Cyclooxygenase expression and prostanoid production in pyloric and duodenal mucosae in dogs after administration of nonsteroidal anti-inflammatory drugs

OBJECTIVE: To assess cyclooxygenase (COX) expression and prostanoid concentrations in pyloric and duodenal mucosae of dogs after administration of nonsteroidal anti-inflammatory drugs (NSAIDs). ANIMALS: 8 healthy dogs. PROCEDURES: Each dog received carprofen (4.4 mg/kg, q 24 h), deracoxib (2 mg/kg, q 24 h), aspirin (10 mg/kg, q 12 h), and placebo (1 dog treat, q 24 h) orally for 3 days (4-week interval between treatments). Before study commencement (baseline) and on day 3 of each treatment, pyloric and duodenal mucosal appearance was assessed endoscopically and biopsy specimens were obtained for histologic examination. Cyclooxygenase-1 and COX-2 protein expressions were assessed via western blotting, and prostanoid concentrations were measured via ELISAs. An ANOVA was used to analyze data. RESULTS: Treatments had no effect on mucosal appearance and ulceration was not evident histologically. In pyloric and duodenal mucosae, COX-1 expression was unaffected by treatments. Cyclooxygenase-2 expression remained unchanged in pyloric mucosa; in duodenal mucosa, aspirin significantly increased COX-2 expression, compared with effects of deracoxib and carprofen. At baseline, total prostaglandin and thromboxane B2 concentrations in pyloric mucosa were significantly greater than those in duodenal mucosa. Aspirin significantly decreased both prostanoid concentrations in both mucosal tissues, compared with other treatments. In pyloric mucosa, carprofen administration significantly decreased total prostaglandin and thromboxane B2 concentrations, compared with deracoxib administration. CONCLUSIONS AND CLINICAL RELEVANCE: In dogs, prostanoid synthesis was greater in pyloric mucosa than it was in duodenal mucosa. Nonselective NSAIDs significantly decreased prostanoid concentrations in these mucosae, compared with the effects of a selective COX-2 NSAID.     

Quantification of Mycobacterium avium subspecies in pig tissues by real-time quantitative PCR

Background

Mycobacterioses in animals cause economical losses and certain Mycobacterium avium subspecies are regarded as potential zoonotic agents. The evaluation of the zoonotic risk caused by M. avium subspecies requires information about the quantities of Mycobacterium strains in infected animals. Because M. avium subspecies in pig tissues are difficult or even impossible to quantify by culturing, we tested the suitability of a culture-independent real-time quantitative PCR (qPCR) assay for this purpose.

Methods

Mycobacterial DNA was extracted from porcine tissues by a novel method and quantified by Mycobacterium genus specific qPCR assay targeting the 16S rRNA gene.

Results

The response of the qPCR assay to the amount of M. avium subspecies avium mixed with porcine liver was linear in the range of approximately log10⁵ to log10⁷Mycobacterium cells per 1 g of liver. The assay was validated with three other M. avium subspecies strains. When the assay was applied to porcine lymph nodes with or without visible lesions related to Mycobacterium avium subspecies infections, around 10⁴–10⁷ mycobacterial genomes per gram of lymph nodes were detected.

Conclusions

The qPCR assay was found to be suitable for the quantification of Mycobacterium avium subspecies in porcine lymph nodes and liver.     

The effect of four anesthetic protocols on the spleen in dogs

Splenic enlargement following administration of barbiturates has been well described in dogs; other agents have not been investigated. This study aimed to compare the effects of four anesthetic protocols on splenic size.
Twenty-four fasted Beagle dogs scheduled for laparotomy were allocated to one of the four groups. Group 1: acepromazine and butorphanol followed by induction with thiopental; Group 2: acepromazine and butorphanol followed by induction with propofol; Group 3: medetomidine and butorphanol followed by induction with propofol; Group 4: medetomidine and butorphanol followed by induction with ketamine and diazepam. Anesthesia was maintained with halothane in oxygen, intravenous fluids were administered. Splenic length, width and height were measured once when the abdomen was opened and again just prior to closure. Spleens were also traced, the image was digitized, and the area was calculated. PCV and total solids were measured before and after pre-medication, after induction, and each time the spleen was measured. Data were analyzed using a Repeated Measures anova with splenic variables indexed by body surface area and dose of induction agent as a covariate.
Area and width of the spleens were less in the dogs of Groups 2 and 3 than in those of the other groups. Splenic area and length did not change significantly during surgery. Dosage of propofol was not significantly different between Groups 2 and 3. Baseline PCV was not significantly different among groups and decreased significantly in all dogs, but at different times. In Groups 1 and 2, the decrease occurred after pre-medication, in Group 3 at induction, and in Group 4 during surgery. A significant decrease in TS occurred in all groups during surgery.
We concluded that the use of propofol resulted in smaller spleen size during surgery than that following the use of thiopental. Multiple factors influenced the PCV.     

The future of antiinflammatory therapy.

The cells and mediators that make up the inflammatory response have the potential to injure tissues and contribute to the pathophysiology of many inflammatory diseases. Strategies to reduce neutrophil migration into sites of inflammation and subsequent activation by inhibiting integrin-mediated adhesion hold promise for successful treatment of a variety of inflammatory diseases. New pharmacologic agents that specifically target prostanoid mediators of inflammation by specifically inhibiting the activity of cyclooxygenase 2 are potent antiinflammatory agents with fewer gastrointestinal side effects than nonspecific cyclooxygenase inhibitors. These areas of antiinflammatory research are rapidly yielding drugs with diverse future applications in equine medicine.     

Antimicrobial susceptibility of bacteria isolated from neonatal foal samples submitted to a New Zealand veterinary pathology laboratory (2004 to 2013)

AIMS: To describe antimicrobial susceptibility, and identify antimicrobial resistance (AMR), in bacteria isolated from New Zealand foals.

METHODS: A database search was performed of submissions to a veterinary pathology laboratory between April 2004 and December 2013 for bacterial culture of samples from foals <3 weeks of age. Culture and susceptibility results were compiled with demographic information. Susceptibility results were as defined for the Kirby-Bauer disk diffusion susceptibility test based on Clinical Laboratory Standards Institute guidelines. Multi-drug resistance (MDR) was defined as non-susceptibility to ≥3 of a panel of antimicrobials (ceftiofur, enrofloxaxin, gentamicin, penicillin, tetracycline, trimethoprim-sulfonamide); penicillin susceptibility was not included for Gram-negative isolates.

RESULTS: Submissions from 102 foals were examined, and 127 bacterial isolates were cultured from 64 (63%) foals. Of the 127 isolates, 32 (25%) were Streptococcus spp., 30 (24%) were Staphylococcus spp., 12 (10%) were Enterococcus spp. and 26 (21%) were Escherichia coli. Of 83 Gram-positive isolates, 57 (69%) were susceptible to penicillin. Over all isolates, 92/126 (73%) were susceptible to gentamicin and 117/126 (93%) to enrofloxacin; 62/82 (76%) of Gram-positive, and 22/42 (52%) of Gram-negative bacteria were susceptible to ceftiofur; 53/81 (65%) of Gram-positive, and 23/44 (52%) of Gram-negative bacteria were susceptible to tetracycline; 59/82 (72%) of Gram-positive, and 23/44 (43%) of Gram-negative bacteria were susceptible to trimethoprim-sulfonamide. Of 126 isolates, 33 (26%) had MDR; >1 isolate with MDR was cultured from 24/64 (38%) foals, and ≥2 isolates with MDR were recovered from 8/64 (13%) foals.

CONCLUSIONS: Multi-drug resistance, including resistance to commonly used antimicrobials, was found in bacterial isolates from foals in New Zealand.

CLINICAL RELEVANCE: The results of this study are of concern from a treatment perspective as they indicate a potential for antimicrobial treatment failure. For future surveillance of AMR and the creation of national guidelines, it is important to record more data on samples submitted for bacterial culture.     

Evaluation of intraperitoneal and subcutaneous lidocaine and bupivacaine for analgesia following ovariohysterectomy in the dog

The role of ketamine (K) in pain management is controversial. It is reported to provide visceral analgesia in cats. This study aimed to assess its somatic actions using a thermal threshold (TT) model. Six cats (four spayed females, two castrated males, 4.3–7.2 kg) participated in the study. The day before each study, the thorax of each of the cats was shaved and a cephalic catheter was placed. TT was measured using a device specifically developed for cats. A heater element and temperature sensor housed in a small probe were held against the thorax of the cats with an elastic band and pressure bladder to assure consistent contact. The skin temperature was recorded before each test, then the heater was activated. When the cat responded by flinching, turning, or jumping, the stimulus was terminated and the threshold temperature was recorded. Treatments were 2 mg kg^?1 of K (10 mg mL^?1), or 0.2 mL kg^?1 of saline (S) IV, given in a randomized cross‐over design with at least 1 week between treatments. The investigator was blinded to the treatment. TT was measured thrice before treatment (baseline threshold) at 15 minutes, then every 30 minutes for 8 hours and once at 24 hours after injection. Data were analyzed using a four‐factor anova . Cats were sedated for 45 minutes following K treatment. There was no difference in baseline TT between treatments (K = 41.9 ± 1.7 °C, S = 41.0 ± 1.45 °C), and no change in TT at any time in the S group. TT increased significantly at 15 and 30 minutes after K, then decreased below baseline values between 210 and 390 minutes, with a nadir of 38.8 ± ± 1.05 °C at 390 minutes. During this time period, cats exhibited normal activity, but responses to thermal stimuli were exaggerated. This study suggested that K caused a delayed onset hyperalgesia in cats.     

Alfaxalone induction dose following administration of medetomidine and butorphanol in the dog

ObjectiveTo determine in dogs the effects of medetomidine and butorphanol, alone and in combination, on the induction dose of alfaxalone and to describe the induction and intubation conditions.Study designProspective, randomized, blinded clinical trial.AnimalsEighty-five client-owned dogs (ASA 1 or 2).MethodsSubjects were block randomized to treatment group according to temperament. The treatment groups were: medetomidine 4 μg kg^?1 (M), butorphanol 0.1 mg kg^?1 (B), or a combination of both (MB), all administered intramuscularly. After 30 minutes, a sedation score was assigned, and alfaxalone 0.5 mg kg^?1 was administered intravenously over 60 seconds by an observer who was unaware of treatment group. Tracheal intubation conditions were assessed and, if tracheal intubation was not possible after 20 seconds, further boluses of 0.2 mg kg^?1 were given every 20 seconds until intubation was achieved. Induction dose and adverse events (sneezing, twitching, paddling, excitement, apnoea and cyanosis) were recorded; induction quality and intubation conditions were scored and recorded.ResultsThe mean dose of alfaxalone required for induction was similar for groups M and B: 1.2 ± 0.4 mg kg^?1. The mean dose requirement for group MB (0.8 ± 0.3 mg kg^?1) was lower than groups M and B (p < 0.0001). Induction dose was not influenced by temperament or level of sedation. Induction and intubation scores did not differ between treatment groups. Adverse events were noted in 16 dogs; there was no association with treatment group, temperament or level of sedation.Conclusions and clinical relevanceMedetomidine and butorphanol administered in combination reduce the anaesthetic induction dose of alfaxalone compared to either agent alone. This difference should be taken into account when using this combination of drugs in a clinical setting.