RUMINANTS

What’s your diagnosis?

Josepha DeLay, Felipe Reggeti, Mike Krystolovich

Stillborn Holstein calf with disproportionate dwarfism (note proportionately shortened limbs, compared to body), hindlimb arthrogryposis, lumbar kyphosis, and shortened maxilla). Dam was a first-calf heifer in poor body condition.

Answer:

Disproportionate dwarfism is a hallmark of congenital nutritional chondrodystrophy associated with maternal micronutrient deficiency during gestation. Manganese deficiency is recognized as a cause of this condition. Liver manganese levels in this fetus were low (0.77 µg/g; ref. 2.0-6.0 µg/g for adult cattle), although manganese levels typically do not reach the adult range until 2-3 wk of age. Further work is needed to determine the normal range of liver manganese in Ontario calves and fetuses.

Disproportionate dwarfism associated with manganese deficiency has been described in calves in Canada, New Zealand, and elsewhere. Joint laxity and swelling is also documented in some affected animals. Low manganese levels in feed have been linked to drought conditions during the previous growing season, as well as to diets inherently low in manganese, including unsupplemented corn silage.

Manganese contributes to pathways of glycosaminoglycan synthesis, and deficiency of this essential micronutrient disrupts normal endochondral ossification and bone development. Kyphosis in this fetus was related to malformation of lumbar vertebrae, suspected to also be associated with micronutrient deficiency here. Resulting spinal cord compression was the likely cause of concurrent arthrogryposis.   AHL

References

McLaren PJ, et al. Chondrodysplastic calves in northeast Victoria. Vet Pathol 2007;44:42-354.

Puls R. Mineral Levels in Animal Health. Clearbrook, BC:Sherpa International, 1994.

Ribble CS, et al. Congenital joint laxity and dwarfism: a feed-associated congenital anomaly of beef calves in Canada. Can Vet J 1989;30:331-338.

White PJ, Windsor PA. Congenital chondrodystrophy of unknown origin in beef herds. Vet J 2012;193:336-343.

---

Copper toxicosis in a dairy goat herd

Murray Hazlett, Talia Fletcher, Felipe Reggeti

A dairy goat herd of ~100 animals experienced 10 sick and 10 dead animals. For the previous 8 mo, the owner reported problems with the doelings that appeared to wax and wane. The goats would go off feed and then deteriorate rapidly. To investigate, a 4-mo-old goat that had recently died was autopsied. It was weak and paddling before death with a mild fever (39.6^oC) and died about 2 h after the producer noticed clinical signs. It had a body condition of 3/5, was mildly dehydrated, and had normal fat and muscle stores. There was pulmonary congestion. Polioencephalomalacia or listeriosis was suspected, and fixed and fresh tissue samples were submitted to the AHL for testing.

Histology showed dissociation of hepatic cords with single-cell necrosis (Fig. 1) and mild diffuse increase in leukocytes in hepatic sinusoids. In brain, there was cerebral cortical edema with the presence of cells compatible with Alzheimer type II cells – these cells are formed usually in the face of liver or colonic damage, and are associated with hyperammonemia. Because of the liver lesions, copper analysis was done on liver, which had levels of 270 µg/g (reference interval [RI] 25 - 150 µg/g) and kidney which had levels of 96 µg/g (RI 3.0 - 6.0 µg/g).

Toxicology results in this case indicate copper toxicosis. In a relatively recent report of copper toxicosis in dairy goats,¹ copper levels in liver and kidney were similar to our case; hepatic necrosis without hemolysis was the main lesion.

After identification of the problem, the producer reported that both the mineral mix and the pelleted feed had been copper supplemented and that the problem resolved after correcting for this.

A 10-yr computer search of AHL pathology records for copper toxicity in goats revealed 11 cases (Table 1). In those cases which had both liver and kidney tested, it can be seen that commonly the relative increase in kidney copper compared to normal levels is much more striking that that seen in liver, which is why diagnosticians commonly prefer to test both of these organs. Hemolysis and jaundice are sometimes, but not always, seen.   AHL

Reference

1. Cornish J, et al. Copper toxicosis in a dairy goat herd. J Am Vet Med Assoc 2007;231:586-589.

Figure 1. Liver, with necrosis of individual hepatocytes (arrows).

Table 1. AHL pathology cases of copper toxicosis in goats.

Breed	Age	History	Submission diagnosis	Liver Cu (25-150 µg/g)	Kidney Cu (3-6 µg/g)
Goat		None given.	Acute hepatic necrosis due to Cu toxicity	1,267	-
Goat		Diarrhea.	Hepatopathy with  nephrosis - r/o Cu	-	-
Saanen	1.5 y	Sudden death.	Acute hepatic necrosis
Pygmy goat	2 y	Weak.	Hepatopathy with elevated renal Cu levels	170	48
Boer goat	3 y	Sudden death.	Hepatic single cell necrosis - compatible with Cu toxicosis	350	-
Nubian	3 y	Sick 8 days. Liver orange.	Hepatopathy - bile stasis and hemoglobinuric nephrosis	190	31
Goat	3.2 y	Sick one day, down in sternal recumbency.	Acute hepatic necrosis	330	150
Mixed-breed goat	4 mo	Sudden death. Weak. Paddling, pupils unresponsive.	Acute hepatic necrosis - Cu toxicosis	270	96
Saanen	2.5 mo	Didn't eat. Ran away when treated. Dead next day.	Periacinar hepatic necrosis - Cu toxicosis	360	190
Caprine	2 y	Found dead. Kidded 2 mo ago.	Nephropathy - probable Cu toxicosis	-	-
Toggenburg	7 mo	Separated from rest of herd. Given horse feed.	Hepatic necrosis due to Cu toxicosis	478	114