Many prey species (including plants) deter predators with defensive chemicals. These defensive chemicals act by rendering the prey's tissues noxious, toxic, or both. Here, I explore how predators cope with the presence of these chemicals in their diet. First, I describe the chemosensory mechanisms by which predators (including herbivores) detect defensive chemicals. Second, I review the mechanisms by which predators either avoid or tolerate defensive chemicals in prey. Third, I examine how effectively free-ranging predators can overcome the chemical defenses of prey. The available evidence indicates that predators have mixed success overcoming these defenses. This conclusion is based on reports of free-ranging predators rejecting unpalatable but harmless prey, or voluntarily ingesting toxic prey.

How Do Predators Cope With Chemically Defended Foods

The history of «slobbers syndrome,» a mycotoxicosis associated with Rhizoctonia leguminicola infestation of pastures and stored forages, is discussed. The chemistry and physiological effects of the two known biologically active alkaloids of R. leguminicola, slaframine and swainsonine, are described. Slaframine administration is generally associated with increased exocrine function, especially salivation. Ingestion of swainsonine may be linked to serious and potentially lethal central nervous system defects similar to that described for locoism. However, the singular effects of these alkaloids do not completely account for the total clinical picture noted in the field during the occurrence of slobbers syndrome. It is possible that this phenomenon is the result of an interaction between both known and unidentified biologically active metabolites of R. leguminicola

The involvement of slaframine and swainsonine in slobbers syndrome: a review.

Pathogenesis and preventive treatment for animal disease due to locoweed poisoning

This paper describes a neurovisceral cytoplasmic storage disease together with neuroaxonal dystrophy and dysmyelinogenesis in two of three new born goats affected with an arthrogryposis-like syndrome. The entity is compared with other conditions in which no substance can be demonstrated in cytoplasmic vacuoles.

Neurovisceral storage and dysmyelinogenesis in neonatal goats

Locoweed poisoning generally occurs in early spring. We evaluated cattle grazing of woolly locoweed (Astragalus mollissimus var. mollissimus Torr.) at Gladstone, N.M., and of white locoweed (Oxytropis sericea Nutt. ex T&G) at Capulin, N.M., through the spring and into early summer as the phenological development of warm-season grasses progressed from dormancy to rapid growth. Diets of 8 mature cows were quantified by bite count at each location. Cattle initially rejected woolly locoweed at Gladstone, even though it was the only green forage available in late March and early April. Gladstone cattle were then restricted to a small 7-ha pasture where high grazing pressure and limited feed forced them to graze woolly locoweed (41% of bites). When these cows returned to a larger pasture of unlimited forage availability, they continued eating woolly locoweed (23% of bites). At Capulin, cattle with a history of eating locoweed (loco-eaters) consumed more white locoweed (23% of bites) thin cattle without a history of eating locoweed (6% of bites) during the April grazing period. When warm-season grasses started rapid growth and locoweed matured in June, cattle ceased grazing both locoweed species.

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G. R. Staker

Papers

Locoweed (Astragalus lentiginosus) poisoning in cattle and horses.