Sudden Death of Feedlot Cattle

Sudden Death of Feedlot Cattle

J. T. Vasconcelos[1]

Texas A&M University Agricultural Research and Extension Center, Amarillo 79106 and Division of Agriculture, West Texas A&M University, Canyon 79106-0001

Unexpected death of feedlot cattle has long been a problem for the feedlot industry. Sudden death syndrome (SDS) is a sporadic, fatal disease of unknown origin in which feedlot cattle are found dead in the pen. Cattle usually succumb to SDS after eating a high-energy diet for at least 100 d (Pierson et al., 1976; Nagaraja et al., 1979). Death has most commonly been associated with digestive upset; however, the etiology and preventive measures are poorly defined. Affected animals simply stop eating, step back and die without clinical signs (Nagaraja et al., 1979). The objective of this review is to discuss SDS and the importance of SDS to cattle feeding operations.

The cause of the SDS is unknown. One of the earliest attempts to identify the cause of SDS was conducted by Pierson et al. (1976). They surveyed different feedlots (407,000 cattle). Of the 4,260 (1%) cattle that died during this period, 1,358 (32%) were categorized as cases of SDS. The most frequent and common causes of sudden death, as determined by necropsy, were bloat, bronchopneumonia, acidosis, hemorrhagic enterocolitis, and IBR. Most cattle that died of SDS were affected with pneumonia, and pneumonia cases were observed to be at least several days in duration and evidently had been overlooked by attendants. Therefore, sudden death may be a misnomer for many long-course diseases. In some instances clinical SDS frequently includes cattle that have been sick, often with pneumonia, for several days (Pierson et al., 1976).

Pierson found that 47% of the sudden deaths were a direct result of respiratory disease. However, Glock and DeGroot (1998) indicated that bronchopneumonia should not be considered a cause of sudden death. If bronchopneumonia is eliminated from the Pierson et al (1976) study, acidosis and bloat would be the most common causes of sudden death.

Overfeeding and erratic feeding may be associated with SDS as a result of acidosis, but the disease does not seem to be simply a process of lactic acidosis (Moxley, 1996). Nagaraja et al. (1998) suggested that ruminal acidosis may be a predisposing factor for SDS. The SDS is more prevalent when management error or adverse weather brings about irregular consumption of feed, leading to overeating (Panciera and Williams, 1986). According to Panciera and Williams (1986), major outbreaks have occurred immediately following the refilling of feeders after periods of enforced fasting. Also, SDS is more prevalent when daytime feed consumption is diminished because of extremely high ambient temperatures, followed by overeating during the cooler night period.

Acidosis is most prevalent following engorgement of large amount of starch or other rapidly fermented carbohydrate. With acute acidosis, ruminal acidity and osmolality increase markedly as acids and glucose accumulate. These can damage the ruminal and intestinal wall, decrease blood pH, and cause dehydration that proves fatal (Owens et al., 1998). Endotoxemia also may play a role in SDS because low pH causes lysis of ruminal microorganisms with liberation and systemic absorption of lipopolysaccharides (Glock and DeGroot, 1998).

Bloat is a frequent factor in sudden death (Glock and DeGroot, 1998); however, bloat is considered an effect rather than a cause of SDS (Nagaraja and Bartley, 1981). The lesions often associated with bloat are equivocal, but frequently are observed in sudden death animals. Postmortem diagnosis of bloat is complicated by continued production of gas by the ruminal microflora (Glock and DeGroot, 1998). Therefore, it is very difficult to distinguish at necropsy antemortem from postmortem bloat (Moxley, 1996).

Various clostridial organisms have been suspected to cause SDS. Some SDS causes in feedlots occur as a result of infections with organisms such as Clostridium chauvoeii and Clostridium novyii. However, the more commonly diagnosed form of clostridial disease, enterotoxemia, is much more difficult to identify and define. Bovine enterotoxemia in the feedlot has been identified as the result of enteric infections with Clostridium perfringens types C and D (Brandini, 1996; Glock and DeGroot, 1998).

It is extremely difficult to identify the cause of death in animals that are assumed to have died from enterotoxemia. The most frequent basis for diagnosis of enterotoxemia is reddened or hemorrhaged areas in the small intestine; however, these often result from other problems, such as postmortem redistribution of blood, salmonellosis, or other causes of segmental or diffuse congestion. Difficulty in identifying the role of clostridial enterotoxemia in sudden death is reflected in questions about the efficacy and value of Clostridium perfringens types C and D vaccines. Although outbreaks of SDS are reported to have been interrupted by vaccination with polyvalent Clostridial toxoid (Panciera and Williams, 1986), other vaccination studies have not shown an affect on SDS rate in feedlot cattle (DeGroot et al., 1997).

Some researchers have maintained that SDS may represent an anaphylactoid hypersensitivity to endotoxins released as result of low ruminal pH (Moxley, 1996). The predominant Gram-negative flora in the rumen provide a large pool of endotoxin (Bartley, 1977), which could induce shock and death if released and absorbed. Shock resulting from endotoxemia following release of massive amounts of endotoxin is unlikely to happen. Alternately, cattle may become sensitized by intermittent exposure to small amounts of ruminal endotoxin. Such hypersensitive cattle may succumb to anaphylactic shock (Nagaraja and Bartley, 1981). Other causes of SDS include riding injuries and liver abscesses. Riding of bulling steers may result in injuries and death (Pierson et al., 1976). Abscesses that rupture into hepatic veins may produce acute septic shock and death (Glock and DeGroot, 1998).

When an animal is found dead without having been previously diagnosed to be ill, it is often difficult to make an accurate diagnosis, even after necropsy examination, because of the absence of clinical findings and epidemiology (Blood et al., 1983). In SDS, clinical signs have not been described because the animal dies suddenly (Nagaraja and Bartley, 1981). The common event is for animals to be observed feeding normally and to be found dead minutes or hours later (Panciera and Williams, 1986). Although the SDS occurs frequently, clinicians are infrequently called to make a necropsy diagnosis. When the clinician is called for a diagnosis, rapid autolysis and the many etiologic agents recovered from tissues have complicated and confused diagnostic proof (Pierson et al., 1976).

Necropsy findings are nonspecific and reflect rapid postmortem autolysis (Panciera and Williams, 1986). Lesions most frequently observed include hemorrhage and edema peritracheal and endotracheal, bloat, and emphysema of muscle and subcutaneous tissue (Pierson et al, 1976; Eyre, 1977; Nagaraja and Bartley, 1981). Tissues posterior to the diaphragm are engorged with blood, the liver and kidney are severely autolyzed, and the lungs are variably congested and edematous (Panciera and Williams, 1986).

Improved management practices may result in reduction of SDS incidence. Cattle should be observed frequently and carefully. Animals must be necropsied, and efforts should be continued in order to identify cattle in early stage of sickness. Professional assistance may be available for employees’ orientation and the necropsies must be conducted by veterinarians. Better diagnostic tools are necessary. An open relationship between feedlots, veterinarians, and nutritionists will assist in defining SDS and working toward a prevention plan for this disease.

Literature Cited

Bartley, E. E. 1977. Sudden death syndrome. Page 29 in Proc. Acad. Vet. Consultants, 1977 Cecil Reedy Workshop on Sudden Death, Amarillo, TX.

Blood, D. C., O. M. Radostists, and J. A. Henderson. 1983. Veterinary Medicine. 6th ed. Pitman Press Ltd., Bath, Great Britain.

Brandini, J. C. 1996. Doenças em bovinos confinados. Tech. Bull. No. 65. ed. EMBRAPA-CNPGC, Campo Grande, Brazil.

DeGroot, B. D., C. E. Dewey, D. D. Griffin, L. J. Perino, R. A. Moxley, and G. L. Hahn. 1997. Effect of booster vaccination with a multivalent clostridial bacterin-toxoid on sudden death syndrome mortality rate among feedlot cattle. J. Am. Vet. Med. Assoc. 211:749-53.

Eyre, P. 1976. Sudden death syndrome. Page 15 in in Proc. Acad. Vet. Consultants, 1976 Cecil Reedy Workshop on Sudden Death, Amarillo, TX.

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Panciera, R. J., and D. E. Williams. 1986. Sudden death syndrome of feeder cattle. Page 955 in Current Veterinary Therapy, Food Animal Practice 2. J. L. Howard, ed. W. B. Saunders Co. Philadelphia, PA.

Pierson, R. E. , R. Jensen, L. H. Lauerman, D. A. Saari, P. M. Braddy, A. E. McChesney, and D. P. Horton. 1976. Sudden death in yearling feedlot cattle. J. Am. Vet. Med. Assoc. 169:527-529.

[1] Correspondence: 6500 Amarillo Blv. West Amarillo, TX 79106 (phone: 806 677 5678; E-mail: ).