Steroidal or lithogenic saponins are a relatively common plant toxin poisoning of ruminants in New South Wales (NSW). Common sources of saponins in NSW include Panicum and Tribulus spp. Regault (1990) reports a case in sheep grazing Bambatsi panic (Panicum coloratum) in the Goondiwindi region of Queensland. McKenzie (2002) lists both Bambatsi panic and Gatton panic (Megathyrsus maximus) as sources of saponins, and Bambatsi panic as an important species for poisoning. Both of these grass species are commonly sown in pasture mixes in northern NSW (Harris et al. 2014). Saponins cause crystal-associated cholangiohepatopathies and secondary photosensitisation. McKenzie (2002) indicated poisoning commonly involves young ruminants, especially lambs grazing stressed pastures or crops.
This paper reports an investigation into saponin poisoning in black-headed Dorper lambs following introduction to mature Bambatsi panic dominated pasture on a property in the Wee Waa district of NSW in March 2018.
Two adjacent 30 ha paddocks were sown in March 2017 with a Bambatsi panic, Gatton panic and Premier digit grass (Digitaria eriantha) mix. Due to conditions at pasture establishment, by the time of poisoning, the pasture consisted of predominantly Bambatsi panic. A small area of Tribulus spp. was present in one paddock but largely absent in the other.
At the time of poisoning the pasture was mature, 40–70 cm high and setting seed. Examination of the paddocks showed heaviest grazing of the Gatton panic, followed by Bambatsi panic. The digit grass was least grazed. These observations suggest the sheep had preferentially grazed the Gatton panic, then the Bambatsi panic. In the one paddock where Tribulus spp. was present, this plant had been heavily grazed suggesting that it had also been selectively grazed by the sheep. Perhaps critically, at the time of introduction there had been 40 mm of rain. As a result, all grasses were actively growing and new green shoots were developing. At the time of paddock inspection this green regrowth from the base of the plants appeared to have been preferentially grazed and the older longer leaves were generally ungrazed.
The black-headed Dorper lambs from two mobs were grazing the adjacent paddocks. One mob consisted of 500 weaned lambs aged 4–8 months. The other mob consisted of 700 Dorper ewes and 900 unweaned lambs aged 4–8 months. The history and grazing management of both paddocks was similar and both mobs were introduced to their respective paddocks on the same day.
Deaths were first noticed 10 days after introduction to the pasture with 24 dead lambs across both mobs. When the deaths commenced was unclear as the mobs had not been checked since introduction. However, the degree of carcass decomposition suggested the first deaths had occurred 5–8 days after introduction. The sheep were immediately removed from the pasture.
At 13 days after introduction 50 lambs had died and another 80–90 were clinically affected. After this point, no previously unaffected lambs developed clinical signs. By 20 days after introduction 90 lambs were dead and 40–50 clinically affected. Deaths continued for two months and eventually almost all clinically affected lambs died (approximately 140 lambs per group). Both mobs of lambs were affected at similar rates. No ewes were observed with clinical signs.
A property investigation was undertaken when deaths were first observed. It included an examination of clinically affected lambs, an autopsy and paddock inspection. Treatment consisted of immediately removing all sheep from the paddocks and placing the lambs in a well-shaded paddock with only dry grasses. The ideal treatment of removal from any direct sunlight was not possible due to the absence of a suitable shed.
Clinically affected lambs showed lethargy, shade seeking and yellowing of mucous membranes. Photosensitisation damage to skin was not a prominent feature (possibly related to protecting black skin).
The autopsy found extensive yellowing of all tissues and a swollen orange liver. Tissue samples were submitted to the NSW Department of Primary Industries State Veterinary Diagnostic Laboratory. Liver histopathology was consistent with saponin poisoning but pathognomonic crystals were not identified, potentially due to autolysis of the tissues. No other possible causes of the clinical signs and gross pathology were identified.
The classic reported conditions for saponin toxicity of Bambatsi and other panic pastures are grazing short pasture that is actively growing, but which has then become moisture stressed (McKenzie 2002). These were the circumstances for an earlier poisoning incident in this flock (10 dead, eight clinically affected from 220 Dorper lambs) that occurred on the same paddocks in December 2017. To manage the risk of future poisonings the owner elected to restrict future grazing by lambs of mature pastures.
In contrast, the March poisonings outlined in this paper demonstrated that poisoning of lambs grazing flowering stands of Bambatsi panic is possible. The observations suggested poisoning can occur if the pasture is actively growing and lambs are able to preferentially graze regrowing shoots. It also demonstrates that poisoning can occur without the pasture showing visible signs of moisture stress.
The role of Gatton panic in this poisoning incident was difficult to quantify. While preferentially grazed, Gatton panic plants were less than one in 20 plants, and as such would have been a small part of the diet. McKenzie (2002) did not categorise Gatton panic as an important species for poisoning. In contrast, Bambatsi panic was categorised as an important species, and it was the major component of the grasses observed to have been grazed.
The following measures were recommended to manage the risk of future poisonings on Bambatsi panic-dominated pastures:
These measures were successful in preventing poisonings for the following five years. This period covered a range of conditions including two years of severe drought and three years of above average rainfall.
The absence of photosensitisation-caused damage to skin as a prominent clinical sign in a case with significant mortalities was unusual but consistent with the current understanding of secondary photosensitisation.
The deep black pigmentation of the head and upper neck of the lambs most likely prevented the most sensitive areas from being affected. However, shade seeking was a prominent feature of the affected lambs.
Further, the absence of skin damage in this case supports the premise that it is liver damage not photosensitisation that kills most lambs with saponin poisoning.
The susceptibility of lambs and the absence of poisoning in adult sheep with Panicum spp. was noted by Button et al. (1987). They also indicated that age-related susceptibility has been used as a management tool for grazing of P. coloratum. In contrast, in both the author’s experience and Button et al. (1987) saponin poisoning from Tribulus spp. affects sheep of all ages.
The literature fails to explain this strong age-related susceptibility. In general, younger sheep are more susceptible to toxicities due to differences in ruminant metabolism and general resilience. However, these differences do not explain the strict immunity of adult animals to Panicum spp. poisoning. The selective grazing, in this case, raises the possibility that differences in grazing behaviour may contribute to this age-related susceptibility.
Overall, the risk factors for poisoning in this case are likely to have been actively growing pasture, the potential for selective grazing of new shoots and grazing by lambs. The grazing management measures outlined earlier may be sufficient to manage these risks, and thus future poisonings on Panicum spp. dominated pastures.