Memory tricks for bacteriology

Cocci: diplococci (pairs — N. meningitidis), streptococci (chains — Strep), staphylococci (clusters like grapes — Staph). Bacilli: single or chains. Spirochetes: flexible spirals (Treponema pallidum, Borrelia). Shape + Gram stain = powerful rapid ID tool.

Gram+: thick peptidoglycan, no outer membrane, retain crystal violet → purple. Examples: Staph, Strep, Enterococcus, Clostridium, Bacillus, Listeria. Gram−: thin peptidoglycan + outer membrane (LPS), lose crystal violet → counterstained pink. Examples: E. coli, Klebsiella, Pseudomonas, Neisseria, H. influenzae.

NAM and NAG alternate in glycan backbone. Transpeptidase (penicillin-binding protein/PBP) forms peptide cross-links. Beta-lactams block PBP → no cross-links → osmotic lysis. Humans lack peptidoglycan → no toxicity. Vancomycin blocks a different step (D-Ala-D-Ala binding).

Transformation: uptake of free DNA (Streptococcus pneumoniae). Transduction: bacteriophage carries genes between cells (cholera toxin, diphtheria toxin). Conjugation: direct cell-to-cell transfer via F pilus — most important for spreading R plasmids carrying multiple resistance genes.

Lipid A is the toxic component — activates macrophages and monocytes, triggers massive cytokine release (TNF-α, IL-1, IL-6). Consequences: fever, hypotension, DIC (disseminated intravascular coagulation). Heat-stable — NOT destroyed by autoclaving. Detected by Limulus amebocyte lysate (LAL) test.

Capsule surrounds the cell wall — polysaccharide (or poly-D-glutamate protein in B. anthracis). Prevents opsonization and phagocytosis. Key encapsulated pathogens: SHiNE SKiS mnemonic. Capsule vaccines (Prevnar 13, Hib) induce protective anticapsular antibodies.

Obligate aerobes: M. tuberculosis (upper lung lobes — highest O₂ in body). Obligate anaerobes: Clostridium, Bacteroides — deep wounds, abscesses, gut. Facultative anaerobes: E. coli, Staph — grow anywhere. Microaerophiles (Campylobacter, H. pylori): low O₂ preferred.

Exotoxins: proteins secreted by living bacteria. Heat-labile, highly specific (botulinum, cholera toxin ↑cAMP, diphtheria toxin blocks EF-2, tetanospasmin). Endotoxins (LPS): from Gram− cell walls, released on cell death. Heat-stable. Causes fever, shock, DIC — not a specific enzyme.

Lag: bacteria adapt to environment — no division. Log (exponential): rapid binary fission — doubling every generation time (E. coli ~20 min; M. tuberculosis ~24 hours). Stationary: nutrients depleted, growth = death rate. Death: population declines. Beta-lactams (cell wall synthesis) only work during active growth.

Bacillus anthracis (anthrax), B. cereus (food poisoning), Clostridium tetani (tetanus), C. botulinum (botulism), C. perfringens (gas gangrene), C. difficile (colitis). Survive heat, drying, UV, most disinfectants. Require autoclave (121°C, 15 min, 15 psi) to destroy.

Mycoplasma pneumoniae: no cell wall → unaffected by beta-lactams; treat with macrolides/doxycycline. Walking pneumonia in young adults. Chlamydia: obligate intracellular — cannot make own ATP. Rickettsia: obligate intracellular — transmitted by arthropods. Legionella: Gram−, but poorly staining — use silver stain; grows in water systems.

S. aureus: catalase+, coagulase+ (distinguishes from CoNS). Golden colonies on blood agar. Toxins: TSST-1 (toxic shock), exfoliatin (scalded skin), PVL (necrotizing pneumonia). MRSA: mecA gene → PBP2a has low beta-lactam affinity → resistant to ALL penicillins and cephalosporins. Treat MRSA: vancomycin, daptomycin, linezolid.