188 Contagious Pleuro-Pneumonia of Goats
THE HISTOPATHOLOGY OF THE LESIONS
Histopathologically, the lesions in the lungs present a very wide variety
of picture, some or all of which may be present in one affected lung.
Pleura.—The pleura is thickened, oedematous, and the capillaries are
engorged in early lesions. A rapid leucocytic invasion of the oedematous
membrane follows. The inter-lobular septa are similarly involved in direct
continuity with the pleura (Plate VIII, figs. 1, 2 and Plate IX, figs. 1 and 2).
The organism is most readily discernible in the infiltrated septa. In late
lesions there is a well-marked fibrosis. (Plate IX, fig. 4).
Lungs.—The lesions in the lungs are peculiar in that the classical stage
of red hepatisation, with rupture of capillaries and massive accumulations of
erythrocytes in the alveoli, the orthodox prelude to grey hepatisation,
seems rarely if ever to occur. The earliest lesion is probably always an
oedema (Plate VIII, figs. 2 and 3) with capillary congestion, which is rapidly
followed by very severe capillary engorgement, but rupture of the capillaries
is not the rule. A rapid invasion of polymorphoneuclear neutrophile
leucocytes and monocytes leads directly to a grey hepatisation (Plate VIII,
figs. 4 and 5 and Plate IX, figs. 1, 2 and 3). This is quite commonly
associated with a persistence of the capillary engorgement, and extensive
areas of what, on histopathological grounds, can only be designated ' grey
hepatisation ' retain a red colour macroscopically as a result of this per-
sistent capillary dilation (Plate VIII, figs. 1 and 4). Vesicles in the oede-
matous stage are often contiguous with vesicles in grey hepatisation (Plate
VIII, fig. 4 and Plate IX, fig. 1). The alveoli in the surrounding hepatised
areas are usually emphysematous (Plate VIII, fig. 3 and Plate IX, fig. 2).
The stage of hepatisation (Plate IX, fig. 3) is followed either by necrosis
with the complete loss of all pulmonary structure, or by organisation (Plate
VIII, fig. 5).
The bronchi manifest no change in the early stages, but become com-
pletely involved later, when they exhibit catarrhal inflammation and fill with
muco-purulent exudate. Bronchiolitis is manifest earlier (Plate VIII, figs.
4 and 5).
The specific organism has several times been evident lying both in the
surface of the mucosa and within the lumen. Oedematous infiltration of the
peribronchial connective tissues is common, and in this as in the infiltrated
septa, the organism is frequently to be found. The oedema is characteristi-
cally followed by massive peribronchial cellular infiltration.
Muscle lesions.—The lesions in the muscles are very similar in principle
to those in the lungs, commencing with oedema with severe capillary congestion,
and terminating in necrosis with complete loss of structure. The oedema
is first evident in the inter-fascicular connective tissues (Plate X, fig. 1),
but rapidly extends to the inter-fibrillar tissues, isolating the individual
muscle fibres (Plate X, fig. 2. Plate X, fig. 3 depicts a cross section
at the intermediate stage). Meanwhile, leucocytes rapidly invade the
involved area, and accummulate in enormous numbers. The muscle fibres
lose their striation, and undergo a ' hyaline' degeneration (Plate X,
figs. 2, 3 and 4). This is followed by their lysis, and peculiar focal concen-
trations of leucocytes are then formed (Plate X, fig. 4). Ultimately,