Porcine hemagglutinating encephalomyelitis is classically described as a nontreatable disease of piglets, characterized by a vomiting and wasting disease (VWD) and/or encephalomyelitis.
The causal betacoronavirus, porcine hemagglutinating encephalomyelitis virus (PHEV), is of a single antigenic type and is the only neurotropic coronavirus that affects swine. PHEV grows in several types of porcine cell cultures, in which it causes syncytia as the cytopathic effect. As indicated by its name, PHEV agglutinates erythrocytes of several animal species. Pigs are the only known natural host, and the virus is not transmissible to people. The virus is spread via respiratory droplets.
Based on virus detection and/or serology, PHEV appears to be highly prevalent in pig populations worldwide. The virus circulates endemically in most breeding herds via ongoing pig-to-pig transmission. Lactogenic immunity is likely transferred from immune sows to piglets during suckling, which protects the offspring until they develop age-associated resistance. Therefore, PHEV clinical outbreaks are rare because infections usually remain subclinical; however, if PHEV enters a susceptible herd, age-dependent clinical manifestations can appear.
Upon infection, 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, PHEV 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.
The two main clinical syndromes of porcine hemagglutinating encephalomyelitis, acute encephalomyelitis and vomiting and wasting disease, are confined almost exclusively to pigs <4 weeks old who failed to receive lactogenic immunity from their dams. Both clinical forms of PHEV infection may be seen during an outbreak on the same farm.
The VWD form has an incubation period of 4–7 days, after which repeated retching and vomiting are observed. Pigs start suckling but soon stop nursing, withdraw from the sow, and vomit the milk they have ingested. They dip their mouths into water bowls but drink little, possibly due to pharyngeal paralysis.
The persistent vomiting results in a rapid decline of condition. Neonatal pigs become dehydrated, cyanotic, comatose, and die. Piglets that survive the initial course of disease continue to vomit, although less frequently than in the early stage of the disease, until they become anorectic and emaciated.
Significant distention of the cranial abdomen can develop during this chronic syndrome. This “wasting” state may persist for 1–6 weeks until the pigs die of starvation. Mortality approaches 100% within the litter, and survivors remain permanently stunted.
The encephalomyelitic form usually starts 4–7 days after birth, with 24–48 hours of intermittent vomiting, which is rarely as severe as the VWD form and does not result in dehydration. After 1–3 days, the piglets develop generalized muscle tremors and hyperesthesia. The affected pigs tend to walk backward, often ending in a dog-sitting position. They soon become weak, nonambulatory, and paddle their limbs. Blindness, opisthotonos, and nystagmus may also occur. After a few days, the piglets become dyspneic, comatose, and die. While unusual, reports from both Taiwan and South Korea have detailed encephalomyelitic PHEV outbreaks in 30- to 50-day-old pigs. Morbidity and mortality of the encephalomyelitic form are high (as much as 100%) in neonatal pigs but both decrease with increasing age.
From onset of disease to disappearance of clinical signs, an outbreak on a farm lasts 2–3 weeks. Disappearance of disease coincides with the development of immunity in sows in late pregnancy, which subsequently protects piglets via maternal antibodies.
Less commonly, PHEV can present as acute influenza-like illness in older pigs and adult swine.
Pigs chronically infected with porcine hemagglutinating encephalomyelitis consistently have cachexia and abdominal distention because 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 the encephalomyelitic form of PHEV and in 20%–60% of pigs with VWD. Neuritis of peripheral sensory ganglia, particularly the trigeminal ganglia, is a common finding. 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.
Observation of 4- to 7-day-old piglets with frequent and persistent vomiting, with or without motor disorders, is highly suggestive of PHEV infection, and laboratory testing should be conducted.
A laboratory diagnosis of porcine hemagglutinating encephalomyelitis can be made routinely by RT-PCR. Successful PHEV isolation from target tissues (brain stem, tonsils, and respiratory tract) generally requires sample collection within 2 days of disease onset, because it is often difficult to isolate the virus from pigs who have been affected for >2–3 days. Direct immunofluorescence staining can be useful for detection of PHEV antigens in tissue sections.
In general, PHEV serology results must be interpreted with an abundance of caution due to the high global prevalence. A significant rise in antibody titer can be demonstrated in paired serum samples, but because of the rather long incubation period, pigs may start to seroconvert 2–3 days after the first clinical signs appear. Therefore, the acute serum must be collected immediately after the onset of disease. The endemic nature of PHEV in most swine herds means antibody titers in older pigs are common; however, PHEV antibody profiling in high-health sow herds can be used to predict the disease risk among new litters.
Because protection from PHEV-related disease in piglets is likely provided by lactogenic immunity supplied by their sows, PHEV is mainly a concern in high-health herds and first-parity litters whose dams may not have been previously exposed to the virus. There is no treatment, and once clinical signs are evident, the disease runs its course. Spontaneous recoveries are rare, and euthanasias are common among neonates. Piglets born from nonimmune sows during the outbreak can be protected with an at-birth injection of either hyperimmune serum or, if this is not available, pooled serum collected from older, immune sows. However, the time lapse between diagnosis and cessation of the disease is usually too short for this procedure to be practically accomplished. Maintaining the virus on the farm (thus retaining naturally induced immunity in the sows) avoids outbreaks in piglets.
Subclinical porcine hemagglutinating encephalomyelitis virus (PHEV) is highly prevalent in most swine herds worldwide.
Although clinical outbreaks are rare, neonatal piglets who do not receive lactogenic antibodies against PHEV may develop either encephalomyelitis or a vomiting and wasting syndrome 4–7 days after exposure.
Once clinical signs appear, there is no specific treatment. Depending on the severity of disease, euthanasia may be indicated.
Lactogenic immunity provided to neonatal pigs by previously exposed sows generally prevents the occurrence of clinical disease, so control should focus on building immunity in breeding sows.