Enzootic Ataxia in a Norwegian Red Deer Herd

Acta vet. scand. 2000, 41, 329-331. BriefCommunication Enzootic Ataxia in a Norwegian Red Deer Herd By K. Handeland and A. Flaeyen National Veterinary Institute, Oslo, Norway In the I960s, a disease characterized clinically October to April they also had access to silage by ataxia and posterior paresis that had for a ad libitum, and, once a week, the animals were long time been recognised in park herds of red given a mineral mixture produced for cattle and deer (Cervus elaphus) in Britain, and in park goat (Felleskjepet ) mixed with concentrates. and wild red deer in Germany, was shown to be The mineral mixture contained 600 mg Cu per associated with demyelination in the spinal kilogram. cord (Barlow & Butler 1964, Terlecki & Done During winter 1996/97 a 1.5-year-old female 1964, Knosel & Schulz 1968). Some of the developed signs of posterior locomotor distur cases also showed nerve cell degeneration and bances. The condition remained stable for necrosis in the brain tissue. Later, enzootic about 8 months after which the animal was de ataxia was reported in deer farms in New Zea stroyed without veterinary inspection. In No land (Wilson et al. 1979), Australia (Peet & vember 1997 a 2.5-year-old female showed Hepworth 1993), China (Yoshikawa et al. 1996) signs of hind limb weakness and unsteadiness and Germany (Geisel et al. 1997). The disease while running. Signs progressed, and the ani occurs in young adult deer. The aetiology is mal was euthanized I month after onset of dis considered multifactorial, but copper (Cu) defi ease. Its head, cervical columna and samples of ciency appears a central factor, and the disease liver and blood were available for laboratory can be efficiently prevented through Cu supple examination. mentation (Wilson et al. 1979). In New Zea The skull was split in the sagittal plane and the land, Cu deficiency has also been suggested as cervical vertebral column was opened from the a cause of osteochondrosis in farmed red deer dorsal. No gross lesions could be found on the calves (Thompson et al. 1994, Audige et al. brain and spinal cord, and the organs were fixed 1995). in 10% buffered formalin . After fixation, tran This paper reports the occurrence of enzootic verse tissue blocks ofthe cerebral hemisphere s, ataxia in a small red deer herd located on a pons, cerebellum and medulla oblongata and 2 dairy farm in the municipality of0len, Horda tranverse tissue blocks per segment of the cer land county, Norway. The herd, comprising vical spinal cord were embedded in paraffin, cut about 15 animals, was established in the late at 5 urn, and stained with haematoxylin and eo 1980s based on locally wild-captured animals. sin (HE) for histopathological examination. Se The animals grazed unfertilised, semi-culti lected sections were stained with luxol fast vated pasture in a 10 hectare enclosure. From blue. The concentration ofCu in the liver tissue Acta vel. scand. vol. 41 no. 3, 2000 330 K. Handeland & A. Flaeyen Figure I . Cross section ofthe cervical spinal cord. Deficit of stainable myelin, and vacuoles with swollen (ar row) or disintegrated (arrowhead) axons and scattered macrophages. HE x 200. and serum were measured using atomic absorp 1964, Terlecki & Done 1964, Knosel & Schulz tion spectroscopy (Jorhem & Engman 1996). 1968), combined with abnormally low Cu lev Histopathological examination revealed bilat els in the liver and serum. erally symmetrical demyelination and axon de The liver is the central storage organ for Cu in generation in the ventral and lateral columns of the body and therefore analysis ofliver samples the cervical spinal cord (Fig. I). Vacuoles or gives the best indication ofthe Cu status (Grace distended myelin sheats surrounding swollen or 1983). The level ofCu in serum is controlled by disintegrated axons and scattered macrophages homeostatic mechanisms and can be normal frequently gave affected areas a spongy appear also when liver Cu levels are low. Thus, the ence. Similar lesions also occurred in white level of Cu in serum declines only after the Cu matter ofthe medulla oblongata, but no consis concentration in the liver has been depleted tent histological findings could be detected (Mackintosh et af. 1986). The Cu liver concen elsewhere in the brain tissue. The concentra tration found in our animal was below the con tions of Cu in the liver tissue and blood serum centration of 100 ,umollkg WMB regarded as were 47 ,umollkgwet matter basis (WMB) and deficient in farmed deer, and lower than 60 6.3,umolll respectively. ,umol/kg considered the «critical» concentra Our diagnosis of enzootic ataxia was made on tion below which enzootic ataxia may occur the basis oftypical clinical signs and histopath (Clark & Hepburn 1986, Mackintosh et al. ological spinal cord lesions (Barlow & Butler 1986). The serum Cu concentration found was Acta vel. scand. vol. 41 no. 3, 2000 Enzootic ataxia in red deer 331 below 8 pmol /I, which is regarded as indicative Geisel 0 , Betzl E. Dahm e E, Schmal W. Hermanns W: of Cu deficiency following liver depletion Enzootic spinal ataxia of fanned fallow and red deer in Southern Bavaria/Germ any, Tierarztl, (Clark & Hepburn 1986, Mackintosh et al. Prax. 1997, 25. 598-604. 1986). Grace ND : Copper (Cu), In: Graze NO (ed): The Cu deficiency can occur as a result ofingesting min eral requirements ofgrazi ng rum inants. N Z. pasture containing an inadequate level of Cu Soc. Anim. Prod . 1983, 9, 56-66. (simple deficiency), or as a result of high levels Jorh em L, Engman J: Determ ination of lead, cad mium , zinc, copper and iron in foodstuffs by of molybdenum, sulphur, iron, and cadmium in atomic absorptio n spectrophotometry after mi the diet reducing the absorption or availability crowave digestion : NMKL Collaboratory study. ofCu (induced Cu deficiency) (Grace 1983). A 1996. Statens Livsmedelverk, Sverige. more complete evaluation of causes requires Knosel H, Schulz L-C: On the pathogenesis of en pasture and soil analyses that were not carried demic paresis (lameness of the hip) in red deer. Berl. Munch . Tierarztl. Wschr. 1968, 8, 92-96. out in our study. However, the reported cases Ma ckintosh CG : Deer health and disease. Acta Vet. occurred during winter, when Cu liver concen Hung . 1998,46,381-394 . trations in farmed deer have been found to de Ma ckin tosh CG, Wilson PR, Beatson NS, Turner K, crease due to low Cu contents in pasture (Mack John stone P: Preliminary report of the liven serum copper relationship in red deer. Proc. Deer intosh et al. 1986). In addition, feeding on Course for Veterinarians 1986, 3, 156-164. silage during winter may have contributed to Peet RL. Hep worth K: Enzoo tic ataxia in red deer, Cu deficiency, as this is usually made from rap Cervus elaphus. Austral. Vet. 1. 1993, 70. 395 idly growing spring grass which tends to be 396. very low in Cu (Mackintosh 1998). Terlecki S, Done J T: Enzoot ic atax ia ofred deer. Brit. Vet. 1. 1964, 120, 31 1-32 I. Thompson KG, Audige L, Arthur DG, Jul ian AF. Orr References MB, McSporran KD, Wilson PR: Osteochondro Audige L, Wilson PR oMorris RS, Davidso n GW: Os sis associated with copper deficiency in young teochondrosis, skeletal abnormalities and en farmed red deer and wapiti x red deer hybrids. N zootic ataxia assoc iated with copper deficiency in Z. Vet. 1. 1994, 42. 137- 143. a fanned red deer (Cervus elap hus) herd . N Z. Wilson PR, Orr MB, Key EL: Enzootic ataxia in red Vet. 1. 1995, 43, 70-76. deer. N Z. Vet. 1. 1979, 2 7. 252-254. Barlow RM, Butler EJ: An ataxic condition in red Yoshikawa H, Sea H, Oyamada Ta, Ogasawara T, deer (Cervus elaphus). 1. Compo Path. 1964, 74, Oyamada To, Yoshikawa T, Wei X. Wang S, Li y'. 5 19-529. Histopathology of enzoo tic ataxia in sika deer Clark RG, Hepburn JD: Deer liver and serum copper (Cervus nippon Temminck). 1. Vet. Med. Sci. levels. Surve illance 1986, 13, 11-14. 1996, 58, 849-854. (Received February 10, 2000; accepted March 20, 2000). Reprints may be obtained from : K. Handel and, Section of Wildlife Diseases, National Veterinary Institute, P.O.Box 8156 Dep., N-033 Oslo, Norway. E-mai l: [email protected]. Acta vet. scand. vol. 41 no. 3, 2000.

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