Page 767 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

726 SECTION | X Avian and Aquatic Toxicology

VetBooks.ir regurgitation, pallor, dark or bright green diarrhea, paresis, allows it to penetrate the blood brain barrier, where the
majority of toxic effects are expressed. Selenium can
seizures, and sudden death. In acute cases, corrosive
modify the toxicity of MeHg by forming nontoxic
lesions in the GI tract leading to associated disturbances,
and injury to the liver, kidneys, and pancreas may be mercury selenium complexes, preventing the attachment
observed. In chronic cases, erythrocyte abnormalities and of mercury with sulfhydryl groups of enzymes and other
anemia may be commonly observed due to oxidative dam- bioligands (Sugiura et al., 1976), when the average molar
age to the erythrocyte hemoglobin and cell membrane pro- ratio Hg:Se is approximately 1.0 1.5 and total mercury
teins (Luttgen et al., 1990). Common findings on gross concentrations exceeded about 50 μg/g as reported in
examination of birds that have died from zinc toxicosis eagles, loons and marine or freshwater fishes (Luten
include greenish, mucoid feces in the ileum, colon, or clo- et al., 1980; Scheuhammer et al., 2008).
aca and wasting of pectoral muscles. Microscopically, pan- Clinical signs due to mercury intoxication are similar
creas may reveal severe apoptosis, loss of acinar structure, in multiple species of birds and are characterized by
necrosis of individual acinar cells, and interstitial fibrosis reduced food intake, emaciation, weakness in wings and
(Wight et al., 1986). Hemosiderosis in the liver, accompa- legs, with difficulty flying, walking, and standing.
nied by hepatic biliary retention and multifocal, necrotizing Reproductively, MeHg exposure leads to shell-less eggs,
hepatitis, may be observed. In GI, hemorrhagic enteritis, decrease in mean egg weight, early embryonic mortality
hemorrhagic ventriculitis, and ventricular koilin degenera- and an increase in unfertilized eggs. Most important path-
tion are noted (Puschner et al., 1999). ological findings in birds are atrophy of fat deposits, mus-
Diagnosis of zinc intoxication can be challenging. cles, demyelination and necrosis of nerves in the
History of exposure (e.g., exposure to a new cage, feeding peripheral and central nervous system, and necrosis of
and/or watering utensils, or metallic toys), radiographic renal tubular epithelium.
imaging, measurement of zinc in plasma/serum (live The diagnosis of mercury intoxication should not be
birds) and liver / kidney (dead birds) and histopathology based on tissue concentrations of mercury alone but nec-
can aid diagnosis. For most psittacines, a physiologic, essarily address corresponding selenium concentrations,
nontoxic zinc concentration in serum or plasma is 2 ppm the presence or absence of compatible clinical signs and
(0.2 mg/dL) or less. However physiologic concentrations necropsy findings. There are no successful treatment
are slightly higher of up to 3.5 ppm (0.35 mg/dL) for approaches reported in birds to reverse damage due to
cockatoos and up to 2.5 ppm (0.25 mg/dL) for eclectus mercury intoxication. Feeding uncontaminated food and
parrots (Puschner et al., 1999). Postmortem, liver zinc water is the most practical approach. Selenium and vita-
concentrations exceeding 100 ppm are toxic. min E supplementation can additionally be utilized to
If a radio-dense zinc object is identified by radiogra- reduce the toxic potential of mercury before the appear-
phy, removal of the zinc source results in the rapid ance of expected signs.
decline of body concentrations. If immediate removal is
not possible or delays are expected, reducing the further Iron
absorption of zinc in the GI tract may be achieved by
administering antacids such as calcium carbonate (Van Increased hepatic iron storage or iron storage disease (ISD)
der Merwe and Tawde, 2009 ). Chelation of zinc is possi- is a serious condition noted in captive birds especially in
ble with CaNa 2 EDTA, although its efficacy and safety in some species belonging to families Paradiseadae (birds-of-
the treatment of zinc intoxication in birds have not been paradise), Ramphastidae (toucans), and Sturnidae (star-
evaluated. lings) (Pavone et al., 2014). Avian species that have been
evolved to tolerate relatively low iron content in their diet
have very efficient iron absorption and do not downregu-
Mercury
late their iron absorption when body stores are saturated or
Mercury exists in nature in different forms ranging from on feeding of high-iron containing diets (Klasing et al.,
inorganic elemental forms to complex organic forms. One 2012). Many commercial diets intended for captive birds
of the most toxic forms is methylercury (MeHg) which is have been formulated using the nutritional requirements of
the major source of intoxication in fish-eating birds such poultry and are not optimal for the low-iron tolerating spe-
as loons, mergansers, and bald eagles. Consumption of cies. In addition, the use of animal byproducts significantly
MeHg-containing diets at environmentally realistic con- affects the nutritional interactions and bioavailability of
centrations has been demonstrated to cause behavioral, iron. Absorption of iron from animal byproducts (heme-
neurological, hormonal, and reproductive changes in based iron sources) may be three times higher than that
birds, fish, and mammals (Scheuhammer et al., 2007). from nonheme products containing equivalent iron concen-
MeHg is metabolized and excreted more slowly than trations. Thus excessive dietary iron, nutritional interac-
other organomercurials. The lipophilic nature of MeHg tions increasing the bioavailability and genetically or