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#1
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Need some QUICK ideas
A fellow volunteer just called to say that his brother's dogs got into some grass clippings that had been sitting around for a couple of weeks, and got really sick from it. One of the dogs (a boxer mix) died from it, and his 145 lbs. GSD is at the vet's and barely hanging on. The vet has started the dog on IV antibiotics, and is doing blood tests. I don't have a lot of information, but the symptoms appear to be lethargy, vomiting and blood in the feces. Phenolic acid, benzoic acid and hydroxyphenylpropionic acids can all be released during plant decay, but they shouldn't be in large enough doses to kill 60 pound dogs. It's been warm here the past week, and it's possible there were mushrooms mixed in there that could be causing this. Don't know if there could be some other fungus or mold that could cause these symptoms. The dog can't be impacted if it is still passing stool, can it? I've asked the owners to check the grass to see if there is anything growing in there, and to call poison control for how to deal with that if they find anything. Any other ideas? Suja |
#2
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Need some QUICK ideas
"Suja" wrote in message: Forgot to mention, no chemicals of any sort was used on the lawn, so that's not it. Suja |
#3
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Need some QUICK ideas
"Suja" wrote in message ... A fellow volunteer just called to say that his brother's dogs got into some grass clippings that had been sitting around for a couple of weeks, and got really sick from it. One of the dogs (a boxer mix) died from it, and his 145 lbs. GSD is at the vet's and barely hanging on. The vet has started the dog on IV antibiotics, and is doing blood tests. I don't have a lot of information, but the symptoms appear to be lethargy, vomiting and blood in the feces. Phenolic acid, benzoic acid and hydroxyphenylpropionic acids can all be released during plant decay, but they shouldn't be in large enough doses to kill 60 pound dogs. It's been warm here the past week, and it's possible there were mushrooms mixed in there that could be causing this. .................yeah, wonder if that isn't it. In which case the liver needs huge support. Do they really think they ate some of the clippings or was the pile just disturbed? Any nasty neighbors? There's a list of fungi present in compost: http://www.annmicro.unimi.it/full/53...oer_53_349.pdf We got bad toads here in FL - any reptiles they could have eaten? But this is silly. She should call ASPCA poison control hotline and open an account. Cripes, hope his pup is OK buglady take out the dog before replying |
#4
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Need some QUICK ideas
"buglady" wrote in message: ................yeah, wonder if that isn't it. In which case the liver needs huge support. Do they really think they ate some of the clippings or was the pile just disturbed? Any nasty neighbors? I think it's no on the nasty neighbors, and they seem absolutely convinced that whatever is causing this is/was in the grass clippings. The symptoms of mushroom poisoning in humans is similar. There's a list of fungi present in compost: http://www.annmicro.unimi.it/full/53...oer_53_349.pdf I'll pass it along. We got bad toads here in FL - any reptiles they could have eaten? Not that I know of. Another avenue to explore, however. But this is silly. She should call ASPCA poison control hotline and open an account. That's what I said, and he said that the thought never occured to them. Cripes, hope his pup is OK Me too. I'll let you know how it turns out. Wonder if necropsy of the dog that died would've given them the answers they're looking for. Suja |
#5
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Need some QUICK ideas
"buglady" wrote in message link.net... This doesn't sound the same, but I will note that gastric lavage was done - and may have saved this dog. Roquefortine can occur in silage: http://www.pubmedcentral.nih.gov/art...i?artid=339273 Acute penitrem A and roquefortine poisoning in a dog A 45-kg, 4-year-old, castrated male, Labrador retriever had vomited once and was presented for lethargy, excessive panting, trembling, and incoordination. That morning, the dog had been outside unsupervised, with access to restaurant garbage. The dog was anxious, ataxic, and full-body tremors were evident. The heart rate was elevated but difficult to determine due to the polypnea. Body temperature was elevated (40.9°C) and both pupils were dilated. Mucous membranes were pink, and capillary refill time (CRT) was normal (1 s). Collection and immediate freezing of the vomitus was requested to help with diagnosis, treatment, and prognosis. Because of the severity of its condition, the dog was to be transferred to an emergency clinic for 24-hour care, but convulsions began before this was possible. Seizures, but no foreleg paddling, and hyperesthesia were controlled by administration of diazepam (Valium 10; Rocher, Mississauga, Ontario), 3 boluses, each 0.22 mg/kg body weight (BW) given, IV, at 3-minute intervals. Lactated Ringer's solution (Baxter, Toronto, Ontario) was administered, IV, at a rate of 90 mL/kg BW/h. All tremor activity ceased after administration of phenobarbitol sodium (Phenobarbitol; Abbott Laboratories, Toronto, Ontario), 2 boluses, each 2.7 mg/kg BW given, IV, at a 5-minute interval. Acute toxicosis was suspected. Because of the possibility of septic shock, or anaphylactic shock, or both, the dog was treated with ampicillin sodium (Ampicillin; Novopharm, Toronto, Ontario), 22.2 mg/kg BW, IV, and tripelennamine HCl (Vetastim; rogar/STB, Montreal, Quebec), 0.5 mL/10 kg BW, IM. In addition, prednisolone sodium succinate (Soludelta Cortef; Upjohn, Orangeville, Ontario), 22.2 mg/kg BW, was given IV. Gastric lavage with warm water was performed, after anesthesia had been induced with a bolus of propofol (Rapinovet; Schering-Plough, Pointe-Claire, Quebec), 2 mg/kg BW, IV, and was maintained with isoflurane (Aerrane; Janssen, Toronto, Ontario). Activated charcoal (50 g) was administered. Hyperthermia was treated by placement of cold wet towels over the animal's body during anesthesia. Heart rate (96 beats/min) and body temperature (38.1?C) were normal before transport to the emergency clinic. Diazepam (Valium; Sabex, Boucherville, Quebec) was administered in an IV drip (0.2 mg/mL) before and during the 30-minute trip. On arrival at the emergency clinic, the dog was panting and had begun to paddle with his forelegs. Rectal temperature (38.5°C), CRT ( 2 s), and mucous membranes were normal. An electrocardiogram revealed a regular cardiac rhythm with an increased heart rate (160 beats/min). The dog was maintained on diazepam, 0.5 mg/kg BW/h, IV, for 4 h. Administration rate was halved at 2-hour intervals during the next 6 h. Intravenous electrolytes (Plasma-lyte 148; Baxter, Toronto, Ontario) were administered, as required. Ampicillin sodium was continued at 22.2 mg/kg BW, IV, q8h, for 24 h. Lateral and dorsoventral thoracic radiographs taken on day 2 revealed signs of aspiration pneumonia. Ampicillin was discontinued and cefoxitin sodium (Cefoxitin; Novopharm, Toronto, Ontario) was prescribed at 22.2 mg/kg BW, IV, q6h, for 24 h, then q8h for 24 h. Pulse oximetry readings of blood oxygen saturation were below normal (80%). Nasal catheterization with 100% oxygen therapy (112 mL/kg BW/min for 20 h) increased blood oxygen saturation to levels greater than 95%. By day 4, the dog was free of abnormal neurological signs and the pneumonia was treated at home with amoxicillin and clavulinic acid (Clavamox; Pfizer, London, Ontario), 11.1 mg/kg BW, PO, q12h, for 14 d. Gross and microscopic examination of the vomitus revealed blades of grass, pieces of raw tenderloin, and a cereal-based substance resembling flour. A thin layer chromatography screen was used for detection of penitrem A (PA), roquefortine (RQ), or strychnine. Significant levels of PA and RQ ( 10 ppm) were identified. Poisoning is the primary differential for a dog with acute onset of vomiting, polypnea, tachycardia, hyperesthesia, and ataxia, followed by lateral recumbency, muscle fasciculations, and seizures. Metaldehyde, mycotoxins, strychnine, zinc phosphide, bromethalin, xanthines, and insecticides must be considered. The history of garbage consumption in this case suggested that mycotoxins or xanthines were the most likely toxins. The dog exhibited mydriasis and tachycardia, clinical signs not associated with insecticides that cause cholinergic stimulation; the lavage contents lacked an acetaldehyde odor, making metaldehyde poisoning unlikely; recovery from bromethalin poisoning rarely occurs in 3 d; and strychnine poisoning is a rare occurrence. Mycotoxins are produced by specific fungus. Only certain species of Aspergillus, Claviceps, and Penicillium produce tremorgenic mycotoxins (1), such as PA and RQ, which can cause uncontrollable neuromuscular activity in vertebrates. Different taxonomic classifications of fungal species have made it difficult for researchers to agree on the species of origin for individual mycotoxins (2,3). On the basis of morphological and physiological properties, Penicillium crustosum and Penicillium roquefortii are now considered the most common producers of PA and RQ, respectively (2). Fungal synthesis of mycotoxins is factor-dependent. For example, an ambient temperature of 25°C and a pH of 5.7 optimize production of PA by P. crustosum. Similarly, a culture medium containing 2% skim milk, potato extract, and 2% lactose induces the highest levels of PA when P. crustosum isolates are incubated for 3 wk (4). Penicillium crustosum may be isolated from several types of food, including meat, fruit, cereal and cereal products, cheese, spices, and nuts (4). Lacking appropriate environmental conditions, fungal mycelia can proliferate but fail to produce a specific mycotoxin. Treatment for PA or RQ toxicosis should begin immediately after obtaining a suspicious history and observation of characteristic clinical signs, which usually begin 30 min to 4 h after ingestion of garbage, depending on the amount of mycotoxin consumed (5,6). Penitrem A intoxication causes ataxia, polypnea, and sustained tremors that may progress to generalized seizures and death (5,6,7). However, as in this case, animals may vomit before any of these clinical signs appear (7). Hyperesthesia may occur, indicated by muscle fasciculations in response to noise (5). Death of the animal can be avoided by administering phenobarbitol immediately to control seizures. Clinical signs may resolve within 12 h (7), but complete recovery may take as long as 21 d (5), depending on the amount of PA absorbed (6). Without treatment, animals receiving more than 0.5 mg/kg BW of PA are likely to die within 3.5 h (6). A minimum toxic dose of PA for the dog has not been determined. Roquefortine intoxication is characterized by vomiting, panting, muscle tremors, paddling, hyperesthesia, and seizures (8). Intravenous diazepam does not alleviate the clinical signs of RQ poisoning as it does similar signs caused by strychnine and metaldehyde poisoning (8). The prognosis for dogs with RQ intoxication depends on how soon the toxin is removed from the stomach. Barbiturate therapy is effective in controlling seizures but may not prevent death if the toxin remains in the stomach (8). A complete recovery occurs within a 24- to 48-hour period following vomiting (8). This dog showed signs typical of both PA and RQ poisoning. Death due to RQ poisoning was likely prevented by early vomiting, and barbiturate therapy probably protected the dog against death due to PA-induced seizures. If RQ levels in the vomitus had been compared with those in the lavage solution, it might have been possible to show that vomiting did protect the dog against fatal intoxication. The effectiveness of activated charcoal in preventing fatality in animals that have ingested RQ is unknown and needs to be investigated. The exact mechanism of action by which PA causes symptoms is uncertain. Data from postmortem examination suggest that some serum enzymes may increase due to hepatic centrolobular changes (congestion and hepatocyte degeneration and necrosis) (6). Lungs and large and small intestine are often hemorrhagic and edematous (6), which may be the result of shock. The primary target of PA may be at the biochemical level, as a neural lesion has not been identified microscopically (9). In vitro research has demonstrated that PA alters central presynaptic release of the excitatory neurotransmitters (NTs) glutamate and aspartate, and the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) (9). In response to PA, release of these NTs by inactive cortical synaptosomes increases, and release by stimulated synaptosomes decreases (9). Synapses at the neuromuscular junction are not affected (9). Research is needed to identify the in vivo synaptic effects and primary site of action of PA. In electrophysiologic and histologic studies in rodents, seizure-sensitive areas (the thalamus and hippocampus) exhibited no abnormalities to account for PA-induced seizures (10). Rather, dose-related lesions of the cerebellar cortex may be implicated. At a dose of 0.5 mg/kg BW of PA, some degeneration of Purkinje cells were observed (10). After inoculation with a low dose of PA, animals appeared to be most severely affected within 30 min and recovered within 24 h (10). High doses of PA caused extensive loss of Purkinje cells and vacuolization of the molecular layer of the cerebellar cortex (10). Lesions of this magnitude caused significant neuromotor deficits that persisted for more than a week (10). Breton et al (10) theorized that the cerebellar lesions are caused by PA's interference with release mechanisms for glutamate and aspartate, the neurotransmitters for the primary excitatory inputs to Purkinje cells. These inputs are believed to be secreting or transmitting GABA (GABAergic). Upon exposure to PA, excitotoxic cell damage to the Purkinje cells occurs. The GABAergic axons of the Purkinje cells form inhibitory synapses with the cerebellar nuclei, which, in turn, activate the cells of the medial thalamic nucleus (10). This may be the mechanism by which lesions in the cerebellum, a structure responsible for motor coordination, cause seizures, a clinical sign specific to thalamocortical damage. No studies have investigated the mechanism of action of RQ. Clinical signs are similar to those of strychnine poisoning. Strychnine competes with glycine at the postsynaptic site in the spinal cord and medulla. Research investigating the site of action of RQ is needed to aid clinicians further in effectively treating affected animals. The possibility of intoxication with PA or RQ may be overlooked by clinicians presented with a dog exhibiting convulsions. A history of garbage consumption and sudden ataxia progressing to generalized tremors and seizures should raise suspicion of intoxication by PA, RQ, or both. Further investigation into the action of PA and RQ will allow veterinarians to make a faster diagnosis and more appropriate selection of treatment. Hillary's (vet from alt.med.vet) class notes on poisonous plants: http://www.hillary.net/school/spring...m.lec.04.20.98 The other thought is that new green plant growth can have a lot of nitrogen - perhaps nitrates. buglady tak eout the dog before replying |
#6
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Need some QUICK ideas
In article , Suja wrote:
Any other ideas? Some time after reading this post I remembered that we were always told not to let the horses eat cut grass because of ..... and I couldn't remember what. It just came to me that it's botulism, which is rare but can get into the grass from dead animals (in this case possibly moles, mice, etc., that met an early demise at the hands of the lawnmower). I'd guess it's a long shot but I don't think it's impossible. -- Melinda Shore - Software longa, hardware brevis - Prouder than ever to be a member of the reality-based community |
#7
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Need some QUICK ideas
"Suja" wrote in message ... Wonder if necropsy of the dog that died would've given them the answers they're looking for. ..........Absolutely - they could have at least looked at stomach contents and the liver. OK more on molds in silage: http://www3.interscience.wiley.com/c.../1382/ABSTRACT Wilted grass and whole-crop maize silages taken from farm silos in northern Germany were analysed for fermentation pattern, mould counts and composition of mycoflora as well as for roquefortine C. In general, increasing DM contents of visibly unmoulded silages resulted in decreasing amounts of volatile fatty acids and a greater portion of samples with a high number of mould propagules. The average mould count of these silages was found to be 1·4×104 cfu g-1, whereas visibly moulded samples contained about 1×108 cfu g-1. Penicillium roqueforti was the predominating fungal species in silages occasionally accompanied by species of the genera Aspergillus, Mucor, Monascus and/or Geotrichum. Penicillium roqueforti was detected in 89% of the visibly moulded and in 85% of the visibly unmoulded samples. Of 24 visibly moulded silages tested, 21 samples contained roquefortine C, a mycotoxin known to be produced by P roqueforti. The highest level of roquefortine C found was 36 mg kg-1 ...........Nothing here but the title, but apparently it does have an effect on the liver: Inhibitory Effects of Roquefortine on Hepatic Cytochromes P450 Aninat, C. Delaforge, M. ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY Bibliographic details 2001, VOL 500, pages 331-334 List of fungal toxins and fungi that produce them: http://www.aerobiology.net/Mycotoxin.html Some fungal toxins and their effects - more useful than one above:: http://www.aerias.org/DesktopDefault...dex=4&tabid=66 ......OK I'm done buglady take out the dog before replying |
#8
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Need some QUICK ideas
"buglady" wrote in message link.net... OK, ONE more! Mycotoxins in sileage - usually a combo: http://www.das.psu.edu/dairynutritio...nts/kuldau.pdf buglady take out the dog before replying |
#9
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Need some QUICK ideas
"Suja" wrote in message ... A fellow volunteer just called to say that his brother's dogs got into some grass clippings that had been sitting around for a couple of weeks, and got really sick from it. One of the dogs (a boxer mix) died from it, and his 145 lbs. GSD is at the vet's and barely hanging on. The vet has started the dog on IV antibiotics, and is doing blood tests. I don't have a lot of information, but the symptoms appear to be lethargy, vomiting and blood in the feces. Phenolic acid, benzoic acid and hydroxyphenylpropionic acids can all be released during plant decay, but they shouldn't be in large enough doses to kill 60 pound dogs. It's been warm here the past week, and it's possible there were mushrooms mixed in there that could be causing this. Don't know if there could be some other fungus or mold that could cause these symptoms. The dog can't be impacted if it is still passing stool, can it? I've asked the owners to check the grass to see if there is anything growing in there, and to call poison control for how to deal with that if they find anything. Any other ideas? Suja - If it isn't too late, if there was clover (I think) or certain weeds growing in the lawn, I believe coumadin or a substance close to it can be formed. In that case the dog needs vitamin K, stat. That would cause internal bleeding and blood in the stool. Abnormal clotting would be evident by blood tests - I think PT/PTT. flick 100785 |
#10
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Need some QUICK ideas - SUJA SUJA
"buglady" wrote in message thlink.net... Have you gotten any feedback on bloodwork and how the pup is doing? buglady take out the dog before replying |
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