John Burns Brooksby CBE: 25 December 1914 - 17 December 1998.

John Brooksby was an outstanding veterinary virologist, who worked at the Animal Virus Disease Research Institute, Pirbright, for 40 years, for 16 of which he was Director of the Institute. He will be remembered for his contributions to the diagnosis of foot-and-mouth disease, for his discovery of four new types, for the classification of subtypes and for fundamental studies of the virus. As Deputy Director and Director he was responsible for programmes on fundamental investigations of foot-and-mouth disease virus and other viruses exotic to the UK and for the application of the results both in the UK and worldwide. His advice on the distribution and the control of foot-and-mouth disease was sought by international organizations and by individual countries and was responsible for reducing the risk of spread of disease.

Comparison of different control strategies for foot-and-mouth disease: a study of the epidemics in Canada in 1951/52, Hampshire in 1967 and Northumberland in 1966.

The measures used to control the epidemics of foot-and-mouth disease in Canada in 1951/52 (29 outbreaks) were compared with those used in the epidemic in Hampshire in 1967 (29 outbreaks). In both epidemics the disease spread more from premises where the disease was reported late and the imposition of quarantine or restrictions on infected premises was delayed. In Hampshire, area restrictions were imposed, susceptible livestock on infected premises and on premises in direct contact were slaughtered, and contacts were traced. In Canada, the initial diagnosis was vesicular stomatitis, no area restrictions were imposed, no tracing was carried out and the animals on infected premises were allowed to recover. However, apart from the disease's spread through infected meat and by unknown or airborne routes, it did not spread from infected premises once quarantine was imposed, partly owing to the low population density of livestock in the area. The effects of the slaughter of infected premises and direct contacts in the Fareham area of Hampshire in 1967 and in the Chathill area of Northumberland in 1966 were compared with what might have happened if, in addition, culling on contiguous premises or culling on premises within 3 km or emergency vaccination had been put into effect. The slaughter of cattle, sheep, goats and pigs on premises within 3 km two days after confirmation of the first outbreak would have resulted in fewer outbreaks and a shorter period to complete slaughter, but more animals would have been slaughtered. In the Chathill area, the slaughter of sheep, goats and pigs only on premises within 3 km two days after confirmation of the first outbreak would not have resulted in fewer outbreaks and more animals would have been slaughtered. Fewer premises and animals would have been slaughtered by a contiguous cull than by a 3 km cull but more than by the slaughter of infected premises and direct contacts. Emergency vaccination within 3 km, providing protection at four days (but not to animals already infected before the development of immunity), would have resulted in the fewest animals being slaughtered and could have reduced the number of outbreaks in the Fareham area by one and in the Chathill area by two or three. All the procedures would have had a greater effect the sooner they were introduced. However, with many foci of infection, priorities for action would have had to have been established. Earlier tracing of the last outbreak in the Fareham area could have shortened the Hampshire epidemic. Surveillance of a farm identified as at risk through animal movements and by the use of an airborne-prediction model could have eliminated the source of further outbreaks in the Chathill area.

Re-assessing the likelihood of airborne spread of foot-and-mouth disease at the start of the 1967-1968 UK foot-and-mouth disease epidemic.

The likelihood of airborne spread of foot-and-mouth disease at the start of the 1967-1968 epidemic is re-assessed in the light of current understanding of airborne disease spread. The findings strongly confirm those made at the time that airborne virus was the most likely cause of the rapid early development of the disease out to 60 km from the source. This conclusion is reached following a detailed epidemiological, meteorological and modelling study using original records and current modelling techniques. The role played by 'lee waves' as the mechanism for the spread is investigated. It is thought that they played little part in influencing the development of the epidemic. A number of lessons learned from the work are drawn, identifying the need for further research on the quantity and characteristics of airborne virus. The results are also used to illustrate what advice would have been available to disease controllers if the outbreak had occurred in 2004.

Weather factors in the prediction of western equine encephalitis epidemics in Manitoba.

Cases of western equine encephalitis in horses in 1987 in western USA and Manitoba, Canada were examined by backward trajectory analysis of winds. Culex tarsalis mosquitoes infected with western equine encephalitis virus could have been carried on southerly winds from Texas and Oklahoma to northern USA and from there to Manitoba. The presence of the Polar front over North Dakota and Minnesota at the end of July would have led to the landing of Cx. tarsalis in Montana and Wisconsin and prevented further carriage into Manitoba. Temperatures in southern Texas during the winter months (average daily maximum temperatures 19.7 degrees C and higher) would have permitted continuous transmission of western equine encephalitis virus by Cx. tarsalis in this area. Weather factors involved in outbreaks from 1975-88 were analysed to see if epidemics in Manitoba (23 or more cases in horses) could be predicted. The conditions for epidemics could be defined as follows: (a) the number of cases in horses in USA was 98 or more, (b) winds were southerly with speeds 45 kmh-1 or higher, and (c) counts of Cx. tarsalis females/light trap per day were 3.2 or higher. There were 3 or fewer cases in Manitoba, when the number of cases in USA was 27 or less, even when Cx. tarsalis counts were higher than 3.2. With Cx. tarsalis counts below 3 and/or unsuitable winds, or the Polar front further south, the number of cases in Manitoba was between 0 and 17, even when the number of cases in USA was from 38-172. Without information on the extent of infection further south, the weather variables would probably be more useful in excluding the possibility of an epidemic in Manitoba than in predicting one.

Temperature and the persistence of viruses in Culicoides spp. during adverse conditions.

The average daily maximum temperature for the coldest month during the winters of 1977-1978 and 1978-1979, when bluetongue (BT) virus overwintered in a cycle between Culicoides spp. and cattle in western Turkey (Aydin and Izmir provinces), was found to be 12.5 degrees C. This temperature agreed with the lowest temperatures found for Culicoides activity and for flight over long distances. Overwintering of BT virus in western Turkey and Lesbos (1979-1980), African horse sickness (AHS) virus in Spain (1987-1990) and BT and epizootic haemorrhagic disease of deer (EHD) viruses in British Columbia (1987-1988) was assessed using the following conditions for survival: maximum temperatures > or = 13 degrees C on 45% of days or more, a weighted "degree day" value of > or = 1.35 of 6 and an average daily maximum temperature of > or = 12.5 degrees C (all for the coldest month) together with a total of 40 days or fewer with maximum temperatures < 13 degrees C and < or = 10 consecutive days with maximum temperatures < 13 degrees C. Using these criteria, overwintering is unlikely to have occurred in Culicoides in Lesbos, Madrid, Toledo, Ciudad Real or British Columbia, but could have taken place in western Turkey (Aydin and Izmir) and southern Spain (Guadalquivir, Guadiana and Tagus Valleys). Isotherms of average daily maximum temperatures of 12.5 degrees C and 18 degrees C for the coldest month were drawn on maps covering various regions of the world, to indicate areas where virus and Culicoides activity could continue during the winter and to compare these areas with the known distribution of BT, EHD, AHS and Akabane infection.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.