An Athlete With Mononucleosis Can Compete Again if All of the Following Are True Except When

• Journal Listing
• Sports Health
• 5.6(3); 2014 May
• PMC4000473

Sports Health. 2014 May; 6(3): 232–238.

Return to Play After Infectious Mononucleosis

Jonathan A. Becker

^†Department of Family and Geriatric Medicine, University of Louisville and Kentucky Ane Health Sports Medicine Fellowship, Louisville, Kentucky

Julie Anne Smith

^‡School of Medicine, University of Louisville, Louisville, Kentucky

Abstract

Context:

Infectious mononucleosis is a disease primarily of adolescence and early adulthood. The gamble of splenic injury and chronic fatigue make return-to-play decisions a claiming for the clinician caring for athletes with infectious mononucleosis.

Testify Acquisition:

Data were obtained from the PubMed and MEDLINE databases through December 2012 past searching for epidemiology, diagnosis, clinical manifestations, management, and the role of the spleen in infectious mononucleosis.

Study Design:

Clinical review.

Level of Evidence:

Level four.

Results:

Infectious mononucleosis is normally encountered in immature athletes. Its disease pattern is variable and tin affect multiple organ systems. Supportive care is the cornerstone, with little function for medications such as corticosteroids. Concrete examination is unreliable for the spleen, and ultrasound imaging has limitations in its ability to guide return-to-play decisions. Exercise does not appear to identify the young athlete at risk for chronic fatigue, but determining who is at take a chance for persistent symptoms is a challenge.

Conclusion:

Return-to-play decisions for the athlete with infectious mononucleosis need to be individualized because of the variable affliction course and lack of evidence-based guidelines.

Keywords: mononucleosis, spleen imaging, splenomegaly, chronic fatigue

The question of when an athlete can render to play post-obit contraction of infectious mononucleosis (IM) is complex because of the serious complication of splenic rupture.^1,43 Splenic injury is rare but may occur spontaneously or with minor abdominal trauma.^26,32 Protecting the athlete from splenic rupture should be at the forefront when making return-to-play decisions. The natural progression of splenic enlargement can exist unpredictable, and splenic dimensions vary with body size and type so the office for ultrasonography is unclear. IM besides carries the run a risk of persistent or chronic symptoms, most notably fatigue, likewise as neurologic, hematologic, cardiac, and respiratory complications.^1,14 The variable presentations and form of this disease pose a claiming for physicians, as evidence-based protocols for return to competition are defective. Therefore, decisions regarding athletic participation should exist made on an private basis.

Epidemiology

Infectious mononucleosis is a self-limiting clinical syndrome typically acquired by the Epstein-Barr virus (EBV).^1,20 Epstein-Barr virus is a fellow member of the herpes virus family that causes benign lymphoproliferative IM but has also been linked to Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma.⁴² Epstein-Barr virus exposure is common worldwide, with xc% to 95% displaying amnesty past adulthood.^six,xx,30,34 Infection with EBV is often clinically silent in babyhood but results in symptomatic illness during adolescence or adulthood.⁴¹ The incidence of IM in the United States is approximately 500 cases per 100,000 persons per year, with the highest incidence in the 15- to 24-year-old age grouping.^seven The incidence is well-nigh negligible by 35 years of historic period.^one,20 Among college students, up to half may be initially seronegative, with 15% of that group eventually developing the disease.^26,34 In that location is no sexual practice predilection for IM.⁴⁵ There is a higher incidence of IM in the white population in comparing with the African American population, believed to be due to before exposure to EBV resulting in subclinical manifestations.^xvi

While moderate exercise can be beneficial to the immune system, the elapsing and intensity of exercise performed by the competitive athlete may impair immune function.^xiv This has been previously described by a "J curve," where exercise tin can initially decrease the charge per unit of affliction merely has a negative issue at more intense levels.^14,19 There is no evidence supporting IM existence more prevalent in the educatee-athlete population in comparison to nonathletes, only their higher incidence of trauma certainly places them at a higher gamble for complications.³⁴

Pathogenesis

Epstein-Barr virus, like other members of the canker virus group, persists within the host in its latent grade. The virus is transmitted via saliva, giving the virus the reputation of a "kissing disease," and has an incubation period of 30 to 50 days.⁴⁵ Epstein-Barr virus targets memory B lymphocytes and induces their proliferation. As a result, a cell-mediated immunity response produces a clonal expansion of T lymphocytes. The cytotoxic T lymphocytes release a multitude of cytokines that cause the classical IM symptoms. Additionally, the T-lymphocyte response produces lymphoid hyperplasia, a marked lymphocytosis, and singular lymphocytes in a peripheral blood smear.²⁶ Lytic infection of tonsillar crypt epithelial cells and B lymphocytes results in viral reproduction and shedding into saliva, which decreases exponentially over the first year of infection only will continue to persist for life.¹³

Clinical Manifestations

The history and physical examination are pertinent for making the correct diagnosis. The long incubation period makes it difficult to determine the source or onset of IM, even so in that location is a classic 3- to 5-day prodromal menstruation consisting of malaise, fatigue, and anorexia. Symptoms and so progress into the classic "triad" of IM—pharyngitis, fever, and lymphadenopathy. At times, the presentation of IM is much more atypical and tin affect many different organ systems. Fatigue and pharyngitis are the most debilitating symptoms and often nowadays every bit the main complaint. The posterior cervical lymph nodes are more commonly involved in IM, with axillary and inguinal lymphadenopathy less likely to occur. Oft, the signs of IM may be subtle, with the athlete presenting with nada more than fatigue, lack of energy, or diminished performance. Other features of IM may include posterior palatine petechiae, jaundice, exudative pharyngitis, rash, and splenomegaly.^{fourteen,29,34}

Posterior palatine petechiae occur in nigh one tertiary of cases and are highly suggestive of IM.^viii This feature distinguishes an acute EBV infection from other causative agents, such as acute herpes simplex virus infection, HIV infection, or streptococcal infection, that could exist included in the differential diagnosis.⁴⁷

Jaundice is rare, occurring in less than x% to 15% of patients.²⁷ However, approximately 90% of patients have mildly elevated liver enzymes facilitating in the diagnosis of IM.³⁶

Exudative pharyngitis and concomitant tonsillar enlargement tin cause obstacle of the airway, leading to devastating consequences.^14,20 The exudation has been described as white, gray, or green and even necrotic in appearance. The enlargement of the tonsil is due to lymphoid hyperplasia and pharyngeal inflammation. Often mistaken for streptococcal pharyngitis, the clinician must be vigilant for clues of IM such as fatigue, the appropriate age grouping, or posterior cervical lymphadenopathy.²⁶ Positive testing for streptococcal pharyngitis does non completely exclude IM, since simultaneous infection may exist seen in up to 30%.²⁹

A rash is seen in nigh 10% to 40% of patients. The rash is transient and generalized with maculopapular, petechial, or urticarial features (Figure 1). This is more commonly seen in a patient who has been treated with penicillin in an effort to eradicate a presumed group A Streptococcus infection. This is almost pathognomonic for IM. Other antibiotic classes have been implicated, but the penicillins are the most widely reported to produce this effect.^13,14

Rash presenting with infectious mononucleosis.^v

Splenomegaly in IM occurs every bit a effect of lymphocytic infiltration enlarging the spleen beyond protection from the rib cage and creating an organ that is susceptible to rupture either spontaneously or traumatically.^26,32 This infiltration may also alter splenic architecture, resulting in a more susceptible construction.^32,43 The ability to determine the presence of splenomegaly by physical examination is unreliable, with i study showing as lilliputian as 17% of cases existence identified on physical test.^1,12,43,45 Ultrasonography is the imaging modality of option.^1,43 Linear measurements are used since measuring spleen book is technically difficult. Additionally, normative data are lacking equally studies take shown that "boilerplate" spleen size tin be variable, so this tool has limitations as far every bit its usefulness in predicting a safe return to play.^19,28,39,43

Since baseline spleen size measurements on competitive athletes are impractical, serial ultrasound measurements may be employed to determine the course of splenomegaly in IM. A report of 19 patients with IM found normal spleen measurements in 84% at 1 month subsequently diagnosis and 100% at two months. In this series, there were no series or baseline measurements, leaving the possibility that the "normal" results may still take been abnormal for that individual.³² In a study where baseline spleen measurements were obtained in a large cohort of athletes, those with IM underwent serial ultrasonography. Top splenic enlargement was typically seen within 2 weeks but, in some, extended to 3.5 weeks. For the majority, splenomegaly resolved in four to six weeks.¹⁸

The long incubation flow and variable nature of the illness can make the job of identifying onset of disease a claiming. The astute stage of IM can resolve as quickly equally 7 days, but usually takes between 2 and iii weeks from the onset of symptoms.^14,45 This is followed by a recovery catamenia that may take up to 2 to three months.^1,14,26 IM is typically self-limiting, but an acute EBV infection is a risk factor for chronic fatigue, with symptoms lasting in excess of half-dozen months.^1,23

Diagnosis

The diagnosis of IM tin can be made through history and physical examination equally well as atypical laboratory findings (Table 1).^1,20,33 The differential diagnosis includes group A streptococcal infection, influenza virus, herpes virus, cytomegalovirus, toxoplasmosis, astute HIV infection, and many more bacterial and viral pathogens.^1,43 Diagnostic criteria for IM (Hoagland criteria) include greater than 50% lymphocytes and at least ten% atypical lymphocytes with fever, pharyngitis, adenoapthy, and a positive serologic exam.¹⁷ The presence of singular lymphocytes has a sensitivity of 75% and a specificity of 92%.^nine Other laboratory findings that could exist suggestive of IM include transient neutropenia, thrombocytopenia, and elevated liver transaminases.^27,45 Anemia is considered a feature of complicated IM and is indicative of autoimmune hemolytic anemia, splenic rupture, aplastic anemia, and even disseminated intravascular coagulation.²⁴

Table ane.

Diagnostic tests for infectious mononucleosis, %^{thirteen,18-21,44}

Test	Sensitivity	Specificity	Positive Predictive Value	Negative Predictive Value
Heterophile antibody—latex agglutination test	87	91	52	ii
Heterophile antibody—solid phase immunoassay	83	97	75	2
Singular lymphocytes ≥10%	75	92	51	3
Atypical lymphocytes ≥50%	66.3	84.5	31	4
VCA IgM and IgG	97	94	64	0.five
PCR for EBV DNA	80	94	95	79

Heterophile antibodies are a characteristic feature of IM.^9,17,33 Epstein-Barr virus stimulates the evolution of immunoglobulin M (IgM) antibodies directed against viral antigens.^9,17 These antibodies then cross-react with antigens found on sheep and equus caballus ruddy cells. Rapid (monospot) tests for these heterophile antibodies are used to screen patients for IM. About 85% to 90% of patients with confirmed IM will demonstrate a positive heterophile test by week 3 of disease.^17,27 Therefore, the first few weeks of illness may effect in a negative heterophile test whereby the fake-negative rate tin can exist as high as 25% in the beginning week and repeated testing is required at a afterward appointment.³² A definitive diagnosis can exist made for IM with more than sensitive tests that detect viral capsid antigens for IgM and IgG antibodies.^24,33 The negative likelihood ratio for detecting viral capsid antigens is 0.03 in comparison with the negative likelihood ratio for the heterophile antibody test, which is 0.xiv to 0.18. Viral capsid antigen testing is useful for patients who initially had a negative heterophile antibody exam.^2,10 Epstein-Barr virus is the causative agent in ninety% of cases of IM, but other viruses rarely produce a "mono syndrome."^eleven The about common agents are cytomegalovirus and toxoplasmosis. The illness would accept the features of IM, but EBV testing would be negative.¹¹

Management and Prevention

There is no specific treatment for IM. Supportive therapy is the mainstay of care, which includes adequate rest, hydration, and analgesics.^xiv,20,33 Over-the-counter hurting medication, such equally anti-inflammatories, is generally sufficient to manage the myalgias and pharyngitis. Acetaminophen is appropriate but used judiciously because of potential liver complications, every bit IM ofttimes causes tiptop in liver role tests.¹⁵ Aspirin should exist avoided because of haemorrhage risks and an association of IM with Reye syndrome in children.^14,33 There is no office for antivirals or antibiotics.^14,15,20,34 Despite the fatigue, there is no role for strict bed rest. For patients with a quick recovery of symptoms, a return to light exercise in as little every bit 2 weeks from the onset of illness may provide a benefit. Shut follow-upwards is recommended to ensure resolution of all symptoms equally the athlete may gamble progression to more chronic symptoms, specifically fatigue.^20,46

The office of corticosteroids in the treatment of IM is of involvement but there is bereft testify to recommend their utilize in unproblematic IM. At that place does not appear to be whatever improvement in elapsing of symptoms or progression to chronic symptoms.^four,44 In spite of this, a significant number of patients are given corticosteroids for symptom control in the absence of the complications of IM.⁴¹ In that location is general consensus that corticosteroids exercise have a part when at that place is airway obstruction equally a result of laryngeal edema.^4,33,41 Other severe complications of IM warranting corticosteroid handling include hepatitis, myocarditis, or hematologic abnormalities.^four,33,41 Risks and benefits must be weighed, as the agin effects of corticosteroids in IM may include infection or even femoral head necrosis.^4,xiv,20,41

Transmission is by close contact via saliva, then isolation is not necessary. Common sense precautions such every bit paw washing and not sharing water bottles are typically acceptable. Unfortunately, the long incubation menstruation tin can confound efforts to forestall infecting others.^17,34 Current advances are beingness made to develop an EBV vaccine. In a stage two trial, vaccine recipients were less likely to have symptoms of IM during principal EBV infection compared with those who were not vaccinated.³⁸ Nonetheless, the recipients were not protected against acquiring EBV.³⁸

Render-to-Play Considerations

At that place is full general consensus that the athlete must be asymptomatic with resolution of symptoms such every bit fever, fatigue, and pharyngitis before they initiate whatsoever render to activity.^xx,31,33 The majority of those with IM volition non feel well enough to pursue activeness during the kickoff weeks of affliction, which makes clinical decisions easier. They ought to be afebrile and well hydrated.^31,33,45 Any business concern for oropharyngeal issues or airway compromise would clearly prohibit any sports participation.^{14,twenty,34,45} Although their level of workout would exist expected to turn down, the athlete should have full resolution of fatigue or risk prolonged symptoms.^ane,34 Resolution of laboratory abnormalities (eg, elevated white claret prison cell counts, abnormal liver function tests) do not play a role in profitable return-to-play decisions.³⁴ It is difficult to predict who is at risk for prolonged symptoms, merely competitive athletes may actually be at a lower level of risk for chronic fatigue.^1,iii,34 Nonetheless, the athlete should "feel good" before considering render to play.^one,iii,34

For those athletes who practice have "early" resolution of symptoms, there is little consensus on the optimal time for render to activity. Keeping in mind that the highest adventure for splenic injury is during the first 21 days of disease, it has not been shown that early return to calorie-free activity causes deleterious furnishings.^21,26,43 The athlete should engage in very light activity at beginning (walking), with a gradual progression to light aerobic activity.^33,36,45 Although information technology may take 2 to 3 months for the athlete to fully recover from IM, it appears they tin initiate activity well before.^ane,34,43,46

The render to activities that place the spleen at risk for injury is a confounding matter. At this time, recommendations vary, and in that location is a lack of evidence-based protocols.^33,45 The concern is the athlete participating in any action that increases intra-abdominal pressure and contact sports that would place the chest or abdomen at risk for trauma.^33,45 In ultrasound studies, top spleen size is typically noted within the commencement 2 weeks of illness, only may extend to three.5 weeks.¹⁸ The majority of spleen injuries occur within the offset 21 days of illness and are exceedingly rare at >28 days.^21,26,43 Fortunately, splenic rupture is rare, occurring in <0.5% of those with IM, just its consequences can be severe.^20,34,43

Almost recommendations support that the athlete with IM should residual for 3 weeks and so brainstorm resumption of light activity.^{i,twenty,25,34} Keeping in mind there is so much individual variability to this disease and the verbal date of onset is often hard to establish, return-to-play recommendations should exist individualized. Ultrasonography may play a function in render-to-play decisions, only the variability in baseline spleen size can limit its utility.^19,28,39,43 Additional factors include the nature of the activity or sport (contact vs noncontact) and the flavor in which the disease occurs (competitive season vs off-flavour). Any return to competition must include a detailed explanation of the risk of splenic injury, since total recovery may take months (Figure 2).

Return-to-play recommendations for infectious mononucleosis (IM). Level of evidence, 4.^{7,9,24,28,32,35,forty,41}

There take been some novel attempts made to protect the spleen from contact for collision sports with a flak jacket²² or a customized protective brace for a college basketball game season.³⁷

Conclusion

Counseling the athlete with IM remains a challenge. The disease has a long latency period, the onset of illness may be difficult to place, and the disease course is variable. In that location is no specific concrete exam finding, laboratory examination, or imaging modality that provides a definitive answer. To minimize complications of IM, return-to-play decisions must be individualized.

Footnotes

The authors study no potential conflicts of involvement in the development and publication of this manuscript.

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