The field pea (Pisum sativum var avense) is a rapid-growing fodder legume. It is high in protein and energy (16-20% crude protein, 60-65% digestible organic matter and 10MJ/kg DM of metabolisable energy ).
Field Pea toxicity in cattle has been described previously on a property in Warwick, SE QLD, as an acute neurological syndrome encompassing a broad range of clinical signs such as hyperaesthesia, circling, aggression, pollakiuria and aimless charging . In 1987, an incident of deranged behaviour and death was reported in a bull grazing a pea crop in Victoria, and other such incidents in that region involving cattle and lambs have been referred to anecdotally .
In mid-August 2012, a property near Burren Junction in the North West of NSW was investigated for a cause of neurological signs in two, twelve month old, homebred Hereford heifers. The animals at risk included forty heifers that had grazed on a ten hectare paddock of field peas (Pisum sativum var arvense) and fodder oats for fourteen days. The peas were sown at the end of May, and were in the pre-flowering stage of growth when consumed. At the time that the neurological signs were noticed, the crop had been extensively grazed by the mob. As a result, all oats had been eaten and the crop of predominantly field peas was grazed to one third of original height. The cattle had previously grazed a large paddock of dry standing summer grasses with short green pick underneath, and still had access to this.
A nearby, similar paddock of field peas was being grazed by cattle with no clinical signs evident. The field peas in this paddock had not been grazed as low.
Fourteen days after being introduced to the paddock, the property owners noticed that a heifer had isolated herself from the mob and appeared to be repeatedly trying to eructate. By that afternoon, the heifer was showing progressively more severe nervous signs, including circling, agitation when approached and repeated flank licking. A second heifer was also beginning to show signs. Upon advice, the mob was moved from this paddock.
The next day, one affected heifer was yarded along with an unaffected companion heifer for examination. The other affected heifer was impossible to muster due to continued neurological symptoms.
Upon distant examination of the heifer alone in a pen, she displayed obvious hyperaesthesia. As agitation increased, this progressed to a grand mal seizure, with the animal prostrate in lateral recumbency for approximately one minute. During recovery from the seizure, the heifer displayed repeated muscular ticks and jaw chomping. There was no suggestion that the heifer was blind, as she could manoeuver around the yards successfully. When the companion heifer was returned to the pen, the affected heifer quickly calmed. The property owners reported that the clinical signs had improved compared to the previous day.
The affected heifer was able to be restrained in the crush together with the companion animal. A clinical examination was performed, with temperature, heart rate, respiratory rate, lung sounds, urine dipstick and mucous membranes all within normal limits.
Blood analysis revealed no evidence of lead poisoning, sporadic bovine encephalomyelitis (Chlamydiophila pecorum), or metabolic disease. Creatine kinase was elevated (5355U/L). GLDH was very mildly elevated (31 U/L). Urea and creatinine levels were within normal limits, however the urea/creatinine ratio was elevated (0.13). Calcium and magnesium levels were within normal range.
The previous case report of Pisum sativum var arvense toxicity written by Reardon and McKenzie suggested that the toxin mode of action is unknown, but may be related to abnormal rumen modification of an enzyme in the pea resulting in a neurotoxin. The toxin also caused a mild liver dysfunction in most cases . All of the cattle in that study recovered after being removed from the field pea paddock.
A histopathology report of the bull that died after displaying similar neurological signs revealed cerebral oedema, which is consistent with the pathogenesis of many toxicities, including ammonia toxicity .
Key features of this case included the affected cattle recovering rapidly after removal from the field pea crop, normal liver enzymes and parameters of kidney function, and slight elevation of the urea/creatinine ratio.
These features are supportive of the aetiology being a protein related toxicity, possibly akin to the non-protein nitrogen neurotoxicities seen in cattle after consumption of ammoniated feeds (also known as Bovine Bonkers Syndrome). This syndrome is characterised by wildly aberrant behaviour as displayed in this case, and is thought to be caused by the formation of 4-methylimidazole through the action of ammonia on soluble carbohydrates in ammoniated feedstuffs .
A case of neurological signs in cattle similar to Bovine Bonkers syndrome has also been reported in Belgium as a result of excessive intake of raw soybeans, which contain high fermentable carbohydrate and protein content as well as high urease activity. Overconsumption of raw soybeans can cause acute carbohydrate fermentation and excessive ammonia release, resulting in ammonia toxicosis and lactic acidosis .
The previous report stated that Pea Mania occurred after consumption of plants in the pre-flowering stage of growth and this case study supports that epidemiological feature. As for the previous report by McKenzie and Reardon, no environmental factors such as water stress can be attributed to the toxicity in this instance, rather heavy grazing of a high concentration of field pea plant .
The possibility should also be considered that an enzyme reaction occurred within the rumen, creating an unknown neurotoxin unrelated to ammonia.
Further investigation into cases of cattle showing "Bovine Bonkers" clinical signs is required, particularly including analysis of ammonia blood levels in affected cattle, or rumen pH sampling.