Cattle deaths occurred at Tarraganda and Wallagoot, near Bega, during February 2009 due to suspected toxic plant ingestion. These were investigated by the Bega-Cobargo private veterinarians and Ian Lugton from the South East Livestock Health and Pest Authority.
The deaths occurred during one of the worst summer dry periods experienced in the Bega valley. Prevailing conditions led stock to graze green forbs at the edge of drying dams and swampy areas. As it transpired, these were dangerous places to go for a green pick after hot weather.
Case 1. On 9 February 2009, the District Veterinarian was called to a Wallagoot property to investigate a mortality incident in heavily pregnant mixed-breed beef cows. On arrival there were three dead cows scattered across a paddock from a mob of 63. Two others were recumbent exhibiting nervous signs. The owner reported that 4 hours earlier only two were dead, two were down and one cow was unsteady on her feet and behaving aggressively. Examination of the two downers found them in lateral recumbency. They demonstrated nystagmus, apparent deafness, lack of menace reflex, trembling and a poor response to peripheral pinching.
This mob of cattle had been moved to the paddock around 40 hours earlier on 7 February. The paddock principally contained hayed-off rough grazing pasture, a few eucalypt trees and some Melaleuca spp. scrub. However, one margin of the paddock was bordered by a large receding lake used to irrigate the nearby racecourse (Figure 1). The edge of this lake had the only green grazing in the paddock, mostly forbs, and these showed signs of being recently heavily grazed. The cattle were also watering in the soupy margins of this shallow lake. The water on the paddock side of the dam was covered with a thin and smelly green-brown scum.
One of the recumbent cows was euthanased by firearm and subjected to a detailed necropsy which included brain removal and blood collection for biochemistry. Gross findings included: high protein levels and blood in urine on Dipstix exam; kidney pallor; ventral interlobular emphysema; tiger striping in the large intestine and rectum; 8 month calf in utero with the uterine wall and cotyledons showing patechial haemorrhages; liver with capsular patechiation and an accumulation of yellow oedematous fluid in the hilar area. There was also evidence of scarring, presumably from fluke damage, but no fluke were found in the liver. By the time this necropsy was completed, the other recumbent cow was dead. A 'keyhole' necropsy on this carcass found the liver to be congested and affected by the same hilar oedema seen in the earlier necropsy.
The available history and evidence suggested hepatic encephalopathy subsequent to plant poisoning. On this basis the paddock was searched for suspect plants. This resulted in several of the forbs from the dam edge and a water/scum sample being taken for identification and examination. The serum was taken to the Bega-Cobargo Veterinary Hospital for 'in house' biochemistry due to the urgency of the situation. The results are shown in Table 1, under the heading of Cow 1. This testing showed several serum enzymes to be significantly elevated suggestive of tissue damage, with the rise in GGT particularly suggestive of liver damage.
The laboratory results from samples submitted to the NSW State Veterinary Laboratory (SVL) found the dam water sample to be free of Microcystis spp. or other blue-green algae. The pathologist commented that any water sample containing the amount of volvox (green algae) water fleas, rotifers and other small aquatic fauna, as this sample did, was most unlikely to be toxic.
Histologically the brain was found to be unremarkable. The kidney showed scattered lymphocytes and plasma cells within the interstitium and protein deposits within the Bowman's capsule of the glomeruli. The liver samples from both cows showed extensive diffuse centrilobular necrosis with scattered cytoplasmic proteinaceous inclusion bodies. Portal fibrosis and biliary hyperplasia consistent with chronic liver fluke lesions were also seen. Other tissues examined were either unremarkable or simply confirmed the gross lesions seen at necropsy.
Three days after the initial mortality event, another cow which became recumbent after calving 2 days earlier was shot because she was too weak to rise. The owner removed the kidney and liver and presented these for examination. The kidney appeared normal, however, the liver showed patechial haemorrhages and a distinct lobular pattern suggestive of necrosis. Over the following fortnight a further five jaundiced cows died, bringing the total mortalities associated with this event to 11/63 (17%).
Case 2. A mortality incident on 14 February 2009 occurred in a mob of fifty 15 month-old Holstein-Friesian heifers grazing a dry paddock on the edge of the Bega River at Tarraganda. The stock had been introduced to the paddock 4 days earlier. The paddock gently sloped from a eucalypt scrub at the elevated end down to the river at the other. Adjacent to the river there were a couple of small depressions that had held water, but were now nearly dry (Figure 2). The heifers were watering on the river. To supplement the dry low digestibility pasture, the heifers were provided with a large rectangular bale of oaten hay of good quality.
The heifers appeared fine when checked on 13 Feburary. The next day 4 heifers were found dead in the vicinity of the drying lakes. One other was recumbent, groaning and depressed. On examination by a practitioner from the Bega-Cobargo Veterinary Hospital, the sick heifer was found to have normal vital signs, mucous membrane colour and faeces.
Blood samples for biochemistry were taken from a fresh carcass and from the recumbent heifer. These were processed at the Veterinary Hospital. The biochemistry results are shown in Table 1. Several serum enzymes were significantly elevated and suggestive of tissue damage, with the rise in GGT particularly suggestive of liver damage. Total bilirubin was also elevated. Two carcasses were necropsied. The investigating veterinarian reported an enlarged liver in one and a spleen with ecchymotic haemorrhages in the other.
Although a range of samples were taken from the carcasses and submitted to the SVL, only histopathology on two livers was requested. This was because the biochemistry was already strongly suggestive of acute liver failure. Histopathology confirmed the presumptive diagnosis. The changes in both livers were described as severe, acute and diffuse hepatocellular centrilobular necrosis with subsequent replacement haemorrhages. A phytogenous toxic insult, green cestrum (Cestrum parqui), was suggested as the cause.
At the end of this incident 5/50 (10%) heifers were dead and another two developed photosensitisation.
Plants under suspicion from Case 1 were taken to the DPI office in Bega to assist with identification and to determine their potential for intoxication. Staff of the DPI also visited the paddocks involved in both cases within days of the deaths to search for suspect plants and to determine which had been grazed.
Plants in common to both sites, and that had been grazed included Persicaria orientalis (Princes feather) (Figure 2), Aster subulatus (Bushy starwort) and Alternanthera denticulata (Lesser Joyweed). Pseudognaphalium luteoalbum (Jersey cudweed) had also been consumed in Case 1, and Persicaria lapathifolia (Pale knotweed) (Figure 3), Eleocharis spp. (Spike rush), Lomandra spp. (Mat rush) and Xanthorrea spp. (Grass tree) had also been consumed in Case 2. None of these plants are considered hepatotoxic in poisonous plant lists (McKenzie, 2012).
However, one plant genus that was growing prolifically at these sites and had been grazed heavily by stock was the Persicaria spp. (Smartweeds or Knotweeds, previously Polygonum spp.). In case 2, these were growing up to 2.0 m tall in shallow water-filled depressions near the river as they dried up (Figure 2). As these plants have been recorded as capable of causing photosensitisation, they were suspected as the cause of the acute hepatotoxicity in these two incidents.
In February 2009 the district was in the grip of a drought with ponds and dams rapidly receding. In December 2008, January and February 2009 the district received 19.0, 13.8 and 0.2 mm of rain respectively. The mean monthly rainfall for these same months is 61.3, 52.6 and 98.9 mm. The highest temperatures for February of 37.6 and 44.4 °C occurred on the fifth and seventh days respectively (Table II). The temperature on the 7th being a February high temperature record for Bega, which has mean maximum temperature of 26.4 °C during this month. This was the day of the Black Saturday bushfires in Victoria.
This is the first time that Persicaria spp. (Polygonacae) have been recorded as responsible for deaths from acute liver failure. However, Keith Newby (pers. comm.), former District Vet, Grafton, previously suspected that the ingestion of large quantities of Persicaria spp. had caused the death of cattle in two incidents at Jackadgery and Upper Copmanhurst. Despite smartweed being common in the mid-north coast area of NSW, associated cases of photosensitisation are uncommon (Ian Poe, Senior District Vet, Kempsey, pers. comm.). In this region smartweeds are widely accepted as a cause of photosensitisation by both veterinarians and producers. However, in the few cases where biochemistry has been conducted there has been no evidence of liver damage.
There are other well recorded phytogenous causes of acute liver failure. These include the blue-green algae (Microcystis aeruginosa), green cestrum (Cestrum parqui), lesser loosestrife (Lythrum hyssopifolia), burrawang (Macrozamia communis), or poison peach (Trema tomentosa). However, none of the aforementioned toxic plants were identified in association with these incidents.
Persicaria spp. have long been suspected of causing photosensitisation in Australian livestock (McKenzie et al, 1988). Because Buckwheat (Fagopyrum esculentum), another member of the Polygonacae, is known to cause primary photosensitisation, this had added to the level of suspicion.
However, in one documented mortality incident in Queensland during late 1986 (McKenzie et al, 1988) elevation of serum GGT (87 IU/l) and depressed albumin levels (23 g/l) were found in photosensitised cattle that had grazed P. lapathifolium and P. orientalis growing on the edge of the receding lake Wivenhoe. The clinical biochemistry suggesting that the photosensitisation was secondary to liver damage. However, a feeding trial of the suspect plants to weaner steers in late January and early February 1987, failed to reproduce disease or to demonstrate any significant changes in serum GGT or albumin. This led the authors to speculate that the toxin involved was either labile in harvested plants or that the concentration of toxin varied over time.
I believe that the concentration of toxin does vary over time. In these two Bega incidents, almost occurring simultaneously, there is presumptive evidence from the weather record to suggest that heat/moisture stress on these two smartweed species (or at least P. orientalis) significantly increased their hepatotoxicity. These poisoning cases were preceded by warm to extremely hot days and warm nights.
The weather records for Gatton, 35 km from Lake Wivenhoe, around the time of the reported mortality incident and subsequent feeding trial (McKenzie et al, 1988) were examined. These records showed that the area experienced hot temperatures, with many days' maxima over 30 oC. However, what was remarkable during the period of the feeding trial, was that 20 mm of rain fell 5 days before the start of the feeding trial, with another 95 mm falling during the 15 days of smartweed harvesting. If similar rainfall occurred at the harvest site, it is unlikely that the smartweed would have been moisture stressed. This could explain the failure of the trial to demonstrate any ill-effects on the stock being fed.
Given these incidents, caution should be advised when stock have access to substantial stands of smartweed. Particular care should be taken when moving stock after or during hot dry weather, especially hungry animals, into paddocks with limited grazing, but with to access stands of smartweed. Such conditions may lead to an outbreak of photosensitisation or possibly to deaths.
An omission during this investigation was to fail to send suspect plants off for identification to the Sydney Botanic Gardens, along with a request that these be kept as voucher specimens. This process assists in confirming the identification of the plants under suspicion and helps in the development of a publication arising from such an investigation.
I kindly acknowledge the valuable assistance provided by Hayden Kingston, District Agronomist, and Rick Jennings, Field Assistant of DPI Bega, and the staff of the Bega-Cobargo Veterinary Practice during this investigation.