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IntroductionLymphogranuloma venereum (LGV) is already endemic in vulnerable populations in several European countries; however, molecular epidemiology data with improved accuracy are necessary to better understand LGV epidemic in these countries. Current strategies to study the molecular epidemiology of LGV cases involve schemes based on a few genetic fragments of Chlamydia trachomatis, which have demonstrated limited discriminatory power for LGV. Therefore, this study aimed to propose a new combination of molecular markers based on the most variable genes of L-genotype genomes to improve the characterization of the current LGV epidemic in Madrid, Spain.MethodsFour genes were selected according to their diversity index (CTLon_0054, CTLon_0087, CTLon_0243 and CTLon_0301) for use in combination with ompA. In silico and experimental studies were performed to compare the previously described multilocus sequence typing (MLST) schemes with our proposal. Moreover, the proposed scheme was applied (n = 68) to analyze the spatio-temporal spread of the LGV cases.ResultsOur proposal demonstrated higher diversity allowing the identification of three main groups compared to the previously published MLST based on hypervariable genes wherein only a single sequence type was identified. The temporal analysis showed that the major cluster was progressively diversifying, revealing a very active transmission chain. Furthermore, an L2b genome identical to that of the origin of the epidemic was detected, suggesting reintroductions or a low screening rate in vulnerable populations. The spatial distribution suggests that the selection and spread of new variants occurs from the central district to the peripheral regions.DiscussionThe scheme proposed in this study has proven to be useful for appropriate discrimination of LGV strains. This study, to our knowledge for the first time, demonstrates a spatio-temporal spread that increases our understanding and identifies areas with special susceptibility for maintenance of the endemic situation of LGV.

Allogeneous selection occurs when an antibiotic selects for resistance to more advanced members of the same family. The mechanisms of allogenous selection are (a) collateral expansion, when the antibiotic expands the gene and gene-containing bacterial populations favoring the emergence of other mutations, inactivating the more advanced antibiotics; (b) collateral selection, when the old antibiotic selects its own resistance but also resistance to more modern drugs; (c) collateral hyper-resistance, when resistance to the old antibiotic selects in higher degree for populations resistant to other antibiotics of the family than to itself; and (d) collateral evolution, when the simultaneous or sequential use of antibiotics of the same family selects for new mutational combinations with novel phenotypes in this family, generally with higher activity (higher inactivation of the antibiotic substrates) or broader spectrum (more antibiotics of the family are inactivated). Note that in some cases, collateral selection derives from collateral evolution. In this article, examples of allogenous selection are provided for the major families of antibiotics. Improvements in minimal inhibitory concentrations with the newest drugs do not necessarily exclude “old” antibiotics of the same family of retaining some selective power for resistance to the newest agents. If this were true, the use of older members of the same drug family would facilitate the emergence of mutational resistance to the younger drugs of the family, which is frequently based on previously established resistance traits. The extensive use of old drugs (particularly in low-income countries and in farming) might be significant for the emergence and selection of resistance to the novel members of the family, becoming a growing source of variation and selection of resistance to the whole family. In terms of future research, it could be advisable to focus antimicrobial drug discovery more on the identification of new targets and new (unique) classes of antimicrobial agents, than on the perpetual chemical exploitation of classic existing ones.

Niches are spaces for the biological units of selection, from cells to complex communities. In a broad sense, “species” are biological units of individuation. Niches do not exist without individual organisms, and every organism has a niche. We use “niche” in the Hutchinsonian sense as an abstraction of a multidimensional environmental space characterized by a variety of conditions, both biotic and abiotic, whose quantitative ranges determine the positive or negative growth rates of the microbial individual, typically a species, but also parts of the communities of species contained in this space. Microbial organisms (“species”) constantly diversify, and such diversification (radiation) depends on the possibility of opening up unexploited or insufficiently exploited niches. Niche exploitation frequently implies “niche construction,” as the colonized niche evolves with time, giving rise to new potential subniches, thereby influencing the selection of a series of new variants in the progeny. The evolution of niches and organisms is the result of reciprocal interacting processes that form a single unified process. Centrifugal microbial diversification expands the limits of the species’ niches while a centripetal or cohesive process occurs simultaneously, mediated by horizontal gene transfers and recombinatorial events, condensing all of the information recovered during the diversifying specialization into “novel organisms” (possible future species), thereby creating a more complex niche, where the selfishness of the new organism(s) establishes a “homeostatic power” limiting the niche’s variation. Once the niche’s full carrying capacity has been reached, reproductive isolation occurs, as no foreign organisms can outcompete the established population/community, thereby facilitating speciation. In the case of individualization-speciation of the microbiota, its contribution to the animal’ gut structure is a type of “niche construction,” the result of crosstalk between the niche (host) and microorganism(s). Lastly, there is a parallelism between the hierarchy of niches and that of microbial individuals. The increasing anthropogenic effects on the biosphere (such as globalization) might reduce the diversity of niches and bacterial individuals, with the potential emergence of highly transmissible multispecialists (which are eventually deleterious) resulting from the homogenization of the microbiosphere, a possibility that should be explored and prevented.