J. F. SHIRLAW AND P. R.
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IYER
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especially that of Turner, apparent mycelial forms can be seen which we consider to be fibrin artefacts.
In our opinion no one has, as yet, devised a method of demonstrating the organism in tissues. This
is all the more remarkable, since it is not difficult to demonstrate the organism in fresh lung films by
the long Giemsa method. Indeed, this is the most direct method of establishing a diagnosis; similar-
ly, the organism can be demonstrated, if less abundantly, in the pleural effusion and we consider
paracentesis with (a) microscopic examination of the effusion and (b) cultural isolation of the organism
a neglected method of direct diagnosis. (2) In lung sections stained by Hiadenhain's iron hæmatoxylin
or by Nicolle's carbol-thionin blue we have seen, at a magnification X 1400 and chiefly within the
stromal exudate, homogeneous clusters of what appear to be the elementary bodies described in
studies on the morphology of the organism. (3) Tissue eosinophilia of a type seen in actinomycotic
lesions is a constant feature of the histopathology of the lung in contagious bovine pleurophneumonia.
The experimental local lesion is a spreading, exudative myositis involving, in some cases, muscles
of the limb, abdomen and even head and neck. The associated lymph glands are grossly œdematous
and intensely hæmorrhagic. On incision, the depth of the lesion is revealed and an amber-coloured
or blood-tinged exudate, flows copiously. The affected muscle is necrotic in appearance and the
stroma conspicuously filled with exudate. In the older lesion, considerable absorption of the exudate,
with organization, gives a typical marbled appearance to the cut surface of the muscle which is slowly
invaded by loose granulomatous tissue originating from the stroma. It is obvious that the local
lesion develops as the lung lesion, i.e. the virus shows a predilection for lymph and blood vessels.
Endarteritis and thrombosis of blood vessels with a similar, but later, thrombosis of lymph channels
occurs, with massive cellular infiltration around the vessels and at the margin of the tissue spaces
which are widely dilated with exudate derived from these vessels. In approximately 5 per cent of
cattle used in serial transmission of the Assam 1 virus, the lesion was non-productive and non-exuda-
tive in type, being purely a localized necrosis of muscle. Further inoculation in hill cattle of a saline
extract of such lesions invariably resulted either in no reaction or a non-progressive reaction. In
three cases of this series, arthritis of the shoulder and knee joints was observed; the joint capsule
contained a sero-fibrinous exudate similar to that seen in the local lesion. The peri-articular tissue
was thickened and somewhat œdematous but the cartilages were unaffected. The lesion was generally
similar to the form of arthritis seen in contagious agalactia of the goat. Specific and advanced lesions
of contagious bovine pleuropheumonia were seen in five cattle of the series, the right lung being involv-
ed in four cases. The causal organism was isolated from three cases (not attempted in the fourth)
and a hill bull inoculated with pleural exudate from the fifth case reacted typically, dying in 24 days.
Fourteen animals of the series exhibited splenic lesions. These hitherto undescribed lesions, together
with the pulmonary lesions are unique in studies in pathogenesis.
The first stage spleen lesion is an elevated, pin-head size hæmorrhagic nodule, subcapsular when
few and present throughout the substance when numerous; the spleen is only moderately enlarged.
The second stage nodule is pearly with a firm, gelatinous texture. Later, the nodule is greyish-
yellow increasing to pea size. The fourth stage nodule closely resembles fibroidt Tubercle. (Plate IX,
fig. 1). There is no encapsulation or coalescence of adjacent nodules. In other cases, the lesions
consist of inter-connected tumour-like masses or granulomata, scattered throughout the spleen pulp
and quite large areas of the organ may be involved (Plate IX, fig. 2). It is evident on histological ex-
amination that the lesions are developmentally identical with those naturally occurring in the lung
or in the experimental local lesion, i.e. the spleen lesion develops from a specific vascular reaction,
which, has no analogy in bovine pathology. The small arterial branches of the malpipghian body
are chiefly affected but every vascular anastosmosis and lymph channel may participate equally.
There is massive round cell migration from the blood vessels and collateral lymph channels, followed
by copious outpouring of fibrinous exudate, the cells thus being swept to the margin of the lession.
The vessel, with thickened walls and actively proliferating endothelium, lies in a wide pool of clear
exudate limited by a dense zone of inflammatory cells. The exudate coagulates and is slowly absorbed
and largely replaced by a loose cellular hyperplasia, but as the fibroblastic reaction is not particularly
marked, there is no definite organization of the lesion with the laying-down of fibrous tissue in quantity;
this may be accounted for by the early tendency of the vessels to thrombosis, and interference with