Variety of bacteria that fight antibiotics

Antibiotics are a great medical invention in the 20th century. They can treat various diseases caused by bacterial infections and have saved countless lives since they came out. But living things are constantly evolving, and so are bacteria. Human beings use antibiotics to kill bacteria in order to treat diseases. Cunning bacteria will do everything in their power to try to fight antibiotics. This phenomenon is bacterial resistance. Today we will take a look at the tricks that scheming bacteria will use in order to survive.

Faced with antibiotics, I was born resistant
Some members of our bacterial family are naturally resistant to specific antibiotics due to their own cell structure or functional characteristics. For example, daptomycin, which is used to treat life-threatening gram-positive bacterial infections, is powerless against gram-negative bacteria that are wordless. The reason is that the plasma membrane composition of these two types of bacteria is different. The cell membrane of gram-negative bacteria is more difficult to be destroyed by daptomycin, so it is naturally resistant. There may also be genes related to drug resistance in the conservative genes of our bacteria. When antibiotics do not appear, these genes are responsible for functions that have nothing to do with drug resistance, but when faced with antibiotics, their existence is like covering us with armor and giving us the ability to resist antibiotics.

I tried my best to change myself in order to gain resistance
If we are not born with the ability to be resistant, we will work very hard the day after tomorrow, or illusion ourselves, or pursue “usage doctrine”-capture the drug resistance genes in other bacteria to obtain drug resistance. There are 4 commonly used methods.

Method 1: Close the door tightly and strictly control the input
Some antibiotics will use the outer membrane porin to enter the bacterial cells. For this reason, we will change the permeability of our own cells and change the gene encoding the porin through mutation. For example, the porins can not be encoded correctly, their expression is inhibited, and the number of production is reduced, and the invasion of antibiotics can also be restricted by replacing the porins.

Means 2: Internal drainage and timely drainage
Sometimes, once antibiotics unfortunately enter our cells, efflux pumps can be used to actively transport them out of the cells to reduce the concentration of intracellular antibiotics. Some efflux pumps have strong recognition specificity and can only discharge a few identifiable antibiotics. Fortunately, other efflux pumps can expel a variety of structurally different substrates from the cell, and when the expression of the efflux pump increases, higher resistance to multiple antibiotics can be achieved.

Means 3: Disguise and not be recognized
When antibiotics attack us by binding to specific targets in our cells, we may mutate and “face” the antibiotic target molecules so that they will not be recognized by antibiotics. In addition to “face changing”, you can also change the shape of the target molecule-adding some “decorative” molecules to prevent the two from combining. Even if the target is unfortunately bound by antibiotics, some smart compatriots can obtain genes similar to the antibiotic target from other bacteria, and serve as substitutes to perform normal functions and continue to thrive.

Method 4: Encounter on a narrow road
Of course, our bacteria are not blindly passive, they will also launch a frontal attack on antibiotics, producing a variety of hydrolytic enzymes to inactivate them. Such enzymes are usually located on one of our secret weapons-plasmids. Plasmid is like a car, it will shuttle and spread between bacteria with hydrolase, so that everyone can get drug resistance. We will even give antibiotics a facelift, adding molecules to modify them, and then shielding their sites of action so that they lose their weapons of attacking us.

We work hard to improve resistance
The above introduced the way we fight alone with antibiotics, and let’s talk about how we attacked antibiotic groups through the interaction between different species in groups.

Hydrolase inactivation, all benefits

Resistant strains can secrete hydrolase to reduce the concentration of antibiotics in the environment, and the concentration of antibiotics drops, from red to yellow or even white

Individuals of our bacteria can inactivate antibiotics by producing hydrolytic enzymes, and when bacteria use the “hydrolysis method” in the community, not only can it escape itself, but other bacteria in the community that were originally shivering will also be affected by environmental antibiotics. The concentration drops and survives.

Hold up the biofilm “protective umbrella”
Bacteria can form a biofilm under certain conditions, allowing the entire community to gather and wrap under a membrane composed of polysaccharides and proteins, just like propping up a “protective umbrella” to keep antibiotics out.

The green resistant strains form a membrane to wrap all the sensitive strains together, keeping the antibiotics out

Inter-species communication and induction complement each other
The bacteria in the community are a big loving group, and they will help each other to improve overall resistance. We can sense various compounds (signal molecules) secreted by other compatriots, complement each other, regulate gene expression, and greatly enhance resistance to resistance.

In addition, the synergy between bacteria and antibiotics can be used at the same time! The ability to resist resistance can be strengthened as a whole!

Sensitive strains receive the signal molecules released by drug-resistant strains, and the resistance of different strains in the community increases overall, and the concentration of antibiotics decreases

Scientists find another way to block drug-resistant bacteria
In the face of bacteria with multiple drug resistance capabilities, scientists have launched a series of snipers:

1. Research and develop new antibiotics, and design an enzyme inhibitor for the necessary way for bacteria to survive, which can not only block their growth and kill the bacteria, but also activate the host immune response, which can be described as a two-pronged approach.

2. “Challenging poison with poison”, that is, following the laws of nature, using the “natural enemy” phage of bacteria to treat drug-resistant bacterial infections. Bacteriophages only invade specific bacteria. Applying them to the treatment of drug-resistant bacterial diseases can implement precise strikes without causing side effects to the human body. This is a current research hotspot.

3. To track and pursue drug-resistant bacteria, scientists use artificial intelligence and machine learning methods to conduct in-depth mining of drug-resistant data, establish a method for predicting antibiotic resistance phenotypes based on gene sequences, and realize rapid detection of bacterial drug resistance .

As teenagers, we should also contribute to the problem of bacterial resistance, raise awareness of bacterial resistance, and use antibiotics correctly and carefully with family members to avoid the spread of bacterial resistance.