Between June and October 2005, 45 laboratory-confirmed type 1 vaccine-derived poliovirus (VDPV) cases were identified on Madura Island in Indonesia. Genetic sequencing data on VDPV isolates were consistent with replication and circulation for up to ϳ2 years. Concurrent circulation with type 1 wild poliovirus (WPV) enabled comparisons of VDPV and WPV cases and found that clinical and epidemiological features of both were similar. Attack rates for VDPV were as high as those for WPV. Of 41 VDPV case patients with known vaccination status, 25 (61%) had received zero oral polio vaccine (OPV) doses. Low population immunity due to low routine OPV coverage in rural areas and the absence of WPV circulation for more than a decade were major predisposing factors for the emergence of VDPV. Suboptimal surveillance and a limited initial immunization response may have contributed to widespread circulation. Sensitive surveillance and prompt high-quality immunization responses are recommended to prevent the spread of VDPVs.Trivalent oral polio vaccine (tOPV), a live vaccine consisting of Sabin attenuated poliovirus strains 1, 2 and 3, is the primary tool for the global eradication of poliovirus. OPV prevents paralytic disease through stimulation of humoral immunity and induces intestinal mucosal immunity that reduces person-to-person transmission, thereby protecting both vaccine recipients and the community. Other advantages of OPV include low cost, easy administration, and suitability for use in mass campaigns in developing countries [1]. However, replicating polioviruses have a high frequency of genetic mutation and recombination with other vaccine serotypes and other enteroviruses [2][3][4][5], which rarely may result in vaccine variants reacquiring the ability of the parent wild strains to cause paralytic polio [6 -8]. In settings with low population immunity, Sabin vaccine strains may be transmitted for an extended period among susceptible carriers, increasing the possibility of emergence and spread of virulent strains [6,9].Vaccine-derived polioviruses (VDPVs) are defined as having at least 1% nucleotide difference from their parent Sabin strains in the VP1 capsid protein region of the poliovirus genome [8]. On the basis of the average rate of poliovirus capsid evolution, a 1% divergence in the VP1 area implies that a virus has replicated for ϳ1 year since administration of the initiating OPV dose. VDPVs are classified into 3 categories: circulating VDPVs (cVDPVs), which are associated with sustained personto-person transmission; immunodeficiency-associated VDPVs (iVDPVs), which have been isolated from immunodeficient persons with prolonged viral infection after exposure to OPV; and ambiguous VDPVs (aVDPVs), which either have been isolated from a single patient without immunodeficiency or are environmental isolates with an unidentified source [8] pines [3,12], China [9,13], Madagascar [14], and the United States [15], among others [8, 16, 17]. In addition to low vaccine coverage, other risk factors for cVDPV emergence and ...

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This project demonstrated that under almost ideal conditions (good hygiene, maintenance of universally high IPV coverage, and corresponding high immunity against polioviruses), no emergence and circulation of VDPV could be detected in a tropical developing country setting.

SUMMARYAn outbreak ofSalmonella typhimuriumDT 124 infection which affected 101 people in England in December 1987 and January 1988 was detected through surveillance of laboratory reports from medical microbiology laboratories of the NHS and PHLS. Within 1 week of noting the increase in reports, epidemiological and microbiological investigations identified a small German salami stick as the vehicle of infection and the product was withdrawn from sale. The epidemiological investigation highlighted the occurrence of a long incubation period, bloody diarrhoea. Prompt recognition and investigation of the outbreak prevented further cases of severe infection.

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