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Journal of veterinary internal medicine2006; 20(6); 1491-1494; doi: 10.1892/0891-6640(2006)20[1491:ccpefa]2.0.co;2

Clinical, clinicopathologic, postmortem examination findings and familial history of 3 Arabians with lavender foal syndrome.

Abstract: No abstract available
Publication Date: 2006-12-26 PubMed ID: 17186871DOI: 10.1892/0891-6640(2006)20[1491:ccpefa]2.0.co;2Google Scholar: Lookup
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Summary

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The research article focuses on a genetic condition known as Lavender Foal Syndrome (LFS) in Arabian foals, detailing the clinical, clinicopathologic, postmortem examination findings, and familial history of three Arabian horses affected by the condition.

Introduction

  • The study presents a detailed investigation of Lavender Foal Syndrome (LFS) in Arabian horses. LFS, also known as dilute lethal, lethal LFS, or coat color dilution lethal, is reportedly an autosomal recessive genetic condition exclusively impacting Arabian foals.

Clinical Examinations

  • The researchers used specific cases to illustrate the manifestation of LFS. They began with the case of an Arabian filly showing serious neurological signs, including spontaneous paddling, head banging, and opisthotonus, immediately after birth. Other noteworthy observations included a dilute lavender coat color and a weak suck reflex.
  • The clinical examination exhibited various neurological signs, although severe abnormalities like hypoproteinemia, hypoalbuminemia, hypoglycemia, and hyponatremia were also identified.
  • The researchers ran a series of tests on clinicopathologic analysis, neurological examination, CBC (Complete Blood Count), and serum biochemistry.

Treatment for LFS

  • Due to the neurological symptoms, treatment was initiated using Diazepam, which resulted in only slight temporary improvement. Additional treatments such as Phenobarbitone and Dexamethasone were also administered but showed limited effects.
  • It was emphasized that there are no treatments specifically recommended for LFS and the condition is deemed fatal within 24-72 hours.

Causes and Differential Diagnoses

  • Several potential causes for neonatal neurological abnormalities, including perinatal asphyxia syndrome (PAS), metabolic disorders, infections, central nervous system malformations, cranial or spinal trauma, and toxins, were considered. Additionally, possible conditions like cerebellar abiotrophy and benign epilepsy were also considered.
  • The neonatal seizure activity, a characteristic of LFS, appeared to be tied with cerebellar signs. However, distinguishing seizure activity in newborn foals could be challenging.

Postmortem Examination Findings

  • Although previous examinations on affected foals indicated an anomalous choroid plexus, central nervous system vacuolization of neurons, and abnormal clumping of melanin on skin biopsy, these abnormalities were not unearthed in the cases under research.
  • No lesions specific to LFS were detected, supporting the contention that LFS is a functional or physiological disorder.

Conclusion

  • The study identified key features of LFS that differentiate it from other causes of neonatal neurological abnormalities – its typical signalment, severe neurological deficits present at birth without evidence of perinatal asphyxia, normal CBC and serum biochemistry results, and the lack of response to therapy.
  • Further investigation to determine the pathophysiology and confirm the genetic basis of the LFS condition was recommended by the researchers.

Cite This Article

APA
Page P, Parker R, Harper C, Guthrie A, Neser J. (2006). Clinical, clinicopathologic, postmortem examination findings and familial history of 3 Arabians with lavender foal syndrome. J Vet Intern Med, 20(6), 1491-1494. https://doi.org/10.1892/0891-6640(2006)20[1491:ccpefa]2.0.co;2

Publication

ISSN: 0891-6640
NlmUniqueID: 8708660
Country: United States
Language: English
Volume: 20
Issue: 6
Pages: 1491-1494

Researcher Affiliations

Page, Patrick
  • Department of Companion Animal Clinical Studies Faculty of Veterinary Science, University of Pretoria, Onderstepoort, South Africa.
Parker, Rissa
    Harper, Cindy
      Guthrie, Alan
        Neser, Johann

          MeSH Terms

          • Animals
          • Fatal Outcome
          • Female
          • Hair / pathology
          • Horse Diseases / genetics
          • Horse Diseases / pathology
          • Horses
          • Neurologic Examination / veterinary
          • Pigmentation / genetics
          • Seizures / etiology
          • Seizures / genetics
          • Seizures / pathology
          • Seizures / veterinary
          • Syndrome

          Citations

          This article has been cited 6 times.
          1. Aleman M, Finno CJ, Weich K, Penedo MCT. Investigation of Known Genetic Mutations of Arabian Horses in Egyptian Arabian Foals with Juvenile Idiopathic Epilepsy. J Vet Intern Med 2018 Jan;32(1):465-468.
            doi: 10.1111/jvim.14873pubmed: 29171123google scholar: lookup
          2. Williams DC, Aleman MR, Brosnan RJ, Fletcher DJ, Holliday TA, Tharp B, Kass PH, Steffey EP, LeCouteur RA. Electroencephalogram of Healthy Horses During Inhaled Anesthesia. J Vet Intern Med 2016 Jan-Feb;30(1):304-8.
            doi: 10.1111/jvim.13613pubmed: 26376458google scholar: lookup
          3. Aleman M, Madigan JE, Williams DC, Holliday TA. Brainstem auditory evoked responses in an equine patient population. Part II: foals. J Vet Intern Med 2014 Jul-Aug;28(4):1318-24.
            doi: 10.1111/jvim.12377pubmed: 24903742google scholar: lookup
          4. Brosnahan MM, Brooks SA, Antczak DF. Equine clinical genomics: A clinician's primer. Equine Vet J 2010 Oct;42(7):658-70.
          5. Webb AA, Cullen CL. Coat color and coat color pattern-related neurologic and neuro-ophthalmic diseases. Can Vet J 2010 Jun;51(6):653-7.
            pubmed: 20808581
          6. Brooks SA, Gabreski N, Miller D, Brisbin A, Brown HE, Streeter C, Mezey J, Cook D, Antczak DF. Whole-genome SNP association in the horse: identification of a deletion in myosin Va responsible for Lavender Foal Syndrome. PLoS Genet 2010 Apr 15;6(4):e1000909.
            doi: 10.1371/journal.pgen.1000909pubmed: 20419149google scholar: lookup