Human Hendra virus infection causes acute and relapsing encephalitis.

AIM: To study the pathology of two cases of human Hendra virus infection, one with no clinical encephalitis and one with relapsing encephalitis. METHODS: Autopsy tissues were investigated by light microscopy, immunohistochemistry and in situ hybridization. RESULTS: In the patient with acute pulmonary syndrome but not clinical acute encephalitis, vasculitis was found in the brain, lung, heart and kidney. Occasionally, viral antigens were demonstrated in vascular walls but multinucleated endothelial syncytia were absent. In the lung, there was severe inflammation, necrosis and viral antigens in type II pneumocytes and macrophages. The rare kidney glomerulus showed inflammation and viral antigens in capillary walls and podocytes. Discrete necrotic/vacuolar plaques in the brain parenchyma were associated with antigens and viral RNA. Brain inflammation was mild although CD68(+) microglia/macrophages were significantly increased. Cytoplasmic viral inclusions and antigens and viral RNA in neurones and ependyma suggested viral replication. In the case of relapsing encephalitis, there was severe widespread meningoencephalitis characterized by neuronal loss, macrophages and other inflammatory cells, reactive blood vessels and perivascular cuffing. Antigens and viral RNA were mainly found in neurones. Vasculitis was absent in all the tissues examined. CONCLUSIONS: The case of acute Hendra virus infection demonstrated evidence of systemic infection and acute encephalitis. The case of relapsing Hendra virus encephalitis showed no signs of extraneural infection but in the brain, extensive inflammation and infected neurones were observed. Hendra virus can cause acute and relapsing encephalitis and the findings suggest that the pathology and pathogenesis are similar to Nipah virus infection.

An historical review of criminal abortion.

Criminal abortion is rarely seen in modern Australia. This historical review examine cases seen in Brisbane during the period 1939 and 1947. Instrumentation or introduction of fluid into the uterus were the common causes of fatalities in this pre-penicillin era.

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.

The application of immunoblotting to the phenotyping of group-specific component.

A sensitive immunoblotting method for the routine detection of group-specific component (GC) from fresh serum, and from control and casework bloodstains has been developed. GC phenotypes were separated in a thin layer polyacrylamide gel by isoelectric focusing, transferred to nitrocellulose by a rapid capillary blotting procedure, and detected using a double antibody enzyme immunoassay. This method is capable of phenotyping 8 ng of GC extracted from bloodstains, a four-fold increase in sensitivity when compared to immunofixation and silverstaining. A total of 2424 casework bloodstains have been analysed and GC phenotypes identified in 78% of samples. The method is suitable for use in routine laboratories and is more sensitive than other methods for GC phenotyping of casework bloodstains.

Prenatal cytogenetic diagnosis--a current audit. A review of 2000 cases of prenatal cytogenetic diagnoses after amniocentesis, and comparisons with early experience.

An audit of 2000 cases of prenatal cytogenetic diagnoses is presented. This comprises two consecutive series of 1000 cases (1974-1980 and 1980-1983). Chromosomal studies were performed after mid-trimester amniocentesis. For both series detailed results of the reasons for referral and the outcome of laboratory studies and pregnancy follow-up (in 95% of cases) are presented. In current practice 75% of prenatal cytogenetic diagnoses were for advanced maternal age. Ten per cent of tests were undertaken because of a family history of Down's syndrome. The detection rate of chromosomal abnormality in prenatal cytogenetic diagnoses was 2.06%. Two per cent of amniotic cell cultures failed to grow, necessitating a repeat amniocentesis. The rate of culture failure due to undefinable causes was 0.55%. Fetal loss after amniocentesis for prenatal cytogenetic diagnosis at 16 weeks' gestation has halved since 1980, with a current miscarriage rate of 0.6% within four weeks of the procedure. One maternal death (as a result of amniotic fluid embolism) and one case of amnionitis occurred in the first series of 1000 consecutive cases (up to 1980), but no such complication has occurred since. Secular trends in the indications for referral, laboratory complications, clinical outcome and diagnostic patterns are presented.

A SCUBA-diving fatality.

An investigation by a Naval Board of Inquiry into the circumstances of a fatal naval diving accident is presented. Although drowning contributed to the fatal outcome, massive arterial gas embolism is thought to have been the principal cause of death, and the value of post-mortem computed tomography scanning for its detection is demonstrated. The possibility is discussed of diver error due to unfamiliarity with equipment and procedures, compounded by nitrogen narcosis. The shortfall in expertise of coronial inquiries into diving deaths is emphasized against a background of increasing popularity of sports diving around Australia. The implications for the offshore industry are obvious and suggest the need for a federal diving inspectorate.

Prenatal diagnosis of chromosomal abnormalities: analysis of 1000 consecutive amniotic fluids.

Cytogenetic studies have been performed on 1,000 amniotic fluid specimens referred for prenatal diagnosis. Two-thirds of the patients had strong clinical indications for prenatal chromosome studies and the remaining one-third were referred because of maternal anxiety or a family history of neural tube defect. A total of 18 affected fetuses were detected in this series (1.8%) and these included 3 male fetuses in patients with a history of sex-linked disorder and 15 fetuses with chromosome abnormalities. The overall culture success rate was 97.4% and the average time taken to obtain sufficient material for initial chromosome analysis was 13 days. Fetal loss within 4 weeks of the amniocentesis was 1.2%.

Fatal oleander poisoning.

A case of fatal poisoning due to the presumed ingestion of leaves and/or fruit of the yellow oleander (Thevetia peruviana) is described. The diagnosis was confirmed by radioimmunoassay using antibodies of differential specificity towards cardiac glycosides. Attention is drawn to the potential usefulness of digoxin assay in suspected cases of oleander poisoning.