Zearalenone intoxication of pigs

Mycotoxicosis due to ingestion of zearalenone was detected on 2 pig farms on the Atherton Tableland in northern Queensland. In one herd of 200 pigs, this resulted from feeding maize which had been stored with a high moisture content. In the other herd of 1400 pigs, it resulted from feeding sorghum grain which was rain affected before harvest. Concentrations of zearalenone in the feeds ranged up to 8 mg/kg. Most prepubertal gilts in the herds displayed enlarged teats and signs of oestrus such as having red, swollen vulvas. In several cases both rectal and vaginal prolapses occurred. On one of the farms, 25 pigs died as a direct result of prolapses. Autopsy of a 3-month-old gilt revealed apparently enlarged ovaries and uterine horns. Sows and boars seemed to be unaffected. Four gilts failed to conceive following mating during the period of zearalenone ingestion, but apart from this and the deaths from prolapses, production of the herds appeared to be unaffected.     

Nitrate poisoning in cattle

Summary

In a series of experiments the effect of administering KNO₂ was studied, during parturition, on the capability of oxygen transport of maternal blood and on oxygen transfer to foetal blood. The following blood parameters were analysed, MHb percentage, pO₂, O₂‐saturation, pH, pCO₂, and (NO₂) in maternal arterial blood (carotid art.) and venous blood (jugular vein) and in foetal arterial blood (umbilical art.) and venous blood (umbilical vein). The relative O₂‐saturation was calculated from the estimated O₂‐saturation by multiplying with the factor Hb (mmol/1) minus MHb (mmol/1), divided by Hb (mmol/1). In addition, blood pressure in the carotid artery, heart rate, and respiration rate in the dam were continuously recorded for some hours.

A dosage of 9 to 12 mg of NO₂/kg body weight intravenously or of 30 mg of NO₂/kg body weight orally to the dam caused much higher MHb percentages and NO₂ contents in the maternal blood than in the foetal blood. In maternal blood the ratio of NO₂ content td MHb percentage was proportional to that in foetal blood. In the arterial blood, MHb percentages were almost as high as in the venous blood. After administering of nitrite, relative O₂‐saturation dropped simultaneously with the increase in methaemoglobin.

Nitrite treatment caused a drop in the maternal blood pressure; heart rate and respiration rate increased. O₂‐saturation in the blood in the umbilical vein was much lower in the animals with nitrite treatment than in those without. These experimental results show clearly that the oxygen capacity of the blood decreases after nitrite treatment. In pregnant cows the oxygen supply to the foetus will be adversely affected after nitrate intake, especially by the lower oxygen transfer via the placenta, though hardly at all by methaemoglobin formation in the foetal blood.

When the oxygen transfer to the foetal blood decreases too sharply, intra‐uterine death and ultimately abortion may result.     

Nitrate poisoning in cattle

Summary In a series of experiments the effect of administering KNO(2) was studied, during parturition, on the capability of oxygen transport of maternal blood and on oxygen transfer to foetal blood. The following blood parameters were analysed, MHb percentage, pO(2), O(2)-saturation, pH, pCO(2), and (NO(2)) in maternal arterial blood (carotid art.) and venous blood (jugular vein) and in foetal arterial blood (umbilical art.) and venous blood (umbilical vein). The relative O(2)-saturation was calculated from the estimated O(2)-saturation by multiplying with the factor Hb (mmol/1) minus MHb (mmol/1), divided by Hb (mmol/1). In addition, blood pressure in the carotid artery, heart rate, and respiration rate in the dam were continuously recorded for some hours. A dosage of 9 to 12 mg of NO(2)/kg body weight intravenously or of 30 mg of NO(2)/kg body weight orally to the dam caused much higher MHb percentages and NO(2) contents in the maternal blood than in the foetal blood. In maternal blood the ratio of NO(2) content td MHb percentage was proportional to that in foetal blood. In the arterial blood, MHb percentages were almost as high as in the venous blood. After administering of nitrite, relative O(2)-saturation dropped simultaneously with the increase in methaemoglobin. Nitrite treatment caused a drop in the maternal blood pressure; heart rate and respiration rate increased. O(2)-saturation in the blood in the umbilical vein was much lower in the animals with nitrite treatment than in those without. These experimental results show clearly that the oxygen capacity of the blood decreases after nitrite treatment. In pregnant cows the oxygen supply to the foetus will be adversely affected after nitrate intake, especially by the lower oxygen transfer via the placenta, though hardly at all by methaemoglobin formation in the foetal blood. When the oxygen transfer to the foetal blood decreases too sharply, intra-uterine death and ultimately abortion may result.     

Chlorpyrifos intoxication in a bull

A mature Brangus bull received the recommended dose of chlorpyrifos and became dull and inappetent 3 days later. Clinical findings included weakness, dehydration, rumen stasis, and rumen distention with fluid and gas. Blood cholinesterase activity was 25% of normal. The bull's condition improved after treatment with pralidoxime, antimicrobials, electrolyte solutions, vitamins, and adsorbents. Five weeks later, the bull had gained weight, the blood cholinesterase activity was 70% of normal, and the results of a semen evaluation indicated he was a satisfactory potential breeder.     

Aluminium intoxication in a dog

Summary

A two‐year‐old male Barsoi dog was presented after a two‐week period of muscle twitching and convulsions during exercise, which worsened to a state of tetraparesis and coma. Removal of a gastric foreign body, containing aluminium, resolved the presenting signs. Parallel with this clinical recovery the elevated serum levels of aluminium decreased to values of two normal control dogs, suggesting that the neurological signs were due to A1 intoxication.     

Suspected levamisole intoxication in calves

CASE HISTORY: A group of 32 Friesian and four Hereford calves, 3–4 months old with body weights between 100–120?kg, were purchased from a weaner sale. On arrival at the property the Hereford calves were treated with a combination anthelmintic containing 2?g/L abamectin and 80?g/L levamisole hydrochloride. Shortly afterwards they developed tremors and frothing from the mouth, and two died overnight. The Friesian calves were treated with the same anthelmintic on the following day, when some showed hypersalivation and frothing from the mouth.

CLINICAL FINDINGS: Examination of the three most severely affected Friesian calves revealed severe nicotinic-type symptoms including hypersalivation, frothing from the mouth, muscle tremors, recumbency, rapid respiration, hyperaesthesia, and central nervous system depression. Other calves showed mild to moderate signs of intoxication including restlessness, tail switching, salivation, tremors, frequent defaecation, mild colic and jaw chomping. Two calves died shortly afterwards. An adverse drug event investigation revealed that the formulation and quality of the anthelmintic was within the correct specification, and that the drench gun was functioning correctly.

DIAGNOSIS: Suspected levamisole intoxication due to a combination of possible overdosing, dehydration, and stress caused by transportation and prolonged yarding.

CLINICAL RELEVANCE: Susceptibility to levamisole toxicity in New Zealand calves can be increased if factors like dehydration or stress are present. Levamisole has a narrow margin of safety, and overdosing in calves can easily occur if the dose rate is not based on their actual weight or health status.     

Accidental salinomycin intoxication in calves

Twenty-four 10- to 16-week-old calves in a dairy herd in Birjand, Iran, inadvertently received an excessive dose of salinomycin mixed with barley grain. There was 58% mortality within 10 d. The calves had high serum AST, LDH, and CK activities; histopathologic lesions in myocardium, liver, and kidneys; and clinical signs associated with acute and congestive heart failure.     

Aluminium intoxication in a dog

A two-year-old male Barsoi dog was presented after a two-week period of muscle twitching and convulsions during exercise, which worsened to a state of tetraparesis and coma. Removal of a gastric foreign body, containing aluminium, resolved the presenting signs. Parallel with this clinical recovery the elevated serum levels of aluminium decreased to values of two normal control dogs, suggesting that the neurological signs were due to A1 intoxication.     

Metaproterenol intoxication in a dog

Intoxication with metaproterenol, a mainly beta-2 selective agonist, was diagnosed in a dog with tachycardia, tachypnea, weakness, vomiting, and a history of exposure to the drug. Electrocardiography and echocardiography disclosed sinus tachycardia with episodes of ventricular tachycardia and exuberant systolic ventricular function, respectively. Administration of the beta blocking drugs propranolol and atenolol led to resolution of the clinical signs. Excessive sympathetic stimulation caused by metaproterenol is an unusual intoxication in dogs.