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SPECIAL TOPICS |
Department of Animal and Food Sciences, Texas Tech University, Lubbock 79409
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Abstract |
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 Top Abstract INTRODUCTIONDEFINITIONSCONTRIBUTIONS TO UNDERSTANDING...FUTURE EFFORTS AND CONCLUSIONSLITERATURE CITED |
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Key Words: acidosis • bloat • liver abscess • polioencephalomalacia • ruminant
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INTRODUCTION |
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TopAbstractINTRODUCTIONDEFINITIONSCONTRIBUTIONS TO UNDERSTANDING...FUTURE EFFORTS AND CONCLUSIONSLITERATURE CITED |
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) indicated that 1.9% of cattle placed in feedlots developed digestive disorders, with slightly greater prevalence in larger feedlots than in smaller ones. The economic effects of these conditions can be significant; Smith (1998) reported that in large feedlots, mortality ranged from 0.17 to 0.42% of inventory per month, with digestive disorders accounting for approximately one-third of mortalities. For the past several decades, the Journal of Animal Science (JAS) has been an important repository for scientific studies on metabolic and digestive disorders in cattle. The research reported in JAS has generally focused on 3 disorders: ruminal acidosis, liver abscesses, and bloat. Another disorder, polioencephalomalacia (PEM), has received less attention in JAS than have the others, but research interest in PEM has increased recently with greater use of distillers coproducts, which can have high S concentrations. Our objective was to summarize the major accomplishments of research published in JAS related to these 4 disorders. A secondary goal was to identify areas for further research.
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DEFINITIONS |
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TopAbstractINTRODUCTIONDEFINITIONSCONTRIBUTIONS TO UNDERSTANDING...FUTURE EFFORTS AND CONCLUSIONSLITERATURE CITED |
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Ruminal acidosis is a common digestive disorder in beef cattle (Nagaraja and Titgemeyer, 2007) that is typically ascribed to excessive consumption of fermentable carbohydrates, which decreases ruminal pH and fosters the production of toxic factors (Slyter, 1976; Owens et al., 1998). Specifically, acute ruminal acidosis is characterized by a ruminal pH of less than 5.0 or 5.2. Low pH and increased free glucose concentrations in the rumen can lead to increased production of VFA and lactic acid (Owens et al., 1998). Increased ruminal osmolality, which negatively affects absorption, and production of endotoxin and amides such as histamine also play a role in the physiological effects of the disorder, which include rumen stasis, diarrhea and dehydration, systemic acidosis, and, in acute cases, cardiovascular and respiratory failure (Huber, 1976). Clinical observations include incoordination, weakness, anorexia, and stools that are soft, gray, and foamy (Glock and DeGroot, 1998). Direct and indirect consequences of acidosis are associated with other disorders such as laminitis, liver abscesses, and PEM (Brent, 1976).
Subacute (or subclinical) acidosis is less well defined than acute acidosis. Owens et al. (1998) noted that a benchmark for subacute acidosis is a ruminal pH of less than 5.6, and that variable feed intake has been associated with the condition. It has been suggested that subacute acidosis is linked to decreased performance and also to rumenitis and thereby to liver abscesses. Despite considerable discussion in the scientific literature about possible negative effects of subacute acidosis, clinical standards for the condition have not been adequately developed.
Liver Abscesses
Liver abscesses are common in feedlot cattle, but the frequency of occurrence varies with diet, season, and geographical location. As noted previously, abscessed livers are generally considered to be associated with both acute and subacute ruminal acidosis. In a JAS review, Ørskov (1986) suggested that a continuous high acid load in the rumen can cause parakeratosis or similar insults to the ruminal wall, leading to clumping and necrosis of papillae. Ulcerative lesions, hairs, and other foreign objects that become embedded in the ruminal epithelium can provide routes of entry into the portal blood for microbes that cause liver abscesses. In another important JAS review, however, Nagaraja and Chengappa (1998) indicated that the exact pathogenic mechanism(s) are not known. Liver abscesses are typically scored according to the severity of the condition (Brown et al., 1975), with categories of A–, A, and A+ frequently reported in the literature. Regardless of severity, abscessed livers are condemned at slaughter, which represents a loss of approximately 2% in carcass weight (Nagaraja and Chengappa, 1998).
Bloat
Bloat occurs when ruminants are prevented from expelling ruminal gas, resulting in pressure on the diaphragm and lungs, which affects breathing and potentially results in death. Bloat is observed in virtually all production settings with cattle and other ruminants, but it is often reported as a problem in feedlot cattle. Free-gas bloat, which is typically a result of physical obstruction or damage to the cardia (or esophagus) or to decreased ruminal motility, occurs in feedlot cattle, but frothy bloat is more common (Cheng et al., 1998). The formation of stable foam in the rumen of feedlot cattle can result in the cardia being covered by foam, which inhibits eructation of gas (Cheng et al., 1998). With the frothy pasture bloat that occurs in ruminants grazing alfalfa or annual winter wheat, a combination of high-forage soluble protein concentrations coupled with rapid fermentation and evolution of gas are thought to contribute to the formation of stable foams.
PEM
This neurological disorder of ruminants tends to occur sporadically. The condition is most common in feedlot cattle, but severe outbreaks have been reported in grazing cattle. Signs of PEM include blindness, incoordination, muscle tremors, and possible recumbence with seizures (Gould, 1998). As noted in the JAS review by Gould (1998), the term PEM is used to describe a specific disorder caused by altered thiamine status and to describe a specific brain lesion that can be caused by various factors, including consumption of excessive amounts of S (particularly sulfates) in water, feed, or both. Cerebrocortical necrosis is synonymous with PEM (Gould, 1998), and characteristic brain lesions are manifest at postmortem examination.
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CONTRIBUTIONS TO UNDERSTANDING RUMINAL AND PHYSIOLOGICAL MECHANISMS AND TO CONTROLLING OR MANAGING METABOLIC AND DIGESTIVE DISORDERS IN CATTLE |
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TopAbstractINTRODUCTIONDEFINITIONSCONTRIBUTIONS TO UNDERSTANDING...FUTURE EFFORTS AND CONCLUSIONSLITERATURE CITED |
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Before 1960.
A search for the word "acidosis" in papers published in JAS before 1960 yielded only 1 citation (Brethour et al., 1958). This paper reported measurements of ruminal pH in sheep as affected by addition of corn oil, alfalfa ash, and NaHCO3 to the diet, but the focus of the paper was not acidosis. Thus, acidosis was not a significant topic of research until confinement feeding of grain-based diets became a standard production method for ruminants.
1960 to 1980.
Relatively inexpensive grain prices fueled a dramatic increase in the number of cattle in feedlots during the early 1960s (Albin, 1971), which coincided with the publication of research on acidosis in JAS in the mid to late 1960s. A common feedlot management practice is to transition (adapt) grass-fed cattle to high-concentrate diets as soon as possible (Elam, 1976). Adaptation to finishing diets is a critical process that can tip the balance in the rumen toward acidosis, and one in which nutritional practices could potentially promote or impair performance and health (Brown et al., 2006). The work of Allison et al. (1964), in which changes were measured in ruminal pH, VFA, and lactate as affected by providing ruminal inoculum from lambs adapted to a diet containing wheat, was one of the early efforts to understand ruminal changes coincident with adaptation to grain-based diets. The relationship between ruminal pH and lactate concentration was observed in other studies from the 1960s and 1970s (Uhart and Carroll, 1967; Telle and Preston, 1971), and Telle and Preston (1971) suggested that lactic acid was the main cause of acidosis.
Detailed reviews of the practical, physiological, and ruminal effects of acidosis (Elam, 1976; Huber, 1976; and Slyter, 1976; respectively) were presented at the Symposium on Acidosis in Feedlot Cattle at the 67th Annual Meeting (1975) of ASAS, in Fort Collins, CO. It also became clear during the 1970s that although glucose concentrations in the rumen are typically very low (Owens et al., 1998), with acidosis, ruminal glucose concentrations can exceed those found in blood (Slyter, 1976; Horn et al., 1979). Production of potentially toxic compounds in the rumen also was considered to play a role in acidosis. Huber (1976) discussed the possible roles of bacterial endotoxin and histamine in acute acidosis; however, Koers et al. (1976) reported that histamine did not seem to play a major role in either subacute or acute acidosis.
In the late 1970s, research efforts focused on understanding how adaptation methods affect ruminal and physiological changes related to acidosis. Effects of dietary roughage concentration on lactate utilization were evaluated by Byers and Goodall (1979), and significant work with different adaptation strategies was published by Fulton et al. (1979a, b). The papers by Fulton et al. (1979a, b) are among the most frequently cited articles in JAS with respect to subacute acidosis, intake variation, and digestive disorders related to consumption of high-grain diets.
1980 to 2000.
During the early 1980s, ionophores began to be used extensively in cattle feeding, and considerable research evaluated the effects of compounds such as monensin and lasalocid, as well as other antibiotic compounds, on acidosis. Inhibitory effects of monensin and lasalocid on Streptococcus bovis and other major lactate-producing ruminal bacteria were documented by Dennis and Nagaraja (1981) and Nagaraja et al. (1981). Using a subacute acidosis challenge model, Burrin and Britton (1986) reported that monensin increased ruminal pH through effects on decreased VFA concentrations, and also noted that ruminal pH was more highly correlated with total VFA concentrations than with lactate. Thiopeptin, an S-containing peptide antibiotic, was active against S. bovis (Muir and Barretto, 1979) and prevented lactic acidosis in sheep after intraruminal administration of ground wheat (Muir et al., 1980).
Research on acidosis increased significantly in the 1990s. Hungate et al. (1952) reported that overgrowth of S. bovis was a major factor in the development of acidosis (see Nagaraja and Titgemeyer, 2007), but the results of Slyter and Rumsey (1991) suggested participation of other opportunistic microbes, including coliforms. Using a model system with ruminally cannulated cattle, Goad et al. (1998) observed that bacterial changes associated with subacute acidosis were similar to those associated with adaptation to grain-based diets and that decreased numbers of ciliated protozoa were indicative of acidosis.
Hibbard et al. (1995) reported that slaframine, a parasympathomimetic that increases salivary flow in cattle, seemed to decrease the effects of subacute acidosis in an experimental model with ruminally cannulated beef cattle, but it did not attenuate acute ruminal acidosis. Owens et al. (1998) suggested that enhanced saliva flow, achieved through increased chewing and rumination time by including long roughage in the diet or by injecting specific chemicals such as slaframine, might decrease the incidence of acidosis.
The role of specific feeds in managing acidosis became of interest in the 1990s, particularly as the availability of digestible fiber coproducts (e.g., corn gluten feed) increased. On the basis of an acidosis challenge model, Krehbiel et al. (1995a) reported that the addition of wet corn gluten feed to grain-based diets should decrease the length of time cattle are subjected to an acid insult. Adding up to 8% tallow or yellow grease to the diet in an acidosis challenge model with ruminally cannulated steers did not decrease subacute acidosis (Krehbiel et al., 1995b).
The review of acidosis by Owens et al. (1998) deserves special note. This paper was a contribution to the "Bud Britton Memorial Symposium on Metabolic Disorders of Feedlot Cattle," that was held at the July 1996 ASAS Annual Meeting in Rapid City, SD. It is consistently among the top 10 most frequently cited JAS articles in HighWire-hosted articles (http://jas.fass.org), and according to Science Citation Index (Thomson Scientific; Thomson Corp., Stamford, CT), it has been cited 174 times since publication. This outstanding article remains a seminal contribution in the area of acidosis in cattle.
2000 to Present.
More recent JAS articles have focused on the considerable variability in the ability of animals to cope with dietary factors that might cause acidosis. Brown et al. (2000) reported that selected serum and plasma metabolites (e.g., amylase activity, cholesterol, K concentrations, and NEFA concentrations) were useful to distinguish between steers classified as experiencing subacute acidosis or not affected in an acidosis challenge model. Nonetheless, a notable finding of the study was that based on ruminal pH, ruminal and plasma lactate concentrations, and DMI, 2 of 5 steers subjected to an acute challenge did not experience acute acidosis and 1 of these 2 steers did not even show signs of subacute acidosis (Brown et al., 2000). The reasons that some animals experience subacute acidosis whereas others seem capable of coping with significant acid loads are still not clear. Schwartzkopf-Genswein et al. (2003) and Bevans et al. (2005) noted that variability among individual animals is high in ruminal pH, feed intake, and feeding behavior. Bevans et al. (2005) suggested that current grain adaptation strategies for preventing acidosis in the pens of cattle are based on responses of the most susceptible individuals, which might not be the most efficient approach, particularly given the variability in individual responses to acidosis challenges. Nonetheless, until methods are developed to identify susceptible individuals, feedlot managers have limited options, and questions remain as to effects of animal-to-animal variability on the potential of cattle to deal with ruminal and metabolic acid loads. Animal variation has long been recognized as important in the study of acidosis, as Allison et al. (1964) stated in their summary: "Thus, it is probable that animal as well as microbial factors are active in regulating tolerance or adaptation to a changed ration."
Whether feedlots can alter feeding management and thereby modify the likelihood of acidosis is open to question. So-called "clean bunk" management programs strive for consumption of all feed offered before the next feeding, with a goal of minimizing daily fluctuations in feed intake by pens of cattle (Galyean and Eng, 1998). Bunk management could have positive effects on the incidence of acidosis if variability in intake is decreased (Schwartzkopf-Genswein et al., 2004). These authors noted that average ruminal pH and time that pH was less than 5.8 were less when intake was intentionally varied by 110% of ad libitum intake for 3 d followed by 90% of ad libitum intake for 3 d; however, feedlot performance was not affected by variable intake. Similarly, Schwartzkopf-Genswein et al. (2003) suggested that cattle on finishing diets adapt physiologically and behaviorally to day-to-day intake variation without negatively affecting performance, but effects of intake variation could be greater during the transition from high-roughage to high-concentrate diets.
Uhart and Carroll (1967) acknowledged that the time required for adaptation without causing animals to go "off-feed" was not well defined, but that most experienced cattle feeders allow at least 3 to 4 wk for the adaptation process. Approximately 40 yr later, feedlot consulting nutritionists continue to recommend an average of 21 d for adaptation, regardless of the method used (Vasconcelos and Galyean, 2007). Practical experience and research also indicate that adapting feedlot cattle with incremental increases in dietary concentrate over the range of approximately 55 to 90% of dietary DM in 14 d or less generally results in decreased performance during adaptation or over the entire feeding period compared with longer adaptation periods (e.g., 21 d; Brown et al., 2006). Readers are referred to Brown et al. (2006) for a detailed review on adaptation of beef cattle to high-concentrate diets.
Liver Abscesses
Before 1960.
Smith (1940), the first to describe in JAS the condemnation of livers because of abscesses, reported that 5.3% of the more than 9.5 million cattle slaughtered in 1940 had livers condemned for abscesses, 1.4% were condemned for distoma (flukes), and 2% were condemned for telangiectasis. Fusobacterium necrophorum, which was believed to be the principal agent responsible for liver abscesses, was isolated from the rumen of beef cattle in 1951 (Robinson et al., 1951), but i.v. injection of the organism failed to induce liver abscesses. Bohman et al. (1957) observed that chlortetracycline decreased the incidence of liver abscesses, which had been reported previously in other journals.
1960 to 1980.
Much of the liver abscess research reported in JAS during the 1960s and early 1970s was conducted as a consequence of research on the effects of feeding all-concentrate diets to feedlot cattle. In an extensive review of the feeding of all-concentrate diets, Wise et al. (1968) noted that such diets were associated with an increased incidence of rumen parakeratosis, liver abscesses, lowered feed intake, founder, and bloat. Indeed, these authors suggested that the rumen parakeratosis-liver abscess complex was the most significant problem associated with the feeding of high-energy diets. Wise et al. (1968) further noted that adding 10 to 15% roughage to feedlot diets was the best method available to prevent rumen parakeratosis. In another significant review during this time period, Brent (1976) described the pathology of liver abscesses and suggested that rumenitis and liver abscesses are inseparable conditions because rumenitis allows microorganisms to enter the portal circulation and infect the liver.
Harvey et al. (1968) evaluated the effects of adding limited roughage of different sources and physical forms to an all-concentrate diet on the performance, ruminal characteristics, and liver abscesses of feedlot steers. Severe rumen parakeratosis was observed in steers fed no roughage or ground rice hulls, but coarse roughage (either whole rice hulls at 5% of the diet or long hay at 1.36 kg/d) improved health of the ruminal epithelium, and fewer steers fed had abscessed livers. Similarly, Haskins et al. (1969) reported that feeding 1.36 kg/(animal·d) of hay with an all-concentrate diet decreased the incidence of rumen parakeratosis and liver abscesses compared with 5% cottonseed hulls, 5% corn cobs, and low levels of oyster shell, sand, and ground polyethylene. Effects of dietary roughage level on liver abscesses were reconfirmed by Colling et al. (1979), who reported that steers fed a diet containing 12% corn silage had fewer liver abscesses (23.2%) than steers fed an all-concentrate diet (61.2%).
The role of antibiotics in controlling liver abscesses was an important topic of research in JAS during the 1960s and 1970s. Haskins et al. (1967) evaluated the effects of different concentrations and sources of protein and the antibiotic bacitracin on the performance, ruminal environment, and liver abscesses of cattle fed all-concentrate diets. Neither protein treatments nor bacitracin decreased the incidence of liver abscesses, but rumen parakeratosis was present in all steers at slaughter, and 72% of livers were abscessed. A marked decrease in abscessed livers (33 vs. 3%) was achieved by feeding 75 to 85 mg/(animal·d) of chlortetracycline (Harvey et al., 1968) in all-concentrate diets. The use of tylosin for control of liver abscesses was reported by Brown et al. (1973), who evaluated 3 levels and 2 formulations of tylosin [50, 75, and 100 mg/(animal·d) of tylosin phosphate and tylosin phosphate urea adduct] and noted an 81.8% decrease in the incidence of liver abscesses, with no difference between tylosin formulations. Subsequently, Brown et al. (1975) compared 75 mg of tylosin and 70 mg of chlortetracycline/(animal·d) in 1,829 animals fed medium- to high-concentrate diets. The incidence of liver abscesses was 56.2% for the control diet, 44.2% for chlortetracycline, and 18.6% for tylosin. Pendlum et al. (1978) observed 14.6 vs. 6.3% abscessed livers when feeding 0 or 75 mg of tylosin/(animal·d), respectively, averaged over monensin levels of 0, 100, and 300 mg/(animal·d). Similarly, Heinemann et al. (1978) observed that tylosin decreased liver abscesses from 29 to 10%, and as in the report by Pendlum et al. (1978), no monensin x tylosin interactions were observed.
1980 to 2000.
Potter et al. (1985) summarized the results of 14 trials in which tylosin (0 or 11 mg/kg) and monensin (0 or 33 mg/kg) were fed and reported that, averaged over monensin concentration, the incidence of liver abscesses decreased from 27 (control cattle) to 9%. Monensin did not affect the incidence of liver abscesses. Rogers et al. (1995) summarized data from trials conducted in several different geographical locations and concluded that virginiamycin at 19.3 or 27.6 mg/kg of the diet decreased the incidence of liver abscesses, a result that might be related to effects of virginiamycin on the growth of lactic acid-producing bacteria (Coe et al., 1999). Nagaraja et al. (1999) concluded that feeding tylosin to prevent liver abscesses did not induce antibiotic resistance in F. necrophorum or Actinomyces pyogenes, but abscesses in cattle fed tylosin were more frequently characterized by a mixed infection of the 2 organisms than in control cattle that were not fed tylosin.
Harman et al. (1989) reported that the incidence of liver abscesses varied with the season cattle were started on feed, being greater for cattle started on feed during fall and winter than for those started in spring and summer. Nonetheless, ADG did not differ between cattle with normal and abscessed livers, but the effect of the severity of the abscesses on ADG was not evaluated. The report by Brink et al. (1990) seems to be the most frequently cited publication on the relationship between liver abscesses and cattle performance. In 4 of 9 experiments, in which the incidence of liver abscesses averaged 24.3%, the presence of an abscess did not affect performance, regardless of severity. In 5 of 9 experiments in which the average incidence of liver abscesses was 43.7%, the presence of severe liver abscesses [A+ according to a slight modification of the Brown et al. (1975) scoring system] negatively affected ADG, DMI, and G:F. Results of the Brink et al. (1990) study are sometimes misstated by ignoring the fact that overall data were not analyzed because of heterogeneity of variance and that abscess severity had no effect in 4 of the 9 studies analyzed.
The complete pathogenesis of liver abscesses was summarized by Nagaraja and Chengappa (1998), an excellent and frequently cited review from the Bud Britton Memorial Symposium. Glock and DeGroot (1998), in a paper from the same symposium, noted that liver abscesses can result in sudden death when abscesses rupture into hepatic veins and produce acute septic shock, but this condition seems to occur rarely.
2000 to Present.
Although several papers have reported the incidence of liver abscesses, no significant research directed specifically toward understanding the development or control of liver abscesses in cattle has been reported in JAS during the last 7 years. According to the 2000 National Beef Quality Audit (McKenna et al., 2002), liver condemnations were 30.3%, of which 44.8% were for abscesses, suggesting that liver abscesses will continue to be a topic of interest.
Bloat
Before 1960.
Pasturing cattle on immature alfalfa or clover has long been recognized as conducive to bloat. Cole et al. (1943) evaluated methods to induce pasture bloat and to control it by various management schemes, including feeding sudangrass hay before cattle were allowed to graze alfalfa. Knapp et al. (1943) identified bloat as a problem in feedlot cattle operations, but indicated that the physiological cause(s) of this condition were not understood. Cole et al. (1945) was one of the first and more complete reviews (222 literature citations) concerning bloat published in JAS. The authors discussed several theories about the causes of bloat, including complete or partial obstruction of the esophagus, ruminal atony, frothiness of the ingesta, and defective eructation. On the basis of their data, Cole et al. (1945) suggested that lack of coarse roughage in the diet to induce eructation was likely the most important cause of bloat.
Parsons et al. (1955) tested a theory supported by data from other laboratories indicating that biochemical or toxic substances caused partial paralysis of the rumen and thereby prevented belching. Results indicated that extracts from bloat-producing forages and samples of ruminal contents from cows that died as a result of acute bloat inhibited motility of isolated segments of rabbit intestine.
Lindahl et al. (1957), Jacobson et al. (1957), and Jacobson et al. (1958) conducted a series of studies on bloat with feedlot cattle. Lindahl et al. (1957) produced frothy bloat with an experimental diet of 61% barley, 22% alfalfa meal, 16% soybean oil meal, and 1% salt, but noted considerable animal-to-animal variation in susceptibility. The authors concluded that factors other than the lack of sufficient coarse roughage were involved in the frothy bloat. Using the bloat-producing diet of Lindahl et al. (1957), Jacobson et al. (1957) developed in vitro methods to evaluate foam stability and measured the occurrence of encapsulated bacteria in the rumen, concluding that frothy bloat resulted from the formation of stable foam that prevented eructation. Jacobson et al. (1958) evaluated proportions of VFA and microbial fermentation of glucose and cellobiose in the rumen of cattle changed from a grass hay plus silage-based diet to a bloat-producing diet. Acetate decreased and propionate increased within the first few weeks after the dietary switch, but changes were variable over time.
Barrentine et al. (1956) compared oral administration of chlortetracycline, oxytetracycline, bacitracin, streptomycin, and penicillin in cattle grazing clover. Penicillin was the only antibiotic that prevented bloat when a single dose was given.
1960 to 1980.
Elam and Davis (1962b) reported on the effects of method of administration, and amount and type of oils and fats on the incidence of feedlot bloat. The addition of tallow to the diet had no effect on incidence of bloat, but adding 4 or 8% mineral oil decreased bloat by 40%. Elam and Davis (1962a) observed no influence of the consumption of salivary salts by feedlot cattle on either the incidence of bloat or on microbial activity as measured by gas production and concentrations of total VFA. Workers in the laboratory of E. E. Bartley at Kansas State University made numerous contributions to our understanding of bloat in cattle. Van Horn and Bartley (1961) and Mishra et al. (1967) demonstrated that adding saliva to frothing ruminal contents in vitro released gas from the foam. Bartley and Yadava (1961) suggested that bloat occurs when salivary secretion is not sufficient to counter foaming agents in feeds, and that mucins derived from animals aided in the prevention of bloat by inhibiting and breaking foams. The same laboratory later isolated ruminal microorganisms and tested mucinolytic activity, reporting that the efficacy of mucin in countering bloat was decreased by the action of mucinolytic microorganisms (Fina et al., 1961; Mishra et al., 1967).
Lippke et al. (1969) developed in vitro-based gas evolution and foam stability indices to assess the bloat potential of alfalfa. Correlations of the indices with bloat scores in cattle ranged from approximately 0.6 to 0.9, suggesting that in vitro methods might be useful to assess the potential for legume bloat.
Poloxalene, a polyoxypropylene polyoxyethylene block polymer patented by E. E. Bartley and G. C. Scott in 1969 (Bartley, 1965; Bartley et al., 1965), effectively prevented legume bloat in cattle. Bartley et al. (1975) subsequently reported that poloxalene also was effective in decreasing the incidence and severity of wheat pasture bloat, and that soluble forage proteins were associated with bloat on wheat pasture. Essig et al. (1972) described changes in pH, VFA, and buffering capacity of bloating and nonbloating cattle grazing clover and also noted that both poloxalene and penicillin were effective for decreasing the incidence and severity of bloat. After the success of poloxalene, several other compounds were tested. Meyer and Bartley (1972) evaluated 235 drugs for their in vitro effects on froth production, surface tension, relative viscosity, and microbial activity, ultimately concluding that none of the drugs adequately controlled feedlot bloat.
1980 to 2000.
Shortly after their approval and widespread use, research conducted with ionophores showed their efficacy for controlling bloat. Bartley et al. (1983) reported that monensin was more effective than lasalocid or salinomycin in controlling legume bloat. In a widely cited review of the effects of monensin on cattle performance, Goodrich et al. (1984) noted that monensin alone or in combination with poloxalene decreased the incidence of legume bloat; however, poloxalene was more effective than monensin. Katz et al. (1986) reported that monensin was more effective than lasalocid for prevention of legume bloat. Branine and Galyean (1990) reported that monensin supplied in a grain-based supplement was effective in decreasing the incidence and severity of wheat pasture bloat.
Using the approach of Cole et al. (1943), Mader et al. (1983) examined the potential of feeding low-quality roughages to decrease wheat pasture bloat. The authors concluded that neither wheat straw nor sorghum sudangrass hay at the levels consumed (approximately 0.2 to 0.25 kg of DM/d) controlled bloat of cattle on wheat pasture.
In an extensive review of research regarding cattle grazing alfalfa pastures or offered fresh alfalfa herbage, poloxalene was the only supplement evaluated that effectively controlled bloat (Majak et al., 1995). Moreover, the authors concluded that bloat was decreased when the legume plant had begun to flower, when cattle were moved to a new pasture in the afternoon, when grazing was continuous vs. interrupted, and when producers were aware that cattle could still bloat on alfalfa after a "killing" frost.
Glock and DeGroot (1998), in a paper from the Bud Britton Memorial Symposium referred to previously, stated that bloat is frequently identified as a factor in sudden death of feedlot cattle. They suggested that the diagnosis of bloat should be based on a postmortem examination of the carcass, as well as evaluation of the ruminal contents, and in particular, ruminal pH. Cheng et al. (1998) published a detailed review of feedlot bloat that also was presented at the Bud Britton Memorial Symposium. They noted that dietary roughage concentration, grain-processing methods, type of cereal grain, feed additives (e.g., ionophores), and dietary adaptation schedules can aid in decreasing the likelihood of bloat in feedlot cattle.
2000 to Present.
In an extensive review of supplementation practices for cattle grazing wheat pasture, Horn et al. (2005) confirmed the efficacy of monensin for decreasing the incidence and severity of wheat pasture bloat, as well its superiority to lasalocid for bloat control. For the most part, research published in JAS since 2000 has largely focused on the use of condensed tannins (CT) to decrease ruminal protein digestion and ruminal bacterial activity, decrease ruminal gas formation, and prevent bloat as a result of CT-plant protein interactions. Min et al. (2005) reported that added CT decreased the rate of in vitro gas production of minced wheat forage samples. Subsequently, Min et al. (2006a) evaluated the effects of CT on in vitro gas production, in vivo ruminal fluid protein fractions, bloat dynamics, and ADG by steers grazing winter wheat, reporting that feeding CT increased ADG and minimized the frequency of bloat. Ruminal fluid supplemented with CT and incubated with minced wheat forage produced less gas and methane in vitro. Min et al. (2006b) assessed the growth of various anaerobic bacterial species as influenced by soluble protein from fresh wheat forage, as well as biofilm formation, changes in ruminal bacterial populations, and bloat potential, by using ruminally cannulated steers. The authors concluded that wheat pasture bloat was associated with increased production of biofilm resulting from changes in the microbial population associated with wheat forage consumption.
As noted by Cheng et al. (1998), grain processing may be related to bloat in feedlot cattle. In a review of the steam-flaking process, Zinn et al. (2002) suggested that the optimal flake density for corn to maximize starch digestion is 0.31 kg/L, and that flaking to less than 0.31 kg/L might increase the rate and extent of ruminal starch digestion, decrease DMI, increase variation in ADG, and predispose cattle to acidosis and bloat.
PEM
Before 1980.
The first "semireview" of PEM in JAS was part of the 1975 symposium on acidosis at the ASAS meetings in Fort Collins, CO (Brent, 1976). Brent (1976) suggested that lactic acidosis was responsible for the ruminal conditions that can lead to development of PEM. Specifically, decreased pH would create optimal conditions for accumulation and activity of bacterial thiaminase. Brent’s laboratory (Lusby and Brent, 1972) developed a continuously infused liquid diet high in readily fermentable carbohydrate that would consistently induce PEM in lambs. Subsequently, Sapienza and Brent (1974) observed that decreasing ruminal thiamine concentrations and development of ruminal thiaminase activity were associated with greater intakes of concentrate by lambs.
1980 to 1990.
Brent and Bartley (1984) discussed some of the hypotheses that could explain the cause(s) of PEM. Of particular note was the thiaminase I hypothesis, in which the enzyme thiaminase I destroys thiamine, producing a thiamine analog that inhibits thiamine-dependent reactions of glycolysis and decarboxylations (Brent and Bartley, 1984). Moreover, the sulfite produced during the reduction of sulfate to sulfide cleaves thiamine at the methylene bridge; thus, high sulfide levels could cause the brain lesions associated with PEM. Because of their role in the prevention of acidosis, Brent and Bartley (1984) suggested that if PEM is related to acidosis, ionophores could potentially help prevent PEM, although experimental evidence to support this hypothesis is still lacking. Brent and Bartley (1984) also suggested that 1 g/(animal·d) of thiamine could be fed for the prevention of PEM in the presence of thiaminase I, but they did not recommend supplemental thiamine as a routine practice.
1990 to Present.
The review article by Gould (1998) from the Bud Britton Memorial Symposium is one of the more complete recent sources of information in JAS about PEM. Although the focus of the article was S-related PEM, definitions and other topics related to PEM were discussed in detail. Sulfate-associated PEM is of economic importance for both pasture and feedlot cattle. Grazing ruminants in parts of the US where water supplies are naturally high in sulfates can develop PEM as a result of H2S production in the rumen. Gould (1998) also described a field method to estimate rumen gas cap H2S concentrations.
With respect to the effect of sulfates on performance of feedlot cattle, Zinn et al. (1997) reported that dietary S concentrations (achieved by adding ammonium sulfate) in excess of 0.2% of the dietary DM decreased ADG, DMI, and efficiency of feedlot heifers. Loneragan et al. (2001) evaluated effects of increasing concentrations of SO4 in the drinking water of feedlot steers, and suggested that a water SO4 concentration of greater than 538 g/L (equivalent to 0.22% SO4 in the diet) was detrimental to performance. Obviously, effects of high-SO4 water vary with season, with the summer months and associated increased water intake increasing the risk for decreased performance and PEM. High feed S concentrations in addition to water SO4 concentrations would be expected to exacerbate the problem.
Galyean and Eng (1998) summarized information presented at the Bud Britton Memorial Symposium. As suggested by Brent (1976) approximately 20 yr earlier, they noted that practical experience indicates a link between PEM and acidosis, so preventing acidosis may decrease the incidence of PEM. Galyean and Eng (1998) also suggested that a greater understanding was needed of the potential role of dietary and water supplies of S in H2S production in the development of PEM, as well as definition of the ruminal H2S concentrations associated with PEM. Recently, Grout et al. (2006) compared the effects of increasing concentrations (up to 4,500 mg of SO4/L) of Na2SO4 or MgSO4 salts in the drinking water and observed decreased water consumption with MgSO4, but not with Na2SO4. Water intake was the primary variable of interest, so DMI and ruminal H2S concentrations were not measured. Nonetheless, results suggest that the chemical form of SO4 in the water or diet might be important relative to effects on performance or development of PEM.
No significant findings on or contributions to controlling or managing PEM were found in JAS, which probably reflects the frequency of occurrence and perceived economic significance of PEM relative to acidosis, liver abscesses, and bloat. As noted previously, increased availability of distillers coproducts that often have high S concentrations will probably spur additional research and publication in the next few years.
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FUTURE EFFORTS AND CONCLUSIONS |
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TopAbstractINTRODUCTIONDEFINITIONSCONTRIBUTIONS TO UNDERSTANDING...FUTURE EFFORTS AND CONCLUSIONSLITERATURE CITED |
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Major contributions that have been published in JAS to understanding metabolic and digestive disorders in cattle are summarized in Figure 1. Although the research published in JAS represents tremendous contributions to our understanding of metabolic and digestive disorders in cattle, gaps in knowledge still exist. Continued efforts to understand the changes in microbial ecology of the rumen during acidosis, bloat, and PEM are needed, and efforts to identify microbial species should be facilitated by use of modern molecular biology techniques. Further work is needed with model systems that allow acidosis to be created predictably, which also should allow more intensive study of genetic and environmental factors affecting the variability in animal responses to ruminal and systemic acid loads. Research on the development of grain varieties with altered rates of nutrient (e.g., starch or protein) digestion designed to modify ruminal acid load or bloat potential should be combined with efforts to define microbial and physiological changes. If the cattle-feeding industry moves toward automated systems for feed delivery, additional data on the effects of feed intake delivery patterns on cattle performance and on ruminal acidity and microbial populations will be needed.
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, in vitro gas production measurements could lead to rapid methods to assess the likelihood of feeds to cause bloat, and might provide a means of assessing ruminal conditions that lead to production of H2S. Further refinement is needed of our understanding of how liver abscesses affect performance by cattle. In addition, with the cattle feeding industry being under increasing pressure to use fewer antibiotics in routine production, alternatives to antibiotics such as tylosin are needed for control of liver abscesses. Perhaps research on the selection of innocuous strains of bacteria that would competitively inhibit F. necrophorum and A. pyogenes might prove useful. With respect to PEM, in vitro and in vivo evaluation of the effects of dietary (particularly distillers coproducts) and water sources and concentrations of S on ruminal H2S production are needed. In this context, further practical evaluation is needed of the value of supplemental thiamine in preventing PEM.
Conclusions
It is clear from our review that JAS has been a significant repository of information related to the physiological consequences of metabolic and digestive disorders in cattle, as well as a leading source of information on management of these problems in the field. Outstanding and frequently cited review articles on these conditions that have been published in JAS have played a significant role in educating students and scientists and in stimulating additional research. Most of these reviews came from symposia held at ASAS annual and sectional meetings. We believe that continued sponsorship of such symposia and the associated publication of high-quality reviews in JAS are vital for the future of ASAS. As ASAS moves into its second century, fostering the open exchange of ideas and research findings will ensure that JAS continues to be a premier resource for information in animal science.
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Footnotes |
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2 Corresponding author: jvasconcelos2{at}unl.edu
Received for publication January 9, 2008. Accepted for publication March 1, 2008.
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LITERATURE CITED |
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TopAbstractINTRODUCTIONDEFINITIONSCONTRIBUTIONS TO UNDERSTANDING...FUTURE EFFORTS AND CONCLUSIONSLITERATURE CITED |
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