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VERTEBRATE TOXIC AGENTS

Free-ranging Australian mammals may be exposed to a range of vertebrate toxic agents (VTA) used for feral predator control (e.g. sodium fluoroacetate (1080), para- aminopropriophenone (PAPP), sodium cyanide).

A range of factors may influence the risks of exposure and poison­ing, including diet, foraging behaviour, bait design and species specific LD50 (mg/kg) (de Tores et al. 2011; Mall- ick et al. 2016). Use of canid-pest ejectors may reduce risk for smaller species (particularly dasyurids as most VTAs are meat-based) such as eastern quoll (Dasyurus viverri- nus); however, larger species, such as the spotted-tailed quoll (D. maculatus) and Tasmanian devil (Sarcophilus harrisii), are predicted to have sufficient jaw pulling power to trigger these devices (Mallick et al. 2016).

Table 19.1. Other plant toxicoses reported in Australian mammals

bgcolor=white>Clinical signs included anorexia, depression, lethargy and jaundice, and photosensitivity dermatitis on the ear pinnae margins, eyelids, muzzle and scrotum. Liver enzymes and bilirubin elevated. Jaundice evident at necropsy. One animal recovered with supportive care, two others died.
Plant and toxin Species affected Clinical signs and treatment
Rhododendron spp.1

Andromedotoxin

Western grey kangaroo (MC) (Macropus fuliginosus) GI pain, inappetence, bradycardia, coughing, dyspnoea, ataxia. Stifle adduction, twisted upper torso, stood with abdomen hunched. Complete recovery following supportive therapy.
Oxalis pes-caprae2~5 (Sour sob)

Calcium oxalate

Eastern ring-tailed possum (MC) (Pseudocheirus peregrinus) Scaly-tailed possum (MC) (Wyulda squamicaudata)

Swamp wallaby (MC) (Wallabia bicolor) Gilbert's potoroo (Potorous gilbertii) Southern hairy-nosed wombat (Lasiorhinus latifrons)

Gross and microscopic lesions in oxalate poisoning are renal: radial pale streaks in the cortex, chronic sclerosing nephrosis and oxalate crystals in tubules associated with epithelial degeneration.
In the Gilbert's potoroo, multifocal acute tubular necrosis and suppurative intratubular nephritis with intratubular crystals (consistent with oxalate). Endstage liver cirrhosis also present.
Taxus baccata6 (Yew)

Taxine

Red-necked wallaby (Notamacropus rufogriseus) Renal, myocardial, hepatic and lung congestion and acute enteritis. Microscopic lesions in the brain indicated circulatory disturbance.
Lantana camara7 (Lantana) Triterpenoids Red kangaroo (MC) (Osphranter rufus)
Parsonsia straminea8 (Monkey rope, Silk pod) Unknown toxin Eastern grey kangaroo (MC) (M. giganteus) Clinical signs included ataxia, grinding of teeth and cerebral oedema.
Duranta erecta4

(Golden dewdrop, Geisha girl) Unknown toxin

Kangaroo (unknown species) Clinical signs included drowsiness.
Camellia sp.9

Unknown toxin

Common brush-tailed possum (Trichosurus vulpecula) Ingestion of blossoms. Clinical signs included diarrhoea, focal hepatic necrosis and death.
Senecio jacobaea4 (Ragwort) Pyrrolizidine alkaloids Pygmy possum (Cercartetus spp.) Hepatosis presumptively related to the feeding of honey from regions with ragwort.
Carrichtera annua10

(Ward's weed)

Glucosinolates

Southern hairy-nosed wombat (Lasiorhinus latifrons) Hepatopathy including megalocytosis, hepatocellular necrosis, bile duct hyperplasia, cholestasis, bridging fibrosis, weight loss, alopecia, anaemia.

1Hough 1997; 2Johnson and Hemsley 2008; 3Ellis etal.

1983; 4Ladds 2009; 5Woolford 2012 pers. comm.; 6Barker etal. 1963; 7Johnson and Jensen 1998; 8Hanger et al. 2001; 9Presidente 1978; 10Camp et al. 2020

MC = managed care.

2.1 Sodium fluoroacetate (1080)

Wildlife mortality may occur as a result of ingestion of 1080 baits used to control vertebrate pests such as Euro­pean rabbits (Oryctolagus cuniculus), pigs (Sus scrofa), European foxes (Vulpes vulpes) and dogs (Canis famil- iaris) or after eating fluoroacetate-containing plants such as Gastrolobium spp. (Speare et al. 1989) and Oxylobium spp. Most of the plant species known to produce this compound are found in the south-west of WA. It is a rapid-acting toxin, impairing cellular respiration, producing CNS anoxia and cardiovascular disturbance. Clinical signs of 1080 poisoning are typically seen about 30 min to 3 hr following ingestion and death may occur within hours to several days. Signs include dyspnoea, tremors, muscle spasms and terminal convulsions.

Concerns about the impact of this poison on non-tar- get species led to investigations into the sensitivity of native wildlife to 1080 (McIlroy 1981a) and species-spe­cific differences in the LD50 of 1080 have been demon­strated (McIlroy 1981b; McIlroy 1982a; McIlroy 1982b;

McIlroy 1983). Susceptibility to poisoning with 1080 depends on a combination of the species of animal, age (juvenile animals appear to be more susceptible) and geo­graphical location (McIlroy 1981a). For example, the western quoll (D. geoffroii), yellow-footed antechinus (Antechinus flavipes) and red-tailed phascogale (Phas- cogale calura), which feed on insects that consume Gas- trolobium leaves, are relatively resistant (Holz 2008), indicating an evolutionary adaption to the toxin.

Macropods can be non-target casualties of baiting campaigns, although historically red-necked wallabies and Tasmanian pademelons (Thylogale billardierii) have been specifically targeted to manage overabundant popu­lations (Vogelnest and Portas 2008).

Many smaller mar­supials, and Australian native and introduced rodents that have been tested, are more sensitive to 1080 poison (McIlroy 1982b). There is no antidote or specific treat­ment; sedation, fluids, activated charcoal and other sup­portive care may be effective.

2.2 Anticoagulant toxins

Anticoagulant poisons can be classified as 1st-generation (warfarin, coumatetralyl, pindone) or 2nd-generation (brodifacoum, difenacoum, bromadiolone). The 1st-gen- eration anticoagulants require multiple doses to exert their effect whereas the 2nd-generation anticoagulants are more toxic and normally only require a single dose to exert their effect, which, in both cases, results in death within 1-2 wks. Anticoagulant rodenticides suppress the vitamin K cycle that occurs in the liver, inhibiting the production of clotting factors in the blood and result in widespread haemorrhage (McLeod and Saunders 2013). Poisoning can occur in non-target species as a result of primary exposure when consuming bait or secondarily through ingestion of poisoned animals.

Pindone, commonly used for controlling European rabbits, can cause accidental toxicity in macropods fol­lowing ingestion of pindone-laced baits. Death secondary to coagulopathy has been observed in macropods, south­ern brown bandicoots (Isoodon obesulus) and common brush-tailed possums, although the latter species is con­sidered relatively resistant (Jolly et al. 1994). Signs in common brush-tailed possums include dyspnoea, exer­cise intolerance, pale or cyanotic oral mucus membranes and haemorrhage into the GIT and lungs. During a mass toxicity episode in several species of macropods, furless PY with extensive subcutaneous and internal haemor­rhages were found dead in the pouch of affected but live females, suggesting pindone was present in the milk (Vogelnest and Portas 2008). In trials on common brush­tailed possums, using brodifacoum, average time to death was 21 d (Littin et al. 2002) with clinical signs of external bleeding, weight loss and lethargy appearing 14 d after ingestion.

Reduced feed intake, lethargy and display of abnormal postures suggest possums experience distress for at least 6 d before death (Littin et al. 2002). Recent common brush-tailed possum cases in Qld exhibited similar clinical signs (Grillo et al. 2016). Some possums, with PCVs ranging from 9 to 12, recovered after treat­ment with blood transfusion and vitamin K injections. Treatment involves correction of the hypovolaemia with crystalloids and/or homologous plasma or blood transfu­sions. Vitamin K (2.5-5 mg/kg) SC and then PO for 14 d (Johnson and Hemsley 2008).

2.3 Cyanide toxicity

Australia and New Zealand are facing resistance to the continued use of 1080 because of animal welfare concerns and other unintended effects such as collateral toxicity in domestic animals and increasing target species tolerance to 1080 poison. As a result, encapsulated cyanide pellets have been trialled to investigate the effectiveness of con­trolling tammar wallabies (N. eugenii) and red-necked wallabies, which are considered a pest in New Zealand. Mean time to death was 13.5 min in tammar wallabies and 22 min for red-necked wallabies. The onset of signs and effects were similar to those previously reported in possums following ingestion of cyanide. Toxin use for pest control will be sustained only if the control tools used are humane. On that basis, cyanide offers an alter­native to other toxins, including 1080, for the control of wallabies in New Zealand as it is fast-acting and breaks down rapidly in the environment (Eason et al. 2010).

2.4 Para-aminopropiophenone (PAPP) toxicity

PAPP is available only for European fox and wild dog control in Australia as meat-based blocks in two sizes (Animal Control Technologies, Somerton, Vic.). When ingested it is absorbed rapidly from the GIT and trans­ported to the liver. Foxes and dogs (and other carnivores) can convert PAPP to a hydroxylated version, PHAPP (para-hydroxyaminopropiophenone), which is the active compound. PHAPP is taken up by erythrocytes where it causes the rapid conversion of haemoglobin to methae­moglobin, leading to anoxia and death with 1-2 hr (McLeod and Saunders 2013).

First visible signs are pallor or cyanosis of mucous membranes and tongue. Lethargy, stupor and deteriorating consciousness occur as methae­moglobin levels approach 55%. Higher levels may cause cardiac arrhythmias, circulatory failure and neurological depression, while levels of 70% and above are usually fatal. The LD50 for foxes and dogs is between 25 and 50 mg/kg (McLeod and Saunders 2013). Of a range of Australian native mammals assessed for the effects of orally administered PAPP, only the southern brown ban­dicoot and spotted-tailed quoll had lower LD50 than dogs (Fisher et al. 2008). The LD50 for fat-tailed dunnarts (Sminthopsis crassicaudata), brown antechinus (A. stuar- tii) and Tasmanian devils were 2-4-fold greater (McLeod and Saunders 2013). Unlike 1080, which is available in various formulations that improve target specificity (e.g. ejectors), in Australia PAPP is only available as meat­based blocks. These would be attractive and palatable to other species. PAPP is absorbed and metabolised rapidly and tissue concentrations of PAPP in poisoned animals are low, therefore the risk of secondary poisoning is also low. Methylene blue given PO or IV can act as an antidote (McLeod and Saunders 2013).

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Source: Vogelnest L., Portas T. (Eds.). Current Therapy in Medicine of Australian Mammals. CSIRO,2025. — 848 p.. 2025

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