Clinical signs and duration of cyanide toxicosis delivered by the M-44 ejector in wild dogs

Sodium cyanide poison is potentially a more humane method to control wild dogs than sodium fluoroacetate (1080) poison. This study quantified the clinical signs and duration of cyanide toxicosis delivered by the M-44 ejector. The device delivered a nominal 0.88 g of sodium cyanide, which caused the animal to loose the menace reflex in a mean of 43 s, and the animal was assumed to have undergone cerebral hypoxia after the last visible breath. The mean time to cerebral hypoxia was 156 s for a vertical pull and 434 s for a side pull. The difference was possibly because some cyanide may be lost in a side pull. There were three distinct phases of cyanide toxicosis: the initial phase was characterised by head shaking, panting and salivation; the immobilisation phase by incontinence, ataxia and loss of the righting reflex; and the cerebral hypoxia phase by a tetanic seizure. Clinical signs that were exhibited in more than one phase of cyanide toxicosis included retching, agonal breathing, vocalisation, vomiting, altered levels of ocular reflex, leg paddling, tonic muscular spasms, respiratory distress and muscle fasciculations of the muzzle.

A field investigation into a suspected outbreak of pyrrolizidine alkaloid toxicosis in horses in western Queensland

A disease outbreak investigation was conducted in western Queensland to investigate a rare suspected outbreak of pyrrolizidine alkaloid (PA) toxicosis in horses. Thirty five of 132 horses depastured on five properties on the Mitchell grass plains of western Queensland died in the first six months of 2010. Clinical–pathological findings were consistent with PA toxicosis. A local variety of Crotalaria medicaginea was the only hepatotoxic plant found growing on affected properties. Pathology reports and departure and arrival dates of two brood mares provided evidence of a pre wet season exposure period. All five affected properties experienced a very dry spring and early summer preceded by a large summer wet season. The outbreak was characterised as a point epidemic with a sudden peak of deaths in March followed by mortalities steadily declining until the end of June. The estimated morbidity (serum IGG > 50 IU/L) rate was 76%. Average crude mortality was 27% but higher in young horses (67%) and brood mares (44%). Logistic regression analysis showed that young horses and brood mares and those grazing denuded pastures in December were most strongly associated with dying whereas those fed hay and/or grain based supplements were less likely to die. This is the first detailed study of an outbreak of PA toxicosis in central western Queensland and the first to provide evidence that environmental determinants were associated with mortality, that the critical exposure period was towards the end of the dry season, that supplementary feeding is protective and that denuded pastures and the horses physiological protein requirement are risk factors.

Young ovine death during hyperimmunization: crotalic envenomation or copper toxicosis?

The unfavorable evolution of a young ovine during hyperimmunization process with Crotalus durissus terrificus venom was investigated in order to differentiate its origin between ophidic envenomation and copper toxicosis. Clinical, laboratory, necroscopic and histological exams as well as evaluation and measurement of heavy metals (copper) in the kidneys and in the liver were carried out. Blood counts revealed anemia and serological tests showed high levels of blood urea nitrogen, creatinine, aspartate aminotransferase, creatine phosphokinase, total bilirubin and indirect bilirubin; which indicates liver, kidney and skeletal muscle damages. At necropsy, the animal presented hepatopathy and nephropathy. Histological examination revealed renal and hepatic features that may imply copper intoxication. Copper levels were 237.8 mu g/g in the liver and 51.2 mu g/g in the kidneys. Although the amount of metal found in both organs was below the level that can cause death, according to the literature, anatomopathological signs were suggestive of copper intoxication. Therefore, the hypothesis of metal toxicosis during the hyperimmunization process became more consistent than the crotalic envenomation one.

Slaframine toxicosis in Brazilian horses causing excessive salivation

Ingestion of food contaminated with slaframine, an alkaloid produced by Rhizoctonia leguminicola, causes a mycotoxicosis, characterised by excessive salivation. Twenty-eight horses demonstrated this clinical sign after the consumption of alfalfa hay which on inspection showed dark patches on many of the stems. The presence of slaframine (1.5 ppm) in this hay was confirmed by gas chromatography and mass spectroscopy. This is the first equine slaframine toxicosis case reported in Brazil.

Copper toxicosis in sheep fed dairy cattle ration in São Paulo, Brazil

Intoxicação crônica por cobre foi observada em um rebanho de 20 ovinos no município de Franca, São Paulo. Três meses após o início do arraçoamento com feno e ração concentrada peletizada para bovinos de leite, seis animais apresentaram anorexia, icterícia severa e urina marrom escura, e vieram a óbito. Diagnosticou-se doença hemolítica com base em sinais clínicos, alterações macroscópicas observadas na necropsia e observações histológicas. À necropsia todos os ovinos apresentaram icterícia severa, fígado amarelado com padrão lobular evidente e rins escuros. As principais alterações histológicas incluíram necrose hepática periacinar e nefrose hemoglobinúrica. Acúmulos de cobre foram demonstrados nos hepatócitos e macrófagos pela coloração rodamina e níveis elevados de cobre mediante espectrofotometria de absorção atômica no soro, fígado e rins de dois ovinos afetados e na ração fornecida.

Retrospective study of salinomycin toxicosis in 66 cats

We examined 66 cats with salinomycin intoxication. Salinomycin caused different LMN signs of varying degrees of severity in all cases. Changes in blood work were unspecific, with the most frequent being increased serum creatine kinase activity, leukocytosis, and increased liver enzymes. Pathological electrodiagnostic findings: fibrillation potentials and positive sharp waves were detected in 10 cases, motor nerve conductance velocity was mildly decreased in 8/12 cats, and sensory nerve conductance velocity and repetitive nerve stimulation were normal in all examined cases. In five cases the peripheral neuropathy was confirmed by pathohistology. Fluid therapy and supportive care were used as therapy and 52 cats recovered completely. The probability for complete remission was significantly different between mildly and severely affected cases. It seems that the severity of clinical signs and prognosis correlate well with the amount of toxin ingested. We conclude that early recognition and decontamination combined with supportive care results in complete recovery.

Inherited copper toxicosis with emphasis on copper toxicosis in Bedlington terriers

Canine copper toxicosis is an important inherited disease in Bedlington terriers, because of its high prevalence rate and similarity to human copper storage disease. It can lead to chronic liver disease and occasional haemolytic anaemia due to impaired copper excretion. The responsible gene for copper toxicosis in Bedlington terriers has been recently identified and was found not to be related to human Wilson's disease gene ATP7B. Although our understanding of copper metabolism in mammals has improved through genetic molecular technology, the diversity of gene mutation related to copper metabolism in animals will help identify the responsible genes for non-Wilsonian copper toxicoses in human. This review paper discusses our knowledge of normal copper metabolism and the pathogenesis, molecular genetics and current research into copper toxicosis in Bedlington terriers, other animals and humans. (C) 2004 Elsevier GmbH. All rights reserved.

Evaluation of haplotypes associated with copper toxicosis in Bedlington Terriers in Australia

Objective-To evaluate the haplotype distribution associated with the copper toxicosis gene and the segregation of the mutated allele in a Bedlington Terrier population in Australia. Animals-131 Bedlington Terriers. Procedure-Samples of DNA and RNA were obtained from each dog. Genetic status of each dog was evaluated by use of the DNA markers C04107; single nucleotide polymorphism (SNP), which was adjacent to exon 2 of Murr1; and a deletion marker for exon 2. A subgroup of the study population was evaluated by use of biochemical and histologic techniques to elucidate the correlation between genotype and phenotype. Results-We identified a recombination between the C04107 marker and Murr1 and a variation in a nucleotide in the splice site of exon 2 in our Bedlington Terrier cohort. Furthermore, we identified a novel haplotype associated with copper toxicosis in this cohort. Conclusions and Clinical Relevance-Our findings indicate that the deletion of exon 2 was not the sole cause of copper toxicosis, although only exon 2 deletion of Murr1 has been responsible for copper toxicosis in Bedlington Terriers. Although we failed to find a novel mutation in our cohort, we identified an affected dog family with an intact exon 2. Furthermore, we found that an SNP in the 5' splicing site of exon 2 may or may not be associated with a novel mutation of the Murr1 gene or other genes. Loss of linkage between the C04107 marker and the Murr1 gene was also identified in a certain family of dogs.

Clinical signs and duration of cyanide toxicosis delivered by the M-44 ejector in wild dogs

Sodium cyanide poison is potentially a more humane method to control wild dogs than sodium fluoroacetate (1080) poison. This study quantified the clinical signs and duration of cyanide toxicosis delivered by the M-44 ejector. The device delivered a nominal 0.88 g of sodium cyanide, which caused the animal to loose the menace reflex in a mean of 43 s, and the animal was assumed to have undergone cerebral hypoxia after the last visible breath. The mean time to cerebral hypoxia was 156 s for a vertical pull and 434 s for a side pull. The difference was possibly because some cyanide may be lost in a side Pull. There were three distinct phases of cyanide toxicosis: the initial phase was characterised by head shaking, panting and salivation; the immobilisation phase by incontinence, ataxia and loss of the righting reflex; and the cerebral hypoxia phase by a tetanic seizure. Clinical signs that were exhibited in more than one phase of cyanide toxicosis included retching, agonal breathing, vocalisation, vomiting, altered levels of ocular reflex, leg paddling, tonic muscular spasms, respiratory distress and muscle fasciculations of the muzzle.

Prospects for whole genome linkage disequilibrium mapping in domestic dog breeds

Linkage disequilibrium (LD) mapping is commonly used as a fine mapping tool in human genome mapping and has been used with some success for initial disease gene isolation in certain isolated in-bred human populations. An understanding of the population history of domestic dog breeds suggests that LD mapping could be routinely utilized in this species for initial genome-wide scans. Such an approach offers significant advantages over traditional linkage analysis. Here, we demonstrate, using canine copper toxicosis in the Bedlington terrier as the model, that LD mapping could be reasonably expected to be a useful strategy in low-resolution, genome-wide scans in pure-bred dogs. Significant LD was demonstrated over distances up to 33.3 cM. It is very unlikely, for a number of reasons discussed, that this result could be extrapolated to the rest of the genome. It is, however, consistent with the expectation given the population structure of canine breeds and, in this breed at least, with the hypothesis that it may be possible to utilize LD in a genome-wide scan. In this study, LD mapping confirmed the location of the copper toxicosis in Bedlington terrier gene (CT-BT) and was able to do so in a population that was refractory to traditional linkage analysis.

The Occurrence and Toxicity of Indospicine to Grazing Animals

Indospicine is a non-proteinogenic amino acid which occurs in Indigofera species with widespread prevalence in grazing pastures across tropical Africa, Asia, Australia, and the Americas. It accumulates in the tissues of grazing livestock after ingestion of Indigofera. It is a competitive inhibitor of arginase and causes both liver degeneration and abortion. Indospicine hepatoxicity occurs universally across animal species but the degree varies considerably between species, with dogs being particularly sensitive. The magnitude of canine sensitivity is such that ingestion of naturally indospicine-contaminated horse and camel meat has caused secondary poisoning of dogs, raising significant industry concern. Indospicine impacts on the health and production of grazing animals per se has been less widely documented. Livestock grazing Indigofera have a chronic and cumulative exposure to this toxin, with such exposure experimentally shown to induce both hepatotoxicity and embryo-lethal effects in cattle and sheep. In extensive pasture systems, where animals are not closely monitored, the resultant toxicosis may well occur after prolonged exposure but either be undetected, or even if detected not be attributable to a particular cause. Indospicine should be considered as a possible cause of animal poor performance, particularly reduced weight gain or reproductive losses, in pastures where Indigofera are prevalent.

In vitro degradation of hepatotoxic indospicine in indigofera spicata by camel foregut fluid

Indospicine toxicosis was reported in sheep, goats and cattle fed on Indigofera, a leguminous plant rich in indospicine. Recent death report on dogs as a result of dietary ingestion of indospicine contaminated camel meat has raised concern about the distribution of this toxin in camels fed on Indigofera. This in vitro study aimed at measuring the degradability of indospicine in Indigofera spicata by camel-foregut fluid and attempted at explaining indospicine accumulation in meat tissue. In the first experiment, in vitro dry matter digestibility and indospicine disappearance were evaluated by using foregut fluid from 15 feral camels. Foregut fluid was collected post mortem from a nearby abattoir. In the second experiment, a composite foregut fluid obtained from three feral camels was used to examine the time-dependent degradation of indospicine. Results indicated that 99 of the dietary indospicine was degraded after 48 h of incubation. The time-dependent degradation study showed rapid degradation (11 µg/h) during the first 18 h of incubation, followed by a much slower rate (2 µg/h) between 18-48 h. Results demonstrated the ability of the camel microbiota to degrade indospicine and suggest the presence of a by-pass mechanism that enables the toxin to escape degradation and reaches the intestine.