This viral disease of young pigs characterized by vomiting, constipation, and anorexia results either in rapid death or chronic emaciation. Motor disorders due to acute encephalomyelitis (hemagglutinating encephalomyelitis) also may be seen during some outbreaks.
Etiology, Epidemiology, and Pathogenesis
The causal coronavirus, hemagglutinating encephalomyelitis virus, is of a single antigenic type, and it grows in several types of porcine cell cultures, in which it causes syncytia. It agglutinates RBC of several animal species. Pigs are the only natural host. The virus is spread via aerosol.
Infection appears to be widespread in North America, western Europe, and Australia. It usually remains subclinical. The virus is endemic in most breeding herds, and a herd immunity exists. Immune sows transfer maternal antibodies to their piglets, which are protected until they have developed an age resistance; thus, clinical outbreaks are rare. However, if the virus enters a susceptible herd with neonatal piglets, morbidity and mortality may be high.
The virus first replicates in the nasal mucosa, tonsils, lungs, and to a very limited extent, in the small intestine. From these sites of entry, the virus invades defined nuclei of the medulla oblongata via the peripheral nervous system and subsequently spreads to the entire brain stem, and possibly to the cerebrum and cerebellum. Vomiting is thought to be caused by viral replication in the vagal sensory ganglion. Wasting is due to vomiting and delayed emptying of the stomach, which is the result of virus-induced lesions in the intramural plexus. Infection of cerebral and cerebellar neurons may rarely cause motor disorders.
Both clinical syndromes, the vomiting and wasting disease (VWD) and the encephalitic forms, are confined almost exclusively to pigs <4 wk old. The VWD form has an incubation period of 4–7 days. Repeated retching and vomiting are seen. Pigs start suckling but soon stop, withdraw from the sow, and vomit the milk they have ingested. They dip their mouths into water bowls but drink little, possibly indicative of pharyngeal paralysis. The persistent vomiting results in a rapid decline of condition. Neonatal pigs become dehydrated, cyanotic, and comatose, and die. Older pigs continue to vomit, although less frequently than in the early stage of the disease. They lose appetite and become emaciated. A large distention of the cranial abdomen can develop. This “wasting” state may persist for 1–6 wk until the pigs die of starvation. Mortality approaches 100% within the litter, and survivors remain permanently stunted.
The encephalomyelitic form also starts with vomiting, usually 4–7 days after birth. Vomiting continues intermittently for 1–2 days, but it is rarely severe and does not result in dehydration. After 1–3 days, generalized muscle tremors and hyperesthesia are seen. The pigs tend to walk backward, often ending in a dog-sitting position. They soon become weak, are unable to rise, and paddle their limbs. Blindness, opisthotonos, and nystagmus also occur. After a few days, they become dyspneic, comatose, and die.
From onset to disappearance, an outbreak on a farm lasts 2–3 wk. Disappearance of disease coincides with the development of immunity in sows in late pregnancy, which subsequently protects piglets via maternal antibodies.
Cachexia and abdominal distention are seen in chronically affected pigs. Their stomachs are dilated and filled with gas. Microscopically, perivascular cuffing, gliosis, and neuronal degeneration are found in the medulla in 70–100% of pigs with nervous signs, and in 20–60% of pigs with VWD. Neuritis of peripheral sensory ganglia, particularly the trigeminal ganglia, is seen regularly. Degeneration of the ganglia of the stomach wall and perivascular cuffing are found in 15–85% of pigs with VWD. The lesions are most pronounced in the pyloric gland area.
A laboratory diagnosis can be made routinely by virus isolation from the brain stem if the pigs are euthanized within 2 days after signs appear. It is difficult to isolate the virus from pigs that have been affected for >2 days.
A significant rise in antibody titer can be demonstrated in paired serum samples. The acute serum sample must be collected immediately after the start of disease, because pigs may already have built up a low antibody titer when the first signs appear.
Differential diagnoses include pseudorabies (see Pseudorabies) and teschovirus encephalomyelitis (see Teschovirus Encephalomyelitis). Respiratory signs in older pigs and abortions in sows are part of a pseudorabies outbreak. In teschovirus encephalomyelitis, older pigs are usually involved.
There is no treatment. Once signs are evident, the disease runs its course. Spontaneous recoveries are rare. Piglets born from nonimmune sows during an outbreak can be protected by injecting, at birth, either hyperimmune serum or serum from sows randomly selected at slaughter. However, the time lapse between diagnosis and cessation of the disease is usually too short for this procedure to be effective. Maintaining the virus on the farm (thus retaining naturally induced immunity in the sows) avoids outbreaks in piglets.
Last full review/revision March 2012 by Maurice B. Pensaert, DVM, MS, PhD