Cantharidin poisoning of emu chicks by ingestion of Pyrota insulata.

Abstract

In April and May 1992, the Texas Veterinary Medical Diagnostic Laboratory (TVMDL) received for necropsy several frozen 1–3-month-old emu chicks from 1 ranching operation. Insects had swarmed to blooms on mesquite trees (Prosopis glandulosa) near the chick barn, and when a cool front arrived, lights were left on inside to encourage the chicks to seek shelter. As dusk fell, the insects were attracted to the lighted area, and they could be seen covering the floor of the barn and other surfaces accessible to the chicks. The history accompanying the birds described the chicks’ avid consumption of the insects. Some chicks remained clinically normal while others became ataxic, vomited beetles, became prostrate, and died. Some survived by vigorous treatment with oral fluids. Submissions to TVMDL consisted of proventricular contents, the frozen carcasses of 4 emu chicks, and a sample of the suspect insects. At necropsy, the esophagus of each bird was congested and edematous, and the proventricular serosa was hemorrhagic. The gizzard linings were sloughed, the intestinal contents were pink and the livers were pale. Tissue samples for histopathologic evaluation were fixed in 10% neutral buffered formalin, processed, embedded, sectioned and stained with hematoxylin and eosin (HE) prior to microscopic examination. Ingesta were examined under a dissecting microscope. Only 1 of the birds had a large volume of intact ingesta, which included fibrous plant material, small pebbles and 1 beetle about 1 cm long. Insect fragments were found in the proventricular and gizzard contents of 2 of the other chicks. Microscopically, the lesions varied in severity within each animal (Fig. 1). In some chicks, areas of the esophageal mucosa were overlaid with a thick coat of mucus (Fig. 1b). In others, there was multifocal epithelial ulceration with diffuse submucosal necrosis and thrombosis of small submucosal blood vessels (Fig. 1c–e). Catarrhal esophagitis and multifocal esophageal ulceration with underlying inflammation and necrosis were suggestive of exposure to a chemical irritant in a solid form, which was consistent with ingestion of a blister beetle, as opposed to a liquid irritant, which would have produced a more uniform lesion. Ingesta and insects were extracted and analyzed for can-