It is not unusual to find an Oleander shrub in the older farm homesteads throughout Australia. The most likely explanation being that it was established as a plant that grows well and thrives under harsh conditions and provides year long greenery. However, this plant also has a somewhat two-pronged reputation as both a possible medical saviour and an efficient killer of many species, including domestic livestock and humans (Galey et al 1996, da Silva et al 2006, www.cancer.org). Oleander was imported around the world by settlers and merchant shipmen, who are rumoured to have used the extract from the plant as a hangover cure. However, anecdote also suggests that those utilising Oleander for medicinal purposes may have regularly come unstuck as any part of the plant is toxic enough to cause death, even if taken as a herbal beverage (Bandara et al 2010). The Oleander species contain a variety of cardiac glycosides including neriifolin, thevetin A, thevetin B and oleandrin. It is suggested that the cardiotonic properties of Oleanders have long been experimented with and utilised, including as an instrument of suicide (da Silva et al 2006), which includes a recently disturbing frequency of cases of self harm involving ingestion of Oleander seeds in developing countries such as Sri Lanka and India (Bandara et al 2010, Eddleston et al 1999).
The scientific accounts of toxicity in livestock are commonly based on circumstantial evidence of exposure and ingestion (Galey et al 1996). However, it has been proposed that the development of a 'thin layer chromatography' technique for detection of oleandrin and an increased awareness of the histological appearance of cardiac lesions may facilitate a more accurate, evidence based approach to diagnosis in cases where substantial circumstantial or physical evidence is lacking (Galey et al 1996). Australian data for Oleander toxicity in livestock is not readily available and although the plant is extremely common in many farm environments the significance of Oleander as a cause of death in livestock is not well documented. Records in the Hume shire have identified Oleander as the cause of death in 4 of 71 cases recorded due to plant toxicity between 1993 and present. This paper will explore the nature of the circumstantial and more definitive evidence for this diagnosis in two of these cases reported in October/November 2010.
Two cases of sudden death in beef cattle were investigated on two properties in the Hume board in October/November 2011. Case one required a systematic approach to differential diagnosis of sudden death due to an initial lack of evidence of exposure to Oleander or other toxin. In case two, a diagnosis was based on physical evidence of presence of Oleander leaves at postmortem and circumstantial evidence of recent access to Oleander. Case one and two resulted in mortality rates of 23.8% and 41.7% respectively. A summary of the progression and findings for each case is presented in Table 1 and discussed.
|Case details||Case 1||Case 2|
|Age affected animals||Approximately 2 years||Approximately 2 years|
|Appropriate vaccination history for signalment (Clostridial)||Yes||Yes|
|Recent endoparasite control||Backline 3 weeks prior to visit||Backline 2 weeks prior to visit|
|Grazing history||Hay in previous 7-10 days, dry paddock feed plus grazing oats/lucerne mix.||Established, improved pasture –annual rye grass dominant|
|Immediate history of animals||Escaped from paddock into laneway 24 hours previously. Returned to paddock after 12-24 hours||Yarded 8 hours and drafted steers and heifers – returned heifers to original paddock and steers to a new paddock – adjacent to yards|
|Reason for initial visit||Sudden death||Sudden death and ill heifers|
|Initial mortality rate||8 of 42 (19.0%)||2 of 24 (8.3%)|
|Final mortality rate||10 of 42 (23.8%)||10 of 24 (41.7%)|
|Timeframe for mortalities||0-3 days||0-10 days|
|Morbidity rate initially||All mortalities||4 of 24 (16.6%)|
|Presentation mortalities||Lateral recumbency, watery blood at eyes, mouth and anus, slightly bloated appearance, some evidence autolysis, no evidence of convulsion etc immediately prior to death||Lateral recumbency, tongue protruding, bloated (carcases 24-48 hours old), and evidence profuse watery faeces.|
|Presentation clinical cases||No cases||Sternal recumbency progressing to lateral recumbency, profuse watery brown/green faeces,|
The initial investigation in case 1 involved an anthrax exclusion (which returned negative results) followed by a systematic approach to rule in or out the main hypotheses and work through differential diagnoses. The collection of information was complicated by the fact that this case occurred on a Monday morning on a large property with multiple people responsible for the stock health and welfare across the weekend. The dead animals were also located both in and outside the paddock (having broken through the gate) and 3 were dead in a public laneway adding a level of complexity to the logistics of the investigation! On receipt of a negative result for anthrax, carcases were submitted to the CSU Veterinary diagnostic laboratory for post mortem. As it appeared that the cattle had only had access to the paddock and the laneway immediately adjacent to the paddock, the primary hypotheses at this stage included (but not limited to) Nitrate/Nitrite, Urea toxicity, lightening strike (recent inclement weather) and hypomagnesaemia.
A full post mortem was conducted on 2 steers in case 1 and samples of aqueous humour were submitted from 4 steers.
Steer 1; The carcase was moderately autolytic and bloated with blood stained discharges present at all external orifices. Visible mucous membranes appeared congested. There was extensive haemorrhage and congestion of the ventral cervical muscles. All body cavities contained excessive volumes of blood stained fluid. The lungs were diffusely congested and multiple eccymotic haemorrhages present in the left ventricular endocardium. Diffuse moderate congestion was evident on the tunica mucosa of the oesophagus distally as far as the thoracic inlet.
Steer 2; The gross appearance was as for steer 1. Both pleural and pericardial cavities contained moderately excessive volumes of red/brown, clear fluid. Blood stained froth was present in the trachea. Ecchymotic to splash haemorrhages were observed in the epicardium, tunica adventitia of the pulmonary artery and ventrally in the greater omentum. The liver appeared moderately congested and friable. There were no other significant findings
Aqueous humour was submitted for biochemical analyses from four steers;
|AQ HU Ca||1.49||1.71||1.6||1.04||1.00-2.40||mmol/l|
|Aq Hum Mg||1.08||1.02||1.01||1.10||0.48-1.50||mmol/l|
(Nitrate was also tested 'cow side' in 'DIPSTIX' (as described by Morton (personal comm) and found to be negative)
The histopathology for both steers post mortemed in case 1 are summarised together for brevity; the histopathology identified myocardial degeneration, severe, diffuse congestion of the lungs with moderate alveolar and interstitial oedema. There was acute periacinar congestion in the liver with no other significant changes detected.
In this case, as animals were available for clinical examination (Table 1), this assisted ascertaining the main organ systems affected. The profuse watery diarrhoea was the main finding associated with severe, acute abdominal pain. Other findings were related to a 'depressed' systemic state and dehydration.
The approach to post mortem in case two was initially focussed on the enteric system based on the presentation in the clinical cases observed. The carcase examined was moderately autolytic. All small intestinal loops appeared reddened and inflamed with some evidence of oedema/thickening of the mucosa. The rumen and omasum were full, abomasum, small and large intestines all appeared relatively empty with watery, brown fetid contents. On opening the rumen contents appeared dry with large amounts of fibrous, partially digested material present. Oleander like leaves were removed from the rumen (15-20 leaves). Other findings were non specific. Thoracic contents appeared relatively normal. Based on these findings no further samples were collected.
The pathologist opinion was that lesions were likely to be of 6-12 hours standing. There was infiltration of neutrophils into Purkinje fibres which is consistent with but not diagnostic of Oleander poisoning. Acute phalaris toxicity may also be implicated. However, the peracute form associated with methyl tryptamine and Β-carboline indoleamines is not recorded as causing cardiac degeneration and the lack of polioencephalomalacia would mitigate against the possibility of an acute syndrome. In clinical pathology urea was slightly elevated and ammonia levels moderately elevated. However, ammonia levels will increase post mortem with an approximate doubling in concentration for every 24 hours post mortem. Outcome; diagnosis not confirmed!
Oleander toxicity was diagnosed based on the recovery of Oleander leaves from the rumen of the heifer at post mortem. No other significant findings were made on post mortem.
ONE DIAGNOSIS DOWN AND ONE TO GO – WE NEED MORE INFORMATION;
On further examination of the environment to which the steers in case 1 were believed to have had access to, it became apparent that a large number (42?) of cattle had actually broken through a second gateway on the lane and had travelled approximately 200 metres to a groups of sheds. This finding was based on the discovery of footprints in mud in an adjacent laneway. Beyond the sheds lay a watercourse with rank phalaris covering an area of approximately 100 square meters. Four silos were also located at the sheds and evidence of concreted DAP was present at the base of one silo. It appeared that a number of animals had also been present in that area (footprints). On further inspection of this area a small number of dried Oleander branches were discovered along with other items of garden waste. In the light of these findings the possibility sudden death caused by Oleander, phalaris toxicity or DAP ingestion needed to be explored further.
The diagnosis in case 2 seemed quickly apparent with clinical signs in sick/dying heifers matching those in the literature for Oleander toxicity (Galey et al 1996), however these are relatively non specific and require supporting evidence of access to the plant. The circumstantial evidence of access to a mature Oleander bush in a laneway on return from the yards and the physical evidence of Oleander type leaves in the rumen of the heifer at post mortem support these clinical findings in this case. The fact that the heifers and steers were drafted and returned to different paddocks via different routes (no steers affected), the heifers were left in the lane to make their own way back to the paddock and would have been hungry, off feed for 7-8 hours, also supports the diagnosis. The lack of gross pathology at post mortem is not unusual. If lesions are found they are commonly consistent with gastroenteric and myocardial damage. Pulmonary oedema and liver damage are often visible and are secondary to cardiac effects leading to congestion in those organs. The timeframe over which mortalities occurred in this case is of considerable interest, with initial mortality rate of 8.3%, an initial morbidity rate of 16.6% and a final mortality rate of 41.7% over a period of 10 days post exposure or ingestion of Oleander. This is considerably different to reports in the literature of 0-36 hours post ingestion (Galey et al 1996). Given that in reports of Oleander toxicity where either animals are examined a considerable time post death or animals have survived for any length of time, remnants of the plant may no longer be evident in ingesta and diagnosis may be reliant on circumstantial and other pathological evidence. In these circumstances testing of intestinal contents for the presence of Oleandrin may be beneficial, particularly in the absence of circumstantial evidence of exposure or ingestion (Galey et al 1996).
The investigation in case 1 was complicated by the fact that on initial enquiry it appeared that the cattle could not have had access to any toxic materials or plants and that there were no clinically affected animals to examine to identify the major systems involved in the subacute case. Continued questioning of farm staff and investigation of the immediate environment of the cattle revealed three possible sources of toxin; Oleander, DAP and phalaris. Examining the pathological evidence; the hyperammonaemia may be a consequence of phalaris toxicoses or possibly ingestion of DAP (no definitive information in literature 1995-present), although this may simply reflect the time frame of post mortem examination post death. The cardiac pathology and histopathology for acute phalaris toxicoses is non specific and not well described in much of the literature which mostly deals with the acute syndrome of sudden death associated with increased ammonia levels in blood and aqueous humour, the pathological findings in the nervous system and the investigation of the phalaris plant for presence of toxic compounds. On the basis of the possibility that there may have been more than one cause of death in the steers and only two of 10 dead were examined, the final diagnosis became a somewhat moot point in this case. However, the consensus was that the most likely cause of death was Oleander toxicity with only 0.005% of an animal's bodyweight in dry Oleander leaves considered fatal (Galey et al 1996) and evidence of possible easy access to the dry plant for all 42 steers. Probably the more valuable outcome for case 1 was the communication to farm workers of the importance of accurate record keeping and communication of stock movements, the need for adequate maintenance of paddock infrastructure and the development of a policy on maintenance of laneways and shed areas including the dumping of garden waste in these areas.
The conclusion on reflection of the investigation of these cases is that where there is substantial circumstantial evidence of Oleander ingestion and cases of sudden death, it is highly likely that Oleander will be implicated. For cases that appear less definitive further evidence of cause may be determined from the pathological investigation and a more intensive investigation of the circumstances of the case.