Page 769 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

728 SECTION | X Avian and Aquatic Toxicology

VetBooks.ir birds are found dead. Grossly, dead animals often have concentrations approach 60% 70% (Osweiler et al.,
Cyanide is a rapidly acting toxicant; most intoxicated
1985). Ambient CO concentrations of 600 ppm for 30 min
cause clinical signs in chickens; concentrations of
bright red blood and multiorgan congestion (Woldemeskel
and Styer, 2010). 2000 ppm or greater are lethal within 1.5 2h (Brown
A diagnosis is based on the history of exposure and and Julian, 2003).
measurement of cyanide in blood, heart, liver, or brain. Diagnosis of CO intoxication is based on a history
Samples should be stored and shipped frozen to avoid the compatible with CO production, compatible clinical signs,
loss of cyanide before analysis. Denying birds access to and measurement of ambient air CO and blood carboxy-
cyanide-contaminated water is the best preventive hemoglobin concentrations. Treatment is generally limited
approach. to provision of fresh air or oxygen; pet birds can be
placed in oxygen cages.
TOXIC GASES
Polytetrafluoroethylene: Teflon
Ammonia
Polytetrafluoroethylene (PTFE) is a synthetic polymer that
Exposure to toxic concentrations of ammonia mostly occur is widely used as a nonstick surface in cookware and as a
in chickens as a result of decomposition of poultry waste coating on heat lamp bulbs. Heated to high temperatures
and poor ventilation in confined poultry houses (Brown ($280 C), PTFE releases toxic pyrolysis products that can

et al., 1997). Ammonia readily dissolves in water to form cause rapid death of birds. Although all birds are likely to
ammonium hydroxide, which is an alkaline irritant. Thus, be susceptible to intoxication, most spontaneous cases
contact with the moist mucous membranes of the eyes and involve pet birds such as cockatiels, parrots, finches, and
respiratory tract results in corneal and epithelial cell dam- budgerigars. PTFE pyrolysis products contain toxic particu-
age. High ambient air concentrations of ammonia lates of respirable size (,1 μm diameter) that can penetrate
(50 75 ppm) reduce feed consumption, growth rate, and the alveoli. Lung damage is believed to be due to direct
egg production in poultry. Toxic air concentrations cause irritation and oxidative damage (Johnston et al., 1996;
keratoconjunctivitis, corneal ulceration, blindness, photo- Wells et al., 1982). Although there is little comparative
phobia, tracheitis, tachypnea, and dyspnea. Prolonged toxicity information among avian species, budgerigars
exposure can result in increased mucous secretion and were more sensitive than quail in one experimental study.
hyperplasia of the bronchiolar and alveolar epithelium. After exposure, the onset of clinical signs is rapid.
Maintenance of adequate ventilation and prompt Eyelid blinking is an early sign and may be related to a
removal of poultry waste alleviate problems associated direct irritant effect on the conjunctiva and cornea. Eyelid
with excessive ammonia. Ambient ammonia air concen- movements could also be secondary to hypoxia-induced
trations should not be greater than 25 ppm for poultry somnolence. Tachypnea, dyspnea, anxiety, cage wire bit-
(Brown and Julian, 2003). ing, incoordination, and inability to perch or stand may be
due to hypoxia secondary to lung damage. In many cases,
the bird may be found dead with no other clinical signs
Carbon Monoxide
noted. Grossly, the lungs are severely edematous, con-
Toxic exposure to carbon monoxide, CO (a product of gested and hemorrhagic. Histologically, there is extensive,
incomplete combustion of hydrocarbon-based fuels) often severe, necrotizing, and hemorrhagic pneumonitis.
results from use of defective gas catalytic or open-flame Amorphous, elongate particles may also be noted (Wells
brooders, furnaces or internal combustion engines in and Slocombe, 1982).
poorly ventilated spaces, or confinement in an operating A diagnosis is generally based on a history of expo-
vehicle with poor ventilation. Of all the species, canaries sure and characteristic postmortem lesions. Currently,
are known to be susceptible to the toxic effects of CO. there is no analytical test available to confirm exposure to
Harris hawks (Buteo unicinctus) are also very sensitive the pyrolysis products. The rapidity of onset of severe
and many deaths have been reported following transport signs and subsequent death most often precludes treat-
in enclosed pick-up trucks (Redig and Arent, 2008). ment. Awareness of the hazard and avoiding housing
CO competes with oxygen to form carboxyhemoglo- birds near PTFE coatings is the best prevention.
bin which reduces the oxygen carrying ability of red
blood cells, and the oxygen dissociation curve shifts to CONCLUDING REMARKS AND FUTURE
the left, resulting in tissue hypoxia. Affected birds exhibit DIRECTIONS
drowsiness, labored breathing, weakness, and ataxia, with
seizures occurring before death (Brown and Julian, 2003). Given the number and diversity of avian species and their
Birds may be found dead when blood carboxyhemoglobin environments and the diversity of chemicals to which