may also be enlarged. Posterior palatine petechiae, jaundice, exudative pharyngitis, rash (commonly seen in a patient who started penicillin for a suspected group A streptococcal infection), and splenomegaly are also possible. Jaundice is uncommon, but 90% of patients have mildly elevated AST and ALT. Exudative pharyngitis can be mistaken for a streptococcal pharyngitis, but concomitant infections do occur in up to 30% of patients. Splenomegaly and increased risk of rupture is concerning for athletes, but routine imaging is not generally regarded as useful in return-to-play decisions. Splenomegaly alone does not predict the risk of rupture. A Monospot test, which detects the presence of heterophile antibodies, is clinically utilized but has a false negative rate of 25% in the first week of illness. Testing for EBV early antigen (EA), IgM, and IgG (to EBV viral capsid antigens) may be useful if Monospot is negative. Atypical lymphocytes have a sensitivity of 75% and a specificity of 92%, and other laboratory abnormalities may include transient neutropenia, thrombocytopenia, and anemia.

Treatment : Treatment is supportive, including rest, hydration, and NSAIDs. In addition, given the negative effects IM can have on the liver, acetaminophen should be used with caution. Moreover, aspirin is best avoided for risk of bleeding and an association of IM with Reye syndrome in pediatric patients. In general, corticosteroids are not needed but may be considered if there is significant laryngeal edema or painful swallowing that interferes with drinking and eating.

Return to Play : Splenic rupture is the most concerning issue while making return-to-play decisions. All athletes should be withheld from competition until their symptoms have resolved. Occasionally, light aerobic activity can be initiated after 14 days if the athlete’s symptoms have resolved, but published guidelines (expert opinion) generally recommend to withhold an athlete from participation for 3 weeks . Some experts advocate holding out contact athletes and anyone with splenomegaly for a total of 4 weeks. Follow-up laboratory results demonstrating normalization are not necessary. Athletes, parents, coaches, and trainers should be educated that in severe cases, it may take up to 3 months to make a full recovery.

Prevention : Hand washing should be encouraged, and teammates should not share water bottles.