NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
188
Rhinosporidiosis in Bovines
growth from a horse in Uraguay. Ayyar [1929 and 1932] in South India
detected the fungus in the nasal growths from two bullocks, one cow and one
pony. It is, therefore, interesting to note that while this disease has been met
with in a small number of equines in different parts of the world, its existence
in bovines has been reported, so far, only from the Madras Presidency.
It has been possible for the present author, during the last six years, to
record rhinosporidiosis in eighteen bovines and one pony in this presidency, in
addition to those already reported by Ayyar [1929]. Ayyar's cases were all
from Tanjore district, but the following table shows that the disease exists in
other districts as well. The fact that twenty-three cases of rhinosporidiosis
(including two equines) in the Madras Presidency have been detected within
a period of eight years indicates that the disease is not so rare among animals
in this part of India as it is supposed to be. The present writer has not found
the disease in cows so far, and most of the cases noted in the table below were
detected while examining nasal washings for nasal schistosomiasis.
*TABLE I
Serial
No.
1
2
3
4
5
6
7
8
9
10
11
12
13
14
Year
1930
1931
1931
1932-33
1933-34
1934-35
1934-35
1934-35
1934-35
1935-36
1935-36
1935-36
1935-36
1936-37
Name of
District
Chingleput
Malabar .
Ramnad .
Tanjore .
Tanjore .
Tanjore .
Tanjore .
Ramnad .
S.Arcot .
Ramnad .
Tanjore .
Ramnad .
Malabar .
Malabar .
Name of
Town
Madras .
Calicut .
Devakottah
Tanjore .
Tanjore .
Tanjore .
Tanjore .
Devakottah
Kallakuruchi
Devakottah
Tanjore .
Rajapala¬
yam.
Calicut .
Calicut .
Kind of
Animal
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Bullock .
Age
. .
. .
7 years .
6 years .
Not avail-
able.
6 years .
7 years .
5 years .
7 years .
8 years .
7 years .
9 years .
7 years .
6 years .
Seat of
Tumour
Nostrils.
Do.
Do.
Entrance to
left nostril.
Nostril.
Nostril.
Nostril.
Nostril.
Nostril.
Nostril.
Nostril.
Nostril.
Nostril.
Nostril.
*In this list, the four cases reported by Ayyar (1929 and 1932) have not been included.
M.
ANANT
NARAYAN
RAO
189
Serial
No.
15
16
17
18
19
Year
1936-37
1936-37
1936-37
1937-38
1937-38
Name of
District
Chingleput.
Chingleput.
Chingleput.
Malabar .
E. Godavari
Name of
Town
Tindivanam
Trivellore .
Saidapet .
Manjeri .
Cocanada .
Kind of
Animal
Bullock .
Bullock .
Bull-cult .
Bullock .
Pony .
Age
8 years .
8 years .
2½ years .
4 years .
aged. .
Seat
Tumour
Nostril.
Nostril.
Nostril.
Nostril.
Nostril.
In the Madras Presidency rhinosporidiosis in man has been reported fairly
frequently from certain districts and it is interesting to note that the bovines
noted above are also from those very districts. So far, all the reported cases
of rhinosporidiosis in animals have been from districts other than the Northern
Circars ; opportunity is now taken to record the first case in a pony at Cocanada,
East Godavari.
No cases of rhinosporidiosis in bovines or equines have been reported
from Northern India. Allen and Dave [1936] state that at their instance, the
Director of Veterinary Services, Central Provinces, issued instructions to his
staff to look for rhinosporidial growths in animals in that province but no cases
were reported. Those authors made enquiries in the Drug district of Central
Provinces and failed to obtain even one infected animal, though they saw
over sixty human beings affected with the disease in Raipur and Drug districts.
This seems interesting as far as it goes, but compared to what obtains in the
Madras Presidency, it seems reasonable to assume that cases of rhinospori-
diosis in bovines or equines have escaped diagnosis till now and it may not
be long before such cases come to light.
2. SITE OF INFECTION
The predilection seat for rhinosporidial growths in animals appears
to be the nasal mucous membrane. In all the bovine and equine cases re-
ported so far, such growths were found only in the lower third of the nasal
cavity. An analysis of the clinical histories of the affected bovines shows
that the growth is either found on the margin of the hole on the nasal septum
made for the nose string or by the side of the sessile lesions of nasal schistoso-
miasis, in the lower third of the nasal cavity. Hence, it would appear that
trauma is a necessary factor for the development of rhinosporidial tumours.
The author learns that in certain parts of Northern India, the system of
puncturing the nasal septum is not in vogue, and that nasal schistosomiasis
exists there. Therefore, there is at least one factor present in causing trauma
in the nose in cattle and adequate investigation may result in demonstrating
the existence of the disease in bovines in that part of India.
190
Rhinosporidiosis
in Bovines
3. SEX AND AGE INCIDENCE
As far as the twenty-one bovines included in the present studies are
concerned, it is interesting to observe that twenty animals or roughly 95 per
cent of the cases were bullocks. In the human beings the incidence of the
disease is very much higher in males than in females and it is found to be the
case in bovines also. This common sex incidence in bovines and in human
beings is somewhat significant and will be discussed later.
The affected animals were all between the ages of four and nine with one
exception, a bull-calf (vide Table I), which was reported to be only 2½ years
old. Bulls and bullocks are put to the plough when they are about 3½ years
of age and their noses are punctured for nose strings when they are about that
age. Cows are very rarely used for ploughing in Southern India and their
nasal septum is seldom punctured for a nose string.
4. DURATION OF THE DISEASE AND RECURRENCE OF THE GROWTHS AFTER
EXCISION
It has not been possible to obtain exact data regarding the total duration
of the disease in bovines, except in one case, a bullock aged about nine years
which was reported to have had the condition for over a period of about five
years.
As regards recurrence of the growths after removal, it has been observed
from some of the available history sheets that the growths re-appear in about
twelve to sixteen months. In a bullock which was kept under observation by
the author, the growth did not recur till eleven months after removal. That
animal was destroyed and its nasal mucous membrane was sectioned and
examined but no Rhinosporidium was detected. It would appear, therefore,
that recurrence depends on whether or not, the diseased tissue has been removed
completely along with the adjoining healthy tissue.
5. CONCURRENT INFECTION
Out of the fifteen animals whose histories are known eight (or 54.4 per
cent) had nasal schistosomiasis as well.
6. CLINICAL FEATURES
The tumours caused by Rhinosporidium in bovines and equines can be
classed under two types, viz. (1) Pedunculated and (2) Sessile. The size of
the growths is seldom bigger than a large playing marble. The sessile types
of tumours are more or less flat and are usually associated with the lesions of
nasal schistosomiasis and appear to be seldom bigger than a double bean.
The growths appear more or less lobulated, soft and spongy. The surfaces
of both types of tumours are dotted over with small white specks which repre-
sent the sporangia or asci of Rhinosporidium. The growths are pink or reddish
in colour and bleed readily when handled. It is interesting to note that in all
the cases observed so far, the lesions were unilateral in the nose.
Ind. Jour. Vety. Sci. & Anim. Husb., Vol. VIII, Part III ]
PLATE VI
FIG. 1.
A small growing ascus. Note the nucleus
as a ring with the nucleolus which is
accentric. × 700
FIG. 2.
Developing asci (Trophozoites). Note the small one
at the bottom of the bigger one. Note the granular
protoplasm, the nucleus and the nucleolus. × 700
FIG. 3.
The central ascus has a thick wall in which the "pore"
is seen. Note the nuclear divisions in the protoplasm.
The ascus on the right shows that condensation of
protoplasm round nuclear bits is in progress. × 200
FIG. 4.
Section of rhinosporidial growth - equine
showing a developing ascus with a thick
wall in which is seen the pore. ×200
PLATE VII
[ Ind. Jour. Vety. Sci. & Anim. Husb., Vol. VIII, Pt. III
FIG. 1.
Section of growth - bovine. A developing ascus in
which the nuclear division is completed. × 200
bits of nuclei is just commencing. Note the pore
on the wall of the ascus. × 200
FIG. 2.
Section of rhinosporidial growth - bovine. A young
ascus in which condensation of protoplasm around
bits of nuclei is just commencing. Note the pore
on the wall of the ascus. × 200
FIG. 3.
A degenerating ascus, the contents of which have
been replaced with tissue cells. Note the section
of a giant cell inside it. × 200
FIG. 4.
An ascus filled with small spores only × 450
192
Rhinosporidiosis in Bovines
the spores are said to escape, is seen in the wall depending upon the orientation
of the ascus in section. The spores in an ascus vary in their sizes ; some of
them are large, and each large spore has a capsule containing a nucleus and
proteinacious granules and the rest are small spores with no capsule and
contain finely granular protoplasm and a nucleus. The large spore measures
8 to 10 µ and the small one 5 to 7 µ.
8. IDENTITY OF THE PARASITE
It is interesting to note that rhinosporidiosis in cattle occurs in such areas
in the Madras Presidency where it is known to exist in man. There appears
to be no difference in the histopathology of the lesion or in the morphology of
the fungus in the material obtained either from man, bovine or equine.
Wenyon [1926] doubts the existence of any specific differences between equine
and human rhinosporidiosis. Ayyar [1932] pointed out that there is a very
close resemblance between the human and bovine lesions as regards the site of
growth, gross appearance of the tumour, its histology and the morphology of
the sporangia, etc. He sent some of his material to Ashworth who confirmed
those findings and said that the discovery of Rhinosporidium in bovines may
throw light on the mode of infection. Allen and Dave [1936] also said that the
sections of rhinosporidial lesions from cattle looked very similar to those from
man. The author could not find any specific difference in the morphology of the
causal organism or in the histopathology of the lesions in men, bovines or
equines. It would appear, therefore, that the causal organism of rhinospo-
ridiosis in man and animals is identical. This conclusion seems to throw light
on the mode of transmission as prophesied by Ashworth and will be discussed
later.
9. DISSEMINATION OF SPORES FROM THE LESIONS
The mature ascus may burst upon the nasal mucous membrane liberating
the spores on its surface or it may burst in the soft tissue. In the former case
the spores get mixed up with the nasal mucus and may be passed outside the
animal body, or as it usually happens in cattle or even in human beings, they
may be swallowed with the nasal mucus to find their way outside the body
through the faeces. If the ascus bursts inside the tissue, the spores remain
in the tissue having to complete their destiny there alone. To complete their
biological destiny outside the animal body, the spores are for obvious reasons
provided with protection and food material which on. the other hand, are not
required by those that are destined to complete their life-history in the tissue,
where protection and food are provided for by the host tissue. It is interesting
to note that the author found in the nasal discharge only the large type of
spores each having proteinacious granules and a capsule. Other workers with
material obtained from human patients, particularly Allen and Dave [1936]
have recorded the presence of only the large spores in the nasal discharge
which is diagnostic of the infestation. Ashworth [1923] and Karunaratne
[1936] said that the smallest developing trophozoite in the tissue measure
Ind. Jour. Vety. Sci. & Anim. Husb., Vol. VIII, Pt. III ]
PLATE VIII
FIG. 1.
The large spores in asci of rhinosporidium. Note the protenaccous
granules and the capsule of each spore. × 750
FIG. 2.
Large spores in nasal discharge. Note the thicker capsule
than in those in asci of the lesion. × 650
M.
ANANT
NARAYAN
RAO
197
3. It is observed that the disease is prevalent both in man and animals in
certain districts of the Madras Presidency.
4. The organism causing the lesions in man and bovines is probably
identical.
5. In cows, as in women, the disease is rarely found, but in men and bul-
locks that take part in ploughing, the incidence of the disease is high.
6. The probability of the existence of a saprophytic form of the fungus is
suggested and discussed.
7. The possibility of dust and water being the medium through which
infection may be carried to healthy individuals is discussed.
ACKNOWLEDGMENTS
I am indebted to Mr. P. T. Saunders, Director of Veterinary Services,
Madras, to Mr. T. J. Hurley, Principal, Madras Veterinary College and to the
Government of Madras for the grant sanctioned for work on Rhinosporidium.
I am grateful to Dr. P. V. Cherian, Dr. Varada Acharya, Rao Bahadur Dr. T. S.
Tirumuti, Dr. A. Vasudevan and Dr. Kurup for the help rendered in supplying
me with fresh and preserved rhinosporidial growths from human beings,
without which it would not have been possible for me to make a comparative
study of the fungus. I am thankful to Mr. K. M. Thomas, Government
Mycologist, Agricultural Research Institute, Coimbatore for kindly arranging
to get the fungus in culture identified. My thanks are also due to Mr. P.
Margabhandu, Veterinary Assistant Surgeon, Tanjore, to my assistants Messrs.
S. Vaidyanatha Mudaliar, K. S. Gopalakrishna Iyer and to Mr. P. Doraswamy
Mudaliar, the artist of the College, for their valuable assistance given to me.
REFERENCES
Allen, F. R. W. K. and Dave, M. L. (1936). Ind. Med. Gaz. 71, 276.
Ashworth, J. N. (1923). Trans. Roy. Soc. Edinburgh. 43, 301.
Ayyer, V. Krishnamurti (1928). Trans. 7th Congress, Far East. Assoc. Trop. Med.
1927, 3, 658.
(1932). I. J. Vet. Sci., & Anim. Husb. 2, 1, 49.
Cordero, E. H. and Vogeslang, E. C. (1928). Bol. Inst. Clin. Quir. 4. Quoted by Allen
and Dave.
Dodge, C. W. (1936). Medical Mycology. Henry Kimpton, London.
STUDIES ON A NATURAL OUTBREAK OF PIGEON-POX
BY
R. L. KAURA, B.V.Sc., M.R.C.V.S.
Offg. Veterinary Research Officer, in-charge Serology
AND
S. GANAPATHY IYER, G.M.V.C.
Veterinary Inspector
Imperial Veterinary Research Institute, Mukteswar-Kumaun
(Received for publication on 2nd March 1938)
(With Plates IX and X)
INTRODUCTION
THERE are few authentic records of the occurrence of bird pox in India.
Since 1934 suspected cases have been examined at this Institute and it is
now possible to state that the disease is a menace to the poultry industry.
Apparently pigeon-pox has not been described in India, and this paper re-
cords the only outbreak that has come to our notice.
In April, 1936, spontaneous cases of what later proved to be pigeon-pox
occurred among the healthy stock of pigeons at this Institute. We had then
fifty-eight pigeons of which twenty-eight were isolated as sick and kept under
close observation for study. Six pigeons died and the rest recovered.
Previous to the occurrence of this outbreak, studies on pigeon-pox and
fowl-pox with reference to their propagation in vivo, the preparation of a vac-
cine from the pigeon-pox virus for use against fowl-pox and routine diagnostic
work on the specimens suspected for fowl-pox were in progress and are being
continued. The seed materials for our stock strains of fowl-pox and pigeon-
pox viruses were obtained in 1934 through the courtesy of the Veterinary
Laboratory, Ministry of Agriculture, Weybridge, England, and an Indian
strain of fowl-pox was later added in 1936.
Marx and Sticker [1902] found that the causative agent of pigeon-pox in
a natural case was a filterable virus which could be successfully passaged
through pigeons but when passaged through the fowl, it became attenuated for
the pigeon even after the first passage. M'Fadyean [1908] reported that in
outbreaks of ' epithelioma contagiosum' various species of domesticated
poultry and pigeons were affected. Dean and Marshall [1909] confirmed the
filtrability of the causative virus in a natural outbreak of ' pigeon diphtheria '.
Jowett [1909] considered that the bird-pox virus would adapt itself to the
particular species of birds in which it might have become implanted, losing
its power to infect any of the other species. Haring and Kofoid. [1911-12]
reported, that fowls could be infected with pigeon-pox and the sera of such
infected fowls could fix the complement to a greater extent than that of normal
(199 )
Ind. Jour. Vety. Sci. & Anim. Husb. Vol. VIII, Pt. III ]
PLATE IX
FIG. 1.
A natural case of pigeon pox showing buccal diphtheritic lesions, wart-like
nodular growths on the upper eyelid and signs of diarrhoea.
FIG. 2.
Head and neck of the same pigeon as in Fig. 1. showing the buccal and cutaneous lesions (magnified)
R. L. KAURA and S. GANAPATHY IYER 201
Material from the buccal lesions has not been used for subinoculation
purpose because it has been established in another paper by the authors [1936]
that in an identical condition in Indian fowls the causal agent of the buccal
diphtheritic lesions and the cutaneous lesions is one and the same filterable
virus.
TRANSMISSION EXPERIMENTS
(a) Experimental transmission of the disease in pigeons.—Five apparently
healthy pigeons that were in contact with the natural cases of pigeon-pox
were soon separated and inoculated on 20th April 1936 with the Indian
strain of pigeon-pox virus as a preliminary experiment (Table I). It
took some weeks before a fresh lot of healthy pigeons could be obtained.
Pox lesions devloped only in Pigeon No. 3 and the remaining four pigeons
resisted the infection
bably due to the varying degree of immunity which
might have developed area result of their having been in contact with the
naturally infected cases before they were segregated or due to their being
naturally immune to this infection as considered by Findlay [1930].
Three weeks after the above experiment, Indian strain of this virus after
passage through Pigeon No. 3 was subinoculated into five healthy pigeons
on 12th May 1936. Of these, four readily took the infection and in one
(Pigeon No. 45) there was no reaction (Table I).
Mixed crusts from Pigeons Nos. 41, 42, 43 and 44 were further passaged
into twelve healthy pigeons on 13th June 1936 with the result that experi-
mental disease was reproduced in ten pigeons and two were found to be re-
sistant (Table I). Subsequent passages of the Indian strain of this virus
were continued in pigeons for the availability of the material for further
work.
Lesions in the experimentally infected pigeons were mostly confined to
the seat of inoculation. Some of these birds developed acute gastro-enteritis
and succumbed and one showed eye lesions as well.
TABLE I
Experimental transmission of the disease in pigeons
Pigeon
No.
1
2
3
Date of inocu-
lation
20th April 1936
20th April 1936
20th April 1936
Inoculum (In-
dian strain of
pigeon-pox from
natural cases)
First passage .
Do. .
Do. .
Result
No reaction .
Do . . .
Reacted . .
Remarks
Originally in contact
with natural cases of
pigeon-pox.
Ditto.
Ditto.
202
Studies on a Natural Outbreak of Pigeon -Pox
TABLE I—contd.
Experimental transmission of the disease in pigeons—contd.
Pigeon
No.
4
5
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
Date of inocu¬
lation
20th April 1936
20th April 1936
12th May 1936
12th May 1936
12th May 1936
12th May 1936
12th May 1936
13th June 1936
13th June 1936
13th June 1936
13th June 1936
13th June 1936
13th June 1936
13th June 1936
13th June 1936
13th June 1936
13th June 1936
13th June 1936
13th June 1936
Inoculum (In-
dian strain of
pigeon-pox from
natural cases)
First passage .
Do. .
Second passage
Do. . .
Do. . .
Do. . .
Do. .
Third passage .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
Result
No reaction
Do. .
Reacted . .
Do. . .
Do. .
Do. .
No reaction
Reacted .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
Do. . .
No reaction .
Do.
. .
Reacted . .
Do. . .
Remarks
Originally in contact
with natural cases of
pigeon-pox.
Ditto.
Died on 1st June 1936.
Died on 6th June 1936.
Died on 30th June 1936.
(showed eye lesions).
Died on 27th July 1936.
Died on 19th July 1936.
Died on 1st July 1936.
Died on 6th February
1936.
(b) Experimental transmission of the disease in fowls.—Three fowls were
at first inoculated with natural pigeon-pox material on 20th April 1936,
R. L. KAURA and S. GANAPATHY IYER 203
(Table II). There was only a transient local congestion of the feather folli-
cles. Although the reaction was not very suggestive of successful trans-
mission of the disease from pigeons to the fowls, yet, their subsequent immunity
test against fowl-pox virus showed that they had developed the immunity.
Doyle and Minett [1927], Findlay [1930] and Irons [1934] obtained similar
results by the inoculation of fowls with pigeon-pox virus. Two control fowls
Nos. 56 and 57 were inoculated with fowl-pox virus alone. They reacted
typically unlike the three fowls that received the Indian strain of pigeon-pox
virus previously.
Four more fowls that were inoculated with the Indian, strain of pigeon-
pox virus from Pigeon No. 3, (Table I) on 13th June 1936, were tested with
our stock fowl-pox virus, along with two healthy controls on 25th June 1936
(Table II). All the fowls that received a dose of the Indian strain of pigeon-
pox virus reacted mildly to it and later resisted the test dose of fowl-pox virus
which produced the disease in the two healthy controls. This showed that
the Indian strain of pigeon-pox virus, like the English strain of the same
virus, can be used as a live vaccine against fowl-pox.
TABLE II
Experimental transmission of the disease in fowls and cross immunity tests with
fowl-pox virus
Fowl
No.
28
29
30
56
57
88
89
90
91
104
105
Date of inocu-
lation with
the Indian
strain of pigeon-
pox virus
20th April 1936
20th April 1936
20th April 1936
. .
. .
13th June 1936
13th June 1936
13th June 1936
13th June 1936
. .
. .
Result of the
inoculation
Mild reaction
Do. . .
Do. . .
. .
. .
Mild reaction
Do. .
Do. .
Do.
. .
. .
Date of im-
munity test
with fowl-pox
virus (English
strain)
6th May 1936
6th May 1936
6th May 1936
6th May 1936
6th May 1936
25th June 1936
25th June 1936
25th June 1936
25th June 1936
25th June 1936
25th June 1936
Result of im-
munity test
No reaction .
Do.
Do.
Reacted
Do.
No reaction .
Do.
Do.
Do.
Reacted
Do.
Remarks
Control.
Do.
Control.
Do.
204
Studies on a Natural Outbreak of Pigeon-Pox
FILTRATION EXPERIMENTS
One per cent saline emulsion of the cutaneous crusts after autolysis at
37°C. for one hour and centrifugation was filtered through an unused Berke¬
feld 'V' candle and Pasteurella avisepticus was added to the virus emulsion
before filtration to control the safety and efficacy of the filter. The
filtration was done under negative pressure at 56 cm. of mercury and it took
about thirty minutes to deliver about 25 c.c. of the filtrate. The filtrate, as ob-
tained above, was tested for bacterial sterility and was found to be sterile.
It was swabbed over the feather follicles of five healthy pigeons (Table III).
Five more pigeons were then inoculated with the unfiltered emulsion to serve
as controls. Four out of the five pigeons inoculated with the filtrate reacted
typically and in one, Pigeon No. 38, there was no reaction. Out of the five
control pigeons, inoculated with the unfiltered material, four reacted and one
was found to be resistant.
TABLE III
Filtration experiments
Pigeon
No.
36
37
38
39
40
41
42
43
44
45
Date of inocula-
tion
12th May 1936
12th May 1936
12th May 1936
12th May 1936
12th May 1936
12th May 1936
12th May 1936
12th May 1936
12th May 1936
12th May 1936
Inoculum
Berkefeld ' V ' filtrate .
Do.
...
Do.
...
Do.
...
Do.
...
Unfiltered emulsion
Do.
...
Do.
...
Do.
...
Do.
...
Result of the inocula-
tion
Reacted.
Do.
No reaction.
Reacted.
Do.
Do.
Do.
Do.
Do.
No reaction.
CROSS IMMUNITY TESTS
(a) Testing the immunity of pigeons, immunized with the English strain of
pigeon-pox virus, against the Indian strain of the same virus.—Five pigeons
immune to the English strain of pigeon-pox virus were tested with the Indian