To describe abnormal clinical signs following duloxetine ingestion in dogs.
364 client-owned dogs that ingested duloxetine.
The American Society for the Prevention of Cruelty to Animals, Animal Poison Control Center electronic database was searched for records of dogs with duloxetine ingestion between January 2012 and December 2016. Data collected included age, body weight, breed, duloxetine exposure and dose, clinical signs, and overall outcome. Clinical signs were categorized as either neurologic, digestive, cardiovascular, respiratory, or metabolic and endocrine. Outcomes were categorized as no clinical signs, fully recovered, died, or unknown.
Clinical signs developed in 55 of the 364 (15.1%) dogs with known ingestion of duloxetine. The most common clinical signs were lethargy (22/55 [40%]), mydriasis (18/55 [33%]), vomiting (11/55 [20%]), and trembling (6/55 [11%]). Dogs that ingested an estimated dose of duloxetine ≥ 20 mg/kg (9.1 mg/lb) were more likely to have had abnormal clinical signs than were dogs that ingested < 20 mg/kg.
CONCLUSIONS AND CLINICAL RELEVANCE
Findings indicated that most dogs in the present study did not have clinical signs associated with ingestion of duloxetine and that development of clinical signs varied by individual dog. Further information is needed to determine toxic dose ranges for duloxetine ingestion in dogs. (J Am Vet Med Assoc 2019;255:1161–1166)
OBJECTIVE To establish the minimum toxic dose of isoniazid in dogs, characterize the clinical signs and outcomes for dogs following isoniazid ingestion, and determine whether IV administration of pyridoxine to dogs with isoniazid toxicosis is protective against death.
DESIGN Retrospective case series.
ANIMALS 137 dogs with isoniazid toxicosis.
PROCEDURES The electronic database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center was reviewed from January 2004 through December 2014 to identify dogs with isoniazid toxicosis. For each dog identified, information extracted from the medical record included signalment, estimated dose of isoniazid ingested, clinical signs, treatment, and outcome. Follow-up communication with pet owners or primary care veterinarians was performed when necessary to obtain missing information.
RESULTS Clinical signs of isoniazid toxicosis were observed in 134 of 137 (98%) dogs and included seizures (n = 104), CNS signs without seizures (94), and gastrointestinal (41), cardiovascular (19), urogenital (4), and respiratory (1) abnormalities. Of the 87 dogs for which the outcome was available, 61 survived, 18 died, and 8 were euthanized. Probability of survival was positively associated with body weight and IV administration of pyridoxine and negatively associated with dose of isoniazid ingested and presence of seizures. Dogs that received pyridoxine IV were 29 times as likely to survive as dogs that did not receive pyridoxine IV.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated rapid diagnosis of isoniazid toxicosis and prompt treatment of affected dogs with pyridoxine and other supportive care were imperative for achieving a successful outcome.
Objective—To evaluate microtiter-plate format ELISAs constructed by use of different diagnostic targets derived from the Ehrlichia ewingii p28 outer membrane protein for detection of E ewingii antibodies in experimentally and naturally infected dogs.
Sample Population—Serum samples from 87 kenneled dogs, 9 dogs experimentally infected with anti-E ewingii, and 180 potentially naturally exposed dogs from Missouri.
Procedures—The capacities of the synthetic peptide and truncated recombinant protein to function as detection reagents in ELISAs were compared by use of PCR assay, western blot analysis, and a full-length recombinant protein ELISA. Diagnostic targets included an E ewingii synthetic peptide (EESP) and 2 recombinant proteins: a full-length E ewingii outer membrane protein (EEp28) and a truncated E ewingii outer membrane protein (EETp28)
Results—A subset of Ehrlichia canis-positive samples cross-reacted in the EEp28 ELISA; none were reactive in the EESP and EETp28 ELISAs. The EESP- and EETp28-based ELISAs detected E ewingii seroconversion at approximately the same time after infection as the EEp28 ELISAs. In afield population, each of the ELISAs identified the same 35 samples as reactive and 27 samples as nonreactive. Anaplasma and E can is peptides used in a commercially available ELISA platform did not detect anti-E ewingii antibodies in experimentally infected dogs.
Conclusions and Clinical Relevance—The EESP and EETp28 ELISAs were suitable for specifically detecting anti-E ewingii antibodies in experimentally and naturally infected dogs. [Am J Vet Res 2010;71:1195-1200)