Page 746 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

VetBooks.ir Chapter 53

Avian Toxicology

Arya Sobhakumari, Robert H. Poppenga and Snehal Tawde

INTRODUCTION relay toxicosis is a more common occurrence in wild
birds than in pet birds or poultry.
There are approximately 30 orders of birds in the Aves
Most commercial poultry are raised in well-controlled
class, with approximately 2000 genera and 10,000 spe-
environments and are provided quality feed and water.
cies. Obviously, such a large class of animals possesses a
Thus, their potential for exposure to toxicants is more
bewildering array of unique physiologic adaptations,
limited. However, poultry can become intoxicated follow-
behaviors, and ecologic niches. Thus, a discussion of a
ing exposure to common feed additives such as
broad topic such as avian toxicology presents a daunting
ionophores, if feed misformulations occur. Obviously,
task. This chapter provides an overview of toxicologic
free-ranging poultry are potentially exposed to a greater
hazards to three subsets of birds: pet and aviary birds,
variety of hazardous chemicals.
poultry and other farm-raised birds, and wild birds. Given
the breadth of the topic, this chapter is not an exhaustive
treatise but, it is hoped, provides an overview of major Physiologic Differences of Birds Relevant
avian toxicologic hazards. to Toxicology
Respiratory System
Environment as a Toxicological Risk The unique physiology of a bird’s respiration makes them
more susceptible to some inhaled toxicants, such as car-
Factors in Birds
bon monoxide (CO) and pyrolysis products from over-
The increase in popularity of pet birds and their confine- heated Teflon. The sensitivity of birds to inhaled
ment in a home environment exposes them to toxicants toxicants brings to mind the image of the canary in the
that poultry and wild birds are unlikely to come into coal mine. Several physiologic differences of birds
contact with, such as the pyrolysis products from Teflon- increase their sensitivity to inhaled toxicants, such as
coated cookware. Alternatively, pet birds can be exposed a higher mass specific minute ventilation, a higher
to toxicants to which poultry and wild birds are also mass specific ventilation of gas-exchange tissues, cross-
exposed but that are in different forms or from different current and countercurrent gas-exchange mechanisms, and
sources. For example, pet birds can be intoxicated by a gas-diffusion barrier one-half the thickness of that of
lead, most often in the form of lead-based paint or lead mammals (Brown and Wang, 1997). These physiologic
objects such as drapery weights or toys, whereas wild adaptations are a result of high metabolic rates of birds
birds are frequently intoxicated following ingestion of and the concomitant need for a high ventilatory capacity.
lead ammunition or lead-containing fishing gear.
Wild birds exist in a much less well-controlled envi- Metabolic System
ronment than do pet birds or poultry and are therefore
A number of studies have examined the metabolism of
exposed to a greater variety of potential toxicants. One
xenobiotics in a variety of avian species and compared
unique aspect of wild bird toxicology is the potential
metabolic capabilities of birds and mammals (Pan and
exposure of wild birds to toxicants via their prey. Raptors
Fouts, 1978; Dalvi et al., 1987). Organophosphate (OP)
and scavengers such as turkey vultures or condors are
insecticides are more toxic to birds than mammals, and
often poisoned as a result of feeding on animal carcasses
the basis for this difference is primarily due to differences
contaminated with pesticides or lead. Thus, secondary or
in OP metabolism. For example, dimethoate is 20 times
Veterinary Toxicology. DOI: http://dx.doi.org/10.1016/B978-0-12-811410-0.00053-2
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