White muscle disease in foals

Gorgi, Alireza A.

White muscle disease in foals

Abstract

White muscle disease, also known as nutritional muscular dystrophy, is a degenerative disease that affects the skeletal and cardiac muscle of foals ranging in age from birth to 11 months. White muscle disease is prevalent in regions with seleniumdeficient soils. Selenium is a component of the enzyme glutathione peroxidase, which protects cell membranes against oxidation. Muscle cell membranes depend on normal body levels of selenium and vitamin E to avoid damage caused by oxygen reactive metabolites that are produced during normal cellular metabolism. (1, 2) A one-day-old colt presented to Cornell University Hospital for Animals with a chief complaint of being recumbent and unable to stand, poor suckling reflex, and discolored urine. Although the mare was 11 days past her expected due date, she had little udder development and milk production. In addition, the mare had retained placenta for 6-10 hours, and the placenta contained diffusely distributed abnormal red areas. On presentation, the foal was extremely depressed, unresponsive, and unable to stand. On physical examination, the foal appeared dehydrated, and a left sided systolic murmur was detected. The muscles were markedly firm to palpation, in special the gluteal muscles. Complete blood cell count (CBC), blood chemistry, acid-base status (ISAT), and urinalysis were performed and the following major problems were noted: neutrophilia with a left shift, mildly elevated packed cell volume, severe hyperkalemia, hyponatremia, hypochloremia, respiratory acidosis, azotemia, hyperglycemia, severely elevated muscle enzymes (CK and AST), and myoglobinuria. Thoracic and abdominal ultrasound examinations were unremarkable. Laboratorial tests for serum selenium and vitamin E levels, and whole blood glutathione-peroxidase (GSH-Px) activity were measured and indicated selenium deficiency. The primary problem list included white muscle disease, septicemia, and neonatal maladjustment syndrome. The foal was treated with fluid therapy, diuretics, broad-spectrum antibiotic therapy, selenium, vitamin E, nasogastric administration of milk, and gastric protectants.

Journal / Series

Senior seminar paper
Seminar SF610.1 2004 G674

Description

Senior seminar (D.V.M.) -- Cornell University, 2004. Includes bibliographical references (leaf (13)).

Sponsorship

Dr. Flaminio. Dr. Gardner, Dr. Figueiredo

Date Issued

2003-09-03

Keywords

Horses -- Diseases -- Case studies

Types

term paper