Reproductive Disease

Stillbirths and mummification of piglets due to porcine parvovirus

Fifteen sows had either aborted or produced dead piglets, out of a herd of 36 sows, since June 2011. The pigs were mainly housed but some sows were turned out during the summer. Four or five aborted at nine weeks gestation in June and then showed poor fertility. More recently, sows had farrowed at term but produced dead, sometimes mummified, piglets as well as some live piglets. No vaccines were used. A single mummified fetus examined at Carmarthen was positive for porcine parvovirus by PCR on fetal liver and heart. Three sows that produced dead pigs were seropositive for porcine parvovirus and seronegative for PRRS. Porcine parvovirus causes stillbirths and mummification but rarely causes abortion. It is likely that some of the reproductive disease reported was due to porcine parvovirus infection and the pattern of disease suggested the introduction of porcine parvovirus into a naïve herd. Vaccination was advised to ensure all the breeding animals were immune.

Respiratory Disease

Actinobacillus suis causing lung lesions typical of Actinobacillus pleuropneumoniae

An unusual diagnosis of pleuropneumonia due to Actinobacillus suis was diagnosed in 13-week-old pigs on an indoor single-source nursery finisher. Respiratory disease with dyspnoea and increasing mortality was reported with 100 of 1,000 pigs affected and 30 deaths in the two weeks prior to submission. Post-mortem examination in both pigs revealed multifocal dark red to purple well-demarcated areas of consolidation with overlying fibrinous pleurisy affecting cranioventral and caudal lung fields. Affected areas were firm and raised, and the cut surfaces were dry and red-black. These gross lesions were suggestive of Actinobacillus pleuropneumoniae infection; however, Actinobacillus suis was isolated in pure and profuse growth from the lungs of both pigs. Histopathology revealed severe subacute to chronic necrotising haemorrhagic bronchointerstitial pneumonia typical of that described with Actinobacillus pleuropneumoniae infection, and also described in Actinobacillus suis. No viral involvement was detected.

Systemic Disease & Miscellaneous

Coal tar poisoning due to clay pigeon remnants

Coal tar poisoning following the ingestion of remnants of clay pigeons was diagnosed at Bury St Edmunds as the cause of four sudden deaths from a group of 35 replacement gilts in one paddock over a ten day period. Post-mortem examination of one gilt revealed yellow-tinged mucous membranes, sclera and subcutaneous connective tissues and a swollen mottled liver (see figure). The hepatopathy and jaundice raised the possibility of coal tar poisoning and farm staff found the clay pigeon remnants. The gilts had been placed on fresh ground and it came to light that clay pigeon shooting had taken place in the past, but was thought to be too long ago to be of concern. The pigs were for breeding and not destined for the food chain; however, a voluntary 28 day period of restriction was agreed and the gilts were moved from the paddock.

Nervous Disease

Congenital tremor type A2 in gilt litters

Two outbreaks of congenital tremor type A2 were diagnosed, both involving piglets born to gilts. Type A2 is believed to be caused by a virus, as yet unidentified. In the first of these, 80% of gilt litters in the first affected batch showed congenital tremor. In each affected litter, the number of piglets showing signs varied from two to the whole litter; in the majority most of the litter was affected. The incidence of congenital tremor rapidly reduced in the four days following farrowing to approximately 20% as piglets recovered rapidly. Most affected piglets survived with the worst affected ones given colostral supplement. All three affected piglets submitted had a constant rhythmic tremor, but were bright and able to stand and walk.

Gross lesions were unremarkable and histopathology with special stains for myelin revealed clinically significant central hypomyelination typical of porcine congenital tremor type A2. In one pig, there was a mild myelin deficit which was reflected in its milder clinical signs. The veterinary surgeon attending the unit reported that litters in the following batch of gilts were also affected, but in the third batch none were affected. Interestingly, gilts in the first affected batch were also the first onto a new gilt mating unit and were kept in a scrape-through system pre and post-service. Later unaffected batches would have been exposed to manure from older gilts and thus able to acclimatise, unlike the first batches.

In the second outbreak, pigs were submitted from a nursery unit after weaning when they were noted to have a rhythmic bouncing tremor, sufficiently severe in one piglet for its hindlimbs to leave the ground. Again, the pigs were bright and alert. Further investigation revealed that some piglets born to gilts at the source breeding unit had been affected with congenital tremor and that these were persistent cases, most piglets having recovered by weaning.

Central spinal hypomyelination consistent with porcine congenital tremor A2 was identified; however, there was also mild non-suppurative panencephalitis which is unusual and merited further testing to rule out ruminant pestivirus involvement. Further investigation is in progress; however, it is thought likely that these lesions reflect the healing process; it is uncommon for us to examine piglets at this age affected with congenital tremor. Reports from the rearing unit indicated that other piglets arriving with congenital tremor had recovered within a week.

Further Reading

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