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Weimer et al., 1991

a True growth yield (g cells/g substrate consumed) calculated in the absence of maintenance. b Maintenance coefficient (g substrate consumed/g cells/h).

a True growth yield (g cells/g substrate consumed) calculated in the absence of maintenance. b Maintenance coefficient (g substrate consumed/g cells/h).

E. Microbial Contributions to Rumen Dysfunction

Under some conditions, the normal ruminal microflora contribute through their activities to certain metabolic diseases (i.e., diseases that are neither infectious nor degenerative and that are preventable by proper feeding and management).

1. Lactic Acidosis

Lactic acidosis is an acute acidification of the rumen resulting from the microbial overproduction of lactic acid (Owens et al., 1998). The condition is often acute in feedlot-finished beef cattle, but subclinical acidosis is also common in high-producing dairy cows (Ostergaard and Sorensen, 1998; Owens et al., 1998). fed diets high in grains, particularly following a switch from diets higher in fiber content. These concentrates are rich in starches and have a relatively poor buffering capacity. The starches are fermented rapidly to lactic acid, primarily by S. bovis, a normal rumen inhabitant. At near-neutral pH, S. bovis produces primarily formic and acetic acids and only small amounts of lactic acid, but during rapid growth carries out a homolactic fermentation producing the D-isomer. The explosive growth of S. bovis outpaces the activities of ruminal lactate consumers (e.g., S. ruminantium, M. elsdenii, as well as some protozoa). As a result, lactic acid levels may increase from normal values of under 1 mM, to reach 20-300 mM. Because the acidity of lactic acid is 10-fold greater (pKa = 3.8) than for the VFAs—acetic, propionic, and butyric acids—(pKa = 4.7-4.8), ruminal pH may drop to 4.5 or below. At high lactic acid concentrations, blood and body tissues attempt to restore proper osmolality to the rumen, leading to a systemic dehydration that may be fatal.

Once acidosis has begun, several factors conspire further to exacerbate the problem (Russell and Hino, 1985). When pH has declined sufficiently, S. bovis maintains its homolactic metabolism even as its growth rate decreases. Reduced pH also inhibits degradation of lactate by S. ruminantium and M. elsdenii and establishes a ruminal niche for other homolactic fermenters such as the facultatively anaerobic lactobacilli.

Even in nonfatal cases, animal health is severely affected. D-lactic acid is absorbed into the bloodstream where it is metabolized more slowly than is the L-isomer. As a result, blood pH decreases and pathologies of other tissues become important (ulceration of the ruminal wall, liver abscess, and foot disorders) (Nocek, 1997; Owens et al., 1998). Low ruminal pH also negatively affects milk production and live weight gain, fiber digestion is inhibited, and feed intake is reduced (Van Soest, 1994).

2. Foamy Bloat

Foamy (or frothy) bloat is an acute condition resulting from formation of a rigid, persistent foam mat at the ruminal liquor surface that prevents normal eructive release of fermentation gases (Clarke and Reid, 1974). It is particularly common in pastured dairy cattle grazing certain lush feeds, especially some legumes (clovers and alfalfa). Gas accumulation results in substantial distension of the reticu-lorumen. In severe cases, this distension can interfere with respiratory function and produce death within an hour of feeding unless strong remedial action (i.e., puncture of the ruminal wall) is taken. Even in cases of mild bloat, dairy production and animal weight gain may be affected substantially because of reduced feed intake.

Plant factors that have been suggested as contributing to induction of bloat include (a) a high content of certain constituents that may contribute to the structure of the foam mat (soluble proteins, pectin, saponins, or certain classes of lipids) and (b) a high rate of fermentation (usually related to high concentration of soluble sugars and an easily digested cell wall). The amount and characteristics of the plant protein appear to be particularly important. Forages containing high levels of condensed tannins (e.g., birdsfoot trefoil) do not cause bloat, and feeding of condensed tannins usually prevents bloat, apparently because of their capacity to precipitate proteins (Tanner et al., 1995). Animal factors are also involved in bloating; there is a clear genetic predisposition toward bloat resistance and bloat sensitivity (Morris et al., 1997). Recent evidence suggests that bloat-resistant cattle have higher levels of bSP30, a salivary protein of unknown function (Rajan et al., 1996).

The involvement of microbes in bloat is controversial (Clarke and Reid,

  1. Microbes certainly are involved to the extent that the ruminal fermentation is responsible for production of methane and carbon dioxide gases and the acids that reduce the ruminal pH and cause release of carbon dioxide from the ruminal bicarbonate pool. More direct roles of individual species of bacteria and protozoa have been difficult to establish. However, microbial involvement is suggested by two lines of evidence: (a) bloat is routinely and effectively inhibited by controlled release of monensin into the rumen (Cameron and Malmo, 1993) and (b) complete switching of ruminal contents between fistulated cattle having a high or low susceptibility to bloat results in a change of susceptibility that is maintained for approximately 24 h before the animal's natural susceptibility or resistance reasserts itself (Clarke and Reid, 1974).
  2. Polioencephalomalacia

Polioencephalomalacia (PEM), also known as cerebrocortical necrosis, is an acute toxicosis that causes destruction of tissues of the central nervous system. It manifests itself in the form of lethargy and sometimes blindness that progress to muscular tremors and coma, with death following within a few days. PEM has been attributed to a thiamin deficiency that may result from elevated levels of thiaminases. More recent data indicate that, in many instances, the condition results from conversion of ingested sulfates to highly toxic hydrogen sulfide (H2S) by sulfate-reducing bacteria (Gould, 1998) (see Sec. IV.D). Sulfate is not normally a component of dairy rations, but it can be present in high concentrations in some groundwaters and surface waters used for watering stock, particularly in the western United States where the disease was first described and is especially common.

F. Microbes in the Causation and Mitigation of Plant Toxicoses

Many wild forages (and a few cultivated ones) contain compounds that have the potential to poison ruminants (James et al., 1988). In some instances, the toxicosis occurs as a result of microbial conversion of a nontoxic plant constituent to a toxic form. Alternatively, microbes may be involved in detoxifying a poisonous agent in the ingested plant. Specific microoganisms have been identified in three different toxicoses: grass tetany, oxalate poisoning, and mimosine poisoning.

1. Grass Tetany

Grass tetany is a type of hypomagnesemia observed in ruminant animals grazing lush pastures, most commonly during periods of cool, cloudy weather in the spring and autumn. Several clinical forms of the disease have been reported (Lit-tledike et al., 1983). Symptoms of the most common type include nervous and

Figure 10 Ruminal metabolism of trans-aconitate, a common component of some forages that is thought to be involved in eliciting grass tetany. The reduced intermediate tricarballylic acid can chelate Mg and is a potent inhibitor of the enzymatic conversion of the tricarboxylic acid cycle intermediate cis-aconitate. Some ruminal bacteria can degrade tricarbyllate to acetate, but only slowly. (From Russell and Forsberg, 1986.)

Figure 10 Ruminal metabolism of trans-aconitate, a common component of some forages that is thought to be involved in eliciting grass tetany. The reduced intermediate tricarballylic acid can chelate Mg and is a potent inhibitor of the enzymatic conversion of the tricarboxylic acid cycle intermediate cis-aconitate. Some ruminal bacteria can degrade tricarbyllate to acetate, but only slowly. (From Russell and Forsberg, 1986.)

excited behavior followed within hours or days by strong convulsions that may lead to coma and death. Several causes of magnesium deficiency have been put forward, including inhibition of Mg uptake by K and formation of MgNH4PO4 precipitates. Alternative, more feasible explanations revolve around trans-aconi-tate (TAA) (Russell and Forsberg, 1986). This compound, an isomer of the tricarboxylic acid cycle intermediate c/s-aconitate, represents up to 7% of the dry weight of some grasses. Although it is itself a potent chelator of Mg2+ in vitro, TAA is also reduced by some ruminal microbes (particularly S. ruminantium) to tricarballylate. This compound is readily absorbed into the bloodstream and acts as both a strong chelator of Mg2+ and as a structural analog of citrate that inhibits the enzymatic conversion of citrate to isocitrate, a key reaction sequence of the oxidative tricarboxylic acid (TCA) cycle (Fig. 10). At least one ruminal bacterium, Acidaminococcus fermentans, can detoxify TAA by stoichimetric conversion to acetate (Cook et al., 1994).

2. Oxalate Poisoning

Oxalate is widely distributed in plants and in some wild forages (e.g., halogeton) and may comprise several percentage of dry weight. Because oxalate is a potent chelator of calcium (and to a lesser extent magnesium), ingestion of these forages can cause hypocalcemia. Oxalate can be metabolized by a dismutation reaction

carried out by Oxalobacter formigenes, a nutritionally specialized gram-negative bacterium unable to use other substrates as energy sources (Allison et al., 1985).

3. Mimosine Poisoning

Mimosine, a nonprotein amino acid, is present in some tropical forages, particularly the shrub Leucaena leucocephale. In the rumen, the pyrridone group of the compound is released and metabolized to the toxic goiterogen 3,4-dihydroxypyri-dine. Resistance to mimosine poisoning is dependent on the ruminal bacterium Synergistes jonesii (Allison et al., 1992). This species has been found in goats from Hawaii and Indonesia, and it has been successfully transferred to ruminants in Australia (Jones and Megarrity, 1986) and the United States (Hammond et al., 1989) where it also confers resistance to mimosine poisoning. In the latter case, the bacterium was maintained in the rumen over a winter during which Leucaena was not fed in the diet of the host cattle; maintenance probably resulted from the bacterium's ability to compete successfully with the native microflora for arginine and a few other amino acids that can serve as growth substrates for this nutritionally specialized bacterium. S. jonesii is unique among ruminal bacteria in that it exhibits a specific geographical distribution.

G. Potential for Altering the Ruminal Fermentation and the Composition of Milk

The ruminal symbiosis has developed over eons in response to selective pressures on both the animal and the ruminal microflora (Van Soest, 1994). The high levels of production achieved in the animal industry have come in part by the use of feeding and management strategies that have placed new challenges on the rumi-nal microflora (e.g., feeding of starches that induce lactic acidosis). Numerous proposals have been put forward to ''improve'' the ruminal fermentation. These proposals have aimed at one or more objectives: (a) increase the rate and extent of digestion of fiber, (b) improve nitrogen availability (either by decreasing the rate and extent of degradation of feed protein or by improving microbial protein synthesis), (c) redirect the microbial fermentation to enhance the amounts or ratios of products that serve as precursors for milk or meat, and (d) detoxify feed or forage components. The microbial ecological principles associated with such proposed alterations have been reviewed by Weimer (1998).

Increasing the rate and extent of fiber digestion is complicated by the nature of the plant cell wall (see Sec. IV.D.1). Introduction of enhanced fibrolytic capabilities by genetic engineering has been touted as a means to improve fiber digestion (Russell and Wilson, 1988). Under normal conditions, cellulose digestion in the rumen appears to be limited by cellulose accessibility and not by properties of the microflora (Waldo et al., 1972; Van Soest, 1973). However, under conditions of low pH most fibrolytic species—particularly the cellulolytics—have lim ited activity. Introduction of fibrolytic activities into acid-tolerant but nonfibro-lytic species may be a viable route to improve fiber digestion as long as the introduced organism can maintain itself in the rumen both at low pH (when competition for fiber may be minimal) and at more normal pH (when competition for fiber would be more intense). A second approach to enhancing the ruminal digestion of fiber involves improvements in plant breeding to produce plant varieties having cell wall structures of improved digestibility (Buxton and Casler, 1993).

Reducing the ruminal degradation of feed protein can be accomplished by a variety of means, including chemical (formaldehyde) or physical (heat) treatment or incorporation of tannins into the diet (Broderick et al., 1991). Alternative means of controlling the microbes—either reducing their proteolytic activity or increasing microbial growth yield—have shown little promise to this point.

Controlling the ratios of fermentation endproducts is already exploited in the beef industry through the use of monensin and other ionophores. These compounds are more effective against gram-positive than gram-negative bacteria. Because these groups contain some of the more notable producers of acetate and propionate, respectively, treatment with monensin has several effects, including increasing ruminal propionate and decreasing ruminal acetate and the acetate/ propionate ratio. This effect, along with an increase in intake, lead to improved gluconeogenesis, feed efficiency, and body weight gain in beef animals (summarized by Goodrich et al., 1984). Effects in heifers have been more equivocal, although monensin does significantly decrease the age at breeding and at calving (Meinert et al., 1992). The opposite strategy to shift the fermentation balance toward acetate production may be useful for dairy animals, as the reduction in ruminal acetate/propionate ratio that occurs in some diets is associated with an undesirable reduction in milkfat levels (Shaver et al., 1986; Woodford and Murphy, 1988; Klusmeyer et al., 1990).

There is considerable interest in redirecting ruminal H2 away from production of methane and toward acetate (Mackie and Bryant, 1994). Although this has not been accomplished practically, recent evidence suggests that yeast may enhance the competitiveness of acetogenic bacteria for H2, although this effect has to this point only been demonstrated in vitro at H2 concentrations well above those found in the rumen (Chaucheyras et al., 1995). Yeasts are an example of a direct-fed microbial agent (or probiotic, a natural strain of microbe that improves digestive function). Incorporation of some yeasts and fungi into ruminant diets improves fiber digestion and milk production (Williams et al., 1991; Wohlt et al., 1991), although the mechanism remains unclear (Martin and Nisbet, 1992). Bacteria may also be useful as probiotics. For example, it has been shown recently that lactic acidosis can be avoided in sheep abruptly switched to a grain diet if the lactate-utilizing bacteria S. ruminantium and M. elsdenii are fed as a probiotic (Wiryawan and Brooker, 1995). The use of probiotics in the dairy industry is expanding, although they have not assumed the same status as in the poultry industry, where bacterial probiotics are widely used to prevent colonization of young chicks with Salmonella infection.

As discussed (see Sec. IV.F.3), implantation of mimosine-degrading bacteria has been proven to confer resistance of ruminant animals to mimosine toxicity. Once established in an animal, these bacteria apparently can be readily transferred to other herd members through normal close contact (Quirk et al., 1988). The probiotic use of other detoxifying organisms holds promise for more productive utilization of toxigenic forages in ruminant diets.

Several milkfat components that have been implicated in having the ability to prevent or reduce the incidence of cancer. Two of these components, butyrate and conjugated linoleic acid, are produced primarily by ruminal bacteria. Butyrate is produced by many common ruminal bacteria (see Table 5). It is maintained at concentrations of several millimolar in the rumen and is efficiently absorbed across the ruminal wall. Among its various metabolic fates is its incorporation into milkfat, where it accounts for 7.5-13.0 mol% of the fatty acids (Parodi, 1996). Butyric acid has been demonstrated to have a variety of anticarcinogenic activities (Parodi, 1996), and its production in the colon of humans on high-fiber diets has been implicated in reducing colon cancer (Mclntyre et al., 1993).

Conjugated linoleic acids (CLAs) are a class of isomers of linoleic acid having conjugated double bonds. CLAs, of which milk fat is the richest natural source, have been reported to have anticarcinogenic, antiatherogenic, and immu-nomodulating activities (reviewed by Parodi, 1996). The most abundant CLA isomer, cis-9, trans-11-octadecandienoic acid, is produced as an intermediate compound in the hydrogenation of linoleic acid by the ruminal fibrolytic bacterium B. fibrisolvens (Kepler et al., 1966). This synthetic activity is in accord with the higher levels of milk CLAs observed in pastured cows whose diets are particularly rich in fiber (Dhiman et al. 1996; Kelley et al., 1998). It appears that CLAs can also be produced by the gut microflora of monogastric animals, as normal rats contain higher amounts of CLAs in their tissues than do germ-free rats (Chin et al., 1994). The higher levels of the linoleic acid substrate that are present in the rumen, purportedly due to hydrolysis of the ruminal bacteria themselves, are thought to explain the unusually high production of CLAs by ruminant animals (Chin et al., 1994).

H. Fermentations in the Hindgut

Hindgut fermentations received very little attention until development of intestinal cannulae permitted quantitative studies. It was long assumed that the extent of digestion that occurs in the hindgut is only a small fraction of that of the total tract. However, the fraction of total tract digestibility that occurs in the hindgut varies with several factors, particularly feed intake (Tamminga, 1993). In cattle fed at high intakes, up to 37% of the total energy digestion can occur in the cecum and large intestine (Zinn and Owens, 1981). Digestion in the hindgut should be of greater importance in high-producing ruminants, which in general have both high levels of feed intake and ruminal pH values sufficiently low to depress fiber digestion and some other microbial activities in the rumen. The microbiology of the hindgut fermentation in ruminants has not been extensively explored, but in many respects probably resembles that of monogastric animals.

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