Navrose Sangha* and Barinder Singh**
*Assistant Professor, Department of Veterinary Pathology, KCVAS, Amritsar, Punjab, India
**Graduate Assistant, Department of Veterinary & Animal Husbandry Extension Education, KCVAS, Amritsar, Punjab, India
Etiology
The most severe type of indigestion, acute rumen acidosis (also known as lactic acidosis, toxic indigestion, grain overload, rumen overload, and acute carbohydrate engorgement of ruminants) is brought on by consuming too much concentrate feed that is rapidly fermentable or by abruptly switching to a diet that contains more finely ground, quickly fermentable feeds, like maize or wheat. When feeder steers are put to whole concentration diets in feedlots as opposed to being gradually switched from high-roughage to high-concentrate feeds, clinical examples of this may take place. Thankfully, dairy cattle don’t experience this issue as frequently, but it has happened when owners have hastily switched to a different type of diet after running out of one. This has historically occurred when cattle owners moved them from pelleted grains with some fibre to finely ground maize or wheat grains, causing ruminal acidosis. Lactic acidosis (both D and L types) can also be brought on by the sudden introduction of highly fermentable small grain silage into the herd. Although it is uncommon in contemporary husbandry systems, rapid, unrestricted, inadvertent access to supplies of extremely appetising cereal grains can nevertheless happen. The outcome is evidence of the cattle’s gluttony and lack of judgement towards these feeds. When cattle are given grain-based silage that has fermented for less than two weeks, ruminal acidosis can also happen. Inadequate TMR mixing is another issue that can result in ruminal lactic acidosis in contemporary dairy management systems (Lorenz and Gentile, 2014). When this happens, feedstuffs used in the TMR may stratify, with cows at one end of the feed line receiving primarily roughage and those at the other receiving primarily high-sugar, high-starch concentrate. Lactic acidosis can also occur in cattle who overconsume grain after unintentionally acquiring access to grain bins. Both the quantity and kind of concentrate are crucial, but even a few pounds of a finely ground concentrate like barley could be hazardous if the cow’s rumen flora is not accustomed to the substance. Because management issues frequently come into play, the herd’s animals frequently exhibit symptoms. To comprehend the symptoms and implement logical treatment, it is imperative to have a fundamental understanding of the pathophysiology of ruminal and lactic acidosis. The easily fermentable, high-sugar, high-starch concentration is broken down into volatile fatty acids and both D- and L-lactic acid within six hours after consumption. The rumen is where the majority of this happens, while the lower GI tract may also produce a sizable amount of D-lactic acid. The D isomer remains and causes D-lactic acidosis, but the L isomer can be used quickly. One of numerous species that cause too much lactic acid production is Streptococcus bovis (Pitta et al., 2014). The pH of the contents of the rumen drops farther towards the acid range as more and more lactic and volatile acids are produced. The rumen pH may drop to 4.5 to 5.0 if there is a enough supply of fast fermentable starch substrate, which would kill most microorganisms except S. bovis. Rumen stasis happens when the lactate and histamine levels are extremely high. S. bovis persists at this low pH and exacerbates the issue by increasing lactic acid production. Rapid acid buildup causes the rumen to osmotically pull water in, drying the cow and promoting systemic L-lactate synthesis through improved anaerobic metabolism. Additionally, the rumen mucosa is harmed by chemical or acid rumenitis, allowing endotoxins and germs to escape into the portal circulation as well as plasma transudation into the rumen.
Clinical Signs
Affected cattle have increased heart rates (90–120 beats per minute) and respiration rates (50–80 breaths per minute), are completely off feed, produce significantly less milk, are dehydrated, and all of these symptoms. They typically have diarrhoea or loose dung, which frequently contains whole grains, a splashy, fully static, and expanded rumen, a chilly skin surface, and a subnormal temperature. Almost always, tachycardia, tachypnea, anorexia, and sadness are present. Animals with the condition are frail, ataxic, and occasionally supine. Cattle that have been badly affected have metabolic acidosis and peripheral acidemia due to dehydration, bicarbonate titration, hypotension, and high levels of D- and L-lactic acid in the rumen and blood (Gressley et al., 2011). Some of the neurologic symptoms and hypotension may be explained by cattle with significant ruminal acidosis having consistently high levels of rumen ammonia and histamine, respectively. Neurologic symptoms could potentially be brought on by abnormally high D-lactate concentrations or a reduction in rumen thiamine synthesis. There may be symptoms including abdominal pain, tachycardia, tachypnea, stumbling, recumbency, a sharp decrease in milk production, coma, and death.
Ancillary Data and Diagnosis
A thorough history of feeding in the herd is combined with clinical symptoms to make the diagnosis of severe ruminal lactic acidosis. A rumen pH of 4.5 to 5.0 will be found in acute cases when rumen fluid is sampled using a stomach tube, a percutaneous left flank puncture, or at necropsy examination in acute fatalities. It is important to note that due to the buffering properties of ingested saliva and plasma dilution of the rumen contents, cattle with severe ruminal acidosis that survive for 24 hours or more frequently have rumen pH values that increase to 5.5 to 7.0 (Ahmed et al., 2002).
Other laboratory assistance include neutropenia with a left shift in the hemogram, significant azotemia, and acid-base and electrolyte readings that frequently represent a metabolic acidosis. This is true even in cases where cows survive for 24 hours or longer after ingesting deadly amounts of grain. Increases in both D- and L-lactic acid cause the systemic acidosis and acidemia. When the causative concentration is present as complete particles in the diarrhoea or loose manure that is passed, this may provide as a clinical diagnostic signal.
Treatment
The veterinarian must decide whether medication therapy will be effective or if a rumenotomy is necessary because treatment is challenging. Additionally, if symptoms have been present for 24 hours or longer, the degree of rumen mucosal injury has already been established, and possible treatments may not have any effect. The therapeutic challenges increase when more than one cow is affected because the potential cost and time commitment of therapy are so great.
Treatment must address the rumen acidosis and make an effort to stop more lactic acid from being produced. If possible, a rumenotomy should be performed and the contents of the rumen evacuated in animals with a rumen pH of 5.0 or less, a heart rate greater than 100 beats per minute, dehydration greater than 8%, and rumen distension and recumbency indicating a severe grain overload. To eliminate as much lactic acid as possible, the rumen is next cleaned with water and repeatedly emptied. Laxatives, new hay in the rumen, rumen transfaunates, if available, parenteral calcium, and IV hydration treatment are used to treat the cow. Hypertonic saline should be the first IV fluid to be administered, followed by balanced electrolyte solutions like lactated Ringer’s solution. If the acidemia is severe (pH <7.15), more sodium bicarbonate should also be supplied (Kmicikewycz et al., 2015).
For the treatment of high prostanoid synthesis and shock, flunixin meglumine should be administered. There are a number of reasons why B vitamins should be given, one of which is that some calves with ruminal acidosis go on to develop polioencephalomalacia. For badly injured livestock, the outlook is not good. For those who survive the initial shock and systemic acidosis, inflammatory lesions in the rumen or microbiome disruption may prevent them from regaining their usual appetite, and they may also experience more severe consequences such liver abscesses and laminitis.
Animals with less severe symptoms and greater rumen pH levels, as well as those whose numbers make rumenotomies impractical, may try alternative therapies. One approach entails inserting a Kingman tube or large-diameter stomach tube and repeatedly flushing the rumen with warm water while using a bilge pump. For this treatment to be effective, it takes several flushes with 10 to 20 gallons of water, and the return flow of fluid must be efficient. After lavage, supportive calcium solutions and IV fluids are given as needed, along with antacids such 2 to 4 quarts of milk of magnesia, activated charcoal, and ruminotorics (Ducharme et al., 2017). Affected cattle shouldn’t be permitted to engorge on water because doing so will just cause their atonic rumen to expand once more. Long-stem hay and free choice water may be made available once rumen activity has returned. Another approach that has been done successfully is to just syphon as much rumen fluid as you can out of the mouth and then give the rumen 1 to 2 pounds of activated charcoal. This seems to work well at binding rumen poisons, like endotoxin. Additionally, sick animals should be given IV fluids that are isotonic and calcium solutions that are supplied by SC (Lean et al., 2014). In order to avoid bacteremia and the development of liver abscesses, cows with moderate to severe rumenitis are typically given penicillin (10,000–20,000 U/kg given intramuscularly [IM] or subcutaneously [SC] once daily for 3-5 days). Antibiotics with a broad spectrum should not be administered since they increase the risk of a fungal overgrowth.
Other therapies are experimental. They consist of antihistamines, stomach-tube-administered penicillin solutions to try and lower the amount of S. bovis organisms in the rumen, and roughage-only meals until the animals are well. Dr. Francis Fox has long advocated the use of subcutaneously injected antihistamines, and a 2014 paper by Golden et al. demonstrates that intraruminal histamine may be noticeably raised in cows with severe clinical ruminal acidosis. Cattle with severe ruminal lactic acidosis that make it through the acute phase and have their rumen pH return to normal are still at risk for complications from the underlying chemical rumenitis. In the following days, bacterial opportunists like Fusobacterium necrophorum may enter the areas of chemical damage, attach to the rumen wall, and cause a bacterial rumenitis that lasts 4 to 7 days. If these previously damaged areas have received intensive treatment with broad spectrum antibiotics or steroids, a mycotic rumenitis may develop. The injured rumen mucosa is invaded by bacterial and mycotic opportunists, who then climb the portal circulation and infect the liver, lungs, and other organs, causing fever and, in rare cases, death (Fubini et al., 2018). The majority of the time, antibiotic medication has little effect on fever brought on by mycotic illness. Seven to fourteen days following the onset of the initial clinical symptoms of lactic acidosis, embolic infections of the brain may result in strange neurologic symptoms.