Bacterial Envelope: Gram Positive and Gram Negative Envelope


Combination of external layers that cover the bacterial cell is known as bacterial envelope. The structure of envelope is greatly different in gram-positive and gram-negative bacteria; in fact, it is this difference that defines these two major sets of bacterial species.

The bacterial envelope usually consists of cytoplasmic membrane, cell wall and slime layer. Many bacterial species are surrounded by capsule as the external layer of cellular envelope.

Gram-Positive Cell Envelope

The envelope of gram-positive bacteria is relatively simple, consisting of two to three main layers: the cytoplasmic membrane, a thick peptidoglycan layer; and sometimes capsule or slime layer.

In the cell wall of gram-positive bacteria there are many sheets of peptidoglycan (40-50 or even more) that embrace about 50% of the cell wall substance. On the contrary, gram-negative bacteria have only one or two sheets of murein that include about 5-10% of the wall contents. In addition, gram-positive microbial cells carry negatively charged teichoic acids that possess toxic activity. Precursors of teichoic acids, lipoteichoic acids, are anchored within the cell membrane of gram-positive bacteria.

Gram-Negative Cell Envelope

The cytoplasmic membrane or the inner membrane in gram-negative bacteria is surrounded by a single planar sheet of peptidoglycan. Peptidoglycan is linked to a complex layer called the outer membrane. An outermost capsule or slime layer may also be present. The space between the inner and outer membrane is termed as periplasmic space.

Gram-negative cell walls include three components that are located outside of the peptidoglycan layer: lipoprotein, and outer membrane with its external leaflet lipopolysaccharide.

Numerous lipoprotein molecules cross-link peptidoglycan and the outer membrane of gram-negative bacteria. They stabilize the joining of outer membrane with peptidoglycan layer.

Lipoprotein is the most exuberant molecule present in gram-negative cells (about 700,000 molecules per 1 cell).

The outer membrane has its inner and outer leaflets.

Inner leaflet is organized similarly to the cytoplasmic membrane. The outer leaflet is composed of lipopolysaccharide (LPS) molecules. Therefore, these leaflets are asymmetrical in structure and their activity is substantially different from standard cytoplasmic membrane.

Unlike typical biologic membranes, outer membrane demonstrates the evident capacity of exclusion of hydrophobic molecules. It is non-ordinary trait for the membrane and helps to protect microbial cells such as enterobacteria from surface-active agents (bile salts and others).

Lipid part of outer membrane is also poorly permeable for hydrophilic molecules. Nevertheless, it has a large set of channels made of special proteins porins that foster passive diffusion of hydrophilic substances with low molecular weight (ions, carbohydrates, amino acids, etc.). In the same vein, the outer membrane is a serious barrier for entry of antibiotic molecules; the latter supports enhanced antibiotic resistance of gram-negative microbial cells.

The level of permeability of the outer membrane strongly depends on species of gram-negative bacteria. For instance, outstanding antibiotic resistance of Pseudomonas aeruginosa is maintained in part by very low permeability of the outer membrane, about 100 times less than membrane permeability of E. coli.

The lipopolysaccharide or LPS of gram-negative bacteria is composed of three parts: central uniform polysaccharide core connected with lipid A on bottom side and with external variable polysaccharide chains generally known as O-antigen. Complex lipid that is called lipid A is attached to inner leaflet of outer membrane by hydrophobic interactions. It is formed within cytoplasmic membrane with next transportation towards the outer membrane. Next it becomes linked to bacterial polysaccharide core.

Lipid A is responsible for high toxicity of LPS for mammals. LPS as endotoxin of gram-negative bacteria retains its toxic activity after degradation of bacterial cell.

The polysaccharide core has very similar composition in all gram-negative bacteria that possess LPS.

Terminal polysaccharide chains, which are composed of variable oligosaccharide residues, play a role of major surface antigen of gram-negative bacteria. Taken together, they are termed as O-antigen. Bacterial antigenic specificity largely depends on oligosaccharide repeatitive units that form the external layer of hydrophilic polysaccharides covering bacterial cells.

The total number of polysaccharide antigenic variations is extremely high (eg, more than 2500 for Salmonella enterica species).

Also LPS supports proper activity of many proteins located within the outer membrane.

Bacterial cells carry special hydrolytic enzymes, or autolysins, that destroy their own peptidoglycan. They comprise peptidases, amidases, and glycosidases. Autolysins actively impact on cell growth and division. They perform degradation and lysis of bacterial cell after its death (autolysis).

Bacteria can lose the cell wall under various external influences. Gram-positive bacteria become lack of the cell wall by treatment of antibiotics, inhibiting cell wall synthesis (eg, beta-lactams) or by lysozyme action. The resulting cells deprived of the cell wall are named as protoplasts. Usually they are spherical in shape, and without capability to next cellular division.

In gram-negative bacteria the degradation of the cell wall ordinarily leads to formation of spheroplasts. Spheroplasts only partially lose their cell walls.

Another particular morphological variations of microorganisms were disignated as L-forms. They look like protoplasts, making spherical or thread-like structures without cell wall. L-forms were discovered in 1935 at the Lister Institute in Great Britain. They are actively generated under the influence of penicillins or in some cases of the division of bacterial cells.

Despite L-forms of bacteria closely resemble protoplasts, they are capable of reproducing and may reverse to initial vegetative state. As deprived of the cell wall, L-forms display increased resistance to several groups of antibiotics. Thus, they are able to extend the infectious process resulting in chronic forms of infection.