Early diagnosis of Murray Valley encephalitis by reverse transcriptase-polymerase chain reaction.

A 4-year-old aboriginal boy developed encephalitis due to Murray Valley encephalitis virus (MVE) following an earlier infection with Kunjin virus (KUN). The illness was severe, resulting in cerebral atrophy and profound physical and intellectual disability. The earlier KUN infection complicated his serological profile and delayed antibody responses to MVE. By contrast, the reverse transcriptase-polymerase chain reaction (RT-PCR) assay detected MVE in serum 3 days after the onset of illness and 4 days before the appearance of MVE-specific IgM. We suggest that MVE-specific RT-PCR provides rapid and specific diagnosis of MVE and should be used more widely for the diagnosis of acute viral encephalitis in cases originating from flavivirus endemic areas.

Primary staphylococcal pneumonia in childhood: a review of 69 cases.

Primary staphylococcal pneumonia is a rapidly progressive illness with well-described clinical and radiological features and a significant mortality rate. This retrospective study of cases diagnosed over a 20 year period at a tertiary paediatric hospital was undertaken to document the epidemiology and assess the management and mortality of the disease. The survey demonstrated that far fewer patients are being seen than formerly and confirmed that this is a disease primarily affecting infants and Aboriginal children. The initial radiological features were not diagnostic in the majority of cases but typical changes appeared in most at some time during the illness. The use of surgical drainage was not associated with a decrease in the duration of fever or length of hospital stay. The mortality rate has improved but remains significant.

What are the mechanisms producing increased ventilation in dead space studies in neonates?

In 21 studies on 15 infants an additional dead space tube produced a significant rise in end-tidal PCO2 and fall in end-tidal PO2, associated with a rise in minute ventilation (228 +/- 77 mL/kg/min at zero, 348 +/- 85 mL/kg/min at one, and 437 +/- 128 mL/kg/min at two anatomical dead spaces). The differences between end-inspiratory and end-expiratory PCO2 and PO2 did not change significantly, suggesting an increase in dead space, but not in alveolar ventilation. In a further 9 babies the rise in ventilation was unchanged when measurements were repeated in 30% oxygen (361 +/- 65 vs. 340 +/- 54 mL/kg/min at one anatomical dead space). Studies on 8 babies, with the added tube ventilated by a fan, showed that a mean 28% of the rise in minute ventilation was due to increased resistance. Although the response to tube breathing in neonates is complex, carbon dioxide appears to be the major factor producing increased ventilation.

Increased paediatric admissions with asthma in Western Australia--a problem of diagnosis?

A study of hospital admissions of paediatric cases with asthma over a 17-year period (1971-1987) in Western Australia was performed retrospectively. Hospital admission rates for asthma increased in all paediatric age-groups with the most dramatic increase occurring in the youngest (zero- to four-years') age-group. This increase in hospital admissions for asthma has been accompanied by a rapid decline in admissions for other paediatric respiratory conditions that share a potential diagnostic overlap with asthma. Hospital admission rates for asthma have reached a plateau at the major paediatric teaching hospital in the State from 1977 and Statewide from 1983. Diagnostic transfer has contributed significantly to the reported increase in hospital admissions for asthma over the past two decades.

Ventilatory response to increased dead spaces in the first week of life.

We have developed a method for quantitatively assessing respiratory control in a group of 10 full-term healthy babies, mean age at test 5 days, by measuring their ventilatory response to added external dead spaces. The dead spaces were equal to 0.5, 1, 2, and 3 anatomic dead spaces (2.2 ml/kg body weight), respectively. Tidal volumes were measured by a nasal mask and a 200-I rigid container. End-tidal CO2 was monitored via a tube in the nostril by a mass spectrometer. Baseline measurements were made during a 10-minute period, after which similar recordings were obtained with each of the dead space tubes. The system was calibrated against a 20-ml syringe. The mean baseline ventilation was 602 ml/minute. On the addition of 0.5, 1, 2, and 3 dead spaces, minute ventilations were increased by 37.5, 74.7, 150.7, and 273.6%, respectively. These increases were due to rises in tidal volume rather than respiratory rate. End-tidal CO2 rose by 1.8 and 4 mmHg on the addition of 2 and 3 dead spaces. When the results were compared with expected minute ventilations--based on the baseline recordings and corrected for the added dead spaces and for changes in anatomic dead space ventilation due to alterations in respiratory rate--the results were within 10% of expected values.

Possible "outbreak" of Kawasaki disease in Victoria.

Kawasaki disease, a multisystem disorder of unknown cause, which primarily affects young children, has been recognized in many countries and previously reported in Melbourne. The condition is usually endemic, but has occasionally been reported in clusters or epidemics. Such an apparent "epidemic" occurred in the winter of 1981. This paper highlights the clinical features, the results of investigations and sequelae of this disorder in the seven children admitted to the Royal Children's Hospital, Melbourne, during that period. Possible aetiological factors were sought, but none was found.