battlefield Superbug fact or fiction?

there is always a risk of spreading disease from one hospital to another in the same town, let alone ones in a different country.

MRSA in Iraq is the same as MRSA in UK - might be a screen, but I havent heard this one.

We casevaced a badly burnt civi from Shabbi Log base on Telic 3, to a burns unit in UK. Considering he'd been cared for in a tented hospital for three weeks, the burns unit was suprised that his wounds were not infected.

 

That's just civilian ignorance. As we know, it doesn't matter what's overhead - it's the way you treat the patient and the wound.

Florence Nightengale proved that in the Crimea.

FF.

 

Do we know its MRSA? Possible but more likely to be something else. Certainly saw MRSA in Iraqi civilian patients on Telic 1, but also on Telic 1 a couple of civilian burns patients were evaced to UK and took with them multi antibiotic resistant Acinetobacter baumanii which led to spread within the admitting burns unit (see link below). This is not a new problem, dealt with something similar in a civi neurosurgical ICU some years in a patient brought back from the eastern Med. Also on Telic 1 saw patients with multi-resistant Klebsiella spp (three or four on one ward), source may have been an Iraqi civi hospital but we couldn't be certain.

http://www.hpa.org.uk/cdr/PDFfiles/2003/cdr4303.pdf

 

just to fling another option in the air but could it be ESBL E-Coli?

 

Interested to know the view on the acinetobacter front - sticky bugger that one, seemingly worse than our old friend Mr S.A. - also reassuring to hear that our mil patients are relatively 'bug free' - I always wondered if our deployment infection control measures seemed to 'work' simply because we did not routinely culture our patients like they do in the NHS! (What you don't know does not hurt you......!) (Did I spell routinely right - no spell check on this thing..(or is there - the truth is out there)(Is that you mother...)

 

I imagine it's Acinetobacter as it's present in the soil all over the Middle East.

It's an absolute sod to get rid off as it survives really well in dust, so will stick to any surface.

Most of it is multi-drug resistant.

It has a predilection for fluid-rich environments which is why I have a patient on ITU with Acinetobacter meningitis.

 

I know from bitter experience its survives well almost anywhere. Yes its a Gram negative and therefore should like moist areas but it doesn't seem to need dust and survives drying very well indeed. In reality it behaves more like a Gram positive. It is intrinsically multi-resistant and detegent and warm water doesn't seem to get rid of it, 1000ppm sodium hypochlorite will destroy it in the environment though. For info at:-

http://www.hpa.org.uk/infections/topics_az/acinetobacter_b/gen_info.htm

 

I'd never heard that before. Does being Gm -ve mean the bacteria thrives more in moist conditions? How? I thought all bacteria (perhaps excepting a few special ones) thrived in moist conditions. Gram staining notwithstanding. Am I wrong? What does the Gram staining matter?

Another question - if the Acinetobacter is wild-type (being in the soil, etc.), how is it become multi-dug resistant? Is this innate resistance? If not, where's it originated from? Even in the antibiotic-washed UK, wild-type Staph aureus is not particularly resistant. Neither is E. coli or TB (excepting in special environments).

This is not a challenge (I am not a microbiologist). Just for my education.

FF.

 

All bacteria need moisture, its a question of degree. As a general rule Gram negatives (Klebsiella, Proteus, Psuedomonas, E.coli etc) do not survive well in a dry environment prefering an abundance of moisture. Acinetobacter is a Gram -ve which thinks its a Gram +ve , i.e. can survive in relatively dry conditions, for example the skin or on a visibly clean and dry environmental surface.
Gram staining seems to be done less and less these days. Still useful in suspected sepsis (CSF, blood etc) as a guide to what might be causing the infection and what to treat it with.
Acinetobacter are intrinsically antibiotic resistant although once in a setting where antibiotics are heavily used (burns unit, ICU etc) they could easily become more resistant. For more info try this link

http://en.wikipedia.org/wiki/Gram_stain

 

That makes sense. I suppose a glycoproteinacous coat would allow a bacterium to survive in harsher conditions.

FF.

P.s., We use Gram staining all the time in urology, albeit in uro-sepsis, but it is easy to get any time in infected urine and aids "semi-blind" antibiotic treatment.

 

I've just learnt more about battlefied infections and infection control in one thread than in the last six years in the AMS!

Not that I mind the usual banter on this forum, but it's great as a non-clinician to get some education here, too.

IF

 

I always though that, couldnt say it, but I always thought that.

 

This story has been going on for a while check the link below:

Sunday Times

The article suggests the CO is Acinetobacter baumannii and even gets a MOD spokesperson to comment on the Superbug problem in returning troops.

Regards.

 

Aarrh - Ye know toooooooo much! (maybe it is and maybe it's not...) Jeeves - pass my heroin x