Infection of humans and horses by a newly described morbillivirus.

OBJECTIVE: To describe the clinical and epidemiological features of an outbreak of a viral infection affecting humans and horses. SETTING: Stables in Hendra, a suburb of Brisbane. SUBJECTS: Affected horses and humans, and at-risk human contacts. RESULTS: A pregnant mare died two days after arrival from a paddock elsewhere in Brisbane. Eight to 11 days later, illness (depression, anorexia, fever, dyspnoea, ataxia, tachycardia, tachypnoea and nasal discharge) was reported among 17 other horses from the same or an adjoining stable. Fourteen horses died or were put down. Five and six days after the index mare's death, a stable-hand and then a horse-trainer, both of whom had had close contact with the sick mare's mucous secretions, developed influenza-like illnesses. The stable-hand recovered but the trainer developed pneumonitis, respiratory failure, renal failure and arterial thrombosis, and died from a cardiac arrest seven days after admission to hospital. A morbillivirus cultured from his kidney was identical to one isolated from the lungs of five affected horses. The two affected humans and eight other horses were seropositive for the infection, which was reproduced in healthy horses following challenge by spleen/lung homogenates from infected horses. There was no serological evidence of infection in 157 humans who had had contact with the stables or the sick horses or humans. CONCLUSIONS: A previously undescribed morbillivirus infected a probable 21 horses and two humans; one human and 14 horses died. That no further cases were detected among humans suggests that the virus was of low infectivity. The source of infection remains undetermined.

Heparin inhibits the immediate response to antigen in the skin and lungs of allergic subjects.

Although heparin is used as an anticoagulant, its biologic function remains unclear. Substantial evidence exists that suggests it may modulate many aspects of immune function and inflammation. We demonstrated, in a double-blind, placebo-controlled, crossover study involving 10 allergic subjects, that a small dose of heparin (25 U/kg) administered intravenously 10 min before challenge reduced the acute cutaneous reaction to 10 allergens and histamine from a group-average sum of mean (+/- SD) wheal diameters at a baseline of 29.9 +/- 10 mm and after normal saline placebo (29.5 +/- 10.7 mm) to after heparin (14.4 +/- 10.4 mm) (p < 0.02, Wilcoxon's signed rank test). In 15 subjects with asthma and dust mite allergy, nebulized heparin 20,000 units administered in a double-blind, placebo-controlled, crossover fashion 10 min before challenge inhibited the bronchospasm induced by inhaled dust mite extract. Log2 of the provocative dose of mite extract causing a 20% fall in FEV1 at baseline was 4.1 +/- 1.5 protein nitrogen units (PNU); after normal saline it was 4.5 +/- 2.0 PNU, and after heparin it was 5.1 +/- 2.5 PNU (p = 0.04). These data suggest heparin may have an inhibitory role in acute mast-cell-mediated allergic inflammation.

Subdural and epidural empyema: diagnostic and therapeutic problems.

OBJECTIVE: A clinical and microbiological review of cases of subdural and epidural empyema. DESIGN, SETTING, PATIENTS: A 10-year retrospective review of patients with subdural and epidural empyema in all Brisbane hospitals with neurosurgical units. In this period there were 14 cases. RESULTS: The paranasal sinuses were the primary focus in 8 of the 14 cases, the middle ear in 3 and a surgical or traumatic wound in 2. One case occurred as a complication of Haemophilus influenzae meningitis. Streptococci, particularly Streptococcus milleri, were the causative organisms in all cases of sinus origin, most of which occurred in the second decade of life. An intracranial collection was considered in the differential diagnosis within 24 hours of admission in all 3 cases of otic origin but in only 2 of the 10 sinus or post-traumatic cases. The most common initial diagnosis was viral or partially-treated bacterial meningitis (8 of 13 cases). The initial computed tomographic (CT) scan was not diagnostic in 3 of 11 patients. No patient was successfully treated without surgery, and all 3 deaths in the series were associated with delayed surgery. CONCLUSIONS: Subdural and epidural empyema is an uncommon condition. The majority of the cases in this series were associated with sinusitis, and Streptococcus milleri was the commonest organism identified. The condition remains a diagnostic challenge; CT scanning cannot be relied upon although the use of intravenous contrast and more modern scanners has improved the diagnostic yield. Surgical drainage and early aggressive antimicrobial therapy are essential to avoid significant morbidity and mortality.

Spatial distribution and prognostic significance of ST segment potential determined by body surface mapping in patients with acute inferior myocardial infarction.

We investigated the mechanism and significance of ST segment changes in inferior infarction by studying 100 patients with acute inferior infarction in whom body surface maps were recorded on admission. The magnitude of the maximum ST segment elevation (denoted Vmax) and magnitude of the maximum ST segment depression (denoted Vmin), as well as the ST depression on the standard 12-lead electrocardiogram were analyzed against morbidity and mortality (at a median follow-up time of 14 months). A value obtained by subtracting Vmax from Vmin correlated (p less than .0002) with outcome. Correlations were also found between Vmin and complications, Vmin and mortality, and between increasing levels of ST depression on the 12-lead electrocardiogram and mortality. The maps were also studied by grouping the 100 ST segment map patterns into five groups by cluster analysis techniques. One group showed marked anterior negativity and had 37% mortality compared with an overall 5% mortality for the remaining groups. The limited arteriographic and autopsy data available indicated that the findings of a diseased artery or arteries corresponded with the results of mapping. The mean map patterns of the five groups showed that, in most patients with inferior infarction, the standard chest leads V1 to V6 are over a region of steep voltage gradient. Small changes in the position of the standard chest lead can cause large changes in the displayed potentials. This study indicates that patients at high risk after acute inferior infarction can be identified by surface mapping on admission to the coronary care unit.