Experimental Copper Deficiency, Chromium Deficiency and Additional Molybdenum Supplementation in Goats – Pathological Findings

Abstract

Secondary copper (Cu) deficiency, chromium (Cr) deficiency and molybdenosis (Mo) has been suggested to cause the "mysterious" moose disease in the southwest of Sweden. The present experiment was performed on goats to investigate the clinical, chemical, and pathological alterations after 20 months feeding of a semi-synthetic diet deficient in Cu and Cr. Four groups were included in the study: control group (n = 4), Cu-deficient group (group 1, n = 4), Cr-deficient group (group 2, n = 2) and Cu+Cr-deficient group (group 3, n = 3). Group 3 was additionally supplemented with tetrathiomolybdate during the last 2 months of the experiment. Main histopathological findings in groups 1 and 3 were the lesions in the liver, characterised by a severe active fibrosis, bile duct proliferation, haemosiderosis and mild necroses. Additionally, degenerative alterations of the exocrine pancreas were prominent in groups 1 and 3. Lesions in group 3 were more pronounced than in group 1. In group 3, the skin showed an atrophic dermatosis, while in group 2 a crusty dermatitis caused by Candida spp. was observed. This study shows that liver, pancreas and skin are mainly affected by a long term deficiency of copper and the findings are complicated by molybdenum application while chromium deficiency produced no histomorphological effects in our study.

Histopathological and biochemical findings of congenital copper deficiency: are these similar to those of caprine arthritis-encephalitis?

“…Aside from cerebral edema, cerebellar hyperplasia in gelatinous material-filled cavities, demyelination in the brain, cerebellum, and medulla spinalis and wallerian degeneration have also been reported in animals with swayback [ 12 ] but this was not seen in our study. On the contrary, we observed neural chromatholysis, pyknosis, and satellitosis in the medulla spinalis similar to that resulting from Cu deficiency as previously reported by different authors [ 3 ].…”

“…Glial cell proliferation was observed in grey matter of the spinal root pyknosis and chromatholysis of the neurons were also noted in the same area. These findings were previously reported in goat kids, lambs, and calves with Cu deficiencies [ 3 , 14 ].…”

Alteration of the Antioxidant Capacity and Gut Microbiota under High Levels of Molybdenum and Green Tea Polyphenols in Laying Hens

“…In ruminants it has been demonstrated that high levels of dietary MO can interfere with microbial metabolism [4,5]; however, information about the effect of MO on the poultry microbiota is limited. In this study, we observed that exposure to high MO levels resulted in lower Firmicutes and higher Proteobacteria abundance, whereas in the TP and MO + TP groups, an increase in Firmicutes abundance and Firmicutes/Bacteroidetes ratio at phylum level was observed.…”

“…However, MO (45 mg/kg BW) can also have negative effects as demonstrated in several studies where rumen microbial metabolism was altered. Moreover, MO (100 mg/kg diet) can interfere with the bioavailability of other trace elements, such as iron (Fe) and zinc (Zn), especially copper (Cu) leading to Cu deficiency [3,4,5,6]. Other adverse effects that have been observed in animals exposed to high dietary levels of MO include poor growth, achromotrichia, severe diarrhea, and anemia [7].…”

Molecular Regulation of Copper Homeostasis in the Male Gonad during the Process of Spermatogenesis

“…Histological analyses have demonstrated that the seminiferous tubules of Cu-deficient animals are less developed. This was mainly explained by the inactivation of the function of the Sertoli cells [48,50,[58][59][60][61]. All these data indicate that copper concentration and metabolism in male gonads must be very tightly regulated, starting from puberty and continuing progressively throughout adult life.…”