The association between ocular squamous cell tumors and various measures of solar radiation was evaluated for 2,775 contemporaneous Hereford cattle. The animals were from 34 herds located in 21 states in the United States and in one Canadian province. Examinations and photographs were made of the eyes of all cows and heifers in a herd; 33 herds were examined between June and August 1957 and 1 herd was examined in 1958. Solar radiation was measured by altitude and mean annual hours of sunshine applying to an individual herd, and global radiation, a cloudiness index, and elevation of nearby National Weather Service stations. All measures of solar radiation provided evidence of a significant association between increasing risks of developing cancer eye and increasing levels of radiation; adjustments were made for possible confounding effects of age and corneoscleral pigmentation. Associations were evident whether affliction was defined as the occurrence of any type of tumor (ie, plaque, papilloma, or carcinoma), or as the occurrence of only papilloma or carcinoma. Average ages of affected cattle also tended to be lower at high radiation levels than at low levels, further supporting the hypothesis that solar radiation has an important role in the development of this disease. In view of the heritability of eye pigmentation and its inhibitory effect on lesions, cancer eye may be controlled by selective breeding for increased pigmentation in and around the eye to afford protection against the harmful effects of incident UV radiation.

Sodium hyaluronate reduces adhesions after tendon repair in rodents and dogs, and has been used in limited clinical trials in people. To evaluate its effect on tendon healing and adhesion formation in horses and to compare these effects with those of a compound of similar viscoelastic properties, a study was performed in horses, using a model of collagenase injection in the flexor tendons within the digital sheath. Eight clinically normal horses were randomly allotted to 2 groups. Adhesion formation between the deep digital flexor tendon and the tendon sheath at the pastern region was induced in the forelimbs of all horses. Using tenoscopic control, a 20-gauge needle was inserted into the deep digital flexor tendon of horses under general anesthesia and 0.2 ml of collagenase (2.5 mg/ml) was injected. The procedure was repeated proximally at 2 other sites, spaced 1.5 cm apart. A biopsy forceps was introduced, and a 5-mm tendon defect was created at each injection site. Group-A horses had 120 mg of sodium hyaluronate (NaHA) gel injected into the tendon sheath of one limb. Group-B horses had methylcellulose gel injected at the same sites. The contralateral limbs of horses in both groups served as surgical, but noninjected, controls. Horses were euthanatized after 8 weeks of stall rest. Ultrasonographic evaluation revealed improved tendon healing after NaHA injection, but no difference in peritendinous adhesion formation. Tendon sheath fluid volume and hyaluronic acid (HA) content were greater in NaHA-treated limbs. Gross pathologic examination revealed considerably fewer and smaller adhesions when limbs were treated with NaHA. However, significant difference in pull-out strengths was not evident between NaHA-treated and control limbs. Histologically, the deep digital flexor tendon from the NaHA-treated limbs had reduced inflammatory cell infiltration, improved tendon structure, and less intratendinous hemorrhage. Treatment with methylcellulose had no significant effect on tendon healing, adhesion size, quantity, or strength or on the volume and composition of the tendon sheath fluid. Sodium hyaluronate, administered intrathecally, appears to have a pharmaceutically beneficial action in this collagenase-induced tendinitis and adhesion model in horses.

Sublethal irradiation of BALB/c mice 4 hours prior to inoculation with 5 X 10(4) virulent Brucella abortus, caused significant (P < 0.01) reductions in bacterial numbers in comparison with numbers in unirradiated controls. Numbers of brucellae in the spleen were significantly lower by 5 days after inoculation and decreased thereafter, so that at 2 and 3 weeks after inoculation, there were up to 1,000-fold fewer organisms in the spleen of irradiated mice. The number of brucellae in the spleen increased in irradiated mice thereafter. The course of events in the liver was similar, but developed more slowly, and peak differences in bacterial numbers were about 1 log less. These phenomena were not attributable to differences in implantation of brucellae in the liver or spleen, nor to an abnormal distribution of organisms in other organs of irradiated mice. Irradiation of mice during the plateau phase of infection also resulted in significant (P < 0.05) reductions in bacterial counts in the spleen during the succeeding 4 weeks. Macrophage activation in the spleen, measured by a Listeria monocytogenes-killing assay, was significantly (P < 0.01) increased by irradiation alone at 1 week after inoculation and at that time was significantly (P < 0.01) greater in B abortus-infected, irradiated mice than in B abortus-infected controls. Histologic, cytologic, and immunologic studies revealed that the decrease in numbers of organisms between 1 and 2 weeks after inoculation in irradiated mice occurred at a time when their immune response to B abortus was suppressed and when numbers of neutrophils and monocytes infiltrating the spleen were significantly (P < 0.01) diminished. The increase in numbers of B abortus in organs of irradiated mice that began after the third week coincided with recovery of the immune response and an increase in numbers of neutrophils and monocytes in the infected organs. The course of B abortus infection was not substantially altered during the first 11 days after inoculation in mice infected at the height of a profound monocytopenia and neutropenia induced by azathioprine, a drug that by itself failed to activate macrophages. We hypothesized that, in irradiated mice, a rapid radiation-induced activation of resident macrophages to a brucellacidal state was coupled with an absence of newly formed monocytes in which virulent strains of B abortus could establish persistent infection, and that as susceptible monocytes emerged in mice recovering from the effects of irradiation, chronic infection became established.

Plasma concentrations of porcine growth hormone (PGH) were similar in healthy pigs and those with atrophic rhinitis (AR), therefore, observed reduced growth rates and feed efficiency in naturally infected pigs with AR were not attributed to low concentrations of plasma PGH. Also, pituitary glands in both groups of pigs were responsive to growth hormone-releasing hormone (GHRH) challenge by increasing PGH secretion. Administration of clonidine hydrochloride to pigs naturally infected with AR failed to elicit any significant change (5.3 +/- 1.4 ng/ml) in the plasma concentration of PGH within a 45-minute bleeding interval. The pretreatment concentrations of PGH were similar in specific-pathogen-free toxin-treated and specific-pathogen-free control groups, but they increased significantly in toxin-treated pigs (20.7 +/- 8.2 ng/ml) within 15 minutes after GHRH injection. Porcine growth hormone release in toxin-treated pigs was variable; however, all pigs did not respond to GHRH administration: 3 responded with an increase in PGH release (35.6 +/- 10.6 ng/ml), 2 did not respond (6.7 +/- 0.5 ng/ml), and 1 had a decrease in PGH release (3.9 ng/ml). Therefore, the observed reduced growth rates reported in the literature may be attributed to factors at the target level of PGH action, such as insufficient or down-regulation of PGH receptors, changes or impaired ability in the PGH receptor-binding characteristics, and inability of PGH receptor complex to transduce signal. Toxins are known to modulate signal transduction pathways. It has been speculated that serotype-D Pasteurella multocida toxin may influence growth by its effect on signal transduction from PGH receptor complex on the cell membrane to the interior of the cell. This would account for the presence of high concentrations of PGH in the plasma and a functionally competent hypophysis cerebri, which responded to GHRH injection that have retarded growth in pigs affected with AR.

A reliable bovine viral diarrhea (BVD) viral antigen was prepared from BVD virus grown on Madin Darby bovine kidney (MDBK) cells by solubilizing the virus with detergent MEGA-10 (decanoyl-N-methylglucamide) followed by removal of hydrophobic proteins with Triton X-100 treatment. By these treatments, problems of high background associated with BVD viral antigen in the enzyme-linked immunosorbent assay (ELISA) were eliminated. With this new antigen, an ELISA was adapted to detect bovine serum antibody against BVD virus. The diagnostic specificity of the assay in 403 bovine sera collected from a BVD virus-free herd was 100%; in 296 bovine sera with serum neutralizing antibody titers of greater than or equal to 1:2, 289 sera were ELISA positive (relative sensitivity of 97.6%), two sera gave false negative reactions (0.7%) and five sera gave suspicious reactions (1.7%). These interpretations were based on positive/negative (P/N) ratio readings, i.e. a P/N ratio of < 1.50, 1.50-1.99 and greater than or equal to 2.00 were interpreted as negative, suspicious and positive reactions, respectively. The ELISA results gave excellent agreement with serum neutralization in detecting both seropositive and seronegative animals (Kappa = 0.994). The ELISA assay was considered to be technically superior to the serum neutralization test for the routine detection of BVD viral antibody in bovine sera.

Electroretinogram (ERG) and visual-evoked potential (VEP) recordings were taken from ten Suffolk-cross sheep. Stimuli for VEP were 1.5 flashes of white light/s; ERG stimuli were single flashes. The ERG measurements of the a and b wave latencies and a-to-b amplitude were measured between the lower eyelid and the vertex, with ground on the nuchal crest. The VEP after monocular stimulation were measured between the nuchal crest and the interorbital line, with ground on the vertex. Measurements consisted of the latencies to seven alternating positive and negative peaks P1, N1 P2, N2, P3, N3 and P4, and six amplitudes, P1-N1, N1-P2, P2-N2, N2-P3, P3-N3 and N3-P4. Average latencies for the a and b waves were 13.6 and 28.2 ms; the mean ab amplitude was 131.68 micromole. Average latencies for the seven VEP peaks were 35.0, 43.1, 52.8, 64.1, 74.5, 90.4 and 112.2 ms. Mean amplitudes ranged from 3.90 to 8.29 microV.

Twenty-six clinically normal colostrum-fed dairy calves were allotted to 5 groups. Calves of groups 1 and 2 served as nonvaccinated controls and were challenge-exposed with variable numbers of organisms. Group-3 calves were vaccinated SC with a modified Salmonella typhimurium bacterin. The bacterin was composed of killed acid-hydrolyzed S typhimurium G30/C21 (Re-mutant) whole cells coated with alkali-hydrolyzed S typhimurium LT-2 lipopolysaccharide, as antigen, and monophosphoryl lipid A, as adjuvant. Calves of groups 4 and 5 were vaccinated with a 2% mineral oil-in-water emulsion containing lipopolysaccharide as antigen and monophosphoryl lipid A and trehalose 6-6'-dimycolate as adjuvants. Calves of groups 3-5 were vaccinated at 2 weeks of age and again at 4 or 6 weeks of age. Adverse reactions were not observed after vaccination. Calves were challenge-exposed orally at 6 or 8 weeks of age with 1.5 X 10(11) (groups 1 and 4), or 3.0 X 10(11) (groups 2, 3, and 5) colony-forming units of S typhimurium UCD 108-11. Mortality after challenge exposure was 2 of 5 group-1 calves; 4 of 5 group-2 calves; 5 of 6 group-3 calves; 1 of 5 group-4 calves; and 4 of 5 group-5 calves. Statistical difference between calves of similarly challenge-exposed groups was not evident, indicating failure of either vaccine to protect calves of this age from oral challenge exposure with virulent S typhimurium.

Blood culture and serologic testing were used to study the prevalence of Trypanosoma cruzi infection in a group of 85 dogs from southern Louisiana rural environment. These dogs were known to have been in contact with wild mammalian hosts of the hemoflagellate. Results were compared with blood culture and serologic test results in 103 dogs from a rural environment and with limited known wild mammalian T cruzi host contact. Serologic test results for the 188 dogs from the rural environment were compared with results for 176 dogs from an urban animal shelter and for 100 household pet dogs from an urban southern Louisiana environment. Blood culture was not performed on urban dogs. Culture results were negative in all dogs from rural environments. Serologic evidence of infection was obtained for 4 of the 85 (4.7%) dogs of rural environment with known host contact. Of 176 dogs from the animal shelter, 4 (2.3%) had high antibody titer to T cruzi, and 11 others had low titer (< 2 adjusted ELISA units [aEU]). Two and 4 dogs of the housed urban and rural groups, respectively, had antibody titer to T cruzi that was < 2 aEU. Results indicate that prevalence for exposure to T cruzi antigen is higher in dogs with high potential contact with the vector and wild mammalian hosts of T cruzi, whether they are from rural or urban environment. Furthermore, results indicate that similar studies on high-risk human populations may be indicated.

Pharmacokinetic determinants of spiramycin and its distribution into the respiratory tract were studied in 2 groups of calves, 4 to 10 weeks old. Group-A calves (n = 4) were used to determine pharmacokinetic variables of spiramycin after IV (15 and 30 mg/kg of body weight) and oral administrations of the drug (30 mg/kg) and to measure distribution of spiramycin into nasal and bronchial secretions. Group-B calves (n = 4) were used to determine distribution of spiramycin into lung tissue and bronchial mucosa. Spiramycin disposition was best described by use of an open 3-compartment model. Mean (+/- SD) elimination half-life was 28.7 +/- 12.3 hours, and steady-state volume of distribution was 23.5 +/- 6.0 L/kg. Bioavailability after oral administration was 4 +/- 3%. High and persistent concentrations of spiramycin were achieved in the respiratory tract tissues and fluids. Tissue-to-plasma concentration ratio was 58 for lung tissue and 18 for bronchial mucosa at 3 hours after spiramycin administration and 137 and 49, respectively at 24 hours. Secretion-toplasma concentration ratio was 4 for nasal secretions and 7 for bronchial secretions, and remained almost constant with time. Thus, spiramycin penetrates well into the respiratory tract, although the value in bronchial secretions is lower than that in lung tissues and bronchial mucosa. Calculations indicate that a loading dose of 45 mg/kg, administered IV, followed by a maintenance dose of 20 mg/kg, IV, once daily is required to maintain active concentrations of spiramycin against bovine pathogens in bronchial secretions.

A comparison of immune variables following lung sensitization with live Pasteurella haemolytica serotype 1 (Ph1)-impregnated agar beads was done in 2 separate trials. The Ph1 immune variables studied were blood bactericidal activity, serum bacteriolysis, total classical complement, and indirect hemagglutination antibody. Each trial had 16 male weanling goats: 6 controls and 10 principals. In trial 1, each goat was surgically catheterized through the trachea, then the material was deposited in a bronchus. The controls received only agar beads and the principals received agar beads impregnated with live Ph1. These goats were studied for 32 days, euthanatized, and necropsied. In trial 2, the controls were each transthoracically injected with agar beads into the left lung and the principals were similarly injected with agar beads impregnated with live Ph1. These goats were studied for 35 days, then challenge exposed transthoracically by injection of Ph1 in saline solution (1.2 X 10(7) CFU/ml) into the right lung. Four days later, they were euthanatized and necropsied. The volume of lung consolidated tissue was an excellent measure of Ph1 immunity. Principal goats generated solid protective immunity to subsequent challenge exposure because minimal or no lung consolidation was observed, whereas large volumes of lung consolidation were seen in the controls. The principal goats in trial 1 gave a weak serum indirect hemagglutination Ph1 antibody response, which was attributed to the bronchial method of depositing the Ph1. The corresponding response of the control group remained negative. The Ph1 agar beads (1 X 10(6) CFU in 0.5 ml) protected the bacteria from immediate phagocytosis and lysis as indicated by the induced pneumonic deaths of 2 principals 5 days later. Also, live Ph1 were isolated on day 32 during necropsy of respiratory tracts of 3 principals. At necropsy, no Ph1 isolates were found in the controls. Bacteriolytic activity was not induced against Ph1 in either control or principal groups in this trial. the study, but antibody titers of the principals increased to a geometric mean of 1:250 seven days after lung injection (1 X 10(5) CFU in 0.5 ml). Serum bacteriolytic titers on day 0 indicated that both principals and controls could be subgrouped to high or low subgroups on the basis of their bacteriolytic activity. The bacteriolytic activities of the controls remained unchanged during the experiment, and neither control subgroup was protected from Ph1 challenge exposure. Bacteriolytic activities of the high and low principal subgroups responded differently to Ph1 agar bead lung injection, but both principal subgroups were protected from lung challenge exposure. The low principal subgroup generated high titers of indirect hemagglutination Ph1 antibody, whereas, the high principal subgroup generated lower antibody titers. Total complement, serum bacteriolytic, and blood bactericidal profiles were similar in the principal group with high bacteriolytic activity. The immune factors that protected 2 principal subgroups did not appear to be associated with Ph1 serum bacteriolysis.