CASE NOTES
Oxalate Poisoning
Samantha Yorke, Veterinary Officer, Dareton
Posted Flock & Herd February 2011
Introduction
Oxalate ingestion produces several syndromes depending on the type of oxalate found in the plant. Oxalates can be found as water soluble oxalates, or can combine with calcium to form water insoluble calcium oxalate. Some of the syndromes that can result include
- Sudden death or chronic renal damage due to the consumption of plants containing high concentrations of soluble oxalates.
- Equine nutritional hyperparathyroidism (aka Big Head) due to insoluble calcium oxalate in the plant.
- Buccal mucosal irritation due to insoluble calcium oxalate crystals in leaves.
This particular case study focuses on acute and chronic oxalate poisoning affecting sheep on a property in the Western division. Home bred merino ewes and lambs and recently introduced Dorper rams experienced oxalate poisoning after consuming New Zealand spinach. Acute toxicity was suspected when merino ewes and lambs were yarded for 48 hours, then, released hungry into a nearby holding paddock which contained large lush patches of New Zealand Spinach and little else. Rapid consumption of large quantities of this plant by three ewes and lambs raised strong suspicion for their sudden deaths overnight. The remaining ewes were not affected. The producer suspected toxicity and did not report it.
Several weeks later, the producer noticed six recently introduced Dorper rams with weight loss, depression and lameness. The rams were running with 100 apparently healthy merino ewes in a 20,000 acre paddock. A three and a half year old Dorper ram took the producers interest. He noted the ram had marked weight loss over 2 months, severe scouring, polyuria, frequent periods of extended recumbency, tailed the mob when mustered and eventually the ram became anorexic.
The clinical pathology and histopathology will be discussed as part of the following discussion which will focus on oxalate poisoning in ruminants, which is one of the most common syndromes of oxalate poisoning in animals. A brief discussion of big head in horses will follow, however, equine nutritional hyperparathyroidism is an anti-nutritive condition rather than a plant poisoning.
Epidemiology
The animal
In a normal situation mature ruminants can usually consume large quantities of oxalates without harm if the young potentially toxic plant is ingested gradually. Gradual introduction of oxalate containing diets allows rumen bacteria to become accustomed to metabolising the oxalate, preventing its systemic uptake. For this reason, ruminants in general can tolerate larger quantities of oxalate in their diet than other animals.
Toxicity generally occurs if the animal
- Consumes too much oxalate too rapidly
- Is unaccustomed to oxalate and thus have few oxalate degrading bacteria
- Experiences a reduction of rumenal microbe activity due to fasting
- Has low dietary calcium
In this case study the ewes may well have been accustomed to oxalates, as it seems to me that the Western division is a world of oxalates. However, the ewes fasting during a management procedure may have reduced the rumen microbial activity and the rapid excessive consumption of the plant may have resulted in their deaths. On the other hand the Dorper rams were recently introduced to the district and their rumen bacteria may not have been accustomed to degrading oxalates predisposing them to chronic poisoning over the merino ewes in the same paddock that appeared healthy. Breed differences may have also played a role as Dorpers differ in their selection of plant species and parts of the plant consumed.
Other predisposing factors include late pregnant and lactating stock and stock in rangelands where access to and control of problem plants can not be restricted.
PLANT FACTORS
The amount of oxalate within the plant varies with
- Plant species: many different species contain varying amounts of oxalate. Some of the plants commonly known to have high levels of oxalate include:
— Soubsob (Oxalis pes caprae)
— Pigweed (Portulaca)
— Soft roly poly (Salsola kali)
— Setaria (Setaria sphacelata) and
— New Zealand spinach (Tetragonia tetragonioides) - The stage of the plants growth. Commonly actively growing leaves contain the greatest concentrations of oxalate. For example with soursob, the young, growing plant contains high levels of oxalate, while mature dry plants contain low levels.
- The local soil and water conditions where the plant grows. Plants that are grown where there is a high level of ground water calcium or fertilizer (such as stock yards) may have higher levels of oxalate.
Pathogenesis
Acute Oxalate Poisoning
- Occurs in sheep and cattle
- Is possible in horses but not a common phenomenon
- Is a consequence of rapid ingestion of large quantities of young actively growing plant
Mode of action
Soluble oxalate has a high affinity for calcium.
When soluble oxalate is absorbed into the systemic circulation it binds calcium ions to form insoluble calcium oxalate. A variety of pathological changes ensue and the animal may experience:
- Hypocalcaemia, impairing normal cell membrane function causing animals to develop muscle weakness and tremors, collapse and die.
- Calcium oxalate crystal formation and accumulation in renal tubules precipitating acute nephrosis and ureamia.
- Calcium oxalate crystal formation in rumenal capillaries, causing rumenitis. Secondary bacterial or fungal invasion of rumenitis lesions may follow.
Additionally, oxalate may have a direct irritant action on lung capillaries resulting in pulmonary oedema.
Chronic Oxalate Poisoning
Continuous ingestion of plants with a high content of soluble oxalates may cause precipitation of insoluble oxalate crystals in the renal tubules, resulting in nephrosis and chronic renal failure.
Usually ruminants grazing high risk pastures such as soursob develop tolerance, however, there is often a low level of oxalate that is absorbed and consequently progressive renal injury and deposition in the kidneys of calcium oxalate crystals ensues. Renal failure develops over 2-12 months and death may occur. It has been reported that up to 25% of sheep may be affected in some flocks grazing soursob.
In ruminants acute and chronic oxalate pathological changes are most common however other syndromes do occur for example:
Urinary calculi - Calcium oxalate urolithiasis is possible in ruminants, but this is not a common sequelae to oxalate poisoning.
Abortion in cattle - the foetuses may display renal oxalosis
Clinical signs
Acute:
Clinical signs are reported to occur within 4 - 48 hours of rapid ingestion. In sheep the clinical signs may be indistinguishable from hypocalcaemia.
Clinical signs may include one or several of the following:
- Anorexia
- Excessive salivation
- Muscle weakness and tremor, particularly facial muscles
- Rumenal atony, slight bloating
- Pollakiuria
- Frothy blood tinged nasal discharge
- Dyspnoea
- Staggering
- Recumbency with head turned into the flank
- Death without struggle
Chronic:
Chronic signs may develop in 1 — 12 months of exposure and include:
- Depressed appetite
- Scouring
- weight loss
- anaemia
- PU/PD
The most severely affected ram in the case study presented with weakness and depression, frequent periods of recumbency and separation from the mob, mucopurulent nasal discharge, PU/PD, scouring, elevated TPR, exercise intolerance and eventually anorexia.
Clinical pathology
Acute
- Hypocalcaemia
- Elevated urea and creatinine
- Proteinuria — reported to be almost diagnostic of the disease in sheep grazing Oxalis.
Chronic
- Albuminuria, haematuria, epithelial casts in the urine
- Elevated urea and creatinine
- Hypoproteinemia
- Anaemia
- Hyperkalemia
Of the eight rams blood tested each had mild to moderate increases in urea and low normal albumin. In the most affected ram, ram number 8, epithelial cell casts were evident, however there was no evidence of crystalluria.
Necropsy and Histopathology
Acute poisoning findings vary and affected animals may have a range of the following:
- Generalised petechial haemorrhages
- Pulmonary oedema, with copious stable froth in the trachea and bronchi
- Marked hyperaemia of the mucosa of the forestomachs and of the lower alimentary tract
- Pale swollen kidneys
- Birefringent rosettes of crystals in the renal tubules and pelvis
Chronic:
- Shrunken, white and fibrotic kidneys, with large numbers of crystals.
- Perirenal oedema
The kidneys from ram number 8 displayed oxalate crystals in many tubules, particularly in the deeper cortex. The tubular epithelium was flattened and tubules were dilated. Other tubules in the cortex and medulla contained necrotic epithelial cells, cellular debris and occasionally macrophages containing brown pigment. Interstitial spaces were widened which partially may have been due to tubule loss.
Diagnosis
- Access, clinical signs, clinical pathology, necropsy
- Assay plants for soluble oxalate content
- Hazardous plants contain > 2.0 � 2.5% soluble oxalate in dry matter
DDX
- Hypocalcaemia — milk fever or abrupt reduction of feed intake
- Grain poisoning — but history of free access to grain is usually available.
Treatment for Acute Poisoning
- IV or SC 25% calcium borogluconate @ 50-100ml (sheep), 300-500ml (cattle)
- Oral fluids
- Prognosis always guarded due to the risk of nephrosis. Various studies in catlle indicate that if cattle survive the acute stages of the disease, they may die several days later from renal nephrosis.
Control
- Provide alternative sources of food
o Avoid access to hazardous plants when animals are hungry.
o Not overstocking. Overgrazing will potentiate oxalate poisoning if there is no other vegetation. - Ample water available to facilitate the elimination of the oxalate
- Prophylactic feeding of dicalcium phosphate before and during high risk exposure is an effective means of reducing losses. High levels of dietary calcium bind oxalate in the rumen as insoluble, non absorbable calcium oxalate.
- Maintain low level access to oxalate in feed to ensure rumenal flora remains adapted Eg; livestock could be gradually introduced to oxalate plants for short periods for at least 4 days by incrementally increasing the time they are allowed to graze the plants, ensuring the animals are not hungry during this process.
Nutritional hyperparathyroidism (Big head)
The Animal
This is a condition where the animal is deprived of calcium in the diet, thus it is an anti-nutritive condition rather than a poisoning. However I will very briefly discuss the condition.
Horses only seem to be affected. Ruminants rumen microbes break down the oxalate, thereby releasing calcium for absorption in the duodenum.
Predisposing causes
Nursing mares and foals tend to be more susceptible due to their increased requirements for calcium.
The Plant
Big head is caused by horses grazing a pasture which is predominantly introduced tropical grass species such as:
- Buffel grass (Cenchrus ciliaris),
- Setaria (Setaria sphacelata) and
- Kikuyu grasses.
Pathogenesis
The insoluble calcium oxalate crystals within the blades of grass prevent calcium absorption in the duodenum. The resultant hypocalcaemia initiates compensatory parathormone secretion, increased osteoclastic activity, bone resorption, remodelling and replacement by fibrous tissue. This facilitates calcium mobilisation elevating blood calcium to the low normal range.
Osteodystrophy can be generalised, however it tends to be accentuated in cancellous bone of the skull, causing a thickened look of the mandible and/or maxilla. Additionally, articular cartilage may degenerate and the periosteal attachments of ligaments to bone may weaken contributing to lameness. In severe cases bowing deformities and multiple folding fractures of affected bones may occur.
Clinical signs
- Develop on average in 6-8 months
- Shifting lameness,
- Appearance of swollen facial bones,
- Loosening of teeth,
- Weight loss.
Pathology
- Increased circulating parathormone
- Normal serum calcium and phosphorus
- Osteodystrophia fibrosa in swollen bones — such as in the mandible and/ or maxilla
- Osteoporosis in long bones
- Parathyroid gland hyperplasia and hypertrophy
- Erosions and pitting of joint surfaces
Treatment
Treatment consists of
- Removing animals from affected pasture
- Calcium and Phosphorus supplementation in a 2:1 ratio for approximately six months
- The prognosis after treatment is good with osteodystrophic and osteoporetic lesions returning to normal form and function.
Prevention and Control
- Avoid grazing horses on predominant introduced tropical grass pastures without mineral supplementation for longer than 4 weeks
- Legumes may supply more calcium in the diet, but tend not to flourish where tropical grasses predominate so supplementation may be preferable.