M. Clauss, E.S. Dierenfeld
Severel cases of copper deficiency in captive wild animals have been described (Senf 1974, Senf and Zscheile 1978, Ashton and others 1979, Zwart and others 1985, Gillespie and others 1995). For one spieces, the bleskbok (Damaliscus doracas phillipsi), a state of deficiency has been demonstrated both in captivity (Jones 1978) and in the wild (Turkstra and others 1978), and this may reflect an unusually high requirement for the element (Direrenfeld and others 1988). The evidence and possibility of genetic differences in the absorption of copper was reviewed by Wiener (1987).
Specific clinical signs which responded to copper supplementation have been noted in yak (Bos grunniens) in two zoological collections. At Whipsnade Wild Animal Park (formerly Whipsnade Zoo), low serum copper concentrations were observated in yak by Ashton and others (1979), who descriebed a range of clinical signs which responded to oral supplementation with the element, including debility, weight loss, anorexia, diarrhoea, hinleg ataxia, alopecia, loss of coat colour including typical white spectacles around the eyes, poor reproductive rate, frequent stillbirths and low neonatal survival (Ashton and others 1979, Hawkey and others 1983, E. J. Flach, personal observation) Haematological changes in these yak included microcytic anaemia, neutrophilia and eosinophilia, possibly due topersistent parasitic infections despite regular anthelmintic treatment (Hawkey and others 1983). Pasture analyses revealed slightly low copper concentrations whitout high molybdenum concentrations (Whipsnade veterinary records 1998), but bactrian camels (Camelus bactrianus) and P’ere David’s deer (Elaphurus davidianus) sharing the same pasture have never displayed clinical signs of deficiency. The yak’concentrate ration has been supplemented with copper for many years, wich has resulted in alleviation of the problems and cases recur only sporadically.
In a yak group kept at the New York Zoological Society (Bronx Zoo) until
1987, low blood copper levels, loss of coat colour, hair loss and hyperkeratotic
skin lesions on the neck, shoulders and withers, were successfully treated
with a special copper-supplemented diet (E. S. Dierenfeld, personal observation).
A dietary mineral supplement with an excessively high iron content was
found to be part of the problem, but the final cause could not be identified.
In 1998, 12 European facilities returned a questionnaire on the subject. In 11 collections, a copper deficiency problem in yak had neither been suspected or identified, nor had similar clinical signs ever been observed. In one collection, however, hyperkeratosis of the neck and rump, and a bad hair contradict the idea that yak have special copper requirements, notwithstanding the lack of detailed knowledge aboutdifferent institutes’ dietary regimes. Alternatively, the report of hyperkeratotic skin lesions, albeit sporadic, may suggest a species peculiarity, not in the requirement for copper, but in the response to copper deprivation.
Reports on yak diseases (Pal 1993, RanaRao and others 1994, Liu and others 1995, Lensch 1996) have not mentioned copper deficiency problems except for the Whipsnade case reported by Li and Wiener (1995). Whitehead (1950) described a syndrome similar to enzootic ataxia in yak at Woburn Zoo in the UK, but not diagnostic investigations were recorded.
Li and Wiener (1995) recorded a seasonal variation in the red blood cell haemoglobin content in yak in China, with a low before and a peak directly after the grazing season; similar results were reported from Siberia. As copper is an important element for red blood cell production, it may be possible that this variation was due to a marginal copper supply in the winter period. Liu and others (1995) revealed very low liver copper levels from apparently healthy yak, with no reports of copper deficiency in yak or other domestic species in the region.
Winter and others (1982) descrided severe losses of free-ranging domestic yak due to pyrrolizidine alkaloid poisoning, and the suspected toxic plants were later identified as Senecio raphanifolius, Senecio biliguatus, Ligularia mortonii, Ligularia amplexiaulis and a then unknown Ligularia species (Winter and others 1994). Apart from pathological changes corresponding to alkaloid poisoning in other species, skin lesione were a consistent and even pathognomonic symptom, although such lesions have not been descriebed in cases of alkaloid poisoning in other animals. The lesions occurred on the nose, the dorsal part of the body and the legs, and symptoms included hair loss. No parasitic or bacterial cause could be demonstrated. The anaemia found in the diseased yak was a more severe and consistent feature than normally reported for alkaloid poisoning. Swick and others (1982) demonstrated that pyrrolizidine alkaloid poisoning causes an increase in liver copper concentrations in rats, and they hypothesised that this was due to a mobilisation of copper from other tissues were marginally copper deficient, the compartmentalisation of copper in the liver, triggered by alkaloid poisoning, may changes in red blood cell count, and with skin lesions seemingly typical for copper-deficient yaks.
In general, the reproductive rate of free-ranging yak is low under normal
grazing and rearing conditions (Li and Wiener 1995). Females are most likely
to calve every two years, and many will have only one annual oestrus, with
much of the relatively low productivity being directly attributed to malnutrition
in winter and early spring (Li and s from Whipsnade suggest that copper
supplementation may have a beneficial influence on fertility: Senf and
Zscheile (1978) reported that the addition of a copper supplement to the
diet af a zoo in a copper-deficient area resulted in improved fertility,
fewer stillbirths, fewer births of immature offspring, intensified rutting
behaviour in males, and an overall improved condition in several ungulate
groups: similar results are also reported by Wiener and sales (1976). A
long-term copper response trial should be undertaken with free-ranging
yak, for exmple, as descriebed by Wikse and others (1992), and probably
with slow release intraruminal devices. Li and Wiener (1995) suggest that
the role of specific minerals should be investigated as possible factors
limiting health and production in yak; copper seems a good choice with
which to start.