Whether there is a relationship between the overuse of antibiotics and the emergence of a large numb

It's definitely related.

Every species has evolved to have the instinct to escape danger and resist threats.

To put it bluntly, most of the mechanism of action of antibiotics is aimed at the destruction of bacterial cell walls and the prevention of the synthesis of 50S large subunits and 30S small subunits of bacteria, all of which are coordinated by specific channel proteins or specific receptors on the surface of bacterial cell walls. However, the use of a large number of antibiotics stimulates the instinct of bacteria to resist threats, and through various gene modulation, the specific channel proteins of the bacterial body are turned off and the specific receptors are lost. Without a site of action, antibiotics lose their effect.

And the most terrifying thing is that bacteria of the same genus can also pass on the gene modulation function of drug resistance through sex pili and plasmids, so that those bacteria who have not been exposed to antibiotics can also develop drug resistance.

The end result is a rampant spread of drug-resistant strains.

Bacterial resistance is divided into natural drug resistance (natural variant resistance to a certain type or class, or several types of antibiotics) and drug-induced resistance!

First of all, for natural drug-resistant strains: We know that there is a balance between the natural and human flora, and the mutual influence of microorganisms will not cause them to overmultiply, so assuming that we do not use antibiotics, then the proportion of natural variant strains and normal strains will be very small, but if a large number of antibiotics are used to kill sensitive strains, and the colonies are to achieve rebalance, there will inevitably be a large number of naturally resistant variants, so the bacterial resistance rate will rise sharply.

In addition, for drug-induced drug resistance, we know that organisms are stressful, antibiotics kill bacteria generally enter the bacterial cell body and bind specifically with the bacterial enzyme to destroy the bacterial cell structure, when the antibiotic molecule enters the bacterial body, the bacteria will be rejected through various functions, such as closing the membrane pore tissue drug molecules enter; Under normal circumstances, these functions have certain limits, but when the antibiotic is used inappropriately (such as insufficient dosage, too poor quality, improper usage, etc.), the bacteria are not killed within the time they should have, resulting in the overexpression of one or several functions of the bacteria, and thus produce mutations to permanently obtain this function, which becomes drug-induced drug-resistant bacteria.

So the overuse of antibiotics is clearly the culprit for the emergence of drug-resistant strains!

No, there are variations of drug resistance in the offspring of bacteria, after the use of the drug, the strong drug resistance individuals will be retained and multiply, and their offspring will still have the mutation of drug resistance, after the drug is used again, the weak drug resistance will be eliminated, and the strong drug resistance individuals will survive and reproduce in large numbers. Such generational choices allow for the accumulation of favorable variation.

The production of passivating enzymes, drug-resistant strains act on antimicrobial drugs by synthesizing a certain passivation enzyme, causing them to lose their antibacterial activity. -Lactamases produce this enzyme in penicillin- and cephalosporin-resistant strains, which can specifically open the drug-lactam ring and completely lose its antimicrobial activity.

Aminoglycoside passivating enzymes, through the action of phosphotransferase, acetyltransferase, and adenosyltransferase, change the molecular structure of antimicrobial drugs and lose their antibacterial activity. Due to the similar structure of aminoglycoside antibiotics, there is obvious cross-resistance.

Chloramphenicol acetyltransferase, an enzyme encoded by a plasmid, inactivates chloramphenicol acetylation; The methylase Staphylococcus aureus carries a drug-resistant plasmid that methylates purines on the 23srRNA in the 50S subunit, creating resistance to erythromycin.

The mechanisms by which bacteria develop resistance to antimicrobial drugs are mainly as follows:

1. Production of passivation enzyme Drug-resistant strains act on antibacterial drugs by synthesizing a certain passivation enzyme to make them lose their antibacterial activity.

1. -lactamase.

This enzyme is produced by penicillin- and cephalosporin-resistant strains, which specifically opens the drug-lactam ring and completely loses its antimicrobial activity. It is divided into four categories;

2. Aminoglycoside passivating enzymes.

Through the action of phosphotransferase, acetyltransferase, and adenosyltransferase, the molecular structure of antimicrobial drugs is changed and the antibacterial activity is lost. Due to the similar structure of aminoglycoside antibiotics, there is obvious cross-resistance.

3. Chloramphenicol acetyltransferase This enzyme is encoded by a plasmid, which makes chloramphenicol acetylated and inactive;

4. Methylase.

Staphylococcus aureus carries a drug-resistant plasmid that methylates purines on the 50sRNA in the 23s subunit, creating resistance to erythromycin.

Second, the target position of the drug action is changed.

1. Streptomycin.

The binding site is the S12 protein on the 30S subunit, and if the configuration of the S12 protein changes, streptomycin cannot bind to it and drug resistance occurs;

2. Erythromycin.

The target site is the L4 or L12 protein of the 50S subunit, and when the ERY gene on the chromosome is mutated, the configuration of the L4 or L12 protein changes, and the resistance to erythromycin will appear;

3. The point of action of rifampicin is the gene of RNA polymerase, and when it is mutated, drug resistance is generated;

4. Penicillin.

The target site is the penicillin-binding protein (PBPS) on the cell membrane, PBPS has enzymatic activity, participates in the synthesis of the cell wall, and is the target site of -lactam antibiotics, bacteria change the structure of PBPS, which can lead to drug resistance;

5. Quinolones.

The target site is DNA gyrase, when the gene mutation causes changes in the enzyme structure to prevent quinolones from entering the target site, which can cause cross-resistance of all quinolone drugs;

6. Sulfonamide bacteria can change the target enzyme of the drug, making it not easy to be killed by antibacterial drugs.

3. Changes in cell wall permeability and active efflux mechanisms.

1. Change cell wall permeability.

Due to the barrier effect of the outer membrane of the cell wall of gram-negative bacteria, it produces a non-specific low level of resistance to some drugs with different structures, which is achieved by changing the permeability of the cell wall.

2. Active efflux mechanism can increase the level of drug resistance due to gene mutations;

For example, Pseudomonas aeruginosa is the cause of resistance to antimicrobials.

1) Poor permeability to antibiotics than other gram-negative bacteria;

2) there is an active efflux mechanism that can excrete tetracyclines, -lactam antibiotics and quinolones from the cell;

3) There were three different efflux systems of the bacterium, naib type, NFXB type and NFXC type, and there were differences in the drug resistance spectrum of each type.

4. The relationship between the use of antimicrobial drugs and bacterial resistance.

The emergence of drug-resistant strains is not directly related to the use of antimicrobials. The role of antimicrobial drugs is simply to select drug-resistant strains and eliminate susceptible strains.

a.Increases metabolic antagonists BInactivation enzyme C. is producedAlteration of bacterial cytoplasmic membrane permeability dChange the target site of the drug action eStrengthen the active outflow system.

It is a genetic mutation caused by environmental influences, and it is a heritable variant! At present, it is believed that the main reason for the emergence of drug-resistant bacteria is that when antibiotics are used for a long time, most of the susceptible strains are constantly killed, and the drug-resistant strains multiply in large numbers to replace the sensitive strains, so that the resistance rate of bacteria to the drug continues to increase!

The impact of antibiotics on bacteria belongs to the environmental impact, causing genetic mutations to have internal and external causes, which belong to external factors, antibiotic orientation changes the bacterial flora, as a result of directional selection! In turn, it is the result of bacteria adapting to the environment!

Genetic mutations. Directional selection.

Genetic mutation Compulsory 2 Chapter 7 has.

Although it is very normal to use antibiotics to treat bacterial infections, if a large number of antibiotics are used, it may bring great harm to the human body. Therefore, when taking medicine, we must use antibiotic drugs reasonably, not use them indiscriminately, and have regular medication, for those who want to take medicine, if the symptoms improve and stop taking medicine, this practice is very wrong.

It is believed that in daily life, if there is a problem of infection caused by bacteria, doctors will prescribe antibiotics to patients. But now there is a phenomenon of antibiotic drugs, there is a problem of abuse of antibiotic drugs all over the world, and even some patients, when they have symptoms of physical discomfort, they will buy antibiotic drugs by themselves. The use of antibiotics is now very common, and this large-scale use has led to a continuous increase in the number of people who have adverse reactions to drugs.

If the abuse of antibiotics may lead to allergies, if the symptoms of allergies are mild, there will be itching or urticaria, but severe cases may cause anaphylactic shock and so on, it is enough to see that if the abuse of antibiotics and allergies are caused, the consequences are very serious. Antibiotics can also cause damage to the body's organs, because antibiotics are mainly metabolized in the liver and then excreted through the kidneys, so it can be seen that antibiotics can cause great damage to the liver and kidneys. Therefore, antibiotics must be used rationally.

Can not be used casually, if the body is not the symptoms must go to the hospital to find a doctor for medical treatment, can not buy drugs in the pharmacy casually, you can use antibiotic drugs also have this, if you can take oral drugs do not need infusion, although the effect of intravenous infusion is more significant, and the response is faster, but the safety of intravenous infusion is low, adverse reactions are likely to occur.

Be sure to follow the doctor's advice, don't abuse, be sure to prescribe the right medicine, if the child is young, try not to use it, be sure to respect the doctor's advice, be aware that the damage to liver function is particularly serious, try not to use drugs in combination.

It should be used reasonably in accordance with the instructions, and you must pay attention to your physical condition, and you also need to go to the hospital for examination, otherwise it will cause certain harm to the body, and the harm is relatively high.

Answer]: The first dose effect refers to the intolerable strong tremor positive response caused by the body not yet adapting to the effect of the drug when some patients take a certain drug for the first time. For example, prazosin and other antihypertensive drugs should be used for the first time**High blood pressure can cause a sudden drop in blood pressure.

Answer: Wang's previous case]: e

This question examines the characteristics of cephalosporins. Cephalosporins belong to the -lactam class of antibiotics and contain -lactam rings, which are easily destroyed by the -lactamase produced by bacteria and lose their antimicrobial pre-trap properties. Therefore, the answer to the sign of remorse is e.

Answer] :d efflux pump is generally an enhanced expression, which increases the efflux of antimicrobial drugs, and the concentration in the bacteria decreases, resulting in drug resistance.