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
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.
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
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.
The amount of oxalate within the plant varies with
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:
Additionally, oxalate may have a direct irritant action on lung capillaries resulting in pulmonary oedema.
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 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:
Chronic signs may develop in 1 — 12 months of exposure and include:
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.
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.
Acute poisoning findings vary and affected animals may have a range of the following:
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.
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.
Nursing mares and foals tend to be more susceptible due to their increased requirements for calcium.
Big head is caused by horses grazing a pasture which is predominantly introduced tropical grass species such as:
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.
Treatment consists of