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There have been many topics covered over the past year since the inception of this microbiology based twitter journal club.  Now it is time to go out of this world and look at how spaceflight affects microbial communities!  With the increasing speculation of manned missions to mars, it is imperative that we know how/if bacteria will be affected by space flight.  The ARTICLE focusses on P. aeruginosa biofilm formation in zero gravity  when travelling on two STS missions.  We will meet on the 25th of June (8pm BST) to discuss our thoughts and give insights to the discussion points listed below:

Aled – @sbi5ar


Understanding the effects of spaceflight on microbial communities is crucial for the success of long-term, manned space missions. Surface-associated bacterial communities, known as biofilms, were abundant on the Mir space station and continue to be a challenge on the International Space Station. The health and safety hazards linked to the development of biofilms are of particular concern due to the suppression of immune function observed during spaceflight. While planktonic cultures of microbes have indicated that spaceflight can lead to increases in growth and virulence, the effects of spaceflight on biofilm development and physiology remain unclear. To address this issue, Pseudomonas aeruginosa was cultured during two Space Shuttle Atlantis missions: STS-132 and STS-135, and the biofilms formed during spaceflight were characterized. Spaceflight was observed to increase the number of viable cells, biofilm biomass, and thickness relative to normal gravity controls. Moreover, the biofilms formed during spaceflight exhibited a column-and-canopy structure that has not been observed on Earth. The increase in the amount of biofilms and the formation of the novel architecture during spaceflight were observed to be independent of carbon source and phosphate concentrations in the media. However, flagella-driven motility was shown to be essential for the formation of this biofilm architecture during spaceflight. These findings represent the first evidence that spaceflight affects community-level behaviors of bacteria and highlight the importance of understanding how both harmful and beneficial human-microbe interactions may be altered during spaceflight.


  1. Was the article well written with enough background information?
  2. Were the methodologies used sufficient to derive the conclusions of the paper?
  3. What experiments would have furthered the conclusions?
  4. What are the large scale implications (if any) back on earth?
  5. What is the future of microbial space travel?

So people here is next week’s paper for discussion.

Microanatomy at Cellular Resolution and Spatial Order of Physiological Differentiation in a Bacterial Biofilm

I had a hard choice and I have decided on one of two stories (the other one was on phages) that caught my attention at the BACNET13 meeting I attended in Poland recently.

The wonderful images produced by the Hengge lab while dissecting the role of c-di-GMP in biofilm formation won. You will need to use the online material as well as the paper for this one.

We have discussed c-di-GMP and Biofilms sometime back and it is a subject that started my own journey into the fascinating world of Caulobacter crescentus as a young Post-Doc. Regine Hengge gave an excellent talk on this story at BACNET. The field of c-di-GMP itself played a central role at this meeting. What was clear to me is that the field has begun to move on from the biochemical characterisation of the components involved to returning to the underlying question of what c-di-GMP is regulating, why and how? Clearly exciting times are ahead for the field.

As per usual our discussion will focus on:

1) Did the paper read well?

2) Could you understand the regulatory network?

3) Would you have done anything differently?

4) where next?

Hello All!

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.

Discussion Points:

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!

Read the rest of this entry »

From the genome of ancient organisms we now move on to ancient therapies for the next #Microtwjc meeting.  This week’s paper (5th June 2012) goes “back to basics” reporting the ability of manuka honey to inhibit Streptococcus pyogenes biofilms and reduce binding to human tissue proteins.

A big thanks needs to go to The Society for General Microbiology (@SocGenMicro) and the journal Microbiology for making this week’s journal open access (until the 7th June 2012).  They have been and will continue to be very supportive of #Microtwjc.

If you have any problems accessing the paper then please let me know!


Streptococcus pyogenes is a problematic organism of clinical significance, whereby infection of skin trauma sites can result in increased patient morbidity and mortality.  The authors first identified the antibacterial effects of manuka honey on both planktonic and biofilm cultures of Group A Streptococcus progenies by growing cells in the presence/absence of manuka honey.  The minimum inhibitory concentration (MIC) was  found to be 20% w/v and the minimum bactericidal concentration (MBC) was found to be 45% w/v with growth analysis showing a dose dependent inhibitory effect.

Having established a bactericidal mode of action, they went on to investigate the effects of manuka honey on biofilms, aggregation, and micro-colony formation.  Manuka honey was effective at permeating established biofilms, killing bacterial cells (reduction in CFU/ml), and reducing the overall biomass of the biofilm (reduction in crystal violet staining).  Microscopy looking at micro-colony formation showed the inability of S. pyogenes to form micro-colonies when grown in sub-lethal concentrations of manuka honey.  Binding of S. pyogenes to human tissue proteins was observed for fibronectin but not fibrinogen at sub-lethal concentrations which were confirmed by end point RT-PCR.

Based on the evidence provided by the authors they conclude that “manuka honey is effective at inhibiting the development of biofilms and disrupting established biofilms of S. pyogenes”.  They go on state that this most likely “mediated by the specific interruption of binding to host tissue ligands” and that manuka honey has potential as a “preventative measure against and treatment for wounds infected with S. pyogenes”.

Discussion Points:

  • Was the paper written clearly and logically with a natural progression of thoughts and ideas through the article?
  • Were the methods robust enough to draw conclusions from?
  • Would you have liked to see any other experiments, maybe some other host tissue proteins tested?
  • Do you agree with the authors closing statements?
  • Finally, is there place for this ancient remedy in modern health care practices?
Relavent Links:
I’ll add new links to the list below so be sure to check back regularly!