Burnout and compassion fatigue are frequently mentioned in relation to veterinary work. Veterinary nursing is a caring profession and those who seek a career within this field do so because of a natural empathetic desire to care for animals. However it is the individuals who are the most caring and empathetic towards others that will be most at risk of experiencing occupational stress when they are confronted with psychologically demanding workplace roles and working environments. Burnout is considered an ‘unintentional end point’ for certain individuals who are exposed to chronic stress within their working environment. When suffering burnout, a person may experience emotional exhaustion, may become more cynical or they may have a reduced sense of personal accomplishment in regards to their own work. Signs of burnout can include increased levels of absenteeism at work, or the working standards of that staff member may decline below that of what would normally be expected of them. This could directly impact on patient care in the veterinary practice. Working in a role that places emotional demands on staff, such as a need to show compassion and empathy towards clients who are emotionally distressed, puts staff at risk from experiencing compassion fatigue. Workplace supports may include appropriate debriefing sessions among willing participants, particularly after an emotionally stressful encounter with a client. Taking personal responsibility for care of one’s own mental and physical health is just as important as taking care of the patient’s health. Personal strategies may include lifestyle changes, adopting a healthier lifestyle, reduction of working hours, and ensuring adequate sleep. Adopting healthy self-care strategies can promote characteristics of

Suffolk sheep carrying theDRB1*1101(previously referred to as-DRB1*0203or G2) allele have been reported to show increased resistance to naturalTeladorsagia circumcinctainfection compared to non-carriers. The objective of this study was to compare the biochemical and physiological responses ofDRB1*1101carrier and non-carrier twin lambs to an experimental infection with 3 × 10⁴L3Teladorsagia circumcincta. The variables studied included worm burden, faecal egg count, abomasal mast cells, IgA, IgE, IgG1 plus IgG2 and haematological parameters at 0, 3, 7, 21 and 35 days post infection (dpi), and duodenal smooth muscle contractility at 0 and 35 dpi.DRB1*1101carrier lambs had significantly lower worm burden, higher mast cell and plasma platelet counts than theDRB1*1101non-carriers (P< 0.05). Before infection, the non-carrier lambs exhibited significantly higher mucosal levels of all antibody isotypes measured compared to the carriers; these levels remained relatively stable over the course of infection in the non-carriers while there was a slow build up of these antibodies in the carriers up to day 21 post infection (pi). TheDRB1*1101non-carrier lambs had a significantly higher plasma lymphocyte count, and produced greater duodenal contractile force relative to the carrier lambs (P< 0.05). There was no significant difference between genotypes in the level of plasma eosinophils, monocytes, neutrophils or FEC. This evidence suggests that resistance conferred byDRB1*1101is acquired rather than innate, depends on worm expulsion rather than fecundity and is dependent on mucosal mast cell proliferation, platelet activation, and IgA and IgE antibody responses.

Objective—To evaluate the effect of body position on barrier pressure at the gastroesophageal junction in anesthetized Greyhounds and to assess alterations in barrier pressure following gastropexy. Animals—8 adult Greyhounds. Procedure—Barrier pressure at the gastroesophageal junction was measured by fast (1 cm/s) and slow (1 cm/10 s) withdrawal of a subminiature strain gauge transducer through the gastroesophageal junction in 8 anesthetized dogs. The effect of body position was measured. Each dog then was placed in right-lateral recumbency, and gastropexy was performed in the left flank. Additional measurements were obtained 1, 5, 10, 20, and 30 minutes after gastropexy. Results—Barrier pressure for dogs positioned in sternal recumbency (mean ± SEM, 1.1 ± 0.53 mm Hg) was significantly less than for dogs positioned in right lateral or left lateral recumbency. Following gastropexy, there was a steady increase in barrier pressure. Thirty minutes after gastropexy, barrier pressure was significantly higher (13.36 ± 3.46 mm Hg), compared with the value before surgery. Conclusions and Clinical Relevance—Barrier pressure in anesthetized dogs is highly variable and influenced by body position. This is most likely the result of anatomic interrelationships between the diaphragm, stomach, and terminal portion of the esophagus. Gastropexy also increases barrier pressure in the immediate postoperative period, which may be clinically relevant in terms of understanding how resolution of gastroesophageal reflux disease associated with hiatal hernia may be affected by gastropexy combined with hernia reduction. (Am J Vet Res 2001;62:1068–1072)

As targeted personalized therapy becomes more widely used in human medicine, clients will expect the veterinary clinician to be able to implement an evidence-based strategy regarding both the prescribing of medicines and also recognition of the potential for adverse drug reactions (ADR) for their pet, at breed and individual level. This review aims to provide an overview of current developments and challenges in pharmacogenetics in medicine for a veterinary audience and to map these to developments in veterinary pharmacogenetics. Pharmacogenetics has been in development over the past 100 years but has been revolutionized following the publication of the human, and then veterinary species genomes. Genetic biomarkers called pharmacogenes have been identified as specific genetic loci on chromosomes which are associated with either positive or adverse drug responses. Pharmacogene variation may be classified according to the associated drug response, such as a change in (1) the pharmacokinetics; (2) the pharmacodynamics; (3) genes in the downstream pathway of the drug or (4) the effect of “off-target” genes resulting in a response that is unrelated to the intended target. There are many barriers to translation of pharmacogenetic information to the clinic, however, in human medicine, international initiatives are promising real change in the delivery of personalized medicine by 2025. We argue that for effective translation into the veterinary clinic, clinicians, international experts, and stakeholders must collaborate to ensure quality assurance and genetic test validation so that animals may also benefit from this genomics revolution.