Cantharidin.

Cantharidin is the toxic component of blister beetles of the genus Epicauta. Cantharidin is a potent vesicant which causes blisters, erosions, and ulcerations in the gastrointestinal and urinary tracts, and can cause myocardial necrosis. Blister beetles are found over most of North America and specifically contaminate alfalfa at harvest. History of alfalfa feeding, with colic, dysuria, hypocalcemia, and hypomagnesemia are suggestive of blister beetle toxicosis. Myocardial damage causes increased serum cardiac troponin 1. Tentative diagnosis can be made by finding the beetles in feed or ingesta. Definitive diagnosis requires detection of cantharidin in urine or gastric contents. Treatment involves ending exposure, decreasing absorption, controlling pain, using gastroprotectants, and fluids and electrolyte replacement. Prognosis is guarded to poor.

Pyrogallol Toxicosis in Horses.

Plants in the maple genus, Acer, and pistachio genus, Pistacia, have been reported to cause acute hemolysis in horses. The cause of hemolysis seems to be metabolism of gallic acids to the potent oxidant pyrogallol by enteric bacteria of the horse. Diagnosis is often tentative and circumstantial. Treatment is symptomatic and supportive and can include detoxification, fluid and electrolyte therapy, supplemental oxygen, and pain control. Corticosteroid and antioxidant therapies do not improve prognosis. Prognosis is guarded to poor but horses that survive 6 days postexposure are expected to recover.

The urban lead (Pb) burden in humans, animals and the natural environment.

Centuries of human activities, particularly housing and transportation practices from the late 19th century through the 1980's, dispersed hundreds of millions of tons of lead into our urban areas. The urban lead burden is evident among humans, wild and domesticated animals, and plants. Animal lead exposures closely mirror and often exceed the lead exposure patterns of their human partners. Some examples: Pigeons in New York City neighborhoods mimicked the lead exposures of neighborhood children, with more contaminated areas associated with higher exposures in both species. Also, immediately following the lead in drinking water crisis in Flint MI in 2015, blood lead levels in pet dogs in Flint were 4 times higher than in surrounding towns. And combining lead's neurotoxicity with urban stress results in well-characterized aggressive behaviors across multiple species. Lead pollution is not distributed evenly across urban areas. Although average US pediatric lead exposures have declined by 90% since the 1970s, there remain well defined neighborhoods where children continue to have toxic lead exposures; animals are poisoned there, too. Those neighborhoods tend to have disproportionate commercial and industrial lead activity; a history of dense traffic; older and deteriorating housing; past and operating landfills, dumps and hazardous waste sites; and often lead contaminated drinking water. The population there tends to be low income and minority. Urban wild and domesticated animals bear that same lead burden. Soil, buildings, dust and even trees constitute huge lead repositories throughout urban areas. Until and unless we begin to address the lead repositories in our cities, the urban lead burden will continue to impose enormous costs distributed disproportionately across the domains of the natural environment. Evidence-based research has shown the efficacy and cost-effectiveness of some US public policies to prevent or reduce these exposures. We end with a series of recommendations to manage lead-safe urban environments.

The role of the veterinary diagnostic toxicologist in apiary health.

Susceptibility of individuals and groups to toxicants depends on complex interactions involving the host, environment, and other exposures. Apiary diagnostic investigation and honey bee health are truly population medicine: the colony is the patient. Here we provide basic information on the application of toxicology to the testing of domestic honey bees, and, in light of recent research, expand on some of the challenges of interpreting analytical chemistry findings as they pertain to hive health. The hive is an efficiently organized system of wax cells used to store brood, honey, and bee bread, and is protected by the bee-procured antimicrobial compound propolis. Toxicants can affect individual workers outside or inside the hive, with disease processes that range from acute to chronic and subclinical to lethal. Toxicants can impact brood and contaminate honey, bee bread, and structural wax. We provide an overview of important natural and synthetic toxicants to which honey bees are exposed; behavioral, husbandry, and external environmental factors influencing exposure; short- and long-term impacts of toxicant exposure on individual bee and colony health; and the convergent impacts of stress, nutrition, infectious disease, and toxicant exposures on colony health. Current and potential future toxicology testing options are included. Common contaminants in apiary products consumed or used by humans (honey, wax, pollen), their sources, and the potential need for product testing are also noted.

Pesticide contamination of beeswax from managed honey bee colonies in New York State.

The New York State (NYS) beekeeping industry generated >$11M worth of honey in 2020 and >$300M in pollination services to agriculture annually. Bees are frequently exposed to pesticides through foraging and husbandry practices. Lipophilic pesticides can remain in beeswax for extended periods. We analyzed for pesticides in wax comb samples collected from NYS apiaries at the end of the growing season, comparing residue numbers and concentrations among beekeepers of different operation scales: commercial beekeepers (>300 colonies), sideliners (50-299 colonies), and hobbyists (<50 colonies). We analyzed samples collected from 72 managed honey bee colonies for 92 insecticides, herbicides, and fungicides by liquid chromatography-tandem mass spectrometry. Pesticides were detected in all samples and included 34 fungicides, 33 insecticides, and 22 herbicides. Each wax sample contained 7-35 different residues (x¯ = 17.8 residues). Wax from colonies managed by commercial beekeepers contained the most residues (x¯ = 21.9 residues), hobbyists were second (x¯ = 16.3 residues), and sideliners had the fewest (x¯ = 11.7 residues). Nearly all wax samples (98.6%) contained the pesticide synergist piperonyl butoxide, most samples (86%) contained common varroacides used to control honey bee parasites, including coumaphos and amitraz breakdown products, and 93.1% contained the fungicide difenoconazole. We detected 34 fungicides, 7 of which were found in 50% or more of the samples. We detected 22 herbicides. We found pesticide contamination of beeswax to be common, with commercial beekeepers experiencing the greatest contamination.

Marijuana toxicosis in 2 donkeys.

Marijuana toxicosis is typically seen by companion animal veterinarians. However, with increased marijuana availability, there is a greater potential for toxicosis in other species. Herein we describe a case of suspected marijuana toxicosis in a female and a male American Mammoth donkey, aged 8 y and 20 y, respectively, fed cannabis buds. Both cases were presented because of depression and lethargy. However, the jenny had ataxia, mild colic, tachycardia, tachypnea, and decreased tongue tone. Plasma samples from the jenny on presentation and 3 d following hospitalization were submitted to the Kansas State Veterinary Diagnostic Laboratory to be screened for cannabinoids using high-pressure liquid chromatography coupled with tandem mass spectroscopy (HPLC-MS/MS). A single serum sample from the jack was taken on presentation and submitted to the Animal Health Diagnostic Center at Cornell University for Δ9-tetrahydrocannabinol (THC) and cannabidiol analysis using HPLC-MS/MS. THC was detected in all samples. Clinical signs were noted 24-36 h after ingestion, which included mild-to-moderate neurologic deficits, mild colic, tachycardia, tachypnea, and decreased tongue tone. Both donkeys recovered uneventfully within 24 h of peak effects. Utilizing a cannabinoid screening assay in collaboration with a veterinary diagnostic laboratory may be useful when an equine practitioner suspects marijuana toxicosis in a patient.

Comparison of two methods for blood lead analysis in cattle: graphite-furnace atomic absorption spectrometry and LeadCare(R) II system.

The current study compared the LeadCare(R) II test kit system with graphite-furnace atomic absorption spectrometry for blood lead (Pb) analysis in 56 cattle accidentally exposed to Pb in the field. Blood Pb concentrations were determined by LeadCare II within 4 hr of collection and after 72 hr of refrigeration. Blood Pb concentrations were determined by atomic absorption spectrometry, and samples that were coagulated (n = 12) were homogenized before analysis. There was strong rank correlation (R(2) = 0.96) between atomic absorption and LeadCare II (within 4 hr of collection), and a conversion formula was determined for values within the observed range (3-91 mcg/dl, although few had values >40 mcg/dl). Median and mean blood pb concentrations for atomic absorption were 7.7 and 15.9 mcg/dl, respectively; for LeadCare II, medians were 5.2 mcg/dl at 4 hr and 4.9 mcg/dl at 72 hr, and means were 12.4 and 11.7, respectively. LeadCare II results at 4 hr strongly correlated with 72 hr results (R(2) = 0.96), but results at 72 hr were lower (P < 0.01). There was no significant difference between coagulated and uncoagulated samples run by atomic absorption. Although there have been several articles that compared LeadCare with other analytical techniques, all were for the original system, not LeadCare II. The present study indicated that LeadCare II results correlated well with atomic absorption over a wide range of blood Pb concentrations and that refrigerating samples for up to 72 hr before LeadCare II analysis was acceptable for clinical purposes.

An investigation of blood selenium concentrations of goats in New York State.

The goal of the current study was to determine the range of blood selenium concentrations in goats in New York State that were fed adequately supplemented diets. Blood samples from mature, juvenile, and neonatal goats from commercial farms, 2 dairy and 2 meat producers, were analyzed via graphite-furnace atomic absorption spectroscopy. Feed samples were analyzed by using inductively coupled argon plasma optical emission spectroscopy to confirm that dietary selenium concentrations were adequate. The ranges of blood selenium concentration obtained were 9.1-49.9 microg/dl for mature goats, 7.6-37.5 microg/dl for juveniles, and 9.7-40.7 microg/dl for neonates.

Comparison of blood lead and blood and plasma δ-aminolevulinic acid concentrations as biomarkers for lead poisoning in cattle.

Lead (Pb) concentrations in whole blood and δ-aminolevulinic acid (ALA) concentrations in plasma and whole blood from 37 cattle with suspected Pb exposure were determined in order to investigate the usefulness of ALA as a biological indicator for Pb poisoning in cattle. Cows were divided into 4 groups based on blood Pb, as follows: <30 ppb (group 1), 30-100 ppb (group 2), 100-300 ppb (group 3), and >300 ppb (group 4). The derivatization reaction for ALA was improved by a greater than 2-fold measure in whole blood and by a 10-fold measure in plasma by adding 75 and 50 µl of 0.1 N HCl, respectively. Blood Pb concentrations ranged from <25 ppb to 1,006 ppb (185.5 ± 254.9 ppb), with 17 samples containing >50 ppb Pb. Delta-aminolevulinic acid concentrations in whole blood and plasma ranged from <62.7 ppb to 96.9 ppb (77.4 ± 8.4 ppb) and from <5.0 ppb to 24.0 ppb (4.6 ± 3.8 ppb), respectively. Whole blood ALA did not correlate with blood lead concentrations in any group. Increase in plasma ALA concentration was dependent on blood Pb concentration. There was no correlation between blood Pb concentration and plasma ALA concentration in group 2 (n  =  4), but correlation coefficients were 0.736 in group 3 and 0.807 in group 4, respectively. The correlation coefficient was increased to 0.851 when groups 3 and 4 were combined. Based on these observations, in cattle, plasma ALA is a more reliable biological biomarker for Pb exposure than is blood ALA.

Polyacrylamide gel ingestion leading to fatal intestinal obstruction in two birds in a zoological collection.

Two birds from a zoological collection suffered fatal intestinal obstruction after each ingested single particles of polyacrylamide gel. Polyacrylamide gel, used in soils for gardening and agriculture, exists as small granules in the dehydrated state but expands markedly upon exposure to water. Polyacrylamide gel might, therefore, be an unrecognized hazard for captive and wild birds and other small animals if consumed.

Analysis of neurofilament concentration in healthy adult horses and utility in the diagnosis of equine protozoal myeloencephalitis and equine motor neuron disease.

Neurofilaments (NFs) are structural proteins of neurons that are released in significant quantities in the cerebrospinal fluid and blood as a result of neuronal degeneration or axonal damage. Therefore, NFs have potential as biomarkers for neurologic disorders. Neural degeneration increases with age and has the potential to confound the utility of NFs as biomarkers in the diagnosis of neurologic disorders. We investigated this relationship in horses with and without neurological diagnosis. While controlling for horse type (draft, pleasure, and racing), we evaluated the relationship between serum heavy-chain phosphorylated neurofilaments (pNF-H) and age, sex, and serum vitamin E concentrations. Serum pNF-H concentrations increased by 0.002 ng/ml for each year increase in age. There were significant differences in the serum pNF-H concentration among the type of activity performed by the horse. The highest serum pNF-H concentration was found in horses performing heavy work activity (racehorse) and with lower serum pNF-H concentration found among light (pleasure riding) and moderate (draft) activity. There was no significant association between the pNF-H concentration and sex or vitamin E concentration. Serum pNF-H concentration was elevated among horses afflicted with EMND and EPM when compared with control horses without evidence of neurologic disorders. Accordingly, serum pNF-H concentration can serve as a useful biomarker to complement the existing diagnostic work-up of horses suspected of having EPM or EMND.

The effects of formalin fixation and tissue embedding of bovine liver on copper, iron, and zinc analysis.

Veterinary analytical chemistry laboratories might be called upon to analyze formalin-fixed or paraffin-embedded tissue samples for trace minerals. The purpose of this study was to determine whether concentrations of copper (Cu), iron (Fe), and zinc (Zn) are comparable among fresh or frozen, formalin-fixed, and paraffin-embedded bovine liver samples on an as-received basis. Three liver sample subtypes (fresh or frozen, formalin-fixed, and paraffin-embedded) from 12 cows were collected and analyzed for Cu, Fe, and Zn concentrations. Concentrations were measured by using inductively coupled argon plasma atomic-emission spectroscopy. There was no significant difference in mineral measurements between fresh or frozen and formalin-fixed samples for Cu and Zn (both P > or = 0.052). The median concentration of Fe was lower in the fresh or frozen samples than in the formalin-fixed samples. However, for every pair of fresh or frozen and paraffin-embedded samples for all 3 minerals, the fresh or frozen sample had a lower measurement than the paraffin-embedded sample (all P = 0.005). Differences in mineral measurements associated with tissue processing did not result in differences in classification (within or outside the reference range) for Fe. However, the classification of Cu and Zn was different up to 25% of the time with fresh or frozen versus formalin-fixed or embedded liver. Although Cu, Fe, and Zn concentrations attained from processed tissue may be useful, they must be evaluated with caution.

Clinicopathologic, histologic, and toxicologic findings in 70 cats inadvertently exposed to pet food contaminated with melamine and cyanuric acid.

OBJECTIVE: To document clinicopathologic, histologic, and toxicologic findings in cats inadvertently exposed to pet food contaminated with melamine and cyanuric acid. DESIGN: Case series. ANIMALS: 70 cats from a single cattery inadvertently fed contaminated food that was the subject of a March 2007 recall. PROCEDURES: Clinical signs, clinicopathologic and histopathologic findings, and results of toxicologic analyses were recorded. RESULTS: Clinical signs were identified in 43 cats and included inappetence, vomiting, polyuria, polydipsia, and lethargy. Azotemia was documented in 38 of the 68 cats for which serum biochemical analyses were performed 7 to 11 days after consumption of the contaminated food. One cat died, and 13 were euthanized. Histologic examination of kidney specimens from 13 cats revealed intratubular crystalluria, tubular necrosis with regeneration, and subcapsular perivascular inflammation characterized by perivascular fibroplasia or fibrosis and inflammation with intravascular fibrin thrombi. Toxicologic analyses revealed melamine and cyanuric acid in samples of cat food, vomitus, urine, and kidneys. CONCLUSIONS AND CLINICAL RELEVANCE: In cats unintentionally fed pet food contaminated with melamine and cyanuric acid, the most consistent clinical and pathologic abnormalities were associated with the urinary tract, specifically tubular necrosis and crystalluria.

Clinical and clinicopathologic features of dogs that consumed foodborne hepatotoxic aflatoxins: 72 cases (2005-2006).

OBJECTIVE: To characterize clinical signs, clinicopathologic features, treatments, and survival in dogs with naturally acquired foodborne aflatoxicosis. DESIGN: Retrospective case series. ANIMALS: 72 dogs that consumed aflatoxin-contaminated commercial dog food. PROCEDURES: Medical records of affected dogs were reviewed. Between December 2005 and March 2006, dogs were identified as having foodborne aflatoxin hepatotoxicosis on the basis of the history of consumption of contaminated food or characteristic histopathologic lesions (subject dog or a recently deceased dog in the same household or kennel). Recorded information included signalment, clinical features, clinicopathologic test results, treatments, and survival. Data were analyzed by survival status. RESULTS: Most dogs were of large breeds from breeding kennels. No significant differences were found in age or weight between 26 (36%) survivor dogs and 46 (64%) nonsurvivor dogs. Severity of clinical signs varied widely; 7 dogs died abruptly. In order of onset, clinical features included anorexia, lethargy, vomiting, jaundice, diarrhea (melena, hematochezia), abdominal effusion, peripheral edema, and terminal encephalopathy and hemorrhagic diathesis. Common clinicopathologic features included coagulopathic and electrolyte disturbances, hypoproteinemia, increased serum liver enzyme activities, hyperbilirubinemia, and hypocholesterolemia. Cytologic hepatocellular lipid vacuolation was confirmed in 11 dogs examined. In comparisons of clinicopathologic test results between survivor and nonsurvivor dogs, only granular cylindruria (7/21 dogs) consistently predicted death. Best early markers of aflatoxicosis were low plasma activities of anticoagulant proteins (protein C, antithrombin) and hypocholesterolemia. Despite aggressive treatment, many but not all severely affected dogs died. CONCLUSIONS AND CLINICAL RELEVANCE: Serum liver enzyme activities and bilirubin concentration were unreliable early markers of aflatoxin hepatotoxicosis in dogs. Hypocholesterolemia and decreased plasma protein C and antithrombin activities may function as exposure biomarkers.

Equine feed contamination and toxicology.

Feed as a cause of poisoning in horses can occur on small or large scales. It is challenging to work up cases of suspected feed contamination, but there are resources available to veterinarians and owners. Feed contamination can be chemical or biological. This article focuses on and provides examples of chemical feed contamination including misformulation, adulteration, and natural contaminants. Additionally, recommendations for feed sampling and diagnostic submission, including legal documentation, are included.

Pet Food Recalls and Pet Food Contaminants in Small Animals: An Update.

Commercial pet foods are usually safe, but incidents of contamination can have a devastating impact on companion animals and their owners. There are numerous possible contaminants ranging from natural contaminants to nutrient imbalances to chemical adulteration, making it impossible to predict what will cause the next pet food recall. Veterinarians involvement with pet food recalls includes examining and treating affected animals, documentation and sample collection, and communicating with pet food manufacturers and regulatory agencies.

Severe Lead Toxicosis in a Lionhead Rabbit.

INTRODUCTION: Lead toxicosis occurs in veterinary patients, with few reports involving rabbits, and no previous reports using oral calcium disodium EDTA. CASE REPORT: A 7-year-old male castrated Lionhead rabbit presented to the Cornell University Hospital for Animals (CUHA) for evaluation after a 2-day history of lethargy and a 2-week history of hyporexia. The patient had been observed pulling paint from the walls of the home, a house built circa 1900, in the months prior to presentation. The patient was moderately anemic with a hematocrit of 21% with red blood cell morphological changes consistent with lead toxicosis, including basophilic stippling, nucleated red blood cells, and polychromasia. Radiographic images of the abdomen revealed excessive accumulation of gas in the gastrointestinal tract in a pattern consistent with gastric stasis and numerous small mineral to metallic opacities in the cecum. The blood lead concentration was 792 µg/dL, confirming the diagnosis of lead toxicosis with secondary gastrointestinal stasis. The rabbit was hospitalized for treatment with oral and subcutaneous calcium disodium EDTA for 4 days and then discharged home to the care of the owners. DISCUSSION: Severe lead toxicosis in a rabbit can be treated successfully with oral and subcutaneous calcium disodium EDTA and aggressive supportive treatment.

Zinc Toxicosis in a Boxer Dog Secondary to Ingestion of Holiday Garland.

INTRODUCTION: Increased admissions occur in small animal veterinary emergency clinics during some holidays, and some of the increased caseload is due to ingestion of toxic substances. This report documents zinc toxicosis contributing to the death of a dog after ingestion of holiday tinsel garland. CASE STUDY: A mature boxer dog presented with a 4-day history of vomiting and diarrhea. Radiodense foreign material was detected in the stomach and removed via gastrotomy. The patient clinically worsened over the next several days with evidence of hemolytic anemia, severe hypernatremia, and an elevated WBC count with a suspected dehiscence of the surgical site and acute renal failure. The serum zinc concentration was moderately elevated. Postmortem findings included surgical dehiscence from the gastrotomy and enterotomy sites, hepatic extramedullary hematopoiesis, hemoglobinuric nephrosis, and pancreatic fibrosis. The foreign material removed from the stomach also contained zinc. DISCUSSION: Ingestion of holiday tinsel garland made from metal-coated plastic film has not previously been implicated in zinc toxicosis. Zinc toxicosis has a good prognosis in veterinary medicine when diagnosed and treated promptly, but the unique source of zinc in this dog contributed to the delay in diagnosis and grave outcome in this case.

Comparison of blood and tissue lead concentrations from cattle with known lead exposure.

Blood lead (Pb) is used to diagnose Pb poisoning and exposure in cattle, but there are limited data comparing circulating Pb with concentrations in beef from the same cattle. This study determines whether there is a correlation between blood Pb and tissue Pb concentrations in accidentally exposed cattle. Pb analyses were carried out on ante-mortem blood and post-mortem tissues (including, if available, brain, liver, skeletal muscle, bone, gastrointestinal contents and kidney, and also foetal tissues from one cow) collected from 13 cattle known to have accidental Pb exposure and from three control cows with no known exposure. Variables from cattle were analysed statistically using a Shapiro-Wilk normality test and non-parametric descriptive and association statistics. Blood Pb from exposed cattle rank-correlated with liver, bone and kidney Pb concentrations, but not with the Pb concentrations of brain, skeletal muscle or gastrointestinal contents. The lowest blood Pb concentration associated with a detectable skeletal muscle Pb concentration (> 0.1 mg kg-1 dry matter) was 4.57 µg dl-1. Based on these findings, we recommend that cattle with blood Pb > 2.5 µg dl-1 be withheld from slaughter and that liver, bone and kidney from all cattle with known Pb exposure be withheld from the human food chain.

Treatment of pieris ingestion in goats with intravenous lipid emulsion.

Seven goats and one ram presented with clinical signs including regurgitation, obtundation, anorexia, apparent pain, and bloat. The animals had escaped from their barn, and it was discovered that they had ingested leaves of Pieris japonica, Japanese pieris, a grayanotoxin-containing plant. Animals were treated with antibiotics, calcium borogluconate, B vitamins, and activated charcoal within the first 24-h postexposure, which was followed by the recovery of the ram and two goats and the death of two goats. Approximately 36 h after Japanese pieris ingestion, one of the three remaining anorectic goats was dosed with intravenous lipid emulsion (ILE). This goat recovered within a few hours. The remaining two goats were given ILE the next day and appeared to recover, but one died a week later of aspiration pneumonia.