title: Equine laminitis: ultrastructural lesions detected 24-30 hours after induction with oligofructose.
abstract: BACKGROUND
  The pathology of equine laminitis has been well-documented 48 h after dosing with oligofructose when clinical lameness and lamellar disintegration is well advanced. Further analysis of the earliest lesions, by collecting lamellar samples at the first sign of foot lameness after oligofructose dosing is required in order to increase understanding of the disease.
  
  
  OBJECTIVE
  To investigate lamellar epidermal hemidesmosome damage and basement membrane dysadhesion by transmission electron microscopy (TEM).
  
  
  METHODS
  Eight clinically normal, mature Standardbred horses were divided randomly into 2 groups of 4. The treatment group were dosed with oligofructose (10 g/kg bwt) and subjected to euthanasia when shifting weight from one foot to other commenced and at the first sign of lameness during walking and turning. This occurred at 24 h in 3 horses and 30 h in one. The sham treatment control group were dosed with water and subjected to euthanasia after 48 h. Lamellar tissues of the front feet were harvested and processed for ultrastructural study using TEM.
  
  
  RESULTS
  Examination by TEM showed excessive waviness of the basement membrane zone and pointed tips of some secondary epidermal lamellae, an ultrastructural lesion typical of laminitis. The average number of hemidesmosomes/microm of basement membrane was decreased and their distance from the centre of the lamina densa of the basement membrane was increased.
  
  
  CONCLUSIONS
  Laminitis lesions are detectable 24 h after oligofructose administration.
  
  
  CONCLUSIONS
  Hindgut events occurring in the first 24 h after dosing have begun the destruction of the hoof lamellar interface. Prevention and treatment strategies should precede lameness if they are to be efficacious.
authors.affiliation: Australian Equine Laminitis Research Unit, School of Veterinary Science, The University of Queensland, Brisbane, 4072 Queensland, Australia.
authors.forename: A R
authors.initials: AR
authors.lastname: Nourian
authors.forename: G I
authors.initials: GI
authors.lastname: Baldwin
authors.forename: A W
authors.initials: AW
authors.lastname: van Eps
authors.forename: C C
authors.initials: CC
authors.lastname: Pollitt
mesh_terms: D000818:Animals; D001485:Basement Membrane / Q000187:drug effects / Q000648:ultrastructure; D005260:Female; D005534:Foot Diseases / Q000139:chemically induced / Q000473:pathology / Q000662:veterinary*; D022002:Hemidesmosomes / Q000187:drug effects / Q000648:ultrastructure; D006724:Hoof and Claw / Q000473:pathology / Q000648:ultrastructure*; D006734:Horse Diseases / Q000139:chemically induced / Q000473:pathology*; D006736:Horses; D007794:Lameness, Animal / Q000139:chemically induced / Q000473:pathology*; D008297:Male; D046529:Microscopy, Electron, Transmission / Q000379:methods / Q000662:veterinary; D009844:Oligosaccharides / Q000494:pharmacology*; D012720:Severity of Illness Index
chemical_list: D009844:Oligosaccharides; C120489:oligofructose