Muscle damage attributable to selenium (Se)/vitamin E deficiencies is known to develop at birth or later in lambs. The purpose of this study was to determine whether and when muscle damage develops in utero. Thirty pregnant ewes maintained on Se-deficient forages from birth were allotted to 3 equal groups. Half of each group was given a single IM injection of 0.056 mg of Se/kg of body weight, 1 month before parturition. At 3 weeks before parturition, cesarean section-derived fetuses from Se-deficient ewes did not have evidence of muscle damage. At 2 weeks before parturition, fetuses from Se-deficient ewes had biochemical evidence of congenital nutritional myopathy, as evidenced by low blood Se concentration (P < 0.05) and by increased plasma creatine kinase (P < 0.001) and lactate dehydrogenase (P < 0.01) activities, compared with fetuses from Se-treated ewes. Thus, for optimal protection of fetuses and newborn lambs in Se-deficient areas, Se should be administered to ewes at least 1 month before parturition.

We tested the hypothesis that lymphocytes from swine with susceptibility to malignant hyperthermia (MH) had calcium extrusion activity higher than unaffected swine. Cytoplasmic concentration of ionized calcium was determined by use of dual emission spectrofluorometry and measurement of the ratio of free to calcium-bound form of the fluorescent calcium dye indo-1. Net calcium accumulation and unidirectional calcium extrusion rate were dependent on intracellular calcium concentration. Calcium extrusion from calcium-loaded lymphocytes was monitored while calcium influx was inhibited by suspending the cells in calcium-free medium with a calcium chelator. Net calcium accumulation of untreated lymphocytes was monitored in calcium-replete medium. A novel method of calculation of ionized calcium was used. This method confirmed our previous findings of lower ionized calcium concentration (86 +/- 40 and 370 +/- 216 nmol/L; P < 0.01) and slower rates of calcium accumulation (39 +/- 16 and 127 +/- 52 nmol/L/min) in untreated lymphocytes from MH-susceptible swine compared with controls. These changes were attributable to calcium extrusion activity two- to three-fold higher in lymphocytes of MH-susceptible swine (154 +/- 36 and 408 +/- 47 nmol/L/min at 175 nmol/L; 972 +/- 111 and 1,690 +/- 505 nmol/L/min at 425 nmol/L). These data were compatible with our model of higher calcium extrusion activity being a compensatory adaptation of MH-susceptible swine lymphocytes to their hypersensitivity to stimuli that increase cytoplasmic calcium concentration.

Cell proliferation kinetic values were established for the hair root matrix of primary anagen follicles of 14 Beagles and 4 Cocker Spaniels with healthy skin and 9 Cocker Spaniels with primary idiopathic seborrhea. Indices were established by intradermal pulse labeling with tritiated thymidine, followed by cutaneous biopsy and autoradiography. The hair root matrix cell labeling index was 23.4 +/- 3.5% for Beagles, 24.4 +/- 4.0% for healthy Cocker Spaniels, and 24.9 +/- 4.3% for seborrheic Cocker Spaniels. These values indicate a rapidly proliferating cell population. Differences among these cell kinetic data for the 3 groups of dogs were not statistically significant. Although significant cell kinetic differences have been reported for other epidermal structures (interfollicular epithelium, upper hair follicle external root sheath, sebaceous glands) in seborrheic Cocker Spaniels, proliferation of hair root matrix cells apparently remains unaffected.

Effects of thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH) on plasma concentrations of thyroid hormones, and effects of ACTH and dexamethasone on plasma concentrations of cortisol, were studied in adult male ferrets. Thirteen ferrets were randomly assigned to test or control groups of eight and five animals, respectively. Combined (test + control groups) mean basal plasma thyroxine (T4) values were different between the TRH (1.81 +/- 0.41 microgram/dl, mean +/- SD) and TSH (2.69 +/- 0.87 microgram/dl) experiments, which were performed 2 months apart. Plasma T4 values significantly (P < 0.05) increased as early as 2 hours (3.37 +/- 1.10 microgram/dl) and remained high until 6 hours (3.45 +/- 0.86 microgram/dl) after IV injection of 1 IU of TSH/ferret. In contrast, IV injection of 500 microgram of TRH/ferret did not induce a significant increase until 6 hours (2.75 +/- 0.79) after injection, and induced side effects of hyperventilation, salivation, vomiting, and sedation. There was no significant increase in triiodothyronine (T3) values following TSH or TRH administration. Combined mean basal plasma cortisol values were not significantly different between ACTH stimulation (1.29 +/- 0.84 microgram/dl) and dexamethasone suppression test (0.74 +/- 0.56 microgram/dl) experiments. Intravenous injection of 0.5 IU of ACTH/ferret induced a significant increase in plasma cortisol concentrations by 30 minutes (5.26 +/- 1.21 microgram/dl), which persisted until 60 minutes (5.17 +/- 1.99 microgram/dl) after injection. Plasma cortisol values significantly decreased as early as 1 hour (0.41 +/- 0.13 microgram/dl), and had further decreased by 5 hours (0.26 +/- 0.15 microgram/dl) following IV injection of 0.2 mg of dexamethasone/ferret. These results indicate that IV injection of 1 IU of TSH/ferret is preferable to IV injection of 500 microgram of TRH/ferret for thyroid function testing in adult male ferrets. Results of this study also indicated that when TRH or TSH is used for the thyroid-stimulation test in male ferrets, plasma T4 concentrations, instead of T3, should be used as the indicator of thyroid response. Additionally, IV injection of 0.5 IU of ACTH and 0.2 mg of dexamethasone may be used in ferrets for the ACTH stimulation and dexamethasone-suppression tests, respectively.

Aminoglycoside nephrotoxicosis (AGNT) was induced in ewes by daily SC administration of gentamicin. Changes in urinary indices of renal function during the development of AGNT are reported. Measurements from timed, volume-measured urine samples were made on days 0, 7, and 8 and included creatinine clearance, total excretion (TE) rates of electrolytes (Na, K, Cl, P) and urine volume. Measurements from free-catch urine samples (without volume measurement) were made daily and included fractional excretion (FE) rate of electrolytes, urine osmolality, and urine-to-serum osmolality and urine-to-serum creatinine ratios. With the onset of AGNT, FE rates of Na, K, Cl, and P increased many fold above baseline values (200 X, 4 to 5 X, 6 to 9 X, and 70 to 95 X, respectively, on days 7 and 8), indicating decreased tubular reabsorption or increased tubular secretion. The increased FE rates were not representative of increases in total electrolyte excretion rates. The total excretion of Na (TE(Na)) was mildly increased, TE(K) was decreased, TE(Cl) was unchanged, and TE(P) was significantly increased on days 7 and 8. Abnormal urinalysis results, glucosuria, and increased FE(P) preceded appreciable increase in serum creatinine concentration. Other abnormal urinary indices of renal function coincided with or followed the increase in serum creatinine concentration. Urinary indices may help characterize renal function associated with the disease state, but did not provide early indication of AGNT.

T-cell-mediated and humoral immune responses were measured in chickens infected with standard and variant strains of infectious bursal disease virus. One-day-old and 3-week-old chickens were infected with these viruses and then given sheep RBC, killed Brucella abortus strain 19, and Newcastle disease virus. Appropriate serologic tests were used to monitor the primary and secondary responses to the antigens. Lymphoblast transformation assays were performed weekly. The response to the infectious bursal disease virus was determined by virus neutralization tests, microscopic examination of bursas, and bursal to body weight ratios. One-day-old chickens had T-cell-mediated and humoral immune suppression with both strains of virus, compared with controls. The lymphoblast transformation responses indicated that the variant strain was significantly (P < 0.05) more suppressive than the standard strain. Three-week-old chickens had humoral immune suppression with the standard strain, but not with the variant strain. The lymphoblast transformation response was transiently suppressed at this age by the variant strain only. During the first week of infection, 1-day-old and 3-week-old chickens had lower neutralizing antibody titers to the variant strain than to the standard strain.

The development of Anaplasma marginale was studied in Dermacentor andersoni nymphs after they had fed on a calf with ascending Anaplasma infection. Gut tissues were collected on day 4 of tick feeding, from newly replete (fed) nymphs and on postfeeding days (PFD) 5, 10, 15, 20, and were processed for light and electron microscopy to determine density of A marginale colonies. Homogenates of gut tissues were prepared from nymphs collected on the same days and inoculated into susceptible, splenectomized calves to test for infectivity. Anaplasma colonies were detected in gut cells on PFD 5, 10, 15, and 20. Although colony density appeared to be higher on PFD 10 and 15, differences were not significant. Nymphal type-1 colonies were detected in highest numbers on PFD 5 and 10, transitional colonies were seen in highest numbers at PFD 10 and 15, and nymphal type-2 colonies were observed only on PFD 20. Gut homogenates that were collected from ticks at 4 days of feeding, when newly replete, and on PFD 20 caused anaplasmosis when injected into susceptible calves, but homogenates made from ticks collected on PFD 5, 10, and 15 were not infective. The data indicate that of the colony types of A marginale that develop in replete nymphs, nymphal type-1 and transitional colonies may contain organisms that are not infective for cattle.

Brain stem auditory-evoked responses were recorded in 9 male and 11 female clinically normal mature dogs, weighing between 2 and 36 kg. Mean wave latency for the entire group of dogs, using 60-dB hearing level click stimuli at 11/s for waves I to VII was: 1.41, 2.21, 2.85, 3.31, 3.71, 5.12, and 6.46 ms, respectively. The mean interpeak latency for waves I and V (IPLIV) was 2.32 ms. Neither gender nor ear effect was detectable. Positive correlation was observed between cranium length, cranium width, nasion-external auditory meatus interval, and body weight for wave-V latency and IPLIV. Such correlation was not documented for wave I. The regression equations for their effects on IPLIV were: cranium length, y = 0.05x + 1.85; cranium width, y = 0.07x + 1.32; nasion-external auditory meatus interval, y = 0.05x + 1.79; and body weight, y =0.05x + 2.15. On the basis of any of the 3 variables of cranium size or body weight, the study population could be classified into groups of large and small dogs, with the large group having significantly (P < 0.05) longer latency for wave V and IPLIV. It is recommended that the effect of size variation in dogs on brain stem auditory-evoked responses should be compensated for by use of the regression equation based on cranium length.

Cartilage retention strengths of laryngoplasty prostheses were compared in larynges of 2-, 3-, and 4-year-old horses, using doubled polyester and expanded polytetrafluoroethylene prostheses. Bilateral laryngoplasties were performed on each of 15 (seven 2-year-old, two 3-year-old, and six 4-year-old) larynges, which were collected at an abbatoir. Prostheses were secured to a mechanical testing machine, and tension causing arytenoid cartilage abduction was applied, until total failure of the cartilage or prosthesis resulted. Tension caused cricoid cartilage failure in 1 specimen, and muscular process cartilage failure in the remainder. There was no significant effect of age, prosthetic material, or side of prosthesis placement on cartilage retention of the prostheses. Additionally, frequency of multiple load-displacement peaks, indicating partial muscular process failure, was not affected by age or prosthetic material variables.

A field strain (87-8363) of bovid herpesvirus-4 (BHV-4) isolated from an aborted bovine fetus was used to inoculate pregnant rabbits. Eleven rabbits in midgestation were alloted to 4 groups consisting of 3 infected groups and 1 control group. Rabbits were inoculated with BHV-4 or mock-infected cell culture preparations via IV, intravaginal, and intrauterine routes. Mild vulvovaginitis and endometritis were observed after intravaginal and IV inoculation of BHV-4, whereas intrauterine inoculation of BHV-4 resulted in abortion of hemorrhagic fetuses and nonsuppurative endometritis. Virus was successfully isolated from organ explants of fetal tissues. Rabbits seroconverted 1 week after infection as detected by results of an indirect immunofluorescence assay.