IF the captain of the Titanic had
paid more heed to the “tip of the
iceberg” concept, the most well-
known disaster in maritime
history may have been averted and
many souls would not have
perished in the icy waters of the
North Atlantic.
This expression has entered into everyday usage to
illustrate an
apparently
small
problem that
hides a
hugely
significant
issue and in
many walks of life businesses and
dreams have foundered because
people forget the importance of the
“tip of the iceberg”.
Equally there is no better
expression to illustrate the problem
of ketosis within the dairy herd.
There are few dairy farmers who
have never had a good cow suffer
from milk drop and inappetence.
Closer examination reveals that
the cow has lost condition since
calving and indeed they may notice a
sweet “pear drop” smell on the
breath of the cow. The cause of this
is the infamous “energy gap” of early
lactation.
To understand this energy gap we
have to go all the way to the dry
period. During this critical period in
the cow’s year she has a large calf
filling her abdomen, reducing the
space that can be occupied by the
rumen; this in turn reduces the
amount of food the cow can eat.
Genetically programmed
At calving the cow is genetically
programmed to produce large
volumes of milk which requires a lot
of energy to produce. At the same
time she is, perhaps, a little sore after
calving, is stressed by having to
change groups and establish herself
in the hierarchy of that group.
Her diet has changed significantly
and the microflora of the rumen is
not able to deal with this change with
maximum efficiency. Thus, it is very
unlikely, even in the best case
scenario, that the modern dairy cow
can eat enough to meet her energy
requirements.
As a consequence she starts to use the fat that she has stored
through late lactation and the dry
period as a source of energy. This
provides her with energy but as a by-
product she produces ketones. If
these reach too high a level then
appetite is suppressed significantly,
milk yields drop and the cow is
deemed to have clinical ketosis.
Treatment involves trying to
reverse the changes by giving
propylene glycol as a glucose
precursor, boosting appetite with
vitamins and trying to reverse some
of the metabolic changes with
steroids. The cow may go on to
develop fatty liver which is very
challenging to treat or she may
respond to treatment but have lower
than expected yields, poorer fertility
and other health problems.
Although fat mobilisation is a
reality for most, if not all modern
dairy cows, not every cow will
develop ketosis. However, some
factors increase the likelihood of
ketosis developing.
Fat cows at dry off have a
reduced dry matter intake throughout
the dry period and this further
suppresses the appetite post-calving.
It is of paramount importance to
manage the late lactation cow to
avoid excessive fat deposition. This is
best done by avoiding a prolonged
lactation (by getting them in calf
earlier) and feeding for yield
(especially difficult in smaller herds
feeding TMR).
Any post-calving problems such
as retained foetal membranes, mastitis
or metritis are also likely to reduce
voluntary food intake after calving
and increase the risk of ketosis. To
avoid post-calving problems careful
management of the transition cow is
essential with regards to mineral
intake, etc. Early detection and
aggressive treatment of any problem
is of paramount importance.
Sub-clinical cases
Now for the “tip of the iceberg”
lesson. For every cow showing signs
of clinical ketosis there will be many
cows who fail to reach their full
potential but do not show clinical
signs. These cows are described as
suffering from sub-clinical ketosis.
They show no signs but are nonetheless held back by the ketones
in their body. Not only will their
yields be reduced but their fertility
will be suppressed and they will be
more prone to other conditions such
as LDAs, mastitis and metritis.
These cows are very difficult to
identify. As a result they often escape
without treatment and end up with a
long calving interval or culled for a
variety of reasons, with scarcely a
thought as to why these problems
have developed.
Glucometer
To detect cows suffering from ketosis
we need to measure the amount of
ketones in the blood. This can be
done using blood samples and a
simple glucometer such as is used by
diabetics.
This works well but is a little bit
of a hassle and requires an ability to
blood sample cows.
Another method is to take a milk
sample and use the wonderfully-
named Rothera’s reagent which turns
pink when ketones are present in the
milk. This is good for clinical ketosis
cases but does not detect many of
the sub-clinical cases. Test sticks that
detect ketones in urine have also been used with some success but it
can be somewhat time-consuming
waiting for a cow to urinate.
Recently Elanco has launched a
test strip that can be used on milk.
As cows are milked at least twice
daily, sample collection is easy and
the strip gives a colour change that
varies in intensity depending on the
amount of ketones present in the
milk. This semi-quantitative test is
quick, easy and accurate enough to
give a measure of the incidence of
ketosis within the herd.
Samples taken from many herds
throughout the UK have shown that
there is an incidence of around one
in three cows in the UK. This is
causing significant financial loss to
the farmer through reduced yields,
increased disease incidence and also
an increased culling rate.
Elanco has also recently launched
a treatment aimed at preventing
ketosis and thus reducing the losses
associated with the problem.
It comes in the form of the
Kexxtone bolus, which is designed to
be given to dairy cows or heifers 3-4
weeks before calving and releases
monensin for 95 days once it’s placed
in the rumen.
