GC105 Medically Important Microbes What Every Doctor Should Know
A foundational medical microbiology framework covering the essential bacteria, viruses, fungi, and parasites that clinicians must recognize for accurate diagnosis, appropriate antimicrobial therapy, and effective infection control.
Medically Important Microbes: What Every Doctor Should Know
This lecture, delivered by Dr. Siddharth Sridhar, is a crash course in systematic classification of medically important microorganisms. The fundamental premise is deceptively simple: you cannot memorize every microbe, but if you build a robust mental classification system, you can slot every new organism into the right place throughout your career [1].
The lecture covers:
- Bacterial classification using Gram stain, morphology, and biochemical tests (catalase, coagulase, hemolysis)
- Clinically important bacteria — Gram-positive cocci, Gram-positive rods, Gram-negative rods, Gram-negative cocci, "unculturable" organisms
- Fungi — yeasts, moulds, dimorphic fungi
- Parasites — protozoa, helminths, ectoparasites
- Virology — organized by clinical syndrome rather than taxonomic classification
How this fits into exams: The Fourth Summative regularly tests organism identification from clinical scenarios (blood culture results, Gram stain findings), antibiotic resistance patterns (MRSA, ESBL, VRE, CPE), and the clinical associations of specific organisms (e.g., S. bovis → colorectal cancer screening). Questions test whether you can link organism → disease → treatment → resistance pattern.
Core Concepts: The Gram Stain as the Foundation
The 'Gram Smear' is the basis of classification of bacteria [1]
The Gram stain is the single most important rapid diagnostic test in clinical microbiology. It takes about 5 minutes and provides two critical pieces of information:
-
Gram reaction: Purple (Gram-positive) vs. Pink (Gram-negative)
- Gram-positive bacteria have a thick peptidoglycan cell wall that retains the crystal violet-iodine complex during alcohol decolorization
- Gram-negative bacteria have a thin peptidoglycan layer plus an outer membrane containing lipopolysaccharide (LPS); they lose the purple dye and pick up the pink counterstain (safranin)
-
Morphology: Cocci (spheres) vs. Rods (bacilli)
- Further arrangement: chains vs. clusters
Why this matters clinically: When a blood culture flags positive, the Gram stain result is the first piece of actionable information. "GPC in clusters" in blood culture triggers a very different antibiotic response (anti-staphylococcal coverage) compared to "GNR" (gram-negative coverage, typically broad-spectrum). The Gram stain bridges the gap between clinical suspicion and culture results (which take 24–48 hours).
| Test | What It Tests | Key Discrimination |
|---|---|---|
| Catalase | Breaks down H₂O₂ → O₂ + H₂O | Staphylococcus (+) vs. Streptococcus (−) |
| Coagulase | Converts fibrinogen → fibrin clot | S. aureus (+) vs. CoNS (−) |
| Hemolysis pattern | Lysis of RBCs on blood agar | Alpha (partial/green), Beta (complete/clear), Gamma (none) |
| Lancefield grouping | Carbohydrate antigen on cell wall | Groups A, B, C, D, G for beta-hemolytic streptococci |
| Oxidase | Cytochrome c oxidase presence | Pseudomonas (+) vs. Enterobacterales (−) |
| Glucose fermentation | Can organism ferment glucose? | Enterobacterales (yes) vs. Non-fermenters (no) |
Section 1: Gram-Positive Cocci (GPC)
1A. Staphylococcus — GPC in Clusters, Catalase Positive
GPC in clusters: Staphylococcus [1]
S. aureus is arguably the single most important pathogenic bacterium you will encounter. It is a commensal of the anterior nares (~30% of population are carriers) but causes a staggering range of infections.
Infections caused by S. aureus [1]:
- Skin/soft tissue infections — cellulitis, abscesses, wound infections
- Abscesses — can occur anywhere (brain, liver, spleen, muscle)
- Native/prosthetic joint septic arthritis
- Osteomyelitis — #1 cause in all age groups
- Pneumonia — post-influenza pneumonia, ventilator-associated pneumonia
- Infective endocarditis — both native and prosthetic valves; acute presentation
- Endovascular infections — mycotic aneurysms, infected grafts
- Surgical site infections
Toxin-mediated diseases [1]:
- Food poisoning by staphylococcal enterotoxin — preformed toxin; onset 1–6 hours; vomiting predominant; self-limiting
- Toxic shock syndrome (TSS) — superantigen (TSST-1) → massive T-cell activation → cytokine storm → shock, diffuse erythroderma, desquamation
- Scalded skin syndrome (SSSS) — exfoliative toxins A and B → cleavage of desmoglein-1 in epidermis; mainly in neonates/young children
Why S. aureus Is Such a Versatile Pathogen
S. aureus produces a remarkable arsenal of virulence factors: protein A (binds Fc portion of IgG, preventing opsonization), coagulase (creates fibrin shield around bacteria), hemolysins, leukocidins (Panton-Valentine leukocidin/PVL in CA-MRSA), and multiple superantigens. This explains why it can cause such diverse diseases — from localized skin abscesses to systemic septic shock.
This table is directly from the lecture and is extremely high yield [1]
| Subtype | Antibiotic Susceptibility | Treatment | Notes |
|---|---|---|---|
| MSSA | Sensitive to most β-lactams | Cloxacillin (first-line) | — |
| HA-MRSA | Resistant to β-lactams; often resistant to other agents (e.g., clindamycin) | Vancomycin, Linezolid, Daptomycin, Ceftaroline | Carriage common in old age home residents & after prolonged hospitalization |
| CA-MRSA | Resistant to β-lactams; often less resistant to non-β-lactam agents | Same as HA-MRSA + any susceptible antibiotic | May carry PVL toxin |
| VISA/VRSA | Intermediate to full resistance to glycopeptides | Linezolid, Daptomycin, Ceftaroline, etc. | Very rare |
Why cloxacillin for MSSA, not amoxicillin? Cloxacillin is a penicillinase-resistant penicillin — S. aureus almost universally produces penicillinase (β-lactamase), so plain penicillin/amoxicillin won't work. But cloxacillin resists this enzyme, making it the drug of choice for MSSA.
Why vancomycin for MRSA? MRSA carries the mecA gene encoding PBP2a (penicillin-binding protein 2a), which has very low affinity for all β-lactams. Vancomycin works by binding D-Ala-D-Ala peptidoglycan precursors — a completely different mechanism that bypasses PBP2a resistance.
HA-MRSA vs. CA-MRSA
HA-MRSA = hospital-associated; multiresistant; typically SCCmec types I-III (large cassette carrying multiple resistance genes). CA-MRSA = community-associated; often susceptible to clindamycin, TMP-SMX; SCCmec types IV-V (smaller); may carry PVL toxin → necrotizing pneumonia, recurrent abscesses. The practical implication: CA-MRSA infections may have more antibiotic options beyond vancomycin.
Usually benign commensals of skin. Single blood culture isolates of CNS usually represent contamination [1]
This is a critical clinical concept. When you see "GPC in clusters" in a single blood culture bottle, you cannot automatically assume infection. Most single CoNS isolates are contaminants from skin flora during phlebotomy.
Exceptions to the "CoNS = contaminant" rule [1]:
| Species | Clinical Significance |
|---|---|
| S. saprophyticus | UTI (especially in young sexually active women) |
| S. lugdunensis | Virulent organism — behaves more like S. aureus; can cause aggressive endocarditis |
| S. epidermidis | Prosthesis/catheter-associated infections (biofilm formation) |
Expert practice tip 1: Whenever your patient has GPC in clusters in blood culture, always repeat at least TWO sets blood culture before making any change in antibiotics [1]
Why repeat two sets? Because if only one bottle grows CoNS, it's likely contamination. If multiple sets (≥ 2 from different venipuncture sites) grow the same CoNS species, genuine bacteremia becomes much more likely — especially in patients with indwelling devices.
1B. Streptococcus — GPC in Chains, Catalase Negative
Organize streptococci in your mind according to their hemolysis pattern. Remember the Lancefield grouping for the beta-hemolytic streptococci [1]
| Hemolysis | Appearance on Blood Agar | Key Species |
|---|---|---|
| Alpha (α) | Partial hemolysis → green discoloration | S. pneumoniae, Viridans group |
| Beta (β) | Complete hemolysis → clear zone | S. pyogenes (GAS), S. agalactiae (GBS) |
| Gamma (γ) | No hemolysis | Enterococcus (classified separately) |
S. pneumoniae (Pneumococcus) [1]:
Causes more than pneumonia: meningitis, septicemia, otitis media, sinusitis [1]
Key points:
- Emergence of strains intermediate or wholly resistant to penicillin — this is clinically important because empiric meningitis treatment with penicillin alone may fail
- Vaccination included in universal program (PCV13 in HK childhood immunization) but doesn't cover all serotypes well — > 90 serotypes exist; vaccine only covers 13 or 23 depending on formulation
- Encapsulated organism → virulence depends on the polysaccharide capsule evading phagocytosis
- Asplenic/hyposplenic patients are at extreme risk for overwhelming pneumococcal sepsis (this connects to the 2021 SAQ Q12c about post-transplant patients with Howell-Jolly bodies [3])
Other Important Streptococci [1]:
| Species | Key Associations |
|---|---|
| Viridans streptococci | Dental caries, infective endocarditis (subacute; on damaged native valves) |
| S. anginosus (S. milleri) | Abscess formation — liver, brain, lung abscesses |
| S. bovis (now: S. gallolyticus, S. infantarius, S. pasteurianus) | Bacteremia, endocarditis; associated with underlying GI malignancy |
| S. suis | Important cause of meningitis & bacteremia in HK — occupational exposure (pig farmers, butchers) |
Expert practice tip 2: Always remember to screen for colorectal cancer in patients with S. bovis bacteremia or IE [1]
S. bovis → Colonoscopy
This is a classic exam question. The mechanism is thought to involve translocation of S. bovis/gallolyticus through a disrupted colonic mucosa harboring a malignancy. Any patient with S. bovis/gallolyticus bacteremia or infective endocarditis MUST be referred for colonoscopy regardless of symptoms. Students frequently forget this association.
S. pyogenes (Group A Streptococcus, GAS) [1]:
- Infections: pharyngitis, scarlet fever, impetigo, cellulitis, necrotizing fasciitis
- Toxin-mediated: Toxic shock syndrome (streptococcal superantigens)
- Post-infectious immune-mediated syndromes:
- Acute rheumatic fever (ARF) — molecular mimicry between M protein and cardiac myosin; follows pharyngitis (NOT skin infections)
- Post-streptococcal glomerulonephritis (PSGN) — immune complex deposition; can follow pharyngitis OR skin infections
S. agalactiae (Group B Streptococcus, GBS) [1]:
- Neonatal sepsis/meningitis, peripartum infections
- Invasive in elderly/immunocompromised
- Cases in HK recently — emerging invasive GBS disease in adults, particularly linked to raw fish consumption in Southeast Asia
Group C & G streptococci [1]:
- Skin and soft tissue infections
Expert practice tip 3: Beta-hemolytic streptococci are sensitive to penicillin [1]
Why is this practice tip so important? Unlike S. aureus (which almost always produces penicillinase), beta-hemolytic streptococci have maintained penicillin susceptibility for decades. This means:
- GAS pharyngitis → Penicillin V orally is first-line
- GAS necrotizing fasciitis → IV penicillin + clindamycin (clindamycin suppresses toxin production)
- You never need to "upgrade" to broader agents for confirmed beta-hemolytic strep
Normal gut flora; mainly opportunistic infections [1]
- E. faecium & E. faecalis most common species
- Diseases: catheter-associated UTI, endocarditis, component of polymicrobial intra-abdominal/biliary infections, line sepsis [1]
Intrinsic Resistance of Enterococcus
Enterococci are intrinsically resistant to cephalosporins [1]. This is a crucial exam fact. If your patient has enterococcal infection, cephalosporins will NOT work — you need ampicillin (for E. faecalis) or vancomycin. This also means that empiric cephalosporin therapy for UTI or intra-abdominal sepsis will NOT cover Enterococcus.
- VRE (vancomycin-resistant Enterococcus) — usually E. faecium; carries vanA or vanB gene
- Treatment: daptomycin, linezolid, tigecycline [1]
- VRE is a major nosocomial MDR organism
Section 2: Gram-Positive Rods (GPR)
2A. Aerobic GPR
Organized from the lecture classification tree [1]
Association with milk & chicken. Causes neonatal meningitis & infections in pregnancy. CNS infections in elderly/immunocompromised [1]
Key pharmacological point:
Resistant to cephalosporins, sensitive to ampicillin [1]
Expert practice tip 4: Consider adding ampicillin for Listeria coverage on top of ceftriaxone if you encounter high-risk patients with meningitis [1]
Why is this practice tip critical? The standard empiric therapy for bacterial meningitis is ceftriaxone (a 3rd-generation cephalosporin). However, Listeria is intrinsically resistant to all cephalosporins because of its unique PBP profile. High-risk groups for Listeria meningitis include:
- Neonates
- Elderly ( > 50 years)
- Pregnant women
- Immunocompromised (transplant recipients, HIV, steroids)
For these patients, you MUST add ampicillin to ceftriaxone. This is directly tested in the 2025 MCQ Q36 [4], where ceftriaxone is the answer for empirical bacterial CNS infection — but the nuance of adding ampicillin for Listeria coverage is important.
- C. diphtheriae: respiratory and cutaneous diphtheria
- Rare in HK due to universal vaccination
- Sore throat with adherent grey pseudo-membrane in oropharynx
- Cervical lymphadenopathy, toxin-mediated cardiac and neurological complications (diphtheria toxin inhibits protein synthesis via ADP-ribosylation of EF-2)
- Other coryneforms: opportunistic pathogens; skin/oral commensals; frequently contaminants
- Opportunistic pathogens causing chronic infections in very immunocompromised patients
- Weakly acid-fast (modified acid-fast stain positive) — distinguishes them from regular GPR
- Nocardia: pulmonary, CNS & cutaneous nocardiosis — think of it in transplant recipients with brain abscess + pulmonary nodules
- Rhodococcus: zoonotic organism; pneumonia, lymphadenopathy, wound infections
Acid-fast bacilli. Gram positive cell structure; does not retain Gram stain well [1]
NOT ALL AFB is TB, not all Mycobacteria are TB [1]
This is a critical conceptual point. When the lab reports "AFB smear positive," students reflexively think TB. But NTM (non-tuberculous mycobacteria) are also acid-fast and are increasingly common, especially in immunocompromised patients.
M. tuberculosis — endemic in HK; covered separately in TB clerkship
Non-Tuberculous Mycobacteria (NTM) [1]:
| Species | Key Association |
|---|---|
| M. marinum | Skin/soft tissue infection among fishermen (aquarium granuloma) |
| M. avium-intracellulare (MAC) | Lung disease in elderly women ("Lady Windermere's syndrome"); disseminated in AIDS with CD4 < 50 |
| M. leprae | Leprosy; cutaneous ± neuronal involvement |
| M. abscessus/chelonae | Fast-growing mycobacteria; various opportunistic infections; notoriously difficult to treat |
The 2024 MCQ Q8 [5] tests this concept: a leukemia patient with persistent neutropenic fever grows AFB from CVC tip and blood — the answer is M. fortuitum (a rapid grower, catheter-related NTM infection), NOT M. tuberculosis or M. leprae.
2B. Anaerobic GPR [1]
| Species | Disease |
|---|---|
| C. perfringens | Gas gangrene, food poisoning, biliary sepsis |
| C. tetani | Tetanus (tetanospasmin → blocks glycine/GABA release → spastic paralysis) |
| C. botulinum | Botulism (blocks ACh release → flaccid paralysis) |
| C. difficile | Pseudomembranous colitis (toxin A & B; associated with antibiotic use, especially clindamycin, fluoroquinolones, broad-spectrum cephalosporins) |
Why spore-forming matters: Spores are extremely resistant to heat, drying, and disinfection. C. difficile spores survive alcohol hand gel — this is why soap and water hand washing is required for C. difficile infection control (alcohol gel insufficient).
- GI and genital tract colonizer
- Causes pulmonary/pelvic/abdominal/cervicofacial actinomycosis
- Infection crossing tissue planes — hallmark feature; forms "sulfur granules"
- Pelvic actinomycosis associated with IUCD use
- Treatment requires prolonged courses of antibiotics (typically 6–12 months of penicillin/amoxicillin)
Section 3: Gram-Negative Organisms
3A. Gram-Negative Rods (GNR) — Aerobic/Facultative Anaerobes
Classify them as: Enterobacterales, Vibrionaceae & related genera, Non-fermenters, Other GNR [1]
| Organisms | Disease Associations |
|---|---|
| E. coli | UTI (#1 cause), intra-abdominal infections, neonatal meningitis (K1 capsule), diarrheal syndromes (ETEC, EHEC, EIEC, EPEC, EAEC) |
| Klebsiella | UTI, pneumonia (lobar, "currant jelly" sputum), liver abscess (K. pneumoniae K1/K2 in diabetics — especially HK/East Asia) |
| Proteus | UTI (urease → alkaline urine → struvite stones), wound infections |
| Enterobacter | Nosocomial infections; AmpC β-lactamase (inducible resistance to 3rd-gen cephalosporins) |
| Citrobacter, Morganella, Serratia | Nosocomial infections |
| Salmonella (non-typhoidal) | Gastroenteritis; bacteremia in immunocompromised |
| Shigella | Dysentery (bloody diarrhea, tenesmus) |
| Yersinia | Y. enterocolitica (mesenteric adenitis mimicking appendicitis), Y. pestis (plague) |
Antibiotic Resistance in Enterobacterales [1]:
ESBL-producers: Resistant to β-lactams except carbapenems [1] CPE (Carbapenemase-producing Enterobacteriaceae) — resistant to carbapenems; extremely limited treatment options
Expert practice tip 5: If you have a patient with documented severe infection due to ESBL +ve Enterobacteriaceae, carbapenems are the antibiotic of choice [1]
ESBL and CPE — The Resistance Ladder
Think of antibiotic resistance as a ladder:
- Wild-type: susceptible to ampicillin, cephalosporins
- AmpC producers: resistant to ampicillin + some cephalosporins; use cefepime or carbapenems
- ESBL: resistant to ALL penicillins and cephalosporins → carbapenems are treatment of choice
- CPE: resistant to carbapenems → may need colistin, ceftazidime-avibactam, or combination therapy
The 2024 SAQ Q12b identifies ESBL-producing E. coli as the most common multidrug-resistant gram-negative bacteria in HK hospital-acquired infections [5]. The 2020 MCQ Q83 also tests this [6].
| Organism | Disease |
|---|---|
| V. cholerae O1 & O139 | Cholera epidemics (rice-water stool, severe dehydration) |
| Non-O1, Non-O139 V. cholerae | Diarrhea (less severe) |
| V. vulnificus | Necrotizing fasciitis — classically in chronic liver disease patients after raw seafood exposure or seawater wound contamination; extremely high mortality |
| V. parahaemolyticus | Food poisoning (seafood) |
| Aeromonas, Plesiomonas | Gastroenteritis, wound infections |
GNR not fermenting glucose or other sugars. Most are environmental bacteria [1]
| Organism | Clinical Significance |
|---|---|
| Pseudomonas aeruginosa | Nosocomial pneumonia (VAP), UTI, wound infections, otitis externa, chronic infections in CF patients; intrinsically resistant to many antibiotics |
| Acinetobacter baumannii | Nosocomial infections; often MDR; ventilator-associated pneumonia |
| Stenotrophomonas maltophilia | Nosocomial; intrinsically resistant to carbapenems; treat with TMP-SMX |
| Burkholderia cepacia complex | Chronic lung infection in CF patients |
| Burkholderia pseudomallei | Severe pneumonia, sepsis syndromes in elderly, often associated with soil exposure (melioidosis — endemic in SE Asia/Northern Australia) |
Key features of non-fermenters:
| Organism | Key Disease Associations |
|---|---|
| Haemophilus influenzae | Hib (type b): severe sepsis, meningitis, epiglottitis — vaccine preventable; Non-typeable Hi: sinusitis, otitis media — no vaccine |
| Legionella pneumophila | Community-acquired pneumonia (atypical CAP; contaminated water systems/cooling towers); diagnose by urinary antigen |
| Campylobacter spp. | Gastroenteritis (most common bacterial cause worldwide); associated with Guillain-Barré syndrome |
| Helicobacter pylori | Gastric ulcers, Ca stomach (Group 1 carcinogen); diagnosed by CLO test, urea breath test [7] |
| Brucella species | Febrile illness, osteoarticular infections (zoonotic; undulant fever) |
| HACEK group | Fastidious organisms; rare cause of infective endocarditis — important for culture-negative endocarditis workup |
Expert practice tip 6: Consider adding metronidazole in patients with severe intraabdominal sepsis to cover Bacteroides fragilis [1]
| Organism | Key Associations |
|---|---|
| Fusobacterium spp. | Lemierre's disease (internal jugular vein thrombophlebitis after pharyngitis), brain abscess |
| Bacteroides fragilis | GI tract colonizer; complicated intra-abdominal infections; increasing antimicrobial resistance |
Why metronidazole? B. fragilis produces β-lactamases making it resistant to many penicillins. Metronidazole is activated under anaerobic conditions (reduced by ferredoxin) to form toxic free radicals that damage bacterial DNA. It is the gold-standard anti-anaerobic drug.
| Organism | Key Features |
|---|---|
| Moraxella catarrhalis | Oral commensal; acute bacterial sinusitis, otitis media; may be implicated in COPD exacerbations |
| N. gonorrhoeae | Gonorrhea; genital and extragenital manifestations; tenosynovitis-arthritis-dermatitis syndrome, Fitz-Hugh-Curtis syndrome, PID, gonococcal ophthalmia neonatorum, rarely gonococcal endocarditis |
| N. meningitidis | Meningococcemia, meningitis; vaccine preventable |
N. meningitidis and Post-Splenectomy Sepsis
N. meningitidis is an encapsulated organism. Patients with functional/anatomic asplenia (e.g., post-BMT with Howell-Jolly bodies on blood smear, as tested in 2021 SAQ Q12c [3]) are at extreme risk for fulminant meningococcal sepsis. Other encapsulated organisms to fear in asplenic patients: S. pneumoniae and H. influenzae type b. Vaccination against all three + antibiotic prophylaxis is mandatory.
These organisms cannot be grown on standard culture media or do not Gram stain well. Diagnosis relies on serology, PCR, or specialized culture.
| Category | Organisms | Key Diseases |
|---|---|---|
| Spirochaetes | Treponema pallidum | Syphilis (primary, secondary, tertiary) |
| Borrelia recurrentis | Relapsing fever | |
| Borrelia burgdorferi | Lyme disease (erythema migrans, arthritis, carditis, neuroborreliosis) | |
| Leptospira | Leptospirosis (Weil's disease: jaundice + renal failure + hemorrhage) | |
| Cell-wall-deficient | Mycoplasma & Ureaplasma | Atypical pneumonia (M. pneumoniae), urethritis (Ureaplasma) |
| Obligate intracellular | Chlamydia & Chlamydophila | C. trachomatis: STI, trachoma, lymphogranuloma venereum; C. pneumoniae: atypical pneumonia; C. psittaci: psittacosis |
| Coxiella burnetii | Q fever (pneumonia, hepatitis, endocarditis) | |
| Rickettsia spp. & Orientia tsutsugamushi | Typhus, spotted fever, scrub typhus | |
| Other | Bartonella quintana | Trench fever |
| Bartonella henselae | Cat-scratch disease |
Section 5: Fungi [1]
| Type | Morphology | Key Examples |
|---|---|---|
| Yeasts | Unicellular, budding | Candida, Cryptococcus, Trichosporon, Malassezia |
| Moulds | Multicellular, hyphae | Dermatophytes, Aspergillus, Zygomycetes, Fusarium |
| Dimorphic | Mould at 25°C, yeast at 37°C | Histoplasma, Blastomyces, Coccidioides, Sporothrix, Paracoccidioides, Penicillium marneffei |
| Special | Unique classification | Pneumocystis jirovecii (atypical fungus; causes PJP in immunocompromised) |
Candida species:
- Mucosal candidiasis (oral thrush, vulvovaginal candidiasis)
- Systemic infections in immunocompromised and ICU patients (candidemia — high mortality)
- Important species: C. albicans (most common), C. parapsilosis (catheter-associated), C. krusei (intrinsically fluconazole-resistant), C. glabrata (often fluconazole-resistant), C. auris (emerging MDR, nosocomial outbreaks)
Cryptococcus neoformans / C. gattii:
- Opportunistic meningitis (chronic, subacute; CSF India ink positive; diagnose by cryptococcal antigen)
- Systemic infections in immunocompromised (especially HIV with CD4 < 100)
Dermatophytes: Tinea pedis, Tinea cruris, Tinea corporis, Onychomycosis
- Trichophyton, Microsporum, Epidermophyton
Invasive moulds:
| Mould | Key Features |
|---|---|
| Aspergillus (A. fumigatus, A. flavus, A. niger) | Invasive aspergillosis in neutropenic patients; allergic bronchopulmonary aspergillosis (ABPA); aspergilloma |
| Zygomycetes (Rhizopus, Mucor) | Rhinocerebral mucormycosis in diabetic ketoacidosis; angioinvasive |
| Fusarium | Disseminated infection in severely neutropenic patients |
All dimorphic fungi follow the rule: "mould in the cold, yeast in the heat" (environmental mould form at 25°C → yeast form at 37°C body temperature). Geographic distribution is key to diagnosis.
| Fungus | Endemic Area | Key Features |
|---|---|---|
| Histoplasma capsulatum | Ohio/Mississippi River valleys, SE Asia | Cave exploring, bird/bat droppings exposure |
| Coccidioides immitis | SW USA, Mexico | "Valley fever"; desert soil exposure |
| Blastomyces dermatitidis | Great Lakes, Ohio/Mississippi | Pulmonary + skin/bone involvement |
| Paracoccidioides brasiliensis | Latin America | "Captain's wheel" yeast form |
| Sporothrix schenckii | Worldwide | Sporotrichosis; rose gardener's disease; lymphocutaneous spread |
| Penicillium marneffei (now Talaromyces marneffei) | SE Asia (including HK) | Important opportunistic infection in HIV in this region |
| Depth | Examples |
|---|---|
| Superficial mycoses | Tinea, onychomycosis, cutaneous candidiasis, pityriasis versicolor |
| Subcutaneous mycoses | Mycetoma, sporotrichosis |
| Deep/systemic mycoses | Invasive aspergillosis, cryptococcal meningitis, disseminated candidiasis, endemic mycoses |
| Category | Organisms | Key Diseases |
|---|---|---|
| Protozoa | Plasmodium (P. falciparum, P. vivax, P. ovale, P. malariae, P. knowlesi) | Malaria (chemoprophylaxis available — 2024 MCQ Q86 [5]) |
| Giardia lamblia | Giardiasis (watery diarrhea, malabsorption) | |
| Entamoeba histolytica | Amoebic dysentery, liver abscess | |
| Naegleria, Acanthamoeba | Primary amoebic meningoencephalitis, keratitis | |
| Toxoplasma gondii | Toxoplasmosis (congenital infection; reactivation in AIDS) | |
| Helminths | Nematodes (roundworms) | Ascaris, hookworm, Strongyloides, Enterobius |
| Trematodes (flukes) | Schistosoma, Clonorchis | |
| Cestodes (tapeworms) | Taenia, Echinococcus | |
| Ectoparasites | Sarcoptes scabiei | Scabies |
| Lice, fleas | Pediculosis |
The lecture explicitly states: learn virology by diagnostic syndromes, NOT by taxonomic classification [1]
Expected to recognize: common viral causes of each syndrome, routes of transmission, infection control; multiple viruses can cause any one syndrome; same virus can cause more than one syndrome [1]
| Viral Syndrome | Important Viral Causes |
|---|---|
| Respiratory tract infection | Rhinovirus, Enterovirus, Coronavirus (HKU1, NL63, OC43, 229E, SARS-CoV-2), Parainfluenza 1-4, RSV, HMPV, Adenovirus, Influenza A & B, Bocavirus |
| Viral hepatitis | HAV, HBV, HCV, HDV, HEV |
| Gastroenteritis | Norovirus, Rotavirus, Adenovirus 40/41, Sapovirus |
| Meningoencephalitis | Enterovirus, HSV-1, VZV, Japanese encephalitis virus, Rabies |
| Myelitis | Enterovirus D68, Poliovirus |
| Myocarditis | Coxsackievirus B, Adenovirus, Parvovirus B19 |
| Viral exanthems/arboviruses | Measles, Rubella, HHV-6, Parvovirus B19, Dengue, Chikungunya, Zika |
| Viral hemorrhagic fever | Ebola, Marburg, Dengue (severe), Crimean-Congo HF |
| HIV and infections in immunocompromised | HIV, CMV, EBV, HHV-8, JC virus, BK virus |
| Cancer-associated viruses | HPV, EBV, HBV, HCV, HHV-8, HTLV-1 |
Respiratory Virus Hierarchy
The lecture presents a gradient of propensity to cause lower respiratory tract illness [1]:
- Upper respiratory predominant: Bocavirus, Rhinovirus/Enterovirus → Coronavirus (seasonal) → Parainfluenza
- Lower respiratory predominant: RSV, HMPV → Adenovirus → Influenza A/B → MERS-CoV, SARS-CoV-2
But any respiratory virus can cause infection of any part of the respiratory tract — e.g., influenza is usually URTI; rhinovirus can trigger asthma attacks; Enterovirus D68 can cause acute lower respiratory illness.
These "expert practice tips" from the lecture are essentially the lecturer's way of flagging high-yield exam points and real-world clinical pearls:
| Tip # | Content | Why It Matters |
|---|---|---|
| 1 | GPC in clusters in blood culture → repeat ≥ 2 sets before changing antibiotics | Distinguishes true S. aureus bacteremia from CoNS contamination |
| 2 | S. bovis bacteremia/IE → screen for colorectal cancer | S. bovis/gallolyticus translocates through disrupted colonic mucosa |
| 3 | Beta-hemolytic streptococci are sensitive to penicillin | No resistance to date; penicillin remains first-line |
| 4 | Add ampicillin to ceftriaxone for Listeria coverage in high-risk meningitis | Listeria is resistant to all cephalosporins |
| 5 | ESBL +ve Enterobacterales → carbapenems are drug of choice | ESBL hydrolyzes all cephalosporins; carbapenems are stable |
| 6 | Add metronidazole for Bacteroides fragilis in severe intra-abdominal sepsis | B. fragilis is β-lactamase producing; metronidazole is the standard anti-anaerobic |
Integration with Past Paper Themes
| Part | Answer | Source |
|---|---|---|
| (a) Most common MDR Gram-positive (contact) | MRSA | GC 105 [1] |
| (b) Most common MDR Gram-negative (contact) | ESBL-producing E. coli | GC 105 [1], GC 104 |
| (c) Most common MDR yeast (contact) | Candida auris | GC 105 [1] |
| (d) Most common bacterial cause of infectious diarrhea (contact, hospital) | C. difficile | GC 105 [1] |
| (e) Three airborne microbes (hospital) | M. tuberculosis, VZV, Measles virus | GC 104 |
| (f) Three bloodborne viruses | HBV, HCV, HIV | GC 104 |
| Timepoint | Expected Organisms | Rationale |
|---|---|---|
| Day 10 (pre-engraftment, profound neutropenia) | S. epidermidis (CoNS), Viridans streptococci, E. coli, Pseudomonas, Klebsiella | Neutropenia → bacteria from gut translocation + skin flora via central line |
| Day 28 (post-engraftment, non-compliant with prophylaxis) | CMV, Aspergillus, PJP (Pneumocystis jirovecii) | Impaired cell-mediated immunity; typical if not taking prophylaxis |
| 4 years post (functional hyposplenism, Howell-Jolly bodies) | S. pneumoniae, N. meningitidis, H. influenzae | Encapsulated organisms; asplenia/hyposplenism post-BMT |
- Answer: M. fortuitum (rapid-growing NTM associated with catheter-related infections)
- NOT M. tuberculosis (unlikely to grow from catheter tip), M. leprae (cannot be cultured), or M. marinum (aquatic exposure)
- Answer: MRSA (historically the most prevalent MDR organism overall in HA hospitals, though ESBL-E. coli is the most common MDR gram-negative)
- Answer: Viridans streptococci (Streptococcus viridans) — bacterial causes predominate in early neutropenia; fungal causes (Aspergillus, Candida) typically emerge after 7+ days of persistent neutropenia, but at day 10 bacteria are still most likely in this MCQ context
- (a) Clinical diagnosis: viral encephalitis/meningoencephalitis
- (c) Infective causes: HSV-1, Japanese encephalitis virus, Enterovirus
- (d) Empirical therapy: IV aciclovir (for HSV encephalitis) ± ceftriaxone (to cover bacterial causes)
1. SAQ: A 70-year-old nursing home resident develops fever and purulent wound discharge after hip replacement surgery. Blood cultures show GPC in clusters.
- (a) What is the most likely organism? → S. aureus (coagulase-positive) or CoNS
- (b) What resistance pattern should you anticipate? → HA-MRSA (nursing home resident)
- (c) What empirical antibiotic would you start? → Vancomycin
- (d) How would you confirm this is not a contaminant? → Repeat ≥ 2 sets blood cultures from different sites
2. SAQ: A 55-year-old man with S. gallolyticus endocarditis.
- What additional investigation is essential? → Colonoscopy (screening for colorectal malignancy)
3. MCQ: Which of the following organisms is intrinsically resistant to cephalosporins?
- A) S. pneumoniae B) E. coli C) Listeria monocytogenes D) S. pyogenes → Answer: C
4. SAQ: Name 3 encapsulated organisms that cause fulminant sepsis in asplenic patients.
- S. pneumoniae, N. meningitidis, H. influenzae type b
5. MCQ: A patient with ESBL-producing E. coli UTI progressing to sepsis. What is the antibiotic of choice?
- Carbapenem (e.g., meropenem, ertapenem)
6. SAQ: Name 3 organisms causing nosocomial diarrhea by contact transmission.
- C. difficile (most common), Norovirus, ESBL-producing Enterobacterales
7. MCQ: An immunocompromised patient develops chronic pneumonia and brain abscess. Weakly acid-fast filamentous organisms are seen on stain. What is the organism?
- Nocardia
8. SAQ: A fishmonger presents with a chronic skin nodule on his hand. AFB stain is positive. What organism is most likely?
- M. marinum
High Yield Summary
The Gram stain divides the bacterial world into a manageable classification tree. For exams, you must be able to:
- Trace the classification: Gram reaction → morphology → catalase/coagulase/hemolysis → species
- Know the key clinical associations for each major organism (S. aureus infections + toxin diseases, S. bovis → CRC, Listeria → cephalosporin resistance, S. suis → HK meningitis, VRE treatment options, ESBL → carbapenems)
- Apply the 6 Expert Practice Tips from this lecture — these are direct exam question stems
- Recognize antibiotic resistance patterns: MSSA → cloxacillin; MRSA → vancomycin; ESBL → carbapenems; VRE → daptomycin/linezolid; Enterococcus intrinsically resistant to cephalosporins; Listeria resistant to cephalosporins
- Not all AFB is TB — NTM species have distinct clinical presentations (M. marinum fishermen, MAC in AIDS, M. abscessus rapid grower)
- Learn virology by clinical syndrome, not taxonomy
- Fungi: Candida auris = emerging MDR nosocomial yeast; Cryptococcus = AIDS meningitis; Aspergillus = neutropenic patients; dimorphic fungi = geographic exposure
- Post-BMT infection timeline: Pre-engraftment (bacteria), Post-engraftment (CMV, fungi), Late (encapsulated organisms in hyposplenism)
Active Recall - Medically Important Microbes
[1] Lecture slides: GC 105. Medically important microbes what every doctor should know.pdf (all slides) [2] Senior notes: Gen Clerk Anaes + Microbiology Summary.pdf (Microbiology section) [3] Past papers: 2021 Fourth Summative SAQ.pdf (Q12 — post-BMT infections) [4] Past papers: 2025 Fourth Summative MCQ.pdf (Q36 — empirical CNS antibiotics) [5] Past papers: 2024 Fourth Summative MCQ.pdf (Q8 — AFB from CVC; Q84 — neutropenic fever; Q86 — malaria prophylaxis); 2024 Fourth Summative SAQ.pdf (Q12 — MDR organisms and transmission) [6] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q82 — neutropenic fever organism; Q83 — most common MDR organism in HK) [7] Senior notes: Block A - Upper abdominal pain_ peptic ulcer; pancreatitis and gallstone.pdf (H. pylori section) [8] Past papers: 2019 Fourth Summative SAQ.pdf (Q10 — encephalitis with seizure)
GC104 Infection Outbreak: Infection Control
An infection outbreak is the occurrence of cases of a particular infectious disease in excess of what is normally expected in a defined community or area, requiring coordinated infection control measures such as surveillance, isolation, and containment to prevent further spread.
GC106 Practical Issues In Antibiotic Use
Practical issues in antibiotic use encompass clinical considerations such as appropriate drug selection, dosing, route of administration, duration of therapy, spectrum of activity, drug interactions, adverse effects, and antibiotic stewardship to optimize efficacy and minimize resistance.