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Wound Infection with Mycobacterium avium: A Complication of Surgical Resection Without Supplementary Medical Therapy in Focal Pulmonary Disease

Tabriz, M. Shamse MD*; Briski, Laurence E. MD†; Camero, Luis G. MD‡; Khatib, Riad MD*

Infectious Diseases in Clinical Practice: September 2006 - Volume 14 - Issue 5 - pp 325-326
doi: 10.1097/
Case Reports

Abstract: Focal Mycobacterium avium-intracellulare complex infection is often discovered after surgical resection of a pulmonary nodule. Although surgery alone is curative, the role of supplementary medical therapy is unknown. We present an immunocompetent patient who developed delayed wound infection after resection and recurred after debridement. It resolved with anti-Mycobacterium avium-intracellulare therapy.

Departments of *Medicine, †Pathology, and ‡Surgery, St. John Hospital & Medical Center, Detroit, MI.

Address correspondence and reprint requests to Riad Khatib, MD, Medical Education, St. John Hospital and Medical Center, 22101 Moross Road, Detroit, MI 48236. E-mail:

Mycobacterium avium-intracellulare complex (MAC) organisms are known to cause chronic pulmonary disease, cervical lymphadenitis, localized soft tissue infection, and rarely, dissemination.1-10 Pulmonary lesions are sometimes encountered incidentally after surgical resection of a "nodule." Surgical treatment of focal infection in the immunocompetent host is often considered adequate.7,8,11 The role of supplementary antimycobacterial therapy in these cases is unclear.11 We report a case of recurrent chest wound infection and maxillary lymphadenitis after resection of a localized pulmonary lesion. This complication required supplementary medical therapy for resolution.

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An otherwise healthy 50-year-old man, with 20-pack year smoking history, presented with cough and hemoptysis for few days without fever, night sweats, or weight loss. A chest radiograph showed left upper lobe density. A computed tomography scan of the chest showed left upper lobe lesion extending to the pleura (Fig. 1). Two of 3 sputum smears showed acid-fast bacilli (AFB). Bronchoscopy showed inflamed mucosa without intraluminal lesion; the results of bronchial washings stains (Gram, AFB, and fungal) were negative, and cytology did not reveal any malignant cell. He was empirically started on isoniazid, rifampin, ethambutal, and pyrazinamide for presumptive pulmonary tuberculosis. The result of tuberculin skin test was negative. All the 3 sputa and the bronchial washings specimen grew MAC. The result of his human immunodeficiency syndrome test was negative. He was thought to have a left upper lobe MAC disease with or without malignancy. Antitubercolosis medications were discontinued after receiving a 3-week course with the plan for an open-lung biopsy. About 4 weeks later, hemoptysis recurred and persisted, necessitating left upper lobe resection. The lesion was densely adherent to the apex of the chest and bled massively. Histopathologic examination showed extensive caseating granulomas. The results of AFB and fungal stains, and cultures were negative. The patient's symptoms were resolved. He was considered to have localized pulmonary MAC lesion that was resected. Perioperative anti-MAC therapy was not prescribed.

Four months later, the wound site and adjacent axilla became painful, swollen, and tender, with minimal drainage of serosanguineous fluid from the wound. Surgical exploration and debridement of the wound and axilla did not reveal abscess formation; the results of the stains and routine cultures of surgical swabs from both sites were negative. He received multiple courses of amoxicillin/clavulanic acid and ciprofloxacin without improvement. A computed tomography scan of the chest, obtained 2 months later, exhibited left axillary's adenopathy and soft tissue inflammation of left chest wall without any new lung lesion (Fig. 2). He then underwent debridement of the wound and excision of the left axillary lymph node. Histopathology of the soft tissues and the node showed caseating granulomas. The results of Gram, AFB, and fungal stains, and cultures were negative. He was considered to have MAC wound infection and lymphadenitis and was started on clarithromycin (500 mg BID), rifabutin (300 mg/d), and ethambutal (15 mg/kg per day). The wound completely healed over a few weeks course. Therapy was continued for a 6-month course. No further recurrences were noted over a 2-year follow-up.

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Although therapy for MAC infection in the immunocompromised host is well standardized, the treatment of choice for localized infection in the immunocompetent host is not well defined.7 The American Thoracic Society published guidelines include medical therapy (a newer macrolide plus ethambutal with or without rifabutin) for chronic pulmonary disease.7 Generally, when surgery is performed in a localized disease, including pulmonary lesions, resection is often considered curative. Rare incidence of bronchopleural fistulas7,8,11 and recurrences of soft tissue lesions were reported, but they were often cured with repeated surgery.6,11 The development of wound infection after resection of a pulmonary lesion has not been described. Our patient developed recurrent granulomatous wound infection after resection of a focal pulmonary lesion. Although no organism was isolated from the surgical samples, the characteristic histopathologic findings and response to therapy suggest that MAC was the etiology. The negative results of the lung and wound cultures were probably due to the use of antibiotics with antimycobacterial activity before surgery. This case illustrates that supplementary medical therapy after resection of focal pulmonary MAC lesion may be beneficial in the immunocompetent host, especially in patients with lesions adherent to the pleura.

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