Copper accumulation in the liver in wildlife occurs primarily because of impaired copper excretion due to chronic portal pathology , excessive dietary intake or overdosing by injection . Inherited defects in copper metabolism have not yet been proven in African wildlife . The primary presentation of copper poisoning is that of hepatic necrosis and / or intravascular hemolysis with methemoglobinemia .
3 . Zinc
severely emaciated with extensive alopecia and thick surface crusting in affected areas ( figure 4 ). Marked thymic atrophy was encountered ( figure 5 ).
On histopathology , there was outspoken cutaneous parakeratosis with heavy colonization of the parakeratotic crust by opportunistic fungi . Following dietary supplementation with trace elements including zinc , these pups showed a dramatic recovery ( figure 6 ).
Analysis of liver for zinc can reflect zinc deficiency but is not a reliable tissue for zinc adequacy . In the bovine calf , liver zinc levels are significantly higher in animals originating from herds that supplement trace minerals compared to those that do not , whether the same applies in African wildlife is unknown at this stage .
Zinc is present in many metalloenzymes and is involved in DNA replication , RNA and protein synthesis , carbohydrate and lipid metabolism , gene expression and appetite regulation . Therefore , the clinical manifestations of zinc imbalances can be severe . Due to zinc ’ s electron configuration , many other metals interact with it and these interactions are frequently involved with both deficiencies ( antagonistic ) or toxicities ( synergistic ). These antagonistic and synergistic influences make interpretation of zinc levels in tissues complicated as both deficiencies and toxicities may occur at apparently normal zinc tissue levels .
Clinical syndromes observed in zinc deficient animals include poor body condition ( decreased efficiency of feed use ), decreased appetite , poor growth rates , rough hair coat , impaired vision , diarrhea , hyperkeratosis ( parakeratotic ), alopecia , abortion , mummification , prolonged birth process ( uterine inertia ), impaired vitamin A metabolism , immunosuppression , thymic atrophy , and in neonate ’ s stiff gait , swelling of the distal extremities and deformed hooves .
Figure 4 : African wild dog puppie showing severe emaciation , alopecia and crusting dermatitis .
Figure 5 : African wild dog puppy thorax cavity opened demonstrating severe thymic atrophy .
In this case of zinc deficiency in a litter of orphaned African wild dog puppies , affected animals presented with cachexia , poor growth rates , crusting dermatitis and mortality . At post-mortem affected puppies were
Figure 6 : African Wild dog puppies post zinc supplementation ( image courtesy of Champion Wildlife )
2017 October 11