Porcine hemagglutinating encephalomyelitis is a viral disease of piglets, characterized by a vomiting and wasting syndrome and/or encephalomyelitis. Although the virus is widespread, outbreaks of the disease are rare because sows pass protective antibodies during nursing. Diagnosis is based on clinical signs (including vomiting, wasting, influenza-like illness, and/or neurological signs) and can be confirmed by viral isolation, immunofluorescence staining of tissues, or PCR assay. There is no treatment or vaccine. Control is focused on building immunity among breeding sows.
Porcine hemagglutinating encephalomyelitis (PHE) is typically described as a nontreatable disease of piglets, characterized by a vomiting and wasting disease (VWD) and/or encephalomyelitis.
Etiology, Epidemiology, and Pathogenesis of Porcine Hemagglutinating Encephalomyelitis
The betacoronavirus that causes PHE, 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 its cytopathic effect is the formation of syncytia. As its name indicates, PHEV also agglutinates erythrocytes. Pigs are the only known natural host, and the virus is not transmissible to humans. The virus is transmitted via respiratory droplets.
Virus detection and serological testing suggest that PHEV is highly prevalent in pig populations worldwide. The virus circulates endemically in most breeding herds via continuous pig-to-pig transmission.
Lactogenic immunity to PHE—ie, transferred from immune sows to piglets during suckling—protects the offspring until they develop age-associated resistance. Therefore, PHE outbreaks are rare because PHEV infections usually remain subclinical. However, if PHEV enters a susceptible herd, age-dependent clinical signs can appear.
Upon infection, PHEV first replicates in the nasal mucosa, tonsils, lungs, and, to a very limited extent, small intestine. From these sites of entry, the virus invades defined nuclei of the medulla oblongata via the peripheral nervous system and then spreads to the entire brainstem, and possibly to the cerebrum and cerebellum.
Vomiting with PHE 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 results from virus-induced lesions in the intramural plexus. Infection of cerebral and cerebellar neurons may cause motor disorders.
Clinical Findings of Porcine Hemagglutinating Encephalomyelitis
The two main forms of PHE—acute encephalomyelitis and VWD—are confined almost exclusively to pigs < 4 weeks old that failed to receive lactogenic immunity from their dams. Both manifestations may occur during a single outbreak on the same farm.
Vomiting and Wasting Disease
The VWD form of PHE 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 because of pharyngeal paralysis.
The persistent vomiting results in a rapid decline of condition. Neonatal pigs become dehydrated, cyanotic, and comatose, and they 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.
Marked distention of the cranial abdomen can develop during this chronic syndrome. This wasting state may persist for 1–6 weeks until the pig dies of starvation. The mortality rate of PHE approaches 100% within a litter, and survivors remain permanently stunted.
Encephalomyelitis
The encephalomyelitic form of PHE usually starts 4–7 days after birth with 24–48 hours of intermittent vomiting, which is rarely as severe as in 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.
Piglets with encephalomyelitic PHE soon become weak and nonambulatory, and they paddle their limbs. Blindness, opisthotonos, and nystagmus may also occur. After a few days, the piglets become dyspneic and comatose, and they die.
Reports from Taiwan and South Korea have detailed rare encephalomyelitic PHE outbreaks in 30- to 50-day-old pigs, but this age range is not typical overall. The morbidity and mortality rates of the encephalomyelitic form are high (up to 100%) in neonatal pigs; however, both rates decrease with increasing age.
From the onset of PHE to the disappearance of clinical signs, outbreaks on farms last 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, PHE can present as acute influenza-like illness in older pigs and adult swine.
Lesions
Pigs chronically infected with PHEV 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 PHE, and in 20%–60% of pigs with the VWD form.
Neuritis of the 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.
Diagnosis of Porcine Hemagglutinating Encephalomyelitis
Presumptive: clinical signs
Definitive: viral isolation, immunofluorescence staining, or PCR assay
Observation of frequent and persistent vomiting in 4- to 7-day-old piglets, with or without motor disorders, is highly suggestive of PHEV infection, and laboratory testing should be conducted.
A laboratory diagnosis of PHE can be made routinely by reverse transcription PCR (RT-PCR). Successful PHEV isolation from target tissues (brainstem, 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 that have been affected for > 2–3 days. Direct immunofluorescence staining can be useful for detection of PHEV antigens in tissue sections.
In general, PHEV serological test results must be interpreted with an abundance of caution because of the high global prevalence of this virus.
A marked rise in PHEV antibody titer can be demonstrated in paired serum samples. Because of the long incubation period, however, 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 that antibody titers in older pigs are common. However, PHEV antibody profiling in healthy sow herds can be used to predict the disease risk among new litters.
Differential diagnoses for PHE include pseudorabies and teschovirus encephalomyelitis. Respiratory signs in older pigs may mimic those of swine influenza.
Treatment and Control of Porcine Hemagglutinating Encephalomyelitis
Treatment: none available
Control: building of immunity in the breeding herd
Because protection from PHEV-related disease in piglets is likely provided by lactogenic immunity supplied by their sows, PHEV is mainly a concern in first-parity litters whose dams may not have been previously exposed to the virus.
There is no treatment for PHE, and once clinical signs are evident, the disease runs its course. Spontaneous recoveries are rare, and affected neonates are commonly euthanized.
Piglets born from nonimmune sows during a PHE outbreak can be protected with an at-birth injection of either hyperimmune serum or, if that 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, rather than attempting to eradicate it, retains the naturally induced PHEV immunity in the sows and avoids outbreaks in piglets.
Key Points
Subclinical porcine hemagglutinating encephalomyelitis virus (PHEV) is highly prevalent in swine herds worldwide.
Although clinical outbreaks are rare, neonatal piglets that 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 PHE, so control should focus on building immunity in breeding sows.
For More Information
Swine Health Information Center fact sheet: Porcine Hemagglutinating Encephalomyelitis Virus
Newport Laboratories: Swine Disease Diagnostic Manual
Mora-Díaz JC, Piñeyro PE, Houston E, Zimmerman J, Giménez-Lirola LG. Porcine hemagglutinating encephalomyelitis virus: a review. Front Vet Sci. 2019;6:53. doi:10.3389/fvets.2019.00053
