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Dr Jillian Kelly, Central West Livestock Health & Pest Authority, Coonamble & Nyngan

Posted Flock & Herd September 2012


Hypersensitivity reactions involving manic behaviour in cattle grazing Field Pea (Pisium sativum),crops, referred to as "Field Pea Mania", have been described infrequently in the literature. The clinical signs are dramatic but short lived, meaning that the veterinarian is often not present to witness them, and must rely on the stock owners’ description. In this case all animals recovered, and aside from injuries sustained during the manic episode, there were no changes on haematology, biochemistry or histopathology of the brain to suggest the cause of the reported clinical signs, making diagnosis challenging.


The property involved in this disease investigation is located approximately 50kms south west of Nyngan. The property consists of black loam, granite and red loam soils. The average rainfall for the property is 18 inches, however in the past year (2010) the farm had received 41 inches. The property runs sheep for wool and meat production, beef cattle and a small amount of opportunistic cropping depending on the season.

Although there was high rainfall in 2011, the rain stopped in February 2011 and it had barely rained since. Hence conditions in September 2011 were quite dry, and pasture feed quality was poor.

The farm does not routinely grow or graze field peas, however they had some field peas stored from a one-off previous crop, and found that there was no market for them, and they were too bitter to feed as a supplementary feed to stock. It was therefore decided to sow the stored field peas into a 1000 acre red loam paddock and graze the crop with freshly calved heifers.

The 70 Hereford heifers had been brought in near the house to be monitored in the lead up to calving, and then as each one calved they were moved over into the field pea paddock. So some of the heifers and their calves had been in the paddock for a month, and some only a few days at the time of the incident.

On Thursday the 22nd of September 2011, the manager of the property drove down on a motorbike to check the heifers. One heifer (Heifer 1) staggered, circled and fell down. She lay there, got up and tried to ‘focus’ as if blind. Then another one (Heifer 2) showed similar signs - got up frothing at the mouth and chomping. The manager's first instinct was to get the heifers out of the paddock, but as he went to move them, another heifer (Heifer 3) bellowed, ran across paddock, fell over and ‘broke’ a hind leg.

Upon moving the mob, Heifers 1 & 2 where still wobbly and had difficulty with food prehension. These recovered completely once out of the field pea paddock, and as of 3 days after the "manic" episode they where grazing normally with the mob in a native pasture paddock. The owner and manager of the farm could not tell them apart from the rest of the mob. Heifer 3 also recovered neurologically but had sustained a major musculoskeletal injury to a hind leg. Despite this, they managed to move her out of the field pea paddock.


I attended the farm on Monday the 26th of September 2011 (4 days after the clinical signs were noticed). Heifer 3 was in sternal recumbency, on a fence line. She was in body condition 3.5/5. The animal was alert and aware of her surroundings. She had vision, a bilateral menace response, no muscle tremors, and her face and head were symmetrical. While in recumbency, her heart rate was 64bpm, lung sounds normal and rumen sounds decreased. Faeces appeared of normal consistency. Her calf was not present. The heifer appeared to have avulsed the left gastrocnemius tendon. She was ambulatory, but the plantar surface of the hock and metatarsus remained in contact with the ground when rising and during weight bearing. The heifer could walk several paces when forced, but quickly became recumbent again.

A paddock inspection revealed a paddock of dry, water-stressed, mature field pea plants with pea pods present. The crop was greener and fresher in the gilgais of the paddock and there was a grey powdery mould on foliage of the plants in these areas. There were surprisingly very few weeds and other plants between the rows of field peas - just red dirt. There was an old haystack that had been opened up to the cattle since they have been in the paddock, but there was little hay left - just straw on the ground. There were no signs of carcasses or other foreign or toxic material in this area. There was a 15% urea block in the paddock, which had also been there since the cattle were put into the paddock.

It was decided that the heifer should be euthanased on welfare grounds (due to the gastrocnemius injury), and a post-mortem be conducted.

Post-mortem findings

On post-mortem, the liver was noticed to be enlarged (approximately 1.5x normal size), dark orange in colour and firmer than normal. The gall bladder was significantly enlarged (holding approximately 800ml of fluid). All other organs were grossly normal on post-mortem.

Blood (pre-mortem); in serum, Lithium Heparin & EDTA tubes; was submitted to the laboratory along with fixed tissues of all major organs, aqueous humour, and fresh spinal cord. The samples were submitted under the National Transmissible Spongiform Encephalopathy (TSE) Surveillance program.

Laboratory Findings

Blood results identified elevations in Fibrinogen 8g/L (3-7), GLDH 51U/L (0-30), AST 250U/L (0-120) and CK 2495U/L (0-300). Blood lead and magnesium levels were normal. The pathologist commented that there was:

"evidence of muscle damage, likely due to trauma and recumbency. The high fibrinogen is suggestive of inflammation, could also be due to trauma. There is no evidence of lead toxicity, metabolic disease or anaemia".

Histopathologic examination of the brain (medulla (obex), caudal cerebellar peduncles, mid brain, cerebrum and cerebellum) and kidney showed no significant findings. The liver had mild fattty hepatocyte degeneration.

The pathologist commented that there were:

"no liver lesions suggestive of aflatoxicosis. Aspergillus clavatus mycotoxin (occurs on sprouting grain and legume seeds) causes nervous signs, but is usually accompanied by brain and spinal cord lesions. There may be other unspecified fungal toxins that cause functional nervous derangement only. TSE negative. No histological lesions suggestive of TSE detected at the brain sites specified in the Australia & New Zealand Standard Diganostic Protcols "TSEs".

A sample of the field pea crop was taken to the local DPI Agronomist, who identified it as Pisium sativum var arvense. It was unclear as to whether the mould on the foliage was significant, and phone calls to many testing laboratories indicated that testing for mycotoxins may be extensive, expensive and ultimately futile.


A diagnosis still had not been made following the property visit, paddock inspection and post-mortem. It was not until I presented this case at the 2012 Production Animal Pathology for Field Veterinarians course, that Field Pea Mania was suggested as the likely cause.

A literature search shows that this condition has been documented twice in the Australian literature, namely by Lenghaus in Victoria in 1987, and Reardon & McKenzie near Warwick in Qld in 2001.

In both of these cases, the crops were dry (or water stressed) when the syndrome was noticed. Reardon & McKenzie noted that the crop in their case received 11mm of rain in the weeks prior to the onset of the manic behaviour. These reported conditions are very similar to those preceding the clinical signs in this case.

Also similar to our case, Reardon & McKenzie ruled out major organ failure, metabolic and infectious causes on blood work during their case. In the case reported by Lenghaus, a post-mortem was performed on a bull that had intermittent convulsions, became comatose and died within 24 hours of becoming unwell. Histopathology of this bull showed cerebral oedema and sporadic cerebral neuronal necrosis. This is different to our case, where there were no abnormalities seen on histopathology of the brain.

In all three cases, the majority of animals that experienced Pea Mania recovered within three days when moved to alternative pasture. Some animals needed to be euthanized due to injuries sustained during the manic episodes.

In both of the previously reported cases, there were no microbial pathogens or endophytes found on or in the plants. This is different to our case, where there was a grey mould noticed on the foliage of the plants. In light of these previous reports, it is thought that the clinical syndrome of Pea Mania is unrelated to this mould but instead that the plant itself generates a toxin, possibly when water stressed and then freshened up with recent rainfall.

Although a rarely reported syndrome, Pea Mania should be considered when any abnormal behaviour is reported by a livestock owner grazing a field pea crop, especially when there is a lack of pathological changes on blood work or post-mortem. As the clinical signs are dramatic and short lived, it would be worthwhile getting farmers to film the animals while the clinical signs are occurring. It would be interesting in future to identify the toxin involved in this clinical syndrome.


  1. Lenghaus C. Peas. Veterinary Pathol. Report (Newsletter, Aust. Soc. Veterinary Pathol.) 1987; 16:13
  2. Reardon CJ, McKenzie RA. Pea mania: deranged behaviour in cattle grazing a pea crop (Pisium sativum var arvense). Australian Veterinary Journal 2002;80:10:617-619


A big thank you to John Glastonbury, Peter Windsor, Robert Barwell and the rest of the 2011 Pathology for Field Veterinarians course who brought Pea Mania up as a probable diagnosis for this case; and to Tim McNee, DPI Agronomist at Nyngan who helped with the identification of the plant.


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