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Epidemiology of Animal Poisonings in Asia Chapter | 4  59




  VetBooks.ir  largest eagles. The total population of the Steller’s Sea-  Arsenic (As)
             Eagle is estimated at 5000 6000 on the island of
                                                                As poisoning due to contamination of groundwater is one
             Hokkaido. Pb poisoning of Steller’s Sea-Eagles in Japan
             was first confirmed in 1996. By 2007, 129 Steller’s and  of the most important causes of heavy metal poisoning in
                                                                domestic animals in several countries. However, other
             White-tailed Eagles died from Pb poisoning. Necropsies
                                                                sources of intoxication include dips, sprays, powders, or
             and radiographs also revealed pieces of Pb from rifle bul-
                                                                vegetation contaminated by pesticides containing As
             lets and from shotgun slugs to be present in the digestive
                                                                (Selby et al., 1977).
             tracts of poisoned eagles, providing evidence that a source
                                                                  Dogs and cattle are intoxicated more frequently than
             of Pb was spent ammunition from Pb-contaminated Sika
                                                                other animals; yet sporadic instances of poisoning have been
             deer carcasses. Reacting to the eagle poisoning issue,
                                                                observed in sheep, cats, horses, and pigs. Reports from
             Hokkaido authorities have regulated the use of Pb rifle
                                                                industrial cattle farm in Iran indicated poisoning is either
             bullets since 2000. Despite the overwhelming evidence
                                                                peracute, acute, or chronic in nature. Frequently the initial
             that Pb ammunition is toxic to wildlife and people and the
                                                                and only indication that a severe problem exists with pera-
             broad support for eliminating its use, it remains widely
                                                                cute poisoning in a cattle herd is dead animals. Chronic
             used by hunters (Saito, 2009). In the United States, Pb
                                                                intoxications are also observed in cattle (Bazargani et al.,
             poisoning is on the decrease due to government
                                                                2007). In two other incidences, acute intoxication of As poi-
             regulations to remove Pb from house paint in 1978.
                                                                soning has been reported in young dog and sheep. As is a
             However, dogs can still be exposed to Pb through roofing
                                                                severe alimentary tract irritant in domestic animals, and
             materials, rug padding, linoleum, and other aged house-
                                                                treatment in most instances are primarily symptom-based
             hold  materials  (https://www.vetary.com/dog/condition/
                                                                and supportive (Selby et al., 1977; Javad et al., 2013).
             lead-poisoning). It may be worth mentioning that
             California, in 2013, passed the first state wide phase-out
             of Pb ammunition for all forms of hunting (Anon, 2016).
                                                                Copper (Cu)
                                                                Cu poisoning is common in various parts of Asia. Acute Cu
             Mercury (Hg)
                                                                toxicity results from ingestion of high Cu feeds, Cu salts,
             Hg toxicosis has been reported in cats, pigs, calves, horses,  pesticides, poultry litter, and other high Cu intakes of
             and laboratory animals (rats, mice, mink, ferrets, and  20 100 mg/kg  in  sheep  and  young  calves,  and
             guinea pigs) but rarely in dogs. Clinical signs and lesions  200 800 mg/kg in adult cattle. Chronic Cu toxicity occurs
             of Hg intoxication depend on the species affected, dose  when high levels of Cu are ingested over a period of time
             obtained, route of administration, chronicity of exposure,  but at doses below the acutely toxic level. Sheep are the
             and the chemical form of the Hg involved (Gupta, 2010b).  most susceptible species to chronic Cu toxicity because their
                A sporadic outbreak of a curious disease occurred  liver cells have a high affinity for Cu and they excrete Cu
             among dairy cattle, from early February to late May  into the bile at a very low rate, leading to a build-up of liver
             1955, in Monbetsu District, Kitami Subprefecture of  Cu concentration over time. One of the most common
             Hokkaido in Japan (Katherine et al., 2010). This disease  causes of toxicity in sheep is the accidental feeding of
             was due to poisoning by ingested linseed meal treated  feedstuffs intended for other livestock. Field investigation of
             with mercurial fungicide, “Ceresan.” The characteristic  one closed herd of 400 mixed-breed dairy goats from India
             symptoms of this disease were dyspnea and depilation;  was examined because of a decrease in milk production and
             out of 29 cases, eight died while two were slaughtered.  increase in mortality rate. Nine animals had died within a
             The general symptoms were fever attack, salivation, diar-  1-month period. Goats were found to have been fed a min-
             rhea, bloody feces, depression and anorexia, lacrimation,  eral mix containing 3050 ppm Cu for 9 months prior to the
             decrease in milk production, and cramps. In addition, par-  onset of Cu toxicosis. Clinical signs were evident only in
             tial and diffusive depilation, eczema, and swelling of the  lactating goats and included anorexia and recumbency.
             skin accompanied by itchiness on the entire body surface  In the most severely affected goats, signs progressed to
             were found. Bronchial catarrh was observed in about half  neurologic abnormalities and death (Cornish et al., 2007;
             of the cases, especially; it was distinct in the severe or  Badiye et al., 2013).
             moderate ones. Anemia on all mucous membranes and
             petechial hemorrhages on the nasal and vaginal mucous
             membranes, cardiac disturbance, and swelling of lymph-  NONMETALS AND METALLOIDS
             nodes were also noted in the severe cases. In some  Selenium (Se)
             instances, epistaxis, bloody milk, and nephritis were also
             observed. In another incidents, renal problems have been  Se has chemical and physical properties intermediate
             reported in dogs (Farrar et al., 1994).            between metals and nonmetals and is similar to those of
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