Category Archives: Confessions of a Microbiologist

“When the patient and the microbiology lab don’t agree”

I am signing out blood culture results. A patient has an E. coli resistant to amoxycillin clavulanate (augmentin) in both their blood culture and urine specimen. I ring up the patient’s doctor to see how the patient is doing. The patient is currently on augmentin but is nevertheless feeling much better, has been switched to oral augmentin and is ready to be discharged home. Hmm… What should I do? Should I change the antibiotic or am I just treating myself rather than the patient…?

Or the patient who develops a post-operative wound infection and they get treated empirically with flucloxacillin, to which they “respond” well, becoming afebrile and the wound discharge dries up. A swab of the wound then grows an MRSA. Should they complete their course of flucloxacillin or should they switch to an antibiotic to which the MRSA is susceptible to?

The joys of being a clinical microbiologist!

These scenarios have a few possible explanations:

  • Some patients will get better from infections, even bacteraemias and septicaemias, whatever you have used to treat them. Not all patients who contracted infections in the pre-antibiotic era succumbed to them.
  • Just because an antibiotic has tested resistant in the lab does not mean there will be no clinical response. Lots of other factors come into play here, e.g. dosage and pharmacokinetics, penetration into site of infection, host immunity, etc.
  • The isolated pathogen is not actually the cause of infection.

Clinical microbiologists are often left in a difficult situation here. Do they listen to the laboratory telling them that the isolate is resistant to an antibiotic, or do they listen to the clinician telling them that the patient is better. And what happens if they listen to the clinician and then the patient takes a turn for the worse…

It is almost a no-win situation. Is it any wonder that older, more experienced clinical microbiologists like myself end up becoming slightly insane!

These scenarios, or something similar happens to me every few weeks. It is not often discussed how to approach this situation, and it is probably glossed over somewhat in clinical microbiologist training. I was certainly never trained how to deal with it. In fact it could even be regarded as something of a taboo subject…

I think the answer lies in a case by case approach, taking into account the type of infection, the pathogenicity of the organism, the degree of resistance to the antibiotic, the reserves of the patient and how unwell they were on presentation, and a multitude of other factors that cannot possibly be learned from a textbook.

There is a lot of science in microbiology, but sometimes experience, intuition and common sense count even more than knowledge. Antimicrobial susceptibility results are important, but they are not the whole story by any stretch of the imagination.

Michael

Apologies for the paucity of posts recently, a combination of busyness and laziness!

 

“A taste of my own medicine”

I hadn’t been feeling quite right since Christmas… Upset stomach, loose bowel motions, no appetite, and worst of all I didn’t even feel like a glass of wine in the evenings! The symptoms weren’t that severe, unfortunately not even bad enough to keep me off work, but they just grumbled on and on…

After a few weeks of this, it was time to call in the help of my microbiology laboratory. And sure enough, the enzyme immunoassay for Giardia was positive on my stool sample. I was quite glad it was positive, because at least I had an answer for my symptoms, but also because I hate unnecessary laboratory testing!

I self-prescribed myself some oral metronidazole (“tut, tut…”),  at the high dose that is recommended for Giardiasis. At the higher dosage, it  is not a particularly pleasant medicine to take. It turned my urine so brown, I found myself checking my eyes for jaundice! It also made my morning coffee taste like dishwater.

I now feel much better, back to my normal incorrigible self. Looking back in retrospect, it was a classic textbook case of giardiasis. I have no idea where I got it from, and will probably never know! I don’t envy those who work in the murky waters of Public Health.

There is no better way of learning than experiencing the disease yourself. I would not recommend this however for lots of other infections. Giardiasis is probably one of the “better” ones to catch.


Giardia lamblia trophozoite

Another good way of learning about a particular infection is to get to find out its history. Giardiasis is fascinating in this respect. Giardia trophozoites were first observed in 1681 by Anthony Leeuwenhoek in his very own stool samples, on his funny looking microscopes. Thus it has to be regarded as one of the first infections to be diagnosed by a “laboratory”.

The name Giardia lamblia was in recognition of a French zoologist, Alfred Giard, and a Czech physician, Vilem Lambl,  who each contributed to the description of giardia trophozoites. Initially called Cercomonas intestinalis, it only became known as Giardia lamblia in 1915. It is also still known as Giardia intestinalis.

“Alfred Giard”

However none of these people mentioned actually made the connection between Giardia lamblia and infectious diarrhoea! In fact it wasn’t actually confirmed as a pathogen until the 1970s.

So my awareness of Giardiasis has now increased considerably, and we should all have a low threshold for testing for it in patients with chronic gastrointestinal upset, unexplained weight loss, failure to thrive, etc.

Apparently 200 million people worldwide are infected with Giardia lamblia, so I am not the only one!

Michael

“Making a difference to gonorrhoea treatment”


For several years now, the core empirical treatment for gonorrhoea has been intramuscular ceftriaxone. This wasn’t always the case, but the resistance rates for both penicillin and ciprofloxacin have crept up to levels that meant using them as empirical antibiotics was no longer a satisfactory option.

N. gonorrhoeae is particularly vulnerable to antibiotic resistance, essentially because it has no hiding place.

There are not many viable options left after ceftriaxone, so we end up using ceftriaxone on everybody with gonorrhoea or suspected gonorrhoea. And as a result we are starting to see ceftriaxone resistance…

Selection pressure…

The solution of course is to avoid using ceftriaxone on every patient for empirical treatment of gonorrhoea. 

And this is now becoming achievable with the release of a commercial rapid diagnostic PCR assay, ResistancePlus® GC ,that not only detects the presence of N. gonorrhoeae (using both OPA and PorA targets), but also looks for the mutation conferring ciprofloxacin resistance (GyrA S91 F).

In the patients who have ciprofloxacin susceptible gonorrhoea, this will allow oral ciprofloxacin to be prescribed in a timely fashion, thus allowing the selection pressure of ceftriaxone on N. gonorrhoeae to be reduced.

This is a great example of how good diagnostic stewardship can lead to good antimicrobial stewardship. Hopefully such advances in molecular diagnostics will prevent the rather ugly scenario of “untreatable gonorrhoea”

Michael