Monthly Archives: February 2017

“Running to stand still…”

When I started working as a Clinical Microbiologist in 2007, anti-NMDA receptor encephalitis had not yet been discovered. The diagnostic test, looking for anti-NMDA receptor antibodies, only appeared commercially around 2010.

Now it is the latest fashionable test to perform…

I am getting old.

The whole area of auto-immune encephalitis has progressed rapidly in the last 10 years, and this potentially treatable cause of encephalitis (options include steroids, IV immunoglobulins, plasma exchange and immunomodulators) is now thought to be similar in prevalence to some viral encephalitides.

Anti-NMDA receptor encephalitis represents the vast majority (approx. 80%) of all cases of autoimmune encephalitis. It usually presents with a short prodromal period followed by a range of symptoms such as auditory and visual hallucinations, delusions, behavioural change, decreased level of consciousness, seizures, and autonomic dysfunction. 

A majority of patients (58%) with anti-NMDA receptor encephalitis will have a CSF leucocytosis(Raised CSF protein and oligoclonal bands are also seen in a proportion of patients.) So testing for anti-NMDA receptor antibodies becomes the obvious default for a patient with a CSF leucocytosis and negative bacterial culture and negative CSF viral PCR…

Other causes of autoimmune encephalitis include unfamiliar names such as anti-LGl1, anti-AMPAR, anti GABA  and anti-CASPR to name but a few. You will likely see these crop up from time to time on CSF request forms.

It is of course not microbiology per se. However we need to know about it as we end up getting the CSF samples and we need to triage the test requests, and deal with the perennial problem of separating a ml or two of CSF for several different tests, which often get sent away to different laboratories…

I didn’t need to worry about these exotic tests 10 years ago. Now I do.

Sometimes it feels like you need to keep running just to stand still…


p.s.  For the academics amongst you, NMDA stands for N-methyl-D-aspartate.

“Reinventing yourself”

In the next generation (20-25 years), the diagnostic microbiology laboratory workforce will be decimated worldwide.

If you are a student, they don’t tell you that at the careers fair…

“You sound like exactly the sort of person we are looking for. Come and “train” for four years in a lecture theatre, and then work in a clinical microbiology laboratory, that is if you are lucky enough to get a job. Unless your Mum and Dad are well off, you will accrue a hefty debt which will likely take you a couple of decades to pay off. However in 20 years time your job will probably not even exist…”

Am I being too harsh?

In terms of general culture based bacteriology, most of it will have gone molecular. Whatever is left of it will be automated, not just partially automated as with the current Kiestra TLA system, but completely automated to include plate interpretation, colony picking, identification, antibiotic susceptibility testing and rule based signout. The whole works…

Most microbiology samples will never touch a laboratory worker’s hands.

Molecular testing will have increased, but on highly automated platforms, processing high volumes of work, with minimum manual input.

Our work will be reduced to oddities and troubleshooting. I would even chance to say that there will be just as many engineers as microbiologists on the laboratory floor.

And then I look at the core components of my own job as a clinical microbiologist…

  • Authorising important results:- This will be done automatically using sophisticated rules based computer algorithms. And they will do it much better than I can.
  • Giving antibiotic advice:- Decision support apps downloaded on clinicians’ smartphones will do this more sensibly than me.
  • Laboratory Management:- I fear there will be nobody left in the lab to manage…
  • Demand management:- Although the process of demand management will be performed by software algorithms, there might still be a little work left for me regarding the initiation and governance of such projects.
  • Anti-microbial stewardship:- Anti-microbial resistance is not going away anytime soon so there may be a continuing role in the governance of such programmes. But the nuts and bolts will be highly automated and app-based.

So I am not overly optimistic about my own long term future. No one is immune…

It is no accident that during conferences I heavily focus  on presentations in molecular diagnostics and demand management. That should help in the short term at least in securing my usefulness. However it is entirely possible I will need to retrain in something completely different before I am done.

I know my job description as a clinical microbiologist will change out of all recognition before I retire. It is not impossible that clinical microbiology as a career entity will cease to exist altogether.

We need to be constantly looking at what we do today, then imagining what we will potentially be doing tomorrow, and preparing for it as best we can…


“Painting Pictures”

A wound swab arrives into the microbiology laboratory..

…Because there are no clinical details we don’t know whether a Gram stain might be worthwhile.

Because there are no clinical details, we don’t know whether to add anaerobic culture or set up a yeast agar for this  swab.

Because there are no clinical details, we don’t know whether this Pseudomonas aeruginosa isolate on the plate is potentially significant…

Microbiology laboratories all over the world (including our own) receive hundreds of wound swabs every day. Often there are no clinical details or only a very cursory acknowledgement to this requirement, such as “?infection”, or “discharging wound”.

You know the story well…

So often we are left to process and report the wound swab with no idea of what is actually wrong with the patient, and what exactly we should be doing with the swab.

In my opinion clinical details involve two main elements, which overlap to a certain extent:

  • Contextualisation- What type of infection are we dealing with here? Taking the example of skin infections; Is it an impetiginous lesion, is it a boil, is it an area of cellulitis, is it a post-surgical wound, is it a burn, etc, etc? By providing clinical context we can start to work out what we are looking for and ascertain the importance of potential pathogens on the agar plates. Is there anything we should know about the patient? Are they immunocompromised? Do they have antibiotic allergies? Are they failing treatment? Is there anything unusual about the clinical presentation? Was it caused by a bite? Was there overseas travel?
  • Justification- Taking the example of skin infections again, most patients with impetigo & boils, along with many other types of uncomplicated skin infections, do not need a wound swab sent to the lab. For most skin infections, swabbing should be the exception, not the rule. So what was it about this particular patient that prompted the clinician to send a wound swab? Was it because the patient failed first line treatment? Was it because they had an associated fever? Was it because the infection was getting rapidly worse?

Here are a few examples of hypothetical clinical details that both contextualise and justify the swab.

  • “Impetiginous lesions on face getting worse despite topical anti-septic treatment. Past history of MRSA colonisation.”
  • “Area of spreading cellulitis L lower leg. Patient diabetic.”
  • “Carbuncle L buttock, patient has an anaphylactic allergy to penicillin.”
  • “Cat scratch to R hand. patient now has fever and increasing erythema. Commenced on amoxycillin-clavulanate.”

It’s not rocket science, nor does it have to be a story.

If the clinician is required to contextualise and justify the laboratory request, then the advantages are two-fold. Not only can the scientist paint a picture in their head of what is going on with the patient, and process accordingly, but also the clinician may start to think twice about why they are sending a particular sample to the laboratory in the first place…