It is difficult in the midst of confusing
and more or less contradictory theories and experiments to arrive at any definite conclusion regarding
In considering the subject it is necessary
to bear in mind two essential features of the affection.
1. Febrile symptoms due to the specific
action of the pneumotoxin or pneumotoxins.
2. Inflammatory exudation.
To this last hypothesis certain of my
observations in pneumonia would appear to lend support
and with the aid of this hypothesis the events taking
place in pneumonia can be best explained.
1. The relative low percentage of the polynuclear leucocytes in the first stage as compared
with Stage 2, is firstly due to the fact that they
are being rapidly lost from the blood; secondly that
they are in the process of development
2.) The relative high percentage of the mononuclear cells in Stage 1, notwithstanding that they
are also thought to a less extent, lost from the
"blood, is diie to increased state of development from
the lymphocytic condition.
3. In stage 2 the process of exudation
is over, or if not, the production of the luucocytes
is proportional to the loss,' the large cells are often
relatively diminished as compared with Stage 1, "because
they have developed into fully formed polynuclear
4. At the crisis the agents which are the
cause of this increased rate of development are antagonised , and a sudden arrest takes place of the
progress. This is evidenced first by increase in
the number of large mononuclear cells, an arrest of
their process of development into the polynuclear fi'rst
taking place, later by a greater relative increase
of the lymphocytes due to a further arrest of development, the conversion of the lymphocyte into the hyaline cells being apparently a simpler and more quickly
accomplished process, than the other.
On no other theory than this can I explain
absolute increase in the number of the mononuclear cells which is often seen at the crisis.
5. A quick decided fall of the luucocyte
count during the acute attack is to be explained as
due to a sudden increased exudation into the lung,
which the haemic leucocytosis is not capable of meeting.
6. Cases occurring without leucocytosis may
be explained by (1) very rapidly extending inflammatory exudation, (S) failure in the production of
leucocytes either due to extreme virulence of the
poison, or a want of proper blood supply to the
leucocyte producing centres. In such cases most of
the polynuclear cells disappear from the blood.
They are probably not destroyed; their loss may be
accounted for by emigration. The cells which remain
in the blood are mostly cells in a transitional stage
between the large mononuclear and polynuclear forms.
In these cases, even the largest hyaline share in the
process of rapid development, and the result of this
is the production of polynuclear cells of a larger
size than normal.