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Locoweed is a perennial herb that grows in clumps with pinnately compound leaves and lacking tendrils. It has blue, white, or purple pea-like flowers and short or long, often inflated pods. Seeds are kidney-shaped and retain vitality for 40+ years. Taxonomy and proper identification are difficult since at least 372 species of Astragalus exist, most being toxic. Astragalus is the largest of the legume forms in the U.S.. 

Toxic principle.  Locoweeds contain one of three toxic fractions.

ü      Miserotoxin, a glycoside, is hydrolyzed in ruminants to a toxic form known as 3-nitropropanol.  Toxicity may be due, in part, to nitrite released from the 3-nitropropanol or to an unknown neurotoxic principle.  A. emoryanus and A. miser are species with high concentrations of miserotoxin.

ü     Swainsonine, an alkaloid found in many locoweeds, inhibits a-mannosidase.  Inhibition  leads to increased lysosomal accumulation of oligosaccharides, resulting in neuronal swelling and vacuolization.  Examples of swainsonine-containing locoweeds include A. lambertii, A. mollisimus, A. lentigenosus, and Oxytropis.

ü     Selenium.  Some species of Astragalus and Oxytropis are selenium accumulators

Toxicity.  Fresh plants are toxic.  The toxicity is gradually lost as the plant dries, except for that of selenium accumulators, which are not affected by drying.  Swainsonine poisoning occurs after 2 weeks or more of ingestion.  Cattle and horses may become habituated to locoweed and seek it out, even when good forages are available.  Swainsonine may be passed in the milk.

Diagnosis

Clinical signs

Miserotoxin

ü      Neurologic signs.  Demyelination of the posterior spinal cord causes incoordination, hypermetria, ataxia and clicking of the dewclaws (a condition known as "cracker heels").

ü      Respiratory signs include emphysema (primarily in sheep), dyspnea and cyanosis.  Sudden collapse and death may occur within 4-24 hours in animals poisoned by large doses

Swainsonin

ü      Neurologic signs.  Affected animals exhibit ataxia, emaciation, staggering, and proprioceptive deficits.  Horses may become belligerent or startle violently as a result of mild stimuli

ü      Emaciation

ü      Vision may be impaired by decreased lacrimation and retinal degeneration

ü     Immunosuppression of the cellular immune system can occur.

ü      Abortions are common in mid to late pregnancy, and teratogenic effects (e.g., contracted tendon) also occur.

ü      Male infertility with reduced spermatogenesis is reported.

Selenium accumulators are discussed in the metals lectures.

Laboratory diagnosis.

Miserotoxin:  non-specific

Swainsonine:  decreased serum a-mannosidase activity combined with ­ alkaline phosphatase activity and  albumin and ¯ T4 and T3.

Lesions

Misertoxin:  gross lesions are not dramatic.  There may be congestion of the liver with some hepatomegaly, pulmonary emphysema and pneumonia and increased amounts of CSF.  Microscopically, lesions include pulmonary alvelolar emphysema, bronchiolar constriction, interlobular edema and fibrosis, Wallerian degeneration in the spinal cord and peripheral nerves.

Swainsonine:  gross lesions are not specific.  However, microscopic lesions are rather dramatic and can be described as neurovisceral cytoplasmic vacuolation.  Vacuoles are observed in organs such as the thyroid gland, pancreas, lymph nodes, lymphocytes and liver.

Treatment

• Often unrewarding

• Remove from source of exposure

• Depending on the length of exposure, damage can be irreversible

• Horses recovered from locoism should be considered unsound