A previously healthy 26-year-old woman presented with a fever and coughing on October 1, 1995. Despite treatment with β -lactam antibiotics at another hospital, she had a high fever, coughing, and dyspnea. A chest roentgenogram showed diffuse infiltrates in both lung fields. On October 9, she was transferred to our hospital.
On admission, a chest X-ray film showed marked diffusely infiltrates in both lung fields and a effusion in the left lung. Arterial blood gas analysis after inhalation of 4 liters per minute of oxygen via a nasal cannula revealed a PaO₂ of 39.0 torr.
Despite treatment with various antibiotics, including minocyclin and γ -globulin, her respiratory condition rapidly deteriorated. She was mechanically ventilated by with intermittent mandatory ventilation and positive end-expiratory pressure, and received antibiotics and methylprednisolone pulse therapy. Her chest X-ray and arterial blood gase findings, gradually improved. The passive hemagglutination titer for Mycoplasma rose from 1: 4 on October 9, to 1: 2,560 on the 14th hospital day. Acute respiratory failure due to Mycoplasma pneumoniae pneumonia was diagnosed. A chest X-ray film obtained 2 months after admission showed linear-reticular shadows in both lung fields and pulmonary-function tests revealed abnormally low vital capacity and diffusing capacity. Examination of a specimen obtained by transbronchial lung biopsy revealed focal intraalveolar exudate with fibrin and macrophages. Very mild interstitial thickening was also noted. The lymphocyte stimulation responses to PPD, PHA, and Con A were low early in the illness and became normal after recovery. Several reports have said that an enhanced pulmonary cellular immune response may be responsible for the development of severe Mycoplasma pneumoniae, resulting in a temporary decrease in the cell-mediated immune response. This case supports that hypothesis. We believe that in severe cases, steroid therapy including pulse therapy should be started as soon as possible.