Superphosphate poisoning of sheep: the role of fluoride

Earlier work confirmed that the fundamental lesion of superphosphate poisoning is an acute toxic tubular nephritis in which both phosphate and fluoride may play a part but their respective roles could not be determined. In this study, sheep poisoned by sodium fluoride (NaF) were compared with sheep poisoned by superphosphate containing approximately 1.5% fluoride. The LD50 of NaF was in the range 100 to 300 mg/kg (45 to 135 mg F/kg). This range is of the same order as the amount of fluoride in a toxic dose of superphosphate (70 to 90 mg F/kg). A lethal dose of NaF caused severe depression, salivation, hyperpnoea, blindness, ataxia and incoordination. Death ensued three to 52 hours after dosing. Acute necrotizing rumino-reticulitis and abomasitis and necrosis of epithelial cells in the proximal convoluted tubules of the kidney were the characteristic lesions of NaF toxicity. Superphosphate poisoning took a more protracted course with depression and diarrhoea as the predominant clinical signs until the terminal coma. As with NaF, the notable lesions were in the gastrointestinal tract and kidneys, but were less severe. Although there were differences in the clinical and pathological manifestations of the two forms of poisoning, the comparable toxic dose of NaF and of the fluoride in a toxic dose of superphosphate, and the similar target organs involved, support the view that fluoride plays a dominant role in the pathogenesis of superphosphate poisoning. It is probable that phosphate plays a contributory role but the nature of the interaction of fluoride and phosphate remains to be established.     

Phosphatic fertiliser poisoning of sheep: Experimental studies

The toxicity of serpentine phosphate and superphosphate for non-pregnant dry ewes, pregnant ewes and lactating ewes was investigated by oral dosing. An attempt was made to reproduce a natural episode of poisoning by exposing pregnant and lactating ewes to topdressed pasture.

A total dose in the range of 1200 to 1800 g of serpentine phosphate was required to kill two ewes and it was concluded that natural episodes of poisoning with this material are unlikely. The toxic process was similar to that caused by superphosphate.

The LD₅₀ of superphosphate was estimated to be in the range of 5 to 6 g/kg and a dose in the range of 200 to 300 g was sufficient to kill most sheep. The apparently greater susceptibility of pregnant and lactating sheep to poisoning suggested by the study of natural outbreaks was not demonstrated in these experiments, but the numbers of experimental animals may have been too small to detect diiering susceptibility.

The clinical disease resembled that seen in natural episodes; anorexia, diarrhoea, progressive depression and death in a period of 5 to 8 days after the start of dosing. Sublethal doses produced a transient diarrhoea and, in two sheep, a severe wool-break.

The principal biochemical changes were hyperphosphataemia and evidence of renal failure (oliguria, uraemia, azotaemia). Gross lesions were not consistently present but included abomasal ulceration and renal cortical swelling and pallor. The histopathological evidence of renal tubular obstruction by flocculant eosinophilic casts was characteristic.     

Phosphatic fertiliser poisoning of sheep: experimental studies

The toxicity of serpentine phosphate and superphosphate for non-pregnant dry ewes, pregnant ewes and lactating ewes was investigated by oral dosing. An attempt was made to reproduce a natural episode of poisoning by exposing pregnant and lactating ewes to topdressed pasture. A total dose in the range of 1200 to 1800 g of serpentine phosphate was required to kill two ewes and it was concluded that natural episodes of poisoning with this material are unlikely. The toxic process was similar to that caused by superphosphate. The LD50 of superphosphate was estimated to be in the range of 5 to 6 g/kg and a dose in the range of 200 to 300 g was sufficient to kill most sheep. The apparently greater susceptibility of pregnant and lactating sheep to poisoning suggested by the study of natural outbreaks was not demonstrated in these experiments, but the numbers of experimental animals may have been too small to detect differing susceptibility. The clinical disease resembled that seen in natural episodes; anorexia, diarrhoea, progressive depression and death in a period of 5 to 8 days after the start of dosing. Sublethal doses produced a transient diarrhoea and, in two sheep, a severe wool-break. The principal biochemical changes were hyperphosphataemia and evidence of renal failure (oliguria, uraemia, azotaemia). Gross lesions were not consistently present but included abomasal ulceration and renal cortical swelling and pallor. The histopathological evidence of renal tubular obstruction by flocculant eosinophilic casts was characteristic.     

Emory milkvetch (Astragalus emoryanus var emoryanus) poisoning in chicks, sheep, and cattle.

A severe outbreak of Emory milkvetch poisoning in cattle and sheep occurred near Roswell, New Mexico, in the spring of 1975. Mortality averaged 2% to 3% and morbidity averaged 15% to 20%. Emory milkvetch collected from the infested area contained miserotoxin measured as 5 to 9 mg of NO2/g of plant (dry weight). Chicks fed extracts of Emory milkvetch showed toxic signs when fed one dose as 300 mg of NO2/kg of body weight, and died within 5 to 8 hours when fed milkvetch as 400 mg of NO2/kg. A sheep fed Emory milkvetch for 7 days in the form of 38 mg of NO2/kg/day developed signs of nitro poisoning on the 7th day. Cattle were poisoned or died when fed Emory milkvetch as 12 to 20 mg of NO2/ig for several days. The toxic signs observed in the field and under experimental conditions were similar.     

The Pathology of Arylmercurial Poisoning in Swine

To produce arylmercurial poisoning, phenylmercuric chloride (PMC) was administered daily to 30 healthy five week-old piglets for periods of up to 90 days. The dosage used ranged from 0.19 to 4.56 mg of mercury (Hg)/kg. Levels exceeding 2.28 mg Hg/kg daily were moderately toxic.

The disease occurring in this intoxication resulted from injury to the kidneys and large intestine. Fetid diarrhea and failure to gain weight were consistent clinical signs. The primary gross lesions were necrotic typhlitis and colitis, and nephrosis. Degeneration and necrosis were found in affected organs. Regeneration was prominent in the proximal convoluted tubules.

The pathology of this disease was similar to that described for mercuric chloride poisoning in other species and, presumably, reflected the ease with which PMC was metabolized to release mercuric ion.

Tissue analysis for mercury suggested that only certain target organs, such as kidney and colon, accumulated significantly high levels of mercury. This, presumably, resulted from rapid metabolism of the compound and excretion of mercuric ion in the kidney and colon. The net effect was to spare other tissues, and to injure the excretory organs when the dose level was sufficiently high.

     

The toxicity of myoporum tetrandrum (Boobialla) and myoporaceous furanoid essential oils for ruminants

Boobialla (Myoporum tetrandrum)leaf contains from 0.25 to 0.5% wet weight of furanoid sesquiterpene essential oils of which the main component is dehydrongaione. The plant was toxic when dosed to calves at equivalent dose rates of oils of from 50 to 134 mg/kg, causing mainly extensive haemorrhagic centrillobular necrosis; and to sheep at equivalent dose rates of oil of from 55 to 66 mg/kg, causing either centrilobular or periportal liver lesions with or without acute pulmonary oedema. An essential oil mixture of similar composition derived from Myoporum deserti produced similar syndromes. In addition, treatment of calves with phenobarbitone or Melaleuca linariifolia essential oils prior to dosing with the Myoporum oils caused periportal hepatic necrosis rather than the centrilobular lesion which occurred usually in this species. The liver lesions found in the experimental calves and sheep respectively, were thus similar to those reported in suspected field cases of Boobialla poisoning in cattle and goats in Western Australia. The liver injury that may be expected in intoxication of livestock by myoporaceous plants containing this type of essential oils can thus be either periportal, midzonal or centrilobular necrosis, depending, probably, on the nutritional regime of the animal immediately prior to consumption of the toxic plant.     

THE ORAL TOXICITY FOR SHEEP OF TRITERPENE ACIDS ISOLATED FROM LANTANA CAMARA

SUMMARY Toxic Lantana camara taxa growing in Queensland all contain the triterpene acids lantadene A, reduced lantadene A and lantadene B. These when dosed as pure compounds orally to sheep were similarly toxic at 65 to 75, 42 to 80 and 200 to 300 mg/kg body weight respectively, causing jaundice, photosensitisation, kidney and liver lesions typical of natural and experimental lantana poisoning. Because of its comparative toxicity and abundance lantadene A is the most significant toxic principle in the plant. Reduced lantadene A because of its low concentration in the leaves (5% of lantadene A) and lantadene B because of its significantly lower toxicity are thus unlikely to be of much importance in the poisoning of ruminants following consumption of the plant. In addition, the structural features of both lantadene A and B molecules given to sheep by the oral route do not conform to the chemical structures previously reported to be required for liver damaging action of the verbenaceous triterpenes administered to rabbits by the intraperitoneal route.     

Toxicity of the lichen secondary metabolite (+)-usnic acid in domestic sheep

Toxicity following ingestion of the vagrant, foliose lichen Xanthoparmelia chlorochroa was identified as the putative etiology in the death of an estimated 400-500 elk on the Red Rim-Daley Wildlife Habitat Management Area in Wyoming during the winter of 2004. A single, unsubstantiated report in 1939 attributed toxicity of X. chlorochroa in cattle and sheep to usnic acid, a common lichen secondary metabolite. To test the hypothesis that usnic acid is the proximate cause of death in animals poisoned by lichen, domestic sheep were dosed PO with (+)-usnic acid. Clinical signs in symptomatic ewes included lethargy, anorexia, and signs indicative of abdominal discomfort. Serum creatine kinase, aspartate aminotransferase, and lactate dehydrogenase activities were considerably elevated in symptomatic sheep. Similarly, only symptomatic ewes exhibited appreciable postmortem lesions consisting of severe degenerative appendicular skeletal myopathy. The median toxic dose (ED(50)) of (+)-usnic acid in domestic sheep was estimated to be between 485 and 647 mg/kg/day for 7 days.     

Macrocyclic lactone toxicity due to abamectin in farm dogs without the ABCB1 gene mutation

Abstract

CASE HISTORY: A 5-year-old entire female Huntaway from a sheep and beef farm was one of four dogs that developed clinical signs including hypersalivation, depression, blindness and ataxia after the death of another dog. A 4-year-old female Huntaway farm dog from a second farm was observed to be sitting down more often than usual on the day after being fed part of a calf carcass that had been treated with an abamectin pour-on.

CLINICAL FINDINGS: The first dog was ataxic and depressed but did respond to sound. The second dog presented with an acute onset of blindness, mydriasis, absence of a menace response, hypersalivation, gait abnormalities (e.g. high stepping gait and ataxia), and depression. Other presenting signs included muscle tremors, dehydration and difficulty eating. No abnormalities were detected from routine haematology and biochemistry. Analysis of samples of plasma from both dogs revealed concentrations of abamectin of 0.149 mg/L and 0.260 mg/L for the first and second dogs, respectively. Buccal swabs taken from the first dog for DNA testing for the ABCB1 gene mutation, gave a negative result.

DIAGNOSIS: In addition to the presenting signs which suggested a toxicosis, both dogs had measurable concentrations of abamectin in plasma confirming exposure.

CLINICAL RELEVANCE: Farm dogs exposed to concentrated pour-on products containing abamectin have been poisoned and recover or die. The product labels do not carry any warnings as to the risk of poisoning to dogs. This paper discusses two incidents affecting six farm dogs, but the authors are aware of more toxicoses in farm dogs exposed to abamectin.     

Establishment of the Rex Rabbit Fluorosis Model and Detection of the Fluoride Content in Organs

In order to study the influence of different doses of sodium fluoride on rex rabbit,rex rabbit fluorosis model was established and the fluorine contents of blood,bone,liver,kidney and other organs in rex rabbit were examined to provide a theoretical reference for the further research. Rex rabbits (age (30±5) days,weight (1.1±0.2) kg) were divided into three groups:Control group,test group Ⅰ (10 mg/(kg·d) NaF group) and test group Ⅱ (20 mg/(kg·d) NaF group). The tests lasted 100 d. The results showed that,on the 100th day,fluoride contents of bone and tooth were significantly different (P<0.05),and they were positively correlated with the time and intake of fluoride;The fluoride contents of kidney and liver were slightly different (P>0.05),and they were not significantly different between both test groups (P>0.05).The fluoride contents of blood were not significantly different between group Ⅰ and group Ⅱ (P>0.05),but both had no significant changes compared with control group (P<0.05). Sodium fluoride as a fluoride source could be used to simulate the natural state of rex rabbit fluorine poisoning. The fluoride accumulating ability in bone and tooth were stronger while the ability in blood,liver and kidney were weaker.     

The effect of shade, shearing and wool type in the protection of Merino sheep from Hypericum perforatum (St John's wort) poisoning

OBJECTIVE: To investigate the roles of shade, fleece length and wool type in the protection of sheep from Hypericum perforatum poisoning. ANIMALS: Adult Merino ewes of superfine, fine and medium wool type. DESIGN: Seventy sheep were divided into seven equal groups. During late spring and summer a series of successive, replicate experiments was conducted, each using one group and lasting 5 days. The sheep carried 14 to 24 weeks wool growth. In each experiment the treatments tested were Hypericum +, sunlight + (n = 7); Hypericum +, sun - (n = 1); Hypericum -, sun + (n = 1); Hypericum -, sun - (n = 1). Next, 24 sheep in two equal groups were used in experiments of similar design to the above. Each group consisted of nine recently (1 to 3 weeks previously) shorn and three wool covered (25 to 26 weeks growth) sheep. The treatments tested were Hypericum +, sunlight +, fleece - (n = 9); Hypericum +, sun -, fleece + (n = 1); Hypericum -, sun +, fleece + (n = 1); Hypericum -, sun -, fleece + (n = 1). PROCEDURES: Finely milled Hypericum was administered by gavage to provide 3 mg hypericin / kg body weight. Sheep were sheltered from direct sunlight or were exposed for 5 h per day for 4 successive post-treatment days. Rectal temperatures were measured immediately before and at the end of each sunlight exposure session. Rectal temperature above 40 degrees C was considered indicative of hypericin poisoning. RESULTS: After Hypericum treatment hypericin poisoning was displayed by 26.5% of woolled sheep that were exposed to sunlight, but by none of those that were fully shaded. In similarly treated but recently shorn sheep 94% displayed hypericin poisoning when exposed to sunlight. In the wool covered group the percentages of poisoned animals based on wool type were: superfine 14%, fine 28.5%, medium 33.3%. In the recently shorn group the percentage for all three approached 100%. CONCLUSIONS: A majority of Merinos with at least 14 weeks wool growth will not be poisoned by a single oral dose of 3 mg hypericin /kg, but because hypericin persists in the blood circulation for several days this safe dose will be lowered by continuous daily ingestion. Sheep with access to substantial areas of shade could safely ingest much greater amounts of hypericin. Wool removal greatly increases the risk of poisoning. Superfine Merinos with a wool cover should be able to ingest more hypericin than comparable, medium wool types, without any increased risk of poisoning. The ability of ruminant livestock to safely ingest Hypericum is probably determined more by the amount of skin protection they have against incident sunlight than by differences in hypericin metabolism and excretion capacity.     

Superphosphate poisoning of sheep: a study of natural outbreaks

Superphosphate poisoning is typically a disease of pregnant and lactating ewes under nutritional stress. Poisoning has been observed only in the late winter and spring. Most episodes occurred when hungry sheep were forced to graze short pastures topdressed within one week prior to the onset of clinical signs. Fine weather which is favourable for the application of fertiliser also favours the occurrence of poisoning.

Clinical signs include anorexia, thirst, diarrhoea, weakness and incoordination. Death usually occurs within 48 hours of the onset of clinical signs. In some outbreaks the presenting signs are those of hypocal- caemia but response to calcium therapy is transient.

Poisoning results iu a toxic tubular nephritis and uraemia.

No satisfactory treatment can be suggested but poisoning can be prevented by avoiding exposure of sheep to topdressed pastures.     

獭兔氟中毒模型的建立及各器官氟含量测定

为研究不同剂量氟化钠对獭兔的影响,试验建立獭兔氟中毒模型并对獭兔血液、骨骼、肝脏、肾脏等器官氟含量进行测定。试验獭兔日龄（30±5） d,体重（1.1±0.2） kg,数量24只,分为3组：对照组、试验Ⅰ组（10 mg/（kg·d）氟化钠组）和试验Ⅱ组（20 mg/（kg·d）氟化钠组）,试验共100 d。结果表明,试验第100天测定的骨骼和牙齿氟含量在各组之间均差异显著（P<0.05）,且骨骼和牙齿的含氟量随时间和摄入氟剂量的增加而递增;肾脏和肝脏氟含量在各组之间均差异不显著（P>0.05）;试验Ⅰ、Ⅱ组间血液氟含量差异不显著（P>0.05）,但都与对照组差异显著（P<0.05）。氟化钠作为氟化物来源可用来建立獭兔自然状态氟中毒症,骨骼和牙齿累积氟能力强,血液、肝脏和肾脏累积氟能力弱。本试验为进一步研究獭兔氟中毒及其防制提供了理论参考。     

Acute lead poisoning in western Canadian cattle — A 16-year retrospective study of diagnostic case records

This study describes the epidemiology of acute lead poisoning in western Canadian cattle over the 16-year period of 1998 to 2013 and reports background bovine tissue lead concentrations. Case records from Prairie Diagnostic Services, Western College of Veterinary Medicine, identified 525 cases of acute lead toxicity over the investigational period. Poisonings were influenced by year (P < 0.0001) and month (P < 0.0001). Submissions were highest in 2009 (15.6%), 2001 (11.2%), and 2006 (9.9%). Most cases were observed during May, June, and July (62.3%). Cattle 6 months of age and younger were frequently poisoned (53.5%; P < 0.0001). Beef breeds were predominantly poisoned. Mean toxic lead concentrations (mg/kg wet weight) in the blood, liver, and kidney were 1.30 ± 1.70 (n = 301), 33.5 ± 80.5 (n = 172), and 56.3 ± 39.7 (n = 61). Mean normal lead concentrations in the blood, liver, and kidney were 0.036 ± 0.003 mg/kg (n= 1081), 0.16 ± 0.63 mg/kg (n = 382), and 0.41 ± 0.62 mg/kg (n = 64).     

Effects of low dose rates of sporidesmin given orally to sheep

Aim: To examine clinical and subclinical effects of sporidesmin administered orally to sheep at very low daily dose rates for periods of 3 to 48 days.

Methods: Two experiments were conducted. In Experiment A, sporidesmin-A was administered orally to groups of 16 sheep at daily dose rates of approximately 0.0042, 0.0083 and 0.0167 mg/kg bodyweight for 48 days. In Experiment B, the highest of these doses was administered orally for 3, 6, 12, 24 or 48 consecutive days. Parameters of production, clinical findings, organ weights and pathological findings were recorded.

Results: In Experiment A, severe liver lesions and photosensitisation were evident as early as 18 days after commencement of daily low-dose administration of sporidesmin, and were associated with significant bodyweight loss. Significant bodyweight loss also occurred in non-photosensitised sporidesmin-treated sheep. Bodyweight reductions were associated with reduced carcass weights and skin weights in treated animals. Sporidesmin administration was also associated with reduced bodyweight gains and pathological changes of the liver, kidney, hepatic lymph nodes, thymus, adrenal gland, heart and spleen. In Experiment B, only moderate changes occurred in a few sheep in the groups dosed with sporidesmin at 0.0167 mg/kg for 3 or 6 days, but major changes were frequently recorded in animals dosed at this rate for 12 days or longer. These comprised changes in the liver and other organs, and photosensitisation typical of the disease, facial eczema. Results are discussed in relation to animal welfare and economic issues associated with this disease.

Conclusions: Sporidesmin caused significant clinical and sub-clinical disease and reduced animal production at relatively low daily dose rates. The effects of repeated daily low-dose administration of sporidesmin appear to be cumulative. There was considerable variation in susceptibility between individual animals.These results emphasise the considerable production losses and animal welfare effects associated with sporidesmin toxicity in sheep.     

Experimental acute yellow-wood (Terminalia oblongata) intoxication in sheep

SUMMARY An aqueous suspension of air-dried, hammer-milled leaf of Terminalla oblongata (yellow-wood) was administered to sheep by gavage, as a single dose of 5 to 20 g (dry weight)/kg body weight. Doses of 15 g/kg, or more, caused depression, Inappetence, abdominal pain and reduced ruminal movements within 24 to 48 h and some sheep also showed dyspnoea, oplsthotonus and champing of the Jaws. Haematology and blood gas and acid-base measurements were unaffected. In sheep given a dose of 12.5 g/kg, or more, plasma osmolality, aspartate aminotransferase activity and potassium and bilirubin concentrations Increased while plasma total protein markedly decreased and plasma sodium concentration and alkaline phosphatase activity remained normal. Most sheep were necropsled 48 h after dosing. The liver showed zonal hepatocellular necrosis, the pattern of which varied with the dose given. No renal lesions were observed, although one sheep given a very high dose became azotaemic and hyperkalaemic. Hydrothorax, hydroperlcardlum and ascltes developed In sheep given doses of 15 or 20 g/kg.     

Reassessment of the toxicity of Hypericum perforatum (St John's wort) for cattle

OBJECTIVE: To investigate the clinical effect of administering sufficient Hypericum perforatum to cattle to deliver quadruple the reported oral toxic dose. ANIMALS: Thirty-six yearling Hereford (n = 18) and Angus (n = 18) steers. DESIGN: A series of six experiments was conducted, each using 12 animals in a 2 x 2 factorial design, with two breeds of cattle (Hereford, Angus) and two dose levels of hypericin, 1.5 mg/kg (treated group) and 0 mg/kg (control group). Each set of 12 steers was used in duplicate experiments, with all animals alternated between treated and control groups. PROCEDURES: Treated groups received finely milled H. perforatum administered orally in gelatin capsules to provide 1.5 mg hypericin/kg body weight. All cattle were then exposed to direct sunlight for 5 h per day for 5 successive days. Rectal temperatures were measured immediately before and at the end of each sunlight exposure session. Rectal temperature above 40 degrees C, together with some other clinical sign of hypericin poisoning, was considered indicative of intoxication. RESULTS: No animals developed a rectal temperature above 40 degrees C or other clinical signs of hypericin poisoning. CONCLUSIONS: While the reported bovine oral toxic dose of 3 g dried plant/kg body weight, for flowering stage, presumed narrow leaved biotype, H. perforatum, is probably correct, the corresponding dose for hypericin of 0.37 mg/kg is incorrect. Based on its known concentration in this plant the toxic dose of hypericin for partially pigmented Hereford-cross cattle is estimated at about 10.5 mg/kg body weight and more than this for fully pigmented cattle. This would imply that cattle of the former type should be about three and a half times better protected against H. perforatum toxicity than are unpigmented, wool protected, Merino sheep. Cattle, particularly if fully pigmented, may have a role in grazing management to control H. perforatum.     

家蚕氟化物中毒后血淋巴中脂质过氧化物和抗氧化物含量及抗氧化酶活性的变化

为了探究氟化物对家蚕的毒理作用,通过给家蚕5龄期幼虫添食NaF,检测氟化物中毒家蚕幼虫血淋巴中脂质过氧化物质丙二醛(MDA)、抗氧化物质谷胱甘肽(GSH)的含量变化以及谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽硫转移酶(GST)等抗氧化物酶的活性变化。正常家蚕幼虫和氟化物中毒家蚕幼虫血淋巴中的MDA含量在5龄期均逐渐下降,但氟化物中毒家蚕的MDA平均浓度比正常家蚕升高了83.77%;GSH含量变化趋势为5龄第1天和第5天较高,第3天较低,但氟化物中毒家蚕5龄期的GSH浓度平均比正常家蚕下降了47.81%;氟化物中毒家蚕5龄期的GSH-Px和GST的平均活性分别比正常家蚕升高63.49%、39.22%,5龄第3天达到最高峰,5龄第1天和第5天较弱。初步分析认为家蚕幼虫血淋巴中MDA和GSH的含量变化以及GSH-Px和GST的活性变化,与家蚕氟化物中毒后体内氧自由基含量上升和脂质过氧化作用增强密切相关,可作为诊断家蚕氟化物中毒的生化指标。     

Carbamate poisoning in a dairy goat herd: Clinicopathological findings and therapeutic approach

Abstract

CASE HISTORY: Approximately 1 hour after the consumption of carnations from a nearby glasshouse 55 animals from a dairy goat herd exhibited signs of possible poisoning.

CLINICAL FINDINGS: Upon clinical examination affected animals exhibited signs of salivation, tympany, tachypnoea, polydipsia, urination, diarrhoea, bradycardia, miosis, tremor and convulsions. As poisoning from an acetylcholinesterase-inhibiting insecticide was suspected, treatment with atropine sulphate was initiated at a dose of 0.3 mg/kg bodyweight. The treatment was repeated for some animals that relapsed, and was effective in all cases, with the exception of one goat kid that died.

DIAGNOSIS: Necropsy of the goat kid showed pulmonary oedema and congestion of internal organs. Toxicological analysis of stomach contents and liver of the dead animal, as well as of the carnations, revealed high concentrations of carbamates.

CLINICAL RELEVANCE: Carbamate poisoning after consumption of polluted feedstuffs or glasshouse products can be fatal for dairy goats. Atropine sulphate, at 0.3 mg/kg, can be useful in treating this condition.     

Assessment of risk of monepantel faecal residues to dung fauna

Objective To evaluate the safety of monepantel and its major metabolite for dung fauna. Monepantel is a new oral anthelmintic drug for use in sheep at a dose of 2.5 mg active ingredient/kg body weight. Hazard (toxicity) is related to the expected exposure. Design The methodology was based on the Organisation for Economic Cooperation and Development (OECD) draft guideline for testing of chemicals, so dung from cattle, not sheep, and eggs of the dung fly, Scathophaga stercoraria and larvae of the dung beetle Aphodius constans were used. Procedures Monepantel or its sulfone metabolite were mixed into bovine faeces in which either dung fly eggs or dung beetle larvae were placed and their development observed. The primary endpoint was survival. Real exposure data (faecal concentrations) for comparison with the generated laboratory data were taken from a kinetics study in sheep dung. Results The no-observed effect concentration (NOEC) for monepantel was >1000 mg/kg substrate for dung flies and 250 mg/kg for dung beetles. The sulfone metabolite was slightly more toxic, with a NOEC of 500 mg/kg for dung flies and 125 mg/kg for dung beetles. Conclusion A comparison of the results to the maximum concentrations of 15 mg monepantel and 4.5 mg sulfone per kg dung observed under an exaggerated dosing regime in sheep indicates that monepantel poses no risk to insect dung fauna when used as recommended. The study is considered valid because representatives of both genera were able to develop in bovine or ovine dung.