An antibiotic is designed to target a molecule inside a bacterium, a molecule related and critical to proliferation or survival.
In presence of an antibiotic, bacterial growth or proliferation is inhibited. Their numbers decrease and so a bacterial infection is controlled.
Yet, not all bacteria die.
Some resist and manage to survive. Some bacterial endure while in the presence of the antibiotic and show resilience. Over time the resilient bacteria grow in numbers and overtake space and medium their lost companions had freed up.
Studies have revealed many mechanisms that can turn a bacterium resistant to the effect of antibiotics. It helps me remember them by grouping them in two.
Group #1 mechanisms: The battle at the gate
The first frontier bacteria battle is its entry into the cell. For the antibiotic to work it must get inside the cell and bind to its target, so bacteria fight hard defending their boundaries prohibiting the antibiotic to enter.
What do bacteria do at this stage in simple words?
· Build new, stronger walls
· Close the entry gates
· Grab them and return them back out
· Secrete inactivating enzymes
Group #2 mechanisms: The battle within
For the antibiotic to work it must bind to its target, so bacteria also fight against this interaction. How?
· They produce abundant amounts of the target molecule. In this case, a portion of the target molecule is inevitably bounded by the antibiotic, nevertheless, another portion remains free from the antibiotic and is available to continue fulfilling its role related to survival.
· They modify the part of the target molecule that binds to the antibiotic. The modification is done in such a way that the target molecule is no longer recognized by the antibiotic, so it is free to function as expected inside the cell.
· They invent a new molecule, a new process to substitute for the activity blocked by the antibiotic (by-pass mechanism).