DISTRIBUTION:
Widely distributed. Growing on nearly all soil types and under most climatic conditions. More than 200 species are found in South Africa; only two are exotic. Mostly in damp conditions in high rainfall areas. Often found as weeds in gardens.
BOTANICAL DESCRIPTION:
General: Annual or perennial herbs, sometimes stemless, often with “corms”, underground stems or stolons or fleshy taproots. Often in small colonies.
Leaves: The leaves are usually trifoliate, but can be simple. Photosensitive (folding back at night like butterfly wings).
Flowers: Bell-shaped flowers in clusters on long slender stalks. Flowers can be in shades of white, pink, red or yellow.
TOXIC PRINCIPLE:
Contains soluble oxalates.
SYNDROMES:
Soluble oxalate poisoning, Primary nephropathy.
SYSTEMS AFFECTED:
Urogenital system.
CLINICAL SIGNS:
Acute poisoning:
• Hypocalcaemia phase: -soon after intake, 2-6 hours
- Weakness
- Paresis to paralysis, semi-comatose, “milk fever” signs.
- Head thrown back onto shoulder
- Bradycardia
- Mortalities
Treatment of these symptoms with Ca-borogluconate gives good results and animals may recover.
• Kidney failure phase: Following day to few days later due to blockage and damage of tubuli by Ca-oxalate crystals resulting in:
- Uraemia: BUN and creatinine increase
- Oliguria or anuria
Treatment of very little value - irreversible condition.
NECROPSY:
Macroscopical findings:
• Hypocalcaemia:
- Nothing significant,
- haemorrhages.
• Nephrosis and Uraemia:
- Ascites, hydrothorax, perirenal and subcutaneous oedema.
- Kidneys pale, oedematous, swollen - nephrosis.
- Ammonia and urea odour (uraemia).
- Haemorrhages in different organs.
- Oedema and haemorrhages in rumen.
HISTOPATHOLOGY:
Typical oxalate crystals in kidney tubules (seen under polarized light) with signs of kidney damage.
TREATMENT: CONTROL:
• Avoid sudden exposure to oxalate containing plants or intake of large quantities.
• Avoid oxalate containing plants as the only food.
• Feed Ca2+ in the form of dicalcium phosphate as a lick (25% or more with salt) or mixed in the supplementary feed.
EPIDEMIOLOGY:
• Acute poisoning happens where:
- unadapted animals suddenly eat a relatively large amount of oxalate containing plants and the oxalates are absorbed into the circulation
- excessive large amounts of oxalates are absorbed in adapted animals which are not able to detoxify all the oxalates in the rumen (e.g. large amounts during droughts).
• Chronic effect characterized by:
Calcium deficiency resulting in:
- bone abnormality,
- poor milk production and
- poor growth.
N.B. Kidney- and bladder stones where oxalates can play a role amongst other things.
