From: MMWR May 19, 2000 / 49(RR05);1-22
These recommendations of the Advisory Committee on
Immunization Practices (ACIP) for poliomyelitis prevention replace those issued in 1997. As
of January 1, 2000, ACIP recommends exclusive use of inactivated
poliovirus vaccine (IPV) for routine childhood polio vaccination in the United States.
All children should receive four doses of IPV at ages 2, 4, and 6--18 months and
4--6 years. Oral poliovirus vaccine (OPV) should be used only in
certain circumstances, which are detailed in these recommendations. Since 1979,
the only indigenous cases of polio reported in the United States have
been associated with the use of the live OPV. Until recently, the benefits of OPV
use (i.e., intestinal immunity, secondary spread) outweighed the risk for
vaccine-associated paralytic poliomyelitis (VAPP) (i.e., one case among 2.4
million vaccine doses distributed). In 1997, to decrease the risk for VAPP but maintain
the benefits of OPV, ACIP recommended replacing the all-OPV schedule with
a sequential schedule of IPV followed by OPV. Since 1997, the global
polio eradication initiative has progressed rapidly, and the likelihood of
poliovirus importation into the United States has decreased substantially. In addition,
the sequential schedule has been well accepted. No declines in
childhood immunization coverage were observed, despite the need for
additional injections. On the basis of these data, ACIP recommended on June 17, 1999,
an all-IPV schedule for routine childhood polio vaccination in the United States
to eliminate the risk for VAPP. ACIP reaffirms its support for the global
polio eradication initiative and the use of OPV as the only vaccine recommended
to eradicate polio from the remaining countries where polio is endemic.
As a result of the introduction of inactivated poliovirus vaccine (IPV) in the
1950s, followed by oral poliovirus vaccine (OPV) in the 1960s, poliomyelitis control has
been achieved in numerous countries worldwide, including the entire Western
Hemisphere (1,2). In the United States, the last indigenously acquired cases of polio caused by
wild poliovirus were detected in 1979 (3). In 1985, the countries of the Americas*
established a goal of regional elimination of wild poliovirus by 1990
(4). In 1988, the World Health Assembly (WHA), which is the directing council of the World Health Organization
(WHO), adopted the goal of global polio eradication by the end of 2000
(5). In the Americas, the last case of polio associated with isolation of wild poliovirus was detected in Peru in
1991 (6). The Western Hemisphere was certified as free from indigenous wild poliovirus
in 1994, an accomplishment achieved by the exclusive use of OPV
(7). The global polio eradication initiative has reduced the number of reported polio cases worldwide by
>80% since the mid-1980s, and worldwide eradication of the disease by the end of 2000 or
soon after appears feasible (8).
Summary of Recent Polio Vaccination Policy in the
Based on the continued occurrence of vaccine-associated paralytic
poliomyelitis (VAPP) in the United States, the absence of indigenous disease, and the sharply
decreased risk for wild poliovirus importation into the United States, the Advisory
Committee on Immunization Practices (ACIP) recommended in June 1996 a change from
an all-OPV schedule for routine childhood poliovirus vaccination to a sequential
IPV-OPV vaccination schedule (i.e., two doses of IPV at ages 2 and 4 months, followed by
two doses of OPV at ages 12--18 months and 4--6 years). These recommendations were
officially accepted by CDC and published in January 1997
(9). The sequential schedule was intended to be a transition policy in place for 3--5 years until eventual adoption of an
all-IPV schedule. At the same time that ACIP recommended a sequential schedule, the
American Academy of Pediatrics (AAP) and the American Academy of Family Physicians
(AAFP) recommended expanded use of IPV, with all-OPV, all-IPV, and sequential IPV-OPV
as equally acceptable options (10,11).
After the successful implementation of expanded IPV use without any
observed declines in childhood immunization coverage
(12,13), AAP and AAFP joined ACIP in January 1999 in recommending that the first two doses of polio vaccine for routine
vaccination be IPV in most circumstances
(14,15). However, an all-IPV schedule was still
needed to eliminate the risk for VAPP while maintaining population immunity. Thus, ACIP
recommended in June 1999 that the all-IPV schedule begin January 1, 2000
(16). Although AAFP concurred with this recommendation, AAP recommended only that the
all-IPV schedule begin during the first 6 months of 2000
The United States can remain free of polio only by maintaining high levels of
population immunity and reducing or eliminating the risk for poliovirus importation.
ACIP strongly reaffirms its support for the global polio eradication initiative, which relies
on OPV in countries where the disease has recently been endemic. This report
provides the scientific and programmatic background for transition to an all-IPV schedule,
presents the current recommendations for polio prevention in the United States, and
summarizes recommendations for OPV use if the U.S. vaccine stockpile is needed for
Characteristics of Poliomyelitis
Poliomyelitis is a highly contagious infectious disease caused by poliovirus, an
enterovirus. Most poliovirus infections are asymptomatic. Symptomatic cases are
typically characterized by two phases --- the first, a nonspecific febrile illness, is followed
(in a small percentage of cases) by aseptic meningitis or paralytic disease. The ratio of
cases of inapparent infection to paralytic disease ranges from 100:1 to 1,000:1.
After a person is exposed to poliovirus, the virus replicates in the oropharynx
and the intestinal tract. Viremia follows, which can result in infection of the central
nervous system. Replication of poliovirus in motor neurons of the anterior horn and brain
stem results in cell destruction and causes the typical clinical manifestations of
paralytic polio. Depending on the sites of paralysis, polio can be classified as spinal, bulbar,
or spino-bulbar disease. Progression to maximum paralysis is rapid (2-4 days), is
usually associated with fever and muscle pain, and rarely continues after the patient's
temperature has returned to normal. Spinal paralysis is typically asymmetric and
more severe proximally than distally. Deep tendon reflexes are absent or diminished.
Bulbar paralysis can compromise respiration and swallowing. Paralytic polio is fatal in
2%--10% of cases. After the acute episode, many patients recover at least some muscle
function and prognosis for recovery can usually be established within 6 months after onset
of paralytic manifestations.
After 30--40 years, 25%--40% of persons who contracted paralytic polio during
childhood can experience muscle pain and exacerbation of existing weakness or
develop new weakness or paralysis. This disease entity, called post-polio syndrome, has
been reported only in persons infected during the era of wild poliovirus circulation.
Risk factors for post-polio syndrome include a) the passage of more time since acute
poliovirus infection, b) the presence of permanent residual impairment after recovery
from the acute illness, and c) being female
Polio is caused by three serotypes of poliovirus --- types 1, 2, and 3. In
countries where poliovirus is still endemic, paralytic disease is most often caused by
poliovirus type 1, less frequently by poliovirus type 3, and least frequently by poliovirus type
2. The virus is transmitted from person to person primarily by direct fecal-oral
contact. However, the virus also can be transmitted by indirect contact with infectious saliva
or feces, or by contaminated sewage or water.
The first paralytic manifestations of polio usually occur 7--21 days from the time
of initial infection (range: 4-30 days). The period of communicability begins after the
virus replicates and is excreted in the oral secretions and feces. This period ends with
termination of viral replication and excretion, usually 4--6 weeks after infection.
After household exposure to wild poliovirus, >90% of susceptible contacts become
infected. Poliovirus infection results in lifelong immunity specific to the infecting viral serotype.
Humans are the only reservoir for poliovirus. Long-term carrier states (i.e.,
excretion of virus by asymptomatic persons >6 months after infection) are rare and
have been reported only in immunodeficient persons
(20,21). Risk factors for paralytic disease include larger inocula of poliovirus, increasing age, pregnancy, strenuous
exercise, tonsillectomy, and intramuscular injections administered while the patient is
infected with poliovirus (22--24).
Secular Trends in Disease and Vaccination Coverage in the United States
In the United States, poliovirus vaccines have eliminated polio caused by wild
poliovirus. The annual number of reported cases of paralytic disease declined from
>20,000 in 1952 to an average of 8--9 cases annually during 1980--1994 (Figure)
(3,25,26). During 1980--1998, a total of 152 cases of paralytic polio were reported, including 144 cases
of VAPP, six imported cases, and two indeterminate cases
(16). Until worldwide polio eradication is achieved, epidemics caused by importation of wild virus to the United
States remain a possibility unless population immunity is maintained by vaccinating
children early in their first year of life. In the United States, outbreaks of polio occurred in
1970, 1972, and 1979 after wild poliovirus was introduced into susceptible populations
that had low levels of vaccination coverage. Vaccination coverage among children in
the United States is at the highest level in history because of ongoing immunization
initiatives. Assessments of the vaccination status of children entering kindergarten and
first grade indicated that 95% had completed primary vaccination against polio during
the 1980--81 school year, and rates continue to be above that level.
Coverage levels among preschool-aged children are lower than the levels at
school entry, but have increased substantially in recent years. Nationally, representative
vaccination coverage rates among children aged 19--35 months are derived from the
Immunization Survey (NIS). Vaccination coverage with at least three doses of
poliovirus vaccine among children in this age group increased from 88% in 1995 to 91% in 1996
and remained >90% in 1997 and 1998 (13).
Serosurveys have identified high levels of population immunity consistent with
these high coverage rates. Based on data from selected surveys, >90% of children,
adolescents, and young adults had detectable antibodies to poliovirus types 1 and 2,
and >85% had antibody to type 3 (27,28). Data from seroprevalence surveys conducted
in two inner-city areas of the United States during 1990--1991 documented that >80% of
all children aged 12--47 months had antibodies to all three poliovirus serotypes. Of the
children who had received at least three doses of OPV, 90% had antibodies to all three
serotypes (29). A serosurvey conducted during 1997--1998 among low-income children
aged 19--35 months living in four U.S. cities reported that 96.8%, 99.8%, and 94.5% were
seropositive to poliovirus types 1, 2, and 3, respectively
Both laboratory surveillance for enteroviruses and surveillance for polio cases
suggest that endemic circulation of indigenous wild polioviruses ceased in the United
States in the 1960s. During the 1970s, genotypic testing (e.g., molecular sequencing or
oligonucleotide fingerprinting) of poliovirus isolates obtained from indigenous cases
(both sporadically occurring and outbreak-associated) in the United States indicated that
these viruses were imported (31). During the 1980s, five cases of polio were classified as
imported. The last imported case, reported in 1993, occurred in a child aged 2 years
who was a resident of Nigeria; the child had been brought to New York for treatment of
paralytic disease acquired in her home country. Laboratory investigations failed to
isolate poliovirus among samples taken from this child after she arrived in the United States.
Recent experience in Canada illustrates the continuing potential for importation
of wild poliovirus into the United States until global eradication is achieved. In 1993
and 1996, health officials in Canada isolated wild poliovirus in stool samples from
residents of Alberta and Ontario. No cases of paralytic polio occurred as a result of these
wild virus importations. The strain isolated in 1993 was linked epidemiologically and
by genomic sequencing to a 1992 polio outbreak in the Netherlands
(32). The isolate obtained in 1996 was from a child who had recently visited India
Inapparent infection with wild poliovirus no longer contributes to either the
establishment or maintenance of poliovirus immunity in the United States because
these viruses no longer circulate in the population. Thus, universal vaccination of infants
and children is the only way to establish and maintain population immunity against polio.
After the widespread use of poliovirus vaccine in the mid-1950s, the incidence
of polio declined rapidly in many industrialized countries. In the United States, the
number of cases of paralytic polio reported each year declined from >20,000 cases in
1952 to <100 cases in the mid-1960s (3). In 1988, the WHA resolved to eradicate polio
globally by 2000 (5). This global resolution followed the regional goal to eliminate polio by
1990, set in 1985 by the countries of the Western Hemisphere. The last case of polio
associated with wild poliovirus isolation was reported from Peru in 1991, and the entire
Western Hemisphere was certified as free from indigenous wild poliovirus by an
International Certification Commission in 1994
(7). The following polio eradication strategies,
which were developed for the Americas, were adopted for worldwide implementation in
all polio-endemic countries (34):
- Achieve and maintain high vaccination coverage with at least three doses of
OPV among infants aged <1 year.
- Develop sensitive systems of epidemiologic and laboratory surveillance,
including acute flaccid paralysis (AFP) surveillance.
- Administer supplemental doses of OPV to all young children (usually those aged
<5 years) during National Immunization Days (NIDs) to rapidly decrease
widespread poliovirus circulation.
- Conduct mopping-up vaccination campaigns (i.e., localized campaigns that
include home-to-home [or boat-to-boat] administration of OPV) in areas at high risk
to eliminate the last remaining chains of poliovirus transmission.
In 1998, global coverage with at least three doses of OPV among infants aged <1
year was 80%. All WHO regions** reported coverage rates of >80%, except the African
Region (AFR), where coverage improved from 32% in 1988 to 53% in 1998
(8). Also in 1998, a total of 90 countries conducted either NIDs (74 countries) or Sub-National Immunization
Days (16 countries). These 90 countries provided supplemental doses of OPV to
approximately 470 million children aged <5 years (i.e., approximately three quarters of the world's
children aged <5 years) (8). In 1999, NIDs were conducted in all 50 polio-endemic
countries. NIDs in the AFR targeted approximately 88 million children aged <5 years
(35). Synchronized NIDs were conducted in 18 countries of the European Region (EUR) and
Eastern Mediterranean Region (EMR), vaccinating 58 million children aged <5 years. Another
257 million children aged <5 years were vaccinated in December 1998 and January 1999
in countries of the EMR (Pakistan), South East Asia Region (SEAR) (Bangladesh,
Bhutan, India, Myanmar, Nepal, and Thailand), and Western Pacific Region (WPR) (China
and Vietnam) (36--40). NIDs in India reached 134 million children, representing the
largest mass campaigns conducted to date. Each round of NIDs in India was conducted in
only one day (41). Mopping-up campaigns have been conducted widely in the countries of
the Americas (including Brazil, Colombia, Mexico, Peru, and several countries in
Central America) and more recently in the Mekong delta area encompassing Cambodia,
Laos, and Vietnam in 1997 and 1998, and in Turkey in 1998
These supplemental immunization activities have been successful in decreasing
the number of reported polio cases globally from 35,251 in 1988 (when the polio
eradication target was adopted) to 6,227 in 1998, a decrease of 82%
(8). This decrease in incidence is even more remarkable considering the progress in implementing sensitive
systems for AFP surveillance, which substantially increased the completeness of
reporting of suspected or confirmed polio cases. To conduct virological surveillance, a global
laboratory network has been established that processes stool specimens in
WHO-accredited laboratories, with both quality and performance monitored closely
Concurrent with the decline in polio incidence, the number of polio-endemic
countries has decreased from >120 in 1988 to approximately 50 in 1998. Approximately
50% of the world's population resides in areas now considered polio-free, including
the Western Hemisphere, WPR (which encompasses China), and EUR. Two large
endemic areas of continued poliovirus transmission exist in South Asia and Sub-Saharan
Africa. Priority countries targeted for accelerated implementation of polio eradication
strategies include seven reservoir countries (Bangladesh, Democratic Republic of the
Congo, Ethiopia, India, Nepal, Nigeria, and Pakistan) and eight countries in conflict
(Afghanistan, Angola, Democratic Republic of the Congo, Liberia, Sierra Leone, Somalia,
Sudan, and Tajikistan) (8). Progress in these countries will be essential to achieve the goal
of global polio eradication by the end of 2000.
Vaccine-Associated Paralytic Poliomyelitis (VAPP)
Cases of VAPP were observed almost immediately after the introduction of
live, attenuated poliovirus vaccines (43,44). Before the sequential IPV-OPV schedule was
introduced, 132 cases of VAPP were reported during 1980--1995 (Figure)
(26; CDC, unpublished data, 2000). Fifty-two cases of paralysis occurred among otherwise healthy
vaccine recipients, 41 cases occurred among healthy close contacts of vaccine
recipients, and 7 cases occurred among persons classified as community contacts (i.e.,
persons from whom vaccine-related poliovirus was isolated but who had not been
vaccinated recently or been in direct contact with vaccine recipients). An additional 32 cases
occurred among persons with immune system abnormalities who received OPV or
had direct contact with an OPV recipient (Table).
The overall risk for VAPP is approximately one case in 2.4 million doses of OPV
vaccine distributed, with a first-dose risk of one case in 750,000 first doses distributed
(Table). Among immunocompetent persons, 83% of cases among vaccine recipients and 63%
of cases among contacts occurred after administration of the first dose (Table)
(3,25,36). Among persons who are not immunodeficient, the risk for VAPP associated with the
first dose of OPV is sevenfold to 21-fold higher than the risk associated with
subsequent doses (25). Immunodeficient persons, particularly those who have B-lymphocyte
disorders that inhibit synthesis of immune globulins (i.e., agammaglobulinemia
and hypogammaglobulinemia), are at greatest risk for VAPP (i.e., 3,200-fold to
6,800-fold greater risk than immunocompetent OPV recipients)
Since implementation of the sequential IPV-OPV schedule in 1997, five cases of
VAPP with onset in 1997 and two cases with onset in 1998 were confirmed. Three of
cases were associated with administration of the first or second dose of OPV to
children who had not previously received IPV, and one of the 1998 cases was associated
with administration of the third dose. Although these data suggest a decline in VAPP
after introduction of the sequential schedule, continued monitoring with additional
observation time is required to confirm these preliminary findings because of potential
delays in reporting (25,46).
Transition to an All-IPV Schedule
Adopting an all-IPV schedule for routine childhood polio vaccination in the
United States is intended to eliminate the risk for VAPP. However, this schedule requires
two additional injections at ages 6--18 months and 4--6 years because no combination
vaccine that includes IPV as a component is licensed in the United States. Because
of concerns regarding potential declines in childhood immunization coverage after
introduction of the sequential IPV-OPV schedule (which required two additional injections
at ages 2 and 4 months), several evaluations were conducted during this transition
period. No evidence exists that childhood vaccination coverage declined because of
these additional injections. In two West Coast health maintenance organizations (HMOs)
with automated recording and tracking systems for vaccination, researchers assessed
the up-to-date vaccination status of infants at age 12 months (i.e., two doses of
poliovirus vaccine, three doses of diphtheria and tetanus toxoids and acellular pertussis
vaccine [DTaP], two doses of Haemophilus influenzae type b vaccine [Hib], and two doses
of hepatitis B vaccine [HepB]). The proportion of children who started the routine
vaccination schedule with IPV ranged from 36%--98% across the HMOs by the third quarter
of 1997. Infants starting with IPV were as likely to be up-to-date as were infants
starting with OPV (12).
Available data from other public-sector clinics showed similar results. In one
inner-city clinic in Philadelphia, 152 children due for their first dose of polio vaccine
received IPV. Of the 145 children who returned to the clinic, 144 received a second dose of
IPV. More than 99% of children due for their third and fourth injections (including IPV)
during a single visit received them as indicated
(47). An evaluation conducted at six public health clinics in one Georgia county also concluded that, of 567 infants who
received their first dose of polio vaccine by age 3 months, 534 (94%) received IPV. Among
these infants, 99.6% were also up-to-date for their first doses of diphtheria and tetanus
toxoids vaccine (DTP), DTaP, Hib, and HepB
(48). More detailed data on compliance with
the recommended vaccination schedules is available from state immunization registries.
Another study reviewed immunization data from children born in Oklahoma
during January 1, 1996--June 30, 1997 (i.e., 36,391 children seen at one of 290 facilities).
The percentage of children who received IPV as their first dose of polio vaccine
increased from <2% of children born in 1996 to 15% of children born in the first quarter of
1997 and to 30% of children born in the second quarter of 1997. However, receipt of IPV
did not impact overall vaccination coverage; 80% of children receiving IPV for their
first dose were up-to-date, as were 80% of children receiving OPV
In 1995, a total of 448,030 doses of IPV were distributed (i.e., approximately 2%
of total poliovirus vaccine doses) in the United States. IPV use increased from 6% of
all polio doses distributed in 1996 to 29% in 1997 and 34% in 1998. Through August
31, 1999, a total of 69% of doses purchased were IPV, indicating increased acceptance
of IPV (18).
INVESTIGATION AND REPORTING OF SUSPECTED POLIOMYELITIS CASES
Each suspected case of polio should prompt an immediate epidemiologic
investigation with collection of laboratory specimens as appropriate (see Laboratory
Methods). If evidence suggests the transmission of wild poliovirus, an active search for
other cases that could have been misdiagnosed initially (e.g., as Guillain-Barré
syndrome [GBS], polyneuritis, or transverse myelitis) should be conducted. Control measures
(including an OPV vaccination campaign to contain further transmission) should be
instituted immediately. If evidence suggests vaccine-related poliovirus, no vaccination
plan should be developed because no outbreaks associated with live, attenuated
vaccine-related poliovirus strains have been documented.
The two most recent outbreaks of polio reported in the United States affected
members of religious groups who object to vaccination (i.e., outbreaks occurred in
1972 among Christian Scientists and in 1979 among members of an Amish
community). Polio should be suspected in any case of acute flaccid paralysis that affects an
unvaccinated member of such a religious group. All such cases should be investigated
promptly (see Surveillance).
CDC conducts national surveillance for polio in collaboration with state and
local health departments. Suspected cases of polio must be reported immediately to local
or state health departments. CDC compiles and summarizes clinical, epidemiologic,
and laboratory data concerning suspected cases. Three independent experts review
the data and determine whether a suspected case meets the clinical case definition of
paralytic polio (i.e., a paralytic illness clinically and epidemiologically compatible with
polio in which a neurologic deficit is present 60 days after onset of symptoms [unless
death has occurred or follow-up status is unknown]). CDC classifies confirmed cases of
paralytic polio as a) associated with either vaccine administration or wild virus
exposure, based on epidemiologic and laboratory criteria, and b) occurring in either a
vaccine recipient or the contact of a recipient, based on OPV exposure data
(25). For the recommended control measures to be undertaken quickly, a preliminary assessment
must ascertain as soon as possible whether a suspected case is likely vaccine-associated
or caused by wild virus (see Case Investigation and Laboratory Methods).
Specimens for virus isolation (e.g, stool, throat swab, and cerebrospinal fluid
[CSF]) and serologic testing must be obtained in a timely manner. The greatest yield for
poliovirus is from stool culture, and timely collection of stool specimens increases the
likelihood of case confirmation. At least two stool specimens and two throat swab
specimens should be obtained from patients who are suspected to have polio.
Specimens should be obtained at least 24 hours apart as early in the course of illness as
possible, ideally within 14 days of onset. Stool specimens collected
>2 months after the onset of
paralytic manifestations are unlikely to yield poliovirus. Throat swabs are less often
positive than stool samples, and virus is rarely detected in CSF. In addition, an
acute-phase serologic specimen should be obtained as early in the course of illness as possible,
and a convalescent-phase specimen should be obtained at least 3 weeks later.
The following tests should be performed on appropriate specimens collected
from persons who have suspected cases of polio: a) isolation of poliovirus in tissue
culture; b) serotyping of a poliovirus isolate as serotype 1, 2, or 3; and c) intratypic
differentiation using DNA/RNA probe hybridization or polymerase chain reaction to
determine whether a poliovirus isolate is associated with a vaccine or wild virus.
Acute-phase and convalescent-phase serum specimens should be tested for
neutralizing antibody to each of the three poliovirus serotypes. A fourfold rise in
antibody titer between appropriately timed acute-phase and convalescent-phase serum
specimens is diagnostic for poliovirus infection. The recently revised standard protocol
for poliovirus serology should be used (50). Commercial laboratories usually
perform complement fixation and other tests. However, assays other than neutralization
are difficult to interpret because of inadequate standardization and relative
insensitivity. The CDC Enterovirus Laboratory is available for consultation and will test
specimens from patients who have suspected polio (i.e., patients with acute paralytic
manifestations). The telephone number for this lab is (404) 639-2749.
INACTIVATED POLIOVIRUS VACCINE (IPV)
IPV was introduced in the United States in 1955 and was used widely until
OPV became available in the early 1960s. Thereafter, the use of IPV rapidly declined to
<2% of all poliovirus vaccine distributed annually in the United States. A method of
producing a more potent IPV with greater antigenic content was developed in 1978 and is
the only type of IPV in use today (51). The first of these more immunogenic vaccines
was licensed in the United States in 1987. Results of studies from several countries
have indicated that the enhanced-potency IPV is more immunogenic for both children
and adults than previous formulations of IPV
Two IPV vaccine products are licensed in the United States,*** although only one
(IPOL®) is both licensed and distributed in the United States. These products and their
descriptions are as follows:
- IPOL®. One dose (0.5 mL administered subcutaneously) consists of the
sterile suspension of three types of poliovirus: type 1 (Mahoney), type 2 (MEF-1),
and type 3 (Saukett). The viruses are grown on Vero cells, a continuous line
of monkey kidney cells, by the microcarrier method. After
concentration, purification, and formaldehyde inactivation, each dose of vaccine contains 40
antigen units of type 1 poliovirus, 8 D antigen units of type 2, and 32 D antigen
units of type 3. Each dose also contains 0.5% of 2-phenoxyethanol and up to 200 ppm
of formaldehyde as preservatives, as well as trace amounts of
neomycin, streptomycin, and polymyxin B used in vaccine production. This vaccine
does not contain thimerosal.
- POLIOVAX®. One dose (0.5 mL administered subcutaneously) consists of
the sterile suspension of three types of poliovirus: type 1 (Mahoney), type 2
(MEF-1), and type 3 (Saukett). The viruses are grown on human diploid (MRC-5)
cell cultures, concentrated, purified, and formaldehyde inactivated. Each dose
of vaccine contains 40 D antigen units of type 1 poliovirus, 8 D antigen units of
type 2, and 32 D antigen units of type 3, as well as 27 ppm formaldehyde, 0.5% of
2-phenoxyethanol, 0.5% of albumin (human), 20 ppm of Tween 80, and <1
ppm of bovine serum. Trace amounts of neomycin and streptomycin can be
present as a result of the production process. This vaccine does not contain thimerosal.
A clinical trial of two preparations of enhanced-potency IPV was completed in
the United States in 1984 (53). Among children who received three doses of one of the
enhanced-potency IPVs at ages 2, 4, and 18 months, 99%--100% had developed serum
antibodies to all three poliovirus types at age 6 months, which was 2 months after
administration of the second dose. The percentage of children who had antibodies to all
three poliovirus serotypes did not increase or decrease during the 14-month period after
the second dose, confirming that seroconversion had occurred in most of the children.
Furthermore, geometric mean antibody titers increased fivefold to tenfold after both
the second and third doses.
Data from subsequent studies have confirmed that 90%--100% of children
develop protective antibodies to all three types of poliovirus after administration of two
doses of the currently available IPV, and 99%--100% develop protective antibodies after
three doses (53--55). Results of studies showing long-term antibody persistence after
three doses of enhanced-potency IPV are not yet available in the United States.
However, data from one study indicated that antibody persisted throughout a 4-year
follow-up period (56). In Sweden, studies of persons who received four doses of an IPV with
lower antigen content than the IPVs licensed in the United States indicated that >90% of
vaccinated persons had serum antibodies to poliovirus 25 years after the fourth dose
(57). One dose of IPV administered to persons during an outbreak of poliovirus type 1
in Senegal during 1986--1987 was 36% effective; the effectiveness of two doses was
Several European countries (e.g., Finland, Netherlands, Sweden, and Iceland)
have relied exclusively on enhanced-potency IPV for routine poliovirus vaccination to
eliminate the disease. More recently, all Canadian provinces have adopted vaccination
schedules relying exclusively on IPV (i.e., five doses at ages 2, 4, 6, and 18 months and
4--6 years), and Ontario has used an all-IPV schedule since 1988
(59). In addition, France has used only IPV since 1983
In countries relying on all-IPV schedules, no increased risk for serious adverse
events has been observed. An extensive review by the Institute of Medicine (IOM) of
adverse events associated with vaccination suggested that no serious adverse events have
been associated with the use of IPV in these countries
(61). Since expanded use of IPV in the United States in 1996, no serious adverse events have been linked to use of IPV
(CDC, unpublished data, 1999).
RECOMMENDATIONS FOR IPV VACCINATION
Recommendations for IPV Vaccination of Children
All children should receive four doses of IPV at ages 2, 4, and 6--18 months and
4--6 years. The first and second doses of IPV are necessary to induce a primary
immune response, and the third and fourth doses ensure "boosting" of antibody titers to
high levels. If accelerated protection is needed, the minimum interval between doses is
4 weeks, although the preferred interval between the second and third doses is 2
months (see Recommendations for IPV Vaccination of Adults). All children who have
received three doses of IPV before age 4 years should receive a fourth dose before or at
school entry. The fourth dose is not needed if the third dose is administered on or after
the fourth birthday.
Incompletely Vaccinated Children
The poliovirus vaccination status of children should be evaluated periodically.
Those who are inadequately protected should complete the recommended vaccination
series. No additional doses are needed if more time than recommended elapses
between doses (e.g., more than 4--8 weeks between the first two doses or more than 2--14
months between the second and third doses).
Scheduling IPV Administration
Until appropriate combination vaccines are available, the administration of IPV
will require additional injections at ages 2 and 4 months. When scheduling IPV
administration, the following options should be considered to decrease the number of
injections at the 2- and 4-month patient visits:
- Administer HepB at birth and ages 1 and 6 months.
- Schedule additional visits if there is reasonable certainty that the child will
be brought back for subsequent vaccination at the recommended ages.
- Use available combination vaccines.
Interchangeability of Vaccines
Children who have initiated the poliovirus vaccination series with one or more
doses of OPV should receive IPV to complete the series. If the vaccines are administered
cording to their licensed indications for minimum ages and intervals between
doses, four doses of OPV or IPV in any combination by age 4--6 years is considered a
complete series, regardless of age at the time of the third dose. A minimum interval of 4
weeks should elapse if IPV is administered after OPV. Available evidence indicates that
persons primed with OPV exhibit a strong mucosal immunogloblulin A response
after boosting with IPV (62).
Administration with Other Vaccines
IPV can be administered simultaneously with other routinely recommended
childhood vaccines. These include DTP, DTaP, Hib, HepB, varicella (chickenpox) vaccine,
and measles-mumps-rubella vaccine.
Recommendations for IPV Vaccination of Adults
Routine poliovirus vaccination of adults (i.e., persons aged
>18 years) residing in the United States is not necessary. Most adults have a minimal risk for exposure
to polioviruses in the United States and most are immune as a result of vaccination
during childhood. Vaccination is recommended for certain adults who are at greater
risk for exposure to polioviruses than the general population, including the following
- Travelers to areas or countries where polio is epidemic or endemic.
- Members of communities or specific population groups with disease caused
by wild polioviruses.
- Laboratory workers who handle specimens that might contain polioviruses.
- Health-care workers who have close contact with patients who might
be excreting wild polioviruses.
- Unvaccinated adults whose children will be receiving oral poliovirus vaccine.
Unvaccinated adults who are at increased risk should receive a primary
vaccination series with IPV. Adults without documentation of vaccination status should be
considered unvaccinated. Two doses of IPV should be administered at intervals of 4--8 weeks;
a third dose should be administered 6--12 months after the second. If three doses of
IPV cannot be administered within the recommended intervals before protection is
needed, the following alternatives are recommended:
- If more than 8 weeks are available before protection is needed, three doses of
IPV should be administered at least 4 weeks apart.
- If fewer than 8 weeks but more than 4 weeks are available before protection
is needed, two doses of IPV should be administered at least 4 weeks apart.
- If fewer than 4 weeks are available before protection is needed, a single dose
of IPV is recommended.
The remaining doses of vaccine should be administered later, at the
recommended intervals, if the person remains at increased risk for exposure to poliovirus. Adults
who have had a primary series of OPV or IPV and who are at increased risk can
receive another dose of IPV. Available data do not indicate the need for more than a
single lifetime booster dose with IPV for adults.
Precautions and Contraindications
Hypersensitivity or Anaphylactic Reactions to IPV or
Antibiotics Contained in IPV
IPV should not be administered to persons who have experienced a severe
allergic (anaphylactic) reaction after a previous dose of IPV or to streptomycin, polymyxin B,
or neomycin. Because IPV contains trace amounts of streptomycin, polymyxin B, and
neomycin, hypersensitivity reactions can occur among persons sensitive to these
antibiotics. No serious adverse events related to use of enhanced-potency IPV have been
Although no adverse effects of IPV have been documented among pregnant
women or their fetuses, vaccination of pregnant women should be avoided on
theoretical grounds. However, if a pregnant woman is at increased risk for infection and
requires immediate protection against polio, IPV can be administered in accordance with
the recommended schedules for adults (see Recommendations for IPV Vaccination
IPV is the only vaccine recommended for vaccination of immunodeficient
persons and their household contacts. Many immunodeficient persons are immune to
polioviruses as a result of previous vaccination or exposure to wild virus when they
were immunocompetent. Administration of IPV to immunodeficient persons is safe.
Although a protective immune response in these persons cannot be ensured, IPV might
confer some protection.
Breastfeeding does not interfere with successful immunization against polio. A
dose of IPV can be administered to a child who has diarrhea. Minor upper respiratory
illnesses with or without fever, mild to moderate local reactions to a previous dose
of vaccine, current antimicrobial therapy, and the convalescent phase of an acute
illness are not contraindications for vaccination
ORAL POLIOVIRUS VACCINE (OPV)
Routine production of OPV in the United States has been discontinued. However,
an emergency stockpile of OPV for polio outbreak control is maintained. Because OPV
is the only vaccine recommended to control outbreaks of polio, this section
describes OPV and indications for its use.
Trivalent OPV contains live attenuated strains of all three poliovirus serotypes.
The viruses are propagated in monkey kidney cell culture. Until introduction of the
sequential IPV-OPV schedule in 1997, OPV was the nation's primary poliovirus vaccine, after
its licensing in the United States in 1963. One dose of OPV (0.5 mL administered
orally from a single dose dispenser) is required to contain a minimum of
106 TCID50 (tissue culture infectious dose) Sabin strain of poliovirus type 1 (LSc 2ab),
105.1 TCID50 Sabin strain of poliovirus type 2 (P712 Ch 2ab), and
105.8 TCID50 Sabin strain of poliovirus
type 3 (Leon 12a1b), balanced in a formulation of 10:1:3, respectively. The OPV
formerly manufactured in the United States**** contained approximately threefold to tenfold
the minimum dose of virus necessary to meet these requirements consistently
(64). Each dose of 0.5 mL also contained <25 µG each of streptomycin and neomycin.
After complete primary vaccination with three doses of OPV,
>95% of recipients develop long-lasting (probably lifelong) immunity to all three poliovirus types.
Approximately 50% of vaccine recipients develop antibodies to all three serotypes after a
single dose of OPV (53). OPV consistently induces immunity of the gastrointestinal tract
that provides a substantial degree of resistance to reinfection with poliovirus. OPV
interferes with subsequent infection by wild poliovirus, a property that is important in
vaccination campaigns to control polio epidemics. Both IPV and OPV induce immunity
of the mucosa of the gastrointestinal tract, but the mucosal immunity induced by OPV
is superior (65,66). Both IPV and OPV are effective in reducing pharyngeal replication
and subsequent transmission of poliovirus by the oral-oral route.
RECOMMENDATIONS FOR OPV VACCINATION
Recommendations for OPV Vaccination for Outbreak Control
As affirmed by ACIP, OPV remains the vaccine of choice for mass vaccination
to control polio outbreaks (16). Data from clinical trials and empirical evidence support
the effectiveness of OPV for outbreak control. The preference for OPV in an outbreak
setting is supported by a) higher seroconversion rates after a single dose of OPV compared
with a single dose of IPV; b) a greater degree of intestinal immunity, which limits
community spread of wild poliovirus; and c) beneficial secondary spread (intestinal shedding)
of vaccine virus, which improves overall protection in the community.
As a live attenuated virus, OPV replicates in the intestinal tract and induces
antibodies in more recipients after a single dose. Thus, OPV can protect more persons who
are susceptible in a population, making it the preferred vaccine for rapid intervention
during an outbreak (53,67). Among persons previously vaccinated with three doses of
IPV or OPV, excretion of poliovirus from the pharynx and the intestine appears most
closely correlated with titers of homologous humoral antibody
(68). Three doses of either IPV or OPV induce protective antibody levels (neutralizing antibody titers >1:8) to all three
serotypes of poliovirus in >95% of infant recipients
(9). Therefore, boosting of immunity with a single dose of OPV or IPV is likely to reduce both pharyngeal and intestinal excretion
of poliovirus, effectively stopping epidemic transmission of wild poliovirus.
Use of OPV for Outbreak Control
OPV has been the vaccine of choice for polio outbreak control. During a polio
outbreak in Albania in 1996, the number of cases decreased 90% within 2 weeks
after administration of a single dose of OPV to >80% of the population aged 0--50 years.
Two weeks after a second round of vaccination with OPV, no additional cases were
observed (69). Rapidly implemented mass vaccination campaigns resulting in high coverage
appears to have been similarly effective in interrupting wild poliovirus outbreaks in
other countries (70).
European countries that rely solely on IPV for routine poliovirus vaccination
(e.g., the Netherlands and Finland) have also used OPV for primary control of
outbreaks. During the 1992--93 polio outbreak in the Netherlands, OPV was offered to members of
a religious community affected by the outbreak (who were largely unvaccinated before
the outbreak) and other persons living in areas affected by the outbreak. IPV was given
to immunized persons outside the outbreak areas to ensure protection in this
population (71). During a 1984--85 polio outbreak in Finland, 1.5 million doses of IPV initially
were administered to children <18 years for immediate boosting of protection
(72). Later, approximately 4.8 million doses of OPV were administered to 95% of the population.
In contrast, mass vaccination with IPV exclusively has had little impact on outbreaks
and has rarely been used since OPV became available
Recommendations for Other Uses of OPV
For the remaining nonemergency supplies of OPV, only the following indications
are acceptable for OPV administration:
- Unvaccinated children who will be traveling in fewer than 4 weeks to areas
where polio is endemic. If OPV is not available, IPV should be administered.
- Children of parents who do not accept the recommended number of
vaccine injections. These children can receive OPV only for the third or fourth dose
or both. In this situation, health-care providers should administer OPV only
after discussing the risk for VAPP with parents or caregivers.
Precautions and Contraindications
Hypersensitivity or Anaphylactic Reactions to OPV
OPV should not be administered to persons who have experienced an
anaphylactic reaction to a previous dose of OPV. Because OPV also contains trace amounts of
neomycin and streptomycin, hypersensitivity reactions can occur in persons sensitive
to these antibiotics.
Although no adverse effects of OPV have been documented among pregnant
women or their fetuses, vaccination of pregnant women should be avoided. However, if a
pregnant woman requires immediate protection against polio, she can receive OPV in
accordance with the recommended schedules for adults (see Use of OPV for
OPV should not be administered to persons who have immunodeficiency
disorders (e.g., severe combined immunodeficiency syndrome, agammaglobulinemia,
or hypogammaglobulinemia) (74--76) because these persons are at substantially
increased risk for VAPP. Similarly, OPV should not be administered to persons with altered
immune systems resulting from malignant disease (e.g., leukemia, lymphoma, or
generalized malignancy) or to persons whose immune systems have been
compromised (e.g., by therapy with corticosteroids, alkylating drugs, antimetabolites, or radiation
or by infection with human immunodeficiency virus [HIV]). OPV should not be used
to vaccinate household contacts of immunodeficient patients; IPV is recommended.
Many immunodeficient persons are immune to polioviruses as a result of previous
vaccination or exposure to wild virus when they were immunocompetent. Although their
risk for paralytic disease could be lower than for persons with congenital or acquired
immunodeficiency disorders, these persons should not receive OPV.
Inadvertent Administration of OPV to Household Contacts
of Immunodeficient Persons
If OPV is inadvertently administered to a household contact of an
immunodeficient person, the OPV recipient should avoid close contact with the immunodeficient
person for approximately 4--6 weeks after vaccination. If this is not feasible, rigorous
hygiene and hand washing after contact with feces (e.g., after diaper changing) and
avoidance of contact with saliva (e.g., sharing food or utensils) can be an acceptable but
probably less effective alternative. Maximum excretion of vaccine virus occurs within 4
weeks after oral vaccination.
Breastfeeding does not interfere with successful immunization against polio. A
dose of OPV can be administered to a child who has mild diarrhea. Minor upper
respiratory illnesses with or without fever, mild to moderate local reactions to a previous dose
of vaccine, current antimicrobial therapy, and the convalescent phase of an acute
illness are not contraindications for vaccination
Vaccine-Associated Paralytic Poliomyelitis (VAPP)
In rare instances, administration of OPV has been associated with paralysis in
healthy recipients and their contacts. No procedures are available for identifying persons
(other than those with immunodeficiency) who are at risk for such adverse reactions.
the risk for VAPP is minimal, vaccinees (or their parents) and their susceptible,
close, personal contacts should be informed of this risk (Table). Administration of OPV
can cause VAPP that results in death, although this is rare
Guillain-Barré Syndrome (GBS)
Available evidence indicates that administration of OPV does not measurably
increase the risk for GBS, a type of ascending inflammatory polyneuritis. Preliminary
findings from two studies in Finland led to a contrary conclusion in a review conducted by IOM
in 1993 (77,78). Investigators in Finland reported an apparent increase in GBS
incidence that was temporally associated with a mass vaccination campaign during which
OPV was administered to children and adults who had previously been vaccinated with
IPV. However, after the IOM review, these data were reanalyzed, and an observational
study was completed in the United States. Neither the reanalysis nor the new study
provided evidence of a causal relationship between OPV administration and GBS
REPORTING OF ADVERSE EVENTS AFTER VACCINATION
The National Childhood Vaccine Injury Act of 1986 requires health-care providers
to report serious adverse events after poliovirus vaccination
(80). Events that must be reported are detailed in the Reportable Events Table of this act and include paralytic
polio and any acute complications or sequelae of paralytic polio. Adverse events should
be reported to the Vaccine Adverse Events Reporting System (VAERS). VAERS
reporting forms and information are available 24 hours a day by calling (800) 822-7967.
Vaccine Injury Compensation Program
The National Vaccine Injury Compensation Program, established by the
National Childhood Vaccine Injury Act of 1986, provides a mechanism through which
compensation can be paid on behalf of a person who died or was injured as a result of
receiving vaccine. A Vaccine Injury Table lists the vaccines covered by this program and the
injuries, disabilities, illnesses, and conditions (including death) for which
compensation can be paid (81). This program provides potential compensation after development
or onset of VAPP in a) an OPV recipient (within 30 days), b) a person in contact with
an OPV vaccinee (no time frame specified), or c) an immunodeficient person (within
6 months). Additional information is available from the National Vaccine Injury
Compensation Program ( 338-2382) or CDC's National Immunization Program Internet
site at the following address: http://www.hrsa.dhhs.gov/bhpr/vicp/vicp.html
In 1997, ACIP recommended using a sequential schedule of IPV followed by OPV
for routine childhood polio vaccination in the United States, replacing the previous
all-OPV vaccination schedule. This change was intended to reduce the risk for VAPP. Since
1997, the global polio eradication initiative has progressed rapidly, and the likelihood of
poliovirus importation into the United States has decreased substantially. The
sequential schedule has been well accepted, and no declines in childhood immunization
coverage have been observed. On the basis of these data, ACIP recommended on June 17,
1999, an all-IPV schedule for routine childhood polio vaccination in the United States to
nate the risk for VAPP. ACIP also reaffirms its support for the global polio
eradication initiative and the use of OPV as the only vaccine recommended to eradicate polio
from the remaining countries where polio is endemic.
- Kim-Farley RJ, Bart KJ, Schonberger LB, et al. Poliomyelitis in the USA: virtual elimination
of disease caused by wild virus. Lancet 1984;2:1315--7.
- Nathanson N, Martin JR. The epidemiology of poliomyelitis: enigmas surrounding
its appearance, epidemicity, and disappearance. Am J Epidemiol 1979;110:672--92.
- Strebel PM, Sutter RW, Cochi SL, et al. Epidemiology of poliomyelitis in the United
States one decade after the last reported case of indigenous wild virus-associated disease.
Clin Infect Dis 1992;14:568--79.
- Pan American Health Organization. PAHO director announces campaign to
eradicate poliomyelitis from the Americas by 1990. Bull Pan Am Health Organ 1985;19:213--5.
- World Health Assembly. Global eradication of poliomyelitis by the year 2000. Geneva:
World Health Organization, 1988 (Resolution WHA 41.28).
- CDC. Update: eradication of paralytic poliomyelitis in the Americas. MMWR 1992;41:681--3.
- CDC. Certification of poliomyelitis elimination---the Americas, 1994. MMWR 1994;43:720--2.
- CDC. Progress toward global poliomyelitis eradication, 1997--1998. MMWR 1999;48:416--21.
- CDC. Poliomyelitis prevention in the United States: introduction of a sequential
vaccination schedule of inactivated poliovirus vaccine followed by oral poliovirus
vaccine. Recommendations of the Advisory Committee on Immunization Practices. MMWR
- American Academy of Pediatrics Committee on Infectious Diseases. Poliomyelitis
prevention: recommendations for use of inactivated and live oral poliovirus vaccines. Pediatrics
- Prevots DR, Strebel PM. Poliomyelitis prevention in the United States: new
recommendations for routine childhood vaccination place greater reliance on inactivated poliovirus
vaccine. Pediatric Annals 1997;26:378--83.
- CDC. Impact of the sequential IPV/OPV schedule on vaccination coverage levels---United
States, 1997. MMWR 1998;47:1017--9.
- CDC. National vaccination coverage levels among children aged 19--35
months---United States,1998. MMWR 1999;48:829--30.
- American Academy of Pediatrics Committee on Infectious Diseases. Poliomyelitis
prevention: revised recommendations for use of inactivated and live oral poliovirus vaccines.
- CDC. Recommended childhood immunization schedule---United States, 1999.
- CDC. Notice to readers. Recommendations of the Advisory Committee on
Immunization Practices: revised recommendations for routine poliomyelitis vaccination. MMWR 1999;48:590.
- CDC. Recommended childhood immunization schedule---United States, 2000.
MMWR 2000;49:35--8, 47.
- American Academy of Pediatrics Committee on Infectious Diseases. Prevention
of poliomyelitis: recommendations for use of only inactivated poliovirus vaccine for
routine immunization. Pediatrics 1999;104:1404--6.
- Ramlow J, Alexander M, LaPorte R, Kaufman NC, Kuller L. Epidemiology of the
post-polio syndrome. Am J Epidemiol 1992;136:769--86.
- CDC. Prolonged poliovirus excretion in an immunodeficient person with
vaccine-associated paralytic poliomyelitis. MMWR 1997;46:641--3.
- Khetsuriani N, Prevots DR, Pallansch M, Kew O. Vaccine-derived poliovirus (VDPV)
persistence among immunodeficient persons with vaccine-associated paralytic poliomyelitis
(VAPP) [Abstract no. 675]. Presented at the 39th Interscience Conference on Antimicrobial
Agents and Chemotherapy, September 26--29, 1999.
- Sutter RW, Patriarca P, Suleiman AJM, et al. Attributable risk of DTP (diphtheria and
toxoids and pertussis vaccine) injection in provoking paralytic poliomyelitis during a
large outbreak in Oman. J Infect Dis 1992;165:444--9.
- Strebel PM, Ion-Nedelcu N, Baughman AL, et al. Intramuscular injections within 30 days
of immunization with oral poliovirus vaccine---a risk factor for vaccine-associated
paralytic poliomyelitis. N Engl J Med 1995:332:500--6.
- Gromeier M, Wimmer E. Mechanism of injury-provoked poliomyelitis. J Virology
- Prevots DR, Sutter RW, Strebel PM, Weibel RE, Cochi SL. Completeness of reporting
for paralytic poliomyelitis, United States, 1980 through 1991. Arch Pediatr Adolesc Med
- CDC. Paralytic poliomyelitisUnited States, 19801994. MMWR 1997;46:79--83.
- Kelley PW, Petruccelli BP, Stehr-Green P, Erickson RL, Mason CJ. The susceptibility of
young adult Americans to vaccine-preventable infections: a national serosurvey of US army
recruits. JAMA 1991;266:2724--9.
- Orenstein WA, Wassilak SGF, Deforest A, Rovira EZ, White J, Etkind P. Seroprevalence
of polio virus antibodies among Massachusetts schoolchildren [Abstract no. 512]. In:
Program and abstracts of the 28th Interscience Conference on Antimicrobial Agents and
Chemotherapy. Washington, DC: American Society for Microbiology, 1988.
- Chen RT, Hausinger S, Dajani AS, et al. Seroprevalence of antibody against poliovirus
in inner-city preschool children: implications for vaccination policy in the United States.
- Prevots R, Pallansch MW, Angellili M, et al. Seroprevalence of poliovirus antibodies
among low SES children aged 19--35 months in 4 cities, United States, 1997--1998 [Abstract
no.158]. Presented at the 39th Interscience Conference on Antimicrobial Agents and
Chemotherapy, September 26--29, 1999.
- Rico-Hesse R, Pallansch MA, Nottay BK, Kew OM. Geographic distribution of wild
poliovirus type 1 genotypes. Virology 1987;160:311--22.
- CDC. Isolation of wild poliovirus type 3 among members of a religious community
objecting to vaccination---Alberta, Canada, 1993. MMWR 1993;42:337--9.
- Ministry of Health Ontario. Wild type poliovirus isolated in Hamilton. Public Health
and Epidemiology Report Ontario 1996;7:1-2.
- Hull HF, Ward NA, Hull BP, Milstien JB, de Quadros C. Paralytic poliomyelitis:
seasoned strategies, disappearing disease. Lancet 1994;343:1331-7.
- CDC. Progress toward poliomyelitis eradication---African Region, 1998--April 1999.
- CDC. Progress toward poliomyelitis eradication in Europe and Central Asian Republics,
1997--May 1998. MMWR 1998;47:504--8.
- CDC. Wild poliovirus transmission in bordering areas of Iran, Iraq, Syria, and Turkey,
1997--June 1998. MMWR 1998;47:588--92.
- CDC. Final stages of poliomyelitis eradication---Western Pacific Region, 1997--1998.
- CDC. Progress toward poliomyelitis eradication---Pakistan, 1994--1998. MMWR 1999;48:121--6.
- CDC. Progress toward poliomyelitis eradication---South East Asia Region, 1997--1998.
MMWR 1999;48:230--2, 39.
- CDC. Progress toward poliomyelitis eradication---India, 1998. MMWR 1998;47:778--81.
- CDC. Status of the Global Laboratory Network for poliomyelitis eradication, 1994--1996.
- Terry LL. The association of cases of poliomyelitis: with the use of type III oral
poliomyelitis vaccines---a technical report. Washington, DC: US Department of Health, Education and
- Henderson DA, Witte JJ, Morris L, Langmuir AD. Paralytic disease associated with oral
polio vaccines. JAMA 1964;190:41--8.
- Sutter RW, Prevots DR. Vaccine-associated paralytic poliomyelitis among
immunodeficient persons. Infect Med 1994;11:426, 429--30, 435--8.
- Prevots DR, Khetsuriani N, Wharton M. Evidence for a decline in the number of
vaccine-associated paralytic poliomyelitis cases in the United States following implementation of
a sequential poliovirus vaccination schedule, 1997--1998. Presented at the 36th annual
meeting of the Infectious Disease Society of America, Denver, Colorado, November 12--15, 1998.
- Melman ST, Ehrlich ES, Klugman D, Nguyen TT, Anbar RD. Parental compliance with
initiation of sequential schedule for infant immunization [Abstract no. 104]. In: Abstracts of the
1998 Pediatric Academic Societies' Annual Meeting. The Woodlands, Texas: American
Pediatric Society/Society for Pediatric Research, 1998.
- Kolasa MS, Desai SN, Bisgard KM, Dibling K, Prevots DR. Impact of the sequential
poliovirus vaccination schedule: a demonstration project. Am J Prev Med 2000;18:1--6.
- Stevenson JM, Chen W, Brown P, Maley M. Implementation and impact of the
ACIP recommended sequential schedule for IPV/OPV [Abstract no. 363]. In: Abstracts of the
1998 Pediatric Academic Societies' Annual Meeting. The Woodlands, Texas: American
Pediatric Society/Society for Pediatric Research, 1998.
- World Health Organization. Report of a WHO informal consultation on polio
neutralizing antibody assays. Geneva: World Health Organization, 1991; publication no.
- van Wezel AL, van der Velden-de-Groot CAM, van Herwaarden JAM. The production
of inactivated poliovaccine on serially cultivated kidney cells from captive-bred monkeys.
3rd General Meeting of ESACT, Oxford, 1979. Dev Biol Stand 1980;46 (special issue):151--8.
- International Association of Biological Standardization. International Symposium
on Reassessment of Inactivated Poliomyelitis Vaccine. Dev Biol Stand 1981;47(special issue).
- McBean AM, Thoms ML, Albrecht P, Cuthie JC, Bernier R. Serologic response to oral
polio vaccine and enhanced-potency inactivated polio vaccines. Am J Epidemiol 1988;128:615--28.
- Faden H, Modlin JF, Thoms ML, McBean AM, Ferdon MB, Ogra PL. Comparative
evaluation of immunization with live attenuated and enhanced-potency inactivated trivalent
poliovirus vaccines in childhood: systemic and local immune responses. J Infect Dis 1990;162:1291--7.
- Modlin JF, Halsey NA, Thoms ML, et al. Humoral and mucosal immunity in infants
induced by three sequential inactivated poliovirus vaccine-live attenuated poliovirus
vaccine immunization schedules. J Infect Dis 1997;175(suppl 1):S228--S234.
- Faden H, Duffy L, Sun M, Shuff C. Long-term immunity to poliovirus in children
immunized with live attenuated and enhanced-potency inactivated trivalent poliovirus vaccine. J
Infect Dis 1993;168:452--4.
- Bottiger M. A study of the sero-immunity that has protected the Swedish population
against poliomyelitis for 25 years. Scand J Infect Dis 1987;19:595--601.
- Robertson SE, Traverso HP, Drucker JA, et al. Clinical efficacy of a new,
enhanced-potency, inactivated poliovirus vaccine. Lancet 1988;1:897--9.
- Varughese P, Carter A, Acres S, Furesz J. Eradication of indigenous poliomyelitis in
Canada: impact of immunization strategies. Can J Public Health 1989;80:363--8.
- Malvy D, Drucker J. Elimination of poliomyelitis in France: epidemiology and vaccine
status. Public Health Rev 1993--94;21:41--9.
- Institute of Medicine. Polio vaccines. In: Stratton KR, Howe CJ, eds. Adverse events
associated with childhood vaccines. Evidence bearing on causality. Washington, DC: National
Academy Press 1994:187210.
- Herremans MPT Tineke, Reimerink JHJ, Buisman AM, Kimman TG, Koopmans MPG.
Induction of mucosal immunity by inactivated poliovirus vaccine is dependent on previous
mucosal contact with live virus. J Immunol 1999;162:5011--8.
- CDC. General recommendations on immunization: recommendations of the Advisory
Committee on Immunization Practices (ACIP). MMWR 1994;43(No. RR-1).
- Patriarca PA, Wright PF, John TJ. Factors affecting the immunogenicity of oral poliovirus
vaccine in developing countries [Review]. Rev Infect Dis 1991;13:926--39.
- Onorato IM, Modlin JF, McBean AM, Thomas ML, Losonsky GA, Bernier RH. Mucosal
immunity induced by enhanced-potency inactivated and oral polio vaccines. J Infect Dis 1991;163:1--6.
- Henry JL, Jaikaran ES, Davies JR, et al. A study of poliovaccination in infancy:
excretion following challenge with live virus by children given killed or living poliovaccine. J
Hyg (Cambridge) 1966;64:105--20.
- Ion-Nedelcu N, Strebel PM, Toma F, et al. Sequential and combined use of inactivated
and oral poliovirus vaccines: Dolj District, Romania, 1992--1994. J Infect Dis 1997;175(suppl
- Nishio O, Ishihara Y, Sakae K, et al. The trend of acquired immunity with live
poliovirus vaccine and the effect of revaccination: follow-up of vaccinees for ten years. J Biol
- Prevots DR, Ciofe M, Sallabanda A, et al. Outbreak of paralytic poliomyelitis in Albania,
1996: high attack rate among adults and apparent interruption of transmission following
a nationwide mass vaccination. Clin Infect Dis 1998;26;419--25.
- Patriarca PA, Sutter RW, Oostvogel PM. Outbreaks of paralytic poliomyelitis, 1976--1995.
J Infect Dis 1997;175(suppl 1):S165--S172.
- Oostvogel PM, van Wijngaarden JK, van der Avoort HGAM, et al. Poliomyelitis outbreak
in an unvaccinated community in the Netherlands, 1992--1993. Lancet 1994;344:665--70.
- Hovi T, Cantell K, Huovilainen A, et al. Outbreak of paralytic poliomyelitis in
Finland: widespread circulation of antigenically altered poliovirus type 3 in a vaccinated
population. Lancet 1986;1:1427--32.
- Poos RS, Nathanson N. Use of poliomyelitis vaccine under epidemic conditions. Report
of outbreak of poliomyelitis among naval personnel and dependents in Hawaii. JAMA
- Nightingale EO. Recommendations for a national policy on poliomyelitis vaccination. N
Engl J Med 1977;297:249--53.
- CDC. Poliomyelitis prevention: recommendations of the Immunization Practices
Advisory Committee (ACIP). MMWR 1982;31:22--6, 31--4.
- CDC. Recommendations of the Immunization Practices Advisory Committee
(ACIP). Poliomyelitis prevention: enhanced-potency inactivated poliomyelitis
vaccine---supplementary statement. MMWR 1987;36:795--8.
- Uhari M, Rantala M. Cluster of childhood Guillain-Barré cases after an oral polio
vaccine campaign. Lancet 1989;2:440--1.
- Kinnunen E, Farkkila M, Hovi T, Juntunen J, Weckstrom P. Incidence of Guillain-Barré
syndrome during a nationwide oral poliovirus vaccine campaign. Neurology 1989;39:1034--6.
- Rantala H, Cherry JD, Shields WD, Uhari M. Epidemiology of Guillain-Barré syndrome
in children: relationship of oral polio vaccine administration to occurrence. J Pediatr
- Chen RT, Rastogi SC, Mullen JR, et al. The Vaccine Adverse Event Reporting System
(VAERS). Vaccine 1994;6:542--50.
- Kitch EW, Evans G, Gopin R. U.S. law. In: Plotkin SA, Orenstein WA, eds. Vaccines.
Third edition. Philadelphia, PA: W.B. Saunders Company, 1998:1165--86.
* Anguilla, Antigua and Barbuda, Argentina, Aruba, Bahamas, Barbados, Belize, Bermuda,
Bolivia, Brazil, Canada, Cayman Islands, Chile, Colombia, Costa Rica, Cuba, Dominica,
Dominican Republic, Ecuador, El Salvador, French Guiana, Grenada, Guadeloupe, Guatemala,
Guyana, Haiti, Honduras, Jamaica, Martinique, Mexico, Montserrat, Netherlands Antilles,
Nicaragua, Panama, Paraguay, Peru, Puerto Rico, Saint Kitts and Nevis, Saint Lucia, Saint Vincent and
the Grenadines, Suriname, Trinidad and Tobago, Turks and Caicos Islands, United States of
America, Uruguay, Venezuela, United Kingdom Virgin Islands, and United States Virgin Islands.
** African Region (AFR), Region of the Americas (AMR), Eastern Mediterranean Region
(EMR), European Region (EUR), South East Asia Region (SEAR), and Western Pacific Region
*** Official names: IPOL® (enhanced-inactivated poliomyelitis vaccine), manufactured and
distributed by Aventis-Pasteur, Swiftwater, Pennsylvania; and POLIOVAX,® manufactured by
Aventis-Pasteur, Ontario, Canada (licensed but not distributed in the United States).
**** Official name: Orimune® (poliovirus vaccine, live, oral, trivalent types 1,2,3
manufactured by Lederle Laboratories, Division of American Cyanamid Company, Pearl River, New York.
Return to top.
Return to top.