Actinobacillus pleuropneumoniae transmission and clinical outbreaks

Abstract

Actinobacillus pleuropneumoniae is a bacterium causing respiratory disease and mortality in pigs. Outbreaks of clinical disease occur regularly in pig farms. More knowledge of the epidemiology of the bacteria in pig populations should contribute to the design of more effective measures for prevention and control. The aims of this thesis were to investigate transmission of A. pleuropneumoniae on pig farms and to study the association between clinical signs and transmission of the bacterium between pigs. Two hypotheses were addressed that could explain the occurrence and course of clinical outbreaks on farms. The first hypothesis is based on the trigger mechanism: the occurrence of clinical outbreaks is explained by simultaneous exposure of already colonised pigs to a trigger. The alternative hypothesis states that clinically diseased pigs transmit A. pleuropneumoniae after which the newly infected pigs rapidly develop clinical signs (transmission mechanism). Based on this thesis the occurrence of clinical outbreaks is best explained by the trigger mechanism. The transmission mechanism is considered unlikely. It was demonstrated experimentally that severely diseased pigs transmitted the bacterium less efficiently to a pen mate than less severely diseased pigs. Moreover, contact infected pigs did not develop clinical signs. In a simulation study based on mathematical transmission models, it was shown that the transmission mechanism needs transmission by diseased pigs to be more than 50-300 times as efficient as transmission by colonised (non-diseased) pigs, which is unlikely considering the result of the experimental studies. Furthermore, the transmission mechanism assumes that rapid transmission across pens is needed to explain the rapid increase of clinical cases across pens observed in the field. However, the transmission rate by colonised pigs across pens was actually very low and experimentally challenged pigs with clinical signs did not infect separately housed sentinel pigs. Finally, farm observations of an outbreak of mild pleuropneumonia in pigs distributed across pens are not in line with the transmission mechanism. According to the trigger mechanism, pigs have to become colonised with A. pleuropneumoniae first, before exposure to a trigger at a later time results in a clinical outbreak. Outbreaks are mostly observed in pigs of twelve weeks or older and it was shown in a field study that even under strict hygienic and animal management measures almost half of the pigs were already colonised at ten weeks of age. The observation of mildly diseased pigs distributed across pens could be explained by the trigger mechanism. Therefore the results of this thesis are more supportive of the trigger mechanism. It is concluded that for prevention of outbreaks, measures have to aim at a reduction of transmission by colonised pigs and the prevention of the occurrence of a trigger, for example by optimising housing conditions. Future research needs to identify methods to reduce colonisation among healthy pigs and to identify effective interventions on the interaction between trigger, bacteria and host.