Rabbit haemorrhagic disease virus 2 (RHDV2 or GI.2, referring to any virus with lagovirus GI.2 structural genes) is a recently emerged calicivirus that causes generalised hepatic necrosis and disseminated intravascular coagulation leading to death in susceptible lagomorphs (rabbits and hares). Previous studies investigating the virulence of RHDV2 have reported conflicting results, with case fatality rates ranging from 0% to 100% even within a single study. Lagoviruses are of particular importance in Australia and New Zealand where they are used as biocontrol agents to manage wild rabbit populations, which threaten over 300 native species and result in economic impacts in excess of $200 million AUD annually to Australian agricultural industries. It is critically important that any pest control method is both highly effective (i.e., virulent, in the context of viral biocontrols) and has minimal animal welfare impacts. To determine whether RHDV2 might be a suitable candidate biocontrol agent, we investigated the virulence and disease progression of a naturally occurring Australian recombinant RHDV2 in both 5-week-old and 11-week-old New Zealand White laboratory rabbits after either high or low dose oral infection. Objective measures of disease progression were recorded through continuous body temperature monitoring collars, continuous activity monitors, and twice daily observations. We observed a 100% case fatality rate in both infected kittens and adult rabbits after either high dose or low dose infection. Clinical signs of disease, such as pyrexia, weight loss, and reduced activity, were evident in the late stages of infection. Clinical disease, i.e., welfare impacts, were limited to the period after the onset of pyrexia, lasting on average 12 h and increasing in severity as disease progressed. These findings confirm the high virulence of this RHDV2 variant in naïve rabbits. While age and infectious dose significantly affected disease progression, the case fatality rate was consistently 100% under all conditions tested.

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Para-aminopropiophenone (PAPP) is a methaemoglobin (MetHb) forming compound used for the lethal control of invasive carnivores and mustelids. By measuring the dose-dependent inhibition of O2 transport arising from the oxidation of haemoglobin (HbFe2+) to MetHb (HbFe3+), we determined the sensitivity of nine bird species to PAPP. A methaemoglobinaemia absorbance index (MAI) was validated in five common bird species to determine thresholds associated with a 99% probability of survival (ST99) and a 50% probability of mortality (LT50). Dose–response trials in high conservation value birds sought MAI values below the ST99 threshold, projecting the LT50 value and avoiding the need for lethal outcomes. Black-backed gull (LT50 = 1784.7) and eastern rosella (LT50 = 1074 mg kg−1) were the most tolerant species, while brown kiwi (LT50 = 8.4 mg kg−1) and weka (LT50 = 9.3 mg kg−1) were the most sensitive. Takahē were of intermediate acute sensitivity (LT50 = 51 mg kg−1), although protracted impacts on haemoglobin were observed in takahē up to 72 h later and associated with PAPP doses as low as 25.6 mg kg−1. In pukeko (LT50 = 138.4 mg kg−1), protracted declines in haemoglobin 72 h later occurred at doses as low as 29.5 mg kg−1, while at higher doses (253 and 112 mg kg−1), deaths resulted after 4–6 days. Based upon PAPP doses that caused acute and protracted responses, we provide estimates for the lowest observable adverse effect level (LOAEL) and no observable effects level (NOEL) for nine bird species.

The introduced Australian brushtail possum is a major vertebrate pest in New Zealand, with impacts on conservation and agriculture being managed largely through poisoning operations. Cholecalciferol (vitamin D3) is registered for use in controlling possums and despite its many advantages it is expensive and relatively inhumane. Combination of a high proportion of aspirin with a low proportion of cholecalciferol was effective in killing high proportions of groups of acclimatised, caged possums: this is attributed to both an unexpectedly high toxicity of the type of cholecalciferol used, and a proposed synergistic mechanism between the two compounds. Death was caused by localised damage to heart ventricles by aspirin, and inhibition of tissue repair by both aspirin and cholecalciferol. The observed toxicosis had lower impact on the welfare of possums than either compound administered alone, particularly aspirin alone. Residue analyses of bait remains in the GI tract suggested a low risk of secondary poisoning by either compound. The combination of cholecalciferol and aspirin has the potential to meet key requirements of cost-effectiveness and humaneness in controlling possum populations, but the effect of the combination in non-target species has yet to be tested.

Context Pindone is used to control rabbits in Australia and New Zealand, but the secondary non-target risks presented by pindone-poisoned rabbits are poorly known. Aims We aimed to generate new data on residual concentrations of pindone in poisoned rabbits for use in a review of the secondary poisoning risks posed to non-target animals in New Zealand. Methods Laboratory rabbits were offered pellet bait containing 0.25 g kg–1 pindone in three trials to simulate a range of bait uptake scenarios: single exposure and low or high chronic exposure. Residual pindone concentrations measured in body tissues of laboratory rabbits that had ingested known exposures of pindone were compared with those in wild rabbit carcasses collected after three pindone-baiting operations. Residues in the faeces of some laboratory rabbits were also measured. Key results Highest concentrations of pindone residues were in the liver and fat tissue of poisoned rabbits, with consistently lower concentrations in muscle tissue. A dose–response relationship between pindone exposure and liver residue concentrations was found only at the highest chronic exposures. Rabbit carcasses collected after field-baiting operations had generally higher pindone residue concentrations than did laboratory rabbits that had ingested known lethal amounts of bait. Unmetabolised pindone was excreted in rabbit faeces. Conclusions The occurrence of the highest residual pindone concentrations in rabbit liver was consistent with the known tissue distribution of anticoagulants in mammals; however, the co-occurrence of similar-range pindone concentrations in rabbit fat has not been previously described. Re-ingestion of soft faecal pellets (caecotrophy) in rabbits that have eaten pindone bait may function as a secondary exposure to increase or prolong their oral exposure to pindone. Some rabbits poisoned following field pindone-baiting operations are likely to have consumed well in excess of a lethal amount of bait. Implications Concentrations of residual pindone in fat and liver of poisoned rabbits suggest that secondary poisoning hazard to some non-target predators and scavengers is high. The lack of field-based assessments of the non-target impacts of pindone is a marked information gap that needs to be addressed.