The bacterial cell wall serves as a robust outer layer, providing the structural integrity necessary for a microbe’s survival. This structure is the basis for classifying bacteria into two broad groups: Gram-positive and Gram-negative. Gram-positive bacteria are characterized by a highly uniform and relatively thick cell wall that directly surrounds the cytoplasmic membrane. This unique architecture protects the cell and defines its interaction with chemicals, including laboratory stains and therapeutic drugs.
Core Structural Components
The defining feature of the Gram-positive cell wall is its thick, multi-layered sheet of peptidoglycan, also known as murein. This mesh-like polymer constitutes 60% to 90% of the wall’s dry weight. This broad, dense structure is typically 20 to 80 nanometers thick, substantially thicker than the layer found in Gram-negative cells. Peptidoglycan is constructed from long glycan chains of alternating N-acetylglucosamine and N-acetylmuramic acid units, which are heavily cross-linked by short peptide bridges.
Interwoven throughout this thick peptidoglycan network are specialized molecules called teichoic acids (TA). These are water-soluble polymers made of repeating units of glycerol or ribitol phosphate. Some teichoic acids are covalently bound directly to the peptidoglycan. Others, known as lipoteichoic acids (LTA), have a lipid anchor that embeds them into the underlying cytoplasmic membrane. Both forms contribute to the cell surface’s negative charge and play roles in adhesion.
Maintaining Cell Integrity
The thick, cross-linked peptidoglycan shell is necessary because it counteracts the immense internal pressure generated by osmosis. The bacterial cytoplasm contains a high concentration of solutes, causing water to continuously flow into the cell. This inward movement creates high internal osmotic pressure, known as turgor pressure, which pushes outward against the cell membrane.
Without a rigid external structure, this high turgor pressure would cause the cell membrane to rupture, resulting in cell lysis. The robust, multi-layered peptidoglycan acts like a pressurized retaining wall, resisting the outward force and preventing the cell from bursting. This mechanical strength also helps maintain the characteristic shape of the bacterium.
Why Gram Positive Bacteria Retain the Stain
The unique structural characteristics of the cell wall explain why Gram-positive bacteria retain the purple Gram stain. The procedure begins when the primary stain, crystal violet, penetrates both cell walls, staining them purple. Iodine, acting as a mordant, is then applied to form a large, insoluble crystal violet-iodine (CV-I) complex within the cell.
Next, a decolorizer, typically ethanol or acetone, is applied. In Gram-positive cells, this alcohol dehydrates the thick, dense peptidoglycan layer, causing the mesh to shrink and tighten. This tightening effectively traps the large CV-I complexes within the multi-layered wall, preventing their elution. The bacteria remain purple even after the application of a pink counterstain like safranin, which cannot penetrate the constricted cell wall.
Targeting the Wall with Antimicrobials
The cell wall’s external location and necessity for survival make it an ideal target for antibacterial therapies. Since the cell wall is unique to bacteria and absent in human cells, drugs that interfere with its synthesis can selectively kill the pathogen without harming the host. A major class of antibiotics, the beta-lactams (including penicillins and cephalosporins), directly exploits this vulnerability.
These drugs function by mimicking the structure of the peptide units involved in peptidoglycan formation. Beta-lactams irreversibly bind to and inactivate penicillin-binding proteins (PBPs). PBPs are transpeptidases responsible for cross-linking the peptidoglycan strands into a strong, rigid mesh. Inhibiting this cross-linking prevents the final assembly of the cell wall, leaving the growing bacterium with a structurally weak outer layer. The compromised wall cannot withstand the high internal turgor pressure, leading rapidly to cell lysis and death.