No abstract

Meningococcal disease is normally suspected on clinical grounds and is confirmed by isolation of Neisseria meningitidis bacteria from blood or cerebrospinal fluid or, more recently, by serology or PCR of cerebrospinal fluid. Achieving confirmation of a clinical diagnosis of meningococcal disease has become more difficult in the last few years. The prehospitalization administration of parenteral benzylpenicillin normally renders blood cultures sterile, and lumbar puncture is undertaken less frequently, especially in young children. We evaluated PCR for the detection of meningococcal DNA in 80 blood samples taken from patients with known or suspected meningococcal disease or from patients with other diagnoses (negative controls). Both the sensitivity and the specificity of the test were 100% for patients with confirmed cases of meningococcal disease when the blood buffy coat was used (83 to 100% sensitivity and 87 to 100% specificity with 95% confidence limits). Positive PCR results could be obtained from both blood buffy coat and serum samples. Sensitivity was unaffected by prior antibiotic treatment. PCR is a rapid, sensitive test that may be used to confirm a diagnosis of meningococcal disease by using peripheral blood samples. Introduction of this test into clinical laboratories may in some cases obviate the need for lumbar puncture to be performed on patients with suspected meningococcal disease. Our results demonstrate that a substantial number of cases of meningococcal disease are not confirmed by conventional techniques and remain undiagnosed. If the PCR test described here was widely applied, the number of cases of meningococcal disease ascertained might rise by as much as 60% greater than that recognized at present. It is likely that we are in a prevaccination era for meningococcal disease. Better case ascertainment is urgently required to assess the need for vaccines, to determine their costs and benefits, and to monitor their efficacies.

The influence of respiration on the flow of blood from the abdominal vena cava into the thorax was studied in 15 patients with pulmonary emphysema and in 10 control subjects without thoracic disease or heart failure. In control subjects, during quiet breathing blood flowed into the thorax throughout the respiratory cycle at a rate which was greatest during inspiration. Simultaneously the transmural pressure of the abdominal vena cava fell and transmural right atrial pressure increased. The same pattern of flow was observed in nine of the patients with emphysema. In the other six patients, however, flow was greatly reduced or completely arrested during inspiration, with simultaneous increase in transmural caval pressure and reduction in transmural atrial pressure. This inspiratory obstruction at the thoracic inlet was associated with gross hyperinflation of the lungs and a low diaphragmatic position. It probably was not the result of the high negative and positive intrathoracic pressures that develop during inspiration and expiration, respectively, in such subjects. It is possible that this phenomenon may account for the peripheral edema that occurs in patients who have emphysema without associated pulmonary hypertension or cardiomegaly.

The pulmonary function of 24 normal subjects ranging in age from 20 to 50 years has been studied at rest and during exercise. At rest there is a significant decrease with age in the pulmonary diffusing capacity and the level of diffusing capacity attained on exercise at any particular oxygen uptake decreases with increasing age. Simultaneous measurements of O2 uptake, ventilation, end tidal O2 and CO2 concentration and calculated alveolar CO2 concentration, using the Bohr equation, show no evidence that any of these measurements are significantly influenced by age. The predicted maximal O2 diffusing capacity ( J. Appl. Physiol. 6: 588, 1954) predicts with fair accuracy the diffusing capacity for carbon monoxide that will be found in any given individual at an O2 uptake of about 2.8 l/min. It correctly predicts the change in CO diffusing capacity with increasing age. Reasons are given for suggesting that the decrease in pulmonary diffusing capacity observed may be explained by a diminution in cardiac output with increasing age. Submitted on November 21, 1958