NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
358 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [ IV, IV.
In both amoebiases and bovine haematuria, one notices a progressively, mild
chronic course with periods of quiescence between exacerbations, and the
occurrence of lesions in apparently healthy cases. Moussu's [1905] case, already
mentioned, was known to suffer from attacks of haematuria for 20 years, and
similar remarkably persistent cases of amoebiasis in man have been encountered.
With regard to the possibility of haematuria and the bladder lesions, as encountered
in cattle, being due to amoebiasis, considerable support is available in relevant
literature. Of the numerous cases of amoebic cystitis associated with haematuria
which have been met with in the diverse races of the world, authorities in
protozoology are prepared to accept notably few cases as genuine amoebic infections,
such as Walton's [1915], Fischer's [1914], and Petzetakis' [1923]. Further
Wirthin's case of amoebic infection of the testis and epididymis has also been
accepted. From the few cases of amoebiases recounted below it will be seen
that the maintenance of an over-critical attitude from theoretical considerations of
protozoology without reference to the nature of the clinical disease or of its lesions,
can no longer be justified.
Commencing with such interesting cases of amoebiases in large animals,
which have not found mention in any of the standard books or in the literature
upon Amoebiases, one finds that Benome [1895]* published an article on " Uber
parasitare Ictero-haematurie der Schafe. Beitrage Zum Studien der Amoebo-
sporidien " and Lehman [1912] dealt with cases of amoebiases in the horse,
cattle and sheep. Lehman showed that in these animals amoebae induce
papillomata and other neoplastic growths. A comparison of the picture of the
warty growths in sheep found by him with Plate XIX, Fig. 2, of this article is very
suggestive. In discussing Lehman's findings, an Indian Veterinarian, Valladares
[1913] makes the remark that "it would be worthwhile keeping a look out with
a view to ascertaining whether the amoebae as the cause of disease in the
domesticated animals exist in India," and the pertinence of that remark has been
illustrated in the present investigation and also in the records by Ware [1916]
and Boyd [1931] upon amoebiasis of dogs in the Madras Presidency.
Turning now to the pathology of human amoebiases, Brown [1910] states
" Not only is the submucosa actively inflamed and infiltrated but the connective
tissue fibres proliferate, and minute buttons of adenoid tissue push up from below
and appear as cluster of wart-like buds on the surface of the mucous membrane.
*
*
*
*
* None of the morbid changes of amoebic dysentery are
more distinctive of the disease than the exudation of pus from minute orifices of
mammillated growths on the mucosa. *
* Many of the epithelial cells are
replaced by mucous cysts." Jurgens found mucoid cysts in his case of chronic
* Original not consulted.
ETIOLOGY OF ENZOOTIC BOVINE HAEMATURIA
359
cystitis. A resume of the early cases where amoebae were found in human urine
has been given by Dobell [1919], and Fiessinger and Parturier [1926] have
reviewed the subject since. In a demonstration before the Royal Society
of Tropical Medicine and Hygiene, Yorke and Adams [1928] described an
interesting case of 'colloid carcinoma' of the splenic flexure of the large intestine,
in the lesions of which the presence of great numbers of Entamoeba histolytica
was proved. Again in an article on " Amoebic granulomas of the large bowel and
their clinical resemblance to carcinoma," Gunn and Howard [1931] describe their
own experience and draw pointed attention to the occurrence of localised tumours
of amoebic origin, which present the clinical and gross pathological picture of
carcinoma. They proceed to cite the previous experience of Desjardins, who
coined the term pseudocancer for cases of amoebiasis resembling cancer but res-
ponding to medicinal treatment. It will not be out of place here to quote Knowles
[1928] who remarks that " it is just possible that amoebic infection with its
consequent irritation may be one of the factors concerned in the production of
primary carcinoma of the liver of man in India.
Again in the case of experimentally infected guinea pigs the occurrence of
lesions resembling neoplasms is definitely known, though to Dobell and O'Connor
[1921] the lesions seen appear to be peculiar.
Having seen how closely the morbid anatomy of bovine haematuria conforms
to the available knowledge on amoebiasis of man and animals, one may turn to
the probable method by which amoebae gain access to the urinary bladder. In
cases of human amoebic cystitis, the question is still obscure. From the
histological features of bovine haematuria, the blood stream appears to be the
chosen route. Secondary infection of the brain, liver and other organs have been
encountered in man, and the parasites have been detected in blood vessels in some
of these cases, but the possibility of the blood circulation playing an important
role in the generalisation of amoebic infection does not appear to have been
considered at all seriously. From the studies in the present cattle disease, the
need of this possibility being investigated is emphasised.
CONCLUSION.
Definite evidence has been put forward in this article to show that the hitherto
obscure enzootic bovine haematuria is a parasitic disease, caused by a large
protozoan parasite. From the characters of the parasite, it appears to belong
to the phylum Rhizopoda resembling Entamoeba histolytica but would appear to be
a new species, for which the designation Entamoeba Kamala n. sp. is proposed.
Results of further work in connection with experimental transmission, cure
etc., which are now in progress will be published in due course.
360 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [ IV, IV.
Acknowledgment. Thanks are due to Mr. Sundar Rao, Artist, for preparing
the photographic plates and to Mr. Ahmed Bux, Assistant Artist, for making the
drawings. The author is indebted to Mr. Krishna Iyer, G.M.V.C., for measuring
the parasites and their cysts from time to time.
REFERENCES.
Allardyce, J. and others (1930). Vet. Bul. 1, 150.
Bonome, A. (1895). Virchows Arch. f. Path. 139, 1.
Boeck, W. C. & Drbohlav, J. (1925). Am. J. Hyg. 5, 371.
Boyd, J. S. K. (1931). J. Roy. Army. Med. Corps. 56, 1.
Brown, W. C. (1910). Amoebic or Tropical Dysentery. London. p. 125.
Bull, L. B. (1929). Australian Vet. J. 5, 60.
—and
others (1932). Enzootic Haematuria of Cattle in South Australia. Coun. Sc. &
Indus. Res., Australia Pamphlet No. 33. Melbourne.
Chieri & Frohlich (1911). J. Chem. Soc. 100, Pt. 2, 1018.
Cleland, J. B. (1911). J. Trop. Vet. Sc. 6, 125.
Craig, J. F. & Kehce, D. (1921). J. Comp. Path. & Ther. 34, 27.
Datta, S. C. A. (1931). Indian Vet. J. 8, 10.
—(1931-32).
An. Rep. Imp. Inst. Vet. Res. Muktesar, 15.
—(1932-33).
Ibid.
Dobell, C. (1919). The Amoebae Living in Man. London, 125.
—&
O'Connor, F. W. (1921). The Intestinal Protozoa of Man. London, 56.
Durin & Unglas (1931). Rec. Med. Vet. 108, 31; also Vet. Bul. 1, 309.
Fiessinger & Parturier (1926) cited by Knowles (1928), 89.
Fleming, R. H. and others (1931). Biol. Abs. 5, 1698.
Garudachar, M. K. (1930). Indian Vet. J.
Ghosh, S. (1933). An. Rep. Calcutta Scl. Trop. Med. 83.
Goetz, H. (1906). Schweizer Arch. f. Tierhlk. 48, 1. Abs. Vet. News. 1907, 4.
Gunn, H. & Howard, N. J. (1931). J. Am. Med. Assn. 97, 166
Hadwen, S. (1911). Proc. Am. Vet. Med. Assn.
—(1913).
Rep. Vet. Dir. Gen. Canada, p. 74.
—(1914).
Ibid. 119 and 136.
—(1917).
J. Am. Vet. Med. Assn. 51, 822.
Ichikawa, (1922). Jap. J. Med. Sc. 1, 63. Abs. Trop. Vet. Bul 1924, 12, 20.
Inchley, (1921). J. Pharm. & Exp. Ther. 18, 237.
Kerr, P. J. (1925). Tr. Far. Eastern Assn. Trop. Med. 1927, 3, 684.
—(1932-33).
An. Rep. C. V. D., Bengal, p. 14.
Knowles, R. (1928). An Introduction to Medical Protozoology, 80.
Law, J. (1901). Veterinary Medicine. Ithaca, 3, 205 & 207.
Lehman, E. (1912). Centbl. Bakt. Orig. 62, 589.
Macgregor, A. D. & others, (1934). The Statesman, New Delhi, 9th Sept.
Miyamoto (1927). Tr. Far. Eastern Assn. Trop. Med., Calcutta, 3, 667.
PLATE XIX.
Fig. 1. Inside of the urinary bladder shows extensive cauliflower-like growths
and two pyriform mucoid cysts.
Fig. 2. Two warty growths in the duodenum, a few inches from the pyloric
end of the abomasum. Microscopically, sections showed resemblance to bladder-
growths and the presence of rare parasites.
PLATE XX
Fig. 1 × 56. Bladder. Junction of healthy and desquamating mucosa. Surface is hæmorrhagc,
undergoing coagulation necrosis under the action of developing parasites situated immediately
subjacent to the degenerating mucosa.
Fig. 2 × 40. Shows extreme dilation and engorgement of the capillaries supplying the mucosa and
submucosa. These capillaries provide seats for the localisation of the parasites.
PLATE XXI.
Fig. 1 × 244. Eirly lesion, reaching nearly to the muscular layer, resembling a ' typical ulcer of
Harris ' of human amœbiasis.
Fig. 2 × 56 shows the nidus of the disease in the submucosa, represented here by a colony of
parasites in a thrombosed and bursting vessel, with secondary changes in the mucosa.
PLATE XXII.
Fig. 1. Bladder mucosa shows considerable proliferation in the centre of the field, it is disposed
into an adenoma-like formation. Submucosa shows so-called angiomatous pools of blood and a focus
of cellular infiltration.
Fig. 2 shows warty papillomatous growths.
PLATE XXIII.
Fig. 1 × 143 shows epithelial nodes in various stages of development and degeneration. The swollen
node, about to be shed, shows a few peauliar nucleated bodies in the thinned central area.
Fig. 2 × 216 shows a colony of large-sized parasites and a double-contoured cyst, localised in an
extremely attenuated epithelial node on the point of bursting.
PLATE XXIV.
Fig. 1 × 335. Blood vessel shows a few parasites in the lumen and wall.
Fig. 2 × 150. Colony of quiescent parasites in broken down blood vessels. Note the subacute
cellular reaction around the parasites.
PLATE XXV.
Fig. 1 × 216. Colony of active parasites in the superficial lesion. Note the cyst, showing one definite,
and two hazy nuclei, with a suggestive empty space.
Fig. 2 × 129. Another colony. Note the lateral prolongation on the large parasite on the top right
hand sides of the field.
PLATE XXVI.
Fig. 1 × 166. Section of the kidney dilated blood vessel shows parasites in the lumen Note the
difference in the appearance of the parasites, compared to the endothelial and other cells in the field.
Fig. 2 × 128. Shows four neighbouring colonies of rapidly multiplying parasites below the bladder
surface. Note two cysts of varying shapes.
PLATE XXVII.
Fig. 1 × 335. High power photograph of a section stained with iron-hæmatoxylin, showing
inclusion bodies inside the parasite.
Fig. 2 × 244. High power photograph showing a colony of large-sized parasites in the superficial
lesion in the bladder. Section was stained intensely by Gram's method. Note the typical character of
the nucleus and the shape of the parasites.
PLATE XXVIII.
Fig. 1. Shows growths in the mucosa and submucosa resembling to an extent adeno-carcinoma.
Fig 2.
Shows
in
filterating
charecter
of
cell-extention
in the depth of the bladder wall.
PLATE XXIX.
Fig. 1 × 56. Low power photograph. Section, of bladder shows two altered vessels. In one, the
parasites still persist, while in the other they have been digested by body tissues.
Fig. 2 × 244. A degenerated area in the duodenal lesion (Plate XIX, Fig. 2) showing a few parasites
With the typical nuclei.
ETIOLOGY OF ENZOOTIC BOVINE HAEMATURIA
361
Moussu, G. & Dollar, J. A. W. (1905). Diseases of Cattle, Sheep, etc. 520, London.
Mustak Husain (1930). U. P Vet. Mag. 19, No. 6, 4.
Ottawa (1930). An. Rep. Vet Dir. Gen. Canada, 40.
Parameswara Ayyar (1922). Madras Vet. J. 16th issue, 4.
Petzetakis, M. (1923), cited by Wenyon (1926). Protozoology, 192.
Piot Bey (1918). Rec. Med. Vet. 94, 631.
Rangaswamy (1922). Madras Vet. J. 14th issue, 1.
Sarvonat & Roubier (1911). J. Chem. Soc. 100, Pt. 2, 815.
Sonsino (1876), cited by Neumann in Parasites and Parasitic Diseases of Domesticated Animals.
London, 1905, 532.
Steyn, D. G. (1933). Onderstepoort J. Vet. Sc. & An. Indus. 1, 439.
Theiler, A. (1929). Health and Nutrition of Animals. Coun. Sc. & Indus, Res., Australia Pamph-
let No. 10, 44.
Valladares, J. F. (1913). Notes on Protozoal Infections in Madras and Central Provinces, Nagpur, 8.
Vet. Bul. (1931). 1,95.
Walton, H. J. (1915). Br. Med. J. 1, 844.
Ware, F. (1916). J. Comp. Path. & Ther. 29,126.
Wirthin, A. S. (1922). J. Infec. Dis. 30, 559.
Yorke & Adams (1928). Tr. Roy. Soc. Trop. Med. & Hyg. 22, 8.
SOME OBSERVATIONS ON THE TRYPANOSOMES OF CATTLE
IN SOUTH INDIA.
BY
M. ANANT NARAYAN RAO,
Lecturer in Parasitology, Madras Veterinary College,
AND
S. VAIDYANATHA MUDALIAR,
Assistant Lecturer.
(Received for publication on 20th. August 1934.)
(With Plates XXX to XXXII and six text-figs.)
CONTENTS.
Introduction . . . . . . . . . . . . . .
Early experimental work on pathogenicity of cattle trypanosonies to horses . .
The identity of the small trypanosomes of cattle in South India . . . . . . . . . . . . . .
Pathogenicity to experimental animals . . . . . . . . . . . . . .
Cross immunity teasts . . . . . . . . . . . . . .
Adhesion phenomenon . . . . . . . . . . . . . .
Reserviours of surra . . . . . . . . . . . . . .
Mechanical transmission by tabanus . . . . . . . . . . . . . .
Observations on the occurence of trypanosomiasis in rinderpest—virus producing
calveas . . . . . . . . . . . . . .
The large trypanosomes in the blood of bovines and buffaloes. (T. theileri
Laveran, 1902) . . . . . . . . . . . . . .
Summary . . . . . . . . . . . . . .
Acknowledgments . . . . . . . . . . . . . .
Pages.
362
363
365
370
374
376
376
384
390
391
394
395
INTRODUCTION.
Only two kinds of trypanosomes have been met with in the blood of cattle in
South India, viz., a large one resembling T. theileri Laveran, 1902, and a smaller one
resembling T. evansi [ Steel 1885 ], and the same two trypanosomes are found in
Northern India. Stirling [ 1920 ] appears to have found trypanosomes resembling
T. congolense Broden, 1904 [ T. dimorphon Laveran and Mesnil, 1904 ], in a bullock
that died in the Central Provinces under conditions suggestive of piroplasmosis, but
the existence of this trypanosome in India has not been confirmed.
In the smaller trypanosome of cattle resembling T. evansi, which is also found
in other animals such as the horse, dog and buffalo, no polymorphism seems to exist.
Whether this smaller trypanosome as found in cattle is pathogenic to them and to
( 362 )
OBSERVATIONS ON TRYPANOSOMES OF CATTLE IN SOUTH INDIA
363
other domesticated animals, particularly to the horse, is a question which is often
asked. Until recently it was commonly believed that such trypanosomes of cattle,
in this part of India, were not very pathogenic to bovines and buffaloes, but with
the increased facilities now available for routine microscopical examination of blood
of cattle in the field, it has been possible to determine that definite outbreaks of
trypanosomiasis do occur in bovines and buffaloes, causing mortality, which varies
according to the severity of the outbreak. Edwards [1928] says that virulent out-
breaks of surra occur among cattle and notably among buffaloes in which the mor-
tality rate may vary from 20 to 80 per cent.
Other workers have shown that there exists some circumstantial evidence that,
under natural conditions, these trypanosomes may be transmitted to horses, from
bovines as reservoirs. But experimental evidence appears to be very meagre to
prove the identity of these monomorphic trypanosomes of cattle and that bovines
act as the reservoirs from which the disease is carried over from one season to the
next, and to the horse, in which surra is fatal.
EARLY EXPERIMENTAL WORK ON PATHOGENICITY OF CATTLE TRYPANOSOMES
TO HORSES.
Lingard [ 1899 ], in his Report on Surra, mentions two horses which, on being
inoculated with cattle trypanosomes, developed clinical symptoms of surra, with the
appearance of the parasites in the peripheral blood. These two cases were briefly
as follows:—
(1) Australian mare, aged.—Inoculated subcutaneously, on 3rd October 1892,
with 0.5 c.c. of blood swarming with trypanosomes taken from a cow.
The latent period occupied 5 days and the temperature gradually rose
during this time, the parasites appearing in the blood on the 6th day.
Death occurred on the 14th day of the disease.
(2) Horse.—Inoculated with 0.5 c. c. of blood swarming with trypanosomes
taken from a cow. Result positive (but no details given).
Presumably on the basis of the two foregoing and perhaps other similar obser-
vations, Lingard [ 1906 ] was led to deduce the following conclusions: "Horses
inoculated with blood in small quantities drawn from plains and hill bovines during
the early stages of the disease, whether the blood be collected during a paroxysm or
an intermission, contract the disease in virulent form, and death may take place
when the infective blood is derived from a plains animal within the short period of
5 days, and when from hill bovines between a period of 19 or more days. When,
however, inoculations are conducted with blood taken at a later stage of the disease,
G 2
364 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [ IV, IV.
from a similar source, the course of the malady in equines is more prolonged, but
equally fatal in its results."
Proof of the pathogenicity of cattle trypanosomes to equines is afforded by the
results of two experiments carried out by Fraser and Symmonds [ 1909 ] in the
Federated Malay States. The full account of these two cases, as given by the
authors, is of sufficient interest to bear quotation :—
(1) "In order to follow the course of the disease in a horse inoculated from
a naturally infected bullock, an Australian mare, 9 years old, about
16 hands high and in excellent condition, was inoculated subcutane-
ously with 1 c.c. of blood from a naturally infected bullock. Seven
days later the temperature of the horse rose to 103°F., and on the
following morning trypanosomes were discovered. Thereafter the
temperature was irregular, a remittent temperature of from two to
five days duration alternated with an interval of one to two days,
when the temperature was either intermittent or normal. During the
last 12 days of the disease, the temperature remained constantly eleva-
ted. On six occasions parasites could not be found, their period of
absence lasting from one to four days. Oedema of the legs was first
noted on the 10th day and by the 13th day was marked; on the 18th
day oedema under the abdomen was observed and later on it extended
along the thorax. An urticarial eruption occurred from time to time.
Loss of condition was pronounced by the 25th day and weakness of
the hindquarters, which was first noticed on the 44th day, became
very evident by the 50th day. On the 62nd day the mare fell down
and did not rise again. Death occurred on the 66th day."
(2) " An Australian gelding, 8 years old, in good condition, was inoculated
subcutaneously with 0.1 c.c. of blood from a naturally infected bullock.
The period of incubation was six days and the disease ran its course in
51 days. The observations as regards parasites and clinical signs were
similar to those in the preceding case, save that oedema was never
present. That this was not due to a different species of trypanosome
was shown by the fact that another horse which was inoculated with
the same strain of trypanosomes developed oedema of the legs, abdo-
men and thorax ".
Fraser also conducted experiments to determine the identity of the trypano
somes encountered in other species of animals and, as a result of these experiments,
came to the conclusion that the trypanosomes " met with in horses, cattle, and dogs
are indistinguishable morphologically and in their pathological effects (and hence
they all belong to the species Trypanosoma evansi)".
OBSERVATIONS ON TRYPANOSOMES OF CATTLE IN SOUTH INDIA
365
THE IDENTITY OF THE SMALLER TRYPANSOME OF CATTLE IN SOUTH INDIA.
(a) Morphology. The general morpological characters of this trypanosome
agree with those described for T. evansi [ Steel 1885 ]. It is monomorphic with a
well developed undulating membrane and a free flagellum. The measurements range
from 18 to 33 µ in length and 1-5 to 2 0 µ in width. The average length is about
25 µ.
(b) Biometry. The idea of the study of biometry was obtained from the work
on Trypanosome Diseases of Domesticated Animals in Uganda by Bruce and his
collaborators [1911] and also from Fig. 196 in " Protozoology" by Wenyon
[1926]. In the latter two curves, one for T. evansi and the other for T. brucei, are
given representing the percentage of trypanosomes in respect to length. It is
presumed that those curves were plotted from smears obtained from animals in
which relapses had occurred. "Wenyon [ 1926 ] suggests that the notch, which
these curves show, is an indication that in such infections two types of trypanosomes
are present—not necessarily two species, but that the one species tends to produce
in its development two main groups of organisms and it is of interest that curves
drawn for T. evansi in white rats also show similar notches. Taliaferro [ 1930 ]
says that in mice, where no crisis occurs, the infected trypanosomes do not come in
contact with the lytic anti-bodies, hence they do not become biologically changed
as they do after each trypanolytic crisis in such hosts as guinea pigs, dogs, etc.
White rats behave exactly like mice in having no crisis when injected with T. evansi,
yet a notch in the curve of lengths of trypanosomes is seen. Even the curves drawn
for relapse strains of a known original, all maintained in different rats, also show a
similar notch in each curve drawn. Curves drawn for a strain maintained in a
guinea pig also show similar notches in the original as well as in those drawn during
each relapse. Hence it would appear that the indication of such a notch, if it is of
any significance, is that these trypanosomes have in them a latent possibility of
variation which may manifest itself even without the action of a trypanolytic anti-
body. Ritz [1914] was able to produce twenty-two variants immunologically different
from the original strain with which he worked and it seems that there are
unknown factors which influence the virulence of the same type of trypanosome
when it is obtained from different sources such as the bullock, dog, or horse, about
which reference will be made later.
The biometric curves discussed in this paper were drawn from a large number
of blood smears from different classes of naturally infected animals, received in this
laboratorÿ, and from the blood smears of experimental animals used in the present
study. Since all these smears were made and stained under similar conditions, it is
suggested that any error due to contraction of the parasite, etc., should be common
to all the organisms drawn for measurement, and can be ignored. Fig. I shows
366 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [ IV, IV.
FIG. I.
Trypanosomes Madras Strains.
Curves in respect of lengths by percentages.
OBSERVATIONS ON TRYPANOSOMES OF CATTLE IN SOUTH INDIA
367
curves for trypanosomes in naturally infected ponies, dogs, cattle and buffaloes.
The similarity in the rise of particular lengths is striking in all these curves. These
curves also show that the average length of 25 µ is common to all and coincides with
the average length of T. evansi. It was also found that the curves drawn for
trypanosomes in experimentally infected ponies resembled those drawn for the
trypanosomes from naturally infected ponies in respect of the average length and
the range of variation in length. (Fig. II). In experimentally infected white
FIG. II.
Tryps: Bovine Strain