June, 1955]
H. G. SEN, B. N. DUTTA AND H. N. RAY 147
Comment. Gross nutritional deficiency of the host could not restrict the multi-
plication of the parasites as compared with the control. This suggests that the
trypanosomes are able to multiply in the absence of some factors which are not
markedly affected during starvation.
DISCUSSION
The observations suggest that on fasting of the host, Trypanosoma evansi infection
responds in a different way from the plasmodia. In contrast to the finding that
starvation of the host infected with rodent or simian plasmodia suppresses the
development of the parasites from the peripheral blood and also does not affect
the normal development of immunity in the host, it has no effect either in suppressing
the infection or in the development of immunity in Trypanosoma evansi infection.
With the progress of fasting an essential factor necessary for the growth of the plas-
modia is gradually depleted from the host tissues or blood with the result that the
plasmodia cannot grow in the host after 8-10 days of continued starvation. McKee
[1951] thought this substance to be some protein bound methionine or PABA or
possibly the peptides of methionine and PABA in the case of P. knowlesi. Our present
experiments suggest that the trypanosomes, on the other hand, require a completely
different factor, the concentration of which is not much altered during starvation.
The explanation and the difference in these varying behaviour of the malaria parasites
and the trypanosomes can be sought in the fact that the trypanosomes are
extracellular organisms depending much on the plasma for their nutrition. It is
probable that as the red cells are depleted from the nutrients and metabolic
constituents at a much rapid rate from the plasma, the malaria parasites grow very
poorly in the starved hosts.
The mechanism of suppression of protozoal infection by starvation is not quite
clear. Several parasites of the intestinal tract can be completely eliminated by
withholding food from the host and in this way it is possible to defaunate termites
and to eliminate rumen ciliates [Cleveland, 1925; Mangold and Krahmer, 1927;
Dogiel and Winogradowa Fedorowa, 1930]. In both the cases a very considerable
decrease in glycogen content of the parasite occurred and it has been attributed
that owing to loss of muscular energy due to depletion in glycogen the parasites
cannot maintain themselves in the gut. Some other intestinal helminths (such as
Ascaridia galli and Raillaetin cesticillus) can be removed between 48 to 96 hours
and the period of starvation needed to eliminate the parasites varied with the different
species [Reid, 1940, 1942a, b, 1944 ; Reid and Ackert 1941]. It is probable
that the elimination of the parasite depends much on the nature of the habitat of
the parasite and the variation in the composition of their environment. It has been
suggested by von Brand [1938] that the tissue parasites can hardly be killed by
the host. But Müller and Simons [1920] found retarded multiplication of pathogenic
trypanosomes in starving hosts. Solazzo [1929], on the other hand, reported that
Trypanosoma brucei could be maintained for several days in starving and not in
fed pigeons. In certain experimental infections caused by rickettsia or virus which
live in the tissues, adverse effects of starvation were observed.
Our present observations suggest that gross nutritional deficiency of the host
could neither alter the course of development of the flagellates, nor affect their
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