Suspected lasalocid poisoning in three dogs

The ionophore lasalocid has been used as a feed additive for broilers chickens and for improving feed efficiency in ruminants. Although dogs appear to be more sensitive to lasalocid intoxication than other species, there is only 1 report in the veterinary literature about lasalocid poisoning in dogs. We describe the clinical signs, treatment and resolution of 3 hunting dogs that developed acute neurological signs consistent with lasalocid poisoning after the consumption of several broilers that had died on a nearby farm.     

A model for ammonia poisoning in cattle

The intravenous infusion of ammonium chloride was used to induce ammonia (NH3) poisoning in cattle. A 1.5 M ammonium chloride solution, buffered to pH 7.0, was infused at 400 mL/h until a convulsive episode occurred and therapy was initiated. Convulsions occurred with 200 to 1200 mL of ammonium solution. The clinical picture and metabolic effects were similar to the natural poisoning; no side effected occurred. The hypermmoniemia caused hyperglycemia, hyperlactemia, hyperkalemia and Intense metabolic acidosis. After treatment there was a sharp decrease in plasma NH3. Within 110 min all steers stood and recovered appetites. The induction of NH3 poisoning in cattle with ammonium chloride offers many advantages over the administration of high po doses of urea.     

Suspected cases of bromocyclen poisoning.

This report summarizes the case histories and tabulates the analytical results from investigations of 8 incidents of suspected bromocyclen poisoning. Interpretation of the results and withdrawal of ALUGAN from the UK market are discussed.     

Salt poisoning in beef cattle

Salt poisoning has been described under various circumstances in adult cattle. Presenting clinical signs in 6 Holstein beef cattle with such poisoning were primarily dysfunction of the central nervous system and included ataxia, opisthotonus, nystagmus, depression, muscle twitching and intermittent convulsions, as well as abdominal pain and polydipsia. Diarrhea occurred in 2, and blindness in 3/6 cattle. Hypernatremia (161.8 - 178.8 mmol/L) and hyperosmolality (331.81 - 366.18 mOsm/L) were present in all animals. To treat the affected cattle, access to fresh water was restricted, vascular volume was expanded with isotonic saline and then hypotonic fluid (5% Dextrose solution) i.v. and dexamethasone im was administered. Although biochemical parameters returned to normal reference ranges, 3/6 affected animals remained blind.     

Acute endosulfan poisoning in cattle

Endosulfan poisoning was observed in cattle where the owner applied the insecticide topically as ectoparasitic control. Two of 11 cattle died in 2 d with rapid and difficult breathing, foamy exudates in the mouth, tremors, exophthalmos and coma. At necropsy, hemorrhages were on the serosal membranes of the visceral organs and lungs, and there was severe edema and emphysema in the lungs. The levels of endosulfan in the liver, kidney, lungs and muscle were 13.1, 4.0, 1.6 and 0.8 ppm, respectively.     

MicroRNAs as serum biomarker for Senecio brasiliensis poisoning in cattle

Senecio spp. is one of the most frequent plant-related poisonings in cattle. Its ingestion generates the disease seneciosis, characterized by hepatic damages. Liver biopsies and serum markers dosage are tools used in diagnosis; however, many breeding cattle are undiagnosed. MicroRNAs are non-coding RNA, stable in biological fluids. Their difference in expression levels may indicate the presence of the poisoning. We analyzed the miRNA profiling to identify potential diagnostic biomarkers for Senecio brasiliensis poisoning. The expression of miR-21, miR-885, miR-122, miR-181b, miR-30a, miR-378, and let-7 f were evaluated in the serum of exposed cattle. At least one histological change was found in liver and lower quantity of albumin and high AST and ALP were also detected. MiRNAs miR-30a, miR-378, miR-21, miR-885, and miR-122 presented significantly higher expression in intoxicated animals than in healthy animals. Furthermore, miR-122, miR-885, and, especially, miR-21 signatures demonstrated high sensitivity and specificity, with potential application for detecting poisoning.     

Nitrate poisoning in cattle fed Chenopodium album hay

Three cows fed Chenopodium album hay died 30 min after showing ataxia, bluish-brown mucous membranes, rapid and difficult breathing, increased heart rates, tremors and coma. Brown-colored and badly coagulated blood was the prominent necropsy finding. Slight pulmonary edema was prominent and all visceral organs were hyperemic. The hay contained 2,500 ppm nitrate-nitrogen and 11 ppm nitrite nitrogen.     

Baccharis megapotamica var Weirii poisoning in Brazilian cattle

Three Holstein heifers died after consumption of Baccharis megapotamica var weirii in southern Brazil. Main histologic lesions included degeneration and necrosis of the epithelium from the forestomachs and of the lymphoid tissue of the spleen and lymph nodes.     

Senecio spp poisoning in cattle in southern Brazil.

Epidemiological, clinical, necropsy and histopathological data were accumulated during the study of 15 outbreaks of Senecio spp poisoning in cattle occurring during the last 3 y in the State of Rio Grande do Sul, Brazil. Morbidity averaged 17% and mortality was virtually 100%. The peak mortality occurred during spring and early summer. The most constant clinical signs included anorexia, depression, tenesmus often followed by rectal prolapse, and rough hair coat. Affected animals remained apart from the rest of the herd, lost weight, presented ascites, and had signs of digestive and neurological disturbances. Icterus, photodermatitis, polydipsia, and dependent subcutaneous edema were occasionally noticed. Two main clinical courses could be distinguished. In the protracted form, progressive weight loss terminated with death within many weeks or months. Alternatively, an acute or subacute course led to death in a few days. In both forms, necropsy and histopathological findings included diffuse fibrosis of the liver, hepatomegalocytosis, and biliary hyperplasia. Extrahepatic lesions included gastrointestinal and mesenteric edema, distension, edema and adenomatoid hyperplasia of the gallbladder, and spongy degeneration of the cerebral white matter. S brasiliensis and S oxyphyllus were the species involved in the field outbreaks.     

Anagallis arvensis poisoning in cattle and sheep in Uruguay

Outbreaks of Anagallis arvensis poisoning were observed from 1994 to 1998 in cattle and sheep in Uruguay during December and January. Cattle morbidity varied between 3.2 and 53.2% and lethality 42.6 and 100%. Sheep morbidity was 2.8 to 42.9% and lethality 81.3 to 100%. Nine outbreaks occurred on barley and wheat stubble, and 1 in a field previousy ploughed but not cultivated. Clinical signs were weakness, staggers, diarrhea (sometimes bloody), coma, and death. Serum levels of creatinine and urea were elevated. Gross lesions were characterized by sc petechiae, fluid in body cavities, mesenteric and perirenal edema, yellowish or pale kidneys with petechiae on the cortex, esophageal erosive lesions or ulcers, and hemorrhagic abomasitis and enteritis. Severe nephrosis was observed histologically. The green plant collected in a field where an outbreak occurred was administered to 2 sheep at doses of 160 and 224 g/kg bw and produced clinical signs and pathology similar to those observed in field cases.     

Suspected environmental poisoning by drugs,household products and pesticides in domestic animals

Animal poisoning by chemicals (pesticides and household products) and drugs is a frequent occurrence and special attention should be paid to this phenomenon to improve prevention and treatment strategies and because of the fundamental role that animals may play as bioindicators. From January 2017 to March 2019 the Poison Control Centre of Milan (CAV) in collaboration with the University of Milan, collected and analyzed epidemiological data on animal poisoning. During this period, the CAV received a total of 442 enquiries on domestic animal poisoning episodes and, among these, 80.3 % were related to chemicals and drugs. Pesticides and drugs were the two major causes of poisoning (34.1 % and 33.5 %, respectively), followed by household products (29.3 %) and other causative agents (3.1 %, n = 11). In conclusion, these findings can provide useful information for the identification and monitoring of known and emerging toxicants, with positive repercussions on human, animal and environmental health.     

Acute poisoning of cattle by fertilizer-contaminated water

Three cases of accidental acute fertilizer poisoning in cattle resulted in substantial death loss. Water hauled in tanks previously contaminated with a nitrogen-based fertilizer was the source in all cases. In 2 cases, analysis of the water measured urea at 1,640 and 2,300 ppm and ammonia-nitrogen at 640 and 750 ppm, respectively. Confirmation of urea toxicosis was made by measurement of toxic levels of ammonia-nitrogen in the rumen contents (>800 ppm) and blood (>8.0 ppm). In Case 3, no urea was detected in the water but ammonia-nitrogen was measured at 1,670 ppm and nitrate at 1.1%. Toxic levels of nitrate were measured in ocular fluid from 2 animals (60 ppm). Rumen contents contained toxic levels of ammonia-nitrogen (300 ppm) and a pH of 8.7. Interpretation of ammonia levels in rumen contents should take into account the source of ammonia as well as the pH since urea is more toxic than some ammonium salts. When the source is unknown, analysis of blood and/or serum ammonia-nitrogen instead of rumen content is recommended. The rapid progression of signs to death with ammonium nitrate poisoning may explain the lower levels of nitrate attained in ocular fluid than observed with pure nitrate intoxications.     

Outbreak of copper poisoning in cattle fed poultry litter

In a feedlot of about 1,000 head of cattle, 146 animals died within a period of a few months affected by a disease characterized by anorexia, icterus, hemoglobinuria, constipation, or diarrhea. The clinical course of the disease lasted a few days. Postmortem findings were generalized icterus and a yellow discolored liver. The kidneys were dark brown, and the urinary bladder was filled with urine of the same dark-brown color. The main histopathological findings were centrolobular coagulative necrosis, apoptosis, bilestasis, and proliferation of bile ducts in the portal space. Changes in the kidneys included nephrosis and the presence of bile and precipitates, and cylinders of albumin and of hemoglobin in the uriniferous tubules. Liver samples, collected from 3 animals on which postmortem examinations were performed, had 2,008, 2,783 and 4,906 ppm copper in their dry matter. Two samples of poultry litter fed to the cattle contained 362 and 323 ppm copper. The green forage that formed the rest of their feed only had 4.7 ppm copper. Copper poisoning was diagnosed, most probably caused by feeding litter from poultry that had been fed a ration treated with copper sulfate to avoid aspergillosis.     

A case of Datisca glomerata poisoning in beef cattle

Six of 175 Angus heifers died after ingesting excessive amounts of Durango root (Datisca glomerata). Animals had rumens full of Durango root, were extremely lethargic, and had diarrhea prior to death. The animals had nonspecific postmortem lesions. This case is discussed in light of previous findings from trials in which Durango root was experimentally fed to cattle.     

A case report of Nerium oleander poisoning in cattle

Nerium oleander leaves caused the death within 36 hours of 7 of 17 cattle which had access to boughs of the plant. Arrhythmia and auriculo-ventricular block at ECG were found in three cattle surviving on day 4. In one animal which died on day 4, postmortem examination revealed subendocardial and abomasal hemorrhages. Epidermic tissues of the leaves of N oleander were found in the rumen content. Recovery occurred in the three animals with marked cardiac signs.     

Oak (Quercus incana) leaf poisoning in cattle.

Oak poisoning occurred in crossbred cattle due to eating immature tender oak (Quercus incana) leaves. Mortality was 70%. The animals exhibited anorexia, severe constipation and brisket edema. The feces were hard, pelleted and coated with blood and mucous. Significant reductions in blood hemoglobin and mean corpuscular hemoglobin, and significant elevations in serum bilirubin were observed. Serum urea nitrogen and creatinine were greatly increased. There was bilirubinuria, proteinuria, hypoproteinemia and hypocalcemia, and greatly increased activities of serum aspartate aminotransferase, lactate dehydrogenase and alkaline phosphatase. The levels of tannins and condensed tannins were 97.7 mg tannic acid equivalent and 5.8 mg catechin equivalent/g of dry leaves. There was extensive nephro- and hepatotoxicity in the affected cattle due to hydrolysable tannins and simple phenols in the oak leaves.     

Lead poisoning in cattle grazing pasture contaminated by industrial waste

Lead poisoning is described in a herd of 120 Nelore cows of which 35 were affected. All affected cows died after a clinical course of 2-7 d with clinical signs related to cortical neurological disturbances. The source of Pb was fumes from a car battery recycling plant which has had a failure in its filtering system. Lead concentrations in liver and kidneys of 2 cows, in soil; and in grass where the cows were held were respectively 39 to 431 ppm, 147 to 431 ppm, and 245 ppm. No significant gross changes were observed. Histopathology revealed of neuronal necrosis, vacuolation of the neuropil and hypertrophy of the vascular endothelium in the cerebral cortices, degeneration of the epithelial cells of renal proximal tubules, and hemosiderosis of kidney, spleen and liver.