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The study by Price et al. highlights the emergence in multidrug resistance S. aureus in a livestock associated lineage, and the subsequent transmission to humans. Of note, the ancestral host of the lineage is predicted to be originally human, raising questions about agricultural practices that may have contributed to the emergence of drug resistance.
There is also a commentary on the paper here: http://mbio.asm.org/content/3/2/e00082-12.full
Looking forward to a good discussion.
I can’t get the export to WordPress function to work on Storify, so just follow the link to see discussion.
The paper this week is from PLoS Genetics, concerning the mechanisms of adaptation of Bartonella spp. to their mammalian hosts.
The PLoS journals give a good accessible overview of there papers so here is the author summary:
Adaptive radiation is the rapid origination of an array of species by the divergent colonization of disparate ecological niches. In the case of pathogenic bacteria, radiations can lead to the emergence of novel human pathogens. Being divergently adapted to a range of different mammalian hosts, including humans as reservoir or incidental hosts, the genus Bartonella represents a suitable model to study genomic mechanisms underpinning divergent adaptation of pathogens. Here we show that two distinct lineages of Bartonella have radiated in parallel, resulting in two arrays of evolutionary distinct species adapted to overlapping sets of mammalian hosts. Such parallelisms display excellent models to reveal insights into the genetic mechanisms underlying these independent evolutionary processes. Our genome-wide analysis identifies a striking evolutionary parallelism in a horizontally-acquired protein secretion system in the two lineages. The parallel evolutionary trajectory of this system in the two lineages is characterized by the convergent origination of a wide array of adaptive functions dedicated to the cellular interaction within the mammalian hosts. The parallel evolution of the two radiating lineages on the ecological as well as on the molecular level suggests that the horizontal acquisition and the functional diversification of the secretion system display an evolutionary key innovation underlying adaptive evolution.
- Were the aims of the study clear?
- Were the findings clearly supported by the data?
- What relevance does understanding the mechanisms driving diversification have for human health?
- Could any additional experiments improve the study?
The authors developed a novel capture array to fish out bacterial DNA from the dental pulp of a plague victim buried in London’s East Smithfield cemetery. The captured sequences were then sequenced and mapped to a contemporary Y. pestis strain. Differences in gene content and synteny, as well as polymorphic sites, were investigated through a combination of BLAST searches and reference-guided assembly of sequence reads. The study concludes that the 14th century strain does not contain any unique polymorphisms, or significant genetic changes, that would make it more virulent than modern strains.
The authors go on to place the 14th century strain in the phylogenetic context of other Yersinia strains, and show that it sits “close to the ancestral node of all extant human pathogenic Y. pestis strains”. Using a Bayesian coalescent method, they estimate a date for the emergence of human-associated Y. pestis to between 1282–1343 AD, calling into question the commonly accepted hypothesis that the earlier Justinian Plague was caused by the same pathogen.
The authors feel that the study of ancient pathogens can inform the study of mechanisms of host adaptation and pandemic spread of modern pathogens. The authors close by stating “At our current resolution, we posit that molecular changes in pathogens are but one component of a constellation of factors contributing to changing infectious disease prevalence and severity, where genetics of the host population, climate, vector dynamics, social conditions and synergistic interactions with concurrent diseases should be foremost in discussions of population susceptibility to infectious disease and host–pathogen relationships with reference to Y. pestis infections.”
- What are the drawbacks of the capture array/sequencing method used?
- Is the method used sufficient to support the conclusions the authors have drawn?
- Do you feel that the study of ancient pathogens is useful for informing the study of contemporary strains?
- Is the conclusion that the causative agent of the Black Death is distinct from earlier supposed plagues convincing?
Links to other relevant discussions
The paper received quite a bit of coverage when it was published, thought I’d link to the NY Times article and the TWiM podcast that discussed a bit about the previous work done.