Dementors and Impostors

Mentoring is a hot topic in academia and the business world; a good mentor being seen as critical to "getting on". I have been fortunate to be mentored in an informal way by many of my seniors over the years; but increasingly, emphasis is laid on setting up a more formal interaction.
Which is great, if you can find the right mentor for you; of which more another day.

A recent blog post which caught my eye sums up the antithesis of the helpful relationship of mentoring; which, with reference to J.K.Rowling, was called dementoring. A mentor builds up, encourages and a dementor sucks the very soul out of you.

Another favourite blogger of mine, @athenedonald, has posted a couple of times on "imposter syndrome"; the feeling that you don't really deserve to be where you are and you will be found out.

I think dementors and imposters are irrevocably linked; most of us will probably feel like an imposter sometimes, but if that feeling becomes the dominant one in our working life then personal satisfaction and productivity are likely to fall. I tweeted in response to the dementors post that I could see analogies to the theories of "positive parenting" and I was only half-joking. Dementors, at their best, could be seen to be like the "Tiger Mother" for whom nothing is ever quite good enough and who uses criticism but never praise to spur ever greater efforts. At their worst, more like the Azkaban variety, they simply run you down because they can.

Jenny Martin describes in the blog linked above how she almost gave up academia as the result of one demotivating experience. Many of us (?most) have been there and probably also got through one bad experience, but what about the daily attrition resulting from chronically dysfunctional interactions?

There has been a flurry of twitter and blog activity this past couple of weeks around the issue of women in STEM: science, technology, engineering and medicine. This is in response to the UK parliamentary select committee report published on 6th February, intended to address the problem of gender imbalance within the STEM subjects in universities: the "leaky pipeline" .

I think dementors and imposters, while definitely not exclusively a female problem, are directly relevant to this issue. In their evidence to the parliamentary select committee,

"The University of Oxford considered that "within many science disciplines, work is organised into large research groups, which are often described as having a 'sink or swim' culture, with few formal reporting or support mechanisms". It stated that "the evidence is that the absence of such mechanisms is largely neutral for men, but has a significant negative effect for women, who place a higher value on structured support"."(1)

In my own field, clinical academic medicine, the leaky pipeline is all too evident.
85% of the UK clinical academic workforce are at Senior lecturer/ Professor level but only 28%/ 16% of these are women, despite the intake in medical school being predominantly female (50-60% for each of the last ten years) (2). One argument runs that the upsurge in women applicants is recent and it will take time for this to filter through; however, women have filled 50% of the places at UK medical schools since 1990 and 40% from 1980-1990, so it is this cohort who would be expected to be providing the clinical academics of today;  even at the most senior levels, and they appear to be consistently under-represented. Lack of adequate role models has been recognised to be a significant disincentive to taking up or continuing a particular career path.

My own experiences, which are hardly extraordinary, are summed up by a recent opinion piece in a UK newspaper, where a senior surgeon chose to deride the contribution of women to UK healthcare, asserting that the feminisation of the profession was harming hospitals and that women chose the "easier" medical specialties, including General Practice (3). There are many things wrong with that particular piece, not least that the author fails to recognise the key importance of General Practice to UK healthcare and the need to increase not decrease recruitment to this specialty, something which is becoming a major problem for the NHS.  The lack of suitable role models, male or female, in the higher echelons of a number of specialties, is not addressed, strangely enough.
A similar attitude prevails in academia where women are more often asked to take up more "female" pastoral or teaching roles, neither of which have high status (and are not acknowledged by that arbiter of UK university activity, the Research Excellence Framework). This compounds the issue of failing to progress to the highest career levels.

It would be great to think that a parliamentary report will lead to some solutions. The optimist in me may continue to think so for a while. The Athena Swan initiative demands that academic institutions identify the barriers and challenges to women in STEM and promote best practice in supporting career equality. It is too soon to say whether this is having significant positive effects. At the worst, it will become another box-ticking exercise as universities ensure questionnaires are filled out and more committees (taking up more time of the limited pool of female academics) convened.

Athena Swan Charter

So what would I do? Firstly, address the need to develop researchers with continuous constructive feedback, starting from the undergraduate level (getting women into the pipeline in the first place is still a serious problem in many areas of STEM). The "macho" culture is a huge disincentive to many women. Recognise the diversity of contributions within the academic environment, pastoral, teaching, administrative and research (REF, I'm looking at you, but also the grant-awarding bodies, for whom you're only ever as good as your last 3 papers), if they are seen as valuable. If not, stop asking anybody to do them! A commitment to appoint talented scientists is right; but there should also be a commitment that they should are effective mentors for others and that if this is not a skill which comes to them naturally, then they need to learn it. There should be little point increasing the academic stature of your institution today without taking a good hard look at whether those academics are securing the future of your institution in 15 years time. Again, the short-termism of the REF and grant-awarding bodies actively mitigates against this. What about adding an extra category to "impact" to include the career development of junior researchers?

This would not only address many of the "women in STEM" issues, but also make academia a better working environment for everybody, thereby increasing productivity. Win-win?

1. http://www.publications.parliament.uk/pa/cm201314/cmselect/cmsctech/701/70107.htm

2. http://www.medschools.ac.uk/AboutUs/Projects/Athena-SWAN/Pages/Women-in-Clinical-Academic-Medicine.aspx

3.http://www.dailymail.co.uk/debate/article-2532461/Why-having-women-doctors-hurting-NHS-A-provovcative-powerful-argument-leading-surgeon.html

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Of tweeps and ivory towers

New year, new calendar, time to think about what conferences I might attend in 2014. As a newly-minted academic, the choice is dizzying. Of course, it would help to have some results to present and my research project is only just getting off the ground, but there are other reasons to go, to see and be seen.


When I was a mere PhD student, there was guidance available on how many conferences I was expected to attend and when to present; as a member of academic staff, there seems to be no guidance at all. Being invited to give a talk remains a far-off possibility.
This is an exciting time in microbiology and particularly antimicrobial resistance research, with more media coverage and funding streams in the past two years than the preceding 20, so there is a lot to talk about.

So far, events which have definite appeal are as diverse as Genomics 2014, the Oxford Bone Infection Conference and the SMBE satellite meeting on reticulated microbial evolution. This is without even mentioning the alphabet soup which signifies the big players in infection research meetings: ECCMID, ICAAC, ASM, FIS, SGM and more.

                                           Key themes in this year's infection conferences

The problem is obvious; even if none of these events overlap with each other, I couldn't possibly attend them all, not while carrying on the "day job" in research, teaching and clinical microbiology. There's also the not-so-small matter of work-life balance.

Do I need to go to conferences at all? The world wide web draws talks and posters to my laptop; I have discovered that almost all the talks from the Federation of Infection Societies' (FIS) 2013 are available freely as videos (here) and many proceedings, including the excellent Beatles and Bioinformatics, are posted on YouTube (link); in that case, they were actually streamed live, so I could watch and listen from the comfort of my office in real time, with no train fares or hotel bills to pay and no difficult childcare juggling. A late-comer to the twittersphere, I have discovered its utility in alerting me to new papers and research projects, traditionally reasons for attending meetings.

                           Not quite ivory: the towers of Coventry, home to the University of Warwick

If I can get all this without leaving my ivory tower, should I go at all? I find myself asking for a cost-benefit analysis of conference attendance. (I may have spent too much time reading clinical guidelines, where cost-benefit analysis is always implicit and usually explicit). Widely reproduced opinions in favour claim that conference attendance is good for the CV, that networking is beneficial and that attending talks outside one's specific subject area broadens knowledge.

What about the costs? Time, travel, accommodation, environmental impact, childcare, family impact... Beyond the personal implications, it has been suggested that conferences also promote presentation of posters containing poor-quality research, which may never make it to peer-reviewed publication, facilitate branding of particular scientific cadres and promote "group-think", whereby the same opinion leaders appear repeatedly on different platforms and the same ideas circulate (1). "Tribes" may form of researchers who meet repeatedly at conferences and become exclusive clubs, inviting each other to talk at yet more conferences and potentially sit on the same grant committees awarding further funding to scientists with more invited talks as a marker of success. Less mobile researchers, those with significant health issues or family commitments which preclude large quantities of travel, or simply those without the funding to subsidise this kind of activity are disadvantaged by their non-attendance.




Putting a price on each of these costs and benefits is impossible and will, of course, be different for every researcher. Which leads me no closer to a solution as to which and how many meetings I should attend and indeed begs the question of whether the whole model of large multi-national medical and scientific conferences is broken and a new way of facilitating scientific discourse should be developed.




1. Are Medical Conferences Useful? And for Whom?
John P. A. Ioannidis, MD, DSc
JAMA. 2012;307(12):1257-1258



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Rise of the Resistance

The growing issue of antibiotic resistance

Today is European antibiotic awareness day. The European center for disease control (ECDC) has published more worrying statistics on the seemingly inexorable rise of multi-resistant gram negative bacteria (here) and is pushing the viewpoint that resistance is everyone's problem.

Sadly, awareness remains low in the public as a whole, although recent press releases from the UK Department of Health and Centers for Communicable Disease Control in the US have led to front page stories.

As a small contribution to public awareness of this problem, I spoke recently on local BBC Radio Coventry and Warwickshire and wrote about it for the public-facing website of my university. I have reproduced that text here.

Rise of the Resistance

“Take care, not antibiotics”, we are urged by NHS England as the flu season comes upon us again. In one of many new experiences since I started at Warwick, in the new Division of Microbiology and Infection, I found myself on BBC local radio talking about some of the background to this slogan and the threat of antibiotic resistance in bacteria. This is a subject close to my heart. As a clinical microbiologist at Heartlands Hospital, I routinely deal with the problems posed to patient care by antibiotic-resistant bacteria; as a researcher, I am trying to understand the spread of antibiotic resistance.

Antibiotic resistance – a cause for concern?

My media interview on the BBC came about as a result of comments from Dr Srinivasan at the Centers for Disease Control and Prevention (CDC) in America. In an interview with Frontline, he stated that both humans and livestock have been overmedicated to such a degree that bacteria are now resistant to antibiotics. This led to a proliferation of media coverage suggesting that we’ve reached a point where antibiotics no longer work.

Antibiotic resistance is a significant cause for concern in the US. Every year, at least two million people become ill with drug-resistant infections. But it’s also a problem globally. A number of medical organisations, including the World Health Organisation (WHO), have warned that the overuse of antibiotics and the resulting evolution of resistant bacteria are causing a public health crisis.

Understandably people found these news reports very alarming. But antibiotics are still wonder drugs, saving hundreds of thousands of lives without question every year. Even penicillin remains incredibly effective in the infections we use it for. However we are seeing more antibiotic resistance than we did 30 years ago and this poses a serious risk to human health. The spread of resistant bacteria in hospitals is a major issue for patients' safety and it’s a problem in hospitals across the UK and Europe.

However, the good news is that many countries are implementing measures to stem this. In the UK as well as launching the “Take care, not antibiotics” public health campaign, the Department of Health published an antibiotic resistance strategy in September. This recommended that we limit the use of antibiotics and fund research not only to develop new antibiotics but also to help us understand why resistance spreads.  

Researching antibiotic resistance

My entry point into the fascinating complexity of this subject is through a bacterium intimately connected with influenza. The bacterium is called Haemophilus influenzae because it was originally found in the lungs of people who had died from the flu. Haemophilus influenzae is not the cause of flu, which is a viral illness. However, much of the mortality from the flu results from the fact that the virus renders a patient’s lungs much more susceptible to bacterial infection. This means that if you have a nasty case of the flu you can become vulnerable and more likely to pick up something else, for example, pneumonia, of which H. Influenzae is an important cause and it’s this that can kill.

A lethal synergy

This relationship between the influenza virus and H. influenzae, is a lethal synergy. It has been observed in clinical cases and elegantly demonstrated in animal models of disease, most recently by Wong and colleagues in the US. Immunisation against H. influenzae type b, or Hib, has been highly successful in virtually eliminating serious illnesses caused by H. influenzae in children. However, not all strains of the bacterium are covered by the vaccine and it is these non-vaccine strains which cause serious disease in an increasingly elderly population. Diseases caused by H. influenzae and other respiratory bacteria, notably Streptococcus pneumoniae, account for up to 75 per cent of the antibiotic consumption in the developed world.

Clever creatures

In common with many other bacteria, H. influenzae has become increasingly antibiotic-resistant in the past few decades. The principal reason for this in Haemophilus is that it has acquired a large segment of DNA, known as a genetic element, with genes encoding resistance to common antibiotics. Bacteria are clever. They can, and do, freely and promiscuously exchange DNA and genetic elements with other members of the same species and other, often very distantly-related, species.

Bacteria have been sharing genes for millennia, but the use and abuse of antibiotics in healthcare, veterinary medicine and agriculture has undoubtedly led to a new breed of super resistant bacteria, resulting in the problems that we face today. The evolution of antibiotic resistance is natural selection in action. The presence of an antibiotic in a person, animal or ecosystem such as waste-water plant, kills all the vulnerable (susceptible) bacteria, leaving open the habitat for resistant bacteria. The presence of the antibiotic can itself promote the sharing of genes and because genetic elements often carry genes for resistance to many antibiotics, this drives the evolution of multiple antibiotic-resistant bacteria.

My research focuses on a particular genetic element, known as an ICE (integrating and conjugating element). This was first detected in H. influenzae but it is stably present in many bacterial species which are separated from H. influenzae by millions of years of evolution. Not all of the elements carry antibiotic resistance genes, rather they seem to be efficient capture and transfer mechanisms for genes which will benefit bacteria in whichever environment they happen to inhabit.

I am using RNA sequencing technology to explore the transfer of this genetic element in response to antibiotics and other stresses common to H. influenzae’s lifestyle, such as the presence of free oxygen radicals and competing bacteria. As the genetic element is present in so many bacterial species, insights gained in this species are likely to apply to a wide range of antibiotic resistant bacteria of profound relevance to human and animal health.

The future of antibiotics

Furthering our understanding of how antibiotic resistance genes spread and what triggers the spread, is vitally important in preserving the utility of the antibiotics in current use. There has been an alarming dearth of new antibiotics developed in recent decades. However, new developments may now be restarting with government and commercial initiatives. Understanding how resistance arises and spreads may enable the conservation of the efficacy of these new antibiotics as long as possible. It may also lead to more intelligent antibiotic design. Potentially the antibiotics of the future will be less likely to cause the spread of resistance.

My research, and that of others working in this field, will help to underpin the strategy outlined by the UK Chief Medical Officer in September to deal with the serious threat of antibiotic resistance to human health. It’s possible that with this work the “end of antibiotics” needn’t become a reality.

Baby steps: starting out as a clinical academic

Sitting in a cold lecture theatre, being inducted into yet another NHS trust, I have for the first time this month, leisure to reflect on my initial 30 days as a clinical academic.

It has, as expected, been a rollercoaster ride. In the last month, I have not only moved into a new office and a new laboratory in a new department, but stepped up from specialist trainee to honorary consultant at one of the biggest NHS trusts in the country and taken on the role as lead for infection teaching in the  new curriculum for the MBChB course at Warwick Medical School.

Piles of paperwork, arcane computer systems, health and safety, one regular and two honorary contracts, all the paraphernalia of a new job doubled.

It has been an exciting few weeks; we inaugurated our brand new department with a symposium packed with great science (see our Storify here), I have some brilliant new colleagues, both clinical and academic and I am beginning to crank up the research. Lectures written, external lecturers cajoled, teaching materials reviewed and supplemented and a whole new virtual learning environment encountered, it makes me slightly breathless just thinking about it. When combined with my "extramural" commitments, it is slightly amazing I (and all the other new starters all over the country) haven't subsided gently into wobbling agar jelly. 

I can, and do, maintain a professional front at work, but like most other employees, I strive for a work-life balance which sits in some sort of equilibrium. In my case, the see-saw is still lurching wildly as we incorporate a house move, an unfinished kitchen, a bike-train-bike commute and, most importantly, two children to settle into new schools, one of them for the first time. I have a multi-coloured spreadsheet containing all the details of who is taking whom, with what, when and where; all of which starts to sound like "Cluedo", but less fun. Nonetheless, an entirely familiar game for working parents.

So why do I do it? Well, the science, as alluded to above, is great (new colleagues blog and tweet @mjpallen, @gingermicrobe, @milja001, @antibugdoc, @MicrobLog_me_uk). It is an exciting time to be dealing with clinical infection and ensuring that "Tomorrow's Doctors" know about and manage infection properly is an important part of my role.

All I have to do now is find time and space to plan and write grant applications which I can get funded....

Resurrecting a lonely blog

This blog has been sadly untended for, gulp, the last 2 years. But, it appears that old blogs never die and my account is still here. I have obviously been far too busy in the 24 months since I last posted to indulge in the narcissistic, but ultimately cathartic activity of committing my thoughts to public scrutiny.

In dire need of some therapeutic composition, I have returned, with the intention of posting quite frequently, if not regularly, on topics microbiological and academic.  I feel like I have plenty to say with two new jobs, a multitude of new colleagues and a lot of research to get to grips with. Whether these will turn out to be mere lonely musings, only time will tell.

Bacteria and the tree of life

Microbial phylogeny: a mouthful to say, let alone consider. I have been doing quite a lot of work on it and get increasingly sucked in to the fascinating complexity and speculations which exist within it. Phylogeny is the study of the tree of life, how all living organisms relate to all others. The only illustration in Darwin's "On the Origin of the Species by Means of Natural Selection," the tree of life has been our starting point for evolutionary theory ever since.

 Phylogenetic tree by Haeckel

Originally, bacteria and other microbes were thought to le outside the tree, to be primitive ,left over life forms. They leave no fossil record and, within living memory, were thought not to have genes as they were already understood in higher organisms. In 1942, in his book, Evolution, the Modern Synthesis, the famous evolutionary theorist, Julian Huxley, excluded bacteria from the evolutionary synthesis because they had no genes as then understood.
It has become clear in the half century since the discovery of DNA, with the explosion of molecular technology which followed it, that microbes have an evolutionary story at least as complex and a great deal more ancient than the "higher" organisms. The whole concept of a tree may be completely irrelevant on a whole organism scale, as most microbes are capable of lateral gene transfer between species, genera and even kingdoms.
One of the (many) problems in dealing with microbial phylogeny is simply the speed with which the accepted wisdom in the field changes. When I was at school (less than 20 years ago), bacteria were part of the kingdom known as Monera; by the time I got to University, they were a kingdom of their own. Now it seems ,they are greater than that ,a domain, or (sounding like something out of science fiction), an Urkingdom!
A lot of this is simply semantics, something in which microbial taxonomists (those responsible for naming and classifying) excel.
Does it matter? Well, yes. Firstly , if we don't understand the simple spread of genes through generations, how can we ever get a handle on how collections of genes, coding for antibiotic resistance, or the lethal factors which turn a fairly nasty but local germ into a worldwide pandemic, spread.
Secondly, bacterial evolution is vital for human evolution. It is now widely accepted that the energy powerhouses of all our cells, mitochondria, are simply intracellular bacteria gone native. An amazing survival strategy for that germ. Microbial evolution drives changes in our food crops, our pests (it is estimated that one genus of bacteria, Wolbachia ,lives inside up to 70% of insect cells) and, of course, the diseases which threaten us daily.
Thirdly, it is becoming clear that the amazing adaptibility of microbes may have a lot to teach us about cliimate change and responses to it. There have been several mass extinctions in geological history; is it possible that somewhere within the genetic history of microbial life there is a molecular "signature" which could tell us what actually happened? There are bacteria which have evolved to deal with almost all possible extreme conditions, but a sudden spread in, for instance, sulphur-metabolising bacteria, 65million years ago, might support the theory that massive volcanic activity killed off the dinosaurs.

Blood loving bug

Bacterial names are usually mouthfuls, usually in one or more classical languages. Many were named a long time ago and their names reflect something early microbiologists found distinctive about them; their shape, or habits.

Haemophilus influenzae (yellow rods) growing on airway cells 

(Image from the Science Museum archive)

Haemophilus influenzae: blood lover of influenza. Misnamed, as it doesn't actually cause influenza (flu). Flu is caused by a virus as many a public health campaign will have told you: antibiotics don't help! But it is a blood lover, requiring components of  blood, ready broken down, for it to survive in the lab. Outside its normal environment (the back of your throat), it's a bit of a wimp. In its own habitat, it is a master of survival, usually harmless and just occasionally a cause of devastating disease: meningitis and blood poisoning. One of the least trumpeted and most quietly effective vaccines of the past 20 years, Hib, has seen potentially fatal Haemophilus disease all but eliminated from the UK's children. On the other hand, Haemophilus causes middle ear infections and infection-related worsening of chronic bronchitis; two troublesome conditions at opposite ends of life, causing misery to many, poor school performance in affected children and lots of healthcare visits and hospital admissions.
Haemophilus, as a result, is responsible for huge numbers of antibiotic prescriptions. Antibiotic resistance is becoming more common, so different antibiotics need to be used, so more resistance arises and so on.
It was the first free-living organism to have its genome (complete genetic code) sequenced, giving us a headstart on understanding its biology and providing the starting point for the massive growth in sequence information which has flooded the scientific world since.
Discovered in the 1890s and present in up to 75% of us at any one time, it is a bacterium which lacks headline appeal but has a lot to teach us about bacteria-human interaction and antibiotic resistance.