Margery L. Kennett
Fairfield Hospital
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Pediatric Infectious Disease Journal | 1988
Gwendolyn L. Gilbert; Kaye E. Dickson; Mary-Jo Waters; Margery L. Kennett; Sally A. Land; Margaret Sneddon
An outbreak of infections caused by enterovirus 71 occurred in southeastern Australia during the winter of 1986. Infection was confirmed by virus isolation or serology in 114 patients, 65 of whom were admitted to hospital. Fifty-one percent of inpatients were infants younger than 12 months old and 85% were younger than 5 years old. Many cases of hand, foot and mouth disease occurred in the community during the epidemic, but 51% (33 of 65) of patients admitted to hospital had central nervous system involvement, often associated with severe symptoms. Six patients had encephalitis and one had a poliomyelitis-like paralytic illness. Various skin manifestations other than hand, foot and mouth disease occurred, especially in young children, and 25 patients had significant respiratory disease including at least 7 with pneumonia. Enterovirus 71 is one of very few viruses that cause hand, foot and mouth disease as well as a variety of other clinical manifestations. The most important of these is meningoencephalitis, which causes significant morbidity, especially in infants and young children.
Archives of Virology | 1994
John C. Hierholzer; Gregory A. Tannock; Connie M. Hierholzer; R. A. Coombs; Margery L. Kennett; P. A. Phillips; Ian D. Gust
SummaryStrains of respiratory syncytial virus from 3 major areas of Australia and Papua New Guinea (PNG) were analyzed for variations in their antigenic and biological properties and in the molecular weights of their major structural proteins. Seventy-eight strains from infants and young children with LRI were collected from 1981–1984. The RSV season in the Australian cities lasted from April through September, with major peaks in July of each year, while the RSV season in tropical PNG was year-round, with small peaks in March and October of each year coinciding with excessive rainfall. Fifty-six strains were analyzed in detail; 40 were typed by time-resolved fluoroimmunoassay with monoclonal antibodies as group A strains and 16 were group B; both groups were concurrent. Three children of one family had sequential RSV infections 13 months apart, and the etiologic group A strain was identical both years in terms of growth and antigenic properties with strain-specific ferret antisera; the second infection was milder in all three children. On average, the group A strains replicated considerably better than group B strains in HEp2 cells, producing 53% more syncytia and 99% higher infectious virus titers in 31% less time in culture. Ten group A and B reference strains exhibited the same growth patterns as the A and B regional strains, respectively. Differences in antigenicity as measured with hyperimmune antisera to prototype Long strain were even greater. Group A strains exhibited a mean 68% greater IFA staining than B strains, a 71% greater EIA reaction, and were neutralized to 69% higher serum titers than B strains. Again, the reference A and B strains included as controls gave patterns identical to those of the regional strains. Finally, the P phosphoprotein had consistently higher molecular weight in A strains (mean 35 900) than B strains (mean 33 100). Small variations in the sizes of the F and G glycoproteins were not sufficient to suggest grouping on this basis.
Journal of Hygiene | 1972
Margery L. Kennett; Anne W. Ellis; F. A. Lewis; Ian D. Gust
During the period October 1968 to March 1969 echovirus type 18 was isolated from 83 patients investigated at Fairfield Hospital for Communicable Diseases, Melbourne. The illnesses most commonly associated with these isolations were aseptic meningitis, and fever with rash.We believe that this is the first report of an epidemic due to echovirus type 18 and the first occasion on which this virus has been shown to produce disease in adults.
Journal of Hygiene | 1986
Zong-Da Meng; Margery L. Kennett; Suzanne M. Rodger; Kaye E. Dickson; Bruce N. Anderson; Ian D. Gust
Forty-one strains of adenovirus type 19/37 (Ad19/37) mainly isolated from patients with keratoconjunctivitis or conjunctivitis between 1974 and 1984 were re-evaluated by serum neutralization (SN), haemagglutination inhibition (HI) and DNA restriction analysis. Of 19 isolates which were neutralized to high titre by antiserum prepared against prototype Ad19, 5 showed cross-reactivity with 32-64 units of Ad37 antiserum, while of 22 strains neutralized by high titre by Ad37 antiserum, 3 showed cross-reactivity with 32 units of Ad19 antiserum. By DNA restriction analysis, all Ad19 isolates were identical to each other and to Ad19A virus. Using endonuclease Bgl 1, three variants were observed among the Ad37 isolates.
Journal of Hygiene | 1981
L. Irving; Margery L. Kennett; F. A. Lewis; Chris Birch; A. Donaldson
A number of adenovirus serotypes have been associated with both sporadic cases and outbreaks of conjunctivitis and pharyngoconjunctival fever but only adenovirus type 8 and adenovirus type 19 have been responsible for wide-spread epidemic kerato-conjunctivitis. In Melbourne, Australia, in the past eight years these two serotypes have been prevalent, resulting in an outbreak of adenovirus type 8 kerato-conjunctivitis in 1976-7 followed by adenovirus type 19 kerato-conjunctivitis in 1978-9. During these two periods of peak incidence, 53 cases of adenovirus type 8 and 43 cases of adenovirus type 19 kerato-conjunctivitis were confirmed by isolation.
Pathology | 1973
Anne W. Ellis; Margery L. Kennett; F. A. Lewis; Ian D. Gust
Summary During 1969‐1970, 12 strains of virus were isolated in cell culture from 9 patients with hand, foot and mouth disease investigated at Fairfield Hospital for Communicable Diseases, Melbourne. The strains, although acid stable and producing an enterovirus‐like cytopathic effect, could not be neutralized, in conventional tube neutralization tests, by antisera to any of the prototype enteroviruses. Immunodiffusion studies and mouse neutralization tests performed on selected isolates showed them to be strains of Coxsackie A16 virus. When suspensions of the strains which had proved difficult to neutralize were treated by sodium deoxycholate or filtered, the difficulty was overcome, suggesting that it had been due to the presence of viral aggregates.
Bulletin of The World Health Organization | 1974
Margery L. Kennett; Christopher J. Birch; F. A. Lewis; A. P. Yung; Stephen Locarnini; Ian D. Gust
Journal of Medical Virology | 1977
Chris Birch; F. A. Lewis; Margery L. Kennett; M. Homola; H. Pritchard; Ian D. Gust
The Medical Journal of Australia | 1985
Oliver B; Ng S; John A. Marshall; Harry B. Greenberg; Ian D. Gust; Cresswell; Ward B; Margery L. Kennett; Christopher J. Birch
Journal of Hygiene | 1981
Margery L. Kennett; A. Donaldson; J. A. Marshall; H. G. Williamson