Case report

Lessons from Mycobacterium avium complex-associated pneumonitis: a case report

Victor Zota¹ , Sheryn M Angelis² , Armando E Fraire¹ , Ciaran McNamee³ , Shasta Kielbasa⁴ and Daniel H Libraty^2,4

¹Department of Pathology, Division of Infectious Disease, University of Massachusetts Medical School, Worcester, MA, USA

²Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA

³Department of Surgery, University of Massachusetts Medical School, Worcester, MA, USA

⁴Center for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester, MA, USA

author email corresponding author email

Journal of Medical Case Reports 2008, 2:152doi:10.1186/1752-1947-2-152

Published:	13 May 2008

Abstract

Introduction

Mycobacterium avium complex (MAC) is an increasingly recognized cause of pulmonary disease in immunocompetent individuals. An acute form of MAC lung disease, MAC-associated pneumonitis, has generally been associated with the use of hot tubs. There is controversy in the literature about whether MAC-associated pneumonitis is a classic hypersensitivity pneumonitis or is a direct manifestation of mycobacterial infection.

Case presentation

We report the second case in the literature of MAC-associated pneumonitis not related to the use of hot tubs. The source of MAC in a 52-year-old immunocompetent patient was an intrapulmonary cyst containing numerous acid-fast bacilli. The patient developed disseminated miliary nodules throughout both lung fields. Histological examination of resected lung tissue revealed well-formed, acid-fast negative granulomas composed predominantly of CD4⁺ T-cells and CD68⁺ histiocytes. The granulomas were strongly positive for tumor necrosis factor-α, a pro-inflammatory cytokine.

Conclusion

The attempt to classify MAC-associated pneumonitis as either a classic hypersensitivity pneumonitis or a direct manifestation of mycobacterial infection is not particularly useful. Our case demonstrates that MAC-associated pneumonitis is characterized by a vigorous T-helper 1-like, pro-inflammatory, immune response to pulmonary mycobacterial infection. The immunopathology provides a rationale for clinical studies of anti-MAC therapy with the addition of anti-inflammatory agents (for example, corticosteroids) to hasten the resolution of infection and symptoms.