Biomedical subjects
Publications and source records attributed to B H Kay.
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The exacerbation of epidemics of Murray Valley encephalitis in southern Australia during 1951 and 1974 was studied retrospectively to determine when viral introduction may have occurred. Data from studies spanning over 30 years were utilized 1) to determine the number of infective Culex annulirostris necessary to cause one clinical case, based on known host-feeding patterns and the subclinical infection rate in man, and 2), using mathematical modeling, to calculate the likely duration of the rural amplification phase. Generalized tables were generated which demonstrated that mosquito longevity, extrinsic incubation period, and duration of the feeding cycle were the most important variables predisposing rapid amplification. Although Murray Valley encephalitis transmission may still occur during adverse conditions when the reproduction rate Z less than 1.0, subtraction of the durations of incubation in man prior to clinical onset and the most likely rural amplification period from the dates of onset of clinical infections during January 1951 and 1974 suggested that amplification commenced around October 9-30 and that any Murray Valley encephalitis introduction had occurred by then. Examination of bird and mosquito dispersal prior to this time suggests that long-range dissemination of the virus from endemic northern Australia was unlikely.
Eleven weanling horses were inoculated with Murray Valley encephalitis and Ross River viruses either by intravenous injection or by the bite of Culex annulirostris or Aedes vigilax mosquitoes infected orally. Five of the 11 horses circulated trace amounts of MVE virus for 1 to 5d and they infected 7/408 Cx annulirostris which subsequently fed on them. Haemagglutination-inhibiting antibody persisted at detectable levels for the 24-week observation period. With Ross River virus, only one of 11 horses inoculated developed a viraemia detectable by inoculation of suckling mice but 5 horses contained virus sufficient to infect 41/383 Cx annulirostris that fed on them 3 to 4 days after inoculation. On primary inoculation with Ross River virus, only 2 horses developed HI antibody but late responses occurred in 3 horses following probable naturally acquired re-infections. With both viruses, most horses remained normal, some developed mild pyrexia and transient clinical signs. This paper, therefore, indicates that horses are unlikely to be efficient amplifiers of either MVE or RR viruses and does little to incriminate them as important pathogens.
Of 11 stains tested in the laboratory with larval Aedes aegypti, Giemsa at dosages of 6 mg/liter for 24 hr and 21 mg/liter for 3 hr proved most satisfactory for in-vivo staining. At these rates, Giemsa caused some mortality especially in first instars of Ae. vigilax, Ae. aegypti and Culex annulirostris but effectively was retained in all adults examined up to 3 days posteclosion. The method was deemed satisfactory for investigations of larval movement of Ae. vigilax, Cx. sitiens and Ae. alternans in salt marsh in southeast Queensland.
In the laboratory, 8.5% and 5.1% of colonized Culex annulirostris from Brisbane and Mildura, Australia respectively were autogenous when reared and maintained on nutrient rich diets. Females reared and/or maintained on poor diets mainly had ovaries at Christophers' stage I and exhibited from 0 to 0.7% autogeny. All autogenous females had previously mated. Insemination rates in the Brisbane and Mildura colonies respectively, were 72.8% and 78.8%. No autogeny was detected in 997 females reared from 7 localities throughout Queensland but this may have been due to their poorer nutritional status (as indicated by wing size) or more likely to a low insemination rate of 0 to 16%. Our laboratory results, particularly with well-fed females, may have little relevance to the field situation, where adults are generally smaller and less well-nourished.
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A total of 142 young animals including 10 domestic and 14 feral pigs, 12 Hereford calves, 12 crossbred and 24 Merino lambs, 11 dogs, 8 domestic and 16 feral rabbits, 14 Grey kangaroos, 9 Agile wallabies and 12 chickens was exposed to infection with 4 strains of Murray Valley encephalitis virus (MVE), mainly using orally infected Culex annulirostris mosquitoes. In terms of their viraemic response, the animals were grouped into high (Grey kangaroos, rabbits), moderate (pigs, dogs, chickens) and low (calves, lambs, Agile wallabies). Recipient Cx annulirostris induced to bite these animals 1-7 d post-inoculation exhibited infection rates up to 95% but usually were much lower. Some animals in which virus was not detected by intracerebral inoculation of suckling mice were capable of infecting up to 5% Cx annulirostris. Haemagglutination-inhibiting antibody (HI) was of high titre and persistent in rabbits and Grey kangaroos but moderated in others, e.g., cattle, sheep, Agile wallabies to be transient and of low titre. Cattle and Merino lambs were often completely non-responsive. This study increases the range of vertebrates that could be considered as maintenance or amplifying hosts of MVE and, on the basis of their HI antibody responses, evaluates them as potential sentinels of infection in Australia.
Orally infected Culex annulirostris or intravenous injections were used to infect 10 Galahs, 15 Sulphur-crested cockatoos, 12 Corellas, 4 Black ducks and 10 wild mice with Murray Valley encephalitis (MVE) virus. The birds produced moderate viraemias of titres of log 10(2.0)-10(6.0) suckling mouse intracerebral (SMIC) LD50/ml for durations of 1-9 d. However, the wild mice developed low grade viraemia for 1-4 d. Recipient Cx annulirostris feeding on viraemic birds sustained infection rates of 0-10% but, by extrapolation from vector competence data, some titres were capable of infecting greater than or equal to 50% of recipient Cx annulirostris. HI antibody responses were moderately high for most birds (reciprocal titres of 1 in 640-2560) by 14 d and usually persisted at detectable levels for 140 d and, in some individuals, for 6 months. However, 6 of 12 Corellas and 1 of 4 Black ducks became seronegative after 42 and 56 d, respectively. As with previously tested animals, any IgM response was absent 4 wks post-infection. The viraemias attained indicate that these bird species may be considered as potential hosts of MVE, but the limited viraemic response of wild mice suggests that they might play only a minor role.
A method employing ANOVA is presented to quantify man-mosquito contact at Kowanyama, based on human bait collections indoors in light, indoors in darkness and outdoors in darkness. No shifts in feeding behavior were noted during the transitional, dry or wet seasons of 1974-75. Anopheles bancroftii fed in significantly greater numbers indoors in darkness; An. amictus, An. annulipes, An. farauti, An. meraukensis, Aedes normanensis, Ae. kochi, Ae. lineatopennis, Ae. vigilax and Culex annulirostris fed outdoors; Mansonia uniformis fed equally well in the 3 situations tested whereas Cx. quinquefasciatus primarily fed indoors.
During March, 1981, a number of cases of dengue fever occurred in Cairns and Townsville, northern Queensland. From October, 1981, an outbreak of the infection was recognized on Thursday Island and, by May 1982, an estimated 38% of residents had been infected. Isolated cases were reported from other towns in northern Queensland and from other islands in the Torres Strait. Clinical presentation varied from that of severe incapacitating illness lasting up to seven days to infections which were confirmed by serological tests, but were not associated with apparent illness. No deaths were reported. Entomological surveys indicated that the domestic breeding vector of dengue, Aedes aegypti, is widely distributed throughout Queensland - southwards to Dirranbandi and westwards to Mornington Island. In some localities, the indices of Ae. aegypti abundance are alarmingly high, but at least in some suburbs of Townsville, it has been effectively controlled.
Australian populations of Culex annulirostris Skuse from 10 localities, Brisbane, Townsville, Cairns, Charleville, Kowanyama (Queensland), Darwin (Northern Territory), Mildura (Victoria) and Port Hedland, Karratha and Mt. Tom Price (Western Australia) showed considerable heterogeneity in response to oral infection with low passage level Murray Valley encephalitis (MVE) and Kunjin (KUN) viruses. However, there was no consistent pattern of either high or low vector efficiency for populations collected from different regions. Overall, Cx annulirostris was a more competent vector of MVE virus than KUN virus, both in oral susceptibility (suckling mouse intracerebral ID50 of 10(1.7)-10(3.9) compared to 10(2.7)-10(4.8)/mosquito, respectively) and in ability to transmit virus to chicks after 10 d extrinsic incubation (50-89% compared to 0-55%). High or low susceptibility with one virus did not correlate with susceptibility for the other. Although these date were probably subject to some seasonal variation, they generally support the view that Cx annulirostris is the principal vector of MVE in Australia. Poor to moderate susceptibility with KUN suggests that (1) it is only a minor vector in some localities, (2) vertebrate hosts have high viraemias or (3) the strain used may have been atypical.
Some 15% of the saltmarsh mosquito, Aedes (Ochlerotatus) vigilax (Skuse) mechanically transmitted the T48 strain of Ross River virus from viraemic donors to uninfected recipient suckling mice. The population tested from near Brisbane was moderately susceptible to infection (ID50=10(4X5+/-0X1) suckling mouse LD50/mosquito) when fed virus diluted in blood on a cotton pledget. Rapid proliferation of the virus in the mosquito allowed transmission from 4 days after ingestion with maximum transmission of 50-57% occurring from 10 days. From assay of Ae vigilax ovaries and of progeny reared from parentally-infected females, preliminary data suggest transovarial transmission as a potential survival method for this virus.
Australian populations of Culex pipiens quinquefasciatus Say from Brisbane, Charleville, Cairns, Kowanyama (Queensland), Darwin (Northern Territory), Mildura (Victoria), and Port Hedland (Western Australia) proved to be either poorly susceptible or refractory to oral infection with low passage level Murray Valley encephalitis, Kunjin, and Ross River viruses. With respect to past or future epidemics of Murray Valley encephalitis or Kunjin (both known to cause clinical encephalitis in man), and of epidemic polyarthritis, this mosquito is viewed as an unlikely vector.
A biting collection on the banks of Ross River included Anopheles farauti, Adedes imprimens and Ae. alboscutellatus, indicating a relict population of rain-forest mosquitoes and confirming two earlier records of An. farauti from Townsville. Aedes aegypti was collected at Townsville airport. Significance of these findings is discussed in relation to changing urban conditions and a proposed international airport.
In laboratory studies, Murray Valley encephalitis virus was transmitted transovarially by orally infected Aedes aegypti to approximately 1.5% of both adult male and female progeny.
Current practices for early warning of activity of Murray Valley encephalitis and other medically-important arboviruses are reviewed with view to improvement. Data from previous papers on Culex annulirostris populations, environmental factors and virus infection rates were reanalysed and the results considered as a basis for prediction and surveillance. This goal will only be achieved with improved national cooperation, a better epidemiological understanding and greater knowledge of the bionomics of the major vector, Culex annulirostris. The improved monitoring system will utilize meteorological, serological and entomological criteria.
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