Accidental monensin sodium intoxication of feedlot cattle

Of 1,994 yearling and 2-year-old cattle in a winter feeding program, 117 died within 42 days of being fed toxic amounts of monensin sodium in a liquid protein supplement. Death losses commenced on the third day after ingestion of a toxic amount in the feed. Clinical signs in cattle that died in less than 9 days included anorexia, pica, diarrhea, depression, mild hindlimb ataxia, and dyspnea. Gross necropsy findings in cattle dying in the acute phase of the illness included hydrothorax, ascites, and pulmonary edema, as well as petechial hemorrhages, edema, and yellow streaking in skeletal and cardiac muscle. Cattle dying after 9 days had gray streaks in heart and skeletal muscle, generalized ventral edema, enlarged, firm, bluish discolored liver, and enlarged heart. Microscopic changes in cattle dying in the acute phase (less than 9 days) consisted of pulmonary edema, congestion, and hemorrhage. Cardiac and skeletal muscle had localized areas of edema, hemorrhage, and coagulative necrosis. In cattle dying after 9 days of illness, the changes included lymphocytic infiltration, sarcolemmal nuclear proliferation, and fibrosis in skeletal and cardiac muscle. Lungs contained increased alveolar macrophages and a few neutrophils. Centrilobular necrosis and mild fibrosis were found in the liver. Changes varied somewhat according to the area of heart or skeletal muscle that was affected. Active muscles, eg, those in the heart ventricles and diaphragm, were altered most severely. Intoxication appeared to be a result of sedimentation of monensin in the molasses carrier to give remarkable concentrations of the substance at the bottom of the holding tank.     

Light and electron microscopic changes in cardiac and skeletal muscle of sheep with experimental monensin toxicosis

Monensin toxicosis was induced in lambs by either a single oral dose of 12 mg/kg or six daily doses of 8 mg/kg. Clinical signs of toxicosis consisted of depression, dyspnea, stiffness of gait, reluctance to move, and recumbency. Serum creatine phosphokinase activity was increased. Samples of skeletal and cardiac muscle were obtained over a six-day period and examined by light and electron microscopy. Light microscopic changes in cardiac and skeletal muscles consisted initially of vacuolation and intracellular edema of muscle cells followed by segmental necrosis. Interstitial fibrosis was present on days 5 and 6 postexposure. Muscle fiber necrosis was more severe in skeletal than cardiac muscles and most severe in sheep given 8 mg/kg of monensin daily. Macrophages were seen only in areas of severe necrosis. The earliest ultrastructural change was severe swelling of mitochondria. Secondary changes consisted of lipid accumulation and myofibrillar alterations. Myoblast proliferation was present as early as four days after initial exposure to monensin.     

Effect of shock strength on survival and acute cardiac damage induced by open-thorax defibrillation of dogs

The safety of open thorax defibrillation with single damped sine-wave shocks and 6-cm-diameter electrodes was evaluated in healthy anesthetized dogs. Twenty-one dogs were allotted to 6 groups: Group A were nonshocked controls and groups B through F were given single shocks of 4-, 7-, 12-, 19-, or 32-fold, respectively, greater than a defibrillation threshold dose (30 mA/g of heart). Immediate postshock death resulted in group F dogs; group A through E dogs survived and were killed after 2 days. The incidence and severity of cardiac morphologic damage increased with shock strength (mild damage occurred in 1 of 3 dogs in group C and in 3 of 4 dogs in group D and severe damage occurred in 2 of 3 dogs in group E). The cardiac lesions were characterized grossly and microscopically. In dogs that died immediately after shocking, damage was apparent as pale circular zones of edema and myofibrillar degeneration in the ventricular free walls beneath the electrode placement sites on the cardiac surface. In the dogs that survived 2 days, the defibrillator-induced areas of myocardial necrosis and calcification were concentrated in arc or ringlike patterns beneath the periphery of the electrode placement sites. All dogs that were studied 2 days after shocking had mild fibrinous pericarditis. Postshock electrocardiographic changes were not good indicators of cardiac damage because the mild epicardial inflammatory reaction associated with the surgical procedure produced large ST and T wave changes which masked any changes associated with myocardial necrosis induced by the electric shocks. It was concluded that a substantial safety margin exists between the required defibrillation threshold shock dose and the large shocks required to produce marked cardiac damage or death in healthy dogs.     

The toxicity of Castanospermum australe seeds for cattle

Two calves given a mean of 16.1 g and 16.4 g ripe Castanospermum australe seeds/kg body weight daily for 13 and 16 days respectively developed haemorrhagic gastroenteritis. The first calf died. The second calf had mild myocardial degeneration and necrosis and mild nephrosis at necropsy. Two calves given a mean of 16.8 g unripe C. australe seeds/kg body weight daily for 18 days remained clinically normal and had mild gastritis at necropsy. The activity of alpha-glucosidase was reduced in the mononuclear cells of peripheral blood and in skeletal muscle. This was attributed to the presence of the indolizidine alkaloid, castanospermine, in the seeds. The toxin causing the gastroenteritis and other lesions is unknown.     

Unexpected death in an adult dog with anomalous origin of the left coronary artery from the pulmonary trunk

A two-year-old female miniature poodle died unexpectedly while romping with its owner. Anomalous origin of the left coronary artery from the left pulmonic sinus was discovered at necropsy. Histologically, the right ventricle was unremarkable, but multifocal to coalescing necrosis and fibrosis occurred in the myocardium and endocardium of the left ventricle. Medial hypertrophy of small muscular pulmonary arteries was observed in the lung. The cardiac lesions were similar to those of children with anomalous origin of the left coronary artery from the pulmonary trunk. Pulmonary hypertension, which is suggested by the pulmonary arterial medial hypertrophy, could have increased left ventricular myocardial perfusion and delayed the ischemic myocardial damage that resulted in the death of this dog.     

Creatine kinase isoenzymes in serum of pigs having myocardial and skeletal muscle necrosis.

Serum creatine kinase (CK) and lactic dehydrogenase (LD) isoenzyme activities were measured in blood serum of pigs having myocardial damage and skeletal muscular lesions. Myocardial and muscular damage was induced by restraint stress provoked by intravenous infusion of a pharmacological restraint (succinylcholine-chloride) during 12 minutes. Pigs of Swedish Landrace and Swedish Landrace X Yorkshire breed, stress-susceptible (halothane-sensitive) and nonreacting pigs were studied. Severe myocardial damage and slight to moderate skeletal muscle necrosis were found 24 hours after restraint stress in the stress-susceptible pigs whereas in nonreacting pigs generally only myocardial lesions of moderate extent were registered. No significant increase was detected in the serum CK-BB (CK-1) or CK-MB (CK-2) activity whereas a pronounced elevation of the CK-MM (CK-3) activity was found, particularly in the stress-sensitive animals. In the myocardial tissue of pigs only a low CK-MD activity was found (about 4-5% CK-MD in addition to CK-MM) and this may explain the low CK-MB activity in serum of pigs subjected to severe myocardial damage. This is further supported by the pronounced increase in the anodal serum fractions LD 1-2 in animals free from skeletal muscular lesions. In the halothane-sensitive pigs skeletal muscle necrosis besides the myocardial lesions contributed to the high levels of CK-MM activity in serum.     

Adult-onset nemaline myopathy in a dog presenting with persistent atrial standstill and primary hypothyroidism

A nine-year-old neutered female mixed breed dog presented for evaluation following a five-day history of lethargy, inappetence, weakness, abdominal distension and generalised muscle atrophy. Persistent vatrial standstill with a junctional rhythm was identified on electrocardiogram. Echocardiogram identified moderate dilation of all cardiac chambers and mild thickening of the mitral and tricuspid valves. Serology was negative for Neospora caninum and Toxoplasma gondii. Permanent pacemaker implantation was performed in addition to endomyocardial and skeletal muscle biopsies. Cryosections from the biceps femoris muscle showed numerous nemaline rod bodies while endomyocardial biopsies were possibly consistent with end-stage myocarditis. Rod bodies have rarely been reported in the veterinary literature. To the authors' knowledge, this is the first report of adult-onset nemaline rod myopathy and hypothyroidism with concurrent cardiac disease in a dog.     

A case of spontaneous myocardial necrosis and cerebral ischemic lesions in a laboratory beagle dog

A beagle dog treated with saline as a control animal in a preclinical study was euthanized due to sudden systemic deterioration. On histopathological examination, contraction band necrosis of myocardial cells was observed widely in the left ventricular wall, including the papillary muscle and apex, and observed slightly in the ventricular septum and left atrium. In the brain, necrosis was observed in neurons and glia of the cerebral cortex, hippocampal pyramidal cells, glial cells of the rostral commissure and Purkinje cells of the cerebellar vermis. It is highly probable that the marked systemic deterioration was caused by cardiac dysfunction due to the spontaneous contraction band necrosis of the myocardial cells, although the pathogenesis of the myocardial lesions remains unclear. Given the distribution of neuronal necrosis in the brain, it is likely that these lesions resulted from the ischemia responsible for acute cardiac failure.     

Inflammation of the cardiac coronary artery in ICR mice

Inflammation of the cardiac coronary artery in ICR mice is occasionally observed in toxicity studies; however, this has not been well explored histologically. Herein, we investigated the detailed histology of the associated lesions in 6–8-week-old ICR mice. Coronary artery inflammation in the right ventricular wall was observed in 10 of 142 mice (7.0%). Histopathological examination revealed hypertrophy of the vascular smooth muscle cells and perivascular infiltration of macrophages in mild cases. In moderate to marked cases, single-cell necrosis of vascular smooth muscle cells, hemorrhage of the tunica media, and fibrinoid necrosis of the vessel wall were observed, in addition to the changes seen in mild cases. Electron microscopic examination of moderate cases revealed a discontinuous internal elastic lamina suggestive of rupture, and vascular smooth muscle cells beneath the elastic lamina showed degeneration and necrosis. These findings suggest that the lesions developed as a rupture of the internal elastic lamina and necrosis of vascular smooth muscle cells, while leaked plasma components caused vascular and perivascular inflammation. In ICR mice, dystrophic calcinosis (DCC) is known to occur rarely in the right ventricle. DCC is defined as focal calcification in necrotic myocardial fibers, the pathogenesis of which is considered to involve ectopic calcification. Since calcification was not observed in any part of the heart, including the inflammation region, the pathophysiology of cardiac arterial inflammation seen in our ICR mice was considered to differ from that of DCC.     

Creatine kinase isoenzymes in bovine tissue

Brain, heart, liver, kidney, spleen, lungs, rumen, abomasum, small intestine, skeletal muscle, and urinary bladder from healthy cattle were analyzed for creatine kinase isoenzymes as a possible aid in the diagnosis of myocardial disease. Creatine kinase was detected in all organs evaluated. In addition, 6 different fluorescing bands were detected by isoenzyme analysis. Large quantities of the same isoenzymes were in cardiac and skeletal muscle, but not in other organs. Creatine kinase isoenzyme analysis does not necessarily indicate cardiac damage, but may narrow the range of tissue damage possibilities to be included in the differential diagnosis.     

Effects of ractopamine on genetically obese and lean pigs

Twenty-eight genetically obese and 24 lean barrows (65.0 and 68.7 kg average BW, respectively) were allotted within genotype to a 16% CP corn-soybean meal basal diet or this basal diet + 20 ppm ractopamine (a phenethanolamine beta-adrenergic agonist) and allowed ad libitum access to feed for 48 d. Compared to lean pigs, obese pigs had lower ADG, gain to feed ratio, longissimus muscle area, predicted amount of muscle, and weights of trimmed loin and ham, ham lean, heart, spleen, kidney and gastrointestinal tract (P less than .05). Obese pigs also had shorter carcass but higher dressing percentage, backfat thickness, fat depth, fat area, untrimmed loin weight and fasting plasma urea N concentration (P less than .05). Dietary supplementation with 20 ppm ractopamine reduced daily feed intake and improved gain to feed ratio in both lean and obese pigs (P less than .05). Pigs fed ractopamine had shorter carcasses, less fat depth and fat area, smaller weights of stomach and colon plus rectum, but higher dressing percentages, longissimus muscle areas, weights of trimmed Boston butts, picnics and loins, ham lean and predicted amounts of muscle than pigs not fed ractopamine (P less than .05). Supplemental ractopamine had no effect on fasting plasma concentrations of urea N, nonesterified fatty acids, triglyceride or glucose (P greater than .05). No genotype x ractopamine interactions for the criteria described above were detected (P greater than .05). These results suggest that ractopamine will improve the efficiency of feed utilization and carcass leanness in swine with different propensities for body fat deposition.     

alpha-Adrenoreceptor stimulation of the systemic circulation in dogs

The influence of phenylephrine (an alpha-adrenoreceptor agonist) on the arterial and venous systems of the systemic circulation was studied in 10 anesthetized dogs during a right ventricular bypass procedure. Phenylephrine (1 microgram X kg-1 of body weight X min-1) produced a significant (P less than 0.001) increase in arterial resistance, no change in venous resistance, and a mild decrease in venous compliance. Seemingly in the clinically normal dog, a dose of phenylephrine sufficient to double total peripheral resistance will redistribute a small amount of blood volume from the venous to arterial systems with a slight decrease in venous return and concomitant attenuation of cardiac output.     

Experimental West Nile virus infection in Eastern Screech Owls (Megascops asio)

Eastern Screech Owls (EASOs) were experimentally infected with the pathogenic New York 1999 strain of West Nile virus (WNV) by subcutaneous injection or per os. Two of nine subcutaneously inoculated birds died or were euthanatized on 8 or 9 days postinfection (DPI) after <24 hr of lethargy and recumbency. All subcutaneously inoculated birds developed levels of viremia that are likely infectious to mosquitoes, with peak viremia levels ranging from 10(5.0) to 10(9.6) plaque-forming units/ml. Despite the viremia, the remaining seven birds did not display signs of illness. All birds alive beyond 5 DPI seroconverted, although the morbid birds demonstrated significantly lower antibody titers than the clinically normal birds. Cagemates of infected birds did not become infected. One of five orally exposed EASOs became viremic and seroconverted, whereas WNV infection in the remaining four birds was not evident. All infected birds shed virus via the oral and cloacal route. Early during infection, WNV targeted skin, spleen, esophagus, and skeletal muscle. The two morbid owls had myocardial and skeletal muscle necrosis and mild encephalitis and nephritis, whereas some of the clinically healthy birds that were sacrificed on 14 DPI had myocardial arteritis and renal phlebitis. WNV is a significant pathogen of EASOs, causing pathologic lesions with varying clinical outcomes.     

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.     

Myocardial damage in dogs affected by heartworm disease (Dirofilaria immitis): Immunohistochemical study of cardiac myoglobin and troponin I in naturally infected dogs

It has recently been reported that dogs affected by canine heartworm disease (Dirofilaria immitis) can show an increase in plasma levels of myoglobin and cardiac troponin I, two markers of muscle/myocardial injury. In order to determine if this increase is due to myocardial damage, the right ventricle of 24 naturally infected dogs was examined by routine histology and immunohistochemistry with anti-myoglobin and anti-cardiac troponin I antibodies. Microscopic lesions included necrosis and myocyte vacuolization, and were associated with loss of staining for one or both proteins. Results confirm that increased levels of myoglobin and cardiac troponin I are indicative of myocardial damage in dogs affected by heartworm disease.     

Safety of ceftiofur sodium administered intramuscularly in horses.

Ceftiofur sodium, a broad-spectrum cephalosporin antibiotic, was evaluated for safe use in horses. Male or female horses were allotted to groups and were given either saline solution (control), or 2.2, 6.6, or 11 mg of an aqueous solution of ceftiofur sodium/kg of body weight/d, IM, for 30 or 31 days. These dosages are expressed in terms of the ceftiofur free acid, and represent 1 to 5 times the proposed therapeutic dosage (2.2 mg/kg/d) administered for 3 times the maximal recommended duration of 10 days. Some of the horses were euthanatized and necropsied on day 31 or 32. The other horses were evaluated for an additional 30 days, and some were euthanatized and necropsied on day 60. The following types of data were collected: clinical observation; physical examination; pelleted food consumption; body weight; hematologic, serum biochemical, and urinalysis findings; organ weight; gross necropsy observations; and histopathologic findings. Ceftiofur sodium was generally well tolerated at the exaggerated doses and treatment durations used in these safety studies. Slight to mild decrease in pelleted food consumption was detected in horses given 6.6 or 11 mg of ceftiofur sodium/kg/d. Decreased food consumption began on day 2 and lasted for approximately 9 to 12 days. Generally, mild skeletal muscle irritation was detected by gross and microscopic examination of the injection sites of horses given ceftiofur sodium. Prevalence and severity of the muscle irritation tended to increase with increasing concentration of the dosing solution.(ABSTRACT TRUNCATED AT 250 WORDS)     

Severe heart muscle degeneration caused by Clostridium perfringens type A in camel calves (Camelus dromedarius).

Clostridium perfringens type A was isolated from different organs and intestines from three to five weeks old camel calves which have died from heart muscle necrosis. No other bacterial pathogens were isolated. Virus isolation on two different cell lines including a fetal camel skin were also negative. Mice which were injected with bacteria free filtrates prepared from intestinal contents of necropsied camel calves died after one to six hours demonstrating the presence of clostridial toxins. Our findings suggest that the cardiac muscle necrosis is caused by Clostridium perfringens type A toxins.     

Pathology of Murine Cytomegalovirus Infection in Newborn Mice. Muscle, Heart and Brown Fat Lesions

Newborn mice were inoculated intracerebrally with murine cytomegalovirus and studies were made of the pathological changes in the striate and cardiac muscle and brown fat. Widespread necrosis was seen in muscle and brown fat in the early stages of the infection. Necrotic lesions became calcified. By 56 days lesions were not resolved in the heart and brown fat but were completely resolved in skeletal muscle.     

Experimental viral myocarditis: parvoviral infection of neonatal pups

Myocarditis was produced in seronegative five-day-old pups by oral and by intraperitoneal inoculation of canine parvovirus. The disease was subclinical. Histologic lesions were compatible with, but less extensive than, those seen in naturally occurring canine parvoviral myocarditis. In pups necropsied 23 days after inoculation, scattered cardiac myocytes contained intranuclear inclusion bodies, and virus-infected myocytes were demonstrated by immunofluorescence. Degeneration and loss of cardiac myocytes usually was not associated with a cellular infiltrate. At 51 days after inoculation, the myocardium contained an extensive lymphocytic infiltrate which was sometimes associated with fragmented myocytes, and was often contiguous with areas of interstitial fibrosis. At 108 days after inoculation, inflammatory lesions had regressed, and there were multifocal areas of myocardial fibrosis.     

The raccoon dog (Nyctereutes procyonoides) as definitive host for Sarcocystis spp. of reindeer (Rangifer tarandus)

A raccoon dog (Nyctereutes procyonoides; Family: Canidae), was given cardiac muscle of reindeer infected with S. grueneri, and started shedding Sarcocystis sporocysts 10 days post feeding. The sporocysts measured 13.9 (12.4–15.7) × 10.1 (9.2–11.2) µm, and were excreted for at least 16 days. The raccoon dog is thus an additional definitive host for S. grueneri (Yakimoff & Sokoloff, 1934) Gjerde, 1984.Another raccoon dog was given skeletal muscle infected with 4 species of Sarcocystis, none of which was S. grueneri. The raccoon dog started shedding Sarcocystis sporocysts on day 10 post feeding, and excreted sporocysts for at least 16 days. The sporocysts measured 14.0 (12.3–15.6) × 10.1 (9.2–11.2) µm, and are considered to be sporocysts of S. tarandivulpes Gjerde, 1984.This is the first record of the raccoon dog as an experimental definitive host for Sarcocystis.