Ant and roach baits
The product names may vary, and the containers may be referred to as chambers, discs, stations, systems, traps, baits, or trays, but most ant and roach baits use an attractant (often peanut butter), a sweetening agent, and bread. And while these baits
once contained compounds that are relatively highly toxic to mammals (e.g. arsenic trioxide, lead arsenate), the most common insecticides used in ant and roach baits today are boric acid, avermectin,
fipronil, hydramethylnon, propoxur, and sulfluramid.1
Because of the low concentration of the insecticide and the small size of the bait, serious toxicosis in mammalian pets ingesting
the baits is not expected.4 In many instances, the risk of foreign body obstruction from the plastic or metal part of the container is of greater concern
than the active ingredients. Signs of ingestion are usually limited to mild GI upset and do not require specific treatment.
The three main types of rodenticides are those containing anticoagulants (warfarin, brodifacoum, diphacinone [also called
diphenadione]), those containing bromethalin, and those containing cholecalciferol.
Anticoagulant rodenticides are probably the most commonly used rodenticides in the world. Ingesting an anticoagulant rodenticide
can block vitamin K-dependent clotting factor synthesis by inhibiting the 2,3-epoxide reductase enzyme, which results in a
coagulopathy three to five days after ingestion (possibly sooner in immature animals).5
Ingesting a bromethalin-containing rodenticide may cause vacuolization and severe spongiosis of the white matter within the
CNS and cerebral edema.6 Bromethalin ingestion can cause signs ranging from tremors and seizures (convulsant syndrome) to weakness and paralysis
(paralytic syndrome). Convulsant syndrome usually occurs at doses of 2.3 mg/kg and higher. Paralytic syndrome is more likely
when a dog ingests a lower dose.6
Ingesting cholecalciferol-containing rodenticides can increase dogs' serum calcium and phosphorus concentrations, potentially
leading to acute renal failure and tissue mineralization.7
Perform gastric decontamination procedures (induce emesis and administer activated charcoal with a cathartic) as soon as possible
after any rodenticide ingestion. Do not induce emesis in symptomatic animals (e.g. bleeding or seizing animals).
Treat anticoagulant-rodenticide ingestion with vitamin K1 orally for 14 to 30 days, depending on the specific active ingredient. It is recommended to evaluate the one-stage prothrombin
time at 48 hours after the last dose of vitamin K1. An alternative to treatment is to monitor the prothrombin time at 48 and 72 hours after ingestion, and if elevated, initiate
vitamin K1 therapy.8 Animals that have developed a coagulopathy may require whole blood or plasma transfusion and oxygen. The prognosis for animals
that have developed a coagulopathy is guarded and depends on the bleeding site.
Because no specific treatment for bromethalin toxicosis is available, aggressive decontamination is critical. If clinical
signs develop, they are difficult to treat, and the patient's prognosis is guarded. Therapy is directed at resolving cerebral
edema and addressing seizures, usually by administering corticosteroids, furosemide, mannitol, and diazepam. Since the cerebral
edema from bromethalin toxicosis is intramyelinic,6 it does not respond well to standard therapy. Mannitol, corticosteroids, and furosemide may temporarily lower cerebrospinal
fluid pressure, but signs often progress once these treatments are discontinued.
In rats, an extract of Ginkgo biloba was shown to reduce the development of cerebral edema and brain lipid peroxidation when administered orally immediately after
gavage with a lethal dose of bromethalin.6 Whether G. biloba or its extracts would influence the development of clinical signs in dogs with bromethalin toxicosis is unknown, but you
may wish to consider it in patients in which other options have been unsuccessful.