Vomiting & wasting disease

Occurrence: Worldwide.
Age affected: Piglets pre-weaning.
Causes: Haemagglutinating encephalomyelitis virus (HEV).
Effects: Mostly no illness, but can be vomiting, weight loss, constipation, inappetence, nervous signs, particularly in piglets.

Causes

The disease is caused by infection of young piglets with haemagglutinating encephalomyelitis virus (HEV), a coronavirus. This RNA virus is stable from pH 3-10 and resembles TGE virus but agglutinates (clumps) chicken red blood cells. There may be some antigenic similarity between the 2 viruses, but they are distinct in serum neutralisation tests. The virus grows in pig kidney cells to form syncytia (fused cells) within 12-16 hours. Cell killed (CPE) is complete in 48 hours. There is only one serotype. After oronasal infection, clinical signs develop within 3-5 days.

Primary viral multiplication takes place in epithelial cells of the tonsil, lung, nasal mucosa and lungs. Virus spreads along nerves to the trigeminal, inferior vagal, superior cervical, solar and dorsal root ganglia and to the intestinal nervous plexuses. The trigeminal and vagal sensory nuclei in the brain stem become infected followed by other nuclei, the cerebrum, cerebellum and the spinal cord. Viral replication in the gastric nervous plexus causes damage and leads to delayed gastric emptying and eventual starvation. Passive colostral immunity protects against infection.

Mode of transmission

Infection spreads throughout the herd in nasal secretions. Maternal immunity protects piglets which have taken colostrum for up to 15 weeks. The virus therefore circulates in older growers and young finishers in which it does not cause clinical disease. Clinical disease occurs in the piglets of non-immune sows, generally those purchased from infection-free herds. Infection appears to spread from herd to herd in carrier pigs.

Clinical signs

Piglets aged between 5 days and 3 weeks are affected. The first signs to be noted are vomiting, huddling of the piglets which may be associated with a rise in temperature, depression, inappetence and constipation. Some affected animals may show signs of encephalomyelitis, e.g. hind leg weakness or difficulties in swallowing. Affected piglets die within 36-28 hours or become progressively emaciated.

The contrast between affected and unaffected piglets in the same litter is striking. Clinical signs in piglets may be preceded by transient fever (to 40.6°C, 105°F) in the sows. Most infections occur in older pigs after maternal antibody has disappeared and are inapparent. The virus has been demonstrated in the Periweaning Failure to Thrive Syndrome (PFTS), but its role is so far not clear.

The disease should be suspected when vomiting, depression and constipation followed by wasting and hairiness develop in piglets aged less than 21 days. Additional evidence comes from post-mortem demonstration. Demonstration of antibody in the sera of wasting piglets and in sera from the mothers of affected litters 14 days after the clinical signs are first noted is also of use. Enteroviruses and Aujeszky’s disease may also cause encephalitis but are more severe and usually also affect older pigs. TGE causes profuse diarrhoea and no encephalitis. 

Postmortem lesions

There are no specific lesions. The intestinal tract is normally empty with scanty faeces and there is pronounced wasting. In 25% of cases a non-suppurative encephalomyelitis is found in the brain by microscopic examination together with perivascular cuffing with mononuclear cells, glial node formation, neuronal degeneration and meningitis which are seen in the grey matter of the mesencephalon, pons, medulla oblongata and in the upper spinal cord. Diagnosis may be confirmed by virus isolation from the respiratory tract, hindbrain and spinal cord of early cases. The CPE can be confirmed as specific by haemagglutination, haemadsorption, serum neutralisation or immunofluorescence. RTPCR testing can confirm the presence of the virus.

Treatment and prevention

There is no treatment and control in non-infected herds depends upon the maintenance of a closed herd or the purchase of stock from herds known to be free from the disease. In infected herds the only preventative measure is to ensure access to colostrum. It is possible that immunity may be stimulated in non-pregnant gilts by feeding affected piglets or the faeces of weaned pigs to them. This procedure may require the permission of a state veterinarian. Disinfection is possible.