[Anticoagulant rodenticide poisoning in dogs: Retrospective analysis of clinical and laboratory diagnostic data]. / Vergiftung mit Cumarinderivaten beim Hund: Retrospektive Analyse klinischer und labordiagnostischer Daten.

OBJECTIVE: In this retrospective study, patient records of dogs suffering from poisoning with coumarin derivatives were evaluated to characterize the clinical appearance more precisely. MATERIAL UND METHODS: Retrospective data analysis included 52 dogs with hemostaseologically proven anticoagulant rodenticide poisoning which were treated as inpatients at the Clinic for Small Animals between September 2011 and October 2018. RESULTS: In only 2 dogs (4%) the intake of poison could be observed with certainty. The most common clinical signs observed were reduced general behavior (79%), pallor of the mucosa (79%), anorexia (60%), and dyspnea/tachypnea (60%). In contrast, macroscopically visible internal and external bleedings occurred less frequently. Initially, all cases showed a highly altered prothrombin time and most patients a considerably prolonged activated partial thromboplastin time. Anemia was present in 75% of patients. All dogs included in the study received initially an intravenous treatment with 10 mg/kg vitamin K1. Pretreatment with 1 mg/kg prednisolone was given for prophylaxis of possible incompatibility reactions. No patient showed signs of anaphylactic reaction. Transfusions of whole blood or concentrated red cells were given to only 10 of the 52 animals; only one received 2 transfusions of erythrocytes. 94% of the animals could be discharged home for outpatient therapy after a median length of hospitalization of 3 days (1-9 days) with physiological or almost physiological coagulation test results. CONCLUSION: Anticoagulant rodenticide poisoning is often associated with non-specific symptoms and good prognosis if treated adequately. CLINICAL RELEVANCE: Coagulation diagnostics is always indicated in cases with unclear disorders. In life-threatening emergencies, immediate intravenous infusion of high-dose vitamin K1 is a very effective treatment and results in a rapid increase in coagulation factor activity.

Selenosis in Ruminants.

Selenium (Se) is a metalloid that exists as a red amorphous powder, reddish crystal, silver-gray crystal, or brown-black solid. Its potency as a nutrient and a toxicant is such that few people have seen the pure element. It is easy to lose sight of the narrow margin between too little and too much. The most common cause of selenosis is accidental or intentional overuse of supplements. Many target organs and effects of Se toxicity are similar to those of Se deficiency, so laboratory confirmation is necessary. Prevention consists of minimizing exposure to seleniferous feedstuffs and optimizing dietary factors that might aggravate selenosis.

MYONECROSIS AND DEATH DUE TO PRESUMED MICROCYSTIN TOXICOSIS IN AMERICAN WHITE PELICANS (PELECANUS ERYTHRORHYNCOS).

Over a period of 5 mo, seven out of eight American white pelicans (Pelecanus erythrorhynchos) housed on a spring-fed pond at a zoo died or were euthanized. Clinical signs included inability to stand, anorexia, and weight loss. Clinicopathologic findings included heterophilic leukocytosis and elevated creatine kinase and aspartate aminotransferase. Histopathologic findings on all pelicans demonstrated severe, chronic, diffuse rhabdomyofiber degeneration and necrosis, making vitamin E deficiency a differential diagnosis despite routine supplementation. Based on tissue and pond water assays for the cyanobacterial toxin, microcystin, toxicosis is suspected as the inciting cause of death in these cases. We hypothesize that vitamin E exhaustion and resultant rhabdomyodegeneration and cardiomyopathy were sequelae to this toxicosis.

Successful management of Heinz body hemolytic anemia associated with leek (Allium ampeloprasum) ingestion in a South American coati (Nasua nasua).

OBJECTIVE: To describe the diagnosis, management, and outcome of Heinz body hemolytic anemia in a South American coati (Nasua nasua) secondary to suspected leek (Allium ampeloprasum) toxicosis. CASE SUMMARY: A South American coati presented with Heinz body hemolytic anemia following addition of leeks to its diet for 2-5 days prior to initial presentation. Administration of a whole blood transfusion from an animal of the same species (conspecific) and supportive care resulted in immediate improvement in clinical signs. Normal behavior fully returned within 6 days of transfusion. Hematological evidence of anemia resolved by 4 weeks and there were no significant features of oxidative injury present by 8 weeks following initial presentation. NEW INFORMATION PROVIDED: This is the first reported case of Heinz body hemolytic anemia, suspected leek toxicosis, and administration of a blood transfusion in this species.

Successful Management of Severe Bromethalin Toxicosis in a Dog.

ABSTRACT The use of bromethalin rodenticides has risen since 2011, and in some states, it is the most common rodenticide ingestion reported to poison control. Although intravenous lipid emulsion (ILE) has been previously reported to lower serum desmethylbromethalin levels in an asymptomatic dog, and repeated mannitol has been investigated in a laboratory setting, there are no published reports of successful treatment of symptomatic bromethalin toxicosis in dogs. A 9 yr old castrated male Norwich terrier was evaluated for obtunded mentation, seizures, cranial nerve deficits, and tetraparesis secondary to bromethalin toxicosis. The patient was treated with ILE, mannitol, and ginkgo biloba and returned to normal neurological function. Bromethalin exposure was confirmed by serum desmethylbromethalin levels. Previous literature indicates that the prognosis for patients who suffer from symptomatic bromethalin toxicosis is poor to grave, and the return to normal neurological function after severe toxicosis has not been reported. ILE, mannitol, and ginkgo biloba are readily available and relatively inexpensive, and in combination may be of benefit in symptomatic bromethalin intoxication.

Acute barium poisoning in a dog after ingestion of handheld fireworks (party sparklers).

OBJECTIVE: To report a case of acute barium poisoning in a dog subsequent to ingestion of a common handheld pyrotechnic (sparkler). CASE SUMMARY: A 5-year-old female neutered German Shorthaired Pointer presented with acute onset of generalized flaccid muscle paralysis and fasciculations, ptyalism, and an irregular heart rhythm. Marked hypokalemia (1.9 mmol/L [mEq/L]; reference range [3.5-5.8 mmol/L [mEq/L]), acidemia (pH 7.20; reference range 7.38-7.44), and hypoventilation (PvCO2 55 mm Hg; reference range 40-50 mm Hg) were present on admission. Treatment consisted of fluid therapy, aggressive IV potassium chloride supplementation, gastric lavage, and oral magnesium sulfate administration. Based on history and clinical presentation, barium intoxication after ingestion of handheld firework (sparklers) was suspected and a serum sample was submitted for barium analysis. The serum barium concentration determined by inductively coupled plasma/mass spectrometry was 2,000 µg/L, a 3 orders of magnitude elevation above previously reported normal values in dogs. Within 18 hours of admission, the clinical signs resolved and the blood potassium concentration normalized. The animal was discharged home 36 hours after admission. On follow-up performed after 1 and 5 years, no health issues were apparent. NEW INFORMATION PROVIDED: To the authors' knowledge, this is the first report of acute, life-threatening barium toxicosis characterized by flaccid paralysis, acidemia, and severe hypokalemia occurring in a dog after ingestion of a popular pyrotechnic (sparkler) containing barium nitrate. Clinical signs may resolve within 24 hours with appropriate supportive care including aggressive potassium supplementation and chelation therapy.

Anticoagulant rodenticide toxicosis causing tracheal collapse in 4 small breed dogs.

OBJECTIVE: To describe 4 cases of tracheal narrowing attributed to tracheal mucosal hemorrhage caused by anticoagulant rodenticide toxicity in breeds predisposed to tracheal collapse. CASE SUMMARY: Over the years 2005-2014, 4 dogs were presented for respiratory distress secondary to diffuse tracheal narrowing. All dogs had possible anticoagulant rodenticide ingestion and prolonged prothrombin time. All dogs received fresh-frozen plasma transfusions, vitamin K1 supplementation, and supportive care. Tracheal narrowing improved on follow-up radiographs in 3 of 4 patients. One of 4 did not have follow-up radiographs performed. All dogs survived. NEW OR UNIQUE INFORMATION PROVIDED: Anticoagulant rodenticide toxicity causing clinical signs consistent with tracheal collapse is a rare but recognized phenomenon that has not been previously reported in breeds prone to tracheal collapse.

Retrospective evaluation of the effectiveness of xylazine for inducing emesis in cats: 48 cats (2011-2015).

OBJECTIVE: To determine the effectiveness of xylazine for the induction of emesis in cats that were suspected of ingesting potentially toxic substances or foreign objects. DESIGN: Retrospective study. SETTING: Private emergency and specialty referral hospital. ANIMALS: Forty-eight client-owned cats that were administered xylazine to induce emesis for decontamination of a toxic substance or expulsion of an ingested foreign object. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The medical records of 48 cats presenting for known or suspected ingestion of foreign material that underwent decontamination with xylazine were reviewed. Signalment, material ingested, dose and route of xylazine administration, success of emesis and recovery of foreign material ingested, use of a reversal agent, and adverse effects were noted. The induction of emesis was successful in 29/48 (60%) of cats. Sedation was the most common adverse effect and was noted in 15/48 (31%) of patients. CONCLUSIONS: Xylazine is safe and reasonably effective at inducing emesis in cats.

Utilização de sal mineral rico em molibdênio na prevenção da intoxicação cúprica acumulativa em ovinos - microminerais hepáticos / Use of molybdenum rich mineral mix in the prevention of cumulative cooper poisoning in sheep - hepatic microminerals

Este estudo avaliou a capacidade de um sal mineral rico em molibdênio (Mo) em prevenir a intoxicação cúprica acumulativa (ICA), mediante a análise das variáveis clínicas e dos teores de cobre (Cu) e Mo hepático. Foram utilizados 25 ovinos cruzados da raça Ile-de-France, aleatoriamente distribuídos igualmente em cinco grupos, em que o grupo 1 recebia dieta contendo 80% de volumoso e 20% de concentrado, os grupos 2 e 3 recebiam 50% de volumoso e 50% de concentrado, e os grupos 4 e 5 recebiam a mesma dieta dos grupos 2 e 3, com a adição diária de 150mg de sulfato de Cu. Os grupos 1, 3 e 5 recebiam sal mineral contendo 300ppm de Mo. Foram realizadas três biópsias hepáticas para determinação de Cu, Mo e Zn. Três ovinos do grupo 4 e um do grupo 5 manifestaram ICA. Não houve diferença na frequência de mortalidade entre os grupos (P=0,56). Os teores de Cu hepático nos ovinos com ICA (2450ppm) foram superiores aos que não intoxicaram (1518ppm). Quanto maior a ingestão de Mo na dieta, menor foi o acúmulo de Cu hepático ao término do experimento (r = -0,72).(AU)

The aim of this project is to evaluate the capacity of a molybdenum-rich mineral salt in the prevention of cumulative cooper poisoning (CCP) in sheep, through clinical and hepatic copper and molybdenum concentrations. Twenty five crossbreed Ile-de-France sheep were randomly distributed equally into five groups. Group 1 received a 80% forage and 20% concentrate diet, groups 2 and 3 received a 50% forage and 50% concentrate diet, and groups 4 and 5 received the same diet as groups 2 and 3 with a daily supplementation of 150 mg of copper sulfate. Groups 1, 3 and 5 received a mineral salt with 300 ppm of molybdenum. Three times during the experiment a liver biopsy was carried out to evaluate the degree of copper accumulation. Three sheep from group 4 and one sheep from group 5 showed a clinical picture of CCP. There was no difference in the frequency of mortality between groups 4 and 5 (P=0.56). The liver copper concentration was higher in sheep with CCP (2450 ppm) compared to sheep that did not present CCP (1518 ppm). The higher the ingestion of molybdenum in the diet the lower the liver copper concentration at the end of the experiment (r=-0.72).(AU)

Evaluation and comparison of xylazine hydrochloride and dexmedetomidine hydrochloride for the induction of emesis in cats: 47 cases (2007-2013).

OBJECTIVE: To evaluate and compare i.m. administration of xylazine hydrochloride and dexmedetomidine hydrochloride for the induction of emesis in cats. DESIGN: Retrospective case series. ANIMALS: 47 cats with a history of suspected ingestion of a toxic substance or foreign material between June 2007 and June 2013. PROCEDURES: Data collected for analysis from the medical records included signalment, drug dose and route of administration, whether a repeated dose of the emetic agent was administered, and outcome (emesis, yes or no). RESULTS: Cats in the 2 treatment groups did not differ with regard to age, sex, or breed distribution. The range of doses of xylazine administered i.m. was 0.36 to 0.64 mg/kg (0.16 to 0.29 mg/lb). The range of doses of dexmedetomidine administered i.m. was 6 to 18 µg/kg (2.7 to 8.2 µg/lb). A repeated dose of xylazine or dexmedetomidine was given to 3 and 1 cats, respectively. Emesis was successfully induced in 24 of the 47 (51.1%) cats. Nine of the 21 (43%) cats that received xylazine vomited and 15 of the 26 (58%) cats that received dexmedetomidine vomited. Percentage of cats that vomited after either drug administration did not differ significantly. CONCLUSIONS AND CLINICAL RELEVANCE: Following i.m. administration in cats, xylazine and dexmedetomidine were similarly effective for induction of emesis, indicating that dexmedetomidine is a comparable alternative to xylazine for this purpose. Prospective studies are needed to determine the optimal i.m. dose of dexmedetomidine for induction of emesis in cats.

Treatment of zinc toxicosis in a dog with chelation using d-penicillamine.

OBJECTIVE: To describe chelation therapy with d-penicillamine for treatment of zinc toxicosis in a dog. CASE SUMMARY: A 1.5-year-old intact female Maltese dog weighing 2.7 kg was presented with acute, progressive anorexia, lethargy, pigmenturia, and melena. The owner reported that the dog had ingested a hook from a dog leash made of a zinc-based alloy 9 days prior. A blood transfusion was administered and an abdominal radiograph revealed a metal-dense foreign body in the stomach. Laboratory findings revealed a serum zinc concentration of 1845.12 µg/dL (reference interval, 70-200 µg/dL) and a decreased hematocrit that remained low despite removal of the zinc foreign body. On day 3, another blood transfusion was performed and d-penicillamine therapy was instituted. After the administration of d-penicillamine, the clinical signs and hemogram progressively improved and the dog was discharged 2 days later. On day 9 after initial presentation, the hematocrit and platelet values were within normal limits and the serum zinc concentration was 280.16 µg/dL. NEW OR UNIQUE INFORMATION PROVIDED: This case demonstrates the use of d-penicillamine in the treatment of zinc toxicosis. Serum zinc concentration appeared to decline more rapidly after administration of d-penicillamine than before chelation therapy. This is the first report to evaluate serial serum zinc concentrations before and during chelation therapy with d-penicillamine.

Assessment of dexmedetomidine and other agents for emesis induction in cats: 43 cases (2009-2014).

OBJECTIVE: To compare the use of dexmedetomidine hydrochloride, xylazine hydrochloride, and hydrogen peroxide for emesis induction in cats. DESIGN: Retrospective case series. ANIMALS: 43 client-owned cats for which emesis induction was attempted because of known or suspected toxicant ingestion or recent ingestion of a string foreign body. PROCEDURES: Data collected from the cats' medical records included type, dose, and route of administration of emetic agent; outcome of attempted emesis induction; time until emesis or postemesis administration of a reversal agent (to counter sedative effects of the emetic agent); and adverse events. RESULTS: Emesis induction was attempted by oral administration of hydrogen peroxide (n = 3) or IM or IV administration of xylazine (25 [including 1 cat that had already received hydrogen peroxide]) or dexmedetomidine (16). No cat that received hydrogen peroxide vomited. Emesis was induced in 11 of 25 xylazine-treated cats and in 13 of 16 dexmedetomidine-treated cats. Dexmedetomidine was more likely to cause vomiting than xylazine (OR, 5.5; 95% confidence interval, 1.1 to 36). The median dose of dexmedetomidine that caused emesis was 7.0 µg/kg (3.2 µg/lb; range, 0.96 to 10.0 µg/kg [0.44 to 4.55 µg/lb]). The elapsed time until emesis or postemesis reversal agent administration was recorded for 5 xylazine-treated cats (median interval, 10 minutes [range, 5 to 175 minutes]) and 10 dexmedetomidine-treated cats (median interval, 5 minutes [range, 1 to 12 minutes]). Sedation was the only adverse effect, occurring in 2 xylazine-treated cats and 1 dexmedetomidine-treated cat. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that dexmedetomidine can be used successfully to induce emesis in cats.

A novel strain of Cellulosimicrobium funkei can biologically detoxify aflatoxin B1 in ducklings.

Two experiments were conducted to screen microorganisms with aflatoxin B1 (AFB1 ) removal potential from soils and to evaluate their ability in reducing the toxic effects of AFB1 in ducklings. In experiment 1, we screened 11 isolates that showed the AFB1 biodegradation ability, and the one exhibited the highest AFB1 removal ability (97%) was characterized and identified as Cellulosimicrobium funkei (C. funkei). In experiment 2, 80 day-old Cherry Valley ducklings were divided into four groups with four replicates of five birds each and were used in a 2 by 2 factorial trial design, in which the main factors included administration of AFB1 versus solvent and C. funkei versus solvent for 2 weeks. The AFB1 treatment significantly decreased the body weight gain, feed intake and impaired feed conversion ratio. AFB1 also decreased serum albumin and total protein concentration, while it increased activities of alanine aminotransferase and aspartate aminotransferase and liver damage in the ducklings. Supplementation of C. funkei alleviated the adverse effects of AFB1 on growth performance, and provided protective effects on the serum biochemical indicators, and decreased hepatic injury in the ducklings. Conclusively, our results suggest that the novel isolated C. funkei strain could be used to mitigate the negative effects of aflatoxicosis in ducklings.

Poisoning of dogs and cats by drugs intended for human use.

One of the main causes of poisoning of small animals is exposure to drugs intended for human use. Poisoning may result from misuse by pet owners, off-label use of medicines or, more frequently, accidental ingestion of drugs that are improperly stored. This review focuses on classes of drugs intended for human use that are most commonly involved in the poisoning of small animals and provides an overview of poisoning episodes reported in the literature. To perform this review a comprehensive search of public databases (PubMed, Web of Science, Scopus, Google Scholar) using key search terms was conducted. Additionally, relevant textbooks and reference lists of articles pertaining to the topic were reviewed to locate additional related articles. Most published information on small animal poisoning by drugs intended for human use was from animal and human poison control centres or from single case reports. The dog was the species most frequently poisoned. The major drugs involved included analgesics (nonsteroidal anti-inflammatory drugs), antihistamines (H1-antihistamines), cardiovascular drugs (calcium channel blockers), central nervous system drugs (selective serotonin reuptake inhibitors, baclofen, benzodiazepines and zolpidem), gastrointestinal drugs (loperamide), nutritional supplements (vitamin D and iron salts) and respiratory drugs (ß2-adrenergic receptor agonists).

Intoxicação por selênio em suínos no Sul do Brasil / Selenium poisoning in swine in southern Brazil

Two outbreaks of poisoning by selenium in swine in southern Brazil are described. Piglets were affected in the post-weaning period, between 27 and 22 days, with mortality rates ranging from 16% to 15.3% (Outbreak 1 and 2 respectively). The pigs had focal symmetrical poliomielomalacia and hoof lesions, which were initially characterized by a reddish line at the coronary band that evolved in surviving pigs to release of the hooves. Clinical signs were observed after six days (Outbreak 1) and 30h (Outbreak 2) after the introduction of feed with high selenium content...

São descritos dois surtos de intoxicação por selênio em suínos na região Sul do Brasil. Foram acometidos leitões em fase de creche, entre 27 e 22 dias, com mortalidade variando de 16% a 15,3% (Surto 1 e 2 respectivamente). Os suínos apresentaram poliomielomalacia simétrica focal e lesões de casco, que inicialmente eram caracterizadas por uma linha avermelhada na borda coronária que evoluía nos suínos sobreviventes para desprendimento do casco. Os sinais clínicos iniciaram após seis dias (Surto 1) e 30 horas (Surto 2) da introdução da ração com alto teor de selênio...

Acute enteral manganese intoxication with hepatic failure due to ingestion of a joint supplement overdose.

Manganese is a ubiquitous, essential trace element and a common ingredient of joint supplement tablets. Little information is known about the inherent toxic potential if ingested at higher doses. A 5-year-old female spayed Pug dog presented for evaluation of vomiting and ataxia after accidental ingestion of approximately 100 joint supplement tablets. The dog developed acute hepatic failure and was euthanized 6 days after presentation due to progression of the disease. Necropsy showed severe acute hepatic necrosis. Liver and kidney samples were submitted for toxicology analysis, results of which showed severely elevated manganese concentrations in the liver and kidneys.

Pathogenesis and preventive treatment for animal disease due to locoweed poisoning.

Locoweeds are perennial herbaceous plants included in Astragalus spp. and Oxytropis spp. that contain the toxic indolizidine alkaloid swainsonine. The livestock that consume locoweed feeding can suffer from a type of toxicity called "locoism." There are aliphatic nitro compounds, selenium, selenium compounds and alkaloids in locoweed. The toxic component in locoweeds has been identified as swainsonine, an indolizidine alkaloid. Swainsonine inhibits lysosomal α-mannosidase and mannosidase II, resulting in altered oligosaccharide degradation and incomplete glycoprotein processing. As a result, livestock that consume locoweeds exhibit several symptoms, including dispirited behavior, staggering gait, chromatopsia, trembling, ataxia, and cellular vacuolar degeneration of most tissues by pathological observation. Locoism results in significant annual economic losses. Recently, locoweed populations have increased domestically in China and abroad, resulting in an increase in the incidence of poisoning. Therefore, in this paper, we review the current research on locoweed, including on species variation, pathogenesis, damage and poisoning prevention measures.

Copper toxicosis in New Zealand White rabbits (Oryctolagus cuniculus).

Six 12- to 14-month-old New Zealand White rabbits were diagnosed with copper toxicosis. These rabbits were part of a group of 110 purchased and shipped overnight for research purposes. On arrival, the group experienced an abrupt diet change. Eight died over 3 weeks and 6 were submitted for postmortem examination. Microscopic findings included severe centrilobular to midzonal hepatocellular necrosis with rhodanine stain-positive copper granules in the remaining hepatocytes. Mild periportal fibrosis and biliary hyperplasia, hemoglobinuric nephrosis, and splenic erythrophagocytosis were also observed. Hepatic copper concentrations were elevated, ranging from 319 to 997 ppm. Clinical disease was not previously observed in younger rabbits gradually transitioned from the supplier's copper-supplemented diet. Copper toxicosis likely occurred in these rabbits from a combination of (1) increased duration of copper supplementation leading to increased hepatocellular stores and (2) stress leading to anorexia and release of hepatocellular copper stores similar to chronic copper toxicosis as described in sheep.

An outbreak of sodium fluoroacetate (1080) intoxication in selenium- and copper-deficient sheep in California.

Sodium fluoroacetate is an organofluorine compound toxic to mammals, insects, and birds, currently registered for use only in livestock protection collars as a predacide in some North American states, with restricted use in California. A flock of 445 lambs and ewes in California were moved into a native pasture on a municipal refuse disposal site. Within 24 hours, 14 ewes were found dead, and the remaining sheep were moved off the site. Both ewes and lambs exhibited disoriented running, followed by apparent blindness, weakness, ataxia, coma, and death. Over the next 4 days, 63 ewes and 80 lambs died with a peak at 3 days after grazing the suspect pasture (157/445, 35% mortality). Two dead 4-month-old lambs and 2 ewes were submitted to the California Animal Health and Food Safety laboratory for necropsy. Grossly, there were bilateral diffuse pulmonary congestion and edema, hydrothorax and hydropericardium with fibrin clots, and multifocally extensive areas of epicardial petechiae, ecchymoses, and pallor. In 1 ewe, there was regional caudodorsal pulmonary hemorrhage and intraluminal tracheal clotted blood. Microscopically in all cases, there was multifocal acute myocardial degeneration and necrosis with nonsuppurative pleocellular myocarditis. Sodium fluoroacetate was detected in kidney from a lamb and a ewe at 27.5 and 12.5 parts per billion, respectively. All sheep were selenium deficient, and concurrent copper deficiency was diagnosed in 3. The pathological and toxicological findings were consistent with 1080 poisoning, possibly exacerbated by micronutrient deficiency. This outbreak raised an alert about the use of restricted products with potential lethal effect in animals in California.

Contents of various elements in the organs of seabirds killed by an oil spill around Tsushima Island, Japan.

Twenty nine oil-soaked birds were collected from around the Coast of Tsushima Island. The contents of eight elements in the livers and kidneys of the birds were investigated. Statistically higher concentrations of vanadium and thallium in the liver and of titanium in the kidney were found in the birds that were found dead compared with those that died after rescued. A significant correlation (r=0.695, P<0.01) was observed only for the molybdenum content between the kidneys and livers from the birds found dead. Although the controls of the eight elements of birds investigated in the present study remain unexplained, some of lower concentration in rescued birds can be blamed on a decrease in food intake of birds. The relation between oil contamination and concentration of elements need to be further explored.