Oxalis species
Loading...
Date
Authors
Botha, C.J. (Christoffel Jacobus)
Venter, Elna
Journal Title
Journal ISSN
Volume Title
Publisher
Abstract
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.
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.
Description
Colour photos. Final web-ready size: JPEG. Photo 1: 22.4 kb, 72 ppi; Photo 2: 9.12 kb, 72 ppi; Photo 3: 21.3 kb, 180 ppi; Photo 4: 26.7 kb, 72 ppi; Photo 5: 28.6 kb, 72 ppi. Original TIFF file housed at the Dept. of Paraclinical Sciences, Section Pharmacology and Toxicology, University of Pretoria.
Keywords
Plant poisoning, Toxicology, Plant poisoning in animals, Poisonous plants, Soluble oxalate, Nephropathy
Sustainable Development Goals
Citation
Botha, CJ & Venter, E 2002, 'Plants poisonous to livestock Southern Africa (CD-ROM)' University of Pretoria, Faculty of Veterinary Science, Dept. of Paraclinical Sciences, Section Pharmacology and Toxicology, Pretoria, South Africa.