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  • Author or Editor: P. G. Todhunter x
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Objective—To determine the clinical characteristics and outcome of foals with septic osteitis of the distal phalanx.

Design—Retrospective case series.

Animals—22 foals.

Procedures—Information obtained from medical records included signalment; clinical, laboratory, and radiographic findings; treatment method; and outcome. Foals included in the study had lameness referable to the foot, radiographic evidence of localized lysis or focal loss of bone density of the distal phalanx, and suppurative discharge or necrosis of the affected bone evident at surgery. Foals with a history or evidence of penetrating wounds or subsolar abscessation were excluded.

Results—Mean age of foals at initial evaluation was 40.8 days (range, 3 to 122 days). Twenty-one (95%) foals had lameness as the primary complaint. Lesions consistent with septic osteitis of the distal phalanx localized to specific areas of the bone on the basis of radiographic and surgical findings were located on the solar margin or toe (14/22 [64%]), extensor process (5/22 [23%]), and palmar or plantar process (3/22 [13%]). Hind limbs (18/26 [69%] affected limbs) were more frequently affected. Two foals had > 1 affected limb, 2 had additional sites of osteomyelitis, and 4 had concurrent septic arthritis. Surgical debridement and regional antimicrobial perfusion were performed during general anesthesia. Extensor process lesions were not debrided. Nineteen of 22 (86%) foals survived to be discharged from hospital, and 16 horses reached racing age. Eleven of 16 had race starts, of which 8 had official race starts and 3 had unofficial race starts.

Conclusions and Clinical Relevance—Septic osteitis of the distal phalanx should be considered as a source of lameness in foals with signs referable to the foot and does not necessarily preclude a career in racing. Although infection may occur secondary to bacterial penetration of the hoof or sole, the distal phalanx should also be considered as a potential site for hematogenous septic arthritis or osteomyelitis in foals.

Full access
in Journal of the American Veterinary Medical Association



To use lipopolysaccharide (LPS) to create synovitis in the midcarpal joint of ponies, and to assess the morphologic, histochemical, and immunohistochemical effects of synovitis on articular cartilage of the third carpal bone.


2- to 3-year-old ponies, 6 control (group 1) and 6 treated (group 2).


Synovitis was induced in 1 midcarpal joint of group-2 ponies by intra-articular injections of LPS (0.02 μg/kg of body weight), morphine (0.1 mg/kg), and saline solution (group 2a) and morphine and saline solution alone in the contralateral midcarpal joint (group 2b). Articular cartilage sections and attached synovial membrane from the third carpal bones were examined by immunohistochemical distribution of interleukin 1β, tumor necrosis factor (TNF)-α, TNF receptors (P55, P75) and 3-B-3(–) epitopes, and by localization of proteoglycans (metachromatic staining). Proteoglycan extracts were assessed by metachromatic staining or western blotting and immunohistochemical staining, using anti-3-B-3 antibodies.


Enhanced immunoreactivity for the cytokines and receptors was found in inflamed synovial membrane and noncalcified cartilage (group 2a more than 2b). Metachromasia of the noncalcified cartilage was greater in group-1 than in group-2a and group-2b specimens. In group 2a, chondrocyte hypertrophy and enhanced immunoreactivity for 3-B-3(–) epitope in areas of increased cytokine immunoreactivity suggested possible phenotypic change of the chondrocytes in response to synovitis. Immunohistochemical analysis by western blotting of proteoglycan extracts indicated strong 3-B-3(–) epitope immunolocalization in group-2a, weaker staining in group-2b, and barely detectable stain in group-1 specimens, which correlated with in situ immunolocalization.


Intra-articular administration of LPS may be used to induce a synovial environment conducive to increased immunoreactivity of interleukin 1β, TNF-α, and its receptors in equine synovial membrane and articular cartilage. These cytokines may be involved in the early phenotypic change of chondrocytes that is believed to occur in osteoarthritis and is characterized in this study by enhanced 3-B-3(–) epitope immunoreactivity and chondrocyte hypertrophy. (Am J Vet Res 1996;57:1080–1093)

Free access
in American Journal of Veterinary Research


Objective—To determine whether a mutation in the fibrillin 2 gene (FBN2) is associated with canine hip dysplasia (CHD) and osteoarthritis in dogs.

Animals—-1,551 dogs.

Procedures—Hip conformation was measured radiographically. The FBN2 was sequenced from genomic DNA of 21 Labrador Retrievers and 2 Greyhounds, and a haplotype in intron 30 of FBN2 was sequenced in 90 additional Labrador Retrievers and 143 dogs of 6 other breeds. Steady-state values of FBN2 mRNA and control genes were measured in hip joint tissues of fourteen 8-month-old Labrador Retriever–Greyhound crossbreeds.

Results—The Labrador Retrievers homozygous for a 10-bp deletion haplotype in intron 30 of FBN2 had significantly worse CHD as measured via higher distraction index and extended-hip joint radiograph score and a lower Norberg angle and dorsolateral subluxation score. Among 143 dogs of 6 other breeds, those homozygous for the same deletion haplotype also had significantly worse radiographic CHD. Among the 14 crossbred dogs, as the dorsolateral subluxation score decreased, the capsular FBN2 mRNA increased significantly. Those dogs with incipient hip joint osteoarthritis had significantly increased capsular FBN2 mRNA, compared with those dogs without osteoarthritis. Dogs homozygous for the FBN2 deletion haplotype had significantly less FBN2 mRNA in their femoral head articular cartilage.

Conclusions and Clinical Relevance—The FBN2 deletion haplotype was associated with CHD. Capsular gene expression of FBN2 was confounded by incipient secondary osteoarthritis in dysplastic hip joints. Genes influencing complex traits in dogs can be identified by genome-wide screening, fine mapping, and candidate gene screening.

Full access
in American Journal of Veterinary Research


Nine dairy herds (mean size, 149 cows) with bulk-tank milk somatic cell counts of < 300,000 cells/ml and > 80% of cows with Dairy Herd Improvement Association linear somatic cell counts ≤ 4 were selected for study. Each herd was monitored for 12 consecutive months. Duplicate quarter-milk specimens were collected from each cow for bacteriologic culturing at beginning of lactation, cessation of lactation, and at the time of each clinical episode of mastitis. Streptococcus agalactiae was never isolated and Staphylococcus aureus was isolated from < 1% of all quarters. There were 554 episodes of clinical mastitis. During the year of study, the incidence rate of clinical mastitis varied from 15.6 to 63.7% of cows among the 9 herds. Mean costs per cow per year in herd for mastitis prevention were: $10 for paper towels, $3 for nonlactating cow treatment, and $10 for teat disinfectants. Mean cost associated with clinical mastitis was $107/episode. Approximately 84% ($90) of the costs attributed to a clinical episode were associated with decreased milk production and nonsalable milk. Costs of medication and professional veterinary fees per clinical episode varied Significantly among the 9 herds. Three of the herds did not have a veterinarian treat a clinical episode of mastitis during the year of study even though 2 of these herds had the first and third highest incidence rates of clinical mastitis. When calculated on a per cow in herd basis, mean costs of $40/cow/year were attributed to clinical mastitis. Our findings suggest that herds that have effectively controlled mastitis caused by contagious pathogens may still have substantial economic losses as a result of clinical mastitis and that losses and even rates of clinical mastitis may vary considerably among such herds.

Free access
in Journal of the American Veterinary Medical Association