A. Pleuropneumoniae

Actinobacillus pleuropneumoniae, the cause of pleuropneumoniae in swine. It is responsible for high morbidity and potentially high mortality, frequently experienced recurrently during late finishing, causing substantial economic losses in the global pork industry.

The peracute and acute forms are easily diagnosed due to the evident and distinct clinical signs and appearance of dead pigs.

The far less distinct clinical signs and low fatality of the subacute form are easily missed and erroneously considered as subclinical; commonly erroneously interpreted as “no pleuropneumonic issues” by farm staff and vets. This partly because A. pleuropneumonia endemic farms also being endemic to other respiratory pathogens, like M. hyopneumoniae, commonly assigned the cause of milder respiratory signs. And partly due to lack of the quality of the on-farm daily monitoring of animals.

However, even truly subclinical pleuropneumonia will involve pathological pneumonic lesions, and despite the lack of clinical signs, average daily weight gain and feed efficiency can be negatively affected.

The chronic form, likely to develop from any form of pleuropneumonia, will further reduce productivity due to pain, reduced respiratory capacity, and reactivation of disease from chronically infected tissues; lesions easily diagnosed via slaughterhouse investigations, like the Ceva lung program (CLP).

Focusing only on clinical signs in an A. pleuropneumoniae endemic farm, where all different manifestations are in principle present in a herd over time, will not reveal the full pleuropneumonic impact. To investigate pleuropneumonia in all its possible manifestations, pathological evaluation of lung lesions appears to be the least biased method. Lung lesion scoring, like the CLP, is considered highly relevant for estimating severity and losses of respiratory disease, such as caused by A. pleuropneumoniae, at the farm level.

In many cases the exact A. pleuropneumoniae infection status of the individual pig production unit is unknown to the farmer and farm vet. However the bacterium is endemic world-wide being present in up to 80–90% of swine farms, up to seven different serovars having been reported on the same farm. The prevalence of serovars varies between countries, regions of countries, and by year of investigation. Particularly the global trade of breeding stock and pigs for finishing will introduce new serovars; endemic serovars are only disappearing by depop-repop eradications.

So far, 19 A. pleuropneumoniae serovars have been classified worldwide. 18 serovars, as serovars 9 and 11 can be considered as one: serovar 9/11, as the difference in the complete capsule polysaccharide CPS) loci is only one amino acid and they have identical toxin profiles (ApxI + ApxII).

Different serovars are considered to have quite variable inherited virulence partly due to different Apx-toxin profiles. However, A. pleuropneumonia is highly adaptable the environmental lining conditions facilitating survival and persistent infection in adverse conditions, in the extreme condition entering the biofilm-stage of hibernation, increased antimicrobial resistance and decreased virulence. In the other end of the scale, it can further upregulate virulence as a response to increase in circulation of host-catecholamine levels. For that reason the same serovar may present itself very differently in terms of virulence under different clinical conditions: a less virulent strain may evoke a highly virulent clinical outbreak and vice versa.

In A. pleuropneumonia endemic farms pleuropneumonic losses are usually seen during finishing, severe clinical outbreaks often in late finishing. This as a combined effect of homogenous maternal immunity, transferred by colostrum, and usually protecting till mid-end nurseries. The downside of colostral antibodies is that they will increasingly reduce A. pleuropneumonia protective response to vaccination. For that reason it is important to estimate optimal time of first vaccination by cross-sectional serology. Usually performed by ELISA titers of the low/no virulent ApxIV exotoxin, unique to A. pleuropneumonia and unique to natural infection; not induced by vaccination.

The three exotoxins: ApxI-III and lipopolysaccharide (LPS) are the virulence factors of major importance both in the development of lung lesions and protective immunity; ApxI, II, and III are, together, the antigens capable of inducing cross-protection.

Several other virulence factors have been described and are under investigation, including membrane proteins, some of which are immunogenic and therefore can add to the vaccine protective capacity.

A serovar-independent A. pleuropneumoniae vaccine with long duration and high protective capacity against pleuropneumonic lung lesions is to be an integral part of any A. pleuropneumoniae control program. Only increasing in importance with the increasing awareness of antimicrobial resistance development as a consequence of routine treatment programs.