@article{larsen_nutter_augspurger_rocke_tomlinson_thomas_stoskopf_2002, title={Clinical features of avian vacuolar myelinopathy in American coots}, volume={221}, ISSN={["0003-1488"]}, DOI={10.2460/javma.2002.221.80}, abstractNote={Abstract
				
					Objective—To characterize clinical features of avian
vacuolar myelinopathy (AVM) in American coots.
				
					Design—Case-control study.
				
					Animals—26 AVM-affected American coots and 12
unaffected coots.
				
					Procedures—Complete physical, neurologic, hematologic,
and plasma biochemical evaluations were
performed. Affected coots received supportive care.
All coots died or were euthanatized, and AVM status
was confirmed via histopathologic findings.
				
					Results—3 severely affected coots were euthanatized
immediately after examination. Seventeen
affected coots were found dead within 7 days of
admission, but 5 affected coots survived > 21 days
and had signs of clinical recovery. Abnormal physical
examination findings appeared to be related to general
debilitation. Ataxia (88%), decreased withdrawal
reflexes (88%), proprioceptive deficits (81%),
decreased vent responses (69%), beak or tongue
weakness (42%), and head tremors (31%), as well as
absent pupillary light responses (46%), anisocoria
(15%), apparent blindness (4%), nystagmus (4%),
and strabismus (4%) were detected. Few gross
abnormalities were detected at necropsy, but histologically,
all AVM-affected coots had severe vacuolation
of white matter of the brain. None of the control
coots had vacuolation.
				
					Conclusions and Clinical Relevance—Although
there was considerable variability in form and severity
of clinical neurologic abnormalities, clinical signs
common in AVM-affected birds were identified.
Clinical recovery of some AVM-affected coots can
occur when supportive care is administered. Until the
etiology is identified, caution should be exercised
when rehabilitating and releasing coots thought to be
affected by AVM. (J Am Vet Med Assoc 2002;221:
80–85)}, number={1}, journal={JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Larsen, RS and Nutter, FB and Augspurger, T and Rocke, TE and Tomlinson, L and Thomas, NJ and Stoskopf, MK}, year={2002}, month={Jul}, pages={80–85} }
 @article{gaskin_schantz_jackson_birkenheuer_tomlinson_gramiccia_levy_steurer_kollmar_hegarty_et al._2002, title={Visceral leishmaniasis in a New York foxhound kennel}, volume={16}, ISSN={["0891-6640"]}, DOI={10.1892/0891-6640(2002)016<0034:VLIANY>2.3.CO;2}, abstractNote={Although endemic throughout much of the world, autochthonous visceral leishmaniasis has been reported on only 3 previous occasions in North America. After diagnosis of visceral leishmaniasis in 4 foxhounds from a kennel in Dutchess County, New York (index kennel), serum and ethylenediamine-tetraacetic acid (EDTA)-anticoagulated blood were collected from the remaining 108 American or cross-bred foxhounds in the index kennel and from 30 Beagles and Basset Hounds that were periodically housed in the index kennel. Samples were analyzed for antibodies to or DNA of tickborne disease pathogens and Leishmania spp. Most dogs had antibodies to Rickettsia spp., Ehrlichia spp., Babesia spp., or some combination of these pathogens but not to Bartonella vinsonii (berkhoffi). However, DNA of rickettsial, ehrlichial, or babesial agents was detected in only 9 dogs. Visceral leishmaniasis was diagnosed in 46 of 112 (41%) foxhounds from the index kennel but was not diagnosed in any of the Beagles and Basset Hounds. A positive Leishmania status was defined by 1 or more of the following criteria: a Leishmania antibody titer > or = 1:64, positive Leishmania polymerase chain reaction (PCR), positive Leishmania culture, or identification of Leishmania amastigotes by cytology or histopathology. The species and zymodeme of Leishmania that infected the foxhounds was determined to be Leishmania infantum MON-1 by isoenzyme electrophoresis. Foxhounds that were > 18 months of age or that had traveled to the southeastern United States were more likely to be diagnosed with visceral leishmaniasis. Transmission of Leishmania spp. in kennel outbreaks may involve exposure to an insect vector, direct transmission, or vertical transmission.}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Gaskin, AA and Schantz, P and Jackson, J and Birkenheuer, A and Tomlinson, L and Gramiccia, M and Levy, M and Steurer, F and Kollmar, E and Hegarty, BC and et al.}, year={2002}, pages={34–44} }
 @article{tomlinson_barker_foster_mcewen_menzies_shewen_2000, title={Naturally occurring lesions of the uterine tube in sheep and serologic evidence of exposure to Chlamydophila abortus}, volume={64}, number={4}, journal={Canadian Journal of Veterinary Research}, author={Tomlinson, L. and Barker, I. K. and Foster, R. A. and McEwen, S. A. and Menzies, P. I. and Shewen, P. E.}, year={2000}, pages={229–231} }