LIVE POLIO IRUS VACCINES

Virologic, Serologic Investigations of Immunization Wi'th Sabin's Strains 257
cent, respectively. It is possible that children
of older-age groups have had previous poliomyelitis
infection experience which was not manifested
by the development of antibody detectable
by the pH test.
At the same time, one must take into account
the fact that younger children are more exposed
to infection with enteric viruses which evidently
prevented good immunologic response to vaccine
strains fed in summer.
In contrast, Type 2 antibody developed in 80.0
per cent of the children under one year of age.
The impression is that younger children are more
susceptible to Type 2 virus or that Type 2 virus
is less inhibited by "wild" enteroviruses present
in the intestinal tract. Type 2 antibody developed
in 56.7 per cent of the children aged one to three
years, in 97.3 per cent of the children three to
seven years, and in 94.1 per cent of the children
seven to 14 years.
Refeeding trivalent live vaccine one month
later did not result in considerable improvement
of the results obtained after first feeding. While
in the L. children's home the percentage of children
acquiring Type 1 antibody after one feeding
did not change one month after refeeding, in
Karaganda some decrease was even found in
numbers of sera with low titers, which was reflected,
though not considerably, in summary results.
In groups of children without pre-vaccination
Type 2 antibody both in the L. children's
home and in the Karaganda region, there was
some increase in the per cent of children developing
Type 2 antibody (11.8 per cent). Greater
changes were observed in increase of Type 3
antibody, especially in the L. children's home
(from 28.9 per cent after first feeding to 48.5
per cent after refeeding). Probably, by the
time of refeeding, the intestinal virus carriage
preventing Type 3 vaccine strain multiplication
had been reduced, which led to more extensive
multiplication of vaccine strains and produced
further rise in antibody levels, which was reflected
in general antibody rise by 16.4 per cent
(Table 23).
Comparison of the results observed one month
and three to four months after two feedings with
trivalent live vaccine from Sabin strains, reveals
a certain reduction in the percentage of children
acquiring Type 1 antibody (by 10.5 per cent)
and a small increase to Type 2 (by 3.4 per cent)
and Type 3 (by 2.6 per cent) poliomyelitis antibody
(Table 24).
The lack of significant improvement of the results
at later periods, and even a certain reduction
of Type 1 antibody, is evidently related to a
drop in titers in cases of incomplete immunity,
as a result of interference by enteric viruses and
of reduced opportunity for contact transmission
of Type 1 and Type 3 viruses inhibited by Type
2 vaccine virus multiplication. As surveys of
vaccine contacts showed, they had predominantly
Type 2 virus carriage, accompanied by antibody
production. Thus, the children were deprived
of additional immunization with Types 1 and 3
poliovirus vaccine.
For investigation of contact transmission of
vaccine polioviruses under conditions of vaccination
with trivalent live vaccine in the summer,
21 of 93 children in children's home L. and
21 of 63 children in children's home R. were left
unvaccinated and in contact with vaccinees.
Virologic investigation of stool specimens during
the period of contact with vaccinees showed
that all children under observation at one time
or another were carriers of enteric viruses of
non-poliomyelitis nature, belonging mainly to
ECHO-8 viruses or Coxsackie B-1. Despite extensive
dissemination of enteric viruses, many
children in contact with vaccinees picked up vaccine
viruses and began to excrete them.
Of 21 children, seven excreted Type 1 poliovirus,
13 Type 2, and 10 Type 3. About half of
the children after contact with the vaccinees became
carriers of all three types of poliovirus. The
greatest frequency of excretion of three vaccine
viruses in the younger children of from five to 16
months was observed before contact as possessing
no antibody to any poliovirus types. Of nine
such children, five excreted Type 1 virus, eight
Type 2, and seven Type 3 virus. Smaller numbers
of children developed antibody: three to
Type 1, seven to Type 2, and three to Type 3.
The other children possessing poliomyelitis antibody
before contact developed rise in titers, particularly
to Type 2 (Figures 10 and 11).
Under conditions of mass virus carriage of
non-poliomyelitis enteroviruses (ECHO -8, 3, 14.
17, 19, and Coxsackie B-1) establishment of vaccine
viruses and serologic response in those vacci-