NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
H. S.
BAWA
3
internal parasites have ever been found in the lungs of the cases examined at autopsy.
No pathogenic organisms have ever been isolated or found on smear examination from
these cases.
ETIOLOGY
The disease is due to an ultra-microscopic and filterable virus which is present in
the pneumonic areas of the affected lungs and in the pleural exudate Every attempt
to cultivate the etiological agent by previous works has always failed. Only recently
Longley [1940] was able to isolate the causative agent and described it as a highly
pleumorphic organism, which in fresh material examined by dark illumination bears
close resemblance to the organism of contagious bovine pleuro-pneumonia, viz.
Asterococcus mycoides and gave the name Borrelomyces peripneumoniae capri.
NATURAL
INFECTION
It is not exactly known how the disease is spread under natural conditions;
mostly the disease is aerogenic in origin. It is most probable that the etiological agent
of all the specific pneumoniae primarily reach the lungs through the bronchial tubes.
The experimental transmission of the disease carried out at Karachi supports the view
that infection is bronchogenic.
EXPERIMENTAL
WORK
These experiments were conducted with a view to determine if the specific
pneumonia of goats found in Sind is identical to that of Madras described by Longley
[1940]. For experimental purposes live affected goats were brought from outside for
the supply of ineffective agent as previous experience had shown that the etiological agent
is very fragile and does not reach the laboratory in potent stage.
PREPARATION OF INOCULA
The goat was killed by cutting the throat. After clipping the skin over the
throat, it was washed with lysol or dettol lotion. The fore limbs were detached from
the throat and deflected then and the skin covering the sternum was reflected. The
ribs were then cut through proximally and distally and the flap so produced reflected
forwards thus exposing the lungs in situ. The pleural exudate was collected by meant
of a sterile syringe, into a sterile glass flask containing glass beads to prevens
coagulation. The suitable portions of the affected lungs (avoiding portion of lungs
which had become friable, dry and necrotic) were collected into a sterile vessel and
cut into small bits; these were then transferred to a sterile mortar and made into a
fine pulp. The pleural exudate is added to the lung pulp and is then mixed with equal
volume of cold normal saline.
TECHNIQUE
FOR
INTRANASAL
INSUFFLATION
For nasal insufflation the De Vilbiss No. 15 atomiser was used with the nozzle
inserted some 2 to 3 inches into the nasal cavity, the source of pressure being the
hand; about 10 c. c of the prepared inocula was sprayed into each nostril and
intermittent pressure on the chest wall was applied during insufflation to enforce deep
respirations.
Experiment No. 1. The experiment was designed to see if local reaction similar
to that described by Longley could be produced by intramuscular inoculation of
prepared inocula.
4
Contagions Pleuropneumonia of Goats
TABLE I
Reaction with material from natural case
Experimental
goat
No.
1
2
Date
7 July 1942
do.
Route
Intramuscularly
do.
Dose
10 c. c.
do.
Remarks
Developed acute swelling at the site which started
to recede on 5th day. Slaughtered.
Showed no reaction. Probably goat had a natural
attack of disease some time and had developed
immunity.
The pieces of affected muscles from goat No. 1 were sent to the Imperial
Veterinary Research Institute, Izatnagar, for histopathological examination. It was
reported that the muscle lesion was identical with that described by Longley [1940].
The experiment (Table I) shows that the intramuscular inoculation of healthy goats
with pleural exudate and lung juice results in a swelling of typical clinical and pathologi-
cal characters.
Experiment No. 2. It was decided in this experiment to administer the inocula
to each of the three experimental goats, by intra-nasal insufflation, direct into the
lung and also by intramuscular route. Into the fourth goat (control) heated inccula was
administered by intra-nasal route. The experiment was designed in order to see by which
route disease could be transmitted.
TABLE II
Reaction with material obtained from donor No. DI from Nawabshah
Experimental
goat
No.
3
4
5
6
Date
20 August
1942
do.
do.
do.
Route
Intra-nasally
Direct into lung
Inlra-muscular at
sholder
Intra-nasally. In-
oculum heated to
60°C. for 30 min-
utes
Dose
20 c. c.
5 c. c.
do.
20 c. c.
Remarks
Temperature rose to 105° on 12th day and to
106° on 13th day. Goat very dull, off feed,
with cough and felt pain on tapping the chest.
Aborted on 18th day. Made complete recovery.
Subsequently used for G. T. V. and on post-
mortem showed old encapsulated pneumonic
lesions.
As soon as the needle was withdrawn the goat
staggered, collapsed and died withing two-
minutes. Postmortem showed, abdominal
organs highly engorged with blood. Blood-
showed rapid coagulation.
On second day at the site of injection there was
swelling heat and pain and goat was going lame.
Goat became normal after six days. Aborted
32nd day.
The goat showed no symptoms or thermal re-
action for 38 days while it was kept under
observation.
H. S. BAWA
5
TABLE III
Reaction with vaccine made from donor goat No. DI
Experimental
goat
No.
7
Date
20 August
1942
6 September
1942
Route
Subcutancously
neck.
Intra-nasally
Dose
1 c. c.
14 c. c. of
virulent
from
Donor
Goat
No. D 2
Remarks
Goat was kept under observation for 17 days
but showed no reaction.
On 28 September, i.e. after 22 days, the goat
showed a rise of temperature to 105.2, dull, off
feed with cough and died on 29 September,
1942. Postmortem showed bilateral pneu-
monia. Costal pleura inflamed and 50 c. c.
of pleural exudate present.
TABLE IV
Reaction with material obtained from donor gout No. 2 from Pithoro
Experimental
goat
No.
8
9
10
Date
6 August 1942
do.
do.
Route
Intra-nasally
Intra-musculuar
at shoulder
Intra-nasally
Dose
20 c. c.
1½ c. c.
heated
to 60°C.
for 30
minutes.
Left
shoulder
unheat
20 c. c.
heated to
60°C for
30 min-
utes.
Remarks
Rise of temperature to 104.6 on 16th Septem-
ber which rose to 106° on 18th September;
goat dull, off feed with cough, and anxious
look. Temperature fell down to 102.8° on
20th September. Goat was slaughtered
on 24th September. About half of the right
side diaphragmatic lobe completely hepatized
and adherent to pleura. Medisternial gland
enlarged. 15 c. c. pleural exudate.
No reaction was seen on the right shoulder.
Painful swelling developed on left shoulder
which caused lameness. Goat aborted on 12th
September, 1942. Died on 16th October
through emaciation. I. V. R. I. reports:
Serum doubtful against A, positive against M.
Was kept under observation till 4th October
1942, but showed no reaction.
6
Contagious Pleuropneumonia of Goats
The results of these experiments (Table II) show that the disease is transmissible
by intra-nasal insufflation. The inoculum is capable of producing local reaction on
intramuscular inoculation. Heating the inoculum to 60°C. for 30 minutes deprives it
of its potency.
Experiment No. 3. This experiment was designed to immunize the goat with
the formalized lung emulsion (the method adopted in the field) and then after .7 days
put her to immunity test with test dose of virulent inocula by intra-nasal route.
The above experiment (Table III) shows that the goat, immunized according to
the method followed in the field, failed to withstand the test dose of virulant inocula
and further proves that the fatal disease can be transmitted by means of intra-nasal
insufflation of the virulent inocula.
Experiment No 4 This experiment was a repetition of experiment No. 1 to see
if the fatal disease could be produced.
This experiment (Table IV) shows that the disease can be transmitted by means
of intranasal insufflation of virulent inocula. Inocula are capable of producing local
reaction on intramuscular inoculation. Virulent inocula if heated to 60°C. for 30 minutes
lose their potency.
Experiment No. 5. This experiment was designed to see if the disease could
be passed on to healthy goats by using inocula prepared from the material obtained
from experimental goat No. 8 which was slaughtered on 24 September 1942.
TABLE V
Reaction with material obtained from experimental goat No. 8
Experimental
goat
No.
11
12
13
Date
24 September
1942
do.
do.
Route
Intra-nasally
Intramuscularly
right shoulder and
thigh
Intra-nasally heat-
ed to 60°C. for 30
minutes
Dose
20 c. c.
10 c. c.
and
5 c. c.
20 c. c.
Remarks
Goat aborted on 6th October 1942. Tempera-
ture shot up to 105° on 16th October. Goat
dull, off feed and with cough. Died on 18th
October.
Apical
and
diaphragmatic
lobes pneumonic. No pleural exudate, pro-
bably it coagulated as postmortem was made
12 hours after death.
Heat, pain and lameness at both sites of inocu-
lation. Goat aborted on 8th October 1942.
Lameness continued for eight days. Died on
19th October. Muscles necrotic at the site of
inoculation. 50 c. c. of pleural exudate
present. No lung lesions.
Kept under observation till 29th October 1942,
but showed no signs of the disease.
These experiments (Table V) show successful second passage of the disease and
again prove that virus loses its potency when heated to 60°C. for 30 minutes.
Experiment No. 6. This experiment was designed to see if active causative agent
is present in pleural exudate or not.
The experiment (Table VI) shows that pleural exudate is very virulent and
can produce fatal local reaction; this experiment further proves that the disease can
be conveyed with material from the experimental goat to the healthy goat.
H.
S.
BAWA
7
TABLE VI
Reaction with pleural exudate obtained from experimental goat No. 7
Experimental
goat
No.
14
Date
29 September
1942
Route
Intra-muscularly
right shoulder
and thigh
Dose
7 c. c.
Remarks
Heat and slight inflammation at the site of injec-
tion on 1st day. Lameness both right fore and
hindllegs. Inflammation very painful, spreading
to the chest and down the fore leg. Goat
unable to support her weight. Died on 5th
October. The muscles necrotic, oedematous,
yellow in colour. There was 50 c. c. of
muscle exudate. Lung on the right side
showed small four focal patches of pneumonia
in diaphragmatic and cardiac lobes.
Experiment No. 7. This experiment was designed to see if the muscular
exudate produced by intramuscular injection of pleural exudate is virulent or not.
TABLE VII
Reaction with muscular exudate obtained from experimental goat No. 14
Experimental
goat
No.
15
Date
5 October
1942
Route
Intra-nasally
Dose
30 c. c.
Remarks
This goat died on 26th October without show-
ing any thermal reaction or other signs of
disease. Postmortem examination showed
10 c. c. of pleural exudate and right dia-
phragmatic and apical lobes pneumonic. Left
side lung was normal.
This experiment (Table VIII) proves that muscular exudate is virulent and is
capable of producing fatal pneumonia.
IMMUNIZATION
For the first time during the year 1938 experimental vaccination was carried
out in the face of an outbreak among 20 goats out of a flock of 173. The material
used for vaccination was a saline emulsion of hepatized lung removed from a naturally
infected goat sacrificed in extremis. The emulsion was formalized to the extent of one
per cent and kept at the room temperature for 36 hours before it was used. Dose
of 1 c c. in the region of neck was given to each animal irrespective of age. Vaccine
was prepared according to Kolayli, Raif, Esim and Arayici [1935]. The temperature
of the goats at the time of inoculation varied between 102° and 03°F. Twenty-four
hours after the vaccination, two goats registered temperatures 104.2° and 106°
respectively. Three of the vaccinated goats died on the 5th, 6th and 7th day after
inoculation. These goats probably were in the incubative stage at the time of
vaccination. Among the unvaccinated lot, 25 goats died. As this field experiment
was inconclusive but showed some signs of success, it was decided to vaccinate the
8
Contagious Pleuropneumonia of Goats
entire flock in the next outbreak in order to see if it was. possible to check the spread
of the disease by this method. During the year 1938-1939 only one outbreak of the
disease was reported; 82 goats had died of the disease, before the experimental
vaccination could be undertaken. Fifty-two healthy incontact goat's were inoculated
with formalized diseased lung emulsion which was kept for 24 hours at room tempe-
rature before being used for vaccination. Only two deaths among the vaccinated goats
were recorded and the disease was brought under control. The results of this experiment
were very encouraging.
Experience gained during the period 1937-1939 showed that the reaction among
the vaccinated goats was not at all severe; it was, therefore, decided to inoculate the
goats immediately after the preparation of the vaccine instead of keeping it at room
temperature for 24 to 36 hours before its use.
During the year 1939-1940 seventy-two goats were inoculated; there were three
deaths among the vaccinated goats.
The maldars gained confidence in this method of control and became eager to
report the disease and were not indifferent as they used to be when no preventive vacci-
nation for this scourage was known.
During the year 1939-40 eight outbreaks were reported and a total number of
831 goats were vaccinated with an average mortality of 3.4 per cent among the
vaccinated During the year 1941-42 a team of veterinary assistant surgeons was
trained in the technique of the preparation of this vaccine and its use; and from the
year 1942 onwards this mode of vaccination has been adopted by the Civil Veterinary
Department, Sind, as a routine measure to check the spread of contagious pleuro-
pneumonia in goats.
Table VIII shows the number of inoculations performed during the years 1937 to
1945.
TABLE VIII
Number of inooculations performed during the years 1937—1945
Years
1937—38
1938—39
1939—40
1940—41
1941—42
1942—43
1943—44
1944—45
No.
of
outbreaks
1
1
1
8
39
51
53
26
No. inoculated
20
52
72
831
5,870
7,127
7,350
9,443
Average
per cent.
mortality.
15.0
5.7
4.3
3 8
1.87
1.32
.36
.4
The figures in Table VIII shows that each year vaccination has become more
and more popular and deaths among the vaccinated ones lesser. The technique
employed in the preparation of the vaccine and its use is given in the Appendix. In
one flock consisting of 400 goats 2 c. c dose of the vaccine was tried instead of
1 c. c. which is the dose usually given in the field. The larger dose was tried to see
if a higher grade of protection could be achieved as it was reported by some veterinary
staff that 1 c. c. dose in some cases did not seem to give sufficient protection
toward off an attack of the disease. The goats showed no untoward reaction on
receiving 2 c. c. of emulsion and no deaths occurred among the vaccinated goats.
REFINING OF HIGH ACID GHEE
By M. A. SAMUEL, K. C. SEN, ZAL R. KOTHAWALLA and NOSHIR N. DASTUR
Imperial Dairy Research Institute, Bangalore
(Received for publication on 27 December 1945)
G HEE produced under clean conditions contains very little of free fatty acids.
The Agmark standards allow free fatty acids to the extent of 2.5 per cent oleic. It is,
however, found that under commercial conditions of production this limit is often
exceeded and ghee with as much as 12 per cent oleic acid is not uncommon. In the
trade such ghee is used to blend good ghee and bring the free fatty acid content to
the prescribed limits. This practice is not sound because ultimately it results in lowering
the quality of the good product also.
By removing the free fatty acids from ghee, it is possible to put an wholesome
product on the market. Such a practice is regularly followed in case of vegetable
oils which even when fresh often contain rather large amounts of free fatty acids. In
the present investigations the possibility of using such methods as can be applicable
to ghee, under the existing trade conditions have been investigated. The work has
been divided for the sake of convenience into two parts. The first part deals
mainly with alkali refining and the second part with refining by the use of basic
adsorbents.
PART I
Before taking up trials with alkali refining, work was carried out to see if a
simpler process could be adopted. As these trials did not give very encouraging results
they have only been briefly described here.
(a) Heating to 120°C. did not lower the content of free fatty acids, though it helped
to improve the flavour of high acid ghee.
(b) Washing with hot water, four times, reduced the acidity of ghee t o the extent
of about 13 per cent. The first wash was most effective in reducing the acidity. Both the
colour and the flavour of ghee were improved by washing.
(c) Washing with hot 3 per cent and 5 per cent solutions of commercial salt gave
the same results as when hot water was used.
(d) Steaming high acid ghee for an hour reduced the acidity by about 2 per cent
and steaming for two hours by about 3 per cent.
(e) Washing ghee three times with an equal volume of ethyl alcohol reduced the
acidity by about 77 per cent.
(f) Trials were carried out to neutralize the acidity with soda ash solution. For
laboratory trials 10 lb. of high acid ghee was used each time. Ghee was warmed to
about 65°C and transferred to a butter-churn. The requisite amount of 4.0 N soda ash
solution was added and the mixture churned for 15 minutes. The contents of the
churn were then transferred to a cream separator, the cream-screw having been
adjusted for maximum fat output. The ghee thus obtained was given three further
washings with warm water to take out all the alkali. Addition of soda ash solution
all at once and in two instalments was tried but no striking difference in the reduction
of acidity or in handling losses was noticed between the two methods. The results
obtained are given in Table I.
11
12
Refining of high acid ghee
It was found that by neutralizing with soda ash, there was a decrease of about
87 per cent in the acidity of original ghee. On refining, the ghee improved in colour
but had a flat flavour. It was noticed that refining tended to raise the Reichert value to a
small extent. A few samples of refined ghee were stored at 37°C. to study if there was any
increase in acidity. The results obtained are given in Table II. It was found
that refined ghe e was quite stable and did not again develop acidity rapidly.
TABLE I
Refining high acid ghee with soda ash solution
Trial No.
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
Nature of treatment
The required quantity of soda ash
solution (4.0N or 21 per cent)
added all at once.
Same as above but soda ash added
in two instalments.
Acidity of ghee
(percentage
oleic acid)
Original
7.75
7.75
77.5
11.86
11.86
10.40
6.99
6.99
6.99
9.22
9.22
9.22
9.22
9.57
9.57
Refined
0.92
1.54
1.29
1.64
1.51
1.76
0.97
069
0.81
1.27
1.18
1.20
1.09
1.12
1.24
Percentage
of
decrease in
acidity
88.1
80.1
83.3
86.1
87.2
83.2
86.1
90.1
88.4
86.2
87.2
87.0
88.1
88.3
87.0
Reichertvalue
Original
...
...
...
...
...
...
...
...
22.37
22.96
22.97
...
...
...
...
Refined
...
...
...
...
...
...
...
...
23.95
23.26
23.04
...
...
...
...
M, A.
SAMUEL
ET.,
AL.
13
TABLE II
Storage of ghee with soda ash solution and its acidity
Serial No.
1
2
3
4
5
6
7
8
Original acidity
6.99 unrefined
0.91
9.22 unrefined
1.27
1.18
9.57 unrefined
1.12
1.24
Values in percentage oleic acid
Acidity after
one
month
6.69
0.98
9.37
1.44
1.31
9.62
1.19
1.34
Acidity after
two
months
6.86
1.04
9.47
1.45
1.36
9.62
1.22
1.33
Acidity after
three
months
6.98
1.10
9.75
1.57
1.49
9.82
1.29
1.45
(g) Trials were carried out to neutralize the acidity with sodium hydroxide
solution. Commercial quality sodium hydroxide was used for these trials. Experiments
were conducted in the same manner as described in section (f) above. Different
strengths of solutions, viz. 2 per cent, 5 per cent, 10 per cent, 15 per cent, 20 per cent
and 25 per cent sodium hydroxide, were used. The alkali was added all at once. The
results obtained are given in Table III.
It was found that the strength of sodium hydroxide solution had a marked
influence on the degree of reduction in acidity. Dilute solutions were more efficient
in removing the acidity. For example, with 2 per cent sodium hydroxide the decrease in
acidity was 98 per cent, while with 25 per cent sodium hydroxide the decrease was 84
per cent A record of handling losses was also kept and is shown in the last column
of Table III. The loss as a rule decreased with the strength of the alkali solution
used. It was also observed that refining with sodium hydroxide produced a ghee with
a flat flavour and a whiter appearence. Reichert values were determined on a few
samples and with the treatment also there was a tendency for the Reichert value to
increase as was the case with soda ash refining.
h) Neutralizing with sodium hydroxide in the presence of sodium chloride was
also tried. During refining trials with alkali and during the first wash with water an
emulsion was formed and it was not easy to separate the fat. The separator bowl required
cleaning repeatedly and the foots as well required reseparation and also the foots
require reseparation. Trials were, therefore, carried out using commercial sodium
chloride
to help in breaking the emulsion. The amount of salt added
was calculated as a percentage of the volume of alkali solution used in refining.
The base of salt at the rate of 5 per cent gave very good results, lower concentration
producing little effect. Salt, dissolved in a little water was added after churning the
ghee with alkali. This treatment greatly helped in minimizing the handling losses as
illustrated in Table V.
14
Refining of high acid ghee
TABLE III
Refining high acid ghee with sodium hydroxide solution
Trial No.
1
2
3
Average
4
5
6
Average
7
8
9
Average
10
11
12
Average
13
14
Average
15
16
17
Average
Percentage of
NaOH used
2.0
„
„
5.0
„
„
10.0
„
„
15.0
„
„
„
„
25.0
„
„
Original acidity
of ghee (in
percentage of
oleic acid)
7.60
7.36
7.36
11.85
11.85
11.85
10.24
10.24
10.24
9.14
9.14
9.14
10.17
10.17
10.17
8.18
8.18
Acidity after
refining
0.30
0.29
0.35
0.31
0.57
0.61
0.66
0.61
1.31
0.99
0.96
109
1.61
1.20
0.90
1.24
1.30
1.07
1.69
1.00
1.44
Percentage of
decrease in acidity
99.2
99.2
95.3
97.9
95.1
94.8
94.4
94.89
87.2
90.3
90.6
89.4
82.3
86.8
90.1
86.4
87.2
89.5
88.3
83.4
87.8
82.4
84.5
Percentage of loss
in handling
24.2
19.0
19.0
20.7
26.2
20.5
23.4
23.4
16.5
19.3
19.3
18.3
17.5
14.7
14.7
15.7
19.3
16.5
17.9
13.7
10.1
12.8
12.2