For most procedures, the lecture uses a single IV dose of cefazolin (a first-generation cephalosporin). ^[1]

Why cefazolin specifically? ^[1][5]

• Spectrum: Excellent activity against S. aureus (MSSA), Streptococcus spp., and common Gram-negative skin flora (E. coli)
• Half-life: ~2 hours — longer than other 1st-gen cephalosporins → fewer redoses needed
• Tissue penetration: Achieves high blood and tissue levels
• Proven efficacy: > 15 years of evidence
• Safety profile: Good; low toxicity

The lecture's PK curve shows serum concentrations after 1 g IV cefazolin remaining above several illustrative organism MIC lines. Read the diagram for its principle, not as a universal promise of 8–9 hours of protection: SSI prevention depends on adequate tissue concentration from incision through closure, and patient weight, procedure length, blood loss, renal function and organism MIC all matter. ^[1][13]

Current dose check: Hong Kong IMPACT 6 lists cefazolin 1–2 g IV with redosing at 4 hours and gives weight-adjusted adult examples (1 g at ≤80 kg, 2 g at 81–120 kg, 3 g above 120 kg). International SHEA/IDSA/APIC guidance uses 2 g up to 120 kg and 3 g above 120 kg. Follow the current institutional procedure-specific protocol rather than memorising the slide's older 1–2 g statement in isolation. ^[13][14]

Rheumatic fever (RF) is a delayed immune-mediated complication of Group A Streptococcus (GAS, Streptococcus pyogenes) infection. The slide's pathogenesis diagram shows GAS adhering to/invading pharyngeal tissue, antigen presentation activating B and T cells, and cross-reactive antibodies/T cells then injuring the heart, joints, brain and skin (molecular mimicry). Carditis can progress over years to chronic rheumatic heart disease (RHD). WHO's 2024 guidance also recognises GAS skin infection in the prevention pathway, especially in endemic settings. ^[1][16]

The pathogenesis chain:

GAS pharyngitis → (1-3 weeks) → Acute Rheumatic Fever → (years) → Chronic Rheumatic Heart Disease

Secondary penicillin prophylaxis blocks new GAS infection and repeat immune injury; it does not directly suppress the established autoimmune response. The lecture's 2003 burden map is historical, but its enduring message is the marked concentration of RHD in underserved and overcrowded populations; it should not be used for current country-level prevalence. ^[1][16]

Acute rheumatic fever is rare nowadays in Hong Kong. ^[1]

Appropriate treatment of group A streptococcal pharyngitis prevents acute rheumatic fever in most cases. ^[1]

The slide stresses microbiological confirmation of suspected GAS pharyngitis rather than treating every sore throat. ^[1]

Patient with confirmed Group A streptococcal pharyngitis should be treated for an entire 10-day period, even though they will likely be asymptomatic after the first few days. ^[1]

Why 10 days? Ten days remains the standard course for oral penicillin or amoxicillin to eradicate GAS and prevent ARF; this does not mean every alternative agent has a 10-day regimen. ^[17]

Treatment of GAS Pharyngitis:

No advantage with broad spectrum penicillins (e.g. ampicillin or amoxycillin) or cephalosporins. ^[1]

Current correction: the slide's "no advantage" line supports stewardship, but amoxicillin is a current recommended first-line drug, not an inappropriate choice. Avoid broader therapy that offers no patient-specific advantage; choose penicillin V or amoxicillin according to the guideline and adherence needs. ^[17]

Post-treatment throat cultures NOT required, EXCEPT: with recurring symptoms; with history of rheumatic fever. ^[1]

An individual with a previous attack of rheumatic fever in whom GAS pharyngitis develops is at high risk for a recurrent attack of rheumatic fever. ^[1]

A GAS infection need not be SYMPTOMATIC to trigger a recurrence — hence "recognition & treatment" is insufficient. ^[1]

Prevention is achieved by continuous antimicrobial prophylaxis with a narrow spectrum penicillin. ^[1]

Why continuous prophylaxis rather than treating each episode? Because:

1. Asymptomatic GAS carriage can trigger recurrence — you can't rely on the patient developing a sore throat
2. Each recurrent episode worsens cardiac damage (cumulative carditis)
3. The risk of recurrence is highest in the first 5 years after an initial attack

Regimen for Secondary Prevention:

Initiate penicillin once acute rheumatic fever or rheumatic heart disease is diagnosed. Starting with a 10-day course of treatment to eradicate carriage. ^[1]

At ARF diagnosis, eradicate any residual GAS regardless of whether pharyngitis or a positive throat test is still present, then continue secondary prophylaxis. IM benzathine penicillin every 3–4 weeks is preferred; oral penicillin V is an alternative when injections are not feasible. ^[16][17]

Individualize depending on each patient situation. ^[1]

Factors increasing risk (= longer prophylaxis):

• Multiple previous attacks
• Shorter interval since last attack
• High exposure to GAS (children, adolescents, teachers, healthcare workers, military)
• Presence of rheumatic carditis

These durations come from the lecture's 2009 AHA table. WHO 2024 notes that evidence for the optimal duration remains limited: use current national/professional guidance and individualise for age, time since last attack, exposure risk, carditis and residual valve disease. ^[16]

The lecture first shows an older "JONES CAFE PAL" graphic, then the 2015 revised Jones criteria. Do not learn the older image literally: "myocarditis," leukocytosis and a history of rheumatism are not the current lists, and Doppler-detected subclinical valvulitis matters. ^[1][17]

For an initial episode, the usual pattern is evidence of preceding GAS infection plus 2 major or 1 major + 2 minor manifestations. Major manifestations are carditis (clinical or subclinical), joint involvement, Sydenham chorea, erythema marginatum and subcutaneous nodules. Risk-group thresholds differ:

• Low-risk population: polyarthritis is major; polyarthralgia is minor; fever ≥38.5°C; ESR ≥60 mm/h or CRP ≥3 mg/dL.
• Moderate/high-risk population: monoarthritis, polyarthritis or polyarthralgia may be major (after excluding other causes); monoarthralgia may be minor; fever ≥38.0°C; ESR ≥30 mm/h or CRP ≥3 mg/dL.
• Prolonged PR is minor only when carditis is not counted as major. Routine echocardiography/Doppler is recommended in all confirmed or suspected cases, even without a murmur. Recurrence may also be diagnosed with 3 minor manifestations after excluding more likely causes. ^[17]

To prevent secondary cases (sporadic case, attack rate ~0.4% among close contacts). ^[1]

Transmission is through respiratory/throat secretions during close or lengthy contact; use droplet precautions for a suspected or confirmed case. ^[1][19]

The image-heavy epidemiology slide combines a historical Asian serogroup/outbreak map, the African "meningitis belt," and a photograph of extensive purpura. Use the map to recognise outbreak geography rather than current serogroup frequencies. A rapidly evolving petechial/purpuric rash with systemic illness is a red flag for meningococcaemia and needs emergency treatment; chemoprophylaxis is for exposed contacts, not treatment of the index patient. ^[1][19]

The pathogenesis pathway from the lecture:

Patient with meningitis → Droplet spread to close contact → Carriage of bacteria in nasopharynx → [PEP blocks here] → Elimination of bacterial carriage

^[1]

Why PEP works: N. meningitidis colonises the nasopharynx. The slide's loop-and-cross diagram shows PEP interrupting carriage and onward transmission, thereby preventing secondary cases. It is not a vaccine substitute and it does not guarantee that an exposed person will remain well, so contacts also need symptom advice. ^[1][19]

Household, childcare and intimate contacts, and anyone directly exposed to the patient's oral/respiratory secretions, need public-health assessment for PEP. ^[1][19]

Medical personnel with unprotected, direct contact with oral secretions (e.g. mouth-to-mouth resuscitation, intubation). ^[1]

Exposure window and exclusions: assess contact during the 7 days before symptom onset until 24 hours after effective therapy began. Routine examination, starting an IV, delivering food/medication, or merely being in the room without secretion exposure is not an occupational exposure. Vaccination does not remove the need for PEP after a qualifying exposure. ^[19]

Start prophylaxis as soon as possible, ideally within 24 hours of identifying the index case. ^[1][19]

One dose: either oral ciprofloxacin or intramuscular ceftriaxone. ^[1]

All three are about 90–95% effective at reducing carriage. Azithromycin is not routine first-line PEP but may be selected by public health when ciprofloxacin-resistant strains are sustained. PEP given more than 14 days after the index patient's illness onset is usually of little or no value. ^[19]

The slide quotes these historical teaching estimates: ^[1]

• Human: > 70%
• Cat bite: 50%
• Dog: < 10%
• Rodent: 2%

Do not use these unreferenced percentages as current absolute risks or as the sole triage rule. Risk varies with depth, site, host, delay and wound care. The useful visual message is that cat teeth create narrow, deep punctures and human bites—especially a clenched-fist injury over an MCP joint—can seed deep structures despite a deceptively small skin wound. ^[1][20]

Clean and copiously irrigate; remove debris/foreign material and debride devitalised tissue. ^[1][20][21]

Explore for possible tendon or bone involvement, possible foreign bodies. ^[1]

The slide says a wound may be closed if cosmetically desirable; current guidance is more selective. ^[1]

Immunization — tetanus, rabies. ^[1]

Antibiotic prophylaxis — if high risk wound and in certain patient groups (e.g. splenectomy). ^[1]

What the procedure photographs add: after adequate analgesia, open an infected cavity enough to irrigate it thoroughly. A 30 mL syringe and splash shield can generate directed irrigation; wear eye/face protection because splatter still occurs. Soaking may loosen clot and debris but is not a substitute for irrigation. ^[1]

Assess neurovascular status and tendon function, explore for joint/tendon/bone involvement or retained tooth/foreign body, and image/refer when deep injury is suspected. Most bite wounds should not be primarily closed; facial wounds are the main exception after copious irrigation, cautious debridement and pre-emptive antibiotics. Hand bites, clenched-fist injuries, deep punctures, established infection or systemic illness warrant urgent surgical/specialist assessment. ^[20]

Consider antibiotic prophylaxis if: ^[1]

• Moderate to severe injury
• Involve bone or joint
• Hand or face bite
• Wound near a prosthetic joint
• Underlying disease (e.g. splenectomy)
• Delayed presentation (the slide uses > 8 hours)

Current risk-based approach: offer/consider prophylaxis for all human bites that draw blood, cat bites that draw blood (or may be deep), and dog/other pet bites with deep puncture/crush injury, contamination, deep-structure penetration, high-risk location, or a high-risk host (including diabetes, immunosuppression, asplenia or decompensated liver disease). A 3-day course is used for prophylaxis in NICE guidance; an infected bite is treatment, usually 5 days with extension/review for deep structural injury. ^[20]

Why splenectomy patients? The spleen is critical for clearing encapsulated bacteria. Capnocytophaga canimorsus (part of oral flora in cats & dogs) can cause rapidly fatal infections in patients without spleen (or immunosuppressed patients). ^[1] This is one route to overwhelming post-splenectomy infection (OPSI). ^[1][20]

The slide's preferred agents are amoxicillin-clavulanate (oral) or ampicillin-sulbactam (IV). ^[1]

Why amoxicillin-clavulanate (Augmentin)? Look at the antimicrobial susceptibility table from the lecture:

^[1]

Amoxicillin-clavulanate is the usual first-choice oral agent because it covers the common aerobic and anaerobic spectrum, including Pasteurella and Eikenella. It is not literally the only possible regimen; allergy, pregnancy, severity, renal function and culture results may require a guideline-supported alternative. First-generation cephalosporins, cloxacillin or a macrolide alone leave important gaps in the slide's susceptibility grid. ^[1][20]

Bite-wound infections may be polymicrobial. Purulent wounds/abscesses are especially likely to contain mixed aerobes and anaerobes; non-purulent infections may yield staphylococci, streptococci or Pasteurella alone, although they too can be polymicrobial. ^[20]

The lecture includes an older CDC tetanus prophylaxis table. Its structure remains useful, with a current immunodeficiency caveat: ^[1][21]

• "Tetanus-prone" wounds: contaminated with dirt, faeces, or saliva; punctures; burns; crush injuries; injuries with necrotic tissue
• Unknown, unvaccinated or incomplete primary series → vaccinate for all wounds; add TIG for dirty/major wounds
• Complete primary series and last dose < 5 years → no booster, regardless of wound type
• Complete series → booster at ≥10 years for clean/minor wounds or ≥5 years for dirty/major wounds
• For dirty/major wounds, also give TIG to people with HIV or severe immunodeficiency, irrespective of the old table's simple dose count

Antibiotics do not prevent tetanus; wound care, vaccination and TIG assessment do. ^[21]

Rabies prophylaxis follows an urgent exposure and public-health risk assessment. ^[1]

The lecture includes the current WHO exposure categories:

• Category I: Touching/feeding animals, intact skin contact → No prophylaxis
• Category II: Nibbling of uncovered skin, minor scratches/abrasions without bleeding → Immediate vaccination
• Category III: Single/multiple transdermal bites or scratches, contamination of mucous membrane/broken skin with saliva → Immediate vaccination + rabies immunoglobulin (RIG)

The 2017 world map and 2004–2018 China provincial map are historical snapshots, not a current travel-risk tool. The separate 2008 US animal-observation table is also jurisdiction-specific: do not transplant its 10-day dog/cat/ferret rule to every country or delay PEP while independently observing an animal. Immediately wash and flush the wound with soap and water, use a virucidal agent if available, and contact local public health/rabies services. For a previously unvaccinated person with a qualifying exposure, PEP includes vaccine and, for category III exposure, rabies immunoglobulin infiltrated into/around the wound; previously vaccinated people do not receive RIG. ^[22][23]

The lecture slide references OPSI and splenectomy patients as a high-risk group for bite wound infection. ^[1]

What the OPSI slide contributes: risk persists lifelong and can progress within hours from non-specific fever/chills to shock and DIC. The slide's old pneumococcal vaccine products/schedule should not be followed literally. Asplenic patients need an up-to-date specialist vaccination and fever plan, education/medical identification, and prompt empirical treatment for fever according to their local protocol. A dog/cat bite deserves early prophylaxis because Capnocytophaga canimorsus can cause fulminant sepsis; "standby" antibiotics must never delay urgent assessment. ^[1][20]