A Novel Presentation of Mycobacterium Avium Complex in a Recipient of a Lung Transplant

A Case Report

Leah Cohen; Jeannette Guarner; William R. Hunt


J Med Case Reports. 2017;11(240) 

In This Article


Complications post lung transplantation raise concern for a broad differential diagnosis depending on the timing after lung transplant. The risk for serious infections is greatest within the first year following transplantation, whereas risk and prevalence of other morbidities, such as chronic rejection and malignancy, is greater after the first year postoperatively.[1] Because our patient was 4 years out of transplant, our greatest concern was that the endobronchial mass would be some type of malignancy, such as squamous cell carcinoma or an unusual presentation of post-transplant lymphoproliferative disorder due to her chronic immunosuppression.[14] There has even been a case report of non-Hodgkin's lymphoma presenting as an endobronchial mass in a patient with cystic fibrosis (CF) 6 years after bilateral lung transplant.[15]

Of importance though, while infectious complications are more common in the first year following lung transplant, they can still occur at any time in the setting of immunosuppression. A group from Duke University published a case series in 2005 of three patients with CMV endobronchial infection presenting as a focal polyp on bronchoscopy.[5] All three patients had received lungs from CMV-positive donors, although not all patients were CMV seronegative prior to transplant. However, all three cases were discovered within the first few months after transplantation. TB has also been the cause of an endobronchial mass in the middle lobe of the right lung in a case of a 27-year-old patient with CF 3 months post lung transplant.[16]

NTM presenting as an endobronchial mass is very rare. There have been a few case reports in scenarios outside lung transplantation that have described NTM presenting as an endobronchial lesion. Several case reports describe this presentation in individuals immunocompromised with human immunodeficiency virus (HIV).[11,12] A third case report recounts this unusual presentation in a 34-year-old Chinese woman without any evidence of immunosuppression.[13] However, while risk factors such as immunosuppression and airway architectural changes certainly increase the risk for NTM infection, presentation of NTM as an endobronchial mass following lung transplantation has not been previously described.

Although the list of NTM that cause disease in humans has increased with the larger number of immunosuppressed patients, MAC continues to be the most commonly isolated.[17] NTM are found in the soil and water, and humans acquire them from the environment, although the actual source is rarely identified. NTM most commonly presents as pleuropulmonary disease in patients with structural lung disease such as chronic obstructive pulmonary disease (COPD), CF, non-CF bronchiectasis, and post-lung transplantation.[17]

NTM infection occurs in 0.46 to 9% of recipients of lung transplant with varying clinical presentation.[9,18] Patients post lung transplant may be completely asymptomatic and have no radiologic evidence of disease with NTM cultured during routine surveillance bronchoscopy.[17] Many transplant centers, including our own, routinely perform surveillance bronchoscopies to evaluate for clinically silent acute rejection.[19] There has been ample literature describing the risk of bronchoscopic contamination with Mycobacterium and risk for transmission.[20] Great care must be taken to ensure pathologic contamination does not occur via diagnostic interventions, particularly in this immunocompromised population. Fortunately, in this case our patient had not required diagnostic bronchoscopy for many years prior to this presentation. NTM infection in the setting of lung transplantation can also be seen with isolated bronchiectasis secondary to bronchiolitis obliterans syndrome (BOS) or chronic rejection. The diagnosis of NTM pulmonary disease requires: a single NTM isolate from a bronchoalveolar lavage or pulmonary biopsy, or isolation of NTM from two separate sputum samples; or clinical pulmonary disease with concomitant radiographic findings.[21]

There is a wide range of chest radiographic findings in NTM pulmonary disease. The cavitary or classic form appears similar to TB on chest radiograph with upper lobe cavitary lesions and endobronchial spread as evidenced by nodules adjacent to foci of disease, atelectasis, and pleural thickening.[17] Unlike TB, the cavities are usually smaller and thin walled. The bronchiectatic or nonclassic form has chest radiographic findings of randomly distributed nodular opacities. CT commonly shows small centrilobular nodules or tree-in-bud opacities with cylindrical bronchiectasis usually in the same lobe.[17] Disseminated disease is commonly seen in patients with HIV and reported radiographic findings include unifocal and unilateral alveolar opacities, mediastinal and hilar lymphadenopathy, cavitation, and pleural effusions.[17] In immunocompromised patients without HIV, such as those post lung transplant, pulmonary infections can manifest as nodules or masses within the lung tissue parenchyma.[17] MAC presenting as an endobronchial tumor-like mass has not been described as a common radiographic presentation in patients post lung transplant.

Treatment of NTM disease depends not only on the species isolated, but also on the patient's symptoms as well as clinical presentation. In the case of MAC, the treatment of patients with nodular bronchiectatic disease usually involves a three-times weekly regimen of a macrolide, ethambutol, and rifampin.[17] For those with cavitary disease or severe nodular/bronchiectatic disease it is recommended to add streptomycin or amikacin early.[21] The treatment should continue for 1 year after a patient becomes culture negative. Sputum cultures are usually collected on a monthly basis to monitor patient response. If MAC is cultured again within the 1 year treatment window, the treatment clock restarts.[21] Because treatment involves a complicated three-drug regimen, therapy for patients who are asymptomatic may not be indicated, especially when they have adverse effects or intolerance to the drugs. However, in the case of a recipient of a lung transplant, treatment is usually recommended given the risk of associated rejection.[8] Our patient initiated three-drug therapy as described above, but due to significant side effects associated with the ethambutol as well as drug–drug interaction with rifampin and her immunosuppression medications, her regimen was adjusted to dual therapy with a macrolide and fluoroquinolone. While she had radiographic resolution of her disease as well as multiple negative sputum cultures, her duration of therapy only lasted for 12 months due to significant gastrointestinal side effects. She was subsequently monitored very closely without return of infectious symptoms. However, this case highlights the difficulties that can arise with an aggressive drug regimen and real-world practicalities compared to clinical recommendations.