Effects of oral administration of metronidazole and doxycycline on olfactory capabilities of explosives detection dogs in: American Journal of Veterinary Research Volume 77 Issue 8 ()

Olfactory acuity is the ability to detect and recognize odorants. In canids, it is expressed as the detection threshold, which is defined as the lowest concentration of a given odorant that can be consistently detected.1 Olfactory dysfunction in up to approximately 24% of affected humans is caused by metabolic derangement or induced by pharmaceuticals,2-4 but the prevalence of olfactory dysfunction in dogs is unknown. Diminished olfaction in dogs reportedly can be caused by canine distemper virus infection,5 parainfluenza virus infection,6 administration of dexamethasone or hydrocortisone,7 and feeding of a diet high in saturated fat.8

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In humans, generalized decreased olfactory acuity (hyposmia) is characterized as type I, II, or III. Type I hyposmia is defined as the inability to correctly recognize and identify odors. Type II hyposmia is a quantitative decrease in the ability to detect odorants, and type III hyposmia is a decrease in estimation of the magnitude of odors. Types I and III cannot be assessed in dogs. Type II hyposmia is the most common form of hyposmia detected in humans following pharmaceutical treatment,1 and it can be evaluated in dogs via a number of laboratory methods, including use of behavioral olfactometry,7-9 electroencephalographic olfactometry,10 and scent-wheel techniques.11-14

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Hyposmia is of concern in working dogs, particularly detection dogs. Consequences of hyposmia could be catastrophic, especially for dogs trained to detect explosives. Pharmaceutical-induced hyposmia often may remain undetected in dogs because affected animals cannot report hyposmia. Therefore, it is important to elucidate whether pharmaceuticals cause olfactory deficits in working dogs so that clinicians can avoid the use of those medications. To the authors’ knowledge, there is only 1 published study7 on the olfactory effects of pharmaceuticals in dogs. Investigators in that study7 found that a high dosage of dexamethasone (2 mg/kg/d) or a combination of hydrocortisone and deoxycorticosterone (0.25 mg/kg/d) decreased olfactory acuity (with or without observable clinical signs) in laboratory dogs after 7 and 18 days of administration, respectively.

Most clinically relevant information on the effects of pharmaceuticals on canine olfaction is extrapolated from human medicine. There is an extensive list of pharmaceuticals that can induce hyposmia in humans. This list includes anesthetics, antihistamines, antimicrobials, antineoplastics, cardiovascular drugs, endocrine drugs, gastrointestinal drugs, neurologic drugs, and NSAIDs.1,15-18 Of particular interest are metronidazole and doxycycline, which are 2 antimicrobials commonly administered to working dogs. Metronidazole is used to treat diarrhea, especially that caused by Giardia spp, which can be transmitted rapidly through working dog kennels. Metronidazole has been associated with taste disorders, specifically a bitter metallic taste, in humans.19 It has also been linked to decreased cognitive function in elderly humans,20 which suggests that it may impact neurologic function. Doxycycline is also commonly administered to working dogs for the prevention and treatment of vector-borne diseases, such as those caused by Ehrlichia spp, Babesia spp, and Rickettsia spp. Doxycycline can cause hyposmia in humans.21 The objective of the study reported here was to evaluate the effects of metronidazole and doxycycline on olfactory capability in dogs. Our hypothesis was that metronidazole and doxycycline would cause degraded olfactory detection capabilities in ED dogs.

Acknowledgments

Supported in part by the Interdepartmental Research Grants Program; the Scott-Richey Research Center, College of Veterinary Medicine; and the Animal Health Disease Research Intramural Grants Program, Auburn University.

The authors declare that there were no conflicts of interest.

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This manuscript was submitted by Dr. Jenkins to the Department of Clinical Sciences at the Auburn University College of Veterinary Medicine as partial fulfillment for a Master of Science degree.

Presented in abstract form at the American College of Veterinary Internal Medicine Forum, Nashville, Tenn, June 2014; and the Canine Science and Technology Conference, Raleigh, NC, July 2014.

The authors thank Dr. Jay Barrett for medical and technical assistance and Terrence Fischer and Pamela Haney for technical assistance.