Confirmed Grayanotoxin Poisoning with Bradycardia from a Gift of Imported Honey.

BACKGROUND: Human grayanotoxin poisoning is distinctly uncommon in North America, as the predominant source of human exposure is honey made by bees pollinating rhododendron species in the Mediterranean. We present a case of confirmed grayanotoxin poisoning from honey imported from Turkey. CASE REPORT: A 61-year-old man developed nausea, lightheadedness, and lost consciousness. Onset was 30 min after the ingestion of honey that was brought to the United States from Turkey. Emergency medical services found him bradycardic, hypotensive, and unresponsive. He was treated with atropine, saline, and oxygen, at which point his heart rate and blood pressure improved, and he regained consciousness. A similar episode several days earlier was followed by a brief unrevealing hospitalization. He was again hospitalized, and had a normal echocardiogram, telemetric monitoring, and complete laboratory studies. Grayanotoxins I and III were subsequently identified in the patient's blood, urine, and honey. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Grayanotoxins are diterpenoids found in rhododendron species, whose clinical effects span multiple organ systems including gastrointestinal, cardiac, and neurologic. Treatment is largely supportive, and a good response to atropine and intravenous fluids has been described. Laboratory confirmation of grayanotoxins is not available in a short enough turnaround time to be clinically useful during immediate management, but confirmatory testing may obviate further unnecessary evaluation. Grayanotoxins are likely to remain a rare source of poisoning in North America, but recurrent bradycardia without alternative etiology should prompt a thorough exposure history, which may reveal, as in this case, a treatable toxicologic etiology.

Fatal bromethalin intoxication in 3 cats and 2 dogs with minimal or no histologic central nervous system spongiform change.

Use of the neurotoxic rodenticide bromethalin has steadily increased since 2011, resulting in an increased incidence of bromethalin intoxications in pets. Presumptive diagnosis of bromethalin toxicosis relies on history of possible rodenticide exposure coupled with compatible neurologic signs or sudden death, and postmortem examination findings that eliminate other causes of death. Diagnosis is confirmed by detecting the metabolite desmethylbromethalin (DMB) in tissues. In experimental models, spongiform change in white matter of the central nervous system (CNS) is the hallmark histologic feature of bromethalin poisoning. We describe fatal bromethalin intoxication in 3 cats and 2 dogs with equivocal or no CNS white matter spongiform change, illustrating that the lesions described in models can be absent in clinical cases of bromethalin intoxication. Cases with history and clinical signs compatible with bromethalin intoxication warrant tissue analysis for DMB even when CNS lesions are not evident.

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.

Evaluation of the toxicity of Adonis aestivalis in calves.

Toxicosis of Adonis aestivalis is well documented in horses, but little is known of its toxicity in cattle. A. aestivalis (summer pheasant's eye) was collected over multiple years, under different growing conditions, and at various stages of maturity, dried, and administered to calves to evaluate the toxicity of A. aestivalis in cattle. Four 300-lb Holstein, and 2 90-lb, preruminating Jersey calves were administered 1% body weight of ground A. aestivalis via a stomach tube and monitored for clinical signs for 2 weeks and 1 week, respectively. The Holstein calves were then fed 0.2 to 1% body weight A. aestivalis daily for 4 to 5 weeks. The Holstein calves had transient, mild cardiac abnormalities during the feeding trial. Mild, transient gastrointestinal and cardiac signs were noted in the preruminating calves. No gross or microscopic lesions were seen on necropsies performed at the end of the study. Based on the results of this study, cattle do not appear to be as susceptible to toxicosis from A. aestivalis as other species, such as horses and pigs.

Acute depigmentation of fertile brown eggs in a commercial layer operation.

Rapid depigmentation of brown eggs is an infrequent but startling event in the commercial egg industry that can result in significant economic losses. Loss of shell pigment in brown-shelled eggs is caused by various factors. In many cases, the exact cause of flock-wide pigment loss remains undetermined. A rapid decline in shell pigmentation was observed in 2 flocks of Hyline brown layers. The lack of evidence of an infectious disease process suggested a feed or management problem. On the basis of a small-scale, "in-house" feeding trial, the feed was identified as the cause of depigmentation. Feed analysis by liquid chromatography with mass spectrometry confirmed the presence of 4,4'-dinitrocarbanilide, a major component of nicarbazin (NCZ). There was no evidence of increased mortality, and only a slight but transient drop in the egg production was observed. Depigmentation effects were rapidly reversed after replacing the feed with NCZ-free feed.