Leucaena (Leucaena leucocephala) is a leguminous tree that is nutritious forage for domestic livestock when ingested in limited amounts. Unfortunately, leucaena contains mimosine, a plant amino acid, that can be toxic when ingested at higher concentrations. Reported toxic effects include alopecia (fur loss), poor body condition, infertility, low birth weight, thyroid gland dysfunction, and organ toxicity. Originally native to Mexico and Central America, leucaena has been introduced throughout the tropics, including Berenty Reserve, Madagascar where it was planted as supplemental browse for livestock. In Berenty, a seasonal syndrome of alopecia in ringtailed lemurs (Lemur catta) is associated with eating leucaena. Although much is known about the toxic effects of leucaena and mimosine on domestic animals and humans, the systemic effects on wildlife had not been studied. In a comparison of lemurs that include leucaena in their diet and those that do not, we found that animals that ingest leucaena absorb mimosine but that ingestion does not affect body condition, cause kidney or liver toxicity, or affect the intestinal tract. Alopecia is due to mimosine's interference of the hair follicle cycle. Leucaena ingestion is associated with higher serum albumin, α-tocopherol, and thyroxine concentrations, suggesting that leucaena may provide some nutritional benefit and that lemurs can detoxify and convert mimosine to a thyroid stimulating metabolite. The primary conservation consequence of leucaena ingestion at Berenty may be increased infant mortality due to the infants' inability cling to their alopecic mothers. The widespread introduction of leucaena throughout the tropics and its rapid spread in secondary forest conditions mean that many other leaf-eating mammals may be including this tree in their diet. Thus, exposure to leucaena should be considered when wildlife health is being evaluated, and the potential effects on wildlife health should be considered when contemplating leucaena introduction into or near wildlife habitat.
Two separate incidents of monensin exposure in horses resulting in toxicosis provided insight into the diagnostic value and interpretive criteria of various biological samples. In case 1, 25 horses broke into a shed and ingested feed that was supplemented with 800 g/ton (880 µg/g) of monensin. Within 48 hr, 1 horse had died, 2 developed cardiac arrhythmias, lethargy, and recumbency, and another was euthanized due to severe deterioration. Minimal histologic lesions were noted in the horse that died peracutely, while another showed characteristic lesions of acute cardiomyocyte degeneration and necrosis. Stomach content, heart, liver, urine, and serum revealed various detectable concentrations of monensin in clinically affected and unaffected horses with known exposure. In case 2, a pastured horse had access to a mineral mix containing 1,600 g/ton (1,760 µg/g) of monensin. Within 48 hr, the horse became symptomatic and was euthanized because of severe respiratory distress. Histologic cardiac lesions were minimal but detectable amounts of monensin were found in blood, heart, liver, and stomach contents. In both cases, monensin toxicosis was confirmed with toxicological analysis. These cases demonstrate an overall lack of correlation of monensin concentrations in various biological samples with clinical outcome. However, serum, urine, blood, liver, heart, and stomach content can be tested to confirm exposure. More importantly, the consistently higher concentrations found in heart tissue suggest this is the most useful diagnostic specimen for postmortem confirmation of toxicosis in horses especially in cases in which associated feed cannot be tested for monensin or in cases with no histologic lesions.
Abstract. Six dogs died after accidental ingestion of cottonseed bedding. No clinical signs of illness were observed prior to death. A full diagnostic workup was performed on one of these dogs. At necropsy, the lungs were congested and edematous, and the liver was firm, congested, and had a marked reticular pattern. There was also moderate ascites. Histopathologic examination revealed multifocal myocardial degeneration and necrosis, severe pulmonary edema, and chronic passive congestion of the lungs, heart, liver, and kidneys. Transmission electron microscopy of the myocardium revealed disruption of myofibrils, chromatin condensation, and disrupted and swollen mitochondria. The cottonseed bedding contained 1,600 mg/kg of free gossypol, a concentration considered toxic for monogastric animals. The stomach content revealed the presence of gossypol, thus confirming ingestion of cottonseed. Gossypol poisoning in dogs is extremely rare and has not yet been associated with cottonseed bedding. This first documented case of gossypol poisoning in a dog, caused by the ingestion of cottonseed bedding, demonstrates how specific toxicological analysis is crucial in reaching an accurate diagnosis.Key words: Cottonseed; dogs; gossypol; high-performance liquid chromatography; toxicosis.Although dogs are highly susceptible to gossypol poisoning, only 1 documented case of natural poisoning following ingestion of cottonseed meal exists. 15 Most cases of gossypol poisoning have been reported in poultry, 8 swine, 7 cattle, 19 sheep, 13 and goats, 4 as whole cottonseed, cottonseed meal, and hulls are commonly fed to livestock as a source of energy, protein, and fiber. Cottonseed contains gossypol, a polyphenolic pigment, which is found in the endosperm of the seeds and in the stems and roots of the cotton plant. 3 In processed forms of cottonseed, gossypol exists as both free and bound forms. The free form of gossypol is toxic to humans and animals and is the primary form found in recently harvested and properly stored whole cottonseed. Free gossypol exists as a racemic mixture of (ϩ) and (Ϫ) enantiomers. The (Ϫ) isomer exerts most of the antiproliferative, cytotoxic, and antifertility effects. 9 The bound form of gossypol, which results from cottonseed processing when gossypol binds to proteins, is considered nontoxic due to its inability to be absorbed through the gastrointestinal tract, although evidence exists that some dissociation can occur in the intestinal tract. Much of the toxicity of gossypol is attributed to a cumulative effect over several weeks to months, although sudden death has been observed and attributed to alteration of myocardial conduction. 13,19 Gossypol toxicity can also result in kidney and hepatic damage, protein malnutrition, reduced weight gain, and reproductive defects. 14 Monogastrics and prefunctional ruminants are more susceptible than adult cattle to gossypol. Although research interest in gossypol toxicity in the veterinary field has mainly focused on its potent cardiotoxic 2 and male antifertility e...
Twenty-six 5-month-old Holstein calves were accidentally exposed to discarded branches of yew bushes (Taxus sp.). Several calves were found dead approximately 24 hr after exposure; however, a few calves died several days after exposure. One calf died 18 days after the initial exposure to Taxus sp. and was examined on the farm via necropsy. Gross lesions included ascites, and dilated and flaccid myocardial ventricles. Sections of formalin-fixed heart were submitted to the Indiana Animal Disease Diagnostic Laboratory for histopathologic examination; fresh rumen contents were submitted for toxicologic testing. Histologically, large areas of myocardium were replaced by fibrous connective tissue, suggesting previous myocardial necrosis. Taxus alkaloids were identified in the rumen contents using gas chromatography-mass spectrometry. Based on the clinical history, the gross and histologic lesions, the identification of Taxus alkaloids in the rumen contents, and lack of exposure to other known cardiotoxic agents, yew toxicity was considered the cause of death in this calf. Ingestion of taxines is known to cause acute and subacute toxicity in human beings and animals; however, a chronic clinical course and severe histologic lesions have not been previously associated with yew toxicity. Although only 1 calf was examined, this case suggests that yew toxicity can result in a prolonged clinical course in cattle and can cause histologic myocardial lesions.
Background: Aflatoxins (AFs) are secondary metabolites of fungi and are one of the causes of toxin-related pet food recalls. An intralaboratory method was previously developed to quantify aflatoxin B1 (AFB1) and aflatoxin M1 (AFM1) in animal liver by HPLC with fluorescence detection. Objective: The aim of this study was to extensively evaluate the method performance with a single-laboratory blinded method test (BMT-S) and a multilaboratory blinded method test (BMT-M). Methods: Blinded tissue samples were prepared by a third-party laboratory and sent out to participating laboratories for both BMT-S and BMT-M. Results: In both tests, participants analyzed blinded samples prepared by an independent laboratory. In the BMT-S, accuracy ranged between 111 and 154% for AFB1 and 113 and 159% for AFM1 within the quantitation range of 0.1–0.5 ng/g. The HorRat values for repeatability ranged between 0.1 and 0.3 for AFB1 and 0.3 and 0.6 for AFM1. In the BMT-M, the interlaboratory accuracy ranged between 77 and 81% for AFB1 and 83 and 85% for AFM1 within the quantitation range of 0.2–10 ng/g. The HorRat values for reproducibility ranged between 0.4 and 0.7 for AFB1 and 0.4 and 0.9 for AFM1. Both recovery and reproducibility were acceptable. Conclusions: BMT-M evaluation demonstrated that the method was suitable for quantitation of aflatoxins B1 and M1 in animal liver between laboratories. Highlights: The BMT-S and BMT-M results demonstrated that the method is rugged and reproducible among the participating laboratories.
Background Aflatoxins (AFs) are common feed contaminants and are one of the common causes of toxin-related pet food poisoning and recalls. Objective Currently, there are no validated methods for the detection and quantitation of aflatoxins in biological matrices to diagnose aflatoxin exposure in live animals. Following a successful intra-laboratory method development to quantify aflatoxin B1 (AFB1) and aflatoxin M1 (AFM1) in animal urine by high-performance liquid chromatography with fluorescence detection (HPLC-FLD), the present study was conducted to extensively evaluate the method performance in an unbiased manner using blinded samples. Method The evaluation included two stages. First, the performance was verified in the method-originating laboratory in a single-laboratory blinded method test (BMT-S) trial followed by a multi-laboratory blinded method test (BMT-M) trial. Results In both trials, accuracy, repeatability, and reproducibility were satisfactory confirming the relatively good ruggedness and robustness of the method and ensuring that it will perform as expected if used by other laboratories in the future. Highlights A simple urine-based diagnostic test method using high-performance liquid chromatography with fluorescence detection that originated in a single laboratory now has passed a multi-laboratory evaluation and is now available to be shared with other diagnostic laboratories for purposes of diagnosing aflatoxin intoxication in animals so better treatment can be rendered.
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