In several recent studies, the clinical suspicion of AC intoxication based on a healthy cat roaming free outdoors suddenly developing typical neurological symptoms correlated well with presence of AC in blood serum samples, indicating that there was a good correlation between clinical suspicion of AC poisoning and correct diagnosis.
Wild mice consume significantly more rodenticide bait than presumed in the EU assessment report (2009) (12) The calculated amount of AC–containing baits consumed by the wild mice after being trapped as described in the Windahl et al. study (1), is close to the expected daily amount feed intake in laboratory mice. Thus, the results in the study contradict the assumption that the mouse will not eat large portions of the poison bait due to its rapid narcotic effect presented in the EU assessment report.
AC metabolism was to our knowledge studied for the first time by Bernhoft et al. (6) and Windahl et al. (1) One glucuronic acid conjugate of AC was detected in feline urine from feline cases of AC– poisoning, however the studies support the theory that deficiency in enzymes responsible for conjugation reaction could make the cats more susceptible and prone to AC poisoning compared to e.g. dogs.
The calculated intake of bait by wild mice and calculated ingested amount of AC in the studied cats after ingesting poisoned mice may result in exposure below the reported LD50 for cats. However, the collected data on exposure of AC show that harmful symptoms may appear at considerably lower doses than LD50 (1). This shows that secondary poisoning of cats from ingestion of mice is possible and that the ingested doses of AC can be fatal due to heat loss, disorientation, and possible anaesthesia. For non-target wild animals that remain in a poisoned state in cold environments, the prognosis is characterised as poor. Results of the studies therefore also highlight the risk of AC poisoning to other non-target species, especially birds of prey that may be even more susceptible than cats.