Recrudescence of infectious bovine rhinotracheitis virus and associated neural changes in calves treated with dexamethasone

Reactivation of infection bovine rhinotracheitis (IBR) virus in calves administered dexamethasone (DM) was studied in 2 experiments. At 2, 3, 5, 15, or 30 months after inoculation of the Los Angeles strain of IBR virus, IV injections of DM were given for 5 consecutive days to induce a recurrent infection (experiment 1). Three months after the 1st treatment, a 2nd recurrent infection was induced, using DM with the same doses as used in experiment 1. The virus was excreted from nasal secretions from the 4th to the 10th day after initial treatment with DM, and from the 6th to the 9th day after the 2nd treatment. On pathologic examination, trigeminal ganglionitis, consisting of many proliferated microglia and inflammatory cells, was observed in all DM-treated calves. Moreover, degeneration of the ganglion cells and neuronophagia were prominent features in the calves after the 2nd recurrent infection. These observations indicated that the trigeminal ganglion may be one of the latent sites of IBR virus in calves after intranasal infection and that calves can develop a recrudescent infection after DM treatment several times during their lifetime.     

Neural changes in recurrent infection of infectious bovine rhinotracheitis virus in calves treated with dexamethasone.

Recurrent infection by infectious bovine rhinotracheitis (IBR) virus was induced in calves by dexamethasone (DM) treatment (given 5 days) at 5 months after primary infection. The virus appeared in nasal secretions of the calves on the 4th day after initiation of DM treatment and continued until the 9th day. The calves were killed on the 1st, 3rd, 4th, 5th, 6th, 7th, 8th, 10th, and 11th days after DM treatment was started for examination by histopathologic and immunofluorescent antibody techniques. The most significant neural change was trigeminal ganglionitis with neuronophagia, which was observed from the 3rd to the 11th day. Significantly, the extent of changes in the trigeminal ganglion and medulla oblongata corresponded to the amount of DM treatment administered. The IBR virus antigen was first observed in the trigeminal ganglion cells, and thereafter, it was detected in the Schwann cells, satellite cells, neuroglia cells, and nasal mucosa until the 10th day. These observations indicate that the IBR virus is capalbe of producing a persistent infection in the trigeminal ganglion and that trigeminal ganglionitis may be a characteristic lesion for inducing the reactivation of lagent IBR virus.     

Effect of infectious bovine rhinotracheitis virus immunization on viral shedding in challenge-exposed calves treated with dexamethasone

Calves not vaccinated with infectious bovine rhinotracheitis virus (IBRV) became latently infected when challenge exposed and treated with dexamethasone (DM). Calves that shed IBRV after DM treatment were considered to be latently infected. Vaccination with a temperature-sensitive intranasal vaccine or with formalinized IBRV in Freund's complete adjuvant (IBRV-FCA) protected some, but not all, calves against latent infection--indicating a role for the immune response in preventing latent infection. That all latently infected calves were not detected after DM treatment was indicated by the fact that after a 2nd DM treatment of 3 calves treated 6 months previously and not found to shed virus, 1 of the calves was latently infected. Latently infected calves were inoculated with successive doses of IBRV-FCA and treated with DM. Nonvaccinated calves shed virus, whereas vaccinated calves similarly treated did not shed virus. Because both groups had a comparable cell-mediated immune response, as determined by blastogenic response to IBRV, but the vaccinated group had significantly higher virus-neutralizing antibody titers, a role for humoral antibody in preventing viral shedding was indicated.     

Effects of inoculations with Eimeria zuernii on young calves treated with decoquinate or narasin with or without dexamethasone

Sixteen 7-week-old Holstein male calves were inoculated with sporulated oocysts of Eimeria zuernii. Four calves (controls) were euthanatized and necropsied at 14 and 20 days after inoculation (DAI). Two calves were treated with 20 mg of dexamethasone (IM) on 13, 14, and 15 DAI and euthanatized and necropsied 17 DAI and 2 calves were given similar treatments and necropsied 20 DAI. The 8 other calves were euthanatized and necropsied 20 DAI. Two were started on the anticoccidial drug decoquinate in feed 13 DAI; 2 others were given decoquinate on the same schedule plus dexamethasone on 13,14, and 15 DAI. Two calves were given the antibiotic narasin in feed beginning 13 DAI and 2 calves were given parasin on the same schedule plus dexamethasone on 13,14, and 15 DAI. All calves, except 2 controls necropsied 14 DAI and 4 calves given decoquinate, discharged moderate-to-large numbers of oocysts in feces and had moderate-to-serve changes in fecal consistency. Histologic examinations revealed large numbers of endogenous stages in tissues of calves treated or not treated with dexamethasone. Few endogenous stages were observed in tissues from calves that were given decoquinate or decoquinate plus dexamethasone. Calves given narasin or narasin plus dexamethasone had moderate-to-large numbers of endogenous stages in the tissues.     

奶牛低血钙症降低中性粒细胞上ORAI1蛋白的表达

旨在研究泌乳初期高产奶牛高发的低血钙症是否影响细胞内Ca~(2+)通路进而影响中性粒细胞活性并增加泌乳初期的炎症反应。尾静脉肝素抗凝采集血液分离中性粒细胞(PMN),采用Western blot检测ORAI1蛋白的表达,利用流式细胞仪测定静息状态下、离子霉素刺激的中性粒细胞表面ORAI1蛋白丰度以及ROS水平。结果显示,健康对照组奶牛中性粒细胞表面ORAI1蛋白丰度与表达水平均显著高于低血钙症试验组。低血钙症中性粒细胞经离子霉素刺激后细胞表面ORAI1蛋白丰度显著高于未经刺激的低血钙症PMN。健康对照组奶牛中性粒细胞中的ROS水平显著低于低血钙症试验组。这些结果表明,奶牛低血钙症降低中性粒细胞内钙离子进入的调控,以及低血钙症能降低中性粒细胞内的ROS水平,导致泌乳初期的炎症反应。     

Cell-mediated immune function in lambs chronically treated with dexamethasone

Crossbred ewe and wether lambs were individually stanchioned in environmentally controlled rooms at 20 degrees C. On d 0, lambs were treated with .04 mg of dexamethasone (DEX; n = 10)/kg of BW or given an equal volume of saline vehicle (SAL; n = 10). Treatment was repeated every 48 h for 14 d. Samples of blood were obtained by puncture of the jugular vein on d 0 (before treatment), 2, 4, 7, 10, and 14. Total and differential leukocyte numbers, lymphocyte blastogenic responses to mitogens, and in vitro production of interleukin-2 (IL-2) were determined. No treatment x day interaction was noted for any of the experimental end points (P greater than .10); therefore, within-day comparisons between DEX- and SAL-treated lambs were not made. However, over all 14 d, DEX-treated lambs had increased (P less than .05) numbers of lymphocytes (6.5 +/- .4 vs 5.1 +/- .4 x 10(3) cells/microliters for SAL) and monocytes (.8 +/- .1 vs .6 +/- .1 x 10(3) cells/microliters for SAL), and these increases contributed to an increase (P less than .01) in total leukocytes (11.2 +/- .5 vs 9.1 +/- .5 x 10(3) cells/microliters for SAL). Lymphocyte blastogenic responses to mitogens were not affected by DEX treatment. Production of IL-2 was reduced (P less than .05) for DEX- (.90 +/- .12 units/ml) compared with SAL-treated lambs (1.27 +/- .13 units/ml). The data suggest that continued treatment of lambs with DEX may result in a modest reduction in production of IL-2, but mitogen-stimulated blastogenic responses of lymphocytes are not reduced by DEX treatment.     

Response of Pasteurella haemolytica to erythromycin and dexamethasone in calves with established infection.

A subcutaneous soft tissue infection model in calves was used to study the in vivo response of Pasteurella haemolytica to erythromycin and dexamethasone. Two tissue chambers were implanted SC in each of 12 calves. At 45 days after implantation, all tissue chambers were inoculated with an erythromycin-sensitive strain of P haemolytica. Starting 24 hours after inoculation, calves were allotted to 4 groups of equal size and a 2 x 2-factorial arrangement of treatments was applied: 3 calves were given erythromycin (30 mg/kg of body weight, IM, for 5 days), 3 calves were given dexamethasone (0.05 mg/kg, IM, for 2 days), 3 calves were given erythromycin and dexamethasone, and the remaining calves served as nontreated controls. Chamber fluids were tested daily, and the response to treatment was measured. Neither erythromycin nor dexamethasone affected viability or growth of bacteria within tissue chambers. Dexamethasone had no effect on the influx of neutrophils into infected chambers. Despite repeated administration of a high dose of erythromycin and attainment of adequate concentration in serum, erythromycin concentration in chamber fluids did not exceed the minimal inhibitory concentration established in vitro. These results indicate that the clinical efficacy of erythromycin against P haemolytica sequestered in consolidated pneumonic lesions may not be well correlated with predictions based on serum pharmacokinetic and in vitro susceptibility data.     

Implications for dosing regimen of enrofloxacin administered concurrently with dexamethasone in febrile buffalo calves

Tropical Animal Health and Production - The objective of the study was to determine the influence of dexamethasone (DXM) on pharmacokinetics (PK) and pharmacodynamics (PD) of enrofloxacin (ENR) for...     

Pathology and residues in veal calves treated experimentally with clenbuterol

Six veal calves were medicated with clenbuterol at 20 μg kg bodyweight⁻¹ day⁻¹ for 42 days before they were slaughtered, to evaluate the lesions and residues in target organs. Compared with six unmedicated calves the most noticeable changes were tracheal dilatation, decreased uterine weight, slight mucous hypersecretion in the uterus and vagina and depletion of liver glycogen. The highest concentrations of clenbuterol (62 to 128 ng/g⁻¹) were recorded in the choroid/retina, and the aqueous humour had the lowest concentration (0·5 to 2·4 ng ml⁻¹). The residue concentrations were higher than the maximum residue level set for clenbuterol (0·5 ng g⁻¹)     

Effect of isoproterenol and dexamethasone on the lipopolysaccharide induced expression of CD11b on bovine neutrophils

The present experiments investigate the changes in expression of CD11b on bovine neutrophils and its modulation by isopropylnoradrenaline (IPN, isoproterenol), dexamethasone (DX), phenylephrine (alpha-agonist) and clenbuterol (beta-agonist). Both IPN and DX caused a dose-dependent inhibition of LPS-induced CD11b expression. A combination of IPN and DX elicited a synergistical decrease of the CD11b expression. Clenbuterol mimicked the effect of IPN, whereas phenylephrine did not. The effect of IPN and DX could at least partly be mediated through a decreased TNF-alpha production by monocytes since tumor necrosis factor-alpha (TNF-alpha) is shown to mediate a dose-dependent CD11b up-regulation. Stimulation of stress hormone receptors partly immuno-suppresses neutrophil functions by inhibition of CD11b expression on the neutrophil surface upon LPS stimulation. This inhibition is probably related to a decrease in TNF-alpha production. A similar mechanism of immuno-suppression could contribute to the higher susceptibility of cattle to Gram-negative bacterial infections of the udder and lung during periods of stress.     

Importance of neutrophils in the pathogenesis of acute pneumonic pasteurellosis in calves

Acute lung injury was induced in 24 calves by intratracheal inoculation with Pasteurella haemolytica. Calves in groups 1 and 2 were neutrophil depleted, using hydroxyurea given IV. Group 1 calves (n = 7) were inoculated intratracheally with saline solution, and group 2 calves (n = 7) were inoculated with P haemolytica. Group 3 calves (n = 7) had normal numbers of neutrophils and were inoculated with P haemolytica. Group 4 calves (n = 3) were treated acutely with hydroxyurea IV, had normal numbers of neutrophils, and were inoculated with P haemolytica. After inoculation, calves with normal numbers of neutrophils (groups 3 and 4) became hypoxemic 2 hours after inoculation, and hypoxemia persisted until necropsy (6 hours after inoculation). These calves also developed tachypnea, bradycardia, neutropenia, and lymphopenia. Lung lesions consisted of necrosis of the alveolar walls, intra-alveolar hemorrhage, and a severe exudative and necrotizing bronchopneumonia, with accumulation of proteinaceous fluid in alveoli and lymphatics. In neutrophil-depleted calves (groups 1 and 2), blood gas values, heart and respiratory rates, and numbers of circulating leukocytes did not change after inoculation with saline solution or with P haemolytica. At necropsy, the lungs of neutrophil-depleted calves were grossly normal. Therefore, neutrophils were required for the acute lung injury induced by P haemolytica. The protective effect of neutrophil depletion was a specific effect of hydroxyurea because calves with high circulating concentrations of hydroxyurea and calves with normal numbers of neutrophils (group 4) developed lung injury.     

Bovine neutrophils treated with chemotactic agents: morphologic changes

Neutrophils were isolated from the peripheral blood of cattle. After the neutrophils were incubated with zymosan-activated serum, the neutrophils changed from spherical to a bipolar shape. Ninety percent of the neutrophils became bipolar in 5 to 10 minutes. Bacterial cell filtrate and casein also induced bipolar shape changes in neutrophils, but N-formyl-L-methionyl-L-leucinyl-L-phenylalanine did not. The neutrophil-shape-change response was a rapid in vitro assay to evaluate early chemotactic events.     

In vitro migration responses of neutrophils from cows and calves

The directional (chemotactic) and random migration activities of neutrophils from cows and newborn and 2-week-old calves were determined by use of the chemotaxis-under-agarose assay. Blood samples were stored for 2, 24, or 48 hours and at 4 or 25 C before testing. During the assay, cells were incubated at 17, 27, or 37 C. The assay was found suitable for testing the directional and random migration activities of neutrophils from cattle. Directional migration of neutrophils was diminished (P less than or equal to 0.05) when cells were incubated at 17 or 27 C, compared with data from incubation at 37 C. Random migration of neutrophils was unaffected by test incubation temperature. Significant (P less than or equal to 0.05) differences were found between cows and calves regarding the percentage number and viability and the directional and random migration activities of neutrophils. Neutrophils from cows were adversely affected to a greater extent by prolonged sample storage times or low storage temperature than were neutrophils from calves. Results indicate that a sample storage time of up to 24 hours, a sample storage temperature of 25 C, and a test incubation temperature of 37 C provided optimal conditions for testing the migratory activities of neutrophils from cattle.     

Muscle protein degradation in bull calves with compensatory growth

Twelve 5-month-old bull calves were allocated to two feeding strategies: AA, 6 calves were fed ad libitum 34 weeks; and RA, 6 calves were fed restrictively for 14 weeks with an intake of 50% of the metabolic energy and protein eaten by the AA calves, followed by ad libitum feeding for 20 weeks. At the end of the 14-week restriction period, and after 2, 5, 8, 11, 14 and 17 weeks of re-alimentation, urine, blood and muscle biopsy samples from M. longissimus dorsi (LD) were collected. The urine was analysed for 3-methylhistidine for determination of the fractional breakdown rate of muscle protein (FBR). The FBR was depressed during restricted feeding (1.4 versus 2.0%/day; P = 0.05), however, during re-alimentation where the calves exerted compensatory growth, the FBR increased and reached a maximum after 5 weeks into this period (3.1 versus 1.9%/day; P < 0.001). The maximal FBR in the RA calves coincided with a maximum concentration of RNA and DNA in LD, and a maximal fractional rate of growth. The activity of μ-calpain in LD and the concentration of IGF-I in serum were decreased at the end of the restriction period but increased as soon as energy was offered ad libitum. The results support the hypothesis that muscle protein turnover is affected by a restriction/re-alimentation feeding strategy, and that muscle protein degradation reaches a maximum during the re-alimentation period, which exceeds that of control animals.