NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
CLINICAL CHART No. 4.
CLINICAL CHART No. 5.
UNUSUAL CASE OF CHRONIC RINDERPEST.
376
characteristic of rinderpest, dying 25 days after the retest inoculation on account
of pleuropneumonia and resuscitated piroplasmosis [chart No. 4].
Of the two animals which were inoculated with splenic pulp, Hill bull No. 791
showed a characteristic thermal reaction starting from the 4th day, inappetence,
diarrhœa and mouth lesions and died on the 12th day after inoculation [chart No. 2].
In the post mortem examination, typical ulcerative lesions of rinderpest were found
in the pharynx, abomasum and the intestines in association with the presence
of coccidia in rectal smears. The other bull No. 688, also inoculated with splenic
pulp on the same day as the above, developed a characteristic thermal reaction
and from the 5th day showed inappetence, diarrhœa and mouth lesions. It suffered
from resuscitated coccidiosis for some time but eventually recovered. It was
retested with 5 c.c. of virulent rinderpest blood (which was proved to be virulent
by inoculation simultaneously into other susceptible bulls), one month and 20 days
after the test inoculation but was found to be refractory to rinderpest [chart
No. 3].
DISCUSSION.
It is seen from the above inoculation experiments that the spleen, collected
from an animal, dying of chronic rinderpest 74 days after the initial
inoculation was infective by inoculation into susceptible bulls, while the blood
was not. The persistence of rinderpest lesions in the alimentary tract with
accompanying infectivity of the spleen over such a long period is remarkable.
From the data given above, there seems to be no doubt that the lesions exhibited
at post mortem examination were due to the infection contracted at the original
inoculation, there being no room for an accidental second infection. The possibility
of rinderpest lesions persisting or reappearing after a long interval, as seen in
this case, would seem to receive strong support from the observation of Delpi
[1928] who found that in a typical case of bovine rinderpest, mouth lesions may be
detected on the 7th day and again at the time of death, i.e., beyond 1½ months
after the date of infective inoculation. Our case is to a degree comparable with
Delpi's cases since the virus in both cases were from attenuated strains: the
former being due to passage through goats, and the latter being due to accidental
degradation during routine passage through cattle.
As has been pointed out in some detail in the Introduction, the virus of
rinderpest is exceptionally fragile and cannot be transported through air and water,
nor can it survive in the soil for any length of time. Vectors such as mosquitos,
lice, ticks or flies have been shown to be incapable of transmitting it under natural
conditions. Although outbreaks occur among wild animals, they cannot be
377 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [II, IV
incriminated as natural carriers of the disease, like jackals in canine piroplasmosis
or certain wild ruminants in Nagana.
Hutyra and Marek [1926] have quoted the following authors for information
bearing on the actual mode of contagion: (a) Ranpach has shown that, out of
doors, the spread of the disease may be prevented by digging a trench around the
infected herd which the animals are unable to pass and that in such cases cattle
on the other side of the trench may remain healthy; (b) Piot Bey found that by
isolating affected cattle for a distance of 10 metres the spread of the disease
to other animals could be prevented; (c) Nencki has shown that in the stable
healthy cattle may be protected from the neighbouring infected animals by simple
board partition. Very recently Cooper [1932] at this Institute has shown that the
introduction of a healthy bull into a stall just vacated by an animal dead of acute
rinderpest and only separated from other infected animals by mere board partitions
may not result in infection (period of observation was 15 days). Again the
experience at Muktesar, where susceptible and infected animals have been
maintained since the very inception of this Institute about 40 years ago, only
a few hundred feet apart on either side of a ridge, is that there has never been
any instance of the disease spreading over to the other side. No steps whatever
are taken to prevent the movement of men and traffic except for the infected
cattle themselves. In his experiments to obtain some exact information regarding
the infectivity of rinderpest by intimate contact, Cooper has found that a contact
of 2 days with animals during the early febrile stage of the disease is not sufficient
for infection and that the most contagious period in the rinderpest syndrome is
between the 5th and 10th days after artificial inoculation. The infected animals
are so sick in the abovementioned most contagious period that it is not likely
that they would move about.
The known facts about the epizootiology of rinderpest can therefore be explain-
ed only by the view that carriers of rinderpest exist among cattle and perhaps also
among other domesticated ruminants which move among cattle and that outbreaks
are started by prolonged contact of susceptible animals with a carrier in the infec-
tive stage but under suitable conditions. However, when an attempt is made to
obtain from published literature, experimental confirmation of this mode of spread
of the disease both the sides of the question appear to be equally well represented.
For, it has already been seen that Ward and collaborators [1914], Boynton [1918],
Ruppert and Wolfel [1921] and Jacotot [1932] (except in a solitary instance) have
all failed to prove the existence of carriers; and that on the other hand, Schern
[1918], Curasson [1920, 1926] and Jacotot [1932] have brought definite findings
which leave no room for any other conclusion than that carriers do exist. The
UNUSUAL CASE OF CHRONIC RINDERPEST.
378
former results are explained by the latter school of thought by saying that carriers
are not at all frequent and that Ward, Rupert and others were not fortunate enough
to encounter them. Our contention is that carriers are not, perhaps, as rare as
supposed although it is not easy to detect them in the ordinary way. For it seems
more than probable that the virus is kept well under control in some remote duct-
less gland or organ, the virus being not detectable in the usual discharges and
excretions until such time as unfavourable conditions of life supervene and upset
the controlling mechanism. One is struck by the remarkable similarity in the
circumstances under which the reported outbreaks in England [1865], Belgium
[1920], Brazil [1921], Romblon [1916], Australia [1925] originated. An invariable
association of a trying voyage on sea for varying periods (exceeding 10 days) with
each one of these cases suggests that this association was certainly more than a
mere coincidence. This suggestion is considerably strengthened since evidence is
available to show that unfavourable conditions of life have an important bearing
on the starting of outbreaks. Apart from the statement of Bliss already quoted
in extenso, the Indian Cattle Plague Commission observed that rinderpest rages
" on seasons of exceptional insalubrity—a drought, a flood or a cyclone—producing
such wholesale havoc and death that agricultural industry was for the time para-
lysed ". Further, McLeod [1869] quotes a letter from the Consul General of
Bessarabia, addressed to the Earl of Clarendon describing the incidence of rinder-
pest in that country where it is permanently prevalent, and endorses the common
belief of principal landowners and cattle breeders to the effect that the origin of
the disease is attributable to " long journeys during great heat of summer across
arid steppes where no pastures nor wholesome water can be found ".
With reference to the question as to which remote gland or organ is best suited
for the greatest longivity of the rinderpest virus the spleen, which has been shown
in our reported case to be virulent even after 74 days of infection, naturally
suggests itself first. There seems to be a consensus of scientific opinion on the
superiority of the spleen as the most serviceable organ for the preparation of
vaccines. Lingard [1906] found that spleen pulp dried for 3, 8, and 59 days retain-
ed its virulence. In the experience of Kakizaki and collaborators [1926] a vaccine
prepared from lymph glands was inferior to that prepared from spleen pulp.
Kelser [1928] found that the blood entering into the preparation of the vaccine
besides having no immunising properties detracts materially from the keeping
qualities of the vaccine. Daubney [1929] states that lymph glands and kidneys
are of lower value than spleen in the formalised vaccine and blood and liver are
valueless. Jacotot [1931] found that the spleen pulp was virulent for a longer
period (7 months) than blood (2 months) when kept under the same condition at
379 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [II, IV
0 C. Although the abomasum was found to be richest in the virus [Jacotot, 1932]
in an animal at the acute stage of the disease, it does not seem to have been used
for the preparation of vaccine. In certain unpublished experiments, which one of
us (V. R. R.) undertook under the direction of the late Director of this Institute
(Dr. Edwards) it was found that chloroform in the concentration of 0.75 per cent.
killed rinderpest virus in blood within 2 hours at body temperature. In similar
experiments Daubney [1929] found that the virus in blood is readily killed by
chloroform and that such killed virus has no antigenic powers. The superiority of
the spleen as vaccine material has been referred to. The retention of immunising
properties in the spleen can be shown to be due not to any preservative added to
the tissues but to be inherent in them, for it is known that glycerine, phenol and
other antiseptic substances even in minute quantities cause rapid deterioration of
the virus (Koch, Semmer, Theiler, etc.). Further Edwards [1924] proved that the
virus of rinderpest is not destroyed but only inactivated by treatment with
0.5 per cent. carbolic acid, since intensive passage through rabbits brought back
its virulence for cattle. An idea of the degree of the tenacity of the virus in the
spleen can be obtained from the fact that it has been found by more than one
worker [Kelser, 1928, Cooper and Menon, 1931] that the spleen retains its vaccinating
properties for about 1 year. This must have been due to the survival of the virus
in the spleen pulp in spite of treatment with chloroform. In fact it has been
suggested that the vaccinating properties are due to the survival of the virus in
minimal quantities. Curasson and Delpi [1929] do not know whether the mainten-
ance of antigenic powers over long periods is due to the spleen being specially rich
in the virus or because it has some special action but they are certain that other
virulent materials such as blood or peritoneal washings when treated with formalin
are uncertain in their immunising powers. It is interesting to note that Jacotot
[1929] has claimed that antiserum prepared against the organ pulp vaccines as
antigen for hyperimmunisation was superior to that prepared against virulent
blood.
As a result of the studies on our case of chronic rinderpest, it is suggested
that the spleen is one of the seats of the virus in a carrier animal, a view which is
considerably supported by the available information on the persistence of the
virus for long periods in the splenic tissue both under experimental conditions and
in the preparation of vaccines and hyperimmune antiserum. It is believed that
in Kelser's vaccine the spleen cells protect the architecture of the virus molecules
from the destructive action of chloroform and that the superiority of Jacotot's
hyperimmune antiserum is due to the spleen cells constantly releasing small quanti-
ties of the virus and maintaining a sustained stimulation on the host's body
UNUSUAL CASE OF
CHRONIC
RINDERPEST.
380
mechanism for the preparation of efficient antibodies. Further, the employment
of a tissue culture of the spleen with a view to cultivate the rinderpest virus in
vitro would appear to be indicated.
REFERENCES.
Angeloff, St. (1917). Arch. †. Wiss. u. Tierh. 43, 383-420
Trop. Vet. Bull. 6, 35-40.
Baldrey, F. S. (1912). Agri. J. Ind. 7, 294.
Beaton, W. G. (1930). J. Comp. Path. and Therap. 43, 301-307.
Bliss, E. L. (1922). Rinderpest and its prevention—Reprint from China Med. J. March 1922,
3 and 12.
Boynton, W. H. (1913). Philipp. J. Sc. (Sec. B). 8, 509.
—
(1916). Philipp. Agri. Rev. 9, 288-336.
Carre and Fraimbault (1898). Ann. deInst. Past. 12, 848.
Claverie (1929). Rec. Med. Vet. Exot. 2, 129-143.
Trop. Vet. Bull. 1930,18, 26.
Conti, P. A., & Van Dac, N. G. (1929). Rec. Med. Vet. Exot. 2, 204-215.
Trop. Vet. Bull. 1930,18, 95.
Cooper, H., & Menon, M. B. (1931). Proc. Ind. Sc. Cong., Nagpur, 354-355.
Cooper, H. (1932). Rinderpest—The transmission of infection by contact. Ind. J. Vet. Sc.
Ani. Husb., 2, 383.
Curasson, G. (1922). Trop. Vet. Bull. 10,49.
—
(1926). Trop. Vet. Bull. 14, 32.
Curasson, G., & Delpi, L. (1929). Trop. Vet. Bull. 17,131.
Daubney, R. (1928). J. Comp. Path. and Therap. 41, 228-248.
—(1929).
Trop. Vet. Bull. 17, 24.
—(1930).
Ann. Rep. Kenya, Vet. Bull. 1931,1, 53.
Delpi, L. (1928). Rev. Gen. Med. Vet. 37, 259-264.
Trop. Vet. Bull. 16,141.
—(1930).
Rev.
Gen. Med. Vet. 39, 138-141.
Trop. Vet. Bull. 18,94.
De Souza (1924). Trop. Vet. Bull. 12, 63.
Dieckerhoff (1890). History of Rinderpest and its literature, Berlin.
du Toit, P. J. (1916). Ztschft. Inf. Krank. 1917,18,181.
Edwards, J. T. (1924). Ann. Rep. Imp. Bact. Lab. Muktesar, 31-33.
—(1930).
The problem of Rinderpest in India. Imp. Inst. Agri. Res. Pusa Bull.
199, Calcutta.
Eggebrecht, M. (1910). Ztschft, Infek. Krank., 7, 54.
Farrel, H. (1869). Cited in the Rep. Ind. Cattle Plagues, 1871, 58.
Ferraro, G. (1917). Perche persiste la peste bovina in Eritrea Moderno Zooiatro, 5, 215-216.
Trop. Vet. Bull. 6,40.
Galambos,(1861). Gyogyaszat cited by Hutyra and Marek (1926), Spec. Path. and Therap. of
diseases of domestic animals.
Gartner, (1920). Berliner Tier. Woch., 43 and 44.
Gilchrist, W. (1848). " Practical Treatise" cited on p. 540 Rep. Ind. Cattle Plagues, 1871,
Haji, C. S. G. (1932). Ind. Vet. J. 9,13.
381 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [II, IV
Hall, G. N. (930) 5th Ann. Rep. Vet. Lab. Nigeria. Vet. Bull. 1931,1, 213.
Hornby, H. E. (1926). Vet. J. 82, 348-355.
Hutchins, E. (1915). Ann. Rep. Dept. Agri. Vet. Div. Uganda Protectorate.
Trop. Vet. Bull. 3,159.
—
(1920). Ann. Rep. Dept Agri. Vet. Div. Uganda Protectorate.
Trop. Vet. Bull. 8, 170.
Hutyra, F. & Marek, J. (1916). Orientalische Rinderpest.
—
(1926). Spec. Path. and Therap. of the diseases of domestic animals; 1,
299-300.
Inowe, T., Harade, S., & Shimizu, T. (1930). Vet. Bull. 1931,1, 53.
Jackson, R. and Cabot, D. A. E. (1930). La resistance du virus de la peste bovine. Bull, de
L'Office Internat. des Epizooties 3, 781.
Jacotot, H. (1927). Trop. Vet. Bull. 15,120.
—
(1929). Trop. Vet. Bull. 17, 129-130.
— (1930).
Bull. Soc. Path. Exot., 23, 904-909.
Vet. Bull, 1931,1, 50.
—
(1931). C. R. Soc. Biol., 106, 206.
Vet. Bull. 1931,1,125.
—
(1932). Ann. Inst. Past., 48, 377 & 648.
Kakizaki, C. & collaborators. (1926). J. Jap. Soc. Vet. Sc., 5, 221-280.
Trop. Vet. Bull. 1927,15, 78 and 158.
Kelser, R. A. (1928). Philipp. J. Sc. (Sec. B), 36, 373-395.
Trop. Vet. Bull. 16, 23.
Koch, R. (1897). Zentralbl. f. Bakt., I, 21, 526.
Law, J. (1902). Vet. Med., 4, 628-629.
Lingard, A. (1899-1903). Note on the different degrees of susceptibility of bovines, buffalose, &c.
—
(1905). Rep. Imp. Bact., 1905-06, 4.
Littlewood, W. (1905). J. Comp. Path. and Therap. 18, 312.
McCall, F. J. (1922). Ann. Rep. Vet. Sc. and Ani. Husb., Tanganyika.
Trop. Vet. Bull. 1924,12, 74.
McLeod, K. (1871) Evidence cited on p. 800 Rep. Ind. Cattle Plagues.
Melanidi, C. & Stylianopoulo, M. (1927). Rev. Gen. Med. Vet., 36, 72-78.
Molinie, J. P. (1931). Rec. Med. Vet. Exot., 4, 5-26.
Vet. Bull. 2, 126.
Mrowka, F. (1914). Studien uber die ostasische Rinderpest, Zts. Infek. krank., 15, 139.
Nencki, (1898). Untersuchungen uber Rinderpest, Zentralbl. f. Bakt., I, 23, 529.
Nicholas, E., and Rinjard, P. (1921). Rec. de Med. Vet., 92, 602.
Nicolle & Adil Bey. (1899). Ann. Inst. Past., 13, 319.
—
(1902). Ann. Inst. Past., 16, 56.
Ono, S. & Kondo, S. (1923). J. Jap. Soc. Vet. Sc., 2,158-161.
Pease, H. T. (1894). C. V. D. Ledger Series No. 1—Rinderpest, p. 3 and also pp. 30-31.
Pool, W.A.,& Doyle, T.M. (1922). Studies in Rinderpest— Memoirs of Department. Agri.
India, Vet. Ser., 3,103-137.
Report on Indian Cattle Plagues (1871). P. 37 & p. 39, pp. 58-59, p. 411.
Rev. Gen. Med. Vet. (1920), 29, 57-583.
Trop. Vet. Bull. 1921,19,31
UNUSUAL CASE OF CHRONIC RINDERPEST.
382
Rickman, W. (1908). Tierzucht und Tierkrankheiten in Deutsch Sudwest Afrika, p. 156.
Roberts, G. A. (1921). J.Am. Med. Assn., 60, 177—185.
Robertson, W. A. N. (1925). Rinderpest in Western Aust alia in 1923.
Trop. Vet. Bull. 13, 22.
Rogers, L. (1900). Rep. on Exptl. investigation of the methods of inoculation against Rinder-
pest, Calcutta, p. 79 & p. 102.
Schein (1924). Ngo-Dinh-Bich and Nauyen-Danglam-Bull. de Vet. L'Indo-China, p. 134,
cited by Topacio (1927).
Scbern, K., & Mavrides (1918). Spontane Heilungen bei Rinderpest, Ztischft.f, Infek. krank,
19, 193-196.
Trop. Vet. Bull. 1918, 7, 186.
Ruppert, F. (1918). Trop. Vet. Bull. 1921, 9,122.
Ruppert, F., & Schern, K. (1921). Berliner Tier. Woch. 37, 85-88.
Trop. Vet. Bull. 9, 21.
Ruppert, F., & Wolfel (1921). Cited in Berliner Tier. Woch., 37, 86.
Sen, S. K (1925). Memoirs of Dept. Agri. Ind., Ent. Ser. 9.
Shilston, A. W. (1917). Memoirs Dept. Agri. Ind., Vet. Ser. 3, No. 1.
Trop. Vet. Bull., 6, 25.
Stirling, R. F.(1932). Vet. J., 88, 192-204.
Stockman, S. (1905). J. Comp. Path. and Therap., 18, 207-210.
Thacker, J. (1866). Cited on p. 543 Rep. Ind. Cattle Plagues (1871).
Theiler, A. (1898). Schweiz, Arch. Tierh. 1897, 39, 49.
—
Deuts. Tier. Woch., 1898, 6, 205.
Todd, C., & White, R. G. (1914). Expts. on Cattle Plague, Cairo.
Topacio, T. (1927). Use of goat virus in Simultaneous inoculation against Rinderpest (Prely.
Report). Philipp. Agri. Rev., 19, 1926.
Ward, A. R., Wood, W. F., Boynton, W. H. (1914). Philipp. J. Sc. (Sec. B.), 9, 49-78.
Trop. Vet. Bull. 2,187.
Youngberg, S. (1917). Philipp. Agri. Rev., 10, 436—447.
Trop. Vet. Bull. 6,124-125.
Zonchello, A. (1917). Il gulhai nel sthel—Clinica Veterinaria, 40, 113 -132.
Trop Vet. Bull, 5, 127.
E
RINDERPEST : TRANSMISSION OF INFECTION BY CONTACT
BY
HUGH COOPER, M.R.C.V.S., I.V.S.,
Veterinary Research Officer, Imperial Institute of Veterinary
Research, Muktesar.
(Received for publication on 24th June 1932.)
The object of this paper is to record the results of a series of experiments per-
formed during the last few years at Muktesar, since the information already ob-
tained is of interest to workers engaged in the control of this disease in India. With
this object in view only, a description is given of the actual experiments and their
main results, and no attempt is made here to discuss the subject in relation to pre-
viously recorded work.
The aim at the outset of the work was to gain certain information concerning
the " serum alone " method of inoculation against rinderpest. Although the infor-
mation originally sought was not obtained, yet, in the light of the experimental
evidence concerning the transmission of the disease that has emerged from the
experiments described below, it is hoped that the original plan of work can be fol-
lowed in a future series of experiments.
In the year 1926 a plan was laid down for the execution of an experiment de-
signed to give information concerning the duration of immunity conferred against
rinderpest by the " serum alone " method of protective inoculation. The results of
earlier work at Muktesar had indicated that under experimental conditions when
cattle were given a protective dose of anti-serum and then at varying intervals
afterwards were injected with rinderpest virus, the immunity did not extend beyond
about nine days. There was reason to think, however, from reports in the " field "
that protection might last somewhat longer under natural conditions of infection.
The plan of the experiment was designed therefore to copy natural conditions
of infection, and to expose cattle to it that had previously received doses of anti-
serum alone at varying intervals before contact was established. The cattle
that received serum were to be turned loose in a shed and be allowed to mix freely
together with other artificially infected animals. The infected cattle were to be
given rinderpest virus at a suitable time before contact occurred in order that they
would be suffering from the clinical disease when the experiment started. They
were to remain in close contact with the cattle that had received serum for two
( 383 )
RIDERPEST : TRANSMISSION BY CONTACT. 384
days, during which time no cleaning of the shed or removal of excreta was to take
place. The object in allowing contact for only two days was to limit the time of
infection so that results could subsequently be read with precision. After the two-
day period was over the infecting animals were to be removed from contact; the
others were to be placed separately in stalls for detailed observation, and the shed
was then to be cleaned and disinfected.
The experiment began on the 28th of September 1926 when a total number of
thirty hill-bred bulls were turned loose in a shed together with four other hill bulls
already reacting to an injection of rinderpest virus. The thirty-three bulls com-
prised six different lots. Six bulls each had received serum 24, 18, 12 and 6 days
earlier ; one lot of six bulls received serum on the day contact began and three bulls
were left uninoculated as controls.
The four infected bulls used consisted of two which had received virulent blood
three days previously. Both of them exhibited fever during the two days of con-
tact, and they both died of acute rinderpest five and six days later respectively.
The other two bulls had received virus eight days before and were showing at the
time of contact severe symptoms and specific lesions of the disease, including
marked buccal ulceration and diarrhœa. One of them actually died, unexpectedly,
of the disease during the night of the 28th September, or the first day of contact,
and the other bull died during the night of the last day, 30th September, having
been removed from contact in the morning of that day.
Observations, including temperature records, were made upon each of the
thirty-three bulls for three weeks after the period of contact, but within the first
few days it became evident that an accidental and naturally contracted foot-and-
mouth disease infection had come into the shed with them. This disease spread
quickly through the animals and complicated the experiment as regards temperature
records and the appearance of buccal lesions to such an extent that, although none
of the cattle died during the period they were under observation, yet it could not
be determined with certainty that none had also contracted rinderpest of mild in-
tensity and recovered from the attack.
It was accordingly decided to submit all of the animals used in the experiment
to an immunity test consisting of an injection of rinderpest virus. They were
tested in batches of six at a time from 27th November 1926 onwards, lasting until
24th December 1926. The results of these tests left no doubt at all that the bulls
had failed to become infected with rinderpest during the earlier period of two days
contact, since although some of them eventually recovered, almost without excep-
tion they exhibited a typical rinderpest reaction, and the majority of them died of
the acute disease.