More on the crisis in veterinary medicine
Ever since I started my career as a poultry veterinarian and professor at the University of California-Davis School of Veterinary Medicine, I have worried about the training veterinary students receive in preventative veterinary medicine and herd and flock health.1 The level of training in population medicine, particularly poultry, for veterinary students in the United States is typically so limited that students who track in small animal medicine often do not have any real exposure to flock or poultry medicine. At the same time, expertise at the university level is being reduced as faculty retire or the administration prioritizes other areas. In my mind, it is imperative to restructure the veterinary medicine curriculum to include preventative veterinary medicine aspects, including population medicine, since these aspects of veterinary medicine are critically important in controlling foreign animal diseases and maintaining food security and safety. A clear example of the lack of poultry medicine training is the poor reputation veterinarians have dealing with poultry cases and the fact that some groups raising poultry look for expertise abroad or through the internet. This topic deserves brainstorming and a clear strategy so that future veterinarians will be prepared to protect animal health and our food supply.
Rodrigo Gallardo, dvm, phd
School of Veterinary Medicine University of California-Davis Davis, Calif
Osburn BI, Kelly AM, Salman MD, et al. Crisis in veterinary medicine (lett). J Am Vet Med Assoc 2021;258:704–706.
African swine fever in wild pigs
I read with interest the recent JAVMA News article on African swine fever (ASF),1 which noted that controlling this disease will require widespread cooperation. The article closed by noting the USDA had reached an agreement with the Canadian Food Inspection Agency on the steps to be taken following detection of ASF that, among other things, dealt with how affected countries should remove feral swine.
In Africa, ASF is maintained in a sylvatic transmission cycle involving warthogs (Phacochoerus africanus) and soft ticks (Ornithodorus spp). Over the past 3 decades, the geographic area of the United States that contains feral swine or European-type wild boars (Sus scrofa) has more than doubled, and in some areas, their numbers have been difficult or impossible to control. In addition, the United States is home to native species of Ornithodorus ticks, although their vector competence is unknown.2 The susceptibility of peccary or javelina (Tayassu tajacu) populations is also unknown. It is critical that swine veterinarians in the United States and Canada prepare for ASF, but it is not clear what preparations are being made to deal with ASF in wild pigs scattered across the wildland portions of 27 states, 3 territories, and 2 provinces when, not if, the disease arrives here. Removal of wild swine does not seem to be a viable option.
The ASF virus is highly infectious and lasts for a considerable period of time (months to years) in urine, feces, blood, carcasses, soils, and prepared and frozen meats; on knives, boots, tires, and other surfaces3; and even in unprocessed bulk-shipped grain.1 When the virus is introduced into an ASF-free wild boar population, epidemics almost always occur, which may lead to a decrease in the wild boar population3 and fade-out of the disease, but reappearance within months is common, likely as a result of wild boars moving within an infected area and contacting the virus in wild boar carcasses.3 Although the virus tends to remain endemic in previously infected areas, it also spreads by movement and contact into unaffected neighboring wild boar groups.3
In some states and provinces, wild pigs are game animals under the jurisdiction of the state or provincial wildlife agency. In others, they are under the jurisdiction of the agriculture agency, and in some, they are considered alternative livestock. Extensive populations of wild swine now live on private properties and on lands under the authority of a variety of federal agencies including, but not limited to, the National Park Service, US Forest Service, Bureau of Land Management, and Department of Defense. Lack of access or infrastructure, differing policies and priorities, and lawsuits may hinder ASF surveillance and control, even during a declared disease emergency. Aggressive hunting in Texas, including helicopter pursuit and the use of automatic rifles, harvests only about 5% of wild pigs yearly, well below their reproductive capacity. Vaccination may prove useful for the swine industry1 but seems unlikely to be effective in wild swine distributed across vast landscapes.
African swine fever is a disease at the wildlife-livestock interface where wildlife are critical potential reservoirs of persistent infection, and any response or control effort must effectively deal with them and the ecology of the disease. With the likelihood that ASF will eventually arrive in North America, perhaps it is time for federal government agencies, swine veterinarians, and state agriculture agencies to start working with wildlife veterinarians, conservationists, and wildlife agencies.
David A. Jessup, dvm, mpvm
Wildlife Health Center University of California-Davis Davis, Calif
- 1. ↑
Cima G. Industry, agencies continue preparing for African swine fever. J Am Vet Med Assoc 2021;258:813–815.
- 2. ↑
Brown VR, Bevins SN. A review of African swine fever and the potential for introduction into the United States and the possibility of subsequent establishment in feral swine and native ticks. Front Vet Sci 2018;5:11.
- 3. ↑
Guberti V, Khomenko S, Masiulis M, et al. African swine fever in wild boar: ecology and biosecurity. FAO Animal Production and Health Manual No. 22. Rome: Food and Agriculture Organization of the United Nations, World Organisation for Animal Health, and European Commission, 2019.
First reported detection of the equine herpesvirus I DNA polymerase 2254C/His752 variant in horses in the United States
Equine herpesvirus 1 (EHV1) is an important viral pathogen of equids that can cause substantial economic losses. Infection causes a spectrum of disease manifestations in horses, including respiratory disease, abortion, neonatal death, and myeloencephalopathy. Although both host and viral factors are important for EHV-1 infection, a single-nucleotide variation within open reading frame 30 (ORF30) that encodes for the viral DNA polymerase (ie, an A-to-G substitution at nucleotide 2254 resulting in replacement of asparagine at residue 752 with aspartic acid) has been shown to be strongly (76% to 86%) associated with neuropathogenicity.5,6
A new EHV-1 variant (strain FR-56628) with cytosine at nucleotide 2254 in ORF30, resulting in an amino acid change to histidine at residue 752, was recently described in France.3 We report here detection of this new EHV-1 variant in samples from 2 horses in the United States, unrelated to the French outbreak, that were submitted to the Pennsylvania Animal Diagnostic Laboratory System in March 2021. The first horse was admitted to the University of Pennsylvania School of Veterinary Medicine large animal hospital at the New Bolton Center with signs consistent with equine herpes myeloencephalopathy (EHM) and was euthanized. Genetic epidemiological studies are ongoing. The second horse was identified around the same time. This horse was febrile, had neurologic signs, and was also euthanized. It had not been at the New Bolton Center but had been in contact with a horse that had been briefly hospitalized during the risk period. Both of these horses were positive for EHV-1 with a real-time PCR assay targeting the glycoprotein B gene (Ct values of 32.78 and 25) but were negative with an allelic-discrimination (2254A>G) real-time PCR assay.4 Consequently, we amplified a 256-base pair fragment of ORF30 flanking nucleotide position 2254,5 and sequences from both horses had 100% identity with the ORF30 sequence for the FR-56628 EHV-1 strain, confirming the presence of cytosine at nucleotide 2254. Because of this identified variation, veterinarians submitting samples to establish a diagnosis of EHV-1 infection should request the use of a PCR assay that targets consensus regions (eg, the glycoprotein B gene) rather than the use of a neuropathogenic strain-typing assay.
Although this viral variant has been detected in multiple other horses epidemiologically linked to the 2 horses with EHM, exposed and infected horses have not always developed clinical signs or died, and most related confirmed cases have had the usual array of clinical signs typical of EHV-1 infection, including pyrexia, vasculitis, edema, and, in some cases, ataxia. However, it could be noteworthy that in the 2 horses euthanized because of EHM, the first clinically apparent sign was hind limb edema, which was noted ≥ 2 days prior to the development of neurologic signs.
To our knowledge, this represents the first reported detection of the EHV-1 2254C genotype in horses unrelated to the reported French outbreak. Further studies are warranted to understand prevalence of this genotype and its impact on the equine industry in North America.
Nagaraja Thirumalapura, bvsc, phd
Deepanker Tewari, bvsc, phd
Aliza Simeone, vmd
Kevin Brightbill, dvm
Bureau of Animal Health Diagnostic Services Harrisburg, Pa
Eman Anis, dvm, phd
Helen Wheeler-Aceto, phd, vmd
Barbara Dallap-Schaer, vmd
New Bolton Center University of Pennsylvania Kennett Square, Pa
- 1. ↑
Nugent J, Birch-Machin I, Smith KC, et al. Analysis of equid herpesvirus 1 strain variation reveals a point mutation of the DNA polymerase strongly associated with neuropathogenic versus nonneuropathogenic disease outbreaks. J Virol 2006;80:4047–4060.
- 2. ↑
Tewari D, Del Piero F, Cieply S, et al. Equine herpesvirus 1 (EHV-1) nucleotide polymorphism determination using formalin fixed tissues in EHV-1 induced abortions and myelopathies with real-time PCR and pyrosequencing. J Virol Methods 2013;193:371–373.
- 3. ↑
Sutton G, Thieulent C, Fortier C, et al. Identification of a new equid herpesvirus 1 DNA polymerase (ORF30) genotype with the isolation of a C2254/H752 strain in French horses showing no major impact on the strain behaviour. Viruses 2020;12:1160.
- 4. ↑
Smith KL, Li Y, Breheny P, et al. New real-time PCR assay using allelic discrimination for detection and differentiation of equine herpesvirus-1 strains with A2254 and G2254 polymorphisms. J Clin Microbiol 2012;50:1981–1988.
- 5. ↑
Lechmann J, Schoster A, Ernstberger M, et al. A novel PCR protocol for detection and differentiation of neuropathogenic and non-neuropathogenic equid alphaherpesvirus 1. J Vet Diagn Invest 2019;31:696–703.
Emerging outbreak of hepatitis in Midwestern horses
We are writing to inform JAVMA readers of a potential emerging outbreak of hepatitis in horses. Recognition of cases in several Midwestern states, including Indiana, Illinois, Kentucky, and Michigan, began in the autumn of 2020 and continues to date. Additionally, a few horses with similar signs have been reported in other areas of the country.
The hallmarks of disease include high fever (39.4°C to 41.7°C [103°F to 107°F]) that may be biphasic or triphasic with 7- to 10-day periods of normothermia between fever cycles. Horses are lethargic and anorectic while febrile, but no localizing signs are present. Affected horses vary in age, breed, and sex, and affected broodmares have given birth to healthy foals. Serum activities of γ-glutamyltransferase and sorbitol dehydrogenase are consistently high, and high aspartate aminotransferase and alkaline phosphatase activities have been documented in some horses. Unconjugated serum bilirubin concentrations are typically high, and serum amyloid A concentration is consistently high (500 to 1,000 mg/dL). Neutrophilia is the most common cytologic abnormality. Toxic neutrophils are present in some horses when initial clinical signs appear. Histologic examination of liver biopsy samples has revealed acute cholangiohepatitis with infiltrations of neutrophils, lymphocytes, and macrophages in some cases and portal hepatitis in others. In some samples obtained during the acute phase of the disease, islands of necrosis are present. At this time, an etiology has not been identified, and results of the following diagnostic tests have been negative in affected horses:
Fecal culture for Salmonella spp.
Anaerobic fecal culture for Clostridium spp.
Fecal PCR assay for Neorickettsia risticii, Clostridioides difficile toxin genes, Lawsonia intracellularis, Salmonella spp, and coronavirus.
Aerobic and anaerobic microbial culture of liver tissue.
Electron microscopic examination of liver tissue.
Virus isolation from liver tissue.
Serum and liver PCR assay for equine parvovirus-hepatitis and nonprimate hepacivirus (ie, equine hepacivirus) in horses from Indiana (up to 70% of affected horses and 30% of unaffected pasture mates from Kentucky have been positive for equine hepacivirus in serum samples).
Whole blood PCR assay for Anaplasma phagocytophilum.
Urine PCR assay and serum antibody titers for Leptospira spp.
Nasal swab PCR assay for equine herpesvirus 1 and 4, equine influenza A, Streptococcus equi subsp equi, equine rhinitis A virus, and equine rhinitis B virus.
Nasal swab, nasopharyngeal swab, and fecal assays for SARS-CoV-2.
The high fevers observed in affected horses typically respond to NSAIDs. It is unclear whether antimicrobial treatment is necessary. In some cases, antimicrobials appeared to have no effect on preventing a second or third cycle of fever; in others, long-term (3 to 4 weeks) antimicrobial treatment has been associated with the prevention of additional fever cycles and normalization of hepatic enzyme activities. Most affected horses make a full clinical recovery with hepatic enzyme activities decreasing over 4 to 12 weeks. However, it is unknown whether hepatic fibrosis will occur in the future as a consequence of hepatitis.
Readers are encouraged to contact Dr. Sandra Taylor if they have suspect cases or questions.
Sandra D. Taylor, dvm, phd
Janice E. Kritchevsky, vmd, ms
Purdue University College of Veterinary Medicine West Lafayette, Ind
Nathan M. Slovis, dvm
Hagyard Equine Medical Institute Lexington, Ky
Pamela A. Wilkins, dvm, phd
Scott M. Austin, dvm, ms
University of Illinois College of Veterinary Medicine Urbana, Ill
Harold C. Schott, dvm, phd
Michigan State University College of Veterinary Medicine East Lansing, Mich