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Cyanide poisoning associated with the feeding of apricot kernels to dairy

cattle

Article  in  The Veterinary record · May 2008

DOI: 10.1136/vr.162.15.488 · Source: PubMed

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Short Communications
Cyanide poisoning
associated with the
feeding of apricot
kernels to dairy cattle
J. Kupper, M. Schuman, R. Wennig,
U. Gorber, A. Mittelholzer, R. Artho,
S. Meyer, H. Kupferschmidt, H. Naegeli
THERE are over 1000 cyanogenic plant species worldwide,
but only a fraction of these contain sufficient amounts of gly-
coside compounds, for example, amygdalin, to release lethal
doses of hydrogen cyanide (HCN) (Galey 1996, Smith 1996,
Casteel 1999, Pickrell and Oehme 2003). After disruption of
the plant integrity by mechanical grinding or chewing, natu-
rally occurring enzymes generate HCN by hydrolysis of glyco-
sides (Poulton and Li 1994). Ruminants are more susceptible
than monogastric animals to cyanide poisoning due to the
additional presence of microbial enzymes in the rumen that
hydrolyse the glycosides. Also, the higher pH in the rumen
compared with the stomach of monogastric species increases
the rate of conversion, thus releasing even more HCN (Smith
1996, Casteel 1999, Radostits and others 1999, Pickrell and
Oehme 2003). The free CN- forms tight complexes with oxi-
dised iron (Fe3+) in cytochrome complexes, leading to inhi-
bition of mitochondrial electron transport, and death due
to deprivation of aerobic energy supplies (Kerns and others
2002, Pickrell and Oehme 2003).
A possible risk factor for cyanide poisoning is associated
with the feeding of unusual by-products of the food industry.
This short communication describes how a mixture of hulls
and seeds (Fig 1), removed from the inner part of the wood-
like pit of apricot fruits, was the source of a unique case of
HCN toxicity in dairy cattle. A farmer obtained large quanti-
ties of soft hulls, separated from apricot kernels used for the
production of a traditional gingerbread cake, from a local
bakery in the area of Appenzell, Switzerland. Unfortunately,
the farmer did not notice the typical smell of bitter almonds
but, initially, all 12 cows demonstrated a strong aversion to
the unusual feed consisting of soft apricot hulls. Eventually,
the feed was made more palatable by the addition of silage
such that, on average, each cow ingested approximately 2 kg
of the toxic material.
The following morning, five of the 12 cows showed acute
tympany, of these, two suffered from nystagmus, profuse sali-
vation, tremor, opisthotonos and dyspnea. These two cows
died within the next 30 minutes and, at the time of death,
showed petechial haemorrhages in the sclera and blood drip-
ping from the anus. The three other cows suffered from ataxia
and became recumbent. The mucosae were light red and the
venous blood was of a distinctive cherry-red colour, reflect-
ing the inability to use oxygen for aerobic metabolism (Kerns
and others 2002, Erdman 2004). These surviving animals
remained anorexic for another 24 hours. Their milk produc-
tion was reduced, but they recovered without treatment. In
view of the transfer of cyanide across the mammary gland
(Soto-Blanco and Górniak 2003), it was recommended that
the residual milk obtained from overtly sick animals should
be discarded.
For quantitative cyanide detection, HCN was converted
into cyanogen chloride by reaction with chloramine (Odoul
and others 1994). The subsequent analysis by gas chroma-
tography-mass spectrometry revealed that the apricot hulls
contained a mean (sd) HCN level of 110 (23) mg/kg. The
amygdalin content of the sample, determined by reverse-
FIG 1: Representative
sample of soft apricot
hulls and some residual
seeds fed to dairy cows
phase liquid chromatography (Hwang and others 2002), dis-
closed 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 pre- Veterinary Record (2008)
viously (Cran 1985, Roder 2001, Suter 2002), confirmatory 162, 488-489
HCN detection is a difficult and tedious procedure. Although
toxic levels of HCN were detected in the present case, the J. Kupper, DVM,
volatility and rapid breakdown of HCN, combined with H. Naegeli, DVM,
the time it normally takes for the samples to be received Institute of Veterinary
and analysed, may invariably lead to false-negative results. Pharmacology and
Therefore, in the search for an alternative approach, the Toxicology,
authors took advantage of a more stable metabolite that can U. Gorber, DVM,
easily be monitored. The majority of HCN (80 per cent) is Department of
detoxified by the enzyme rhodanese in the liver, producing Farm Animals,
a thiocyanate metabolite that is excreted mainly through University of Zurich,
the kidneys with a half-life of up to three days in human Winterthurerstrasse
beings (Gurnsey and others 1977, Erdman 2004). In the 260, CH-8057 Zurich,
present study, the serum thiocyanate level was determined Switzerland
in blood samples obtained from three surviving cows 24 M. Schuman, PhD,
hours after the initial deaths. The procedure (Lundquist and R. Wennig, PhD,
others 1979) involved an ion exchange clean-up to remove National Health
interfering matrix components. After elution with sodium Laboratory, Toxicology
perchlorate, the thiocyanate concentration was determined Division, University
by a quantitative colorimetric reaction in the presence of of Luxembourg,
sodium hypochlorite and barbituric acid, yielding a deriva- Luxembourg
tive with peak absorption at a wavelength of 580 nm. The A. Mittelholzer, DVM,
thiocyanate concentrations in the cows (145, 209 and 211 R. Artho, DVM,
µmol/l) exceeded the reference range determined for human S. Meyer, DVM,
blood (15 to 70 µmol/l) and reached the same high concen- Veterinary Practice,
trations as those found in severe cases of cyanide poisonings Appenzell, Switzerland
in human beings (Singh and others 1989). A healthy cow H. Kupferschmidt, MD,
in the neighbourhood had a serum thiocyanate level of 52 Swiss Toxicological
µmol/l, suggesting a similar normal range in cattle to that Information Centre,
in humans. This view was supported when, one month later, Zurich, Switzerland
the thiocyanate serum concentration of the three cows was
measured again and the values were 50 54, and 60 µmol/l. Dr Kupper is also at Swiss
It was concluded that the conversion of HCN to thiocyanate Toxicological Information
provides a potentially useful diagnostic marker to confirm Centre, Zurich,
suspected exposures to cyanide or cyanogenic glycosides in Switzerland
The Veterinary Record, April 12, 2008

livestock. However, alternative sources of increased thiocy-
anate levels should be considered, including the ingestion
of rapeseed meal with a high glucosinolate content (Bell
1984).
A commonly recommended treatment for cyanide poi-
soning (Radostits and others 1999, Roder 2001) consists of
the slow intravenous injection of sodium nitrite (20 per cent
solution, up to 22 mg/kg bodyweight) followed by sodium
thiosulfate (20 per cent, up to 660 mg/kg bodyweight). The
purpose of sodium nitrite is to oxidise the ferrous iron (Fe2+)
of haemoglobin, generating methaemoglobin. The resulting
ferric iron (Fe3+) combines with CN to form cyanmethae-
moglobin, thus restoring the activity of mitochondrial cyto-
chrome complexes involved in aerobic respiration. Sodium
thiosulfate provides the rate-limiting sulphur moiety to
accelerate the enzymatic conversion of CN into the less toxic
thiocyanate metabolite.
There have been several previous reports of acute tox-
icity in human beings resulting from the consumption of
apricot kernels (Sayre and Kaymakcalavu 1964, Rubino and
Davidoff 1979, Suchard and others 1998). The Committee on
Toxicity of Chemicals in Food, Consumer Products and the
Environment of the Food Standards Agency (FSA) has issued
a risk assessment study for amygdalin and similar cyanogenic
glycosides present in foods (FSA 2006). The study concluded
that it is appropriate to apply a tolerable daily intake for the
human population of 0·02 mg cyanide/kg bodyweight/day,
which represents an intake of approximately one to two apri-
cot kernels per day.
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