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

The slide's MSSA/healthcare-associated MRSA/community-associated MRSA table is useful historically, but the categories now overlap. Exposure setting and PVL status do not select treatment by themselves; infection site, severity, source control and susceptibility results do.

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.

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 one blood-culture bottle, you cannot decide from morphology alone: it may be S. aureus, which is clinically important, or a CoNS contaminant. A CoNS isolated from only one of multiple properly collected sets is often contamination, but the patient's condition, device/prosthesis, species, number and timing of positive bottles and repeat cultures all matter ^[10].

Exceptions to the "CoNS = contaminant" rule ^[1]:

Safe practice update: obtain two or more properly collected sets from separate venepunctures before antibiotics when this is feasible, but never delay urgent treatment in an unstable patient. A positive S. aureus blood culture should not be dismissed as routine contamination; repeat cultures help document clearance, while source control and evaluation for metastatic infection/endocarditis are central ^[11]. Repeated recovery of the same CoNS from separate sets, especially with a compatible device or prosthesis, supports true bacteraemia.

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 is included in immunisation programmes, but formulations and schedules change; check the current local schedule rather than memorising the lecture's PCV13/PPSV23-era numbers. No formulation covers every pneumococcal serotype.
• 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]:

Expert practice tip 2: Always remember to screen for colorectal cancer in patients with S. bovis bacteremia or IE ^[1]

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) — an immune-mediated sequela; classically follows pharyngitis, but current CDC guidance recognises that it can follow GAS skin infection as well ^[12]
  • 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

Lecture pearl, narrowed safely: GAS remains susceptible to penicillin and cephalosporins ^[12]

Why is this practice tip so important? Unlike S. aureus (which commonly produces penicillinase), GAS has maintained penicillin susceptibility. This means:

• GAS pharyngitis → Penicillin V orally is first-line
• GAS necrotizing fasciitis → IV penicillin + clindamycin (clindamycin suppresses toxin production)
• Macrolide and clindamycin resistance varies geographically, so susceptibility/local guidance matters; do not generalise the GAS statement to every beta-haemolytic streptococcus or every syndrome ^[12]

• Widely distributed in environment, e.g., soil ^[1]
• B. anthracis: anthrax (cutaneous, pulmonary, GI)
• B. cereus: food poisoning (two syndromes: emetic type from reheated rice — preformed toxin; diarrheal type)
• Bacillus in blood cultures is most often a contaminant ^[1] — similar principle to CoNS

Foodborne exposure is broad (including unpasteurised dairy and ready-to-eat foods). Causes pregnancy-associated and neonatal infection, and invasive CNS/septic disease in older or immunocompromised people ^[13]

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
• Older adults (risk rises particularly from about 65 years; local meningitis protocols define empiric-treatment thresholds differently)
• Pregnant women
• Immunocompromised (transplant recipients, HIV, steroids)

For a patient whose age, immune state, pregnancy status or clinical context creates meaningful Listeria risk, add IV ampicillin/amoxicillin according to the current local meningitis protocol; ceftriaxone does not cover Listeria. Do not use the slide's fixed age greater than 50 years as a universal rule, and never delay urgent empiric treatment while debating the cutoff ^[14].

• 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)
  • Do not wait for confirmation when respiratory diphtheria is suspected: institute droplet precautions, notify public health and arrange antitoxin plus penicillin or erythromycin promptly; cultures and toxigenicity testing still matter ^[15]
• Other coryneforms: opportunistic pathogens; skin/oral commensals; frequently contaminants

The slide groups these opportunists, but their images should not be read as identical morphology:

• Nocardia: branching, beaded filamentous Gram-positive organisms that are variably/weakly acid-fast on a modified stain; pulmonary, CNS and cutaneous nocardiosis, especially in immunocompromised hosts
• Rhodococcus equi: pleomorphic Gram-positive coccobacilli that may be weakly acid-fast, but are not hyphae; classically cause cavitating pneumonia and disseminated disease in immunocompromised people and have an equine/soil association

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]: NTM conventionally excludes the M. tuberculosis complex, M. leprae complex and M. ulcerans ^[16]. An environmental NTM isolate is not automatically disease; pulmonary diagnosis integrates symptoms, imaging and microbiology, often including at least two sputum cultures with the same species.

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.

Why spore-forming matters: C. difficile spores persist in the environment and resist alcohol. Gloves/gowns and effective environmental sporicidal cleaning are therefore crucial. CDC still prefers alcohol-based hand rub in most routine clinical situations, including care of patients with CDI, unless hands are visibly soiled; soap and water is encouraged when hands are soiled and during outbreaks. “Alcohol gel is always forbidden for CDI” is too absolute ^[17].

• GI and genital tract colonizer
• Causes pulmonary/pelvic/abdominal/cervicofacial actinomycosis
• Infection crossing tissue planes — hallmark feature; forms "sulfur granules"
• Pelvic actinomycosis can be associated with prolonged intrauterine-device use, but incidental cervical-smear colonisation is not the same as invasive disease
• Treatment commonly uses penicillin-class therapy plus drainage/debridement when needed; duration is individualised by site, extent, response and adequacy of source control rather than automatically 6–12 months

Classify them as: Enterobacterales, Vibrionaceae & related genera, Non-fermenters, Other GNR ^[1]

Reading the classification slide: the first branch separates aerobic/facultative rods from anaerobic oral/gut rods; the aerobic branch then separates fermenting Enterobacterales, curved/water-associated Vibrionaceae, non-fermenters and miscellaneous fastidious rods. “Enterobacteriaceae” in the older slide is narrower than the modern order Enterobacterales.

Antibiotic Resistance in Enterobacterales ^[1]:

Current terminology: ESBL-producing Enterobacterales hydrolyse many penicillins, oxyimino-cephalosporins and aztreonam but not cephamycins or carbapenems; the final phenotype still depends on additional mechanisms. “CPE” is now expanded to carbapenemase-producing Enterobacterales, within the broader category of carbapenem-resistant Enterobacterales (CRE).

GNR not fermenting glucose or other sugars. Most are environmental bacteria ^[1]

Key features of non-fermenters:

• Mainly nosocomial infections: pneumonia, wound infections, prosthesis-associated ^[1]
• Can be highly resistant to antibiotics ^[1]

Safe update: severe complicated intra-abdominal infection needs prompt source control and an empiric regimen with appropriate enteric Gram-negative and anaerobic activity. Add metronidazole to a regimen that lacks anaerobic cover (for example ceftriaxone), but do not automatically add it to piperacillin-tazobactam or a carbapenem, which already cover B. fragilis ^[19].

Why metronidazole can work: it is reduced in anaerobic organisms to reactive intermediates that damage DNA. It is one useful anti-anaerobic component, not the only acceptable drug and not a substitute for drainage/debridement.