Assessing the sustainability of anticoagulant-based rodent control for wildlife conservation in New Zealand : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Conservation Biology at Massey University, Palmerston North, New Zealand
Brodifacoum is used extensively to control invasive rodent pest populations in New Zealand.
However, there are major concerns regarding non-target poisoning due to brodifacoum, its
high persistence and risk of emergence of resistance in targeted rodents. In the present study,
I assessed brodifacoum resistance in ship rats and house mice using blood-clotting response
(BCR) tests. Mature ship rats of both sexes were live trapped from Akatarawa forest, an area of
no known anticoagulant use history in Wellington. A ranging study was performed whereby
healthy ship rats were administered increasing doses of brodifacoum to calculate the effective
dose, which in ship rats is considered to be the dose giving a 3.6-fold increase in blood-clotting
time (this proportional increase is referred to as the International Normalised Ratio, or INR).
An unexpectedly high effective dose of 2.9 and 3.8 mg/kg was calculated for male and female
ship rats respectively. The calculated effective dose was used to access brodifacoum
susceptibility in ship rats captured from nine areas of known brodifacoum use history in the
Wellington region and Palmerston North. A total of 54 ship rats were successfully tested, and
there was a significant decrease in INR with increasing number of years of brodifacoum use in
an area. Despite this evidence of anticoagulant resistance revealed by BCR tests, no mutations
conferring anticoagulant resistance were found in VKORC1 gene sequences in tested ship rats.
This suggests that resistance may be caused by other pathways.
Similarly, BCR tests were performed in house mice using the effective dose from
published literature, i.e. 0.52 mg/kg for males and 0.46 mg/kg for females. Twenty out of 26
house mice assessed were found to be resistant to administered dose of brodifacoum,
meaning the INR was >5. However, no relationship was observed between the INR value and
the number of years of brodifacoum use in an area. Seven of the tested mice were found to
have a non-synonymous mutation, Tyr139Cys in exon 3 of the VKORC1 gene. The house mouse
individuals carrying this mutation are known to be fully resistance to all first-generation
anticoagulants and a second-generation anticoagulant, bromadiolone, but only minor
resistance is known to occur towards more potent second-generation anticoagulants.
At present, only technical resistance to brodifacoum has been reported in ship rats and house
mice, and brodifacoum may still be used effectively to control these rodent populations.
However, continual use of brodifacoum may encourage further resistance. Effective long-term
control of anticoagulant-resistant populations can only be achieved by use of alternative non-