Reemergence of Recombinant Vaccine–derived Polioviruses in Healthy Children, Madagascar

To the Editor: Poliomyelitis outbreaks caused by pathogenic vaccine-derived polioviruses (VDPVs) are primarily a result of low polio vaccine coverage. Low coverage enables interhuman circulation of polioviruses (PVs) from the oral polio vaccine (OPV), and it enables genetic drift of the viruses and their subsequent reversion to neurovirulent phenotypes (1). Polio outbreaks associated with type 2 or 3 VDPVs (VDPV2s or VDPV3s) were reported in 2001– 2002 and 2005 in Toliara Province in southern Madagascar (2,3). These VDPVs were found in patients with acute flaccid paralysis (AFP) and in healthy children who were contacts of the patients with AFP (2,4). The genomes of these VDPVs belong to several independent, complex mosaic recombinant lineages composed of sequences derived from vaccine polioviruses and other co-circulating species C human enteroviruses (human EV-C) (4,5). The 2001–2002 and 2005 outbreaks in Toliara Province were stopped after rapid and efficient OPV vaccination campaigns. No polio cases have been detected in Madagascar since 2005. However, OPV coverage fluctuates in Toliara Province. In June 2011, to determine if VDPVs were circulating in the province, we collected fecal samples from 616 healthy residents <5 years of age (Madagascar Ethics Committee agreement 011-MSANP/ CE). Sample extracts were used to inoculate human RD and HEp-2c cells and mouse L cells expressing the human poliovirus cellular receptor CD155 (L20B cells) (6). Of the 616 samples, 238 induced cytopathogenic effects in human cells, of which 20 also induced cytopathogenic effects in L20B cells; the latter samples were confirmed by reverse transcription PCR molecular testing (7) to contain PV strains. All PV isolates originated from children who had not received OPV in the 30 days before samples were collected. We sequenced the genomic regions encoding the capsid viral protein (VP1) of the 20 isolates confirmed to contain PV strains: 3 type 2 PV isolates showed >0.5% nt sequence divergence from the type 2 OPV strain (Sabin 2) and were thus identified as potentially pathogenic VDPV2s.