Multinodular pulmonary fibrosis in five horses

CASE DESCRIPTION: 5 horses were evaluated because of decreased appetite, weight loss, fever, cough, tachypnea, and respiratory distress. CLINICAL FINDINGS: Tachycardia, tachypnea, increased respiratory effort, lethargy, fever, poor body condition, and nasal discharge were detected in various combinations on initial physical examination. Evaluation of the lower portion of the respiratory tract via radiography and ultrasonography revealed a severe nodular interstitial pattern. Histologic examination of lung tissue revealed interstitial expansion of alveolar parenchyma with collagen, intraluminal accumulation of neutrophils and macrophages within the alveoli, and occasional intranuclear inclusion bodies within alveolar macrophages. Equine herpesvirus type 5 was detected in samples of lung tissue, bronchoalveolar lavage fluid, or both via polymerase chain reaction assay in all cases. A diagnosis of equine multinodular pulmonary fibrosis (EMPF) was established. TREATMENT AND OUTCOME: Horses were provided supportive treatment and were administered a variety of medications including corticosteroids and acyclovir. Two horses survived and returned to their previous level of activity. Three horses were euthanized because of either deterioration of clinical condition (n=2) or failure to improve within 4 weeks of initiation of treatment (1). CLINICAL RELEVANCE: EMPF should be considered as a differential diagnosis for adult horses with interstitial pneumonia and should be suspected on the basis of characteristic radiographic, ultrasonographic, and histopathologic findings. Equine herpesvirus type 5 is found in association with EMPF; although the exact pathogenic role this virus plays in EMPF is unknown, equine herpesvirus type 5 may be an etiologic agent or cofactor in the development of EMPF.     

Effect of short-duration overnight cattle kraaling on grass production in a southern African savanna

Ranch owners in eastern and southern Africa have embraced a new rangeland management practice of keeping cattle overnight in temporary livestock corrals (hereafter referred to as kraals) within rangelands for short durations (for example, one week) to improve grass production. To better understand the influence of this practice on the grass community, we determined grass species diversity, richness, biomass and quality (crude protein, fibre, rumen fermentation and metabolisable energy) from a chronosequence consisting of kraals abandoned 1, 2, 3 and 4 years prior to the study and compared them to the surrounding vegetation. Grass species diversity, richness, biomass and quality were higher in abandoned kraals than the surrounding vegetation. Grass biomass increased five-fold in the first year of kraal abandonment and thereafter declined three-fold after four years. Metabolisable energy, a measure of grass nutritive value, increased from 8.92 to 11.90 MJ kg?1 with kraaling. The number of grass species also increased with kraaling. Palatable grass species, such as Urochloa mosambicensis and Panicum maximum, were more abundant in abandoned kraal sites than the surrounding vegetation. We conclude that short-duration overnight cattle kraaling improves grass quality and biomass.     

Investigation into the causes of aspirin resistance in healthy dogs

Antiplatelet effects of acetylsalicylic acid (ASA, aspirin) may be poor in some individuals. Additionally, no method exists for predicting poor ASA response (resistance) in individual dogs. This study's main objective was to determine whether poor ASA response results from pharmacodynamic or pharmacokinetic causes. ASA concentrations causing 50% inhibition of platelet aggregation (in vitro IC50) were determined using whole blood collected from 21 drug‐free healthy dogs to evaluate intrinsic sensitivity of platelets to ASA. Dogs were then administered ASA at 4 mg/kg once orally. Percent decrease in platelet aggregation from baseline, and plasma ASA and salicylic acid (SA) concentrations (expressed as AUC values) were measured for up to 3 hr. By 3 hr, 13/21 (62%) dogs showed >50% aggregation inhibition, while 8/21 (38%) dogs showed <50% inhibition. Aggregation inhibition values were negatively correlated with in vitro IC50 values (Rs = ?0.49; p = 0.028) and positively correlated with ASA concentrations (Rs = 0.48; p = 0.03). Furthermore, ASA concentrations were strongly negatively correlated (Rs = ?0.88; p < 0.001) with SA/ASA concentration ratios, an index of ASA metabolism to SA by esterase enzymes. Multiple linear regression analysis indicated that 59% (p < 0.001) of interindividual variability in aggregation inhibition was explained by in vitro IC50 values (29% of variability) and ASA concentrations (29% of variability). Consequently, poor in vivo ASA response in these dogs resulted from both pharmacodynamic (decreased platelet sensitivity) and pharmacokinetic (lower ASA concentrations) causes. Lower ASA concentrations may be explained by reduced bioavailability associated with higher esterase activities.     

Tamoxifen induces apoptosis and inhibits respiratory burst in equine neutrophils independently of estrogen receptors

Neutrophils play an important role in the exacerbation and maintenance of severe equine asthma; persistent neutrophil activity and delayed apoptosis can be harmful to surrounding tissues. Tamoxifen (TX) is a nonsteroidal estrogen receptor modulator with immunomodulatory effects and induces early apoptosis of blood and bronchoalveolar lavage neutrophils from horses with acute lung inflammation. This study investigated if the in vitro effects of tamoxifen are produced by its action on nuclear (α and β) and membrane (GPR30) estrogen receptors in healthy equine neutrophils. Results showed that TX inhibits neutrophil respiratory burst induced by opsonized zymosan in a dose‐dependent manner. Nuclear (17‐β‐Estradiol) and GPR30 cell membrane (G1) estrogen receptor agonists and their antagonists (ICI 182,780 and G15, respectively) do not block or reproduce the effect of TX. Therefore, TX does not inhibit respiratory burst through estrogen receptors. TX (8.5 μM) also increased phosphatidylserine translocation, a marker of early apoptosis, which did not occur with any of the estrogen receptor agonists or antagonists . Thus, tamoxifen generates dose‐dependent inhibition of respiratory burst and increased early apoptosis in healthy equine neutrophils, independently of nuclear or membrane estrogen receptors. Further studies are necessary to explore the signaling pathways of tamoxifen‐induced ROS inhibition and phosphatidylserine translocation.     

Considerations for analysis of time-to-event outcomes subject to competing risks in veterinary clinical studies

In veterinary medicine, prospective clinical trials are increasingly utilized to address questions regarding effectiveness of therapies and patient prognosis. A large number of these trials involve time-to-event (TTE) endpoints, which require special methods of analysis to handle data in which not all subjects are observed to have the event of interest. Analyses and interpretation of the results can be further complicated when an endpoint of interest is not observed in some patients because they incur a competing risk, such as death from an unrelated cause. Competing risks have been the source of confusion in many epidemiologic analyses leading to the potential for misinterpretation. In this article, we review key considerations for the TTE analysis in the setting of competing risks. We briefly review standard TTE tools, namely Kaplan–Meier survival curves and Cox regression. In the setting of outcomes with competing risks, we provide guidance on the appropriate analysis techniques, such as cumulative incidence curves, to estimate the risk of an event of interest. We also describe a common pitfall of treating competing risks as censoring in Kaplan–Meier survival curve analysis, which can overestimate the event rate of interest. We describe two common regression methods that examine associated risk factors in the presence of competing risks and highlight the different research questions these methods address. This article provides an introductory overview and illustrates concepts with examples from veterinary trials and with example data sets.     

Sorption-desorption of flucarbazone and propoxycarbazone and their benzenesulfonamide and triazolinone metabolites in two soils

Sorption-desorption interactions of pesticides with soil determine the availability of pesticides in soil for transport, plant uptake and microbial degradation. These interactions are affected by the physical and chemical properties of the pesticide and soil and, for some pesticides, their residence time in the soil. While sorption-desorption of many herbicides has been characterised, very little work in this area has been done on herbicide metabolites. The objective of this study was to characterise sorption-desorption of two sulfonylaminocarbonyltriazolinone herbicides, flucarbazone and propoxycarbazone, and their benzenesulfonamide and triazolinone metabolites in two soils with different physical and chemical properties. K(f) values for all four chemicals were greater in clay loam soil, which had higher organic carbon and clay contents than loamy sand. K(f-oc) ranged from 29 to 119 for the herbicides and from 42 to 84 for the metabolites. Desorption was hysteretic in every case. Lower desorption in the more sorptive system might indicate that hysteresis can be attributed to irreversible binding of the molecules to soil surfaces. These data show the importance of characterisation of both sorption and desorption of herbicide residues in soil, particularly in the case of prediction of herbicide residue transport. In this case, potential transport of sulfonylaminocarbonyltriazolinone herbicide metabolites would be overpredicted if parent chemical soil sorption values were used to predict transport.     

Seasonal Sulfate Deposition and Export Patterns for a Small Appalachian Watershed

Sulfate deposition and exports from 1988–92 were analyzed for a small headwater catchment in north-central West Virginia. Annual sulfate inputs, estimated by applying throughfall-adjusted ratios to bulk deposition values, and outputs were approximately equal for the five years. Annual mean throughfall-adjusted deposition and export loads were 55.78 and 55.48 kg ha-1, respectively. While these results indicate the watershed has reached sulfate equilibrium relative to current deposition levels, seasonal sulfate accumulations and deficits were evident. Deposition and exports averaged 5.61 and 2.49 kg ha-1 mo-1, respectively, during the growing season, and 3.69 and 5.22 kg ha-1 mo-1 during the dormant season. Sulfur accumulated within the soil during the growing season because inputs of wet and dry sulfur deposition were high while outputs were negligible. The latter was due largely to the lack of runoff resulting from high evapotranspirational demands. By contrast, net sulfate losses occurred during dormant seasons, primarily due to high runoff, even though inputs declined during this season. Researchers working on other watersheds have interpreted similar input/output patterns to mean that sulfate accumulated during the growing season is the source of sulfate exported during the dormant season. However, radioisotopic evidence from a companion study on this watershed showed that some labeled sulfate applied to the watershed more than a year earlier was still present in the organic and mineral soil layers at the point of application (with some as soluble sulfate), and in soil water dispersed throughout the watershed. Its presence indicates that dormant season exports can originate from sulfate deposited over longer periods than just the previous growing season or even previous year. Volume-weighted concentrations in soil leachate suggest that dormant-season sulfate losses resulted from progressive depletion of the anion through the soil profile. During the fall and early winter, soluble sulfate was depleted in the upper soil horizons; in later winter, depletion occurred in the lower horizons.