Now in a fully updated seventh edition, Plumb's Veterinary Drug Handbook remains the most complete source of drug information relevant for animals available. Providing referenced dosing recommendations in each monograph, this book offers doses for a wide range of species, including dogs, cats, exotic animals, and farm animals, in a single resource. The book also includes detail on key aspects for appropriate use of each drug, including pharmacology, pharmacokinetics, contraindications, adverse effects, safety during pregnancy or nursing, overdoses, drug interactions, monitoring, chemistry and stability, storage, compatibility, and available products. The seventh edition adds 22 new drug monographs, as well as updated dosages and information for existing drugs. A noteworthy feature is the Prescriber Highlights section found at the beginning of each monograph that allows readers a quick method of finding important information for that drug. This is the 8 1/2 x 11-inch desk size, offering enhanced readability and ease of use; Plumb's Veterinary Drug Handbook is also available in the convenient 5 by 8-inch pocket size and as a mobile version. Plumb's exhaustive one-volume coverage of drugs approved for veterinary species and non-approved (human) drugs that are used in veterinary practices today make this book an essential reference for veterinarians, veterinary technicians, veterinary pharmacologists, pharmacists with veterinary patients, animal research or zoological facilities, and libraries that serve these groups.

Plumb's Veterinary Drug Handbook

In a world that is increasingly perturbed by humans, the need to understand ecosystems is urgent. Attaching measuring devices to wild animals is often the only way to acquire vital life-history information on larger, charismatic species, and on cryptic species that do not lend themselves to observation. However, the ethics of acceptable practice for attached devices are poorly defined. Here, we consider the need for further research and attempt to identify a system that allows animal restraint practices and device-induced effects to be quantified and monitored, so that ethics committees can have a defined scale on which to base decisions.

Measuring devices on wild animals: what constitutes acceptable practice?

Dehorning or disbudding in cattle is performed for a variety of reasons using various methods. Pain associated with this procedure has been mostly evaluated through behavioral, physiologic, and neuroendocrine changes following dehorning. Analgesics, including local nerve blockades, anti-inflammatories, and opioids have demonstrated an effective attenuation of the cortisol response. The administration of sedatives with analgesic properties has been indicated in the attenuation of the acute phase of pain associated with dehorning. Following a literature review, this article recommends a multimodal approach to analgesia for dehorning procedures, including the use of a local anesthetic and anti-inflammatory and, when possible, a sedative-analgesic.

Bovine dehorning: assessing pain and providing analgesic management.

Southern elephant seals (Miroungo leonina) were immobilised with a mixture of tiletamine and zolazepam administered intravenously at a mean (sd) dose rate of 0.46 (0.08) mg/kg. This dose provided a satisfactory degree of anaesthesia with no side effects, and the induction, duration and recovery times were short. The mean (sd) induction time was 26 (9) seconds and the mean level of anaesthesia was 4.4 units on an eight-point scale. Male seals were given less drug than female seals, remained immobilised for shorter periods and recovered sooner. The mean (sd) dose of drug administered to males was 0.44 (0.06) mg/kg and to females 0.48 (0.08) mg/kg, and the mean (sd) duration times were 14.9 (4.5) minutes and 16.1 (5.3) minutes. The mean (sd) time taken to recover from immobilisation was 14.5 (4.6) minutes for males and 15.7 (5.3) minutes for females. Physiological condition and size significantly affected the duration of anaesthesia. Thin seals remained immobilised for 18 (7) minutes whereas fatter seals remained immobilised for 15 (4) minutes (P<0.0001).

Field immobilisation of southern elephant seals with intravenous tiletamine and zolazepam

T ability to sense pain (nociception) is lifesaving. Without it, tissue trauma would not be detected, potentially resulting in the development of more severe tissue injury and infection. Severe tissue injury and infection can initiate a systemic inflammatory response syndrome that results in multiple organ failure and death. In humans, congenital insensitivity to pain results in extensive tissue damage typified by destruction of the joints, pressure ulcers, and muscle ischemia in addition to self-induced mutilation. Most humans afflicted with this condition die within the first or second decade of life because of overwhelming infections. Therefore, the pain-detecting system has a vital life-sustaining role, and it is the key warning system for alerting an animal to the presence of potential tissue-damaging stimuli, which results in initiation of protective physiologic, somatic motor, and behavioral responses to maintain the integrity of the body. Typically, most noxious stimuli (mechanical, thermal, chemical, and electrical) are transient, non–tissue-damaging events that generate pain (physiologic pain) by activating high-threshold pain receptors (nociceptors) located on the terminal ends of thinly myelinated or unmyelinated peripheral Aδ and C nerve fibers. A noxious stimulus is transduced into electrical impulses that are transmitted to the dorsal horn of the spinal cord, thereby initiating the release of glutamate from presynaptic nerve terminals. Glutamate activates postsynaptic AMPA and KA receptors. The AMPA and KA receptors are the primary mediators of fast excitatory pain transmission (Figure 1). Sensory processing is subsequently controlled by electrical impulses generated in local spinal cord segmental circuits and by descending tonic and phasic facilitatory and inhibitory influences originating from the brain. If tissue damage occurs despite the activities of this defensive system, changes in pain sensitivity occur that help to protect the animal from and prevent further injury. Severe tissue injury (trauma, surgery, or inflammation) or sustained nociceptive input (trauma) increases glutamate release from the presynaptic nerve terminals and results in increases in neuronal activity of the superficial dorsal horn and removal of Mg from NMDARs (named on the basis of the synthetic agonist that activates them). The activation and modulation of NMDARs by the excitatory neurotransmitter glutamate are believed to be key components in the development of central sensitization and secondary hyperalgesia and in the consequent amplification of the pain response. Increases in sensitivity to noxious or non-noxious stimuli (hypersensitivity) are recognized as allodynia and hyperalgesia. Allodynia is pain caused by a stimulus that does not normally provoke pain. Depending on the severity and duration of noxious stimuli, allodynia or hyperalgesia may spread from the site of injury (primary hyperalgesia) to surrounding noninjured tissues (secondary hyperalgesia). Primary hyperalgesia can be caused by a reduction in the threshold (peripheral sensitization) of normally high-threshold peripheral nociceptors. Peripheral sensitization is caused by the generation of inflammatory mediators, including prostaglandins, bradykinin, cytokines, neuropeptides, and nerve growth factors (collectively referred to as a sensitizing soup). Many of these sensitizing agents also activate quiescent (so-called silent or sleeping) nociceptors, thereby magnifying the pain response to nonpainful stimuli. Intense or sustained peripheral stimuli can also effect changes in the excitability of neurons located in the dorsal horn of the spinal cord. Temporal summation and cumulative depolarization (ie, wind-up) of impulses transmitted by pain fibers amplify and facilitate neuronal activity in dorsal horn neurons, leading to central sensitization (Figure 1). Clinically, central sensitization contributes to the development of allodynia and hypersensitivity at the site of injury (primary hyperalgesia) and further expands the extent of the painful area to noninjured tissue (secondary hyperalgesia). Peripheral and central sensitizations are responsible for primary and secondary hyperalgesia and contribute to the development of pain memory and

Prevention of central sensitization and pain by N-methyl-D-aspartate receptor antagonists

Review: Telazol – a review of its pharmacology and use in veterinary medicine

The purpose of this study was to assess safety and alterations in body fluid concentrations of voriconazole in normal horses on days 7 and 14 following once daily dose of 4 mg/kg of voriconazole orally for 14 days. Body fluid drug concentrations were determined by the use of high performance liquid chromatography (HPLC). On day 7, mean voriconazole concentrations of plasma, peritoneal, synovial and cerebrospinal fluids, aqueous humor, epithelial lining fluid (ELF), and urine were 1.47 ± 0.63, 0.61 ± 0.22, 0.70 ± 0.20, 0.62 ± 0.26, 0.55 ± 0.32, 79.45 ± 69.4, and 1.83 ± 0.44 μg/mL respectively. Mean voriconazole concentrations in the plasma, peritoneal, synovial and cerebrospinal fluids, aqueous humor, ELF and urine on day 14 were 1.60 ± 0.37, 1.02 ± 0.27, 0.86 ± 0.25, 0.64 ± 0.21, 0.68 ± 0.13, 47.76 ± 45.4 and 3.34 ± 2.17 respectively. Voriconazole concentrations in the bronchoalveolar cell pellet were below the limit of detection. There was no statistically significant difference between voriconazole concentrations of body fluids when comparing days 7 and 14. Results indicated that voriconazole distributes widely into body fluids.

Distribution of voriconazole in seven body fluids of adult horses after repeated oral dosing

Sellers, G., Lin, H. C., G. Riddell, M. G., Ravis, W. R., Lin, Y. J., Duran, S. H., Givens, M.D. Pharmacokinetics of ketamine in plasma and milk of mature Holstein cows. J. vet. Pharmacol. Therap. 33, 480–484.



The purpose of this study was to evaluate the pharmacokinetics of ketamine in mature Holstein cows following administration of a single intravenous (i.v.) dose. Plasma and milk concentrations were determined using a high-performance liquid chromatography assay. Pharmacokinetic parameters were estimated using a noncompartmental method. Following i.v. administration, plasma Tmax was 0.083 h and plasma Cmax was 18 135 ± 22 720 ng/mL. Plasma AUC was 4484 ± 1,398 ng·h/mL. Plasma t½β was 1.80 ± 0.50 h and mean residence time was 0.794 ± 0.318 h with total body clearance of 1.29 ± 0.70 L/h/kg. The mean plasma steady-state volume of distribution was calculated as 0.990 ± 0.530 L/kg and volume of distribution based on area was calculated as 3.23 ± 1.51 L/kg. The last measurable time for ketamine detection in plasma was 8.0 h with a mean concentration of 24.9 ± 11.8 ng/mL. Milk Tmax was detected at 0.67 ± 0.26 h with Cmax of 2495 ± 904 ng/mL. Milk AUC till the last time was 6593 ± 2617 ng·h/mL with mean AUC milk to AUC plasma ratio of 1.99 ± 2.15. The last measurable time that ketamine was detected in milk was 44 ± 10.0 h with a mean concentration of 16.0 ± 9.0 ng/mL.

Pharmacokinetics of ketamine in plasma and milk of mature Holstein cows.

Effect of PO Administered Gabapentin on Chronic Lameness in Horses

Isoflurane and sevoflurane are the two most commonly used inhalation anesthetics in veterinary medicin e today. This study compared the anesthetic effects between isoflurane and sevoflurane in 17 calves undergoing surgery for placement of portal and jugular vein cannulas. Using a randomized control trial, calves were assig ned to receive sevoflurane or isoflurane. Anesthesia was i nduced with xylazine and ketamine then maintained with the assigned inhalation anesthetic. Parameters for hear t rate, respiratory rate, indirect blood pressures, oxygen hemoglobin saturation and end-tidal carbon dioxide were monitored and recorded during surgery. The anesthetic concentrations of the vaporizers were adjusted acco rding to the calves’ responses, e.g., blood pressur e, eye position, respiratory and heart rate, to surgical s timulation. Upon discontinuation of the inhalation anesthetic, calves were placed in sternal recumbency and recovery variables including time to extubation, time to first movement, attempts to stand and time to standing were observed and recorded. Statistical analysis was performed using a two-sample t-test on the recorded variables . There were no statistical differences between iso flurane and sevoflurane for any of the parameters recorded duri ng anesthetic maintenance or recovery. The results of this study showed a faster time to first movement and extubation, 3.38±1.85 min and 11.75±3.73 min for sevoflurane compared to 7.56±5.34 min and 15.56±8.69 min for isoflurane, respectively. Attempts to stand were 3.00 ±2.14 for sevoflurane and 3.22±1.79 for isoflurane. Thoug h the time to standing during recovery was not stat istically different between anesthetics, the values did indic ate a quicker trend of recovery from sevoflurane. B oth inhalation anesthetics produced comparable anesthet ic qualities and there were no statistical differen ces between the parameters recorded during maintenance of anesthesia. On the basis of the reported results, sevofl urane and isoflurane are suitable inhalation anesthetics for use in calves. However, present cost of sevoflurane is a limiting factor for its use in food animals.

Comparison of Isoflurane and Sevoflurane Anesthesia in Holstein Calves for Placement of Portal and Jugular Vein Cannulas

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