SWINE A. Pleuropneumoniae
Actinobacillus pleuropneumoniae is the bacterium responsible for pleuropneumonia in swine. It causes high morbidity and, at times, significant mortality, particularly during the late finishing period. This recurrent disease leads to substantial economic losses in the global pork industry.
The peracute and acute forms are easily diagnosed due to their evident and distinct clinical signs, as well as the characteristic appearance of deceased pigs, which help distinguish the two forms.
The far less distinct clinical signs and low fatality of the subacute form are easily missed and mistakenly considered as subclinical; commonly interpreted as “no pleuropneumonic issues” by farm staff and vets. This is partly because A. pleuropneumonia endemic farms are often co-infected with other respiratory pathogens, like M. hyopneumoniae, which is often the cause of milder respiratory symptoms. This can also be partly attributed to the lack of quality 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 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 on an A. pleuropneumoniae endemic farm, where all different clinical manifestations are typically present in a herd over time, will not reveal the full impact of the disease. 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 from respiratory disease caused by A. pleuropneumoniae, at the farm level.
In many cases, the exact A. pleuropneumoniae infection status of the individual pig is unknown to the farmer and farm vet. However, the bacterium is endemic worldwide, being present in up to 80–90% of swine farms, with seven different serovars (variation of bacteria strain) having been reported on farms. The prevalence of serovars varies between countries, regions of countries, and by year of investigation. Particularly, the global trade of breeding stock and finishing pigs will introduce new serovars; endemic serovars are only disappearing by depopulation/repopulation eradications.
So far, 19 A. pleuropneumoniae serovars have been classified worldwide. There are technically only 18 serovars, however 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 variable inherited virulence (level of ability to damage host) partly due to different Apx-toxin profiles. “However, A. pleuropneumoniae is highly adaptable to environmental conditions, enabling its survival and persistence even under adverse circumstances. In extreme cases, it can enter a biofilm-associated hibernation stage, characterized by increased antimicrobial resistance and reduced virulence. Conversely, the bacterium can also upregulate its virulence in response to elevated host catecholamine levels – hormones responsible for the fight-or flight response. As a result, the same serovar may present with varying degrees of virulence under different clinical conditions—a typically low-virulence strain may trigger a severe outbreak, while a more virulent strain may cause only mild disease.
In A. pleuropneumonia endemic farms, pleuropneumonic losses are usually seen during finishing, and severe clinical outbreaks are often seen in late finishing. This is the result of homogenous maternal immunity, transferred by antibodies in the colostrum, providing immunity until closer to the end of the nursery period. The downside of antibodies from colostrum 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.