Haemorraghic Bowel Syndrome (HBS) has become more and more prevalent on dairies. HBS is characterized by sudden death of afflicted animals, often with little or no sign of health problems. Upon autopsy, animals show signs of severe bleeding in the small intestine.
The cause of HBS is unknown; however, some evidence suggests this is a multifactorial problem. Several predisposing conditions may need to combine before a problem erupts. These conditions include acidosis and high levels of starch reaching the small intestine. Their interactions are examined in the following article.
Prevention is the preferred course of action, as treatment is seldom successful. A number of nutritional interventions are possible; these are detailed in the article.
Source: International Dairy Topics #3 2005
It is a true balancing act to provide proper nutrition to high producing dairy cattle while also keeping their digestive systems healthy. Dairy cattle can experience stress at freshening, during environmental changes, with changes in grouping, and when rations change. Stress can trigger digestive problems. Poor intake and inconsistent eating patterns often result in more rumen acidosis. Higher ration energy density can help cows obtain the energy they need for high milk production. But, high energy diets generally result in more rumen acidosis. In the last 10 years, there has been an increase in the number of sudden deaths on dairy farms, particularly due to haemorrhagic bowel syndrome. This has caused nutritionists and veterinarians to begin focusing more attention on intestinal health as well as rumen health. Rumen acidosis (chronic acidosis) occurs when the pH of the rumen drops below 5.6. When the rumen microbes ferment feed, they produce acids. If this acid builds up, rumen pH drops and inhibits microbial growth. At low rumen pH, the concentration of hydrogen ions outside the rumen microbes increases and hydrogen ions leak inside the microbes. In order to maintain near neutral pH within their cells, the microbes must expend additional energy to get rid of the hydrogen ions.
This process results in less energy available for the microbes to use to grow. Those microbes that ferment fibre are especially affected. Intake declines and becomes variable, fibre digestibility is reduced, and rumen microbial protein production is limited by rumen acidosis. Cows typically have diarrhoea and are lethargic. Metabolic acidosis (systemic or acute acidosis) occurs when rumen pH drops below 5.2 and the cow’s blood becomes acidic (below a pH of 7.35). Just like the rumen microbes, the cells of the cow’s body do not work as well in acid. The activity of body enzymes is also negatively affected by low blood pH. Acidic blood cannot carry as much oxygen. The cow’s feet, being at the farthest points of the cow’s body, receive the least oxygen. This results in swelling of the feet. Endotoxins produced in the rumen also promote the release of histamines that further contribute to swelling and inflammation. Pressure between the hoof wall and bone inside results in the pain, haemorrhages, and ulcers associated with laminitis. Laminitis is defined as an inflammation of the sensitive tissues (lamellae) that are located in between the outside wall of the hoof and the coffin bone (on the inside).
Causes and prevention
The rumen microbes ferment starches and sugars to form volatile fatty acids(VFA), primarily propionate. VFA’s are absorbed from the rumen and used as a source of energy by cows. Excessive accumulation of propionate in the rumen reduces pH and encourages the growth of lactate producing microbes. Abrupt increases in grain intake also result in more lactate production. Lactate is a stronger acid. Its accumulation in the rumen further reduces pH, resulting in rumen acidosis. It is not only the amount of dietary starches and sugars that affects rumen acid levels but also the type of starch and processing. At the same level of total dietary starch and sugar, one ration containing a large amount of sugars and fast fermenting starches such as barley, high moisture corn, or bakery product may result in acidosis, whereas a ration containing a more slowly degradable starch like cornmeal may not. Heat and pressure make starches more rapidly fermentable. For high energetic efficiency, a high extent of starch availability is desired but a slow rate of availability helps with acidosis control. Starch intake can be controlled by substituting products such as soy hulls, beet pulp, and wheat midds for starchy feeds. These feeds contain more soluble fibre and create less rumen acid. Providing adequate soluble and rumen degradable protein in the ration to ferment in conjunction with starch will also help to increase microbial protein production and reduce the formation of acid in the rumen. It is the accumulation of acid in the rumen that is the problem. Volatile fatty acids are absorbed from the rumen via the rumen papillae.
The rumen papillae of dry cows are reduced in size and absorptive capacity because little or no grain is typically fed during the dry period. Slowly increasing dietary starch and sugar over the three weeks before and three weeks after freshening will help control the increase in acid production to a rate more similar to the growth rate of the rumen papillae. Fibre counteracts the acid produced from the digestion of starches and sugars by its own intrinsic buffering capacity as well as by stimulating saliva production to buffer the rumen. Cows regurgitate and chew fibre to produce saliva. It has been estimated that cows make over 3kg of the buffer (like sodium bicarbonate) each day. Fibre also stimulates the movement of rumen contents to increase the absorption of acid out of the rumen. It is generally recommended that 15%of the particles in the diet should exceed 1.5 inches (3.8cm) in length.
Additives for acidosis control
- Yeast and microbial products
Studies have shown that yeast products can increase the growth of lactate utilising bacteria to stabilise rumen pH and enhance microbial growth. These products also provide co-factors such as B vitamins, enzymes, and isoacids that may further stimulate growth of the rumen bacteria. Live yeast cells may also use up any oxygen present in the rumen and consume lactate, helping to stimulate rumen bacterial growth. Yeast products have been found to be especially helpful during times of dietary change and intake fluctuation. Researchers at the University of California found that dairy cows that were fed a yeast product maintained their normal eating pattern until a time closer to calving (seven days rather than 10 days prepartum) and then regained a normal eating pattern sooner after calving (14 days rather than 20 days postpartum).
Buffers, such as sodium bicarbonate (Bicarb) or sodium sesquicarbonate (Scarb), can be added to rations. Buffers can help to increase and stabilise dry matter intake, in-crease rumen microbial protein production, and improve fibre digestion. Their inclusion rate is generally at 1-1.5% of the ration dry matter.
Sudden death syndrome
Many sudden deaths that occur in cows are associated with digestive problems. With sudden death syndrome, cows having no previous signs of illness usually die at night with no signs of pain or struggle. Acidosis, bloat, endotoxaemia, and enterotoxaemia may all be involved in sudden deaths. Unfortunately, no one has all the answers to this problem but it seems reasonable to associate some sudden deaths with the growth of undesirable organisms.
Normally, concentrations of glucose in the rumen are low. Researchers have found, however, that glucose concentrations can be higher when acidotic conditions exist in the rumen. It is not known if this is simply the result of a fast breakdown of dietary starch or if the microbes reduce their usage of glucose during acidosis. Some undesirable microbes such as coliforms and amino acid degrading microbes grow better on glucose and release endotoxins. Endotoxins are part of the cell wall of Gram negative bacteria like coliforms. They are released when the bacteria die and then they go into the animal’s bloodstream. The toxins can cause blood clots to form, interrupt blood flow to organs, and decrease blood pressure. Endotoxins can cause blood acidosis, shock and death. Coliforms have been associated with sudden death in cattle.
Haemorrhagic bowel syndrome
In the last 10 years haemorrhagic bowel syndrome (HBS), also known as haemorrhagic jejunal syndrome (HJS), acute haemorrhagic enteritis, clostridial enterotoxaemia, overeating disease, and dead gut, has become a greater concern in regards to sudden death of both dairy and beef cattle in the US. A 2002 US Department of Agriculture survey found that over one third of large dairy farms (500 cows) had at least one case of HBS in the previous five years. Reports indicate that the frequency of the problem is increasing in the US. Since the fatality rate of cows with HBS has been estimated at 85%, HBS is an economic concern even when the incidence rate is low. Cows that show no signs of previous health problems die within 24 to 36 hours. Cows may show signs of abdominal pain and may have either constipation or bloody diarrhoea. Early postmortem examination of cattle with HBS shows intestinal lesions with haemorrhages and clots that block the flow of ingested feed. Death is the result of the obstructed bowel, blood loss, as well as the resulting anaemia.
Overeating disease or enterotoxaemia in sheep is generally thought to be caused by Clostridium perfringens Types C and D. The 7-way vaccine given to cattle is designed to protect against Blackleg and Blackleg type disease as well as Clostridium perfringens Types B, C, and D. Despite widespread usage of this vaccine, some researchers question its value for controlling HBS in cattle. Vaccinated animals have died of HBS with acute Clostridium perfringens infections. Using new laboratory techniques, some researchers have concluded that Types B, C and D might not be involved in many HBS cases. Researchers have cultured intestinal contents soon after death of cows having HBS and found large numbers of the bacteria called Clostridium perfringens Type A. These bacteria normally occupy the cow’s intestine. They generally divide slowly and cause no problems. It is thought that problems can occur when these organisms suddenly grow very fast and produce toxins that facilitate the production of intestinal lesions. Clostridium perfringens Type A will grow very fast if it has the nutrients to do so and the environment is right. These bacteria are able to break down starch. If a large amount of starch reaches the intestine and intestinal pH changes, this can trigger growth. If a cow consumes a large meal, the motility of the intestinal tract may be slowed.
This situation may also increase growth of the bacteria. Researchers have found a positive relationship between rumen acidosis, which facilitates the passage of more starch to the cow’s intestine, and HBS. Although many scientists have found Clostridium perfringens Type A in cows with HBS, with one study finding it in 85% of the cases examined, it is not known if it is the primary cause of the disease or if it grows as a secondary response to something else. One group of scientists has associated HBS with feeding mouldy forage or grain. They found higher levels of Aspergillus fumigatus, a common soil microbe, in the blood of cows with HBS, but they did not show that mouldy feeds directly cause HBS. A different initial cause of HBS, such as a nutritional issue that allows intestinal haemorrhaging, may increase the bloodstream load of Aspergillus fumigatus spores, which then cause bloodstream infections. Natural solutions for controlling sudden death syndrome include:
When feeding high producing dairy cattle, we must not forget the basics of making sure acidosis is controlled, feeding is consistent, grain kernels are being digested in the rumen, and mouldy feed is not fed. If the nutrition theory is correct, subclinical rumen acidosis is likely one of the main causes of sudden death syndrome. Many times simply adding more effective fibre, reducing overall starch levels in the ration, and more carefully and accurately mixing the ration can significantly reduce problems. It is interesting that dietary manipulation has been shown to reduce the shedding of coliform in cattle manure. Escherichia coli O157:H7 has been known to cause illness and death in humans who have consumed ground beef, fruits, vegetables, or water contaminated with cattle faeces. It has been found that increases in fermentation acids in the intestine of beef cattle and the resulting decreases in intestinal pH promote the growth of acid resistant E. coli that can better survive in the human digestive tract. When cattle were fed hay for one week before slaughter, their colons were less acidic and fewer acid resistant E. coli as well as fewer numbers of E. coli O157: H7 were shed in their manure.
We must recognise that even with good dietary management, high producing dairy cows digest a significant amount of ration nutrients in their intestines. This situation increases their risk of experiencing HBS. So, after taking all steps to control sub-clinical rumen acidosis, it may be beneficial to use microbial additives to improve the animal’s balance of intestinal bacteria as well as to bind the toxins potentially produced by undesirable bacteria. It may not be essential to know which organisms contribute to sudden death syndrome if the focus is on preventing the overgrowth of any undesirable organism and controlling the production of toxins and their damage. Feeding a direct fed microbial product composed of 10 billion CFU’s of lactobacillus bacteria in addition to mannan oligosaccharides appeared to reduce the incidence of HBS in some high producing dairy herds. Lactobacillus bacteria can survive through the digestive tract and have beneficial effects in the intestine. They have been shown to be particularly beneficial in humans and in young calves. Lactobacillus bacteria produce organic acids (like lactic and acetic acid) that lower intestinal pH and the oxidation/reduction potential to reduce the growth of undesirable bacteria. They also can produce specific proteins that can inhibit the growth of other bacteria. Lactobacillus bacteria have been found to reduce the numbers of salmonella, E. coli and Clostridium perfringens in laboratory cultures. Recent research has also shown that Lactobacillus acidophilus can reduce the shedding of Escherichia coli O157:H7 from feedlot calves infected with the organism. Lactobacillus bacteria may simply outcompete the undesirable bacteria in digestion rate and rate of attachment to intestinal villi. Lactobacillus bacteria can also change the form of intestinal bile to inhibit the growth of pathogens. Finally, lactobacillus bacteria have been known to reduce the level of amines. Amines can irritate the intestinal tract and cause diarrhoea.
Quicker defence response
Mannan oligosaccharides are fragments of yeast cell walls. The antigenic nature of mannans may stimulate antibody function so that when an animal is exposed to a pathogen challenge, the defensive response may be quicker and more effective. Many intestinal pathogens specifically attach to mannans and can be taken out of the intestine in this way rather than attaching to the intestinal wall to do damage. A Scandinavian research journal reported that a similar product called fructo-oligosaccharides prevented the growth of Clostridium difficile. The toxins produced by undesirable intestinal bacteria must be absorbed into the intestinal tract in order to do their damage. Mannan oligosaccharides may absorb and directly reduce toxin loads in the intestine by taking them out of the cow’s body. Mannan oligosaccharides have been very effective in improving health and performance of calves, turkeys, chickens, and pigs. Penn State University researchers found that mannan oligosaccharide supplementation in milk replacer for dairy calves improved faecal scores and reduced scours to the same extent as additional antibiotics in milk replacer. An organism called Lawsonia intracellularis often infects pigs and causes HBS problems.
In the USA, antibiotics are typically used to control these infections but some nutritionists have found that inclusion of mannan oligosaccharides in the diet can reduce the need for these antibiotics. The benefits of proper nutrition and microbial additives for digestive health are exciting. Research continues to be done on microbial additives. This will hopefully help everyone to be more confident about their usage in the future.