Chronic Lymphocytic Enteritis Associated with Wasting and Copper Deficiency in Intensively Managed Muskoxen (Ovibos moschatus)
From 1990 through 1994, a captive herd of musk ox (Ovibos moschatus) experienced substantial losses in all age and sex groups. Adults showed two primary patterns of mortality: sudden death without warning or within 24–72 hours of recumbency, and a chronic wasting syndrome. The principal necropsy findings in the acute cases were an enlarged, pale liver and a chronic lymphocytic enteritis with villous atrophy. Livers were small and dark in the chronic form. Liver copper levels were between 1–8 ppm. Dietary changes and discontinuation of an in-feed anticoccidial medication resulted in an improvement in condition of the herd and a substantial reduction in mortality.
From 1990 through 1994, the Musk Ox Farm in Palmer, AK experienced substantial losses in all age and sex groups. Adults showed two primary patterns of mortality: 1) A sudden death syndrome which frequently presented as unexpected death with no prior clinical signs, or sudden onset recumbency followed by death within 24–72 hours. These animals were generally in good body condition with abundant internal body fat and an enlarged, pale liver. There was a distinctive clustering of these cases in the late summer and early fall. 2) A chronic wasting syndrome characterized by progressive weight loss for 6–18 months, sometimes with a brief recovery period. These animals usually showed facial hair loss, dry brittle discolored hair coats, and periodic drooling. Dead animals had abundant body fat but showed marked muscle wasting. The liver in these animals was dark and slightly smaller than normal.
Both types of mortality had the following common pathologic features: a chronic lymphocytic enteritis with villous atrophy, atrophy of the exocrine pancreas, splenic hemosiderosis, abundant internal body fat, loss of alveolar bone with tooth root abscesses, and extremely low liver copper levels (1–8 ppm). An aggressive plan of diagnostics was implemented with a careful analysis of herd records. Bacteriologic, virologic, and parasitologic investigations were unrevealing. Affected animals showed mild anemia and haptoglobin was not detected in serum of affected animals. Serum copper levels were not indicative of tissue levels. Ceruloplasmin levels were not evaluated. By fall 1993, over 95% of the herd showed symptoms of the chronic wasting syndrome. Although, animals dying suddenly in early fall were considered at necropsy to be in good body condition, herd records indicated that poor weight gains and slight declines occurred in all but one animal during the summer, a time of maximal weight gain in muskoxen. In addition to adult losses, the herd was experiencing high losses due to abortion, stillbirth, and calf mortalities.
We believe that the different clinical presentations in the adults represent various nutritional deficiencies that were secondary to the chronic enteritis. Copper deficiency and a protein losing enteropathy were identified in these animals, but multiple vitamin deficiencies may also have been present. Although a definitive etiologic agent was never identified we propose that the intestinal lesion was the result of a chronic irritant.
Management changes included:
1. An overall reduction in quantity of pelleted feed.
2. Pelleted feed offered three times weekly instead of everyday.
3. A larger amount of browse was offered starting in summer 1994.
4. Decoquinate (Decoxx®, Rhone-Poulenc, Atlanta, GA, USA), an anticoccidial drug incorporated into this herd’s pelleted ration (0.02%) in 1990, was removed on November 1, 1993.
The overall herd condition improved over the summer of 1994 and winter 1995. Starting in 1996, the annual adult mortality rate decreased to less than 1%. Unfortunately, too many management changes were implemented to determine which was most effective. However, based on experience with muskoxen at the Institute of Arctic Biology, we suspect that the reduction in quantity and frequency of feeding pellets coupled with the increase in browse was insufficient to produce such a dramatic change in herd health. The chronic feeding of decoquinate is more likely to have induced the changes seen. Long-term feeding is not recommended by the manufacturer.
A similar problem to the sudden death pattern described above occurred in spring 1991 at the Large Animal Research Station, Institute of Arctic Biology. Two male muskoxen died unexpectedly following a 2-day course of illness. These animals had mild-moderate muscle wasting, abundant internal body fat, and a markedly enlarged, pale liver. There was marked lipid accumulation within hepatocytes and bile stasis. Liver copper levels were 1 and 2 ppm. Unlike in the farm herd, there was no enteritis in either of these animals. Pasture and hay trace mineral analyses were not available for that time period. However, subsequent analyses in 1994 indicated that the pasture housing these two animals becomes severely deficient in copper and cobalt by mid-August and the hay obtained from the Fairbanks/Delta Junction areas was equally deficient. For these two animals we suspect that a primary nutritional deficiency occurred with resultant lesions closely resembling ovine white-liver disease. Unfortunately, elemental cobalt levels are of little value and samples were not available for vitamin B12 or metabolite analyses.
In conclusion, these disease investigations emphasize the importance of careful dietary management in captive muskoxen. Additionally, this work suggests that both primary and secondary copper deficiency can occur in captive muskoxen. Although requirements are unknown, both muskox facilities currently feed 35–45 ppm of copper in their pelleted rations. Specific dietary manipulations are underway to better evaluate copper requirements in this species.