Thymic hyperplasia causing right ventricular outflow tract compression following treatment for oesophageal rupture in an Arabian colt

True thymic hyperplasia has been reported sporadically in the human literature as an immunological rebound phenomenon following immunosuppressive treatment or disease. There are limited accounts in domestic species, mainly following vaccination, and thymic hyperplasia has not been a recognised condition in the horse to date. This report details a case of true thymic hyperplasia in a 10-week-old Arabian colt diagnosed by histopathology of core biopsy samples. The colt developed pulmonary stenosis caused by compression due to a space occupying lesion in the cranial mediastinum following a 3-month history of hospitalisation for treatment of traumatic oesophageal rupture with perioesophageal abscess formation. Diagnostic imaging of the cranial mediastinum was indicative of a thymic mass, and histopathology confirmed the mass was normal (hyperplastic) thymic tissue. The colt was treated with a tapering dose of corticosteroids, which led to involution of the hyperplastic tissue and resolution of pulmonary artery compression. Thymic hyperplasia may be an unrecognised sequela to chronic inflammation in horses and was only identified in this case when the size was sufficient to compress right cardiac outflow.     

Leukoencephalomalacia in a horse induced by fumonisin B1 isolated from Fusarium moniliforme

Each of two horses was dosed by stomach tube with culture material on maize of Fusarium moniliforme MRC 826. One horse developed severe hepatosis and mild oedema of the brain after 6 doses of 2.5 g of culture material/kg body mass/day in 7 days. The second horse, in a similar experiment but at a dosage rate of 1.25 g/kg/day, developed mild hepatosis and moderate oedema of the brain. In both animals the brain oedema was particularly noticeable in the medulla oblongata. The mycotoxin fumonisin B1 was extracted and purified from the culture material of F. moniliforme MRC, 826 which contained approximately 1 g/kg of this compound. A horse was injected intravenously 7 times from Day 0-Day 9 with 0.125 mg of fumonisin B1/kg body mass/day. Clinical signs of neurotoxicosis, which appeared on Day 8, included nervousness followed by apathy, a wide-based stance, trembling, ataxia, reluctance to move, paresis of the lower lip and tongue, and an inability to eat or drink. Euthanasia was performed on the horse on Day 10 while the animal was in a tetanic convulsion. The principal lesions were severe oedema of the brain and early, bilaterally symmetrical, focal necrosis in the medulla oblongata. This report provides experimental evidence that fumonisin B1, produced by F. moniliforme, causes equine leukoencephalomalacia.     

Computed tomographic morphology of the synovial invaginations of the distal sesamoid bone of the horse

The morphological features of the distal border synovial invaginations (SI) of the distal sesamoid bone (DSB) in horses were described by the use of computed tomography (CT). Transverse CT images were obtained on 50 cadaver forefeet from 25 Warmblood horses. Dorsal and sagittal planes were reformatted. The CT images allowed the evaluation of the number, shape, depth of penetration and direction of the SI into the bone. The total number of SI was 295 (mean 5.9). The number of invaginations in a particular DSB ranged from 3 (n = 3), 4 (n = 6), 5 (n = 11), 6 (n = 12), 7 (n = 13), 8 (n = 3), 9 (n = 1) to 11 (n = 1). The shape of the SI was 'conical' (n = 118), 'linear' (n = 109), 'lollipop' (n = 38) or 'branched' (n = 30). Penetration of the SI into the DSB was 'mild' in 195 cases, 'moderate' in 67 cases and 'deep' in 33 cases. The SI ran in a 'straight', 'dorsoproximal' and 'palmaroproximal' direction in 187, 28 and 80 cases, respectively. In only six DSBs, all SI ran in the same direction. The images obtained in this study may serve as reference for the radiographic evaluation of these SI.     

Study of osteogenesis in adult sheep on a high and a low calcium ration by means of fluorescing bone markers

The rate of osteogenesis was studied in 8 non-pregnant, non-lactating Friesian dairy sheep, 3–6 years old, by means of a treatment with 3 different bone seeking agents. Four sheep were fed a low calcium ration (LCa : 1.8 g Ca/d) and four other sheep a high calcium ration (HCa : 12.7 g Ca/d). The bone markers, oxytetracycline-HCl, alizarine-complexon and demeclocycline-HCl, were administred at intervals of 6 weeks, and the sheep were killed 1 week after administration of the last marker. In undecalcified cross sections from the middle of ribs 2, 10 and 12, and from the proximal and distal parts of rib 10, the numbers of labelled osteons and the number of osteons with 1, 2 or 3 markers were counted under fluorescent microscopy.In the ribs of sheep from the LCa group, the number of labelled osteons and the quantity of labels per osteon tended to be higher than those of sheep from the HCa group. When osteogenic activity was compared in the different sites of ribs analysed, lowest osteogenic activity was observed in the proximal part of the 10th rib.The use of fluorescing markers offers the possibility of studying osteogenic activity over a certain period of time in adult sheep.     

Familial non-rcd1 generalised retinal degeneration in Irish setters

Four Irish setters were diagnosed with bilateral retinal degeneration and cataracts at an age ranging from six to 11 years. In three of these dogs, progressive night blindness was reported from an age of eight to 11 years. In the fourth dog, aged six, no signs of visual impairment had been noticed. In all four dogs, the rod-cone dysplasia type 1 (rcd1) mutation was excluded as a cause, using an allele-specific PCR. From their three-generation pedigrees, a familial relationship was detected in three out of four dogs, which were also related to four additional Irish setter dogs with a history and clinical signs suggestive of late-onset progressive retinal degeneration. These results suggest the existence of a possibly hereditary, late-onset, progressive retinal atrophy in the Irish setter breed, that is distinct from rcd1.     

Veterinary school admission interviews, part 3: strategies for increasing interview validity

The veterinary school admission interview is a widely used selection tool, yet concerns persist about its reliability, validity, and cost. Relative to medicine, optometry, and dentistry schools, veterinary schools have been more likely to conduct panel interviews and to fix the interview's weight in selection decisions, strategies that increase interview validity. This article provides strategies for further increasing the veterinary school interview's validity. Interview reliability and validity studies point to key strategies the veterinary school admissions committee can implement before the interview: (1) establishing the interview's purpose(s); (2) conducting a "job" analysis to identify desirable candidate skills, knowledge, and attributes; (3) developing a structured and panel interview where interviewers, if possible, are blind to other admission data; (4) training interviewers; (5) setting a reasonable interview schedule; and (6) determining methods for analyzing applicant data. During the interview, interviewers should proceed through a structured series of steps: (1) open the interview with a specified agenda; (2) probe for information using structured questions and anchored rating scales; (3) close the interview to allow for candidate questions; and (4) evaluate the interview data. After the interview, the admissions committee should (1) analyze the interview data within and across interviewers and (2) analyze the data across all selection tools in order to assign relative weights to the selection tools.     

Inhibitory effects of the beta-adrenergic receptor agonist zilpaterol on the LPS-induced production of TNF-alpha in vitro and in vivo

In this study the anti-inflammatory properties of zilpaterol, a beta2-adrenergic receptor (AR) agonist specifically developed as a growth promoter in cattle were investigated. Although zilpaterol has a different structure compared with the beta2-AR agonists known to date, it was noted that it was able to bind to both the beta2-AR (Ki = 1.1 x 10(-6)) and the beta1-AR (Ki = 1.0 x 10(-5)). Using lipopolysaccharide (LPS)-exposed U937 macrophages, the production of cyclic adenosine-3',5'-cyclic monophosphate (cAMP) and tumor necrosis factor alpha (TNF-alpha) were investigated. Zilpaterol inhibited TNF-alpha release and induced intracellular cAMP levels in a dose-dependent manner. The inhibition of TNF-alpha release and induction of cAMP production was mainly mediated via the beta2-AR, as indicated by addition of beta1- and beta2-specific antagonists. The effects of zilpaterol were investigated in LPS-treated male Wistar rats after pretreatment with zilpaterol. Zilpaterol dosed at 500 microg/kg body weight reduced the TNF-alpha plasma levels. In conclusion, zilpaterol is a beta2-adrenergic agonist and an inhibitor of TNF-alpha production induced by LPS both in vivo and in vitro.