Murphy, G. M.

St George, T. D.

University of Queensland eSpace

Paper 3.29
An alternative view on the hypocalcaemia of cows
St. George, T.O. and Murphy, G.M.
Proceedings of The Australian Association of Cattle \Jreterinarians 2001
Pages 30-39
An invitation was received to present our research on milk fever at the Australian Veterinary "'
Association's Animal Conference in Melbourne 14-18 May 2001 .Al Powerpoint presentation was
developed using the multicolour graphs of the haematology and biochemistry developed for this
thesis. It was only possible to publish black and white representations of these illustrations for the
proceedings paper, which follows. The data used for the milk fever aspects was drawn from that
used for paper 3.28. However, a small amount of additional data V'ias used
Date: /.;3/1P.l
T.O. St. George

Paper 3.29
signs. Iron and zinc levels fell. Plasma glucose
rose initially to a peak of up to 5.1 mM/L then fell.
Plasma phosphate fell as low as 0.97 mM/L. In
addition, the blood ammonia level rose, as did the
pH while the partial pressure of CO2 fell especially
in periods of rapid breathing during fever phases.
Plasma fibrinogen levels doubled in the recovery
phase. The haematological changes are very
characteristic with a neutrophilia overshadowing a
Iymphopaenia and an oesinopaenia. A fall in
lymphocyte numbers that is very characteristic of
virus infections occurred. Non esterified fatty acid
rose approximately ten-fold during fever (II). In
earlier experiments most enzyme systems assayed
showed minor change (15). Most of the
biochemical changes illustrated occur in stress as
well as in inflammation (16) (Table I).
could not be closely related to calving; A heifer
sampled in the same herd did not show disturbances
in haematology at calving.
A third group of four cows (3rd to 10th calvers)
were placed in stalls and were fitted with catheters
and allowed to settle down. Feed consumption was
monitored daily. An intensive period of blood
sampling was started when calving appeared
imminent. Three cows did not develop milk fever
(Figures 2,3,4). One cow developed characteristic
paresis 9 h after calving (Figure 5). The cow with
milk fever responded to calcium borogluconate
treatment. The general observations (21) on the
four cows can be sununarised:
The clinical signs related to hypocalcaemia in
ephemeral fever are reversible by calciU!D
borogluconate as they are in milk fever. However,
unless anti-inflammatory treatment is also given
many relapse (9,17). The hypocalcaemia is a
secondary effect of an underlying inflammation and
specific treatment with calcium borogluconate is
recommended only as a supplement to treatment
with anti-inflammatory drugs as a life saving
measure.
.rumination ceased for 2 to 5 h before calving.
.all cows lost some appetite in the 24 h prior to
calving but ate avidly within 24 h post calving.
The cow with milk fever did not eat until after
treatment (Figure 6).
.plasma calcium levels began to fall I to 3 days
before calving to reach plasma Ca .s 2.0 mM/L,
within the wide range where clinical milk fever
can occur.
.plasma fibrinogen levels rose, zinc and
inorganic phosphate levels fell.
.plasma glucose rose to a peak at parturition then
fell rapidly to below normal.
.plasma iron showed a variable response.
.plasma pH rose.
Parturition and Milk Fever
The biochemical spectrum accompanying
ephemeral fever was developed progressively over
a decade. We reached the point where comparison
with the biochemistry of milk fever was essential to
discover what differences existed from those
accompanying milk fever. Very little data was
found for normal calving or milk fever (18,19,20).
A comprehensive panel of biochemistry and
haematology bracketing normal calving did not
exist.
Neutrophil numbers peaked close to the peak of
rectal temperatures. Lymphocyte numbers also
rose. Eosinophils disappeared for a 24 h period
spanning the calving process.
Taken together, the spectrum of biochemical change
that occurred in the group of four multiparous cows
in the periparturient period was similar to that found
in ephemeral fever with a calcium demand (Figure
I). Neutrophilia and oesinopaenia were similar but
lymphocyte numbers rose instead of falling as they
do in ephemeral fever. Peaks in body temperature
were not as high. The changes from normal
occurred earlier in the cow with milk fever and for a
more protracted period than in those without milk
fever. The variable rectal temperature in milk fever
reported by Fenwick (22) during clinical milk fever
would depend on when it was measured in relation
to the peak above normal.
The first attempts were to carry out biochemical
tests on the blood taken from milk fever cases
before treatment and again 3 to 5 days later (21).
This showed clearly a wide range of calcium levels
at the acute stage (0.4 to 2.1 mM/L). Zinc and iron
levels were lower than normal. A relative
neutrophilia occurred in all cases. Fibrinogen levels
were elevated.
In an attempt to establjsh what pattern occurred in
multiparous cows calving nonnally, blood analyses
were carried out on samples taken daily during the
period spanning calving for three cows in a dairy
herd. The results showed disturbances in zinc, iron,
copper as well as in calcium. Again, a relative
neutrophilia was noted plus high fibrinogen (two to
three times nonnal in the second sample).
However, with once a day sampling the changes
Implications for Milk Fever
In the peri parturient period in multiparous cows:
.there is a wide range of biochemical dyscrasias
in multiparous cows in the periparturient period
that are concurrent with, not consequential to, a
fall in plasma calcium (Table 1).
(i.I~Convention Centre, 14-18 May, 2001 31
Paper 3.29
any point in the spinal cord up to the brain. The
spinal cords of a few downers have been examined
in ephemeral fever. In brief, areas of demyelination
were found in the cervical spinal cord {C I to C3)
(24, TD StGeorge, GM Murphy and MWH Hill
unpublished data). An interesting point about the
unpublished case was that the steer had relatively
small falls in plasma calciwn (0.3 mM/L) and, when
it was killed in extremis 3 days after fever had
terminated, plasma calciwn values were normal.
Only one publication recording demyelination in the
spinal cord in a milk fever case has been found
(25). Two separate causes could also operate in
milk fever as spinal cords are seldom examined in
chronic milk fever paresis.
Table 1 Comparison BEF/milk fever.
Acute paresis
responsive to CBG
Chronic paresis
unresponsive to CBG
Rumen motility
Body temperature
+ +
.J,
tt
J.
iJ.
iii
.1-
.1-
tt
t
J,
Neutrophils
Lymphocytes
Oesinophils
Plasma
Iron
Zinc
Copper
Calcium
.I.
.I.
t
.1..1.
,j,
,j,
t
,j,
Conclusions
Once the value of calcium gluconate treatment for
milk fever was established in the 1930s (26) an
assumption was made that a fall in plasma calcium
was the prime lesion. Our contention is that
inflammation can playa role in the initiation of a
secondary hypocalcaemia and other biochemical
dyscrasias associated with parturition as well as
impending lactation. This contention does not
invalidate the regimes that have evolved to diminish
the prevalence of milk fever (I).
I
, ;
.
J.
tJ.
t
.J,
t.J,
t
Phosphate
Glucose
Fibrinogen
t
tt
t
t
Ammonia
pH There is much to be done to extend the range of
blood parameters measured in the periparturient
period. The cows, whose biochemistry and
haematology is illustrated here, were multiparous.
The close observations should be repeated on first
calf heifers which are reputed not to suffer from
milk fever.
Paresis has two separate causes in ephemeral fever,
one biochemical (hypocalcaemia) and one due to
neural changes. "Downer" cows might also not be a
direct consequence of low plasma calcium but
concurrent loss of myelin.
References
1 Hibbs JW (1950) Milk fever (parturient paresis)
in dairy cows -a review. J DairySci 33:758-789.
2. StGeorge TD, Uren MF and Zakrzewski H (1986)
The pathogenesis and n-eatrnent of bovine ephemeral
fever. Arbovirus Research in Australia, Proceedings
Fourth Symposium May 6-9, 1986, CSIRO/QIMR,
Brisbane, Ausn-alia. (StGeorge, T.D., Kay, B.H., and
Blok, J., Eds) pp.303-307.
3 Murphy GM, StGeorge ill, Guerrini V, Collins
RG, Uren MF and Doolan DL (1987) Trace
elements and macro electrolyte behaviour during
inflammatory diseases in cattle and sheep.
Proceedings 6th International symposium on Trace
Elements, Asilomar, Monterey, California.
.the overall picture near calving is characteristic
of a systemic inflammation which is more severe
in the cow which developed milk fever.
.periods of mild fever preceded parturition.
.treatment with calcium borogluconate changed
only two of the biochemical abnormalities.
Overall biochemical normality is therefore not
achieved by this treatment.
.a neutrophilia and oesinopaenia occurred
consistent with the biochemistry characteristic
of inflammation.
.blood pH does not rise as high or for as long as
in ephemeral fever with short periods of
overbreathing (Figures 7,8).
.a lymphocyte response indicated antigenic
stimulus close to calving.
.the clinical picture of milk fever seen by
clinicians is only a small part of the syndrome.
.it is possible that the reason that heifers do not
experience milk fever or lose appetite (23) is
that they have not been sensitised by exposure to
foetal proteins during earlier calvings.
.non-steroidal anti-inflammatory drugs should be
tried experimentally in prevention and
treatment.
"Downers"
Nerve conduction, causing loss of hindquarter
control, can fail due to a lower plasma calcium
level, as discussed ,or due to physical interruption at
(f)c~ Melbourne Conference Proceedings32


Paper 3.29
Calving cow
1800
~g/L
1600 iron
1400
1200
Copper1000
800
Zinc
600
400
3.0 9
8
7
mM/L Glucose mM/L
2.5
Calcium
6
5
2.0
Phosphate
,.J.
1.5 4Ulucose '""
3
2
1.0
Magnesium
0.5 1
12 Leucocytes xl 09/L
1\10
8
cympnocytes
6
4
Neutrophils ~
2
Eosinophils -0
40.0 Temperature Co
39.5
39.0
38.5
38.°52 " Au 12 -4--4", -44 -.-':>0 -w, -'v -L.. -Lv -,oJ -
Hours (calving at time 0)
4 12 16 ,J
FIGURE 2. Haematological and biochemical changes in a cow having its 3rd calf
~~
Convention Centre, 14-18 May, 2001 35

Paper 3.29
Paper 3.29
Calving cow with milk fever Calcium
borogluconale3000 J.1g/L
2500
2000
i Copper
I;:;;v ~ ..:..V'/1500
~ ~~~~~
1000
I~.A
500
Linc
0
4.0 11
10
9
8
7
6
5
4
3
2
1
mM/L Glucose mM/L
3.5
3.0
CalciumGlucoseCalcium
2.5
,
2.0
1/"", 
I
, Phosphate,~"'::::::::::
~
~1.5
1.0
'-- ,- 
- Magnesium0.5
8 Leucocytes xl 09/L
6
NeutTophils
4
""'--Lymphocytes2
Eosinophils
0
40.5 Temperature CO
40.0
A39.5 r:-
i
39.0
l -
38.5
38.0
, 
4 8 12 ..~ 20 2..
-4CS -44 -4U -~o : -~d -~.. -~V -'V -i~
Hours (calving at time 0)
FIGURE 5. Haematological and biochemical changes in a cow having its 3rd calf and
affected by milk fever ueated with calcium borogluconate nine hours after calving
(f;4c~ Melbourne Conference Proceeding38
Paper 3.29
20
15
0>
~
"0 10
Q)
Q)
u..
5
-6 -4 -2 0
Days
2 4 6
Figure 6 Daily feed consumption in a multiparous co,.' that developed milk fever compared with one that did not
Figure 7. Panial pressure of carbon dioxide in blood and effect on pH in an ephemeral fever
Calving cow with milk fever
Calcium
Calving borogluconate
OCO2 mmHg
7.50 60
oH
~
55
7.45
50
7.40 45
40
7.35
35
7.30 30
-52 -48 -44 -40 -36 -32 -28 -24 -20 -16 -12 -8 -4 0
Hours (calving at time 0)
4 8 12 16 20 24
Figure 8 Partial pressure of carbon dioxide in blood and effect on pH in a milk fever case
(i:~Convention Centre, 14-18 May, 2001 39
I


An alternative view on the hypocalcaemia of cows

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An alternative view on the hypocalcaemia of cows

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