NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
346
An
Outbreak of Equine Encephalomyelitis
After these cerebral symptoms had subsided, the animal developed hemiplegia
with a tendency to go round in a circle. The condition of the animal got
steadily worse and it succumbed three weeks later.
In most cases, the symptoms of paraplegia were seen to progress only to
a point after which they became stationary. There was no loss of appetite
or other disturbance of health and such animals would perhaps have lived
indefinitely, had they not been destroyed.
It may be stated that while a febrile phase of a few days' duration, prior
to the onset of symptoms of paresis, is considered to be a characteristic feature
of equine encephalomyelitis of virus origin, in none of the horses which were
involved in this outbreak was any rise of temperature at any stage of the
disease noted (except in No. 12 already referred to, the result probably of
violent struggling and excitement). The outbreak that occurred during the
winter of 1937-38 was also characterized by an entire absence of any pyrexial
phase, a feature which serves to distinguish these outbreaks sharply from
those which occurred at Multan and in Kashmir.
In practically all cases there was some degree of retention of the urine
amounting in the worst affected cases to complete suppression. In the
majority of cases the urine was definitely thick and gluey due to the presence
of a large amount of mucus and this character is of some diagnostic importance.
None of the animals revealed any interference with the function of the
anal sphincter.
In one case the paralysis also involved the retractor muscles of the penis
which used to hang down out of the sheath.
Swelling of the near hind fetlock was seen in one case, while one case
(No. 13) also showed, coincident with the attack of paraplegia, a filaria worm
in the near eye which, however, disappeared before any operative treatment
could be carried out. Later, this animal went completely blind in this eye,
though it recovered from the paraplegia.
A similar worm was also seen in another horse, involved in the 1937-38
outbreak, but its removal failed to bring about any amelioration of the symp-
toms.
In all the animals the appetite remained normal throughout and though
some of them were kept under observation for months, none showed any
signs of muscular atrophy or skin lesions, indicative of trophic disturbances.
There was no loss of sensation in the hind limbs in any of the animals nor was
any hypersensitiveness elicited on application of pressure over the loins.
Briefly summarized, the symptoms in the majority of the animals were
mainly those of paraplegia of varying degrees combined with the retention,
either partial or complete, of urine in the worst affected cases. In acute
cases, the brain was also affected, especially in the earlier stages.
LAKSHMI
SAHAI
347
TREATMENT
Routine treatment with potassium iodide, Nux Vomica, arsenic, etc., com-
bined with other symptomatic treatment was carried out in all cases but
without any beneficial results. Two horses (Nos. 8 and 13) in which the
attack was relatively mild recovered but recovery in these animals may
have been spontaneous rather than due to any treatment adopted.
On the assumption that the trouble might prove to be encephalomyelitis
(of virus origin), before the results of transmission experiments were known,
the treatment of all the affected animals was carried out on the lines adopted
by Mosley, Heane and Shirlaw [1934] in the Multan outbreak but without
any appreciable benefit. Cases which occurred subsequently were also treated
in the same way. This treatment was as follows :—
About a pound of mag. sulph was administered per stomach tube and at the
same time the animal was given an enema and catheter passed if there was
any evidence of retention of urine. This was repeated as often as necessary.
Small quantities of mag. sulph (4 oz.) were given daily on subsequent days.
Injections of hexamine in doses of 25 grm. dissolved in about 60 c. c. of water
were given intravenously on six consecutive days. Forced exercise was given
daily to all animals that could walk.
By the time this treatment could be carried out horses Nos. 12 and 52
had already died. The Commandant's horse, which was the worst affected
at the time, showed some improvement in the beginning but later the condi-
tion relapsed and the animal had to be destroyed, when it could no longer
stand even with the support of slings. In the less severely affected cases also
there was no improvement.
Trials carried out with the hexamine treatment in the 1937-38 outbreak
showed that the drug is of some value especially in the earlier stages, as a
surprisingly quick recovery was obtained in some cases following the adminis-
tration of this drug, but on the whole it may be stated that once the symptoms
have become established and definite degenerative changes have occurred
in the central nervous system the prognosis is bad and there is no specific
remedy that could be relied upon to effect a cure.
POST MORTEM FINDINGS
Post mortem examination was carried out on nine horses, of which two
had died naturally and seven had been destroyed because there appeared no
hope of their recovery. They may be classified as three acute and six subacute
cases.
Briefly speaking, it may be stated that the post mortem findings in all those
animals less severely affected were almost of an entirely negative character,
but definite lesions were seen in the more acute cases. These consisted of
petechial haemorrhages on the serous membranes, on the surface of the spleen,
in the endocardium (one case) and on the serous coat of the large intestine.
348
An Outbreak of Equine Encephalomyelitis
The liver was found to be fatty in two cases, while congestion and petechial
haemorrhages were seen in the kidneys in practically all cases. In all cases in
which there was no retention of the urine the bladder was found to be normal,
but in those with any degree of suppression of the urine it was either found to
be enormously distended or shrunken in size to a small volume, with a greatly-
thickened wall due to infiltration with new granulomatous tissue, consequent
on the irritation set up by cystitis. In such cases the bladder contained only
a small quantity of a thick oily urine of an offensive odour and with a quantity
of a thick greenish-coloured sediment composed of precipitated mineral matter
adhering to the mucosa, which on its removal was found to be thickly studded
with haemorrhages.
Exactly similar changes in the bladder had been seen in horse No. 80
which had been attacked in 1935.
The brains and spinal cords of all the animals that were destroyed were
carefully examined but except for a few petechial haemorrhages, here and
there, in the cord and some evidence of softening especially in the lumbar
region not much in the way of naked-eye changes was seen.
HISTOPATHOLOGICAL CHANGES
Pathological tissues from a number of cases were sent to Mukteswar for
histological examination. The findings were more or less identical in each
case and they may be briefly summarized as follows :—
Spinal cord.—Congestion of the meningeal vessels. Marked gliosis,
especially of the grey matter. Degenerative changes with
perivascular haemorrhages in the grey matter which also showed
some degree of infiltration (glia) around the central canal which
appeared dilated.
Cerebrum.—Congestion of meningeal vessels. Gliosis with micros-
copic haemorrhages, some of which were perivascular. Neuro¬
nophagia. Slight cuffing of blood vessels.
Kidney.—Deep congestion. Slight interstitial changes. The tubules
showed early degenerative changes, and even necrosis in places.
The glomeruli were congested, and showed leucocytic infiltra-
tion.
Urinary bladder (in a protracted case with thickening of the wall).—Marked
congestion. The mucous membrane highly petechiated and
hyperplastic with desquamative and necrotic changes on the
free edge. The mucosal surface showed Gram-positive bacteria
and deposit of blood pigment, and in some places the entire
mucosa had been desquamated. A few foci of lymphocytic
infiltration were present in the submucosa.
350
An Outbreak of Equine Encephalomyelitis
A pony injected by the author locally with 10 c. c. of brain emulsion from
a horse that had been destroyed after a severe illness lasting for about three
months also failed to develop the disease, while an attempt to infect another
pony by injecting it intrathecally and intranasally with 40-50 c. c. of cerebro-
spinal fluid taken from horses involved in the 1937-38 outbreak yielded no
better results.
It will thus be seen that the results of transmission experiments on guinea-
pigs, rabbits and ponies have been too uncertain and inconsistent to justify
any definite conclusions about the virus origin of the malady, though in view
of the known difficulty of transmitting equine encephalomyelitis experi-
mentally, such a possibility cannot be entirely excluded. Nevertheless, one
cannot help thinking that if a virus was the real cause of the trouble the per-
centage of successes should have been greater than that obtained in the ex-
perimental transmission work. It is also well known that in carrying out
experiments with brain tissue great care is necessary both with regard to the
technique and the material used as otherwise quite misleading results may
be obtained.
It is proposed to carry out further experiments when some of the horses
involved in the present outbreak (1937-38) are destroyed.
The possibility of a mineral imbalance as a factor in the etiology of the
condition has not been overlooked and at the request of the Imperial Veteri-
nary Research Institute, Mukteswar, which is engaged in an investigation of
this disease and other similar diseases from this point of view, samples of
serum and fodder were supplied for analysis, but the results so far to hand do
not reveal any abnormality in the calcium and phosphorus contents of these
materials of such a consistent nature as to warrant any definite conclusions.
It is proposed to pursue the investigation from this point of view as and when
opportunity occurs.
While on this subject, the possibility of cold as a probable factor in the
causation of the condition must be mentioned, for it was observed that the
majority of the cases in the 1936-37 outbreak (as also those in the 1937-38
outbreak) were among horses tethered on the side of the stables exposed to
the cold westerly winds, while very few cases were seen among horses tied on
the other side. It is not improbable that cold acts as an important predispos-
ing factor in the causation of the condition, tending to lower the vitality of the
animal and rendering it susceptible to attack by the specific cause whatever
that might be. Support is lent to this view by the fact that in both the out-
breaks which have occurred at Jamshedpur so far the disease has shown a
definite seasonal incidence. The first cases are usually seen to arise about
October or November and the disease tends spontaneously to subside about
February or March with the onset of the warmer weather. The outbreaks at
Multan and in Kashmir also occurred during the colder part of the year though
the exact relationship between them and the disease in this Province has not
LAKSHMI
SAHAI
351
been established. It must, however, be admitted that the greater incidence
of the disease at this time of the year may be explained on other grounds as
well.
DISCUSSION AND CONCLUSION
In the foregoing, an account has been given of an outbreak of equine
encephalomyelitis among the Mounted Military Police horses at Jamshedpur
in the year 1936-37 supported by brief references to another outbreak in
1937-38, and of the steps taken to establish a diagnosis. The possibility of a
virus, of vegetable poisoning and of mineral imbalance in the causation of the
condition has been discussed but the results have either been wholly negative
or not sufficiently definite to justify one in pronouncing a definite opinion.
Certain points of resemblance between this outbreak and those at Multan and
in Kashmir have been stressed. At the same time attention has been drawn
to the important points of difference between them, such as the absence of a
definite pyrexial phase in the outbreaks in this Province, the almost negative
results of transmission experiments, and the disappointing results obtained
with hexamine treatment which was reported to have given good results in
the Multan and Kashmir outbreaks, especially in the latter. It is not improb-
able that the encephalomyelitis occurring in this Province is not a virus malady
at all, but one due to some other cause.
ACKNOWLEDGMENT
Thanks are due to the Director, the Imperial Veterinary Research Insti-
tute, Mukteswar, for much help in the laboratory side of this investigation.
REFERENCES
Kak, Prem Nath (1937). An outbreak of Equine Encephalomyelitis. Ind. Vety.
J. 14, 11-15.
Maclister, G. H. K. (1917). ' Kumri ' Combined Diffuse Sclerosis and Central
Poliomyelitis of Horses. Mem. Dept. Agri. Ind. Vet. Ser, Vol. 8, No. II.
Mosley, H. S., Heane, C. W. and Shirlaw, J. F. (1934). Incidence of Equine
Encephalomyelitis in an Indian Cavalry Regiment. J. Roy. Army.
Vet. Cor. 6, 159-172.
DISEASES TRANSMITTED BY THE INDIAN SPECIES OF
TICKS AND THE POSSIBILITY OF THEIR PREVEN-
TION THROUGH BIOLOGICAL CONTROL*
BY
M. SHARIF, D.Sc. (PANJAB),PH.D. (CANTAB.), F.L.S. (LOND.)
Entomologist
Haffkine Institute, Parel, Bombay
(Received for publication on 17th May, 1938)
INTRODUCTION
COMPARED with what is known in other countries about tick-borne
diseases, very little appears to be on record in India. As to the amount of
loss due to tick-borne diseases in India there is no record. In a country, where
no importance is attached to the loss of human life through diseases trasmitted
by arthropods, one should not expect any consideration for cattle and other
domestic animals. This article is not intended to be an exclusively original
contribution, but it is put forward in the hope of enlisting further active in-
terest in these parasites and the diseases which they transmit in India. India
offers a rich field for investigators to study the various aspects of tick-
borne diseases which have hitherto remained unsolved, and which are unques-
tionably of vital importance to the stock-breeders.
The tick fauna of India as in other tropical and sub-tropical countries
is very rich and is represented by eleven genera and about seventy species.
They are found on all kinds of domestic and wild animals like mammals,
birds, snakes, lizards and tortoises, and they also attack man. Economically
nine species listed in Appendix A are of considerable importance. They
attack, the domestic animals in India in large numbers and thus they are the
chief live-stock pests. In addition there are twenty-six species listed in
Appendix B, which have been found on domestic animals but nobody knows
as to the importance of the rôle they play in the economy of domestic animals
in nature. Very little is known as to the life-history of even the commonest
species and the rôle they play in the spread of diseases in India.
The number of Indian species is larger than that which is recorded from
the United States of America, where about forty species have been listed so
far [Bishopp, 1935]. In the latter country the tick problem attracted
attention as early as the last decade of the nineteenth century ; with the
result that a large number of workers took interest in ticks, and with the
increase of the knowledge of them a progressively large number of tick-
borne diseases began to be known. Keeping in view, the ecological conditions
* Read at the Silver Jubilee Session of the Indian Science Congress Association at
Calcutta, 1938.
( 353 )
M.
SHARIF
357
who is not well versed in ticks. The present author had since long suspicion
that D. auratus is the real vector of the Tick typhus fever in India and R.
haemaphysaloides may play some part in the transmission of the disease.
Marseilles fever (la fièvre boutonneuse), whose causal agent is Rickettsia
conori Brumpt, is transmitted by R. sanguineus [Brumpt, 1930] and has been
reported from several places on the Mediterranean coast. The tropical Tick
typhus fever in Kenya according to Roberts [ 1935 ] is also transmitted by
R. sanguineus. This disease according to Symes and Roberts [1936] is
identical with Marseilles fever.
Rocky Mountain spotted fever which is due to Dermacentroxenus rickettsi
(Wolbach) is present in thirteen states of the United States of America, where
according to Cooley [ 1932 ], more than 4,260 persons have suffered up to
1928 from this disease with an average mortality of about 17.11 per cent.
According to Parker, Philip and Jellison [1933] the transmission tests of
this disease with R. sanguineus over a period of two years have shown that
it is a very efficient vector under experimental conditions.
Spirochaetosis.—The tick-transmitted spirochaetosis in man causes relaps-
ing fever. Ornithodoros savignyi (Audouin), which is almost certainly the
vector of the relapsing fever due to Spirochaeta duttoni Novy and Knapp in
Somaliland and Abyssinia, is found in India. The causal agent of the Central
Asiatic [Khodukin and Sofiev, 1932 ] and Persian relapsing fever is Spiro-
chaeta persica Dschunkowsky and its chief vector is Ornithodoros papillipes
(Birula) though according to some O. lahorensis can also transmit this disease.
Sergent and Levy [ 1935 ] found that R. sanguineus can transmit experiment-
ally and in nature in Algeria the Spanish relapsing fever due to Spirochaeta
hispanica de Buen.
Spirochaetosis of domestic fowls which is due to Spirochaeta anserina
Sakharoff is transmitted by Argas persicus all over the world. It is a very
fatal disease and it may kill all fowls in a yard in a few days. According to
Rajagopalan [ 1936 ] this disease is very common in India.
Spirochaeta theileri (Laveran) which is non-pathogenic is found in cattle
of India [Lingard, 1907]. Brumpt [1919] succeeded in infecting cattle in
France with this species by feeding Boophilus australis on them from Brazil.
In the North Caucasus B. annulatus subsp. calcaratus transmits it [ Yaki-
moff, Belawine, Rastégaieff and Schlüpikoff, 1929 ].
Bacterial diseases.—Tularaemia or Rabbit fever a disease due to Pasteurella
tularense, has been recorded from the United States of America and Japan.
It is primarily a disease of wild rodents but human infection is of purely acci-
dental nature. According to Parker [ 1934 ] the causal agent can survive
from larva to adult in R. sanguineus.
According to Basu [ 1930], the chicken cholera or fowl plague due to
Pasteurella avicida can possibly be acquired by eating infected individuals of
A. persicus. Faddeeva [ 1932 ] obtained 23.6 per cent success in transmitting
N
358
Diseases Transmitted by the Indian Species of Ticks
plague experimentally by A. persicus at Saratov. The causal agent remained
alive and effective up to 110 days in the body of the tick.
Tick paralysis.—According to some observers the salivary secretion of
ticks contains toxins and cases of tick paralysis in some animals are generally
explained on the basis of their presence. Tick paralysis has been reported from
the United States of America and Australia both in man and domesticated
animals. The ticks attach themselves to the body usually on the base of
the head or along the spinal column which results in paralysis which progresses
upwards and if the tick is not removed the end is fatal. Ixodes holocyclus
Neumann, which is found in India, causes extremely common and fatal para-
lysis of dogs, cats, calves, lambs and children in Australia.
According to Regendanz and Reichenow [ 1931], the poison causing tick
paralysis is especially formed in the female of R. sanguineus during the process
of egg development. They experimentally showed that injections of eggs
or ovaries of this tick just before oviposition gave rise in dogs to symptoms
similar to those of tick paralysis. Mlinac and Oswald [ 1936 ] working in
Jugoslavia showed that similarly injections of extracts of eggs of H. (H.)
aegyptium, I. ricinus, Haemaphysalis cinnabarina var. punctata can cause
tick paralysis. According to Rastégaieff [ 1936, 1] O. lahorensis caused fatal
tick paralysis in a sheep in Russia.
Virus diseases.—Amongst the virus diseases the louping-ill according to
MacLeod and Gordon [ 1932 ] is transmitted by Ixodes ricinus in England,
Scotland and Wales. This tick also transmits the causal agent of the " Tick-
borne fever of sheep," [ MacLeod and Gordon, 1933] in sheep, pigs and goats.
Rinderpest, a virus disease, which causes 35 per cent mortality of cattle
in India, although there is no positive proof of its transmission by ticks,
yet it may possibly be transmitted by ticks as it has been shown by De Souza
[ 1924 ] that specimens of Boophilus annulatus (Say) which had engorged
themselves upon an animal infected with rinderpest maintained the virus
at full virulence for seven days. In view of this, there is a possibility of the
direct transmission of the disease by ticks. In India as pointed out before
(p. 355) its complication with piroplasmosis may increase the percentage of
mortality.
To give an idea of the extent to which the species of ticks found in India
can be concerned in transmission of diseases, the author has listed in
Appendix C those Indian species which have been incriminated to transmit
diseases either in India or outside India.
BIOLOGICAL CONTROL
There is no doubt that ticks are comparatively free from the attacks of para-
sites and predaceous enemies on account of their passing a portion of their life
concealed within the fur, feathers or scales of their hosts. Unfavourable
climatic conditions are mainly responsible for keeping their number in check.
Ticks have natural enemies both predaceous and parasitic. The study of