LIVE POLIO IRUS VACCINES

DISCUSSION
CHAIRMAN LÉPINE: The papers by Dr. Sabin
and Dr. Ramos Alvarez are now open for discussion.
DR. MELNICK: Dr. Sabin showed that after
the mass feeding in Toluca polio isolations
dropped from 11 to 1 per cent, but not to zero.
I should like to hear whether he might predict
how long it will remain at this low level. Even
if it dropped to zero, how long might it be before
live viruses came into the community and caused
reinfection? If wild viruses do come in, 1 believe
Dr. Sabin's data showed that reinfections
will occur. His paper indicated that immunity
reached close to 100 per cent of the population
by the age of four. Yet, even in this community,
the immune mothers carried poliovirus to the
extent of about 5 per cent. The viruses which
they carried, as I recall, belonged to all three
polio types and not just to one.
I should also like to raise the question of how
we might prevent the reintroduction of polioviruses
into mass vaccinated communities if we
already know that immune persons can carry
virus again, and perhaps again and again.
DR. SABIN: The first marked reduction occurred
after a single feeding of trivalent vaccine. The
second feeding was given to only a small number
of children, and was not a mass feeding.
Whether or not the second trivalent feeding
would have reduced the dissemination of polioviruses
to a still lower level is something which
may be expected but has not been demonstrated.
But, as an indication of what nature itself does,
we can look at the reported cases of poliomyelitis
in the city of Toluca, which I think throws some
light on the question. The pattern in Toluca,
which is a city on trade routes with many people
passing through it, is almost comparable to the
pattern of measles. That is, you have one year
with a high incidence and the next year with a
very low incidence, followed by another year with
a very high incidence.
That has been the pattern of recent years.
This indicates that even after a period of high
410
natural dissemination, which is associated with a
high incidence of paralytic cases, there develop
enough resistant intestinal tracts to stop the dissemination
of the Type 1 poliovirus responsible
for most of the clinical cases to such an extent
that the following year there are very few cases
-when I say very few, two to three has been
the pattern-until additional children who are
not immune come into the community.
The point about the mothers: I myself remarked
that it seemed to me somewhat peculiar
that, in a population in which presumably they
would be exposed repeatedly, 5 per cent of the
mothers should still be found to be carriers of
poliovirus. But to be a carrier of polio is not
an all-or-nothing affair as regards capacity to
transmit virus. A person may become infected
and yet may not be able to transmit.
It is quite possible, on the basis of many previous
studies, that the young children who are
primarily infected and excrete large amounts
of virus are chiefly responsible for continuing
dissemination. They can disseminate it to a
number of others, including mothers, who may
then have only low levels of multiplication. This
is also comparable to experiences which many
bacteriologists and epidemiologists have recorded
for dysentery. It is not enough to be a carrier of
dysentery. A person who has a few dysentery
bacilli is not a disseminator, a person who has a
million per gram is a disseminator.
The very fact that such marked reduction in
dissemination could be achieved by a single feeding
of trivalent vaccine indicates that we have
to repeat it, as I said, in order to produce not
only more immunization but also more intestinal
resistance. Whether or not, and to what extent,
such massive immunization will achieve, by continuing
programs, the blockade to natural dissemination
of polioviruses is something the virus
laboratories will have to continue working on for
the next few years and give us the answer. That
available evidence warrants the attempt to eliminate
naturally occurring polioviruses by this
technique is to me beyond doubt,