Additional toxins for feral pig (Sus scrofa) control: Identifying and testing Achilles' heels

Abstract

A literature review was conducted in order to identify unique weaknesses in the physiology or metabolism of pigs that could be targeted with specific chemicals (i.e. an ‘Achilles’ heel’ search). A promising weakness identified was the species’ susceptibility to methaemoglobin-forming compounds, most likely related to their uniquely low levels of methaemoglobin reductase. Further examination revealed that sodium nitrite is a cost-effective, readily available methaemoglobin-forming compound that is highly toxic to domestic pigs, which has caused numerous accidental poisonings. Pen trials on pigs showed that sodium nitrite delivered by gavage (>90 mg kg−1) and freely consumed in bait (>400 mg kg−1) caused rapid and lethal rises in methaemoglobin. Sodium nitrite appeared to be more humane than currently used toxins, with deaths following bait consumption being considerably quicker and with fewer symptoms (within 80 min of clinical signs beginning; clinical signs including infrequent vomiting, lethargy, ataxia and dyspnoea). The review also identified a second deficiency in the metabolism of pigs, namely high sensitivity to selective inhibition of cytochrome P450 liver enzymes. This leads to potentially lethal interactions between various drugs, such as two antibiotics, monensin and tiamulin. A pen trial confirmed that the antibiotic combination in a single gavage dose was reliably and rapidly lethal to pigs. However, its utility as a pig toxin is low, because it was unpalatable to pigs when delivered in bait and appeared to cause pain and suffering (leading to the early termination of pen trials). The findings presented here demonstrate the potential of sodium nitrite as an additional feral pig toxin.