Chapter 14 Collapse and Sudden Death
The ruminant or horse that collapses and dies within 24 hours while being observed or is found dead with no premonitory signs of illness is often a diagnostic challenge. In these situations clients often are distressed and frequently pressure the veterinarian to declare an immediate diagnosis. Sudden death in the absence of observed clinical illness is usually the most perplexing. Obligation to clients necessitates a systematic approach to derive a specific causative diagnosis, to determine the source and extent of the problem, and to recommend corrective measures. These goals are best accomplished by delineating the characteristics of normal animals within the herd and analyzing the distribution of the disease with respect to time, place, and a variety of exposure factors and environmental influences. These factors are then correlated with necropsy results and additional diagnostic testing.
Collapse is easily identified as a state of extreme prostration and depression. However, sudden death has a somewhat tenuous meaning, lending itself to subjective impression. The timing parameter used to define sudden death ranges from 1 to 24 hours from the onset of the fatal episode. Some veterinarians restrict the definition to a narrower time span. The 12- to 24-hour interval is sometimes selected to coincide with the frequency of owner observation of the livestock. For our purposes sudden death means clinically unexplained, rapid death (12 to 24 hours) occurring during normal activity in apparently healthy animals. Generally a condition of this nature is associated with fatal dysfunction of the cardiovascular, nervous, respiratory, or gastrointestinal (GI) system. In addition, perturbations in general cellular metabolism (cyanide or hydrogen sulfide) may result in peracute death.
The causes of sudden death are investigated in much the same way as for any disease. The accompanying tables of differential diagnoses include infectious, metabolic, nutritional, physical, cardiovascular, toxic, and miscellaneous causes of sudden death. Diagnostic laboratories provide an array of tests and analytic procedures based on the needs of veterinarians in their service areas. Use of these facilities to support a definitive diagnosis is essential in sudden death cases. Diagnosis is rarely based on a single item of evidence and usually requires input from multiple testing procedures. Unless the cause of death is apparent, some important considerations required for effective use of a diagnostic laboratory include the following:
Foal actinobacillosis is an acute fulminant septicemia caused by Actinobacillus equuli, a gram-negative bacterium found in the upper respiratory tract, feces, and genital tract of normal adult horses. Predisposing factors to foal septicemia with any agent include prematurity, failure of passive transfer, dam malnourishment during gestation, and environmental stress. A characteristic histologic finding is multiple bacterial emboli in renal glomerular capillaries without inflammatory infiltrate in neonatal foals. Acute anthrax may be rapidly fatal to horses after a period of excitement, depression, convulsions, and coma. Isolating the causative agent from blood confirms the diagnosis. Babesiosis is an erythrocytic parasite that may cause death within 24 hours. Identification of the organism in blood smears or complement fixation testing for parasite antibodies confirms the diagnosis.
Box 14-1 Infectious Causes of Collapse and Sudden Death in Horses
* Likely to involve several animals.
Acute clostridial disease involving Clostridium septicum, Clostridium chauvoei, Clostridium novyi, and Clostridium perfringens, has been associated with intramuscular injections of various parenterals such as ivermectin, vitamin B complex, prostaglandin, antihistamines, and flunixin meglumine when asepsis has been ignored. Clostridial myopathies also are associated with deep stab or puncture wounds. Botulism in foals (shaker foal syndrome) is caused by Clostridium botulinum, (usually type B). Toxin may sometimes be demonstrated in feed and gut contents. The organism may be cultured from tissues or gut contents in toxico-infectious cases. Clostridium sordellii, should be suspected in cases of foals having a history of colic, bloody diarrhea, and death within a few hours.1 C. perfringens, type C may induce a hemorrhagic enterotoxemia and death in foals as young as 4 days.2 Severe intestinal lesions are caused by the beta-toxin produced by this species. Organisms may be demonstrated in smears of intestinal contents. C. perfringens, type D also induces sudden death in the most aggressive foals in group-feeding situations. Similar enterotoxemia also has been associated with toxin-producing Clostridium difficile,3 and Bacteroides fragilis.,4
Equine monocytic ehrlichiosis (Potomac fever), caused by Ehrlichia risticii, is a severe colitis with diarrhea and dehydration, followed by ileus, endotoxemia, and death in adult horses. Diagnosis is based on clinical findings and antibody and antigen detection using immunofluorescent antibody (IFA) and enzyme-linked immunosorbent assay (ELISA) methods, respectively. Guttural pouch mycosis often results in nonfatal intermittent unilateral epistaxis. Occasionally a single episode of severe epistaxis from rupture of an aneurysm in the internal carotid artery may result in sudden death. Necropsy reveals blood in the nasal passages and guttural pouch with a diphtheritic plaque in the dorsocaudal aspect of the medial compartment. Salmonellosis is responsible for many cases of acute enterocolitis, especially when several animals are involved. The peracute syndrome may resemble colitis-X in mature horses with a course of 6 to 12 hours. Horses may die before diarrhea develops. Postmortem diagnosis is based on isolation of Salmonella, species from bowel contents, bowel wall, and/or associated lymph nodes. Tyzzer’s disease is a rapidly developing fatal hepatitis of foals. The incidence is sporadic, and, because of the peracute development, clinical signs may not be observed before death. Diagnosis is based on histologic demonstration of the bacilli in bundles within hepatocytes surrounding necrotic areas.
Infectious causes of sudden death range from acute septicemias and toxemias to rupture and release of abscess contents into the systemic circulation (Box 14-2). A liver abscess rupturing into the caudal vena cava; endocarditis, especially of the right atrioventricular valve, with subsequent pulmonary thromboembolism; and the rupture of a pituitary abscess are occasional causes of sudden death in individual animals. Acute anthrax and the clostridial infections, as well as ingestion of their preformed toxins, are more common causes of sudden death in ruminants. Anaplasmosis may cause sudden death in mature cattle under stress, without apparent icterus. In these cases anthrax may be mistaken for anaplasmosis because of the gross enlargement of the spleen. Anaplasma, organisms may be demonstrated in blood smears, whereas newer diagnostic methods involve indirect fluorescent antibody and DNA probes. Of all domestic animals, cattle are the most susceptible to clostridial infections in which tissue invasion is present (blackleg). Because of this, vaccination status is important to ascertain. In addition, a fluorescent antibody test and isolation of the bacterium confirm the diagnosis. C. perfringens, of various types is responsible for heavy losses caused by enterotoxemia in calves, lambs, kids, and feedlot cattle in apparent good health and on full feed. C. perfringens, type D has been associated with focal symmetric encephalomalacia in lambs.5 Coliform, mastitis may result in peracute systemic disease and rapid death if not treated early. Diagnosis is based on culture of the organism from the affected gland. Leptospira, may cause an acute septicemia with hemolytic anemia and rapid death in young ruminants. Demonstration of leptospires in fresh urine or by immunohistochemical staining of tissues may assist in making the diagnosis. The course of listeriosis in sheep and goats is rapid, and death may occur in 4 to 48 hours after the appearance of clinical signs.6 Bacteriologic culture (isolation) or immunohistochemical staining of the organism in tissues is diagnostic. Acute fascioliasis (Fasciola hepatica), occurs seasonally in sheep and may cause sudden death within 6 weeks of initial infection. Anaerobic conditions induced by flukes in hepatic parenchyma predispose ruminants to the highly fatal clostridial hepatopathies such as Clostridium hemolyticum, infection. Evidence of fluke infection is grossly visible. Peracute malignant catarrhal fever (MCF) is a sporadic cause of sudden death in cattle that is usually associated with contacting ovine carriers, but most animals with MCF have diarrhea, keratitis, and other obvious clinical signs for days before death occurs. A septicemic form of mycoplasmosis has induced rapid death in kids.7 Isolation of the causative organism is diagnostic. Sudden death is the usual manifestation of septicemic pasteurellosis in lambs. Pseudorabies is a consideration in sudden death cases of ruminants having contact with infected swineherds in the Midwestern United States. Brain for microscopic examination and virus isolation should be submitted to confirm the diagnosis. Acute septicemic salmonellosis mainly affects young ruminants and may result in death within 24 hours. Acute septic metritis usually occurs secondary to complications of parturition. Endotoxic shock and rapid death may occur in severe cases. Thromboembolic meningoencephalomyelitis caused by Haemophilus somnus, is a peracute septicemic disease of young calves. Many cattle die without showing clinical signs. It may be associated with prior respiratory problems in the herd or feedlot. Typical lesions or isolation of the causative organism is diagnostic. Adult lymphosarcoma associated with bovine leukemia virus can be a cause of sudden cardiac death when neoplastic cells infiltrate the cardiac conduction system.
Box 14-2 Infectious and Parasitic Causes of Collapse and Sudden Death in Ruminants
B, Bovine; C, caprine; O, ovine.
* Likely to involve several animals.
Hypocalcemia in horses is most common in lactating mares, but it also occurs after transit. Animals may develop tetany, synchronous diaphragmatic flutter (thumps), muscle tremors, and sweating. Low serum calcium is diagnostic. White muscle disease (nutritional myodegeneration) is associated with selenium and vitamin E deficiency. Sudden death in adult horses after severe exercise is attributed to degenerative lesions in cardiac and skeletal musculature. Death in foals may occur within hours from pulmonary edema and heart failure. Diagnosis is based on measuring whole blood and/or liver selenium and vitamin E concentrations.
Metabolic and nutritional diseases often are not considered in cases of sudden death. The primary lesion in a disorder of cattle known as “falling disease” is progressive fibrosis of the myocardium. Sudden deaths characteristic of the disease are attributed to exercise-induced heart failure.8 Rapid development of hypocalcemia usually is associated with the onset of lactation in cattle, with stressful circumstances in older lactating ewes, or with transport associated with fasting and weather stress. Hypomagnesemia also may develop under similar conditions, especially in ewes and cows in heavy lactation and on lush grass pastures. Polioencephalomalacia occurs most commonly in animals raised under intensive production techniques and can sometimes be traced to excessive sulfates in the diet and/or water. The clinical course tends to be most rapid in sheep. Severe cases of ruminal lactic acidosis, especially in animals unaccustomed to high levels of soluble carbohydrate in the diet, may induce death within 24 hours. Nutritional myodegeneration of the heart is a frequent cause of sudden death in young ruminants born to dams fed selenium-deficient diets during gestation. Diagnosis is based on histopathology and measurement of liver selenium concentration. Some cases of sudden death associated with myocardial necrosis are idiopathic.9
Diagnosis of sudden death caused by cardiovascular failure depends on a careful and methodic technique (Box 14-3). Usually a single animal is affected. Necropsy is necessary to identify the location and characteristics of the lesion, and further analysis may be necessary to establish the exact cause of death. Aortic ring (root) rupture in stallions usually is seen early in the breeding season, occurring immediately after servicing a mare. Rupture of the aorta may occur just distal to the aortic valve, resulting in cardiac tamponade and rapid death. Acute central nervous system embolism results from detached thrombi originating from endocarditic lesions or accidental intracarotid injection. Cerebral hematoma also can result from intracarotid injection. Endocarditis, especially of the aortic valve, may result in coronary thromboembolism and myocardial infarction. Coronary occlusion as a result of damage induced by Strongylus vulgaris, larvae can be diagnosed by the presence of the larvae in the coronary thrombus. Massive abdominal or thoracic hemorrhage is found at necropsy, and the cause may be difficult to ascertain.10 Racehorses mostly die from severe hemorrhage in the thorax. Myocarditis in horses up to 4 years of age resulting from recent respiratory infection may be diagnosed with histopathologic examination. Pericardial rupture and the associated heart damage is a result of violent trauma. Splenic rupture and fatal hemorrhage rarely occur because of the protection afforded by the thoracic wall. Massive thrombi of verminous origin have been observed in young horses that die suddenly while exercising. Uterine arterial rupture involving ovarian, uteroovarian, uterine, or external iliac arteries is observed in older mares, with death ensuing in 30 minutes to 20 hours’ postpartum.
Fatal air embolism can result from any open vein above the heart. Open needles or catheters and severe head wounds involving teeth and sinuses have resulted in sudden death from air emboli. Air is aspirated into the vein by the Venturi effect from blood surging past a portal and creating the necessary negative pressure to aspirate air into the vein. Between 700 and 6000 mL of air may produce a fatal air embolus in the right cardiac ventricle, where it obstructs the pulmonary artery. Cecal or colonic rupture in parturient mares results in sudden death within 8 hours.11
Physical causes of sudden death often display gross evidence indicative of the diagnosis. Abomasal bloat occurs in calves and lambs drinking excessive quantities of warm milk replacer at infrequent intervals. Abomasal ulcers occasionally may perforate and cause rapid death in calves or adult cattle. Ruminal bloat is one of the more common physical causes of sudden death in intensively raised ruminants. When differentiating postmortem from antemortem bloat, note that bloat is the primary cause of death when there is congestion and hemorrhage in the anterior parts of the carcass and edema in the scrotal and ventral perineal areas. Bloat and hypersalivation are the most consistent clinical signs seen in cases of choke. Attempts to swallow firm fruits, tubers, or green ears of corn may occlude the esophagus and result in rapid ruminal tympany and death.
Sudden death is a major concern in feedlots because most such deaths occur in cattle near market weight. GI disturbances are seen with a high frequency in cattle in the late stages of the feeding program. Sudden death is the result of interactions among factors such as rumen acidosis, bloat, and endotoxemia.
Exposure to high-voltage currents in the form of lightning or electrical transmission wires may cause instantaneous death. The diagnosis of lightning strike is based on a history of an electrical storm, linear singe marks, food in the mouth, several animals dead in the same vicinity, and evidence of lightning damage in the immediate environment. Gunshot wounds may be deliberate or accidental, but in any case involving sudden death the head or heart is the usual target. Bullets may pass through or lodge in obscure locations, making retrieval difficult. Radiography can assist in locating a bullet. Heatstroke is a sporadic condition characterized by hyperthermia and collapse. High humidity, dehydration, obesity, and poor heat tolerance associated with young or old age are all factors that predispose animals to overheating. Summer slump induced by consumption of endophyte-infected fescue potentiates the heat intolerance. Internal bleeding may cause sudden death when a uterine artery is ruptured during parturition. This is readily apparent on necropsy. Tracheal edema, or “honker” syndrome, of feeder cattle is seen sporadically in feedlot cattle of the southern plains during hot weather. The pathoanatomic basis of this syndrome is extensive edema of the mucosa and submucosa of the lower trachea, with attendant dyspnea and obstructive asphyxiation. Increased respiratory movements stimulated by hot weather or exercise trigger the clinical illness, especially in heavy cattle during the latter part of the feeding period.12 Traumatic reticuloperitonitis or reticulopericarditis is associated with lack of oral discrimination in cattle. Sudden death occurs because of acute hemorrhage or dysrhythmia when the heart is punctured.
Toxic causes of sudden death are frequently related to management practices. An increase in specific disease syndromes or sudden death in a population of livestock with common potential exposures suggests involvement of a toxicant. Investigation of the premises and a familiarity with poisonous plants and pesticides used in the practice area should help narrow the list of possible causative agents (Box 14-4).
Horses ingesting a lethal dose of the avicide 4-aminopyridine have died within 2 hours of the onset of clinical signs. Diagnosis is based on chemical analysis of stomach contents. Fatal doses of arsenic-containing pesticides may induce cardiovascular collapse and death in horses within hours of ingestion. The presence of edema and fluid in the GI tract suggests the diagnosis, and chemical analysis of GI tract contents, liver, or kidney confirms it. Black flies swarm where swiftly flowing water provides the aeration necessary for the development of larvae. Massive attacks of these blood-sucking insects can rapidly kill livestock because a toxin present in the saliva of the flies increases capillary permeability.13 Cantharidin poisoning can occur after ingestion of 4 to 5 g of blister beetles. Lesions suggestive of cantharidin toxicosis include blistering and ulceration of mucous membranes of the GI and urinary tracts and myocardial degeneration and necrosis. Sustained hypocalcemia and hypomagnesemia are features of the clinical pathology consistent with blister beetle poisoning. Identification of blister beetles in the hay and chemical analysis of urine and GI contents are suitable for diagnostic confirmation. In the past, ferrous fumarate, present in digestive inoculate and administered to foals immediately after birth, resulted in death in some cases in 12 to 96 hours. This illustrates the acute toxicity of iron to young animals in particular. Lesions induced were those of gross liver damage. Fusarium moniliforme,–contaminated corn causes rapid death in horses after the sudden onset of bizarre neurologic deficits and behavioral effects. The lesion of this mycotoxin-induced leukoencephalomalacia is liquefactive necrosis in the subcortical white matter.
High intravenous doses of insulin14 and potassium15 induce sudden death without significant lesions. Chemical detection is often overlooked and very difficult to perform and interpret in cases of deliberate poisoning. Immediate analysis of blood and circumstantial evidence of needle punctures in the jugular furrow are of diagnostic value. Monensin is quite toxic to horses, and fatal poisoning can occur within 12 hours of ingestion of poultry feed containing 100 g/ton or cattle premixes containing 300 g/ton. Lesions related to heart failure are seen on postmortem examination. Tissues collected for microscopic examination should include heart and diaphragm. Chemical analysis of feed samples and stomach contents will confirm exposure. Toxic gases such as nitrogen dioxide, hydrogen sulfide, and carbon monoxide may be responsible for sudden death in horses housed in poorly ventilated buildings with associated gas sources nearby. Organophosphate and carbamate insecticides may induce acute intoxication and death within hours. Diagnosis is based on a history of exposure, determination of acetylcholinesterase activity in the caudate nucleus of the brain, and chemical detection of specific compounds in gut contents.
Circumstances surrounding toxic plant ingestion and diagnosis of intoxication are described in the ruminant section of this chapter. Ingestion of wilted Acer rubrum, (red maple) leaves may induce massive methemoglobinemia, causing marked tissue anoxia and death.16 Red maple poisoning usually occurs during the late summer and early fall when trees are in full leaf. Ready access to wilted leaves follows windstorms. Ricinus communis, or castor bean, is also unique to this section. Seeds of this plant contain a phytotoxin called ricin, which causes severe enteritis and rapid death in horses. About 150 beans (50 g) are sufficient to kill a 450-kg horse. Diagnosis can be verified by finding a toxic amount of ingested seeds in the gut contents.
Intoxication of livestock is frequently suggested as a simple explanation for very complex situations involving sudden death. Suspicions are warranted when a large number of animals die suddenly within a short time. Toxicants should be considered when the appearance of a disease or sudden death is temporally associated with a change in the environment (Box 14-5). An accurate diagnosis in many of these cases requires qualitative and quantitative analyses for suspect poisons. Selecting toxicants for which to analyze requires reasoned judgment supported by an extensive investigation of the environment and postmortem findings.
Box 14-5 Toxic Causes of Collapse and Sudden Death in Ruminants*
* Likely to involve several animals.
The avicide 4-aminopyridine usually is formulated with corn, making it a palatable poison for nontarget herbivorous livestock. Diagnosis is confirmed by chemical analysis of rumen contents or urine. Anticoagulant intoxication may induce sudden death when hemorrhage occurs in the cranial vault, abdominal cavity, pericardial sac, mediastinum, or thorax. The antemortem or postmortem sample for chemical analysis is whole blood or liver. Failure to detect an anticoagulant is not unusual because of the time lag between consumption and presence of the clotting defects, as well as the metabolism of the compound. Arsenic derivatives are a significant hazard to ruminants, especially in areas where such chemicals are widely used as cotton desiccants. Postmortem findings are consistent with microvascular injury to the GI tract. Diagnosis is confirmed by chemical analysis of rumen contents, liver, or kidney. In rare cases large doses of botulinum toxin may cause sudden death in ruminants. Sources of the toxin include the bones of dead animals eaten by osteophagic livestock, poultry carcasses in manure fed to cattle, stagnant pond water, animal tissues in silage or baled hay, and improperly ensiled silage or haylage.
Acetylcholinesterase-inhibiting agents such as the carbamate and organophosphate pesticides can kill livestock within hours. Agricultural practices result in the use of these pesticides in close proximity to livestock. This situation may lead to disaster. Acetylcholinesterase activity in the caudate nucleus of the brain is readily determined and interpreted, and specific compounds may be identified in rumen contents. Toxic gases such as carbon monoxide, hydrogen sulfide, and nitrogen dioxide become important differentials for sudden death in ruminants housed in poorly ventilated buildings, particularly over waste pits. Chlorinated hydrocarbon pesticides do not enjoy the widespread use they once did; however, old containers remain in obscure locations on many farms. When acute intoxication with these compounds is suspected, samples for analysis should include liver, brain, and rumen contents. In subacute cases fat and milk are appropriate samples. Copper toxicosis is a frequent cause of sudden death in sheep and has been reported in cattle fed chicken litter.17 Cattle feeds normally contain twice as much copper as sheep feeds and may cause copper toxicosis in sheep. Copper from treated fence posts also may poison sheep that either chew the posts or ingest contaminated forage in the vicinity. Samples required for chemical confirmation consist of whole blood or serum and liver. Close proximity of livestock to petroleum exploration and production activities in the major oil-producing states results in a variety of clinical problems, including sudden death.18 Consumption of the more volatile petroleum constituents may induce rapid bloating and coating of the respiratory membrane when these substances are aspirated into the lungs. Gossypol toxicosis reportedly causes death without premonitory signs in calves (occasionally cows) and lambs fed cottonseed products containing this toxic pigment.19,20 Poisoning appears abruptly after livestock have been fed the gossypol-containing ration for a period of weeks to months. Sudden death is attributed to heart failure. Postmortem examination reveals edema, centrilobular hepatic necrosis, and an enlarged heart. Ionophores may induce sudden death in species exposed to large overdoses, but delayed death is the usual course. Conditions conducive to lethal overdose include insufficient mixing or top dressing with monensin- or lasalocid-supplemented mineral. Degenerative-to-necrotic lesions in the heart are compatible with a diagnosis of ionophore poisoning.
Acute lead intoxication is another differential from the list of possibilities in sudden death cases. Lead poisoning is the most common toxicosis in cattle. Blood, liver, and kidneys are suitable specimens for lead analysis. Metaldehyde is an uncommon poison for ruminants; however, intoxication in cattle has occurred in low wetland areas where the chemical is used as a molluscicide. The palatability of metaldehyde baits promotes ingestion. Ammoniation of high-quality forage such as forage sorghum and Sudan grass, cereal grain, brome, and fescue hays is responsible for bovine bonkers syndrome, reportedly caused by the formation of 4-methyl-imidazole.21 This sporadic intoxication causes central nervous system derangement and rapid death in cows and nursing calves. Ruminants may be poisoned by nicotine sulfate from ingestion of solution, treated foliage, and food or water from contaminated containers. The onset and progression of the syndrome are rapid, and death may occur within hours. Detection of nicotine in urine is easily performed by most toxicology laboratories. Iatrogenic selenium toxicosis and death in young ruminants can result from parenteral administration of excess doses. Rapid onset of violent tetanic seizures ending in death characterizes strychnine toxicosis. Samples suitable for chemical analysis include rumen contents, liver, and urine.
Urea toxicosis is a frequent cause of sudden death in feedlot livestock. In one particular case, 48 feedlot steers died within 2 days of delivery of a new lot of feed supplemented with urea.22 Unusually high rumen pH, excess ammonia in serum, rumen contents, and eyeball fluid support the diagnosis. Water deprivation, with attendant sodium ion intoxication, is a known cause of sudden death in ruminants.23 Some cases occur in hot weather, but frozen water supplies in cold weather can be equally as devastating.
Poisonous plant problems frequently present a unique set of circumstances associated with their ingestion. Overgrazing of pastures is probably the most significant factor affecting the ingestion of toxic plants. Other situations conducive to poisonous plant ingestion include lack of suitable forage in periods of drought and the incorporation of toxic forbs in hay or greenchop. Plants normally avoided because of poor palatability may become acceptable when frosted or sprayed with herbicide. Toxic plants also may be the first green plant available early in the spring, when livestock are hungry for anything green and succulent. Livestock trailed or transported for long distances without food or water and then suddenly introduced to new pasture may fail to avoid toxic plants and often will eat anything within immediate reach. In general, diagnosis of plant poisoning is based on availability, grazing evidence or presence in the hay, and the existence of plant parts in the rumen contents. Diagnostic lesions are usually lacking, and analytic methods for toxic components are severely limited.
Aconitum, species (monkshood) rarely are a cause of sudden death because of their limited availability. Delphinium, species (larkspur), however, are closely related to monkshood and are responsible for more cattle losses in the western United States than any other poisonous plant. Larkspur grows in dense stands in the mountainous West and is readily consumed, especially during an early stage of growth. Mature stands are less palatable and not as toxic. Cattle poisoned by larkspur often are found close to a stand, collapsed and bloated. Death from the cardiotoxic and neuromuscular blocking effects may occur within a few hours of ingestion. Sheep are less susceptible to larkspur and are seldom poisoned by it, partly because of their different grazing habits.24 Asclepias, species (milkweed) contain either cardioactive glycosides or neurotoxic compounds.25 The most toxic species reside in the western and southwestern United States. These plants are not very palatable but are somewhat less objectionable when dried. Livestock will graze them in a drought, but the biggest problem is contamination of hay or greenchop. Blue-green algae may cause sudden death in all classes of livestock within minutes of ingestion of toxins from certain neurotoxic species. Toxins from other hepatotoxic species may require 24 hours to induce death. Toxic blooms occur sporadically during certain environmental conditions of late summer and fall. Diagnosis is usually based on a history of exposure to a concentrated bloom, but some laboratories perform chemical and bioassays.
Calycanthus, species (bubby bush) contain an alkaloid similar in structure and mechanism of action to strychnine. These species are of minor importance to the livestock industry in the Southeast and West but have induced death in cattle. Seeds and other plant parts may be identified in rumen contents. Cicuta, species (water hemlock) may induce violent convulsions and death within an hour. Intoxication is most common in early spring, when plants growing along waterways are easily uprooted and the tuberous parts are eaten. A single root system from a large plant can kill a cow. This is one of the most toxic plants in North America, and it has been responsible for the deaths of numerous livestock and humans. Conium maculatum, (poison hemlock) grows throughout the United States. Cattle are most sensitive, and sheep are relatively resistant. Poisoning is usually associated with heavily grazed pastures.
Cyanogenic glycosides are present at toxic concentrations in more than 250 plant genera, including Sorghum, Prunus, Triglochin, and Linum,. Ruminants are especially susceptible to these glycosides, as they possess the microorganism enzyme systems necessary for rapid liberation of hydrocyanic acid. Death may occur within 15 to 30 minutes of ingestion. Hyperoxygenated venous blood will be cherry red and slow to clot, and rumen contents may have the odor of almond extract. Samples of forage, blood, and rumen contents should be collected immediately, placed in airtight containers, and frozen for analysis. Negative results are often questionable because of the highly volatile nature of hydrogen cyanide. Drymaria pachyphylla, (inkweed) has caused sudden death in cattle in the southwestern United States. The differential diagnosis in this part of the country includes anthrax. Diagnosis is based on examination of rumen contents for plant parts.
Halogeton glomeratus, is a soluble oxalate-containing plant that grows best in disturbed soil along roadsides in the western intermountain states. Sarcobatus vermiculata, (greasewood) grows in semiarid regions of the West. It also contains toxic levels of soluble oxalate. Unadapted sheep are most frequently intoxicated with these plants, and death may occur within 9 to 11 hours of onset of intoxication. Sudden death results from hypocalcemia and inhibition of cellular respiration. Postmortem findings include hemorrhagic rumenitis, hydrothorax, ascites, and the presence of oxalate crystals in the kidney and rumen wall. Kalmia, species (laurel) are an occasional problem in winter or early spring, when they are the only conspicuously green plant available. Laurel grows in the wild in the eastern and western regions of the United States. Death may occur in 12 to 14 hours. Fragments of glossy, leathery leaves may be visible in rumen contents. Kochia scoparia, (summer cypress or burning bush) sporadically causes a thiamine-responsive polioencephalomalacia in cattle. Laburnum anagyroides, (golden chain tree) is a large ornamental shrub considered to be the second most poisonous plant in Great Britain. It also grows in much of the United States. The shrub contains quinolizidine alkaloids that may induce rapid death from respiratory failure. Lupinus, is a genus with about 200 species in North America. There is considerable seasonal variation in toxicity, with the toxic species presenting a problem when plants are very immature or when they have reached the seedpod stage. Acute intoxication and rapid death are likely only when large quantities of seeds are ingested within a short time. Toxic species cause more deaths in sheep than any other plant in Montana, Idaho, and Utah. Improperly cured hay and silage derived from Melilotus, species (white and yellow sweet clover) may cause sudden death in cattle when hemorrhage occurs in the cranial vault, pericardial sac, mediastinum, or thorax. Induction of the disease requires consumption of the moldy forage for several weeks to allow sufficient depletion of vitamin K—dependent clotting factors. Nerium, species (oleander) are widely cultivated in the South and West. Toxic in the green or dry state, these plants may border hay fields, and significant mortality of livestock may occur when dropped leaves or trimmings are incorporated into forage. Livestock often are poisoned when prunings are mixed with grass clippings and the bitter taste is disguised. Diagnosis is based on evidence of consumption and identification of plant parts in rumen contents.
The genus Nicotiana, contains toxic species of wild and cultivated tobacco. Poor palatability usually hinders consumption; however, opportunities for intoxication and death sometimes occur in areas of the West where forage is scarce and in parts of the country where tobacco is cultivated. Nitrate-accumulating plants include certain annuals, weeds, and cool-season crops and grasses. Notable examples include pigweed, lamb’s-quarters, Sudan grass, and oat hay. Under the right environmental conditions most plants can accumulate toxic concentrations of nitrate. Plant-associated nitrate poisoning is a serious problem only in ruminants because of the nitrate-reducing ability of rumen microbes. Onset of nitrate intoxication is rapid, and death may result within 6 to 24 hours of rapid ingestion of a toxic dose. Diagnosis is based on a brownish cast to the viscera and blood, together with chemical analysis of serum, aqueous humor, and forage for nitrate concentration.
Acute bovine pulmonary emphysema is associated with an abrupt change from dry range forage to lush green pasture high in L-tryptophan concentration. Less commonly, the pulmonary toxins of Perilla frutescens, (perilla mint) can induce dyspnea and death in a few hours. Necropsy reveals incomplete collapse of lungs that are heavy and firm, with froth-filled airways. Histologic examination shows a proliferation of type II pneumocytes. Phalaris, species (canary grass) recently were reported to have caused sudden collapse and death of sheep in California.26 Sheep that had been grazing a field containing canary grass were herded a short distance when six ewes collapsed and died. Bilaterally symmetric, greenish-grey discoloration was seen in the midbrain. The same gross discoloration also was seen in the renal cortex. Microscopic examination confirmed the presence of intracytoplasmic accumulation of this granular pigment. Solanum, species (nightshades) grow throughout the United States, especially in waste areas and overgrazed pastures. Rapid ingestion of large quantities of highly toxic fruit can result in coma and rapid death. Taxus, species (yew) poisoning in ruminants commonly results in sudden death. Poisoning is most likely to occur when ruminants are pastured adjacent to residential areas where yew is a common ornamental shrub. Diagnosis is based on evidence of exposure and identification of yew leaves in rumen contents. Xanthium, species (cocklebur) are most toxic at the cotyledonary stage of growth. These species may induce death in calves within 12 hours of onset of clinical intoxication. Hypoglycemia and centrilobular hepatic necrosis are consistent findings. Zigadenus, species (death camas) are of major importance to sheep grazing on western ranges. These plants begin growth in early spring, presenting a significant hazard at this time.27
Allergic reactions capable of causing sudden death include rupture of warble fly larvae. Warble fly larvae are seldom able to penetrate equine skin, and the fully matured larvae either die or are killed when the horse is saddled or harnessed. Anaphylactic shock results, and pulmonary edema and foam in the airways are found on necropsy. Penicillin or other antibiotics may cause an anaphylactic reaction with a similar outcome.
Perinatal sudden death may occur in foals as a result of meningeal hemorrhage caused by birth trauma. The sudden onset of profuse, watery diarrhea and rapid development of hypovolemic shock characterize colitis-X. A severe necrotic typhlitis is seen at necropsy, with destruction of colonic and cecal mucosa. Diaphragmatic rupture and hernia are associated with violent exercise or trauma, with or without bowel herniation. Electrocution occurs when a horse chews through or comes into contact with an uninsulated hot wire while well grounded. Death is instantaneous, usually with negative necropsy findings. Lightning strike may reveal burning or singeing of skin, hair, or underlying tissue. GI maladies that may cause sudden death include volvulus, intussusception, torsion, incarceration, gastric rupture from grain overload, tympanites, and small intestine rupture from ascarid impaction.
Gunshot wounds may be another cause of sudden death that is surprisingly difficult to verify, as bullet retrieval is necessary to establish the diagnosis. Finding the bullet lodged in tissue is a time-consuming task at best. Heat or work stress is seen in horses in hot, poorly ventilated quarters or in poorly conditioned horses overworked in hot, humid weather. Collapse and coma are followed by death in a few hours. Necropsy reveals skeletal and cardiac muscle damage, GI ulceration, and renal necrosis. In pregnancy, unrecognized and untreated torsion of the gravid uterus may result in sudden death.
Exercise-induced respiratory tract injury may cause sudden death in well-conditioned horses.28 Epistaxis and pulmonary hemorrhage occur at the peak of training, with most cases being of little concern. However, in fatal cases horses that die immediately after exercise often have subpleural hemorrhages in the caudal lung lobes, and rupture of these hematomas has resulted in extensive intrathoracic hemorrhage and sudden death. Rupture of lung tissue while exercising also may result in fatal hemorrhage.
Serum sickness (acute hepatitis) can be traced to administration of biologics of equine origin 50 to 90 days before the onset of clinical signs. Death may occur within 12 to 48 hours. The main lesion seen is liver necrosis with discoloration and accentuation of the lobular pattern on the cut surface. Fracture of the junction between the basisphenoid and basioccipital bone usually results from rearing over backward and striking the poll on the ground.
Fatal anaphylaxis occurs in sensitized animals after parenteral use of drugs or vaccines. This is most common with the penicillins and vaccines containing gram-negative bacteria or cell walls. Anaphylactic shock also may be an outcome of blood transfusion reactions. Immune-mediated hemolytic anemia (neonatal isoerythrolysis) from ingestion of colostrum-containing antibodies against a neonate’s erythrocytes may induce sudden death if the specific antibody concentration is sufficiently high. A sudden death syndrome occurs in feeder cattle on high-concentrate diets. It usually occurs in warmer months and is limited to cattle fed high-concentrate rations for several weeks.29 A malignant tumor that has been associated with sudden death is the thymoma, or thymic lymphosarcoma, seen most commonly in old goats. It appears as a large, pale, fleshy mass in the cranial mediastinum.30
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