70
Para. 40
As far as I can gather, the low fever commences about the end of the first,
second or third month of the illness ; and it tends to cease, I think, in nine
months or more from the onset of the disease. It is probable that the low fever
sets in earliest in the severest infections.
It seems both convenient and accurate to select the low fever as the sign
of the second stage ; it is easily detected by the thermometer, and should repre-
sent the degree of the secondary effects, to which entirely, and not to the
parasites themselves, I ascribe it (paragraph 32).
The parasitic invasion, however, probably lasts well into the second stage,
ever decreasing according to its duration. At the same time the system feels
the toxic effect of the parasites less and less ; but suffers more and more from
the residual condition of the organs and the low fever.
The melanin is, I think, constantly being eliminated as it is deposited ;
and some months after it ceases to be deposited, that is, after the invasion is
exhausted, it is probably got rid of altogether in many cases. Judging from
Case 71 this may be accomplished in seven months from the onset.
There seems to be a rapid fall in the number of red corpuscles after each
parasitic exacerbation, with a corresponding recuperation afterwards; but
in the second and third stages the anæmia seems to me to remain constant,
being maintained by the secondary effects. Kelsch and Kiener note this in
paludism in general. I fancy that the yellow pigment results more from the
anæmia due to the secondary effects, than from that due to the parasites them-
selves.
Edema may appear early in the second stage, but more commonly toward
the end of it.
The end of the second stage, when the system exhausted after the severe
illness lies prostrate to intercurrent affections, seems to be the most dangerous
epoch. Now, too, if any considerable number of ankylostomes are present, they
must begin to make themselves heavily felt. Death is actually caused in most
cases by dysentery, diarrhœa or pneumonia ; but in many ankylostomes and
even other worms have played an important part in the final scenes.
I can give no evidence regarding darkening of the skin.
I was not able, in the short time at my disposal for the enquiry, to assure
myself regarding the species of the malarial parasite which causes kala-azar,
or even whether the disease is caused by a single species (paragraph 21).
Whatever species it may be due to, however, I conceive the disease to be a
form of paludism in which the infection falls with a very heavy incidence on
the spleen and liver, especially the latter. It is, in fact, the secondary symptoms
—the enlargement of these organs and the low fever—which are the gravest
feature of this disease and which, I think, are the chief cause of the exceptional
mortality. It is well-known that in some localities and in some races the
parasites effect these organs but little ; in others much. Why this should be
we cannot say. But the fact remains that kala-azar is principally a manifes-
tation of the secondary results of malarial fever.
I will add here some remarks of Dr. Daniels on the sections examined by
him (paragraph 17). "The minute anatomy," he writes, "shows merely evi-
dence of a hæmolytic disease. Direct evidence of malaria, i.e., black pigment,
is wanting in some of the cases. If the hæmolysis, of which the yellow pig-
mentary deposits give evidence, be the result of malaria, this must be of some
form in which the hæmolysis is quite out of proportion to the melanosis or
direct product of the organism, and would, therefore, probably indicate a specific
form of parasite differing at any rate in its chemical activities from that met
with in British Guiana. The absence of fatty changes and the different dis-
position of the pigmentary and ferruginous granules prevent any support from
the structure of the organs being given to the theory of ankylostomiasis."
It appears possible to me, however, that the evidences of hæmolysis
referred to here are not so much the effect of a particular parasite with special
chemical activities, as of the great secondary enlargement of the organs and
the concomitant low fever. If these cause anæmia, as they most certainly do,
they may be expected also to yield evidences of hæmolysis.
By such a theory the yellow pigment would be a result, not a cause, of the
enlargement of the organs. In Case 75, for instance, the spleen was greatly
enlarged, congested and tender ; yet post mortem it was found to contain no