Biomedical subjects
Publications and source records attributed to A M Murphy.
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The enzyme-linked immunosorbent assay (ELISA) was used to detect leptospire-specific immunoglobulin M (IgM) and IgG in the sera of patients infected with leptospiral serovars hardjo, pomona, or copenhageni. All patients produced specific IgM and IgG detectable by ELISA. In contrast, only a few patients produced IgG agglutinins whereas all produced IgM agglutinins. The specificity and sensitivity of the test suggest that the ELISA anti-IgM technique is a suitable method for detecting leptospiral antibodies in human sera for diagnostic and epidemiological purposes.
The IgM globulin response has been measured following the onset of primary Q fever infections. A complement fixation test method was used to measure the IgM after separation by ultracentrifugation in a sucrose density gradient. Specific IgM was demonstrable between 2 and 10 wk after onset of symptoms. The test can be used to confirm a recent infection when only a 'convalescent' blood specimen has been collected and will be useful in the assessment of workers' compensation claims.
At least 2000 persons were involved in an Australia-wide outbreak of oyster-associated food poisoning in June and July, 1978. At the time, this episode presented a major health risk to the community as a whole and has subsequently posed a serious economic problem for the oyster farming and distributing industry. Although bacteriological investigations indicated some batches of oysters were contaminated by sewage, no bacterial cause could be established. The causative organism was shown to be Norwalk virus, a known cause of acute non-bacterial gastroenteritis. This virus was found in 39% of faecal specimens examined by electron microscopy and an antibody response was demonstrated by immune electron microscopy in 75% of paired sera tested. Norwalk virus has not been identified previously outside the United States of America and has not been linked to food-borne gastroenteritis before. Purification of oysters and other measures have been instituted to prevent a recurrence of the outbreak.
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A case of fatal pneumonia caused by adenovirus type 7 in an adult is reported. This virus was isolated from the lung tissue, and typical inclusion bodies were found in histological sections. Death due to adenovirus pneumonia in adults appears to be extremely rare.
An outbreak of acute gastroenteritis occurred in a primary school southwest of Sydney in August, 1977. Two hundred and eight pupils and nine teachers were affected over a one-month period. Electron microscopy revealed parvovirus-like particles in faecal extracts of 14 of 23 persons tested during the acute phase of illness. The virus was still present in the faeces of four individuals six weeks later. The appearance of specific antibodies was demonstrated by immune electron microscopy in five persons. No other cause for the outbreak could be found despite exhaustive investigations.
Faecal specimens from 628 newborn babies in the nurseries of six metropolitan hospitals were examined by electron microscopy for rotaviruses. 304 babies (49%) were found to be excreting virus. All those infected were in five nurseries; viruses were not detected in specimens from the sixth nursery. Two nurseries were studied for 9 mo and another for 11 mo and rotaviruses were found consistently in 40-50% of stools examined. There was no seasonal variation. None of the neonates under the age of one day were infected but by the age of three to four days approximately 50% were excreting virus. Most of those shedding virus were symptom-free but 84 (28%) had diarrhoea. Persisting endemic rotavirus infection is apparently common in hospital nurseries in Sydney. The virus is probably transmitted by environmental spread from neonate to neonate.
During the 1976 influenza epidemic, the incidence and severity of attack by A/Victoria/3/75 strain were studied in 312 participants who were divided into two groups: in Group 1 were 216 participants who had a history of laboratory-proven infection by one of the earlier strains of Hong Kong subtype; in Group 2 were 96 participants who had no known history of such prior infection. No participant in either group received influenza vaccine. The efficacy of clinical immunity, acquired as a result of prior infection by an earlier Hong Kong subtype strain, was judged by comparing the findings in Group 1 and Group 2. Incidence of laboratory-proven A/Victoria/3/75 infection was found to be 27% in Group 2 (26 cases confirmed) and 10.6% in Group 1 (23 cases confirmed). Among Group 1 members, the incidence was highest in those with the longest interval since prior Hong Kong subtype infection. Severe influenzal illness was seen in 14 of the 26 proven cases in Group 2, and in only three of the 23 proven cases in Group 1. The prior infection in these three had been by A/Hong Kong/1/68 strain in 1969-1970. Thus in Group 1, severe influenzal illness was not observed until six years or more had passed since prior infection (and three episodes of antigenic drift had intervened). Results suggested that low serum antibody levels may be unreliable as indicators of clinical immunity. Preepidemic sera of 99 members of Group 1 and 82 members of Group 2 showed no HAI antibody to A/Victoria/3/75 (titre less than 8), but the incidence of laboratory-proven A/Victoria/3/75 infection among these individuals was lower in Group 1 (19%) than in Group 2 (30.5%).
After type A influenza virus had undergone major antigenic change in mid 1968, it was noted that individuals previously infected by strains of the old subtype (Asian), especially late strains, appeared to be unexpectedly resistant to clinical attack by the new subtype (Hong Kong). Prospective studies have since shown that, during the A/England/42/72 influenza epidemic of 1972, in which the incidence was approximately 7% in the community, clinical influenza due to this virus was not found in 229 subjects previously confirmed as having had A/Hong Kong/1/68 influenza, even though vaccine which had been effective against A/Hong Kong/1/68 was ineffective against A/England/42/72. During the A/Port Chalmers/1/73 influenza epidemic of 1974, clinical influenza resulting from Port Chalmers virus was not found in a closely monitored group of 176 unvaccinated subjects previously infected by A/Hong Kong/1/68 or A/England/42/72, although laboratory studies demonstrated Port Chalmers infection in five of these (2-8%). By contrast, among 99 subjects who had no such history of earlier infection, 22 developed laboratory-proven Port Chalmers influenza and most of them had typical illness.
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By means of electron microscopy and ultracentrifugation techniques rotavirus-like particles have been found in 84 of 269 specimens of faeces collected from infants and young children admitted to the Royal Alexandra Hospital for Children, Camperdown, N.S.W. during the usual winter outbreak of infantile gastroenteritis. Morphologically intact viruses were also found in faecal specimens stored at -20 degrees C for up to nine years. Rotaviruses were found in specimens collected from five newborn infants with diarrhoea, and in a subsequent survey of the nursery when 23 neonates without diarrhoea were present, 12 (52 %) were found to be excreting virus. Morphologically similar viruses were found in six of 16 faecal specimens from newborn calves with gastroenteritis (scours), and an antigenic relationship between the rotaviruses of human and bovine origin has been demonstrated.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.