Effects of Subchronic Copper Poisoning on Cecal Histology and Its Microflora in Chickens

Copper (Cu) is an important trace element with a two-sided effect on the growth performance of animals, which depends on the timing and dosage of Cu addition, etc. The purpose of this study was to determine the effects of oral copper sulfate (CuSO4, 350 ppm) on growth performance, cecal morphology, and its microflora of chickens (n = 60) after 30, 60, and 90 days. The results showed that after 90 days of copper exposure, the chickens lost weight, the cecum mucosa was detached, and vacuolation and inflammatory infiltration occurred at the base of the lamina propria. In addition, using the 16S rDNA sequencing method, we observed that copper exposure changed the richness and diversity of intestinal microorganisms. At the phylum level, Proteobacteria and Actinobacteria both significantly increased, while Bacteroidetes significantly decreased in the Cu group compared with control check (CK) group. At the genus level, the relative abundance of Rikenellaceae_RC9_gut_group decreased significantly, while Ruminococcaceae_UCG-014, Lachnoclostridium, and [Eubacterium]_coprostanoligenes_group increased significantly after copper exposure, and the change in microflora was most significant at 90 days. Moreover, the relevance of genus-level bacteria was altered. PICRUST analysis revealed potential metabolic changes associated with copper exposure, such as Staphylococcus aureus infection and metabolic disorders of nutrients. To sum up, these data show that subchronic copper exposure not only affects the growth and development of chickens but also causes the imbalance of intestinal microflora, which may further induce metabolic disorders in chickens.

Spontaneously Occurring Chronic Copper Toxicosis in Pattanam Breed of Sheep

Background: Copper (Cu), an essential trace element, is toxic if consumed in excessive amounts. Ruminants, particularly sheep, are highly susceptible to chronic copper poisoning and cause acute death. Spontaneous copper poisoning in sheep was reported from many parts of the world however limited reports are available from India. Hence the present investigation was undertaken to report the occurrence of chronic copper poisoning in an intensively maintained Pattanam breed of sheep flock and its therapeutic management. Methods: An investigation was carried out to ascertain the possible cause of increased mortality in an intensively maintained 130 male lambs aged between 8 to 10 month old belongs to Pattanam breed during the month of September 2020 following death of 21 animals within a period of 15 days. Affected flock was inspected and samples were collected for biochemical analysis, toxicological, bacteriological and pathological examination.Result: Affected animals showed depression, anorexia, jaundice, hemoglobinurea and accelerated breathing. At necropsy, the dead animals showed generalized icterus, lung edema, yellow to orange coloured liver and gun metal kidney. Histopathological lesions include lung edema, centrilobular hepatic necrosis, bile stasis, renal tubular necrosis and formation of tubular cast. Toxicological analysis of liver revealed the copper level of 781 mg/kg dry matter basis. Source of copper was identified as a commercial mineral mixture supplement intended for cattle was supplemented along with concentrate feed. The flock was treated with chelating agent (D-penicllamine) and supportive therapies.

Copper poisoning in sheep

This article examines the causes and effects of copper poisoning in sheep. Whether the poisoning is acute or chronic depends on the clinical symptoms seen. Sometimes haemolytic crisis is observed leading to jaundice and dark coloured urine and the condition can lead easily to death. Strategies to minimise the copper intake of animals are essential to prevent more damage to the initial animals and to others.

Chronic copper poisoning in beef cattle in the state of Mato Grosso, Brazil

ABSTRACT: Copper is an essential micromineral in animal feed; however, when consumed in excess, it can cause liver necrosis, hemolytic crisis, hemoglobinuric nephrosis and death in cattle. Although uncommon in this species, copper poisoning occurs as a result of exacerbated supplementation, deficiency of antagonist microminerals, or previous liver lesions. An outbreak of chronic copper poisoning is reported in semi-confined cattle after supplementation with 50 mg/Kg of dry matter copper. The cattle showed clinical signs characterized by anorexia, motor incoordination, loss of balance, jaundice, brownish or black urine, diarrhea and death, or were found dead, 10 to 302 days after consumption. Of the 35 cattle that died, 20 underwent necropsy, whose frequent findings were jaundice, enlarged liver with evident lobular pattern, black kidneys, and urinary bladder with brownish to blackish content. Microscopically, the liver showed vacuolar degeneration and/or zonal hepatocellular centrilobular or paracentral coagulative necrosis, in addition to cholestasis, mild periacinal fibrosis, apoptotic bodies, and mild to moderate mononuclear inflammation. Degeneration and necrosis of the tubular epithelium and intratubular hemoglobin cylinders were observed in the kidneys. Copper levels in the liver and kidneys ranged from 5,901.24 to 28,373.14 μmol/kg and from 303.72 to 14,021 μmol/kg, respectively. In conclusion, copper poisoning due to excessive nutritional supplementation is an important cause of jaundice, hemoglobinuria, and death in semi-confined cattle.