CASE NOTES


Pyrrolizidine Alkaloid Poisning in Cattle - Case 2

Bruce Watt, SDV, Tablelands LHPA (Bathurst) and David Payten, 'Kaloola', Darbys Falls Road, Cowra

Posted Flock & Herd August 2010

INTRODUCTION

Across Australia, the main plant genera with appreciable quantities of pyrrolizidine alkaloids (PA) are Senecio, Crotalaria, Heliotropium, Amsinkia and Echium (Seawright, 1982). However, across the southern agricultural belt of NSW only Heliotropium europaeum (common heliotrope or potato weed) and Echium plantagineum (synonym E. lycopsis), (Patersons curse) are significant sources of PAs. Vast numbers of sheep in southern Australia are unavoidably exposed to heliotrope (Culvenor, 1978 cited by Seawright, 1982) and some degree of PA-associated liver damage is often considered normal.

Clinical hepatopathy is also diagnosed routinely in these areas especially in crossbred and British breed sheep. As cattle are considered to be in the order of ten (Seawright, 1982) to forty (Radostits et al, 2007) times more susceptible to PA intoxication than sheep, it is surprising that bovine PA intoxication is not diagnosed more frequently.

CASE REPORT

One of us (DP) was called in late May 2009 after a cattle producer from near Cowra on the central west slopes of NSW progressively lost 12 of 22 mature Angus cows. The cows, in good body condition had commenced dying in mid April 2009 and deaths continued intermittently. The owner runs numerous mobs and in total runs 400-500 breeding cows. Deaths occurred only in the mob of cows that had been grazing in the one 40 hectare paddock for at least a year.

One cow, seen with neurological signs was treated by DP for hypomagnesaemia but failed to respond. The second of us, (BW) visited the property on the 25th May 2009 for further investigation. At this time there were no fresh deaths and the remaining cattle appeared normal. Cattle had grazed this paddock for 20-30 years without similar problems being recalled. It was a conventional paddock with improved, naturalised pasture of predominately barley grass and subterranean clover. No potentially toxic plants were noted in sufficient abundance to be of concern.

At the time of examination, pasture was short and green but moisture stressed. Most deaths occurred along the western fence line. However, there were no rubbish dumps or old batteries in the paddock, which was watered by troughed town water and an earth dam. There was no evidence of blue-green algae in the dam. Neither the paddock nor the cattle had received any unusual treatments in the last few months.

The freshest carcase, a cow that was estimated to have died three days before, was anthrax PCR-negative. The owner commented, however, that due to summer rain, this paddock grew a dense stand of common heliotrope over the summer and the cows had little choice but to eat it.

Dead cow
Most deaths occurred along the western fence line, suggesting aimless wandering

The owner moved the cows from the paddock about a week before the visit on date made by BW, but two had died subsequently.

On the 27th May 2009, the owner called because another cow in the mob had become sick. The owner commented that she became weak and mildly aggressive then became recumbent. She died just before the arrival of BW.

NECROPSY FINDINGS (CASE 1)

The most significant post-mortem findings on this mature Angus cow in condition score 2.5 included widespread serosal haemorrhages and marked oedema of the mesenteric tissues. The liver appeared small for a cow of this size and was of firm consistency.On the cut surface the liver parenchyma was of normal colour but appeared mottled. The gall bladder was grossly distended.

BACTERIOLOGY, BIOCHEMISTRY ON CASE 1

Rumen content and serum were negative for Clostridium botulinum toxin, types C and D. Unclotted blood obtained from the freshly dead cow was submitted for biochemistry.

Normal Case 1
GGT (biliary system) <30 439
GLDH (hepatocytes) <30 63.1
AST (non-specific) <130 468
ALP <300 584
Bilirubin <10 89
Ca 2.00-3.00 1.63
Mg 0.5-1.5 1.06
Albumin 28-38 22
Globulin 24-40 46

The elevated liver enzymes and bilirubin and depressed albumin levels are consistent with a hepatopathy. Pathologist Steven Hum suggested that the low calcium might be a pseudohypocalcaemia given the low albumin. Given that the blood sample was collected from the jugular vein soon after death it may be necessary to treat these results with caution.

PATHOLOGY

The pathologist reported that the liver showed congestion, multifocal oedema, and prominent diffuse portal necrosis with some bile duct proliferation. There was scattered acute hepatocellular necrosis and moderate diffuse fatty degeneration. The diagnosis was of a severe diffuse subacute hepatopathy, highly suggestive of a toxic aetiology.

DIAGNOSIS

Based on the history of prolonged grazing of heliotrope, clinical signs consistent with hepatic encephalopathy, the pattern of steady losses, necropsy, biochemical and histopathological findings, and in the absence of an alternative, a diagnosis of subacute hepatopathy from pyrrolizidine alkaloid toxicosis was made.

DISCUSSION

Despite their greater sensitivity to PAs and their potential exposure, in our experience PA poisoning (or more correctly poisoning from the toxic pyrrolic metabolites of PAs, Radostits et al, 2007) is less common in cattle than sheep. This is consistent with the observations of Seawright (1982) who considered that heliotrope might not be as palatable for cattle as it is for sheep. It may also be because cattle are less likely to be grazed on heliotrope infested summer cropping paddocks.

However, BW has seen several cases of hepatopathy in cattle in the Condobolin district in which pathologists have not mentioned the megalocytosis that characterises the liver pathology of PA intoxication in sheep. Megalocytosis is indicative of the antimitotic effects of chronic PA intoxication but is not pathognomonic (Cullen, 2007). Additionally, a long latent period before megalocytosis develops poses 'difficulties in interpretation' (Jubb and Kennedy, 1970). Again presumably, if cattle are subacutely intoxicated and die within this latent period then megalocytosis will not be a feature of the pathology.

Given the plethora of potential bovine liver toxins, a non-specific description of the microscopic lesions adds to the clinician's challenge of ascribing an aetiological agent to the disease.

BW has seen several cases of PA poisoning in crossbred sheep in which losses have occurred in a sporadic pattern over several months. Others have noted the onset of illness 'many months after the animals have been removed from toxic pastures' (Radostitis et al, 2007).

Based on this experience, the owner in this case was advised that deaths could continue and treatment options were limited. One suggestion was to sell the remainder of the mob for slaughter. The owner opted not to do this to avoid the risk of cattle becoming sick in transit to and from the saleyards. The losses did continue, and several months later only four cows remained alive. By September, the owner considered that the losses had ceased.

These losses represent an 80% mortality rate over four months months commencing two to three months after grazing of the heliotrope had finished.

Hepatic encephalopathy seems to be more of a feature of subacute to chronic PA intoxication in horses and cattle than sheep. The names 'walk-about' (and Kimberley horse disease) for the manifestation of this disease in northern Australia and 'walking disease' of cattle and horses in the US (Jubb and Kennedy, 1970) attest to the fixed ambulation that is sometimes a feature of an encephalopathy.

Cattle that walk aimlessly tend to die pressed against objects or after being obstructed by fences. A feature of this case is that many of the cattle died against a fence. BW has also seen this pattern in lead intoxicated cattle. Diarrhoea, straining and rectal prolapses, also features of PA intoxication in cattle were not observed or reported in this outbreak. Secondary copper poisoning associated with PA hepatopathy in sheep is not a feature of the disease in cattle.

Common heliotrope grows in profusion on stubbles, fallows and degraded pastures after summer rains. It is normal practice to control weeds on summer stubbles and fallows with herbicides as these weeds deplete soil nutrients and water prior to a winter crop. In this instance, the intoxication occurred in a long term pasture that had been set stocked. Set stocking is practised in part because mob sizes are smaller and more convenient to handle. However, set stocking also depletes perennial species and favours annuals. Annualised pastures are therefore much more likely to support heliotrope after summer rains.

REFERENCES

  1. Seawright AA, Animal Health in Australia, Vol. 2 Chemical and Plant Poisons. Australian Government Publishing Service. Canberra, 1982
  2. Cullen (2007) Liver, Biliary system and Exocrine Pancreas Chapter 8 in Pathological Basis of Veterinary disease Fourth Edition edited by McGavin MD and Zachary JF, p 444
  3. Jubb KVF and Kennedy PC and Palmer N. (1970). Pathology of Domestic Animals, 2nd Edition, p 217
  4. Radostits OM, Gay CC, Hinchcliff KW and Constable PD. (2007). Veterinary Medicine, 10th Edition, p 1879

 


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