Application of admissions criteria to applicants with practice versus non-practice career goals in North American schools /colleges of veterinary medicine.

PURPOSE: The study was intended to determine whether North American veterinary schools/colleges apply admissions criteria differently to applicants with practice versus non-practice career goals. METHODOLOGY: A written questionnaire with seven queries on admissions criteria was sent to the associate deans for academic affairs at each of the 31 North American veterinary schools/colleges. RESULTS: Questionnaires were completed and returned by 25 of the 31 institutions. The responses were summarized and individual comments were compiled. For veterinary and animal experience, similar amounts but different types of experiences were acceptable to most institutions for applicants with practice versus non-practice career goals. The required pre-veterinary course work was not different for the two groups of applicants. The backgrounds of mentors providing written evaluations were often allowed to be different for the two groups of applicants. The responses expected in applicant interviews were different for the two groups for queries related to veterinary and career experiences and knowledge of specific career areas but were similar for various basic qualities and skills expected of all applicants. CONCLUSION: Although institutions vary, North American veterinary schools/colleges tend to apply admissions criteria differently to applicants with practice versus non-practice goals, except for pre-veterinary course requirements.

Suppressive effect of serum from pigs and dogs fed a diet deficient in vitamin E and selenium on lymphocyte proliferation.

The effect of sera collected from either pigs or dogs previously fed a vitamin E (vit E)- and selenium (Se)-deficient diet on in vitro lymphocyte blastogenesis response to mitogens was studied. Porcine sera were obtained from pigs used in 2 different trials. In I trial, 4-wk-old pigs received either a basal diet deficient in vit E and Se or the basal diet supplemented with Vit E, Se or Vit E and Se. Pigs were maintained on their respective diet for 25 d. Canine sera were collected from pups maintained on a deficient diet for 8 wk. Four dogs and 4 pigs maintained on a commercial diet were used as donors of peripheral blood lymphocytes (PBL). The addition of sera from pigs or dogs maintained on a vit E- and Se-deficient diet markedly suppressed both porcine and canine PBL response to mitogens. Porcine PBL blastogenesis was also suppressed when porcine or canine sera were added 8, 24 or 48 h after the beginning of the incubation period to culture containing 1% of fetal bovine serum (FBS). However, the suppressive effect caused by porcine sera was less severe than the one due to canine sera. Addition of 1% FBS in the cultures was sufficient to eliminate the suppression caused by the presence of sera from pigs fed a vit E- and Se-deficient diet. Other attempts to restore the lymphocyte response to mitogens by the addition of indomethacin, diethylcarbamazine or eicosatetraynoic acid, inhibitors of prostaglandin and/or leukotriene synthesis, were not successful. Because of the severe suppression caused by sera from animals maintained on a vit E- and Se-deficient diet on the in vitro response of lymphocytes to mitogenic stimulations, it is very important to take precautions to avoid such deficiency. In vivo suppression of immunocompetent cells to antigenic stimulations may impair the capacity of the host to control infections.

Etiologic factors and pathologic alterations in selenium-vitamin E deficiency and excess in animals and humans.

The etiology of selenium-vitamin E (Se-E) deficiency diseases may be complex. Many of the syndromes involve combined deficiency of selenium and vitamin E. Selenium moves into the animal and human food chain from soil and plants, which may contain inadequate amounts of the nutrient in many areas of the world. Vitamin E may be in low concentration in many animal feeds unless supplements are added. Some syndromes, such as steatitis in cats, result from an increased requirement of vitamin E in diets that contain large amounts of polyunsaturated fatty acids, and these diseases will only respond to vitamin E administration. Deficiency syndromes in animals owing to pure Se deficiency are infrequent and have been produced mainly by laboratory studies utilizing extreme deficiency conditions. Other factors that may affect the occurrence of these deficiency diseases are concurrent dietary deficiency of S-containing amino acids, bioavailability of different forms of dietary Se, intake of compounds that antagonize Se (e.g., silver salts), and exposure to various prooxidant substances (e.g., iron compounds, oxygen, ozone, and various drugs).

Serum chemistry alterations, including creatine kinase isoenzymes, in furazolidone toxicosis of ducklings: preliminary findings.

Furazolidone induces a cardiotoxicosis when fed in toxic concentrations to newly hatched ducklings. This preliminary experiment was designed to determine if creatine kinase (CK) isoenzymic activities or other serum analytes would be useful as indicators of these cardiac alterations. Sera from 12 ducklings (six fed a control ration and six fed the control ration with 700 mg furazolidone added per kg of feed [700 ppm] for 28 days) were analyzed for CK isoenzymic activities, electrolytes, nitrogenous metabolites, hepatic enzymic activities, bilirubin, and glucose. Statistically significant differences between control and treated groups were detected for creatine kinase MB (CK-MB, cardiac muscle origin) isoenzymic activity and bilirubin, potassium, calcium, and total carbon dioxide concentrations. Differences other than CK-MB isoenzymic activity were generally explained by factors related to the toxicosis or sample handling. These findings suggest that CK-MB isoenzymic activity may be useful to detect and monitor the progress of cardiac injury in furazolidone toxicosis, thereby increasing the usefulness of this model of dilated cardiomyopathy. Our findings, analyzed on the Kodak Ektachem 700 Dry Chemistry Analyzer, are compared with serum chemistry values reported in the literature.

Early clinical and morphologic alterations in the pathogenesis of furazolidone-induced toxicosis in ducklings.

Clinical and pathologic alterations during the development of furazolidone-induced toxicosis were investigated in a group of 35 newly hatched male Pekin ducklings fed a ration containing 700 mg of furazolidone/kg of feed for 27 days. A control group (n = 25) was fed the same ration without added furazolidone. Every 3 days, ducklings were weighted and palpated for ascites and 3 were chosen at random for euthanasia to determine the severity of lesions and to obtain hearts for gross measurements and ultrastructural study. Clinical alterations in treated ducklings consisted of decreased feed consumption with lower weight gain and nervous signs. Gross pathologic alterations included cardiomegaly with dilatation of all chambers and thinning of the myocardium, pericardial effusion, pulmonary edema and congestion, ascites, and testicular enlargement. Gross lesions were not observed before day 8. The earliest lesion (day 9) was cardiac chamber dilatation, with the left ventricle and left atrium most commonly and most severely dilated. Hearts from ducklings euthanatized on days 6, 12, 18, 24, and 27 were examined ultrastructurally. Myofibrillar lysis was first observed on day 12 in 1 duckling (of 3) and in at least 1 duckling from subsequent euthanasia periods. Myofibrillar lysis did not appear to be uniform among the cardiac chambers.

Reversibility of furazolidone-induced cardiotoxicosis in ducklings.

Furazolidone cardiotoxicosis was induced in 2 groups (FZ and FZ-CR groups) of newly hatched male Pekin ducklings (100/group) by feeding a ration containing 650 mg of furazolidone/kg of feed (ppm) for 28 days. A third group (control ration, CR group; n = 100) was fed the same ration without furazolidone. On day 28, the control ration was initiated for the FZ-CR group initially given the furazolidone-containing ration, to allow recovery from the effects of the drug, whereas ducklings of the FZ group continued to consume the furazolidone-containing ration. Biweekly, beginning with week 4, ducklings were euthanatized to assess severity of gross lesions and to obtain sections of myocardium for histologic and ultrastructural examination. Clinical evidence (increased weight gain, increased feed consumption, decreased mortality, reduced prevalence of palpable ascites) of regression of cardiotoxicosis of ducklings of the FZ-CR group was nearly complete by day 56 (28 days after cessation of furazolidone intake). Likewise, regression of gross lesions, as measured by overall prevalence of gross lesions, left ventricular volume, and ascites prevalence and severity, were also essentially complete by day 56. Myofibrillar lysis was not seen in sections from the heart (examined ultrastructurally) obtained from ducklings of the CR group that were euthanatized on day 28, 56, or 98. Myofibrillar lysis was detected in all ducklings (4/4) fed furazolidone (FZ and FZ-CR groups) and euthanatized on day 28. Myofibrillar lysis was not seen in the heart of ducklings of the FZ-CR group that were euthanatized on day 56 or 98. Myofibrillar lysis was detected in the heart from all ducklings of the FZ group that were euthanatized on day 56.(ABSTRACT TRUNCATED AT 250 WORDS)

Cellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.

The effects of dietary restriction of vitamin E (Vit E) and selenium (Se) on lymphocyte proliferation, natural killer (NK) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), and on burst respiratory response of stimulated granulocytes as measured by chemiluminescence (CL) were studied in pigs. Six male weanling pigs were maintained for 25 d on a torula yeast-based diet containing no measurable amount of alpha-tocopherol and less than .02 mg of Se per kilogram of feed. Six others received the same basal diet supplemented with 33 IU of DL-alpha-tocopheryl acetate and .2 mg of Se per kilogram of feed. All pigs were inoculated with Salmonella typhisuis on d 21 of the feeding period and killed on d 25. Tests to measure cellular immune functions were performed on cells isolated from blood samples taken on d 21 and 25. After 21 d of feeding, lymphocyte blastogenesis responses to phytohemagglutinin, concanavalin A, and pokeweed mitogen in pigs fed the Vit E- and Se-deficient diet were normal compared with the response in pigs fed the supplemented diet. Moreover, the cytotoxic activity of NK cells, the ADCC response, and the CL response of granulocytes were not affected. After 25 d, a marked suppression of lymphocyte response to mitogens occurred in pigs fed the Vit E- and Se-deficient diet when the cells were cultured in the presence of autologous serum. When fetal bovine serum replaced autologous serum in the cultures, no suppression was observed. No effect on NK activity and ADCC was observed, whereas the CL peak response of granulocytes tended to be higher in pigs fed the deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Ultrastructural alterations in furazolidone-induced cystic testicular degeneration in ducklings.

Cystic testicular degeneration was induced in groups of ducklings by feeding furazolidone at 250, 400, 550, or 750 mg per kilogram of feed (ppm) for 4 weeks. In normal ducklings, tall, columnar Sertoli cells predominated in the seminiferous epithelium. In treated ducklings, the mildest ultrastructural alteration was cytoplasmic vacuolation of Sertoli cells. In birds with more severely affected tubules, cytoplasmic vacuolation was more severe and the cells were cuboidal or rounded. The rounded cells desquamated into the tubular lumens, eventually undergoing cytolysis. In birds with the most severely affected tubules, only extensively flattened epithelial cells lined the extremely dilated seminiferous tubules. The interstitium was edematous and compacted between the expanded tubules. Many of the testicular ultrastructural alterations in furazolidone-intoxicated ducklings were similar to those described in the testicles of sodium-intoxicated cockerels.

Cystic testicular degeneration in furazolidone toxicosis of sexually immature ducks.

Cystic testicular tubular dilatation was seen in ducklings fed a ration containing furazolidone at 250, 400, 550, or 700 ppm for 28 days. Gross evidence of cystic testicular dilatation was observed at necropsy in 16% (32/203) of the ducklings that survived to the end of the study. Gross testicular lesions consisted of various degrees of enlargement with increased translucency in moderately to severely enlarged testicles. Histological evidence of cystic testicular dilatation was present in 45% (41/91) of the testicles examined. Histologically, the tubules were in various states of dilatation with attenuation of the seminiferous epithelium proportional to the severity of dilatation. In the most severely affected testicles, tubules were greatly dilated, distorted, and fluid-filled, with extensively flattened epithelium visible on the inner margin of the tubule as a thin rim of cytoplasm with a protuberant nucleus. Interstitial tissues were compressed to thin septa between the dilated tubules.

Furazolidone-induced injury in the isolated perfused chicken heart.

The Langendorff isolated heart preparation was adapted to determine the effect of furazolidone (0.5 and 2 micrograms/ml of perfusate) on hearts of 3-week-old broiler chickens. Following 115 minutes of perfusion, both concentrations of furazolidone caused approximately a two-fold increase in myocardial vascular resistance and a six-fold increase in lactate dehydrogenase release into the effluent fluid, compared with a control perfused group of isolated hearts (P less than 0.01). Ultrastructural alteration differences were not found between the drug-treated and control groups. It was concluded that: (i) furazolidone, at concentrations only moderately above therapeutic plasma concentrations, caused detrimental changes in myocardial vascular resistance and lactate dehydrogenase release and (ii) the isolated chicken heart preparation is an example of a cost-effective, reliable laboratory tool for screening potential cardiotoxins.

Effects of dexamethasone elution on tissue reaction around stimulating electrodes of endocardial pacing leads in dogs.

A pair of endocardial pacemaker leads, identical except for the presence or absence of dexamethasone elution from the distal stimulating electrode, was implanted into the right ventricle of each of 12 dogs for either 3 weeks (n = six pairs) or 6 weeks (n = six pairs). Fibrous connective tissue sheaths (0.04 to 0.20 mm thick) formed around the distal porous-surfaced stimulating electrodes because of proliferation of endocardial connective tissue and adherence and organization of thrombus. Connective tissue sheaths were composed of fibroblasts within an abundant collagen matrix and contained scattered macrophages, lymphocytes, plasma cells, and mast cells. Connective tissue sheaths around dexamethasone-eluting leads were thinner (p less than 0.03), less cellular (p less than 0.10), and had fewer mast cells (p less than 0.10) than corresponding nonsteroid leads. There was mild multifocal interstitial fibrosis, myofiber atrophy, and myofibrillar lysis in the adjacent myocardium. Thresholds for electrical stimulation of the myocardium were consistently lower for pacing leads with dexamethasone-eluting stimulating electrodes than for leads without dexamethasone.

Sequential ultrastructural changes of the pancreas in zinc toxicosis in ducklings.

The sequential ultrastructural alterations of the pancreas in zinc toxicosis were examined in ducklings fed 2500 ppm Zn (as ZnSO4) for 56 days. From days 3 to 17, acinar cells had cytoplasmic vacuoles that contained electron-dense, zymogen-like material and increased autophagocytosis. Other changes were swollen mitochondria and dilatation, vesiculation, degranulation and intracisternal sequestration of rough endoplasmic reticulum. Apoptosis was the predominant form of cell deletion. By day 10, acinar cellular atrophy and interstitial fibrosis were noted. Islets appeared normal. After day 19, the pancreas consisted of ductlike structures embedded in fibrous connective tissue with a minimal inflammatory cell response. These ductlike structures were lined by attenuated to cuboidal, atrophic acinar cells. Many cells contained granular, electron-dense cytoplasmic debris that served as a marker of previous cell damage. This ultrastructural study provides support for a previously proposed theory that ductlike structures (tubular complexes) arise by atrophy and dedifferentiation of acinar cells.

Paired comparisons of steroid-eluting and nonsteroid endocardial pacemaker leads in dogs: electrical performance and morphologic alterations.

The effects of steroid elution from endocardial pacemaker electrodes on electrical performance and the thickness and cellularity of the reactive fibrous connective tissue formed around the stimulating electrode (peri-electrode tissue) were determined. Comparison was made with a nonsteroid electrode implanted in the same cardiac chamber (right ventricle) in each of six dogs for 6 weeks. Paired Students' t-tests showed that steroid-eluting leads had significantly (P less than .05): (1) lower voltage stimulation thresholds (as determined in sequential measurements made on the conscious animals during the experiment and on the anesthetized dogs at termination of the study); (2) less fibrous connective tissue formation around the electrode surfaces; and (3) fewer cells per unit area of peri-electrode fibrous connective tissue. There were also fewer (P less than .10) mast cells in the reactive connective tissue surrounding steroid-eluting leads. The thinner reactive connective tissue surrounding the steroid-eluting electrodes was correlated with lower voltage stimulation thresholds (r = 0.7, P less than .01). This is consistent with the hypothesis that the effect of the peri-electrode connective tissue is to increase the virtual surface area of the electrode, decreasing current density in adjacent stimulatable tissue. The relatively fewer total cells and mast cells in the peri-electrode connective tissue of the steroid-eluting electrodes suggest that the observed differences in fibrous connective tissue thickness, and therefore voltage stimulation threshold, may be related to a relatively decreased population of inflammatory cells due to the anti-inflammatory properties of the steroid.

Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and/or vitamin E.

Modulation of acute monensin toxicosis in swine was evaluated in 2 studies. In study 1, 56 weanling male pigs were allotted to 14 groups of 4 each. Pigs in 7 groups were given tiamulin in the drinking water (to supply 7.7 mg/kg of body weight/day) for 3 days before and for 2 days after monensin administration. Monensin was given as a single oral dose (at 0, 7.5, 15, 25, 50, 75, or 100 mg/kg) to pigs in groups with or without tiamulin exposure. Prominent acute clinical signs of monensin toxicosis (hypermetria, hind limb ataxia, paresis, knuckling of hind limbs, and recumbency) developed by 2 to 6 hours after dosing in pigs given 15 or 25 mg of monensin/kg with tiamulin exposure, but not in pigs given the 15 or 25 mg of monensin/kg without tiamulin exposure. Also, the extent of monensin-induced skeletal muscle damage at 4 days after monensin dosing was enhanced in pigs given 7.5, 15, or 25 mg of monensin/kg and exposed to tiamulin. In study 2, 48 weanling male pigs were allotted to 8 groups of 6 each. Four groups of pigs were given 20 mg of monensin/kg orally, and 4 groups were given 100 mg of monensin/kg orally. For each monensin dose, a group was treated 24 hours before monensin administration with (i) selenium (Se)-vitamin E preparation, 0.25 mg of Se and 68 IU of d-alpha-tocopheryl acetate (vitamin E)/kg, IM; (ii) vitamin E only, 68 IU of d-alpha-tocopheryl acetate/kg; (iii) Se only, 0.25 mg of Se/kg; or (iv) vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Furazolidone-associated cardiomyopathy in two Indiana flocks of ducklings.

Furazolidone (FZ)-induced congestive cardiomyopathy was diagnosed as the cause of high mortality and unthriftiness in two flocks of white pekin ducklings. Cumulative mortality at 7 weeks of age was 10.0-14.4%. Samples of FZ-supplemented feeds fed to flocks 1 and 2 from day 1 to day 14 had 140 and 150 mg FZ/kg, respectively. Both flocks had various degrees of water restriction. Clinically, the ducklings had dyspnea, incoordination, and abdominal distention. Necropsy findings included pulmonary edema and congestion, ascites, atrophic congested livers covered with sheets of fibrin, and cardiac enlargement with biventricular dilatation. Cardiac alterations were minimal by light microscopy. Ultrastructurally, scattered myocytes had myofibrillar lysis. These outbreaks occurred following intake of FZ at therapeutic dosages and emphasize the high susceptibility of young ducklings to FZ cardiotoxicity.

Ultrastructural changes in inherited cardiac calcinosis of DBA/2 mice.

Cardiac dystrophic calcinosis, an inherited condition in DBA/2 mice, produced extensive calcific lesions in the right ventricular myoepicardium of affected mice. The morphogenesis of the cardiac alterations was evaluated by microscopic and ultrastructural studies. The initial event was necrosis and mineralization of subepicardial myocytes. Mineral deposits were seen as dense granular and spicular deposits in mitochondria only, mitochondria and adjacent sarcoplasm, or the entire sarcoplasm in necrotic myocytes. In mature myoepicardial calcific lesions, the remnants of necrotic myocytes were seen as scattered dense masses of mineralized debris with surrounding fibroplasia and occasional macrophages and giant cells. Male weanling DBA/2 mice (n = 135) were fed either a commercial diet adequate in selenium-vitamin E (Se-E) content, or a basal semipurified Se-E-deficient diet with or without silver acetate for 15, 20 or 25 weeks. Cardiac calcinosis severity seemed to increase in mice which developed concurrent Se-E deficiency. Cardiac calcinosis in the DBA/2 mouse is a useful model of cardiac calcification.

Myocardial diseases of animals.

In this review we have attempted a comprehensive compilation of the cardiac morphologic changes that occur in spontaneous and experimental myocardial diseases of animals. Our coverage addresses diseases of mammals and birds and includes these diseases found in both domesticated and wild animals. A similar review of the myocardial diseases in this broad range of animal species has not been attempted previously. We have summarized and illustrated the gross, microscopic, and ultrastructural alterations for these myocardial diseases; and, whenever possible, we have reviewed their biochemical pathogenesis. We have arranged the myocardial diseases for presentation and discussion according to an etiologic classification with seven categories. These include a group of idiopathic or primary cardiomyopathies recognized in man (hypertrophic, dilated, and restrictive types) and a large group of secondary cardiomyopathies with known causes, such as inherited tendency; nutritional deficiency; toxicity; physical injury and shock; endocrine disorders, and myocarditides of viral, bacterial, and protozoal causation. Considerable overlap exists between each of the etiologic groups in the spectrum of pathologic alterations seen in the myocardium. These include various degenerative changes, myocyte necrosis, and inflammatory lesions. However, some diseases show rather characteristic myocardial alterations such as vacuolar degeneration in anthracycline cardiotoxicity, myofibrillar lysis in furazolidone cardiotoxicity, calcification in calcinosis of mice, glycogen accumulation in the glycogenoses, lipofuscinosis in cattle, fatty degeneration in erucic acid cardiotoxicity, myofiber disarray in hypertrophic cardiomyopathy, and lymphocytic inflammation with inclusion bodies in canine parvoviral myocarditis. The myocardial diseases represent the largest group in the spectrum of spontaneous cardiac diseases of animals. Pericardial and endocardial diseases and congential cardiac diseases are seen less frequently; and, in contrast to man, coronary artery disease and myocardial ischemia are rather infrequent in animals. The present review shows clearly that the spectrum of myocardial diseases in animals is enlarging and that many newly recognized diseases are emerging and assuming considerable importance. For example, various heritable cardiomyopathies have recently been described in the KK mouse, cattle, and rats. Increasingly recognized myocardial diseases include cardiomyopathies in cats, dogs, and birds; anthracycline cardiotoxicity; furazolidone cardiotoxicity; ionophore cardiotoxicity; myocardial damage associated with central nervous system injuries; myocardial hypertrophy in

Myocardial ultrastructural alterations in ducklings with isoproterenol-induced cardiotoxicosis.

Fifty-two, 8-week-old, male White Pekin ducklings (Anas platyrhynchos domesticus) were allotted into control (n = 7) and isoproterenol-injected groups (n = 45). One control duck and 5 to 7 isoproterenol-injected (200 mg/kg of body weight) ducklings were euthanatized at postinjection hours (PIH) 1, 12, and 24 and at postinjection days (PID) 2, 4, 7, and 14. The left ventricular myocardium was examined, using electron microscopy. The earliest ultrastructural alteration in damaged myocytes was myofibrillar lysis at PIH 12. At PIH 24, affected myocytes had necrosis with mineralization of mitochondria. By PID 2, macrophages had invaded into areas of myocardial necrosis, mineralization was prominent in myocyte mitochondria, and dedifferentiated myocytes with reduced numbers of myofibrils, increased numbers of polysomes, large nuclei, and prominent nucleoli were first observed. The primary myocardial finding at PID 4, 7, and 14 was 2 populations of sublethally damaged myocytes. One population of injured myocytes had numerous polysomes in the sarcoplasm and large nuclei with prominent nucleoli, indicating attempts at repair of myofibrillar damage. The 2nd population of myocytes with myofibrillar lysis did not have morphologic evidence of myofibrillar repair. Therefore, the sequential ultrastructural alterations of damage and repair induced by isoproterenol in the duckling myocardium provided model for comparative studies of cardiotoxicity.