Drugs and Toxins With Effect on Body Temperature

Phenothiazine tranquilizers are a recognized cause of loss of ability to control body temperature.²⁸ Conversely, α₂-adrenergic agonist sedatives (e.g., detomidine, xyalzine) have been shown to induce tachypnea and decrease body temperature in febrile horses.²⁹ The potential mechanism for the antipyrexic effect of α₂-adrenergic agonist drugs may be related to their ability to decrease prostaglandin E₂ production by the hypothalamus.^29-30 Erythromycin may induce hyperthermia during hot weather, particularly in foals.^31-32 This side effect has been attributed to a reaction to erythromycin itself or to an alteration of the foal's thermoregulatory system by mechanisms not yet described.³² Other drugs that have been associated with increase in body temperature in large animals are summarized in Box 4.1.

Certain toxins and drugs may act to increase body tem­perature by causing an increase in metabolic work (Boxes 4.2 and 4.3). For example, chlorophenols and nitrophenols, used as herbicides and wood preservatives, cause uncoupling of oxidative phosphorylation within mitochondria and lead to rapid extreme rises in body temperature.³⁴ Chronic and/or low-level exposure to these compounds may manifest clinically as hyperthermia.

Tall fescue infected with the endophyte Neotyphodium coenophialum contains vasoactive ergopeptine alkaloids that

■ BOX 4.2

Toxins Associated With Increased Temperature in the Horse

Blister beetle (cantharidin)

Selenium Arsenic Mercury Chlorinated hydrocarbons Dinitrophenol Propylene glycol

Trichloroethylene extracted feed

Plant Toxins

Pyrrolizidine alkaloid-containing plants Algae

Castor bean (Ricinus species) Water hemlock (Cicuta species) Jimson weed (Datura stramonium) Mycotoxicosis

■ BOX 4.3

Toxins Associated With Increased Temperature in Ruminants

Arsenic

Selenium

Mercury

Zinc

Crude oil, kerosine, coal oil

Qrganochlorine, chlorinated hydrocarbons Iodine

Paraquat Dinitrophenol

Propylene glycol Trichloroethylene-extracted feeds

Halothane toxicity (C)

Plant Toxins

Fescue toxicosis (B)

Ergot (Claviceps) (B)

Pyrrolizidine alkaloid-containing plants, algae Brassica species (mustards, crucifers, cress) Bracken fern

Castor bean

Water hemlock

Milkweed (Asclepias species) (B, Q)

Buttercup (Caltha palustris and Ranunculus species) (Q) Rhododendron (C, Q)

Gossypol toxicity (B) Jimson weed (Datura stramonium)

B, Bovine; C, caprine; O, ovine.

cause vasoconstriction and reduced blood flow to the skin of ruminants.³⁵ These alkaloids also induce bronchoconstriction and pulmonary vasoconstriction, which further compromise ruminants’ ability to lose heat, especially during hot environ­mental conditions.³⁵ Affected animals have a poor appetite and other indications of poor performance recognized as part of the syndrome of fescue toxicosis, or “summer slump.”³⁵ A related endophyte infesting perennial ryegrass has been found to produce a similar hyperthermic condition in the western United States.³⁶ Clavicepspurpurea infestations of annual or perennial ryegrass and of cereal grain heads have also been reported to produce a similar hyperthermic syndrome, which may lead to heat prostration and death when ambient temperatures are high.^{37 39}

Cattle affected by any of these ergopeptine alkaloids have few to no clinical signs when environmental conditions are cool and heat loss mechanisms are not challenged.