The authors report the case of a 26 year old woman with acute anterior poliomyelitis contracted during the vaccination of her baby. Despite having been herself vaccinated in infancy she was not protected against the poliovirus. The clinical interest of this uncommon case is a severe paralytic state with definitive paraplegia. The authors suggest serologic testing of patients born before 1967 especially if they are at risk of encountering the virus.

Poliomyelitis caused by wild poliovirus has been virtually nonexistent in the United States since 1980, and vaccine-associated paralytic poliomyelitis (VAPP) has emerged as the predominant form of the disease. We reviewed national surveillance data on poliomyelitis for 1960-1989 to assess the changing risks of wild-virus, vaccine-associated, and imported paralytic disease; we also sought to characterize the epidemiology of poliomyelitis for the period 1980-1989. The risk of VAPP has remained exceedingly low but stable since the mid-1960s, with approximately 1 case occurring per 2.5 million doses of oral poliovirus vaccine (OPV) distributed during 1980-1989. Since 1980 no indigenous cases of wild-virus disease, 80 cases of VAPP, and five cases of imported disease have been reported in the United States. Three distinct groups are at risk of vaccine-associated disease: recipients of OPV (usually infants receiving their first dose), persons in contact with OPV recipients (mostly unvaccinated or inadequately vaccinated adults), and immunologically abnormal individuals. Overall, 93% of cases in OPV recipients and 76% of vaccine-associated cases have been related to administration of the first or second dose of OPV. Our findings suggest that adoption of a sequential vaccination schedule (inactivated poliovirus vaccine followed by OPV) would be effective in decreasing the risk of VAPP while retaining the proven public health benefits of OPV.

Paralytic poliomyelitis is rare in the United States because of the success of universal childhood immunization and the Global Polio Eradication Initiative. Poliovirus vaccine was introduced in the 1950s. Since then, the United States has eliminated indigenous wild poliovirus transmission, controlled imported wild poliovirus cases, and, through a vaccine policy change (i.e., from live, attenuated oral polio vaccine [OPV] to inactivated polio vaccine [IPV]), eliminated vaccine-associated paralytic polio (VAPP) cases. The most recent VAPP case occurred in 1999. The primary risk for paralytic polio for U.S. residents is through travel to countries where polio remains endemic or where polio outbreaks are occurring. This report describes the first known occurrence of imported VAPP in an unvaccinated U.S. adult who traveled abroad, where she likely was exposed through contact with an infant recently vaccinated with OPV. This case highlights the previously unrecognized risk for paralytic polio among unvaccinated persons exposed to OPV during travel abroad.

Although acute flaccid paralysis is a manifestation observed in several neurologic and muscular disorders, vaccine-associated paralytic poliomyelitis (VAPP) is an exceedingly rare etiology. In the clinical setting of acute flaccid paralysis, MRI is useful in differentiating between VAPP and other conditions. Additionally, MRI can assess the extent of lesions. However, reports on MRI findings in VAPP are scarce in the pediatric radiology literature. We report a Brazilian infant who developed VAPP 40 days after receiving the first dose of oral polio vaccine (OPV). MR images of the cervical and thoracic spinal cord showed lesions involving the anterior horn cell, with increased signal intensity on T2-weighted sequences. We would like to emphasize the importance of considering VAPP as a differential diagnosis in patients with acute flaccid paralysis and an MRI showing involvement of medulla oblongata or spinal cord, particularly in countries where OPV is extensively administered.

From January, 1988, to March, 1989, a widespread outbreak (118 cases) of poliomyelitis type 1 occurred in Oman. Incidence of paralytic disease was highest in children younger than 2 years (87/100,000) despite an immunisation programme that recently had raised coverage with 3 doses of oral poliovirus vaccine (OPV) among 12-month-old children from 67% to 87%. We did a case-control study (70 case-patients, 692 age-matched controls) to estimate the clinical efficacy of OPV, assessed the immunogenicity of OPV and extent of poliovirus spread by serology, retrospectively evaluated the cold chain and vaccine potency, and sought the origin of the outbreak strain by genomic sequencing. 3 doses of OPV reduced the risk of paralysis by 91%; vaccine failures could not be explained by failures in the cold chain nor on suboptimum vaccine potency. Cases and controls had virtually identical type 1 neutralising antibody profiles, suggesting that poliovirus type 1 circulation was widespread. Genomic sequencing indicated that the outbreak strain had been recently imported from South Asia and was distinguishable from isolates indigenous to the Middle East. Accumulation of enough children to sustain the outbreak seems to have been due to previous success of the immunisation programme in reducing spread of endemic strains, suboptimum efficacy of OPV, and delay in completing the primary immunisation series until 7 months of age. Additionally, the estimated attack rate of infection among children aged 9-23 months exceeded 25% in some regions, suggesting that a substantial proportion of fully vaccinated children had been involved in the chain of transmission.

We report a case of vaccine-associated paralytic poliomyelitis (VAPP) in Bahrain. The case occurred in an 8-week-old infant who had received a dose of oral polio vaccine (OPV) 7 days after birth. She was in contact with two vaccinees who had received OPV during the national immunisation campaign conducted 10 days before her birth. Specimens from the infant were sent to the WHO Collaborating Centre for Virus Reference and Research Laboratory for serological testing and virus detection, including genomic sequencing. Clinical and virological features are presented of a case of VAPP caused by the Sabin 3 strain of poliovirus that had reverted towards neurovirulence. The case represents one in 51,879 first doses of OPV distributed between 1995 and 1998. In order to reduce further the risk of VAPP, the dose of OPV at birth has been discontinued and a sequential schedule of inactivated polio vaccine (IPV) followed by OPV will be recommended.

Oral poliovirus vaccine (OPV) can cause, in extremely rare cases vaccine-associated paralytic poliomyelitis in recipients, or contacts of vaccinees. Three cases of vaccine-associated paralytic poliomyelitis (two contacts and one recipient) occurred in the Bourgas region of Bulgaria in the spring of 2006. The first two cases, notified as acute flaccid paralysis, were 55 days old unvaccinated twin brothers, having been in contact with vaccinees. The third case concerned a 4-month-old infant who had received the first OPV dose 37 days prior to the onset of illness. Complete clinical, epidemiological, virological, serological and molecular investigations of the children with paralysis and their contacts were undertaken. In all the three cases type 3 polioviruses were isolated from fecal samples and characterized as Sabin-like poliovirus strains. Type 3 polioviruses isolated from the twin brothers demonstrated by sequence analysis U-to-C back mutation at nt 472 of the 5' UTR, known to correlate with neurovirulence, and mutation in the VP1 region. Type 3 poliovirus isolated from the third child demonstrated in the 3D sequenced region a recombination with Sabin type 1 poliovirus. In the latter region, three silent mutations and one, resulting in amino acid substitution, were also observed. The clinical, epidemiological and virological data and the neurological sequelae observed 60 days following the onset of paralysis, confirmed the diagnosis of vaccine-associated paralytic poliomyelitis in all the three patients.

Paralytic poliomyelitis presenting with quadriparesis, transient encephalitis and bulbar symptoms in 2 patients in close contact with recently vaccinated children with trivalent live oral polio vaccine is described. Symmetrical lower motor neuron involvement of deltoid muscles with electromyographic confirmation was found. Upper motor neuron signs, with symmetrical hyperactive deep tendon reflexes developed in the lower extremities. Poliovirus Type-2 vaccine-like strain was cultured from one patient and both patients showed significant antibody titers rises to poliovirus. Attention is drawn to the possible clinical differences between vaccine associated poliomelitis and the usual features found in wild strain poliomyelitis. It is suggested that in selected cases, non-immunized contacts be given inactivated polio-vaccine when the vaccinees are immunized with the live oral-vaccine.

We encountered an adult patient with acute anterior poliomyelitis (AAP), whose monoparesis developed 28 days after his son's immunization with oral poliovirus vaccine (OPV). Neurological and electrophysiological examinations suggested that his muscular wasting of the left lower limb was due to a lower motor neuron disorder, and magnetic resonance imaging revealed the responsible lesion in the left anterior horn at the thoracolumbar junction. His stool was found to include poliovirus type 3, mainly originating from Sabin 3 by neutrization antibody and PCR-restriction fragment length polymorphism method. This indicated that the AAP resulted from contact with his son. This patient raises the question about OPV in polio-free countries.

Poliomyelitis associated with live strain vaccine is defined as the paralytic form of the acute anterior poliomyelitis related to the vaccine strain. Since these strains behave similarly to the wild-type virus, we can differentiate, epidemiologically, two types of vaccine-associated poliomyelitis: cases in which the patient was vaccinated and cases in which the patient had had contact with vaccinated individuals. We herein present the case of an unvaccinated child, with a clinical picture of an acute anterior poliomyelitis associated with the live strain vaccine, whose brother received the Sabin vaccine 20 days before the onset of the symptoms. Vaccine strain of the type 3 poliovirus was isolated in fecal culture and a presented mutation in nucleotide 472 (C-->U) in the 5' non-coding region, which is strongly related to the higher strain virulence.