Bacterial Structure & Function MCQ

Bacterial structure rewards a small map: how the cell wall is built (which the Gram stain reveals), what sits on the surface (capsule, pili, flagella), how some species armor themselves as spores, what oxygen they tolerate, and how they trade genes (including resistance). Each of these has a dental face. The cell wall is why penicillin works and why salivary lysozyme matters; the Gram-negative outer membrane carries the endotoxin that drives the inflammation of a necrotic pulp; spores are the reason instruments are autoclaved rather than wiped; and horizontal gene transfer is why careless antibiotic use is harmful.

Gram Stain and the Cell Wall

• The Gram stain sorts bacteria by cell wall structure. Gram-positive cells have a thick peptidoglycan layer that traps the crystal violet and stains purple; Gram-negative cells have thin peptidoglycan and decolorize, then take the pink safranin counterstain.
• Gram-negative bacteria add an outer membrane whose outer leaflet is lipopolysaccharide (LPS). The lipid A portion of LPS is endotoxin, which triggers fever, inflammation, and, in large amounts, septic shock.
• Gram-positive walls carry teichoic and lipoteichoic acids, which contribute to attachment and to the inflammatory response.
• Peptidoglycan is a mesh of sugar chains cross-linked by short peptides. Penicillins and cephalosporins block the cross-linking (transpeptidase) step, and lysozyme in saliva and tears cleaves the sugar backbone directly.

Surface Structures: Capsule, Pili, and Flagella

• The capsule is a usually polysaccharide layer outside the wall. It is antiphagocytic, hiding the cell from neutrophils and macrophages, and is a major virulence factor for encapsulated organisms.
• Pili (fimbriae) are short surface fibers used for adhesion, the first step in colonizing teeth and mucosa. The longer sex pilus mediates conjugation, the direct transfer of DNA between bacteria.
• Flagella provide motility, letting some bacteria swim toward nutrients; the spirochetes of periodontitis move with internal (axial) filaments.
• A loose slime layer or glycocalyx lets bacteria stick together and to surfaces, the foundation of biofilm such as dental plaque.

Endospores and Sterilization

• A few Gram-positive genera, notably Bacillus and Clostridium, form endospores: dormant, metabolically inactive cells with a tough keratin-like coat.
• Spores resist heat, drying, ultraviolet light, and most chemical disinfectants, surviving conditions that kill ordinary (vegetative) cells.
• Because spores survive surface wiping and many liquid disinfectants, true sterilization of dental instruments requires the autoclave (steam under pressure, typically 121 C).
• Spore-forming biological indicators (spore strips) are the standard way to confirm that a sterilizer is actually killing the most resistant organisms.

Oxygen Requirements and Growth

• Obligate aerobes need oxygen to grow (for example, Mycobacterium tuberculosis and Pseudomonas). Obligate anaerobes are poisoned by oxygen and grow only where it is absent.
• Facultative anaerobes, such as most streptococci and E. coli, use oxygen when present but can ferment without it, which is why they thrive in many environments including the mouth.
• Aerotolerant organisms ignore oxygen and ferment regardless; microaerophiles need only a little oxygen.
• Anaerobes are damaged by oxygen because they lack protective enzymes (catalase, superoxide dismutase) that detoxify the reactive oxygen species aerobic metabolism creates.

Bacterial Genetics and How Resistance Spreads

• Bacteria carry their main genome as a single circular chromosome, plus small extrachromosomal plasmids. Plasmids often carry antibiotic-resistance genes (R factors) and can copy themselves independently.
• Horizontal gene transfer spreads genes between cells three ways: transformation (uptake of naked DNA from the environment), transduction (DNA carried by a bacteriophage), and conjugation (direct transfer through a sex pilus, often of a plasmid).
• Resistance also arises by spontaneous mutation, then antibiotic exposure selects the resistant survivors, letting them outgrow the rest.
• A common resistance mechanism against penicillins is the enzyme beta-lactamase (penicillinase), which breaks the drug's beta-lactam ring; pairing amoxicillin with clavulanic acid blocks that enzyme.