• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Scientist finds link between antibiotics, bacterial biofilms and chronic infections

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
Scientist finds link between antibiotics, bacterial biofilms and chronic infections

July 10, 2014

scientistfin.png

The bacteria called non-typeable Haemophilus influenzae are a common cause of infection in the upper respiratory tract. By attaching to surfaces in the body the bacteria form a biofilm... Wu et al. have reported that when the bacteria encounter non-lethal amounts of specific antibiotics they are stimulated to form a bioiflm, a structure that causes chronic infection and which can be highly resistant to antibotics. Credit: Paul Webster, Ph.D.


Researchers from the University of Southern California and the Oak Crest Institute of Science have discovered the link between antibiotics and bacterial biofilm formation leading to chronic lung, sinus and ear infections. The study results, published in the current issue of PLOS ONE, illustrate how bacterial biofilms can actually thrive, rather than decrease, when given low doses of antibiotics.

"This research addresses the long standing issues surrounding chronic ear infections and why some children experience repeated ear infections even after antibiotic treatment," said Paul Webster, PhD, lead author, senior staff scientist at USC and senior faculty at the Oak Crest Institute of Science. "Once the biofilm forms, it becomes stronger with each treatment of antibiotics."

During the study, non-typeable Haemophilus influenzae (NTHi) bacteria a common pathogen of humans was exposed to non-lethal doses of ampicillin, a class of antibiotics commonly used to treat respiratory, sinus and ear infections, or other beta-lactam antibiotics. The dose of the antibiotic was not enough to kill the bacteria which allowed the bacteria to react to the antibiotic by producing glycogen, a complex sugar often used by bacteria as a food source, to produce stronger biofilms when grown in the laboratory.

Biofilms are highly structured communities of microorganisms that attach to one another and to surfaces. The microorganisms group together and form a slimy, polysaccharide cover. This layer is highly protective for the organisms within it, and when new bacteria are produced they stay within the slimy layer. With the introduction of antibiotic-produced glycogen, the biofilms have an almost endless food source that can be used once antibiotic exposure has ended...

Read more at: http://phys.org/news/2014-07-scientist-link-antibiotics-bacterial-biofilms.html#jCp

Beta- Lactam Antibiotics Stimulate Biofilm Formation in Non-Typeable Haemophilus influenzae by Up-Regulating Carbohydrate Metabolism

Abstract
Non-typeable Haemophilus influenzae (NTHi) is a common acute otitis media pathogen, with an incidence that is increased by previous antibiotic treatment.

NTHi is also an emerging causative agent of other chronic infections in humans, some linked to morbidity, and all of which impose substantial treatment costs.

In this study we explore the possibility that antibiotic exposure may stimulate biofilm formation by NTHi bacteria.

We discovered that sub-inhibitory concentrations of beta-lactam antibiotic (i.e., amounts that partially inhibit bacterial growth) stimulated the biofilm-forming ability of NTHi strains, an effect that was strain and antibiotic dependent.

When exposed to sub-inhibitory concentrations of beta-lactam antibiotics NTHi strains produced tightly packed biofilms with decreased numbers of culturable bacteria but increased biomass.

The ratio of protein per unit weight of biofilm decreased as a result of antibiotic exposure. Antibiotic-stimulated biofilms had altered ultrastructure, and genes involved in glycogen production and transporter function were up regulated in response to antibiotic exposure.

Down-regulated genes were linked to multiple metabolic processes but not those involved in stress response.

Antibiotic-stimulated biofilm bacteria were more resistant to a lethal dose (10 µg/mL) of cefuroxime.

Our results suggest that beta-lactam antibiotic exposure may act as a signaling molecule that promotes transformation into the biofilm phenotype.

Loss of viable bacteria, increase in biofilm biomass and decreased protein production coupled with a concomitant up-regulation of genes involved with glycogen production might result in a biofilm of sessile, metabolically inactive bacteria sustained by stored glycogen.

These biofilms may protect surviving bacteria from subsequent antibiotic challenges, and act as a reservoir of viable bacteria once antibiotic exposure has ended.

Received: December 1, 2013; Accepted: May 12, 2014; Published: July 9, 2014