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Bilateral Pleural Effusions and Right
Pneumothorax in a 25-Year-Old Man*
Eric J. Olafsson, MD; Chris C. Naum, MD, FCCP;
George A. Sarosi, MD, FCCP; and John G. Mastronarde, MD, FCCP
(CHEST 2004; 126:986 –992)
man presented to the hospital with a
A 6-h25-year-old
history of acute-onset, right-sided back pain.
He reported increasing dyspnea in the preceding 5
to 7 days. He had a chronic dry cough that had not
changed over the previous year. He denied hemoptysis, weight loss, or appetite change, but had night
sweats during the prior week or two. The patient also
reported subjective fevers, but denied chills.
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.
*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,
Manuscript received August 14, 2003; revision accepted November 10, 2003.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail:
[email protected]).
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: [email protected]
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/␮L, 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/␮L (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.
Hospital Course
Two days after hospital admission, the patient
failed to show clinical improvement. HIV assay was
negative. Purified protein derivative developed induration at 14 mm. A CT scan of the chest was
performed (Figs 2– 4). The CT revealed small hydropneumothoraces in the apex of both lungs, as well as
a small, loculated hydropneumothorax in the right
base. There was a large left pleural effusion. Furthermore, airspace opacification was identified in
posterior right upper lobe and posterior left upper
lobe, superior segment of the right lower lobe and
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Pulmonary and Critical Care Pearls
Figure 1. Anteroposterior chest radiograph (at the time of hospital admission) showing bilateral
pleural effusions and a right pneumothorax.
right lung base, and was thought to be compatible
with infection or prior inflammation. A 13-mm
lymph node in the subcarinal region and a 12-mm
node in the right paratracheal area were noted.
Additionally, some of the above noted areas were
associated with cylindrical bronchiectasis, consistent
with a more chronic process. There were also regions
of tree-in-bud appearance noted in the right upper
lobe and right lower lobe.
A thoracentesis was performed on the left,
Figure 2. CT scan of the chest (2 days after hospital admission) reveals right upper lobe
hydropneumothoraces and a small left hydropneumothorax.
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987
Figure 3. CT scan of the chest (2 days after hospital admission) shows bilateral hydropneumothoraces
and a left upper lobe cavitary lesion. The right upper lobe has airspace consolidation. There is a right
pleural effusion, as well as a right hemithorax chest tube.
revealing a cell count of 2,273 WBCs/␮L, of which
90% were lymphocytes. Chemistry analysis
showed a glucose level of 96 mg/dL, lactate dehydrogenase of 416 U/L, and protein of 4.3 g/dL.
Again, stains were negative for AFB and fungi, as
were the bacterial cultures. A closed pleural biopsy was then performed on the left. The pathologic diagnosis was necrotizing granulomatous inflammation with vasculitis. Special stains for fungi
and AFB were negative.
Figure 4. CT scan of the chest (2 days after hospital admission) revealing a large left pleural effusion
and associated compressive atelectasis. The right hemithorax has basilar airspace disease and a
hydropneumothorax.
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Pulmonary and Critical Care Pearls
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
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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?
CHEST / 126 / 3 / SEPTEMBER, 2004
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989
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 HIVpositive 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 HIVnegative 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.
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Pulmonary and Critical Care Pearls
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
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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.
Clinical Pearls
1. The differential diagnosis of a chronic chest
infection presenting with pleural effusion would include M tuberculosis and the nontuberculous mycobacteria, nocardiosis, actinomycosis, blastomycosis,
and coccidioidomycosis.
2. Cryptococcosis, histoplasmosis, and aspergillosis rarely have pleural involvement.
3. M kansasii has not been isolated from soil or
natural water supplies, so it is not considered an
environmental contaminant. Hence, when recovered,
it should be considered a pathogen.
4. Radiographic presentation of M kansasii is also
similar to tuberculosis, with cavitation and tree-inbud appearance in the posterior segments of the
upper lobes being typical findings. Bronchiectasis is
often seen, but is not the predominant finding on
chest CT scan.
5. M kansasii often presents with unilateral (usually right-sided) disease and rarely with pleural
effusions.
6. Recommended therapy for M kansasii includes
isoniazid, rifampin, and ethambutol, and should be
continued for 18 months, with 12 of those months
after sputum culture findings become negative.
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Pulmonary and Critical Care Pearls