NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
342 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [ I, IV
In trial III, 800 units of insulin were injected in twenty-five minutes. Marked
muscular tremors developed in five minutes, followed by profuse watery nasal ex-
cretions which dripped into the manger. This condition lasted for about fifteen
minutes, after which the animal appeared normal.
In no case was there any suggestion of paralysis or coma.
THE EFFECT OF HYPOCALCEMIA IN COWS.
The previous experiment demonstrated to our satisfaction that hypoglycemia
could not be responsible for milk fever symptoms.
Speculating on the theory that a hypocalcemia is a factor in the cause of milk
fever, it was thought that it should be possible to produce artificial conditions
simulating milk fever by displacing the calcium. It was therefore decided to
produce hypocalcemia to determine definitely whether or not this condition alone
would produce symptoms analogous to milk fever. It is well known that sodium
citrate reacts with ionized calcium in the blood to form unionizable calcium citrate,
and thus displaces the ionized calcium in the blood.
Intravenous injection of sufficient sodium citrate should lower the ionized
calcium of the blood and produce hypocalcemia, which should demonstrate whether
or not a low blood-calcium alone can produce symptoms analogous to milk fever.
The first part of this work was to try the effect of sodium citrate injected in-
travenously into rabbits. The injection of 4.5 cc of a 1 per cent. solution of
sodium citrate produced no noticeable effect in a rabbit weighing 1810 grams.
Two cc of an 8 per cent. solution of sodium citrate injected slowly into the
posterior auricular vein of a rabbit weighing 1500 grams produced tetany and
prostration in about 30 seconds. The injection of 2 cc of an 8 per cent. solution
of calcium chlorid restored the animal in one minute. The experiment was re-
peated with two other rabbits with the same results. A 20 per cent. solution of
sodium citrate was slowly injected into the posterior auricular vein of a rabbit.
As the injection progressed, the rabbit went into violent tetany and then into
complete anesthesia. A 20 per cent. solution of calcium chlorid was then injected,
which brought about complete recovery in less than one minute. This experiment
was repeated several times with the same results.
After the preliminary experiments on rabbits, cows were used for the experi-
ments. A 20 per cent. sodium citrate was used in all cases. In each case it was
injected into the jugular vein. Seven experiments on five cows were conducted at
HYPOGLYCEMIA AND HYPOCALCEMIA IN COW
343
TABLE I.
Typical observations of hypocalcemia produced by intravenous injection of sodium citrate.
Time
1-43 p.m.
1-48 p.m.
1-59 p.m.
2-08 p.m.
2-17 p.m.
2-22 p.m.
2-25 p.m.
2-28 p.m.
Injected Sodium
Citrate (20 per
cent. Solution)
(cc)
30
30
30
60
30
60
0
Injected Calcium
Chlorid (20 per
cent. Solution)
(cc)
60
0
Observation
No clinical symptoms.
Slightly dull eye; lost alertness.
Ears drooped; shook hoad; slight paralysis
over loin.
Anesthesia of skin over the loin; barely able to
walk.
Paralysis extending forward; dyspnea.
At 2.24 went down; completely paralyzed;
marked dyspnea ; animal considered in ex-
tremis.
Back on her feet ; apparently normal in all
respects.
the University Farm, Saint Paul: two experiments on one high-grade Holstein
cow, four experiments on three pure-bred Jersey cows, and one experiment on a
pure-bred Guernsey cow. Table I gives the details for one experiment on a grade
Holstein cow, which is typical of dairy cows.
The injection of 30 cc of a 20 per cent. sodium citrate solution had no visible
effect. Subsequent injections caused a drooping of the ears followed by a stagger-
ing gait as a result of inco-ordination of the hind legs. Further injections caused
complete paralysis from the lumbar region posteriorly, while the animal still re-
tained more or less control of the head and fore legs. The eyes, however, became
glassy and starey. Further injections caused the animal to develop complete
paralysis with marked dyspnea. An intravenous injection of a 20 per cent. solu-
tion of calcium chlorid effected a rapid and complete recovery.
Table II gives a summary of the experiments, performed at University Farm,
with injection of sodium citrate, giving the amounts injected and the time over
which the injections took place, together with the amounts of calcium chlorid
solution injected and the time for recovery. Similar experiments were conducted
by one of us (E. A. H.) at Iowa State College.
344 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [ I, IV
The first animal used in this series of experiments was a grade Holstein cow.
This animal withstood the intravenous injection of 400 cc of 20 per cent. sodium
citrate solution. Although this did produce decided muscular tremors, the animal
remained on its feet. The sodium citrate solution was injected by means of a 40-cc
syringe over a period of twenty minutes. No calcium chlorid was administered to
this animal.
TABLE II.
Summary of experiments with intravenous injection of sodium citrate into cows of
dairy lype.
Cow
E 81
E 81
141
143
143
547
171
Amount of
Sodium Citrate
to produce
Paralysis
(cc)
240
240
250
210
270
210
110
Time from 1st
Injection to Last
(Minutes)
39
34
17
9
14
9
—
Amount of Calcium
Chlorid Injected
(cc)
60
None
60
60
60
60
90
Time for Recovery
(Minutes)
3
Slow spontaneous
recovery.
2½
1½
1½
1½
1¼
Two grade Shorthorn cows were subsequently killed by the rapid injection,
under pressure, of 800 and 600 cc respectively, of sodium citrate solution. Both
animals failed to respond to the injection of 800 cc of a 20 per cent. solution of
calcium chlorid.
Another grade Shorthorn cow which was to be used for anatomy dissection
was given 640 cc of the sodium citrate solution into the jugular vein by means of
a 40-cc syringe over a period of 32 minutes at which time the animal went down.
This was preceded by a period of excitement, muscular tremors and inco-ordination.
There was also a marked expiratory dyspnea present. This animal was allowed to
remain in the recumbent position without being given the calcium chlorid treat-
ment. Forty-five minutes later, the animal was urged to get up but walked with
a decidedly stilted gait and showed signs of tetany and inco-ordination. The ani-
mal was again put down by the intravenous injection of 160 cc of the sodium,
citrate solution. The animal was then bled out, preparatory to embalming. A
sample of blood was collected from this animal which was only partially coagulated
HYPOGLYCEMIA AND HYPOCALCEMIA IN COW
345
in 40 minutes. Smears of this blood showed crenated red blood cells and anisocy-
tosis.
Another cow, a grade Shorthorn was given 500 cc of sodium citrate solution
over a period of 20 minutes, at which time the animal went down. She showed
muscular tremors, although the expiratory dyspnea was absent. In one and one-
half minutes after the animal went down, 120 cc of a 20 per cent. solution of
calcium chlorid was injected intravenously and in three minutes the symptoms
produced by the sodium citrate had entirely disappeared.
The next animal, a grade Shorthorn cow, was injected with 360 cc of the
sodium citrate solution intravenously and in three and one-half minutes the animal
was down. She made attempts to rise but there was a lack of co-ordination. The
pupils were greatly dilated, there was a marked expiratory dyspnea and the act
of breathing was accomplished with considerable noise. Nine minutes after the
animal went down, 60 cc of calcium chlorid solution was administered intraven-
ously. The pupils immediately constricted down to normal, the dyspnea and
noise of breathing ceased and all the symptoms produced by the injection of the
sodium citrate disappeared at once.
The next subject was considerably more of a dairy type than were the preced-
ing animals. This cow received 420 cc of sodium citrate solution intravenously
over a period of seven minutes, which caused the animal to go down. This cow
did not show the muscular tremors of the previous cases, although a marked expi-
ratory dyspnea was present. The condition in this case more closely simulated
that found in milk fever cases. There was present the comatose condition so
characteristic of milk fever. After the animal had been in this condition for
twenty minutes, 100 cc of calcium chlorid solution was administered by intraven-
ous injection. The respiratory symptoms disappeared at once, although the coma
persisted. Sixty cc more of the calcium chlorid solution was given and in five
minutes the animal got up on its feet, and at first was unsteady but, after taking a
few steps, appeared apparently normal.
DISCUSSION AND CONCLUSIONS.
Hypoglycemia.—The data presented bring out two important considerations.
1. Hypoglycemia is not analogous to milk fever symptoms.
2. The bovine tolerates a much lower blood-sugar level than is reported for
other species.
The rather prolonged cases of hypoglycemia, going as low as 17 mg. per 100 cc
in trial II, should dispel any question as to low blood-sugar being a cause of partu-
rient paresis.
346 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [ I, IV
Hypocalcemia.—From these experiments it is noted that beef types apparently
react somewhat differently than dairy types. The beef animals gave some evidence
of tetany, while only one of the dairy animals showed any symptoms that could be
likened to tetany. This was with a pure-bred Guernsey in a strange environment
when a demonstration was given before a large group. With beef types, apparent-
ly, hypocalcemia may produce symptoms more analogous to tetany.
Before the symptoms of hypocalcemia become too pronounced, the animal
may effect a rather rapid spontaneous recovery. If only sufficient sodium citrate
is injected to cause a marked staggering gait, spontaneous recovery is effected in a
short time. Whether this is effected through an oxidation of the citrate radical of
the calcium citrate and thus freeing the calcium ions or whether it is due to the
release of calcium ions from the body stores, is not known.
The administration of calcium chlorid requires care and skill. Calcium chlorid
in 20 per cent. solution must be given intravenously. If not carefully administer-
ed, varying amounts of the solution will be deposited in the tissues, which may
result in edema, abscessation, necrosis and phlebitis.
THE INFLUENCE OF DIET UPON THE COURSE OF COCCI -
DIOSIS INFECTION IN CHICKENS,
(Reprinted from Poultry and Poultry Husbandry, dated 14th August 1931.)
[ Observations made at the Southern Table Poultry Experimental Station, at
Wye College, which tend to show that in Coccidiosis in Chickens the diet of birds
exerts a material influence upon the ailment. This is perhaps the first experi-
ment which so " strongly indicates that the nature of the ration plays a vital
part in determining whether chickens are going to withstand or succumb to
Coccidiosis infection, an infection which the great majority of chickens are
exposed to ".]
When a diet definitely deficient in certain essentials is fed to animals, clearly
defined symptoms of disease and pathological changes occur. Where disease is
caused by living organisms which are parasitic upon the animal body it is probable
that the nature of the diet may play contributory part in lessening or aggravating
the condition, but the function of diet in this respect is as yet not clearly
defined. Should the course of disease be influenced by diets which are not in the
strict sense deficient but considered as coming within the sphere of normal, the
question becomes one of practical moment.
These notes are concerned with observations made at the Southern Table
Poultry Experimental Station, Wye, which tend to show that in coccidiosis of
chickens the diet of the birds exerts a material influence upon the disease.
The contributory cause of outbreaks of coccidiosis is often obscure, though a
variety of plausible explanations may be advanced to account for outbreaks of the
disease. The soundness of these explanations is generally doubtful, and it has to
be remembered that with this disease care must be exercised to avoid placing
importance upon a factor which may be purely coincidental.
Every year coccidiosis causes a heavy mortality among fowls, but despite this
and the scientific interest of the problem comparatively few investigations of a
fundamental nature have been made upon the disease, and authoritative knowledge
is scanty regarding such aspects of the question as the plurality of species of
coccidia, the pathogenicity of possible different species, the lesions these produce
in the host bird, the resistance of the host to the invasive and destructive action
( 347 )
H
348 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [ I, IV
of the parasites under different environmental condition, and the question of
acquired resistance or immunity on the part of the host.
However, it may be accepted that more than one species of coccidium exist
and that these probably vary in their pathogenicity; further, there are indications
that birds are capable of building up a resistance to infection as the result of a
previous attack of the disease, and that as far as is known there is no very definite
increase in resistance due to age alone. Again it is known that if reinfection of the
bird is prevented the disease runs a remarkably rapid course, and that from the
time of the birds ingesting the sporulating oocyst to the disappearance of the
infection is a matter of not more than 10 to 14 days.
The longevity and great viability of the sporulated oocyst, the infective stage
of the parasite, is well known, and practical measures for the prevention of the
disease have been formulated with a view to keeping young chicks off ground or
pasture upon which poultry have been running and which probably contaminated,
and chicks are confined to the narrow limits of the brooder house and possibly a
sun porch. But unless the chicks are kept on wire floors it is very questionable
whether the exposure to infection in the brooder house is not as great as, or some-
times even greater than, would be the exposure were the chicks allowed to range
over an area of grass. This is because, if infection of the ground outside the
brooder house or on the farm exists, it is virtually impossible, under farming
conditions to prevent the infection reaching the chicks in the brooder, and once
infection is acquired by the chicks, the small area in the brooder will rapidly become
heavily contaminated.
Nevertheless, apparently good results have followed the adaptation of the
more confined system of rearing, and the losses attributed to coccidiosis have in
many instances diminished. Is this improvement due to the adoption of the
enclosed system or is it merely coincidental and is it possible that any change in
the treatment of the chicks was made about the same time, that might have a
bearing upon the course of the disease, e.g., a change of feeding, say, from a wet to
a dry mash, etc.? These questions are worthy of consideration.
The suspicion that diet might have some bearing upon coccidiosis infection
arose from the experience of this year's chicken rearing at the Southern Table
Poultry Experimental Station, Wye. For the past three years the brooder-house and
sunporch system has been used for rearing chicks in their first eight weeks of life,
and there has been no suspicion that during this period the chickens had been
infected with coccidiosis. A number of deaths certainly occurred but these were
not considered in excess of the usual wastage caused by unknown and unspecified
causes and they excited no alarm.
INFLUENCE OF DIET UPON COCCIDIOSIS IN CHICKENS
349
Previous to the introduction of the confined brooder-house there had been
definite loss from coccidiosis among the young chicks in the late summer and
autumn hatchings.
In 1931 a change was made in the feeding of certain of the chicks. These
were given a ration which was calculated to supply growth and maintenance
requirements but not fat, in other words a store ration. This was fed for the first
time to a batch of 100 chicks. These chicks commenced to die at the end of the
third week, and by the end of the sixth week the majority were dead and the
survivors were unthrifty and worthless. One or two of the dead chicks were sent
to the Ministry's laboratory at Weybridge and a diagnosis of coccidiosis was
returned. Meantime other chicks kept under comparable conditions, but receiving
the customary ration fed at the Institute continued to behave apparently normally,
and though a number of these animals died, they were too few to excite suspicion,
and the cause of these deaths was not ascertained. At first it was thought that the
chicks fed upon the store ration and which died from coccidiosis must have been
accidentally exposed to a heavy infection, and fresh houses were selected which had
been free from all poultry for a period of twelve months, and into these houses
batches of newly-hatched chickens were placed. These were again fed the two
rations in order to test their relative merits as regards growth in the chicks, etc.,
but again the experiment was upset in as dramatic a manner as on the former
occasion, chicks fed on the store ration rapidly dying while the others survived.
The results of feeding this store ration were so striking, though along an entirely
different line from that intended at the commencement of the experiment, that it
was considered of sufficient interest to follow the course indicated and ascertain as
far as possible if the ration alone did play such a vital part in the incidence of the
disease. Accordingly, with the supervision of the Veterinary Department of the
South-Eastern Agricultural College, a further experiment was planned under
what appeared more controlled but still farming conditions. The plan of the
experiment was as follows:—Six hover houses and sun parlours were selected. In
none of these had there ever been chickens with a known history of coccidiosis.
These houses were grouped in pairs. One pair was scrubbed out, disinfected, and
sterilised as far as possible with a blow lamp. The second pair was scrubbed out
and disinfected only. The last pair was scrubbed, disinfected and blow-lamped,
and then infected with coccidia by spreading a mixture of droppings of infected
chicks equally upon the floors and brushing these out after 24 hours.
Into each prepared house 94 chicks all from one hatching were placed. The
chicks in one house of each pair were fed upon the store ration, those in the
remaining three houses were fed the institute ration. The results which followed
H 2
350 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [ I, IV
were practically identical with what had previously been experienced. These are
herewith tabulated:—
Ration
Store ration .
Store ration .
Store ration .
Normal Insti-
tute Ration.
Normal Inst-
tute Ration.
Normal Insti-
tute Ration.
House
Disinfected and
blow-lamped.
Disinfected
Disinfected,
blow-lamped
and reinfect-
ed.
Disinfected and
blow-lamped.
Disinfected
Disinfected,
blow-lamped
and reinfect-
ed.
Number of chicks which died per week.
1st
wk.
0
0
0
0
0
0
2nd
wk.
0
0
0
0
0
0
3rd
wk.
0
0
0
0
0
0
4th
wk.
3
20
6
2
1
3
5th
wk.
34
29
67
4
0
11
6th
wk.
40
28
12
1
1
4
7th
wk.
8
5
4
1
5
2
8th wk.
Survivors un-
thrifty, killed.
Survivors un-
thrifty, killed.
Survivors un-
thrifty, killed.
2
1
1
9th wk.
4
unthrifty
killed, remain-
der sent to
fatten.
3
unthrifty
killed, remain-
der sent to
fatten.
4
unthrifty
killed, remain-
der sent to
fatten.
This time, however, all the chicks which died were examined at the College
Veterinary Laboratory. An interesting and important point established by these
examinations was the fact that the deaths which occurred among the chickens fed
the normal Institute ration were also due to coccidiosis in the majority of instances.
Had these post-mortem examinations not been made it is probable that the
mortalities would not have excited comment and the presence of coccidiosis infec-
tion would have remained undetected.
In none of the houses did deaths commence until the fourth week, and it was
during the fifth and sixth weeks that the death-rate reached its peak and the post-
mortem examinations showed acute coccidiosis infection. Thereafter the deaths
diminished and a number of the chickens dies as a result of the coccidiosis infection,
though the acute disease had run its course. This was indicated by the emaciation
of the chicks and the presence of firm casts in the caeca, though microscopical
examination of these casts and of portions of the intestine showed few or no
oocysts.
INFLUENCE OF DIET UPON COCCIDIOSIS IN CHICKENS
351
By the end of the seventh week 256 birds out of 272 birds fed upon the store
ration had perished and the remainder were too unthrifty to make further rearing
profitable. As against this, at the end of the eighth week only 39 birds fed upon
the usual Institute ration had died from disease. The following week 11 were killed
because of being unthrifty and 22 birds were drafted into the fattening pens.
The deliberate infection of pens had little effect upon the course of the
epizootic, and the experiment illustrates in no uncertain manner the impossibility
of excluding coccidiosis from brooder houses under ordinary farming conditions,
even though all ordinary precautions are taken. That deaths did not commence
until the fourth week suggests that the initial infection of the chicks was not a
heavy one, and it was only after recontamination of the houses by the chickens'
droppings commenced that the infection became sufficiently severe to kill the
chicks.
Finally, the experiment strongly indicates that the nature of the ration plays a
vital part in determining whether chickens are going to withstand or succumb to
coccidiosis infection, an infection which the great majority of chickens are exposed
to.
It is hoped that the necessary aid may be available to continue this investiga-
tion both under controlled laboratory conditions and in the field, where the import-
ant factor or factors in the diet may be arrived at by adequately planned experi-
ment, and further knowledge concerning the relationship between the parasite and
the host obtained.
[ Speaking of coccidiosis in the informative paper he read to the National Poultry
Parliament at Scarborough, Mr. Y. Watanabe said :—I am already quite certain
that this disease can, to a very great extent, be both prevented and controlled by a
skilled poultryman. I cannot deal fully with such a big subject at the present
moment, but summarised quite briefly, I have reason to think that the coccidia can
go through the necessary cycle for their reproduction only in the unhealthy intestines
of an overfed chick. Where the insides of young chicks are kept healthy by their
having periods of rest from feeding, where in other words, young chicks are fed by a
highly skilled attendant who keeps them lively for each feed and also keeps the
litter free from the musty left-overs of the meal before, the chicks have the very
highest resistant powers against coccidiosis, since the coccidia cannot reproduce
themselves in the healthy intestines. This theory explains the successful way in
which coccidiosis has been controlled by removing chicks to clean ground or by the
continual relittering of intensive brooder houses.]