Mycobacterium chimaera lung infection and empyema in a patient without cardiopulmonary bypass

Abstract

Mycobacterium chimaera is a nontuberculous mycobacterium that belongs to the Mycobacterium avium complex. Invasive infections are very rare and have been associated with contaminated heater-cooler water systems used during cardiopulmonary bypass. There is usually a long latency period and patients have nonspecific symptoms that can result in a delayed diagnosis or misdiagnosis. We report a case of M. chimaera infection in a man who presented with worsening shortness of breath and was found to have pleural effusion. The patient did not have any history of cardiopulmonary bypass surgery, which raises concerns about community spread of this rare infection and needs further investigation in the general population. Furthermore, he had a history of sarcoidosis and was on immunosuppressive medications, which might suggest that immunosuppressed patients can acquire this infection without the described risk factors.

Mycobacterium chimaera is a nontuberculous waterborne mycobacterium belonging to the Mycobacterium avium complex. It was first proposed as a distinct organism from the Mycobacterium avium complex by Tortoli et al in 2004 based on a unique mycolic acid pattern. The organism acts as an opportunistic pathogen that can spread through the inhalation of aerosolized particles. Usually, patients are immunocompromised or have underlying respiratory diseases.^1,2 The first cases of infection were described following cardiothoracic surgery by Achermann et al in 2013.³ We hereby present an 82-year-old patient who was found to have a pulmonary infection with M. chimaera without any prior history of cardiopulmonary surgery. To the best of our knowledge, this is the first reported case of M. chimaera infection without any history of cardiopulmonary surgery.

CASE DESCRIPTION

An 82-year-old white man with prior sarcoidosis was brought to the emergency department with complaints of worsening dyspnea for almost a year. Dyspnea was associated with productive cough and sputum. The patient denied having chest pain, palpitations, dizziness, fever, night sweats, rigors, chills, or hemoptysis. He had a long-standing history of sarcoidosis, for which he was taking prednisone and methotrexate. His blood pressure was 131/73 mm Hg; heart rate, 72 beats/min; respiratory rate, 15 breaths/min; temperature, 36.1°C; and oxygen saturation, 98% with oxygen at 2 L/min via nasal cannula.

Initial laboratory tests showed a normal complete blood count, renal function tests, liver function tests, and troponins. Chest x-ray revealed chronic bilateral upper lobe fibrotic changes and minimal left-sided pleural effusion (Figure 1). The patient was started empirically on intravenous ceftriaxone, azithromycin, and steroids. A high-resolution computed tomography (CT) scan of the chest demonstrated bilateral confluent parenchymal scarring with reticular densities and traction bronchiectasis (Figure 2). It also showed a new loculated pleural effusion on the left side and a minimal right-sided pleural effusion. Methotrexate was discontinued. An echocardiogram showed an ejection fraction of 60% with right ventricular pressure of 30 mm Hg.

Figure 1.

Chest x-ray showing bilateral chronic fibrotic changes with loculated left-sided pleural effusion.

Figure 2.

CT of the chest (high-resolution reconstruction) showing bilateral pleural effusions (blue arrows) with traction bronchiectasis changes.

After 3 days of hospitalization, the patient did not improve clinically and a CT-guided thoracentesis was performed, which was consistent with exudate (pleural fluid protein to serum protein ratio of 0.7, pleural fluid lactate dehydrogenase [LDH]/serum LDH ratio of 0.8, pleural fluid LDH 463 IU/L, serum LDH 98 IU/L). Gram stain of the pleural fluid showed many polymorphonuclear leukocytes along with beaded gram-positive, acid-fast bacilli. Due to high suspicion of pulmonary nocardiosis, antibiotics were changed to intravenous trimethoprim/sulfamethoxazole. After almost 28 days, cultures grew M. chimaera intracellular group. Therefore, the antibiotics were tailored to amikacin, clarithromycin, ethambutol, and rifampin while awaiting sensitivity results. The sensitivity report showed that the organism was sensitive to ethambutol, rifampin, and clarithromycin and resistant to ciprofloxacin, streptomycin, linezolid, and amikacin. Therefore, amikacin was discontinued. The patient was also referred for an ophthalmologic examination to rule out any ophthalmologic involvement and was supposed to receive a prolonged course of ethambutol. His dyspnea started improving after 2 weeks and he completed antibiotics for almost 12 months and had a complete resolution of infection with repeated negative cultures. There has been no recurrence of symptoms or infection to date.

DISCUSSION

M. chimaera is a nonpigmented acid-fast mycobacterium that can take up to 6 to 8 weeks to grow. It has a distinguished highly lipophilic cell wall and a low number of porins.^1,4 Currently, differentiation and identification require gene sequencing and a high-performance liquid chromatography profile. Almost all the patients reported with M. chimaera infection in the literature had a history of cardiac bypass surgery. However, our patient is unique in having M. chimaera infection without this risk factor.

Cough, low-grade fever, and shortness of breath are the usual presenting complaints and are often treated as nontuberculous infections initially. Laboratory abnormalities can include pancytopenia with elevated alkaline phosphatase and hypoalbuminemia, especially in disseminated disease.⁵ The Infectious Diseases Society of America/American Thoracic Society usually recommend at least two samples from sputum or one from bronchoalveolar lavage for culture. The diagnostic sensitivity of one positive blood culture is estimated at 68%.^5,6 The radiological pattern can be similar to active tuberculosis.

Kohler et al reported 10 cases of disseminated M. chimaera; all had prior cardiac bypass surgeries and four were initially misdiagnosed with sarcoidosis.⁷ Ocular findings such as chorioretinitis were also commonly seen in patients with disseminated M. chimaera infection.⁸ Specific treatment guidelines are lacking in the literature. Nevertheless, the class 1 recommendation for treatment is combination therapy with azithromycin (or clarithromycin) plus ethambutol and rifampicin. A minimum 12-month duration of an antibiotics regimen is usually required after sputum conversion for patients with lung disease. Treatment can be modified based on HIV testing and sensitivity. For macrolide-resistant severe lung disease, parenteral amikacin can also be used.^1,5,9

In conclusion, M. chimaera has a strong association with a previous history of cardiopulmonary bypass. The lack of this history in our patient raises concern of community spread of M. chimaera. Moreover, de Melo Carvalho et al reported M. chimaera infection in an immunocompromised patient with B-cell lymphoma.¹⁰ This case and our patient’s history of being on steroids for sarcoidosis suggest that immunocompromised patients can have M. chimaera infection; however, further clinical evidence is needed.