In the clinic and on the website, I often encounter patients who ask questions about bacterial L-types. In patients with urinary tract infections, sometimes repeated negative plain bacterial cultures may be recommended by the doctor for a hypertonic culture to clarify the presence or absence of L-type bacteria. So what is L-type bacteria? The following is an introduction to L-type bacteria, which I hope will be helpful. The creation of type L bacteria and the origin of the name Type L bacteria, in fact, is also bacteria, but, is a kind of bacteria with different morphology from ordinary bacteria, this kind of bacteria due to some effects, the most common effect is the induction of antibiotics, and from the original ordinary bacteria into the cell wall mutilated bacteria. Because this variant was discovered in the Lister Institute of Medical Research (Lister is a famous microbiologist in England), it was named after its first letter, so it is called L bacteria. What is the difference between L-type bacteria and common bacteria? After the change of bacterial morphology, its biological characteristics also changed: (1) hypertonicity: only in the hypertonic environment can grow, not in the ordinary medium; because it has lost the strong wall, only a layer of cytoplasmic membrane, so in the non-hyperosmotic environment, the bacterium will quickly lyse and die; such as L-type bacteria in distilled water 3min will be will be lysed, 2h after disappearing, in 0.1% ~ 0.2% sodium chloride solution, after 15min, bacteria reduced by 90%, while in 2% ~ 15% sodium chloride solution, the bacterium is no change; Ancestrality: This is an important biological property; when the inhibition, destruction of the bacterium wall factors removed, L bacteria and restore the integrity of the cell wall, back to the parental strain, and have the characteristics of the parental strain, which This is the ancestrality. Ancestrality can be divided into the following two kinds, namely ① variable L bacteria: when the inhibition, destruction of the cell wall factors removed quickly back to the parental strain of L bacteria is called; clinical isolation of this type; usually just formed or light cell wall defects of L bacteria is easier to ancestral, the cell wall is completely absent, it is not easy to ancestral; ② stable L bacteria: when the inhibition, destruction of the cell wall factors removed, after many generations still maintain the characteristics of L bacteria is called; ② stable L bacteria: when the inhibition, destruction of the cell wall factors removed, after many generations still maintain the characteristics of L bacteria is called; ② stable L bacteria: when the inhibition, destruction of the cell wall factors removed, after many generations still maintain the characteristics of L bacteria is called. L bacteria are called L bacteria; strictly speaking, only this type of bacteria can be called L bacteria; weak antigenicity: the main antigen of bacteria in the cell wall and its surface appendages, once the wall is missing, it will lead to a great reduction in antigenicity, or even disappear; L bacteria can survive in the host’s body and resist the host’s defense mechanism; it has antigenicity, but weak antigenicity, so it can escape the host immune system self-defense This is the reason for the longevity of L. aeruginosa in the host. The pathogenicity of L. aeruginosa is the same as that of the common bacteria, which can cause infections in various parts of the human body and cause recurrent episodes of chronic disease. However, L-type bacteria can only cause disease if it adheres to human cells, and although its adhesion is weak, only 1/10 of that of the parental strain, the adhesion time is very long. Usually the parental strain contains polysaccharide substances in the wall, which can act as chemotaxis, so the peripheral leukocytes will increase after infection, but L-type bacteria because there is no wall, that is, there is no polysaccharide substances, so the peripheral leukocytes are still within the normal range after infection, which often leads to misdiagnosis and is worth noting; but neutrophils can be seen in the toxic particles, and the bone marrow can show signs of infection. This type of bacteria is widely present. Anyone with prolonged fever and no bacterial growth in common culture, so that the diagnosis is unknown, must think of two possibilities: one is the infection of L bacteria; the other is the infection of anaerobic bacteria. In this regard, both cultures must be done to avoid misdiagnosis or missed diagnosis. The virulence of the bacterium is lower than the parental strain, so there is often no acute process, and the strain is preserved in the host for a long time, making the patient a persistent source of infection. The selection of antimicrobial drugs for type I infections After the parental strain becomes an L strain, its drug sensitivity also changes greatly, so we have to choose antimicrobial drugs for the characteristics of L bacteria. Because the bacterial wall is absent or mutilated, it cannot take drugs that act on the bacterial wall, such as penicillins and cephalosporins, but the latter are often effective in clinical application, probably because the bacterial wall is not completely defective. These antibiotics can only destroy their parental strains, but they are not effective for those who have lost their walls and become L strains, and will continue to induce L strains, resulting in prolonged illness; this can be selected for antibiotics that are effective for both the wall and the plasma membrane, such as vancomycin, chloramphenicol and neomycin; antibiotics that act on the plasma membrane and interfere with protein synthesis can be selected, such as amikacin, gentamicin, tobramycin and small nootropic antibiotics. Aminoglycoside antibacterial drugs, such as amikacin, gentamicin, tobramycin, and minor norfloxacin, which have a stronger killing effect on L strains than on parental strains, especially the former is stable to most aminoglycoside blunting enzymes and is less likely to produce resistance despite the high frequency of clinical use; macrolides and tetracyclines, such as erythromycin, roxithromycin, spiramycin, and doxorubicin and memantine, respectively, can also be selected, and all of these antibiotics can inhibit bacterial protein The formation of quinolones, such as ofloxacin, levofloxacin, etc. are to inhibit the nucleic acid nucleation of the pathogenic bacteria, so as to play a bactericidal effect; should not choose to act on the plasma membrane of the phospholipids of antibacterial drugs, such as polymyxin B, because the wall and plasma membrane of G + bacteria are lack of phospholipids, so these antibiotics are ineffective against L strains and their parental strains. The drug sensitivity of L bacteria is often different from the parental strains, it can produce resistance, the original type and dose of antibacterial drugs will not work, you must change the drug, increase the dose to be effective; β-lactam-induced L bacteria, its pathogenicity and its virulence are weaker, so that the symptoms are more moderate / or some relief, but after the drug is stopped, L bacteria and return to the parental strains, the virulence increased, the symptoms are manifested again, this is This is called “rebound”; therefore, treatment must be long-term, especially for sepsis. After the parental bacterial resistant strains are transformed into L strains, the resistant R plasmids on the cell wall are usually lost due to wall defects, and the resistance cannot be restored after reversion; however, whether the R plasmids are lost or not depends on the degree of wall loss, and when the DNA encoding the resistance still exists in combination, the resistance will continue to exist. Therefore, usually when applying antibiotics, it is necessary to use a combination of therapies, combined administration, relatively long courses of treatment and large doses.