A large outbreak of poliomyelitis, with 463 laboratoryconfirmed and 47 polio-compatible cases, took place in 2010 in Tajikistan. Phylogenetic analysis of the viral VP1 gene suggested a single importation of wild poliovirus type 1 from India in late 2009, its further circulation in Tajikistan and expansion into neighbouring countries, namely Kazakhstan, Russia, Turkmenistan and Uzbekistan. Whole-genome sequencing of 14 isolates revealed recombination events with enterovirus C with cross-overs within the P2 region. Viruses with one class of recombinant genomes co-circulated with the parental virus, and representatives of both caused paralytic poliomyelitis. Serological analysis of 327 sera from acute flaccid paralysis cases as well as from patients with other diagnoses and from healthy people demonstrated inadequate immunity against polio in the years preceding the outbreak. Evidence was obtained suggesting that vaccination against poliomyelitis, in rare cases, may not prevent the disease. Factors contributing to the peculiarities of this outbreak are discussed. The outbreak emphasises the necessity of continued vaccination against polio and the need, at least in risk areas, of quality control of this vaccination through well planned serological surveillance.

IMPORTANCEThe oral poliovirus vaccine largely contributed to the nearly complete disappearance of poliovirus-caused poliomyelitis. Being generally safe, it can, in some cases, result in a paralytic disease. Two types of such outcomes are distinguished: those caused by slightly diverged (Sabin-like) viruses on the one hand and those caused by significantly diverged VDPVs on the other. This classification is based on the number of mutations in the viral genome region encoding a viral structural protein. Until now, only sporadic poliomyelitis cases due to Sabin-like polioviruses had been described, and in distinction from the VDPV-triggered outbreaks, they did not require broad-scale epidemiological responses. Here, an unusual outbreak of poliomyelitis caused by a Sabin-like virus is reported, which had an exceptionally high disease/infection ratio. This outbreak blurred the borderline between Sabin-like polioviruses and VDPVs both in pathogenicity and in the kind of responses required, as well as underscoring important gaps in understanding the pathogenicity, epidemiology, and evolution of vaccine-derived polioviruses.A s a result of the implementation of the Global Polio Eradication Initiative launched by the World Health Organization (WHO) in 1988, the worldwide incidence of paralytic poliomyelitis decreased by approximately 2 orders of magnitude. The success has been due largely to the use of two outstanding vaccines: the Salk inactivated polio vaccine (IPV) and Sabin live oral polio vaccine (OPV). Notwithstanding their obvious merits, these vaccines have drawbacks: the former fails to trigger a robust intestinal immunity and is unable therefore to prevent transmission of wild polioviruses, whereas the latter can be associated, although quite rarely, with cases of paralytic poliomyelitis, a circumstance especially important now that the incidence of the disease caused by wild polioviruses has substantially decreased.Two situations linked to the OPV-associated polio cases are usually distinguished. The disease may be triggered in vaccine recipients or their contacts by the original or slightly evolved (Sabinlike) vaccine viruses soon after the vaccination (1). Such cases are referred to as vaccine-associated paralytic poliomyelitis (VAPP).Other cases might be caused by markedly diverged vaccine viruses after their cryptic circulation or hidden evolution in a single organism before showing up. Such viruses are dubbed vaccine-derived polioviruses (VDPVs) (2). The current official criterion to classify an OPV-originated virus as a VDPV are the presence of 10 or more mutations in the region encoding the viral capsid protein

The risk of VAPP exists if OPV remains in the vaccination schedule.