Abstract:
Paraquat is a bipyridylium non-selective contact herbicide commonly used worldwide. When
ingestion occurs by humans and animals either accidentally, intentionally or maliciously,
paraquat selectively accumulates in the lungs resulting in the production of oxygen-free
radicals, causing membrane damage and cell death. Intoxicated subjects typically show
progressive and fatal pulmonary haemorrhage, collapse and oedema. In individuals surviving
the acute phase, pulmonary fibrosis develops. Gastrointestinal-, renal- and central nervous
system clinical signs may also occur. Owing to the lack of effective treatment and absence of an
antidote, the prognosis is poor. The clinical presentation, clinicopathological findings and
treatment are briefly described of three dogs from one South African household, intoxicated
with paraquat. Macroscopic and microscopic lesions in one dog that was necropsied, as well
as pulmonary ultrastructure are detailed and illustrated for academic reference. All dogs
presented with tachypnoea and dyspnoea 2–3 days after accidental paraquat ingestion.
Treatment was aimed at reducing gastrointestinal absorption, enhancing elimination by
diuresis and avoiding further oxidative damage by administration of antioxidants. All dogs,
however, became progressively hypoxic despite treatment and were euthanised. Paraquat
toxicity should be a differential diagnosis in dogs with unexplained progressive respiratory
and gastrointestinal signs and renal failure. The local veterinary profession should be aware of
accidental or intentional paraquat toxicity of animals. Existing literature, variations possible in
canine clinical signs, measured parameters, lesions, as well as possible treatments, promising
experimental antidotes and management options are discussed.
