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Atypical Pneumonia in Active Patients

Clues, Causes, and Return to Play

Thomas J. Melham, MD

Internal Medicine Series Editor: Donald M. Christie, Jr, MD


In Brief: Atypical pneumonias can affect young, otherwise healthy individuals who have close contact with one another, such as athletes in team sports. Symptoms, which often progress gradually, may mimic an upper respiratory tract infection. Mycoplasma, chlamydia, and legionella organisms, along with certain viruses, are the usual atypical pneumonia agents, and antimicrobial therapies are recommended. Because complications, though rare, can be protracted, affect athletic performance, and result in sudden death, return-to-play guidelines should be cautious and patient- and sport-specific.

Atypical pneumonia is commonly categorized as community-acquired pneumonia (CAP) and may differ both clinically and radiographically from classic lobar, or "typical," pneumonia caused by bacteria (1-7). Also known as "walking pneumonia," atypical pneumonia is usually found in relatively young, otherwise healthy individuals. Predisposing factors can put many active patients at risk. Especially in 18- to 40-year-olds, these include close contact with a number of people (as in team travel or dormitory living), time of year, possible overtraining, and being debilitated from hectic schedules that leave little time for sleep.

Pneumonia remains the leading cause of death from infection (8) and is one of the leading causes of infection-related mortality in the United States (5). "Atypical" pneumonias are not necessarily less virulent to those infected than are "typical" pneumonias (5).

Clinical Clues for Diagnosis

The following case report illustrates clues suggesting an atypical pneumonia.

Case report. A 22-year-old male college football player presented at the student health center during football season with a 1- to 2-week history of nonproductive cough, malaise, low-grade fever, and a mild sore throat. He had been seen at the center a week earlier. At that time an upper respiratory tract infection had been diagnosed, and a beta-lactam antibiotic prescribed. He had also been instructed to return if he was not better after 3 to 5 days. At the time of this second visit, symptoms had not abated and he was occasionally coughing up thin, slightly discolored sputum.

On examination he appeared tired and more ill than expected. His temperature was 100.8°F (38.2°C), his blood pressure was 118/76 mm Hg, and his pulse was 78 per minute. He had postnasal drip and erythema of the tympanic membranes with no effusion or exudate. On auscultation, he had coarse, diffuse breath sounds that did not clear with cough, and faint wheezing was detected in the posterior mid to lower lobes. There was no dullness on percussion. Heart, abdomen, and skin examinations were unremarkable. Laboratory tests showed a white blood cell count of 12,800 cells/mm3, with a slight elevation of segmented neutrophils. Sputum Gram's stain was negative for a predominant pathogen and showed a few polymorphonuclear leukocytes.

The clinical findings suggested atypical pneumonia, and antibiotic coverage was changed from the beta-lactam to a newer macrolide. The patient began to improve after 5 days, and by day 12 of the antimicrobial therapy, all symptoms had resolved. One week later he was allowed to resume daily light workouts consisting of bicycling and running, starting at about 50% of his usual training level, with no full sprinting and no contact. He was allowed to increase his activity by about 25% over 3 days as long as no problems arose. He had no recurrence of symptoms during this week of light training, and was allowed to return to play.

Discussion. Specific clues, both pulmonary and extrapulmonary, may help to differentiate atypical (nonbacterial) from typical (bacterial) pneumonia (table 1: not shown). Like the patient in the case report, patients who have atypical pneumonia usually begin having symptoms of an upper respiratory tract infection, often with a sore throat that may progress after a few days to a cough. Slowly progressing symptoms might include a low-grade fever, generalized muscle aches and pains, and a nonproductive cough or scant sputum production with no predominant pathogen seen on Gram's stain. Fatigue and malaise may also be present. Some rhinorrhea is present in 25% to 50% of patients. Chest radiographs (figure 1: not shown) may reveal a patchy infiltrate. Extrapulmonary manifestations may include abdominal pain, headache, diarrhea, and, in up to about 20% of patients, ear pain.

While much overlap occurs in the presentation of various pneumonias (table 2), the physician treating active patients who have pneumonia should be on the lookout for atypical pneumonias when the patient has associated ear pain, headache, abdominal pain, diarrhea, mental confusion, or a rash. Clinical presentation, however, is only approximately 40% accurate in distinguishing typical from atypical pneumonias, and in clinical practice a causative organism is identified in only about 50% of all pneumonia cases (5).

Table 2. Distinguishing Signs and Symptoms of Pneumonia Caused by Common Atypical Organisms*

OrganismPossible Characteristics

Mycoplasma pneumoniae Arthritis
Cough (dry, nonproductive)
Diffuse lower lobe infiltrates
Erythema multiforme**
Otitis media or bullous myringitis
Chlamydia pneumoniaeConjunctivitis
Cough (dry, nonproductive)
Diffuse lower lobe infiltrates
Legionella pneumophila Diarrhea
High fever
Mental status changes
Relative bradycardia
Renal impairment
Influenza or parainfluenza viruses Chills
Muscle aches
Sore throat

*Significant symptom overlap exists between forms of atypical pneumonia; neither individual characteristics nor the cluster of characteristics is diagnostic unless otherwise noted.

**Pathognomonic in the setting of pneumonia.

Causative Organisms

Mycoplasma, chlamydia, legionella, and viruses are the usual agents of atypical pneumonia. (table 3: not shown. For a more complete listing of microorganisms that may be implicated in causing pneumonia, refer to Principles and Practice of Infectious Diseases(16).) In children and adolescents aged 5 to 20, Mycoplasma pneumoniae causes 30% to 60% of CAP. M pneumoniae probably causes the majority of cases of CAP in people under 40, while Chlamydia pneumoniae causes 6% to 17% of CAP (4).

A variety of typical and atypical organisms may cause CAP (5,8-12). Infectious agents that can cause pneumonia in a relatively young and healthy athletic population are more likely to be atypical (nonclassical) organisms; typical bacterial pneumonia occurs more often in older patients who have underlying lung disease or other debilitating conditions such as diabetes, alcoholism, seizure disorder, or stroke.

The agents causing atypical pneumonias are further subclassified by some authors as zoonotic or nonzoonotic. The atypical nonzoonotic agents include Legionella pneumophila, C pneumoniae, and M pneumoniae. The atypical zoonotic agents include Coxiella burnetii (Q fever), Francisella tularensis (tularemia), and Chlamydia psittaci (psittacosis).

Clues to specific agents may include travel history, sexual contacts, risky behavior patterns, and exposure to animal or human carriers. Keep in mind that pneumonias caused by Pneumocystis carinii and Mycobacterium tuberculosis are on the rise, and there have been recent reports of a Hantavirus outbreak.

Specific Forms of CAP

The following discussion is limited to the more common entities that are likely to be encountered by physicians who provide healthcare to athletes. Antimicrobial therapies are included here; see table 4 (not shown) for dosage.

Mycoplasma pneumoniae. The mycoplasmas are the smallest free-living organisms. M pneumoniae (also called Eaton agent or pleuropneumonia-like organism [PPLO]) was one of the organisms originally found to cause atypical pneumonia. It is spread from human to human primarily via aerosolization and contact with infected droplets. M pneumoniae pneumonia is most common in the fall and winter months, but is seen year-round both epidemically and endemically, with outbreaks every 4 to 7 years (11). It is more common in children and young adults, and has an incubation period of 3 weeks (7,8).

Patients' symptoms may begin with a low-grade fever, mild sore throat, and ear pain. Muscle pain, headache, diarrhea, and a dry cough or slight nonpurulent sputum production are also seen. Abnormal breath sounds may be heard on chest auscultation. These patients commonly have sinusitis, otitis, or bullous myringitis. Erythema multiforme is rare but quite specific for M pneumoniae if seen in a patient with pneumonia. Rare complications include meningoencephalitis, Guillain-Barré syndrome, mononeuritis multiplex, pericarditis, and myocarditis (13,14).

With M pneumoniae infection, the erythrocyte sedimentation rate may be slightly elevated, and a mild leukocytosis may be present, usually less than 15,000 cells/mm3. Sputum Gram's stain may show a few polymorphonuclear white blood cells and usually no bacteria. Cold agglutinins are present in about 75% of patients in a titer of 1:64 or more. A chest radiograph typically demonstrates a patchy unilateral infiltrate in the lower lobes; rarely, a pleural effusion will be seen. M pneumoniae can be cultured with special media, but this is not routine (11). A polymerase chain reaction (PCR) test for M pneumoniae and other atypical pneumonia organisms is available through Specialty Labs (Santa Monica, California). These relatively expensive tests are performed on Thursdays, and results are available within 24 hours.

Treatment is a 2- to 3-week course of erythromycin, azithromycin, clarithromycin, dirithromycin, or doxycycline (8,11,15,16). Patients continue to be infectious for weeks, even after starting antibiotics, and may have a persistent cough for 6 weeks (4). Radiographic findings may be evident for months. In addition, pneumonia caused by M pneumoniae has been implicated in the onset of asthma in adults.

Chlamydia pneumoniae. C pneumoniae (also called TWAR agent) was initially isolated from the conjunctivae of a child in Taiwan (TW-183) and from the pharynx of a University of Washington student (AR-39).

C pneumoniae, like other chlamydia, is an obligate intracellular organism containing both DNA and RNA. The mode of infection is from human to human, most likely via respiratory secretions, with no animal reservoir. The infection is uncommon in children—epidemics occur mainly in college students and military recruits. Reinfection is common and has been linked to coronary artery disease (3).

Initially, C pneumoniae may manifest with pharyngitis, hoarseness, nonproductive cough, and usually fever. The gradual onset of symptoms over days to weeks may appear biphasic, or as two separate infections. Patients may also have sinusitis or rhinitis and, rarely, pleuritic chest pain. They may also have arthralgias, myalgias, or headache. Rhonchi and rales may be heard on chest auscultation.

With C pneumoniae infection, the erythrocyte sedimentation rate is elevated, but the white blood cell count may be normal or elevated. Chest radiographs demonstrate a nonspecific interstitial lower lobe or funnel-shaped infiltrate. Pleural effusions are small and infrequent. C pneumoniae does not grow well in culture. Recent infection can be identified by serologically measuring a single high titer or a four-fold rise in antibody titers of either IgM (2 to 4 weeks) or IgG (6 to 8 weeks). The PCR test can also detect C pneumoniae.

Treatment is with doxycycline, erythromycin, azithromycin, or clarithromycin for 14 days (8,11,15,16). Strains resistant to erythromycin have developed, and the newer macrolides are effective for such cases. Recovery is slow. Both the cough and malaise may persist, with retreatment occasionally indicated.

Legionella pneumophila. The L pneumophila species of legionella is implicated in up to 15% of CAP cases (4). L pneumophila is an aerobic gram-negative bacillus, and it can be grown in nonstandard culture media. Legionellas grow best in warm fresh-water environments such as water heaters and humidifiers. Transmission of the organism is via inhalation of aerosols or aspiration of infected liquids, and the incubation period is 2 to 10 days. It is more common in older people, smokers, patients with lung disease, and those who use corticosteroids.

Pontiac fever is a less severe, nonpneumonic form of the infection. Common symptoms include dry cough, coryza, headache, muscle pain, low-grade fever, and malaise. The pneumonic form, also called legionnaire's disease, has the same flu-like symptoms but with a higher fever (102°F to 105°F [38.9°C to 40.6°C]), rigors, and relative bradycardia. Purulent sputum may develop later with hemoptysis, pleuritic chest pain, and/or dyspnea. Abnormal breath sounds may be heard. Patients may have watery diarrhea and abdominal pain, with occasional nausea and vomiting, and they may also be delirious. Although rare, proteinuria, microscopic hematuria, renal insufficiency, pericarditis, endocarditis, myocarditis, or pancreatitis may occur.

Helpful laboratory findings include elevated transaminases, hypophosphatemia (which specifically points to legionella), mild leukocytosis primarily with polymorphonuclear cells, and hyponatremia. Sputum Gram's stain demonstrates polymorphonuclear leukocytes or monocytes, but no bacteria. The chest radiograph shows a patchy unilateral infiltrate that characteristically will progress rapidly and asymmetrically. The diagnosis can be established rapidly via direct fluorescent antibody staining of tissue or fluid, although some cross-reactivity can occur with Bacteroides fragilis and Pseudomonas species. Both a urinary antigen test and serologic testing are available for legionella. A single antibody titer of greater than or equal to 1:256, or a fourfold rise in titer between acute and convalescent phases, confirms the diagnosis. The PCR test is also effective for diagnosing L pneumophila.

Treatment is with erythromycin plus rifampin, azithromycin, clarithromycin, pefloxacin, ciprofloxacin, ofloxacin, or trimethoprim-sulfamethoxazole (1,8,15,16). For seriously ill patients, treatment may be needed for up to 4 weeks.

Influenza and parainfluenza virus. Outbreaks of pneumonia caused by influenza viruses usually occur in the winter months of December to March and are transmitted via respiratory particles. Parainfluenza virus is more common in late summer and fall. These viral pneumonias typically begin with fever, chills, sore throat, and muscle aches. Diffuse reticular infiltrates are often noted on chest radiographs. A rapid influenza antigen test may be helpful but is not universally available. Influenza A is far more common than influenza B in causing pneumonia; however, influenza B more often sets the stage for bacterial superinfection, especially with staphylococcal pneumonia.

Treatment for influenza A is amantadine (first line) or rimantadine. Neither is useful for influenza B. Vaccination is still the best option for preventing both influenza A and B, despite the persistent and false belief that the vaccine can cause the illness (8,11). Some advocate use of these antimicrobials for the prevention of influenza A infection, but not in otherwise healthy individuals (15). Physicians should advise their active patients, especially those who are members of traveling winter sports teams, to receive the seasonal trivalent vaccine.

Other Causes and Treatments

Usually, empiric antibiotic therapy is successful in treating the more common agents causing pneumonia in the young, athletic population. If a patient is not responding appropriately, consider more esoteric causes of infection, such as mycoses (coccidioidomycosis, histoplasmosis, and cryptococcosis); with the increase in HIV infection, don't overlook the possibility of tuberculosis or Pneumocystis carinii (see "Tuberculosis in a Young Baseball Player," September, page 112). Also, consider respiratory syncytial virus since it can mimic asthma, influenza, or colds in this age-group.

Return-to-Play Criteria

Once the diagnosis of atypical pneumonia is made and appropriate treatment undertaken, the physician must direct convalescence and return to play. Physicians must be especially attuned to an athlete's need to return to practice and competition as soon as possible.

The literature yields no data regarding when athletes with pneumonia, atypical or typical, should be allowed to return to play. However, return-to-play criteria and recommendations have been published (17-19) pertaining to patients who have upper respiratory tract illnesses, systemic illnesses like mononucleosis, and other seemingly less severe types of infection.

These studies (17-19) have demonstrated the adverse effects of an upper respiratory tract illness on pulmonary, cardiac, and skeletal muscle function. Lung compliance, diffusion capacity, FVC, FEV1, and flow rate are all decreased in an infected athlete while at rest, and respiratory muscle weakness is present. These findings persist for 7 to 10 days after infection; full recovery is seen by 14 days. Infections cause decreased activity of important enzymes in both skeletal and cardiac muscle, decreased muscle glycogen utilization, and ultrastructural abnormalities distinguishable by electron microscopy. In athletes who report having myalgia, decreases in muscle performance correlate well with the amount of pain (18).

Febrile subjects show a decrease in isometric and dynamic strength as well as endurance. Stroke volume is decreased both during and after a fever. With fever, cardiac output is maintained by an increased heart rate; however, cardiac output decreases in the early postfebrile recovery period. Decrease in cardiac output correlates well with the degree of fever (17-19).

Finally, although complications are rare, they can significantly affect performance, be very protracted, and may even result in sudden death. Physicians who treat athletes are recognizing postinfection fatigue syndrome and athletes' loss of form even after minor illnesses, as well as the possibility of postviral or postmycoplasma myocarditis or pericarditis, which in turn may increase the risk of acute arrhythmias leading to sudden cardiac death (13,14,18).

Most athletes can begin a light workout at approximately 50% of normal intensity 7 days after complete resolution of all systemic signs and symptoms, gradually increasing activity over the ensuing 7 days if no problems arise. Resumption of full exercise after atypical pneumonia should not begin before 10 to 14 days after complete resolution of all systemic signs and symptoms. However, for those athletes who have viral infections with myalgias and fever including suspected or confirmed coxsackievirus or influenza pneumonia, resumption of full training should not begin until 4 weeks after all systemic signs and symptoms have resolved, to avoid incurring cardiac complications. Although cardiac complications are rare, because of possible pericarditis or myocarditis associated with M pneumoniae, one might advise an athlete who has been severely ill to wait 4 weeks to resume full training if a true M pneumoniae infection has been documented (13,14).

Deconditioning begins as early as 4 to 5 days after onset of inactivity in otherwise healthy athletes. Reconditioning must proceed at a gradual, progressive pace that avoids inadvertent soft-tissue injury. Above all else, the physician treating active patients should individualize recommendations for the convalescent and retraining period according to the patient's preexisting fitness level and the type and severity of the atypical pneumonia.


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Dr Melham is a sports medicine physician at the Central Indiana Orthopedics and Sports Medicine Clinic in Muncie, Indiana. He was formerly medical director of the Indiana State University student health center and of the Sports Plus sports medicine clinic at the Columbia Terre Haute Regional Hospital, and was team physician for several Terre Haute, Indiana, area high schools and colleges. He is a member of the American Medical Society for Sports Medicine (AMSSM) and the American College of Sports Medicine (ACSM). Dr Christie practices internal medicine and sports medicine at the Community Health Plan in Poughkeepsie, New York, is a charter member of the AMSSM, and is a fellow of the ACSM and the American College of Physicians. He holds a certificate of added qualifications in sports medicine. Address correspondence to Thomas J. Melham, MD, Central Indiana Orthopedics and Sports Medicine, State Rd 3, So Hills Plaza, 113 S Memorial Dr, New Castle, IN 47362-4947; e-mail to [email protected].