Actinobacillus pleuropneumoniae is the causative agent of porcine pleuropneumonia, an economically important endemic bacterial disease of pigs worldwide (Bossé and others 2002). Epidemiologically, serotyping is the gold standard method, with A pleuropneumoniae being classified into 16 different serovars (1 to 4, 5a, 5b, 6 to 15) based on the presence of surface carbohydrates, principally of the capsule. The prevalence of different serovars varies from country to country (Dubreuil and others 2000). Classically, the serovar of an isolate is determined immunologically using polyclonal serum obtained from animals (typically rabbits) that have been immunised with killed whole cells of a reference strain of the relevant serovar. Such immunological-based methods have limitations, in particular, cross-reactivity between serovars. Cross-reactivity has been reported between serovars 1, 9 and 11, between serovars 4 and 7 and between serovars 3, 6 and 8 (Zhou and others 2008). To circumvent this cross-reactivity, investigators have devised multiplex PCRs for the simultaneous identification of sero
APXIVA is an RTX toxin of Actinobacillus pleuropneumoniae that is a candidate antigen to differentiate infected from vaccinated animals (DIVA). Insertion of ISApl1 into the apxIVA gene is known to compromise an APXIVA-based DIVA approach, as is potentially a TGG to TGA mutation in the apxIVA gene. ISApl1 was found in 63/349 (18.1%) A. pleuropneumoniae isolates from England and Wales including serovars 2, 3, 6-8 and 12. No ISApl1 insertions into apxIVA were found. Only two serovar 3 isolates contained the TGG to TGA mutation. We conclude that an ApxIVA-based DIVA approach would potentially be viable in England and Wales.
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