59
Paras. 31 & 32
The frequent discovery of crescents in kala-dukh appears to me, in the
light of my experience of paludism among natives, to be rather remarkable
In my regiment at Secunderabad almost all first attacks of æstivo-autumnal
fever were followed by crescents if large doses of quinine had not been given ;
but as second and third attacks developed the crescents always tended to become
less numerous. Attention to the subject was forced on me, by my researches
on the mosquito theory, which require crescents for various experiments. I have
attributed this to the gradual establishment of immunity which, though it can
scarcely affect the full-grown organisms, may inhibit their formation, especially
if, as Mannaberg thinks, they are due to syzygies of two young parasites in one
corpuscle. Many of the æstivo-autumnal cases at Nowgong gave no crescents.
In some of them this may have been due to quinine ; in other and older cases
such as cases 16, 23, 24, 36, 38 and 44, their absence can scarcely have been
caused by this. Season may have something to do with the matter—Brown's
researches were carried on in April, mine in autumn. But I am certainly
of opinion that with poor natives of India, the older the case the fewer are the
crescents as a rule.
Another point also may have an important bearing on the questions at
issue. Mannaberg has suggested the existence of an æstivo-autumnal parasite,
the fever cycle of which is entirely unpigmented, and Marchoux depicts
unpigmented sporulating forms in his paper on Senegal fevers [22]. If crescents
ceased to be produced in such fevers, the inference is that all black pigment
would cease to be formed. In Nowgong, however, I found no unpigmented
sporulating forms in the spleen.
I think, then, that we may safely conclude that with an unpigmented
quotidian, or a parasite producing few crescents, or an ordinary tertian or
quartan parasite, the melanin is likely to disappear earlier than with the
remaining varieties.
32. Secondary Effects Of the Invasion.—I propose to deal very shortly
with this point. As a matter of fact, we have little knowledge of the precise
cause of many of the phenomena attending the invasion. The exact nature
of the toxin (if there be one), that of much of the anæmia present and of the
enlargement of the organs, cannot yet be considered as entirely elucidated ;
though, of course, many reasonable inferences, such as the irritation of the organs
by the yellow pigment, have been drawn.* Putting etiology aside, the associa-
tion of anæmia, enlargement of the spleen and liver, and so on, with paludism
is one of the best known facts in medicine ; to these symptoms, epistaxis, darken-
ing of the skin, œdema, first of the feet and then of the face, ascites, dilatation of
some of the superficial abdominal veins, progressive emaciation, and the
frequency of inter-current attacks of diarrhœa, dysentery, cancrum oris, pneumo-
nia, and so on, must be added. All these, symptoms of kala-azar, are recognised
everywhere to be also symptoms of paludism and, therefore, need not all be
examined here. A word, however, remains to be said on a point or two.
I have already mentioned that the enlargement of the organs in the worst
cases of kala-azar seen by me, was not more extreme than in some cases of
paludism seen in other parts of India. It is not so much the extremity of the
enlargement found as the constancy of great enlargement in all established cases,
which seems to be one of the leading features of kala-azar. Primâ facie,
however, this is only a question of degree. See also Bogers [4, page 41].
I agree with other observers that extreme anæmia is not necessarily a leading
symptom of kala-azar and that, when it occurs, it suggests ankylostomiasis as
a complication.
Practically only the low fever, which is certainly not generally recognised
as a symptom of paludism, remains to be considered. I have cited (paragraphs.
26 and 27) Vandyke Carter, Kelsch and Kiener and Daniels, to show that such
a thing really may and does exist in what is thought everywhere to be paludism.
We must now endeavour to explain it.
In my cases of kala-azar it was obvious that, apart from the absence of
parasites and melanin, this fever was not being caused by the actual parasitic
invasion—the curve was not a malarial curve.
* Note.—I have often thought that melanin may be more nearly concerned in those processes than is
imagined. At the moment it is set free, the access begins, and when it is taken up by the phagocytes the fever
ceases ; while it is just those organs where it is most largely deposited which are the seat of future trouble.
I 2