Enzootic pneumonia is caused by Mycoplasma hyopneumoniae. It is widespread in pig populations and endemic in most herds throughout the world. As an uncomplicated infection in well-housed and well-managed pigs it is relatively unimportant and has only a mild effect on the pig. However if there are other infections present particularly App, Hps, Pasteurella, PRRS or SI, the pneumonia can become more complex with serious effects on the pig.
EP always attacks the lower areas of each lung lobe causing consolidation. The extent of this consolidation in each lobe is scored out of either 5 or 10 depending upon the lobe affected. Thus a severely affected pig with all lobes involved would score 55. This scoring system can be used to assess the severity of disease and its effects on the pig.
If more than 15% of lungs are affected it is highly probable that EP is present in the population. Herds that do not carry M. hyopneumoniae rarely show consolidated lesions in more than 1 % and even then they are very small.
If EP is not present in the growing population then the effects of the other respiratory pathogens are greatly reduced. It is therefore considered a primary pathogen that opens up the lung to other infections.
Clinical signs of enzootic pneumonia only occur in the lactating sow and piglets when the disease has been introduced into a fully susceptible herd for the first time. The breakdown of disease usually takes place over 6 to 8 weeks with sows coming into the farrowing house continuing to be affected.
There is a widely held but erroneous belief that sows and gilts will become carriers and pass this infection to their next litters. They may do so early on and their piglets may cough but by the time they farrow again 4 to 5 months later they will have eliminated the infection and will provide a solid immunity to their piglets via colostrum. If weaning is at 3 to 4 weeks, subsequent litters are not likely to become infected until after weaning.
Symptoms
All pigs
It usually has an incubation period of two to eight weeks before clinical signs are seen but may be longer. Acute disease is normally only seen in new break-downs of disease.
Over the first six to eight weeks after it enters there may be: (This picture however is extremely variable).
- Severe acute pneumonia.
- Dehydration.
- Heavy breathing.
- Coughing, prolonged.
- Respiratory distress.
- Fever.
- High mortality across all ages of stock.
- Chronic disease is the normal picture when the organism has been present in the herd for some considerable time.
Maternal antibody is passed via colostrum to the piglets. It disappears from seven to twelve weeks of age after which clinical signs start to appear including:
- A prolonged non-productive cough, at least seven to eight coughs per episode, is a common sign around this time, with some pigs breathing heavily (“thumps”).
- 30 to 70% of pigs will have lung lesions at slaughter.
Causes / Contributing factors
- It is commonly transmitted through the movement of carrier pigs.
- Wind-borne infection for up to 3km (2 miles) if the climatic conditions are right. The organism dies quickly outside the pig, particularly when dried.
- Incoming pigs.
Increased clinical disease is associated with the following;
- Overcrowding and large group sizes.
- Less than 3 cu.m.air space per pig and 0.7 sq.m. floor space per pig.
- Houses that are too wide for good air flow control.
- Variable temperatures and poor insulation.
- Variable wind speeds and chilling.
- Low temperature, low humidity environments.
- High levels of carbon dioxide and ammonia.
- High dust and bacteria levels in the air.
- Pig movement, stress and mixing.
- Housing with a continuous throughput of pigs.
- Other concurrent diseases particularly PRRS, App, flu, and aujeszky’s disease.
- Poor nutrition and dietary changes at susceptible times.
Diagnosis
This is based on the clinical picture and examination of the lungs at post-mortem examination or at slaughter, combined sometimes with histology of the lesions. However, these do not provide a specific diagnosis and in the herds supplying breeding stock or in special cases (e.g. litigation) it may be necessary to confirm the diagnosis by carrying out one or more of the following tests: Serological (ELISA) tests, microscopic examination of stained touch preparations (TPs) of the cut surface of the lungs, fluorescent antibody tests (FATs), polymerase chain reaction (PCRs) tests and finally culture and identification of Mycoplasma hyopneumoniae.
These tests are becoming more widely available and some diagnostic laboratories cannot do them. The PCR is probably the most sensitive. FAT, serology and cultures are used in Denmark, but only FATs are available in many laboratories.
EP must be differentiated from Flu, PRRS, Hps and other mycoplasma infections. Laboratory tests are required to differentiate them. Furthermore, all or some of these may occur as mixed infections together with Mycoplasma hyopneumoniae.