Summary

This document provides a detailed overview of gossypol poisoning and its effects, including etiology, clinical presentation, diagnosis, and management in animal health. The study details the effects and pathogenesis in various tissues and systems and describes potential preventive measures and supportive therapy.

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Gossypol Poisoning I.SEMATOVICA Jelgava, 2021 Etiology Gossypol, the predominant pigment and probably the major toxic ingredient in the cotton plant (Gossypium spp). Gossypol content of cottonseeds varies from a trace to >6% and is affected by...

Gossypol Poisoning I.SEMATOVICA Jelgava, 2021 Etiology Gossypol, the predominant pigment and probably the major toxic ingredient in the cotton plant (Gossypium spp). Gossypol content of cottonseeds varies from a trace to >6% and is affected by plant species and variety and by environmental factors such as climate, soil type, and fertilization. Cottonseed meal is marketed with 50%–90% protein, depending on the intended use. Lipid-soluble gossypol is readily absorbed from the GI tract. Gossypol also affects enzymatic reactions critical for many biologic processes, including the ability of cells to respond to oxidative stress and inhibition of oxygen release from hemoglobin. Conjugation, metabolism, and urinary excretion of gossypol is limited; most is eliminated in the feces. Introduction usually chronic, cumulative, and sometimes insidious toxicosis can affect high-producing dairy cows with high feed intake L because these cows eat more protein https://www.msdvetmanual.com/toxicology/gossypol-poisoning/overview-of-gossypol-poisoning?query=poisoning%20selenium Patogenesis Fat soluble, completely absorbed from the intestine, bounds to proteins (lysine) and Fe in the blood. Accumulates in the body. Excreted mainly in faeces and milk. Clinical Findings effects on the cardiac, hepatic, renal, reproductive, or other systems; hepatotoxicity can be a primary effect from direct damage to hepatocytes or metabolism of phenolic compounds to reactive intermediates, or liver necrosis may be secondary to congestive heart failure, inhibits glutathione-S-transferase, impairing the liver’s ability to metabolize xenobiotic compounds, anemia, increased RBC fragility, decreased oxygen release from oxyhemoglobin, reproductive disorders, diarea, hemoglobinuria, reduced growth rate, weight loss, weakness, anorexia, and increased susceptibility to stress Lesions non-specific enlarged, flabby, pale, streaked, and mottled heart with pale myocardial streaking, enlarged and dilated ventricules, and valvular edema may be evident. skeletal muscles may also be pale. a froth-filled trachea and edematous, congested lungs are common, with interstitial pulmonary edema and markedly edematous interlobular septa, the kidneys, spleen, and other splanchnic organs may be congested, possibly with petechiae; mild renal tubular nephrosis may be present. Hemoglobinuria and edema and hyperemia of the visceral mucosa may develop. Diagnosis History//anamnesis; signs, especially sudden death or chronic dyspnea, affecting multiple animals within a group; lesions - cardiomyopathy and hepatopathy, with increased amounts of fluids in various body cavities; no response to antibiotic therapy; the presence of significant concentrations of free gossypol in the diet; aanalysis of dietary components for free gossypol must be correlated with history, clinical signs, and postmortem findings. Differential diagnoses other poisonings, nutritional or metabolic disorders, hypophosphatemia Postpartum infectious diseases Prevention, Treatment, and Control no effective treatment for gossypol poisoning; adsorbents such as activated charcoal and saline cathartics are of little value because of the chronic exposure and cumulative nature of gossypol; if gossypol toxicity is suspected, all cottonseed products should be removed; extent of toxic cardiopathy; a high-quality diet supplemented with lysine, methionine, and fat- soluble vitamins should be included in supportive therapy. selenium or copper deficiencies may potentiate gossypol toxicosis.

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