मवेशी में जीर्ण और अर्धजीर्ण रयूमि‍नल एसिडोसिस

Ruminal acidosis is a fermentative disorder of the ruminants in which the ruminal pH decreases below the normal range. The condition is usually associated with the ingestion of large amounts of highly fermentable starch rich feeds. Feeding high grain diets to the dairy cows by the farmers for maximum milk production increases the risk of acidosis which can reduce milk production and affects the health of the cow.

The nature of ruminal acidosis ranges from life-threatening peracute forms to subacute chronic illness. In peracute cases severe metabolic acidosis and toxaemia may occur leading to recumbancy, coma and death within few hours.

Acute ruminal acidosis is a serious condition, occurs quickly and characterised by the anorexia, abdominal pain, rapid breathing, diarrhoea, dehydration, ruminal hypotony, staggering, recumbancy and severe depression in ruminal pH. The subacute form is less intense but more common in the herd.

During subacute ruminal acidosis the pH depression is slight and the clinical sign are poorly expressed which may go unnoticed for longer. The subacute cases has long-term devastating health and economic impacts to the dairy farmers due to reduced feed digestibility and absorption, reduced milk yield and fat percentage, weight loss, lameness and various other health complications so the periodic monitoring of the herd is necessary for early diagnosis.

The acute acidosis, in addition to the above losses, may pose immediate threat to the survivability of the animal.

Cause and Pathogenesis of Ruminal acidosis

The acute form of acidosis is also called grain engorgement or ruminitis or ruminal lactic acidosis and generally occurs due to sudden ingestion of large amounts of highly fermentable starch rich feeds. In acute form of ruminal acidosis the ruminal pH generally reaches below 5.2 due to accumulation of lactic acid. In case of subacute ruminal acidosis the low ruminal pH is caused by excessive accumulation of volatile fatty acids (VFAs) without persistent lactic acid accumulation and is mostly restored by the animal's own physiological response but its repeated occurrence makes the animal susceptible to acute ruminal acidosis. When the ruminal pH stays in the range of 5.2 and 6 for a prolonged period of time it is categorised into the subacute ruminal acidosis.  

The different causes of the ruminal acidosis generally includes feeding of high concentrate and low roughage diet, shifting from high forage to high concentrate diet i.e. feeding of comparatively high grain diets to dairy cows which are adapted mainly to forage diets, feeding very finely chopped forage, diet composed of highly fermented feeds and high moisture content. Grains like wheat and barley are more fermentable than corn and sorghum. Grain processing improves starch ruminal degradation and consequently increases the incidence of acidosis. Increased environmental temperature also poses threat to ruminal acidosis.

Ruminoreticulum consists of numerous microbes including interdependent population of bacteria, protozoa and fungi. These microbes cause anaerobic fermentation of the carbohydrate to form volatile fatty acids (VFA). The population of different ruminal microbe increase or decrease with the quantity and quality of feed. Different microbes require different optimum pH for their activity in rumino – reticulum and proliferate more near their optimal pH such as cellulolytic bacteria require pH 6.2 or more, lactate producing bacteria like Streptococcus bovis and Lactobacillus spp proliferate at pH below 5.8 and flourish fastly when ruminal pH dips below five.

During the anaerobic fermentation of the carbohydrate, lactic acid is an intermediate product formed transiently and in low concentration. Lactate utilising propionate bacteria utilises the lactic acid to produce propionate. An abrupt feeding of large quantity of easily digestible starch rich diet like wheat and barley or other cereal grains leads to the rapid proliferation of amylolytic bacteria which causes the production of large amount of lactic acid. Lactic acid is several times much stronger acid than VFA.

Ruminal protozoa feed on starch as well as ruminal bacteria and try to curb their over proliferation but lowered ruminal pH (below pH 5.5) is hostile to protozoa and fungi and populations of these microbe fall precipitously. Rapid accumulation of lactic acid in the rumen causes decrease in ruminal pH which further provides more favourable environment to the lactate producing bacteria to populate and a vicious cycle starts in the rumen resulting in ruminal acidosis which may lead to systemic acidosis and the condition is called carbohydrate engorgement or grain overload.

Such type of dietary shift initially causes increase in total VFA production so the pH of the rumen tends to decrease. This causes activation of ruminal receptors leading to decrease in ruminal motility so as to adjust the rate of VFA production. But the decreased motility results in decreased rumination and saliva production. Saliva contains the bicarbonate buffer which is important in maintaining normal ruminal pH. The pH of the rumen varies depending on the type of diet with a range from 6-7. The pH above 5.7 is considered normal. When the ruminal pH is maintained above 5.5, lactate generally does not accumulate and there remains a balance between the lactate producers and lactate users.

When then pH drops down further cellulolytic bacteria begins to die (below pH 5.7) and there is rapid proliferation of lactate producing bacteria. Streptococcus bovis which is the important causative agent is capable of rapid growth on starch-based substrates and produces lactic acid. The net effect of the sudden dietary change is a switch from predominantly VFA production to lactate production. Osmolality of rumen increases. Increased osmolality of rumen leads to fluid sequestration from general circulation to the rumen leading to dehydration.

Increased ruminal acidity causes damage to the ruminal epithelium and rumen papillae that can slough leading to the entry of various pathogenic organisms in the systemic circulation. These bacteria may cause liver abscesses. If the ruminal bacteria clear the liver they may colonize in other parts of body like the lungs, heart or kidneys which may cause serious complications of respective organs.

Rumenitis is the fundamental lesion of ruminal acidosis. Change in absorption occurs. The dying bacteria release endotoxins that enter the systemic circulation. Histamines are released. Severe diarrhoea, dehydration and endotoxins may lead to cardiovascular collapse, shock and death. Laminitis, abscess in the liver or other organs, polioencephalomalacia, hypocalcaemia or hypomagnesaemia are the common findings that may be observed in many animals even after recovery from ruminal acidosis. Polioencephalomalacia occurs due to thiamine deficiency. T

he reason of the lesions of laminitis generally observed after the recovery of ruminal pH is not well established.  Ruminal wall may get thickened after healing so nutrient absorption may be retarded for months even after the recovery from the disease that may lead to poor performance of the animal. Immunity is also suppressed.

Diagnosis of Ruminal acidosis

The acute cases are diagnosed on the basis of the history of sudden dietary changes, anorexia, diarrhoea, dehydration, ruminal hypotony or atony, bloat (excessive accumulation of gas), increased pulse, increased heart rate, increased respiratory rate, panting, lethargy, thirst, lameness, kicking at belly and decreased ruminal pH to about 5.2 or lower.

There is no typical clinical sign in subacute ruminal acidosis. Dairy herds with chronic and subacute acidosis can be diagnosed on the basis of various observations including the history of quantity and quality of feed intake, reduction in feed intake, lethargy, decreased percentage of herd (less than 50%) in actively chewing stage, gas bubbles in the faeces with decreased faecal consistency, faeces may be  light coloured with altered smell, smearing around the perineum, presence of undigested grain or fibre in the faeces, decreased milk production, decreased milk fat percentage, poor body condition in spite of adequate energy intake, weight loss, laminitis, increased respiratory rate, heart rate, body temperature and decreased rate of rumen contraction.

Laminitis may be associated with hoof overgrowth, sole abscesses or ulcers. The manure of healthy cattle contains only few forage particles whose size should not be greater than half an inch. Watery and foamy manure indicates the abnormal fermentation.

There cannot be an exact demarcating value of ruminal pH for diagnosis of ruminal acidosis; however a ruminal pH of below 5.7 indicates the developing problem of ruminal acidosis.  In a suspected herd of subacute acidosis, rumenocentesis (rumen sample may be taken with a hypodermic needle) on 12 animals should be done and if three or more have a pH of 5.5 or less then corrective measures against ruminal acidosis should be taken in the herd. Samples should be collected at 4-8 hours after a TMR meal or 2-4 hours after the feeding of concentrate portion of ration.

Herd showing characteristic clinical signs can be suggestive of subacute acidosis, but each sign by itself could have several other reasons and differential diagnosis should be overruled before reaching a final conclusion for example low milk fat % is frequently observed during acidosis, but can occur due to excess ration fat, ionophores, and several other reasons.

On the other hand many herds with normal average milk fat % have significant acidosis problems. Early lactation cows are quite sensitive to ruminal acidosis. Ruminitis, liver absession, polioencephalomalacia, epistaxis and hypocalcemia are the secondary disorders which may be found as a result of ruminal acidosis.  Heart rate in a cow with clinical ruminal acidosis may be used as a prognostic indicator. Cattle suffering from ruminal acidosis, with a heart rate greater than 120 beats per minute generally have a grave prognosis.

Prevention and Treatment of Ruminal acidosis

• Proper diet balancing or feeding management, control of ruminal pH and the fermentation process are the basis to prevent ruminal acidosis.
• The diet containing proper balance of fiber and nonfiber carbohydrates should be given to the ruminants. Growth of lactic acid utilising ruminal bacteria e.g., Megasphaera elsdenii,  Propionibacterium spp. is relatively slow and these bacteria need sufficient time to adapt to dietary changes. Any dietary formulations based on grain rich diet should be gradually provided over a period of time in weeks. This gives sufficient time for the resident lactate utilising bacteria and amylolytic bacteria to populate so that they can keep up with the growth of streptococcus bovis and prevent acidosis.
• Cattle which are not accustomed to high grain diets may get severely affected or die whereas accustomed cattle may develop even no clinical sign. In adapted cows, these bacteria ensure the rapid metabolism of the produced lactic acid thereby preventing lactic acid from accumulating in the rumen. During acidosis roughage should be increased and concentrate feeding should be restricted.
• The particle size of the fodder should be optimum. The reduction in the forage particle size decreases ruminal pH because reduced forage particle size does not stimulate saliva production sufficiently. Ionophores like monensin, salinomycin, lasalocid and other rumen modifiers like tylosin and virginiamycin and yeast culture (saccharomyces cerevisiae) has been used for prevention of subclinical acidosis.
• Monensin/ tylosin combination and virginiamycin are effective in controlling rumen fermentation and ruminal acidosis and these antibiotics should be given to the herd gradually and not suddenly.
• Probiotics containing lactate utilizing bacteria like Megasphaera elsdenii, Selenomonas ruminantium should be used both for preventive and treatment purpose. Oral antacid like sodium bicarbonate or milk of magnesia is used for prevention and treatment of ruminal acidosis.
• The animal should be treated based on the severity of the disease. The mild cases should be treated by oral antacid and electrolyte solutions. Non steroidal antiinflamatory drugs may be given to relieve pain.
• Concentrate feeding should be withheld during ruminal acidosis. The severe cases should be treated by giving intravenous, hypertonic saline solutions. Avoid fluids containing lactate such as Ringer lactate.
• Animal should be given balanced electrolyte solution and sufficient water to recover hydration. Lavaging the rumen with stomach tube and transfaunation from a healthy animal is beneficial.
• Antibiotics like Penicillin, tylosin or potentiated sulphonamides or tetracycline has been used to prevent secondary infections.
• Flunixin meglumine should be given intravenously for endotoxaemia. Antihistamines should be given. Calcium and magnesium should be included in the treatment for preventing secondary hypocalcaemia and hypomagnesaemia.
• Vitamin B complex especially thiamine should be given to prevent polioencephalomalacia.
• In more severe cases ruminotomy may be performed and contents of the rumen should be evacuated and replaced by the ruminal contents obtained from several other healthy cattle.

Authors:

MK Tripathi¹, PC Chandran², S Dayal³, S Mondal⁴ and A. Dey⁵

^{1, 2}Scientist, ³Senior Scientist, ⁵Principal Scientist

Division of Livestock and Fishery Management,

ICAR Research Complex for Eastern Region, ICAR Parisar, P.O Bihar Veterinary College Patna, 800014.

⁴Principal Scientist, National Institute of Animal Nutrition and Physiology, Bangalore

Email- This email address is being protected from spambots. You need JavaScript enabled to view it.