In the last blog, Biofilms: Establishing the colony.. we saw how the biofilm is formed. In this and the next blogs, we shall see the connection of the biofilm with the health problems.

Biofilms: The Troublemaker

Biofilms are real troublemakers to humans life in many ways. Different industries like wineries, diary, seafood based industries are all affected by the biofilms (Read more here). But the major concern is their association with various human diseases and ailments like bacterial endocarditis, cystic fibrosis, infectious kidney stones, and many more. Their success in causing health problems can be attributed to their ability to dodge the antibiotics and the immune system.

Let’s see how the biofilms outplay these two very important rescuers of human ailments, with today’s post focussing on the ways bacteria in biofilm escape the attack of the antibiotics.

1. Biofilms and antibiotic resistance.

The bacteria as a community within the biofilm gains antibiotic resistance. It’s more like “divided we fall united we stand.” The bacteria maybe susceptible to a certain antibiotic in its planktonic mode, but become resistant when a part of the biofilm. The extracellular polymeric substances (EPS) which is composed of polysaccharides, proteins, nucleic acids resists the diffusion of the antibiotics within the biofilm. These molecules are charged and hold the antibiotic molecule limiting their movement into the matrix. Hence the antibiotic may not reach the bacteria at all, specially in the interiors of the biofilm.

Some biofilms are heterogenous and contain different bacterial sps. This heterogeneity, makes the choice of antibiotic difficult. As a single antibiotic would not be effective against all the different types of bacteria a biofilm may be containing.

E.g. Aminoglycosides is effective against aerobes but not anaerobes.

Biofilms are also heterogenous with respect to the environment, there are micro-environments which differ in the pH, concentration of oxygen, and so on. The lack of certain nutrients causes the bacterial cells to either become dormant or persistent. Dormant cells are the ones in which the metabolic activities have stopped to conserve energy and persister cells have slow growth rate and can escape being killed by antibiotics. These subpopulation of cells become resistant to antibiotics and allows the biofilm to flourish again once the favourable conditions return. That is these cells make the biofilm infection recalcitrant and hence difficult to treat.

Another phenomenon which takes place within canopy of the extracellular matrix is horizontal gene transfer via conjugation. The antibiotic resistance genes also gets transferred during this process, which allows the bacteria to thrive within the biofilm, even in the presence of the antibiotic.

E.g. In cystic fibrosis, overproduction of cephalosporinase AmpC enzymes confers P. aeruginosa resistance to antibiotics.

Some proteins called efflux pumps and membrane channels (porins) also play a role in the antibiotic resistance. The efflux pumps expels nearly all class of antibiotics from the cell. Role of efflux pump in biofilm resistance has been witnessed in several microorganisms like Escherichia coli, Pseudomonas aeruginosa, Candida albicans and so on

Opposite to efflux pumps, certain transmembrane channels called the porins (more here) lets in certain hydrophobic molecules, including some antibiotics, into the cell. Any mutation in the genes encoding these proteins hinders the entry of the antibiotics into the cell, and hence endows the cell with resistance to antibiotics. Such mutated porin proteins are common features of biofilms.

Eg. OprD, a porin present in P. aeruginosa transports basic amino acids into the cells. The non-functional OprD is associated to resistance to imipenem and carbapenem.

2. Biofilms and Immune System.

The immune system also, like antibiotics, are dodged by bacteria in biofilms. The immune cells need to recognize the different surface molecules of the bacterial cell. These structures are concealed by the components of the EPS matrix and other mechanisms, which shall be discussed in the next post.

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Please read other posts by The Biotech Notes:

Monoclonal Antibody: HATs off

Let’s go FISH’ ing

Clinical Trials (P-1).