PubMed Health⌕ Search

Biomedical subjects

R F Sellers

Publications and source records attributed to R F Sellers.

At least 19 recordsLinked to original sources
PubMed1991

Possible introduction of epizootic hemorrhagic disease of deer virus (serotype 2) and bluetongue virus (serotype 11) into British Columbia in 1987 and 1988 by infected Culicoides carried on the wind.

Outbreaks of epizootic hemorrhagic disease of deer and of bluetongue began in British Columbia in August and October 1987 respectively and recrudescence of infection by both viruses was detected the following year in August. Weather records for up to 18 days before the initial outbreaks of disease, isolation of virus or seroconversion were examined to determine if the viruses could have been introduced by infected Culicoides carried on the wind. Data on temperature, rainfall, wind speed and direction and pressure together with backward trajectory analysis showed that there were suitable winds which could have introduced Culicoides infected with epizootic hemorrhagic disease of deer virus on 13 August 1987 (14 days before disease was observed), Culicoides infected with bluetongue virus on 1 October 1987 (7 days before virus was isolated and 13 days before disease in sheep) and Culicoides infected with bluetongue or epizootic hemorrhagic disease of deer viruses on 20 July 1988 (15 days before seroconversion was detected). The arrival on 13 August 1987 coincided with the passage of a cold front and rain and that on 1 October 1987 with a fall in temperature and calm winds. The source of the Culicoides before arrival could have been the Okanogan Valley as far south as the junction of the Okanogan and Columbia rivers in Washington, USA. Flight would have been at temperatures of 12.6 degrees C or higher and at heights up to 1.5 km.

Animals↗
PubMed1990

Trajectory analysis of winds and vesicular stomatitis in North America, 1982-5.

Outbreaks of vesicular stomatitis, serotype New Jersey, during epidemics in the United States and northern Mexico, 1982-5, were examined by backward trajectories of winds to investigate spread and possible sources. The outbreaks selected for analysis did not involve introduction of disease by infected animals. The findings indicate that wind could have been responsible for carrying infection from northern Mexico to Arizona and New Mexico and thence to Colorado and Utah and on to Wyoming, Idaho and Montana. The results of these analyses are consistent with the findings from T1 RNAse fingerprinting of virus isolates from outbreaks during the epidemics. The arrival of the trajectories was associated with the passage of a front and rain or passage of a front alone or rain alone. At the time of the trajectories temperatures of 10 degrees C and higher were recorded at heights up to 2500-3500 m. Introduction by airborne particles would appear unlikely as it would have required a source of at least 10(5) infectious units per minute per animal. Vesicular stomatitis virus had been isolated from Simulium and Culicoides during the epidemic with amounts of virus from Simulium sufficient to suggest biological transmission. The possibility of Simulium infected with vesicular stomatitis virus being carried downwind to introduce disease is discussed in relation to the behaviour of Simulium and the pathogenesis of vesicular stomatitis in large animals.

Air Movements↗
PubMed1990

Trajectory analysis of winds and eastern equine encephalitis in USA, 1980-5.

Backward trajectories of winds were determined to identify possible sources of eastern equine encephalitis virus associated with isolation of virus from mosquitoes or birds or outbreaks in horses between 1980 and 1985 in Maryland, New Jersey, New York and Michigan, USA. The results of the trajectory analyses suggested that eastern equine encephalitis virus could have been carried by infected mosquitoes on surface winds at temperatures 13 degrees C or higher from North Carolina north-eastwards along the Atlantic Coast to Maryland and New Jersey and thence to upstate New York and from western Kentucky to Michigan. Landing of mosquitoes was associated with the presence of a cold front and rain leading to variations in the location and timing of outbreaks from year to year. The mosquito responsible was most likely to have been Culiseta melanura, but Coquillettidia perturbans and Aedes sollicitans could also have been involved. There may be a continual cycle of eastern equine encephalitis virus in mosquitoes and birds in south-eastern USA, from where the virus could be distributed by infected mosquitoes on the wind along the Gulf and Atlantic Coasts and up the Mississippi Valley.

Air Movements↗
PubMed1990

Airborne spread of foot-and-mouth disease in Saskatchewan, Canada, 1951-1952.

Farms affected with foot-and-mouth disease during the epidemic in Saskatchewan, in 1951-1952, for which the origin of virus was not known or uncertain, were studied to determine if infection could have been introduced by the airborne route. A short-range Gaussian plume dispersion model was used to estimate the concentration of virus downwind and the dose available for individual animals. The investigation suggested that a large virus source due to infected pigs in a feedlot in January 1952 could have been responsible for airborne dispersion northwestwards downwind to farms up to 20 km distant. Subsequent spread from these farms was to neighboring farms and was influenced by the local topography of a creek. The dispersion model could be used for predicting airborne spread if foot-and-mouth disease should occur.

Air Microbiology↗
PubMed1990

The epidemic of foot-and-mouth disease in Saskatchewan, Canada, 1951-1952.

The epidemic of foot-and-mouth disease in Saskatchewan in 1951 and 1952 was studied in order to determine origins of outbreaks and methods of spread. The epidemic was initially considered to be vesicular stomatitis and foot-and-mouth disease was not recognized until February 1952, three months after the initial infection. The reports prepared at that time were reviewed in order to obtain details of the numbers of animals infected and the source and date of infection for the outbreaks. Methods of spread were rated according to their likelihood. The introduction of infection by an immigrant through his clothes as well as by sausage was possible. The sequence of events from the first outbreak to the spread from a feedlot/packing plant and from a dairy farm, which failed to report the disease, were clarified. Methods of spread included movement of animals, animal products and people and the airborne route. Milk delivery and artificial insemination did not result in spread of infection. The quarantine of affected farms reduced spread by animals and deterred visits by people. The original diagnosis of vesicular stomatitis was due to misinterpretation of a lesion in an inoculated horse. Laboratory tests established the presence of foot-and-mouth disease. The limited extent of the epidemic, despite the delay in diagnosis, is attributed to (i) the low density of cattle, (ii) few infected pigs and hence less airborne virus and (iii) absence of waste food feeding and milk collection in addition to the limited quarantine imposed.

Animals↗
PubMed1989

Trajectory analysis and bluetongue virus serotype 2 in Florida 1982.

Examination of Northern Hemisphere synoptic charts and computation of backward trajectories indicated that Culicoides infected with bluetongue virus serotype 2 could have been carried on the wind and brought the virus to Florida on the afternoon of August 19, 1982 after leaving northern Cuba the previous evening. Flight would have occurred at a height of 1-1.5 km at temperatures of 15-17 degrees C. The distance of 500 km from northern Cuba to Ona would have been covered in 20 h at an average speed of 25 km h-1. Computation of trajectories indicated that a second electropherotype, Ona B, was unlikely to have been introduced by infected Culicoides.

Animals↗
PubMed1989

Eastern equine encephalitis in Quebec and Connecticut, 1972: introduction by infected mosquitoes on the wind?

In 1972 there were outbreaks of eastern equine encephalitis in the Eastern Townships, Quebec, Canada and in Connecticut, USA. Climatic data including Northern Hemisphere synoptic charts were examined. The findings indicate that the virus could have been brought to Lac Brome by infected mosquitoes carried on surface winds from Meriden, Connecticut, on the night of August 22-23, 1972. The distance of 400 km would have been covered in 14-16 h at a speed of 25-30 km h-1 and at a temperature of 15 degrees C and higher. The first case was recorded 13 days later on September 5, 1972. The outbreak at Meriden, Connecticut started on August 21, 1972. On August 7, 1972 southwesterly winds blew along the Atlantic coast at heights up to 1.5 km. Infected mosquitoes could have been carried on the wind from Cape May, New Jersey, Delaware-Maryland-Virginia peninsula, North Carolina or Georgia. Flights would have been at 17 degrees-20 degrees C and lasted 5-6, 9-10, 14-16 and 20-26 h depending on the origin. The arrival on August 8, 1972 coincided with a cold front moving from the northwest through Connecticut. Culiseta melanura is regarded as the mosquito species most likely to have been involved in the transmission of infection.

Air Movements↗
PubMed1988

Impact of climate on western equine encephalitis in Manitoba, Minnesota and North Dakota, 1980-1983.

Information was collected on confirmed outbreaks of western equine encephalitis (WEE) in North America east of the Rockies for 1981 and 1983 (epidemic years) and 1980 and 1982 (non-epidemic years). The initial pattern of outbreaks in Manitoba, Minnesota and North Dakota was determined for each year. Backward (and in some instances forward) wind trajectories were computed for each day 4-15 days (incubation period) before the initial outbreaks of WEE in a given area of province or state. During these years the timing and location of WEE outbreaks in horses and man, seroconversion in chickens, the maximum Culex tarsalis counts at Winnipeg and first isolation of WEE virus from C. tarsalis could be correlated with trajectories of winds from states further south within acceptable intervals. It is suggested that C. tarsalis mosquitoes infected with WEE virus are carried on the wind from Texas on the Gulf of Mexico, where they continue to breed during the northern winter months, to northern Texas and Oklahoma in the spring. In May, June and July C. tarsalis are carried north on southerly winds from these states through Kansas and Nebraska to North Dakota, Minnesota, Wisconsin and Manitoba. Distances of 1250-1350 km are traversed in 18-24 h at heights up to 1.5 km with temperatures greater than or equal to 13 degrees C. Landing takes place where the warm southerly winds meet cold fronts associated with rain. Convergence leads to concentration of C. tarsalis and determines where outbreaks occur. It is possible that return of new generations of C. tarsalis to the south may occur later in the year. The development of an epidemic of WEE in the northern states and provinces would appear to depend on (i) suitable trajectories from the south in June and July with temperatures greater than or equal to 13 degrees C meeting cold fronts with rain, (ii) sufficient C. tarsalis infected with WEE virus at source, carried on the wind and locally, (iii) C. tarsalis biting horses and man, (iv) maintenance of local mosquito populations in August and (v) susceptible hosts (birds) at source and susceptible hosts (horses and man) locally. Possible methods of prediction involving determination of trajectories, identification of C. tarsalis blood meals, measuring seroconversion in calves are discussed in addition to the methods already in use.

Animals↗
PubMed1987

Possible windborne spread of myxomatosis to England in 1953.

An analysis of the meterological conditions showed that the first outbreaks of myxomatosis in S.E. England in 1953 could have resulted from wind carriage of insects infected with myxoma virus from northern France. South-easterly winds on the night 11-12 August would have carried the insects 120-160 km from the Départements of Nord, Pas de Calais and Somme across the English Channel to near Edenbridge, Kent. The flight would have taken 6.5-8.5 h at wind speeds of 15-22 km h-1. On the night 11-12 August, temperatures increased with height (inversion) up to 500 m; at ground level temperature was around 19 degrees C and at 500 m was 25 degrees C. Insects would have travelled up to the top of the inversion arriving on 12 August as the inversion declined. Two or possibly three generations of infection would have taken place before the disease was seen around the middle of September 1953. The most likely insect was the mosquito Anopheles atroparvus which breeds along the coastal marshes of England and northern France and which has been shown experimentally and in the field to transmit myxoma virus mechanically.

Air Movements↗
PubMed1985

Possible windborne spread to western Turkey of bluetongue virus in 1977 and of Akabane virus in 1979.

An outbreak of bluetongue in sheep started in the Menderes valley, Aydin Province, Western Turkey, in October 1977. The severity of the disease indicated that it had not been there before but had been introduced into the area. Analysis showed that, while it was possible for the virus to have been brought into the area by movement of infected animals, there was also a period of south-easterly winds which could have carried infected midges from Cyprus, where bluetongue was present. During the night of 14-15 October 1977, south-easterly winds could have brought midges infected with bluetongue virus for the 15 h flight at a height possibly of 500 m and at temperatures of about 20 degrees C. A depression moving north-eastwards accompanied by rain may have affected the landing of midges in the Menderes valley on the morning of 15 October. An outbreak of arthrogryposis-hydranencephaly in newly born calves occurred in March-May 1980, also in the Menderes valley, Aydin Province. The severity of the outbreak indicated that Akabane virus had not been in the area before but had been introduced in September-November the previous year. While infected animals could have brought the virus into the area, analysis based on the probable time of infection of pregnant dams showed that easterly winds at the end of September or beginning of October 1979 could have brought insects infected with Akabane virus into the Menderes valley from eastern Turkey or northern Syria. These analyses illustrate the use of meteorological data to backtrack to possible sources and to identify the time of infection.

Air Movements↗
PubMed1983

Serological studies of Australian and Papua New Guinean cattle and Australian sheep for the presence of antibodies against bluetongue group viruses.

Following isolation of a virus (CSIRO19) from insects in Australia and its identification as bluetongue virus serotype 20 (BTV20), a nationwide survey of antibodies in cattle and sheep sera was undertaken. Initial studies using the serum neutralization (SN) test showed that the distribution of BTV20 antibodies in cattle was confined to the northern part of Australia. Group-reactive antibody tests (agar gel diffusion precipitin, AGDP, and complement-fixation, CF) showed group-reactive cattle sera south of the BTV20 zone (northern Australia), and southwards from Queensland to New South Wales. Very few group-reactive sheep sera (45 out of 16213) were found and these were of doubtful epidemiological significance. Some of these BTV group-reactive, BTV20-negative, sera were tested in SN tests against BTV1 to 17 and Ibaraki (IBA) virus. The results indicated that BTV1, or a closely related orbivirus, was active in cattle in Queensland, northern Western Australia, and New South Wales, and that antibody to BTV15 was present in some of the cattle sera in northern Western Australia and the Northern Territory. Antibody to IBA virus was present in some cattle sera in Queensland, northern Western Australia and New South Wales. SN antibody titres greater than or equal to 60 were also found to a number of other BTV serotypes in cattle sera in northern Western Australia and Queensland (principally, BTV2 and BTV7). Low level reactions were commonly observed against these and a number of other BTV serotypes, often in the same serum samples. Further, 22% of the group-reactive cattle sera did not react with any of the viruses in the SN tests. Such results were difficult to interpret in terms of known Australian BTV or BTV-related isolates.

Animals↗
PubMed1982

Long distance transport of foot-and-mouth disease virus over the sea.

The conditions required for the transport of foot-and-mouth disease (FMD) virus in the atmosphere over long distances and in sufficient concentrations to cause infection in exposed animals are described. Using these factors a series of 23 outbreaks of FMD in Europe, where the original outbreaks were separated from later outbreaks by sea passage, have been investigated. The findings obtained support the hypothesis that under certain conditions the airborne transmission of FMD over a long sea passage is possible.

Air Microbiology↗
PubMed1980

Weather, host and vector--their interplay in the spread of insect-borne animal virus diseases.

The spread of insect-borne animal virus diseases is influenced by a number of factors. Hosts migrate, move or are conveyed over long distances: vectors are carried on the wind for varying distances in search of hosts and breeding sites; weather and climate affect hosts and vectors through temperature, moisture and wind. As parasites of host and vector, viruses are carried by animals, birds and insects, and their spread can be correlated with the migration of hosts and the carriage of vectors on winds associated with the movements of the Intertropical Convergence Zone (ITCZ) and warm winds to the north and south of the limits of the ITCZ. The virus is often transmitted from a local cycle to a migratory cycle and back again.Examples of insect-borne virus diseases and their spread are analysed. Japanese, Murray Valley, Western equine, Eastern equine and St Louis encephalitis represent viruses transmitted by mosquito-bird or pig cycles.THE AREAS EXPERIENCING INFECTION WITH THESE VIRUSES CAN BE DIVIDED INTO A NUMBER OF ZONES: A, B, C, D, E and F. In zone A there is a continuous cycle of virus in host and vector throughout the year; in zone B, there is an upsurge in the cycle during the wet season, but the cycle continues during the dry season; there is movement of infected vectors between and within zones A and B on the ITCZ and the virus is introduced to zone C by infected vectors on warm winds; persistence may occur in zone C if conditions are right. In zone D, virus is introduced each year by infected vectors on warm winds and the arrival of the virus coincides with the presence of susceptible nestling birds and susceptible piglets. The disappearance of virus occurs at the time when migrating mosquitoes and birds are returning to warmer climates. The virus is introduced to zone E only on occasions every 5-10 years when conditions are suitable. Infected hosts introduced to zone F do not lead to circulation of virus, since the climate is unsuitable for vectors. Zones A, B and C correspond to endemic and zones D and E to epidemic conditions.Similar zones can be recognized for African horse sickness, bluetongue, Ibaraki disease and bovine ephemeral fever - examples of diseases transmitted in a midge-mammal cycle. In zones A and B viruses are transported by infected midges carried on the wind in association with the movement of ITCZ and undergo cycles in young animals. In these zones and in zone C there is a continual movement of midges on the warm wind between one area and another, colonizing new sites or reinforcing populations of midges already present. Virus is introduced at times into fringe areas (zones D and E) and, as there is little resistance in the host, gives rise to clinical signs of disease. In some areas there is persistence during adverse conditions; in others, the virus is carried back to the endemic zones by infected midges or vectors.Examples of viruses maintained in a mosquito/biting fly-mammal cycle are Venezuelan equine encephalitis and vesicular stomatitis. These viruses enter a migratory cycle from a local cycle and the vectors in the migratory cycle are carried over long distances on the wind. Further examples of virus spread by movement of vectors include West Nile, Rift Valley fever, yellow fever, epizootic haemorrhagic disease of deer and Akabane viruses.In devising means of control it is essential to decide the relationship of host, vector and virus and the nature of the zone in which the area to be controlled lies. Because of the continual risk of reintroduction of infected vectors, it is preferable to protect the host by dipping, spraying or by vaccination rather than attempting to eliminate the local population of insects.

African Horse Sickness↗