There is well defined syndrome associated with the ingestion of Birdsville Indigo (Indigofera linnaei) or Creeping Indigo (Indigofera spicata). Birdsville Indigo occurs across a large part of central and northern Australia. It also occurs throughout southeast Asia. Creeping Indigo is found in the south eastern USA, particularly in Florida. Creeping indigo toxicity was recently reported in Hawaii. It is suggested that abnormal signs occur after 2 weeks consumption of 4.5 kg of green plant daily. Most poisoning in the US occur in summer and early autumn.
Recently there has been severe disease seen in dogs fed horse meat contaminated with Birdsville Indigo toxins.
Toxins
The plants contain 2 important toxins. The first is indospicine, which inhibits the production of nitric oxide. Nitric oxide is important for neurotransmission as well as maintenance of blood vessel tone (vasomotor tone). It is thought that indospicine is responsible for many of the non-neurologic signs of poisoning, such as mucosal and ocular ulceration, and liver damage. Indospicine is a non-protein amino acid. It is toxic to the liver because of antagonism to the essential amino acid arginine, with which it competes. Horses, in contrast to dogs, are relatively resistant to the liver damage.
The second toxin is 3-nitroprionate (3-NPA), which blocks the TCA (Krebs) cycle by irreversibly blocking succinate dehydrogenase, the enzyme that catalyses the oxidation of succinate into fumarate (the 6th step in the cycle). 3-NPA is thought to be responsible for most of the neurologic signs of poisoning.
Signs of poisoning
Non-neurological signs. Common signs include a loss of appetite, weight loss, elevated heart and respiratory rates, and dehydration. The eyes are commonly affected with ulceration of the cornea, corneal opacities, watery discharge from the eyes (epiphora), and squinting. There is severe ulceration of the tongue and gums leading to profuse salivation (ptyalism) or foaming from the mouth, and feed retention in the cheeks (quidding), and halitosis.
Neurological Signs. Earliest signs of poisoning include lethargy with lowered head carriage progressing to behaviours including compulsive circling and head pressing. There may be a loss of balance with head and neck twisted to one side. Nystagmus and rhythmic blinking may be present. The gait also becomes abnormal with incoordination (ataxia) and paresis (weakness) in all four limbs, sometimes a pacing gait with toe dragging. There may be a hypermetric, goose-stepping gait in the forelimbs. Affected horses may adopt an abnormal posture at rest. Horses can continue to progress leading to recumbency with an inability to rise, loss of consciousness, seizures and eventually death.
Diagnosis and Management
The diagnosis is based on the spectrum of signs described above with access to the offending plant. In Florida they measure indospicine levels, but this is not available commercially.
Animals that are removed from the pasture typically recover completely, with the exception of some persistent gait abnormalities. Dietary supplementation with arginine-rich feeds is recommended, including peanut meal, lucerne/alfalfa chaff, and gelatin. Intravenous infusions of L-arginine (20% in saline) have been tried but positive effects remain speculative.
Dogs are very sensitive to the effects of indospicine where a severe hepatopathy results.
Tags: Neurology; Toxicities