Cyanide poisoning associated with the feeding of apricot kernels to dairy cattle

Abstract

phase liquid chromatography (Hwang and others 2002), disclosed another 300 (36) mg/kg of HCN equivalents. Because the sample had been stored and shipped at room temperature in containers that were not tightly closed, it is likely that the original material contained even higher HCN levels and that much of this toxic gas had been lost from the specimen before analysis. The 2 kg or more of toxic feed ingested by each affected cow translates to at least 820 mg of HCN equivalents, approaching the reported lethal dose of 2 mg/kg bodyweight (Radostits and others 1999).The characteristic clinical signs, in conjunction with the consumption of appropriate plant material, are comparable to intoxication due to cyanogenic glycosides. As noted previously (Cran 1985, Roder 2001, Suter 2002, confirmatory HCN detection is a difficult and tedious procedure. Although toxic levels of HCN were detected in the present case, the volatility and rapid breakdown of HCN, combined with the time it normally takes for the samples to be received and analysed, may invariably lead to false-negative results. Therefore, in the search for an alternative approach, the authors took advantage of a more stable metabolite that can easily be monitored. The majority of HCN (80 per cent) is detoxified by the enzyme rhodanese in the liver, producing a thiocyanate metabolite that is excreted mainly through the kidneys with a half-life of up to three days in human beings (Gurnsey and others 1977, Erdman 2004). In the present study, the serum thiocyanate level was determined in blood samples obtained from three surviving cows 24 hours after the initial deaths. The procedure (Lundquist and others 1979) involved an ion exchange clean-up to remove interfering matrix components. After elution with sodium perchlorate, the thiocyanate concentration was determined by a quantitative colorimetric reaction in the presence of sodium hypochlorite and barbituric acid, yielding a derivative with peak absorption at a wavelength of 580 nm. The thiocyanate concentrations in the cows (145, 209 and 211 µmol/l) exceeded the reference range determined for human blood (15 to 70 µmol/l) and reached the same high concentrations as those found in severe cases of cyanide poisonings in human beings (Singh and others 1989). A healthy cow in the neighbourhood had a serum thiocyanate level of 52 µmol/l, suggesting a similar normal range in cattle to that in humans. This view was supported when, one month later, the thiocyanate serum concentration of the three cows was measured again and the values were 50 54, and 60 µmol/l. It was concluded that the conversion of HCN to thiocyanate provides a potentially useful diagnostic marker to confirm suspected exposures to cyanide or cyanogenic glycosides in

Cyanide poisoning caused by ingestion of apricot seeds

“…12 Sudden clinical deterioration and a bitter almond smell on the breath associated with metabolic acidosis support the diagnosis of apricot seed poisoning. 2,4 Diagnosis is further aided by a secondary symptom of bright red venous blood owing to cellular hypoxia and decreased SaO 2 -SVO 2 . 13,14 In suspected cases, diagnosis can be confirmed by measuring the blood cyanide level but the analysis takes several hours or longer to complete.…”

“…If the level of 40% is exceeded, methylene blue should be used. 2,3 The potential for serious toxicity limits the use of the cyanide antidote kit in pre-hospital empirical treatment of suspected cyanide poisoning. Highdose hydroxocobalamin alone differs from the other antidotes in that, in usual antidotal doses, it has not been associated with clinically significant toxicity.…”

“…2 In Turkey, cyanogenic glycosides are known as amygdaline and are present in the seeds of bitter almond, peach, cherry, apple and apricot. [1][2][3] Most cases of cyanogenic intoxication in Turkey are related to ingestion of apricot seeds by children. 1,4 This study reviews 13 children with cyanide intoxication owing to consumption of apricot seeds.…”

Accumulation Pattern of Amygdalin and Prunasin and Its Correlation with Fruit and Kernel Agronomic Characteristics during Apricot (Prunus armeniaca L.) Kernel Development

“…Clinical symptoms of acute cyanide poisoning, which usually occur less than 1 min after inhalation and within a few minutes after ingestion, include rapid respiration, a drop in blood pressure, rapid pulse, headache, dizziness, vomiting, abdominal pain, diarrhea, mental confusion, stupor, blue discoloration of the skin due to lack of oxygen (cyanosis), twitching and convulsions to coma and death [19][20][21]. A series of poisoning cases (adults, children, livestock) has been reported from the ingestion of bitter apricot kernels [21][22][23][24][25][26][27][28]. Long-term exposure to sublethal concentrations of cyanogenic glycosides can present ongoing health issues, such as Konzo, an irreversible motor neuron disease with clinical signs including the inability to walk, limited arm movement, and speech difficulties [29,30].…”

Rosaceae Juss.

“…Introduced Old In some instances seeds within the pits are a greater risk than leaves. In another instance, a mixture of soft hulls and apricot seeds from a bakery were fed to dairy cattle, resulting in illness in 5 of 12 cows and the death of 2 (Kupper et al 2008). Apricot seeds, which are sold in health food stores, oftentimes without appropriate warnings, are a health risk.…”