Collapse Versus Sudden Death

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.

Approach to Diagnosis of Sudden 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 on the basis of veterinarians’ needs in their service areas. Use of these facilities to support a definitive diagnosis is essential in sudden death cases.

Recently, a specific postmortem examination protocol intended to identify etiology in instances of sudden death and exercise-associated sudden death (EASD) in racehorses was developed and described by the California Animal Health and Food Safety Laboratory System-University of California, Davis.¹ The three principal goals of that protocol include performance of a complete postmortem examination for each case to attempt to establish the cause of EASD, standardization of histopatho­logic examination of the heart in cases of EASD (so that results would be compared over time and between institutions), and description of the toxicology screens performed at that institu­tion for cases of EASD.¹

Diagnosis is rarely based on a single item of evidence and usually requires input from multiple testing procedures.

1. A detailed history, which consists of the herd incidence, management changes, past medical problems, vaccination records, new additions to the herd, a complete description of the environment (e.g., recent lightning, flooding?), and assessment of the frequency of animal observations. Owners and managers may not be candid for fear of being considered negligent. Inconsistencies among involved parties should be carefully evaluated. Recent changes in management practices should be scrutinized, including feeding habits and whether there have been any illnesses in comingled animals. Animals trailed or transported for long distances or introduced onto unfamiliar ranges may be poisoned by plant species normally avoided by indigenous livestock or infected by a novel locally endemic infectious agent against which the animal had insufficient immunity. The likelihood of foul play should be considered without creating undue alarm. Assigning blame should be left to the discretion of owners. Consideration of disgruntled former employees and equine insurance claims are particularly critical situations that may have legal implications. The precise cause of death is crucial for insured livestock (mostly horses) because of exclusion clauses in many insurance policies. Heavily insured horses should be subjected to a detailed, documented, and witnessed diagnostic evaluation by an unbiased specialist, wherever possible. Toxicologic testing is especially critical in these cases. Scrutiny of the environment before the carcass is moved is necessary to eliminate questionable procedures in insurance claim cases. Evidence of struggling in the immediate area indicates a more protracted illness in contrast to collapse and death without a struggle. Suspicions should be aroused when evidence suggests that the carcass may have been dragged or carried to the current location.

2. Communication with the diagnostic laboratory before specimen collection should be undertaken to ensure that necessary samples are identified, correctly handled, and transported in accordance with the laboratory’s current standard operating procedures. In light of the fact that many cases of sudden death result from central nervous system dysfunction, it is necessary to remove the brain for examina­tion. Busy practitioners frequently do not take the time to remove this organ. Furthermore, there is a higher-than- normal probability of a poison being involved in sudden death cases, especially in equine insurance claims. For toxicologic examination, toxicants remaining in the GI tract must be considered, together with those in the major excre­tory organs, liver, and kidneys. Again, an active dialogue with laboratory personnel should facilitate appropriate specimen collection and handling in order to maximize the probability of a positive diagnostic outcome.

3. The correct quantity and method of preservation of the sample depends on the specific test. Medicolegal cases demand that stringent photographic and written documentation, witnessing, and chain-of-custody protocol be followed during necropsy and sample collection. The quantity of the sample is par­ticularly important for chemical analysis. Sending insufficient quantities of sample may preclude multiple testing procedures. In general, 100 to 200 g of tissue or ingesta, 50 mL of urine, all fluid from both eyes, and 5 to 10 mL of blood or serum suffice for most analytic procedures. A midsagittal cut through the brain is performed to allow freezing of one half for chemi­cal analysis and formalin preservation of the other. When poisoning is suspected, samples from possible sources such as feed, water, baits, poisonous plants, and suspect materi­als should be submitted. Usually 1 kg of each is adequate. Samples submitted for chemical analysis should be frozen in individual containers and labeled with patient identification data, date, location, and specific identity of the specimen (type of tissue).

Causes of Collapse and Sudden Death

Infectious Causes of Sudden Death in Horses

Foal actinobacillosis is an acute fulminant septicemia caused by Actinobacillus equuli, a gram-negative bacterial pathogen found in the upper respiratory tract, feces, and genital tract of normal adult horses (Box 14.1). Many other bacteria can also cause bacteremia/septicemia. Predisposing factors to foal septicemia with any agent include prematurity/dysmaturity, failure of passive transfer, maladjustment, dam malnourishment/ illness during gestation, and adverse environmental conditions. A characteristic histopathologic finding is multiple bacterial emboli in renal glomerular capillaries without inflammatory infiltrate in neonatal foals. Acute hemorrhagic necrotizing enterocolitis, sometimes associated with Clostridial infection, may cause sudden death in foals in the absence of other clinical signs.

Acute anthrax may be rapidly fatal to horses (following a period of excitement, depression, convulsions, and coma). Isolating the causative agent from blood confirms the diagnosis. Babesiosis/Theileriasis is caused by an intraerythrocytic parasite that may cause death within 24 hours. Identification of the organism in blood smears, complement fixation testing for parasite antibodies, or polymerase chain reaction (PCR) testing confirms the diagnosis.

Death may result from clostridial myonecrosis associated with infection at intramuscular injection sites by Clostridium

■ BOX 14.1

Infectious Causes of Collapse and Sudden Death in Horses

Peracute typhlocolitis (any cause) Babesiosis/Theileriasis

Botulism^a

Clostridial myopathy

Clostridium difficile enterocolitis

Clostridium perfringens enterotoxemia

Clostridium sordellii dysentery Guttural pouch mycosis

Hemorrhagic enterotoxemia in foals

Neonatal septicemia

Neonatal diarrhea

Neorickettsia risticii infection (Potomac horse fever) Salmonellosis^a

Theiler disease (serum hepatitis) Tyzzer disease

^aLikely to involve several animals.

septicum, Clostridium chauvoei, Clostridium novyi, or Clostridium perfringens; various parenteral agents such as ivermectin, vitamin B complex, vitamin E, prostaglandin, antihistamines, and flunixin meglumine have been implicated in this regard. Clostridial myopathies are also associated with deep stab or puncture wounds. Toxicoinfectious botulism (shaker foal syndrome) is caused by Clostridium botulinum (usually type B or C) and is more common in specific (endemic) geographic locations. Clostridium botulinum spores can be identified in approximately 80% of affected foals. The neurotoxin may sometimes be demonstrated in gut contents. Although rapid death (within a few hours) was attributed to Clostridium sordellii enteritis in foals with colic and bloody diarrhea in one study,² C. perfringens type C is a more common cause of hemorrhagic enteritis, enterotoxemia, and peracute death in foals as young as 4 days.³ Diagnosis may be supported by bacteriologic culturing, the demonstration of alpha and beta toxins in fresh intestinal samples, and identification of large numbers of clostridia (large gram-positive bacilli) in smears of intestinal contents. C. perfringens type D also induces sudden death in the most aggressive foals in group-feeding situations. Similar enterotoxemia has also been associated with toxin­producing Clostridium difficile^ and Bacteroides fragilis.⁵ Death of foals resulting from hemorrhagic necrotizing enterocolitis as a result of infection by C. difficile has been increasingly reported in recent years.

Peracute death may result from severe disease associated with infection by Neorickettsia risticii (Potomac horse fever or Shasta River Crud). More commonly, N. risticii infection results in severe colitis, fever, systemic inflammation, diarrhea, dehydration, ileus, colic, and laminitis in adult horses. Diagnosis of N. risticii infection is based on PCR testing to demonstrate

N. risticii DNA in whole blood and feces.

Guttural pouch mycosis often results in nonfatal intermittent unilateral epistaxis or dysphagia. Occasionally a single episode of severe epistaxis from hemorrhage from the internal carotid artery may result in unanticipated death from exsanguination. Necropsy reveals blood in the nasal passages and guttural pouch with fungal plaques on the surface of the affected artery, usually at the dorsocaudal aspect of the medial compartment. In fatal cases, the local exterior environment of the carcass will be contaminated with blood that has clearly issued from one or both nostrils.

Acute infection of the central nervous system by either West Nile virus (WNV) or equine herpesvirus 1 (EHV-1) may simply present as unexpected death in susceptible individu­als. Diagnostic corroboration for these conditions is based on histopathologic characterizations, immunohistochemistry (WNV), and PCR testing.

Infectious and Parasitic Causes of Sudden Death in Ruminants

Infectious causes of sudden death range from acute septicemia and toxemia 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 PCR testing. Of all domestic animals, cattle are the most susceptible to clostridial infections in which tissue invasion is present (blackleg). Therefore it is important to ascertain the vaccination status of affected animals. In addition, a

■ BOX 14.2

Infectious and Parasitic Causes of Collapse and Sudden Death in Ruminants

Abscess rupture at liver hilus or pituitary

Anaplasmosis^a (B)

Anthrax^a

Black disease, infectious necrotic hepatitis

Blackleg

Botulism^a

Bovine lymphosarcoma

Clostridium hemolyticum, bacillary hemoglobinuria, redwater^a

Clostridium perfringens, enterotoxemia Coliform mastitis

Endocarditis

Leptospirosis

Listeriosis (C, O)

Liver flukes (O)

Malignant catarrhal fever (B)

Mycoplasmosis (C)

Neonatal septicemia

Neonatal diarrhea

Pasteurellosis, septicemic^a (O)

Pseudorabies

Salmonellosis^a

Septic metritis

Thromboembolic meningoencephalomyelitis^a caused by His- tophilus somni (B)

^aLikely to involve several animals.

B, Bovine; C, caprine; O, ovine. 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.⁶ 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. Leptospirae may cause an acute septicemia with hemolytic anemia and rapid death in young ruminants. Demonstration of leptospires in fresh urine, immunohistochemical staining of tissues, or PCR testing 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.⁷ 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. Individual animals with chronic or severe endoparasitism may present as acute collapse or sudden death if they are maintained in a herd/flock. This is especially true for South American camelids. 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 was reported to cause rapid death in kids.⁸ 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 and feral hogs 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 Histophilus somni 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.

Metabolic and Nutritional Causes of Sudden Death in Horses

Hypocalcemia is commonly associated with lactation (“lactation tetany”), transport (“transit tetany”), and exhaustion during or following endurance work. Affected animals develop tetany, synchronous diaphragmatic flutter (“thumps”), muscle tremors, sweating, and ileus. Diagnosis is based on demonstration of hypocalcemia in the face of typical clinical signs. White muscle disease (nutritional myodegeneration) is associated with selenium and vitamin E deficiency. Sudden death in affected adult horses after severe exercise may be attributed to degenerative lesions in cardiac and skeletal musculature. Death in foals may occur within hours of birth as a result of heart failure and pulmonary edema. Diagnosis of nutritional myodegeneration is based on histopathologic findings and measurement of whole blood and/ or liver selenium and vitamin E concentrations. Unanticipated death may result from cardiotoxic hyperkalemia in Quarter Horses (and related breeds) affected with hyperkalemic periodic paralysis (HyPP). HyPP is a genetic disease that more commonly results in episodes of muscle weakness and/or stertorous breathing. Diagnosis of HyPP status (unaffected/heterozygous/homozygous) is straightforward and based on genetic testing. However, the determination as to whether unexpected death resulted specifically from hyperkalemia is less straightforward and may be based on a combination of genetic testing (tissue obtained postmortem), ruling out other plausible etiologies (including postmortem examination), and the demonstration of elevated potassium concentration in ocular fluids (compared with controls).⁹

Metabolic and Nutritional Causes of Sudden Death in Ruminants

Metabolic and nutritional diseases are not often 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.¹⁰ Rapid development of hypocalcemia is usually 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 may also 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.¹¹

Cardiovascular Causes of Sudden Death in Horses

As a category, cardiovascular conditions likely represent the most common cause of unanticipated death in horses. Diagnosis of sudden death caused by cardiovascular failure depends on a careful and organized methodological approach (Box 14.3).¹ In most instances, 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.

Disorders of the equine cardiovascular system that might lead to unanticipated death may be categorized into those conditions in which death results from a fatal rhythm distur­bance (ventricular tachycardia, ventricular flutter, ventricular fibrillation, complete atrioventricular block, or asystole); conditions in which death results from acute myocardial failure (acute decompensation of chronic heart failure, acute onset of severe valvular insufficiency [e.g., chordal rupture], or acute

■ BOX 14.3

Cardiovascular Causes of Collapse and Sudden Death in Horses

Aortic ring (root) rupture

Central nervous system embolism

Coronary occlusion

Endocarditis

Massive abdominal or thoracic hemorrhage

Myocarditis

Pericardial rupture

Splenic rupture

Thrombi of verminous origin

Uterine arterial rupture myocardial ischemia/necrosis); and conditions in which heart function is compromised by tamponade (viral, bacterial, or idiopathic pericarditis, trauma).¹² Cardiac-related death may result suddenly from several intoxications (myocardial plant toxicities including yew (Taxus spp.), oleander (Nerium olean­der), foxglove (Digitalis spp.), summer pheasant’s eye (Adonis aestivalis), box elder (Acer spp.), and marsh mallow (Malva parviflora). Cardiac death may also result from intoxication by ionophore antibiotics (as contaminants from the bovine feed industry), cantharidin toxicity (blister beetle poisoning), and snake envenomation (Crotalus spp. Viperidae).¹² In rare instances, marked hyperkalemia (hyperkalemic cardiotoxicity) may be responsible for death in horses affected with HyPP. Penetrat­ing chest wounds or iatrogenic damage to the equine heart (cardiac catheterization) may provoke fatal arrhythmia or cause severe hemorrhage with fatal outcomes. External or internal exsanguination represents an important cause of unanticipated death, and several specific syndromes have been described: cardiac rupture (with cardiac tamponade); rupture of either the pulmonary artery or aorta (with or without tamponade); carotid artery rupture in the guttural pouch may lead to the unanticipated death of horses affected with guttural pouch mycosis; and rupture of the cranial mesenteric artery at its origin consequent to damage resulting from Strongylus vulgaris larval migration is presently a rare cause of fatal internal hemorrhage following widespread use of ivermectin. Peripartum uterine arterial rupture involving ovarian, utero-ovarian, uterine, or external iliac arteries is sometimes observed in older mares, with death ensuing in 30 minutes to 20 hours. Pulmonary artery rupture may lead to death in horses that are affected with exercise-induced pulmonary hemorrhage or pulmonary hypertension for any cause. Brain hemorrhage may cause death, especially in horses that have “flipped over backwards” and fractured the basioccipital/basisphenoid bones at the base of the skull.

Aortic sinus of Valsalva aneurysms or tears in the aortic root are well-recognized conditions in breeding stallions, often leading to sudden death, especially early in the breeding season, often occurring immediately after servicing a mare.¹² Rupture of the aorta may occur just distal to the aortic valve, resulting in cardiac tamponade and rapid death. Aortopulmonary fistulation in conjunction with aortic rupture is quite common in the Friesian breed; aortic rupture and aortopulmonary fistulation should be included in the differential diagnosis when Friesian horses are presented with a history of recurrent false colic, coughing, sustained tachycardia, and/or peripheral edema.^12,13 Cardiovascular diseases including myocardial lesions (hemor­rhage, swelling, fibrosis, and infarction), aortic root rupture, and abdominal large artery rupture were identified as common explanations for sudden/unexpected death in Japanese stallions.¹⁴ Acute central nervous system embolism results from detached thromboemboli originating from vegetative lesions on heart valves affected with bacterial endocarditis or from accidental intracarotid injection. Cerebral hematoma may also result from inadvertent intracarotid injections. Endocarditis, especially of the aortic valve, may result in coronary thromboembolism and myocardial infarction, albeit rarely. Coronary artery occlusion resulting from damage induced by migrating S. vulgaris larvae is 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.¹⁵ 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 may result from violent trauma. Splenic rupture with fatal hemorrhage occurs rarely 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.

Physical Causes of Sudden Death in Horses

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 ventricle, where it obstructs the pulmonary artery. Cecal or colonic rupture in periparturient mares may lead to death within 8 hours.¹⁶

Physical Causes of Sudden Death in Ruminants Physical causes of sudden death typically 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 may occasionally 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 being found dead in the vicinity, and evidence of light­ning damage in the immediate environment. Gunshot wounds may be deliberate or accidental; death resulting from gunshot injury typically involves either the head or heart. Bullets may pass through or lodge in obscure locations, making retrieval difficult. Radiography can assist in confirming and 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. Fleeced animals such as sheep and South American camelids often succumb to heatstroke if the time of shearing is not appropriate. “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.¹⁷ Traumatic reticuloperitonitis or reticulopericarditis result from poor oral discrimination behavior in cattle. Sudden death in these cases may result from acute hemorrhage or dysrhythmia if the heart is affected by foreign body migration (cardiac puncture may occur).

Toxic Causes of Sudden Death in Horses

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

■ BOX 14.4

Toxic Causes of Collapse and Sudden Death in Horses^a

4-Aminopyridine (Avitrol), an avicide Arsenic

Black flies Cantharidin*

Ferrous fumarate

Fusarium moniliforme-associated mycotoxicosis Insulin and potassium

Monensin^a

Nitrogen dioxide

Organophosphate and carbamate insecticides

Toxic plants

Acer rubrum (red maple)

Acer negundo (female box elder)

Blue-green algae^a

Cicuta spp. (water hemlock)

Conium maculatum (poison hemlock)

Cyanogenic plants

Melilotus spp. (sweet clover)

Nerium spp. (oleander)

Nicotiana spp. (tobacco)

Ricinus communis (castor bean)

Taxus spp. (Japanese yew)

^aLikely to involve several animals.

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 arsenic toxicosis, 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.¹⁸ 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 insulin¹⁹ and potassium⁹ induce sudden death without significant lesions. Chemical detection is often overlooked and difficult to perform and interpret in cases of deliberate poisoning. Immediate analysis of blood and circumstantial evidence of needle punctures (blood stains) in the jugular furrow may be 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 and other Acer spp. may induce massive methemoglobinemia, causing marked tissue anoxia and death.²⁰ 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. 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.

Toxic Causes of Sudden Death in Ruminants

Intoxication of livestock is frequently suggested as a simple explanation for 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.

The avicide 4-aminopyridine is usually 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. When agricultural strategy results in the deployment of these pesticides in close proximity to livestock, the situation may be disastrous. 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

■ BOX 14.5

Toxic Causes of Collapse and Sudden Death in Ruminants^a

4-Aminopyridine (Avitrol), an avicide Anticoagulants

Arsenic Botulism^a Carbamates Carbon monoxide

Chlorinated hydrocarbons Copper (B, O)

Crude oil

Gossypol^a

Hydrogen sulfide gas^a

Ionophores^a Lead^a

Metaldehyde

4-Methyl-imidazole, bovine bonkers syndrome (B, O) Nicotine sulfate

Nitrogen dioxide gas^a Organophosphates Selenium, parenteral overdose Strychnine

Urea, nonprotein nitrogen^a

Water deprivation, sodium ion toxicity

Toxic plants

Aconium spp. (monkshood) Asclepias spp. (milkweed) Blue-green algae^a Calycanthus fertilis (bubby bush) (B) Cicuta spp. (water hemlock) Conium maculatum (poison hemlock) Cyanogenic plants Delphinium spp. (larkspur) (B) Drymaria pachyphylla (inkweed) Halogeton glomeratus (halogeton) (O, B) Kalmia spp. (laurels)

Kochia scoparia (summer cypress) Laburnum anagyroides (golden chain tree) Lupinus spp. (lupine) (O) Melilotus spp. (sweet clover) Nerium spp. (oleander) Nicotiana spp. (tobacco) Nitrate-accumulating plants Perilla frutescens (perilla mint) Phalaris spp. (canary grass) (O) Sarcobatus vermiculata (greasewood) (B, O) Solanum spp. (nightshades) Taxus spp. (Japanese yew) Xanthium spp. (cocklebur) (B, O) Zigadenus spp. (death camas) (O)

^aLikely to involve several animals.

B, Bovine; O, ovine.

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.²¹ 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.²² 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.^23,24 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.²5 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.²⁶ 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.²⁷ 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 green chop. Plants normally avoided because of poor palat- ability may become acceptable when frosted or sprayed with herbicide. Toxic plants may also 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 spp. (monkshood) are rarely a cause of sudden death because of their limited availability. Delphinium spp. (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 are often 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.²⁸ Asclepias spp. (milkweed) contain either car­dioactive glycosides or neurotoxic compounds.²⁹ 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 green chop. 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 biological assays.

Calycanthus spp. (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 spp. (water hemlock) may induce violent convulsions and death within an hour of consumption. 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 because 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 by 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 spp. (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 polioencepha- lomalacia 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 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 spp. (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 spp. (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 are often 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 spp. (canary grass) have been reported to have caused sudden collapse and death of sheep in Califor­nia.³⁰ Sheep that had been grazing a field containing canary grass were herded a short distance when six ewes collapsed and died. Bilaterally symmetric, greenish-gray discoloration was seen in the midbrain. The same gross discoloration was also seen in the renal cortex. Microscopic examination confirmed the presence of intracytoplasmic accumulation of this granular pigment. Solanum spp. (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 spp. (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 spp. (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 spp. (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.³¹

Miscellaneous Causes of Sudden Death in Horses

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. The ruptured larvae induce anaphylactic shock and pulmonary edema. Foam in the airways is 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 conditions that may cause sudden death include volvulus, intussusception, torsion, strangulation, tympany, and small intestine rupture from ascarid impaction (in foals). Gastric rupture may cause sudden and unexpected death; in one study, rupture of the stomach was predominantly attributed to either idiopathic causes or as a complication of gastric impaction.³²

Gunshot wounds may be another cause of sudden death that is surprisingly difficult to verify, because bullet retrieval is necessary to establish the diagnosis. Tracking and finding a small metal object 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.³³ Exercise-induced pulmonary hemorrhage occurs during race training or competition, with most cases being of little acute concern. In severe cases, horses may die during or immediately after exercise with extensive hemorrhage (especially the caudal lung lobes) evident at necropsy.

Serum hepatitis (Theiler disease, viral hepatitis) may result from administration of biologics of equine origin 50 to 90 days before the onset of clinical signs, including fever, jaundice, and hepatoencephalopathy. In severe cases, 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. Recently, several viral pathogens have been implicated in the etiology of Theiler disease.^34,35 Fracture of the junction between the basisphenoid and the basioccipital bone usually results from rearing over backward and striking the poll on the ground.

Sudden and Unexpected Death in Equine Athletes

Emphasis placed on the postmortem diagnosis of cause of death and risk factors for death in racehorse communities has led to several retrospective studies on this topic in recent years.^36-38 Consistently, most racehorse deaths result from catastrophic musculoskeletal injuries (serious accidents) with limb fracture being the most common circumstance leading to death among all racehorses. Other fatalities are classified as unexpected or sudden death, in association with exercise (racing or training) or occurring spontaneously in the absence of physical exertion. The pathologist may or may not be able to conclude definitively that any observed lesions are necessarily the cause of death (e.g., observed abnormalities may represent unrelated comorbidities or could even result from agonal breathing). Although often presumed to result from acute cardiac, cardiovascular, or cardiorespiratory failure, the importance of a complete and structured postmortem examination cannot be overstated.¹ Results and conclusions from postmortem examinations at different institutions (and over time within the same institution) will be easier to compare if a recently described standardized protocol gains broad acceptance.¹

In one recent study, postmortem findings and cause of death were retrospectively reported over a 13-year period for 963 horses examined for the Ontario Racing Commission Death Registry.³⁶ In that study, unexpected or sudden death that occurred during or immediately following exercise accounted for 31% of performance-related deaths, most commonly resulting from cardiopulmonary lesions (pulmonary hemorrhage was the most common explanation). The most frequent causes of death or significant postmortem findings in horses dying suddenly during exercise were classified as respiratory (50%), cardiovas­cular (22%), and undetermined (20%). Less frequently, skull fracture, sepsis, encephalitis, dyshemostasis, and hemorrhage were reported in a handful of cases. Pulmonary hemorrhage (such as exercise-induced pulmonary hemorrhage) represented 93% of respiratory explanations. Acute heart failure and pulmo­nary hypertension resulting from postexercise arrhythmia may lead to pulmonary hemorrhage, cardiopulmonary failure, and sudden death in racehorses.³⁹ Hemopericardium (pericardial tamponade), hemothorax, and hemoabdomen represented 82% of cardiovascular cases. For example, aortic rupture is a well-recognized cause of sudden death in this species and likely results from increased aortic pressure during strenuous physical activity, as reported previously.⁴⁰

As mentioned earlier, a cause of death was not established for 20% of sudden death cases because explanatory lesions could not be identified postmortem. In those cases, it was speculated that cardiac arrhythmia may have led to death. Injection-associated death was identified in 4% of the study population.³⁶ The proportional mortality rate for exercise-associated sudden death among all breeds was 9% (157 of 1708). Death result­ing from injected drugs occurred in 38 of 377 horses (10%) whose deaths were unrelated to exercise and in 38 of 963 of all horses (4%) horses in that study.³⁶ In most instances, collapse followed by seizure or death occurred during or immediately following the injection. Untoward clinical reactions led to euthanasia for a number of other injected horses that died. Various drugs and combinations of drugs were implicated in this study and included amino acid supplements; antibiotics (penicillin, trimethoprim-sulfadiazine, gentamicin); unspeci­fied iron preparations; dimethyl sulfoxide (DMSO); mannitol; vitamin E-selenium preparations; other nonspecified vitamins; testosterone; other anabolic steroids; estrogen; calcium; pen- tosane polysulfate; Sarapin; trichlormethiazide-dexamethasone acetate; n-butyl alcohol; and prednisone.³⁶ Although specific necropsy-identified lesions that satisfactorily explained death in these cases were not identified, both pulmonary edema and/ or congestion with variable hemorrhage were often identified. Suspicion of an inadvertent intracarotid injection was based on the presence of cerebral edema, malacia, and vasculitis in one case. Furthermore, evidence of sepsis identified during postmortem examination implied that death may have resulted from the intravenous administration of contaminated solutions in three additional cases.

Bit-induced asphyxia (partial or complete) was recently suggested to contribute to the risk of sudden death in race- horses.⁴¹ In that work, the author contended that both sudden/ unexpected death and catastrophic musculoskeletal injury result from bit-induced asphyxia, a potentially preventable situation in racehorses.⁴¹

Miscellaneous Causes of Sudden Death in Ruminants

Fatal anaphylaxis occurs in sensitized animals after parenteral administration of drugs or vaccines. This is most common with the penicillins. Vaccines containing gram-negative bacteria or cell walls may cause an endotoxemic reaction that looks similar to anaphylaxis. Anaphylactic shock may also be an outcome of blood transfusion reactions. Immune-mediated hemolytic anemia (neonatal isoerythrolysis) from ingestion of colostrum­containing alloantibodies 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.⁴² 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.⁴³