Concept
- Resident microbes live on surfaces open to the outside world
- Composition is semi-permanent
- Shifts with major life events (birth, diet, antibiotics, aging)
- Internal sterile sites
- Blood
- Internal organs
- Stomach (acid-sterilized)
Site-by-Site Residents
| Site | Dominant | Other notable |
|---|---|---|
| Skin, outer ear, distal urethra | S. epidermidis | S. aureus, diphtheroids, streptococci, yeasts (Candida) |
| Anterior nares | S. aureus | S. epidermidis, diphtheroids |
| Oropharynx | Viridans streptococci (incl. S. mutans) | Non-pathogenic Neisseria, unencapsulated H. influenzae, C. albicans |
| Gingival crevices | Oral anaerobes | Prevotella, Fusobacterium, Actinomyces, Bacteroides |
| Colon (adult) | Bacteroides/Prevotella (anaerobes outnumber all) | E. coli, Bifidobacterium, Enterococcus faecalis, Eubacterium |
| Colon (breast-fed infant) | Bifidobacterium | Lactobacillus, streptococci |
| Vagina | Lactobacillus | Streptococci, Gram-negative rods, yeasts, Veillonella |
Helpful Roles
- Barrier effect
- Occupy attachment sites
- Consume local nutrients
- Chemical defense
- Keep local pH unfavorable to invaders
- Nutrition
- Make vitamin K
- Make B-complex vitamins
Harmful Roles (Endogenous Disease)
- Right organism, wrong place
- Fecal flora β urinary tract
- Skin flora β catheter/prosthesis
- Host defenses fall
- Overgrowth, e.g., oral candidiasis (thrush)
- Vaginal group B strep colonization occurs in about 15β20% of women.
- Passage through the birth canal can seed neonatal sepsis or meningitis.
- E. coli from fecal flora can do the same.
- S. mutans makes a sticky glucan biofilm that cements oral bacteria to enamel (plaque).
Terminology
| Term | Meaning |
|---|---|
| Bacteremia | Bacteria in blood, no overt illness |
| Septicemia | Bacteria multiplying in blood with symptoms |
| Endogenous infection | Caused by the host's own flora |
| Exogenous infection | Acquired from environment, person, animal, or food |
| Family names | End in "-aceae" |
| Genus/species | Italicized; genus may be abbreviated |
| Class | Behavior | Examples |
|---|---|---|
| Obligate aerobe |
| Mycobacterium, Pseudomonas, Bacillus |
| Microaerophile |
| Campylobacter, Helicobacter |
| Facultative anaerobe |
| Most bacteria, e.g., Enterobacteriaceae |
| Obligate anaerobe |
| Actinomyces, Bacteroides, Clostridium |
Why Oxygen Kills Anaerobes
Oβ reducedβSuperoxide / peroxideβNo SOD / catalaseβOxidative cell damage
- Anaerobes thrive in dead, poorly perfused tissue.
- Aminoglycosides work poorly against anaerobes because uptake needs oxygen-dependent transport.
Gram Stain Sequence
1 Β· Crystal violetβ
2 Β· Iodine (mordant)β
3 Β· Alcohol/acetone washβ
4 Β· Safranin counterstain
| Step | Gram-positive | Gram-negative |
|---|---|---|
| Crystal violet | Purple | Purple |
| Iodine | Purple (large complex trapped) | Purple (complex forms) |
| Decolorizer | Stays purple | Loses color |
| Safranin | Purple | Pink-red |
Structural Basis
- Gram-positive
- Thick peptidoglycan
- Dehydrates with alcohol, locks dye complex in
- Gram-negative
- Thin peptidoglycan plus outer membrane
- Alcohol dissolves outer membrane, dye escapes
Rules That Save Time
- Nearly all cocci are Gram-positive
- Exceptions: Neisseria, Moraxella, Veillonella
- Every spore-former is Gram-positive (Bacillus, Clostridium)
- Tissue-modified Gram stains give a pale red background
Acid-Fast Stain (ZiehlβNeelsen / Kinyoun)
| Step | Acid-fast | Non-acid-fast |
|---|---|---|
| Carbol fuchsin (+ heat in ZN) | Red | Red |
| Acid-alcohol wash | Stays red | Colorless |
| Methylene blue | Red | Blue |
- Heat drives dye through the waxy mycolic-acid wall
- Acid-fast organisms
- Mycobacterium (fully)
- Nocardia (partially, weak acid-fast)
- Protozoan oocysts: Cryptosporidium, Cystoisospora, Cyclospora
- Background cells and sputum stain blue
Organisms That Stain Poorly or Not at All
| Group | Reason | Wall type |
|---|---|---|
| Mycobacterium | Waxy wall repels dye | Gram-positive |
| Spirochetes | Too thin to see color | Gram-negative |
| Chlamydiae | Tiny, intracellular | Gram-negative |
| Rickettsiae | Tiny, intracellular | Gram-negative |
| Legionella | Faint unless counterstain is prolonged | Gram-negative |
| Mycoplasma | No cell wall at all | None |
Gram-Positive
| Shape | Genera |
|---|---|
| Cocci | Staphylococcus, Streptococcus, Enterococcus |
| Rods, aerobic/facultative | Bacillus, Listeria, Corynebacterium, Nocardia, Mycobacterium |
| Rods, anaerobic | Actinomyces, Clostridium, Cutibacterium, Lactobacillus |
Gram-Negative
| Shape / group | Genera |
|---|---|
| Cocci | Neisseria, Moraxella |
| Non-enteric rods | Pseudomonas, Burkholderia, Acinetobacter, Eikenella, Kingella, Haemophilus, Bartonella, Legionella, Brucella, Bordetella, Francisella, Capnocytophaga, Pasteurella |
| Curved / helical | Campylobacter, Helicobacter, Vibrio |
| Enterobacteriaceae | Escherichia, Shigella, Salmonella, Klebsiella, Proteus, Yersinia, Serratia, Citrobacter, Enterobacter (plus Aeromonas listed alongside) |
| Anaerobic rods | Bacteroides, Prevotella, Porphyromonas, Fusobacterium |
| Gram-variable rods | Gardnerella, Mobiluncus |
| Spirochetes | Treponema, Borrelia, Leptospira |
Do Not Gram-Stain Well
| Family | Genera |
|---|---|
| Mycoplasmataceae | Mycoplasma, Ureaplasma |
| Rickettsiaceae | Rickettsia, Ehrlichia, Coxiella |
| Chlamydiaceae | Chlamydia, Chlamydophila |
- Obligate intracellular or wall-less organisms need non-Gram methods (serology, PCR, special culture).
Decision Pathway
Gram+ coccusβ catalase test
Catalase +βStaphylococcusβ coagulase
Coagulase + β S. aureus
Coagulase β β CoNSβ novobiocinSensitive β S. epidermidisResistant β S. saprophyticus
Catalase ββStrep / Enterococcusβ hemolysis pattern
Ξ² (clear)β bacitracinSensitive β S. pyogenesResistant β S. agalactiae
Ξ± (green)β optochin / bileSensitive, soluble β S. pneumoniaeResistant, insoluble β viridans
Ξ³ (none)βEnterococcus (bile-esculin +)
Comparison of Key Species
| Species | Catalase | Coagulase | Hemolysis | Lab discriminators |
|---|---|---|---|---|
| S. aureus | + | + | Ξ² | Ferments mannitol; salt-tolerant; golden colonies |
| S. epidermidis | + | β | none | Novobiocin-S; biofilm former |
| S. saprophyticus | + | β | none | Novobiocin-R |
| S. pyogenes (GAS) | β | β | Ξ² | Bacitracin-S; PYR + |
| S. agalactiae (GBS) | β | β | Ξ² | Bacitracin-R; CAMP +; hippurate + |
| S. pneumoniae | β | β | Ξ± | Optochin-S; bile-soluble |
| Viridans group | β | β | Ξ± | Optochin-R; bile-insoluble; PYR β |
| Enterococcus | β | β | variable / Ξ³ | PYR +; grows in bile and 6.5% NaCl |
Hemolysis key
- Ξ² = complete clearing around colony
- Ξ± = partial, greenish discoloration
- Ξ³ = no hemolysis
- Staph and strep cause overlapping diseases (skin infection, endocarditis), so lab discriminators decide the answer.
- Staph appear in clusters; strep and enterococci appear in chains or pairs.
Genus Profile
- Gram-positive cocci in grape-like clusters
- Catalase-positive
- Medically relevant species
- S. aureus
- S. epidermidis
- S. saprophyticus
S. aureus
Identification
- Golden colonies on blood agar
- Ξ²-hemolytic
- Coagulase-positive (only staph that is)
- Ferments mannitol on mannitol-salt agar
Reservoir
- Skin
- Anterior nares (about 25% carriers)
Transmission
- Hand contact
- Respiratory droplets
- Surgical wounds
- Food contaminated by handlers (custard pastries, potato salad, cured meats)
Risk Factors
- Surgery or open wounds
- Foreign material (tampons, packing, sutures)
- Severe neutropenia (ANC <500/Β΅L)
- Injection drug use
- Chronic granulomatous disease
- Cystic fibrosis
Virulence Factors
| Factor | Action |
|---|---|
| Protein A | Binds Fc of IgG β blocks opsonization/phagocytosis |
| Coagulase | Converts fibrinogen β fibrin; walls off lesions |
| Enterotoxins | Heat-stable; preformed in food; act rapidly |
| TSST-1 | Superantigen β polyclonal T-cell activation β cytokine storm |
| Exfoliatins | Cleave epidermal adhesion proteins β skin peeling, bullae |
| Ξ±-toxin / PantonβValentine leukocidin | Pore-forming cytolysins; PVL is phage-encoded and tied to severe MRSA |
Disease Spectrum
| Disease | Key features | Driver |
|---|---|---|
| Food poisoning |
| Preformed enterotoxins |
| Acute endocarditis |
| Fibrin-platelet vegetation, cytolysins |
| Abscess, mastitis |
| Coagulase, cytolysins |
| Toxic shock syndrome |
| TSST-1 |
| Impetigo (bullous) |
| Exfoliatins |
| Scalded skin syndrome |
| Exfoliatins |
| Pneumonia |
| Cytolysins, coagulase |
| Osteomyelitis |
| Cytolysins |
| Septic arthritis |
| Cytolysins |
| Surgical-site infection |
| Coagulase, exfoliatins Β± TSST |
- Osteomyelitis: S. aureus is the default; sickle cell disease shifts the answer to Salmonella.
- Staph enterotoxin food poisoning has no fever-driven invasion; the toxin is already in the food.
- Toxin-mediated syndromes (TSS, SSSS) can occur with a tiny, localized infection.
Treatment
| Situation | Choice |
|---|---|
| Methicillin-susceptible (MSSA) | Nafcillin or oxacillin (penicillinase-resistant) |
| MRSA | Vancomycin |
| VISA / VRSA | Quinupristinβdalfopristin, among other alternatives |
| Topical / nasal decolonization | Mupirocin |
| Food poisoning | Supportive only |
Coagulase-Negative Species
| Feature | S. epidermidis | S. saprophyticus |
|---|---|---|
| Novobiocin | Sensitive | Resistant |
| Habitat | Skin | Genitourinary tract |
| Key trait | Biofilm on plastic | Adheres to urothelium |
| Disease |
|
|
- A blood culture with a single coag-negative staph is often a contaminant.
- Prosthetic material plus coag-negative staph points to S. epidermidis.
Genus Profile
- Gram-positive cocci in chains or pairs
- Catalase-negative
- Lancefield grouping uses cell-wall carbohydrate antigens (groups AβO)
- Exceptions to grouping
- S. pneumoniae is typed by capsule
- Viridans streptococci are not groupable
- GAS subtyped by M protein
Group A: S. pyogenes
Identification
- Ξ²-hemolytic
- Bacitracin-sensitive
- PYR-positive
Reservoir / spread
- Human throat and skin
- Droplets and direct contact
Virulence
- Hyaluronic acid capsule
- Poorly immunogenic (self-mimicry)
- M protein
- Antiphagocytic
- Linked to rheumatic fever and glomerulonephritis
- Streptolysin O (immunogenic, oxygen-labile)
- Streptolysin S (non-immunogenic, oxygen-stable)
Spreading enzymes
| Factor | Effect |
|---|---|
| Streptokinase | Dissolves fibrin clots |
| DNase | Thins pus, helps lesion extension |
| Hyaluronidase | Breaks down connective-tissue matrix |
| Pyrogenic (erythrogenic) exotoxins AβC | Phage-encoded superantigens β fever and scarlet fever rash |
GAS Disease Map
| Category | Entity | Features |
|---|---|---|
| Suppurative | Pharyngitis | Sudden sore throat, fever, headache, tonsillar exudate, tender anterior cervical nodes |
| Scarlet fever | Pharyngitis plus fine blanching sandpaper rash, circumoral pallor, strawberry tongue; palms/soles usually spared | |
| Impetigo / pyoderma | Honey-colored crusted skin lesions | |
| Other invasive | Cellulitis, erysipelas, necrotizing fasciitis, lymphangitis, puerperal sepsis | Rapid spread via spreading enzymes |
| Non-suppurative | Rheumatic fever |
|
| Post-strep glomerulonephritis |
|
Diagnosis
- Rapid antigen test misses roughly 25% β culture negatives
- ASO titer above ~200 IU supports rheumatic fever
- Anti-DNase B and anti-hyaluronidase titers support glomerulonephritis (skin-source too)
Management
- Treatment: Ξ²-lactam; macrolide if penicillin-allergic
- Prevention: prolonged antibiotic prophylaxis (at least 5 years) after rheumatic fever
- Treating strep throat prevents rheumatic fever but does not reliably prevent glomerulonephritis.
- Skin-source GAS gives glomerulonephritis but not rheumatic fever.
Group B: S. agalactiae
Identification
- Ξ²-hemolytic
- Bacitracin-resistant
- Hippurate hydrolysis +
- CAMP test +
- CAMP factor enhances S. aureus hemolysis
- Gives an arrowhead-shaped zone
Reservoir
- Vagina (15β20% of women)
- Lower GI tract
Pathogenesis / disease
- Capsule, Ξ²-hemolysin, CAMP factor
- Passed to newborn during delivery
- Higher risk with prolonged membrane rupture
- Leading cause of neonatal sepsis and meningitis
- Treatment: penicillin or ampicillin (Β± aminoglycoside or cephalosporin initially in neonates)
- Prevention
- Intrapartum prophylaxis if vaginal/rectal culture positive
- Also for prior GBS-affected infant or prolonged rupture
S. pneumoniae
Identification
- Ξ±-hemolytic
- Lancet-shaped diplococci
- Optochin-sensitive
- Bile-soluble
- Quellung reaction: capsule swells with type-specific antiserum
Reservoir
- Upper respiratory tract (nasopharyngeal carriage)
- Droplet spread; not highly contagious
Risk factors
- Recent influenza or measles
- COPD
- Heart failure
- Alcoholism
- Asplenia (overwhelming sepsis)
Virulence
- Polysaccharide capsule (dominant)
- IgA protease
- Teichoic acid, peptidoglycan (CNS inflammation)
- Pneumolysin: injures epithelium, blunts burst and complement
Diseases
| Disease | Details |
|---|---|
| Lobar pneumonia | Most common cause of community pneumonia; shaking chills, high fever, lobar consolidation, rusty blood-tinged sputum |
| Meningitis | Most common adult cause; CSF: neutrophils β, glucose β, protein β |
| Otitis media / sinusitis | Most common bacterial cause in children |
| Sepsis in asplenia | Encapsulated organism not cleared without spleen |
Diagnosis
- Gram stain and culture of sputum or CSF
- Urinary antigen test
- Latex agglutination for capsular antigen in CSF
Treatment
- Pneumonia: Ξ²-lactam
- Meningitis: ceftriaxone or cefotaxime plus vancomycin if resistance is common locally
- Otitis/sinusitis (children): amoxicillin
Prevention
- Immunity is serotype-specific (>80 capsule types)
- Conjugate vaccine (children)
- 13-valent in the older formulation
- Protein-conjugated β T-cell help β strong infant response
- Polysaccharide vaccine (adults)
- 23 serotypes
- Given at β₯65 y and to at-risk groups
Viridans Streptococci
Identification
- Ξ±-hemolytic
- Optochin-resistant
- Bile-insoluble
- PYR-negative
Members
- S. mutans, S. sanguinis (mouth)
- S. gallolyticus (formerly S. bovis; colon)
Pathogenesis
- Dextran/glucan biofilm sticks to enamel
- Same sticky matrix glues to damaged valves and forms vegetations
- Vegetation shields bacteria from immune clearance
- Source is endogenous
| Disease | Details |
|---|---|
| Dental caries | S. mutans plaque; acid from sugar fermentation erodes enamel |
| Subacute endocarditis | Abnormal or prosthetic valve + bacteremia after dental work; fatigue, low fever, night sweats, weight loss, splinter hemorrhages |
| S. gallolyticus bacteremia | Prompt colonoscopy to look for colon cancer |
- Treatment: penicillin G (Β± aminoglycoside) for endocarditis
- Prevention: antibiotic prophylaxis before dental procedures in high-risk valve patients
- Acute valve infection with rapid destruction β S. aureus.
- Subacute course on a diseased valve after dental work β viridans strep.
- Elderly man with endocarditis after GU/GI procedure β Enterococcus.
Features
- E. faecalis and E. faecium
- Group D Gram-positive cocci, pairs/short chains
- Catalase-negative
- PYR-positive
- Variable hemolysis
- Hydrolyze esculin with 40% bile β black bile-esculin agar
- Grow in 6.5% NaCl
Ecology
- Colon, sometimes urethra and female genital tract
- Endogenous spread
- Bile and salt tolerance β survive in gut and biliary tree
Pathogenesis Chain
GI/GU instrumentationβBacteremiaβPreviously damaged valveβSubacute endocarditis
Diseases
- Urinary tract infection
- Biliary tract infection
- Subacute endocarditis (often older adults with valve damage)
Therapy & Resistance
- Intrinsically resistant to many drugs
- Cephalosporins are ineffective
- Low-level resistance β ampicillin Β± gentamicin or streptomycin (synergy)
- Vancomycin-resistant enterococci (VRE)
- No dependable first-line option in some strains
- VanA mechanism
- Cell-wall precursor terminal D-Ala-D-Ala is swapped for D-Ala-D-lactate
- Precursor still builds wall but vancomycin cannot bind
- Prevention: prophylaxis (penicillin + gentamicin) before GI/GU manipulation in high-risk valve patients
- Bile-esculin positive plus salt-tolerant separates enterococci from non-enterococcal group D strep.
- Penicillin alone is not reliably bactericidal for enterococcal endocarditis.
| Genus | Spores | Aerobic growth | Exotoxin disease | Facultative intracellular | Acid-fast | Branching |
|---|---|---|---|---|---|---|
| Bacillus | + | + | + | β | β | β |
| Clostridium | + | β (anaerobe) | + | β | β | β |
| Listeria | β | + | β | + | β | β |
| Corynebacterium | β | + | + | β | β | β |
| Actinomyces | β | β (anaerobe) | β | β | β | + |
| Nocardia | β | + | β | β | partial | + |
| Mycobacterium | β | + | β | + | + | β |
- Only Bacillus and Clostridium form spores.
- Branching filamentous rods: Actinomyces (anaerobic, not acid-fast) versus Nocardia (aerobic, partially acid-fast).
- Gram-positive rods that make toxins: Bacillus, Clostridium, Corynebacterium.
B. anthracis
Features
- Large, square-ended (boxcar) Gram-positive rods
- Spore-forming, aerobic
- Capsule is poly-D-glutamic acid (a polypeptide)
- Bioterrorism concern
Source and spread
- Reservoir: livestock, hides, wool, soil
- Contact with infected animal products
- Inhaled spores (occupational or deliberate release)
Anthrax Toxin Components
| Component | Role |
|---|---|
| Protective antigen (PA) | Binding/translocation unit; delivers LF and EF into cells |
| Lethal factor (LF) | Zinc protease; kills cells |
| Edema factor (EF) | Calmodulin-activated adenylate cyclase β βcAMP β edema |
- Capsule is antiphagocytic
Clinical Forms
| Form | Course |
|---|---|
| Cutaneous | Papule β vesicle β painless black eschar with surrounding edema; regional nodes; best prognosis |
| Inhalational (woolsorter's) | Flu-like start β abrupt respiratory failure, hemorrhagic mediastinitis, shock; high mortality |
| Gastrointestinal (rare) | Vomiting, bloody diarrhea, GI obstruction |
- Diagnosis
- Widened mediastinum on chest X-ray
- Gram stain/culture of blood, lesion, or secretions
- PCR, serology
- Treatment: ciprofloxacin or doxycycline
- Resistance genes to some agents have been engineered or transferred
- Prevention
- Acellular toxoid-based vaccine for high-risk groups
- Raxibacumab for prophylaxis/treatment (anti-PA antibody)
B. cereus
- Spore-forming; found widely in the environment
- Food-borne intoxication
- Linked to starchy foods held warm (reheated fried rice, buffets)
- Eye infection after trauma (rare)
| Syndrome | Toxin | Timing | Picture |
|---|---|---|---|
| Emetic | Preformed, heat-stable | 1β6 h | Vomiting predominates (resembles staph food poisoning) |
| Diarrheal | Made in the gut; heat-labile, βcAMP | 8β18 h | Watery, nonbloody diarrhea (resembles ETEC) |
- Diagnosis: clinical; culture of implicated food
- Treatment: supportive; vancomycin for ocular infection
Overview
- Anaerobic, Gram-positive, spore-forming rods
- Pathogens
- C. tetani
- C. botulinum
- C. perfringens
- C. septicum
- C. difficile (now Clostridioides)
- Most disease is toxin-driven
C. tetani
Source
- Soil reservoir
- Puncture wounds, crush injuries, burns, bites
- Needs low tissue oxygen to germinate
Toxin pathway
Spores germinateβTetanospasminβRetrograde axonal transportβSpinal inhibitory neuronsββ glycine/GABA release
Result
- Motor neurons fire unopposed
- Spastic paralysis
- Trismus (lockjaw)
- Risus sardonicus
- Opisthotonos
- Painful generalized spasms
- Diagnosis: clinical; organism seldom cultured
- Treatment
- Human tetanus immune globulin
- Metronidazole (or penicillin)
- Benzodiazepines for spasm
- Wound debridement; delay closure
- Airway support
- Prevention
- Toxoid vaccine (formalin-inactivated toxin)
- Wound care (disinfectants do not kill spores)
Wound Prophylaxis Matrix
| Vaccination history | Clean, minor wound | Dirty / tetanus-prone wound |
|---|---|---|
| Primary series incomplete or unknown | Vaccine | Vaccine + immune globulin |
| Primary series complete | Booster if >10 y since last | Booster if >5 y since last |
- Tetanus-prone features
- Burns, frostbite, crush or missile injuries
- Devitalized tissue
- Soil, feces, saliva contamination
- Wound older than ~6 h or deeper than ~1 cm
C. botulinum
- Soil and dust spores
- Germinate in warm, low-acid, anaerobic, nutrient-rich conditions
- Toxin
- AβB polypeptide neurotoxin; types A, B (and E) most often cause human disease
- Phage-encoded
- Heat-labile (inactivated by boiling food)
- Absorbed β blood β peripheral cholinergic nerve endings
- Blocks acetylcholine release (cleaves SNARE proteins)
- Flaccid, descending paralysis
| Feature | Adult / foodborne | Infant |
|---|---|---|
| Acquisition | Preformed toxin in poorly processed canned low-acid food | Spores ingested (honey, dust) β colonize gut β toxin made in vivo |
| Presentation | Blurred vision, diplopia, dysphagia, dizziness, weakness, constipation within 1β2 days | Constipation, weak suck and cry, hypotonia (floppy), may progress to respiratory failure |
| Toxin found in | Suspect food (also serum) | Stool, serum |
| Treatment | Ventilatory support; antitoxin | Intensive supportive care; human-derived botulism immune globulin; avoid antibiotics |
| Prevention | Proper canning; heating home-canned foods | No honey before age 1 year |
- Tetanus gives spastic paralysis; botulism gives flaccid paralysis.
- Botulism is afebrile with clear mental status and descending weakness.
C. perfringens
Features
- Large, nonmotile rods; spores uncommon in tissue
- Rapid fermentation (gas) in milk medium
- Double zone of hemolysis on blood agar
- Reservoir: soil and human colon
Toxins
- Ξ±-toxin (phospholipase C / lecithinase)
- Destroys cell membranes (RBC, WBC, platelets, endothelium)
- Drives hemolysis and tissue necrosis
- Nagler reaction: lecithinase halo on egg-yolk agar is blocked by antitoxin
- Many additional tissue-damaging toxins
- Enterotoxin (gut) β ion transport disruption β watery diarrhea
| Disease | Details |
|---|---|
| Gas gangrene (myonecrosis) |
|
| Food poisoning |
|
- Diagnosis: clinical (imaging may show tissue gas)
- Treatment: urgent surgical debridement; penicillin + clindamycin; hyperbaric oxygen as adjunct
- Prevention: thorough debridement and prophylaxis in dirty wounds
C. septicum
- Anaerobic Gram-positive rod
- Endogenous origin
- Spontaneous gangrene/sepsis in patients with colon cancer
C. difficile
- Colon is the reservoir; endogenous or hospital/nursing-home spread
- Toxins
- Toxin A: enterotoxin β mucosal damage, fluid secretion, neutrophil recruitment
- Toxin B: cytotoxin β cytopathic cell injury
- Trigger: antibiotic disruption of normal flora
- Classic culprits: clindamycin, cephalosporins, ampicillin/amoxicillin, fluoroquinolones
- Disease
- Diarrhea, colitis
- Pseudomembranous colitis (yellow-white plaques on colonoscopy)
- Diagnosis
- Stool toxin or toxin-gene detection
- Culture alone is not diagnostic (organism can colonize)
- Treatment
- Stop the inciting antibiotic when possible
- Oral vancomycin or fidaxomicin; metronidazole in selected cases
- Fecal microbiota transplant for recurrent disease
- Prevention
- Restrict broad-spectrum antibiotics
- Isolate symptomatic patients, contact precautions
- Soap-and-water handwashing (alcohol gel does not kill spores)
- Sporicidal environmental cleaning
| Clue | Think |
|---|---|
| Foul vomiting 2β6 h after custard or potato salad | S. aureus enterotoxin |
| Fever, hypotension, palm/sole peeling, tampon | TSST-1 (S. aureus) |
| Catheter or prosthetic device infection, novobiocin-S | S. epidermidis |
| Young sexually active woman, cystitis, novobiocin-R | S. saprophyticus |
| Sore throat then joint pain and carditis | GAS β rheumatic fever |
| Cola-colored urine, edema after skin or throat infection | GAS β glomerulonephritis |
| Newborn sepsis/meningitis, CAMP + | GBS |
| Rusty sputum, lobar consolidation, optochin-S | S. pneumoniae |
| Dental procedure then subacute valve infection | Viridans streptococci |
| Endocarditis after urinary/GI procedure in older man | Enterococcus |
| Black eschar or widened mediastinum | B. anthracis |
| Vomiting within hours of reheated fried rice | B. cereus (emetic) |
| Dirty wound, lockjaw, spasms | C. tetani |
| Home-canned vegetables, descending flaccid paralysis; infant with honey | C. botulinum |
| Crepitus, severe pain, necrotic wound | C. perfringens |
| Diarrhea after antibiotics, pseudomembranes | C. difficile |
- Catalase separates staph (+) from strep/enterococci (β).
- Coagulase separates S. aureus from other staph.
- Bacitracin separates GAS (S) from GBS (R).
- Optochin and bile solubility separate pneumococcus from viridans.
- Toxins explain most of the clostridial syndromes; spores explain why disinfectants fail.