Changes

Milk fat depression is a poor and insensitive indicator of subacute ruminal acidosis in dairy herds. Cows and herds with severe subacute ruminal acidosis may have normal milk fat tests. Thus, it is vitally important not to exclude the diagnosis in a dairy herd that has a normal milk-fat test.  

Milk fat depression is a poor and insensitive indicator of subacute ruminal acidosis in dairy herds. Cows and herds with severe subacute ruminal acidosis may have normal milk fat tests. Thus, it is vitally important not to exclude the diagnosis in a dairy herd that has a normal milk-fat test.  

===Clinical Signs===

===Clinical Signs===

 

Loose faeces with excessive faecal soiling of hindquarters. Closer examination of the faeces may revela fibrin casts, undigested cereal grains and long fibres. Cows swishing their tails when there are no flies due to gut and or urine irritation. Reduction in milk butterfat. Reduction in milk yoeld. with cows not milking to expectation. REduction in DMI. Individual animals variably go off their food with a consequent reduction in milk yeild. Cows spilling their cud whilts ruminating. Increased incidence of nutritional-related diseases, such as NEB/acetonaemia, LDAs, poor fertility, lameness and other peri-parturient diseases e.g. mastitis.

The major clinical manifestation is reduced or cyclic feed intake, or both. Other associated signs include decreased efficiency of milk production, reduced fat test, poor body condition score despite adequate energy intake, unexplained diarrhea, and episodes of laminitis. High rates of culling or unexplained deaths may be noted in the herd. Sporadic nosebleeds due to caudal vena cava syndrome may also be observed. The clinical signs are delayed and insidious. Actual episodes of low ruminal pH are not identified; in fact, by the time an animal is observed to be off-feed, its ruminal pH has probably been restored to normal. Diarrhea may follow periods of low ruminal pH; however, this finding is subtle and difficult to evaluate.

gTroup having loose faeces. This occurs following the

 

One consequence of feeding excessive amounts of rapidly fermentable carbohydrates in conjunction with inadequate fiber to ruminants is subacute ruminal acidosis, characterized by periods of low ruminal pH, depressed feed intake, and subsequent health problems. Chronic disease conditions secondary to subacute ruminal acidosis can negate the production gains accomplished by high grain feeding. Dairy cattle, feedlot cattle, and feedlot sheep are all at high risk for developing this condition. Although dairy cattle are typically fed diets that are higher in forage and fiber compared with feedlot animals, this advantage is offset by their much higher dry-matter intakes.

of foodstuff's. However, if colonic pH falls

Depressed dry-matter intake becomes especially evident if ruminal pH falls to <~5.5. Intake depression may be mediated by pH receptors and/or osmolality receptors in the rumen. Inflammation of the ruminal epithelium (rumenitis) could cause pain and contribute to intake depression during subacute ruminal acidosis.

excessively. the colonic flora is killed off and hind gut

fermentation ceases, reSsulting in the production of

* Fibrin casts in the faeces. This is indicative of severe

* Excessive faecal soiling, especially of the tail, udder

and rump;Cow's swishing their tails in the absence of flies. This is

likely to be associated with irritation caLused by the production

ot' acidic urine and faeces. Tail swishing leads to

rump faecal soiling, a common finding in affected herds;

* Rumlleni hypomotility and hypophagia. Individual cows

will be seen to be 'off their food' with no other clear

within 24 to 48 hours; this is attributable to a

reduction in appetite, accompanied by a tendency to

* Cows 'dropping the cud' while ruminatincy;

* Reduced feed efficiency (Krajcarski-Hunt and others

with the subsequent passag-e of undigested foodstuLffs

in the t'aeces. It is common in such situations for blame to be attributed to the feedstuff quality rather than

on farms where the problem is continuously present);

* Reduced milk butterfat. There is some debate on the

precise aetiology of reduced milk butterfat. Traditionally,

production from dietary neutral detergent fibre (NDF),

mechanism behind reduced milk fat (Bauman and Griinari

2001). However, since rumen pH is dependent on the

in the diet, and milk fat is dependent on the amount of

NDF in the diet, it is possible to have a situation where

butterfat levels are acceptable in the face of a ruminal acidosis

if the fibre being fed is too short to be effective;

* Increased numbers of cases of digestive disease,

* Laminitis. SARA predisposes to laminitis (Nordlund

2000). Affected herds may have a high prevalence of foot

lameness. However, there is a time lag between the period

of nutritional insult and the resultant lameness. While the

laminitis has not been elucidated, it may involve the products

of colonic fermentation rather than SARA per se;

* Reduced dry matter intake (Garrett and others 1999);

* Excessive weight loss in early lactation. This can

occur as cows affected by SARA fail to increase their

dry matter intake as a coping strategy for negative energy

* Poor reproductive performance. This is a reflection

* Environmental mastitis. Levels may be increased due

to poor hygiene and a reduction in the cow's immune

function. Negative energy balance occurring secondarily

to SARA is recognised as impacting

===Pathology===

===Pathology===