Cereal Overload: also referred to as cereal overeating and rumen acidosis.
This is an acute condition with high mortality that occurs when animals engorge on feed material high in starch or other rapidly fermentable carbohydrates. This could occur when animals get loose in a feed store for example.
The result is a decrease in ruminal pH due to an increase in lactic acid concentration. This occurs due to rapid growth of organisms such as Streptococcus bovis and Lactobacilli which overgrow other species whose growth causes an acid environment to develop.
As a result of cereal overeating carbohydrate fermentation progresses rapidly and the growth of Streptococcus bovis and Lactobacilli increase rapidly. They produce lactic acid which causes a decrease in pH of the rumen fluid and this suppresses the growth of other organisms.
The decreasing pH also establishes a self-perpetuating cycle that eventually causes the growth of S. bovis to slow down and Lactobacillus species overgrow other organisms.
At this stage the rumen contents become foul smelling as the acid environment causes epithelial cell death resulting in the development of necrotic lesions and an ulcerated mucosa.
This disease syndrome can be very severe: the animal displays an enlarged
abdomen, ruminal stasis, toxaemia arising from rumen mucosa necrosis, weakness
and a striking metabolic acidosis. Death may ensue rapidly if the condition
is left untreated.
Another condition that can result is the low milk fat syndrome.
Investigations into this syndrome extend back many years with few recent advances and few uncontested hard facts.
The condition is associated with an increase in propionate production and a decrease in acetate production in the rumen resulting from feeding high grain-low fibre diets.
Many feel that this is the cause of the syndrome since increased availability of glucose to the mammary gland (due to increased hepatic gluconeogenesis from propionate) results in a decreased fat content of the milk.
Acetate is used for lipid biosynthesis in the mammary gland, and increased glucose availability seems to inhibit this process. Supplementary acetate however isn't always effective in reversing low milk fat content.
Not enough is known about the effects of decreased acetate availability to the mammary gland occurring at the same time as increased glucose availability to account for the changes that are seen in milk production.
Two other disease complexes of adult ruminants related to energy metabolism have been identified. They are:-
Acetonaemia which occurs in early lactation in high yielding dairy cows and Pregnancy Toxaemia which occurs in late pregnancy in ewes carrying twins.
Both diseases are disorders of intermediary metabolism characterised by remarkably elevated blood ketone body concentrations and an increase in plasma free fatty acids.
Both diseases seem to be due to an inability of the mother to make enough glucose to supply the needs for lactogenesis in the case of acetonaemia and foetal demands in pregnancy toxaemia.
Liver glycogen levels are low in both syndromes and rapid ketogenesis is the necessary corollary to the high rates of gluconeogenesis that are occurring in the livers of these animals under these conditions.
(You should be able to explain why high rates of hepatic ketogenesis are associated with high rates of gluconeogenesis)
Understanding of the pathogenesis of these diseases is poor because despite their similarities, there are also marked differences which are not explained by our knowledge of the derangements of energy metabolism that have been studied to date.
For example, without treatment virtually all acetonaemic cows recover completely whereas without treatment, virtually all ewes with pregnancy toxaemia die.
In this context it is notable that the chances of a ewe's survival is increased if she aborts or lambs. This can be rationalised by recognising that in either event there is relief of the glucose drain on the mother.
This is probably not the whole story however, because giving glucose to the ewe reduces her survival rate and giving glucocorticoids (that enhance gluconeogenesis in the liver) also worsens the prognosis for the ewe.
Understanding of the involvement of glucocorticoids in pregnancy toxaemia is complicated because sheep pregnant with twins become toxaemic most often in adverse weather conditions where they may be subjected to chilling as well as food deprivation.
These "stressful" conditions result in increased production of glucocorticoid hormones by the ewes' own adrenal glands.
Indeed there are reports which show that the adrenal glands of sheep that have died of pregnancy toxaemia are massively enlarged when compared to those of other animals.
In the case of acetonaemia, glucose therapy and more particularly massive doses of glucocorticoids give the most consistent improvement in the cow's condition with few relapses.
So it appears that the two diseases have dissimilar aetiologies.
In summary, pregnancy toxaemia is a complex metabolic derangement resulting from acute stress and high glucose demand while acetonaemia is more nearly a straight forward case of failure to meet abnormally high glucose demands. Hence acetonaemia responds well to rational therapies such as glucocorticoid administration.
The onset of acetonaemia relates well to the developing hypoglycaemia and this in itself causes anorexia in cows.
This causes lactation to decrease so demand for extra glucose decreases, hence the spontaneous recovery seen in a high proportion of cases.
Other differences between the two conditions are also striking.
For example, deliberately depriving a ewe pregnant with twins of food produces a syndrome which closely simulates pregnancy toxaemia whereas this is not the case with acetonaemia.
Similarly the best way to prevent a ewe pregnant with twins from getting pregnancy toxaemia is to maintain her on an increasing plane of nutrition during later pregnancy.
In contrast, the correlation between feeding management of the cow and the incidence of acetonaemia is poor.
In summary, more is known about how to prevent pregnancy
toxaemia than to treat it and more is known about how to treat acetonaemia
than to prevent it.