A Form L is a bacterial variant lacking cell wall (PC) or defective PC. It is studied for the first time in Streptobacillus moniliformis, where it is observed that spontaneously produces a series of variants capable of reproducing in the form of small filterable elements lacking PC or with defective PC.
These microorganisms are called Forms L (L: comes from Lister Institute, London). These bacteria have a colonial morphology very similar to that of Mycoplasmas.
Forms L can also occur in other bacteria, provided that the synthesis of PC is altered. Training The formation of Forms L is favored by the action of Penicillin, by lytic enzymes that digest peptidoglycan or by high concentrations of salts as occurs with most Gram-positive bacteria. Some Gram-negative bacteria can be converted to Forms L in media with normal or physiological osmolarity.
Forms L are the morphological equivalent of Protoplasts and Spheroplasts, although the term Forms L is limited to organisms capable of multiplication. Some Forms L, if the inducing agent is removed, can revert to the original form (transient variant). Others are stable L shapes.
For many years it was believed that the L Forms were Mycoplasmas, but they differ from them because:
a) Some L shapes can re-own PC (unstable shapes). Mycoplasmas never have PCs.
(b) The cell membranes of the L-forms lack sterols and / or carotenoids, unlike Mycoplasmas in which these substances provide stiffness to their cell membrane.
c) Analysis of nucleic acid homology shows that these two groups have no taxonomic linkage. The similarity of their colonies and the morphological similarity is due to the absence of PC.
d) The L forms of some bacterial species require a concentration of salts in the medium that functions as an osmotic stabilizer to maintain cell integrity. Role in the pathogenesis of these bacterial variants or L-forms It is observed that in vivo there may exist the necessary components for the formation of Forms L. Some antibiotics are capable of altering the synthesis of PC; also antibodies specific to the Complement and serum lysozyme or lysosomal hydrolases that degrade the PC. These bacteria can be resistant to antibiotics that act on the PC and can remain in a state of latency by being phagocytosed without being destroyed.
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