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After week 12 of MicroTwJC there was a request for a Salmonella paper, having just read the paper below it saved me the bother of thinking for myself! It is a very interesting paper investigating an upsurge in invasive non-typhoidal Salmonella (iNTS) in the context of historical isolates. This allowed them to put a time frame on the emergence of the strain. The authors note that the lineages thought to be responsible for this iNTS surge was emerging around the same time as HIV. Since iNTS is associated with immune suppression the authors raise a suggestive eyebrow at a relationship between these infectious disease events.
I hope there is something there to keep virologists interested. Has anyone done BEAST analysis? Would be great to hear from you in the comments or on the night.
The paper was very kindly made Open Access by the people at Nature Genetics, in fact the editor of the paper is part of the twitterati and is planning on joining us for this weeks session!
Anyway, I hope to have time to knock up a quick blog post summarising the findings, picking out weaknesses and thinking about how this work might apply more broadly. Will post here as and when.
Hope you can join us!
Title: Intracontinental spread of human invasive Salmonella Typhimurium pathovariants in sub-Saharan Africa
Abstract: A highly invasive form of non-typhoidal Salmonella (iNTS) disease has recently been documented in many countries in sub-Saharan Africa. The most common Salmonella enterica serovar causing this disease is Typhimurium (Salmonella Typhimurium). We applied whole-genome sequence–based phylogenetic methods to define the population structure of sub-Saharan African invasive Salmonella Typhimurium isolates and compared these to global Salmonella Typhimurium populations. Notably, the vast majority of sub-Saharan invasive Salmonella Typhimurium isolates fell within two closely related, highly clustered phylogenetic lineages that we estimate emerged independently ~52 and ~35 years ago in close temporal association with the current HIV pandemic. Clonal replacement of isolates from lineage I by those from lineage II was potentially influenced by the use of chloramphenicol for the treatment of iNTS disease. Our analysis suggests that iNTS disease is in part an epidemic in sub-Saharan Africa caused by highly related Salmonella Typhimurium lineages that may have occupied new niches associated with a compromised human population and antibiotic treatment.
It was a great session on Tues so thanks everyone 🙂
The transcript can now be found here
Sorry for the delay in getting this weeks #microtwjc paper up on the site. It has been a busy month of conferences culminating in the 6th ASM Conference on Biofilms which finished yesterday. In light of this we have a biofilm paper for you all to enjoy. The one we had originally selected is not available freely so we had to go with a different paper (but it is just as good!).
The paper can be found here: CLICK
The Pseudomonas aeruginosa Reference Stain PA14 Displays Increased Virulence Due to a Mutation in ladS
Pseudomonas aeruginosa is a pathogen that causes acute and chronic infections in a variety of hosts. The pathogenic potential of P. aeruginosa is strain-dependent. PA14 is a highly virulent strain that causes disease in a wide range of organisms, whereas PAO1 is moderately virulent. Although PA14 carries pathogenicity islands that are absent in PAO1, the presence or absence of specific gene clusters is not predictive of virulence. Here, we show that the virulent strain PA14 has an acquired mutation in the ladS gene. This mutation has a deleterious impact on biofilm, while it results in elevated type III secretion system (T3SS) activity and increased cytotoxicity towards mammalian cells. These phenotypes can be reverted by repairing the ladS mutation on the PA14 genome. The RetS/LadS/GacS signaling cascade is associated with virulence and the switch between acute and chronic infections. RetS is a sensor that down-regulates biofilm formation and up-regulates the T3SS. Mutations in retS are acquired in strains isolated from chronically infected cystic fibrosis patients and lead to hyperbiofilm formation and reduced cytotoxicity. Conversely, the LadS sensor promotes biofilm formation and represses the T3SS. We conclude that the ladS mutation is partly responsible for the high cytotoxicity of PA14, and our findings corroborate the central role of RetS and LadS in the switch between acute and chronic infections. Given the extensive use of the reference strain PA14 in infection and virulence models, the bias caused by the ladS mutation on the observed phenotypes will be crucial to consider in future research.
1) Is the paper well written?
2) Are the aims of the paper clear?
3) Do the authors address the aims of the paper, was the data conclusive enough?
4) What additional experiments would you like to see done to support this paper?
A Little Bit on the Side:
Hillary Lappin-Scott gave a mesmerising account of some of the achievements Bill Costerton made through his career as the #FatherOfBiofilms. Having first identified biofilms in fast flowing streams, he then went on to show that they impact on almost every system, from industrial to ecological, and medical applications.
I thought it would be a great idea to say in 2 or 3 tweets (using 1/3, 2/3, and 3/3 to start each tweet) on biofilms in your own particular area! (sorry virologists, I’m not sure what your equivalent would be!). If we did this at the end of the meeting it won’t impinge on the discussion and may broaden our own horizons on the implications of the organisms we work with.
Have a great weekend and see you all next week!