Megaesophagus can occur as a congenital, idiopathic or acquired lesion, but the ASPCA Animal Poison Control Center warns that some toxins have the potential to cause megaesophagus as well.
Megaesophagus secondary to a toxin should be considered in dogs with a history of exposure to any of the following toxins and/or who are showing signs of toxicosis with any of the following toxins.
Botulism (Clostridium botulinum) results from the ingestion of preformed clostridium botulinum type C neurotoxin contained in carrion or spoiled foodstuffs. Signs can appear from a few hours to six days after toxin ingestion.
The botulism toxin causes megaesophagus with regurgitation as well as acute flaccid paralysis with retention of tail wagging.
Tetanus (Clostridium tetani) typically results when the spores are introduced through a wound, puncture or parturition. Signs typically occur from five days to three weeks after exposure.
Animals with tetanus can develop megaesophagus and an esophageal hiatal hernia, and there is a risk of regurgitation and aspiration pneumonia secondary to megaesophagus.
Lead is a heavy metal that can cause gastrointestinal and neurologic signs. Megaesophagus has been reported rarely as a sequelae in cats with chronic lead toxicosis.
Organophosphate toxicosis has been reported to cause megaesophagus in llamas. It could be considered as a rule out in animals with OP exposure, or those showing SLUDDE or nicotinic signs.
Thallium is a heavy metal. Ingestion of mycoplasma agar plates is the most common cause of thallium toxicosis, since thallium-based pesticides were banned in the US in 1972.
Thallium typically causes alopecia, hyperkeratosis, GI upset, cataracts and neuronal dysfunction. In cats it can also cause hepatotoxicity and bone marrow suppression.
Australian tiger snake (Notechis scutatus) is native to Australia and Tasmania. It is an elapid that is highly venomous and can cause paralysis, myalgia, hemolysis, rhabdomyolysis, and renal failure.
A published report with four cases of megaesophagus in dogs shows that in the three dogs who survived, the megaesophagus resolved. The pathogenesis is unknown, but it is thought that myonecrosis of striated muscle may be the cause, rather than neuropathy, due to a lack of other neuropathic signs.
Megaesophagus has not been reported in cats with Australian Tiger Snake envomation, possibly because their esophagus contains smooth muscle, which is not affected by the myotoxic components of the venom.