Microbiology System
Microbiology
High-yield microbiology for USMLE Step 1/2/3 — gram staining logic, infectious populations, STIs, UTIs, respiratory pathogens, antimicrobial mechanisms, and resistance patterns, extracted from Divine Intervention and organized for exam performance.
Bacterial Infections & Gram Staining
Every microbiology question roots itself in organism identity — gram stain, shape, and the clinical population determine the bug before you even read the answer choices. Staph aureus is the universal predator of immune-compromised hosts; encapsulated organisms exploit the asplenic. Knowing which organism owns which niche is the entire game.
EP586
Quick and Dirty Microbiology Associations for Step 1–3
- Endocarditis — organism by valve and host: Staph aureus attacks any valve (normal or abnormal). Strep viridans / Strep mutans attacks abnormal valves after dental procedures. IV drug users → tricuspid valve (veins drain to right heart first)
- Normal flora by site: Nose → Staph aureus (treat nasal colonization with mupirocin). Skin → Staph epidermidis. GI tract → anaerobes + E. coli. Vagina → Lactobacillus (25% colonized by Group B Strep)
- Botulism by mechanism: Infant/neonate (honey exposure, no GI flora → C. botulinum colonizes and produces toxin). Adult foodborne (pre-formed toxin). Wound botulism (direct inoculation). All = flaccid paralysis, hypotonia, decreased cry
- Candidiasis triggers: Post-antibiotic (kills vaginal flora → Candida overgrows). SGLT2 inhibitors (glucosuria → sweet vaginal environment). Diabetes. Treat with oral azole
- Group B Strep (Strep agalactiae): #1 cause of sepsis and meningitis in neonates (first 20 days). Screen pregnant women 35–37 weeks. Give prophylaxis at labor onset (not before). Treat with ampicillin/amoxicillin/penicillin
- Listeria monocytogenes: Meningitis in neonates, age >50, immunocompromised. Drug of choice = ampicillin. Add to empiric meningitis regimen for neonates and patients >50
Endocarditis — Organism Selection Logic
| Clinical Context | Most Likely Organism | Key Mechanism |
|---|---|---|
| IV drug user, tricuspid valve | Staph aureus | Injected bugs → vein → right heart → tricuspid. Can embolize → septic PE |
| Dental procedure, abnormal valve | Strep viridans / Strep mutans | Transient bacteremia from oral flora. Normal valves usually not infected |
| Prosthetic valve, <60 days post-op | Staph epidermidis | Coagulase-negative staph from surgical inoculation |
| Any host, any valve | Staph aureus | Most common overall cause; virulent enough to attack normal valves |
| GI/GU procedure, older adult | Enterococcus | Fecal flora entering bloodstream; requires amoxicillin prophylaxis |
Endocarditis Work-Up Sequence
Blood cultures first (always) → TEE (transesophageal echo) to visualize vegetation → narrow antibiotics per culture → watch for septic emboli (PE from tricuspid; stroke, MI, renal infarcts from left-sided). IV drug user with new murmur + tricuspid vegetation = classic NBME scenario.
Botulism — Three Mechanisms Compared
| Type | Host | Mechanism | Classic Clue |
|---|---|---|---|
| Infant | <12 months | Honey ingested → spores germinate in gut (no flora yet) → toxin produced in vivo | Floppy baby, decreased cry, constipation, head lag |
| Foodborne | Any | Pre-formed toxin in home-canned foods → ingested directly | Outbreak after eating preserved food; descending paralysis |
| Wound | IV drug users, trauma | Spores inoculated into wound → toxin produced locally | No GI symptoms; may have fever from wound infection |
All forms: C. botulinum toxin cleaves SNARE proteins → blocks ACh release at NMJ → flaccid paralysis. Autonomic symptoms (dilated pupils, constipation, urinary retention) precede motor paralysis. Treat: supportive + antitoxin for foodborne/wound types.
Normal Flora Quick Reference
| Site | Dominant Organisms | Clinical Pearl |
|---|---|---|
| Nose | Staph aureus (colonizes ~30% of people) | Mupirocin to nares reduces MRSA risk before hospitalization |
| Skin | Staph epidermidis, Propionibacterium acnes | Staph epi = most common prosthetic device infection |
| Oropharynx | Strep viridans, Neisseria, anaerobes | Strep viridans → endocarditis after dental procedures |
| GI tract (colon) | Bacteroides fragilis, E. coli, Enterococcus | Explains empiric regimens targeting gram-neg + anaerobes for abdominal infections |
| Vagina | Lactobacillus (dominant), Group B Strep (25%) | Estrogen maintains Lactobacillus; loss (menopause, antibiotics) → UTI/candida risk |
EP437
Infectious Populations — IV Drug Users
- Screening priorities: All IV drug users → screen for Hep B, Hep C, and HIV. The drug rarely causes the infection — the unsterile technique does
- Tricuspid endocarditis: IV drugs → vein → right atrium → tricuspid valve (first valve encountered). Staph aureus. Blood cultures first, then TEE. Risk: septic pulmonary emboli from tricuspid vegetations
- Septic arthritis: Hematogenous spread of Staph aureus from injection → joint. Next step = arthrocentesis (WBC count in synovial fluid). Treat with IV antibiotics
- Osteomyelitis: Staph aureus hematogenous spread. Spinal osteomyelitis = pinpoint vertebral tenderness + fever. Treat with weeks of IV antibiotics (not oral). Sternoclavicular osteomyelitis = direct inoculation if injecting into chest area
- FSGS (nephrotic syndrome): IV drug use → focal segmental glomerulosclerosis → T-cell mediated podocyte damage → proteinuria → edema → activated RAAS
- Necrotizing fasciitis: Red, exquisitely tender extremity, high fever → must debride + protein synthesis inhibitor (clindamycin) to stop toxin production. Systemic amyloidosis from chronic injection → restrictive cardiomyopathy, macroglossia, renal failure
IV Drug User — Complete Infection Profile
| Presentation | Diagnosis | Bug | Key Next Step |
|---|---|---|---|
| Fever + new murmur | Endocarditis (tricuspid) | Staph aureus | Blood cultures → TEE |
| Jaundice + elevated AST/ALT | Viral hepatitis (B or C) | HBV, HCV | Screen with serology |
| Hot, swollen joint + fever | Septic arthritis | Staph aureus | Arthrocentesis (joint tap) |
| Vertebral tenderness + fever + elevated ESR | Spinal osteomyelitis | Staph aureus | MRI spine → IV antibiotics for weeks |
| Exquisitely tender, red limb + high fever | Necrotizing fasciitis | Polymicrobial / GAS | Surgical debridement + clindamycin |
| Massive edema + proteinuria | FSGS (nephrotic syndrome) | N/A — T-cell mediated | Steroids; address underlying use |
| Breast/chest cellulitis (no breastfeeding) | Cellulitis from breast injection | Staph aureus | Antibiotics; rule out mastitis |
| Restrictive cardiomyopathy + macroglossia | Systemic amyloidosis | Serum amyloid A | Chronic inflammation → AA amyloid |
Osteomyelitis — IV vs Oral Antibiotics
Always give IV antibiotics for osteomyelitis on NBME exams. IV drug users with osteomyelitis need weeks of IV therapy for adequate tissue penetration. The distractor is an oral option — do not select it. Similarly: meningitis → IV; herpes encephalitis → IV acyclovir; vomiting patient → IV route regardless of infection.
Hematogenous vs Direct Inoculation Osteomyelitis
Hematogenous = infection arrives via bloodstream (long bones in children, vertebrae in adults/IVDUs). Direct inoculation = infection enters from adjacent site (diabetic foot ulcer → underlying bone; IV drug user who injects at sternum → sternoclavicular osteomyelitis). If the osteomyelitis is near an injection site, think direct inoculation.
EP623
Last Minute Microbiology Review for Step 2 and 3
- Osteomyelitis — organism by host: Most common = Staph aureus (post-surgical, post-trauma). Sickle cell disease = Salmonella (USMLE rule — do not deviate). If no Salmonella in the answer, then Staph aureus
- MRSA drugs — complete list: Vancomycin (cell wall, DLA→DLAC resistance). Linezolid (50S inhibitor, also covers VRE, also an MAOI → serotonin syndrome risk). Daptomycin. Clindamycin. Doxycycline (especially skin MRSA). TMP-SMX / Bactrim
- Community-acquired pneumonia organisms: Strep pneumo = #1 overall cause in adults. NBME avoids naming it directly — gives "gram-positive cocci" or "encapsulated organism." Treatment: beta-lactam + macrolide (amoxicillin + azithromycin), or respiratory fluoroquinolone (levofloxacin)
- Neonatal sepsis / meningitis: First 20 days of life → Group B Strep (Strep agalactiae) is #1. Listeria also high risk. GBS prophylaxis: give intrapartum (not before labor begins) — ampicillin/penicillin at onset of labor
- Listeria empiric coverage: Add ampicillin to empiric meningitis regimen for neonates and patients >50. Ceftriaxone + vancomycin + ampicillin is the full empiric regimen for those populations
- Linezolid — dual hazard: Covers MRSA and VRE. Also an MAOI → adding SSRIs, SNRIs, or other serotonergic drugs can cause serotonin syndrome (hyperreflexia, myoclonus, hyperthermia)
Osteomyelitis — Host-Based Bug Selection
| Host / Setting | Bug | Mechanism |
|---|---|---|
| Most adults (post-surgical, post-trauma) | Staph aureus | Hematogenous spread or direct inoculation |
| Sickle cell disease | Salmonella (first), then Staph aureus | Splenic dysfunction → can't clear encapsulated and intracellular bugs |
| IV drug user, vertebral | Staph aureus | Hematogenous; classic IVDU complication |
| Diabetic foot ulcer | Polymicrobial / Staph aureus | Direct inoculation from contiguous ulcer |
| Nail puncture through shoe | Pseudomonas aeruginosa | Pseudomonas loves moist environments → sneaker inner soles |
| Neonatal | Group B Strep / Staph aureus | Hematogenous from bacteremia |
MRSA Treatment Options — Priority Order
| Drug | Class | Key Caveat |
|---|---|---|
| Vancomycin | Glycopeptide cell wall inhibitor | Resistance: DLA→DLAC substitution. Red Man syndrome with rapid infusion (not allergy — slow the drip) |
| Linezolid | 50S ribosomal protein synthesis inhibitor | Also covers VRE. MAOI activity → serotonin syndrome if combined with SSRIs/SNRIs |
| Daptomycin | Lipopeptide (membrane disruption) | Inactivated by pulmonary surfactant — do NOT use for pneumonia. Good for bacteremia and skin |
| Clindamycin | 50S inhibitor | Covers MRSA and anaerobes. Strong association with C. diff colitis |
| Doxycycline | 30S inhibitor (tetracycline) | Good for MRSA skin infections in outpatient setting |
| TMP-SMX (Bactrim) | Folate synthesis inhibitor | Good for MRSA skin infections. Also causes hyperkalemia (ENaC blocker) and oxidative hemolysis in G6PD |
Linezolid + Serotonergic Drugs = Serotonin Syndrome
Linezolid inhibits monoamine oxidase → blocks serotonin breakdown. Adding an SSRI, SNRI, tramadol, or meperidine can precipitate serotonin syndrome: hyperreflexia, myoclonus, hyperthermia, agitation, diaphoresis. Classic NBME trap — patient on linezolid for MRSA gets prescribed sertraline for depression.
Respiratory Pathogens
Pneumonia classification follows an exposure-then-organism logic: community vs hospital vs immunocompromised host vs CF patient each has a predictable bug list. The atypicals (Mycoplasma, Legionella, Chlamydia) walk in with "walking pneumonia" features — interstitial pattern, gradual onset, lack of lobar consolidation. TB and endemic fungi follow geography and immune status.
EP461
Floridly HY Antibiotic Review — Atypicals, TB & Antifungals
- Walking pneumonia (atypical): Low-grade fever, non-productive cough, interstitial infiltrates, age 20–40, lasting days-to-weeks. Most common cause = Mycoplasma pneumoniae. Treat: azithromycin (macrolide) or doxycycline
- Legionella pneumophila: Water exposure (humidifiers, HVAC, hotel water towers), heavy smokers, institutional outbreaks. Treat with macrolides (azithromycin, erythromycin) or respiratory fluoroquinolones. Key: Legionella does NOT gram stain and requires special charcoal yeast extract media
- Active TB treatment: RIPE — Rifampin, Isoniazid, Pyrazinamide, Ethambutol for 2 months, then Rifampin + Isoniazid for 4 more months. Add vitamin B6 (pyridoxine) with isoniazid to prevent peripheral neuropathy
- Latent TB: Positive PPD or IGRA + normal chest X-ray + no symptoms. Treat with isoniazid + B6 alone (9 months)
- Antifungal selection: Invasive aspergillosis → voriconazole (first line), amphotericin B (second line). Mucormycosis → amphotericin B (drug of choice). Cryptococcal meningitis → amphotericin B + flucytosine (induction), then fluconazole (maintenance 9–12 months). Endemic fungi (histoplasma, coccidioides) → itraconazole
- Ethambutol toxicity: Optic neuropathy → red-green colorblindness. Also used for Mycobacterium avium complex (MAC) — triple regimen: clarithromycin + ethambutol + rifampin
Pneumonia Bug by Population
| Population | Most Likely Bug | Treatment |
|---|---|---|
| Healthy adult, community-acquired | Strep pneumo (#1) | Amoxicillin + azithromycin OR levofloxacin |
| Young adult, "walking," interstitial | Mycoplasma pneumoniae | Azithromycin or doxycycline |
| Water/HVAC exposure, smoker | Legionella pneumophila | Macrolide or fluoroquinolone |
| Hospital-acquired (>48 hrs admission) | Gram-negative rods (Klebsiella, Pseudomonas, E. coli) | Piperacillin-tazobactam ± vancomycin |
| CF patient, age >20 | Pseudomonas aeruginosa | Antipseudomonal agents; inhaled tobramycin prophylaxis |
| HIV, CD4 <200 | Pneumocystis jirovecii (PCP) | TMP-SMX (treatment and prophylaxis) |
| HIV, CD4 <50, immunosuppressed | Cryptococcus, MAC, CMV | Depends on organism (see antifungal/antibiotic selection) |
| Immunocompromised, neutropenic | Aspergillus fumigatus | Voriconazole |
TB Drug Toxicities — Must Know
| Drug | Key Toxicity | Mechanism |
|---|---|---|
| Rifampin | Red-orange urine/tears/secretions; hepatotoxic; CYP450 inducer | Induces CYP450 → decreases levels of many co-administered drugs (OCPs, warfarin) |
| Isoniazid (INH) | Peripheral neuropathy; hepatotoxic; drug-induced lupus; B6 deficiency | Inhibits B6 activation enzyme; treat with pyridoxine. Slow acetylators have higher toxicity |
| Pyrazinamide | Hyperuricemia (gout) | Inhibits urate secretion in renal tubule |
| Ethambutol | Optic neuritis → red-green colorblindness | Unknown mechanism; monitor visual acuity and color vision |
Rifampin as Prophylaxis
Rifampin is used as close-contact prophylaxis for Neisseria meningitidis exposure (preferred agent; alternatives: ciprofloxacin, ceftriaxone for pregnant women). Also used for H. influenzae close-contact prophylaxis. Remember: rifampin is also part of many endocarditis regimens (vancomycin + gentamicin + rifampin) and treats leprosy (dapsone + rifampin + clofazimine).
Antifungal Drug Selection
| Infection | First Line | Key Notes |
|---|---|---|
| Invasive aspergillosis | Voriconazole | Second line: amphotericin B. Never use fluconazole (no aspergillus coverage) |
| Mucormycosis | Amphotericin B | Also surgical debridement of necrotic tissue. Occurs in diabetics, DKA, iron-overloaded patients |
| Cryptococcal meningitis (HIV) | Ampho B + flucytosine (induction) → fluconazole (maintenance) | CD4 <100. India ink stain of CSF. Increased opening pressure on LP |
| Histoplasmosis / Coccidioidomycosis | Itraconazole (mild-moderate) | Severe: amphotericin B. Endemic fungi from geographic exposures |
| Tinea (skin/superficial) | Topical azole | For tinea capitis and onychomycosis: oral terbinafine or griseofulvin (penetrates keratin) |
| Candidiasis (vaginal/oral/systemic) | Oral azole (fluconazole) | Systemic / neutropenic: caspofungin or amphotericin B |
EP570
The Clutch Skin and Soft Tissue Infections Podcast
- Erysipelas vs Cellulitis: Erysipelas = face, sharply demarcated elevated red lesion. Cellulitis = lower extremities, flat, poorly demarcated. Both caused primarily by Group A Strep (Strep pyogenes); treat with cell wall inhibitors (penicillin, amoxicillin, cefalexin). Mild → oral; systemic signs → IV
- Impetigo: Honey-colored (golden-yellow) crusted papules on skin. Most common cause = Staph aureus (#1), Group A Strep (#2). Treatment = topical mupirocin (drug of choice)
- Mycobacterium marinum: Nodular skin infection tracking along lymphatics in aquarium workers, fish farmers, swimmers. Treat with clarithromycin + rifampin + ethambutol
- Sporotrichosis (Sporothrix schenckii): Nodular lesions on extremities in gardeners, landscapers, soil exposure. "Rose gardener's disease." Treat with itraconazole. Key differentiator from M. marinum: soil/plant exposure vs water/fish exposure
- Necrotizing fasciitis: Exquisitely tender, rapidly spreading red skin, high fever, systemic toxicity. Requires emergency surgical debridement + clindamycin (protein synthesis inhibitor to halt toxin production). Failure to debride = death
- Pilonidal cyst: Painful lesion / mass above the intergluteal cleft. Management = incision and drainage alone. No antibiotics required unless cellulitis present
Skin Infection Differential — Key Distinguishers
| Infection | Location | Borders | Bug | Treatment|
|---|---|---|---|---|
| Erysipelas | Face (mostly) | Sharp, elevated, bright red | Group A Strep (#1), Staph aureus (#2) | Penicillin / amoxicillin / cefalexin; IV if systemic |
| Cellulitis | Lower extremities (mostly) | Flat, poorly defined | Group A Strep, Staph aureus | Same antibiotics; IV if leukocytosis/fever/sepsis |
| Impetigo | Face / extremities | Honey-colored crusts, not raised | Staph aureus (#1), Strep pyogenes (#2) | Topical mupirocin |
| Folliculitis / furunculosis | Hair follicle | Central hair, pustular | Staph aureus | Warm compresses; I&D for large furuncle |
| Necrotizing fasciitis | Any extremity / perineum | Spreading rapidly; crepitus | Polymicrobial or Group A Strep | Emergency debridement + clindamycin + broad coverage |
Oral vs IV Antibiotics — When to Escalate
Mild infection + no systemic signs → oral cell wall inhibitor. Systemic signs present (temp >102, leukocytosis, tachycardia, hypotension, elevated lactate) → IV therapy. This rule applies to erysipelas, cellulitis, and most other skin infections on NBME exams.
Mycobacterium marinum vs Sporotrichosis — Side by Side
| M. marinum | Sporotrichosis (S. schenckii) | |
|---|---|---|
| Exposure | Water, fish tanks, aquariums, swimming pools | Soil, plants, thorns (rose gardeners, landscapers) |
| Morphology | Nodular lesions tracking along lymphatics | Nodular lesions tracking along lymphatics (sporotrichoid pattern) |
| Treatment | Clarithromycin + rifampin + ethambutol | Itraconazole |
| Bug type | Mycobacterium (non-tuberculous) | Dimorphic fungus |
RR 66EP351
Encapsulated Organisms, Sickle Cell Sepsis & GBS
- Sickle cell + pneumonia / sepsis: Auto-splenectomy → cannot fight encapsulated organisms. Strep pneumo (#1 cause of sepsis in sickle cell). African-American child + high fever + gram-positive diplococci = pneumococcal pneumonia. Treat: ceftriaxone / cefotaxime
- Encapsulated organisms (SHIN): Strep pneumo, H. influenzae, influenza (not bacteria), Neisseria meningitidis. Asplenic patients are vulnerable to all. Prophylactic penicillin in sickle cell children until age 5
- Rheumatic fever — post-Strep sequela: 6 weeks after Group A Strep pharyngitis → migratory polyarthritis, carditis (mitral stenosis), Sydenham chorea, erythema marginatum, Aschoff bodies on biopsy. Treat: penicillin + NSAID. Biggest risk factor for mitral stenosis
- GBS (Guillain-Barré): Ascending paralysis after mucosal infection (GI or respiratory — not only Campylobacter anymore). CSF: albuminocytologic dissociation (markedly elevated protein, 0–3 WBCs). Treat: IVIG or plasmapheresis. Risk: respiratory failure from diaphragm involvement
- Penicillin prophylaxis indications: Sickle cell (age <5), recurrent rheumatic fever. Rheumatic fever = molecular mimicry — Group A Strep antigens mimic cardiac/basal ganglia proteins → autoantibodies attack host
Asplenia and Encapsulated Organisms
The spleen clears encapsulated bacteria via opsonization and phagocytosis. Without a functional spleen (sickle cell auto-infarction, surgical splenectomy, functional asplenia), the patient cannot mount an adequate response. SHIN organisms = most dangerous: Strep pneumo, H. influenzae type b, Influenza virus, Neisseria meningitidis.
| Asplenic Population | Most Dangerous Bug | Prophylaxis |
|---|---|---|
| Sickle cell, age <5 | Strep pneumo (#1) | Daily penicillin prophylaxis until age 5 |
| Surgical splenectomy | Strep pneumo, H. flu, N. meningitidis | Vaccines (pneumococcal, MenACWY, Hib); consider penicillin prophylaxis |
Rheumatic Fever — JONES Criteria
| Major Criteria (JONES) | Minor Criteria |
|---|---|
| J — Joints (migratory polyarthritis) | Fever, elevated ESR/CRP, prolonged PR interval |
| O — Carditis (pancarditis; mitral > aortic) | Prior rheumatic fever history |
| N — Nodules (subcutaneous) | |
| E — Erythema marginatum | |
| S — Sydenham chorea (involuntary movements) |
Need 2 major OR 1 major + 2 minor, plus evidence of prior Group A Strep infection (elevated ASO titer). Aschoff bodies = pathognomonic biopsy finding — multinucleated giant cells in myocardium.
GBS vs ITP — Post-Viral Confusion
Both follow mucosal infection in children. GBS: ascending weakness 2–3 weeks after respiratory/GI illness → albuminocytologic dissociation on LP → IVIG/plasmapheresis. ITP: thrombocytopenia (not weakness) 10 days after URI → autoantibodies against GP2b3a → treat with steroids → IVIG → splenectomy.
GI & Enteric Pathogens
GI infections sort by the type of diarrhea (bloody vs watery vs inflammatory), the timeline, and the exposure source. Knowing which bugs produce pre-formed toxins versus require live organism colonization changes everything — because it changes incubation time, treatment, and the need for antibiotics at all. C. diff is the post-antibiotic colonizer; H. pylori is the peptic ulcer driver; the Salmonella/Shigella/E. coli family maps to geographic and foodborne risk.
EP461
GI Infections — Metronidazole, Anaerobes & H. pylori
- Metronidazole (GET GAP on the metro): G = Gardnerella vaginalis (bacterial vaginosis). E = Entamoeba histolytica (bloody diarrhea + liver abscess). T = Trichomonas vaginalis. G = Giardia lamblia (traveler's diarrhea, IgA deficiency). A = Anaerobes (including BV above/below diaphragm). P = additional parasites. Disulfiram-like effect — no alcohol
- C. difficile treatment: First line = oral vancomycin OR fidaxomicin (not metronidazole anymore). Risk factor = prior antibiotic use (clindamycin classic). Toxic megacolon = complication (transverse colon >6 cm). Treat: NPO + surgery if necrosis signs
- H. pylori triple therapy: Clarithromycin + amoxicillin + PPI. Quadruple therapy: metronidazole + bismuth + tetracycline + PPI. Amoxicillin = aminopenicillin component
- Bacterial vaginosis (Gardnerella): Fishy odor, clue cells, vaginal pH >4.5. Treat with metronidazole or clindamycin
- Clindamycin — coverage profile: Anaerobes (above AND below diaphragm — forget the "above = clinda, below = metro" oversimplification). Also covers MRSA. Strong C. diff association (wipes out normal anaerobic flora). Used for necrotizing fasciitis (protein synthesis inhibitor halts toxin production)
- Trichomoniasis: Motile protozoa on wet prep, vaginal pH >4.5. Treat both partners with metronidazole or tinidazole
Diarrheal Illness — Organism Selection
| Type | Bug | Mechanism | Clue |
|---|---|---|---|
| Watery, rapid onset (1–8 hrs) | Staph aureus (pre-formed toxin) | Heat-stable enterotoxin; no organism needed to grow | Potato salad, mayo; no fever; resolves in 24 hrs |
| Watery, 8–16 hrs | Bacillus cereus (rice) | Two toxins: emetic (early) and diarrheal (late) | Reheated fried rice; biphasic illness |
| Watery, 18–36 hrs | Clostridium perfringens | Toxin produced after ingestion | Reheated meat dishes |
| Bloody diarrhea | EHEC (E. coli O157:H7), Shigella, Salmonella, Campylobacter, C. diff, Entamoeba | Mucosal invasion or toxin-mediated hemorrhage | HUS with EHEC; no antibiotics for EHEC (may precipitate HUS) |
| Traveler's diarrhea (short) | Enterotoxigenic E. coli (ETEC) | Heat-labile toxin (activates adenylyl cyclase → ↑cAMP) | Mexico, developing world travel; watery, no blood |
| Traveler's diarrhea (weeks) | Giardia lamblia | Duodenal attachment; steatorrhea; bloating | IgA deficiency risk; campers; metronidazole |
| Post-antibiotic diarrhea | C. difficile | Spore germination after antibiotic kills normal flora | Clindamycin classic trigger; pseudomembranes; oral vancomycin |
EHEC — Never Give Antibiotics
E. coli O157:H7 causes bloody diarrhea and can progress to Hemolytic Uremic Syndrome (HUS): microangiopathic hemolytic anemia + thrombocytopenia + acute kidney injury. Giving antibiotics causes bacterial lysis → shiga toxin flood → worsens HUS. Treatment is supportive only. TTP has same triad but also has fever + neurologic symptoms (pentad).
C. difficile — Management Hierarchy
- First episode, non-severe: Oral vancomycin 125 mg QID × 10 days OR fidaxomicin 200 mg BID × 10 days
- Severe (WBC >15,000 or creatinine >1.5x baseline): Oral vancomycin 500 mg QID ± IV metronidazole
- Fulminant / toxic megacolon: IV metronidazole + oral vancomycin; surgical consultation for colectomy
- Recurrent C. diff: Consider fecal microbiota transplant (FMT). Also bezlotoxumab as adjunct
- Trigger drugs: Clindamycin (classic), fluoroquinolones, cephalosporins — any broad-spectrum disrupting anaerobic flora
RR 81EP408
Pseudomonas Infections, Ascending Cholangitis & GI Emergencies
- Pseudomonas — special niches: Contact lens wearers → bacterial conjunctivitis. Otitis externa (#1 cause). CF patients age >20 (#1 cause of pneumonia). Nail puncture through shoe → osteomyelitis. Immunocompromised / neutropenic → serious infections. Treat with antipseudomonal agents (pip-tazo, cefepime, ceftazidime, carbapenems, aminoglycosides, fluoroquinolones)
- Ascending cholangitis: Charcot's triad = fever + RUQ pain + jaundice. Retained CBD stone after cholecystectomy → bacteria migrate up bile ducts. Treatment = ERCP (diagnostic + therapeutic) + IV antibiotics (ampicillin + gentamicin + metronidazole covering gram-neg and anaerobes)
- Cholecystitis vs cholangitis: Cholecystitis = cystic duct obstruction → fever + RUQ pain, NO jaundice (bile still flows through CBD). Cholangitis = CBD obstruction → fever + RUQ pain + JAUNDICE. Choledocholithiasis = CBD stone, no fever, just RUQ pain + jaundice
- Ludwig angina: Cellulitis of submandibular and sublingual spaces. Causes airway obstruction. May require emergency intubation (like epiglottitis). Often after dental infection
- Bacterial conjunctivitis: Thick purulent discharge, crusting. Staph aureus = most common. Contact lens user = Pseudomonas
- Pyrogens review: IL-1, IL-6, TNF-alpha → fever. IL-8, LTB4, C5a → neutrophil chemotaxis. TNF-alpha maintains granulomas (TNF inhibitors like adalimumab → granulomatous diseases worsen)
Biliary Pathology — Three-Way Distinction
| Cholecystitis | Choledocholithiasis | Ascending Cholangitis | |
|---|---|---|---|
| Obstructed duct | Cystic duct | Common bile duct | Common bile duct |
| Fever | Yes | No | Yes |
| RUQ pain | Yes | Yes | Yes |
| Jaundice | No (bile still flows) | Yes (CBD blocked) | Yes (CBD blocked) |
| Diagnosis | RUQ ultrasound (gallstones + wall thickening) | RUQ ultrasound / MRCP | ERCP (diagnostic + therapeutic) |
| Treatment | Cholecystectomy; antibiotics if complicated | ERCP to remove stone | ERCP + ampicillin/gentamicin/metronidazole IV |
Key Rule: Jaundice = Common Bile Duct
If bile still flows through the hepatic duct and common bile duct, there will be no jaundice. Therefore: fever + RUQ pain alone = cholecystitis (cystic duct). Add jaundice = CBD is involved (choledocholithiasis or cholangitis). Fever differentiates cholangitis from simple choledocholithiasis.
Pseudomonas — Complete Infection Profile
| Clinical Setting | Infection Type | Treatment |
|---|---|---|
| Contact lens user | Bacterial conjunctivitis (corneal ulcer risk) | Fluoroquinolone eye drops |
| Swimmer's ear | Otitis externa | Acetic acid drops or fluoroquinolone ear drops |
| CF patient, age >20 | Pneumonia | Inhaled tobramycin prophylaxis; antipseudomonal agents |
| Nail puncture through rubber sole | Osteomyelitis (foot) | Ciprofloxacin or anti-pseudomonal penicillin |
| Neutropenic fever | Bacteremia / pneumonia | Antipseudomonal agent is mandatory (cefepime, piperacillin-tazobactam) |
| Diabetic patient | Malignant otitis externa, wound infections | Antipseudomonal agents based on severity |