Suspected monensin toxicosis in feedlot cattle

Suspected monensin toxicosis was seen in feedlot cattle aged 6 to 9 months. Twenty cattle died following inclusion of monensin in the feed at 400g/tonne, which was 13 times the recommended level. The deaths occurred over 2 weeks. Clinical signs were inappetance, respiratory distress and sudden death. Post-mortem features were those of right-sided heart failure and included dependent subcutaneous oedema, ascites, hydrothorax, and periancinar hepatocyte congestion and necrosis. However, in contrast to previous reports no myocardial necrosis was found, but focal skeletal muscle necrosis was observed. Additional findings were marked pulmonary oedema accompanied by fibrin and erythrocyte exudation into alveoli and interlobular lymphatics. From these findings it appears that monensin, as well as affecting both cardiac and skeletal muscle, has a primary effect on lung vasculature.     

Aflatoxin B1 toxicosis in dairy calves pretreated with selenium-vitamin E

Effects of a single IM injection of selenium-vitamin E (Se-E; 5 mg of Se + 68 IU of alpha-tocopherol/60 kg of body weight) as a pretreatment 14 days before an oral dose of aflatoxin B1 (1.0 mg/kg) were studied in 24 dairy calves. Treatment groups were designated as follows: group 1 = no Se-E or aflatoxin B1 (control); group 2 = Se-E supplementation only; group 3 = aflatoxin B1 dose only; and group 4 = Se-E supplementation before aflatoxin B1 dose. Clinical signs of toxicosis in aflatoxin B1-treated calves included anorexia, ataxia, rough haircoats, increased respiration rates, dyspnea, dehydration, and nasal discharge. Packed-cell volume, RBC, WBC, and hemoglobin were increased in aflatoxin-treated calves. Significant increases in serum aspartate aminotransferase (P less than 0.05) and gamma-glutamyl-transferase (P less than 0.001) activities and prothrombin times (P less than 0.001) were observed in aflatoxin-treated calves, indicating that there was hepatic involvement. Although aflatoxin exposure caused a significant decrease in body weight (P less than 0.01) and feed intake (P less than 0.001) in treatment groups 3 and 4, Se was demonstrated to interact significantly (P less than 0.001) with aflatoxin B1 for feed intake, causing an improved feed intake in treatment group 4 calves.     

Pathologic changes associated with experimental lasalocid and monensin toxicosis in cattle

The acute toxicity of lasalocid and monensin was studied in 36 Holstein steers. The cattle were given (orally) a single dosage of lasalocid (1, 10, 50, or 100 mg/kg of body weight) or monensin (25 mg/kg of body weight) or rice hulls. Animals were observed once a day until they died or were euthanatized at 32 days after the dose was given. All cattle were necropsied. Heart, kidney, adrenal gland, liver, spleen, pancreas, lungs, brain, sciatic nerve, skeletal muscle, small intestine, large intestine, and rumen tissue sections, stained with hematoxylin and eosin, were studied microscopically. Lasalocid was lethal at dosages of 50 and 100 mg/kg, and monensin was lethal at the dosage given (25 mg/kg). Cattle dying of lasalocid and monensin toxicoses had gross and microscopic lesions consistent with cardiomyopathy. Dilated heart or petechial and ecchymotic hemorrhages were observed with both drugs. Microscopically, multifocal areas of myocyte necrosis were observed. Those cattle that died within 3 days of dosing with either drug had a marked degranulation of pancreatic acinar cells. Changes were not observed in any other tissues.     

Effect of selenium-vitamin E on adriamycin-induced cardiomyopathy in rabbits

Administration of selenium-vitamin E (Se-E) to weanling rabbits chronically treated with adriamycin (ADR) resulted in decreased incidence and severity of cardiomyopathy and decreased cumulative mortality during a 10-week experiment. However, Se-E did not protect against extracardiac lesions or against a number of clinicopathologic alterations induced by chronic ADR toxicosis. Histopathologic alterations of ADR-induced cardiomyopathy were concentrated periarterially in the free and septal walls of the left ventricle. Initial vacuolar degeneration of injured cardiac muscle cells was followed by myofibrillar lysis and eventual cell death with subsequent interstitial fibrosis. Ultrastructurally, degenerated cardiac muscle cells had 3 prominent alterations: (1) sarcoplasmic vacuolization caused by distention of elements of sarcoplasmic reticulum and T-tubules, (2) degeneration of mitochondria forming large myelin figures from disrupted membranes, and (3) lysis of myofibrils producing granular sarcoplasmic masses. Severely injured fibers were necrotic and macrophages invaded to remove cellular debris. The interstitium was distended by edema and increased amounts of collagen. Extracardiac lesions in rabbits with chronic ADR toxicosis included the usually recognized alterations involving cell-renewal systems in kidney, testis, bone marrow, skin, and alimentary tract, as well as vacuolar degeneration of skeletal muscle and focal loss of pancreatic tissue, with ensuing pancreatic fibrosis and fat necrosis. Deaths in ADR-treated rabbits usually were precipitated by terminal septic embolism. The partial protection afforded by Se-E against ADR-induced cardiomyopathy may be associated with stabilization of the membranes of injured muscle cells or with prevention of ADR-induced inhibition of coenzyme Q10-dependent mitochondrial enzymes.     

Review of monensin toxicosis in horses

Results of experimental studiesindicate that horses are much more sensitive to monensin toxicity than cattle. Single dose studies by gavage with mycelial monensin resulted in an estimated LD₅₀ of 1.38 mg/kg of body weight. Subacute feeding studies indicate that horses will tolerate the highest use level for cattle of 33 ppm without any evidence of toxicity. Evidence of intoxication was apparent with the highest use level for chickens of 121 ppm.In pasture supplement studies, horses ate supplement containing high levels of nonensin upon initial exposure which resulted in toxicity and/or death. Following initial exposure to sublethal levels, consumption of monensin containing supplements was negligible.The clinical signs of toxicity includedpartial to complete anorexia, colicky pain, sweating and tachycardia, uneasiness, polyuria, progressive ataxia, recumbency with frequent attempts to rise and thrashing of the limbs followed by death. Examination at necropsy of animals that die soon after initial exposure to monensin may show no significant lesions, otherwise hemorrhage and pale areas in the heart with transudation into body cavities may be seen. Evidence of degenerative cardiomyopathy and congestive heart failure may be observed on histopathologic examination. Increased activities of muscle origin enzymes may also be found.The results of controlled studiesand evidence from field reports indicated that the greatest risk of intoxication was upon initial exposure to feed or supplement containing monensin. Feed mistakes and mixing errors were the two most common causes of monensin toxicity in field cases.     

Acute monensin toxicosis in broiler breeder chickens

Peracute onset of disease was reported in a 42-wk-old broiler breeder flock that was presented by error with feed containing monensin at approximately seven times the approved level for broiler chickens. Morbidity and mortality were extremely high, and the affected chickens displayed feed refusal, decreased water consumption, and severe paralysis that ranged from abnormal gait to a complete inability to move. During the first 10 days postingestion of the suspect feed, mortality in hens reached 13.7% and 70.9% in the roosters. Hen day production decreased from 67% to 3% in the same period of time. A total of 638 g/ton of monensin was detected in suspect feed samples by one laboratory and 740 g/ton in a second laboratory. Twenty-one days after removal of the suspect feed, the mortality rate returned to normal levels in both hens and roosters, albeit feed consumption and egg production remained extremely low, which prompted the company involved to eliminate the flock.     

Effect of increasing monensin sodium levels in diets with virginiamycin on the finishing of Nellore cattle

This study evaluated the effect of increasing levels of monensin sodium (MON) in diets with virginiamycin (VM) on the finishing of feedlot cattle. Two hundred and eighty intact male Nellore cattle (348 ± 32 kg body weight, 22 months) received one of the following five diets: control diet (without additives); diet containing VM (25 mg per kg dry matter) combined with 0 (MON0), 10 (MON10), 20 (MON20) or 30 (MON30) mg MON per kg dry matter. During adaptation (28 days), the MON0 diet increased dietary net energy for maintenance and gain compared to the control diet (P = 0.04). The combination of additives linearly reduced dry matter intake, body weight and average daily gain (P < 0.01). Considering the total study period (110 days), there was a trend of greater net energy intake for maintenance (P = 0.09) and hot carcass weight (P = 0.06) for animals fed MON0 compared to the control diet. The combination of additives linearly reduced dry matter intake (P = 0.04) and linearly increased gain : feed and dietary net energy for maintenance and gain (P < 0.01). The combination of VM with MON at a dose of 30 mg/kg dry matter is recommended for Nellore feedlot cattle because it improves the efficiency of energy utilization.     

Arsenic toxicosis and suspected chromium toxicosis in a herd of cattle

Arsenic toxicosis and suspected chromium toxicosis were diagnosed in a herd of cattle that ingested ashes from lumber treated with copper, chromium, and arsenic. Findings included peracute death, depression, ataxia, weakness, recumbency, and watery diarrhea. Chemical analyses of liver, kidney, abomasal contents, rumen contents, and ashes revealed high concentrations of arsenic and chromium. Histologically, specimens of abomasum and duodenum had diffuse mucosal degeneration and engorged capillaries. Epithelial cells of the proximal convoluted tubules and distal collecting tubules of the kidney were swollen and had mild granular cytoplasmic degeneration. Burning lumber treated with copper, chromium, and arsenic does not remove the heavy metals from them, and ingestion of the ashes from the wood constitutes a hazard to livestock health.     

Ethylene glycol toxicosis in cattle.

A 1-month-old Jersey calf died of oxalate nephropathy. The calf had access to antifreeze (ethylene glycol) 3 days prior to death. Since ethylene glycol toxicosis had not been reported in cattle, the effects or oral administration of ethylene glycol were studied in 7 calves and 3 cows. The toxic dose ranged from 2 to 10 ml of ethylene glycol per kg of body weight. Clinical signs were increased respiration, staggering gait, paraparesis, depression and later, recumbency and death. Hemoglobinuria and epistaxis were seen at doses of 10mg/kg of body weight. Azotemia, hypocalcemia and neutrophilia were constant findings whereas acidosis, plasma hyperosmolality and hemolytic anemia were seen in the animals receiving the higher doses. A diagnosis of ethylene glycol toxicosis must be based upon a history of ingestion and the presence of calcium oxalate crystals in body tissues (especially the kidney and brain).     

Influence of monensin on the performance of cattle

Performance data on nearly 16,000 head of cattle that were used in trials to document effects of monensin on feedlot cattle were summarized. Cattle fed monensin-containing diets gained 1.6% faster, consumed 6.4% less feed and required 7.5% less feed/100 kg gain than cattle fed control diets. Monensin resulted in the greatest improvement in feed/gain at 2.9 Mcal metabolizable energy (ME)/kg diet dry matter (DM). Within the range of monensin concentrations used in the trials that were summarized (31.8 +/- 7.5 mg/kg DM), high monensin concentrations did not improve feed/gain over that obtained with lower concentrations. Carcass characteristics were not significantly influenced by monensin. Responses of cattle to monensin and implants were additive. Energy metabolism data suggested that monensin improved digestibility of DM, reduced fasting heat production and increased dietary net energy maintenance (NEm) values more than it increased net energy gain (NEg) values. Data showing the response of cattle to monensin when fed various dietary protein concentrations or sources of supplemental N suggested that monensin had a protein sparing effect. Monensin has also been shown to reduce lactic acid production, aid in the control of coccidia and bloat and to be toxic to face and horn fly larva in feces of monensin-fed cattle. In pasture trials, monensin improved daily gains. When fed to beef cows, monensin reduced amounts of feed required to maintain cow weight.     

Acute monensin toxicosis in sheep: light and electron microscopic changes

Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.     

Effect of monensin withdrawal on rumen fermentation,methanogenesis and microbial populations in cattle

This study was designed to obtain information on the residual influence of dietary monensin on ruminant fermentation, methanogenesis and bacterial population. Three ruminally cannulated crossbreed heifers (14 months old, 363 ± 11 kg) were fed Italian ryegrass straw and concentrate supplemented with monensin for 21 days before sampling. Rumen fluid samples were collected for analysis of short chain fatty acid (SCFA) profiles, monensin concentration, methanogens and rumen bacterial density. Post‐feeding rumen fluid was also collected to determine in vitro gas production. Monensin was eliminated from the rumen fluid within 3 days. The composition of SCFA varied after elimination of monensin, while total production of SCFA was 1.78 times higher than on the first day. Methane production increased 7 days after monensin administration ceased, whereas hydrogen production decreased. The methanogens and rumen bacterial copy numbers were unaffected by the withdrawal of monensin.     

牛尿素中毒的治疗体会

尿素中毒在兽医临床上较多见。笔者曾治疗6例病牛,皆因误食多量尿素后发病,经及时抢救均痊愈,现将解毒方法总结如下。