More severe illness such as abrupt onset of fever, headache, myalgia and malaise ^[3][4]

Why the distinction matters: Influenza has specific antiviral treatment (oseltamivir/zanamivir, most effective if started within 48 hours of symptom onset) and carries a much higher risk of serious complications, especially in the elderly, pregnant women, young children, and immunocompromised patients ^[1].

GAS tonsillopharyngitis is usually not accompanied by nasal symptoms ^[3][4]

This is a critical distinguishing point: the common cold is a nasal-predominant illness, whereas streptococcal pharyngitis is a throat-predominant illness with minimal nasal symptoms.

Suggestive features from Adrian Lui notes ^[1]: previous close exposure to strep throat, sudden onset sore throat with little viral symptoms (rhinorrhea, cough, hoarseness), exudative tonsillitis, tender anterior cervical LNs, fever, ± headache and abdominal pain

Why it matters: GAS pharyngitis requires antibiotics (penicillin V or amoxicillin) to prevent rheumatic fever (still relevant in Hong Kong and endemic regions) and peritonsillar abscess. The common cold does not need antibiotics.

The Centor criteria (modified McIsaac) help estimate the probability of GAS pharyngitis: fever > 38°C, tonsillar exudate, tender anterior cervical LAP, absence of cough. Each criterion scores 1 point. Absence of cough is a "negative" finding that actually supports GAS — because cough suggests viral URTI, not bacterial pharyngitis.

Pertussis classically begins with mild cough and coryza but the cough gradually increases and becomes paroxysmal ^[3][4]

Key distinguishing features ^[1]: cough spasms, vomiting with cough, no fever

Why pertussis can fool you: The catarrhal phase is essentially indistinguishable from acute coryza. The clue comes when the cough doesn't improve after 7–10 days and instead escalates into paroxysms. In adolescents/adults with waning vaccine immunity, the presentation may be atypical — just a prolonged cough without the classic whoop.

Diagnosis: nasopharyngeal swab for culture or PCR ^[1].

Differentiated from common cold by persistence, increased severity or worsening of symptoms ^[3][4]

Prolonged ( > 10–14d) URI symptoms + ≥ 2 of facial/sinus pain (especially if aggravated by postural changes or Valsalva's manoeuvre), purulent nasal discharge, fever ^[1]

Three clinical patterns suggest bacterial superinfection rather than a simple viral cold:

1. Persistent symptoms ≥ 10 days without improvement
2. "Double worsening" — initial improvement followed by new/worsening symptoms (new fever, worsening nasal discharge)
3. Severe onset — high fever ≥ 39°C with purulent nasal discharge for ≥ 3 consecutive days

Why sinusitis complicates acute coryza: Viral infection → mucosal oedema → ostial obstruction → mucus stasis → secondary bacterial overgrowth (S. pneumoniae, H. influenzae, M. catarrhalis) ^[5].

Stridor, "barking" or "croupy cough", hoarseness, ± fever ^[8]

Why is the cough barking? Subglottic oedema narrows the airway just below the vocal cords → turbulent airflow through this narrowed segment produces the characteristic harsh, barking quality. Inspiratory stridor occurs because the extrathoracic trachea tends to collapse further during inspiration (negative intraluminal pressure), worsening the obstruction.

Alteration in voice, severe sore throat with dysphagia, stridor, drooling ^[1][2]

This is a medical emergency. The epiglottis swells to obstruct the airway.

Cause: Historically Haemophilus influenzae type b (Hib) — now rare in vaccinated populations. In Hong Kong, Hib vaccine is part of the Childhood Immunisation Programme. Adult cases are more often caused by S. aureus, S. pneumoniae, or S. pyogenes.

In the current Hong Kong context, SARS-CoV-2 must always be considered when a patient presents with acute coryza symptoms. Omicron and subsequent subvariants tend to cause upper-airway-predominant symptoms (sore throat, rhinorrhoea, congestion) that are clinically indistinguishable from the common cold. Distinguishing features (when present) include anosmia/ageusia (less common with newer variants), more significant fatigue, and exposure history. Rapid antigen testing clarifies the diagnosis.

Allergic, seasonal or vasomotor rhinitis ^[3][4]

Why allergic rhinitis mimics a cold: Both involve nasal mucosal oedema and rhinorrhoea. However, in allergic rhinitis the mechanism is IgE-mediated mast cell degranulation (Type I hypersensitivity) rather than viral cytokine release. Mast cell mediators (histamine, leukotrienes) cause the same downstream effects (vasodilation, increased vascular permeability, mucus secretion, nerve stimulation) but with prominent itch (histamine acting on H₁ receptors on sensory nerves) — itch is the distinguishing symptom.

• Chronic rhinorrhoea and congestion triggered by temperature changes, strong odours, humidity, smoke, spicy food
• No itch, no atopic associations, no fever
• Mechanism: autonomic nervous system dysregulation of nasal vasculature → excessive parasympathetic-driven secretion and vasodilation
• Typically perennial rather than seasonal

In a young child with unilateral, foul-smelling, purulent (± blood-stained) nasal discharge — think foreign body. Acute coryza causes bilateral symptoms. A unilateral presentation should always trigger consideration of a foreign body, especially in children aged 2–5 years.

Anatomical predisposing factors: deviated septum, polyp, tumour ^[5]

• Nasal polyps — chronic unilateral or bilateral nasal obstruction and hyposmia; associated with aspirin-exacerbated respiratory disease (Samter's triad: asthma + nasal polyps + aspirin sensitivity)
• Nasopharyngeal carcinoma (NPC) — important in Hong Kong (high prevalence in Southern Chinese). Presents with unilateral nasal obstruction, blood-stained post-nasal drip, unilateral serous otitis media, and cervical lymphadenopathy. Must be considered in any adult with persistent unilateral nasal symptoms.
• Adenoid hypertrophy — chronic nasal obstruction, mouth breathing, snoring in children; can be confused with chronic/recurrent colds

• Acute bronchiolitis ^[8] — common in infants < 2 years (peak 2–6 months)
• Usually caused by RSV
• Starts with coryzal symptoms then progresses to tachypnoea, subcostal/intercostal recession, fine crackles, wheeze, feeding difficulty
• Distinguished from a cold by respiratory distress and lower airway signs

• Pneumonia ^[8] — tachypnoea, fever, crepitations, bronchial breathing, chest indrawing
• Can follow a viral URTI (secondary bacterial pneumonia)
• CXR shows consolidation

• Reactive airway/asthma ^[8] — triggered by URTI (rhinovirus is #1 trigger)
• Seasonal and diurnal variation, association with rhinitis, posture, "clearing of throat", triggers ^[8]
• Wheeze, cough (especially nocturnal), chest tightness; responds to bronchodilators
• In a child presenting with a "cold" that progresses to persistent wheezing, always investigate for asthma

• Extension of URTI to the tracheobronchial tree
• Retrosternal chest tightness, productive cough, low-grade fever
• No focal consolidation on examination or CXR (differentiates from pneumonia)

• Symptoms or signs of ARS < 10 days that are not worsening ^[3][4]
• Essentially indistinguishable from acute coryza — represents the sinus component of the common cold
• No specific investigations needed

Score interpretation ^[10]:

• −1 to 1 points (risk of strep throat < 10%) → no antibiotics or throat culture necessary
• 2 to 3 points (risk 15–32%) → antibiotics if throat culture positive
• 4 to 5 points (risk ~56%) → treat empirically with antibiotics

The key insight: absence of cough is a Centor criterion that supports GAS pharyngitis. If the patient has prominent cough and nasal symptoms, the probability of GAS drops sharply — this is more likely viral URTI/acute coryza.

Why do we use NP aspirate/swab rather than a throat swab for respiratory viruses? The nasopharynx is the primary site of viral replication for most respiratory viruses. The viral load is highest here, giving the best diagnostic yield. Throat swabs have lower sensitivity for viruses like influenza and RSV.

Blood tests are not indicated for uncomplicated acute coryza. They become relevant when considering complications or alternative diagnoses:

Why is CT preferred over plain X-ray for sinusitis? Plain films have poor sensitivity, especially for ethmoid sinus disease (the ethmoid cells overlap with other structures on plain radiographs). CT provides excellent bony detail and can show mucosal thickening, air-fluid levels, and ostiomeatal complex obstruction with far greater anatomical precision. However, CT is not routinely indicated for uncomplicated acute rhinosinusitis — it is reserved for cases with suspected complications or chronic/recurrent disease.

These are examination findings that function as diagnostic tools:

1. Viral infection of the nasopharyngeal mucosa → inflammatory oedema extends to the mucosa lining the Eustachian tube
2. The Eustachian tube in children is shorter, more horizontal, and more flaccid than in adults → predisposes to dysfunction
3. Mucosal swelling → Eustachian tube obstruction → negative pressure develops in the middle ear (trapped air is absorbed by middle ear mucosa) → serous fluid accumulates (effusion)
4. Stasis of fluid + impaired mucociliary clearance → bacterial translocation from the nasopharynx up through the Eustachian tube into the sterile middle ear space
5. Common pathogens: S. pneumoniae, non-typeable H. influenzae, M. catarrhalis (the same organisms that cause ABRS — because they originate from the same nasopharyngeal flora)
6. Bacterial proliferation in the middle ear effusion → acute suppurative otitis media (pus behind the tympanic membrane)

• Otalgia — the most common symptom; in pre-verbal children manifests as ear pulling, irritability, inconsolable crying
• Otorrhoea — purulent discharge if the tympanic membrane perforates (actually provides pain relief as pressure is released)
• Hearing loss — conductive; due to fluid/pus dampening TM vibration
• Dizziness — inner ear irritation from adjacent middle ear infection
• Fever — may be new-onset or recurrent after initial improvement (the "double worsening" pattern)

• Otoscopy: bulging, erythematous, opaque tympanic membrane ± purulent effusion visible behind TM ± spontaneous perforation with otorrhoea

• Many mild cases resolve spontaneously (watchful waiting for 48–72 hours in children > 2 years with unilateral, non-severe AOM)
• Antibiotics (amoxicillin first-line) indicated for: bilateral AOM in < 2 years, AOM with otorrhoea, severe symptoms (fever ≥ 39°C, severe otalgia), no improvement after observation
• Analgesics (paracetamol/ibuprofen) for pain

• Shorter, more horizontal Eustachian tube → easier bacterial ascent
• Larger adenoids → physical obstruction of Eustachian tube orifice
• Immature immune system → more frequent and prolonged viral URTIs
• More frequent nasopharyngeal colonisation with otopathogens

1. Viral infection → mucosal oedema of the nasal cavity and sinus ostia (especially the ostiomeatal complex draining the maxillary, anterior ethmoid, and frontal sinuses)
2. Ostial obstruction → trapped mucus within the sinus cavity → impaired drainage and mucociliary clearance
3. Stagnant mucus in a warm, moist, enclosed space → ideal medium for secondary bacterial overgrowth
4. Common pathogens: S. pneumoniae, H. influenzae, M. catarrhalis (same trio as AOM)
5. Bacterial infection → purulent sinusitis with intense mucosal inflammation, further oedema, and potentially pressure symptoms (facial pain)

The initial phase (viral rhinosinusitis) is essentially part of the common cold itself — most colds involve some degree of sinus mucosal inflammation visible on CT. Only a small fraction (estimated 0.5–2% of viral URTIs in adults, slightly higher in children) progress to acute bacterial rhinosinusitis (ABRS).

• Persistent nasal congestion and purulent discharge beyond 10 days
• Facial pain/pressure (maxillary = cheek/upper teeth; frontal = forehead; ethmoid = between/behind eyes)
• Post-nasal drip with cough
• Hyposmia/anosmia
• Fever (new-onset or recurrent)

This is where things become genuinely dangerous. The paranasal sinuses are anatomically adjacent to the orbit and the anterior cranial fossa. Infection can spread by direct extension, venous drainage (valveless diploic veins and ophthalmic veins connecting to the cavernous sinus), or through bony erosion.

Complications of acute bacterial rhinosinusitis ^[12]:

• Orbital cellulitis, abscess
• Cavernous sinus thrombosis
• Intracranial infection: meningitis, encephalitis, abscess

• Most relevant in infants < 2 years (peak 2–6 months)
• Caused predominantly by RSV (~60–80% of cases)
• Pathophysiology: virus spreads from the upper airway down to the bronchioles → epithelial necrosis → inflammatory cell infiltration and oedema of the bronchiolar wall → mucus plugging of small airways → air trapping (ball-valve mechanism: air enters on inspiration but cannot exit on expiration) + atelectasis (complete obstruction)
• Clinical course: starts as acute coryza (rhinitis, congestion, cough for 1–3 days) → progresses to tachypnoea, subcostal/intercostal recession, wheeze, fine crackles, feeding difficulty, apnoeas (especially in ex-premature infants)
• Management: mainly supportive (oxygen, hydration, nasal suctioning); no proven role for bronchodilators, steroids, or antibiotics in typical bronchiolitis

Long-term sequela: reactive airway disease (recurrent wheezing) is a common sequela reported after bronchiolitis episodes ^[13].

• Viral pneumonia: direct extension of respiratory virus (influenza, RSV, parainfluenza, adenovirus) to the alveoli → diffuse alveolar damage, interstitial inflammation
• Secondary bacterial pneumonia: viral infection damages airway epithelium and impairs mucociliary clearance → creates portal of entry for bacteria (S. pneumoniae, S. aureus, H. influenzae) → consolidation
• Clue: persistent or new-onset high fever after initial improvement, productive cough with purulent sputum, tachypnoea, focal chest signs (crackles, bronchial breathing, dullness to percussion)

• Extension of viral inflammation to the trachea and large bronchi
• Retrosternal chest tightness, productive cough, low-grade fever
• Distinguished from pneumonia by absence of focal consolidation on examination and CXR
• Self-limiting; supportive management

1. Viral URTI (rhinovirus is the #1 trigger for asthma exacerbations, responsible for ~60–80% of virus-induced exacerbations in both children and adults) → direct infection of bronchial epithelium
2. Damaged epithelium releases alarmins (IL-25, IL-33, TSLP — thymic stromal lymphopoietin)
3. Alarmins activate type 2 innate lymphoid cells (ILC2s) and Th2 lymphocytes → amplification of type 2 inflammation → IL-4, IL-5, IL-13 production
4. IL-5 → eosinophil recruitment and activation → release of eosinophil granule proteins (major basic protein, eosinophil cationic protein) → further epithelial damage
5. IL-13 → goblet cell hyperplasia (mucus hypersecretion) + smooth muscle contraction
6. Overall: bronchospasm + mucosal oedema + mucus plugging → acute airway obstruction → wheeze, cough, SOB, chest tightness

• A patient with known asthma who develops a "cold" and then experiences worsening wheeze, nocturnal cough, and decreasing PEFR
• RSV and parainfluenza may cause wheezing → prompt investigation for asthma if persistent ^[1][2]

• Step up asthma controller therapy (increase ICS dose ± add SABA as reliever)
• Systemic corticosteroids if moderate–severe exacerbation
• Optimise URTI treatment (supportive)

• Viral infection causes damage to the bronchial epithelium → exposes subepithelial vagal sensory nerve endings (C-fibres)
• Transient receptor potential (TRP) channels on these nerve endings become sensitised ("upregulated") by inflammatory mediators
• Even after the virus is cleared and mucosal inflammation subsides, these nerve endings remain hyperexcitable for weeks → persistent cough reflex triggered by minimal stimuli (cold air, talking, laughing, deep breathing)
• No evidence of ongoing infection — sputum culture and CXR are typically normal
• Duration: can persist for 3–8 weeks after the acute illness

• Reassurance — explain the mechanism (nerve hypersensitivity, not ongoing infection)
• No antibiotics (there is no bacterial infection)
• Time → resolves spontaneously
• If very bothersome: trial of inhaled ipratropium (blocks the parasympathetic limb of the cough reflex) or low-dose inhaled corticosteroid (reduces residual airway inflammation)
• If cough persists beyond 8 weeks → investigate for other causes (asthma, GERD, ACEi-related cough, pertussis)