Hepatopathy following consumption of a commercially available blue-green algae dietary supplement in a dog.

BACKGROUND: Dietary supplement use in both human and animals to augment overall health continues to increase and represents a potential health risk due to the lack of safety regulations imposed on the manufacturers. Because there are no requirements for demonstrating safety and efficacy prior to marketing, dietary supplements may contain potentially toxic contaminants such as hepatotoxic microcystins produced by several species of blue-green algae. CASE PRESENTATION: An 11-year-old female spayed 8.95 kg Pug dog was initially presented for poor appetite, lethargy polyuria, polydipsia, and an inability to get comfortable. Markedly increased liver enzyme activities were detected with no corresponding abnormalities evident on abdominal ultrasound. A few days later the liver enzyme activities were persistently increased and the dog was coagulopathic indicating substantial liver dysfunction. The dog was hospitalized for further care consisting of oral S-adenosylmethionine, silybin, vitamin K, and ursodeoxycholic acid, as well as intravenous ampicillin sodium/sulbactam sodium, dolasetron, N-acetylcysteine, metoclopramide, and intravenous fluids. Improvement of the hepatopathy and the dog's clinical status was noted over the next three days. Assessment of the dog's diet revealed the use of a commercially available blue-green algae dietary supplement for three-and-a-half weeks prior to hospitalization. The supplement was submitted for toxicology testing and revealed the presence of hepatotoxic microcystins (MCs), MC-LR and MC-LA. Use of the supplement was discontinued and follow-up evaluation over the next few weeks revealed a complete resolution of the hepatopathy. CONCLUSIONS: To the authors' knowledge, this is the first case report of microcystin intoxication in a dog after using a commercially available blue-green algae dietary supplement. Veterinarians should recognize the potential harm that these supplements may cause and know that with intervention, recovery is possible. In addition, more prudent oversight of dietary supplement use is recommended for our companion animals to prevent adverse events/intoxications.

Triiodothyronine or Antioxidants Block the Inhibitory Effects of BDE-47 and BDE-49 on Axonal Growth in Rat Hippocampal Neuron-Glia Co-Cultures.

We previously demonstrated that polybrominated diphenyl ethers (PBDEs) inhibit the growth of axons in primary rat hippocampal neurons. Here, we test the hypothesis that PBDE effects on axonal morphogenesis are mediated by thyroid hormone and/or reactive oxygen species (ROS)-dependent mechanisms. Axonal growth and ROS were quantified in primary neuronal-glial co-cultures dissociated from neonatal rat hippocampi exposed to nM concentrations of BDE-47 or BDE-49 in the absence or presence of triiodothyronine (T3; 3-30 nM), N-acetyl-cysteine (NAC; 100 µM), or α-tocopherol (100 µM). Co-exposure to T3 or either antioxidant prevented inhibition of axonal growth in hippocampal cultures exposed to BDE-47 or BDE-49. T3 supplementation in cultures not exposed to PBDEs did not alter axonal growth. T3 did, however, prevent PBDE-induced ROS generation and alterations in mitochondrial metabolism. Collectively, our data indicate that PBDEs inhibit axonal growth via ROS-dependent mechanisms, and that T3 protects axonal growth by inhibiting PBDE-induced ROS. These observations suggest that co-exposure to endocrine disruptors that decrease TH signaling in the brain may increase vulnerability to the adverse effects of developmental PBDE exposure on axonal morphogenesis.

Debromoaplysiatoxin as the Causative Agent of Dermatitis in a Dog after Exposure to Freshwater in California.

Contamination of recreational waters with cyanobacterial toxins continues to increase and presents a risk to animals and humans. Although cases of acute hepato- and neurotoxicoses in dogs following cyanotoxin exposure exist, no reports of skin-related reactions in dogs exist. A 5-year-old female spayed 34 kg Bracco Italiano was initially presented for rapid onset of severe pruritus and urticaria. Marked excoriation and erythema were noted over the chest and neck, while urticaria was noted in the inguinal regions and ventral abdomen. Initial basic dermatology work-up excluded parasitic, fungal, and bacterial organisms. Due to the severity and progression of urticaria, the dog received IV dexamethasone and IM diphenhydramine. Improvement of the urticaria and the dog's clinical status was noted over the next 45 min. Assessment of the dog's environment revealed access to a lake on the property with visible algal bloom. Water from the lake was submitted for toxicology testing and revealed the presence of debromoaplysiatoxin. Access to the lake was discontinued and follow-up evaluation over the next few weeks revealed a complete resolution of the skin irritation. To the authors' knowledge, this is the first case report of debromoaplysiatoxin exposure in a dog after swimming in cyanobacteria-contaminated water. Veterinarians should recognize the potential harm that contaminated waters may cause in terms of dermal, hepatic, and neurological conditions. In addition, more prudent oversight of contaminated recreational waters is recommended for animals and humans to prevent adverse events and intoxications.

Method for the detection of desmethylbromethalin in animal tissue samples for the determination of bromethalin exposure.

Bromethalin, a potent neurotoxin, is widely available for use as a rodenticide. As access to other rodenticides is reduced due to regulatory pressure, the use of bromethalin is likely to increase with a concomitant increase in poisonings in nontarget animals. Analytical methods for the detection of bromethalin residues in animals suspected to have been exposed to this rodenticide are needed to support post-mortem diagnosis of toxicosis. This paper describes a novel method for the analysis of desmethylbromethalin (DMB), bromethalin's toxic metabolite, in tissue samples such as liver, brain, and adipose. Samples were extracted with 5% ethanol in ethyl acetate, and an aliquot of the extract was evaporated dry, reconstituted, and analyzed by reverse phase ultrahigh-performance liquid chromatography-mass spectrometry. The mass spectrometer utilized electrospray ionization in negative ion mode with multiple reaction monitoring. This method was qualitatively validated at a level of 1.0 ng/g in liver tissue. The quantitative potential of the method was also evaluated, and a method detection limit of 0.35 ng/g wet weight was determined in fat tissue. DMB was detected in tissue samples from animals suspected to have been poisoned by this compound. To the authors' knowledge, there have been no other methods reported for analysis of DMB in tissue samples using LC-MS/MS.

An outbreak of thyroid hyperplasia (goiter) with high mortality in budgerigars (Melopsittacus undulatus).

An outbreak of goiter with high morbidity and mortality in a flock of budgerigars (Melopsittacus undulatus) in California is described. Forty-five out of 400 adult birds exhibited signs of illness, weight loss, and enlargement in the crop area; 15 of the 45 birds died over a 2-3-month period. Diet consisted of a commercial mixture with the addition of broccoli, whole oats, and carrots, but no minerals or supplements. Six budgerigars were subjected to necropsy; all 6 birds had severely enlarged thyroid glands. Thyroid follicular hyperplasia was histologically observed in all birds examined, while granulomatous thyroiditis and microfollicular adenoma were observed in 2 birds, respectively. Virological, bacteriological, parasitological, and heavy metal analyses were negative or within normal limits. The total iodine in the thyroid glands of affected birds was measured by inductively coupled plasma-mass spectrometry. Following iodine supplementation and removal of broccoli from the diet, the owner reported weight gain and a reduced death rate among clinically affected birds; no additional birds became sick. The presence of broccoli with its iodine-binding ability and the complete lack of added minerals in the diet of these animals were thought to be the predisposing factors for the outbreak in the present study. Outbreaks of goiter accompanied by high mortality are rare in any species and, to the best of the authors' knowledge, have not been described previously in any avian species. Recognition of this condition may help improve medical, welfare, and trade standards concerning this species.

Lead exposure from backyard chicken eggs: a public health risk?

Although the USA has made significant strides in reducing lead exposure, new and emerging sources are raising cause for public concern. Recent reports of finding lead in eggs from chickens raised in urban gardens has highlighted the need to consider the potential health risks of consuming eggs from backyard chickens. Following the detection of 0.33 µg/g lead in the edible portion of eggs submitted for lead analysis from a backyard chicken owner, further investigation was conducted to determine the source and extent of lead exposure in the flock. Several birds, almost two dozen eggs, and environmental samples were submitted to the California Animal Health and Food Safety Laboratory for further testing. Lead was detected in the blood, liver, kidney, and bone at varying concentrations in all birds but was not detected in the muscle tissue. All egg shells contained detectable amounts of lead, while only a little over half of the edible portion of the eggs contained lead. The detected concentrations in the edible portion approached or exceeded the recommended threshold of lead consumption per day that should not be exceeded by young children if a child consumed one average-sized egg. Peeling paint from a wooded structure adjacent to the flock's coop was the likely lead source containing 3,700 µg/g lead. Thus, removal of the chickens from the source and periodic testing of eggs for lead were recommended. This case illustrates the need for consumers and health care workers to be aware of potential sources for lead exposure such as backyard chickens.

Bromethalin poisoning in a raccoon (Procyon lotor): diagnostic considerations and relevance to nontarget wildlife.

Submission of a raccoon (Procyon lotor) for necropsy following exhaustion at a California wildlife care center revealed minimal gross pathologic changes and only mild vacuolar changes in the white matter of the brain. Turquoise granular material was noted in the gastrointestinal tract and was submitted for toxicological testing along with portions of the brain, liver, kidney, and mesenteric and perirenal adipose tissues. Testing of the turquoise material for 7 anticoagulant rodenticides, strychnine, 4-aminopyridine, starlicide, and salts revealed none of these compounds; however, desmethylbromethalin was detected by high-performance liquid chromatography-tandem mass spectrometry. Other tissues were subsequently analyzed; the mesenteric and perirenal adipose tissues contained desmethylbromethalin. Desmethylbromethalin is the active metabolite of bromethalin, uncouples oxidative phosphorylation, and results in cerebral edema. Bromethalin is a rodenticide that is visually indistinguishable from many other rodenticides, making identification of poisonings by appearance alone nearly impossible. Based on the pathological and toxicological findings, a diagnosis of bromethalin toxicosis was established. In cases of wildlife species with unknown deaths or inconsistent clinical signs with normal or minimal histological findings, bromethalin toxicosis should be considered as a differential. Adipose tissue is the tissue of choice and can be easily harvested from a live or deceased animal to help confirm or rule out bromethalin exposure or intoxication.

Diagnostic value of tissue monensin concentrations in horses following toxicosis.

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.