SUBACUTE RUMINAL ACIDOSIS (SARA) IN COWS: CAUSES, CONSEQUENCES AND PREVENTION

Dr. R. Selvakkumar

M.V.Sc., Ph.D., Associate Professor
Department of Livestock Production Management
Veterinary College and Research Institute – Theni-625602

Cattle belong to Ruminant animals andare adapted to digest and metabolize predominantly forage diets. But a high grain diet is must for the high yielding animals to meet their huge requirement. High amount of grain diet with inadequate fibre portion will lead to ruminal acidosis. Acidosis is a condition during which the alkali is decreased in body fluids relative to the acid (hydrogen ion) content. Two forms of acidosis is

  1. Acute ruminal acidosis 
  2. Subacute ruminal acidosis (SARA) 

Acidosis can be present in different forms, ranging from acute life-threatening forms to sub-acute illness, which is difficult to detect. Sudden increase of grains with low fibre will lead to acute form of acidosis and gradual and prolonged use of high grain with low fibre will chronically affect the animal and result in Sub Acute Ruminal Acidosis (SARA). 

The ruminal pH of the animals affected by SARA will be reduced and this will affect the normal ruminal function and thus will result in impairment of production performance. Decreased efficiency of milk production, impaired cow health and high rates of culling are some consequences of SARA. Feedlot cattle and small ruminants are at risk of developing this condition. SARA can be easily preventable by excellent feeding management and proper diet formulation.

In acute ruminal acidosis the pH depression is more, clinical signs more prominent and is common in feedlots, whereas SARA is more common on dairy farms and in SARA the pH depression is apparently due to the total accumulation of volatile fatty acids alone and is not due to lactic acid accumulation. 

Rumen

The rumen is the largest of four compartments in the ruminant stomach. The rumen acts as a storage or holding vat for feed. It is also a fermentation vat and is the site of microbial activity.  Billions of microorganisms are present in ruminal contents consisting of bacteria, protozoa, and fungi. This microorganism needs a pH range between 5.8 and 6.4 for their normal function.  Volatile fatty acids (VFA) are the end product of rumen fermentation and they are utilised for milk production. The concentrations of VFAs within the rumen are regulated by a balance between production and removal via absorption. VFA is absorbed across the rumen wall, due to a differential gradient, with the pH of the blood being higher than the pH of the rumen.           

The VFA are passively absorbed by finger-like papillae that project away from the rumen wall. These papillae provide a huge surface area during the period of excess VFA production by increase in length. This will increase the surface area and absorptive capacity, which protects the animal from acid accumulation in the rumen. But, this physiological feature is not helpful during the sudden introduction of an easily fermentable carbohydrate rich diet in huge amounts.   

 SARA

For normal ruminal function, a pH between 6.0-6.4 is essential. Feeding of grain diet with readily fermentable carbohydrates that are rapidly broken down by ruminal bacteria, leading to the production of volatile fatty acids (VFA) and lactic acid. The imbalance between the production and absorption of VFA affects the ruminal pH. Sudden increase in the production VFA will result in depression of ruminal pH below 5.5-5.6.  

Prolonged use of grains with readily fermentable carbohydrate is characterized by extended periods of depressed ruminal pH below 5.5-5.6.  A lower pH means higher the acidity. For ideal ruminal fermentation and digestion, ruminal pH should lie between 6.0 and 6.4 is must. But, pH fluctuation is noticed immediately before and after feed is quite normal even in the cattle with a regular diet. Fluctuations of 0.5 to 1.0 pH units within a 24-hour period are common. This kind of fluctuation is only for short periods during the day and can be easily balanced.

The definition of SARA is based on a time period during which the rumen pH is below a certain threshold. Although, there is no general agreement on the pH threshold for SARA, the two main definitions indicate 5.24 hours below 5.8 (Zebeli et al., 2008) and 3 hours below 5.6 (Plaizier at al. 2008).  

Causes of SARA

  • Excessive carbohydrate feeding and low dietary fibre. Long fibre particles (> 4 mm) stimulate chewing activity and result in normal  saliva production. Saliva has a buffering effect in the rumen.
  • Excessive long and unpalatable feed causes the cow to consume a diet that is low in physically effective fibre (Oetzel, 2007).
  • Failure to adapt to rapid diet changes.  Rumen bacterial population and rumen papillae   need time to be ready to digest large amounts of carbohydrates and consequently to absorb large amounts of VFAs.

Cows in the following category are more prone to SARA  

  • Early lactation: During dry period, the pregnant  animals are fed with lower energy diets and the rumen bacterial population and  rumen papillae are adapted to this condition and face difficulty when the feeding regimen is changed from dry period to lactational ration.
  • Primiparous cows: These animals were never exposed to a lactation diet before and face difficulty like the above situation.
  • Heat stress: blood bicarbonate concentrations increase respiratory rate during heat stress and this will result in   decreasing ruminal buffer capacity of the animal.
  • Inappropriate ration calculation and management: wrong dry matter calculation,in wrong feeding management also a predisposing factor for SARA.

Pathophysiology of SARA

  • Decreased Ruminal pH favours the proliferation of  Streptococcus bovis  and thus will result in  shifts to lactate instead of VFA production. Lactic acid production at a very high rate that exceeds the rumen absorption capacity will further increase the acidity level in rumen.  
  • In subacute ruminal acidosis the number of bacterial species in the rumen is reduced due to the lower pH range. Further, protozoal populations are limited at lower ruminal pH.
  • Due to the Reduction of bacteria and protozoa population, ruminal microflora are  less able to maintain normal ruminal pH during periods of sudden dietary change.  
  • The ruminal epithelial cells are more vulnerable to the chemical damage by acids. Higher acidity of rumen may lead to rumenitis, as well as erosion and ulceration of the ruminal epithelium.  
  • Laminitis and subsequent hoof overgrowth, sole abscesses, and sole ulcers associated with SARA. These problems generally take   weeks or months to appear in affected cows.
  • Subacute or chronic laminitis has been described in SARA affected cows and the clinical signs are discoloration of the hoof, sole hemorrhages, sole ulceration and misshapen hooves.The  molecules like histamine, LPS and lactic acid, are released into the bloodstream during SARA and they  play an important role in the laminitis etiology, weakening the hoof tissue and predisposing the animals to lameness.  
  • Due to the excess production of VFA, receptors in ruminal epithelium send signals to the brain to reduce the rumen motility and end in ruminal atony.
  • Increased osmotic pressure inside the rumen due to the accumulation of organic acids and glucose will result in water flux towards the rumen. This is known as hydrorumen. In this condition animals show diarrhoea, which will complicate the hydroelectrolytic balance of the affected animal. Feces may appear foamy with gas bubbles and whole cereal grains as well as higher amounts of undigested fibre materials also noticed.

How to minimize/ Prevent SARA in cows:

  • For SARA, there is no specific treatment. Providing the cows, a balanced diet in terms of amount and degradability of carbohydrate and quantity and size of fibre. Feeding management plays a vital role in minimizing the risk of SARA. Adding of long-fiber particles in the diet decreases the risk of subacute ruminal acidosis by encouraging saliva production during chewing and by increasing rumination after feeding.
  • Diets should be formulated in such a way to provide adequate buffering, through appropriate feedstuff selection or addition of dietary buffers such as sodium bicarbonate and potassium carbonate. 
  • Proper distribution of small and large feed particles will result in a lower the possibilities of selective feeding.
  • Provide sufficient feeding space to avoid feed competition and the consumption of large meals.
  • Supplementing the diet with direct-fed microbials will enhance lactate use in the rumen and decrease the risk of subacute ruminal acidosis. Yeasts, Propionibacterium, lactobacilli, and enterococci have been used for the above purpose.