Volume 22 • Issue 03 • 2018
PART 03
COMMON PRODUCTION DISEASES:
KETOSIS OR ACETONAEMIA
Ketosis or acetonaemia
Ketosis in dairy cows can broadly be classified
into either type I or type II ketosis, based on
the underlying pathophysiology, with some
similarities to that of type I and type II diabetes.
Type I ketosis is a metabolic disorder of
high yielding lactating dairy cows caused b y
an imbalance in the energy metabolism. It
is characterized by ketonaemia, ketonuria,
hypoglycaemia, depression and anorexia. It is
most often seen from the third to the sixth week
of lactation.
The key factor in the occurrence of ketosis
in dairies, is sufficient intake of a properly
balanced ration (Dry Matter Intake). Feedbunk
management, as mentioned before in the case of
hypocalcaemia, is of particular importance.
Type I ketosis can be sub-classified into primary
and secondary, where primary ketosis occurs due
to a severe negative energy balance (NEB) that
leads to a substrate (oxaloacetate) deficiency
in the absence of any other disease. Secondary
ketosis is the accumulation of ketone bodies in
the body due to anorexia secondary to a disease
process. Any disease process that reduces dry
matter intake (DMI) in early lactation may cause
secondary ketosis.
The prevalence of primary ketosis is relatively
low in southern Africa. Subclinical ketosis can
often be detected in cows from high producing
dairy herds if body fluids are tested for ketone
bodies. Most cases occur between the 3rd and
6th week of lactation.
Many cases (50%) will spontaneously recover
within days and mortalities are rare loss of
production is more important, especially where
cows do not respond well to treatment.
High producing cows and cows in their 3rd
lactation and older have an increased risk for type
I ketosis.
Physiological background
Carbohydrates and fibre compounds in the
feed are broken down in the rumen by rumen
microbes. The end products of rumen digestion
are the volatile fatty acids acetate (average 70%),
propionate (average 20%) and butyrate (average
10%).
Propionate can enter the citric acid cycle (CAC)
directly and its carbon atoms can move through
the cycle to enter the gluconeogenic pathway to
form new glucose (propionate is thus glucogenic).
Acetate may also enter the CAC through acetyl
CoA (small amounts) but only if there is enough
C4 atoms (oxaloacetate) available in the CAC.
Most of the acetate will, however, be used in fat
synthesis, or if the body is in a catabolic state
with fat being broken down, acetate will be used
to form ketone bodies (aceto acetate, ß hydroxy
butyric acid and acetone). Aceto-acetate and ß
hydroxy butyrate have 4-carbon atoms, but they
cannot be interchanged with the C4 units in the
CAC. Acetone is a C3 compound that is formed
slowly and spontaneously from aceto-acetate.
Ketone bodies form an important energy source.
They can enter the CAC via acetate and be oxidized
for energy in heart, kidney, skeletal muscle and
lactating mammary glands if there is sufficient
C4 units (oxalo-acetate) available. If the C4 units
concentration of the mitochondria becomes
sufficiently depleted, there will not be enough C4
units to condense with C2 (acetyl CoA) to allow
the initiation of the CAC. When this occurs, C2
units accumulate in the mitochondria and are
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