Multiple cases of life-threatening adenovirus pneumonia in a mental health care center.

Eighteen cases of pneumonia developed during an outbreak of adenovirus infection in a chronic psychiatric care facility. The six patients most severely affected were admitted to the intensive care unit (ICU) at our institution. Four of these patients developed septic shock. We report the presentation, disease progression, and response to treatment of these patients. Clinical features consisted of high fever, nonproductive cough, and dense lower lobe infiltrates. Laboratory abnormalities included transient fall in white blood cell and platelet counts, and elevations of transaminases, lactate dehydrogenase (LDH), and creatinine phosphokinase (CPK). Five patients were intubated for hypoxemia and four developed the acute respiratory distress syndrome (ARDS) and septic shock (mean cardiac output, 14.1 +/- 1.3 L/min; cardiac index, 6.4 +/- 0.4 L/min/min2; systemic vascular resistance, 326 +/- 107 dyne cm/s2). All patients recovered and were discharged back to the chronic care facility except for one patient with chronic renal failure who died 2 mo after admission. Adenovirus (serotype 35) was isolated from the respiratory secretions of five patients and antibody titers increased 6-fold in the other. These patients constitute the largest series of patients with ARDS and septic shock caused by adenovirus pneumonia and the first outbreak of multiple cases of adenovirus pneumonia in immunocompetent civilian adults occurring from a single source.

Cardiopulmonary responses to chronic hypoxia in transgenic mice that overexpress ANP.

Elevated plasma atrial natriuretic peptide (ANP) levels have been shown to blunt pulmonary hemodynamic responses to chronic hypoxia, but whether elevated circulating ANP levels negatively feedback on cardiac expression of the ANP gene is unknown. Using a recently developed strain of transgenic mouse (TTR-ANF) that expresses a transthyretin promoter-ANP fusion gene in the liver, we studied the effect of chronically elevated plasma ANP levels on cardiac hypertrophic and pulmonary hemodynamic responses and expression of the endogenous cardiac ANP gene during chronic hypoxia. Plasma ANP levels were 10-fold higher in TTR-ANF mice than in their non-transgenic littermates. After 3 wk of hypobaric hypoxia (0.5 atm), right ventricular hypertrophy and pulmonary hypertension had developed in both groups of mice, but TTR-ANF mice had lower right ventricle-to-left ventricle plus septum weight ratios (0.39 +/- 0.01 vs. 0.45 +/- 0.02), right ventricular systolic pressures (25 +/- 2 vs. 29 +/- 2 mmHg), and lung dry weight-to-body weight ratios (0.48 +/- 0.03 vs. 0.57 +/- 0.01 mg/g) and less muscularization of peripheral pulmonary vessels (8.3 +/- 1.4 vs. 17.4 +/- 2.5%) than nontransgenic controls. Right atrial and ventricular steady-state ANP mRNA levels were the same in both groups of mice under normoxic and hypoxic conditions despite much higher plasma ANP levels and less pulmonary hypertension in TTR-ANF mice. We conclude that chronically elevated plasma ANP levels attenuate the development of hypoxic pulmonary hypertension in mice but do not suppress cardiac expression of the endogenous ANP gene under normoxic conditions nor blunt the upregulation of right ventricular ANP expression during chronic hypoxia.