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* From the Division of Pulmonary, Allergy, Critical Care and Occupational Medicine (Drs. Olafsson, Sarosi, and Mastronarde), Indiana University School of Medicine, Indianapolis; and Respiratory and Critical Care Consultants (Dr. Naum), Methodist Hospital, Indianapolis, IN
Correspondence to: Eric J. Olafsson, MD, VAMC, c/o Nedra Huett, Division of Pulmonary Medicine, 481 W Tenth St (111P), Indianapolis, IN 46202; e-mail: ejolafsson{at}yahoo.com
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The patient was taking no medications, and his only medical history was a severe viral infection at age 2 that required temporary tracheostomy. The patient did not know any other details of that illness. He was employed as a machinist in a factory. He quit smoking 3 weeks before hospital admission after a 6-pack-year history. The patient denied using illicit drugs, injection drugs, or alcohol.
Physical Examination
Temperature was 38.7°C, heart rate was 129 beats/min, respiration rate was 24 breaths/min, BP was 117/75 mm Hg, and resting oxygen saturation was 92% on room air. The patient appeared in minimal distress and was speaking in full sentences during the interview. Examination of head, ears, eyes, nose, and throat was unremarkable. There was no lymphadenopathy of the neck or supraclavicular regions. Chest examination revealed bibasilar rales and hyperresonance over the right hemithorax. There was no clubbing of the extremities, no hepatosplenomegaly and the remainder of the physical examination was within normal limits.
Laboratory Data
The WBC count was 7,600/µL, with a differential of 79% neutrophils, 10% lymphocytes, and 10% monocytes. The hemoglobin, platelet count, serum electrolytes, renal function, and urinalysis were all normal. The sedimentation rate was 33 mm/h. The chest radiograph revealed a large right pneumothorax and bilateral pleural effusions (Fig 1
). A chest tube was placed in the right superior hemithorax to re-expand the lung and obtain a sample of pleural fluid for analysis. The amber-colored fluid contained 3,700 WBCs/µL (with a differential of 46% neutrophils, 48% lymphocytes, and 6% monocytes). Chemistry studies revealed a glucose of 50 mg/dL, lactate dehydrogenase of 768 U/L (serum lactate dehydrogenase, 198 U/L), and protein of 5.0 g/dL (serum protein, 6.6 g/dL). Stains for acid-fast bacilli (AFB) and fungi were negative, and the Gram stain revealed 4+ WBCs but no organisms. Culture findings for bacteria were subsequently negative. The patient was admitted to the hospital.
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The patient was then started on a four-drug regimen of isoniazid, rifampin, ethambutol, and pyrazinamide. His right pneumothorax had resolved, and his chest tube was discontinued. Next, a diagnostic bronchoscopy was performed. The airways were mildly edematous diffusely, but no endobronchial lesions were observed. A mild-to-moderate amount of purulent secretions were observed in the right upper lobe. A BAL was performed.
What infectious agents should be included in the differential diagnosis of this patient with fevers, cough, pneumothorax, and bilateral pleural effusions?
Diagnosis: Mycobacterium kansasii
Although numerous pulmonary pathogens present with pleural involvement, the differential diagnosis of chronic pulmonary infections involving the pleura is more limited. Mycobacterium tuberculosis and the nontuberculous mycobacteria, nocardiosis, actinomycosis, blastomycosis and coccidioidomycosis are all reported to cause chronic parenchymal infection that can involve the pleural space. Conversely, cryptococcosis, histoplasmosis, and aspergillosis rarely have pleural involvement accompanying a chronic parenchymal infection.
M kansasii is part of a group of organisms known as nontuberculous mycobacteria (NTM). Typically found in the environment (ie, tap water, soil), these organisms have been known to cause disease in humans for a half century. There appears to be a predilection for NTM in the immunosuppressed population, but these organisms can also cause disease in immunocompetent individuals. Mycobacterium avium complex is the most common isolated NTM, with Mycobacterium fortuitum next and M kansasii third most common.
The prevalence of M kansasii appears to be rising in the HIV era. A population-based laboratory surveillance study in California from 1992 through 1996 by Bloch et al found an incidence of 2.4 cases per 100,000 people. This study identified 270 total cases of M kansasii, of which 69% were found in HIV-positive patients. HIV-negative patients tended to be older (median age, 61 years vs 39 years) and white (62% as opposed to 49%). Lower socioeconomic status and homelessness also appeared to be risk factors for M kansasii infection, as did male sex and a history of tobacco abuse.
Nearly all of the NTM are ubiquitous in the environment. M kansasii is somewhat different than the other NTM in that it has not been found in soil or natural water supplies. Instead, this organism has been isolated repeatedly from tap water in cities where M kansasii is endemic. A study by Steadham in Texas revealed M kansasii to be most often found in urban areas. Hence, because M kansasii is not an environmental contaminant or colonizer, it is considered a pathogen, indicative of disease, when recovered.
Microbiologically, M kansasii is readily identified in the laboratory. This organism has a characteristic long bacillus appearance on acid-fast smears. It may also have a "beading" appearance, which may serve as a clue pointing toward M kansasii instead of M tuberculosis.
Clinically, M kansasii pulmonary infection presents similar to tuberculosis. In 1999, Menziez presented evidence that there is cross reactivity between M tuberculosis and NTM antigens, leading to a false-positive purified protein derivative in some NTM patients. Cough with sputum and night sweats are two of the most frequent symptoms. Chest pain, hemoptysis, and weight loss are quite common. Insidious onset is more common than an acute presentation. Affected patients often have underlying lung disease as a risk factor for M kansasii infection. For instance, Bloch et al reported in their population-based study that only 40% of all HIV-negative patients with M kansasii pulmonary disease had no preexisting medical condition. COPD is the most common associated illness. A history of previous tuberculosis, pneumoconiosis or bronchiectasis (which this patient had) may also provide the proper environment for M kansasii.
Radiologic findings in M kansasii infection may be similar to tuberculosis. Cavitation (which is noted in 75 to 95% of M kansasii cases) and disease in the posterior segments of the upper lobes are the usual features. However, studies have shown some differences in the presentation between the two organisms. For instance, patients with M kansasii infection usually have unilateral disease with right-sided predominance with only 20% of cases being bilateral. Furthermore, cavities tend to be smaller, there is less lower lobe involvement and pleural effusions are less common than in patients with tuberculosis. Unfortunately, none of these differences are specific enough to allow a definitive diagnosis based on radiologic examination alone. Hollings et al recently compared the radiographic findings of Mycobacterium avium intracellulare with M kansasii, and reported M avium intracellulare to have greater degrees of bronchiectasis and frequent centrilobular nodules. M kansasii patients also were noted to have bronchiectasis; however, cavities, a tree-in-bud pattern, and preexisting emphysema were more prominent CT findings. Whether M kansasii causes bronchiectasis or finds bronchiectatic airways a convenient place to prosper remains unclear.
The pneumothorax and pleural effusions in this case are clearly unusual. Review of the literature finds pleural effusions to be rare in M kansasii infections. A study by Christensen et al from 1978 examined the initial radiographic appearance of 187 cases of M kansasii. Only 4% (seven cases) had a defined edge of pleural thickening or fluid blunting a lateral or posterior costophrenic sulcus. In all previous studies in the past 20 years that described the initial radiographic appearance of M kansasii (combined n = 132), there were no reports of pleural effusion as a finding on presentation. In addition, this is the first case report we are aware of that describes a pneumothorax as a finding on presentation of M kansasii.
Diagnosis of M kansasii can be made using the American Thoracic Society (ATS) criteria. The criteria apply to patients with appropriate radiologic findings (ie, cavitary disease, parenchymal infiltrates, or bronchiectasis on CT). One of the three following possibilities must also be met: (1) from three sputum samples or bronchoscopy washes (in the previous 12 months), there must be three positive culture findings with negative AFB smears or two positive culture findings with one positive AFB smear; (2) if only one bronchoscopy wash is available, there must be a positive culture finding with a 2+, 3+, or 4+ AFB smear or 2+, 3+, or 4+ growth on solid media; and (3) if sputum samples or bronchoscopy washes are not diagnostic, there must be a transbronchial lung biopsy or lung biopsy growing M kansasii or a biopsy with pathologic findings of mycobacterial histopathologic features (ie, granulomatous inflammation and/or AFB), and at least one sputum sample or bronchial washing with evidence of M kansasii.
However, not all patients with M kansasii will meet the ATS criteria, specifically, the requirement for isolation of NTM from multiple respiratory specimens. Patients with an abnormal chest radiograph and AFB smear-positive sputum are likely to be initiated on an antituberculosis regimen, which is also active against M kansasii. Thus, subsequent specimens are less likely to be positive for M kansasii. Several studies have suggested that in the appropriate clinical setting, one culture-positive specimen is sufficient for diagnosis of M kansasii.
Treatment of M kansasii involves many of the same antimicrobial agents as therapy for tuberculosis. The recommendation of the ATS for immunocompetent patients is treatment with isoniazid, rifampin, and ethambutol for 18 months, with 12 of those months after sputum culture findings become negative. If rifampin is not tolerated or the organism is rifampin resistant, clarithromycin with sulfamethoxazole may be a reasonable alternative. Most M kansasii strains are resistant to the achievable serum levels of pyrazinamide, so this is not an alternative. The regimen is complicated in HIV-positive individuals by drug interactions involving the protease inhibitors and nonnucleoside reverse transcriptase inhibitors. Depending on the antiretroviral regimen, rifabutin is often substituted for rifampin and clarithromycin is added.
The present patient fits the clinical profile for M kansasii infection. He was a smoker whose symptoms included cough and night sweats. He also has underlying lung disease, as his chest CT revealed regions of bronchiectasis. The etiology of the bronchiectasis is unclear, though he did have the history of a severe viral infection as a young child, which required a tracheostomy. Cultures from the BAL fluid grew M kansasii, as did the culture of the original pleural fluid obtained at the time of chest tube placement on hospital admission. After the chest tube was placed, an air leak persisted for 2 days, indicating a bronchopleural fistula may have been present initially. The air leak stopped spontaneously after 2 days. The chest tube was discontinued 6 days after it was placed. At the time of discharge, the chest radiograph showed a small, right apical loculated pleural air collection. This air collection had not changed in appearance from the chest radiograph obtained just hours before the chest tube was removed. The patient improved clinically on the regimen of isoniazid, rifampin and ethambutol (pyrazinamide was dropped once M kansasii infection was diagnosed). However, a follow-up chest radiograph done 6 weeks after discharge revealed evidence of increasing loculated pleural fluid in the right posterior hemithorax. The patient underwent a decortication procedure at that time, during which gross pus was drained from the pleural space. The intraoperative cultures subsequently grew Fusobacterium varium. Presently, he is doing well on his three-drug regimen after 6 months of therapy.
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Received for publication August 14, 2003. Accepted for publication November 10, 2003.
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