Author: Kristīne Maķe
Nowadays, most people know what bacterial infections are and how to treat them “correctly”. Anyone working in the medical field is aware of the mechanisms bacteria can use to become our body’s worst enemy. Even for people outside of the medical world, the word “infection” is not alien. Thanks to the technological advances of the 21st century, any person can easily search for and find the reason for an illness for self-educational purposes. The causes of sickness are not a mystery or a conspiracy of pharmaceutical companies – each illness has its own certain, well-defined reason for being that a person can even sometimes control.
Wait, did I just read that correctly – control it?
Exactly, control it! All thanks to our famous friends and modern panacea – antibacterials, a.k.a. antibiotics! Their use has become so wide-spread that one cannot remember the first moment we started to look for the “antibacterial effect” note on ordinary hand soaps. Long story short, the fight against the main threat of well-being in humans is gaining momentum.
However, bacteria, despite making up one of the lowest and least complex levels in evolutionary development, are not as foolish as one would think. Over time, microbiology as a science has evolved by thoroughly exploring how populations of plankton, a type of free-living bacteria, expand and grow. This can be seen in the rapid spread of other bacteria throughout the human organism, reaching many organs. Because of this, scientists have acquired a better understanding of the basics of bacterial development, as well as identified vital processes that take place within the bacteria. Any medical student can remember the moment they first tried to understand how the PDP (penicillin-binding protein, the protein which is used by the penicillin antibiotic for attaching to the bacteria) can give germs the ability to become resistant to antibiotics.
Bacteria don’t always move freely through the human body. Scientists have observed that bacterial migration is a forced condition, and that microbes try to spend as little time as possible in a “floating” state.
In around 99% of cases, microbes prefer not to move anywhere and colonize some surface;  for example, in the human body most bacteria choose heart valves, the urinary tract or the bladder.
The fastest bacteria cover artificial surfaces – implants, tracheal tubes, etc.  This kind of lifestyle is called sedentary or seated. Having reached this point, the reader may assume that, when establishing their place of residence, bacteria colonize a surface as a thin layer, in a similar way to dust. However, microorganisms have developed different ways to perform this task. How, exactly?
Once they have chosen to adopt a sedentary form, different bacteria merge into a single population to form yeast-like or colonial compositions. Then, in order to protect themselves from the attacks of the immune system of the human body, a thick and durable protective substance, called extracellular polymeric substance, is produced around it.  This shell is composed of many different types of molecules, such as proteins (around 2%, including enzymes), DNA (less than 1%), polysaccharides (1-2%) and RNA (less than 1%). Most of the shell is made up of water (around 97%).  The combination of these bacteria, along with the produced polymeric substance around them, is called a microbial biofilm.
When one investigates how these bacteria can all live under one roof, one discovers a special and complex social behavior – a sense of quorum. This social behavior begins when a megalopolis of different species occurs, i.e. when the density of bacteria under one biofilm exceeds a critical value.  Because of the sense of a quorum, one bacterial species is capable of dominating over all the other species present in the biofilm, using special signals.  This is needed to create a single bacterial cluster with signal molecules, whose aim is to achieve the same goals. For example, a microbial biofilm is capable of developing specific virulence factors (i.e., factors that ensure the ability of bacteria to infect another organism) or to develop insusceptibility (i.e., resistance) to antibiotics. 
So how does antibiotic resistance develop?
Resistance to antibiotics is in this case a phenomenon of bacterial properties. Biofilms contain bacteria species that exhibit resistance that is three times stronger than in planktonic bacteria. When the antibiotic destroys the upper layer of the biofilm, a small population of surviving bacteria can very quickly restore the number of microorganisms, also increasing the overall resistance of the biofilm in the process. 
In addition, there are additional factors that determine the development of resistance in a given biofilm:
- The microbial biofilm substance has the ability to reduce antibiotic penetration into the biofilm itself. This is done in two ways: by physically slowing the diffusion of antibiotics through the matrix, and by reaction of the matrix components with chemical antibiotic components. In other words, there are many antidotes capable of inactivating antibiotics within the biofilm. [3, 5]
- Bacteria present in biofilms are characterized by slow growth rates. As a result, ampicillin, one of the most commonly used antibiotics in clinical practice, is capable of destroying bacteria located on the periphery of the biofilm, while bacteria inside the biofilm survive. This is because bacteria growing deep within the biofilm do not get enough nutrients and oxygen, so their growth rate is decreased. Such slow-growing bacteria have reduced metabolic activity, which results in reduced susceptibility to antibiotics. [3, 5]
In conclusion, modern knowledge about microbial biofilms requires newer diagnostic methods and treatments that will help to detect and destroy the bacteria in a timely manner. It goes without saying that the most effective treatment is to understand not only antibiotic resistance mechanisms, but also the mechanisms by which a bacteria can attach to a surface and is able to organize a well-ordered colony of millions of other microorganisms around it.
Article sources: Garrett, T. R. 2008. Bacterial adhesion and biofilms on surfaces. Progress in Natural Science. 18 (9): 1049-1056.  Kazakova J., Maķe K., The bacteriological colonisation of intubation tubes in intensive care unit. Rīga Stradiņš University International Student Conference 2018. 50 (abstr).  Pace J. L., Rupp M. E., Finch R. G. Biofilms, Infection, and Antimicrobial Therapy. Miami: Taylor & Francis Group, 2006. 520 p.  Jamal M., Tasneem U., Hussain T., Andleeb S., Bacterial Biofilm: Its Composition, Formation and Role in Human Infections.  Vanzieleghem, T. 2015. Les Biofilms Bactériens en Milieu Hospitalier: Des Réservoirs de Pathogènes? HYGIÈNES. 23 (3): 109-116.  Gostev, V., Sidorenko, S. 2010. Bacterial biofilms and infections. Journal Infectology. 2 (3): 4-15. (In Russ.)
Cover picture: http://nationswell.com/bacteria-oil-eating-halomonas-illinois-basin/
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