Mark P. Dagleish and Amy L. Robinson With the exception of chronic wasting disease, individual neurological diseases of deer are not considered a major cause of morbidity or mortality. However, under certain conditions, they can result in alarming losses within a herd and as the clinical signs of different neurological diseases are frequently similar, it is important to know which are common and under what circumstances they may occur. This chapter describes the more common and/or important neurological diseases of wild free-ranging and farmed deer that have been reported and some that have been the subject of experimental challenges. Enzootic ataxia is a chronic progressive paretic disorder caused by a leucomyelopathy of young adult deer. The condition has been described in red deer, wapiti (Cervus elaphus canadensis), sika deer and fallow deer, as well as several crossed species of deer. Enzootic ataxia has been known for over a hundred years in the deer parks of Europe and more recently in New Zealand. The disorder has also been recognised in farmed and free-ranging deer. As the pathological lesions are similar to swayback of sheep, copper deficiency is considered to be the principal cause of the disease. However, liver copper levels in deer are highly variable, and the relationship between liver copper reserves and serum copper is complex. Furthermore, red deer have been shown to be especially vulnerable to deficiencies in copper and selenium in their first year of life. Deer with enzootic ataxia, in both the United Kingdom and New Zealand, usually have serum levels less than 8 µmol/l and liver levels less than 60 µmol/kg wet weight, together or alone. Previous studies suggest that wapiti may be more likely to develop disease than red or cross-bred deer when grazed on pastures with marginal copper status. Furthermore, intestinal copper absorption and metabolism may be compromised by high levels of ingested molybdenum, iron, sulphur or zinc, especially the former, resulting in secondary copper deficiency. Herd morbidity is normally low, typically <1%, and can reach up to 20%, but morbidity of >13% has been recorded occasionally in the United Kingdom. It is rarely seen in calves less than six months old or deer over two years old. The disease is most often observed in late summer or autumn, where animals are at grass in the absence of supplementation. The clinical signs are insidious in onset and have been attributed to defective proprioception. Clinical signs and progression may take many months to develop and begin with stiffness and disinclination to move, progressing to incoordination and eventual paralysis of the hind limbs. Affected animals may be recognised initially by unsteadiness on rising and a sagging of the hindquarters to one side. Affected animals appear to be unaware of, or unable to correct, this abnormality even when moved at a brisk trot. There is no evidence of pain and exercise does result in appreciable exacerbation of the ataxia. The clinical course to total recumbency may take two years with episodes of temporary or partial remission. The only consistent pathological changes are microscopic, non-inflammatory and confined to the central nervous system. The primary lesions are confined to the long spinal tracts, which undergo demyelination and Wallerian-type axonal degeneration. Chromatolysis may be found in the neurones of some lower brain stem nuclei and the grey matter of the spinal cord. In severe copper deficiencies, bone and joint problems have been reported, such as osteochondrosis and spontaneous fractures. Clinical diagnosis of enzootic ataxia is based on progressive neurological disease characterised, principally, by hind limb ataxia and may be supported by low copper levels in serum and/or liver tissue. Serum copper levels of less than 8 µmol/l and liver copper levels of less than 100 µmol/kg wet weight (fresh tissue; given a wet weight % of 28, this would be equivalent to liver copper <30 µmol/kg dry matter) are suggestive of copper deficiency. Blood samples are of limited benefit because blood copper levels will remain broadly within normal values until all reserves have been depleted. Generally, spinal cord lesions in enzootic ataxia are purely microscopic; therefore, no gross lesions are visible at postmortem examination. See Chapter 5 for more information about trace element analyses in park deer. To detect copper deficiency in a herd with suspected enzootic ataxia it is necessary to examine a minimum of 10 serum samples for statistical reasons. If copper deficiency on a farm is severe then diagnosis by serum or tissue analysis may be possible in all seasons. However, during winter copper uptake in deer falls and, for this reason, deficiency may be seasonal. Therefore, sample analysis in late winter–spring is necessary to detect seasonal deficiency. When interpreting copper levels, it is important to note that liver copper levels are higher in neonates and fall rapidly during the first six months of life and low blood copper levels provide a good indication of acute copper deficiency, but not necessarily of dysfunction. Definitive diagnosis requires a thorough and detailed histological examination of the brain and spinal cord as the microscopic liver lesions are non-specific. There are several reports that copper supplementation (in the diet or as a bolus) may arrest the development of disease in mildly affected animals and may prevent new cases. Animals with advanced clinical disease and, therefore, severe pathological lesions are highly unlikely to recover. Clostridium tetani is an environmental soilborne, sporulating, Gram-positive, anaerobic, rod-shaped bacterium. Infection and resultant disease result from contamination of a wound with spores that then germinate and proliferate rapidly under anaerobic conditions producing tetanus toxin (TeNT; syn. tetanospasmin). This extremely potent product diffuses from the site of infection and enters the nervous system via neuromuscular junctions. The toxin undergoes retrograde transportation up the axons to reach its site of action, the inhibitory interneurons that regulate motor neurones, resulting in progressive spastic paralysis. Tetanus has (rarely) been reported in red deer and fallow deer, the latter after castration using a rubber ring. Cases usually occur between 3 and 10 days after wound contamination. Clinical signs are typical of progressive spastic paralysis and, initially, animals become slightly stiff, unwilling to move and then develop a fine muscle tremor. This is followed 12–24 hours later by a severe general stiffness of the limbs, head and neck together with hyperaesthesia and muscle spasms. Mastication becomes difficult and the animal drools saliva. Recumbency, opisthotonos, convulsions and death due to respiratory failure follow. An initial diagnosis is made from the typical clinical signs of progressive spastic paralysis when these are observed. Attempts can be made to isolate C. tetani from wounds. The main differential diagnosis is strychnine poisoning. Treatment is often unsuccessful and the prognosis is poor. Identification of the wound site is often difficult, but opening and flushing with dilute hydrogen peroxide, taking into account any welfare concerns, along with administration of parenteral penicillin, tetanus antitoxin and sedation to reduce muscle tetany to avoid asphyxia can be attempted. To prevent disease, in the event of animals being put at risk or cases occurring, the stock should be vaccinated with two doses of tetanus toxoid not less than six weeks apart and thereafter annually in areas of high risk. Meningoencephalitis as a result of bacterial and, less commonly, a fungal infection occurs in deer as in other ruminants. Bacteria reported as causing meningoencephalitis in deer include Streptococcus spp., Staphylococcus spp., Salmonella spp., Escherichia coli, Listeria monocytogenes and Actinomyces spp. Although the disease is frequently haematogenous in origin and appears to be spontaneous, a greater frequency of meningoencephalitis occurs in male deer associated with antler growth and can follow cutaneous abrasions and subcutaneous infections adjacent to antler pedicles. Males appear to be most susceptible during the period following the shedding of velvet until the antlers are cast. Typically, pyrexia is present. Diffuse meningitis results in reduced resorption of cerebrospinal fluid, associated with inflammation and oedema, and increased intracranial pressure. Therefore, any initial hyperexcitability is usually rapidly replaced by depression and apparent blindness. If the disease is not treated successfully, animals develop hyperreflexia and hyperaesthesia, followed by recumbency, stupor, coma and death. Acute meningoencephalitis may result in either sudden death or a brief period of recumbency accompanied by thrashing leading rapidly to coma and death. Focal meningoencephalitis, which may progress to abscessation, will cause varied clinical signs dependent upon both the stage of illness and the area of the brain affected; these signs may include circling, rotation or deviation of the head, ptosis, drooping of an ear, retention of cud and anisocoria. Spinal lesions will affect both motor and sensory functions. With listeriosis, animals may be found dead. When clinical signs are observed, initially there may be drooping of an ear and an inability to follow the herd. Subsequently, animals stagger and circle, but if kept quiet periods of apparent normality may be observed. These give way to incoordination, blindness and head pressing followed by recumbency, opisthotonos and death.
Chapter 23
Neurological Diseases in Deer
Major Diseases
Enzootic Ataxia
Cause
Clinical Signs
Pathology
Diagnosis
Treatment
Minor Conditions
Tetanus
Clinical Signs
Diagnosis
Treatment
Prevention
Meningoencephalitis Including Listeriosis
Cause
Clinical Signs
Pathology
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