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Unknown Porcine Neurological Syndrome

By: Dr Edgar Ortmann, Howick Veterinary Clinic
Clinical history
A pig herd was depopulated in early 2006 and for six weeks there were no pigs on farm. First pregnant gilts arrived mid July 2006. These started farrowing in the first week of October and 70% of litters had mummies. Numerous sows failed to farrow, until induced with prostaglandins. They then produced whole litters of mummies. Numerous weak piglets were born, some showing congenital tremor. Initial pre-weaning mortality was 15 to 20%.

The farmer noticed some piglets as early as seven to ten days of age showing signs of incoordination of hind legs and bilateral cataracts. Over time older pigs were seen “leopard-crawling”. The initial paresis progressed to an ascending paralysis. These had come out of numerous litters. All affected pigs were alert and had normal appetites. I presumed that Pocine Parvovirus was present in this herd (no test available in SA) and PCV2 was present clinically.
Gross examination

Clinical signs at presentation for autopsy were neurological signs including head bobbing, head tilt, muscle fasciculation, hindquarter weakness frequently collapsing to a dog sitting position and knuckling of the forelimbs (traumatic skin erosions on carpi). There were bilateral cataracts and suggestions of a uveitis. Another unusual finding was that these weaners were totally avocal with no grunting or screaming, even when handled.
In general the histopathology of the eye, central nervous system and spinal cord were degenerative rather than inflammatory. The ocular pathology was that of primary cataracts with no retinal lesions.  Brain lesions were characterised by marked gliosis in the granular layer of the hippocampus and marked depletion and loss of Purkinje cells in the cerebellar folia. In the spinal cord there was demyelinisation with Wallerian degeneration, while in the recurrent laryngeal nerves a few swollen axons were observed.
This pathology would explain the neurological syndrome observed and the laryngeal nerve pathology might be associated with the aphonia noted.
Further lab analysis
A thorough investigation of potential viral aetiologies including porcine paramyxovirus, enteroviruses, African Swine Fever, Classical Swine Fever, encephalomyocarditis virus, PRRSV, PCV-2 proved negative. Microbiological cultures of fresh brain tissue were unrewarding. A full heavy metal screen on liver tissue from affected pigs was run (lithium, beryllium, boron, titanium, vanadium, chromium, manganese, iron, cobalt, nickel, copper, zinc, arsenic, bromine, selenium, rubidium, strontium, molybdenum, cadmium, tin, antimony, tellurium, iodine, cesium, barium, lanthonum, tungsten, platinum, mercury, thallium, lead, bismith, uranium). All elements appeared to be within normal limits.
Sometimes we come across strange conditions, which we cannot explain. Exhaustive laboratory tests can be very expensive and usually one has to curtail further testing and investigative measures due to financial constraints. This condition has not yet been described in any veterinary literature. Consultation with pathologists via the AAVLD (American Pathology Labs) listserv and at the Faculty of Veterinary Science has failed to link this syndrome to any particular aetiological agent. The possibilities are either toxic, or a potential in-utero viral infection.
Symptoms on the farm disappeared after 18 months and in total about 50 cases were noted. Interestingly, a second farm also having undergone a depop-repop came up with the same symptoms, but only eight cases were recorded. Further testing was undertaken on this farm, also to no avail. Thankfully, the symptoms disappeared on this farm as well.
I would like to encourage farmers and veterinarians to be on the look out for similar symptoms.

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