Paraquat intoxication and associated pathological findings in three dogs in South Africa

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.

FIGURE 1

Tongue of paraquat-poisoned dog showing activated charcoal blackening, necrosis, dorsal tip epithelial sloughing, ulcerations and erosions.

FIGURE 2

Dorsal view of dog lungs showing diffuse extreme dark congestion, oedema, lack of aeration and liver-like appearance: paraquat toxicity.

FIGURE 3

Low magnification of paraquat-induced extreme diffuse pulmonary congestion (star), high protein alveolar oedema (arrowheads) and honeycomb pattern of dilated respiratory bronchioles (arrowheads) and alveolar ducts with surrounding alveolar collapse (star) (HE x 40). Bronchiolar epithelium showing hyperplasia as well as degeneration, necrosis and desquamation into the bronchiolar lumens (horizontal arrows).

FIGURE 4

Interruption of the typical lamellar pattern (arrows) of the secretory vesicles of type II pneumocytes by the deposition of electron-dense material (electron microscopy/ EM).

FIGURE 5

Ultrastructurally visible break (bracket) in a septal membrane with exposure of the interstitial tissue and collagen (star) underlying the alveolar lumen.

FIGURE 6

Fibrin deposits (arrows), desquamated pneumocytes (stars) and cellular debris in the alveolar lumen (EM).

FIGURE 7

Fibroblast (1) within the alveolar septum and an intra-alveolar fibroblast (2) in an area of septal membrane (arrows) disruption. Note dilated endoplasmic reticulum in fibroblasts and interstitial collagen fibrils (stars) (EM).