J. F. SHIRLAW                                           307

These two infections, though clinically somewhat comparable, run an
entirely different course in haemocytological observations, although patholo-
gically comparable in the end result. In a P. canis infection there is an early
invasion, anisocytosis and destruction of the erythrocytes. The serum is ting-
ed, sometimes deeply, with haemoglobin liberated from the breaking down of
erythrocytes and there is an increase of the corpuscular sedimentation rate.

In a P. gibsoni infection, there may be an early and transient invasion of
the erythrocytes. There is, however, no anisocytosis and destruction of the
erythrocytes in the circulating blood, and no evidence of liberated haemoglobin
in the serum. (These observations are enhanced by the fact that in a P.
canis infection, haemoglobinuria is a characteristic symptom, whereas, in a
P. gibsoni infection, this symptom is never noted.)

At the same time, there is an increased fragility of the erythrocytes in a
P. canis, which is absent in a P. gibsoni infection.

It has already been noted that in an experimentally produced P. gibsoni
infection, the histiocytes of spleen origin (reticulo-endothelial) early make
their appearance. In a true P. canis infection, there is no such evidence of an
early involvement of the reticulo-endothelial system. Anaemic changes occur
during the latter phase of the infection and are obviously prompted by the
stimulus provided by the erythrocyte destruction and loss. It is believed,
from these observations, that P. gibsoni is essentially a parasite of the reticulo-
endothelium, unlike P. canis which appears primarily as a parasite of the
erythrocytes.

On this basis, apart from the experimental pathological evidence which
has been produced, it is possible to explain the infrequency of P. gibsoni in
the circulating blood and even its total absence during the course of the disease.
And it is then possible to understand the reluctance to accept ' Lahore
Canine Fever' as a P. gibsoni infection.

In addition to this consideration, previous workers have been impressed
by the dysenteric symptoms, accompanied by rapid wasting, which, are not
infrequent. It is, apparently, these symptoms which have prompted several
workers to consider the disease ' Canine Enteric Fever'.

Osmand Bodman and Cooper (unpublished work) noted intestinal
ulceration as one of the prominent lesions in their investigations, and it was
from such cases that they obtain the Salmonella strains mentioned earlier in
this note. Symons [1926] and Clive Webb [1906] have drawn attention,
however, to the frequency with which dysentery and intestinal ulceration
complicate the syndrome of an authentic P. gibsoni infection. It is certain that
a few dogs normally harbour Salmonella strains and it is possible that under
the stress of debility induced by the primary protozoan infection, these orga-
nisms, potentially latent, assume a pathogenic role. Against this possibility,
however, must be mentioned the fact that such cases fail to give a positive
Widal test against the Salmonella strains isolated.