Age affected: Newborn.
Causes: Genetic; Classical Swine Fever virus; other viruses; poisoning.
Effects: Trembling, shaking, poor growth, death.
Congenital tremor can be inherited, caused by infectious disease, result from toxicity or be of unknown cause. The condition is divided into Types A I-V, those with gross or microscopic changes in the brain or spinal cord and Type B with no visible changes. Congenital tremor Types AI and AII result from infection of the developing foetus by a virus at the time the cerebellum is developing (10-50 days of gestation).
Congenital tremor AI is caused by the virus of classical swine fever and affected pigs carry the virus for 90 days and can shed virus for 56 days. Congenital tremor AII can be caused by another pestivirus (Atypical Porcine Pestivirus, APPv) which has been isolated from brain tissue of affected pigs and shown to be present for up to 5 months in surviving members of an affected litter.
Congenital tremor AIII is the most important inherited type and is a sex-linked recessive condition appearing in male Landrace pigs and carried by the sow. It results in a reduction in the myelination (insulation) of nerve fibres. Congenital tremor AIV is also inherited and occurs in British Saddlebacks. Congenital tremor AV is caused by exposure to Trichlofon or Neguvon between days 45 and 79 or gestation. The causes of congenital tremor Type B are currently unknown.
Both AI and AII are caused by transplacental infection. In the case of classical swine fever, the sow or other members of the herd are usually affected by illness and can be sources of infection, and the virus can be transmitted in the semen. APPv does not appear to cause disease in adults and semen transmission has not yet been identified.
In AI (classical swine fever), more than 40% of pigs are affected within a litter and many litters are affected for up to 4 months, with medium to high mortality. There is no sex or breed effect. It does not recur in litters from the same parents. Piglets show muscular tremor, ataxia and inability to stand and suck. The tremor is still noticeable after 2-3 weeks.
In AII, a high proportion of litters are affected over a period of 4 months and more than 80% of piglets are born with tremor but little mortality occurs. There is no sex or breed effect and no recurrence. Slight tremor remains after 6-8 weeks.
In AIII, severe, coarse tremors of the head and forequarters with undulation of the hindquarters occur in male Landrace piglets. It recurs in successive litters and most affected piglets die. A faint tremor of the head and shoulders remains in adult Landrace boars.
AIV causes recurring high mortality in 25% of successive affected litters in British Saddleback pigs.
AV affects a high proportion of litters for more than a month. 900-100% of piglets of both sexes within affected litters may be born with rhythmic tremor, may stumble and fall and have difficulty in sucking.
Congenital tremor is immediately identifiable by the tremors seen in new born piglets. The types are distinguished by their clinical signs and their occurrence on a farm. When a high proportion of litters is affected and the condition is present in piglets of both sexes born to sows of any breed or to hybrid animals, then the infectious tremors, AI and AII and the toxic AV are likely.
If low mortality is present, the condition is likely to be AII. In AV there is usually a history of organophosphorus treatment and the outbreak lasts for only a month. AI causes high mortality and it is probable there would be other signs of swine fever on the farm. Cerebellar hypoplasia (reduction in size) is present at post-mortem examination in all 3 conditions. Laboratory confirmation is necessary and swine fever virus or antibody confirms AI. Circovirus type II may be present in AII and the microscopic findings should distinguish AV. Congenital tremors AI:I and AIV are associated with a particular breed and recur in successive litters. AIII is sex-linked and occurs only in male Landrace pigs. Type B congenital tremors do not fit the above categories and have no anatomical or obvious microscopic changes.
Cerebellar hypoplasia (reduction in size) is present at post-mortem examination in all three conditions. Laboratory confirmation is necessary and swine fever virus or antibody to it confirms AI. APPV may be present in AII and the microscopic findings should distinguish AV.
The first occurrence of an infectious congenital tremor in a herd should be notified to the state veterinarian to confirm that classical swine fever is absent. If it is present (AI), the normal process of isolation, slaughter, disinfection and restocking will take place. In the other congenital tremors, including type B, priority must be given to the support of the piglets until the tremors disappear.
Piglets should be kept warm, but straw bedding should be avoided as it leads to entanglement and increased risk of crushing. They should be fed individually until able to suck and should be killed humanely if paralysis results or if sores develop. Control depends upon the type of disease.
There are currently no vaccines for congenital tremor AII, and a herd outbreak may have to run its course. AIII can be prevented in the short term by preventing further matings of the boar and sow involved and by crossing with another breed. A breeding policy which reduces occurrence can be considered. A similar policy can be adopted with other hereditary tremors. AV can be prevented by avoidance of the use of organophosphorus products between days 45 and 79 of gestation
Consultation with the state veterinary service is essential once congenital tremor has been identified, because of the possibility, however remote, that swine fever is present.