LIVE POLIO IRUS VACCINES

Discussion
157
Discussion 157
One of the points I made from the text was
that the lack of interference was manifested in
one way by the simultaneous entrance into a
youngest child had not yet had an opportunity to
become infected with Coxsackie B 2 , or whether
the child had naturally terminated his Coxsackie
household of the vaccine strain and a wild virus infection. At any rate, this child immediately
strain. Dr. Fox and I have spoken about this,
and in each instance, of course, the vaccine virus
and the wild virus invaded a different individual
in the same household.
Without more detailed serologic information
on these people, I believe that this frequent happening
may actually be a circumstantial indication
of interference, because there was in these
instances often no continued intrafamilial dissemination
of either the vaccine strain or the
wild virus. Therefore, this might be interpreted
as the manifestation of interference, rather than
of the absence of interference.
We have a number of household examples in
which the children who are actually excreting the
wild virus at the time of vaccine administration
did not become infected, whereas other children
in the household did become infected. To give
an example, in one vaccine-fed household consisting
of seven children, whose ages and immunity
status to polio 3 are shown below, stools
were collected on the day before vaccine feeding,
and five of them were found to be excreting Cocksackie
B 2 as follows:
AGE OF
CHILD
12
11
9
6
5
4
3
P3
IMMUNITY
I__
u
S
S
S
S
S
S
I
VIRUS ISOLATIONS ON
INDICATED DAY
0 4 8 12
0
B 2
B2
B2
B 2
B2
0
o
o
3
B2
B2
B2
3
o
3
3
B2
B2
o
3
The serial records of virus isolations following
feeding of vaccine on the fourth day, the eighth
day, and the twelfth day following vaccine feeding
are briefly summarized.
Unfortunately, we do not have Coxsackie B2
serology, so it is difficult to know what the immune
status of these individuals was to Coxsackie
B2. I do not know, for example, whether the
0
3
3
0
0
3
3
became infected with the vaccine virus. Some of
the others gradually terminated their B 2 virus
and became infected. Two of them never became
infected with poliovirus Type 3. We have a number
of such family episodes that suggest to me
the role of interference.
DR. GEAR: 1 should like to ask Dr. Gelfand
whether these enterovirus infections caused any
clinical manifestations, and if so, whether these in
any way embarrassed him or those responsible
for the feeding?
DR. GELFAND: There were no symptoms whatsoever
from any of the children in the study
which could be possibly related to enterovirus infection
during the entire three months. We were
fortunate.
DR. BODIAN: This admirable study reported by
Dr. Gelfand raises interesting questions. I
should like to comment on two.
First of all, I recall that a few weeks ago Dr.
Sabin took me severely to task for suggesting
that placebo studies were feasible in relation to
the evaluation of live virus vaccine.
It seems to me that the results of this study
suggest that this possibility should be examined
again. Certainly, the evidence of spread is not
such as to suggest that spread alone would eliminate
any possibility of carrying on a controlled
evaluation of the effectiveness of live poliovirus
vaccines.
I wish to point out that either placebo studies
or matched control studies have the further advantage
that one is able to control the laboratory
methods and the results of laboratory methods.
Therefore, I merely wish to put in my bid again
for consideration of the continued use of this
type of study wherever possible.
The second point I should like to refer to is
this: In the studies just reported, we have rates
of reinfection with the Type 3 virus, due either to
the vaccine virus or to wild viruses, which 1
calculated very roughly to be about 14 per cent.
This is reminiscent of the animal work that
was being done in the late 1940's at Michigan