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

Adenoviruses usually cause asymptomatic or mild infection, but occasionally they produce various severe syndromes including neurological disorders. Association of adenovirus infection with acute flaccid paralysis has been investigated. Shedding of adenovirus with feces was detected in 1.05% of young children (mostly infants) with acute flaccid paralysis syndrome versus 0.42% in healthy contact children (P < 0.01). However, 85% of adenoviruses in the pediatric AFP patients belonged to HAdV-C species, which does not have a known neuropathogenic potential. Also, 40% of adenoviruses were isolated from patients with consequently established diagnosis of traumatic neuritis at the discharge, which was not compatible with virus ethology of neurological lesions. Higher adenovirus prevalence in young neurological patients could be affected by an underlying immune deficiency or by congestion in children's hospitals. Indeed, among 70 patients (40 infants, 30 adults) with primary immune deficiencies, asymptomatic shedding of adenoviruses was found in 10-17%; in one adult patient a mixture of HAdV-C2 and HAdV-D15 persisted for several months. Adenoviruses also could be detected in feces of 12% and 57% of healthy young children from two orphanages, respectively. A significant fraction of samples in these groups contained adenovirus mixtures. Therefore, immune deficiencies and congested groups in children's facilities (orphanages and hospitals) could affect significantly the prevalence of adenovirus shedding. The role of adenoviruses in AFP requires further study.

Significantly divergent polioviruses (VDPV) derived from the oral poliovirus vaccine (OPV) from Sabin strains, like wild polioviruses, are capable of prolonged transmission and neuropathology. This is mainly shown for VDPV type 2. Here we describe a molecular-epidemiological investigation of a case of VDPV type 3 circulation leading to paralytic poliomyelitis in a child in an orphanage, where OPV has not been used. Samples of feces and blood serum from the patient and 52 contacts from the same orphanage were collected twice and investigated. The complete genome sequencing was performed for five polioviruses isolated from the patient and three contact children. The level of divergence of the genomes of the isolates corresponded to approximately 9–10 months of evolution. The presence of 61 common substitutions in all isolates indicated a common intermediate progenitor. The possibility of VDPV3 transmission from the excretor to susceptible recipients (unvaccinated against polio or vaccinated with inactivated poliovirus vaccine, IPV) with subsequent circulation in a closed children’s group was demonstrated. The study of the blood sera of orphanage residents at least twice vaccinated with IPV revealed the absence of neutralizing antibodies against at least two poliovirus serotypes in almost 20% of children. Therefore, a complete rejection of OPV vaccination can lead to a critical decrease in collective immunity level. The development of new poliovirus vaccines that create mucosal immunity for the adequate replacement of OPV from Sabin strains is necessary.

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

Проанализированы данные эпизоотологического и эпидемиологического обследования очагов туляремии на территориях 85 субъектов Российской Федерации. О циркуляции и активности инфекции в регионах судили по сведениям о положительных находках при исследовании мелких млекопитающих, иксодовых клещей, комаров, слепней и других объектов внешней среды, полученных при помощи иммунологических и молекулярногенетических методов исследования, по данным о выделении культур возбудителя туляремии и заболеваемости людей. В 2015 г. в стране зарегистрирован 71 случай заболевания человека туляремией. Дана краткая характеристика активности природных очагов туляремии и эпидемической ситуации на территории Российской Федерации в 2015 г. Показаны субъекты Российской Федерации, в которых низкий объем вакцинопрофилактики. Представлена дифференциация территорий по риску заболевания инфекцией в 2016 г.