Infection dynamics and acute phase response of an Actinobacillus pleuropneumoniae field isolate of moderate virulence in pigs

•A. pleuropneumoniae infection with an isolate of moderate virulence was evaluated.•Specific antibodies, acute phase proteins and inflammatory cytokines were examined.•IL-6, serum A amyloid, C-reactive protein and haptoglobin were over-expressed.•Our results are of interest in the study of the pathogenesis of this disease.

Actinobacillus pleuropneumoniae, the causative agent of porcine contagious pleuropneumonia (PCP), causes significant economic losses associated mainly with growth stunting of animals. Although serotypes can be distinguished according to their virulence, most of the studies are focused in A. pleuropneumoniae infections with virulent serotypes. There is little information regarding the role of acute phase proteins (APPs) and proinflammatory cytokines in infections with isolates of mild or moderate virulence. Thus, the present study aims to evaluate the kinetics of infection with an A. pleuropneumoniae serotype 6 (Ap6) field isolate of moderate virulence and the changes in the serum concentration of specific antibodies and different APPs and proinflammatory cytokines. Control animals showed no clinical signs or lesions throughout the study. Infected animals showed increased rectal temperature, respiratory distress and depression from 24 hpi, and typical gross and microscopic lesions of PCP from 6 hpi onwards. Ap6 was isolated from nasal swabs of four out of five inoculated animals at 24 hpi, and from nasal swabs, tonsil and lung samples from all inoculated animals at 72 hpi. Specific antibodies against Ap6 or changes in the serum concentration of IL-1β, IL-10 and TNF-α were not detected throughout the study. The serum concentration of IL-6 increased from 6 hpi as well as serum A amyloid, C-reactive protein and haptoglobin from 24 hpi onwards. Our results highlight the onset of the acute phase response after the infection with a field isolate of A. pleuropneumoniae of moderate virulence from 24 hpi onwards which may be of interest in the study of the pathogenesis of this disease.