Pasteurella haemolytica A1 and Bovine Respiratory Disease: Pathogenesis

The severe fibrinonecrotic pneumonia associated with pneumonic pasteurellosis usually results from colonization of the lower respiratory tract by Pasteurella haemolytica biotype A, serotype 1(A1). Despite recent research efforts, the authors lack a detailed understanding of the interactions and host response to P. haemolytica in the respiratory tract. The authors hypothesize that management and environmental stress factors or viral infection alters the upper respiratory tract (URT) epithelium allowing P. haemolytica to colonize the epithelium. Once the URT is colonized, large numbers of organisms enter the lung where they interact with alveolar macrophages. Endotoxin, released from the bacteria, crosses the alveolar wall where it activates pulmonary intravascular macrophages, endothelium, neutrophils, lymphocytes, platelets, complement, and Hageman factor leading to complex interactions of cells and mediators. It is the progression of this inflammatory response with neutrophil influx that is ultimately responsible for the pulmonary injury. Leukotoxin is a major virulence factor of P. haemolytica that allows it to survive by destroying phagocytic cells. At subcytolytic concentrations it may also enhance the inflammatory response by activating cells to produce mediators and release reactive oxygen metabolites and proteases.     

IOHEXOL AND IOPAMIDOL MYELOGRAPHY IN THE DOG: A CLINICAL TRIAL COMPARING ADVERSE EFFECTS AND MYELOGRAPHIC QUALITY

In a blind clinical trial, adverse effects after iohexol and iopamidol myelography were evaluated in 151 dogs. Eighty-one dogs were given iohexol (240 mgI/ml) and 70 dogs were given iopamidol (200 mgI/ml) by pre-determined assignment. Each dog was evaluated postmyelographically for seizures, hyperthermia, prolonged recovery from anesthesia and intensification of pre-existing neural signs. Myelographic quality was evaluated with a subjective scoring method. In comparing iohexol and iopamidol groups, there was not a statistically significant difference in the incidence of adverse effects or in myelographic quality. Iopamidol and iohexol appeared to be equally efficacious for routine canine myelography.     

A potential early clinical phenotype of necrotizing meningoencephalitis in genetically at‐risk pug dogs

BackgroundNecrotizing meningoencephalitis (NME) in the pug dogs is a fatal neuroinflammatory disease associated with rapid progression and poor response to conventional immunosuppressive therapy. Diagnosis is typically made after severe neurological abnormalities have manifested.Hypothesis/ObjectivePug dogs at genetic risk for NME might manifest neurological abnormalities before developing pathognomonic clinical signs of NME.AnimalsThirty‐six pug dogs less than 4 years of age asymptomatic for NME.MethodsProspective observational cohort study with germline genome‐wide genotyping. Neurological examinations were performed 4 weeks apart to document reproducible findings of central nervous system disease. Magnetic resonance imaging, cerebrospinal fluid analysis, and testing for infectious diseases were performed in all pugs with reproducible abnormalities detected on neurological examination.ResultsThe overall risk allele frequency in this cohort was 40%; 5 (14%) dogs were high risk, 19 (53%) dogs were medium risk, and 12 (33%) dogs were low genetic risk for NME. Reproducible abnormalities detected on neurological examination were identified in 8/24 (33%) genetically at‐risk dogs and 0/12 (0%) low risk dogs. Clinical abnormalities included multifocal spinal pain in 8/8, reduced menace response in 5/8, and lateralizing postural reaction deficits in 5/8 pugs. There was a strong association between genotype risk and the presence of this clinical phenotype (P = .03).Conclusions and Clinical ImportanceOur findings suggest the presence of a novel early clinical phenotype of NME in apparently asymptomatic genetically at‐risk pugs which might be used to plan early diagnostic and therapeutic clinical trials.     

Rainfall Interception by Singleleaf Piñon and Utah Juniper: Implications for Stand-Level Effective Precipitation

The expansion of piñon and juniper trees into sagebrush steppe and the infilling of historic woodlands has caused a reduction in the cover and density of the understory vegetation. Water is the limiting factor in these systems; therefore, quantifying redistribution of water resources by tree species is critical to understanding the dynamics of these formerly sagebrush-dominated rangelands. Tree canopy interception may have a significant role in reducing the amount of rainfall that reaches the ground beneath the tree, thereby reducing the amount of available soil moisture. We measured canopy interception of rainfall by singleleaf piñon (Pinus monophylla Torr. & Frém.) and Utah juniper (Juniperus osteosperma [Torr.] Little) across a gradient of storm sizes. Simulated rainfall was used to quantify interception and effective precipitation during 130 rainfall events ranging in size from 2.2 to 25.9 mm hr^? 1 on 19 trees of each species. Effective precipitation was defined as the sum of throughfall and stemflow beneath tree canopies. Canopy interception averaged 44.6% (± 27.0%) with no significant difference between the two species. Tree allometrics including height, diameter at breast height, stump diameter, canopy area, live crown height, and width were measured and used as predictor variables. The best fit predictive model of effective precipitation under canopy was described by stump diameter and gross precipitation (R² = 0.744, P < 0.0001). An alternative management model based on canopy area and gross precipitation predicted effective precipitation with similar accuracy (R² = 0.741, P < 0.0001). Canopy area can be derived from various remote sensing techniques, allowing these results to be extrapolated to larger spatial scales to quantify the effect of increasing tree canopy cover on rainfall interception loss and potential implications for the water budget.     

Cyclooxygenase (COX) inhibitors and the intestine

Nonsteroidal anti-inflammatory drugs (NSAIDs) have long been used for the treatment of pain and inflammation because of their inhibitory effects on cyclooxygenase (COX). For almost as long as NSAIDs have been in use, multiple adverse effects have been noted. Assessment of many of these adverse effects have been complicated because of the discovery of multiple splice variants of the cox gene, and a greater array of COX inhibitors, especially the COX-2 selective inhibitors have become available. Some of these adverse effects cannot be readily explained by the effect of these drugs on COX. This has sparked a new field of investigation into the COX-independent effects of the COX inhibitors. The major noncyclooxygenase targets of the COX inhibitors of particular relevance to inflammation and the gastrointestinal tract are phosphatidylinositol 3'-kinase Akt signaling, uncoupling of oxidative phosphorylation, PPARgamma, nuclear factor KB, mitogen activated protein kinases, and heat shock proteins.