NationalLibraryOfScotland/medical-history-of-british-india huggingface dataset:
THE ETIOLOGY OF BURSATI
229
analogy should be kept in mind, since certain well-known but hitherto unaccount-
able clinical facts of Bursati can now be explained on this view.
In the light of the present histological findings, Bursati, at any rate as it
occurs in India, appears to be a single disease entity, the presence of moulds in
open sores having no significance ; for, it has been shown above that the diagnos-
tic lesions of Bursati are represented by the kunkurs and that they are, histologi-
cally speaking, typical helminthic nodules, the same nematode larvae of Habro-
nema spp. having been demonstrated consistently as forming the inciting nucleus
for the production of the nodular lesions. There need now be no doubt, therefore,
regarding the helminthic as also the habronemic origin of Bursati.
With regard to the mode of infection, the position is more unsatisfactory. A
perusal of the Bursati literature shows that the fly transmission theory has been
held by the natives of India from as early a date as 1820, and that among the other
old theories, it was believed to be a blood disease [Ubique, 1877 and Ferris, 1881].
In the case of cutaneous habronemiasis, as known in different parts of the world,
the hypothesis current at present is that these helminthic granulomata are caused
by the deposition of the habronema larvae in wounds by flies. Although the
current view is undoubtedly an improvement on the old Indian belief, it will be
seen from what is stated below that it is still unacceptable, since it fails to provide
a satisfactory explanation for the known facts regarding Bursati. Contrarily,
however, it will be realised that from a consideration of certain clinical peculiari-
ties of the disease, which have been emphasised by most observers, one cannot
resist the belief that the disease is more than a mere local infection, although
there are little or no constitutional symptoms. Notable among the protagonists of
what may, for brevity, be called the fly theory, are Railliet and Henry [1915], who
suggested that habronema larvae penetrate the skin in the same manner as the
larvae of ankylostomes, but from the experimental work of several other workers,
it appears that these larvae are not able to penetrate the equine skin even when
the epidermis alone is damaged. Margarinos Torres [1924], however, claims to
have proved that the larvae of Habronema muscae, if deposited in wounds of a
guinea-pig. are able to reach the lungs, it being an organ for which they appear to
have a marked preference. The failure on the part of the present writer [1931] to
transmit the disease through the agency of flies receives support from Holmes
[1914], who states " I am unaware of recorded cases of transmission of the sore
from horse to horse by means of outside agencies ", and also in the statement of
Spooner Hart [1873]: '' Practice and time have afforded ample proof of the non-
contagiousness of Bursati, for my bursatied subjects stand among other animals
and I have never seen any ill effects ensue ". The statements quoted here and the
230 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [III, III.
general experience that in the following year or years " animals once affected with
the disease are almost certain to have it recur " (Kerr, 1829) at the same seat or
in sites far away, where there have been no wounds, to the exclusion of other
animals, indicate that the mechanism underlying the production of natural cases
of the disease is not so simple as the current fly-transmission theory would imply.
The exclusion of other animals is remarkable, since infected flies undoubtedly have
access to all animals housed in a particular stable, where there had been a case or
cases previously. Further, it is known that the prevention of contamination of
wounds from infected flies and the local application of numerous otherwise very
efficient drugs, have failed in the hands of many workers to prevent the recrudes-
cence of the sores in certain parts several years in successions, or of fresh sores
in other parts of an effected subject; but the available information shows that the
larvae in the skin lesions soon die out, i.e., within a month of implication. Again,
that bursati sores persist during the whole of the special season, which is several
times longer than one month, is known. The control and cure of Bursati should
have been achieved by now by the prevention of reinfection by bandaging or appli-
cation of fly-repellents, like Van Saceghem's [1918] Plaster of Paris and Naphthalene
preparation, if the fly theory represented a true picture of the essential pathogenic
process; but the unfortunate fact that Bursati is still incurable, recurrence is
common and destruction of affected cases is still practised, shows that fly trans-
mission is not the usual method. The work of Margarinos Torres [1924] however
proves that occasionally the migration of larva, deposited in a superficial wound,
may take place.
The possibility of infection taking place through the general circulation, which
has already been suggested by Laulanie [1884] in the case of Summer Sores, offers an
interesting alternative, following naturally as a corollary to the significant histo-
pathological findings, referred to above. That the clinical peculiarities of Bursati
are such that one cannot resist the belief that the disease is more than a mere local
infection has already been stated and a consideration of expressions, such as, a
" bursati diathesis " [Collins, 1874], " peculiar conditions of the patient's system "
[Smith, 1879], " constitutional predisposition of the disease " ["Max ", 1876] used
by several workers, makes it obvious that a certain subjective factor is indispensable
to the production of the sores. The subjective factor or " bursati diathesis " would
seem to resolve itself into the infestation of the equine stomach through the inter-
mediary agency of flies and the consequent floating of the migratory worm larvae in
the general circulation. Some of the earliest observations, such as " the poison
appears to be carried to other parts of the body " [Meyrick, 1878] would point to the
intervention of the general circulation, and the same is again supported by the com-
THE ETIOLOGY OF BURSATI
231
mencement. of the growths as an intact tumour, or the lesions being first observable in
the subcutis with extension outwards later, a feature which has been affirmed by
several keen observers.
The first definite case of so-called internal bursati involving the lung, in associa-
tion with the skin lesions and the presence of Habronema in the stomach has been
described earlier in this article. A correct decision upon whether there really exists
any relationship between habronemiasis involving different functional systems, such
as cutaneous, pulmonary or gastric, in the same animal is important, since an
affirmative verdict would add considerable support to the new theory elaborated
herein, viz., an internal origin of Bursati. It would appear to be the opinion of
Roubaud and Descazeaux [1921] that each is a separate entity, being produced by
infected flies, alighting on abrasions, or nostrils or on the lips, as the case may be.
Further they believe that ingestion of parasitized flies also may cause the gastric
affection. But the above-mentioned case of internal bursati is comparable to the
experience of several other workers. For instance, Drouin [1902] observed the
simultaneous involvement of the skin and the lung in Summer Sores. In Belpel's
[1925] experience in Italy, skin lesions were associated with the presence of the
worm in the stomach, and finally Dieulouard [1926] working in Brazil, found that
of 20 horses, showing pulmonary habronemiasis, 19 showed evidence of having had
Summer Sores at some time during their life, and that the lung lesions occurred
only in animals showing evidence of skin involvement. The migratory propensities
of Habronema larvae have been demonstrated by Margarinos Torres [1924], and the
association of various forms of habronemiasis in the same animal as observed by
several workers, has been remarked upon.
It seems that the presence of the migratory worm larvae in the general circu-
lation cannot by itself produce the disease. There still remains the need of a
further factor, injury or contusion, in order that thrombus formation may take
place in the capillaries, enabling the arrest of the worm larvae in embolic masses.
Bursati growths would therefore appear to be formed only in seats, liable to much
risk of successive contusion and injuries, and a breach of the surface may also serve
the same purpose, the actual lesions of Bursati being due to an effort of the host
tissues to get rid of the embolic masses. Even a deep excision of the growths by
the surgical method and a rigid insistence upon the retention of a bandage has
failed in the hands of many workers, and the reason is not far to seek. The
sectioning of blood vessels in the surgical operation leads to clot-formation and
consequently bursati sores. In short, the writer feels justified in advancing the
view, that in a majority of cases the habronema larvae are transported through the
232 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [III, III.
general circulation to certain parts of the body, where they are arrested owing to
previous thrombus formation, and not deposited on existing wounds by the fly.
Turning now to the specific identity of the Habronema responsible for Bursati in
India, H. muscae appears to be the most probable. It may be noted that in France
and Australia, H. megastoma is incriminated as the causal agent of Summer Sores
and Swamp Cancer, and that in Brazil, Margarinos Torres [1923] considers " H
muscae is the most important and perhaps the only cause of the disease ", and Van
Saceghem [1917] believes the same to be true in Zambi in the Congo. That the
measurements and character of the anterior end of the larvae, as seen in sections of
the skin and again in sections of the prepuce lesion conforms to those of H. muscae
has been mentioned earlier in this article. The occurrence of the same species of
the worm to the exclusion of other species in the stomach of a case, which showed
both pulmonary and cutaneous habronemiasis, appears to be more than a mere
coincidence. The experience in India would therefore support that of the Brazilian
worker and of Van Saceghem [1917 ].
In regard to the probable intermediaries, certain native flies, six muscid and
one sarcophagid of Queensland [Johnston, 1920], Drosophilid flies in Ceylon
[ Crawford, 1926 ], have been incriminated in addition to the usual Musca domestica
and Stomaxys calcitrans and recently Patton [ 1932 ] has stated : " Musca crassiros-
tris is a probable transmitter of Habronema in India, for I have found these nema-
todes developing in it ". In addition to being related to " special districts " and
" special seasons ", Bursati has been called a disease of ''special circumstances"
by Burke [ 1881 ], and though the precise factors are as yet imperfectly understood,
the occurrence of particular species of Habronema and of the appropriate flies in
the same locality now seem indispensable to the production of Bursati. The fact
that the sores, after having manifested considerable resistance to treatment, tend
to disappear spontaneously at the approach of the winter indicates that the supply
of the larvae is no longer continued. That a close relationship must exist between
the cycle of evolution of the bursati Habronema and the life-history of its inter-
mediate host is obvious from the work of Ransom [1913, Hill, 1920 ] and others:
and until the evolutionary stages of the worm in relation to the fly in question have
been worked out, month by month, the factors responsible for the bursati, season
and districts, will not be understood. A scheme of evolution has been given by
Roubaud and Descazeaux [ 1921 ], but as far as the writer is aware, this has still
to be confirmed. As a result of histological studies upon sections of H. megostoma
tumours, from about 20 cases, collected at different times during a number of
years, the author could obtain no proof for the view originally advanced by Des-
THE ETIOLOGY OF BURSATI
233
cazeaux that the female parent probably brings forth young but once during a
period of 12 months.
From what has been said above, it will be realised that the effective control
and cure of Bursati must depend upon the eradication of the Habronema worms
from both the definitive and intermediate hosts, disposal of equine faeces and intra-
venous administration of drugs like Tartar Emetic and Novarsenobenzol.
CONCLUSIONS.
The present investigation reveals the nature of Bursati known in India since
1829. It is a habronemic granuloma of equines, most probably due to H. muscae
Carter, involving the skin and internal organs such as the lung. The disease is
more than a mere local infection, the causative larvae exhibiting considerable mig-
ratory powers. In the majority of cases, skin lesions would appear to be produced
through the general circulation, wound infection playing an insignificant role.
ACKNOWLEDGMENTS.
The thanks of the author are due to Mr. G. D. Bhalerao, M.Sc., Helmintholo-
gist at this Institute, for identifying the helminth larvae, discovered in the course
of this investigation, and to Mr. J. Sunder Rao, Artist, for the execution of the
illustrations.
REFERENCES.
Allen, H. (1923). Vet. J. 79, 24-27.
Baylis, H. A. (1929). A Manual of Helminthology, Ldn., 226.
Belpel, M. J. (1925). Rev. Vet. 77, 5-24.
Abs. Trop. Vet. Bull. 13, 93 & 123.
Bull, L. (1916). J. Comp. Path. Therap. 29, 187-193.
Burke, R. W. (1881). Vet. J. 13, 16-22.
—
(1884). Vet. J. 19, 85-87,158.
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(1888). Vet. J. 27, 166-168.
—
(1892). Tropical Diseases of the horse and ox, Jubbulpore, Preface VI, 70.
Carougeau, (1909). Cited by Holmes (1914) Rec. Med. Vet., 94,191.
Collins, F. F. (1874). Veterinarian, 47, 791-792.
Crawford, (1926). J. Comp. Path. Therap. 38, 321.
Datta, S. (1931). Proc. 18th Ind. Sc. Cong., Nagpur.
—
(1933). Ind. J. Vet. Sc. Ani. Husb. 3, 1-28.
C
234 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [III, III.
Descazeaux, M. J. (1915). Ralliet's Report, Bull. Soc. Cent. Med. Vet. 91.
Abs. Trop. Vet. Bull. 4, 468-486.
—
(1921). Rev. Med. Vet., 107, 489.
Abs. Trop. Vet. Bull. 10, 119.
Dieulouard, (1926). Rec. Med. Vet. 105, 206-212.
Drouin, (1902). Bull. Soc. Cent. Med. Vet. 91, 654.
Ferris, (1881). Vet. J. 13, 333-335.
Fish, P. A. (1895-96). 12th and 13th Ann. Rep. Bur. Ani. Indust., 229.
Freeborn, Hart & Howell, (1927). Abst. J. Parasit. 13, 220.
Gaiger, S. H. (1915). Vet. Rec. 28, 129-130.
Hill, (1920). Proc. Roy. Soc. Vict., 31. (New series) 11-76.
Abs. Trop. Vet. Bull. 1920, 8, 198-202.
Rev. App. Entom. 7, 118-120.
Hodgkins, J. R. (1924). J. Trop. Vet. Sc. 5, 357.
Holmes, J. D. E. (1914). Bursati, Mem. Dep. Agri. Ind. Vet. Ser. 2, No. 5.
Jackson,C. (1842). Veterinarian, 15, 257-258.
Johnston, T. H. (1920). Abs. Trap. Vet. Bull. 10, 119.
Proc. Roy. Soc., Queensland, 32, 61-88.
Kerr, J. (1829). Veterinarian, 2, 419-420.
Laulanie, (1884). Bull. Soc. Cent. Med. Vet. 61, 72.
Lewis, J. C., and Seddon, H. R. (1918). J. Comp. Path Therap. 31, 87-94.
Lingard, A. (1905). Observations on Filaria embryos found in the general circulation in
Equidae and Bovidae, Fasciculus I, Bursati Ldn.
Malik, M. (1931). Vet. J. 87, 578-580.
Margarinos Torres, C. (1923). C. R. Soc. Biol. 89, 767-768.
—
(1924). Rev. App. Ent. Ser. B. 12, 2 & 68.
—
(1925). Rev. App. Ent. Ser. B. 13, 135.
"Max", (1876). Vet. J. 3, 338.
Meyrick, J. (1878). Vet. J. 7, 318.
Nunn, J. (1896). Vet. J. 42, 346.
Patton, W. S. (1932). Ann. Trop. Med. Parasit. 26, 348.
Railliet, A. & Henry, A. (1915). Bull. Soc. Path. Exot. 8, 695-704.
Ransom, B. H. (1913). Bull. No. 163, U. S. A. Bur. Ani. Indust.
Rivolta, (1868). Cited by Holmes (1914).
Roubaud, E., & Descazeaux, J. (1921). Bull. Soc. Path. Exot. 15, 471-506.
Abs. Trop. Vet. Bull. 10, 9.
—
(1922). Bull. Soc. Path. Exot. 15, 572-574.
Abs. Trop. Vet. Bull. 10, 9 & 119.
Sen, S. K. (1927). Agri. J. Ind., 22, 281.
Smith, F. (1879). Vet. J, 9, 300 & 383.
THE ETIOLOGY OF BURSATI
235
Smith, F. (1884). Vet. J. 19,16.
—
(1885). Quart. J. Vet. Sc. Ind. 3,121-125.
Also J. Comp. Path. Therap., 1891, 4, 123-131.
Smith, Theobald. (1893-94). 10th and 11th Ann. Rep. Bur. Ani. Indust.
Spitz, G. (1920). Trap. Vet. Bull. 8, 202.
Spooner, Hart. (1873). Veterinarian, 46, 386.
Steel, J. (1881). Vet. J. 13, 237.
—
(1884). Vet. J. 18,132.
Ubique, (1877). Vet. J. 5, 25.
Van Saceghem, (1917). Trop. Vet. Bull. 5, 248.
—
(1918). Rev. App. Entom. 6, 202, & Trop. Vet. Bull. 6, 171-173.
—
(1919). Rev. App. Entom. 7,157.
DESCRIPTION OF MICROPHOTOGRAPHS.
Plate XIV, fig. 1.—Low power photograph of a section of bursati growth, removed from the
angle of the mouth, showing a typical habronemic abscess in the early lymphocytic
stage. In the central degenerated area, both longitudinal and cross-sections of the larvao
can be seen. The histological picture resembles very closely that of early gastric
abscesses, due to H. megastoma.
Fig, 2.—Low power photograph illustrating the essential lesion of Bursati, characterised by a
cross-section of the parasite, enclosed in a blood vessel, around which a lymphocytic
infiltration can be seen arranged in the form of a nodule. This is the earliest stage in
the formation of the kunkur.
Plate XV, fig. 1.—Section of a bursati growth, removed from the limb, showing a coiled larva
in a dilated vessel. Note the sharp outline of the lumen and that the concentration
of the toxic effect on the vessel wall diminishes from the centre outwards.
Fig. 2.—Same as PI. XIV, fig. 2 but under a higher magnification. The worm larva is seen
here at its primary seat of operation, the lumen of a capillary vessel.
Plate XVI, fig. 1.—Low power photograph of an exceptional section of a growth. Superficial
cutis shows degenerative changes, with a slight involvement of two epithelial papillae in
the centre of the field. Sub-epithelial layer is practically unaffected, excepting for slight
eosinophile infiltration.
Fig. 2.—Low power photograph of a bursati section. An elongated kunkur, which is more
extensive in the depth of the growth than towards the surface, is seen here, having been
formed along the course of one of the dilated perpendicular vessels. Note the partial
loss of staining affinities of the major portion of the field, compared to the darker and
healthier portion on the left.
Plate XVII, fig. 1.—Low power photograph. On the left, four kunkurs are to be seen. In
the case of the lowest kunkur, the centrally situated blood vessel can be seen, as also the
diffusion of the toxin for the same distance in all directions, giving a more or less
rounded appearance to the kunkur.
Fig 2.—Low power photograph, showing two kunkurs in a bursati section. The left one is
practically free to be evacuated from the fistula in the mother tissue. The right one
has been formed in a hair follicle, the hair root having already been destroyed.
c 2
236 THE INDIAN JOURNAL OF VETERINARY SCIENCE AND ANIMAL HUSBANDRY [III, III.
Plate XVIII, fig. 1.—The essential structure of an elongated kunkur, partially detached from
the mother tissue is to be seen. Eosinophil leucocytes are the most predominant cells
in this growth. Longitudinal section of the worm larva, with its transverse striation
can be seen occupying the blood vessel, which forms the nucleus for the production of
this kunkur.
Fig. 2.—Section of a bursati growth, showing a healthy worm in a healthy vessel. Only the
perivascular lymphocytic reaction is in evidence here. This stage is followed successively
by the stages represented by PI. XIX, fig. 1 and PI. XVIII, fig. 1.
Plate XIX, fig. 1.—Longitudinal section of a larva lying free in a blood vessel. Diffusive
action of the toxin can be judged by the homogeneous appearance of the border around
the vessel.
Fig. 2.—Photograph of a Habronema larva in a bursati section. The posterior end of the worm
is directed to the right, the anus being easily visible.
Fig. 3.—Photograph of the anterior end of a Habronema larva, obtained from a bursati section.
The cylindrical vestibule is clearly seen.
PLATE XIV.
FIG. 1. × 30.
FIG. 2. × 56.
PLATE XV.
FIG. 1. × 140.
FIG. 2. × 554.
PLATE XVI.
FIG. 1. × 14.
FIG. 2. × 14.
PLATE XVII.
FIG. 1. × 13.
FIG. 2. × 13.
PLATE XVIII.
FIG. 1. × 85.
FIG. 2. × 132.
PLATE XIX.
FIG. 1.
× 128.
FIG. 2.
× 280.
FIG.
3. ×
300.
CERCARIA HURLEYI, N. SP.
BY
M. ANANT NARAYAN RAO,
Lecturer in Parasitology, Madras Veterinary College.
(Received for publication on 8th April 1933.)
(With Plate XX.)
This pharyngeal longifurcate cercaria was obtained from seven snails of the
species Limnea leuteola (Lamarck), out of 710 collected from the Spur tank, Egmore,
during the last quarter of the year 1931. This kind of larval trematode has not
been found in any other kind of fresh water snails collected from the Spur Tank.
The cercariae occur in long slender sporocysts in the digestive gland of the
snail, and often the sporocyst wall is seen bulging in places in which a large number
of cercariae are massed together. It was not possible to obtain a complete
sporocyst, but it would appear that the larvae escape by bursting open the wall at
the bulges.
The cercariae that were discharged by the snail in water were chosen for study.
Each larva is a powerful swimmer, though small in size. It appeared to be nega-
tively phototrophic. The body is an elongate cylinder measuring 1.0 × 0.04 mm.
The tail stem is 0.08 × 0.02 mm., and each furcal ramus is 0.15 mm. in length.
The body and tail are spinose. The cercaria has two pale yellow eye spots, in
front of the ventral sucker. On the body there are four setae on each side,
and on the tail there are six of such setae. Each seta originates from a refractile
granule. In the body there are two suckers. The oral sucker, with its pile of
circular muscle fibres, simulates a protrusible anterior penetrating organ. The
ventral sucker, which is a little wider in diameter than the other, is situated a little
behind the middle of the body. It is well developed and its cuticular lining is
armed with three rows of short and stout spines.
The alimentary canal is well developed. There is a short prepharynx, a small
muscular pharyngeal bulb, followed by a long œsophagus of a thin calibre, and this
bifurcates in front of the ventral sucker into two intestinal ceca which reach almost
to the posterior end of the body.
There is a pair of small penetration glands on either side of the ventral sucker,
on its anterolateral aspects. The anterior gland is the larger of the two, in each set,
and contains coarsely granular oxphilic contents and the posterior gland has fine
granules basophylic in reaction. The ducts from both these glands pass forwards
( 237 )