Nutrition has been identified as a major contributing factor to dairy cattle health status as related to multifactor diseases including rumen acidosis and laminitis. These conditions lead to low milk production, poor health and low reproduction (Ref…). Rumen acidosis is generally diagnosed when the level of rumen pH drops below the physiological range caused by excessive intake of rapidly fermentable carbohydrates and inadequate buffering (Ref…). Such conditions have long been recognized as contributing to the etiology of laminitis (Nocek, 1997), although the exact relationship between rumen acidosis and laminitis is not yet known. However, it is speculated that toxic substances released by bacteria in the rumen might play a role. Nocek (1997) described the pathogenesis of laminitis as a vascular disturbance in the corium of the hoof cause by vasoactive substances leading to corium degeneration and a breakdown of the laminar region associated with the dermal-epidermal junction. However, it is not yet clear how these substances are involved and whether they trigger laminitis or are just metabolites released during laminitis. One possible mechanism might be that toxic compounds are released from the rumen into the circulation (Nocek, 1997). These compounds then directly or indirectly trigger an intricate pathological response in the blood vessels in the corium of the hoof. This review paper will focus on the relationship of rumen acidosis, bacteria toxins and the etiology of laminitis in an effort to prove or disprove the theory.
Rumen acidosis and Laminitis
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Rumen acidosis is one of the most serious health problems facing the world wide dairy industry today (Ref..). It is believed to be caused by the ingestion of greater than normal quantities of ruminally fermented carbohydrates which are low in fiber. This ingestion of large quantities of carbohydrates increase milk production but also causes an increase in the growth rate of all bacteria. These events result in an increase level of volatile fatty acids (VFA) and lactic acids produced in the rumen with a concomitant decrease in rumen pH. These finding are supported by many studies (Gozho et al., 2007; Emmanuel et al., 2008; Zebeli et al., 2009, 2011; Pilachai et al., 2012) showed that increasing starch proportion in the ration related to a decline in rumen pH. In the study of Emmauel et al. (2008), Zebeli et al. (2009) showed that feeding dairy cows with 30% and 40% barley grain in the diets resulted in a decrease rumen pH below the physiological range (<6.0). This is in line with the study of Zebeli et al. (2011) that feeding diets containing >30% concentrate was associated with a decline in rumen pH below 6 from 8-12 h after morning feeding. Pilachai et al. (2012) also demonstrated that feeding with high amounts of concentrate rich in rapidly degradable starch (cassava and corn starch) induced a decline in rumen pH below 5.6 more than 6 h a day.
Rumen acidosis can be divided into two forms; sub- and acute (Enemark et al., 2002; Oetzel, 2003), although the two forms are similar in etiology, they are somewhat different clinically. Acute rumen acidosis is a condition in which the rumen pH depresses due to an accumulation of lactic acid in the rumen (Owens et al., 1998), while sub-acute rumen acidosis (SARA) is generally defined as periods of moderately depressed rumen pH, which are apparently due to the total accumulation of VFA alone and is not due to lactic acid accumulation (Oetzel et al., 1999). However, there is no agreement on which rumen pH depression specifically defines rumen acidosis primarily due to variability in techniques used in the diagnosis of the disease (Plaizier et al., 2008). Several rumen pH thresholds (e.g., 6.0, 5.8, 5.6, and 5.5) have been used to define rumen acidosis (Kleen et al., 2003; Krause and Oetzel, 2005; Plaizier et al., 2008). Currently, the definition of SARA (Gozho et al., 2005; Khafipour et al., 2009; Li et al., 2012; Pilachai et al., 2012) is the thresholds of rumen pH below 5.6 for at least 180 min/day. Therefore, this pH threshold will use to define rumen acidosis in this review.
It is generally accepted that laminitis has multiple causes with several potential factors primarily associated with the occurrence of laminitis to include rumen acidosis (Nocek, 1997; Ossent and Lischer, 1998), but the exact cause of laminitis is not known. However, it has been speculated that a prolonged acidic condition in the rumen accompanied by excessive intake of high rapidly fermentable carbohydrates is related in some way to the occurrence of laminitis (Bent, 1976; Nocek, 1997; Nagaraja and Titgeyer, 2007; Plaizer et al., 2008). This is in line with the study of Thoefner et al. (2004), who induced laminitis in heifers by way of an oral dose of 13, 17 or 21 g/kg of oligofructose, resulting in a decrease of rumen pH below 5.5 Four of the six heifers given oligofrustose developed signs of laminitis. Another study by Danscher et al. (2009, 2010) showed a decreased rumen pH below 4.0 and 4.3, respectively in heifers receiving 17 g/kg of oligifructose. In these studies, all eight heifers and nine of the ten heifers given oligofructose, respectively developed signs of laminitis such as hoof plain, weight shifting and lameness (Table 1).
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A recent study by Pilachai et al. (2012) demonstrated that feeding high amounts of concentrate rich in dietary starch (i.e. cassava and corn) and low roughage resulted in a decrease rumen pH below 5.6 for at least 6 h a day, with three of the four cows observed with clinical signs of laminitis. These results are consistent with the study conducted by our team (un-publish data), who found that rumen pH was below 5.6 at all time after feeding 10.5 kg DM of concentrate contained 40.3% of cassava meal and 1.5 kg of rice straw. Four out of the six test cows displayed marked reactions of weight shifting and swelling over the coronary band. Interestingly, rumen pH of those laminitis-animals decreased below 5.6 for several times a day while some of them had a pH lower than 5 (Table 1).
Table 1. Rumen pH, the occurrence of laminitis and dietary in experimental laminitis induction
Thoefner et al. (2004)
(0,13,17 and 21 g/kg BW)
Ranged pH of 6.0-4.5 Mean pH of <5.5
(Hoof pain and lameness score)
Danscher et al. (2009)
Mean pH of 4.3±0.07
Acute laminitis (Locomotion score, hoof test and weight shifting)
Danscher et al. (2010)
Rumen pH of <4.0
Acute laminitis, hoof test and weight shifting)
Pilachai et al. (2012)
Diet (F:C of 12.5:87.5)
Diet 1, 2, 3 and 4 contained 4.6, 18.3, 32.4 and 46.2% cassava meal, respectively
Mean pH of <5.6
(Weight shifting and coronary band evaluation)
R. Pilachai (un-publish data)
Diet (F:C of 12.5:87.5)
Diet contained 46.3% cassava meal
Mean pH of 5.06
(Weight shifting and coronary band evaluation)
Rumen acidosis and bacterial toxins
Generally, a high level of microbial toxins and toxic substances in the rumen fluid are usually observed during long episodes of low pH. Many studies (Andersen, 1994; Gozho et al., 2005; 2006; 2007; Khafipour et al., 2009a; 2009b; Pilachai et al., 2012) demonstrated that a low rumen pH was associated with the release of toxic substances such as endotoxin or lippolysaccharide (LPS) and histamine in the rumen fluid (Table 2). In a previous study of Andersen et al. (1994) found that increasing the amount of concentrate feeding from 3 to 6 kg/d lead to a drop in rumen pH from 6.5 to 5.7 however, the concentration of endotoxin increased from 118-1,599 EU/ml. In another study conducted by Gozho et al. (2005, 2006, 2007) found that reduced rumen pH <5.6 more than 181 h/d caused by reducing the roughage and concentrate ratios feeding resulted in elevated concentrations of LPS in the rumen fluid. In addition, Emmauel et al. (2008), Zebeli et al. (2009, 2011) demonstrated that increasing the proportion of grain barley more than 30% in the dairy rations suppressed rumen pH values to below 6.0, while the concentration of rumen LPS also increased. These are in line with the recent study conducted by Khafipour et al. (2009a, 2009b) which showed that the concentrations of LPS in rumen fluid increases 3.8 and 3.5 times during episodes of rumen pH lower than 5.6 at 279 and 505 min/d, respectively. Li et al. (2012) found that increasing the time where the rumen pH was below 5.6 (from 56.4 to 299 min/d), rumen LPS concentrations increased from 10,405 EU/ml to 168,391 EU/ml. Pilachai et al. (2012) also showed that when rumen pH falls below 5.6 at least 6 h/d, the concentrations of LPS in the rumen fluid was 40,300 EU/ml. These finding are supported by a recent meta-analysis conducted by Zebeli et al. (2012) demonstrated a negative relationship between daily mean rumen pH and the concentration of endotoxin (R2=0.38). This study indicated that when rumen pH was lower than 6 for more than 96.5 min/d the results were a linear increase in the level of endotoxin in the rumen fluid.
Table 2. Dietary characteristics, rumen pH and the concentration of lipopolysaccharide (LPS) and histamine in rumen fluid of the experimental induction of rumen acidosis cows