Jonathan H. Foreman

A multicenter, matched case-control study of risk factors for equine laminitis

Risk factors for equine laminitis were examined in a prospective case-control study of the 258 cases seen at six collaborating veterinary teaching hospitals over a 32-month period. Case-control pairs were matched on institution, clinician, and season of diagnosis. The 90% of case-control pairs (78 acute, 155 chronic) that had complete data for age, gender, and breed were used in separate conditional logistic-regression models for acute and chronic laminitis. There was an increase in risk for horses with acute laminitis from 5 to 7 years of age (OR 4.7, 95% CI 1.3-16) and from 13 to 31 years of age (OR 3.9, 95% CI 1.3-12) (both compared to <5 years); risk was increased for chronic laminitis from 10 to 14 years (OR 3, 95% CI 1.4-6.8) and from 15 to 38 years (OR 2.9, 95% CI 1.4-6.1) (both compared to <6 years). Mares - but not stallions - were more likely than geldings to develop acute laminitis (OR 2.6, 95% CI 1.1-6.2) and chronic laminitis (OR 2.0, 95% CI 1.1-3.6). In the small acute-laminitis data set, the breed variable was collapsed into three categories: Thoroughbred (THB, reference), the Quarter Horse (QH), and other (non-QH-THB). The non-QH-THB group was at increased risk of acute laminitis (OR 3.8, 95% CI 1.2-11.8). For the seven breed-group categories used in the chronic-laminitis model, however, all non-THB breed groups appeared significantly at risk as compared to the THB, with odds ratios ranging from 3.3 (95% CI 1.3-8.30) for the QH to 9.1 (95% CI 2.1-39.3) for ponies.

The Exhausted Horse Syndrome

Exhaustion occurs in most equestrian sports, but it is more frequent in events that require sustained endurance work such as endurance racing, three-day eventing, trial riding, and hunting. Exhaustion is also more likely when an unfit, unacclimatized, or unsound horse is exercised. Mechanisms that contribute to exhaustion include heat retention, fluid and electrolyte loss, acid-base imbalance, and intramuscular glycogen depletion. Clinical signs include elevated temperature, pulse, and respiratory rate; depression; anorexia; unwillingness to continue to exercise; dehydration; weakness; stiffness; hypovolemic shock; exertional myopathy; synchronous diaphragmatic flutter; atrial fibrillation; diarrhea; colic; and laminitis. Treatment includes stopping exercise; rapid cooling; rapid large volume intravenous or oral fluid administration; and nonsteroidal anti-inflammatory drug administration.

Neurologic abnormalities and cerebrospinal fluid changes in horses administered fumonisin B1 intravenously

The objective of this experiment was to characterize a dose-dependent toxic effect of fumonisin B1 (FB1) and to document initial neurologic signs, clinical progression, and terminal cerebrospinal fluid (CSF) changes in horses administered FB1 IV. Seventeen healthy horses were administered 0.00 (n = 4), 0.01 (n = 3), 0.05 (n = 3), 0.10 (n = 3), or 0.20 mg (n = 4) of purified FB1 IV q24h. When neurologic abnormalities observed by a masked observer became severe, atlanto-occipital CSF taps were performed and CSF pressure, cell count, cytology, protein, albumin and glucose concentrations, and creatine kinase activity were measured. Changes in CSF and number of days to 1st observation of neurologic abnormalities were compared between doses by ANOVA, with the level of significance set at P < .05. Control horses and low-dose horses (0.01 mg/kg) remained neurologically normal. In higher dose FB1-treated horses (n = 10), initial clinical signs (days 4-10) included hindlimb ataxia, delayed forelimb placing, and decreased tongue tone and movement. Hindlimb and trunkal ataxia, depression, hyperesthesia, and intermittent dementia gradually became apparent. When data from all horses with neurologic abnormalities were pooled (0.05-0.20 mg/kg FB1), mild clinical signs (mean day 6.3) occurred significantly earlier than did more severe (mean day 8.9) clinical signs (P = .009). Neurologic horses had high CSF protein, albumin, and IgG concentrations and increased albumin quotients (P < .05). It was concluded that FB1-induced neurologic and CSF changes in a dose-dependent manner, with a no-observable-limit of 0.01 mg FB1/kg IV q24h for 28 days. The neurologic and CSF changes were consistent with vasogenic cerebral edema.

Multicenter case-control study of signalment, diagnostic features, and outcome associated with cervical vertebral malformation-malarticulation in horses

OBJECTIVE To compare signalment of horses with cervical vertebral malformation-malarticulation (CVM) with that of control horses and to describe results of clinical examination, diagnostic imaging and necropsy findings, and reported outcome in horses with CVM. DESIGN Retrospective case-control study. ANIMALS 270 horses with CVM and 608 control horses admitted to 6 veterinary hospitals from 1992 through 2007. PROCEDURES Medical records of participating hospitals were reviewed to identify horses with CVM (ie, case horses) and contemporaneous control (non-CVM-affected) horses that were admitted for treatment. Signalment was compared between case horses and control horses. Results of clinical examination, laboratory and diagnostic imaging findings, necropsy results, and outcome were assessed for horses with CVM. RESULTS Case horses were younger (median age, 2 years) than were control horses (median age, 7 years). Thoroughbreds, warmbloods, and Tennessee Walking Horses were overrepresented in the CVM group. Gait asymmetry and cervical hyperesthesia were frequently detected in horses with CVM. Vertebral canal stenosis and articular process osteophytosis were commonly observed at necropsy; agreement between the results of radiographic or myelographic analysis and detection of lesions at necropsy was 65% to 71% and 67% to 78%, respectively. Of 263 horses with CVM for which outcome was recorded, 1 died and 172 (65.4%) were euthanatized. CONCLUSIONS AND CLINICAL RELEVANCE Odds of a diagnosis of CVM were greater in young horses and horses of specific breeds. Detection of gait asymmetry and cervical hyperesthesia were frequently reported in association with CVM. Accurate diagnosis of lesions associated with CVM by use of radiography and myelography can be challenging.

Lameness and heart rate elevation in the exercising horse

Summary Seven, healthy, conditioned, Quarter Horse mares with previous treadmill experience were each fitted with an adjustable heart bar shoe on the left front foot and a counterbalanced bar shoe on the right front foot. Three treatments were studied: sound, slightly lame, and obviously lame at a trot. Each subject performed one standardized exercise test (SET) daily on three consecutive days. Each subject underwent one treatment during a SET. Treatment order was randomly assigned. The SET consisted of a 5-rain exercise period at 3.2 m/sec on a treadmill at an 11% grade. Heart rate (HR) was determined at rest, 20 rain after the induction of lameness before the SET, during the last 30 sec of the SET, and at 0.5, 1, 2, 3, 4, 5, 10, 20, 30, 40, and 60 min postexercise. The Students paired t test was used to compare HR means for the three treatments at each monitoring interval. Heart rate was higher in slightly lame trials compared to sound trials as rest and at 0.5 through 10 and 30 through 60 min postexercise (P

Phenylbutazone and flunixin meglumine used singly or in combination in experimental lameness in horses

REASON FOR PERFORMING STUDY Using an adjustable heart bar shoe model of foot pain, the objective of this study was to test the hypothesis that the combined use of phenylbutazone (PBZ) and flunixin meglumine (FM) would prove more efficacious in alleviating lameness than either drug alone. MATERIALS AND METHODS One hour after induction of lameness at weekly intervals, 8 healthy adult Thoroughbred horses randomly underwent one of 4 i.v. treatments: saline (SAL) placebo (1 ml/45 kg bwt), PBZ (4.4 mg/kg bwt), FM (1.1 mg/kg bwt) or PBZ+FM (at the same dosages as given individually). Heart rate (HR) and lameness score (LS) responses were assessed in a blinded manner every 20 min for 5 h after lameness induction and then hourly for 12 h after treatment. Jugular venous blood samples were obtained at -1, 0, 0.05, 1, 2, 4, 6, 8, 10 and 12 h and subsequently analysed for drug concentrations. Repeated measures ANOVA and post hoc Tukeys test were used to identify analgesic effects at a significance level of P<0.05. RESULTS Heart rate was lower in all nonsteroidal anti-inflammatory drug (NSAID)-treated trials from 2 h to 10 h post treatment (P<0.05). Analgesic effects of FM and PBZ+FM, as evidenced by decreases in HR, lasted for 12 h post treatment (P<0.05). Lameness score decreased earlier in PBZ and PBZ+FM trials than in FM trials (P<0.05) and the analgesic effect on LS lasted for 12 h post treatment for all NSAID trials (P<0.05). Peak PBZ plasma concentration was 73.7 ± 6.0 and 77.9 ± 5.5 µg/ml. Peak FM concentration was 12.0 ± 0.8 and 13.7 ± 1.0 µg/ml. CONCLUSIONS It was concluded that the combination of PBZ+FM was not more effective than either PBZ or FM alone. These data do not support the hypothesis that the combination is more efficacious at these dosages than either drug alone in this model of acute foot pain.

Effects of single-dose intravenous phenylbutazone on experimentally induced, reversible lameness in the horse.

The objective was to test the hypothesis that phenylbutazone (PBZ) alleviates lameness in an adjustable heart bar shoe model of equine foot pain. Eight Quarter Horse mares underwent 4-weekly treatments randomly: 0.9% saline placebo (SAL: 1 mL/45 kg body weight i.v.) with no lameness; SAL with lameness; PBZ (4.4 mg/kg body weight i.v.) with no lameness; and PBZ with lameness. Blinded heart rate (HR) and lameness score (LS) were assessed every 20 min for 2 h and then hourly through 9 h. At 1 h SAL or PBZ was administered. Jugular venous samples were obtained at hours 0, 1, 2, 4, 6, and 8 and were evaluated for packed cell volume (PCV), cortisol, and drug concentrations. Repeated measures anova and t-tests were used to identify PBZ effects at a significance level of P<0.05. PBZ-treated LS was lower 2-8 h post-treatment, and HR was lower from 2 through 6 h post-treatment (P<0.05). Phenylbutazone did not change PCV and had minimal effect on cortisol. Mean plasma PBZ and oxyphenbutazone concentrations 7 h after treatment were 7.2-7.5 and 1.6-1.9 microg/mL, respectively. It was concluded that PBZ was efficacious in alleviating lameness in this model. Cortisol and PCV were not discriminating enough to distinguish between PBZ-treated and SAL-treated trials.

Necrotizing Mycotic Vasculitis with Cerebral Infarction Caused by Aspergillus niger in a Horse with Acute Typhlocolitis

An 18-year-old Morgan mare was presented to the Veterinary Medical Teaching Hospital, University of Illinois, with a 10-day history of watery diarrhea, depression, and dysphagia. On admission, the animal was severely dehydrated, depressed, and unable to swallow and had no clinical signs of diarrhea. The respiratory and heart rate and body temperature were within normal limits. Following fluid therapy, the mare developed severe watery diarrhea and continued to be depressed, incoordinated, and dysphagic. The animal died on the fourth day after admission and was sent to the Laboratories of Veterinary Diagnostic Medicine for necropsy. Gross postmortem findings were consistent with an acute cerebral infarction in the right cerebral hemisphere, an acute necrotizing typhlocolitis, multifocal petechial and ecchymotic hemorrhages, enlarged and congested pars intermedia of the pituitary gland, and marked bilateral adrenocortical hyperplasia with multifocal areas of necrosis and hemorrhage. Histologic evaluation of the affected brain demonstrated an area of coagulative necrosis of the gray matter, with hemorrhage, vasculitis, and thrombosis. There were many fungal hyphae 3.5–6.0 μm, pale basophilic, septate, and occasionally branching at 45° present in the arterial walls and throughout the necrotic tissue. Immunohistochemical analysis revealed Aspergillus niger as the etiologic agent responsible for the mycotic vasculitis and infarction in the brain. Bacteria culture and immunohistochemical staining of the colon and cecum failed to demonstrate specific pathogens.

Efficacy of single-dose intravenous phenylbutazone and flunixin meglumine before, during and after exercise in an experimental reversible model of foot lameness in horses.

REASONS FOR PERFORMING STUDY Objective blinded efficacy data during exercise are lacking on the use of single-dose i.v. nonsteroidal anti-inflammatory drugs (NSAIDs) before, during and after exercise. HYPOTHESIS Single i.v. doses of either phenylbutazone (PBZ) or flunixin meglumine (FM) would prove more efficacious than negative saline control (SAL) before, during and after exercise in a reversible model of foot lameness. METHODS Six Quarter Horse mares had lameness induced by tightening a set screw against a heart bar shoe 1 h prior to treatment. Randomised blinded treatments included PBZ (4.4 mg/kg bwt i.v.), FM (1.1 mg/kg bwt i.v.), and SAL (1 ml/45 kg i.v.). Heart rate and lameness score (LS) were recorded at rest; every 20 min after lameness induction for 5 h and at the end of 2 min treadmill workloads of 2 and 4 m/s. Heart rate was also recorded from 0.5-60 min post exercise. Results were compared using RM ANOVA and Student-Newman-Keuls test (HR) and Wilcoxon signed rank test (%ΔLS) with significance set at P < 0.05. RESULTS Pre-exercise mean HR was decreased for both NSAIDs compared to SAL from 1:20-4 h post treatment (P < 0.05). Pre-exercise mean %ΔLS was decreased for PBZ (1:20-4 h) and FM (1-4 h) compared to SAL (P < 0.01). With exercise, there were no HR differences between treatments (P > 0.05), but mean %ΔLS was decreased for both NSAIDs compared to SAL (P < 0.01). Mean recovery HR was decreased for PBZ and FM from 1-60 min compared to SAL (P < 0.05). CONCLUSIONS PBZ and FM demonstrated definitive clinical efficacy after single i.v. doses before, during and after exercise. Use of single i.v. doses during competition may mask lameness and may affect the ability of judges in determining the soundness of horses in competition.

Changes in blood gases and electrolytes of horses given varying doses of sodium bicarbonate

Summary Eight Quarter Horse mares, ranging in age from 5–15 years were used in a 4-week Latin-Square design experiment in which pairs of horses were given 0, 333, 666, or 1000 mg/Kg body weight of sodium bicarbonate (NaHCO 3 ) via nasogastric tube once weekly. Blood samples were drawn immediately before nasogastric intubation and then in one-hour increments for eight hours and once again at twenty-six hours after intubation. Blood pH, HCO 3 − , PCO 2 , and PO 2 and the serum electrolytes, Na + , K + , Cl − and Ca ++ were determined. Each treatment with NaHCO 3 produced an increase (p 3 − within two hours post-intubation, and an increase (p 2 within four hours. Peak mean values for pH, HCO 3 − , and PCO 2 were reached between four and six hours after intubation for all NaHCO 3 treatments and remained elevated through eight hours after intubation. Serum Na + was elevated (p + and Cl − were reduced (p 3 administration. All blood gas and serum electrolyte changes were found to return to near baseline levels by 26 hours after intubation. The fact that peak mean pH and HCO 3 − values were not reached until up to four hours after NaHCO 3 administration is important to consider when developing regulations for pre-race blood gas testing.