Overview of Porcine Hemagglutinating Encephalomyelitis
(Vomiting and wasting disease, Coronaviral encephalomyelitis)
Porcine hemagglutinating encephalomyelitis, a viral disease of young pigs, is characterized by vomiting, constipation, and anorexia and results either in rapid death or chronic emaciation (vomiting and wasting). Also, motor disorders due to acute encephalomyelitis (hemagglutinating encephalomyelitis) are often seen during field outbreaks.
The causal coronavirus, porcine hemagglutinating encephalomyelitis virus (PHEV), is of a single antigenic type, and it grows in several types of porcine cell cultures, in which it causes syncytia. It agglutinates RBCs of several animal species. Pigs are the only natural host. The virus is spread via aerosol. It has no public health significance.
Based on virus detection and/or serology, PHEV Infection has been reported from several countries in Europe and from North and South America (Argentina), Australia, and Asia (China, Taiwan, South Korea); thus, it appears to be widespread. The virus is endemic in most breeding herds, and a herd immunity exists. The infection usually remains subclinical. 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 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. More recently, some outbreaks have been reported from Taiwan and South Korea in which pigs 30–50 days old showed motor disorders. Morbidity and mortality of the encephalomyelitic form are high (as much as 100%) in neonatal pigs but both decrease with increasing age. Both clinical forms of PHEV infection may be seen during an outbreak on the same farm.
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 and, to be successful, the pigs are preferably euthanized within 2 days after signs appear. It is difficult to isolate the virus from pigs that have been affected for >2–3 days. Other diagnostic techniques, based on antigen or nucleic acid (RT-PCR) detection, have been developed and applied recently.
A significant rise in antibody titer can be demonstrated in paired serum samples. Because of the rather long incubation period, pigs may start to build up a low antibody titer 2–3 days after the first signs appear. Therefore, the acute serum must be collected immediately after disease starts.
There is no treatment. Once signs are evident, the disease runs its course. Spontaneous recoveries are rare. Piglets born from nonimmune sows during the outbreak can be protected by being injected, at birth, either with hyperimmune serum or, if this is not available, with pooled serum collected from older sows at a slaughterhouse. 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.