BAKTEERIYHDYSKUNNAT KROONISTEN INFEKTIOIDEN TAUSTALLA?

[Bb]

Lähettäjä: Soijuv Lähetetty: 24.5.2004 10:27

Artikkelin mukaan bakteerit kommunikoivat keskenään ja muodostavat yhdyskuntia (biofilms), jotka ovat antibiooteille erittäin vastustuskykyisiä. Tällaiset bakteeriyhdyskunnat kykenevät aiheuttamaan eri puolilla elimistöä vakavia infektioita. Joidenkin arvioiden mukaan ne saattavat olla syypäinä suurimpaan osaan kroonisista bakteerien aiheuttamista infektioista.

Normaalit antibiootit kuten penisilliinit ja erytromysiini eivät niihin juurikaan tehoa, sillä ne on suunniteltu tuhoamaan nopeasti kasvavia ja jakautuvia bakteereita. Bakteerit kykenivät muodostamaan biofilmin fmtC -geenin avulla. Tutkijat ovat löytäneet useita kemiallisia yhdisteitä joilla tämän geenin toiminta kyetään estämään. Tällöin mikrobin herkkyys antibiooteille saadaan mahdollisesti palautettua.


Biofilms - Intricate bacterial colonies

http://www.msnbc.com/news/858649.asp?0cv=CB10

Now scientists have discovered that bacteria talk to one another constantly, often cooperating in the construction of intricate communities, known as biofilms, that allow them to thrive in ways they never could as single-celled individuals.

Unfortunately, these bustling bacterial cities often create debilitating or life-threatening infections inside the human body. But scientists hope that disrupting bacterial communications might offer a new way of treating these infections. Costerton estimated that biofilms account for the majority of chronic bacterial infections.

Microbiologists first realized the importance of biofilms about a decade ago, when Costerton and several colleagues began using a new kind of microscope to look at slimy masses of bacteria such as Pseudomonas aeruginosa, which clogs the lungs of cystic fibrosis patients. In 1991, the scientists demonstrated that they were not just undifferentiated clumps, but intricate structures threaded with pores and channels for transporting nutrients in and waste out. The bacteria were embedded in a sticky protective goo that stuck them to one another and just about anything else that might be around.

Their layered structure makes biofilms hard to kill with traditional antibiotics, which often cannot penetrate beyond the outermost suburbs of a bacterial settlement.

More importantly, current drugs such as penicillin and erythromycin were designed to work against rapidly growing and dividing cells. But most of the bacteria in biofilms are hunkered down in a semi-dormant state, making them much harder to kill with existing drugs. Recent studies also show that bacteria also synchronize their behavior when they create a biofilm, simultaneously turning on different genes than they use while floating around. And many of those genes make them even more resistant to traditional antibiotics.

"The entire conglomerate changes its gene expression at once," Bassler said. "Hundreds of genes switch from on to off or off to on."

In September, Microbia scientists announced that Staphylococcus aureus - a cause of food poisoning, pneumonia,toxic shock syndrome and many other infections - bolsters itself against antibiotics when it forms a biofilm by turning on a gene called fmtC. When the researchers disabled the fmtC gene by mutating the bacteria, the microbes' sensitivity to antibiotics returned.

That experiment suggests a drug that blocks the effects of fmtC might prove effective against biofilm infections. Henderson said Microbia has already found a number of chemical compounds that appear to do just that.