INTRODUCTION: Mycoplasma pneumoniae is a common cause of community-acquired pneumonia, particularly in young adults who are otherwise healthy, and usually causes mild respiratory disease. A very small percentage of patients with M. pneumoniae infection require hospitalization and only a small number of those patients have severe disease necessitating mechanical ventilation. We report a fatal case of a young woman who presented with acute respiratory distress syndrome (ARDS) secondary to Mycoplasma pneumoniae infection.
CASE PRESENTATION: 27 yo woman with no significant past medical history presented with three weeks of fever and malaise and three days of progressive shortness of breath. On admission, she was tachycardic and hypoxic with diffuse bilateral infiltrates on chest x-ray (CXR). Computed tomography (CT) of her chest showed scattered areas of lower lobe consolidation and ground glass opacities. She was started on non-invasive positive pressure ventilation and broad spectrum antimicrobials, including atypical and influenza coverage, for a presumed bacterial pneumonia superimposed on an influenza infection. She developed ARDS and required intubation and mechanical ventilation. On hospital day eight, she had an open lung biopsy that showed diffuse alveolar damage (DAD). As culture results were negative, she was empirically treated with steroids. Clinical deterioration continued, including multi-system organ failure with acute kidney injury, shock liver, diffuse gastrointestinal bleeding, disseminated intravascular coagulation and seizure activity. On hospital day seventeen, brain death was confirmed and she was pronounced dead. Extensive culture and serologic studies to isolate an infectious agent were negative, including blood, urine, sputum and lung biopsy cultures as well as tests for HIV, influenza A and B, H1N1, Legionella, viral titers and rheumatological studies. The only positive studies were two sets of elevated mycoplasma IgM and IgG titers. Major findings at autopsy were DAD, consistent with the clinical diagnosis of ARDS, and acute hemorrhagic leukoencephalopathy (AHLE). The autopsy concluded that ARDS secondary to M. pneumoniae infection was the most likely cause of her death.
DISCUSSIONS: Mycoplasma pneumoniae usually causes mild disease, but there are reports of it causing severe and life-threatening disease, manifesting as ARDS, bronchiolitis obliterans and necrotizing pneumonia. The diagnosis of M. pneumoniae infection is often made serologically; cultures are historically less sensitive due to long incubation times and show growth in as little as 40% of cases. The mechanism by which M. pneumoniae produces pulmonary infiltrates is thought to be related to mononuclear cell migration into the airways, inducing macrophages to release cytokines and development of a mononuclear cell inflammatory response including CD4+ T cells, B cells and plasmocytes. Based on this theory, corticosteroids may down-regulate the cell-mediated immune response and reduce immune-medicated pulmonary injury seen in mycoplasma infections. The autopsy also revealed AHLE, a progressive demyelinating condition of the central nervous system that is often associated with a prodromal febrile illness and upper respiratory infection, including M. pneumoniae infection.
CONCLUSION: Mycoplasma pneumoniae infection is a rare cause of ARDS and has been associated with multi-system organ failure and death, despite adequate treatment with appropriate antibiotics. It is unknown if treatment with antibiotics in an earlier stage of the disease could prevent the devastating respiratory failure seen in a very small sub-group of patients with this infection. Although steroids did not affect the outcome in our patient, treatment with corticosteroids may, in theory, be helpful because they can down-regulate the cell-mediated immune response and may be beneficial in patients with ARDS secondary to Mycoplasma pneumoniae infection.
DISCLOSURE: Sarah Tapyrik, No Financial Disclosure Information; No Product/Research Disclosure Information