Prussic acid Poisoning 'Geilsiekte'
By Dr Mackie Hobson BSc(Agric),BVSc

Prussic acid Poisoning ‘Geilsiekte’

Farmers speak about ‘prussic acid’, ‘geilsiekte’, ‘droë geilsiekte’, ‘opblaasgeilsiekte’, ‘blousuurvergiftiging’ and ‘opblaaskrimpsiekte’ relating to cyanide (HCN) poisoning.

Prussic acid poisoning must be considered a possibility in any acute death in Angora goats (sheep and cattle).

Under what conditions is prussic acid poisoning likely to occur?

Prussic acid poisoning is most likely to occur when grazing occurs:

• After plant wilting (berg winds, frost)
• Soon after a drought is broken by rain.
• Plants that have regrown following tissue damage from livestock trampling or mowing.
• Following high temperatures or water stress

The limp, green or partially wilted yellowed leaves are the most dangerous as they can also be sweet and more palatable. Once the plant material regains the moisture or dries out it loses its toxicity.

What causes the plants to become poisonous?

Wilting occurs when the plant loses water faster than the roots can replace it. In the same way frost damages the plant cells and the water is no longer available to the plant. Under these conditions cyanogenic glucosides are formed by the plant. Mastication of potentially cyanogenic plants is important in releasing the cyanogenic glycosides (cyanide) from plant cell vacuoles. In the rumen the glucosides are broken down by enzymes (β-glucosidase and hydroxynitrilelyase) present in the rumen microflora. A rumen pH of ~6.5–7 favours conversion of the cyanogenic glycosides to cyanide.

Which plants and grasses are involved?

There are certain plants under specific environmental conditions that will contain variable amounts of glucosides. In the karoo plants that may be grazed by goats under intensive and extensive conditions.

Included in the list by Kellerman, Mönnig en Veldman.

Kweek (Cynodon species)                              Oats                                                    Lucerne                                 

  Rooigras’                                                            ‘Steekgras’                                               Daisy spp  ( Asteraceae spp, Osteospermum spp,Dimorphoceta spp)

 Other plants listed include the Sorghum spp, wheat, maize,  some Acacia spp pods (kameeldoring, papierbasdoring, haakdoring), Sudan grass, Johnson grass, Eucalyptus cladocalyx, Manihot exculenta (Cassava)

Symptoms:

High level Acute cyanide poisoning:

Signs generally occur within 15–20 min to a few hours after animals eat the plant material and survival after onset of clinical signs is rarely longer than a few hours.

• Excitement can be displayed initially
• Rapid and deep respiration (Dyspnoea)
• High heart rate (Tachycardia)
• Bright red mucous membranes, become cyanotic terminally
• The classic "bitter almond" breath smell may be present
• Salivation
• Lacrimation (excess tears)
• Passing of urine and faeces may occur
• Muscle fasciculation, trembling
• Animals may stagger and struggle before collapse.
• Progression to generalized spasms and coma before death.

Low level or chronic cyanide poisoning syndromes:

Chronic, low-level cyanide (cyanogenic glycoside) exposure can be associated with neuropathy syndromes.

• Cystitis ataxia syndrome (also described in ruminants) is associated with diffuse nerve fibre degeneration in the lateral and ventral funiculi of the spinal cord and brain stem
• Posterior ataxia or incoordination
• May progress to irreversible flaccid paralysis (photo).
• Cystitis secondary to urinary incontinence and hind limb urine scalding and alopecia.
• Death, although uncommon, is often associated with pyelonephritis.
• Late-term abortion and musculoskeletal teratogenesis may also occur.

Chronic cyanogenic glycoside poisoning may also present as hypothyroidism

Diagnosis

Appropriate history, clinical signs, post-mortem findings, and demonstration of HCN in rumen contents or other diagnostic specimens support a diagnosis of cyanide poisoning.

Samples

• Rumen content
• Liver
• Brain
• Heparinized blood in ante mortem sampling

Differential diagnoses include poisonings by nitrate or nitrite, urea, organophosphate, diseases and other toxins that cause sudden death. However, nitrate poisoning usually occurs several hours after the animal has eaten high nitrate forage, and the animal’s blood is dark chocolate brown in contrast to the red venous blood of the prussic acid-poisoned animal.

Treatment

• Intravenous injection of 1.2% sodium nitrate (20mg/kg body weight) over 3-4 minutes and 7.4% sodium thiosulfate (500mg/kg)
• Oral doses of Hypo 30 g in 100 ml of water. The animals may require repeated intravenous doses. Sodium thiosulphate in a high dose can be effective when given up to 30 minutes after the ingestion of a toxic dose of cyanide, but it must be given as soon as possible.
• Activated charcoal at a dose of 2 g/kg live weight. A large dose is essential to effectively adsorb and bind the excess plant toxins in the rumen
• Vitamin B12 is also used as a cyanide antidote. Hydroxocobalamin detoxifies cyanide by binding to it and forming cyanocobalamin (ie, another decoy receptor approach), which is then excreted in urine.
• Other alternative antidotes in clinical development and use worldwide include dicobalt-ethylenediaminetetraacetic acid (EDTA) and α−ketoglutaric acid.

Prevention if worried the ‘kweek’ or ‘daisy’ veld may be poisonous?

• Hypo in the drinking water 1-2 g/litre (100-200g per 100 litres)
• Turn a goat of little value into the land and observe it for 2–3 hours. If the goat shows no signs of poisoning, the remainder of the stock may be allowed to graze.
• Also, provide a source of starchy feed such as grain concentrate to reduce the potential for poisoning.
• Animals should be fed before first turning out to pasture; hungry animals may consume forage too rapidly to detoxify HCN released in the rumen.
• Goats should be turned out to new pasture later in the day if frost. Avoid grazing certain potential toxic plants after winds or excess heat.

Post Mortem

• Venous blood is classically described as being "bright cherry red"; this colour rapidly fades after death or if the blood is exposed to the atmosphere. Whole blood clotting may be slow or not occur.
• Cyanotic blue mucous membranes
• A generalized dark coloration of skeletal muscle
• Bloat, rumen may be distended with gas.
• In some cases the odour of “bitter almonds” may be detected after opening.
• Agonal haemorrhages of the heart may be seen
• Liver, serosal surfaces, tracheal mucosa, and lungs may be congested or haemorrhagic;
• Froth may be seen in respiratory passages

Rumen contents may provide a positive sodium picrate paper test (or positive results on other rapid cyanide test strip systems.

Chronic ‘cystitis ataxia toxidromes’ are characterized by opportunistic bacterial cystitis with or without pyelonephritis and diffuse nerve fibre degeneration in the lateral and ventral funiculi of the spinal cord and brain stem. Hind limb urine scalding and alopecia may be present.

Dr Mackie Hobson

References

1.C.D. Allison, Extension Range Management Specialist.R.D. Baker, Extension Agronomist

College of Agriculture, Consumer and Environmental Sciences, New Mexico State University

2. Luginbuhl, J-M. 2006. Pastures for Meat Goats
3. 2014 by Rhian B. Cope,
4. Kellerman, T.S., Coetzer, J.A.W., Naude, T.W. and Botha, C.J. 2005. Plant Poisonings and Mycotoxicosies of Livestock in Southern Africa.

5.Mönnig, H.O. en Veldman, F.J. 1975. Handboek oor Veesiektes. Tafelberg uitgewers. ISBN 0 624 00359 0

6 Dr. Faffa Malan, Veeartskonsultant