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Foot-and-mouth disease (FMD) is one of the most important animal diseases hindering livestock production in Thailand. In this study, a temporal and spatial analysis at the subdistrict level was performed on FMD outbreak reports in Thailand from 2011 to 2018. Risk factors associated with FMD outbreaks were furthermore investigated using generalized estimating equations. The results showed that the incidence of FMD outbreaks was the highest in 2016 and was affected by season, with a peak in FMD outbreaks occurring in the rainy-winter season, during October to December. FMD outbreaks were mostly distributed in small clusters within a few subdistricts. Some high-risk areas with repeated outbreaks were detected in the central regions. Risk factors, including the increase of subdistrict's size of the dairy population, beef population or pig population, the low percentage of forest area, subdistricts in the provinces adjacent to Malaysia, the presence of a livestock market and the occurrence of an FMD outbreak in a neighbouring subdistrict in the previous month significantly increased the odds of having an FMD outbreak. The increase in proximity to the nearest subdistrict with an FMD outbreak in the previous month decreased the odds of having FMD outbreaks. This study helped to identify high-risk areas and periods of FMD outbreaks in Thailand. Together with the identified risk factors, its results can be used to optimize the FMD control programme in Thailand and in other countries having a similar livestock industry and FMD situation., (© 2022 The Authors. Transboundary and Emerging Diseases published by Wiley-VCH GmbH.)

Two lungworm outbreaks in dairy herds were investigated in order to estimate the resulting economic costs. On the two farms, with 110 and 95 cows, total costs were estimated at €159 and €167 per cow, respectively. Overall, milk production reduced by 15 to 20 per cent during the outbreaks. Five cows died on one farm, while on the other farm seven cows died as a result of the lungworm outbreak. On one farm, 51.7 per cent of the total costs was due to reduced milk production and 33.1 per cent was due to disposal of dead animals. On the other farm, it was 36.3 and 50.9 per cent, respectively. The remaining 13 to 15 per cent of the total costs were due to extra inseminations, laboratory diagnosis and treatments. The history and development of the outbreaks are described. One lesson from these outbreaks is that recognising that potentially lungworm-naïve animals are to be introduced into the adult herd allows for timely measures (for example, vaccination) to prevent a lungworm outbreak.

This study calculates the financial consequences of the bluetongue serotype 8 (BTV8) epidemics of 2006 and 2007 in the Netherlands. We constructed a deterministic economic model that is compatible with the Dutch livestock production systems for cattle, sheep and goats. Two hundred cattle farms and 270 sheep farms were infected with BTV8 in the epidemic of 2006, whereas 30,417 cattle farms, 45,022 sheep farms and 35,278 goat farms were estimated to be infected in the epidemic of 2007. The net costs (costs minus benefits) of the BTV8 epidemic of 2006 (BT2006) was estimated at 32.4 million Euros. The net costs of the BTV8 epidemic of 2007 (BT2007) was valued at 164-175 million Euros, depending on the mortality and morbidity rates for cattle used. The losses account for 2%, 10% and 11% of the gross value of the primary production within Dutch pasture-based livestock farming that equals 1.6 billion Euros. Control measures accounted for 91% of the net costs of the BT2006, while diagnostic costs represented 7%. By contrast, for the BT2007 92% of the net costs were in the form of production losses and veterinary treatment fees, while only 6% were related to control measures. Furthermore, the control costs dropped from 29,630 in BT2006 to 10,990 in BT2007 mainly due to the costly indoor housing that was not obligatory during the BT2007 epidemic. The cattle sector suffered 88% and 85% of the net costs for the BT2006 and BT2007, respectively; the highest of all sectors.

The build up of lungworm infections was studied in four groups of calves. Calves of Group 1 were infected experimentally with 6 x 10 larvae during the first 3 weeks after turnout. The pasture of Group 2 was contaminated with approximately 35,000 larvae in June and the pasture of Group 3 with approximately 1.3 million larvae in August. Group 4 served as the helminth free control group for challenge infections with 5,000 larvae in October. In Group 1 faecal larval counts increased 5 weeks after the beginning of patency and decreased after another 3 weeks, indicating the development of immunity after the second lungworm generation. In contrast, the development of immunity in Groups 2 and 3 occurred after the first lungworm generation as maximal faecal larval counts were seen within 3.5 weeks after the beginning of patency. Infection levels were highest in Group 3 which was the only group showing clinical signs. These signs became worse after oxfendazole treatment.

The causes of outbreaks of lungworm disease were determined from the herd histories of 25 affected herds of young cattle. The results indicate that light pasture contamination by carriers and subsequent auto-infections are the most prominent cause of lungworm disease, followed by heavy pasture contamination by carriers. Overwintered pasture infections seem to play a minor role. Adult dairy cows seem to be the predominant carrier animal when light pasture infections are concerned. Heavy pasture infections are almost always caused by calves and yearlings.

An experiment was carried out to study the build-up of infection and development of immunity against Dictyocaulus viviparus infections in calves. Six groups of four calves were used. Groups 1-5 grazed on separate pastures and Group 6 served as a permanently housed control group. To simulate 'low' and 'very low' overwintered pasture infectivity, Groups 1 and 2 were infected experimentally six times with ten and two larvae, respectively, during the first 3 weeks on pasture in May. From the middle of July, Groups 2-4 were experimentally infected six times in 3 weeks with 10, 10 and 100 larvae, respectively, to simulate 'low' and 'moderate' pasture contamination by carriers. Group 5 served as a non-infected pasture control group. After housing of Groups 1-5 in October, all calves were treated with oxfendazole and challenged with 5000 larvae of D. viviparus to evaluate the development of immunity. The results showed a similar population build-up of lungworm infections in Groups 1-4. After the beginning of patency, 24-35 days after primary infection, an increase in faecal larval counts occurred 31-35 days later as a result of re-infection. For Group 2, this was only true when the infections with a total of 12 larvae in May were ignored, as these did not result in patent infections. Faecal larval counts were highest in Group 4, which was the only group with mild signs of lungworm disease occurring in the re-infection period. The worm counts at necropsy showed the development of immunity in Groups 1-4 but not in Group 5. This is consistent with the fact that Group 5 did not develop patent lungworm infections throughout the grazing season.

An experiment was carried out with three groups of grazing calves and one housed control group to study the effect of rotational grazing for periods of 1 and 2 weeks on the build up of lungworm and gastro-intestinal nematode infections respectively. The experiment demonstrated that rotational grazing for periods of 1 week on six plots prevented the build-up of heavy lungworm infections. A build up of heavier lungworm infections was observed in a group that was rotationally grazed for periods of 2 weeks on three plots and a group which remained on one plot throughout the grazing season; there was no difference between these two groups. In all three situations, there was an adequate development of immunity against D. viviparus, as measured by worm recovery after challenge infection at the end of the experiment in comparison with worm recovery of the similarly challenged control group. Neither rotational grazing scheme protected the calves against gastrointestinal helminthiasis, because tracer calves, which grazed for 4 days only in August or October, acquired infections which would have resulted in severe illness or even death if necropsy had been postponed for a week.