Page 1007 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Cyanogenic Glycoside Containing Plants Chapter | 64 939

VetBooks.ir source by which the cyanide becomes bound and then risk of poisoning (Knight and Walter, 2001). Proper cur-
ing of hay and silage and allowing adequate time before
excreted. In acutely poisoned animals and humans treat-
ment must be readily available and quickly administered
feeding will reduce toxic levels of CN.
soon after exposure to prevent death. In the case of ani- Treatment in animals is often futile and involves the
mals it is very difficult to prevent death if a lethal dose rapid inactivation and removal of CN by metabolizing to a
has been ingested unless all the necessary tools and anti- nontoxic product or complexing it with other compounds
dotes are readily available and someone experienced with to facilitate urinary excretion (Burrows and Tyrl, 2013).
treatment is present. Intravenous administration of sodium nitrite (10 20 mg/
kg) and sodium thiosulfate (250 500 mg/kg) is an antidote
but should be administered slowly to prevent secondary
DIAGNOSIS AND PATHOLOGY toxicosis. The mechanism associated with this treatment
OF CYANIDE POISONING involves sodium nitrite conversion of hemoglobin to met-
hemoglobin, which has a greater affinity for CN subse-
Diagnosis of acute versus chronic CN poisoning involve
quently producing cyanmethemoglobin. This reaction
multiple and different diagnostic techniques or histopatho-
restores the cytochrome oxidase system critical for cellular
logical analysis. Characteristic cherry red venous blood
respiration. The sodium thiosulfate in the presence of the
and bright pink mucous membranes is strongly indicative
rhodanese enzyme rapidly complexes the CN molecule
of acute HCN exposure. Upon necropsy the blood clotting
cleaved from the cyanmethemoglobin to a form relatively
time is prolonged, muscle tissues are dark and congested
nontoxic sodium thiocyanate, which is excreted in the urine
and internal organs are congested and cyanotic.
(Salkowski and Penney, 1994). However, this sodium thio-
Hemorrhage is often observed in lungs, heart and other
cyanate is the intermediate that interferes with iodine
organs. A characteristic “bitter almond” smell in rumen
metabolism potential causing goiter. However, goiter is
contents upon opening the gastro intestinal tract is another
easily resolved with iodine supplementation.
important clue of CN poisoning (Burrows and Tyrl, 2013).
If CN is suspected, rumen content, liver, and blood
samples should be collected immediately and frozen as CN CONCLUDING REMARKS AND FUTURE
is rapidly lost from animal tissues. Plant material from the
location where poisoning occurs should also be collected DIRECTIONS
and frozen. Suspected plant material containing 200 ppm Appropriate management of grazing systems to avoid
HCN is potentially toxic and liver or blood levels greater introducing livestock to potentially toxic plants will help
than 1 ppm HCN is highly suggestive of cyanide poison- prevent or reduce animal losses. Knowledge and under-
ing. The most diagnostically significant tissues for CN con-
standing what plants are in pastures and what conditions
firmation is brain and ventricular myocardium and levels
and risks are associated with forages. For example, timing
of 100 μg/100 g wet tissue are diagnostic (Ballantyne,
when livestock are introduced to sudan grass pastures is
1983). CN-containing plant identification, evidence of
important. Allowing sudan to grow to at least 2 ft tall
grazing these plants and positive CN analysis of tissues is
before grazing, avoid grazing frozen or damaged crops,
conclusive evidence that CN poisoning occurred.
and proper curing of hay or ensiling of cut forages will
reduce risk. Selection of low CN cultivars will further
reduce risk. Long-term maintenance of horses on sudan
PREVENTION AND TREATMENT
grass hay or other forages with low levels of CN is dis-
OF CN POISONING
couraged. In people, proper preparation of cassava and
Understanding the potential threat of plants containing other CN-containing foods and avoidance of daily, long-
cyanogenic glycosides provides a significant advantage term ingestion of these foods will reduce the risk of neu-
for producers to avoid animal losses or clinical disease. rological effects. Cyanide-containing plants are ubiquitous
New cultivars for animal forages and human foods have and with knowledge of the potential risk of poisoning one
been developed over the last several years. However, low should be able to avoid poisoning of animals and people.
level cyanide ingestion is still a threat for chronic disease.
Selection of low CN-containing cultivars is a method to
reduce disease but cassava still needs to be properly pre- REFERENCES
pared. Forage samples submitted for CN analysis can
Adams, L.G., Dollahite, J.W., Romane, W.M., 1969. Cystitis and ataxia
reduce risk, however time of sample collection and meth- associated with sorghum ingestion in horses. J. Am. Vet. Med.
ods of preparation for analysis may influence CN content Assoc. 155, 518 524.
and should be noted. Allowing sudan grasses to grow to Balagopalan, C., Padmaja, G., Nanda, S., et al., 1988. Cassava in Food,
at least 2 ft tall before grazing or harvesting will reduce Feed and Industry. CRC Press, Boca Raton, FL, pp. 224.