Key footnotes from the lecture:

• The slide uses * to mark “good anti-anaerobic activity,” but the mark must be interpreted at the exact drug/organism level. Penicillin G is active against some susceptible anaerobes; ceftazidime-avibactam should not be relied on for anaerobic coverage; and no class-wide asterisk replaces susceptibility and source-specific guidance.
• Beta-lactamase inhibitors include avibactam, clavulanate, sulbactam, tazobactam

The beta-lactams form the backbone of antibiotic therapy. Understanding their spectrum progression is essential:

Penicillin G (strep only)
→ Cloxacillin (adds staph)
→ Ampicillin/Amoxicillin (adds some Gram −ve)
→ Amox-clav (adds β-lactamase producers + anaerobes)
→ Cefuroxime (2GC: broader Gram −ve)
→ Ceftriaxone (3GC: much broader Gram −ve)
→ Ceftazidime (3GC + non-fermenters like Pseudomonas)
→ Cefepime (4GC: Gram +ve back + Gram −ve)
→ Pip-Tazo (broadest BLBLI, anti-Pseudomonal + anaerobes)
→ Carbapenems (broadest of all β-lactams)

Ask yourself these questions before prescribing empirically:

1. Is there a good reason (justification) to use antibiotic empirically?
2. Is the patient very ill? Are the signs/symptoms getting worse?
3. Is the patient very young, very old, or immunocompromised?
4. Always explain the follow-up actions to the patient. ^[1]

The pyramid is labelled “an illustration only.” It places cefuroxime/amoxicillin-clavulanate/fluoroquinolones at the broad base, piperacillin-tazobactam above them, and carbapenems at the apex, with escalation and de-escalation arrows in both directions. The teaching is dynamic review, not a fixed “sicker patient = carbapenem” ladder:

1. assess syndrome and severity;
2. review previous cultures, recent antibiotics, healthcare exposure, source and local resistance;
3. obtain appropriate cultures without delaying urgent therapy;
4. start the narrowest regimen that safely covers the credible pathogens; and
5. review at 48–72 hours to stop, narrow, target, switch route, or broaden only if the evidence requires it.

Current Hong Kong IMPACT guidance should take precedence over the illustrative brand-name pyramid (IMPACT, empirical therapy).

Uncomplicated cystitis is the most common UTI in outpatient settings. ^[1]

First-line treatment:

• Nitrofurantoin (the lecture specifically highlights this as the preferred agent)

Why nitrofurantoin?

• Concentrated in urine → high urinary levels, low systemic levels
• Low resistance rates among E. coli (even when resistance to other agents is high)
• Minimal impact on gut flora → less collateral damage
• Limitation: Only works for LOWER UTI (cystitis). It does NOT achieve adequate tissue/blood levels, so it is useless for pyelonephritis or systemic infections ^[1]

Request urine culture if:

• Recurrent UTI
• Complicated UTI
• Failure to respond
• Children
• Pregnant women
• Postmenopausal women ^[1]

How to use the list: the slide highlights situations in which culture is more likely to change management. It is not a timeless rule that every child, man, or postmenopausal patient follows the same pathway. Obtain culture for pyelonephritis, pregnancy, recurrent/complicated infection, treatment failure, or another current local indication; classic uncomplicated cystitis can often be managed empirically.

The arrows highlight leukocyte esterase and nitrite, and the manufacturer's chart shows that the pads are read at different times (approximately 2 minutes for leukocytes and 60 seconds for nitrite in the pictured product).

• Leukocyte esterase is a surrogate for pyuria; it supports inflammation but is not specific for bacterial UTI.
• Nitrite supports nitrate-reducing bacteriuria, but a negative result does not exclude UTI (short bladder dwell time, low dietary nitrate, dilute urine, or a non-nitrate-reducing organism can produce a false negative).
• Interpret the strip with symptoms and specimen quality. A positive dipstick alone is not a reason to treat asymptomatic bacteriuria outside recognised exceptions.

The lecture's 15% annotation refers to the proportion with a multidrug-resistant phenotype in a 2007 Hong Kong outpatient dataset, not “15% resistance to common oral antibiotics.” In that historical table, resistance was 60.1% to ampicillin, 34% to co-trimoxazole and 22.1% to ciprofloxacin, versus 2.2% to amoxicillin-clavulanate, 2.5% to nitrofurantoin and 0.4% to fosfomycin. A second graph (2014–2018, > 6,000 outpatient isolates) shows increasing levofloxacin non-susceptibility with age (about 19% in children to about 40% at ≥75 years), while nitrofurantoin non-susceptibility remains much lower (about 1–4%). These are historical lecture datasets, not today's antibiogram; use current local susceptibility data (IMPACT outpatient antibiogram).

This is why:

• Nitrofurantoin remains first-line — resistance rates remain low
• Amoxicillin-clavulanate and fluoroquinolones have higher resistance rates in HK
• Elderly patients (postmenopausal women, older men) have higher resistance rates due to prior antibiotic exposure and healthcare contact

Q17: Empirical treatment of uncomplicated cystitis in a 30-year-old woman → Answer: Nitrofurantoin (H) ^[3]

URTI (also called common cold) – viral infection of nasal mucosa, nasopharynx, oropharynx (tonsils), larynx, paranasal sinuses. ^[1]

Symptoms: Fever, systemic symptoms, running nose, nasal obstruction, cough, hoarseness, sore throat

Treatment is symptomatic. Antibiotic has NO role in URTI. ^[1]

Educate the patient about the natural course:

• Worse on initial 2–3 days, then improve
• Illness may be prolonged – 1+ week
• Yellow nasal discharge and phlegm is COMMON (from inflammation) ^[1]

Viral infection, as an extension of URTI. ^[1] Main symptom: retrosternal discomfort and severe cough. Treatment: symptomatic. ^[1]

DDx for severe and persistent cough > 2 weeks:

• Asthma (airway hypersensitivity)
• Pertussis
• Tuberculosis ^[1]

Why this matters: Acute bronchitis is one of the most over-prescribed conditions. The lecture is explicit: it is viral, and antibiotics are NOT indicated. However, if cough persists > 2 weeks, you must think beyond simple viral illness.

The slide contrasts uncomplicated viral bronchitis with suspected bacterial pneumonia. Pneumonia itself can be bacterial, viral, fungal, or mixed; antibiotics are indicated when bacterial pneumonia is suspected, not for every radiographic pneumonia automatically.

Clinical features that distinguish pneumonia from viral bronchitis:

• Abnormal vital signs (tachycardia, tachypnea, persistent high fever)
• Asymmetrical lung sounds or signs of consolidation
• May need referral for a chest X-ray ^[1]

Why is this distinction critical? Because the whole point of this lecture section is: most respiratory infections are viral and don't need antibiotics, BUT pneumonia is the important bacterial exception. You must be able to clinically distinguish the two.

The slide's pulse-oximeter image adds oxygen saturation to the assessment. In otherwise healthy adults, pneumonia is less likely when vital signs are normal (heart rate < 100/min, respiratory rate < 24/min, temperature < 38°C) and there are no focal consolidation findings; hypoxaemia, abnormal observations, or focal signs should prompt further assessment (CDC adult outpatient guidance).

The following slide reproduces Hong Kong IMPACT advice for non-hospitalised CAP: oral amoxicillin-clavulanate or high-dose amoxicillin, with doxycycline when atypical coverage is indicated; levofloxacin is an alternative for penicillin allergy. The visual also warns that a macrolide, tetracycline, or co-trimoxazole should not be used alone for empirical CAP in Hong Kong. Use the live guideline and patient-specific assessment rather than memorising a screenshot (IMPACT CAP guidance).

Causative agents:

• EBV (Epstein-Barr virus), Adenovirus → viral
• Streptococcus pyogenes (Group A Streptococcus) → bacterial ^[1]

May not be possible to distinguish viral from bacterial tonsillitis clinically. ^[1]

This is a key teaching point. The lecture presents the Centor/McIsaac criteria and rapid antigen testing as tools to help differentiate:

Modified Centor (McIsaac) Criteria for GAS Pharyngitis

Interpretation:

• Score 0–1: No testing, no antibiotics (viral overwhelmingly likely)
• Score 2–3: Perform rapid antigen test → treat if positive
• Score ≥ 4: Higher probability of GAS → test rather than treating from symptoms alone where testing is available

The pictured lateral-flow rapid antigen device is read at 5 minutes (and not after 10 minutes); actual timing and interpretation are product-specific. A visible control line is required, while a test line with a control line is positive. ^[1]

Antibiotic of choice for GAS pharyngitis:

Penicillin V (oral) — a narrow-spectrum first-line option ^[1][3]

Why Penicillin V?

• GAS has NEVER developed resistance to penicillin
• Narrow spectrum → minimal collateral damage
• Cheap and effective
• Duration is guideline- and formulation-specific. The Hong Kong CHP table reproduced on slide 28 lists 5–7 days for penicillin V or amoxicillin, whereas some international regimens use 10 days. Follow the current local regimen; do not infer a universal duration from older teaching.

The 2025 IDSA update recommends using a clinical score to decide who should be tested, chiefly to identify low-risk patients in whom testing is unlikely to help. A high score is not, by itself, proof of GAS or a universal mandate for empirical antibiotics (IDSA 2025 GAS guideline).

2025 Past Paper Q20: Treatment of group A streptococcal pharyngitis → Answer: Penicillin V (I) ^[3]

Sinusitis is COMMON in viral URTI. ^[1] It will resolve with symptomatic treatment. ^[1] Symptoms may linger for weeks in patients with underlying allergic sinusitis. ^[1]

Only very few patients need antibiotics. ^[1] When antibiotics ARE indicated → Amoxicillin ^[1]

When to consider antibiotics for sinusitis:

• Symptoms persist > 10 days without improvement
• Severe symptoms (high fever ≥ 39°C, purulent nasal discharge, facial pain) lasting ≥ 3 consecutive days
• "Double worsening" — symptoms that were improving then suddenly worsen

Most sinusitis is viral. The sinuses are anatomically connected to the nasal passages, so any viral URTI causes mucosal inflammation in the sinuses. This is NOT bacterial sinusitis and does NOT need antibiotics.

The 70% (2 weeks), 40% (1 month), 20% (2 months), and 10% (3 months) persistence figures shown on slide 35 come from a 1980 cohort. They teach that residual effusion after AOM is common and not “treatment failure,” but they should be labelled historical rather than used as a contemporary prediction for an individual child.

Key principles from the prophylaxis lecture that connect here ^[4]:

• Surgical prophylaxis: cefazolin is common for many clean procedures, but agent and timing are procedure-specific; most prophylaxis is started within 60 minutes before incision, while drugs requiring a longer infusion (for example vancomycin) are started earlier. Do not extend prophylaxis merely because a drain remains.
• Vancomycin for penicillin allergy or high MRSA incidence
• Cefuroxime + metronidazole for colorectal surgery (need anaerobic coverage)
• Bite wound prophylaxis: Amoxicillin-clavulanate

Key connections ^[6]:

• ESBL-producing Enterobacteriaceae → carbapenems are the drug of choice for severe infections
• MRSA → vancomycin, linezolid, or ceftaroline
• Intrinsic resistance examples:
  • Salmonella: intrinsically resistant to cefuroxime (active in-vitro but NOT in-vivo)
  • Morganella, Providencia, Proteus: intrinsically resistant to nitrofurantoin
  • Listeria: intrinsically resistant to 3rd gen cephalosporins (must add ampicillin)

Q85 (2023): Mycoplasma pneumoniae detected → Which antibiotic class? → Answer: C. Macrolides ^[5]

Why? Mycoplasma lacks a cell wall → beta-lactams (which target cell wall synthesis) are useless. Macrolides, tetracyclines, and fluoroquinolones work against Mycoplasma because they target protein synthesis or DNA replication.

From the pediatric leukemia and hematology lectures ^[7]:

• Medical emergency → empirical broad-spectrum antibiotics ASAP (within 1–2 hours)
• Must cover Pseudomonas aeruginosa
• Typical regimen: Piperacillin-tazobactam or cefepime or meropenem