Context The last case of poliomyelitis in the United States due to indigenously
acquired wild poliovirus occurred in 1979; however, as a consequence of oral
poliovirus vaccine (OPV) use that began in 1961, an average of 9 cases of
vaccine-associated paralytic poliomyelitis (VAPP) were confirmed each year
from 1961 through 1989. To reduce the VAPP burden, national vaccination policy
changed in 1997 from reliance on OPV to options for a sequential schedule
of inactivated poliovirus vaccine (IPV) followed by OPV. In 2000, an exclusive
IPV schedule was adopted.
Objective To review the epidemiology of paralytic poliomyelitis and document the
association between the vaccine schedule changes and VAPP in the United States.
Design and Setting Review of national surveillance data from 1990 through 2003 for cases
of confirmed paralytic poliomyelitis.
Main Outcome Measures Number of confirmed paralytic poliomyelitis cases, including VAPP, and
ratio of VAPP cases to number of doses of OPV distributed that occurred before,
during, and after implementation of policy changes.
Results From 1990 through 1999, 61 cases of paralytic poliomyelitis were reported;
59 (97%) of these were VAPP (1 case per 2.9 million OPV doses distributed),
1 case was imported, and 1 case was indeterminate. Thirteen cases occurred
during the 1997-1999 transitional policy period and were associated with the
all-OPV schedule; none occurred with the IPV-OPV schedule. No cases occurred
after the United States implemented the all-IPV policy in 2000. The last imported
poliomyelitis case occurred in 1993 and the last case of VAPP occurred in
Conclusion The change in polio vaccination policy from OPV to exclusive use of
IPV was successfully implemented; this change led to the elimination of VAPP
in the United States.
In 1952, 3 years before the licensure of the first poliomyelitis vaccine,
more than 21 000 cases of paralytic poliomyelitis were documented in
the United States.1 The use of inactivated
poliovirus vaccine (IPV) and, later, oral poliovirus vaccine (OPV) led to
a precipitous drop in reported cases of poliomyelitis.2 The
last cases of poliomyelitis caused by indigenously acquired wild poliovirus
occurred in 1979 during an outbreak following importation from Canada.3 Genetic studies of poliovirus isolates from the 1970s
suggested that endemic circulation of wild polioviruses in the United States
may have ceased by the late 1960s, and subsequent sporadic cases and small
outbreaks due to wild poliovirus during the 1970s probably represented importations
from neighboring countries.4
Monovalent OPV type 3 became available in 1961 in the United States.
Trivalent OPV (offering protection against the 3 poliovirus serotypes) was
licensed in the United States in 1963 and became the vaccine of choice for
prevention of poliomyelitis in the United States and most of the world.5 Oral poliovirus vaccine was considered superior to
IPV because of provision of better intestinal immunity, ability to indirectly
vaccinate susceptible contacts through transmission of vaccine polioviruses,
ease of administration, and lower costs. However, a serious consequence of
the use of this live-virus vaccine, vaccine-associated paralytic poliomyelitis
(VAPP), was recognized as early as 1962.6,7 From
1961 through 1989, an average of 9 cases of VAPP (range, 1-25 cases) were
confirmed each year.8-10
In 1988, the World Health Assembly resolved to eradicate poliomyelitis
globally by 2000.11 Universal implementation
of polio eradication strategies substantially reduced the risk of poliovirus
importation into the United States.12 In response
to the changing risk-benefit profile associated with OPV use, the Institute
of Medicine conducted independent evaluations on polio vaccine policy options
in the United States in 1977 and 1988,13,14 and
in 1995, participated in a policy review initiated by the Centers for Disease
Control and Prevention (CDC) and the Advisory Committee on Immunization Practices.15 The discussion of changing reliance from OPV to IPV
led to national debates in the mid 1990s.16 It
was thought that the potential for reduced compliance due to higher costs
and the increased number of injections associated with IPV, coupled with possible
reduced mucosal immunity in IPV recipients, could lead to wild poliovirus
However, as the likelihood of wild poliovirus importations declined,
the risk of VAPP with routine use of OPV became more difficult to justify.
In June 1996, a policy change was made when the Advisory Committee on Immunization
Practices recommended a transition to IPV by first introducing a sequential
vaccination schedule of 2 doses of IPV followed by 2 doses of OPV.17 This schedule was predicted to reduce the number
of VAPP cases by 53%, with the greatest impact on recipients.19 However,
more flexible policy options were supported by the American Academy of Pediatrics
(AAP) and the American Academy of Family Physicians (AAFP) that allowed for
an all-OPV schedule or an all-IPV schedule, provided parents were educated
about the decision.18,20 In January
1999, the AAP and AAFP revised their recommendations to state that only IPV
should be administered for doses 1 and 2, citing that VAPP continued to be
associated with the all-OPV schedule21 and
that the vaccine options were not always presented to patients and parents.20 Further progress toward global polio eradication
and the desire to eliminate VAPP prompted all policy-setting groups to recommend
that an all-IPV schedule be implemented in 2000.22,23
This report reviews national poliomyelitis surveillance data in the
United States from 1990 through 2003, describes the epidemiology of poliomyelitis,
and assesses the impact of the poliomyelitis vaccine policy changes on the
occurrence of paralytic poliomyelitis in the United States.
The CDC has maintained national poliomyelitis surveillance since 1955.
This system relies on voluntary reporting of suspected cases from health care
providers and laboratories through local and state health departments to the
CDC, the Vaccine Adverse Events Reporting System, and the National Vaccine
Injury Compensation Program.10,24,25 Suspected
cases are investigated and demographic, clinical, epidemiologic, and virologic
data are collected. We reviewed paralytic poliomyelitis cases reported in
the United States for 1990 through 2003.
National Immunization Survey (NIS) data for 1995 through 2002 were accessed
to obtain vaccination coverage information and estimates of the proportion
of children who received IPV or OPV26; NIS
is an ongoing random-digit-dial telephone survey that provides national estimates
of vaccine coverage among children aged 19 to 35 months. We obtained the number
of OPV doses distributed in the 1990s from CDC Biologics Surveillance (CDC,
unpublished data, January 2003).
Case Definition and Classification
The Council of State and Territorial Epidemiologists defines a clinical
case of paralytic poliomyelitis as an acute onset of flaccid paralysis in
1 or more limbs, with decreased or absent tendon reflexes in the affected
limbs, without apparent cause, and without sensory or cognitive loss. Confirmed
cases are those that meet the clinical case definition and in which neurologic
deficit continues to be present 60 days after onset of symptoms, unless death
has occurred or follow-up status is unknown.27 Isolation
of poliovirus is helpful but not necessary to confirm a case of paralytic
poliomyelitis, and isolation of poliovirus itself does not confirm diagnosis.
An expert committee of physicians, not affiliated with the CDC, reviews suspected
cases to determine whether they meet the definition for a confirmed case of
Confirmed cases of paralytic poliomyelitis are classified according
to the 4 main categories of the Epidemiologic and Laboratory Classification
of Paralytic Poliomyelitis Cases system: sporadic (immunologically normal),
epidemic, immunologically abnormal, and imported.28 Each
of these categories is subdivided and includes a vaccine-associated subcategory.
A paralytic poliomyelitis case is classified as VAPP if there is a temporal
association between OPV receipt or contact with an OPV recipient and onset
Although laboratory technology evolved during the study period, polioviruses
were isolated and identified using conventional procedures of inoculation
of processed specimens onto susceptible cell cultures.29 Isolates
were then determined to be vaccine-related by 1 of several standard molecular
To estimate rates for VAPP in the 1990s before the implementation of
the sequential schedule, we used a previously described method to calculate
the ratio of VAPP cases per number of OPV doses distributed.33 We
compared ratios of VAPP following exposure with the first OPV dose to ratios
of VAPP following a subsequent dose. To estimate the number of first doses
of OPV administered during 1990-1996, we used the annual number of births
in the United States, obtained from the National Vital Statistics System,34 with the assumption that every child born before
1997 received at least a first dose of OPV. To estimate the number of subsequent
OPV doses administered, we subtracted the estimated number of first OPV doses
from the number of all OPV doses distributed. During the sequential period
(1997-1999), we could no longer assume that all infants received OPV; for
this period, we used NIS data to estimate the percentage of infants who received
a first dose of OPV. National Immunization Survey data were not used for the
1990-1996 period because these data were not available before 1995.
To calculate the risk of VAPP among immunologically abnormal children
younger than 1 year, we estimated that 390 children are born each year with
primary immunodeficiency disease (1 case per 10 000 births).35 We calculated the risk of VAPP for children with
primary-type immunodeficiency because this type of immunodeficiency disease
is a known risk factor for VAPP, whereas VAPP is not known to be associated
with acquired immunodeficiency, such as human immunodeficiency virus infection.36
Impact of Vaccine Policy Change
We compared the frequency of VAPP per year before the polio vaccine
schedule change (1990-1996) with the frequency of VAPP while the sequential
schedule was in effect (1998 and 1999) and determined the percentage reduction
in the number of cases between the 2 periods. Vaccine-associated paralytic
poliomyelitis cases with onset in 1997 were noted but not included in this
analysis because we considered this a transition year between changes in the
polio vaccine policies.
One hundred thirty suspected poliomyelitis cases were reported for 1990-2003.
Sixty-one (47%) of these were confirmed as paralytic poliomyelitis (Table 1), 59 of which were classified as VAPP.
Of the 2 cases not associated with OPV, neither had virus isolated: 1 case
(1993), in a girl who arrived ill from Nigeria, was classified as imported-indeterminate
and 1 case (1991), in a teenaged Mexican-born boy, was classified as sporadic-indeterminate.
The last imported poliomyelitis case occurred in 1993 and the last VAPP case
in 1999 (Figure 1).
Of the 59 cases of confirmed VAPP, 43 (73%) were classified as sporadic
in immunocompetent persons: 27 (46%) in OPV recipients, 13 (22%) in contacts
of OPV recipients, and 3 (5%) in persons with unknown history of OPV exposure
(community-acquired cases). Sixteen cases (27%) occurred in immunologically
abnormal persons: 14 in recipients of OPV, and 2 in contacts. The immunologically
abnormal cases all had primary immunodeficiency disease but none were known
to have the disease prior to administration of OPV.
Forty-seven (80%) of the 59 VAPP cases had cultures performed for virus
isolation; of these, 39 cases (83%) had vaccinelike poliovirus isolated. Poliovirus
types 2 and 3 were isolated with similar frequencies. Type 3 poliovirus was
the most common type isolated from sporadic cases (52%), whereas type 2 poliovirus
was isolated from 73% of immunologically abnormal individuals.
Thirty-five (59%) of the VAPP cases occurred in males. Cases of VAPP
were reported from 25 states. The highest number was reported in California,
with 10 cases (17%), followed by Texas, with 6 cases (10%); 1 case occurred
overseas at a US military base.
Twenty-five (93%) of the 27 sporadic cases in vaccine recipients occurred
in infants; median age at onset was 3 months (range, 2 months to 5 years).
The median age among the 13 sporadic cases among contacts was 27 years (range,
2 months to 69 years); only 2 (15%) occurred in infants. The median age of
cases among immunologically abnormal recipients was 5.5 months (range, 2-19
months), whereas cases among immunologically abnormal contacts ranged in age
from 1 month to 57 years, with a median of 29 years. The 3 sporadic community-acquired
cases had a median age of 6 years (range, 9 months to 34 years).
The first OPV dose was associated with paralytic poliomyelitis in 23
(85%) of the 27 sporadic cases among recipients and was the implicated dose
in 7 (54%) of 13 sporadic cases among contacts but in only 5 (31%) of the
16 immunologically abnormal cases (Table 2).
In terms of vaccination status of sporadic contact and community-acquired
cases, 10 (63%) of 16 had no history or an unknown history of poliomyelitis
The interval from vaccine exposure to onset of paralysis in OPV recipients
was 26 days (range, 3-61 days). In cases among contacts of vaccine recipients,
when the exposure date was known, the median interval was 28 days (range,
10-39 days). The median interval of 63 days (range, 2-398 days) was much longer
for immunologically abnormal cases.
At 60 days after onset of illness, the following outcomes were documented
among the 59 VAPP cases: 11 (19%) had minor sequelae such as foot drop, 31
(53%) had major sequelae involving 2 limbs, 13 (22%) had severe sequelae in
3 or more limbs and/or respiratory involvement, and 3 (5%) had died; 1 case
status was unknown.
Estimation of VAPP Ratios
In 1990-1996, an average of 20 million doses of OPV were distributed
per year, after which the distribution declined to 10 million doses in 1999.
No doses have been distributed since 1999 (Figure
2). The overall ratio was 1 VAPP case per 2.9 million doses of OPV
distributed, or 0.34 cases per 1 million doses of OPV distributed. The ratio
of VAPP associated with the first dose of OPV was 1 case per 0.9 million doses,
a 6.6-fold greater risk than that following exposure to subsequent doses.
Immunocompetent recipients were 25 times more likely to develop VAPP after
the first dose than after subsequent doses (Table
3). Overall, immunologically abnormal persons had a high risk for
VAPP, with 3077 cases annually per 1 million population with primary immunodeficiency
Impact of Vaccine Policy Change
The sequential schedule was increasingly accepted each year. Based on
NIS data, an estimated 54% of infants received OPV as their first dose of
poliovirus vaccine in 1997, 29% in 1998, and only 9% in 1999. An estimated
53% received OPV as their second dose in 1997, 31% in 1998, and 10% in 1999.
Coverage with 2 doses of poliovirus vaccine among 13-month-old children reported
by the NIS was 93.4% in 1997, 93.8% in 1998, and 94.6% in 1999. Coverage continued
to increase slightly each year and reached 95.2% in 2002.26 No
imported cases of paralytic poliomyelitis have been confirmed since implementation
of the sequential schedule. During 1997-1999, 13 VAPP cases occurred, 7 in
1997 and 3 each in 1998 and 1999. None of these cases occurred in persons
who had followed the sequential IPV-OPV or all-IPV schedules. Nine cases occurred
in OPV recipients (6 of which were associated with a first OPV dose), 2 among
contacts of OPV recipients (who had not followed the sequential schedule),
and 2 among immunologically abnormal OPV recipients (both associated with
a second dose).
Comparing 1990-1996 with 1998-1999, the average number of VAPP cases
per year decreased from 6.6 to 3.0, a reduction of 54.3% (Table 4). The average number of cases among sporadic recipients
was similar during the 2 periods. The average number of sporadic contact cases
decreased from 1.6 per year to 0.5 per year, a reduction of 68%; community-acquired
cases decreased by 100%. Immunologically abnormal cases decreased from an
average of 2 per year to 0, a reduction of 100%. The proportion of contact
cases changed from 65% of the sporadic cases during 1990-1996 to 14% of the
sporadic cases in 1998-1999.
In response to the declining risk of poliomyelitis balanced against
the continued occurrence of VAPP each year, the United States transitioned
from OPV to exclusive use of IPV, the most contentious change in vaccination
policy made since OPV replaced IPV in the early 1960s. The transition was
gradually accepted with no decreases in vaccination coverage or increases
in adverse events.37-40 Following
this change, all forms of poliomyelitis have been eliminated in the United
States; the last imported case occurred in 1993 and the last VAPP case in
1999. The only threats from polio in the United States are from laboratories
and the few remaining polio-endemic areas in Africa and Asia.
Globally, estimates for overall risk of VAPP are reported as cases of
VAPP per number of OPV doses distributed. Our overall estimate of 1 VAPP case
per 2.9 million OPV doses distributed during 1990-1999 is similar to other
published US studies and data from other industrialized countries, as is our
finding that there is a substantially higher risk of VAPP in immunocompetent
children following the first dose of OPV compared with subsequent doses.10,11,33,41,42 Our
estimate of 1 contact VAPP case per 13.3 million OPV doses distributed, however,
is more than 50% lower than that estimated for the United States in the 1970s
and 1980s, perhaps because of increasing immunization coverage during the
past 2 to 3 decades. The distribution of the poliovirus serotypes that were
isolated, with type 2 being the predominant type in immunodeficient cases
and type 3 in immunocompetent cases, is also consistent with previous findings
but is not fully understood.
No cases of VAPP were confirmed in persons who followed the IPV-OPV
schedule, which is greater than the predicted reduction of 53%. Contrary to
expectations, the schedule options appeared to provide most benefit in preventing
contact, community-acquired, and immunodeficient cases, with no change in
the risk of sporadic recipient cases. However, the short period that the sequential
schedule was in effect and the rarity of VAPP occurrence in the 3 years make
comparisons with data from the previous decades difficult. The predicted reduction
assumed that the IPV-OPV schedule was the only acceptable schedule and that
it was followed uniformly.19 We speculate that
the decline in cases among those exposed to an OPV recipient (contact and
community-acquired) may be due to the fact that IPV-vaccinated infants shed
less virus for shorter periods when later given OPV.
Our method of calculating VAPP risk using OPV doses distributed and
US births may underestimate the risk in recipients. Until 1996, we assumed
that all OPV doses distributed each year were administered and that all infants
received at least 1 dose. Certainly, not all doses were administered, and
an analysis of the data from the NIS demonstrated that about 1.6% of children
born in 1992-1996 received no dose of poliomyelitis vaccine. For estimated
doses during the sequential schedule period, we used available data from the
NIS; therefore, our estimated denominator for case–to–vaccine
dose ratio calculations may be more accurate than those previously reported.
Although the United States does not conduct active surveillance for
paralytic poliomyelitis cases but instead relies on clinicians investigating
suspected poliomyelitis cases to conduct an appropriate clinical workup for
poliovirus and notify the local or state health department, no evidence suggests
that cases of paralytic poliomyelitis have been missed. On the contrary, the
US poliomyelitis case definition may detect paralytic illnesses with causes
other than poliovirus, especially cases in which no poliovirus was isolated.
Acute flaccid paralysis cases unrelated to poliovirus infection may have been
misdiagnosed as poliomyelitis; furthermore, confirmed poliomyelitis cases
may have been misclassified as vaccine-associated.
Delays in reporting or confirmation of cases may result in previously
unidentified cases of VAPP being reported. In 1992, Strebel et al10 reported 81 VAPP cases for 1980-1989. Since that
report, an additional 13 cases have been confirmed for that period; 6 of these
were reported by the National Vaccine Injury Compensation Program after the
program was initiated.24 Although we cannot
be certain that no other cases will be reported in the United States, as of
September 2004, the CDC currently has no suspected cases that are pending
confirmation. The completeness of reporting was estimated at 81% in 1994 and
85% in 1996; it is unlikely that completeness has changed.24,25 Any
VAPP occurring after 1999 would most likely be imported from a country still
Elimination of VAPP is an important public health accomplishment in
the United States. However, it is crucial that the United States continue
to maintain high vaccination coverage and a sensitive surveillance system
to rapidly detect and respond to cases of suspected paralytic poliomyelitis,
either from imported virus or from possible breaches in laboratory containment
that could introduce laboratory strains. Poliovirus—from any source—that
reaches communities with low vaccine coverage may result in endemic or epidemic
Corresponding Author: Lorraine N. Alexander,
RN, MPH, Centers for Disease Control and Prevention, 1600 Clifton Rd, MS E-61,
Atlanta, GA 30333 (firstname.lastname@example.org).
Author Contributions: Ms Alexander had full
access to all polio case data in the study and Dr Santibanez to National Immunization
Survey data and each takes responsibility for the integrity of these data,
respectively, and the accuracy of the data analysis.
Study concept and design: Alexander, Seward, Wharton,
Acquisition of data: Alexander, Pallansch,
Kew, Prevots, Strebel, Cono, Sutter.
Analysis and interpretation of data: Alexander,
Seward, Santibanez, Pallansch, Prevots, Orenstein, Sutter.
Drafting of the manuscript: Alexander, Seward,
Santibanez, Prevots, Sutter.
Critical revision of the manuscript for important
intellectual content: Alexander, Seward, Santibanez,
Pallansch, Kew, Prevots, Strebel, Cono, Wharton, Orenstein, Sutter.
Statistical analysis: Alexander, Santibanez.
Administrative, technical, or material support:
Pallansch, Prevots, Strebel, Cono, Wharton, Orenstein.
Study supervision: Seward, Sutter.
Acknowledgment: We thank the following individuals
from the National Immunization Program at the CDC: Rex Ellington, for providing
Biologics Surveillance data, Barry Sirotkin, MSC, for maintaining historical
data, Mary McCauley, MTSc, for editorial comments, and Patti Smith, for assistance
with graphics. We greatly appreciate the expert review panel physicians Catherine
Wilfert, MD, Robert Eiben, MD, and Howard Lipton, MD, who have dedicated many
hours over the decades in reviewing clinical poliomyelitis cases. We also
acknowledge the members of the Advisory Committee on Immunization Practices
involved with the polio policy changes discussed in this article for their
involvment in making a difficult public health policy decision.
Centers for Disease Control. CDC Annual Summary: Reported Morbidity and Mortality
in the United States. Atlanta, Ga: Centers for Disease Control; 1981
Schonberger LB, Sullivan-Bolyai JZ, Bryan JA. Poliomyelitis in the United States. Adv Neurol
. 1978;19:217-227217252Google Scholar
Centers for Disease Control. Poliomyelitis—United States, 1975-1984. MMWR Morb Mortal Wkly Rep
. 1986;35:180-1823081788Google Scholar
Rico-Hesse R, Pallansch MA, Nottay BK, Kew OM. Geographic distribution of wild poliovirus type 1 genotypes. Virology
. 1987;160:311-3222821678Google ScholarCrossref
Sutter R, Cochi S, Melnick J. Live attenuated poliovirus vaccines. In: Orenstein WA, ed. Vaccines. Philadelphia,
Pa: WB Saunders Co; 1999:364-408
Luther T. The Association of Cases of Poliomyelitis With the
Use of Type III Oral Polio Vaccines. Washington, DC: US Dept of Health, Education, and Welfare; 1962:1-8
Henderson DA, Witte JJ, Morris L, Langmuir AD. Paralytic disease associated with oral polio vaccines. JAMA
. 1964;190:41-4814197143Google ScholarCrossref
Schonberger LB, McGowan JE Jr, Gregg MB. Vaccine-associated poliomyelitis in the United States, 1961-1972. Am J Epidemiol
. 1976;104:202-211181984Google Scholar
Nkowane BM, Wassilak SG, Orenstein WA.
et al. Vaccine-associated paralytic poliomyelitis. JAMA
. 1987;257:1335-13403029445Google ScholarCrossref
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;14:568-5791554844Google ScholarCrossref
Esteves K. Safety of oral poliomyelitis vaccine. Bull World Health Organ
. 1988;66:739-7463266113Google Scholar
Centers for Disease Control and Prevention. Global Polio Eradication Initiative strategic plan, 2004. MMWR Morb Mortal Wkly Rep
. 2004;53:107-10814961005Google Scholar
Institute of Medicine. Evaluation of Poliomyelitis Vaccines. Washington, DC: National Academy Press; 1977:75
Institute of Medicine. An Evaluation of Poliomyelitis Vaccine Policy Options. Washington, DC: National Academy of Sciences; 1988
Institute of Medicine. Vaccine Safety Forum: Options for Poliomyelitis Vaccination
in the United States: Workshop Summary. Washington, DC: National Academy Press; 1996
Poliomyelitis prevention in the United States: introduction of a sequential
vaccination schedule of inactivated poliovirus vaccine followed by oral
poliovirus vaccine. MMWR Recomm Rep
1-25[erratum appears in MMWR Morb Mortal Wkly Rep. 1997;46:183]
American Academy of Pediatrics Committee on Infectious Diseases. Poliomyelitis prevention: recommendations for use of inactivated poliovirus
vaccine and live oral poliovirus vaccine. Pediatrics
. 1997;99:300-3059024465Google ScholarCrossref
Kohberger RC, Sutter RW, Rhodes PH. Modeling the five immunization schedule options. Presented at: Institute of Medicine Polio Workshop; June 7, 1995;
Zimmerman RK, Spann SJ. Poliovirus vaccine options. Am Fam Physician
. 1999;59:113-1189917578Google Scholar
American Academy of Pediatrics Committee on Infectious Diseases. Poliomyelitis prevention: revised recommendations for use of inactivated
and live oral poliovirus vaccines. Pediatrics
. 1999;103:171-1729917460Google ScholarCrossref
American Academy of Pediatrics Committee on Infectious Diseases. Prevention of poliomyelitis: recommendations for use of only inactivated
poliovirus vaccine for routine immunization. Pediatrics
. 1999;104:1404-140610585998Google ScholarCrossref
Poliomyelitis prevention in the United States—updated recommendations
of the Advisory Committee on Immunization Practices. MMWR Recomm Rep
. 2000;49:1-22Google Scholar
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
. 1994;148:479-4858180638Google ScholarCrossref
Weibel RE, Benor DE. Reporting vaccine-associated paralytic poliomyelitis. Am J Public Health
. 1996;86:734-7378629730Google ScholarCrossref
Centers for Disease Control and Prevention. Case definitions for infectious conditions under public health surveillance. MMWR Recomm Rep
Sutter RW, Brink EW, Cochi SL.
et al. A new epidemiologic and laboratory classification system for paralytic
poliomyelitis cases. Am J Public Health
. 1989;79:495-4982929811Google ScholarCrossref
Schmidt N. Cell culture procedures for diagnostic virology. In: Emmons R, ed. Diagnostic Procedures for Viral,
Rickettsial and Chlamydial Infections. Washington, DC: American Public
Health Association; 1989:51-100
Nottay BK, Kew OM, Hatch MH, Heyward JT, Obijeski JF. Molecular variation of type 1 vaccine-related and wild polioviruses
during replication in humans. Virology
. 1981;108:405-4236258294Google ScholarCrossref
De L, Nottay B, Yang CF, Holloway BP, Pallansch M, Kew O. Identification of vaccine-related polioviruses by hybridization with
specific RNA probes. J Clin Microbiol
. 1995;33:562-5717751358Google Scholar
Yang CF, De L, Holloway BP, Pallansch MA, Kew OM. Detection and identification of vaccine-related polioviruses by the
polymerase chain reaction. Virus Res
. 1991;20:159-1791659060Google ScholarCrossref
Paralytic poliomyelitis—United States, 1980-1994. MMWR Morb Mortal Wkly Rep
. 1997;46:79-839048844Google Scholar
Ventura SJ, Martin J, Curtin M, Menacker F, Hamilton BE. Births: final data for 1999. Natl Vital Stat Rep
. 2001;49:1-10011341112Google Scholar
Lindegren ML, Kobrynski L, Rasmussen SA.
et al. Applying public health strategies to primary immunodeficiency diseases:
a potential approach to genetic disorders. MMWR Recomm Rep
. 2004;53:1-2914724556Google Scholar
Sutter R, Prevots D. Vaccine-associated paralytic poliomyelitis among immunodeficient persons. Infect Med
. 1994;11:426, 429-430, 435-438Google Scholar
Wattigney WA, Mootrey GT, Braun MM, Chen RT. Surveillance for poliovirus vaccine adverse events, 1991 to 1998. Pediatrics
. 2001;107:E8311331733Google ScholarCrossref
Kolasa MS, Bisgard KM, Prevots DR, Desai SN, Dibling K. Parental attitudes toward multiple poliovirus injections following
a provider recommendation. Public Health Rep
. 2001;116:282-28812037256Google Scholar
Impact of the sequential IPV/OPV schedule on vaccination coverage levels—United
States, 1997. MMWR Morb Mortal Wkly Rep
. 1998;47:1017-10199853937Google Scholar
Taylor JA, Darden PM, Brooks DA.
et al. Impact of the change to inactivated poliovirus vaccine on the immunization
status of young children in the United States. Pediatrics
. 2001;107:E9011389288Google ScholarCrossref
Varughese PV, Carter AO, Acres SE, Furesz J. Eradication of indigenous poliomyelitis in Canada. Can J Public Health
. 1989;80:363-3682804867Google Scholar
Joce R, Wood D, Brown D, Begg N. Paralytic poliomyelitis in England and Wales, 1985-91. BMJ
. 1992;305:79-821322218Google ScholarCrossref