Analyze Diet

Topic:Necrosis

Necrosis in horses refers to the localized death of cells or tissues within the body, often resulting from factors such as injury, infection, or compromised blood supply. This pathological process can affect various tissues, including skin, muscle, and internal organs. Necrosis may manifest as visible lesions, swelling, or tissue discoloration, and can lead to further complications if not addressed. Understanding the underlying causes and mechanisms of necrosis is important for effective management and treatment in equine veterinary practice. This page compiles peer-reviewed research studies and scholarly articles that explore the causes, mechanisms, and implications of necrosis in horses, providing insights into diagnostic and therapeutic approaches.
Phenylbutazone toxicosis in the horse: a clinical study.
Journal of the American Veterinary Medical Association    March 15, 1984   Volume 184, Issue 6 699-703 
Collins LG, Tyler DE.In a retrospective study of 269 horses that had been treated with phenylbutazone, horses receiving less than or equal to 8.8 mg/kg of body weight/day for less than or equal to 4 days or 2 to 4 mg/kg of body weight/day for up to 50 days remained clinically normal. Anorexia, depression, colic, hypoproteinemia, diarrhea, melena, weight loss, ventral edema, petechial hemorrhages of mucous membranes, oral and gastrointestinal tract erosions and ulcers, renal papillary necrosis, and death were among the complications seen in horses that had received greater than 8.8 mg/kg of body weight/day. In 2 ca...
Suspected hepatotoxicity in neonatal foals: preliminary report of an emerging syndrome.
The Veterinary record    February 4, 1984   Volume 114, Issue 5 115-117 doi: 10.1136/vr.114.5.115
Mullaney TP, Brown CM, Watson GL, Brandt LA.An apparently new and emerging fatal hepatic disease affecting foals is described. Characteristics included evidence of hepatic failure, marked biliary hyperplasia, hepatocellular necrosis and occasionally fibrosis. Generally, the features of the disease appear to differ markedly from other hepatic diseases of neonatal foals.
[Skin necrosis in a horse as a consequence of a disinfection accident].
Tierarztliche Praxis    January 1, 1984   Volume 12, Issue 1 45-48 
Stanek C.No abstract available
Toxic hepatopathy in neonatal foals.
Veterinary pathology    January 1, 1984   Volume 21, Issue 1 3-9 doi: 10.1177/030098588402100102
Acland HM, Mann PC, Robertson JL, Divers TJ, Lichtensteiger CA, Whitlock RH.Six foals of three different breeds, born to healthy mares, appeared normal at birth, and died at two to five days of age with icterus, ataxia, head pressing, and terminal hepatic coma. Their livers were less than one-half normal weight. Most of the liver was dark red-brown and slightly rubbery. Histologically, these areas were characterized by severe bile ductule proliferation, mild portal tract fibrosis, and massive hepatocellular necrosis and lobular collapse. A small proportion of the liver, usually on the peripheral part of the lobes, was grossly light brown and slightly raised. Histologi...
Verminous (Strongylus vulgaris) myelitis in a donkey.
The Cornell veterinarian    January 1, 1984   Volume 74, Issue 1 30-37 
Mayhew IG, Brewer BD, Reinhard MK, Greiner EC.A fifth stage Strongylus vulgaris migrated through the spinal cord of a 2-year-old, male donkey resulting in progressive paraparesis and then tetraplegia. A profound neutrophilic pleocytosis was detected on analysis of cerebrospinal fluid. The parasite appeared to have entered the mid-lumbar spinal cord, migrated to the cranial thoracic segments, exited, then re-entered the spinal cord a few segments craniad. It then traveled further cranially and was found in the third cervical spinal cord segment. Some parts of the lesion were remarkably free from tissue necrosis, hemorrhage and inflammation...
Toxic hepatic failure in newborn foals.
Journal of the American Veterinary Medical Association    December 15, 1983   Volume 183, Issue 12 1407-1413 
Divers TJ, Warner A, Vaala WE, Whitlock RH, Acland HA, Mansmann RA, Palmer JE.Eight foals, 2 to 5 days of age, with similar clinical signs and laboratory and pathologic findings, died from hepatic failure. The predominant clinical signs were depression and icterus. Abnormally high values were found for plasma ammonia content, aromatic-to-branch-chain amino acid ratio, total serum bilirubin content, gamma glutamyl transferase activity, alkaline phosphatase activity, and PCV; partial thromboplastin time and prothrombin time were prolonged. Some foals had high sorbitol dehydrogenase activity. These laboratory findings were suggestive of subacute hepatic disease and failure...
Renal medullary crest necrosis associated with phenylbutazone therapy in horses.
Veterinary pathology    November 1, 1983   Volume 20, Issue 6 662-669 doi: 10.1177/030098588302000602
Read WK.Thirty-five cases of renal medullary crest necrosis morphologically similar to the renal papillary necrosis of analgesic nephropathy as described in man and rats are reported in horses receiving maintenance dosages of phenylbutazone. The primary lesion is a well-demarcated focal medullary necrosis resulting in sequestration of fragments of the renal crest. Renal cortical lesions are considered secondary to the medullary necrosis and consist of segmental pallor as a result of tubular dilatation, filtrate retention, and interstitial edema. Ischemia in concert with phenylbutazone is suggested as ...
Acute experimentally induced aflatoxicosis in the weanling pony.
American journal of veterinary research    November 1, 1983   Volume 44, Issue 11 2110-2114 
Bortell R, Asquith RL, Edds GT, Simpson CF, Aller WW.Nineteen weanling ponies and 1 adult pony were given a single oral dose of aflatoxin B1 (AFB1). Dosages were: 0, 0.5, 1, 2, 4, 5, 6, and 7.4 mg of AFB1/kg of body weight. Vital signs were monitored, and whole blood and serum collected for analysis of serum enzymes, prothrombin time, blood cell counts, and serum urea nitrogen. Ponies that died were examined for gross lesions, and tissues were collected for histopathologic examination and analysis of AFB1 and AFM1 residues. Two of the 4 ponies given the 2 mg/kg dose and all ponies given the larger dosages died within 76 hours. Clinical signs inc...
Ulcerative duodenitis in foals.
Veterinary pathology    November 1, 1983   Volume 20, Issue 6 653-661 doi: 10.1177/030098588302000601
Acland HM, Gunson DE, Gillette DM.Seven foals aged 18 days to 3 1/2 months had either single or multiple full-circumference segments or long antimesenteric bands of necrotizing duodenitis, sharply delineated from adjacent viable duodenum. Perforation of the necrotic wall had occurred in all foals, leading to acute fibrinous peritonitis. On the mucosal surface severe diffuse, acute inflammation and ulceration involved the anterior half of the duodenum. Two further foals, aged 28 and 30 days, had lesions that are believed to be a chronic form of this disease. Both foals had a thickened duodenal wall, with large areas of mucosa r...
Palatal myositis in horses with dorsal displacement of the soft palate.
Journal of the American Veterinary Medical Association    October 1, 1983   Volume 183, Issue 7 781-785 
Blythe LL, Cardinet GH, Meagher DM, Brown MP, Wheat JD.The histologic and histochemical features of palatine muscles from 53 horses were studied; 25 of the horses were racehorses that had upper airway obstruction associated with dorsal displacement of the soft palate and 28 of the horses did not have any respiratory disorders and served as controls. Pathologic features observed included myonecrosis, phagocytosis, mononuclear cell infiltration of perimysial connective tissue, alkaline phosphatase-positive myofibers, and myofibers with cytoarchitectural changes that included irregular staining of the intermyofibrillar sarcoplasm and sarcoplasmic mas...
Chronic necrotizing vasculitis in a horse.
Journal of the American Veterinary Medical Association    September 1, 1983   Volume 183, Issue 5 579-582 
Morris DD, Miller WH, Goldschmidt MH, Trenka-Benthin S.No abstract available
Renal papillary necrosis in horses after phenylbutazone and water deprivation.
Veterinary pathology    September 1, 1983   Volume 20, Issue 5 603-610 doi: 10.1177/030098588302000512
Gunson DE, Soma LR.Acute renal papillary necrosis occurred in five horses given normal therapeutic doses of phenylbutazone and deprived of water for 36 to 48 hours prior to euthanasia. Five horses given phenylbutazone alone and four horses subjected to water deprivation alone did not develop papillary necrosis. Urinalyses were normal prior to water deprivation, and also after water deprivation in the horses that did not receive phenylbutazone, but the water-deprived, phenylbutazone-treated horses had many red blood cells, transitional epithelial cells, and large numbers of oxalate crystals in their urine. Ulcera...
Nodular necrobiosis in a horse.
Australian veterinary journal    May 1, 1983   Volume 60, Issue 5 148 doi: 10.1111/j.1751-0813.1983.tb05929.x
Nicholls TJ, Arnold KS, Johnston KG.No abstract available
Effects of large doses of phenylbutazone administration to horses.
American journal of veterinary research    May 1, 1983   Volume 44, Issue 5 774-780 
MacKay RJ, French TW, Nguyen HT, Mayhew IG.The effects of large doses of phenylbutazone were evaluated in clinically normal horses. The drug was given to 4 groups of 2 horses each at the rate of 30 mg/kg of body weight, orally, or 30, 15, or 8 mg/kg IV daily for up to 2 weeks. All horses became anorectic and depressed after 2 to 4 phenylbutazone treatments, and the horses given 15 or 30 mg/kg died on or between days 4 and 7 of treatment. A decrease in total blood neutrophil count occurred in all horses, and was associated with toxic left shift in horses given the 2 larger dosage schedules. The horses also had progressive increases in s...
Morphologic and biochemical changes in cartilage of foals treated with dexamethasone.
The Cornell veterinarian    April 1, 1983   Volume 73, Issue 2 170-192 
Glade MJ, Krook L, Schryver HF, Hintz HF.Epiphyseal and articular cartilages were examined in pony foals treated with intramuscular injections of either 0.5 mg dexamethasone per 100 kg bodyweight daily for 3, 8 or 11 months, or 5.0 mg per 100 kg for 11 months, and in horse foals treated with 5.0 mg per 100 kg for 20 weeks. The proximal femoral growth plates exhibited increased spatial separation between chondrocyte columns, narrowed zones of disorganized columnar and hypertrophic cartilage, abnormal penetration of hypertrophic cartilage by metaphyseal capillaries, retained cartilage in the spongiosa, distal terminal plate formation, ...
A morphological study of the lesions of African horsesickness.
The Onderstepoort journal of veterinary research    March 1, 1983   Volume 50, Issue 1 7-24 
Newsholme SJ.Gross, histological and ultrastructural findings are described in 6 natural cases and in 2 experimental cases of African horsesickness. From the gross lesions the cases were divisible into 2 groups which represented the previously described pulmonary and mixed forms of the disease. Histologically, abundance of fibrin and inflammatory cells in oedematous lung suggests that the pulmonary lesion is an exudative pneumonia. Lymphoid depletion and necrosis in germinal centres were consistently present. Electron microscopy failed to demonstrate virus particles or virus-associated structures in the ti...
Renal papillary necrosis in horses.
Journal of the American Veterinary Medical Association    February 1, 1983   Volume 182, Issue 3 263-266 
Gunson DE.No abstract available
Clostridium perfringens cellulitis and immune-mediated hemolytic anemia in a horse.
Journal of the American Veterinary Medical Association    February 1, 1983   Volume 182, Issue 3 251-254 
Reef VB.A 10-year-old Quarter Horse mare was referred for evaluation and treatment of a large pectoral skin slough and hemoglobinuria. The skin slough was secondary to Clostridium perfringens cellulitis and associated gas gangrene. Cold hemagglutinin disease was diagnosed and was suspected to be secondary to C perfringens septicemia. The autoimmune hemolytic anemia, severe intravascular hemolysis, and hemoglobinuria were treated with dexamethasone and hydrocortisone. The infection was treated with 20 X 10(6) units of sodium penicillin, IV, 4 times daily, and the wound was debrided. When the mare relap...
Pathologic changes in 3-methylindole-induced equine bronchiolitis.
The American journal of pathology    February 1, 1983   Volume 110, Issue 2 209-218 
Turk MA, Breeze RG, Gallina AM.The pathologic features of bronchiolitis were studied in horses and ponies from 30 minutes to 27 days after an oral dose of 3-methylindole (3MI). From 30 minutes to 3 hours, lesions were limited to nonciliated bronchiolar epithelial (Clara) cells, which lost apical caps and cytoplasmic granules and had dilated smooth endoplasmic reticulum (SER). At 12 hours, necrotic Clara cells were exfoliated; degeneration and necrosis were evident, in bronchiolar ciliated cells. Rare epithelial cells with hyperplastic SER appeared on the denuded basal lamina at 24 hours. Inflammatory cells, epithelia, fibro...
Ischaemic necrosis of the jejunum of a horse caused by a penetrating foreign body.
Equine veterinary journal    January 1, 1983   Volume 15, Issue 1 66-68 doi: 10.1111/j.2042-3306.1983.tb01712.x
Davies JV.No abstract available
Hemolytic anemia and fibrinoid change of renal vessels in a horse.
Journal of the American Veterinary Medical Association    October 1, 1982   Volume 181, Issue 7 716-717 
MacLachlan NJ, Divers TJ.No abstract available
3-methylindole-induced pulmonary toxicosis in ponies.
American journal of veterinary research    April 1, 1982   Volume 43, Issue 4 603-607 
Derksen FJ, Robinson NE, Slocombe RF, Hill RE.In unanesthetized ponies, arterial blood gas tensions, pulmonary mechanics, and lung volumes were determined before and 24 to 48 hours after oral administration of 500 ml of corn oil or 100 mg of 3-methylindole (3MI)/kg of body weight in 500 ml of corn oil. In the latter group, variables were also measured after bilateral cervical vagotomy. Respiratory rate and minute ventilation were increased by 3MI treatment and decreased after vagotomy, suggesting that the tachypnea induced by 3MI was vagally mediated. The arterial O2 tension (PaO2) was unaffected but arterial CO2 tension (PaCO2) decreased...
Hemolytic anemia in horses after the ingestion of red maple leaves.
Journal of the American Veterinary Medical Association    February 1, 1982   Volume 180, Issue 3 300-302 
Divers TJ, George LW, George JW.Signs of acute hemolytic anemia developed in 4 adult horses from 2 Georgia farms 3 to 4 days after the ingestion of wilted leaves from cut red maple trees (Acer rubrum). Clinical findings included weakness, polypnea, tachycardia, depression, icterus, cyanosis, and brownish discoloration of the blood and urine. Blood changes included methemoglobinemia, free plasma hemoglobin, decreased pcv, and Heinz bodies in erythrocytes. These findings plus hemoglobinuria suggested intravascular hemolysis. Three of the 4 horses diet 5 to 7 days after ingestion of the leaves. Gross pathologic changes included...
Myocardial necrosis secondary to neural lesions in domestic animals.
Journal of the American Veterinary Medical Association    January 15, 1982   Volume 180, Issue 2 144-148 
King JM, Roth L, Haschek WM.Focal myocardial necrosis secondary to neural lesions was diagnosed in 2 dogs and 1 horse. In each case, the neural lesions were traumatic in origin. Spinal cord injury was evident in 1 dog; brain damage was evident in the other dog and presumably in the horse. Retrospective analysis of necropsy material showed that many species were affected, without apparent age or sex predisposition. Central nervous system injury resulting from trauma, infection or space-occupying lesions was associated with acute myocardial necrosis in all cases. The myocardial necrosis was rarely fatal; however, it did ca...
Chlamydia psittaci induced pneumonia in a horse.
The Cornell veterinarian    January 1, 1982   Volume 72, Issue 1 92-97 
McChesney SL, England JJ, McChesney AE.An agent lethal to embryonated chicken eggs was isolated from lung tissues of a quarter horse mare with a fatal respiratory disease. The lesions induced in embryonated chicken eggs, the tinctoral properties, the ultrastructural morphology, the resistance of the organism to sodium sulfadiazine, and the presence of a chlamydial complement fixing antigen, identify this isolate as a member of the family Chlamydiaceae and suggest the agent to be Chlamydia psittaci. Two Shetland ponies experimentally infected with the isolated agent developed subclinical infection as demonstrated by an increase in c...
Observations on vascular accidents in the central nervous system of neonatal foals.
Journal of reproduction and fertility. Supplement    January 1, 1982   Volume 32 569-575 
Mayhew IG.A technique for the subarachnoid perfusion-fixation of the central nervous system was developed to help identify various significant vascular accidents (SVAs) in the central nervous system (CNS) of 24 neonatal foals submitted for necropsy. SVAs, comprising subarachnoid, parenchymal and nerve root haemorrhages, and oedema and necrosis, occurred in 17 foals, more frequently in the spinal cord than the brain. They occurred as frequently in premature foals as in those born at full term, in foals born dead as in foals born alive, and in foals born following dystocia with an assisted delivery as in ...
Glucocorticoid-induced inhibition of osteolysis and the development of osteopetrosis, osteonecrosis and osteoporosis.
The Cornell veterinarian    January 1, 1982   Volume 72, Issue 1 76-91 
Glade MJ, Krook L.Changes in the developing femoral epiphysis, especially those concerning the osteocytes, were examined in pony foals systemically treated with daily intramuscular injections of either 0.5 or 5.0 mg of dexamethasone per 100 kg bodyweight for either 3, 8 or 11 months. Midsagittal sections of proximal femur from animals treated for 3 months contained significantly more bone tissue subchondrally and epiphyseally than did sections from untreated ponies. Large portions of the bone tissue appeared necrotic, although osteoblasts and patent capillaries were abundant. After 8 months the bone sections re...
Postanesthetic myonecrosis in horses.
The Canadian veterinary journal = La revue veterinaire canadienne    December 1, 1981   Volume 22, Issue 12 367-371 
Friend SC.Two horses died of massive myonecrosis following surgery. The hematological, biochemical and pathological changes are described and compared with those previously reported in the literature.
Toxicity of Cassia occidentalis in the horse.
Veterinary and human toxicology    December 1, 1981   Volume 23, Issue 6 416-417 
Martin BW, Terry MK, Bridges CH, Bailey EM.Three Shetland ponies were given a single oral dose of ground Cassia occidentalis seeds in aqueous suspension. The clinical signs observed resembled those seen in naturally occurring and experimental cases in cattle. The syndrome was characterized by an afebrile course, incoordination, recumbency and death. Elevations of blood alkaline phosphatase, CPK, LDH, and SGOT were observed. Although muscle lesions were not seen grossly, microscopic lesions included segmental necrosis of skeletal muscle fibers. The findings were regarded as sufficiently characteristic of C. occidentalis poisoning to be ...
Endotoxemia following experimental intestinal strangulation obstruction in ponies. Moore JN, White NA, Berg JN, Trim CM, Garner HE.Experimental small intestinal strangulation obstruction was produced in anesthetized ponies. The limulus amoebocyte lysate test demonstrated the presence of endotoxin in the general circulation 60 and 120 minutes following restoration of mesenteric blood flow. Mucosal degeneration, with loss of villus epithelial cells, was demonstrated coincident with endotoxemia. The findings were consistent with an ischemia-mediated alteration in the intestinal barrier to endotoxin.