Cyanide poisoning in cattle from Dysphania glomulifera (red crumbweed): Using the internet for rapid plant identification and diagnostic advice: Case Report

A 300-strong Angus-Brahman cattle herd near Springsure, central Queensland, was being fed Acacia shirleyi (lancewood) browse during drought and crossed a 5-hectare, previously burnt area with an almost pure growth of Dysphania glomulifera subspecies glomulifera (red crumbweed) on their way to drinking water. Forty cows died of cyanide poisoning over 2 days before further access to the plant was prevented. A digital image of a plant specimen made on a flat-bed scanner and transmitted by email was used to identify D glomulifera. Specific advice on the plant's poisonous properties and management of the case was then provided by email within 2 hours of an initial telephone call by the field veterinarian to the laboratory some 600 km away. The conventional method using physical transport of a pressed dried plant specimen to confirm the identification took 5 days. D glomulifera was identified in the rumen of one of two cows necropsied. The cyanogenic potential of D glomulifera measured 4 days after collection from the site of cattle deaths was 18,600 mg HCN/kg in dry matter. The lethal dose of D glomulifera for a 420 kg cow was estimated as 150 to 190 g wet weight. The plant also contained 4.8% KNO3 equivalent in dry matter, but nitrate-nitrite poisoning was not involved in the deaths.

Species differences in acrylonitrile metabolism and toxicity between experimental animals and humans based on observations in human accidental poisonings

The high acute toxicity of acrylonitrile may be a result of its intrinsic biological reactivity or of its metabolite cyanide. Intravenous N-acetylcysteine has been recommended for treatment of accidental intoxications in acrylonitrile workers, but such recommendations vary internationally. Acrylonitrile is metabolized in humans and experimental animals via two competing pathways; the glutathione-dependent pathway is considered to represent an avenue of detoxication whilst the oxidative pathway leads to a genotoxic epoxide, cyanoethylene oxide, and to elimination of cyanide. Cases of acute acrylonitrile overexposure or intoxication have occurred within persons having industrial contact with acrylonitrile; the route of exposure was by inhalation and/or by skin contact. The combined observations lead to the conclusion of a much higher impact of the oxidative metabolism of acrylonitrile in humans than in rodents. This is confirmed by differences in the clinical picture of acute life-threatening intoxications in both species, as well as by differential efficacies of antidotes. A combination of N-acetylcysteine with sodium thiosulfate seems an appropriate measure for antidote therapy of acute acrylonitrile intoxications. Clinical observations also highlight the practical importance of human individual susceptibility differences. Furthermore, differential adduct monitoring, assessing protein adducts with different rates of decay, enables the development of more elaborated biological monitoring strategies for the surveillance of workers with potential acrylonitrile contact.

Teor de ácido cianídrico e taxa de crescimento do híbrido de sorgo x capim sudão durante o outono

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

An ecological assessment of secondary poisoning risk in the Australian sugarcane industry

Rodenticide use in agriculture can lead to the secondary poisoning of avian predators. Currently the Australian sugarcane industry has two rodenticides, Racumin® and Rattoff®, available for in-crop use but, like many agricultural industries, it lacks an ecologically-based method of determining the potential secondary poisoning risk the use of these rodenticides poses to avian predators. The material presented in this thesis addresses this by: a. determining where predator/prey interactions take place in sugar producing districts; b. quantifying the amount of rodenticide available to avian predators and the probability of encounter; and c. developing a stochastic model that allows secondary poisoning risk under various rodenticide application scenarios to be investigated. Results demonstrate that predator/prey interactions are highly constrained by environmental structure. Rodents used crops that provided high levels of canopy cover and therefore predator protection and poorly utilised open canopy areas. In contrast, raptors over-utilised areas with low canopy cover and low rodent densities, but which provided high accessibility to prey. Given this pattern of habitat use, and that industry baiting protocols preclude rodenticide application in open canopy crops, these results indicate that secondary poisoning can only occur if poisoned rodents leave closed canopy crops and become available for predation in open canopy areas. Results further demonstrate that after in-crop rodenticide application, only a small proportion of rodents available in open areas are poisoned and that these rodents carry low levels of toxicant. Coupled with the low level of rodenticide use in the sugar industry, the high toxic threshold raptors have to these toxicants and the low probability of encountering poisoned rodents, results indicate that the risk of secondary poisoning events occurring is minimal. A stochastic model was developed to investigate the effect of manipulating factors that might influence secondary poisoning hazard in a sugarcane agro-ecosystem. These simulations further suggest that in all but extreme scenarios, the risk of secondary poisoning is also minimal. Collectively, these studies demonstrate that secondary poisoning of avian predators associated with the use of the currently available rodenticides in Australian sugar producing districts is minimal. Further, the ecologically-based method of assessing secondary poisoning risk developed in this thesis has broader applications in other agricultural systems where rodenticide use may pose risks to avian predators.

Investigation of a food poisoning outbreak due to nitrite contained in cooked peanut [一起因食用煮花生米引起亚硝酸盐中毒的调查报告]

Two workers were hospitalised with similar symptoms. Information was gathered from patients, doctors, colleagues and food seller. Laboratory tests were undertaken on remaining food and vomits. We identified the source food and toxin responsible for this outbreak, and subsequently helped doctors to treat these patients. The intake was estimated to be over the fatal limit but both were fully recovered after treatment. Abstract in Chinese 2001年11月20日，寿光市植物油厂的2名装卸工人因食用花生米引起亚硝酸盐急性中毒，现报告如下。 1 中毒经过 11月20日下午，市植物油厂装卸工人秦×下班后，到本厂职工食堂买了馒头、大米稀饭和少许咸菜，然后到厂外买了1瓶白酒，又到个体菜摊李×处买了2元钱的煮花生米，约400g。17：40与同事江×一同在宿舍内饮酒吃饭，其中花生米大部分被秦×吃掉，江×吃得少。18：30左右秦×在装卸过程中出现双腿发软、恶心、呕吐、呼吸困难、视物模糊，江×随后也出现类似症状，2人被迅速送往寿光市人民医院进行抢救。到医院时已进入昏迷状态，查体可见全身皮肤粘膜青紫、手指脚趾发黑，经吸氧并心电监护、应用美兰静推后，江×症状减轻，于次日出院；秦×因中毒严重，于次日脱离危险，11月23日痊愈出院。……

Physostigmine for promethazine poisoning

Experience suggests that the central anticholinergic action of promethazine is a major element in the toxic effects following overdosage. Physostigmine seems to be a direct antidote at doses within the safe therapeutic range; side-effects, if they become a problem, can be treated with intravenous atropine.

Poisoning for production: how effective is fox baiting in south-eastern Australia?

1. The European red fox Vulpes vulpes represents a continuing threat to both livestock and native vertebrates in Australia, and is commonly managed by setting ground-level baits impregnated with 1080 (sodium fluoroacetate) poison. However, the long-term effectiveness of such control campaigns is likely to be limited due to the ability of foxes to disperse over considerable distances and to swiftly recolonize areas from where they had been removed. 2. To investigate the effectiveness of fox baiting in a production landscape, we assessed the potential for foxes to reinvade baited farm property areas within the jurisdiction of the Molong Rural Lands Protection Board (RLPB), an area of 815 000 ha on the central tablelands of New South Wales, Australia. The spatial distribution and timing of fox baiting campaigns between 1998 and 2002 was estimated from RLPB records and mapped using Geographical Information System software. The effectiveness of the control campaign was assessed on the basis of the likely immigration of foxes from non-baited farms using immigration distances calculated from published relationships between dispersal distance and home range size. 3. Few landholders undertook baiting campaigns in any given year, and the area baited was always so small that no baited property would have been sufficiently far from an unbaited property to have been immune from immigrating individuals. It is likely, therefore, that immigration onto farms negated any long-term effects of baiting operations. This study highlights some of the key deficiencies in current baiting practices in south-eastern Australia and suggests that pest management programmes should be monitored using such methods to ensure they achieve their goals.

Pimelea trichostachya poisoning (St George disease) in horses

A dense population of Pimelea trichostachya plants (Family Thymelaeaceae) in pasture poisoned a horse herd in southern inland Queensland in October-November 2005. Plant density was 2 to 45 g wet weight/m2 (mean 16 g/m2) from 5 to 69 plants/m2 (mean 38 plants/m2) representing 3 to 20% (mean 9%) of the volume of pasture on offer. Ten of 35 mares, fillies and geldings were affected. Clinical signs were loss of body weight, profound lethargy, serous nasal discharge, severe watery diarrhoea and subcutaneous oedema of the intermandibular space, chest and ventral midline. Pathological findings were anaemia, leucocytopenia, hypoproteinaemia, dilatation of the right ventricle of the heart, dilated hepatic portal veins and periportal hepatic sinusoids (peliosis hepatis), alimentary mucosal hyperaemia and oedema of mesenteric lymph nodes. Cattle grazing the same pasture were affected by Pimelea poisoning simultaneously. Removal of the horses to Pimelea-free pasture initiated recovery. The one other incident of this syndrome, previously only recognised in cattle in Australia, occurred in horses, in South Australia in 2002, with access to a dense Pimelea simplex population.

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.

Early harvest and ensilage of forage sorghum infected with ergot (Claviceps africana) reduces the risk of livestock poisoning.

Sorghum ergot produces dihydroergosine (DHES) and related alkaloids, which cause hyperthermia in cattle. Proportions of infected panicles (grain heads), leaves and stems were determined in two forage sorghum crops extensively infected 2 to 4 weeks prior to sampling and the panicles were assayed for DHES. Composite samples from each crop, plus a third grain variety crop, were coarsely chopped and half of each sealed in plastic buckets for 6 weeks to simulate ensilation. The worst-infected panicles contained up to 55 mg DHES/kg, but dilution reduced average concentrations of DHES in crops to approximately 1 mg/kg, a relatively safe level for cattle. Ensilation significantly (P = 0.043) reduced mean DHES concentrations from 0.85 to 0.46 mg/kg.

Reduced risk of acute poisoning in Australian cattle from used motor oils after introduction of lead-free petrol.

Lead (Pb) poisoning of cattle has been relatively common in Australia and sump oil has been identified as an important cause of Pb toxicity for cattle because they seem to have a tendency to drink it. Lead-free petrol has been available in Australia since 1975, so the aim of this study was to assess the current risk to cattle from drinking used automotive oils. Sump or gear box oil was collected from 56 vehicles being serviced. The low levels of Pb found suggest that the removal of leaded petrol from the Australian market as a public health measure has benefited cattle by eliminating the risk of acute poisoning from used engine oil.

Norsesquiterpene Glycosides in Bracken Ferns (Pteridium esculentum and Pteridium aquilinum subsp wightianum) from Eastern Australia: Reassessed Poisoning Risk to Animals.

Austral bracken Pteridium esculentum contains three unstable norsesquiterpene glycosides: ptaquiloside, ptesculento-side, and caudatoside, in variable proportions. The concentration of each of the glycosides was determined in this study as their respective degradation products, pterosin B, pterosin G and pterosin A, by HPLC-UV analysis. Samples of P. esculentum collected from six sites in eastern Australia contained up to 17 mg of total glycoside/g DW, with both ptaquiloside and ptesculentoside present as major components accompanied by smaller amounts of caudatoside. Ratios of ptaquiloside to ptesculentoside varied from 1:3 to 4:3, but in all Australian samples ptesculentoside was a significant component. This profile differed substantially from that of P. esculentum from New Zealand, which contained only small amounts of both ptesculentoside and caudatoside, with ptaquiloside as the dominant component. A similar profile with ptaquiloside as the dominant glycoside was obtained for Pteridium aquilinum subsp. wightianum (previously P. revolutum) from northern Queensland and also P. aquilinum from European sources. Ptesculentoside has chemical reactivity similar to that of ptaquiloside and presumably biological activity similar to that of this potent carcinogen. The presence of this additional reactive glycoside in Australian P. esculentum implies greater toxicity for consuming animals than previously estimated from ptaquiloside content alone.