Outbreak of Polio 2

Outbreak of Polio 2
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Wild poliovirus has remained endemic in northern Nigeria because of low coverage achieved in the routine immunization program and in supplementary immunization activities (SIAs). An outbreak of infection involving 315 cases of type 2 circulating vaccine-derived poliovirus (cVDPV2; .1% divergent from Sabin 2) occurred during July 2005–June 2010, a period when 23 of 34 SIAs used monovalent or bivalent oral poliovirus vaccine (OPV) lacking Sabin 2. In addition, 21 ‘‘pre-VDPV2’’ (0.5%–1.0% divergent) cases occurred during this period. Both cVDPV and pre-VDPV cases were clinically indistinguishable from cases due to wild poliovirus. The monthly incidence of cases increased sharply in early 2009, as more children aged without trivalent OPV SIAs. Cumulative state incidence of pre-VDPV2/cVDPV2 was correlated with low childhood immunization against poliovirus type 2 assessed by various means. Strengthened routine immunization programs in countries with suboptimal coverage and balanced use of OPV formulations in SIAs are necessary to minimize risks of VDPV emergence and circulation. The cornerstone of the Global Polio Eradication Initiative is immunization of children with multiple doses of oral poliovirus vaccine (OPV), via both routine immunization (RI) and supplementary immunization activities (SIAs) [1]. The key advantages of OPV are ease of administration and efficient induction of mucosal immunity, thereby limiting poliovirus shedding and person-to-person transmission [2]. Through widespread implementation of this approach and with standardized virologic surveillance, indigenous wild poliovirus (WPV) transmission has stopped in all but 4 countries (Nigeria, Pakistan, Afghanistan, and India) [1]. WPV type 2 (WPV2) circulation apparently stopped in Africa in the mid-1990s (F. Adu and C. Koffi; unpublished data), and WPV2 was last detected (in India) in 1999 [3]. Despite its advantages, OPV use carries the infrequent risks of vaccine-associated paralytic poliomyelitis among OPV recipients and their direct contacts [2] and the emergence of genetically divergent vaccine-derived polioviruses (VDPVs) [4, 5], both a consequence of selection against the attenuated phenotype during intestinal replication [6]. VDPVs are operationally defined as OPV-related isolates having .1% nucleotide (nt) sequence divergence from the parental OPV strain in the 900-nt region encoding the major capsid surface protein, VP1 [4, 5]. This arbitrary demarcation represents 1 year of poliovirus (PV) replication after administration of the initiating OPV dose [7], substantially longer than the normal postvaccination excretion period of 4–6 weeks [2, 8]. VDPVs are further Received 7 July 2010; accepted 22 October 2010. Potential conflicts of interest: none reported. Reprints or correspondence: Steven Wassilak, MD, 1600 Clifton Rd. N.E., Mail Stop E-05, Atlanta, GA 30333 (sgw1@cdc.gov). The Journal of Infectious Diseases 2011;203:898–909 Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2011. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/byc/2.5), which permits unrestricted nonommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. 1537-6613/2011/2037-0001$15.00 DOI: 10.1093/infdis/jiq140 898 d JID 2011:203 (1 April) d Wassilak et al. by guest on November 27, 2015 http://jid.oxfordjournals.org/ Downloaded from categorized as circulating (cVDPVs) when there is clear evidence of transmission beyond close contacts [4, 5]. cVDPV outbreaks have occurred in settings of widening susceptibility to >1 poliovirus serotype in association with weak RI programs and in locations where the corresponding WPVs of the same serotype have been eliminated [4, 5, 9, 10]. The risk of cVDPV emergence appears to be highest for the Sabin type 2 (Sabin 2) OPV strain [4, 5, 10], particularly in areas with high densities of nonimmune persons, poor sanitation, and tropical or subtropical climates [11]. Northern Nigeria had remained a major reservoir for WPV1 and WPV3 [12, 13], leading to extensive international spread of WPV1 in 2003–2006 [14] and 2008–2009 [13, 15] and limited WPV3 international spread in 2008–2009 [13, 15]. Low trivalent OPV (tOPV) coverage in the RI program, suspension of SIAs in some states in 2003–2004, and low coverage in SIAs have contributed to ongoing WPV transmission [14]. To more efficiently stop WPV1 and WPV3 transmission, monovalent OPV type 1 (mOPV1) was regularly used in SIAs starting in March 2006, and mOPV3 was intermittently used starting in July 2007 [12, 13]. During the period July 2005–June 2010, 11 of 34 SIA rounds in northern Nigeria used tOPV, including only 4 rounds during the period March 2006–April 2009. In 2002, a case involving VDPV type 2 (VDPV2) was detected in Plateau state, but no related cases involving VDPV2 or any other VDPVs were detected over the next 4 years [16]. In August 2006, virologic investigations detected a cluster of acute flaccid paralysis (AFP) cases associated with Sabin 2-related isolates in northern Nigeria; sequence analysis revealed that the isolates were VDPVs [17]. Retrospective analyses found an early outbreak isolate in 2005, and continued screening through mid- 2010 detected a total of 315 VDPV2 case isolates. We found an additional 21 cases with ‘‘pre-VDPV2’’ isolates (0.5%–1% VP1 divergent from Sabin 2), sporadically found in settings of high OPV coverage. Here, we describe epidemiologic characteristics of the outbreak of cVDPV2 infection in Nigeria during the period from July 2005 through 30 June 2010, constituting the largest and second-longest known cVDPV-associated outbreak [5, 17-21]. Furthermore, in accord with the findings of Jenkins et al [21], we compare clinical features of both VDPV2- and pre-VDPV2– associated cases with WPV and non-polio AFP (NP-AFP) cases. We then assess risks of the emergence and spread of cVDPV2 in northern Nigeria and discuss measures needed to prevent further cVDPV outbreaks. METHODS Background Nigeria, the most populous country in Africa (population, 140 million) [22], has a population growth rate of 2.4% [23]. Population densities (national mean, 152 persons/km2 ) vary widely by state and are highest in the states of the tropical south (median, 390 persons/km2 ; highest, 2162 persons/km2 [in Lagos Figure 1. Map of Nigeria showing state geopolitical zones and popula

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