NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
J. F.
SHIRLAW
347
one or two symptoms which may be common to other diseases. Diagnosis in
these cases must, eventually, unless the disease develops further, depend on
pathological examination and demonstration of specific lesions in the central
nervous system.
Equine encephalomyelitis, like rabies, follows no precise syndrome, even
if text-book descriptions might lead one to believe so. Every veterinary
officer in India knows how frequently cases of atypical rabies are encountered
and how easily a mistaken diagnosis may be made. These remarks apply
equally, if not more forcibly, to sporadic cases of equine encephalomyelitis.
The writer, however, looks upon the examination of the urine—which must
be examined while fresh—by the guiacum or spectroscopic method, as a practi-
cally infallible means of diagnosing atypical, sporadic cases. Blood is always
found and bile pigment only slightly less frequently.
As an instance of the difficulties in diagnosis encountered in a typical
sporadic cases, the following case may be cited. A horse was admitted at
night—sporadic cases are usually, for some reason, manifest at nightfall—
suffering from what was diagnosed as acute nephritis. In the morning, it was
down and comatose, with signs around it of struggling during the night. The
writer examined the kidneys and could detect no evidence of nephritis. There
were, however, renal lesions which he has come to consider as specific of equine
encephalomyelitis. This animal represented what was, undoubtedly, an
atypical case of the disease under review. It is unfortunate that nerve tissues
were not available for examination.
V.—PATHOLOGICAL STUDIES
Earlier observers commented on the comparative absence of lesions in
this disease. Some mention was made of gastro-enteritis as a fairly constant
feature and it is probably due to this that a toxicological theory of causation
found favour. In a few instances, hæmorrhages in the brain or cord were
noted. The complete absence of lesions was regarded by many as the peculiar
feature of the disease.
The writer, in his original report (1934), briefly enumerated the lesions
which he encountered in his investigations at Multan. A critical analysis of
the protocols of the fourteen cases referred to gives an indication of the vari-
ability of lesions which may be encountered, even in peracute clinical cases of
the same type.
Horse 156.—Congestion of meningeal vessels of brain and cord. Punctate
hæmorrhages in grey matter. Kidneys congested. Patchy enteritis, small
intestine.
Horse 159.—Mild enteritis ; renal congestion; spleen slightly enlarged;
congestion of meningeal vessels ; punctate hæmorrhages in grey matter of
brain and cord. Streptococcus melanogenes isolated.
Horse 332.—Blood shows little tendency to coagulate ; intense congestion
of meningeal vessels over cerebral cortex, cerebellum and cord; spleen consider-
ably enlarged ; mucous membrane of urinary bladder highly congested ; slight
cystitis ; kidneys congested ; mild congestion of gastro-intestinal tract.
J. F. SHIRLAW 353
that equine encephalomyelitis is caused by the ingestion of toxic forage and
this idea of fodder poisoning is one that is still held in many quarters. This
theory may be briefly disposed of by stating that:—
(a) Examination of the stomach ingesta of all horses succumbing
to the disease was negative for group alkaloid test.
(b) A series of rabbits and guinea-pigs fed on these samples ad lib.
remained free from any symptom, toxic or otherwise.
(c) The withholding of suspected forage and its replacement by fresh
supplies did not result in any cessation of the disease.
(d) Samples of forage appeared perfectly sound and were free from
mouldy decomposition and poisonous seeds, (e.g. Abrus pre-
catorius). The feed was carefully balanced and there was no
probability of a cereal (phytic acid) poisoning.
(e) The grasses and grains fed to horses during the Multan outbreak
were examined by competent agricultural botanists who could
detect no potentially poisonous species.
(f) The same forage from exactly the same source of supply, was
fed to other cavalry regiments, which remained entirely free
from disease.
(g) There is no proof that forage poisoning, whatever that term may
mean, can be responsible for pathological lesions in the central
nervous system of the type described.
The toxic etiology of the disease was one seriously considered by the
writer and finally abandoned in favour of a virus theory, in view of the fact
that the disease on epizootological and pathological grounds was strictly
comparable with a variety of forms of equine ancephalomyelitis, in many of
which the existence of a virus has been proved.
The earliest experiments were performed on horses, aged army casters
being the only animals available, and in rabbits and guinea-pigs. The results
of a successful subdural transmission in horses has been recorded [ Mosley,
Hean and Shirlaw, 1934]. The clinical syndrome of these two cases was
typical of the affection. On post-mortem examination, specific lesions of
equine encephalomyelitis were found in the central nervous system and the
kidney. Mention has also been made of the failure to reproduce the disease
in horses by intrathecal inoculation of brain emulsion. This failure was
anticipated. The resistance to passage of virus particles on part of the
meningo-encephalic barrier is well known.
The first series of rabbits and guinea-pigs was inoculated as follows :—
Small portions of brain were removed immediately after destruction of
hopeless cases (Multan outbreak) and rushed to the laboratory at Lahore
in thermos flasks packed with ice. The tisssue invariably arrived in a frozen
state and small pieces of representative areas of the brain were quickly
triturated in saline and sterile sand. After being allowed to settle in the
refrigerator for eight hours, the supernatant fluid was aspirated. This con-
stituted the inoculum. Rabbits and guinea-pigs, two for each specimen,
were trephined and subdurally inoculated with 0.1 c.c. of the inoculum, the
procedure being the same as for the propagation of rabies virus in the
manufacture of Semple's vaccine.
354
Equine Encephalomyelitis in India
The mortality due to the technique was nil. Several guinea-pigs and
rabbits died within a period of three to eight days, but as they showed no
nervous symptoms, it was not considered, at that time, that a specific en-
cephalomyelitis had been transmitted. The brain and cord were, fortunately,
removed and fixed in each case. It was a surprise, therefore, to find, on
histopathological examination of the brain and spinal cord of these cases,
precise lesions of encephalomyelitis and this finding naturally led to the
planning of more carefully observed experiments.
It proved easy to obtain fresh inoculation material, as from this time,
reports of sporadic cases of equine encephalomyelitis were frequent.
EXPERIMENTAL
Transmission Experiments : material—Multan outbreak
(All inoculations consisted of 0.1 c.c. hippocampus major emulsion—
unless otherwise stated)
—
Guinea pig 110 . . . .
Rabbit 109 . . . . .
Rabbit 150 . . . . .
Rabbit 151 . . . . .
Rabbit 154 . . . . .
Guinea pig 159 . . . . .
Rabbit 155 . . . . .
Rabbit 156 . . . . .
Rabbit 173 . . . . .
Rabbit 170 . . . . .
Guinea pig 158 . . . . .
Rabbit 172 . . . . .
Rabbit 157 . . . . .
Rabbit 140 . . . . .
Rabbit 141 . . . . .
Rabbit 148 . . . . .
Rabbit 169 . . . . .
Rabbit 149 . . . . .
Source of inculum
5 c.c. spinal fluid
from Horse 627,
subcut.
Do. . .
Horse 288 . .
Horse 288 . .
Rabbit 151 . .
Horse 515 . .
Rabbit 151 . .
Horse 515 . .
Horse 286 . .
Horse 416 . .
Horse 515 . .
Horse 286 . .
Horse 515 . .
Horse 84 . .
Horse 84 . .
Horse 154 . .
Horse 416 . .
Horse 154 . .
Date
of
inoculation
26-11-33
Do.
25-1-34
25-1-34
29-1-34
30-1-34
29-1-34
30-1-34
11-2-34
9-2-34
30-1-34
11-2-34
30-1-34
11-1-34
11-1-34
22-1-34
9-2-34
22-1-34
Period
observed
26-1-34
Do.
29-1-34
29-1-34
1-2-34
2-2-34
2-2-34
3-2-34
13-2-34
17-2-34
1-3-34
27-3-34
27-3-34
27-3-34
27-3-34
27-3-34
27-3-34
27-3-34
Result
No reaction
Do.
Died—E. E.
Do.
Died.
Died—E. E.
Do.
Do.
Do.
Do.
Do.
No reaction
Do.
Do.
Do.
Do.
Do.
Do.
These results appear somewhat inconclusive. Fifteen rabbits were
inoculated and only seven reacted. None showed any nervous symptoms,
yet all were completely flaccid and recumbent several hours before death,
with absence of all reflexes. The criticism may be made that too short an
interval elapsed between the inoculation and death. The average period
was four and a half days. The fact remains, however, that none of these,
rabbits showed, on post-mortem examination, any sign of injury to the brain
as the result of inoculation. The brain and spinal cord of these animals were
severally affected with lesions of encephalomyelitis identical with those seen
in the subjects whence the inoculum was derived, and haemorrhagic lesions,
with no involvement of the parenchyma, were noticed in the kidney. The
fact that only seven rabbits reacted, in face of what must be considered
J. F. SHIRLAW 355
a virulent inoculum, cannot be explained. It may be mentioned that no
case of spontaneous occurrence of a specific neurotropic virus infection had
ever been noted in the rabbit stock. No group virus immunity could explain
the phenomenon. The supposition that a mild degree of cerebral irritation
had been induced with a resultant flaring up of a latent but specific virus is
one that had no support.
The results of guinea-pig inoculations correspond in all essential details
with those in rabbits. Two out of three guinea-pigs died with similar and
more intense lesions than those noted in rabbits. It will be seen that both
guinea-pigs injected subdurally died, with an average period between inocu-
lation and death of three days. The lesions in the spinal cords of both guinea-
pigs were peracute and the inflammation was entirely monocellular. It will
also be noted that one serial transmission was made, with successful result
between rabbits 151 and 155.
The second set of transmission experiments was carried out with materials
from three horses which developed paraplegia some months after the cessation
of the main outbreak affecting the horses of the 13th D. C. O. Lancers, and
after the regiment, stationed at Jullundur, had been declared free of the
disease.
Horse 62 developed paraplegia at Khanewal on 7th December 1933
and made an apparent recovery. On 4th October 1934 this animal showed
complete incoordination of the posterior limbs with incontinence of urine,
which progressed till destruction was necessitated.
Horse 233 was a similar case. Pyrexia was noted at Multan on 30th
January 1934 and this animal was discharged cured three days later. On
4th October 1934 (the date of a general veterinary inspection of the regiment)
lack of coordination and incontinence of urine was noted.
Horse 527 developed paraplegia at Khanewal on 24th November 1933
and was a precisely comparable case. These three animals were destroyed
at Lahore and the brain and cord used for inoculation experiments in rabbits
and guinea-pigs. The technique employed was that of Nicolau and Galloway
in their studies of Borna disease.
Transmission Experiments : material—Jullundur cases
(All inoculations were made subdurally with 0.1 c.c. hippocampus major
emulsion)
—
Rabbit 197 . . . . .
Guinea pig 198 . . . . .
Rabbit 199
.
.
.
.
.
Guinea pig 201
.
.
.
.
.
Rabbit 200
.
.
.
.
.
Source of inoculum
Horse 62 . .
Do. . .
Do. . .
Do. . .
Do. . .
Date
of
inoculation
21-1-35
21-1-35
21-1-35
21-1-35
21-1-35
Period
observed
22-3-35
24-1-35
24-1-35
16-2-35
(25 days).
22-3-35
Result
Lived.
Died—traumatic menin-
gitis
Died—Pneumonia and
enteritis. E. E. ne-
gative.
Died—E. E.
Lived.
356
Equine Encephalomyelitis in India
Transmission Experiments : material— Jullundur cases—contd
—
Guinea pig 202
.
.
.
.
Rabbit 229
.
.
.
.
Rabbit 230
.
.
.
.
Guinea pig 227
.
.
.
.
Guinea pig 228
.
.
.
.
Rabbit 341
.
.
.
.
Babbit 342
.
.
.
.
Rabbit 327
.
.
.
.
Rabbit 328
.
.
.
.
Guinea pig 329
.
.
.
.
Guinea pig 330
.
.
.
.
Babbit 331
.
.
.
.
Babbit 332
.
.
.
.
Guinea pig 333
.
.
.
.
Guinea pig 334
.
.
.
.
Source of inoculum
Horse 62 . .
Horse 233 . .
Do. . .
Do. . .
Do. . .
G. P. 227 . .
Do. . .
Horse 527 . .
Do. . .
Do. . .
Do. . .
Horse 527 (with
filtered.
Berkfield
V emulsion).
Do. . .
Do. . .
Do. . .
Date of
inoculation
21-1-35
19-2-35
19-2-35
19-2-35
19-2-35
13-3-35
13-3-35
7-3-35
7-3-35
7-3-35
7-3-35
7-3-35
7-3-35
7-3-35
7-3-35
Period
observed
25-2-35
(33 days).
1-5-35
1-5-35
13-3-35
(22 days).
14-3-35
(23 days).
25-5-35
25-5-35
1-6-35
1-6-35
5-4-35
(30 days).
5-4-35
(30 days).
1-6-35
1-6-35
3-4-35
(28 days).
7-4-35
(32 days).
Result
Died—E. E.
Lived.
Do.
Died—E. E.
Do.
Lived.
Do.
Do.
Do.
Died—E. E.
Do.
Lived.
Do.
Died—E. E.
Do.
The brain tissue, hippocampus major, of Horse 527 was refrigerated for one
week at —5°C. and the following transmissions were effected with 0 .1 c.c.
of the emulsion, subdurally.)
Rabbit 337
.
.
.
.
.
.
.
.
.
.
Rabbit 338
.
.
.
.
.
.
.
.
.
.
Guinea pig 339 . . . . . . . . . .
Guinea pig 340 . . . . . . . . . .
Date
of
inoculation
15-3-35
(unfiltered).
15-3-35
(filtered).
15-3-35
(unfiltered).
15-3-35
(filtered).
Period
observed
1-6-35
1-6-35
7-4-35
(23 days).
9-4-35
(25days).
Result
Lived.
Do.
Died—E. E.
Do.
The concluding set of experiments of this nature were conducted with
braix and cord material received from three horses (A-40, A-84 and C-318)
which died during an outbreak of typical equine encephalomyelitis (mild)
which occurred in the horses of the 7th Light Cavalry stationed at Loralai
during the winter of 1935-36.
358
Equine Encephalomyelitis in India
Results of intranasal inoculation of white mice with brain emulsion from a
natural case of equine encephalomyelitis
Date of inoculation
22-1-36
26-1-36
10-3-36
7-4-36
25-4-36
7-5-36
12-6-36
29-7-36
4-8-36
8-8-36
58, unfiltered
Died 20 days
68
Died 39 days
86
Died 29 days
60, filtered
Died. 7 days
Animal number
140
Died, 3 days.
146
Died, 45 days.
171
Died, 26 days.
3
Died, 18 days.
15
Died, 12 days.
19
Died, 34 days.
26
Died, 45 days.
47
Died, 3 days.
52
Died, 3 days.
61, filtered
Died 3 days
66, filtered
Died 14 days
69, filtered
Died 17 days
71, filtered
Died 26 days
NOTE.—Lesions of encephalomyelitis were found on histopathologieal examination
of the brain and cord in every case,
J. F. SHIRLAW
361
is an opinion that has been tentatively stated and equally denied
by clinicians of experience. They are similar diseases in that
they both affect the central nervous system of the horse, and
in diseases affecting such a highly organized system, the diversity
of the type of lesion and the functional expression is the feature
to be considered. It is only on an accurate study of the re-
active phenomena, in conjunction with detailed study of the
nervous lesions, that any attempt can logically be made to
correlate these two diseases of apparent dissimilar nature.
" Kumri and equine encephalomyelitis have much in common epi-
zootologically. Incidence is largely controlled by seasonal
variation and climatic factors. On purely clinical con-
siderations, Kumri possesses a well defined train of symptoms
with little variation. Equine encephalomyelitis is more variable
in its outward expression, varying between manifestations of
acute cerebral symptoms (true encephalitis) and mild exhibi-
tions, usually progressive, of symptoms referable to the spinal
cord (true myelitis). In naturally occurring outbreaks of
equine encephalomyelitis it is usual to encounter cases pursuing
a course which is indistinguishable from classic Kumri.
" Pathologically, the two diseases are characterized by an absence of
gross anatomic change. Occasionally, in both diseases, tissue
haemorrhages, especially haemorrhage in and around the spinal
cord, are encountered, although the latter are more common
in the fulminating type of encephalitis. It is in the central
nervous system that the features are found that justify the
assertion that Kumri and equine encephalomyelitis, if not
actually identical, are at least most intimately related. Study
of the histopathology of the spinal cord and brain reveals a
similarity of lesions so striking that little doubt remains, that,
in both diseases, there is a common factor producing a common
effect varying only in degree. The etiology of Kumri and
equine encephalomyelitis remains obscure but since there is a
pronounced neurological similarity to certain diseases of the
human subject, of virus origin, considerable importance
attaches to the possibility of a neurotropic virus being of
etiological significance."
The terms ' Kumri' (lit. sprained back) and ' paraplegia ', which is
merely the symptom of a lesion of the spinal cord or higher nerve centres,
are obviously ones that should now be abandoned in favour of the more
precise and comprehensive term of equine encephalomyelitis, which, as in
other countries, has been shown to be caused by a neurotropic virus.
DISCUSSION
Equine encephalomyelitis in India bears, apparently, a close relation
to the Moussu—Marchand type of the disease because (a) the disease shows
a tendency to be ' septicaemic ', (b) haemorrhages are of frequent occur-
rence, (c) transmission experiments yield results which are not always uniform,
366
Equine Encephalomyelitis in India
2. The disease is caused by a neurotropic filtrable virus which can readily
be transmitted to susceptible small animals, as well as the horse, with the
production of classic lesions.
3. Equine encephalomyelitis manifests three types during the course of
an outbreak, cerebral, spinal and mixed cerebro-spinal.
4. Kumri is a form of encephalomyelitis in which the disease mainly
assumes a spinal form, although acute cerebral types are not uncommon.
REFERENCES
Burke, R. W. (1897). Veterinarian 70, 263 and 570.
Howitt, B. F. (1932). Jour. Inf. Dis. 51, 493 and 565.
Hupbauer, A. (1933). Wien. Tierarztl. Mschr. 20.
Hurst, E. W. (1934). Jour. Exp. Med. 59, 529.
—
Jour. Path. & Bact. 34, 331.
—
Jour. Compar. Path. & Ther. 44, 4, 231.
—(1935).
Lancet, 2, 697.
—(1936).
Brain. 59, 1.
Landsteiner, K. and Popper, E. (1909). Ztschr.f. Imm. 2, 377.
Lingard, A. (1896). Rept. on an outbreak of Surra and Filariasis at Karnal (App. D. and
E. equine paralysis).
Macalister, G. H. K. (1917). Mem. Dept. Agric. Ind. 8, 2.
Meyer, K. F. (1932). Ann. Int. Med. 6, 5, 1.
—(1934).
Zschr. Infekt. Haust., 45, 81.
—,
Hering, C. M., and Howitt, B. F. (1913). Science, 74.
Mosley, H. S., Heane, C. W. and Shirlaw, J. F. (1934). Jour. R. A. V. C., 5, 159.
Moussu, R. and Marchand, L. (1924). Rec. de Med. Vet. 100, 1, 5 and 65.
Nicolau, S. and Galloway, I. A., 1928. Sp. Repr. Ser. Med. Res. Counc. 121.
Poyser, R. (1885). Vet. Jour. 20, 167.
Rivers, T. M., Sprunt, D. H. and Berry, G. P. (1933). Jour. Exp. Med. 58, 39.
Sahai, L. (1938). Ind. Jour. Vet. Sci. 8, 4, 341.
Sartin, W. (1878). Vet. Jour. 8, 76.
Simpson, K. S. and Banerji, P. C. (1932). Ind. Jour. Vet. Sci. 2, 59.
Zwick, W. (1925). Berl. tierarztl. Wchnschr. 41, 453.
Zwick, W., Seifried, O. and Witte, J. (1926). Ztschr.f. Infekt. d. Haust, 30, 42.
THE POSSIBLE EXISTENCE OF FOWL PARALYSIS
(NEUROLYMPHOMATOSIS GALLINARUM) IN
INDIA
BY
R. L. KAURA, B.V.Sc., M.R.C.V.S.
Assistant Animal Husbandry Commissioner with the Government of India
O UTBREAKS of paralysis in fowls have appeared in Germany, Holland,
America, Canada, British Isles and in many other countries, which
suggest that this disease is world-wide in its distribution. In India the disease
has been reported from Bombay by Mohey Deen [1933] who concluded that
fowl paralysis (wry neck) was due to calcium deficiency, from Hyderabad by
Mahajan [1934] who reported it as polyneuritis in fowls, from Mysore by
Krishniengar [1937] who described it as neurolymphomatosis gallinarum and
from the Central Provinces by Bachan Singh [1940] who described it as leg
weakness in poultry due to nutritional deficiency. Kaura and Ganapathy
Iyer [1937] have described paralysis of legs, wings, head and neck in poultry due
to Ranikhet disease virus which apparently became neurotropic in type. Para-
lysis occurring as a result of parasitic infestation is also not uncommon. Un-
fortunately very little trouble has been taken to differentiate and classify the
various types of paralysis and the possibility of a simultaneous occurrence of
true fowl paralysis (neurolymphomatosis gallinarum) in the same bird where
some other diagnosis has been given, has been over-looked.
It is possible that the disease may exist in provinces and states but,
other than those mentioned in the preceeding paragraph possibly owing to the
comparatively small amount of attention that has been paid to the diseases
of poultry in the past, it has not yet been brought to light. Also it should be
noted that in the case of this disease, in which the symptoms vary according to
the nerves and organs involved, it may be necessary to hold a histopathologi-
cal examination before arriving at a definite diagnosis. The special cell which
infiltrates and swells the nerves in cases of fowl paralysis is not normally en-
countered in any quantity in the body tissues but if this fowl paralysis cell
does multiply and accumulate then there is formed a modified tumour called
a lymphoma ; hence the term ' neurolymphomatosis gallinarum', i.e. a swel-
ling of the nerves of the fowl by lymphocyte-like cells. The degree of infiltra-
tion of a nerve by these cells determines the extent of destruction of the nerve
fibre caused by pressure. These cells can affect not only nerves of legs and
wings but any nerve in the body, e.g. nerves of gastro-intestinal tract etc., or
in fact any part of the body, e.g. eyes, ovary, liver, kidneys, lungs, brain,
spinal cord etc., with consequent symptoms. If an accumulation of such
tumour cells does not affect the nerves, paralysis will not occur and the
chief symptom by which the disease can be recognized is missing.
Therefore, instead of the term ' neurolymphomatosis gallinarum ', Warrack
( 367 )
372
Possible Existence of Fowl Paralysis
REFERENCES
Bachan Singh (1940). Ann. Rep. Vet. Invest. Officer, C. P. and Berar, p. 9.
Barker, C. W. (1939). Cornell Vet. 29, 41.
Bayon(1932). Vet. Rec. 12, 457.
Blakemore, F. and Dalling, T. (1939). Proc. 7th World Poul. Congr. p. 282.
Crammer (1920). Brit. J. Expt. Path. 1, 184.
Eardmann and Haagen (1928). Deutsche Med. Wchnschr. 53, 796.
Fritzsche, K. (1937). Z. Infenkt. Hanst. 54, 124.
Funk (1914). Lancet 1, 98.
Kaura, R. L. and Ganapathy Iyer, S. (1937). I. C. A. R. Misc. Bull. No. 15, p. 5.
Krishiengar, K. (1937). Ann. Adm. Rep. C. V. D., Mysore, p. 10.
Mahajan, M. R. (1934). Ann. Rep. Vet. Invest. Officer, Hyderabad, p. 2.
Mohey Deen, M. (1933). Ind. Vet. J. 9, 205.
Pappenheimer, Dunn and Seidlin (1929). J. Exp. Med. 49, 87.
Plimmer, Rosedale, Raymond and Lowndes (1927), Biochem. J. 21, 1141.
Seagar, E. A. (1933), Harper Adams Utility Poult. J. 18, 627.
Tanniguchi (1928). Fukuoka-Ikwedaigaku-Zasshi
I, 59, 1,131.
Warrack and Dalling (1932). Vet. J. 88, 28.
Williams, J. K., Gildow, E. M. and Lampman, C. E. (1938). U. S. Egg and Poul Mag.
Jan. 1938, p. 24.