Tuesday, 22 December 2009

Christmas trees: Don't let them stay past 7th night


A small study carried out in 2007 identified fresh natural Christmas trees as a source of mold in the domestic environment.

Twelve times during a two week period, researchers measured mold counts in a room containing a live Christmas tree, beginning when the tree was brought inside and decorated. The tree was located 10 feet from a heat vent, and the indoor temperature was maintained at between 65 and 68 degrees.
For the first three days, counts remained at 800 spores per cubic meter of air, then began escalating, rising to a maximum of 5,000 spores per cubic meter by day 14, when the tree was taken down.
Airborne mold spores are known to be an irritant to people sensitised to mold spores and this could have a bad effect on the health of people suffering from severe allergy, allergic bronchopulmonary aspergillosis (ABPA) and others.

For those people perhaps an artificial tree is the best idea. If artificial Christmas trees are not acceptable then make sure the tree is removed from the room after a week at the most and ensure that the tree has been cut very recently (they are often cut more than a week in advance)!

Merry Christmas to one and all!

Thursday, 17 December 2009

Aspergilloma & biofilms

Aspergilloma are characteristically balls of fungi contained within cavities in tissue. Most commonly this is in lung tissue, often thought to be formed in pre-existing cavities as most patients seem to have a history of lung damage e.g resulting from tuberculosis.

Aspergilloma can be treated with antifungal medication but this is usually as a way to contain the fungal ball rather than to try to eradicate it - the ball can be very resistant to systemic medication and a cure often requires its complete removal.

Why is a fungal ball so difficult to penetrate? One reason is possibly that there is no circulation of blood through the ball so there is nothing to carry the drug into the ball. Another reason is becoming clearer as the latest research starts to offer clues.

Many micro-organisms are known to secrete a tough slimy substance under some growth conditions and to aggregate together to form a biofilm (see fig). Some are known to do that in response to antibiotics, as if there is some protection to be had from this structure.

It has been known for some time that Aspergillus fumigatus forms a biofilm when growing on an agar surface (Beauvais et al., 2007). This paper shows that the biofilm is produced at the surface of an aspergilloma while growing within the human patient. The fungal ball largely consists of what look like dead fungal hyphae with some viable cells at the periphery of the ball - the structure of the dead hyphae are reminiscent of fungi that have used up all available nutrients and died.

Could it be then that the ability to get an antifungal drug within the fungal ball is not as important as it would be to just penetrate the surface as most of the deeper lying cells are already dead?
Why isn't this happening already as that is where the richest blood supply exists already?
One reason is that the biofilm slime is notoriously impermeable to antifungal drugs - once we can get antifungals through that barrier we might be making headway.

Loussert et.al. show that A.fumigatus growing on an agar plate produces a different biofilm slime compared with when it is growing as an aspergilloma. When it grows within a lung as an aspergilloma it produces extra components. When it grows as an invasive aspergillosis (not as a ball) it produces a biofilm slime but the slime is different when compared with that associated with an aspergilloma.

Biofilms are well known to have a role in resistance to antifungals (d'Enfert. 2006) so perhaps they are performing the same function for aspergillomas? Careful attention is needed to assess which antifungal drugs are better at penetrating the type of biofilm secreted by an aspergilloma, and which are likely to penetrate the slime produced by an invasive aspergillosis.

Friday, 11 December 2009

Use of copper fittings to reduce microbial contamination


The environment we live in direct contact with is thought to be a major 'store' for infection. Surfaces we touch can easily provide a route for cross-infection from patient to patient in hospitals.

Examples of surfaces that can carry infection include taps, toilet flush handles, toilet seats, door handles and so on. Traditionally these are made from metal and usually from stainless steel as this has been seen as providing a very easy to clean surface which get frequent disinfection via wiping with a disinfectant.

This study carried out at Selly Oak Hospital in Birmingham, UK showed that replacing door handles, toilet seats and taps with copper fittings markedly reduced the microbial contamination of those surfaces.
The copper has been shown to be toxic to many microbes including Aspergillus and other fungi, preventing growth and killing any fungi or bacteria that land on them without the need for additional antiseptic fluids.

The implications of this finding go beyond touchable surfaces as it is known that mould growing within poorly maintained air conditioning units can be a major problem. Perhaps components like these could be made out of copper or coated in copper as a precaution?
Perhaps sink traps and other fittings used in hospitals should be made out of copper instead of plastic?

Tuesday, 1 December 2009

Antifungal drug resistance caused by agricultural use of azoles?


Azole antifungals (itraconazole, voriconazole, posaconazole) are depended on in medical clinics to treat fungal infections. They are effective but the nature of the infection often means that the patients has to take the medication for long periods of time. Improvement is usually achieved but after a while progress can slow and it is often found that a strain of the fungus has grown out which is resistant to that antifungal drug.

Fungi can develop resistance to antifungal drugs naturally over time but it is a rare event and once it happens there is no know mechanism for the fungus to transfer the resistance genes to other fungi - something that is common in bacteria. This limits the frequency of resistance arising anew in fungi.

Where does the resistance come from? For resistant strains to multiply the fungus must come into contact with antifungals and thus encourage resistant strains grow out. Apart from in a patient undergoing antifungal treatment where does that happen? A recent paper (Science 326:1173 (2009)) strongly suggests that one place that this happens is when crops are treated with antifungal azoles in order to prevent fungal spoilage. Antifungal azoles are known to be used on a very large scale on orchards, vineyards and some grain crops in europe so this would be a good place for resistance to emerge.

Spores from strains of Aspergillus that are resistant to some antifungals have been found close to Radboud University Nijmegen Medical Centre in the Netherlands suggesting that they could be breathed in by patients. The type of mutation found in fungi that infected patients was also found in most of the fungi isolated outside the hospital in soils.  This adds up to a strong possibility that those patients breathed in fungi that were already resistant to the antifungals used in the clinic when they were breathed in. 94% of the clinical isolates at Nijmegen and 69% at other Dutch centres carried the same mutation, suggesting a single event or single cause of the resistance found.

The situation in Radboud University Nijmegen Medical Centre seems to be different to that in the National Aspergillosis Centre Manchester, UK as in Manchester there was a range of different mutations in strains which suggested that there were several different original events that caused those mutations.

The true situation is still not completely clear and the results found in the Netherlands might not be representative of the pattern of resistance everywhere but as the original paper states, this is enough to require us to think carefully about allowing the large scale use of azoles in agriculture.

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