Veterinary Dental Photobiomodulation: Assessing Post-Treatment Gingival Inflammation in Canines.

Objective: This research aims to determine the effect photobiomodulation treatment has on oral inflammation after routine dental prophylaxis in canines. Background: Photobiomodulation therapy after dental procedures has been documented to reduce inflammation in human and animal models. Methods: Canines were randomly assigned into three groups: control group (CG; n = 15), left side treated group (LTG; n = 15), and right side treated group (RTG; n = 15). The canines in the treatment groups received four points of irradiation [GaAlInP-650 nm, continuous wave (CW), 0.1 W, 0.2 W/cm2, 100 sec, 10 J, 20 J/cm2]. The gingiva was evaluated by a veterinary investigator blinded to the treatment groups for erythema and edema on the day following treatment. Student's t-test and Student's paired t-test were used for data analysis. Results: Reductions in composite inflammation (p = 0.008) and erythema (p = 0.030) were observed in the LTG relative to the CG at the location of the left dental arcade. Reductions in composite inflammation (p = 0.025) and erythema (p = 0.013) were also observed in the combined treated arcades of the LTG and RTG when compared to the CG. Conclusions: The results indicate that the canines who received a single photobiomodulation treatment on the left dental arcade demonstrated a decrease in inflammation and erythema.

Caseous lymphadenitis outbreak in a small ruminant herd.

BACKGROUND: Caseous lymphadenitis (CLA) is a chronic disease caused by the bacterium Corynebacterium pseudotuberculosis that affects small ruminants worldwide. AIM: The objective of this case report is to describe an outbreak of CLA that occurred at the California State Polytechnic University, Pomona, in the summer of 2019 and the management strategies employed therein to contain the spread. METHODS: After careful physical screening, blood serum samples from the entire herd (n = 218 sheep, n = 32 goats) were tested using the synergistic hemolysis inhibition test to reveal antibodies present. RESULTS: Animals with titer counts above 1:64 and/or containing CLA lesions were isolated and culled (n = 33 sheep,n = 4 goats) within 2 weeks of testing. Female sheep (n = 160) had higher titer counts and were culled at a much higher rate than male sheep (n = 58) (20% vs. 1.72%), whereas male goats (n = 9) more often had high titer counts and were culled as opposed to female goats (n = 23) (33.33% vs. 4.35%). CONCLUSION: Vaccines were administered to the remainder of the herd following culling. Additional management strategies were employed, the outcome of which was a zero recurrence through August 2021.

Quantifying body surface temperature differences in canine coat types using infrared thermography.

Infrared thermography (IRT) has been used to assess the health of canines by measuring surface temperatures. However, little is known about the effect hair coat differences has on expected surface temperature in healthy canines under the influence of hair coat differences. The aim of this study was to identify the influence of coat characteristics in body surface temperature (BST) in canines (Canis lupus familiaris). To determine the changes in BST, an infrared thermal imaging camera (i.e. FLIR B400) was used. Thermal images of the left and right sides of privately-owned dogs (n = 50) were acquired. Each animal acclimated in an indoor environment away from direct sunlight (23 ±â€¯2.0 °C) for 15 min, and images were taken at a distance 0.67 ±â€¯0.24 m. Regions of interest (ROIs) of mean surface temperatures were examined across the lateral surface of each animal. No statistical differences were detected based on laterality (P = 0.08). Mean BSTs were categorized by each dog's hair coat type: short coat (SC), curly coat (CC), long coat (LC), and double coat (DC). These BSTs were then analyzed using two-way analysis of variance, or ANOVA, (Shapiro-Wilk) and pairwise comparison. SC animals had the highest BST (31.77 ±â€¯0.19 °C; P < 0.001) whereas LC (28.14 ±â€¯0.31 °C; P < 0.001) and DC animals (28.25 ±â€¯0.23 °C; P < 0.001) were lower in BST. CC animals portrayed intermediate BST (29.85 ±â€¯0.33 °C; P < 0.001). The Pearson correlation and one-way ANOVA between rectal temperature and BST and coat type were not statistically significant (r = -0.24 and P = 0.07, respectively). Results indicate that short-haired dogs exhibit a more drastic increase in BST (approximately 2 °C) in comparison to other dogs and this should be considered in future clinical applications.

Photobiomodulation as an Inflammatory Therapeutic Following Dental Prophylaxis in Canines.

Objective: The aim of this study was to determine if a single photobiomodulation treatment can reduce oral erythema and edema following routine dental prophylaxis in canines. Background: Photobiomodulation therapy has been documented to accelerate healing time through mitigation of erythema and edema in human and veterinary patients. Methods: Canine patients were randomly assigned into three groups: CG (Control, n = 9, mock gingiva treatment without irradiation), LTG (left side treated, n = 8, irradiation of left upper and lower dental arcade), and RTG (right side treated, n = 7, irradiation of right upper and lower dental arcade). Immediately following anesthetized dental prophylaxis, the canines in the RTG and LTG received four points of irradiation (GaAlInP-650 nm, continuous wave, 0.1 W, 0.2 W/cm2, 100 sec, 10 J, 20 J/cm2). Erythema and edema along the gingival surface of each dental arcade were scored 24 h after treatment by a blinded veterinary evaluator. Analysis of variance and Bonferroni correction were used for data analysis. Results: Using a composite evaluation, there was significantly lower inflammation scores for the RTG (p = 0.017) and LTG (p = 0.025) relative to the CG at the location of the lower right dental arcade. Evaluating erythema individually, a significant reduction was found in the LTG (p = 0.049) when compared with the CG for the lower left dental arcade. Conclusions: Despite the limitations in this study, the canines who received a single photobiomodulation treatment demonstrated some degree of reduction in oral inflammation and erythema following dental prophylaxis.

Magnetic Resonance Imaging Appearance and Mechanism of Action of Five Hemostatic Agents Used in Neurosurgery.

OBJECTIVE: To describe the magnetic resonance (MR) image appearance of 5 hemostatic agents placed in the brain, and to review their clinical application. STUDY DESIGN: Descriptive ex vivo and in vivo study. ANIMALS: Canine cadavers (n=4), client-owned dogs (n=4). METHODS: Heads from 4 canine cadavers were used, each with 5 hemostatic agents placed in specific locations in the brain. Hemostatic agents were used in their native form in 2 cadaveric brains, and in 2 others the materials were saturated with fresh whole blood prior to placement to mimic application in a field of active hemorrhage. The heads underwent MR imaging and the images were reviewed. Postoperative MRI images from 4 dogs undergoing brain tumor resection were retrospectively reviewed and compared to the images from the cadavers. All clinical cases and cadaveric specimens underwent surgical closure prior to MR imaging including placement of titanium mesh over the craniotomy defect with a dural graft of porcine small intestinal submucosa (SIS) sealed with Tisseel (fibrin sealant). RESULTS: The SIS and Tisseel used in the dural graft were consistently indistinguishable from the surrounding tissues on MR images. The MR imaging appearance of the remaining 4 hemostatic agents (Gelfoam, Avitene, Surgicel, and Floseal) placed on the surface or in the parenchyma of canine brain, varied with MR sequence weighting and blood saturation. CONCLUSION: Accurate evaluation of the degree of brain tumor resection on postoperative MR images requires careful differentiation between hemorrhage, residual tumor, and hemostatic agents implanted.

Chronic nicotine and ethanol exposure both disrupt central ventilatory responses to hypoxia in bullfrog tadpoles.

The central hypoxic ventilatory response (HVR) comprises a reduction in ventilatory activity that follows a peripherally mediated ventilatory augmentation. Chronic early developmental exposure to nicotine or ethanol are both known to impair the peripherally mediated HVR, and nicotine impairs the central HVR, but the effect of ethanol on the central HVR has not been investigated. Additionally, chronic nicotine and ethanol exposure are known to impair ventilatory responses to hypercapnia in bullfrog tadpoles but HVRs have not been tested. Here early and late metamorphic tadpoles were exposed to either 30 µg/L nicotine or 0.15-0.05 g/dL ethanol for 10 wk. Tadpole brainstems were then isolated and the neurocorrelates of ventilation were monitored in vitro over 180 min of hypoxia (PO2=5.05±1.04 kPa). Both nicotine and ethanol exposure disrupted central HVRs. Nicotine impairments were dependent on development. Central HVRs were impaired only in early metamorphic nicotine-exposed tadpoles. Both early and late metamorphic ethanol-exposed tadpoles failed to exhibit central HVRs. Thus, central HVRs are impaired following both nicotine and ethanol exposure. Such failure to decrease ventilatory activity during hypoxia indicates that central hypoxic ventilatory depression is an active suppression of neural activity in response to hypoxia rather than a metabolic consequence of O2 limitation, and that exposure to ethanol (across development) or nicotine (during early development) disrupts mechanisms that normally induce active ventilatory depression.

Chronic, but not acute, ethanol exposure impairs central hypercapnic ventilatory drive in bullfrog tadpoles.

Chronic ethanol exposure early in development is deleterious to neural development and may impair responses to ventilatory stimuli (ventilatory drive) that maintain homeostasis. Central hypercapnic ventilatory drive (CHVD) increases ventilation to ensure pH homeostasis and accommodate the metabolic production of CO(2). We tested the hypothesis that chronic ethanol exposure impairs CHVD in bullfrog tadpoles. Early and late metamorphic tadpoles were exposed in vivo to 0.12-0.06 g/dL ethanol for either 3- or 10-wk durations. Brainstems from these animals were isolated and the neural correlates of ventilation were recorded in vitro during superfusion with normocapnic (1.5% CO(2):98.5% O(2)) and hypercapnic (5.0% CO(2):95.0% O(2)) artificial cerebral spinal fluid. Normocapnic neuroventilation was unaffected by chronic ethanol exposure. The typical response to hypercapnia, an increase in lung burst frequency, was lost following 10 but not 3 wk of ethanol exposure in both early and late metamorphic tadpoles. The neuroventilatory effects of chronic ethanol exposure were distinguishable from those of acute central ethanol (0.08 g/dL) exposure, which attenuated early metamorphic tadpole normocapnic neuroventilation, but had no effect on tadpole CHVD. Thus, 10 wk of ethanol exposure both early and late in metamorphosis impairs CHVD in bullfrog tadpoles.

Assessment of blood pool, soft tissue, and skeletal uptake of sodium fluoride F 18 with positron emission tomography-computed tomography in four clinically normal dogs.

OBJECTIVE: To determine the ideal interval to image acquisition after IV injection of sodium fluoride F 18 ((18)F-NaF) and evaluate biodistribution of the radiopharmaceutical in clinically normal skeletally immature dogs. ANIMALS: 4 female dogs. PROCEDURES: Each dog was anesthetized for evaluation with a commercial hybrid positron emission tomography (PET)-CT instrument. A low-radiation dose, whole-body CT scan was acquired first. An IV injection of (18)F-NaF (0.14 mCi/kg) was administered, and a dynamic PET scan centered over the heart and liver was acquired during a period of 120 minutes. Uptake of (18)F-NaF in the blood pool, soft tissues, and skeletal structures was evaluated via region of interest analysis to derive standardized uptake values and time-activity curves, which were used to determine the optimal postinjection time for skeletal image acquisition. Biodistribution was also assessed from a final whole-body PET-CT scan acquired after the dynamic scan. RESULTS: Time-activity curves revealed a rapid decrease in the amount of radiopharmaceutical in the blood pool and soft tissues and a rapid increase in the amount of radiopharmaceutical in bones soon after injection. At 50 minutes after injection, the greatest difference in uptake between soft tissues and bones was detected, with continued subtle increase in uptake in the bones. Uptake of (18)F-NaF was slightly increased at growth plates and open ossification centers, compared with that at other parts of the bone. CONCLUSIONS AND CLINICAL RELEVANCE: At 50 minutes after IV injection of (18)F-NaF at the dose evaluated, PET-CT yielded excellent bone-to-background ratio images for evaluation of the skeletal system in dogs.

Neuroplasticity of the central hypercapnic ventilatory response: teratogen-induced impairment and subsequent recovery during development.

Neuroventilation is highly plastic and exposure to either of two distinct teratogens, nicotine or ethanol, during development results in a similar loss of the neuroventilatory response to hypercapnia in bullfrog tadpoles. Whether this functional deficit is permanent or transient following nicotine or ethanol exposure was unknown. Here, we tested the persistence of hypercapnic neuroventilatory response impairments in tadpoles exposed to either 30 microg/L nicotine or 0.12-0.06 g/dL ethanol for 10 weeks. Brainstem breathing-related neural activity was assessed in tadpoles allowed to develop teratogen-free after either nicotine or ethanol exposure. Nicotine-exposed animals responded normally to hypercapnia after a 3-week teratogen-free period but the hypercapnic response in ethanol-exposed tadpoles remained impaired. Tadpoles allowed to develop for only 1 week nicotine free after chronic exposure were unable to respond to hypercapnia. The hypercapnic response of ethanol-exposed tadpoles returned by 6 weeks following chronic ethanol exposure. These findings suggest that some nicotine- and ethanol-induced impairments can be resolved during early development. Understanding both the disruptive effects of nicotine and ethanol exposure and how impaired responses return when teratogen exposure stops may offer insight on the function and plasticity of respiratory control.

Cholinergic sensitivity of the developing bullfrog (Rana catesbeiana) does not explain vulnerability to chronic nicotine exposure.

Juvenile bullfrogs previously identified as highly sensitive to acute nicotine, demonstrated normal neuroventilation following 3 wk of chronic nicotine exposure. Acute bath application of 1 microM galantamine, an acetylcholinesterase inhibitor, significantly attenuated both bullfrog normocapnic neuroventilation and response to hypercapnia in a fashion similar to that of acute nicotine. This would suggest that the developmental increase in nicotine sensitivity does not enhance vulnerability to chronic exposure, and that acute nicotine acts via endogenous acetylcholine pathways to depress neuroventilation and hypercapnic drive.

Nicotine elicits a developmentally dependent depression in bullfrog neuroventilatory response to CO(2).

Nicotine exposure is associated with numerous neurodevelopmental aberrations, including impairment of the neuroventilatory response to hypercapnia in bullfrog tadpoles and mouse neonates following prolonged developmental exposure. It is unclear how acute nicotine exposure affects neuroventilation and the neuroventilatory response to hypercapnia, or how these effects might differ from those of chronic exposure. In this study the neural correlates of ventilation were recorded from in vitro brainstem preparations derived from early and late metamorphic tadpoles and juvenile bullfrogs. Lung and gill/buccal breath parameters were compared during control (=0), 18, 50, 100, and 200microg/L nicotine conditions, applied during normocapnia (1.5% CO(2)) and hypercapnia (5.0% CO(2)). All preparations demonstrated a reduction in normocapnic lung burst frequency and an attenuated hypercapnic response during acute nicotine treatment. The concentrations necessary to elicit both of these responses decreased from 200microg/L nicotine in early metamorphic tadpole brainstems to 18microg/L nicotine in juvenile bullfrog brainstems, which suggests a developmental increase in acute nicotine sensitivity that is distinguishable from the developmental changes in vulnerability to chronic nicotine exposure. In summary, acute nicotine exposure impaired central CO(2) response, attenuated rather than enhanced respiratory drive, and had more pronounced effects at progressively lower concentrations as development proceeded through metamorphosis.

Timing and duration of developmental nicotine exposure contribute to attenuation of the tadpole hypercapnic neuroventilatory response.

The ability for air-breathing vertebrates to adjust ventilation in response to increased CO(2) (hypercapnia) is fundamental to maintaining pH homeostasis. Developmental nicotine exposure has been shown to impair tadpole neuroventilatory responses to hypercapnia following 8-12 weeks of exposure. It is not clear, however, to what extent the timing of exposure during development and/or the duration over which the exposure takes place contribute to this impairment. Here, tadpoles were exposed to 30 microg/L of nicotine for 3- or 10-week durations, either early or late in tadpole development. Correlates of tadpole lung neuroventilation were monitored during normocapnic (1.5% CO(2)) and hypercapnic (5% CO(2)) conditions of isolated brainstems. Preparations derived from early metamorphic tadpoles failed to increase lung neuroventilation in response to hypercapnia whether they had been exposed to nicotine for 3 or 10 weeks. Preparations derived from late metamorphic tadpoles failed to respond to hypercapnia after being exposed to nicotine for 10 weeks. These results suggest that both the developmental timing and duration of exposure are important when considering nicotine's effect on the hypercapnic neuroventilatory response.