Bacterial outer membrane vesicles (OMVs) mediate critical bacterium-bacterium and host-microbial interactions that influence pathogenesis through multiple mechanisms, including the elicitation of inflammatory responses, delivery of virulence factors, and enhancement of biofilm formation. As such, there is a growing interest in understanding the underlying mechanisms of OMV production.

The role of Salmonella virulence factor (VF) allelic variation in modulating pathogenesis or host specificity has only been demonstrated in a few cases, mostly through serendipitous findings. Virulence factor (VF) alleles from Salmonella enterica subsp. enterica genomes were compared to identify potential associations with the host-adapted invasive serovars Typhi, Dublin, Choleraesuis, and Gallinarum, and with the broad host-range intestinal serovars Typhimurium, Enteritidis, and Newport. Through a bioinformatics analysis of 500 Salmonella genomes, we have identified allelic variants of 70 VFs, many of which are associated with either one of the four host-adapted invasive Salmonella serovars or one of the three broad host-range intestinal serovars. In addition, associations between specific VF alleles and intra-serovar clusters, sequence types (STs) and/or host-adapted FimH adhesins were identified. Moreover, new allelic VF associations with non-typhoidal S. Enteritidis and S. Typhimurium (NTS) or invasive NTS (iNTS) were detected. By analogy to the previously shown association of specific FimH adhesin alleles with optimal binding by host adapted Salmonella serovars, lineages or strains, we predict that some of the identified association of other VF alleles with host-adapted serovars, lineages or strains will reflect specific contributions to host adaptation and/or pathogenesis. The identification of these allelic associations will support investigations of the biological impact of VF alleles and better characterize the role of allelic variation in Salmonella pathogenesis. Most relevant functional experiments will test the potential causal contribution of the detected FimH-associated VF variants in host adapted virulence.

Salmonella enterica remains a leading foodborne bacterial pathogen in the United States; infected livestock serve often as the source of contaminated food products. A study estimated that over a billion Salmonella gastroenteritis cases and up to 33 million typhoid cases occur annually worldwide, with 3.5 million deaths. Although many Salmonella strains with a broad host range present preferential associations with certain host species, it is not clear what determines the various levels of host adaptation. Here, causal properties of host associations were determined with allelic variants of three colonization factors of S. enterica serovar Newport, a most frequent zoonotic serovar. This is the first study that related not only individual but also a small group of host-associated gene variants with functional properties that cooperate to determine the level of host-adapted virulence. The detected associations should help to identify sources of Salmonella infections in both humans and animals.

Outbreaks of invasive pneumococcal disease (IPD) caused by Streptococcus pneumoniae serotype 12F were observed in two neighboring regions of rural Alaska in 2003 to 2006 and 2006 to 2008. IPD surveillance data from 1986 to 2009 and carriage survey data from 1998 to 2004 and 2008 to 2009 were reviewed to identify patterns of serotype 12F transmission. Pulsed-field gel electrophoresis was performed on all available isolates, and selected isolates were characterized by additional genetic subtyping methods. Serotype 12F IPD occurred in two waves in Alaska between 1986 and 2008. While cases of disease occurred nearly every year in Anchorage, in rural regions, 12F IPD occurred with rates 10- to 20-fold higher than those in Anchorage, often with many years between disease peaks and generally caused by a single predominant genetic clone. Carriage occurred predominantly in adults, except early in the rural outbreaks, when most carriage was in persons <18 years old. In rural regions, carriage of 12F disappeared completely after outbreaks. Different 12F clones appear to have been introduced episodically into rural populations, spread widely in young, immunologically naïve populations (leading to outbreaks of IPD lasting 1 to 3 years), and then disappeared rapidly from the population. Larger population centers might have been the reservoir for these clones. This epidemiologic pattern is consistent with a highly virulent, but immunogenic, form of pneumococcus.

Currently, the epidemic process is considered a complex multilevel system, which involves the suborganismic (i.e., tissue, cellular, and molecular), organismic, and socio-ecosystem (population). In the human population, many pathogenic microorganisms circulate and may cause disease in humans simultaneously. As a rule, they exist in an associated state a universal phenomenon for the vast majority of representatives of the microworld. However, possible interrelationships between them and their reflection in the epidemic development process and its `manifestations, as a rule, has not been taken into account. In this study, based on an analysis of publications on the results of our own research by the authors and world literature, at the sub-organism level of the epidemic process there is an active inter- and intraspecies interaction among representatives of different types of microorganisms, realized through integration-competitive mechanisms. This interaction is reflected both at the organism and population levels of the epidemic process. Therefore, when conducting epidemiological studies, an integrative approach is needed to take into account processes happening at a suborganism level. Understanding that microorganisms actively interact with each other will significantly increase our ability to develop new approaches to protect organisms from infections, as well as adequately predict the occurrence and development of an epidemic.