Analyze Diet

Topic:Poisoning

Poisoning in horses refers to the ingestion, inhalation, or absorption of toxic substances that can adversely affect their health. These substances may include plants, chemicals, medications, or environmental toxins. Poisoning can lead to a range of clinical signs, from mild gastrointestinal upset to severe neurological or systemic effects, depending on the toxin involved. Common toxic substances for horses include certain plants like oleander and yew, heavy metals such as lead and arsenic, and specific pesticides or herbicides. This page compiles peer-reviewed research studies and scholarly articles that investigate the causes, effects, diagnosis, and management of poisoning in horses.
Blister beetle poisoning in horses.
Journal of the American Veterinary Medical Association    July 1, 1978   Volume 173, Issue 1 75-77 
Schoeb TR, Panciera RJ.Case records of 21 horses with acute illness following ingestion of hay containing dead striped blister beetles (Epicauta spp) were selected for review. Abdominal pain, fever, depression, frequent urination, shock, and, occasionally, synchronous diaphragmatic flutter characterized clinical illness. Hematologic findings included hemoconcentration, neutrophilic leukocytosis, and hypocalcemia. Hematuria and low urine specific gravity were abnormal urinalysis results. Sloughing of the epithelium of the esophageal part of the stomach, hemorrhagic and ulcerative cystitis, enterocolitis, and myocardi...
Ergot toxicosis.
Modern veterinary practice    June 1, 1978   Volume 59, Issue 6 463-464 
Lindley WH.No abstract available
Chronic lead poisoning in horses.
American journal of veterinary research    June 1, 1978   Volume 39, Issue 6 961-964 
Dollahite JW, Younger RL, Crookshank HR, Jones LP, Petersen HD.Lead acetate was fed to 4 groups of 2 horses each to study chronic lead intoxication. A 5th group of 3 horses was maintained as controls. The leas was fed in capsules, with the minimum dosage of 6.25 mg/kg/day of lead as lead acetate (group I). The dose was increased from group I through group IV in an approximate geometric series, with each group being given about 125% of the dose given the previous group. These doses were given for 105 days, a period designated as phase 1. Since clinical signs were not observed after 105 days, the doses were increased and fed for an additional 190 days (days...
Acute bracken fern poisoning in a 14-month-old horse.
Veterinary medicine, small animal clinician : VM, SAC    March 1, 1978   Volume 73, Issue 3 295-296 
Kelleway RA, Geovjian L.No abstract available
Pyrrolizidine alkaloid poisoning of horses.
Australian veterinary journal    March 1, 1978   Volume 54, Issue 3 150 doi: 10.1111/j.1751-0813.1978.tb05536.x
Seaman JT.No abstract available
A review of recent trends in animal poisoning.
The British veterinary journal    March 1, 1978   Volume 134, Issue 2 128-145 doi: 10.1016/s0007-1935(17)33537-6
Humphreys DJ.No abstract available
Rodenticide toxicosis in a horse.
Journal of the American Veterinary Medical Association    February 1, 1978   Volume 172, Issue 3 270-271 
Russel SH, Monin T, Edwards WC.No abstract available
Clinical signs and chemical confirmation of 4-aminopyridine poisoning in horses.
American journal of veterinary research    February 1, 1978   Volume 39, Issue 2 329-331 
Ray AC, Dwyer JN, Fambro GW, Reagor JC.4-Aminopyridine poisoning in horses was diagnosed. Specific methods, utilizing thin-layer and high-performance liquid chromatography, were developed for determining the compound in stomach contents and corn bait. The lethal dose was estimated at 2 to 3 mg/kg of body weight.
Pesticide poisonings in domestic animals.
Modern veterinary practice    November 1, 1977   Volume 58, Issue 11 913-920 
Maddy KT, Riddle LC.No abstract available
An outbreak of Swainsona poisoning in horses.
Australian veterinary journal    September 1, 1977   Volume 53, Issue 9 446-447 doi: 10.1111/j.1751-0813.1977.tb05496.x
O'Sullivan BM, Goodwin JA.On 6 properties in south-western Queensland an outbreak of nervous disease occurred horses due to ingestion of Swainsonia (Darling pea). Loss of condition, depression, hyperaesthesia and hyperexcitability were seen in affected horses. At autopsy of 2 horses generalised c ytoplasmic vacuolation was seen in the neurones of the central nervous system and in the liver, adrenal and thyroid. The clinical and pathological features were similar to those described in horses suffering from Swainsona poisoning in Australia and Astragalus and Oxytropis in North America.
Bromide intoxication of horses, goats, and cattle.
Journal of the American Veterinary Medical Association    September 1, 1977   Volume 171, Issue 5 446-448 
Knight HD, Costner GC.During the summer and fall of 1973, a few horses, goats, and cattle in the Napa Valley of California became intoxicated by bromide via the ingestion of volunteer oat hay that had been cut from a field treated with methyl bromide, a soil fumigant. The bromide content of the hay ranged from 6,00 to 8,400 ppm. Signs of intoxication were lethargy, weakness, and ataxia. Animals experimentally fed the contaminated hay developed signs of intoxication between the 7th and 9th days.
Clinical application of cerebrospinal fluid creatine phosphokinase determination.
Journal of the American Veterinary Medical Association    July 15, 1977   Volume 171, Issue 2 200-202 
Wilson JW.Creatine phosphokinase activity was determined in cerebrospinal fluid samples submitted for analysis from 126 animals suspected of having central nervous system disease. Values less than 1 sigma unit/ml were obtained on 32 samples and values less than or equal to 1 sigma unit/ml were obtained on 94 samples. The creatine phosphokinase values were increased in all cases of feline toxoplasmosis and feline infectious peritonitis. From other cases, especially seizure disorders and suspected poisonings, and apparent aid in prognosis for future cases was identified.
[Mold intoxication in a horse (short communication)].
DTW. Deutsche tierarztliche Wochenschrift    May 5, 1977   Volume 84, Issue 5 176-177 
Ahlswede L, Heintzelmann-Gröngröft B.No abstract available
Veterinary toxicology: the epidemiology of poisonings in domestic animals.
Clinical toxicology    January 1, 1977   Volume 10, Issue 1 1-21 doi: 10.3109/15563657708987956
Oehme FW.Animals are constantly exposed to a wide variety of foreign chemicals, many of which are potentially toxic and some of which result in the clinical poisonings. Pesticides are applied on or around animals for the control of insects and rodents. These chemicals may be placed in areas without regard for accessibility to household pets and domestic livestock. Insecticides, herbicides, and fungicides are routinely and haphazardly applied to animal and environmental surfaces alike with apparent disregard for differences in absorptive capability. Fortunately, newer herbicides and fungicides are relat...
Acorn poisoning.
The Veterinary record    December 4, 1976   Volume 99, Issue 23 465-466 doi: 10.1136/vr.99.23.465
Daniels MG.No abstract available
[Poisoning with meta (metaldehyde) in a horse].
Schweizer Archiv fur Tierheilkunde    December 1, 1976   Volume 118, Issue 12 557-558 
Grandchamp G.No abstract available
Evaluation of monensin toxicity in the horse.
Journal of the American Veterinary Medical Association    November 15, 1976   Volume 169, Issue 10 1098-1100 
Matsuoka T.Gelded horses of mixed breeding, ranging in weight between 360 and 455 kg, were fed pellets that contained monensin at concentrations of 279, 124, 31, and 0 ppm. Of 2 horses fed 279 ppm (253 g/T), both died. Of 3 horses fed 125 ppm (113 g/T), 1 died; feed intake was reduced in the 2 survivors. Of 3 horses fed 31 ppm (28 g/T), 1 had a transitory reduction in feed intake and the other 2 remained clinically normal. The 2 horses fed 0 ppm remained clinically normal. Monensin was also given to horses by gavage, at dosages of 1, 2, 3, 4, or 20 mg/kg of body weight. The LD50 was estimated to be betwe...
Acorn poisoning.
The Veterinary record    November 13, 1976   Volume 99, Issue 20 403-404 doi: 10.1136/vr.99.20.403
Broughton JE.No abstract available
Acorn poisoning.
The Veterinary record    October 23, 1976   Volume 99, Issue 17 343 doi: 10.1136/vr.99.17.343-a
Wharmby MJ.No abstract available
A possible case of equine aflatoxicosis.
Clinical toxicology    January 1, 1976   Volume 9, Issue 2 251-254 doi: 10.3109/15563657608988128
Greene HJ, Oehme FW.No abstract available
Presumptive quaternary ammonium intoxication in a pony.
Journal of the American Veterinary Medical Association    January 1, 1976   Volume 168, Issue 1 60 
Skand DL.No abstract available
Fusariotoxicosis from barley in British Columbia. I. Natural occurrence and diagnosis.
Canadian journal of comparative medicine : Revue canadienne de medecine comparee    January 1, 1976   Volume 40, Issue 1 12-15 
Greenway JA, Puls R.Clinical sickness was observed in domestic ducks, geese, horses and swine during October 1973. All species showed upper alimentary distress with mortalities occurring in the geese. Barley derived from a common source had been fed. Examination of the barley revealed invasion by Fusarium spp and detection of a high level of dermatitic fusariotoxins.
Letter: Monensin sodium in horses.
The Veterinary record    August 16, 1975   Volume 97, Issue 7 137-138 doi: 10.1136/vr.97.7.137
Stoker JW.No abstract available
Tetrachlorodibenzodioxin: an accidental poisoning episode in horse arenas.
Science (New York, N.Y.)    May 26, 1975   Volume 188, Issue 4189 738-740 doi: 10.1126/science.1168366
Carter CD, Kimbrough RD, Liddle JA, Cline RE, Zack MM, Barthel WF, Koehler RE, Phillips PE.Tetrachlorodibenzodioxin was identified as the apparent cause of an outbreak of poisoning in humans, horses, and other animals. Exposure was related to the spraying of contaminated waste oil on riding arenas for dust control. The contamination resulted from improper disposal of a toxic industrial waste. The pathologic effects and chemical identification of tetrachlorodibenzodioxin are described.
Metaldehyde poisoning in three horses.
Modern veterinary practice    May 1, 1975   Volume 56, Issue 5 336-337 
Harris WF.Three horses exhibited nervous and cardiopulmonary signs after ingestins small amounts of metaldehyde, and 2 died in 3 to 5 hours. A colt given 0.1 mg/kg was similarly affected and died.
Spongy degeneration in the central nervous system of domestic animals. Part III: Occurrence and pathogenesis hepatocerebral disease caused by hyperammonaemia.
Acta neuropathologica    January 1, 1975   Volume 31, Issue 4 343-351 doi: 10.1007/BF00687929
Hooper PT.Severe spongy degeneration of the central nervous system (CNS) was seen in 11 cattle, 19 sheep, 4 pigs and 1 goat, associated with a variety of hepatic diseases, particularly those caused by hepatotoxic pyrrolizidine alkaloids. It was also seen in a milder form in 2 of 8 horses examined, 1 dog of 5 dogs examined, and in 1 rabbit only of a large number of laboratory animals examined. This paper reports results of experiments which confirmed initially that the CNS disease cold be caused by pyrrolizidine alkaloid intoxication. This was done by poisoning lambs with lasiocarpine. As the disease was...
Poisons: could what you don’t know kill your patients?
Modern veterinary practice    December 1, 1974   Volume 55, Issue 12 941-944 
Harris WF.No abstract available
Correspondence: Accidental poisoning.
The Veterinary record    October 19, 1974   Volume 95, Issue 16 375-376 doi: 10.1136/vr.95.16.375
Thorpe RM.No abstract available
Cyanide poisoning in horses.
Veterinary medicine, small animal clinician : VM, SAC    September 1, 1974   Volume 69, Issue 9 1166-1167 
Prodjoharjono S.No abstract available
Hypercalcaemia and mineralisation of non-osseous tissues in horses due to vitamin-D toxicity.
Zentralblatt fur Veterinarmedizin. Reihe A    August 1, 1974   Volume 21, Issue 8 638-643 doi: 10.1111/j.1439-0442.1974.tb01348.x
Muylle E, Oyaert W, De Roose P, Van Den Hende C.No abstract available