Mycobacterium fortuitum Infection Presenting as Community-acquired Pneumonia in an Immunocompetent Host

Abstract

Mycobacterium fortuitum is a rapidly growing environmental mycobacteria, frequently isolated from water, dust, and soil, which commonly causes infection in the presence of underlying disease or immunosuppression. Skin, soft tissue, and bones are important sites of M. fortuitum, but it may colonize in the respiratory tract as well. We report the case of an otherwise healthy man who presented with signs and symptoms of community-acquired pneumonia. He was diagnosed as having primary infection with M. fortuitum and treated with multidrug antibacterial therapy. Our case confirms that M. fortuitum poses a threat not only to patients with immune defects but also to immunocompetent hosts. Flexible bronchoscopy or a transthoracic needle aspiration may be required to confirm the diagnosis.

Nontuberculous mycobacteria (NTM) are ubiquitous environmental pathogens that can cause a broad range of diseases. With the emergence of AIDS and the increasing use of immunosuppressives, the incidence of NTM-associated diseases has risen dramatically.¹

Although contact with such environmental mycobacteria is frequent, overt disease is uncommon because of their low virulence. Disease usually develops in immunocompromised patients but also involves healthy individuals occasionally.¹ We report a case of NTM infection in an immunocompetent patient who presented with signs and symptoms of community-acquired pneumonia, which was eventually diagnosed as Mycobacterium fortuitum infection by a combination of sputum studies, flexible bronchoscopy (FB), and transthoracic needle aspiration (TTNA).

CASE REPORT

A 57-year-old man with a 30 pack-year smoking history was admitted with high fever, fatigue, cough, and myalgia for a duration of 2 weeks and was placed on clarithromycin (1000 mg/d) since developing fever. He had recently traveled to Africa and had received prophylaxis with tetracycline and ciprofloxacin during his stay. He received isoniazid (INH) for latent tuberculosis 25 years earlier because of active contact with a patient with tuberculosis. There was no history of HIV infection or immunosuppressive therapy.

His temperature was 38.2°C, heart rate was 100/min, and there were fine crackles at the base of the left lung. Erythrocyte sedimentation rate was 68 mm for the first hour (0 to 20 mm/h), white blood cell count was 8900 mL/μL (4.5 to 10,000 mL/μL), and C-reactive protein was 271 mg/L (0 to 10 mg/L). His chest radiograph was unremarkable. Chest computed tomographic (CT) scan showed a consolidation involving the posterior segments of the left lower lobe (LLL). In FB, purulent secretions emitting from the LLL were noticed. Bronchoalveolar lavage (BAL) and transbronchial biopsies were obtained. He was placed on empiric imipenem (4×500 mg/d) and doxycycline (2×100 mg/d). Ziehll-Neelsen staining was negative for acid-fast bacilli (AFB) on 3 consecutive sputum and BAL specimens. BAL cultures grew Streptococcus vestibularis, which was sensitive to ceftriaxone. His treatment was switched to ceftriaxone (2 g/d), which was administered intravenously. He was discharged on the fifth day from the hospital on cefixime (400 mg/d). Five days after discharge, he was readmitted with fatigue, dyspnea, and fever. His C-reactive protein level had decreased to 50 mg/L, but erythrocyte sedmentation rate was 88 mm/h. There was a slight improvement of infiltrates on his CT scan. He was placed on moxifloxacin (400 mg/d).

His fever persisted for the next 10 days. A repeat CT scan showed persistence of a nonhomogenous consolidation and a mass-like infiltrate involving the LLL (Fig. 1). A CT-guided TTNA of the lesion showed a caseating granulomatous inflammation without AFB (Fig. 2). His treatment was modified to INH (300 mg/d), rifampicin (600 mg/d), pyrazinamide (2000 mg/d), and ethambutol (1500 mg/d).

FIGURE 1.: The repeat computed tomographic scan of the chest showing the left lower lobe infiltrate.

FIGURE 2.: Transthoracic needle aspiration biopsy showing (A) noncaseating granuloma (hematoxylin and eosin stain) and (B) negative Ziehl-Neelsen stain for acid-fast bacilli.

During the first week of his treatment, a positive BACTEC culture signal was observed in 1 of his sputum samples. After inoculation of the positive culture with p-nitro-acetylamino-hydroxypropiophenonone, it was recorded as “p-nitro-acetylamino-hydroxypropiophenonone-resistant Mycobacterium.” After subtyping with polymerase chain reaction, it was reported as M. fortuitum. His antibiotic regimen was switched with ciprofloxacin (1000 mg), clarithromycin (1000 mg), and trimethoprim sulfametoxazol (320/1600 mg), daily. Sensitivity studies showed that the organism was resistant to INH, rifampicin, pyrazinamide, ethambutol, streptomycin, oflaxacin, and canamycin, and was sensitive to capriomycin, ciprofloxacin, clarithromycin, and amikacin. A repeat CT scan in the first month of therapy showed a near-total resolution of the infiltrates. His treatment was continued for 12 months until the last negative sputum culture.

DISCUSSION

M. fortuitum is a ubiquitous, rapidly growing organism that can be found in soil, tap water, or dust. When isolated from human sources it usually reflects colonization rather than infection.² It can cause skin and soft-tissue infections after penetrating trauma or punch biopsy.³ It has also been implicated in causing infections after thoracoabdominal surgeries and pacemaker insertions.^4–6M. fortuitum has also been known to cause diffuse lymphadenitis.⁷

The respiratory infections with M. fortuitum are rare in an immunocompetent host and are mostly associated with underlying primary lung conditions, such as chronic obstructive pulmonary disease, cystic fibrosis, bronchiectasis, malignancies, or cavities from healed M. tuberculosis infection.⁸

Our case is unique in the fact that the patient was immunocompetent without any underlying primary lung condition. He was indeed an active smoker, yet was not known to have chronic obstructive pulmonary disease or its symptoms. On the basis of his radiologic studies, we doubt that his present illness was related to his latent M. tuberculosis infection. Positive BAL culture for S. vestibularis was most likely a contaminant. Reviewing the literature, we could not find any correlation between his travel and the infection. We suspect that our patient suffered with primary lung infection with M. fortuitum.

The isolation of all NTM species from a respiratory sample is insufficient evidence for establishing the diagnosis of the disease. One must rely on clinical, radiographic, and bacteriologic criteria as described in the American Thoracic Society guidelines to confirm the diagnosis.⁹ Our case fulfilled the criteria with positive sputum culture for M. fortuitum and the biopsy showed caseating granulomatous inflammation without AFB.

M. fortuitum isolates are susceptible to multiple oral antimicrobial agents, including macrolides, quinolones, doxycycline, minocycline, and sulfonamides. Drug susceptibilities for this species are important for guiding effective therapy.⁹ All isolates of M. fortuitum contain some resistance to macrolides. Thus, despite susceptible minimal inhibitory concentrations seen in 80% of the isolates for clarithomycin, macrolides should be used with caution. The treatment should include at least 2 agents with in vitro activity against the organism and should be continued for 12 months after the last negative sputum culture. The selection of the agent is usually dictated by the patient's tolerance.⁹

Mortality because of localized M. fortuitum infection is rare. Death may result from extensive pulmonary or disseminated disease in immunocompromised patients.¹⁰

In summary, primary lung infection from M. fortuitum is rare. Yet, it should be included in the differential diagnosis of lung infiltrates in an immunocompetent host. A high index of suspicion is required, particularly in patients with a travel history to countries with high endemic mycobacterial infections. Invasive procedures such as FB or TTNA may be required to confirm the diagnosis. Advanced bacteriologic studies help select appropriate treatment and achieve successful outcome.