Sildenafil-induced priapism in a dog : an unusual case report.

BACKGROUND: Priapism is defined as erection that lasts for more than 4 h without sexual stimulation. There are various causes of priapism, but there are no reports of sildenafil-induced priapism in dogs. In human medicine, there were no pre-marketing reports of priapism caused by sildenafil, but post-marketing surveillance has shown that it is rare. In cases of pulmonary hypertension in dogs, sildenafil is the first-line drug of choice for symptomatic relief. CASE PRESENTATION: An 11-year-old neutered male Maltese dog that presented with tachypnea and cough was diagnosed with myxomatous mitral valve disease, American College of Veterinary Internal Medicine (ACVIM) stage C, and was treated medically. Eighteen months after the diagnosis, severe pulmonary hypertension occurred due to left heart disease. At 20 months postdiagnosis, pleural effusion occurred, and sildenafil (2 mg/kg twice daily) was added to the existing treatment. Two weeks later, the dyspnea recurred, confirming pleural fluid recurrence, and sildenafil was increased to 2 mg/kg thrice daily. One day later, the patient developed persistent erections and penile pain. Penile amputation and urethrostomy were recommended but were refused; therefore, analgesia and palliative care were provided. The patient died of acute dyspnea 22 months after the first presentation, with no specific priapism recurrence at the time of death. CONCLUSION: To the best of our knowledge, this is the first report of sildenafil-induced priapism in a dog with pulmonary hypertension.

[Mycotoxin intoxication in 54 dogs after ingestion of walnuts]. / Mykotoxinvergiftung nach Walnussaufnahme bei 54 Hunden.

OBJECTIVE: The aim of this retrospective study was to decribe the intoxication with tremorgenic mycotoxins subsequent to the ingestion of walnuts in a large population of dogs and the evaluation of the development of the clinical signs under the initiated treatment. MATERIAL AND METHODS: The study included 54 dogs exhibiting signs of tremor, hyperesthesia, hyperthermia and ataxia, in particular a few hours following observed ingestion of walnuts or its justified suspicion. RESULTS: The patients were presented to the clinic mostly during winter and spring. Fifty-three of 54 dogs were hospitalized for symptomatic, decontaminating and eliminating therapy (98%). Symptomatic treatment comprised of anticonvulsant therapy in 14 dogs (26%) and an antiemetic therapy in for half of the patients (n=27; 50%). A forced emesis for decontamination was undertaken in only 6 patients due to the severity of their neurological symptoms (11%). For further decontamination, an oral administration of activated charcoal after improvement of clinical signs (n=39; 72%). The majority of dogs (n=45; 83%) additionally received an intravenous lipid therapy for toxin elimination and isotonic crystalloid solution to compensate fluid losses. There were no side effects observed following the administration of intravenous lipid therapy. The majority of dogs were hospitalized for a duration of 2 days (n=44; 81%). In most dogs, examination was unremarkable on the day of their release (n=39; 72%). Potential long-term sequelae of the intoxication were not recorded in any patient. CONCLUSION: Due to the lipophilic nature of mycotoxins, the use of intravenous lipid therapy may considered for toxin elimination purposes. The prognosis of mycotoxin intoxication following walnut ingestion is good with decontamination and elimination measures. CLINICAL RELEVANCE: In the case of unspecific neurological signs such as tremor, ataxia and hyperesthesia as well as a corresponding preliminary report, an intoxication with mycotoxin-containing walnuts should be considered.

Abdominal radiographic features of anticoagulant rodenticide toxicity in 14 dogs and 2 cats.

Background: Anticoagulant rodenticide toxicity is commonly encountered in veterinary practice that can result in internal bleeding. We have observed dogs with retroperitoneal hemorrhage secondary to anticoagulant rodenticide toxicity. However, abdominal radiographic changes in dogs with rodenticide toxicity have not been studied and retroperitoneal hemorrhage secondary to rodenticide toxicity has rarely been reported. Aim: The objective is to describe abdominal radiographic features of anticoagulant rodenticide toxicity and concurrent thoracic radiographic changes in dogs and cats. Methods: Dogs and cats diagnosed with rodenticide toxicity and with available abdominal radiographs were included in this retrospective analysis. Board-certified radiologists reviewed the abdominal and thoracic radiographs. Evaluation of abdominal radiographic changes included assessment of peritoneal or retroperitoneal effusion, subcutaneous hemorrhage, and internal hemorrhage of abdominal organs. Results: Fourteen dogs and two cats with confirmed rodenticide toxicity were included in the study. In dogs, retroperitoneal effusion (28.6%) was the most commonly observed abdominal radiographic change, followed by peritoneal effusion (14.3%). Thoracic radiographic changes in dogs included pleural effusion (63.6%) and mediastinal widening (63.6%) as the most common findings, followed by pulmonary hemorrhage (36.4%) and tracheal narrowing (36.4%). Subcutaneous hemorrhage or edema (9.1%) was also noted. No abdominal radiographic changes consistent with hemorrhage secondary to rodenticide toxicity were noted in the two cats. Conclusion: Based on our findings, it is suggested that rodenticide toxicity may result in retroperitoneal effusion even in the absence of thoracic disease. Therefore, abdominal radiographs may be valuable when suspecting hemorrhage due to coagulopathy. However, abdominal radiographic changes associated with rodenticide toxicity are considered rare in cats.

Clinical methemoglobinemia secondary to administration of hydroxyurea at therapeutic doses in a dog.

Methemoglobinemia secondary to administration of hydroxyurea is only reported in veterinary medicine as a result of accidental ingestion of high doses, and once at therapeutic dose in human medicine. A 2.5-year-old female spayed mixed breed dog was presented for acute signs of neurologic disease and diagnosed with severe erythrocytosis without an identified underlying cause, leading to suspicion of polycythemia vera. The dog was managed with phlebotomies, supportive care, and administration of hydroxyurea. Within 2 h of administration of hydroxyurea (37 mg/kg) administration, respiratory distress with cyanosis, and methemoglobinemia developed. Signs resolved within 24 h but recurred after a second administration of lower dosage of hydroxyurea (17 mg/kg) 20 days later. The dog remained asymptomatic except for mild cyanosis but was humanely euthanized for lack of relevant improvement of signs of neurologic disease. This case report documents the repeated occurrence of methemoglobinemia in a dog after administration of hydroxyurea at therapeutic doses.

[Acute poisonings in dogs - a retrospective case study over 5 years]. / Akute Vergiftungen bei Hunden ­ Falluntersuchung über einen Zeitraum von 5 Jahren.

OBJECTIVE: The aim of this retrospective study was to analyze the clinical signs, confirmed or suspected toxicants, treatments and outcomes of poisoning cases in dogs presented over a 5-year period to the emergency service of a small animal referral center. MATERIAL AND METHODS: Medical records of 634 dogs were evaluated for a history of confirmed or presumed poisoning, suspected toxicant, clinical signs, treatment, and patient outcome. The probability of poisoning was graded based on the patient history, clinical findings, toxicologic examination and - in some cases - investigation of gastrointestinal contents. RESULTS: Most dogs were hospitalized (77%) due to poisoning with mostly unknown toxicants (33%), food residues (18%), rodenticides (10%), tremorgenic mycotoxins (8%), medications (7%) and various plants (7%), followed by recreational drugs (5%), chemicals (4%), molluscicides (3%), antiparasitics (2%), feces (2%), nuts (2%), or toxins of animal origin (1%). Patients were presented predominantly showing neurologic signs (56%), reduced general condition (39%), and cardiovascular or hydration status abnormalities (26%). The survival rate was 97%. Most dogs were clinically unremarkable at the time of hospital discharge (70%). An additional 18% of the survivors had no apparent complications by the time of discharge. Toxicant-related complications (20.5%) included hemorrhage (4%), hepatic (4%), renal (4%), respiratory (3%), gastrointestinal (3%), cardiovascular (3%), and/or central nervous system (3%) complications, or clinically relevant hypoglycemia (0.3%). CONCLUSION AND CLINICAL RELEVANCE: In the present study, poisoning in dogs was mostly associated with the ingestion of food residues, but the causative toxicant remained unidentified in many cases. Neurological signs were the major clinical presentation. The survival rate (97%) in this study was higher compared to those reported by other investigators.

Successful treatment of bifenthrin toxicosis using therapeutic plasma exchange.

OBJECTIVE: To describe a case of bifenthrin toxicosis in a dog with a successful outcome following the use of therapeutic plasma exchange (TPE) and intralipid therapy. CASE SUMMARY: An 8-month-old female neutered poodle mix dog ingested an unknown amount of powered bifenthrin, which resulted in acutely altered mentation, cranial nerve deficits, and intractable tremors that persisted in severity despite aggressive medical management to include intravenous fluids, intravenous lipid emulsion, anticonvulsant medications, and methocarbamol. TPE was initiated after lack of significant clinical improvement 12 hours after initial presentation. The dog underwent cardiopulmonary arrest (CPA) following approximately 1 plasma volume equivalent exchange. The dog was successfully resuscitated and showed marked improvement 12 hours postarrest and post-TPE treatment. Serum bifenthrin concentrations were analyzed prior to TPE (445.38 ng/mL) and ∼10 hours after TPE (51.18 ng/mL), which resulted in an 89% reduction in serum bifenthrin concentration. NEW INFORMATION: TPE may be a promising adjunctive therapeutic modality for bifenthrin toxicosis in dogs.

Cyanide toxicity secondary to apricot (Prunus armeniaca) kernel meal ingestion in a canine.

Cyanide is one of the most rapidly acting, lethal poisons in human and veterinary medicine. This case report discusses a novel case of cyanide toxicity from apricot (Prunus armeniaca) kernel ingestion in a canine and alternative treatment modalities. A 9.5-year-old female spayed Golden Retriever presented for vomiting and collapse after ingestion of apricot kernel meal. Laboratory findings, including a high anion gap metabolic acidosis with severe hyperlactatemia, clinical signs, and known ingestion of apricot kernels, were suggestive of cyanide toxicity. The dog was treated with crystalloid and synthetic colloids for stabilization and antidote therapy with hydroxocobalamin. The dog's metabolic acidosis and hyperlactemia worsened despite antidote therapy, and the dog progressed to CPA during gastric decontamination efforts. The dog did not respond to CPR efforts. This report will review the mechanism of cyanide toxicity, treatment options, and considerations for future cases.

Pamidronate-induced irreversible symptomatic hypocalcemia in a dog with hypercalcemia after glucocorticoid withdrawal: a case report.

BACKGROUND: Pamidronate is used for the treatment of hypercalcemia. However, a rare but potential adverse event of pamidronate treatment is hypocalcemia. This report describes an unusual case of severe, irreversible hypocalcemia after a single injection of pamidronate for the treatment of hypercalcemia due to glucocorticoid withdrawal in a dog. CASE PRESENTATION: An 11-year-old castrated male Maltese dog presented with anorexia, vomiting, and diarrhea (day 0). The patient had calcinosis cutis throughout the body, calcification of intraabdominal organs, mild azotemia, and severe hypercalcemia. The severe calcification was attributed to long-term glucocorticoid administration, which was discontinued 1 month before presentation. Fluid therapy, diuretics, calcitonin, and a single intravenous injection of pamidronate were used for the treatment of hypercalcemia. On day 14, normocalcemia was achieved, but renal failure occurred. On day 20, severe and irreversible hypocalcemia occurred, and on day 42, the patient was euthanized at the owner's request because of worsened hypocalcemia and renal failure. CONCLUSIONS: Although hypocalcemia is an extremely rare adverse event of bisphosphonate treatment, bisphosphonates like pamidronate can result in potentially life-threatening conditions according to the patient's underlying conditions. Therefore, the patient's condition should be closely monitored and any underlying conditions should be carefully evaluated before initiating the treatment for hypercalcemia using pamidronate.

Acute manganese toxicosis related to joint health supplement ingestion in two dogs.

Two unrelated dogs residing in the same house including an 11-year-old, female spayed, mixed breed dog and a 7-year-old, female spayed, mixed breed dog ingested approximately 75 capsules of a human joint health supplement (Ligaplex I; Standard Process, WI, USA). A total of 2,062 mg of manganese was ingested between both dogs. Dog 1 developed acute fulminant liver failure and a severe coagulopathy that led to hepatic fractures and exsanguination from hemoabdomen. The estimated maximum time from ingestion of the joint health supplement to death was 36 to 48 h. Histologic examination revealed severe periportal hepatic necrosis with mild evidence of preexisiting liver disease and renal tubular epithelial necrosis. Manganese concentrations in liver and kidney tissue were severely increased. Dog 2 developed a severe acute liver injury and was hospitalized for 6 days. Therapies provided during hospitalization included intravenous fluids, maropitant, pantoprazole, N-acetylcysteine, vitamin C, S-adenosylmethionine, and silybin. The dog was treated long-term with S-adenosylmethionine, silybin, ursodiol, and vitamin C. Clinical and biochemical resolution occurred on the recheck examination that took place on day 44. The veterinary literature is comprised of only 2 reports containing 3 dogs that describe acute manganese intoxication. Here, we provide a detailed description of 2 dogs that developed manganese-induced toxicosis after ingestion of a human joint health supplement.

Anticoagulant rodenticide toxicity in dogs: A retrospective study of 349 confirmed cases in Saskatchewan.

Objective: To evaluate the signalment and clinical, laboratory, treatment, and outcome features of dogs diagnosed with anticoagulant rodenticide (AR) intoxication in Saskatchewan. Animals: We studied 349 dogs. Procedure: Medical records from the Veterinary Medical Centre (Saskatoon, Saskatchewan) between 1999 and 2022 were reviewed. Cases were included if they met at least 1 of the following criteria: owner witnessed the dog ingesting an AR; AR was seen in the vomitus when emesis was induced; the dog had clinical signs of coagulopathy, with elevation of PT ± aPTT that normalized after vitamin K1 therapy, in the presence of appropriate clinical and paraclinical data and the absence of other causes of hypocoagulable state determined by the primary clinician. Results: Fifty-three percent of cases were seen between July and October. Most dogs (61%) came from an urban setting. Ninety-two percent of dogs ingested a 2nd-generation AR and the most frequent toxin was bromadiolone. Clinical signs were reported in 30% of AR intoxications and included lethargy (86%), dyspnea (55%), and evidence of external hemorrhage (44%). The most common site of hemorrhage was the pleural space, accounting for 43% of hemorrhage sites. Consumptive thrombocytopenia was reported in 24% of dogs with evidence of AR-induced hemorrhage, with moderate (platelet count < 60 K/µL) and marked (< 30 K/µL) thrombocytopenia in 7/12 and 2/12 dogs, respectively. Blood products were administered to 84% of dogs with AR-induced hemorrhage; the most common product administered was fresh frozen plasma (56% of cases). Among dogs with AR-induced hemorrhage, those that received blood products were more likely to survive to discharge (81%) compared to those that did not (19%) (P = 0.017). Eighty-six percent of dogs with AR-induced hemorrhage survived to discharge. Conclusion and clinical relevance: The pleural space was the most common site of hemorrhage. Moderate thrombocytopenia was a common finding. Eighty-six percent of dogs with AR-induced hemorrhage survived to discharge.

Toxicité des rodenticides anticoagulants chez les chiens : étude rétrospective de 349 cas confirmés en Saskatchewan. Objectif: Évaluer le signalement et les caractéristiques cliniques, de laboratoire, de traitement et de résultats des chiens diagnostiqués avec une intoxication par un rodenticide anticoagulant (AR) en Saskatchewan. Animaux: Nous avons étudié 349 chiens. Procédure: Les dossiers médicaux du Veterinary Medical Centre (Saskatoon, Saskatchewan) entre 1999 et 2022 ont été examinés. Les cas ont été inclus s'ils répondaient à au moins 1 des critères suivants : le propriétaire a vu le chien ingérer un AR; de l'AR a été observée dans les vomissures lorsque des vomissements ont été provoqués; le chien présentait des signes cliniques de coagulopathie, avec une élévation du PT ± aPTT qui s'est normalisée après un traitement par la vitamine K1, en présence de données cliniques et paracliniques appropriées et en l'absence d'autres causes d'état hypocoagulable déterminées par le clinicien initial. Résultats: Cinquante-trois pour cent des cas ont été observés entre juillet et octobre. La plupart des chiens (61 %) venaient d'un milieu urbain. Quatre-vingt-douze pour cent des chiens ont ingéré un AR de 2e génération et la toxine la plus fréquente était la bromadiolone. Des signes cliniques ont été rapportés dans 30 % des intoxications par AR et incluaient de la léthargie (86 %), de la dyspnée (55 %) et des signes d'hémorragie externe (44 %). Le site d'hémorragie le plus fréquent était l'espace pleural, représentant 43 % des sites d'hémorragie. Une thrombocytopénie de consommation a été rapportée chez 24 % des chiens présentant des signes d'hémorragie induite par l'AR, avec une thrombocytopénie modérée (nombre de plaquettes < 60 K/µL) et marquée (< 30 K/µL) chez 7 chiens sur 12 et 2 chiens sur 12, respectivement. Des produits sanguins ont été administrés à 84 % des chiens présentant une hémorragie induite par l'AR; le produit le plus fréquemment administré était le plasma frais congelé (56 % des cas). Parmi les chiens présentant une hémorragie induite par l'AR, ceux qui ont reçu des produits sanguins étaient plus susceptibles de survivre jusqu'à leur congé (81 %) que ceux qui n'en ont pas reçu (19 %) (P = 0,017). Quatre-vingt-six pour cent des chiens présentant une hémorragie induite par l'AR ont survécu jusqu'à leur sortie. Conclusion et pertinence clinique: L'espace pleural était le site d'hémorragie le plus fréquent. Une thrombocytopénie modérée était fréquente. Quatre-vingt-six pour cent des chiens présentant une hémorragie induite par l'AR ont survécu jusqu'à leur sortie.(Traduit par Dr Serge Messier).

Neurological adverse effects of isoxazoline exposure in cats and dogs.

BACKGROUND: Isoxazolines are rarely reported to be associated with neurological adverse events in cats and dogs, but information about the onset and duration of neurological signs is lacking in the summary of product characteristics of these medicines. METHODS: The Veterinary Poisons Information Service and the Dutch Poisons Information Center databases were searched using the Veterinary Dictionary for Drug-Related Affairs terms for ataxia, muscle tremor, convulsions or hyperesthesia in cats and dogs exposed to isoxazolines. RESULTS: There were 22 cases with and 57 cases without outcome information, mostly involving fluralaner or sarolaner. In both groups, muscle tremors and convulsions were the most common signs. In dogs, neurological signs occurred with oral therapeutic dose and overdosage. In cats, most fluralaner cases involved therapeutic topical exposure, and all sarolaner cases involved oral exposure. In all cases with outcome information, the animals recovered. LIMITATIONS: Cases discussed with poison centres tend to involve more severe signs. CONCLUSION: The true incidence of neurological adverse effects from isoxazolines remains unclear. The delay between the administration and onset of signs can be long, and the association may be missed. A lack of timing information in the summary of product characteristics could also contribute to missed attribution of adverse effects.

Vincristine-induced adverse events related to body weight in dogs treated for lymphoma.

BACKGROUND: Traditional dosing of chemotherapy drugs based on body surface area may overdose small dogs, leading to an increased frequency of adverse events (AEs). HYPOTHESIS/OBJECTIVES: Evaluate the frequency of hematologic and gastrointestinal AEs in dogs with newly diagnosed lymphoma treated with vincristine weighing ≤15 kg in comparison to dogs weighing >15 kg. We hypothesized that dogs weighing ≤15 kg would experience a higher frequency of AEs. ANIMALS: One hundred and thirty-eight dogs with newly diagnosed lymphoma were treated with vincristine. METHODS: A multicenter retrospective study reviewing hematologic data and medical record information. Complete blood counts were performed no more than 24 hours before vincristine administration and then between 4 and 8 days post-administration. Data were evaluated using logistic regression or ordinal logistic regression. RESULTS: Thirty-eight dogs weighing ≤15 kg and 100 dogs weighing >15 kg were included. The median vincristine dose for both groups was 0.6 mg/m2. Seventeen (12.3%) instances of neutropenia occurred with no significant difference in overall frequency or grade between groups. Thirty initially asymptomatic substage A dogs (29.4%) experienced gastrointestinal AEs. Because of the widespread use of gastrointestinal supportive care medications, statistical comparison between groups could not be performed. Seven instances of hospitalization occurred (5.0%) and the risk of hospitalization did not differ significantly between groups (P = .37). CONCLUSIONS AND CLINICAL IMPORTANCE: Vincristine dosed at ≤0.6 mg/m2 does not increase the risk of hematologic AEs in dogs weighing ≤15 kg.

Systemic absorption and gastrointestinal adverse effects from topical ketorolac and diclofenac ophthalmic solutions in healthy dogs.

OBJECTIVE: To investigate systemic absorption and gastrointestinal (GI) adverse effects of topical ketorolac 0.5% and diclofenac 0.1% ophthalmic solutions. ANIMALS: 11 healthy purpose-bred Beagles. METHODS: Dogs were randomly assigned to receive either ketorolac (n = 6) or diclofenac (5), 1 drop in both eyes 4 times daily for 28 days. Upper GI endoscopy was performed on days 0 and 29 with mucosal lesion scores (0 to 7) assigned to each region evaluated. Plasma samples were collected on days 14, 21, and 28 for measurement of diclofenac and ketorolac using high-performance liquid chromatography-mass spectrometry. RESULTS: GI erosions and/or ulcers developed in all ketorolac-treated dogs and 1 of 5 diclofenac-treated dogs. Post-treatment mucosal lesion score for the antrum was higher in the ketorolac group than in the diclofenac group (P = .006) but not significantly different for any other region. Post-treatment antral mucosal lesion scores were significantly related to plasma ketorolac concentrations (P < .001). Ketorolac and diclofenac were detected in the plasma at all time points (median ketorolac day 14, 191 ng/mL; day 21, 173.5 ng/mL; and day 28, 179.5 ng/mL; and median diclofenac day 14, 21.1 ng/mL; day 21, 20.6 ng/mL; day 28, 27.5 ng/mL). Vomiting and decreased appetite events were observed uncommonly and were not significantly different between treatment groups. CLINICAL RELEVANCE: GI ulceration and erosion developed after ophthalmic administration of ketorolac and diclofenac, with higher plasma concentrations and more severe GI lesions associated with ketorolac. Clients should be alerted to this potential risk with ophthalmic use and informed to watch for systemic clinical signs that would warrant veterinary reevaluation.

Clinical examination findings and electrolyte abnormalities of dogs with marijuana/tetrahydrocannabinol toxicity: 223 cases (January 2017-July 2021).

OBJECTIVE: The goal of this study was to describe the historical, physical, neurologic, and clinicopathologic findings in dogs with a definitive diagnosis of marijuana/tetrahydrocannabinol toxicity. ANIMALS: A total of 223 dogs with known ingestion of marijuana or a positive tetrahydrocannabinol result on human urine multidrug test. METHODS: Retrospective study from January 2017 to July 2021. RESULTS: Median age was 1 year (1 month to 12 years). A common history was becoming acutely neurologic after going outside or to a public place (62/223 [27.8%]). Most owners denied possibility of exposure (152/223 [68%]). Median vitals were normal, but hyperthermia (38/212 [22.6%]), tachycardia (82/222 [37%]), and systemic hypertension (37/61 [60.7%]) were common abnormalities. The most common clinical signs included ataxia (197/223 [88.3%]), hyperesthesia (168/223 [75.3%]), urinary incontinence (102/223 [45.7%]), lethargy (140/223 [62.5%]), and vomiting (58/223 [26%]). The most common combinations of neurologic signs included ataxia and hyperesthesia (157/223 [70.4%]) and ataxia, hyperesthesia, and urinary incontinence (81/223 [36.3%]). Mild hyperkalemia (39/76 [51.3%]) and mild hypercalcemia (53/67 [79.1%]) were common. Twenty-two dogs were hospitalized. Survival was 100%. CLINICAL RELEVANCE: A common presentation for marijuana toxicosis included young dogs with acute ataxia and hyperesthesia, with and without urinary incontinence, after going outside or to a public place. Vitals were often normal, but hyperthermia, tachycardia, and hypertension were common. Bloodwork was mostly normal, but mild hyperkalemia and mild ionized hypercalcemia were common. Marijuana should be high on the differential list with these history, physical examination, neurologic, and electrolyte abnormalities, regardless of owner denial or negative human urine multidrug test.

Effect of Bacillus subtilis and Bacillus coagulans spores on induced allergic contact dermatitis in dogs.

BACKGROUND: Probiotic strains have the potential to modulate immune responses, reduce intestinal inflammation, normalize intestinal mucosal function and decrease allergic reactions. OBJECTIVE: This study aimed to investigate the effect of oral probiotic supplements containing Bacillus subtilis and Bacillus coagulans spores on clinical symptoms, haematological factors and immune responses to allergic contact dermatitis in dogs induced by dinitrochlorobenzene (DNCB). METHODS: DNCB was injected subcutaneously into the scapular region of 20 healthy adult dogs of both sexes, divided into four groups, to induce experimental allergic contact dermatitis. Dogs in Group 1 received food without probiotics or medication. Oral prednisolone was administered to Group 2 for 30 days at a dosage of 0.25 mg/kg every other day. The dogs in Group 3 were treated with a combination of oral prednisolone and probiotics. The dogs in Group 4 were fed daily with a mixture of 109 B. subtilis and B. coagulans bacteria for 30 days. The immune system responses and related gene expression were analysed in the treated animals. RESULTS: The administration of probiotics for 30 days resulted in a reduction in clinical symptoms and duration of wound repair. The probiotics treatment also significantly increased the serum bactericidal effects against Staphylococcus aureus and Escherichia coli. It enhanced both the classic and alternative activity of the complement, as well as lysozyme activity. Additionally, the probiotics led to higher total immunoglobulin levels and significant reductions in anti-trypsin and C-reactive protein levels. Furthermore, the expression of IgE, induction of interferon-gamma and IL-4 genes were also reduced. CONCLUSIONS: According to the results, B. subtilis and B. coagulans can be further investigated as a viable alternative to corticosteroids in treating allergic contact dermatitis in dogs.

Dental erosion following clopidogrel administration in a dog: A case-based study.

A 10-year-old neutered male Chihuahua presented with unilateral dental erosion that occurred after several months of oral medications mixed with honey. A pH test was performed on all oral medications administered to the dogs to determine the cause of enamel erosion. Among the medications, the only acidic medication was clopidogrel (pH 2.65). To evaluate the effect of clopidogrel on the tooth surface under the same conditions as in the present patient, an additional preliminary study was designed in which two extracted teeth of another dog were immersed in a clopidogrel-honey mixture or only in honey. After a 3-week soaking of the extracted tooth in the clopidogrel-honey mixture, field-emission scanning electron microscope analysis revealed a rougher surface, whereas energy-dispersive X-ray spectroscopy analysis showed a reduced Ca/C ratio compared to the control tooth. In this case, prolonged exposure of the tooth surface to clopidogrel may be a cause of dental erosion.

Immune-mediated polyarthritis and anterior uveitis secondary to zonisamide administration in a dog with refractory epilepsy.

The objective of this article is to describe a case of suspected zonisamide-induced immune-mediated polyarthritis (IMPA) and anterior uveitis in a dog. A 7-year-old male neutered Siberian Husky with a history of refractory idiopathic epilepsy was presented for cluster seizures. Following the addition of zonisamide to the antiepileptic regime, the dog developed new IMPA and anterior uveitis. Within a few weeks of discontinuation of the zonisamide, the dog's IMPA and anterior uveitis resolved. These immune-mediated conditions were thus presumed to be an idiosyncratic reaction to zonisamide. To our knowledge, this is the first report of IMPA and anterior uveitis in dogs associated with zonisamide administration at its recommended dose.

Urinary and household chemical exposures in pet dogs with urothelial cell carcinoma.

Urothelial cell carcinoma (UCC) has been linked to environmental chemical exposures in people, but these risk factors are not well understood in dogs with UCC. We hypothesised that household chemical exposures contribute to the risk of UCC in pet dogs. This prospective cross-sectional case-control study included 37 dogs with UCC and 37 unaffected breed-, sex-, and age-matched controls. Dog owners completed an environmental questionnaire and household samples were collected and analysed for arsenic (in tap water and room dust) and acrolein (in room air). Urine samples from UCC dogs, control dogs, and consenting owners were analysed for inorganic arsenic species, the acrolein metabolite 3-HPMA, and the phenoxy herbicide 2,4-D. Public data on chlorination byproducts (total trihalomethanes) in municipal drinking water were also compared between case and control households. Dogs with UCC were more likely to swim in a pool (15.2%) compared with control dogs (0%) (OR 1.69, 95% CI = 1.69-∞; p = .02). Dogs with UCC also had more than 4-fold higher reported municipal water concentrations of chlorination byproducts (median 28.0 ppb) compared with controls (median 6.9 ppb; p < .0001). Dust arsenic concentrations were unexpectedly lower in case households (median 0.277 ng/cm2) compared with control households (median 0.401 ng/cm2; p = .0002). Other outcomes were not significantly different between groups. These data suggest that dog owners, especially those of breeds known to be at higher risk for UCC, consider limiting access to swimming pools and installing water filtration units that remove total trihalomethanes.