Age affected: Growers/finishers.
Causes: Any combination of: PRRSv, mycoplasma, influenza virus, PRCV and management/ environment factors.
Effects: Increased culls, deaths, coughing, breathing difficulty.
Post-weaning Respiratory Disease Complex (PRDC)
The post-weaning respiratory disease complex results from the presence of a variable number of respiratory diseases in a herd which infect the weaned pig as maternal antibody levels decline, and as exposure to infection occurs. Individual agents involved include porcine reproductive and respiratory syndrome (PRRS) virus, porcine respiratory corona virus (PRCV), swine influenza (SI) virus, Aujeszky’s disease virus where it is still present and the bacteria Actinobacillus pleuropneumoniae (pleuropneumonia) and Mycoplasma hyopneumoniae (Enzootic pneumonia) accompanied by Pasteurella multocida which invades any lung lesion.
The underlying process is best understood by considering the three viruses. PRRS infects the pig when maternal antibody declines at 3-6 weeks of age and eliminates the alveolar macrophages which defend the lung against bacteria and causes a mild interstitial pneumonia. It is followed by, or accompanied by, PRCv infection which infects the surviving/recovering macrophages and reduces their ability to attack bacteria and also produces mild pneumonia.
Finally, at 3-4 months of age, influenza virus attacks the lining of the bronchi and trachea and reduces the ability of the respiratory tract to clear infection and produces mild pneumonia. When pleuropneumonia infection occurs at 6-8 weeks or enzootic pneumonia develops, the lung defences are weak and a complex disease results.
Transmission of the components of this complex is principally by pig to pig contact or by aerosol. The order of infection is outlined above, and the occurrence, timing and severity of the condition depend upon the agents present and the husbandry conditions. In particular, it is most severe in single airspaces which are continuously stocked with susceptible pigs unprotected against the agents present. The condition can only be transmitted to other farms when the agents concerned are present in sufficient number and if the management system allows.
PRDC develops after piglets have been weaned and mixed in herds which are infected by some or all of the above agents, usually from 4-6 weeks of age onwards. Affected piglets develop fever, coughing and laboured breathing, lose condition and may die, sometimes with congested (blue) ears, snout and tail. During this period, the appetite and growth rates are depressed and affected animals lose condition or grow slowly.
A variable proportion of them recover completely, but some remain stunted for weeks and may grow slowly until finishing. Affected animals may not only eat less but may not drink at the peak of the condition. In some cases the clinical signs of an individual disease such as pleuropneumonia may be identifiable with its fever, prostration, respiratory distress and rapid death and dramatic loss of condition. The disease complex may be triggered by entry to a particular house or occur in every house on a unit, and the atmosphere (especially ammonia levels) and temperature may contribute to the condition.
A diagnosis of PRDC is easily made on clinical grounds alone on the basis that respiratory disease with features of more than one infection is occurring repeatedly in pigs which have been weaned and mixed. As the condition is a mixture of the individual diseases present on a unit together with environmental factors such as ammonia, the components should be identified in order to plan control measures.
Blood samples should be taken for serological analysis. The presence of individual agents can be confirmed. Serological profiles can then be prepared for conditions such as PRRS and enzootic pneumonia on a herd or house basis to determine the point at which maternal antibody disappears and active infection occurs.
Post-mortem examination provides further information as animals may have lesions suggesting that enzootic pneumonia or pleuropneumonia are important. Systemic changes, such as enlarged carcase lymph nodes, pale liver and tan lungs which do not deflate, suggest the presence of the post-weaning multisystemic wasting syndrome. Identification of all the agents present may require detailed laboratory investigation of pneumonic lung from different stages of the disease and include microscopical examination, followed by testing with specialised reagents for the agents or their nucleic acids.
Antimicrobial treatment should be given for the bacterial component of the condition. Treatment by injection should be given to animals which may not be eating or drinking using tetracyclines, amoxicillin:clavulanic acid or ceftiofur against the pleuropneumonia or pasteurella components.
Water medication with a wider spectrum of antimicrobials can be used for treatment of affected groups. Treatment for animals at risk can be in the feed, but the development of disease may reduce feed intake and necessitate injection of the worst affected animals. Support affected pigs by improving temperatures and ventilation and ensuring access to water and feed for depressed individuals. The conditions can be prevented or reduced in severity by improving ventilation and reducing group sizes, operating all-in, all-out systems of husbandry for affected houses and introducing isowean or separate site management. The husbandry measures should be complemented by vaccination against the individual components of the condition.
Protection against enzootic pneumonia and Glässer’s Disease can be in place before the disease develops and pleuropneumonia and influenza vaccination can also be given. The recent introduction of attenuated PRRS vaccines for weaners may prevent the development of this component. The effects of all interventions should be monitored and the prevalence of the condition on a farm can be monitored at slaughter by recording the residual lesions present.