Short-Term Mesquite Pod Consumption by Goats Does Not Induce Toxicity

Goats, unlike cattle, disperse few viable mesquite (Prosopis glandulosa Torr.) seeds in feces. However, there is some evidence that goats may suffer from toxicosis from overingestion of mesquite pods. We assessed the likelihood that short-term ingestion of mesquite pods would induce toxicosis in goats. Twenty-four goats were randomly allocated to one of four treatments with treatments fed different concentrations (0%, 30%, 60%, or 90% of the diet) of whole mesquite pods fed with alfalfa pellets. The mixture of mesquite pods and alfalfa pellets was fed for 12 d to 14 d. Because there were only 12 pens available for the study, two trials were used so that all 24 goats could be housed in individual pens. Intake, serum metabolite levels, and fecal output were measured to assess physiological status. In Trial 1, intake and fecal output decreased on days 12 through 14 for goats consuming a diet of 90% mesquite pods. In the second trial, intake and fecal output were similar across days of feeding within each treatment, but the trial only lasted 12 d. Serum metabolite levels remained within normal levels irrespective of the amount of mesquite pods in the diet in both trials. Goats appear to be able to consume mesquite pods on a short-term basis without experiencing toxicosis.     

Transmission of bovine viral diarrhea virus to adult goats from persistently infected cattle.

The transmission of bovine viral diarrhea virus (BVDV) from persistently infected (PI) heifers to adult seronegative goats was examined in this study. Ten seronegative adult goats were exposed to 4 PI heifers. None of the goats developed any clinical signs but all goats seroconverted by 42 days after exposure to the PI cattle. Results indicate that goats are susceptible to BVDV infection when housed with PI cattle.     

Acute, fatal illness in cattle exposed to boron fertilizer

Twenty-six cows died after accidental exposure to boron fertilizer. Cows developed diarrhea, weakness, ataxia, signs of depression, and died, usually within a few hours. Seizure-like behavior was noticed in 2 cows, and 2 were suspected of aborting. High boron concentrations in tissues from affected cows confirmed ingestion of an appreciable amount of boron fertilizer. In an attempt to confirm the diagnosis of boron poisoning, boron fertilizer was administered to goats. A kid goat given 3.6 g of fertilizer/kg of body weight developed clinical signs similar to those seen in the cattle. Boron compounds such as sodium borate and boric acid have been considered generally nontoxic, and reports of livestock toxicosis are uncommon. This case report suggests that these compounds may be palatable under certain circumstances leading to ingestion of toxic quantities.     

Toxicity and tissue residue depletion of levamisole hydrochloride in young goats

Toxicity and tissue residue depletion studies were conducted in young goats, using an oral drench formulation of levamisole hydrochloride. In the target animal toxicity study, 3 groups of 5 goats each were given levamisole orally to provide approximately 11.88, 23.76, or 35.64 mg of levamisole HCl/kg/d for 3 consecutive days; a fourth group of 5 goats served as untreated controls. Blood samples were taken for analysis of levamisole 1 day prior to dosing and 1, 2, 3, 4, and 7 days following the third dose. At the 35.64-mg/kg dose, 2 of 5 goats responded with typical cholinergic signs of toxicosis on each of the 3 days of dosing. The times for the onset of clinical signs of toxicosis ranged from 18 to 63 minutes, with an average duration of 32 minutes. Administration of 23.76 mg of levamisole HCl/kg resulted in hyperactive behavior in 1 of 5 goats only on the first day of dosing; no abnormal behavior was observed in any of the 5 goats following the second or third dose of levamisole HCl at 23.76 mg/kg. Untoward effects were not seen in the 5 goats dosed at 11.88 mg of levamisole HCl/kg or in the controls during the 3-day dosing period or in the following 7-day observation period. Overall, the observed signs of toxicosis did not become more severe, affect more goats, or persist for a longer period on subsequent dosing days.(ABSTRACT TRUNCATED AT 250 WORDS)     

Death associated with parenteral administration of copper disodium edetate in calves

Copper disodium edetate in recommended doses was apparently responsible for the deaths of one calf and clinical signs of toxicosis in 5 others on one farm, and 7 deaths and clinical signs of toxicosis in a number of others on another ranch. Signs of hyperexcitability, hypermetria, hindlimb weakness, head pressing, depression, and opisthotonos occurred 6 to 24 hours after injections and preceded death by 1 to 2 days. Necropsy and histologic examination revealed massive liver necrosis. High blood concentrations of liver enzymes in affected cattle that did not die indicated that they had liver damage. High blood concentration of iron in cattle that died indicated possible interaction of copper and iron.     

Neurohistologic and ultrastructural lesions in cattle experimentally intoxicated with the plant Prosopis juliflora

Intoxication by pods of Prosopis juliflora (mesquite beans) causes an impairment of cranial nerve function in cattle and goats. In goats, vacuolation of neurons in the trigeminal motor nuclei has been reported. To study the lesions in cattle caused by consumption of P. juliflora pods and dry ground pods, eight 6- to 12-month-old male cattle were divided into 4 groups: group 1 was fed a ration containing 50% of pods; groups 2 and 3 received a ration containing 50 and 75% of dry ground pods, respectively; group 4 was the control. After 200 days, all cattle were killed and sampled for histologic evaluation. Samples of the trigeminal motor nucleus were examined by electron microscopy. All cattle from groups 1, 2, and 3 showed clinical signs resulting from impaired function of cranial nerves V, IX, X, and XII, starting 45-75 days after consumption of the plant. The main histologic lesions were vacuolation and loss of neurons in trigeminal motor nuclei and other motor cranial nerve nuclei with Wallerian-like degeneration in the cranial nerves. Mild denervation atrophy was observed in the masseter and other masticatory muscles. On electron microscopy, neurons of the trigeminal nuclei had markedly swollen mitochondria, with the mitochondrial cristae displaced peripherally, disoriented and disintegrating. Intoxication by P. juliflora seems to have a novel pathogenesis, characterized by a selective, primary, chronic, and progressive injury to mitochondria of neurons of the trigeminal and other cranial nerve nuclei. Cranial nerve degeneration and denervation atrophy of the muscles occurs as a consequence of the neuronal lesion.     

Caprine aflatoxicosis: experimental disease and clinical pathologic changes

Groups of 8 male crossbreed domestic goats were given 3 dosage levels of aflatoxin B1 [(AFB1) mg/kg of body weight/day] orally: 0.1 for 34 days; 0.2 for 18 days; or 0.4 for 10 days. Clinical condition, feed consumption, and selected blood values were determined. Clinical signs of toxicosis included decreased feed consumption, slight-to-moderate loss of body weight, mucopurulent nasal discharge, dyspnea, coughing, lethargy, icterus, diarrhea (4 goats), and subnormal body temperature 24 to 48 hours before death. Clinicopathologic changes included increases in total RBC count, PCV, hemoglobin concentration, serum bilirubin concentration, and serum activities of aspartate aminotransferase, isocitric dehydrogenase, and ornithine carbamyl transferase. Goats given the 2 smaller dosage levels of AFB1 had slight increases of serum total protein (TP) concentration compared with control goats, but goats given the larger dosage levels of AFB1 initially had a slight decrease in TP. Aflatoxin had little effect on total WBC count. Serum alanine aminotransferase (ALT) activities in goats given the 2 larger dosage levels of AFB1 were similar to those of control goats, but goats given the smallest dosage level of AFB1 had increased serum ALT activities. Aflatoxin did not produce consistent dose-related changes in serum alkaline phosphatase activities. Seemingly, goats are susceptible to aflatoxin. Onset of clinical signs was dose-related. Onset and magnitude of increases in PCV, hemoglobin concentration, serum bilirubin concentration, and activities of serum aspartate aminotransferase, ornithine carbamyl transferase, and isocitric dehydrogenase were dose-related. Changes in TP and activities of serum ALT and alkaline phosphatase were neither dose-related nor were they potentially useful indicators of toxicosis.     

Oak leaf (Quercus pyrenaica) poisoning in cattle

Three experiments were conducted to study the clinical and pathological findings associated with poisoning in cattle due to ingestion of young oak leaves (OL) and the main factors responsible for toxicosis. In Experiment 1, six 1.4 year-old bulls were fed up to 5 kg of young OL per animal per day and showed no signs of toxicity, apart from a slight proteinuria. In Experiment 2, another six 1.4 year-old bulls were first subjected to severe feed restriction for eight days and then fed a higher amount of OL (approx. 10 kg) daily. A marked increase of serum creatinine and blood urea (BUN) was detected in urine as well as clinical signs consistent with renal failure. At necropsy, animals showed gastrointestinal ulcers and kidney tubular necrosis. Since these results suggested a crucial role of the feed restricting period, a third experiment was conducted administering the same amount of young OL as in Experiment 1, but adding the severe feed restricting period as in Experiment 2. There was a wide variation in clinical signs, with one bull showing clinical signs and lesions, another recovering after showing mild clinical signs and high levels of creatinine and BUN, and the third appearing clinically normal. The relevance of restriction access to food in the development of OL toxicosis appears to be critical because the intoxication was only elicited when the OL administration was preceded by a severe feed restricting period.     

Chlorpyrifos Toxicosis in Two Cats

Organophosphate compounds are widely employed for control of external parasites in cats and for control of insects in homes and yards. Chlorpyrifos is a long-acting organophosphate (OP) available for use as a systemically and topically acting parasiticide and insecticide in cattle. Its use on cats is not recommended, and no previous clinical cases of toxicosis have been described. Two cases of chronic chlorpyrifos toxicosis in cats are presented and pathophysiology as well as treatment are discussed. The cats had been showing signs of chronic organophosphate toxicosis before diazepam administration. Signs of acute organophosphate toxicosis were precipitated after diazepam was given. Treatment with pralidoxime chloride (2-PAM) and atropine was attempted. Response to treatment was dramatic and complete recovery was achieved with six injections of pralidoxime and atropine administration.     

Neurologic disease putatively associated with ingestion of Solanum viarum in goats

Several Nubian-cross goats were evaluated because of chronic progressive neurologic disease. Physical and neurologic examination revealed signs consistent with diffuse cerebellar disease. Neurologic signs included generalized hyperresponsiveness, fine head tremors, wide-based posture, dysmetria, weakness, and horizontal nystagmus. No clinical improvement was noted after removing goats from affected enclosures. Histologic examination of cerebellar tissues revealed extensive vacuolation within the cytoplasm of Purkinje cells. The clinical and histologic lesions resembled closely findings that were associated with ingestion of Solanum spp in cattle and goats. Examination of enclosures revealed Solanum viarum (tropical soda apple) that had been heavily consumed by the goat herd. We hypothesized that ingestion of S. viarum caused the neurologic disorder.     

Compensatory weight gain in steers recovered from oak bud toxicosis

Cattle that had recovered from clinical oak bud toxicosis (as assessed by normal BUN and serum creatinine values and good appetite) performed better than did clinically normal herdmates when weight gain and feed efficiency were compared. Both groups had a rate of weight gain (oak bud-exposed cattle, 1.76 kg/steer/d; control cattle, 1.57 kg/steer/d) that exceeded the feedlot mean value (approximately 1.4 kg/d) for cattle (of similar starting weight and diet) that had zeranol implants, and the difference was significant (P less than 0.005) for both groups. The difference in weight gain performance of oak bud-exposed cattle, compared with control cattle, was not highly significant; however, the improved feed efficiency was significantly (P less than 0.05) better than that in controls (2.57 kg of feed/kg of weight gain vs 3 kg of feed/kg of weight gain). On the basis of accepted criteria (increased rate of weight gain and efficiency of feed conversion), the group of oak bud-exposed cattle of this study had compensatory weight gain. Thus, cattle with good evidence of clinical recovery from oak bud toxicosis can be expected to perform in the feedlot at least as well as cattle not exposed to oak bud toxicosis, and may have compensatory weight gain.     

Copper toxicosis in a dairy goat herd

CASE DESCRIPTION: A closed herd of 400 mixed-breed dairy goats was examined because of a decrease in milk production and increase in mortality rate. Nine animals had died within a 1-month period. CLINICAL FINDINGS: Clinical signs were evident only in lactating goats and included anorexia and recumbency. In the most severely affected goats, signs progressed to neurologic abnormalities and death. Serum aspartate aminotransferase activity, gamma-glutamyltransferase activity, and total bilirubin concentration were high in clinically affected does, but no evidence of hemolysis was found. A diagnosis of copper toxicosis was made on the basis of high liver and kidney copper concentrations and histologic evidence of hepatic necrosis. Goats were found to have been fed a mineral mix containing 3,050 ppm copper for 9 months prior to the onset of copper toxicosis. Overall, there was no consistent relationship between serum hepatic enzyme activities, serum copper concentration, and liver copper concentration. TREATMENT AND OUTCOME: Clinically affected goats were treated with penicillamine, ammonium molybdate, sodium thiosulfate, and vitamin E. Penicillamine increased urine copper excretion in treated does versus untreated control animals. An increased incidence of infectious disease was identified in the herd 9 months later. Liver vitamin E concentration was low in 10 of the 12 goats that underwent necropsy. CLINICAL RELEVANCE: Findings suggested that penicillamine may be an effective treatment for goats with copper toxicosis. Production losses months after the diagnosis was made suggested that the intoxication had a prolonged animal welfare and economic impacts.     

Copper toxicosis in cattle fed chicken litter

Cattle from 2 herds developed copper toxicosis after the ingestion of chicken litter. The affected animals were adult Holstein cows and crossbred steers that ate 9 to 16 kg of litter/day. These cattle developed a sudden onset of weakness, depression, anorexia, icteric mucous membranes, and dark reddish brown urine. Liver copper concentrations in 2 cattle (1 from each herd) were 436 and 730 ppm. Results of copper analyses of chicken litter ranged from 620 to 920 ppm. Sodium molybdate and sodium thiosulfate were added to the ration of the dairy herd. Two cows with clinical signs of copper toxicosis recovered after being given additional sodium molybdate and thiosulfate supplements, orally.     

Inorganic arsenic toxicosis in a beef herd

Over a 44-day period, 4 of 5 affected calves in a 170-head herd of beef cattle died after exhibiting clinical signs of lethargy, ataxia, anorexia, and diarrhea. Histopathological examination of tissues and toxicological analysis of a suspicious powder discovered in the pasture confirmed arsenic trioxide toxicosis.     

Suspected dimethoate toxicity in cattle

Dimethoate, an organophosphorus insecticide, was the suspected cause of toxicosis in a group of young cattle grazing on pasture that had been sprayed 6 weeks before the onset of clinical signs. Affected animals had primarily nicotinic signs, such as muscle twitching, stiffness, weakness and paralysis, though muscarinic signs, such as diarrhea, salivation and pollakiuria, were also observed. Whole blood acetylcholinesterase activity was depressed in 3 animals. The atypical clinical syndrome and poor response to treatment with atropine and other anticholinergics may have been due to coexistent hypomagnesemia.     

Black walnut toxicosis in ten horses

Black walnut toxicosis was diagnosed in 10 horses at one stable. The time from exposure to shavings to development of clinical signs was 8 to 12 hours. Most common clinical signs were moderate to severe laminitis (Obel grade 2 or 3), pitting edema of the distal portion of the limbs, and rapid respiratory rate. Two horses had clinical signs of colic and 2 other horses had anorexia and lethargy. All 10 horses recovered without complications.     

Lead concentrations in blood and milk from periparturient dairy heifers seven months after an episode of acute lead toxicosis

In September 1988, 100 of 300 yearling dairy heifers developed blindness, tachypnea, foaming at the mouth, chewing, and facial fasciculations. Twenty-five animals died. Lead toxicosis was diagnosed based on the clinical signs and the presence of excessive concentrations of lead in whole blood, liver, kidney, and rumen contents of affected animals. The source of the lead was sudan grass silage that had been contaminated by soil that contained up to 77,000 mg/kg of lead. Lead concentrations were determined approximately 7 months after the acute episode of lead toxicosis. Whole blood and milk samples were obtained from heifers and a group of control cows 2 weeks prior to (blood only), at the time of, and 2 and 4 weeks after freshening. No lead was found in any of the milk samples (detection limit = 0.055 mg/liter). Animals that had been severely affected by lead toxicosis experienced a transient increase in whole blood lead concentrations at freshening that was not high enough to be considered toxic. No similar increases in blood lead were observed for control cows or heifers that had experienced milder toxicosis. These findings suggest that at parturition lead is mobilized into the blood of cattle previously exposed to excessive lead.     

The role of nitric oxide in Listeria encephalitis of ruminants and in rats intracisternally infected with Listeria monocytogenes

Listeria monocytogenes is a Gram-positive facultative intracellular bacteria which infects a wide range of hosts. In ruminants, infection with L. monocytogenes frequently causes encephalitis, which is usually fatal in sheep and goat, while cattle often recover with antibiotic therapy. Since the role of NO in the control of Listeria is controversial, we have studied the expression of iNOS in the brains of cattle, sheep and goats which had succumbed to listeria encephalitis. iNOS was demonstrated in decreasing intensity in the M phi of microabscesses from cattle, sheep and goat. iNOS expression was accompanied by NT in the microabscesses of cattle, but was only present to a low degree in sheep and was absent in goats. This is indirect evidence for differences in the ability to produce NO in the three species. Presence of iNOS and NT were inversely correlated with the numbers of bacteria. While microabscesses of goats contained high amounts of L. monocytogenes they occurred only rarely in cattle. To corroborate our hypothesis that NO is involved in the control of listeria encephalitis a new animal model was developed. Eleven day old infant rats were infected intracisternally with a low dose of L. monocytogenes. This resulted in a transient meningoencephalitis with moderate clinical signs and low mortality. Listeria proliferated strongly in the inflammatory lesions during the first days of infection, reached a peak at day 4 and were eliminated until day 7. The presence of bacteria was closely accompanied by high numbers of iNOS-expressing M phi and the formation of NT. Administration of the iNOS inhibitor L-NIL or the radical scavenger PBN resulted in rapid death of the treated animals. However, the increase in bacterial numbers was one order of magnitude higher for animals treated with PBN compared with L-NIL administration. This shows that NO plays an important role in the control of a brain infection with Listeria, but suggests that reactive oxidants other than NO are also involved. In conclusion, our findings point to a possible involvement of the differences in the ability to express iNOS and subsequent NO production in the different clinical outcome of listeria encephalitis in cattle and small ruminants.     

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.