In recent years, the resistance of Gram-positive bacteria to various antibiotics is increasing

, and the mechanism of resistance is discussed.

staphylococcus: methicillin-resistant staphylococcus aureus (M R SA) is one of the most important pathogens of nosocomial infection. M R SA is resistant to all B2 lactams, macrolides, tetracyclines, lincomycin, chloramphenicol, gentamicin, etc., except for penicillin. M R SA has both inherent < P > resistance in chromosomal DNA and acquired resistance in plasmid DNA. Although its inherent resistance to < P > drugs is relatively stable, compared with acquired drug resistance, its frequency is less, and it is in a secondary position in the control of clinical drug-resistant bacteria. Some people have tracked and observed the outbreak of infection < P > in the hospital, and think that the spread of R 2 plasmid among different strains is the main reason for its < P >. The main mechanisms of drug resistance of Staphylococcus are as follows: ① Penicillinase-mediated: The resistance of Staphylococcus to penicillin G is mainly due to the production of plasmid-mediated penicillinase.

Penicillinase is attached to the surface of bacteria (belonging to extracellular enzyme), and it is resistant mainly by hydrolyzing extracellular

penicillin and reducing the intracellular drug concentration of enzyme-producing strains and adjacent non-enzyme-producing strains.

Because penicillin can induce bacteria to produce a large number of enzymes, even a large dose of penicillin

can't treat the infection caused by this kind of enzyme-producing strain. Clinically, it was also found that

some borderline drug-resistant staphylococci, whose drug resistance mechanism may be that the bacteria produce too much B2 endo

amidase (if B2 lactamase inhibitor is added, the bacteria can become sensitive

). In addition, individual strains can produce another B2 lactam to hydrolyze methicillin. ②

m ecA gene mediation: it is the main drug resistance mechanism of M R SA. Drug-resistant bacteria obtained the m ecA gene that sensitive < P > susceptible bacteria did not have, which encoded a unique PBP2a, and its affinity with B2

lactam antibiotics decreased, resulting in drug resistance. ③ Active efflux < P > System mediation: The multi-drug resistance of Staphylococcus aureus is based on active efflux. N-O-RA protein, which mediates the resistance of Staphylococcus aureus to fluoroquinolones, has been proved to be a multi-drug excretion transporter. The multi-resistance of Staphylococcus aureus to various chemical disinfectants < P > is determined by sm r, qacA, qacB and qacBC genes.

Enterococci: Vancomycin-resistant enterococci and faeces were first reported in Britain in 1988. In 1993, it was reported in the United States that vancomycin-resistant enterococci increased from < P > 1.13% in 1979 to 71.7%. Vancomycin-resistant enterococci account for 5% ~ < P > 6% in China. ① Mechanism of resistance to penicillin: Enterococcus is usually a drug-resistant strain. It is resistant to

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to avoid throat injury, and extubation should be done as soon as the condition permits. ④ Strengthen the nursing of tracheal intubation < P >. After the children return to ICU, the tracheal intubation should be firmly fixed, the distance between the incisor and the tracheal intubation should be noted, and the shift should be strictly changed to prevent the tracheal intubation from shifting or falling out. ⑤ Fully calm down. 25m g of midazolam and 5 mg of morphine < P > were added into 51m l of normal saline and injected intravenously with a micro-injection pump < P > (2 ~ 3 ml h), which was stopped 1 hours before extubation, and the sedative effect was remarkable. ⑥

Humidify the airway effectively during the catheter, so as to prevent airway mucosal damage

injury caused by dryness. ⑦ Before extubation, push dexamethasone 5m g; For children with catheter length < P >, intravenous drip of hydrocortisone 5m g.

kg 1 hour before extubation can improve the whole body condition and relieve local edema.

the drug mechanism is that enterococcus can produce a special kind of PB P5, and its affinity with penicillin is reduced, which leads to drug resistance, which is more common in Enterococcus faecium. In addition, bacteria occasionally produce a large amount of penicillinase, which causes drug resistance. ② drug resistance mechanism of aminoglycosides: the change of cell

wall permeability leads to moderate drug resistance, but it is sensitive to penicillin combined with streptomycin

, resulting in high drug resistance, and this strain is still resistant to

penicillin+aminoglycosides. ③ Mechanism of resistance to vancomycin: Vancomycin < P > is a hydrophobic compound with high molecular weight. It can combine with the carboxyl terminal d2alanyl 2d2alanine of the glycopeptide < P > precursor of pentapeptide on the cell wall of enterococcus to form a complex, which can prevent the transglycosylation and peptide conversion reactions required for the polymerization of glycopeptide < P > and inhibit the cell wall < P > biosynthesis of enterococcus. The precursor end of the cell wall peptide sugar of vancomycin-resistant enterococci changed < P > to d2alanyl 2D 2 lactate, which made vancomycin unable to bind to it, so it could not < P > inhibit the synthesis of its cell wall. ④ the mechanism of resistance to fluoroquinolones: clinical

after the application of fluoroquinolones (shaprofloxacin, levofloxacin, etc.), bacterial rotation

enzyme can rapidly mutate and produce drug resistance. Vancomycin-resistant enterococci are often < P > resistant to erythromycin, tetracycline and other antibiotics at the same time, and the resistance genes are transferred between different strains through plasmids. Recently, it has been confirmed that vancomycin resistance can be transferred from enterococcus to staphylococcus, and many scholars predict that it is only a matter of time before vancomycin-resistant Staphylococcus aureus appears.

Pneumococcus: The drug resistance mechanism of pneumococcus is the change of PB P of pneumococcus.

Only one PBP reduces the affinity, while the other PBP does not change. This PBP cannot

perform its physiological function in cell synthesis. The reason is that in the process of cell wall synthesis, all kinds of PBPs must cooperate with each other and coordinate with each other. However, only one change of PBP < P > will destroy this cooperation mode and fail to form viable cells. Therefore, the drug-resistant strains in clinical < P > beds often have several PBP changes at the same time. Different drug-resistant strains have different changes in PBP

and molecular weight, thus forming different types of PBP. After < P > in 1981s, the third-generation cephalosporin-resistant strains appeared, and the mechanism was as follows: the mutant strain produced by selective pressure of penicillin < P > and other B2 lactams, its PBP2X hair changed < P >; ② the selection of cephalosporins changed PBP2X (551 amino acids in region 551 and

PBP1a).