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Veterinary pathology2000; 37(6); 672-676; doi: 10.1354/vp.37-6-672

Fatal nonneurological EHV-1 infection in a yearling filly.

Abstract: A case of fatal nonneurological equine herpesvirus 1 (EHV-1) infection in a yearling filly is described. Gross lesions included extensive pulmonary edema, prominent laryngeal lymphoid follicles, and congestion and edema of the dorsal third ventricle choroid plexus. Histologically, there was vasculitis, hemorrhage, and edema in the lungs and dorsal third ventricle choroid plexus as well as mild intestinal crypt necrosis with occasional intranuclear inclusion bodies. The perivascular and vascular inflammatory infiltrates were comprised mainly of T lymphocytes and macrophages. EHV-1 antigen was identified within the nucleus and cytoplasm of endothelial cells, dendritic-like cells of the pharyngeal lymphoid follicles, pharyngeal glandular epithelium, crypt enterocytes, and monocytes. Attempted virus isolation was negative. Weak seroconversion for EHV-1 was observed. Herpesvirus-like particles were identified within pharyngeal endothelial cells by transmission electron microscopy. Polymerase chain reaction amplified 369 and 188 base-pair fragments specific for EHV-1. The scarcity of pathognomonic viral inclusions and lesions in this case suggests that this disease may not be recognized, particularly in situations when ancillary laboratory procedures are limited.
Publication Date: 2000-12-06 PubMed ID: 11105961DOI: 10.1354/vp.37-6-672Google Scholar: Lookup
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Summary

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This research article describes a unique case of a fatal, non-neurological equine herpesvirus 1 (EHV-1) infection in a year-old female horse, which presented many physical and histological abnormalities. The analysis suggests that this type of EHV-1 infection may go unrecognized due to the scarcity of typical viral indicators and limitations in laboratory procedures.

Fatal EHV-1 Infection

  • The study primarily deals with the investigation of a fatal case – a yearling filly was infected with a nonneurological version of EHV-1. This is unusual because EHV-1 typically induces neurological symptoms.
  • The infection in this case led to death, marking the severity of the situation.

Clinical Analysis and Observations

  • During the examination, the filly was found to have an array of gross lesions including pulmonary edema (fluid accumulation in the lungs), pronounced laryngeal lymphoid follicles (probably indicating an immune response), and congestion and edema in the dorsal third ventricle choroid plexus, a part of the brain.
  • On a microscopic level, examination revealed vasculitis (inflammation of the blood vessels), hemorrhage (bleeding), and edema in the lung cells and in the choroid plexus in the brain. A mild intestinal crypt necrosis (death of intestinal cells) was also observed with occasional intranuclear inclusion bodies (a sign of viral infections).

Characteristics of Inflammatory Infiltrates

  • The vascular and perivascular tissue showed a high presence of T lymphocytes and macrophages, cells actively participating in the immune response, indicating an inflammatory reaction to the infection.

Presence and Identification of EHV-1 Antigen

  • The researchers were able to identify EHV-1 antigen within the nucleus and cytoplasm of endothelial cells, dendritic-like cells of the pharyngeal lymphoid follicles, glandular epithelium cells in the pharynx, crypt enterocytes, and monocytes.
  • Despite the identification of EHV-1 antigens, attempts to isolate the virus were unsuccessful.
  • A weak seroconversion for EHV-1 was observed, meaning there was an increase in detectable antibodies specific to EHV-1 in the filly’s blood.

Detection Methods

  • Researchers used transmission electron microscopy to identify herpesvirus-like particles within pharyngeal endothelial cells.
  • Further, polymerase chain reaction (PCR) tests amplified 369 and 188 base-pair fragments specific to EHV-1, confirming the presence of the virus.

Unrecognized Disease

  • The article concludes by voicing the concern that this form of disease might go unrecognized. This is due to the scarcity of pathognomonic viral inclusions (unique cellular changes accompanying certain diseases) and lesions typically associated with viral infections.
  • The under-recognition of this type of infection could also be exacerbated by limited additional laboratory procedures, thus making diagnostics challenging.

Cite This Article

APA
Del Piero F, Wilkins PA, Timoney PJ, Kadushin J, Vogelbacker H, Lee JW, Berkowitz SJ, La Perle KM. (2000). Fatal nonneurological EHV-1 infection in a yearling filly. Vet Pathol, 37(6), 672-676. https://doi.org/10.1354/vp.37-6-672

Publication

ISSN: 0300-9858
NlmUniqueID: 0312020
Country: United States
Language: English
Volume: 37
Issue: 6
Pages: 672-676

Researcher Affiliations

Del Piero, F
  • School of Veterinary Medicine, University of Pennsylvania, New Bolton Center 19348-1692, USA. fdp@vet.upenn.edu
Wilkins, P A
    Timoney, P J
      Kadushin, J
        Vogelbacker, H
          Lee, J W
            Berkowitz, S J
              La Perle, K M

                MeSH Terms

                • Animals
                • Choroid Plexus / pathology
                • Fatal Outcome
                • Female
                • Herpesviridae Infections / pathology
                • Herpesviridae Infections / veterinary
                • Herpesvirus 1, Equid / isolation & purification
                • Horse Diseases / pathology
                • Horses
                • Immunohistochemistry / veterinary
                • Intestine, Small / pathology
                • Lung / pathology
                • Pharynx / pathology
                • Polymerase Chain Reaction / veterinary
                • Vasculitis / complications
                • Vasculitis / pathology
                • Vasculitis / veterinary

                Citations

                This article has been cited 1 times.
                1. Dayaram A, Seeber PA, Greenwood AD. Environmental Detection and Potential Transmission of Equine Herpesviruses. Pathogens 2021 Apr 1;10(4).
                  doi: 10.3390/pathogens10040423pubmed: 33916280google scholar: lookup