Anticoagulant rodenticide exposure and toxicosis in four species of birds of prey presented to a wildlife clinic in Massachusetts, 2006-2010

Mortalities among birds of prey from anticoagulant rodenticide (AR) toxicosis have been documented in several countries. Reports on extent of exposure within regions of the United States are limited. This study investigated AR exposure and toxicosis in four species of birds of prey (red-tailed hawks [Buteo jamaicensis], barred owls [Strix varia], eastern screech owls [Megascops asio] and great horned owls [Bubo virginianus]) presented to a wildlife clinic in Massachusetts. The aims of this study are to document the proportion of these four species that died or were euthanized due to their presenting injuries that had detectable amounts of ARs in liver tissue; to identify and quantify ARs present; to describe clinical, postmortem, and histopathologic signs of toxicosis; to evaluate potential sublethal effects of AR exposure; and to associate liver AR level with toxicosis. Birds included in the study were sampled without regard to signs of AR toxicosis. Postmortem examinations were conducted, and liver samples were analyzed for AR residues. Of 161 birds tested, 86% had AR residues in liver tissue. The second-generation AR (SGAR) brodifacoum was identified in 99% of positive birds. Mortality from AR toxicosis was diagnosed in 6% of birds. No indications of sublethal effects of exposure were found, and no association between liver brodifacoum level and signs of toxicosis was apparent. Given the high proportion of birds in this study exposed to ARs, specifically brodifacoum, continued monitoring is warranted as new U.S. Environmental Protection Agency regulations on the sale and use of SGARs are enacted.     

Comparison of two heavy metal chelators for treatment of lead toxicosis in cockatiels

OBJECTIVE: To compare efficacy and safety of meso-2,3-dimercaptosuccinic acid (DMSA) and Ca EDTA for treatment of experimentally induced lead toxicosis in cockatiels (Nymphicus hollandicus). ANIMALS: 137 (69 females, 68 males) healthy cockatiels between 6 months and 8 years old. PROCEDURE: Lead toxicosis was induced by placing lead shot in the gastrointestinal tract. Treatment with Ca EDTA (40 mg/kg of body weight, IM, q 12 h), DMSA (40 or 80 mg/kg, PO, q 12 h), and sodium sulfate salts (SSS; 0.5 mg/kg, PO, q 48 h) was initiated 4 days after induction of lead toxicosis. Blood lead concentrations were determined, using atomic absorption spectrophotometry. Number of birds surviving and blood lead concentrations were compared among groups. RESULTS: In Phase II of the study, administration of DMSA and Ca EDTA significantly decreased blood lead concentrations when used alone or in combination in birds with lead toxicosis. Addition of SSS did not result in further decreases in lead concentrations. Eight of 12 (66.7%) birds without lead toxicosis given 80 mg of DMSA/kg did not survive to the end of the study. Lesions related to treatment with chelating agents were not detected during necropsy. CONCLUSIONS AND CLINICAL RELEVANCE: DMSA and Ca EDTA are effective chelating agents in cockatiels. Because DMSA is administered orally, it may be easier than other chelating agents for bird owners to administer at home. However, the narrow margin of safety of DMSA indicates that this agent should be used with caution.     

Peripheral neuropathy in a turkey vulture with lead toxicosis

Clinical, electromyographic, and pathologic findings characteristic of lead toxicosis were detected in a turkey vulture (Cathartes aura). The bird had generalized lower motor neuron dysfunction that progressed over 5 days. Electromyography revealed diffuse denervation potentials and a presumed decrement in the sciatic-tibial nerve conduction velocity. Histologic examination of peripheral nerves obtained at necropsy revealed changes that could be compatible with lead-induced neuropathy. Lead toxicosis was confirmed by determination of blood lead concentrations. Lead toxicosis causing neurologic disorders in birds has been described. However, this report emphasizes the effects of lead on the peripheral nervous system and demonstrates the use of electromyography for diagnosis of peripheral neuropathy in birds.     

Vitamin A toxicosis in a lorikeet flock.

Vitamin A toxicosis has recently been recognized as a concern for granivorous birds such as cockatiels (Nymphicus hollandicus) and nectarivorous birds such as lorikeets. Such birds have little exposure to performed vitamin A in their wild diet, relying on carotene conversion to supply their vitamin A needs. Multiple clinical problems arose in a lorikeet flock when excessive vitamin A supplementation was used.     

Mushroom toxicosis in dogs in general practice causing gastroenteritis,ptyalism and elevated serum lipase activity

Mushroom toxicosis is rarely diagnosed in dogs and is poorly reported in the veterinary literature. This report suggests that mushroom toxicosis is a potentially under‐diagnosed condition in first opinion practice in the UK. Nine dogs with clinical signs consistent with mushroom toxicosis were identified from the records of an out‐of‐hours emergency service between August 2010 and January 2011. Four dogs were later excluded because of clinical inconsistencies. Clinical signs included acute profuse ptyalism (5/5), diarrhoea (5/5), vomiting (4/5), hypovolaemia (4/5), stuporous (3/5) or obtunded mentation (1/5), miosis (2/5) and hypothermia (2/5). Serum lipase activity was elevated in 4/4 dogs; canine‐specific pancreatic lipase was elevated in the remaining dog. Four dogs recovered with aggressive intravenous fluid therapy, analgesia and supportive care; the remaining dog was euthanased due to severe clinical signs and financial constraints. Mushroom toxicosis is an important differential diagnosis for acute gastroenteritis and one possible cause of some cases of “Seasonal Canine Illness”. Affected dogs may demonstrate elevated pancreatic enzymes and mushroom toxicosis should be considered in cases of elevated lipase or abnormal semi‐quantitative canine‐specific pancreatic lipase activities.     

Psittacine plasma concentrations of elements: daily fluctuations and clinical implications.

During the past 2 decades, the potential for excessive exposure of pet birds to zinc has become a concern for many pet bird owners. Ideally, avian zinc toxicosis is diagnosed on the basis of history of exposure to zinc, radiographic evidence of ingested metal, occurrence of melena, detection of an elevated plasma zinc concentration, and response to treatment. However, most pet birds suspected of having zinc toxicosis present with vague signs and lack of radiographic evidence; therefore, the diagnosis relies on the presence of an elevated plasma zinc concentration. A question was, is there a significant diurnal variation in the zinc concentration in psittacine birds and could this be clinically relevant? Because studies in other species have shown that zinc is not the only element that shows a diurnal variation, the authors examined 13 other plasma elements including arsenic, cadmium, calcium, cobalt, copper, iodine, iron, magnesium, manganese, molybdenum, potassium, selenium, and total phosphorus. Fifteen adult psittacine birds housed in the same aviary were used in this study. Three blood samples, separated by 4 hours, were taken from the right jugular vein in each bird. All elements were measured in plasma. Zinc, copper, and molybdenum revealed diurnal fluctuations. The results of this study suggest that interpretation of clinical samples may be more complicated than previously believed. Furthermore, on the basis of the results of this study, it is possible that some avian reference ranges may need to be reexamined.     

Relationships between demographic variables and lead toxicosis in cattle evaluated at North American veterinary teaching hospitals

OBJECTIVE: To determine associations between age, sex, breed, and month and year of admission and the diagnosis of lead toxicosis in cattle. DESIGN: Retrospective case-control study. Sample Population-Records of all cattle evaluated at North American veterinary teaching hospitals during the years 1963 to 2002, which were available through the Veterinary Medical Database. PROCEDURES: Logistic regression was used to evaluate the associations between postulated risk factors and the occurrence of lead toxicosis in cattle and predict the occurrence of the diagnosis of lead toxicosis in cattle. RESULTS: 413 cases of lead intoxication and 202,363 control cattle were identified and met the inclusion criteria. Cattle < 4 years of age were at increased risk for the diagnosis of lead intoxication relative to cattle > or = 4 years of age. Cattle > or = 2 months and < 6 months of age had the greatest risk for lead intoxication (odds ratio, 12.3). Angus cattle were at greater risk for toxicosis (odds ratio, 1.95), compared with other breeds. The risk of lead toxicosis was greater before 1985 (odds ratio, 1.94) than the risk thereafter. The risk of lead toxicosis diagnosis was greatest in the months of May, June, July, and August. CONCLUSIONS AND CLINICAL RELEVANCE: Lead toxicosis in cattle was associated with age < 4 years and the Angus breed. A seasonal pattern existed with peak occurrence in the late spring and summer. The occurrence of lead toxicosis has declined over time.     

Benzimidazole Toxicosis in Rabbits: 13 Cases (2003 to 2011)

The objective of this study was to evaluate both clinical and histologic anomalies associated with suspected benzimidazole toxicosis in rabbits. Histopathologic records were reviewed from rabbit cases that were diagnosed with suspected benzimidazole toxicosis at 2 specialty pathology services. Medical records were also solicited from veterinarians who treated rabbits with suspected benzimidazole toxicosis. In all, 13 cases were included in this retrospective study. Histologically, presumed radiomimetic lesions of benzimidazole toxicosis were noted in 3 cases. An additional 10 cases exhibited lesions suggestive of benzimidazole toxicosis. Common clinical signs observed in the study of rabbits included inappetence, lethargy, hemorrhage, and death. One rabbit with suspected benzimidazole toxicosis survived. Benzimidazoles should be used judiciously in rabbits at published doses only after the owners are knowledgeable of the potential health risks associated with this class of drugs. The prognosis for rabbits with suspected benzimidazole toxicosis is poor, but supportive care resulted in the survival of 1 suspected case in this study.     

Suspected lead toxicosis in a captive goshawk.

Lead toxicosis was diagnosed in a 3-week-old male goshawk after evaluation of the history, clinical signs, radiographic lesions, and laboratory values. Treatment with Ca-EDTA and supportive measures was successful. The presumed source of lead was from birds that had been shot with a pellet gun and used for food.     

Endrin toxicosis in a cat

Endrin toxicosis was believed responsible for the sudden death of a cat. Stomach contents contained bird remains, and chemical analysis revealed 233 micrograms of endrin/g. The cat's owner had been using an avicide on the premises just before the cat's death. Endrin is an effective pesticide for control of insects, rodents, and birds. It poses a problem with secondary poisoning in other animals.     

Chlorpyrifos Toxicosis in Two Cats

Organophosphate compounds are widely employed for control of external parasites in cats and for control of insects in homes and yards. Chlorpyrifos is a long-acting organophosphate (OP) available for use as a systemically and topically acting parasiticide and insecticide in cattle. Its use on cats is not recommended, and no previous clinical cases of toxicosis have been described. Two cases of chronic chlorpyrifos toxicosis in cats are presented and pathophysiology as well as treatment are discussed. The cats had been showing signs of chronic organophosphate toxicosis before diazepam administration. Signs of acute organophosphate toxicosis were precipitated after diazepam was given. Treatment with pralidoxime chloride (2-PAM) and atropine was attempted. Response to treatment was dramatic and complete recovery was achieved with six injections of pralidoxime and atropine administration.     

Clinical signs of cardiovascular effects secondary to suspected pimobendan toxicosis in five dogs

The purpose of this study was to review the medical records of dogs that were either suspected or known to have ingested large doses of pimobendan and to describe the clinical signs associated with pimobendan toxicosis. The database of Pet Poison Helpline, an animal poison control center located in Minneapolis, MN, was searched for cases involving pimobendan toxicosis from Nov 2004 to Apr 2010. In total, 98 cases were identified. Of those, seven dogs that ingested between 2.6 mg/kg and 21.3 mg/kg were selected for further evaluation. Clinical signs consisted of cardiovascular abnormalities, including severe tachycardia (4/7), hypotension (2/7), and hypertension (2/7). In two dogs, no clinical signs were seen. Despite a wide safety profile, large overdoses of pimobendan may present risks for individual pets. Prompt decontamination, including emesis induction and the administration of activated charcoal, is advised in the asymptomatic patient. Symptomatic and supportive care should include the use of IV fluid therapy to treat hypotension and address hydration requirements and blood pressure and electrocardiogram monitoring with high-dose toxicosis. Practitioners should be aware of the clinical signs associated with high-dose pimobendan toxicosis. Of the dogs reported herein, all were hospitalized, responded to supportive care, and survived to discharge within 24 hr of exposure.     

The individual and combined effects of citrinin and ochratoxin A in broiler chicks

Citrinin (CTN) and ochratoxin A (OA) were fed alone and in combination to broilers from day of hatch until 3 weeks of age. Dietary concentrations of 300 micrograms CTN/g and 3.0 micrograms OA/g were used. Birds fed CTN had significantly (P less than or equal to 0.05) lower body weights than controls on days 14 and 21 and increased water consumption on days 7, 14, and 21. Birds fed OA had significantly lower body weights than controls on days 7, 14, and 21 and increased water consumption on day 14. Birds fed CTN and OA in combination had lower body weights than controls and increased water consumption during the experiment, but the alterations were intermediate in severity when compared with those in birds fed CTN or OA alone. Birds fed OA alone or combined with CTN had higher liver and kidney weights than controls, but birds fed CTN alone had only higher kidney weights. Birds fed both CTN and OA had concentrations of serum constituents similar to those in birds fed OA alone, except the levels of cholesterol and triglycerides were not significantly different from those in the controls. Histological evaluation of the kidney indicated no lesions in birds fed CTN alone, but birds fed OA, alone or in combination with CTN, had increased tubular casts and tubular hyperplasia compared with controls. These data suggest that there were no additive or synergistic toxic interactions when 300 micrograms CTN/g and 3.0 micrograms OA/g were fed simultaneously to broiler chicks for 3 weeks. However, the severe growth depression resulting from OA and the increased water consumption associated with CTN toxicosis were ameliorated when CTN and OA were fed in combination. These data may be useful in diagnosing field cases of mycotoxicosis where both CTN and OA are involved.     

Normal and toxic zinc concentrations in serum/plasma and liver of psittacines with respect to genus differences.

Determination of zinc concentration in serum/plasma and tissue of caged and aviary birds is commonly requested by practitioners because of an increased awareness of zinc toxicity. However, interpretation of zinc levels is often based on normal zinc concentrations established for poultry. Also, it is likely that intergenus differences exist in normal zinc concentrations of pet birds. In an attempt to determine normal and toxic concentration ranges, zinc concentrations in liver (n = 276) and serum/plasma (n = 260) collected from psittacines between 1990 and 1998 were analyzed. Zinc concentrations were determined by inductively coupled argon plasma emission spectroscopy analysis. The results were categorized by genus and, when available, by history. Birds that were diagnosed with zinc toxicosis (on the basis of history, clinical examination, pathology, and laboratory findings) were exempt and not included in establishing normal ranges. The results indicate that important differences occur with respect to genera. For example, cockatoos and Eclectus parrots have higher normal zinc concentrations in serum or plasma than other psittacines. In addition, analysis of all the submitted cases suggests that potentially toxic zinc concentrations in livers of psittacines can be well below the range considered toxic in chickens (> 200 ppm).     

Pancreatic atrophy due to zinc toxicosis in two African ostriches (Struthio camelus)

Two of three captive adult African ostriches exhibited inappetance and weakness. In spite of treatment, the two birds were euthanized because of lack of clinical improvement. Postmortem examination demonstrated exocrine pancreatic degeneration, necrosis, and atrophy. Grossly, one ostrich had a markedly diminished pancreatic mass. Histologically, there was massive pancreatic acinar (exocrine) atrophy, marked interstitial fibrosis, and tubular complex formation in one animal, and the second ostrich had active pancreatic acinar necrosis. Toxicologic testing revealed markedly elevated liver zinc levels in the first two birds, whereas the third ostrich had normal serum levels of zinc and continues without apparent disease. This form of zinc toxicosis, while previously reported in different avian species, has been only rarely described in ratites.     

The postmortem diagnosis of cholecalciferol toxicosis: a novel approach and differentiation from ethylene glycol toxicosis.

The objectives of this study were to develop a novel approach to postmortem diagnosis of cholecalciferol (CCF) toxicosis in dogs using kidney, bile, and urine samples, and to differentiate CCF from ethylene glycol (EG) toxicosis. To achieve these objectives, specimens collected from 2 previous laboratory studies in which dogs were given a single oral toxic dose of CCF (8.0 mg/kg) were used. For EG toxicosis, historical data from the previous 13 years (1985-1998) were reviewed and confirmed cases of EG toxicosis were selected. The historical data were used to compare trace mineral concentrations, specifically of calcium and phosphorus to differentiate between intoxications caused by CCF from that caused by EG in dogs. Kidneys, bile, and urine from dogs that died of CCF toxicosis were analyzed for 25 monohydroxy vitamin D3 (25(OH)D3) and 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) and compared to known control unexposed dogs. Results of this study show that biliary and renal 25(OH)D3 concentrations and renal calcium to phosphorus ratio are of diagnostic value in dogs exposed to toxic concentrations of CCF. The renal calcium to phosphorus ratio was <0.1 in normal dogs, 0.4-0.9 in dogs that died of CCF toxicosis, and >2.5 in dogs that died of EG toxicosis.     

Lead toxicosis in cats-a review

Although the incidence of lead toxicosis in small animals continues to decrease, it remains a significant malady. We have reviewed the literature of the past 45 years, which revealed 70 cases involving cats. Sources, signs, diagnosis, pathology and treatment of feline lead toxicosis are reviewed. In 84% of these cases the source of lead was old paint usually from home renovation. The most common signs in cats are anorexia, vomiting, and seizures. The younger individuals seem more likely to show CNS signs. Since signs are often vague, lead toxicosis may be significantly under diagnosed in cats. The gold standard of diagnostic tests is blood lead concentration, although it does not necessarily correlate with total body burden of lead or with metabolic effects including clinical signs. Diagnostic tests including erythropoietic protoporphyrin (EPP), urine aminolevulinic acid, and others are discussed. Gross findings on necropsy are few and include a yellow-brown discoloration of the liver often with a nutmeg-like appearance. Histological examination may reveal pathognomonic inclusion bodies in liver and renal tissues. Characteristic histological changes in the CNS include neuronal necrosis and demyelination. Treatment of lead toxicosis in cats, as in any species, involves removing the exposure, decontaminating the individual and the environment, supportive care and chelation therapy. The most recently available chelator is succimer (meso 2,3-dimercaptosuccinic acid). Succimer given orally is well tolerated and has a wide margin of safety. A high index of suspicion of lead toxicosis is warranted in cats since they often present with vague and non-specific signs. With any consistent history owners need to be asked about home renovation. Early diagnosis and treatment affords a good prognosis.     

Inherited copper toxicosis in the Bedlington terrier: a report of two clinical cases

The clinical signs, laboratory findings and pathological changes are described in two cases of inherited copper toxicosis in the Bedlington terrier. The first case presented with acute signs of depression, vomiting, anorexia, weight loss and jaundice while the second case followed a more chronic course with less severe clinical signs which included weight loss and ascites. Both dogs had elevated circulating levels of alanine aminotransferase (ALT), however other haematological and biochemical parameters, while reflecting liver involvement, varied between the two cases. Chemical analysis of the liver revealed elevated copper levels in both cases (951·7 and 1093·4 μg/g wet weight respectively; normal less than 150 μg/g). These levels, however, are less than some affected but asymptomatic Bedlington terriers. Pathologically the first case had micronodular cirrhosis, while the second had focal hepatitis with fibrosis. Both dogs showed vacuolation of the white matter in the cerebrum, cerebellum, midbrain and medulla. Attention is drawn to the similarities and differences between copper toxicosis in the Bedlington terrier and Wilson's disease in man.     

An unusual incidence of neurological disease affecting horses during a drought

The clinical, pathological and epidemiological factors were investigated in 12 horses presenting with severe neurological signs. Although the cases involved differing central (n = 1), spinal cord (n = 4) and peripheral nerve (n = 7) deficits in a number of instances, there were similar pathological findings. The possibility of a unifying aetiological factor, such as a toxicosis, is discussed because of the pathological similarities and as the cases appeared during an unusually long dry period.     

5-Fluorouracil Toxicosis in the Dog

Twenty-six cases of accidental 5-fluorouracil (5-FU) ingestions by dogs were reviewed from phone calls to the Illinois Animal Poison Information Center. Cases were collected from January 1, 1987 to December 31, 1988. Of the 26 calls involving 5-FU exposures, 12 were classified as "toxicosis," 13 as "suspected toxicosis," and one as "exposure." Dogs were the only species involved in 5-FU cases received during this time. Accurate estimates of the amount of 5-FU ingested by dogs could be made in 17 cases. Ingestion of more than 20 mg/kg of 5-FU was associated with the development of toxicosis. None of the 12 dogs that ingested oral doses in excess of 43 mg/kg (estimated) survived. Clinical signs associated with 5-FU poisoning in the dog were death, seizures, vomiting (with and without blood), tremors, diarrhea (with and without blood), ataxia, and depression. Clinical signs generally developed within 45 to 60 minutes after exposure, and deaths occurred 6 to 16 hours after ingestion.