Case Presentation: A 34 yo Hispanic male with recently diagnosed AIDS (CD4 <20) presented to our hospital with fevers, chills, shortness of breath, and hemoptysis. Patient initially presented one month ago with similar symptoms at an outside hospital (OSH). CT Thorax showed bilateral pleural effusions with diffuse patchy groundglass and consolidative opacities. CT Abdomen/Pelvis demonstrated diffuse retroperitoneal and mesenteric lymphadenopathy. Mycobacterium tuberculosis was ruled out with three negative AFB stains, and patient was discharged with a course of amoxicillin. Two weeks later, patient was readmitted to the OSH due to worsening symptoms. At this time, AFB sputum culture from initial admission returned positive. Patient was started on rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE). Shortly after discharge, patient presented to our hospital for continued shortness of breath and hemoptysis. Pulmonology and Infectious Disease were consulted and agreed that AFB culture positivity one week after collection suggested disseminated Mycobacterium avium complex (MAC) which was confirmed by DNA probe. RIPE was discontinued, and treatment for MAC was initiated with rifabutin, ethambutol, and clarithromycin. Diagnostic bronchoscopy demonstrated diffuse alveolar hemorrhage (DAH). PCP-DFA was negative, and there was no evidence of pulmonary Kaposi’s sarcoma. Broad-spectrum antibiotics were given for a possible secondary bacterial etiology, but the patient continued to deteriorate. Rheumatology was consulted to evaluate for a possible autoimmune etiology of DAH. Although serologies were negative and a urinalysis did not show active sediment, IV Solumedrol was given. Despite maximal treatment, patient’s clinical picture continued to worsen. The final diagnosis was determined to be DAH secondary to disseminated MAC.
Discussion: The most common causes of DAH are systemic autoimmune diseases. Infectious disease, however, should be considered early in the differential diagnosis of DAH, especially in patients who are immunocompromised. It is well-established that early targeted antimicrobial therapy improves survival. The most common infections causing DAH include influenza A, dengue, leptospirosis, malaria, and S. aureus pneumonia. While MAC has been associated with alveolar damage, we describe the first case of DAH secondary to disseminated MAC.
Conclusions: DAH is a life-threatening syndrome characterized by bleeding into the alveolar spaces of the lungs. DAH is most commonly caused by capillaritis associated with systemic autoimmune diseases such as anti-neutrophil antibody-associated vasculitis, systemic lupus erythematosus, and anti-glomerular basement membrane disease. DAH can less commonly result from alveolar damage due to infection, inhalation, or cytotoxic drug therapy. Here we present a case that has not been described in current literature: DAH caused by disseminated MAC.