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Common Infections in the Collegiate Athlete
Common Infections in the Collegiate Athlete Jason M. Blaylock, MD, and Catherine F. Decker, MD, FACP, FIDSA Infectious diseases account for a significant proportion of medical conditions that occur in the athlete. As athletes, particularly those at the collegiate level, travel frequently, live in close quarters, and share workout facilities, they are frequently exposed to various infectious pathogens. In addition, the high-risk behavior of some athletes may put them at risk for infections with sexually transmitted diseases (STDs).
Infectious Mononucleosis Infectious mononucleosis (IM) is a common medical condition that afflicts thousands of athletes each year. While acute illness has a classic presentation, the clinical course is often variable with a wide range of symptom severity. Most patients with IM recover uneventfully. However, the rare complication of splenic rupture presents the clinician with difficult decisions regarding when the athlete should return to play. Accurate diagnosis of IM will provide the athlete with anticipation of expected duration of illness and limits on participation in sports. Epidemiology. Epstein-Barr virus (EBV or human herpes virus 4) is a DNA herpes virus that is primarily transmitted from exposure to oropharyngeal secretions of infected individuals through food sharing, kissing, or other intimate contact.1 Intermittent asymptomatic shedding through the oropharyngeal secretions can occur. Peak incidence occurs in the 15to 20-year-old age group, most of which experience significant symptoms. The development of symptomatic IM in adults over age 35 is uncommon due in part to the high likelihood of prior exposures at a young age and/or subclinical disease. Nearly 95% of adults eventually develop antibodies to EBV. College populations experience the highest morbidity from IM, with approximately 30%-50% of students remaining susceptible to infection at the start of college, 1%-3% acquiring the disease each year, and an average rate of infection approaching 15% over the course of their Dis Mon 2010;56:422-435 0011-5029/2010 $36.00 ⫹ 0 doi:10.1016/j.disamonth.2010.05.003 422
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college career.2 This high rate of infection is likely due to close living situations, decreased attention to hygiene, and increased sexual contact and exposures. Sexual intercourse may enhance acquisition of EBV among college students, as EBV can be found in semen and cervical secretions; however, it is difficult to determine whether EBV transmission occurred through related sexual behaviors such as “deep kissing.”3 Clinical Presentation and Diagnosis. The incubation period for EBV ranges from 30 to 50 days, thus making source identification difficult among athletes. In addition, oral shedding has been shown to persist at significant levels for over 32 weeks, predisposing to a prolonged period of infectivity, especially in the setting of close contacts.4 Classic IM is characterized by sore throat, fever, and cervical lymphadenopathy (posterior ⬎ anterior nodes). Some patients may not have all classic features on presentation. Oftentimes, a prodromal period of headache, malaise, and fever can occur and can last up to 3 weeks. Pharyngitis, present in 80% of cases, is typically the most incapacitating feature of the disease and is exudative in one third of these cases. Palatal petechiae and rash may be present and associated splenic enlargement may cause vague abdominal discomfort. Most healthy patients will have resolution of symptoms in 4-8 weeks.5 Laboratory diagnosis is suggested serologically by the appearance of heterophile antibodies (positive monospot test), although the false-negative rate may be 25%, particularly during the first week of illness. If the clinical suspicion for IM is still high and monospot is negative, EBV serology should be obtained. An IgM and IgG antibody to viral capsule antigen is highly sensitive and specific in this situation. Other routine laboratory testing may be helpful, including an elevated white blood cell count with a predominance of lymphocytes. Atypical lymphocytes may account for up to 30% of lymphocytes. Elevations of liver-associated enzymes may be seen in up to 90% of patients. Treatment. The mainstay of treatment for uncomplicated acute IM is symptom relief and supportive care. In healthy young adults, IM is self-limited. Many have symptoms for less than a week with the majority returning to their usual health within a month. Use of acetaminophen for comfort, maintenance of fluids and hydration, and rest during the acute illness is helpful. Antiviral therapy has been extensively studied and is not recommended. While short-term suppression of viral shedding has been demonstrated with acyclovir, a meta-analysis of 5 randomized controlled trials of acyclovir failed to show a clinical benefit.6,7 No controlled studies have evaluated the efficacy of corticosteroids in symptom relief or prevention of complications. In general, steroids should be limited to patients with complications such as severe hepatitis, myocarditis, hemoDM, July 2010
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lytic uremic syndrome, neurologic complications, or those at risk of airway obstruction from tonsillar enlargement.5,8 Complications. Complications in IM occasionally occur and include splenic rupture, Guillian-Barre syndrome,9 hemolytic uremic syndrome,10 meningitis, neuritis,11 aplastic anemia, disseminated intravascular coagulation, and severe tonsillar enlargement resulting in respiratory compromise.12-14 Perhaps the most controversial issue with regard to IM in the athlete is the clinical significance and management of the enlarged spleen. Splenomegaly from lymphocytic infiltration of the spleen may occur in 50%60% of cases of IM. The spleen may be enlarged at least 2- to 3-fold and splenic rupture is estimated to occur in approximately 0.1%-0.2% of IM cases. Nearly all splenic ruptures occur between the 4th and 21st day of symptomatic illness.2 In 1 study reviewing splenic rupture among college athletes, 70% of cases occurred in football players. Other high-risk athletes included hockey, lacrosse, rugby, and basketball players, in addition to judo, karate, and boxing participants.15 While concern of splenic rupture is a major consideration for limiting athletes in returning to strenuous sports, it is interesting that some studies report that more than half of IM-related splenic ruptures were spontaneous without notable prior trauma.13 Physical examination alone is not reliable to exclude splenomegaly in IM cases and cannot be used to guide “return-to-play” decisions. In a prospective study, the presence of positive palpation and percussion signs had a combined sensitivity of only 46%.16 In addition, accurate assessment of splenic sizes might be further complicated by the variable dimensions and well-developed abdominal musculature of collegiate athletes. It is also difficult to define splenic enlargement radiographically given the wide variability in normal spleen size of the collegiate athlete. One study found that 3.8% of college freshmen had palpable splenomegaly on physical examination that was not related to body habitus.17 Furthermore, a prospective study demonstrated significant variability of normal splenic size among 631 collegiate athletes. Over 7% of these athletes met radiographic criteria for splenomegaly at baseline, with a splenic length of over 13 cm.18 Thus, the provider should interpret single sonographic measurements with caution given the wide variability in spleen size seen among athletes. In fact, one should consider obtaining serial measurements of the spleen when making the decision to allow an athlete with IM and initial splenomegaly to return to active participation in sports. Return to Play. As athletes usually experience a period of utter incapacitation during their illness, it is usually not difficult to convince 424
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them to rest during this period. It is more difficult to continue to restrict their play when they are feeling better. To date, there are no welldesigned large clinical trials to assist providers in the difficult decision to return an athlete to a contact sport after they are symptomatically improved. Aerobic capacity does not appear to be altered once the febrile episode has resolved, and prolonged bed rest does not seem to be indicated for the individual recovering from IM.19 In fact, the current consensus is that light noncontact activities may resume at 3 weeks from symptom onset in most patients, assuming the avoidance of activities capable of causing chest or abdominal trauma.13 The ultimate decision of when to return the athlete to more strenuous contact sports following an acute IM illness is controversial. Previous recommendations have varied from convalescing for 3 weeks to 6 months after onset of initial symptoms.20 Given that most recent studies have shown that most splenic ruptures occur within 3 weeks of development of IM, it seems reasonable to prohibit activity during this time. However, it is important to note that cases of splenic rupture have occurred up to 4-7 weeks, and thus, the risk of this complication persists.21 The ideal time for allowing return to full participation in strenuous contact sports is when splenomegaly has resolved, which as has been previously discussed may be difficult to determine without serial imaging. It is important that the athlete be educated regarding the likely timeframe for occurrence of splenic rupture and the signs of possible rupture including pain or fullness in left upper quadrant or presence of left shoulder pain. The aggressive nature of the contact sport should also be considered, as the more strenuous contact sports (football, gymnastics, rugby, hockey, lacrosse, wrestling, diving, basketball) or sports-associated increased abdominal pressure (weightlifting) may carry a higher risk of splenic injury.2 Most recommend in this situation to wait a minimum of 4 weeks after onset of illness as long as there is no evidence of a palpable spleen or enlarged spleen. A clinical algorithm for management of athletes with IM has previously been proposed13 (Fig 1). The ultimate decision for return to play in athletes with splenomegaly beyond 7 weeks should be individualized and based on clinical judgment.
Meningitis While the majority of meningitis cases in athletes are self-limited and viral in origin, the rare cases of bacterial meningitis are associated with significant morbidity and mortality, particularly when there is a delay in early recognition. Therefore, it is crucial to distinguish between these 2 etiologies early in their course to ensure prompt and DM, July 2010
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FIG 1. Proposed algorithm for avoiding splenic rupture in athletes returning to play following infectious mononucleosis. Adapted from Auwaerter PG. Infectious mononucleosis: return to play. Clin Sports Med. 2004;23:485-497 (Color version of figure is available online.)
appropriate management. In addition, given the close physical contact among athletic teams, it is important to know how to reduce the risk of transmission of these pathogens through infection-control practices, post exposure antibiotic administration when indicated, and immunization. Epidemiology. Acute meningitis is clinically defined as a syndrome characterized by the onset of meningeal symptoms such as fever, headache, and neck stiffness over the course of hours to days and may be caused by a wide variety of organisms. Most cases of aseptic meningitis are viral in etiology. The organisms most commonly identified among athletes include the Enteroviruses (echovirus, coxsackie viruses, and the numbered enteroviruses). Most aseptic meningitis cases in the literature have occurred in high school athletes; however, the college athlete is 426
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likely just as susceptible to infection.22-26 Outbreaks on athletic teams have been attributed to enteroviruses, specifically coxsackieviruses and echoviruses. Athletes on these teams were at increased risk for contracting the virus once it was introduced to the team when compared with other athletic teams at the same schools who did not have reported index cases.26 Characteristics of aseptic meningitis identified in these outbreaks are consistent with the seasonal and epidemiologic patterns of enteroviral infections with outbreaks in football players occurring predominantly in the summer and early fall and mode of spread through the fecal-oral route. Transmission was person to person and probably associated with poor hygienic practices (eg, oral contamination of shared water sources and drinking containers).27 While regular and moderate exercise training may improve the ability of the immune system to protect the host from infection, there are data to suggest that exhaustive exercise, as seen with strenuous collegiate athletics, may weaken the immune system and increase the risk for infection.28 While bacterial meningitis is less common in the college athlete, it portends a much poorer prognosis than viral meningitis and has been associated with neurologic complications such as seizures, hearing loss, cranial nerve palsies, and impaired cognition or speech. The most common organisms isolated in the otherwise healthy young adult population include Neisseria meningitidis and Streptococcus pneumoniae. Widespread implementation of universal vaccination against Haemophilus influenza has drastically decreased the incidence of meningitis due to this organism. In a review of 296 episodes of community-acquired bacterial meningitis in adults, S. pneumoniae and N. meningitidis comprised 50% of isolated organisms with a hospital mortality rate as high as 25% despite appropriate therapy.29 In addition, it appears that S. pneumoniae is associated with an overall poorer prognosis and is marked by more complications than N. meningitidis.30,31 Reports of pneumococcal or meningococcal cases in athletes are rare but reported. Outbreaks of meningococcal meningitis are well documented, while pneumococcal disease is sporadic in occurrence. Eleven cases of Type C N. meningitidis were identified following an international youth soccer tournament, while 7 cases were identified in a rugby football team, which was found to have N. meningitidis carriage rate of 29%.32,33 More recently, a case of Type B N. meningitidis was identified at a European Youth Olympic Sports Festival in Spain, which created prophylaxis and surveillance problems when 1500 athletes traveled back to 43 countries within the at-risk incubation period.34 DM, July 2010
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Other less common causes of meningitis should be considered based on exposure history and individual cases. Aseptic presentations can occur with various drugs, malignancies, Lyme disease, rickettsial disease, and herpes simplex virus infections of the central nervous system.35 The largest outbreak of leptospirosis reported in the USA to date resulted from ingestion of contaminated lake water by athletes during a triathlon in Springfield, Illinois. In this outbreak, 98 patients met the definition for a suspected case, and the most common symptoms were suggestive of meningitis, including fevers, headaches, and myalgias.36 An unusual and fatal case of primary amebic meningoencephalitis caused by Naegleria fowleri occurred in an 11-year-old boy who swam in a local river in southern Georgia.37 Clinical Presentation and Diagnosis. Differentiating between viral and bacterial meningitis can be difficult at the time of initial presentation. The onset of meningitis may be acute (⬍24 hours) or subacute occurring over 1-7 days. Oftentimes, the triad of fever, headache, and meningismus is not recognized or may be absent in the young adult.38 Other accompanying symptoms may include nausea, vomiting, pharyngitis, diarrhea, photophobia, or other neurologic symptoms ranging from mental status changes to seizures or coma. The course may rapidly progress or be indolent in nature, particularly if the patient has been partially treated with oral antibiotics. Physical examination alone may not distinguish aseptic from bacterial causes of meningitis; however, a complete neurologic examination is useful for identifying focal neurologic deficits or papilledema, which may indicate a cerebral mass or encephalitis. While assessing for the feasibility of and safety of performing a lumbar puncture and if a bacterial etiology is suspected, a set of blood cultures should be obtained immediately as approximately 50%-70% of patients with untreated bacterial meningitis will have positive blood cultures.38,39 Cerebrospinal fluid (CSF) analysis is the most important laboratory test for excluding bacterial meningitis. CSF should be evaluated for opening pressure, cell count, protein, glucose, aerobic culture, and gram stain. Characteristics of CSF that should heighten suspicion for a bacterial cause include white blood cells elevated to ⬎1000 cells/mm3 with a neutrophil predominance, glucose concentration ⬍40 mg/dL, and protein concentration ⬎50 mg/dL.40 In contrast, viral or aseptic meningitis is marked by a mild to moderate mononuclear pleocytosis (white blood cells rarely ⬎1000 cells/mm3) with a normal to minimally decreased glucose concentration and a normal to mildly increased protein concentration. Occasionally, there is an initial polymorphonuclear predominance, but this generally converts to mononuclear cells within 8-48 hours.35 Opening 428
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pressures are usually elevated in the range of 200-500 mm H2O in acute bacterial meningitis; cases of aseptic meningitis usually have a normal to slightly elevated opening pressure. The initial gram stain of CSF yields an accurate diagnosis in 60%-90% of cases of bacterial meningitis. S. pneumoniae is identified much more frequently via gram stain than is N. meningitidis (90% and 50%, respectively).40 CSF cultures are positive in 70%-80% of patients who have not received prior antimicrobial therapy. Polymerase chain reaction (PCR) studies can be useful in detection of enteroviruses in acute aseptic meningitis and are more sensitive than viral culture.41 A rapid diagnosis of enteroviral meningitis may shorten hospitalizations, decrease antibiotic use, and reduce need for other testing. Empiric antibiotic therapy should not be delayed while attempting to perform a lumbar puncture. While the risk of cerebral herniation always exists in the setting of an intracranial mass or increased intracranial pressure, there is no conclusive evidence to support neuroimaging before performing a lumbar puncture,42 except in certain instances outlined by the Infectious Disease Society of America, which includes the immunocompromised hosts, those with history of CNS disease, associated new-onset seizure, evidence of papilledema, abnormal level of consciousness, or focal neurologic deficits.40 Ultimately, the decision to obtain neuroimaging before diagnostic lumbar puncture should be based on clinical history and physical examination findings. Treatment. Various studies have shown that poor outcome is associated with a high bacterial load before initiation of antimicrobial therapy. Delayed CSF sterilization after 24 hours of therapy increases the risk of neurologic sequelae.43,44 Retrospective studies have demonstrated that early administration of antimicrobial therapy reduces mortality45 and improves overall neurologic outcome and sequelae.46 Empiric antimicrobial therapy in the college athlete with meningitis should include vancomycin plus a third-generation cephalosporin (ceftriaxone or cefotaxime) for coverage of the most likely bacterial pathogens, S. pneumoniae and N. meningitides.40 When viral meningitis is highly suspected in a well-established team outbreak, athletes with minimal/mild symptoms can be treated at home with supportive care. In a case in which meningococcal infection is highly suspected, prehospital treatment with intramuscular benzylpenicillin or ceftriaxone should be considered, if available.47 Antibiotics should be modified based on CSF culture results. The efficacy of adjunctive corticosteroid in bacterial meningitis remains controversial. In the adult population, a placebo-controlled, double-blind multicenter trial found that dexamethasone (10 mg q6h for 4 days, first dose given 15-20 minutes before antimicrobial use) was associated with DM, July 2010
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decreased morbidity and mortality in adults with pneumococcal meningitis (but not among patients with meningococcal disease).48 Based on available evidence to date, the Infectious Disease Society of America continues to recommend use of dexamethasone in adults with suspected or proven pneumococcal meningitis. There are no data to support adjunctive corticosteroids in nonpneumococcal meningitis; however, it is recognized that some authorities would initiate dexamethasone in these cases given that the etiology of bacterial meningitis is not always determined.40 Return to Play. Currently, there are no guidelines for return to play for the athlete recovering from acute meningitis. However, the participant should not return to the playing field until complete resolution of symptoms. In the setting of viral meningitis, the period of symptom recovery can be expected to last several days to a few weeks, with a gradual return to full activity expected. In contrast, the decision to return to play following bacterial meningitis depends more on the presence of secondary neurologic sequelae and comorbidities. Given the high incidence of sensorineural deafness in bacterial meningitis survivors, formal hearing testing is recommended.31 In addition, neuropsychologic evaluation as well as long-term multidisciplinary rehabilitation is often required for survivors with end organ damage, limb amputation, and severe neurologic sequelae. Prevention. Prevention of the spread of meningitis to others is crucial, as evidenced by reported infection rates ranging from 30% to 60% among high school football teams. Most bacterial meningitis cases can be prevented with proper vaccination of collegiate athletes upon enrollment to school. Most athletes fall into subgroups for which the Centers for Disease Control and Prevention (CDC) recommend immunization. College students residing in dorms have an at least 3 times greater relative risk for contracting meningococcal infection than students living off campus. The meningococcal conjugate vaccine, a tetravalent vaccine containing capsular polysaccharides from serogroups A, C, Y, and W-135, is preferred for individuals aged 11-55 years old.49 All persons who are at high risk for contracting meningococcal meningitis should obtain a booster vaccine every 5 years.50 As pneumococcal meningitis is a sporadic and uncommon occurrence, pneumococcal vaccination is not recommended in young healthy adults. Universal precautions should always be enforced, to include frequent hand washing and availability of adequate soap dispensers throughout sports training facilities. Sports teams including managers and training personnel should avoid sharing cups or using communal squeeze bottles. Disinfection of team equipment, 430
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shower facilities, and all common areas should be performed. It is important to ensure appropriate reporting of the outbreak to school and local public health authorities, as this allows for documentation of the outbreak as well as provides a concise report to minimize panic in the community.51 Placing infected and/or symptomatic players on mandatory bed rest is crucial. Given the frequent, close contact that occurs among collegiate athletes during practices, travel, and while staying in dormitories, it is prudent to administer chemoprophylaxis to any teammates of an index case of meningococcal meningitis. A single intramuscular dose of ceftriaxone, single oral dose of ciprofloxacin, or a 2-day oral course of rifampin have all been found effective for prophylaxis and eradication of nasopharyngeal carriage in the case of meningococcal disease. Chemoprophylaxis is not recommended after exposure to a case of pneumococcal meningitis.
Sexually Transmitted Diseases Athletes appear to be more likely than nonathletes to engage in such risk-taking behaviors as consuming greater amounts of alcohol, decreased use of condoms and other contraception, and increased number of sexual partners.52 These behaviors likely contribute to the increased prevalence of STDs in this age group. As sports medicine physicians are often the sole health care professional that athletes routinely see throughout collegiate play, they have an important role in the identification of STDs. The rates of various STDs in this young otherwise healthy patient population are quite high. When screening for STDs during preparticipation sports examinations, 1 study found the prevalence of chlamydial and gonococcal infections in young men to be 2.8% and 0.7%, respectively; while in young women, the prevalence was 6.5% and 2.0%, respectively. Of even more concern was the fact that 93.1% of those infected were asymptomatic and up to 25% did not receive documented treatment.53 Improved screening among this young population seems imperative in preventing transmission. Recommendations from the 2006 updated STD guidelines published by the CDC identify 5 intervention strategies that can be applied to decrease the risk of acquisition and transmission of STDs: education on sexual behavior, identification of asymptomatic individuals, diagnosis and treatment of infected individuals, counseling of sexual partners of persons who have an STD, and preexposure vaccination, if applicable.54 These interventions should be followed to decrease the acquisition and transmission of STDs among collegiate athletes. The diagnosis and treatment guidelines for STDs are well established and accessible through the CDC.54 However, determining when to allow DM, July 2010
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the athlete to return to full participation will be further discussed. In the case of an uncomplicated chlamydial or gonorrheal urethritis/cervicitis/ rectal disease, little, if any, time away from competition is needed. However, with pelvic inflammatory disease, epididymitis, or disseminated gonorrheal disease, convalescence from athletics should continue until resolution of symptoms. Additional time is required for recovery and physical therapy following diagnosis and treatment of a septic joint, and this should be assessed on an individual basis.8 The NCAA has established guidelines regarding play restrictions for wrestlers, who are more prone to acquisition and transmission of such STDs as human papillomaviruses and herpes simplex viruses through skin to skin contact.55 These guidelines can be applied to other contact sports as well. With regards to communicable skin diseases, infectious skin conditions that cannot be adequately protected should be considered for medical disqualification. These recommendations are discussed elsewhere (skin and soft tissue infections in the athlete) in this monograph.
Conclusions As collegiate athletes are at high risk for the acquisition and transmission of various infectious diseases, it is important to provide appropriate primary and secondary prevention techniques in an effort to curtail the spread of disease. It is paramount that providers ensure that athletes are up to date on all vaccinations, adhere to good hygiene practices, are appropriately educated about safe sex practices, and have access to timely prophylaxis with medications if needed.
Disclaimer The opinions and assertions contained herein are those of the authors and are not to be construed as official or as reflecting the views of the Department of Defense, the Department of the Navy, or the naval services at large. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the U.S. Department of the Army or the U.S. Department of Defense.
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Infectious Mononucleosis Infectious mononucleosis (IM) is a common medical condition that afflicts thousands of athletes each year. While acute illness has a classic presentation, the clinical course is often variable with a wide range of symptom severity. Most patients with IM recover uneventfully. However, the rare complication of splenic rupture presents the clinician with difficult decisions regarding when the athlete should return to play. Accurate diagnosis of IM will provide the athlete with anticipation of expected duration of illness and limits on participation in sports. Epidemiology. Epstein-Barr virus (EBV or human herpes virus 4) is a DNA herpes virus that is primarily transmitted from exposure to oropharyngeal secretions of infected individuals through food sharing, kissing, or other intimate contact.1 Intermittent asymptomatic shedding through the oropharyngeal secretions can occur. Peak incidence occurs in the 15to 20-year-old age group, most of which experience significant symptoms. The development of symptomatic IM in adults over age 35 is uncommon due in part to the high likelihood of prior exposures at a young age and/or subclinical disease. Nearly 95% of adults eventually develop antibodies to EBV. College populations experience the highest morbidity from IM, with approximately 30%-50% of students remaining susceptible to infection at the start of college, 1%-3% acquiring the disease each year, and an average rate of infection approaching 15% over the course of their Dis Mon 2010;56:422-435 0011-5029/2010 $36.00 ⫹ 0 doi:10.1016/j.disamonth.2010.05.003 422
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college career.2 This high rate of infection is likely due to close living situations, decreased attention to hygiene, and increased sexual contact and exposures. Sexual intercourse may enhance acquisition of EBV among college students, as EBV can be found in semen and cervical secretions; however, it is difficult to determine whether EBV transmission occurred through related sexual behaviors such as “deep kissing.”3 Clinical Presentation and Diagnosis. The incubation period for EBV ranges from 30 to 50 days, thus making source identification difficult among athletes. In addition, oral shedding has been shown to persist at significant levels for over 32 weeks, predisposing to a prolonged period of infectivity, especially in the setting of close contacts.4 Classic IM is characterized by sore throat, fever, and cervical lymphadenopathy (posterior ⬎ anterior nodes). Some patients may not have all classic features on presentation. Oftentimes, a prodromal period of headache, malaise, and fever can occur and can last up to 3 weeks. Pharyngitis, present in 80% of cases, is typically the most incapacitating feature of the disease and is exudative in one third of these cases. Palatal petechiae and rash may be present and associated splenic enlargement may cause vague abdominal discomfort. Most healthy patients will have resolution of symptoms in 4-8 weeks.5 Laboratory diagnosis is suggested serologically by the appearance of heterophile antibodies (positive monospot test), although the false-negative rate may be 25%, particularly during the first week of illness. If the clinical suspicion for IM is still high and monospot is negative, EBV serology should be obtained. An IgM and IgG antibody to viral capsule antigen is highly sensitive and specific in this situation. Other routine laboratory testing may be helpful, including an elevated white blood cell count with a predominance of lymphocytes. Atypical lymphocytes may account for up to 30% of lymphocytes. Elevations of liver-associated enzymes may be seen in up to 90% of patients. Treatment. The mainstay of treatment for uncomplicated acute IM is symptom relief and supportive care. In healthy young adults, IM is self-limited. Many have symptoms for less than a week with the majority returning to their usual health within a month. Use of acetaminophen for comfort, maintenance of fluids and hydration, and rest during the acute illness is helpful. Antiviral therapy has been extensively studied and is not recommended. While short-term suppression of viral shedding has been demonstrated with acyclovir, a meta-analysis of 5 randomized controlled trials of acyclovir failed to show a clinical benefit.6,7 No controlled studies have evaluated the efficacy of corticosteroids in symptom relief or prevention of complications. In general, steroids should be limited to patients with complications such as severe hepatitis, myocarditis, hemoDM, July 2010
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lytic uremic syndrome, neurologic complications, or those at risk of airway obstruction from tonsillar enlargement.5,8 Complications. Complications in IM occasionally occur and include splenic rupture, Guillian-Barre syndrome,9 hemolytic uremic syndrome,10 meningitis, neuritis,11 aplastic anemia, disseminated intravascular coagulation, and severe tonsillar enlargement resulting in respiratory compromise.12-14 Perhaps the most controversial issue with regard to IM in the athlete is the clinical significance and management of the enlarged spleen. Splenomegaly from lymphocytic infiltration of the spleen may occur in 50%60% of cases of IM. The spleen may be enlarged at least 2- to 3-fold and splenic rupture is estimated to occur in approximately 0.1%-0.2% of IM cases. Nearly all splenic ruptures occur between the 4th and 21st day of symptomatic illness.2 In 1 study reviewing splenic rupture among college athletes, 70% of cases occurred in football players. Other high-risk athletes included hockey, lacrosse, rugby, and basketball players, in addition to judo, karate, and boxing participants.15 While concern of splenic rupture is a major consideration for limiting athletes in returning to strenuous sports, it is interesting that some studies report that more than half of IM-related splenic ruptures were spontaneous without notable prior trauma.13 Physical examination alone is not reliable to exclude splenomegaly in IM cases and cannot be used to guide “return-to-play” decisions. In a prospective study, the presence of positive palpation and percussion signs had a combined sensitivity of only 46%.16 In addition, accurate assessment of splenic sizes might be further complicated by the variable dimensions and well-developed abdominal musculature of collegiate athletes. It is also difficult to define splenic enlargement radiographically given the wide variability in normal spleen size of the collegiate athlete. One study found that 3.8% of college freshmen had palpable splenomegaly on physical examination that was not related to body habitus.17 Furthermore, a prospective study demonstrated significant variability of normal splenic size among 631 collegiate athletes. Over 7% of these athletes met radiographic criteria for splenomegaly at baseline, with a splenic length of over 13 cm.18 Thus, the provider should interpret single sonographic measurements with caution given the wide variability in spleen size seen among athletes. In fact, one should consider obtaining serial measurements of the spleen when making the decision to allow an athlete with IM and initial splenomegaly to return to active participation in sports. Return to Play. As athletes usually experience a period of utter incapacitation during their illness, it is usually not difficult to convince 424
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them to rest during this period. It is more difficult to continue to restrict their play when they are feeling better. To date, there are no welldesigned large clinical trials to assist providers in the difficult decision to return an athlete to a contact sport after they are symptomatically improved. Aerobic capacity does not appear to be altered once the febrile episode has resolved, and prolonged bed rest does not seem to be indicated for the individual recovering from IM.19 In fact, the current consensus is that light noncontact activities may resume at 3 weeks from symptom onset in most patients, assuming the avoidance of activities capable of causing chest or abdominal trauma.13 The ultimate decision of when to return the athlete to more strenuous contact sports following an acute IM illness is controversial. Previous recommendations have varied from convalescing for 3 weeks to 6 months after onset of initial symptoms.20 Given that most recent studies have shown that most splenic ruptures occur within 3 weeks of development of IM, it seems reasonable to prohibit activity during this time. However, it is important to note that cases of splenic rupture have occurred up to 4-7 weeks, and thus, the risk of this complication persists.21 The ideal time for allowing return to full participation in strenuous contact sports is when splenomegaly has resolved, which as has been previously discussed may be difficult to determine without serial imaging. It is important that the athlete be educated regarding the likely timeframe for occurrence of splenic rupture and the signs of possible rupture including pain or fullness in left upper quadrant or presence of left shoulder pain. The aggressive nature of the contact sport should also be considered, as the more strenuous contact sports (football, gymnastics, rugby, hockey, lacrosse, wrestling, diving, basketball) or sports-associated increased abdominal pressure (weightlifting) may carry a higher risk of splenic injury.2 Most recommend in this situation to wait a minimum of 4 weeks after onset of illness as long as there is no evidence of a palpable spleen or enlarged spleen. A clinical algorithm for management of athletes with IM has previously been proposed13 (Fig 1). The ultimate decision for return to play in athletes with splenomegaly beyond 7 weeks should be individualized and based on clinical judgment.
Meningitis While the majority of meningitis cases in athletes are self-limited and viral in origin, the rare cases of bacterial meningitis are associated with significant morbidity and mortality, particularly when there is a delay in early recognition. Therefore, it is crucial to distinguish between these 2 etiologies early in their course to ensure prompt and DM, July 2010
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FIG 1. Proposed algorithm for avoiding splenic rupture in athletes returning to play following infectious mononucleosis. Adapted from Auwaerter PG. Infectious mononucleosis: return to play. Clin Sports Med. 2004;23:485-497 (Color version of figure is available online.)
appropriate management. In addition, given the close physical contact among athletic teams, it is important to know how to reduce the risk of transmission of these pathogens through infection-control practices, post exposure antibiotic administration when indicated, and immunization. Epidemiology. Acute meningitis is clinically defined as a syndrome characterized by the onset of meningeal symptoms such as fever, headache, and neck stiffness over the course of hours to days and may be caused by a wide variety of organisms. Most cases of aseptic meningitis are viral in etiology. The organisms most commonly identified among athletes include the Enteroviruses (echovirus, coxsackie viruses, and the numbered enteroviruses). Most aseptic meningitis cases in the literature have occurred in high school athletes; however, the college athlete is 426
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likely just as susceptible to infection.22-26 Outbreaks on athletic teams have been attributed to enteroviruses, specifically coxsackieviruses and echoviruses. Athletes on these teams were at increased risk for contracting the virus once it was introduced to the team when compared with other athletic teams at the same schools who did not have reported index cases.26 Characteristics of aseptic meningitis identified in these outbreaks are consistent with the seasonal and epidemiologic patterns of enteroviral infections with outbreaks in football players occurring predominantly in the summer and early fall and mode of spread through the fecal-oral route. Transmission was person to person and probably associated with poor hygienic practices (eg, oral contamination of shared water sources and drinking containers).27 While regular and moderate exercise training may improve the ability of the immune system to protect the host from infection, there are data to suggest that exhaustive exercise, as seen with strenuous collegiate athletics, may weaken the immune system and increase the risk for infection.28 While bacterial meningitis is less common in the college athlete, it portends a much poorer prognosis than viral meningitis and has been associated with neurologic complications such as seizures, hearing loss, cranial nerve palsies, and impaired cognition or speech. The most common organisms isolated in the otherwise healthy young adult population include Neisseria meningitidis and Streptococcus pneumoniae. Widespread implementation of universal vaccination against Haemophilus influenza has drastically decreased the incidence of meningitis due to this organism. In a review of 296 episodes of community-acquired bacterial meningitis in adults, S. pneumoniae and N. meningitidis comprised 50% of isolated organisms with a hospital mortality rate as high as 25% despite appropriate therapy.29 In addition, it appears that S. pneumoniae is associated with an overall poorer prognosis and is marked by more complications than N. meningitidis.30,31 Reports of pneumococcal or meningococcal cases in athletes are rare but reported. Outbreaks of meningococcal meningitis are well documented, while pneumococcal disease is sporadic in occurrence. Eleven cases of Type C N. meningitidis were identified following an international youth soccer tournament, while 7 cases were identified in a rugby football team, which was found to have N. meningitidis carriage rate of 29%.32,33 More recently, a case of Type B N. meningitidis was identified at a European Youth Olympic Sports Festival in Spain, which created prophylaxis and surveillance problems when 1500 athletes traveled back to 43 countries within the at-risk incubation period.34 DM, July 2010
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Other less common causes of meningitis should be considered based on exposure history and individual cases. Aseptic presentations can occur with various drugs, malignancies, Lyme disease, rickettsial disease, and herpes simplex virus infections of the central nervous system.35 The largest outbreak of leptospirosis reported in the USA to date resulted from ingestion of contaminated lake water by athletes during a triathlon in Springfield, Illinois. In this outbreak, 98 patients met the definition for a suspected case, and the most common symptoms were suggestive of meningitis, including fevers, headaches, and myalgias.36 An unusual and fatal case of primary amebic meningoencephalitis caused by Naegleria fowleri occurred in an 11-year-old boy who swam in a local river in southern Georgia.37 Clinical Presentation and Diagnosis. Differentiating between viral and bacterial meningitis can be difficult at the time of initial presentation. The onset of meningitis may be acute (⬍24 hours) or subacute occurring over 1-7 days. Oftentimes, the triad of fever, headache, and meningismus is not recognized or may be absent in the young adult.38 Other accompanying symptoms may include nausea, vomiting, pharyngitis, diarrhea, photophobia, or other neurologic symptoms ranging from mental status changes to seizures or coma. The course may rapidly progress or be indolent in nature, particularly if the patient has been partially treated with oral antibiotics. Physical examination alone may not distinguish aseptic from bacterial causes of meningitis; however, a complete neurologic examination is useful for identifying focal neurologic deficits or papilledema, which may indicate a cerebral mass or encephalitis. While assessing for the feasibility of and safety of performing a lumbar puncture and if a bacterial etiology is suspected, a set of blood cultures should be obtained immediately as approximately 50%-70% of patients with untreated bacterial meningitis will have positive blood cultures.38,39 Cerebrospinal fluid (CSF) analysis is the most important laboratory test for excluding bacterial meningitis. CSF should be evaluated for opening pressure, cell count, protein, glucose, aerobic culture, and gram stain. Characteristics of CSF that should heighten suspicion for a bacterial cause include white blood cells elevated to ⬎1000 cells/mm3 with a neutrophil predominance, glucose concentration ⬍40 mg/dL, and protein concentration ⬎50 mg/dL.40 In contrast, viral or aseptic meningitis is marked by a mild to moderate mononuclear pleocytosis (white blood cells rarely ⬎1000 cells/mm3) with a normal to minimally decreased glucose concentration and a normal to mildly increased protein concentration. Occasionally, there is an initial polymorphonuclear predominance, but this generally converts to mononuclear cells within 8-48 hours.35 Opening 428
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pressures are usually elevated in the range of 200-500 mm H2O in acute bacterial meningitis; cases of aseptic meningitis usually have a normal to slightly elevated opening pressure. The initial gram stain of CSF yields an accurate diagnosis in 60%-90% of cases of bacterial meningitis. S. pneumoniae is identified much more frequently via gram stain than is N. meningitidis (90% and 50%, respectively).40 CSF cultures are positive in 70%-80% of patients who have not received prior antimicrobial therapy. Polymerase chain reaction (PCR) studies can be useful in detection of enteroviruses in acute aseptic meningitis and are more sensitive than viral culture.41 A rapid diagnosis of enteroviral meningitis may shorten hospitalizations, decrease antibiotic use, and reduce need for other testing. Empiric antibiotic therapy should not be delayed while attempting to perform a lumbar puncture. While the risk of cerebral herniation always exists in the setting of an intracranial mass or increased intracranial pressure, there is no conclusive evidence to support neuroimaging before performing a lumbar puncture,42 except in certain instances outlined by the Infectious Disease Society of America, which includes the immunocompromised hosts, those with history of CNS disease, associated new-onset seizure, evidence of papilledema, abnormal level of consciousness, or focal neurologic deficits.40 Ultimately, the decision to obtain neuroimaging before diagnostic lumbar puncture should be based on clinical history and physical examination findings. Treatment. Various studies have shown that poor outcome is associated with a high bacterial load before initiation of antimicrobial therapy. Delayed CSF sterilization after 24 hours of therapy increases the risk of neurologic sequelae.43,44 Retrospective studies have demonstrated that early administration of antimicrobial therapy reduces mortality45 and improves overall neurologic outcome and sequelae.46 Empiric antimicrobial therapy in the college athlete with meningitis should include vancomycin plus a third-generation cephalosporin (ceftriaxone or cefotaxime) for coverage of the most likely bacterial pathogens, S. pneumoniae and N. meningitides.40 When viral meningitis is highly suspected in a well-established team outbreak, athletes with minimal/mild symptoms can be treated at home with supportive care. In a case in which meningococcal infection is highly suspected, prehospital treatment with intramuscular benzylpenicillin or ceftriaxone should be considered, if available.47 Antibiotics should be modified based on CSF culture results. The efficacy of adjunctive corticosteroid in bacterial meningitis remains controversial. In the adult population, a placebo-controlled, double-blind multicenter trial found that dexamethasone (10 mg q6h for 4 days, first dose given 15-20 minutes before antimicrobial use) was associated with DM, July 2010
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decreased morbidity and mortality in adults with pneumococcal meningitis (but not among patients with meningococcal disease).48 Based on available evidence to date, the Infectious Disease Society of America continues to recommend use of dexamethasone in adults with suspected or proven pneumococcal meningitis. There are no data to support adjunctive corticosteroids in nonpneumococcal meningitis; however, it is recognized that some authorities would initiate dexamethasone in these cases given that the etiology of bacterial meningitis is not always determined.40 Return to Play. Currently, there are no guidelines for return to play for the athlete recovering from acute meningitis. However, the participant should not return to the playing field until complete resolution of symptoms. In the setting of viral meningitis, the period of symptom recovery can be expected to last several days to a few weeks, with a gradual return to full activity expected. In contrast, the decision to return to play following bacterial meningitis depends more on the presence of secondary neurologic sequelae and comorbidities. Given the high incidence of sensorineural deafness in bacterial meningitis survivors, formal hearing testing is recommended.31 In addition, neuropsychologic evaluation as well as long-term multidisciplinary rehabilitation is often required for survivors with end organ damage, limb amputation, and severe neurologic sequelae. Prevention. Prevention of the spread of meningitis to others is crucial, as evidenced by reported infection rates ranging from 30% to 60% among high school football teams. Most bacterial meningitis cases can be prevented with proper vaccination of collegiate athletes upon enrollment to school. Most athletes fall into subgroups for which the Centers for Disease Control and Prevention (CDC) recommend immunization. College students residing in dorms have an at least 3 times greater relative risk for contracting meningococcal infection than students living off campus. The meningococcal conjugate vaccine, a tetravalent vaccine containing capsular polysaccharides from serogroups A, C, Y, and W-135, is preferred for individuals aged 11-55 years old.49 All persons who are at high risk for contracting meningococcal meningitis should obtain a booster vaccine every 5 years.50 As pneumococcal meningitis is a sporadic and uncommon occurrence, pneumococcal vaccination is not recommended in young healthy adults. Universal precautions should always be enforced, to include frequent hand washing and availability of adequate soap dispensers throughout sports training facilities. Sports teams including managers and training personnel should avoid sharing cups or using communal squeeze bottles. Disinfection of team equipment, 430
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shower facilities, and all common areas should be performed. It is important to ensure appropriate reporting of the outbreak to school and local public health authorities, as this allows for documentation of the outbreak as well as provides a concise report to minimize panic in the community.51 Placing infected and/or symptomatic players on mandatory bed rest is crucial. Given the frequent, close contact that occurs among collegiate athletes during practices, travel, and while staying in dormitories, it is prudent to administer chemoprophylaxis to any teammates of an index case of meningococcal meningitis. A single intramuscular dose of ceftriaxone, single oral dose of ciprofloxacin, or a 2-day oral course of rifampin have all been found effective for prophylaxis and eradication of nasopharyngeal carriage in the case of meningococcal disease. Chemoprophylaxis is not recommended after exposure to a case of pneumococcal meningitis.
Sexually Transmitted Diseases Athletes appear to be more likely than nonathletes to engage in such risk-taking behaviors as consuming greater amounts of alcohol, decreased use of condoms and other contraception, and increased number of sexual partners.52 These behaviors likely contribute to the increased prevalence of STDs in this age group. As sports medicine physicians are often the sole health care professional that athletes routinely see throughout collegiate play, they have an important role in the identification of STDs. The rates of various STDs in this young otherwise healthy patient population are quite high. When screening for STDs during preparticipation sports examinations, 1 study found the prevalence of chlamydial and gonococcal infections in young men to be 2.8% and 0.7%, respectively; while in young women, the prevalence was 6.5% and 2.0%, respectively. Of even more concern was the fact that 93.1% of those infected were asymptomatic and up to 25% did not receive documented treatment.53 Improved screening among this young population seems imperative in preventing transmission. Recommendations from the 2006 updated STD guidelines published by the CDC identify 5 intervention strategies that can be applied to decrease the risk of acquisition and transmission of STDs: education on sexual behavior, identification of asymptomatic individuals, diagnosis and treatment of infected individuals, counseling of sexual partners of persons who have an STD, and preexposure vaccination, if applicable.54 These interventions should be followed to decrease the acquisition and transmission of STDs among collegiate athletes. The diagnosis and treatment guidelines for STDs are well established and accessible through the CDC.54 However, determining when to allow DM, July 2010
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the athlete to return to full participation will be further discussed. In the case of an uncomplicated chlamydial or gonorrheal urethritis/cervicitis/ rectal disease, little, if any, time away from competition is needed. However, with pelvic inflammatory disease, epididymitis, or disseminated gonorrheal disease, convalescence from athletics should continue until resolution of symptoms. Additional time is required for recovery and physical therapy following diagnosis and treatment of a septic joint, and this should be assessed on an individual basis.8 The NCAA has established guidelines regarding play restrictions for wrestlers, who are more prone to acquisition and transmission of such STDs as human papillomaviruses and herpes simplex viruses through skin to skin contact.55 These guidelines can be applied to other contact sports as well. With regards to communicable skin diseases, infectious skin conditions that cannot be adequately protected should be considered for medical disqualification. These recommendations are discussed elsewhere (skin and soft tissue infections in the athlete) in this monograph.
Conclusions As collegiate athletes are at high risk for the acquisition and transmission of various infectious diseases, it is important to provide appropriate primary and secondary prevention techniques in an effort to curtail the spread of disease. It is paramount that providers ensure that athletes are up to date on all vaccinations, adhere to good hygiene practices, are appropriately educated about safe sex practices, and have access to timely prophylaxis with medications if needed.
Disclaimer The opinions and assertions contained herein are those of the authors and are not to be construed as official or as reflecting the views of the Department of Defense, the Department of the Navy, or the naval services at large. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the U.S. Department of the Army or the U.S. Department of Defense.
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