14.2 Bacteria
Key Takeaways
- Gram-positive organisms have a thick peptidoglycan wall with teichoic acids and no outer membrane; Gram-negative organisms have a thin wall plus an outer membrane whose lipid A is endotoxin.
- Endotoxin (LPS lipid A) is heat-stable, encoded on the chromosome, and triggers TNF/IL-1 shock; exotoxins are proteins, often plasmid- or phage-encoded, and are immunogenic enough to make toxoids.
- Horizontal gene transfer is transformation (naked DNA), transduction (phage), or conjugation (pilus/plasmid). MRSA is altered PBP2a (mecA); many β-lactamases destroy the ring instead.
- Staphylococcus aureus is catalase-positive and coagulase-positive and is the classic agent of acute osteomyelitis and septic discitis; Mycobacterium tuberculosis is acid-fast and seeds vertebral bodies as Pott disease.
- Capsules of S. pneumoniae, H. influenzae type b, and N. meningitidis resist phagocytosis until opsonized; asplenic hosts and unvaccinated infants are the high-risk reservoirs for those bacteremias.
Bacteria as 18% of the Microbiology domain
Quick Answer: Crystal violet–iodine–alcohol–safranin. Purple = thick peptidoglycan Gram-positive; pink = outer-membrane Gram-negative with LPS. Spores (dipicolinate) survive boiling; capsules antiphagocytic; acid-fast mycolic acids. Exotoxins are proteins; endotoxin is lipid A. Conjugation moves plasmids. Match organism to Gram morphology, key toxin, and reservoir.
Envelope, stain, spore, and special walls
A bacterium is a prokaryote: no nucleus, 70S ribosomes (30S + 50S), peptidoglycan (except Mycoplasma), and a nucleoid. Peptidoglycan is repeating N-acetylglucosamine–N-acetylmuramic acid chains cross-linked by peptides. Transpeptidases (penicillin-binding proteins) make those cross-links; β-lactams bind them.
Gram stain sequence: (1) crystal violet, (2) iodine mordant (forms a complex in the wall), (3) alcohol/acetone decolorizer, (4) safranin counterstain. Gram-positive cells retain the violet complex. Gram-negative cells lose it and take safranin. Never say “Gram-positive means pathogenic.”
| Feature | Gram-positive | Gram-negative |
|---|---|---|
| Peptidoglycan | Thick, multilayer | Thin |
| Outer membrane | Absent | Present; contains LPS |
| Periplasm | Minimal | Prominent (β-lactamases live here) |
| Teichoic / lipoteichoic acids | Present | Absent |
| Endotoxin | No LPS (lipoteichoic acids can inflame, but lipid A is the exam endotoxin) | Lipid A of LPS |
| Lysozyme / penicillin | Generally more vulnerable | Outer membrane slows many drugs |
LPS has three parts: O antigen (serologic diversity, polysaccharide), core, and lipid A (the toxic moiety). Lipid A is released especially when cells lyse; it stimulates TLR4 and dumps TNF and IL-1 → fever, shock, DIC. That is endotoxin.
Acid-fast organisms (Mycobacterium, Nocardia partially) have mycolic acids. Carbolfuchsin binds; acid-alcohol does not decolorize. Gram stain poorly. Mycoplasma and Ureaplasma have no cell wall—they do not Gram-stain, are penicillin-resistant, and need sterols. Spirochetes (Treponema, Borrelia, Leptospira) are too thin for conventional Gram; use dark-field, silver, or serology.
Capsules are usually polysaccharide (exception: Bacillus anthracis poly-D-glutamate polypeptide). Capsules are antiphagocytic until IgG/C3b opsonizes them. Quellung reaction: capsule swells with type-specific antibody. Biofilms (polysaccharide matrix on hardware, teeth, S. epidermidis catheters) hide bacteria from neutrophils and antibiotics.
Spores (Bacillus, Clostridium) are metabolically dormant, dehydrated, and packed with calcium dipicolinate. They survive boiling, desiccation, and many disinfectants; autoclave steam under pressure is the sterilization standard. Spores are not a reproductive form—one vegetative cell, one spore, one germinated cell.
Pili/fimbriae mediate attachment and, for sex pili, conjugation. Flagella confer motility and H antigen. Plasmid DNA is extra-chromosomal and mobile. Glycocalyx slime is a looser capsule-like layer.
Oxygen and biochemistry (use these as ID keys, not as a biochemistry course):
| Test / trait | Meaning |
|---|---|
| Catalase | Staphylococci + vs streptococci/enterococci − (breaks H2O2) |
| Coagulase | S. aureus + vs most other staphylococci − |
| Oxidase | Pseudomonas, Neisseria, Campylobacter, Vibrio typically + |
| Lactose fermentation | E. coli and Klebsiella +; Salmonella and Shigella − on MacConkey |
| Hemolysis | β complete (S. pyogenes, S. aureus); α partial (S. pneumoniae, viridans); γ none |
| Obligate aerobe | M. tuberculosis, Nocardia, Bordetella, Pseudomonas |
| Obligate anaerobe | Clostridia, Bacteroides; superoxide dismutase/catalase poor |
| Facultative | Most enterobacterales, staphylococci |
| Microaerophile | Campylobacter, Helicobacter |
Resistance, genetics, antigenicity, pathogenicity
Chromosomal mutation can alter a drug target (ribosomal protein, DNA gyrase, PBP). Horizontal transfer moves whole cassettes faster than mutation:
| Mechanism | Vehicle | High-yield example |
|---|---|---|
| Transformation | Naked DNA from lysed cells | S. pneumoniae, H. influenzae, Neisseria competence |
| Transduction | Bacteriophage packages bacterial DNA | Specialized transduction of diphtheria, Shiga-like, cholera, botulinum (some), erythrogenic toxins—lysogeny |
| Conjugation | Sex pilus; F plasmid or conjugative resistance plasmid | Vancomycin-resistance plasmids; many Gram-negative β-lactamases |
| Transposition | Mobile insertion sequences | Spread of resistance genes onto plasmids |
Resistance biochemistries to name: (1) enzymatic destruction (β-lactamase, aminoglycoside-modifying enzymes), (2) altered target (mecA → PBP2a in MRSA; vanA ligase remodeling peptidoglycan termini in VRE; mutated PBPs in penicillin-resistant pneumococcus), (3) decreased uptake / efflux (porin loss and pumps in Pseudomonas), (4) metabolic bypass (sulfonamide-resistant folate enzymes). Penicillinase-resistant penicillins (methicillin class) were built for staphylococcal β-lactamase; MRSA ignores them because the target changed, not because a new β-lactamase appeared.
Antigenicity. Serologic typing uses O (LPS), H (flagella), K (capsule). Antigenic variation of gonococcal pili and Borrelia surface proteins lets the organism outrun antibody. Group A strep M protein is both a virulence factor (antiphagocytic, binds factor H) and the mimic that drives rheumatic carditis.
Pathogenicity is the capacity to cause disease. Virulence factors are the tools:
| Factor | Role |
|---|---|
| Adhesins / pili | Colonization (EPEC bundle-forming pili; gonococcal pili) |
| Capsule | Avoid phagocytosis |
| Invasins | Enter cells (Listeria internalin; Salmonella type III secretion) |
| Siderophores | Steal iron |
| IgA protease | Colonize mucosa (S. pneumoniae, H. influenzae, Neisseria) |
| Biofilm | Persistence on devices and bone |
| Exotoxins | Proteins with specific targets |
| Endotoxin | LPS lipid A shock |
| Superantigens | Non-specific T-cell explosion |
Exotoxin versus endotoxin is a table you should be able to write from memory:
| Exotoxin | Endotoxin | |
|---|---|---|
| Chemistry | Protein | LPS lipid A |
| Organisms | Gram-positive and Gram-negative | Gram-negative (and Listeria has a related discussion, but LPS is Gram-neg) |
| Genetics | Often phage or plasmid | Chromosomal LPS operon |
| Heat | Often labile (exception: staphylococcal enterotoxin, heat-stable) | Stable |
| Vaccine | Toxoid possible | No practical toxoid |
| Disease style | Specific (lockjaw, rice-water stool, gray membrane) | Fever, shock, DIC, neutropenia then leukocytosis |
ADP-ribosylating exotoxins to pair: diphtheria toxin and Pseudomonas exotoxin A inactivate EF-2; cholera toxin and ETEC LT ADP-ribosylate Gs → ↑cAMP in enterocytes; pertussis toxin ADP-ribosylates Gi → ↑cAMP in respiratory epithelium and immune cells. Shiga toxin and EHEC Shiga-like toxin remove a base from 28S rRNA (not ADP-ribosylation) and can trigger HUS. Tetanospasmin is a protease that cleaves synaptobrevin in inhibitory (GABA/glycine) Renshaw circuits → spastic paralysis. Botulinum toxins cleave SNARE proteins at the neuromuscular junction → flaccid paralysis. C. perfringens α-toxin is a lecithinase (phospholipase C). TSST-1 and staphylococcal enterotoxins are superantigens.
Koch-style logic on a stem: isolate, Gram morphology, catalase/coagulase or lactose/oxidase, then toxin or capsule. Do not jump to a drug brand; Part I is the organism and the mechanism.
High-yield communicable diseases by organism
Memorize a short clinical signature per organism, not a textbook chapter. Group by stain and shape.
Gram-positive cocci
| Organism | Keys | Disease / hook |
|---|---|---|
| Staphylococcus aureus | Catalase+, coagulase+, protein A (binds IgG Fc), β-hemolytic | Abscess, cellulitis, osteomyelitis, septic discitis, septic arthritis, endocarditis, scalded skin (exfoliatin), food poisoning (preformed enterotoxin), TSS |
| S. epidermidis | Coagulase−, novobiocin sensitive | Biofilm on prostheses and catheters |
| S. saprophyticus | Coagulase−, novobiocin resistant | Young-woman UTI |
| Streptococcus pyogenes (GAS) | Catalase−, β-hemolytic, bacitracin sensitive, M protein, SLO | Pharyngitis, impetigo, erysipelas, scarlet fever, necrotizing fasciitis; sequelae rheumatic fever, PSGN |
| S. agalactiae (GBS) | Hippurate, CAMP | Neonatal sepsis/meningitis; maternal vaginal reservoir |
| S. pneumoniae | α-hemolytic, optochin sensitive, bile soluble, IgA protease, capsule | Lobar pneumonia, otitis, sinusitis, meningitis |
| Viridans streptococci | Optochin resistant | Dental caries (S. mutans); subacute endocarditis after dental bacteremia |
| Enterococcus | Group D, grows in 6.5% NaCl | UTI, endocarditis; VRE |
Gram-positive rods
| Organism | Keys | Disease |
|---|---|---|
| Bacillus anthracis | Spore, polypeptide capsule, edema + lethal toxins | Cutaneous eschar; pulmonary woolsorter |
| B. cereus | Spore, enterotoxins | Emetic fried-rice; diarrheal forms |
| Clostridium tetani | Spore, tetanospasmin | Spastic paralysis, risus sardonicus; soil/puncture |
| C. botulinum | Spore, botulinum toxin | Flaccid paralysis; canned food; infant honey |
| C. perfringens | Spore, α-toxin | Gas gangrene; late-onset food poisoning |
| C. difficile | Spore, TcdA/TcdB | Antibiotic-associated colitis; healthcare reservoir |
| Corynebacterium diphtheriae | Clubbed, ADP-ribosyl EF-2 | Pseudomembrane, myocarditis, neuropathy |
| Listeria monocytogenes | Tumbling, actin rockets, cold growth | Deli/soft cheese; pregnancy loss; neonatal meningitis |
| Actinomyces israelii | Anaerobe, sulfur granules | Cervicofacial sinus tracts |
| Nocardia | Aerobic, partially acid-fast | Pulmonary/brain abscess in immunocompromised |
Gram-negative cocci and coccobacilli
| Organism | Keys | Disease |
|---|---|---|
| Neisseria meningitidis | Maltose fermenter, capsule, LOS | Meningitis, Waterhouse–Friderichsen; respiratory droplets; college/military |
| N. gonorrhoeae | Maltose non-fermenter, pili variation | Urethritis, PID, septic arthritis in young adults, ophthalmia neonatorum |
| Moraxella catarrhalis | Oxidase+ | Otitis, COPD exacerbations |
| Haemophilus influenzae | Factors X (heme) and V (NAD), capsule type b | Epiglottitis, meningitis in unvaccinated children; otitis (nontypeable) |
| Bordetella pertussis | Pertussis toxin, tracheal cytotoxin | Whooping cough; respiratory droplets |
| Pasteurella multocida | Cat/dog bite | Rapid cellulitis |
| Francisella tularensis | Tick/rabbit, facultative intracellular | Ulceroglandular tularemia |
| Brucella | Unpasteurized dairy, facultative intracellular | Undulant fever |
Enteric and other Gram-negative rods
| Organism | Keys | Disease / transmission |
|---|---|---|
| ETEC | LT/ST enterotoxins | Traveler’s diarrhea; fecal–oral |
| EHEC O157:H7 | Shiga-like toxin, does not ferment sorbitol | Bloody diarrhea, HUS; undercooked beef |
| Salmonella enterica nontyphoid | Motile, H2S | Food-borne gastroenteritis; eggs/poultry; can seed osteomyelitis in sickle cell |
| S. typhi | Vi capsule, human-only | Typhoid; gallbladder carrier |
| Shigella | Nonmotile, very low ID50 | Dysentery; fecal–oral; no animal reservoir |
| Klebsiella pneumoniae | Mucoid capsule, current-jelly sputum | Alcoholics, aspiration pneumonia, UTI |
| Proteus | Swarming, urease | Struvite stones |
| Yersinia pestis | Flea, bipolar staining | Bubonic/pneumonic plague; rodent reservoir |
| Y. enterocolitica | Cold-enriched | Mesenteric adenitis mimicking appendicitis; milk/pork |
| Pseudomonas aeruginosa | Oxidase+, pyocyanin, grape odor, EF-2 toxin | Burns, ventilators, osteomyelitis in puncture-through-shoe, ecthyma |
| Vibrio cholerae | Oxidase+, alkaline TCBS, Gs toxin | Rice-water stool; water/seafood |
| Campylobacter jejuni | 42 °C, microaerophile, comma | Bloody diarrhea; poultry; Guillain–Barré |
| Helicobacter pylori | Urease+ | Ulcer, gastric adenocarcinoma, MALT lymphoma |
| Legionella pneumophila | Charcoal yeast, silver stain | Aerosol from water systems; hyponatremia pneumonia |
| Bacteroides fragilis | Anaerobe, capsule | Mixed GI abscess |
Spirochetes, mycobacteria, obligate intracellular, wall-less
| Organism | Keys | Disease / transmission |
|---|---|---|
| Treponema pallidum | Dark-field; VDRL/RPR screen, treponemal confirm | Syphilis stages; sexual; transplacental |
| Borrelia burgdorferi | Ixodes tick; mouse/deer | Lyme: erythema migrans, AV block, arthritis, neuropathy |
| Leptospira interrogans | Spirochete, animal urine | Weil disease; water sports |
| Mycobacterium tuberculosis | Acid-fast, cord factor, aerobe | Primary Ghon complex; reactivation apices; Pott vertebral infection |
| M. leprae | Cool skin, armadillo | Tuberculoid (Th1) vs lepromatous (Th2) leprosy |
| Chlamydia trachomatis | EB infectious / RB replicative; no muramic acid in wall | NGU, PID, LGV, trachoma, neonatal pneumonia; reactive arthritis |
| Chlamydophila pneumoniae / psittaci | Atypical pneumonia | Person-to-person vs birds (psittacosis) |
| Rickettsia rickettsii | Tick, vasculitis | Rocky Mountain spotted fever |
| Coxiella burnetii | Spore-like, unpasteurized milk/aerosol, no vector required | Q fever pneumonia/hepatitis |
| Mycoplasma pneumoniae | No wall, cold agglutinins | Walking pneumonia in young adults |
Osteomyelitis pattern worth an extra line: S. aureus is the default in any age after neonates. Sickle-cell patients add Salmonella. IV drug use and vertebral involvement still often S. aureus, with Gram-negatives in some series. Puncture through a sneaker: Pseudomonas. Tuberculosis prefers thoracolumbar vertebral bodies and discs late. Those are reservoir-plus-pathogen facts, not surgical technique.
Reservoirs and modes of transmission
A reservoir is where the organism normally lives and multiplies. A source is the immediate origin of the case. Modes are contact (direct, fomite), droplets, airborne droplet nuclei, fecal–oral, vector-borne, vertical, and zoonotic.
| Pattern | Organisms to attach | |---|---|---| | Human-only reservoir | S. typhi, Shigella, N. gonorrhoeae, M. leprae, T. pallidum, C. diphtheriae | | Soil spores | C. tetani, C. botulinum, B. anthracis (also animal hides) | | Water / aerosol | Legionella, V. cholerae, Leptospira (animal urine in water) | | Poultry / eggs | Salmonella, Campylobacter | | Unpasteurized dairy | Listeria, Brucella, Coxiella, M. bovis | | Tick | B. burgdorferi, R. rickettsii, F. tularensis (also rabbit) | | Flea | Y. pestis | | Cat bite / scratch | Pasteurella; Bartonella henselae (scratch) | | Respiratory droplets / airborne | M. tuberculosis (airborne nuclei), N. meningitidis, B. pertussis, S. pneumoniae | | Sexual | N. gonorrhoeae, C. trachomatis, T. pallidum | | Vertical | GBS, Listeria, T. pallidum, N. gonorrhoeae ophthalmic | | Healthcare / spores on hands | C. difficile; MRSA contact |
Carriers matter: S. aureus in the nares, S. typhi in the gallbladder, S. pyogenes in the pharynx. Normal flora that become pathogens when they move: viridans strep (blood), B. fragilis (peritoneum), E. coli (urine). Infectious dose is lowest for Shigella (acid-resistant) and higher for Vibrio (acid-sensitive—antacids raise risk).
Sterilization versus disinfection is scored more heavily in epidemiology (/study-guides/nbce-part1/microbiology-eukaryotes-epidemiology/epidemiology-disease-control); here remember that spores force autoclave thinking and that mycolic-acid walls and biofilms change what a surface wipe can do.
Bacteria items on Part I are matching questions in disguise: stain and structure, toxin biochemistry, gene-transfer route, then reservoir. If you can tell S. aureus from S. pyogenes from S. pneumoniae from M. tuberculosis with their musculoskeletal complications, you have covered the chiropractic-relevant edge of this 18% topic without wandering into Part II management.
Compared with Gram-negative rods, a typical Gram-positive coccus is correctly described by which envelope features?
Which statement correctly identifies bacterial endotoxin?
Which organism lacks peptidoglycan, cannot be classified by Gram stain, is resistant to β-lactam antibiotics, and is a classic cause of atypical pneumonia with cold-agglutinin IgM?