Found in pigs worldwide, Hemagglutinating Encephalomyelitis Virus (HEV) infection has been largely ignored for decades, but the disease is still present and causes clinical problems. HEV was first linked to neurological disease in baby pigs in Ontario, Canada in 1962. Shortly thereafter, it was also identified as the cause of a postweaning syndrome of anorexia, lethargy and depression that was called Vomiting and Wasting Disease.
HEV is an RNA virus. HEV is a serologic Group 2 coronavirus different from the serologic Group 1 coronaviruses that include Transmissible gastroenteritis virus (TGEV) and porcine respiratory coronavirus (PRCV). Bovine coronavirus is more closely related to HEV. HEV only infects pigs.
Researchers at different institutions have been able to reproduce both clinical syndromes by experimentally infecting pigs with HEV. HEV replicates in the nasal cavity and tonsils and is also subsequently found in lung, stomach and small intestine. HEV is thought to spread to the brain through sensory nerves. Inflammation of nerves in the stomach is associated with the Vomiting and Wasting Disease in postweaning pigs.
HEV should be considered when failure-to-thrive syndromes are observed in pigs pre- or postweaning. The virus is thought to be present in most swine herds without causing clinical disease. The virus is being detected most often in nursery pigs from farms with an inappetence and lethargy syndrome. Vomiting has rarely been reported as a clinical sign.
Typically, pigs quit eating, get thin and die with no evident gross lesions. Generally 1-4% of pigs have been affected postweaning. We have seen this syndrome in herds that are negative for porcine reproductive and respiratory syndrome virus (PRRSV) and in pigs that are negative for porcine circovirus Type 2 (PCV2) by polymerase chain reaction (PCR) test.
Microscopic lesions we have seen in recent cases of postweaning failure-to-thrive syndromes have included rhinitis (inflammation of the nasal turbinates), and inflammation of nerves in the stomach wall at the pylorus. Tonsil has been the best sample for virus detection by HEV PCR, especially early in the course of disease.
HEV is more easily detected in acutely affected pigs and has been difficult to detect in chronically affected pigs. The virus has been detected by HEV PCR in the following tissues in descending order of frequency: 1) tonsil, 2) nasal turbinate, 3) stomach, 4) lung and 5) small intestine. Genetic sequencing of portions of recently detected HEVs indicates the virus is closely related to historic HEV viruses.
A hemagglutination inhibition (HI) serology test is available and has been useful in evaluating clinical cases. Pigs with low or no titer at weaning appear to be candidates to develop clinical disease. In comparison to serum HEV titers in pigs at weaning, pigs with chronic clinical disease will show evidence of seroconversion to infection. Low titers and low seroprevalence in breeding herds have been typical for most herd profiles.
In comparison to other RNA viruses such as PRRSV and swine influenza virus, this disease appears to maintain a low seroprevalence in the breeding herd as well as a relatively low level of clinical disease in postweaning pigs (1-4%).
Young pigs are supposed to be protected from clinical disease by colostral antibodies. There is also supposed to be an age-associated resistance to clinical disease as active immunity develops from natural exposure in pigs 8-16-weeks of age. HEV is thought to maintain itself in the breeding herd by natural exposure; however, recent breeding herd serologic surveys we have done have not shown this. There are no commercial vaccines.
There are numerous disease processes that can cause a failure-to-thrive syndrome in pigs postweaning. HEV should be considered as a clinical rule-out and included in routine diagnostic testing.
Kurt Rossow, DVM
University of Minnesota Veterinary Diagnostic Laboratory
rosso003@umn.edu