Lead toxicosis in a captive urban rock pigeon (Columba livia)
Emily Brouwer, Markus Luckwaldt
Animal Health Laboratory, University of Guelph, Guelph, ON (Brouwer); Greenwood Park Animal Hospital, Toronto, ON (Luckwaldt)
AHL Newsletter 2023; 27(3):16.
A captive wild rock pigeon (Columba livia) was submitted to the Animal Health Laboratory for postmortem examination. The bird was initially examined six days prior to death for severe crop stasis and distension. At the time of examination, the bird was markedly underweight with pectoral muscle atrophy and a distended crop. Cytology of crop contents identified large numbers of spore-forming bacilli. A wet mount of the crop wash was negative for Gram positive bacilli and trichomonads. Based on these findings, the bird was prescribed a course of amoxicillin/clavulanic acid and trimethoprim sulfamethoxazole. At a recheck examination two days later, there was no improvement in the bird’s condition and a bacterial culture swab was collected and submitted for aerobic and anaerobic culture. The bird died four days following the recheck examination.
On external postmortem examination, the bird was noted to be in poor body condition, with markedly atrophic pectoral muscle mass. The crop was markedly distended, and tan mash-type feed was adherent to the beak and the cere. There was green staining and mild urate pasting around the vent.
Internally, the crop was thin walled and contained abundant mash-type feed. The proventriculus was flaccid and empty. The gizzard contained several small smooth fragments of metal, a small screw, and a piece of thin-gauge copper wire that was embedded into the gizzard and surrounded by fibrosis (Fig. 1). The koilin was stained dark green. Internal fat stores were absent. Based on the gross findings of multiple metallic foreign bodies in combination with presumptive neuropathic paralysis of the crop, liver was sent for quantitative lead levels and routine tissues were sampled for histology.
Figure 1. Multiple foreign bodies removed from ventriculus.
On microscopic examination, the renal tubular epithelium frequently contained round, amphophilic and acid-fast intranuclear inclusion bodies, typical of lead (Fig. 2). There was accumulation of abundant brown granular pigment within hepatocytes. There was also a focus of inflammation in one section of lung that was compatible with aspiration pneumonia. Subtle vacuolation was noted in the brain, as well as dilation of myelin sheaths in the peripheral nerves. Toxicological testing identified significantly elevated liver lead levels at 73 micrograms/g (normal reference intervals in chickens 0.1-0.5 mg/g), and therefore, lead toxicosis was confirmed.
Figure 2. Kidney, H&E, 60X. Intranuclear inclusion bodies in renal tubular epithelium (left).
Kidney, Ziehl-Neelsen, 60X. Acid-fast intranuclear inclusion bodies in renal tubular epithelium (right).
Lead poisoning is well described in avian species who consume lead in the form of various environmental contaminants, including: paint, lead ammunition, fishing weights, grease, or contaminated foliage (typically near smelters, mines, waste dumps, or along roadsides). It is suspected that columbiform birds consume metallic fragments from the environment to serve as grit, as opposed to raptor species who tend to ingest metallic fragments from the gut of prey species. Once ingested, the lead is rapidly absorbed into the bloodstream, redistributed to the soft tissues, particularly the kidneys and liver, and subsequently deposited in bone.
The elevated blood lead levels impact various metabolic functions, including sulfhydryl-containing enzyme activity and mitochondrial function, eventually leading to neurotoxicity, anemia and gastrointestinal dysfunction. Clinical signs of lead intoxication in birds include weakness, altered mentation, tremors/seizures, regurgitation, loss of condition, muscular atrophy, and green discolouration of the urates. Antemortem diagnosis can be made by assessing blood lead levels, and radiographs can be performed to identify metallic foreign bodies in the gastrointestinal tract. Treatment typically involves removing the source of lead from the gastrointestinal tract, followed by chelation. When there is extensive tissue damage, particularly with neurological involvement, treatment is typically unsuccessful. AHL
References
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