Acid indigestion

It is also known as ruminal acidosis, acute carbohydrate engorgement, rumen over load or lactic acidosis. Ingestion of large quantities of highly fermentable carbohydrate leads to the excessive production of lactic acid in the rumen of cattle, buffaloes, sheep and goat, and drop in ruminal pH. It is characterized by severe toxemia, dehydration, ruminal stasis, recumbency and high mortality rate.

Etiology: Most common cause of acid indigestion is accidental ingestion of highly fermentable feed such as wheat, barley or maize by animal to which they are not accustomed. Less common causative agents are bread, molasses, gur, grapes, apples and potatoes.

Pathogenesis: Finely ground or crushed grains are considered toxic, which exposes a larger surface area and starch component of grain to ruminal microflora. Ingestion of excessive quantity of fermentable carbohydrate change rumen microbes. There is an increase in the number of lactic acid producing bacteria Streptococcus bovis thus producing a large quantity of lactic acid, which decreases rumen pH (5 or less) causing destruction of cellulolytic bacteria and protozoa. Low pH permits the Lactobacilli to produce large quantity of D and L forms of lactic acid enhancing the ruminal osmolarity, thereby withdrawing water from the circulation to result in haemo-concentration and dehydration. At pH 5, there is ruminal stasis. Some strains of Lactobacilli in rumen produce histamine by decarboxylation of histidine. The neurological signs develop as a result of thiamine deficiency occurring due to thiaminase enzyme production by microorganisms. Renal blood flow and glomerular filtration rate decreases causing anuria. Chemical rumenitis is the result of high concentration of lactic acid. Animal may die at this stage by shock.

Clinical signs: The amount and nature of grains consumed by the animal determines the severity of the disease. It is more severe with the finely ground than the whole grains. Within few hours of grain engorgement, there is distended rumen, abdominal pain, and kicking at the belly. In mild cases, animal shows the signs of inappetance to anorexia. Animal is seen in the recumbency in severe form. There is staggering gait, absence of rumination and soft to watery faeces. Ruminal movements are sluggish or absent with increased and shallow respiration. Faeces may contain undigested grains. Absence of faeces and heart rate above 120/min  indicate poor prognosis. Animal is dehydrated and its body temperature is slightly elevated. There is laminitis resulting in stiff gait. Nervous signs consist of depression or coma. Apparent blindness may be seen in some animals. On auscultation of rumen, gurgling sounds may be heard. In early stage there is frequent urination but later on there is anuria. Pressing of head and grinding of teeth are shown by the affected animal.

Laboratory diagnosis: The rumen pH in ruminal acidosis varies between 5 and 6, sometimes less than 5, as against normal ruminal pH between 6.5 and 6.8. Microscopic examination of rumen fluid may reveal predominance of Gram positive bacteria, low concentration to complete absence of protozoa, reduced protozoal motility and absence of protozoal iodophillic activity. PCV (packed cell volume) rises to over 45 % demonstrating hemoconcentration. Urine is concentrated and acidic.

Diagnosis: Diagnosis is based upon the history of excessive consumption of concentrate ration. Severe cases may resemble hypocalcaemia but the later is associated with hard faeces and no marked dehydration. Diffuse peritonitis is accompanied by abdominal pain, leukocytosis and neutrophilia.

Treatment: Mild cases usually recover without treatment. Ruminal and systemic acidosis is required to be corrected and further production of lactic acid should be prevented. Restore fluid and electrolyte losses and rumen motility. Rumen lavage by infusing warm water and then siphoning out the rumen contents reduces the acid producing feed material. Rumenotomy may be required in severe cases. If rumen contents can not be emptied, administer several liters of water to decrease the rumen hypertonicity and treat with 20 to 50 million units of penicillin or 1 to 2 g neomycin or 2 to 4 g chloramphenicol orally to control the growth of lactic acid producing bacteria. The systemic acidosis can be corrected by giving 1.3 to 5% sodium bicarbonate solution intravenously. Cud transfer (5 to 8 liters of rumen fluid) may also be done to restore ruminal flora and fauna for early recovery. Alkalizers like sodium bicarbonate, magnesium oxide or magnesium hydroxide may be given to neutralize ruminal acidity. Antihistaminics should be given intramuscularly. Liver tonics, rumenotorics and thiamine may also be required. Water supply of the animal should be restricted for 12-24 h, if animal has ingested excessive grains but has not developed the symptoms.