A potential early clinical phenotype of necrotizing meningoencephalitis in genetically at-risk pug dogs.


Journal

Journal of veterinary internal medicine
ISSN: 1939-1676
Titre abrégé: J Vet Intern Med
Pays: United States
ID NLM: 8708660

Informations de publication

Date de publication:
Jul 2022
Historique:
received: 24 02 2022
accepted: 04 05 2022
pubmed: 28 5 2022
medline: 27 7 2022
entrez: 27 5 2022
Statut: ppublish

Résumé

Necrotizing meningoencephalitis (NME) in the pug dogs is a fatal neuroinflammatory disease associated with rapid progression and poor response to conventional immunosuppressive therapy. Diagnosis is typically made after severe neurological abnormalities have manifested. Pug dogs at genetic risk for NME might manifest neurological abnormalities before developing pathognomonic clinical signs of NME. Thirty-six pug dogs less than 4 years of age asymptomatic for NME. Prospective observational cohort study with germline genome-wide genotyping. Neurological examinations were performed 4 weeks apart to document reproducible findings of central nervous system disease. Magnetic resonance imaging, cerebrospinal fluid analysis, and testing for infectious diseases were performed in all pugs with reproducible abnormalities detected on neurological examination. The overall risk allele frequency in this cohort was 40%; 5 (14%) dogs were high risk, 19 (53%) dogs were medium risk, and 12 (33%) dogs were low genetic risk for NME. Reproducible abnormalities detected on neurological examination were identified in 8/24 (33%) genetically at-risk dogs and 0/12 (0%) low risk dogs. Clinical abnormalities included multifocal spinal pain in 8/8, reduced menace response in 5/8, and lateralizing postural reaction deficits in 5/8 pugs. There was a strong association between genotype risk and the presence of this clinical phenotype (P = .03). Our findings suggest the presence of a novel early clinical phenotype of NME in apparently asymptomatic genetically at-risk pugs which might be used to plan early diagnostic and therapeutic clinical trials.

Sections du résumé

BACKGROUND BACKGROUND
Necrotizing meningoencephalitis (NME) in the pug dogs is a fatal neuroinflammatory disease associated with rapid progression and poor response to conventional immunosuppressive therapy. Diagnosis is typically made after severe neurological abnormalities have manifested.
HYPOTHESIS/OBJECTIVE OBJECTIVE
Pug dogs at genetic risk for NME might manifest neurological abnormalities before developing pathognomonic clinical signs of NME.
ANIMALS METHODS
Thirty-six pug dogs less than 4 years of age asymptomatic for NME.
METHODS METHODS
Prospective observational cohort study with germline genome-wide genotyping. Neurological examinations were performed 4 weeks apart to document reproducible findings of central nervous system disease. Magnetic resonance imaging, cerebrospinal fluid analysis, and testing for infectious diseases were performed in all pugs with reproducible abnormalities detected on neurological examination.
RESULTS RESULTS
The overall risk allele frequency in this cohort was 40%; 5 (14%) dogs were high risk, 19 (53%) dogs were medium risk, and 12 (33%) dogs were low genetic risk for NME. Reproducible abnormalities detected on neurological examination were identified in 8/24 (33%) genetically at-risk dogs and 0/12 (0%) low risk dogs. Clinical abnormalities included multifocal spinal pain in 8/8, reduced menace response in 5/8, and lateralizing postural reaction deficits in 5/8 pugs. There was a strong association between genotype risk and the presence of this clinical phenotype (P = .03).
CONCLUSIONS AND CLINICAL IMPORTANCE CONCLUSIONS
Our findings suggest the presence of a novel early clinical phenotype of NME in apparently asymptomatic genetically at-risk pugs which might be used to plan early diagnostic and therapeutic clinical trials.

Identifiants

pubmed: 35621070
doi: 10.1111/jvim.16444
pmc: PMC9308433
doi:

Types de publication

Journal Article Observational Study, Veterinary

Langues

eng

Sous-ensembles de citation

IM

Pagination

1382-1389

Informations de copyright

© 2022 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.

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Auteurs

Rebecca Windsor (R)

Ethos Veterinary Health, Woburn, Massachusetts, USA.
Ethos Discovery (501c.3.), San Diego, California, USA.

Samuel Stewart (S)

Ethos Veterinary Health, Woburn, Massachusetts, USA.
Ethos Discovery (501c.3.), San Diego, California, USA.

Jessica Schmidt (J)

Ethos Veterinary Health, Woburn, Massachusetts, USA.

Mario Mosqueda (M)

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona, USA.

Ignazio Piras (I)

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona, USA.

Stefan M Keller (SM)

Department of Pathology, Microbiology, Immunology, University of California, Davis, Davis, California, USA.

Briana Steinmetz (B)

Ethos Veterinary Health, Woburn, Massachusetts, USA.
Ethos Discovery (501c.3.), San Diego, California, USA.

Dori L Borjesson (DL)

Department of Pathology, Microbiology, Immunology, University of California, Davis, Davis, California, USA.

Matthew Huentelman (M)

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona, USA.

Chand Khanna (C)

Ethos Veterinary Health, Woburn, Massachusetts, USA.
Ethos Discovery (501c.3.), San Diego, California, USA.

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