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A case of Lemierre's syndrome is reported. Although Fusobacterium species are commonly associated with this presentation, Prevotella bivia was the causative micro-organism identified in this case. The finding that disseminated anaerobic sepsis followed primary EBV infection led to the construction of a hypothetical model of infection.

Dyspnoea differs between subjects with chronic obstructive pulmonary disease (COPD) and asthma, partly because the underlying mechanisms for bronchoconstriction differ. This study investigated the possible role of inflammation and the contribution of clinical variables on dyspnoea in subjects with COPD and asthma. Forty-eight smoking subjects with COPD and 21 nonsmoking subjects with asthma, were challenged with adenosine 5'-monophosphate (AMP) and methacholine. The Borg score was assessed before and after each challenge. Mean increases in Borg score (per percentage decrease in baseline forced expiratory volume in one second (FEV1)) were significantly smaller in COPD than in asthma (p<0.01), values being 0.055 and 0.045 in COPD and 0.122 and 0.093 in asthma respectively. This difference was largely due to the fact that one-third of the subjects with COPD did not increase their Borg score during bronchoconstriction. The increase in Borg tended to be larger during AMP than during methacholine challenge, both in asthma and COPD. Changes in Borg scores were explained by age in COPD and by the Borg score before AMP challenge in asthma. The authors conclude that perception of dyspnoea during adenosine 5'-monophosphate and methacholine induced bronchoconstriction is lower in chronic obstructive pulmonary disease than in asthma and that age contributes to this difference. As adenosine 5'-monophosphate is regarded as an indirect marker of airway inflammation, the results suggest that inflammation is not important because both groups showed similar responses on such provocations.

To investigate the genetic susceptibility to asthma, we developed an algorithm to classify the phenotype of each family member enrolled in a family study on the genetics of asthma. This algorithm was applied to 92, two- and three-generation families, identified through a subject (proband) with asthma first diagnosed 25 yr previously. The algorithm consisted of five classes based on the presence or absence of bronchial hyperresponsiveness (BHR), respiratory symptoms, smoking, airways obstruction, and bronchodilator reversibility. All family members were classified as: (1) definite asthma; (2) probable asthma; (3) unclassifiable airway disease; (4) chronic obstructive pulmonary disease (COPD); (5) unaffected (without clinical evidence of asthma and COPD). Thirteen of the 92 probands (14%) could not be classified as asthmatic when retested 25 yr later because of loss of BHR, loss of bronchodilator reversibility, or a current history of cigarette smoking. Of the 265 first-degree offspring, 49 (18%) were classified as having definite asthma (Class 1), and 22 (8%) as probable asthma (Class 2). A large number of offspring with clinical evidence of asthma did not have a prior physician's diagnosis of asthma, and offspring in Class 1 (definite asthma), with and without a physician's diagnosis, had similar clinical and physiologic characteristics. These results support the usefulness of this approach to classify subjects with asthma for genetic epidemiologic studies and show that reliance on a prior physician's diagnosis may result in misclassification or underdiagnosis. Characterization of the offspring in this family study showed that there is familial clustering, which supports the presence of a hereditary component in asthma.

Disease progression and efficacy of fungistatic treatment in pulmonary aspergilloma (PA) are difficult to monitor. The usefulness of chest tomography, IgG-ELISA serology, double immunodiffusion, and IgG-immunoblotting was assessed in monitoring disease progression and efficacy of itraconazole treatment during a 9-yr follow-up of a patient with two exacerbations of PA. A rise in IgG-ELISA titer coincided with a recrudescence of clinical symptoms, whereas a decrease after treatment paralleled clinical improvement. IgG-binding to a 32-kD serine protease and to 60- and 94-kD proteins produced with collagen-containing culture medium closely corresponded with IgG-ELISA titers. IgG-binding to a 40-kD metalloprotease remained at very low levels until symptoms and fungal growth became well advanced, when a sharp rise was seen. Responses to all antigens rapidly diminished after the start of successful treatment with itraconazole. Serology may be a useful adjunct in the monitoring of disease progression and the efficacy of itraconazole treatment in patients with PA. IgG-binding to individual fungal proteins shows subtle differences in kinetics. Immunologic responses to fungal proteases raised with collagen-containing culture media may reflect fungal proteolytic involvement during disease progression and treatment more closely than responses to proteins raised with conventional media.

Between 1973 and 1986, 19 patients were treated on 21 occasions for life-threatening attacks of asthma. Twelve times mechanical ventilation was needed. None of the patients died. Most of the patients had been recognized as severely asthmatic before the life-threatening attack. Thirteen out of the 19 patients had previously been admitted with a severe asthmatic attack. All patients, except one, were already using maintenance treatment, and 17 had previously been referred to a pulmonologist. During follow-up the bronchial obstruction was, in most cases, fully reversible while using a rather extensive maintenance treatment (maximum forced expiratory volume in one second (FEV1), 69-138% of predicted). Recently, 17 of the 19 patients were reinvestigated, while in stable phase. The patients who had been mechanically ventilated were significantly more sensitive to inhaled histamine than the patients who had not been mechanically ventilated. This was not explained by any difference in basal FEV1 % pred or dosage of corticosteroids. A very low provocation concentration of histamine producing a 20% fall in FEV1 (PC20) may indicate the risk of a severe, life-threatening attack of asthma.