Gait Changes Vary among Horses with Naturally Occurring Osteoarthritis Following Intra-articular Administration of Autologous Platelet-Rich Plasma.

Mechanisms to reduce lameness associated with osteoarthritis (OA) are vital to equine health and performance. This study was designed to quantify response to autologous, intra-articular platelet-rich plasma (PRP) in horses with OA. Kinetic gait analysis was performed on 12 horses with unilateral forelimb lameness and OA in the same limb before and after intra-articular anesthesia (IAA). Radiographs and kinetic data were obtained before and 6 and 16 weeks after PRP administration to same joint, 4 weeks after IAA. Statistical evaluations included filtration effect on platelet concentration, relationship between kinetic variable changes after IAA versus PRP in the affected limb, and associations between response to PRP and response to IAA, platelet concentration, and radiographic OA. A positive response to IAA or PRP was defined as ≥5% improvement in peak vertical force, vertical impulse, or breaking impulse of the affected limb. Out of 10 horses that responded to IAA, 3 responded to PRP at both time points and 4 responded at one. Of the two horses that did not respond to IAA, one responded to PRP at both time points. Filtration increased platelet concentration significantly. The relationship between kinetic variable alterations of the affected limb after IAA and PRP was not significant, and response to PRP was not associated with response to IAA, platelet concentration, or radiographic OA. Changes in kinetic variables following IAA in joints with naturally occurring OA provide a custom standard to assess intra-articular therapy. Kinetic gait changes after intra-articular PRP are variable in horses with moderate to severe forelimb OA.

Intestinal bacterial overgrowth includes potential pathogens in the carbohydrate overload models of equine acute laminitis.

Carbohydrate overload models of equine acute laminitis are used to study the development of lameness. It is hypothesized that a diet-induced shift in cecal bacterial communities contributes to the development of the pro-inflammatory state that progresses to laminar failure. It is proposed that vasoactive amines, protease activators and endotoxin, all bacterial derived bioactive metabolites, play a role in disease development. Questions regarding the oral bioavailability of many of the bacterial derived bioactive metabolites remain. This study evaluates the possibility that a carbohydrate-induced overgrowth of potentially pathogenic cecal bacteria occurs and that bacterial translocation contributes toward the development of the pro-inflammatory state. Two groups of mixed-breed horses were used, those with laminitis induced by cornstarch (n=6) or oligofructan (n=6) and non-laminitic controls (n=8). Cecal fluid and tissue homogenates of extra-intestinal sites including the laminae were used to enumerate Gram-negative and -positive bacteria. Horses that developed Obel grade2 lameness, revealed a significant overgrowth of potentially pathogenic Gram-positive and Gram-negative intestinal bacteria within the cecal fluid. Although colonization of extra-intestinal sites with potentially pathogenic bacteria was not detected, results of this study indicate that cecal/colonic lymphadenopathy and eosinophilia develop in horses progressing to lameness. It is hypothesized that the pro-inflammatory state in carbohydrate overload models of equine acute laminitis is driven by an immune response to the rapid overgrowth of Gram-positive and Gram-negative cecal bacterial communities in the gut. Further equine research is indicated to study the immunological response, involving the lymphatic system that develops in the model.

Clenbuterol toxicosis in three Quarter Horse racehorses after administration of a compounded product.

CASE DESCRIPTION: 3 Quarter Horse racehorses were examined for suspected clenbuterol overdose 12 to 24 hours after administration by mouth of a compounded clenbuterol product. CLINICAL FINDINGS: All horses developed sinus tachycardia, muscle tremors, hyperhidrosis, and colic. Abnormalities on serum biochemical analysis included hyperglycemia, azotemia, and high creatine kinase activity. The presence of clenbuterol in the serum of all 3 horses and in the product administered was confirmed and quantified by use of liquid chromatography-electrospray tandem mass spectrometry. TREATMENT AND OUTCOME: Propranolol (0.01 mg/kg [0.005 mg/lb], IV) was administered to all 3 horses for antagonism of ß-adrenergic effects and caused a transient decrease in heart rate in all patients. All horses also received crystalloid fluids IV and other supportive treatment measures. Two horses were euthanatized (2 and 4 days after admission) because of complications. One horse recovered and was discharged 4 days after admission to the hospital. In the 2 nonsurviving horses, skeletal and cardiac muscle necrosis was evident at necropsy, and tissue clenbuterol concentrations were highest in the liver. CLINICAL RELEVANCE: Clenbuterol is a ß(2)-adrenergic receptor agonist licensed for veterinary use as a bronchodilator. At doses ≥ 10² µg/kg (4.5 µg/lb), in excess of those normally prescribed, ß-adrenergic stimulation by clenbuterol may cause sustained tachycardia, muscle tremors, hyperglycemia, and cardiac and skeletal muscle necrosis. Laminitis, acute renal failure, rhabdomyolysis, and cardiomyopathy were fatal complications associated with clenbuterol overdose in 2 horses in the present report. At the dose administered, propranolol was effective for short-term control of sinus tachycardia, but it did not alleviate all clinical signs in patients in the present report. These cases demonstrated the risks associated with the use of nonprescribed compounded medications for which the ingredients may be unknown.

Detection and comparison of nitric oxide in clinically healthy horses and those with naturally acquired strangulating large colon volvulus.

The objective of the study was to determine whether nitric oxide (NO) is present in clinically healthy horses (control) under basal conditions, and if it increases secondary to naturally acquired strangulating large colon volvulus (affected). Eleven affected horses and 10 controls were studied. Jugular venous blood, abdominal fluid, and urine were collected. The NO concentrations were standardized to the creatinine concentration in the respective samples. A biopsy specimen collected from the large colon pelvic flexure at surgery was divided into subsections for processing for inducible nitric synthase (iNOS) and nitrotyrosine (NT) immunohistochemical staining and reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemical staining. There were no significant differences in plasma, abdominal fluid, or urine NO concentrations between affected and control horses. There was a significant decrease in submucosal arteriolar and venular endothelium, submucosal plexus, mucosal leukocyte, mucosal and musclaris vasculature, and myenteric plexus NADPH diaphorase staining in affected versus control horses. There was a significant increase in iNOS staining in mucosal leukocytes and vasculature in affected versus control horses. Other than a greater number of positively stained mucosal leukocytes in affected horses, there were no significant differences between affected and control horses for NT staining. The presence of NADPH diaphorase staining in the endothelium and submucosal neurons suggests endothelial and neuronal NOS are present under basal conditions in the large colon of horses. Increased iNOS and NT staining in mucosal leukocytes of affected horses suggests involvement of the NO pathway in large colon volvulus. The reasons for the lack of a significant difference in plasma, abdominal fluid, and urine NO concentrations between affected and control horses are unknown.

Abomasal ulceration and abomaso-pleural fistula in an 11-month-old beefmaster bull.

An 11-month-old, beefmaster bull presented with anorexia and signs of respiratory disease. Physical examination, thoracic ultrasonography and radiography, and pleural fluid analysis indicated pericarditis and septic neutrophilic pleuropneumonia. Postmortem findings were abomasal adherence to the diaphragm, a fibrotic fistulous tract connecting the abomasum and pleural cavity, granulomatous abomasitis, granulomatous pericarditis, and fibrinonecrotic pleuritis.