Pharyngitis and tonsillitis are inflammatory conditions of the pharynx and palatine tonsils, most commonly caused by viral or bacterial (notably group A streptococcal) infections, presenting with sore throat, odynophagia, and tonsillar erythema or exudates.

Exam domain	One-glance essentials
Definition / diagnosis	*>90% of acute sore throat is viral; pharyngitis/tonsillitis = inflammation of pharynx ± palatine tonsils, most commonly infectious (viral >> bacterial) ^[1]^[2] GAS pharyngitis* is the most important bacterial cause (peak age 5–15) due to risk of acute rheumatic fever, preventable with timely antibiotics ^[3]^[4] *Exudates can mean viral or bacterial* — EBV, adenovirus, HSV all produce exudates; never equate exudate with bacterial aetiology ^[1]^[5]
Epidemiology / risks	GAS pharyngitis peaks age 5–15 years; rare <3 years; crowded settings (schools, military) ↑ transmission ^[6]^[5] In Hong Kong, persistent unilateral sore throat + cervical LN in adults → must exclude NPC (Southern Chinese association) ^[7]^[8] *Erythromycin resistance in HK is 40–50%* — impacts antibiotic choice for penicillin-allergic patients ^[9]
Core mechanism	GAS M protein → molecular mimicry with cardiac myosin/valve glycoproteins → cross-reactive T-cells → pancarditis (ARF) 2–4 weeks post-infection ^[10]^[11] GAS → immune complex deposition in glomeruli → PSGN 1–3 weeks later; distinct from ARF pathway ^[12]^[13] *Only pharyngeal GAS causes ARF; skin GAS does NOT cause ARF but CAN cause PSGN* ^[4]^[14] Suppurative complications arise from direct local spread through pharyngeal fascial planes → peritonsillar/parapharyngeal/retropharyngeal abscess ^[14]^[15]
Clinical picture	GAS clues: sudden onset sore throat, tonsillar exudate, tender anterior cervical LN, fever, *absence of cough/rhinorrhoea* — best single discriminator from viral URTI ^[3]^[2] Viral clues: cough, rhinorrhoea, conjunctivitis, hoarseness, oral ulcers — presence of nasal symptoms argues against GAS ^[16]^[2] EBV-IM: severe exudative tonsillitis + posterior cervical LN + splenomegaly + atypical lymphocytes; amoxicillin → maculopapular rash ^[17]^[18] *Peritonsillar abscess (quinsy): unilateral peritonsillar swelling, uvula deviation, trismus*, muffled "hot potato" voice — surgical emergency ^[15]^[19]
Investigations	Centor criteria (CENT): Cough absent, Exudate, Nodes (anterior cervical), Temperature; *McIsaac: +1 if <15 y, −1 if >44 y; score 0–1 → no test/Abx, 2–3 → RADT ± culture, 4–5 → test-and-treat ^[3]^[5] RADT: specificity ≥95% (positive = reliable); sensitivity 70–90% → negative RADT in children needs backup throat culture* (gold standard, 90–95% sensitive) ^[5]^[20] *ASLO/anti-DNase B* rise >2 weeks — used retrospectively for ARF/PSGN, NOT for acute diagnosis; *persistently low C3 >8 weeks* post-PSGN → consider lupus nephritis or MPGN ^[13]^[21] *10–25% asymptomatic GAS carriage* — positive swab + pharyngitis ≠ GAS pharyngitis; clinical correlation essential ^[5]^[22]
Management	Viral pharyngitis → supportive care only (analgesia, hydration); confirmed GAS → penicillin V or amoxicillin × 10 days (GAS has no penicillin resistance) ^[23]^[2] *Penicillin allergy → 1st-gen cephalosporin (non-anaphylactic) or azithromycin/clindamycin (anaphylactic); avoid erythromycin in HK due to high resistance ^[9]^[23] Peritonsillar abscess → IV antibiotics + drainage* (needle aspiration or incision & drainage) ± interval tonsillectomy; *tonsillectomy indications: Paradise criteria, OSA, quinsy unresponsive to drainage, suspected malignancy* ^[15]^[24] EBV/IM → supportive care, AVOID amoxicillin, avoid contact sports for ≥3 weeks (splenic rupture risk) ^[17]^[25]
Complications	Suppurative: peritonsillar/parapharyngeal/retropharyngeal abscess, Lemierre syndrome (IJV thrombophlebitis), necrotising fasciitis, septicaemia ^[14]^[4] Non-suppurative immune-mediated: ARF (2–4 wk), PSGN (1–3 wk), scarlet fever, PANDAS, guttate psoriasis; *ARF preventable by Abx within 9 days; PSGN prevention by Abx is NOT proven* ^[4]^[26] *RHD is the most common/severe ARF sequela; develops 10–20 years later; MV most commonly affected; MS is the most common chronic pathology* — warfarin (not NOAC) for AF in MS ^[11]^[27] Jones criteria (JONES): Joints (migratory polyarthritis), carditis, Nodules (subcutaneous), Erythema marginatum, Sydenham chorea; requires 2 major OR 1 major + 2 minor + evidence of preceding GAS ^[4]^[10]
Prevention / follow-up	*Primary ARF prevention: treat GAS pharyngitis with penicillin within the 9-day window* from symptom onset ^[28]^[9] *Secondary ARF prophylaxis: monthly IM benzathine penicillin G — duration depends on valve involvement (years to lifelong) ^[9]^[28] Tonsillectomy contraindications*: bleeding disorder, high anaesthetic risk, atlantoaxial instability (Down syndrome, RA); secondary haemorrhage day 5–14 is the most common serious complication ^[24]^[29]
Exam traps	*Exudate ≠ bacterial* — treating all exudative pharyngitis with antibiotics is a classic exam error; *empiric Abx NOT recommended* as clinical features alone achieve only ~50% accuracy ^[1]^[5] Synpharyngitic haematuria (concurrent) = IgA nephropathy vs post-pharyngitic haematuria (1–3 wk delay) = PSGN — timing is the key discriminator ^[30]^[12] Unilateral tonsillar enlargement in an adult = malignancy until proven otherwise (lymphoma, SCC); persistent sore throat >3 weeks requires urgent investigation ^[7]^[8] *Amoxicillin in suspected EBV → diffuse maculopapular rash* — always consider IM before prescribing aminopenicillins for exudative tonsillitis in adolescents ^[17]^[25]

References

^[1] Lecture slides: GC 021. Upper respiratory tract infections.pdf, p.25 (Sore throat — viral > 90%, emergency/serious/pitfalls, exudates viral or bacterial) ^[2] Senior notes: Ryan Ho Respiratory, p.48–51 (Section 3.1.1 URTI and 3.1.1.2 Bacterial Pharyngitis) ^[3] Senior notes: Ryan Ho Respiratory, p.51 (Section 3.1.1.2 Bacterial Pharyngitis — Centor criteria, diagnostic testing) ^[4] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.126, 129 (GAS complications — suppurative and non-suppurative; Jones criteria; necrotising fasciitis; septicaemia) ^[5] Senior notes: Adrian Lui Pediatrics Notes, p.157 (Centor criteria, RADT, throat culture, carrier state, empiric treatment caveat) ^[6] Senior notes: Adrian Lui Pediatrics Notes, p.154–157 (Section 5.2.1 Respiratory Infections) ^[7] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai), p.201 and p.255 (Neck mass DDx; Oropharyngeal SCC) ^[8] Lecture slides: GC 015. Imaging of the head and neck.pdf, p.39 (Inflammatory/infectious, neoplastic, congenital neck masses) ^[9] Senior notes: Gen Clerk Anaes + Microbiology Summary, p.13–14 (Primary and secondary prevention of rheumatic fever; penicillin prophylaxis; erythromycin resistance in HK) ^[10] Senior notes: Ryan Ho Cardiology, p.146 (Section 3.3.1 Rheumatic Heart Disease / Acute Rheumatic Fever) ^[11] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai), p.444 and MBBS Final MB (Pediatrics) (Felix PY Lai), p.303 (ARF/RHD overview, pathogenesis, epidemiology Rule of 3) ^[12] Senior notes: Ryan Ho Urogenital, p.66 (PSGN — clinical features, timeline, prognosis) ^[13] Senior notes: Block A - Glomerular and Tubulo-interstitial Diseases and AKI, p.19 (PSGN investigations — C3, ASLO, persistently low C3) ^[14] Senior notes: Ryan Ho Respiratory, p.49, 51–52 (Section 3.1.1 URTI complications; 3.1.1.2 Bacterial Pharyngitis — suppurative and non-suppurative complications) ^[15] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf, p.43 (Peritonsillar abscess / Quinsy) ^[16] Lecture slides: GC 021. Upper respiratory tract infections.pdf, p.25 and p.28 (Sore Throat; Hoarseness) ^[17] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.31 and MBBS Final MB (Medicine) (Felix PY Lai), p.1810–1812 (Infectious mononucleosis) ^[18] Senior notes: Ryan Ho Haemtology, p.87; Ryan Ho Fundamentals, p.395 (Generalised lymphadenopathy: EBV posterior > anterior cervical) ^[19] Lecture slides: GC 021. Upper respiratory tract infections.pdf, p.25 (Sore throat — serious causes include abscess/quinsy) ^[20] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.130 (Diagnostic criteria for GAS pharyngitis, swab technique, physical examination) ^[21] Senior notes: Ryan Ho Fundamentals, p.360; Ryan Ho Urogenital, p.63 (Nephritic syndrome workup — ASLO, complement, throat swab) ^[22] Senior notes: Adrian Lui Pediatrics Notes, p.157 (Centor criteria, RADT, carrier state) ^[23] Senior notes: Ryan Ho Respiratory, p.51–52 (Section 3.1.1.2 Bacterial Pharyngitis — Abx treatment, goals, complications) ^[24] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.133 (Tonsillectomy indications and contraindications) ^[25] Senior notes: Block A - Generalised Lymphadenopathy, p.2–3 (DDx of atypical lymphocytosis / IM-like syndrome) ^[26] Senior notes: Block A - Dermatology PBL 1.pdf, p.17 (Strep pharyngitis → guttate psoriasis) ^[27] Senior notes: Block A - Three Cases of Dyspnea, p.3 (Mitral stenosis in RHD — warfarin not NOAC) ^[28] Senior notes: Gen Clerk Anaes + Microbiology Summary, p.13 (ARF primary and secondary prevention) ^[29] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.134 (Tonsillectomy complications — immediate, early, late) ^[30] Senior notes: Ryan Ho Urogenital, p.59 (IgA nephropathy — synpharyngitic haematuria)

Pharyngitis and Tonsillitis

Pharyngitis refers to inflammation of the pharynx (the muscular tube extending from the posterior nasal passages to the oesophagus and larynx). Tonsillitis is inflammation specifically of the palatine tonsils — the paired lymphoid aggregates sitting within the tonsillar fossae (between the palatopharyngeal and palatoglossal arches). In practice, the two conditions overlap enormously because the tonsils are part of the pharynx, and the term tonsillopharyngitis (or simply "sore throat") is used when both structures are inflamed simultaneously, which is the most common clinical presentation ^[1]^[2].

Breaking down the terminology:

Pharynx (Greek pharynx = throat)
-itis = inflammation
Tonsil (Latin tonsilla = a stake/pointed structure — refers to their almond-shaped appearance)

The condition can be acute (< 2 weeks, by far the most common) or chronic/recurrent (repeated episodes or persistent low-grade inflammation).

One of the most common reasons for primary care consultations worldwide, accounting for ~2–4% of all GP/ED visits ^[2].
Most common of all communicable diseases: ~80% of respiratory infections are URTIs ^[2].
Age distribution: Peak incidence in children aged 5–15 years for bacterial (GAS) pharyngitis; viral pharyngitis affects all ages but is most frequent in younger children (average ~5–8 URTIs/year in the first few years of life) ^[2]^[3].
Seasonality: Viral pharyngitis peaks in autumn and winter; GAS pharyngitis peaks in late winter and early spring in temperate climates.
Hong Kong context: Because of the subtropical humid climate, high population density, and overcrowded living conditions, respiratory infections including pharyngitis are extremely common year-round. Streptococcus pharyngitis remains relevant because of the risk of rheumatic heart disease — although incidence has decreased due to good antibiotic management, it has not been eliminated in Hong Kong ^[4]. Additionally, nasopharyngeal carcinoma (NPC) presenting with sore throat/referred otalgia must always be considered in a southern Chinese patient — this is a "don't miss" diagnosis.

High Yield: In Hong Kong, always consider NPC in an adult with persistent unilateral sore throat/otalgia + cervical lymphadenopathy, especially if Cantonese and male.

3. Anatomy and Function

The pharynx is divided into three regions (superior to inferior):

Region	Boundaries	Key Structures
Nasopharynx	Skull base → soft palate	Adenoids (pharyngeal tonsil), Eustachian tube openings, fossa of Rosenmüller (common site of NPC)
Oropharynx	Soft palate → hyoid bone (level of epiglottis tip)	Palatine tonsils, base of tongue (lingual tonsil), posterior pharyngeal wall, soft palate, uvula
Hypopharynx (Laryngopharynx)	Hyoid → lower border of cricoid cartilage	Pyriform fossae, postcricoid area, posterior pharyngeal wall

The pharynx is a common pathway for both the respiratory and alimentary tracts.
It is lined by stratified squamous epithelium (oropharynx and hypopharynx) — this mucosa is directly exposed to ingested material, inspired air, and pathogens, making it vulnerable to infection and irritation.

The palatine tonsils sit in the tonsillar fossa between the anterior pillar (palatoglossal arch) and posterior pillar (palatopharyngeal arch).
They are part of Waldeyer's lymphoid ring, which also includes:
- Pharyngeal tonsil (adenoids) — nasopharynx
- Lingual tonsil — base of tongue
- Tubal tonsils — around Eustachian tube openings
Function: Waldeyer's ring is a ring of mucosa-associated lymphoid tissue (MALT) acting as the first line of immunological defence against inhaled and ingested pathogens. The tonsils sample antigens via their crypts (deep invaginations of epithelium that increase surface area for antigen exposure) and initiate adaptive immune responses (B-cell/T-cell activation, IgA production).

Feature	Detail
Arterial supply	Tonsillar branch of facial artery (main supply), ascending pharyngeal artery, dorsal lingual artery, ascending palatine artery, lesser palatine artery
Venous drainage	Peritonsillar venous plexus → lingual and pharyngeal veins → internal jugular vein
Lymphatic drainage	Jugulodigastric node (tonsillar node, a/k/a upper deep cervical node at angle of mandible) — this is why a tender, enlarged jugulodigastric node is classic for tonsillitis
Sensory innervation	Glossopharyngeal nerve (CN IX) — explains referred otalgia (via tympanic branch of CN IX / Jacobson's nerve)

High Yield: Referred otalgia in pharyngitis/tonsillitis occurs because CN IX supplies both the tonsillar fossa and the middle ear (tympanic plexus). Pain signals from the inflamed tonsil are misinterpreted by the brain as coming from the ear.

Peritonsillar space: Potential space between the tonsillar capsule and the superior constrictor muscle → site of peritonsillar abscess (quinsy) ^[5].
Parapharyngeal space: Lateral to the superior constrictor; infection can spread here.
Retropharyngeal space: Between the pharyngeal constrictors and prevertebral fascia; more common in children (retropharyngeal lymph nodes atrophy by age ~4).
Danger space: Behind the retropharyngeal space, extends from skull base to posterior mediastinum — explains why deep neck space infections can cause mediastinitis (a life-threatening complication).

4. Etiology

Causes of acute pharyngitis ^[1]^[2]:

Category	Agents	Approximate Frequency
Viral (majority, 25–45% identifiable, true proportion likely higher)	Adenovirus, rhinovirus, coronavirus, enterovirus, influenza, parainfluenza, RSV	Most common overall
Bacterial	Group A streptococcus (GAS, S. pyogenes) (5–15%); others: group C/G streptococcus, Fusobacterium necrophorum, Arcanobacterium haemolyticum, Mycoplasma spp, Chlamydia spp, Corynebacterium diphtheriae	GAS is the most important bacterial cause
Uncommon	HIV, other STIs (N. gonorrhoeae, syphilis), EBV, Herpesviridae	Must consider in right context
Non-infectious	Allergic rhinitis, GERD, smoking, exposure to dry air	Often chronic/recurrent

Viruses account for the majority of acute pharyngitis/tonsillitis cases, especially in children < 5 years.

Virus	Key Features
Rhinovirus	Most common cause of the common cold; mild pharyngitis with prominent nasal symptoms
Adenovirus	Pharyngoconjunctival fever: pharyngitis + conjunctivitis + fever; highly contagious; common in children
Influenza / Parainfluenza	Pharyngitis as part of systemic illness (fever, myalgia, malaise)
EBV (Infectious Mononucleosis)	Severe exudative tonsillitis + posterior > anterior cervical lymphadenopathy + splenomegaly + atypical lymphocytes; characteristic ampicillin-induced rash if misdiagnosed as bacterial and given amoxicillin ^[6]
Coxsackievirus A (Enterovirus)	Herpangina: small vesicles/ulcers on posterior pharynx, soft palate; Hand-foot-mouth disease: oral vesicles + vesicular rash on palms/soles
HSV-1	Gingivostomatitis: multiple shallow, painful ulcers on anterior oral mucosa, lips, gingiva
HIV	Acute retroviral syndrome: pharyngitis + fever + lymphadenopathy + rash; ask about risk factors
Coronavirus (including SARS-CoV-2)	Sore throat as part of URTI; COVID-19 variants commonly present with pharyngitis

4.3 Bacterial Pharyngitis/Tonsillitis

The most clinically important cause of bacterial pharyngitis because of its non-suppurative complications (acute rheumatic fever, post-streptococcal glomerulonephritis) and suppurative complications (peritonsillar abscess, retropharyngeal abscess, cervical lymphadenitis).
GAS = Group A Streptococcus (S. pyogenes) ^[4].
Transmission: respiratory droplets and direct contact; highly contagious in close-contact settings (schools, families, military barracks).
Peak age: 5–15 years; uncommon in children < 3 years (who tend to have "streptococcal fever" without localised pharyngitis).

Why GAS Matters

GAS pharyngitis is the only common cause of sore throat where antibiotic treatment is clearly indicated — not primarily to shorten the illness (though it does by ~1 day), but to prevent acute rheumatic fever (ARF). Antibiotics must be started within 9 days of symptom onset to prevent ARF. This is the entire rationale for distinguishing GAS from viral pharyngitis.

Organism	Notes
Group C and G Streptococcus	Can cause pharyngitis similar to GAS but NOT associated with rheumatic fever
Fusobacterium necrophorum	Anaerobic Gram-negative rod; causes pharyngitis in adolescents/young adults; associated with Lemierre syndrome (septic thrombophlebitis of the internal jugular vein → septic emboli to lungs) — a rare but serious "don't miss" diagnosis ^[1]
Arcanobacterium haemolyticum	Pharyngitis + diffuse maculopapular rash (mimics scarlet fever); more common in adolescents
Corynebacterium diphtheriae	Diphtheria: severe pharyngitis with grey/white pseudomembrane adherent to the pharynx + "bull neck" lymphadenopathy + toxin-mediated myocarditis/neuropathy; now rare due to vaccination but must be considered in unvaccinated/immigrant patients
Neisseria gonorrhoeae	Gonococcal pharyngitis: often asymptomatic or mild; consider in sexually active patients with orogenital contact

Oropharyngeal candidiasis (thrush): white, curd-like plaques on oral/pharyngeal mucosa; occurs in immunosuppressed (HIV, steroid inhalers, chemotherapy), neonates, and denture wearers. Not a true "pharyngitis" but enters the differential of sore throat with white patches.

Cause	Mechanism
Allergic rhinitis	Post-nasal drip irritates pharyngeal mucosa
GERD / Laryngopharyngeal reflux	Acid/pepsin irritation of posterior pharynx/larynx
Smoking	Direct chemical irritation and mucosal drying
Dry air / mouth breathing	Mucosal desiccation
Post-intubation	Mechanical trauma to pharyngeal/laryngeal mucosa
Tumours	NPC, oropharyngeal SCC, lymphoma

Factors increasing susceptibility and severity of URTIs ^[3]:

Underlying chronic illness
Immunocompromised
Malnutrition
Smoking
Close contact / overcrowding (schools, dormitories)
Winter season / cold weather (for viral causes)
Young age (immature immune system, smaller airway)

5. Pathophysiology

Symptoms of common cold (including viral pharyngitis) are due to the innate immune response rather than direct viral damage to the respiratory tract ^[3].

The sequence:

Viral deposition on nasal or conjunctival mucosa → attachment to receptors on epithelial cells in the nasopharynx → entry into cells ^[3].
Infected cells release cytokines and chemokines (IL-1, IL-6, IL-8, TNF-α, interferons) → attracts polymorphonuclear cells (PMNs) ^[3].
Increased vascular permeability and release of albumin and bradykinin → oedema, rhinitis, and sore throat ^[3].
Mucosal oedema + increased secretions → nasal congestion, rhinorrhoea, post-nasal drip.
Pharyngeal mucosal inflammation → sore throat, erythema.
Mucociliary clearance is slow → accumulation of PMNs in nasal secretions → colour of nasal discharge correlates with PMN content ^[3]:
- White: small amount of PMNs
- Yellow: increase in PMNs
- Green: increase in PMNs and PMN enzymatic activity (myeloperoxidase)

Common Misconception

The colour of nasal discharge does NOT correlate with the necessity of antibiotic use. Coloured nasal discharge is a normal self-limited phase of an uncomplicated common cold. Purulence alone cannot distinguish between a cold and a sinus infection ^[3]. This is one of the most common reasons for inappropriate antibiotic prescriptions.

The pathophysiology of GAS pharyngitis involves both direct tissue invasion and immune-mediated damage:

Adhesion: GAS uses M protein (a major virulence factor) and lipoteichoic acid to adhere to pharyngeal epithelial cells. M protein also resists phagocytosis by inhibiting complement activation.
Invasion and local tissue destruction: GAS produces multiple exotoxins and enzymes:
- Streptolysin O and S: Lyse host cells (leukocytes, erythrocytes) → tissue necrosis, pus formation
- Hyaluronidase: Breaks down connective tissue → facilitates spread
- Streptokinase: Activates plasminogen → dissolves fibrin clots → facilitates spread
- DNase (streptodornase): Liquefies pus (breaks down DNA from dead cells)
- Pyrogenic exotoxins (SpeA, SpeB, SpeC): Superantigens → massive T-cell activation → systemic toxicity; responsible for scarlet fever rash and streptococcal toxic shock syndrome
Host immune response: Intense neutrophilic infiltration → exudate (the tonsillar exudate you see clinically is pus = dead neutrophils + bacteria + cellular debris).
Lymph node reaction: Draining lymph nodes (anterior cervical / jugulodigastric) become enlarged and tender due to reactive lymphoid hyperplasia.

Acute Rheumatic Fever (ARF): Molecular mimicry — delayed immune response to infection with certain strains of GAS where cross-reactive antibodies (anti-M protein) target cardiac proteins → inflammation in endocardium, myocardium, and pericardium ^[4].
Post-streptococcal glomerulonephritis (PSGN): Immune complex deposition in glomeruli → complement activation → glomerular inflammation (typically 1–3 weeks after pharyngitis).
Peritonsillar abscess: Direct spread of infection through the tonsillar capsule into the peritonsillar space → collection of pus between tonsillar capsule and superior constrictor ^[5].

6. Classification

Type	Definition
Acute	< 2 weeks; single episode
Recurrent	≥ 7 episodes/year, or ≥ 5/year for 2 consecutive years, or ≥ 3/year for 3 consecutive years (Paradise criteria for tonsillectomy consideration)
Chronic	Persistent sore throat > 3 months; often due to chronic tonsillitis (cryptic tonsils harbouring bacteria), post-nasal drip, GERD, or malignancy

Category	Examples
Viral	Rhinovirus, adenovirus, EBV, influenza, coronavirus, enterovirus, parainfluenza, RSV, HSV, HIV
Bacterial	GAS (most important), Group C/G strep, F. necrophorum, A. haemolyticum, C. diphtheriae, N. gonorrhoeae
Fungal	Candida spp. (usually immunocompromised)
Non-infectious	Allergic, GERD, smoking, tumours, post-nasal drip

Type	Site
Pharyngitis	Posterior pharyngeal wall predominantly
Tonsillitis	Palatine tonsils predominantly
Tonsillopharyngitis	Both (most common clinical presentation)
Adenoiditis	Pharyngeal tonsil (nasopharynx); mainly in children
Adenotonsillitis	Both adenoids and palatine tonsils

Pattern	Description	Typical Causes
Erythematous (catarrhal)	Diffuse redness without exudate	Most viral causes
Exudative	White/yellow patches or exudate on tonsils	GAS, EBV, adenovirus (note: exudate is NOT exclusive to bacteria)
Membranous	Adherent grey/white membrane, bleeds when removed	Diphtheria, Vincent's angina
Vesicular/Ulcerative	Vesicles or ulcers on pharynx/soft palate	Herpangina (Coxsackie A), HSV, hand-foot-mouth disease

7. Clinical Features

Symptom	Pathophysiological Basis	Viral vs GAS Clues
Sore throat (odynophagia)	Mucosal inflammation → stimulation of pain receptors (CN IX, X) in pharyngeal mucosa; bradykinin and prostaglandin release from inflammatory cascade	Acute onset of sore throat favours GAS ^[1]; gradual onset with coryzal prodrome favours viral
Dysphagia	Pharyngeal/tonsillar oedema + pain → reluctance/difficulty swallowing	Severe dysphagia with drooling → consider peritonsillar abscess or epiglottitis (red flag)
Fever	Pyrogens (IL-1, IL-6, TNF-α, PGE2) → hypothalamic set-point elevation	Low-grade fever in viral; higher fever (>38.3°C) more suggestive of GAS
Headache	Systemic cytokine release; meningeal irritation from fever	Common in both but more prominent with GAS
Abdominal pain	Mesenteric lymphadenitis (reactive) due to systemic immune response; common in children with GAS	Fever, headache, abdominal pain in GAS pharyngitis settings ^[1]
Malaise, anorexia	Systemic cytokine effects (IL-1, TNF-α → sickness behaviour)	Non-specific
Nausea/vomiting	Mesenteric lymphadenitis + systemic inflammation; vagal stimulation from pharyngeal irritation	± Vomiting in GAS ^[1]; more common in children
Referred otalgia	CN IX (glossopharyngeal nerve) supplies both tonsillar fossa and middle ear (tympanic plexus) → pain from tonsil is "referred" to the ear	Non-specific but important — always examine the pharynx in a patient complaining of ear pain with a normal tympanic membrane
Cough	Post-nasal drip irritating larynx; direct viral laryngotracheitis	Absence of cough is a Centor criterion favouring GAS; cough suggests viral ^[1]
Nasal symptoms (congestion, rhinorrhoea, sneezing)	Viral infection of nasal mucosa → mucosal oedema + secretions	Nasal symptoms favour viral pharyngitis ^[1]
Hoarseness	Laryngeal involvement (laryngitis) — viral causes extend to larynx	Hoarseness and other coryzal symptoms favour viral ^[1]
Conjunctivitis	Adenovirus has tropism for conjunctival epithelium	Conjunctivitis strongly favours viral (pharyngoconjunctival fever) ^[1]

Sign	Pathophysiological Basis	Clinical Significance
Pharyngeal/tonsillar erythema	Vasodilatation + inflammatory infiltrate in submucosa	Non-specific; present in both viral and bacterial
Tonsillar exudate	Neutrophilic exudate (pus) filling tonsillar crypts	Exudative tonsillitis is a Centor criterion ^[1]; however, EBV and adenovirus can also cause impressive exudate — exudate is not pathognomonic for bacteria
Tonsillar enlargement (hypertrophy)	Reactive lymphoid hyperplasia + oedema	Graded 0–4 (0 = within fossa; 4 = tonsils touching/"kissing tonsils"); bilateral symmetrical enlargement is typical of infection
Tender anterior cervical lymphadenopathy	Reactive lymphoid hyperplasia in draining nodes (jugulodigastric/anterior cervical chain) due to antigen presentation from infected tonsils	Prominent tender anterior cervical adenopathy is a Centor criterion for GAS ^[1]; posterior > anterior cervical lymphadenopathy suggests EBV ^[6]
Palatal petechiae	Capillary fragility + thrombocytopenia (in EBV) or local vasculitis	Classically seen in GAS and EBV; relatively specific for these diagnoses
Uvular oedema	Spread of inflammation to uvula → oedema	Can be seen in GAS pharyngitis
"Strawberry tongue"	Erythematous papillae visible through white coating (white strawberry) → coating desquamates leaving beefy red tongue (red strawberry)	Pathognomonic for scarlet fever (GAS + pyrogenic exotoxin)
Scarlatiniform rash	Pyrogenic exotoxins (superantigens) from GAS → widespread T-cell activation → erythematous, sandpaper-textured rash with Pastia lines (linear petechiae in skin folds) and circumoral pallor	± Rash: scarlatiniform rash, urticaria in GAS ^[1]
Oral vesicles/ulcers	Viral cytopathic effect on epithelial cells → cell death → vesicle/ulcer formation	± Oral ulcers, viral exanthem favours viral ^[1]; herpangina has vesicles on POSTERIOR pharynx; HSV has vesicles/ulcers on ANTERIOR oral cavity
Splenomegaly	Reticuloendothelial hyperplasia in infectious mononucleosis (EBV-driven B-cell proliferation → splenic lymphoid hyperplasia)	If present with exudative tonsillitis → strongly consider EBV
Hepatomegaly	Hepatic involvement in EBV infection	Supports EBV diagnosis
Unilateral peritonsillar swelling with uvula deviation	Collection of pus between tonsillar capsule and superior constrictor ^[5] → mass effect pushes uvula to contralateral side	Peritonsillar abscess (quinsy); symptoms similar to tonsillitis but usually more severe; muffled ("hot potato") voice; airway obstruction risk ^[5]
Trismus	Inflammation/spasm of pterygoid muscles adjacent to the peritonsillar space	Trismus is a key sign of peritonsillar abscess ^[5]; also seen in parapharyngeal abscess
"Bull neck"	Massive cervical lymphadenopathy + soft tissue oedema	Think diphtheria or severe deep neck space infection
Grey pseudomembrane	Diphtheria toxin causes epithelial necrosis → fibrin + necrotic tissue + bacteria form an adherent membrane; bleeds when forcibly removed	Diphtheria — a "don't miss" diagnosis

Feature	Favouring GAS	Favouring Viral
Onset	Acute, sudden	Gradual
Coryzal symptoms	Absent (no cough, rhinorrhoea, hoarseness)	Present (cough, runny nose, hoarseness, conjunctivitis)
Sore throat	Severe	Variable
Exudate	Present	May be present (EBV, adenovirus) or absent
Fever	High (>38.3°C)	Low-grade or absent
Anterior cervical LN	Tender, enlarged	Less prominent
Rash	Scarlatiniform	Viral exanthem, oral ulcers
Age	5–15 years peak	All ages
Season	Late winter/early spring	Autumn/winter
Contact history	Prior close exposure to GAS (esp familial) ^[1]	Exposure to URI contacts
Abdominal symptoms	Headache, abdominal pain, vomiting	Less common

High Yield — Centor Criteria (Mnemonic: CENT — Cough absent, Exudate, Nodes, Temperature)

7.4 Specific Clinical Patterns by Etiology

Triad: severe exudative tonsillitis + posterior cervical lymphadenopathy (posterior > anterior) + splenomegaly
Atypical lymphocytes on blood film ("Downey cells")
Ampicillin/amoxicillin rash: If amoxicillin is given (misdiagnosed as bacterial tonsillitis), ~90% develop a widespread maculopapular rash — this is NOT a true penicillin allergy but rather an immune-mediated reaction
Fatigue may persist for weeks to months

Mainly affects children < 10 years
Small vesicles and shallow ulcers on posterior pharynx, soft palate, tonsillar pillars (spares anterior mouth — key distinction from HSV)
Self-limiting in 7–10 days

Grey/white pseudomembrane firmly adherent to pharynx (bleeds if removed)
"Bull neck" — severe cervical lymphadenopathy + soft tissue oedema
Toxin-mediated: myocarditis (arrhythmias, heart failure) and neuropathy (palatal palsy → nasal regurgitation, limb weakness)
Now rare in HK due to DTP vaccination but must be considered in unimmunised/travellers

Peritonsillar abscess: Collection of pus between tonsillar capsule and superior constrictor ^[5]

Symptoms: Similar to tonsillitis but usually more severe ^[5]
Muffled voice ("hot potato voice") ^[5]
Airway obstruction ^[5]
Signs:
- Unilateral peritonsillar swelling ^[5]
- Deviation of uvula (to the contralateral side) ^[5]
- Trismus (difficulty opening mouth due to pterygoid muscle spasm) ^[5]

Strep pharyngitis → guttate psoriasis, raindrop appearance — this is a well-known association where molecular mimicry between streptococcal M protein and keratin triggers a widespread T-cell–mediated skin reaction ^[7].

Feature	Viral	GAS	EBV	Diphtheria	Peritonsillar Abscess
Age	Any	5–15	Adolescents/young adults	Any (unvaccinated)	Adolescents/young adults
Onset	Gradual	Sudden	Insidious (1–2 weeks)	Insidious	Acute on chronic
Coryzal symptoms	✓	✗	±	✗	✗
Exudate	±	✓	✓✓ (thick, white)	Grey membrane	±
Lymphadenopathy	Mild, generalised	Anterior cervical	Posterior cervical + generalised	"Bull neck"	Ipsilateral, tender
Rash	Viral exanthem	Scarlatiniform	Amoxicillin rash	-	-
Trismus	✗	✗	✗	✗	✓
Uvula deviation	✗	✗	✗	✗	✓
Splenomegaly	✗	✗	✓	✗	✗

High Yield Summary

Most pharyngitis is viral — antibiotics are NOT indicated unless GAS is confirmed or strongly suspected.
GAS pharyngitis is the most important bacterial cause because of the risk of acute rheumatic fever (preventable with antibiotics within 9 days).
Centor criteria (CENT): Cough absent, Exudate, Nodes (anterior cervical), Temperature (fever) — each scores 1 point; used to guide need for testing/empirical treatment.
Viral clues: Cough, rhinorrhoea, conjunctivitis, hoarseness, oral ulcers.
GAS clues: Sudden onset, exudate, tender anterior cervical lymphadenopathy, fever, absence of cough, scarlatiniform rash, age 5–15.
EBV clues: Severe exudative tonsillitis + posterior cervical lymphadenopathy + splenomegaly + atypical lymphocytes; avoid amoxicillin (causes rash).
Peritonsillar abscess (quinsy): Unilateral peritonsillar swelling, uvula deviation, trismus, muffled voice — a surgical emergency requiring drainage.
Diphtheria: Grey pseudomembrane + bull neck + myocarditis/neuropathy — consider in unvaccinated patients.
In Hong Kong: Always consider NPC in adults with persistent unilateral sore throat + cervical lymphadenopathy.
Molecular mimicry explains ARF: GAS M protein cross-reacts with cardiac proteins → pancarditis.
Referred otalgia in pharyngitis is via CN IX (glossopharyngeal nerve).
Coloured nasal discharge ≠ need for antibiotics — it reflects PMN enzymatic activity, not bacterial infection.

Active Recall - Pharyngitis and Tonsillitis (Definition, Epidemiology, Etiology, Pathophysiology, Clinical Features)

Differential Diagnosis of Pharyngitis and Tonsillitis

When a patient presents with a "sore throat," the diagnostic challenge is threefold:

Is it truly pharyngitis/tonsillitis, or is the sore throat coming from somewhere else? (e.g., referred pain, post-nasal drip, GERD, foreign body)
If it IS pharyngitis/tonsillitis, what is the cause? (viral vs. bacterial vs. other)
Is there a serious or "don't miss" diagnosis? (peritonsillar abscess, epiglottitis, diphtheria, malignancy, HIV seroconversion)

This framework maps directly onto the GC lecture slide classification ^[8]:

> 90% of acute sore throat is due to viral URIs ^[8]

Emergency: acute epiglottitis (drooling of saliva) ^[8]

Serious: bacterial tonsillitis, abscess (quinsy), TB, lymphoma ^[8]

Pitfalls: postnasal drip, irritation, foreign body, infectious mononucleosis ^[8]

Enlarged tonsils are normal in children ^[8]

Exudates can mean viral or bacterial ^[8]

GC High Yield — Exudate Does NOT Equal Bacteria

A very common student mistake is equating tonsillar exudate with bacterial infection and prescribing antibiotics. Exudates can mean viral or bacterial ^[8]. EBV, adenovirus, and even HSV can produce impressive exudates. Always use the full clinical picture (Centor criteria, epidemiology, associated features) before deciding on antibiotics.

9.2 Master Differential Diagnosis Table

The differential can be organised into infectious (the majority) and non-infectious causes, with a separate category for "don't miss" / red-flag diagnoses.

Diagnosis	Key Distinguishing Features	Why It Matters
Viral pharyngitis (rhinovirus, coronavirus, parainfluenza, RSV, adenovirus)	Cough, nasal symptoms (congestion, discharge, sneezes), conjunctivitis, hoarseness and other coryzal symptoms, ± oral ulcers, viral exanthem ^[1]^[2]; gradual onset; low-grade fever	Most common cause (> 90%); self-limiting; no antibiotics needed
GAS pharyngitis (S. pyogenes)	Acute onset of sore throat; exudative tonsillitis; prominent tender anterior cervical adenopathy; fever, headache, abdominal pain; ± scarlatiniform rash; absence of cough/coryzal symptoms; prior close exposure to GAS (esp familial) ^[1]^[2]	Risk of ARF and PSGN; only common indication for antibiotics
Infectious mononucleosis (EBV)	Triad of fever, tonsillar pharyngitis, and lymphadenopathy ^[9]; posterior cervical lymphadenopathy (posterior > anterior) ^[9]; splenomegaly; atypical lymphocytes; ampicillin/amoxicillin rash; peak age 15–24 years	Pitfall ^[8] — often misdiagnosed as bacterial tonsillitis; avoid amoxicillin; risk of splenic rupture
EBV-negative mononucleosis-like illness	10% of mononucleosis syndrome not caused by EBV; agents include CMV, HIV, HHV-6, HHV-7, HBV, adenovirus, rubella, toxoplasmosis ^[9]; CMV-IM is often milder and self-limited	Diagnostic testing is particularly important if the patient is pregnant since CMV, HIV and toxoplasmosis have adverse effects on pregnancy outcomes ^[9]
Herpangina (Coxsackievirus A)	Small vesicles/ulcers on posterior pharynx and soft palate; children < 10; summer/autumn	Self-limiting; distinguish from HSV (anterior oral lesions)
HSV gingivostomatitis	Multiple shallow painful ulcers on anterior oral mucosa, lips, gingiva; vesicles on erythematous base	Primary HSV-1 in children; self-limiting but can be severe in immunocompromised
Hand-foot-mouth disease (Coxsackie A16, EV-A71)	Oral vesicles/ulcers + characteristic vesicular rash on palms and soles; children < 5	Usually self-limiting; EV-A71 can rarely cause brainstem encephalitis
Diphtheria (C. diphtheriae)	Grey/white adherent pseudomembrane that bleeds on removal; "bull neck"; toxin → myocarditis, neuropathy	Rare in HK due to vaccination; serious cause ^[8]; consider in unvaccinated/immigrant
Group C/G streptococcus	Clinically indistinguishable from GAS pharyngitis	NOT associated with ARF (no molecular mimicry with cardiac proteins)
Fusobacterium necrophorum	Pharyngitis in adolescents/young adults → Lemierre syndrome (septic IJV thrombophlebitis → septic pulmonary emboli)	"Don't miss" — triad of sore throat → neck swelling/tenderness → respiratory symptoms
Arcanobacterium haemolyticum	Pharyngitis + diffuse maculopapular rash (mimics scarlet fever); adolescents	Often misdiagnosed as GAS with scarlet fever
Gonococcal pharyngitis (N. gonorrhoeae)	Often asymptomatic or mild sore throat; orogenital contact history	Must ask about sexual history; requires specific culture/NAAT
Syphilitic pharyngitis	Mucous patches (painless, greyish) on oral/pharyngeal mucosa in secondary syphilis; ± diffuse rash including palms/soles	STI screening in high-risk patients
Acute HIV seroconversion (acute retroviral syndrome)	Pharyngitis + fever + generalised lymphadenopathy + maculopapular rash + mucosal ulceration; 2–6 weeks after exposure	Pitfall ^[8] — high viral load, highly infectious; ask about risk factors
Peritonsillar abscess (quinsy)	Unilateral peritonsillar swelling; deviation of uvula; trismus; muffled voice; symptoms similar to tonsillitis but usually more severe; airway obstruction ^[5]	Serious cause ^[8]; requires urgent drainage
Parapharyngeal / retropharyngeal abscess	Deep neck space infection; severe systemic toxicity; neck stiffness/swelling; torticollis (retropharyngeal); may follow tonsillitis or dental infection	Life-threatening — risk of airway compromise and mediastinitis via danger space
TB	Chronic sore throat; cervical lymphadenopathy (matted, non-tender); constitutional symptoms (night sweats, weight loss); oropharyngeal ulceration	Serious cause ^[8]; important in HK (endemic area)
Oropharyngeal candidiasis	White curd-like plaques, easily scraped off; immunosuppressed (HIV, inhaled steroids, chemotherapy)	Suggests underlying immunodeficiency if in otherwise healthy adult

Diagnosis	Key Distinguishing Features	Why It Enters the DDx
Post-nasal drip	Chronic/recurrent sore throat worse on waking; associated nasal congestion, rhinorrhoea, throat clearing, "tickle" sensation	Pitfall ^[8] — often overlooked; from allergic rhinitis or chronic sinusitis
Irritation (smoking, dry air, chemicals)	Chronic sore throat; occupational/environmental exposure; no fever/exudate	Pitfall ^[8]; history is key
Foreign body	Acute onset after eating (classically fish bone in HK); localised sharp pain; odynophagia	Pitfall ^[8]; lateral soft-tissue neck X-ray or flexible nasolaryngoscopy to locate
GERD / Laryngopharyngeal reflux	Chronic sore throat; globus sensation; hoarseness; worse after meals/lying down; heartburn may or may not be present	Non-infectious; responds to PPI trial
Allergic rhinitis	Pruritus of eyes, nose, palates, ears; watery rhinorrhoea; sneezing; nasal congestion; postnasal drip ^[1]	Sore throat is secondary to post-nasal drip and mouth breathing
Aphthous ulceration	Recurrent painful shallow ulcers on non-keratinised oral mucosa; no fever	Not true pharyngitis but enters DDx of oral/pharyngeal pain
Drug-induced	Mononucleosis syndrome with atypical lymphocytosis can be induced by anticonvulsants (phenytoin, carbamazepine) or antibiotics (isoniazid, minocycline) ^[9]	Mimics infectious mononucleosis; always check drug history

Diagnosis	Key Distinguishing Features	Why It Must Not Be Missed
Acute epiglottitis	Emergency; drooling of saliva ^[8]; severe sore throat with dysphagia disproportionate to pharyngeal findings; muffled "hot potato" voice; stridor; child sits in "tripod position"; adults may have subtler presentation	Airway emergency — can progress to complete obstruction within hours
Lymphoma	Serious cause ^[8]; asymmetric tonsillar enlargement (unilateral > bilateral); firm, non-tender tonsil ± cervical lymphadenopathy; B symptoms (fever, weight loss, night sweats)	Tonsils and tongue base may be the presenting site for a lymphoma ^[10]
Oropharyngeal / tonsillar SCC	Persistent unilateral sore throat/ulceration; otalgia (referred via CN IX/X); risk factors: HPV 16/18, smoking, alcoholism ^[10]; 5Ss: Smoking, Spirits, Sharp teeth, Sex (male/oral), Spicy food ^[10]	Malignancy — early diagnosis improves prognosis
Nasopharyngeal carcinoma (NPC)	Persistent sore throat + unilateral serous otitis media (blocked Eustachian tube) + posterior cervical lymphadenopathy; epistaxis; Cantonese/Southern Chinese male; EBV-associated	Endemic in HK — "don't miss" in any Southern Chinese adult with persistent unilateral symptoms
Ludwig's angina	Bilateral submandibular/sublingual space infection (usually from dental infection); "woody" floor of mouth; tongue elevation; drooling; stridor	Rapid airway compromise — surgical emergency
Lemierre syndrome	Post-pharyngitis septic thrombophlebitis of IJV → septic emboli to lungs; tender lateral neck swelling; rigors; pleuritic chest pain	Rare but lethal if missed; F. necrophorum
Kawasaki disease (children)	Fever ≥ 5 days + pharyngeal erythema (strawberry tongue) + bilateral non-exudative conjunctivitis + polymorphous rash + extremity changes + cervical lymphadenopathy	Risk of coronary artery aneurysms; must not be dismissed as "tonsillitis" in a child with prolonged fever
Agranulocytosis	Severe sore throat + oral/pharyngeal ulceration/necrosis + high fever + absence of pus (no neutrophils to form pus)	Drug-induced (carbimazole, clozapine, methotrexate); check urgent FBC

9.3 Differential Diagnosis of Specific Clinical Patterns

Think: GAS, EBV, adenovirus, diphtheria, A. haemolyticum, Vincent angina (fusospirochetal infection — ulcerative, fetid breath)

Exudates can mean viral or bacterial ^[8] — never assume bacterial based on exudate alone.

Think: Herpangina (posterior), HSV (anterior), hand-foot-mouth disease, aphthous ulcers, acute HIV

Rash Pattern	Think...
Scarlatiniform (sandpaper)	GAS (scarlet fever), A. haemolyticum
Maculopapular (after amoxicillin)	EBV — ampicillin rash
Palms and soles involvement	Secondary syphilis
Maculopapular + generalised lymphadenopathy	Acute HIV seroconversion
Raindrop / guttate lesions	Strep pharyngitis → guttate psoriasis ^[7] (post-infective, not acute pharyngitis itself)

This is a red flag — always consider:

Peritonsillar abscess (quinsy) ^[5]^[8]
Lymphoma ^[8]^[10]
Tonsillar SCC ^[10]
Parapharyngeal abscess (bulge of lateral pharyngeal wall)

High Yield: Bilateral symmetrical tonsillar enlargement in a child is usually reactive and benign (enlarged tonsils are normal in children ^[8]). Unilateral tonsillar enlargement in an adult is malignancy until proven otherwise.

If the sore throat does not resolve, reassess and consider:

Malignancy: NPC, oropharyngeal SCC, lymphoma
Chronic tonsillitis: recurrent episodes with tonsillar crypts harbouring biofilms
TB ^[8]
Post-nasal drip / allergic rhinitis
GERD / laryngopharyngeal reflux
Foreign body ^[8]
HIV (chronic pharyngeal candidiasis as a marker)
Agranulocytosis

Because pharyngitis often coexists with other URTI syndromes, you must differentiate among the URTI spectrum ^[1]^[2]^[3]:

Condition	Suggestive Features
Common cold	Nasal symptoms (rhinorrhoea), cough, hoarseness, conjunctivitis ^[1]
Bacterial pharyngitis	Previous close exposure to strep throat, sudden onset sore throat with little viral symptoms (rhinorrhoea, cough, hoarseness), exudative tonsillitis, tender anterior cervical LNs, fever, ± headache and abdominal pain ^[1]
Rhinosinusitis	Prolonged ( > 10–14d) URI symptoms + ≥ 2 of facial/sinus pain (esp if aggravated by postural changes or Valsalva manoeuvre), purulent nasal discharge, fever ^[1]
Influenza	Viral URI symptoms + systemic features (fever up to 40°C, myalgia, arthralgia, malaise) ± other system involvement (pneumonia, GE, CNS infections) ^[1]
Non-infectious rhinitis	Pruritus of eyes, nose, palates, ears; watery rhinorrhoea; sneezing; nasal congestion; postnasal drip ^[1]
Acute bronchitis	Preceding viral URI symptoms with prominent cough and wheezes but not a/w features of pneumonia (e.g. fever, tachypnoea, crepitations, lung consolidation) ^[1]

GAS tonsillopharyngitis is usually not accompanied by nasal symptoms ^[3] — this is the single most useful clinical clue to distinguish it from viral URTI.

Pertussis classically begins with mild cough and coryza but the cough gradually increases and becomes paroxysmal ^[3] — don't forget it in the differential of a child with persistent cough that started as a "sore throat."

When the presenting complaint includes hoarseness along with sore throat:

Hoarseness indicates pathology in the larynx ^[8]

Most likely viral URI if acute ^[8]

Differential diagnosis: vocal cord polyps/nodules ^[8]

Serious causes: acute epiglottitis, croup, carcinoma of the larynx ^[8]

Pitfalls: sputum; laryngeal injury/compression; trauma from intubation ^[8]

Pharyngitis can coexist with — or be confused with — a neck mass. The lecture slides on imaging classify neck masses as ^[11]:

Inflammatory/infectious masses: cellulitis, abscess, reactive adenitis; dental infection, pharyngitis, sialadenitis ^[11]

Neoplastic masses: malignant adenopathy from head and neck cancer (oropharyngeal, nasopharyngeal, parotid); cystic nodal metastases; benign masses (schwannoma, paraganglioma, lipoma) ^[11]

Congenital masses: branchial cleft cyst, venous malformation ^[11]

Key point: a 2nd branchial cleft cyst can become infected during a URTI, presenting as a laterally placed neck mass with pharyngitis symptoms. Its sinus tract travels through deep structures of the neck and opens into the tonsillar fossa ^[10] — so it can mimic a peritonsillar abscess.

Because EBV-IM is a classic pitfall ^[8] and commonly tested:

Infectious mononucleosis is characterised by a triad of fever, tonsillar pharyngitis and lymphadenopathy ^[9].

Differential diagnosis of infectious mononucleosis-like syndrome / atypical lymphocytosis ^[12]:

Category	Agents
Viral infections	EBV, CMV, HIV, acute viral hepatitis ^[12]
Bacterial infections	Atypical organisms: Mycoplasma pneumoniae, Legionella pneumophila, Salmonella spp., Rickettsia spp. ^[12]
Mycobacterial	Disseminated TB ^[12]
Fungal	Dimorphic fungi (Talaromyces marneffei) ^[12] — important in HK/Southern China
Parasitic	Toxoplasma gondii ^[12]
Drug reactions	Phenytoin, carbamazepine, isoniazid, minocycline ^[9]^[12]

Don't Confuse Atypical Lymphocytes with Blasts

Acute lymphoblastic leukaemia: the blasts can mimic atypical lymphocytes if you don't look at the blood film clearly ^[12]. Always have a haematologist review the film if in doubt. The clinical context differs — ALL presents with pancytopenia and bone marrow failure features (anaemia, infections, bleeding), not just pharyngitis.

GAS pharyngitis vs EBV IM: Classically, GAS/scarlet fever presents with anterior cervical lymphadenopathy, compared with posterior cervical lymphadenopathy in IM ^[9].

When evaluating a patient with pharyngitis, certain associated conditions must be actively sought:

Association	Explanation
Post-streptococcal glomerulonephritis (PSGN)	Antecedent GAS infection occurring 7d–12w before onset of PSGN; usually 1–3w after pharyngitis ^[13]; presents with haematuria, oedema, hypertension
Acute rheumatic fever	Delayed immune response to GAS; cross-reactive antibodies target cardiac proteins; preceded by strep throat 2–3w before ^[4]
Guttate psoriasis	Strep pharyngitis → guttate psoriasis, raindrop appearance ^[7]; occurs 1–2 weeks after GAS pharyngitis
Erythema nodosum	Streptococcus pharyngitis is a known trigger for erythema nodosum (tender nodules on bilateral shins) ^[14]
Reactive arthritis	Can follow GAS and other infections
PANDAS	Paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections — tics and OCD following GAS pharyngitis
IgA nephropathy	Recurrent synpharyngitic haematuria — gross haematuria occurring simultaneously with pharyngitis (not delayed like PSGN) ^[15]

Synpharyngitic vs Post-pharyngitic Haematuria

IgA nephropathy: haematuria occurs at the same time as the pharyngitis (synpharyngitic, within 1–2 days) because pre-formed IgA immune complexes deposit in glomeruli immediately upon mucosal infection.

PSGN: haematuria is delayed by 1–3 weeks after pharyngitis because time is needed for immune complex formation against streptococcal antigens + complement fixation.

This temporal distinction is a classic exam discriminator.

High Yield Summary — Differential Diagnosis of Pharyngitis and Tonsillitis

> 90% of acute sore throat is due to viral URIs — the default diagnosis is viral unless proven otherwise.
Centor criteria (CENT) guide the need for GAS testing/empirical antibiotics, but exudates can mean viral or bacterial — never treat based on exudate alone.
Red-flag / "don't miss" diagnoses: acute epiglottitis (drooling, stridor), peritonsillar abscess (trismus, uvula deviation), deep neck space abscess, lymphoma (unilateral tonsillar mass), NPC (Southern Chinese, unilateral ear/nose symptoms), diphtheria (pseudomembrane), Lemierre syndrome (post-pharyngitis IJV thrombophlebitis), agranulocytosis (ulceration without pus).
EBV-IM is a classic pitfall — posterior cervical LN, splenomegaly, atypical lymphocytes, amoxicillin rash.
Synpharyngitic haematuria (concurrent with pharyngitis) = IgA nephropathy; post-pharyngitic haematuria (1–3 weeks later) = PSGN.
Unilateral tonsillar enlargement in an adult = malignancy until proven otherwise (lymphoma, SCC, minor salivary gland tumour).
GAS pharyngitis is usually NOT accompanied by nasal symptoms — the best single clinical clue to distinguish from viral URTI.
Persistent sore throat > 3 weeks: must exclude malignancy (NPC, oropharyngeal SCC, lymphoma), TB, HIV, foreign body.

Active Recall - Differential Diagnosis of Pharyngitis and Tonsillitis

References

^[1] Senior notes: Ryan Ho Respiratory, p.48–51 (Section 3.1.1 URTI and 3.1.1.2 Bacterial Pharyngitis) ^[2] Senior notes: Adrian Lui Pediatrics Notes, p.154–157 (Section 5.2.1 Respiratory Infections) ^[3] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai), p.120–122 (Differential diagnosis of URTI) ^[4] Senior notes: Ryan Ho Cardiology, p.146 (Section 3.3.1 Rheumatic Heart Disease / Acute Rheumatic Fever) ^[5] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf, p.43 (Peritonsillar abscess / Quinsy) ^[7] Senior notes: Block A - Dermatology PBL 1.pdf, p.17 (Strep pharyngitis → guttate psoriasis) ^[8] Lecture slides: GC 021. Upper respiratory tract infections.pdf, p.25 and p.28 (Sore Throat; Hoarseness) ^[9] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.31 and MBBS Final MB (Medicine) (Felix PY Lai), p.1810–1812 (Infectious mononucleosis) ^[10] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai), p.201 and p.255 (Neck mass DDx; Oropharyngeal SCC) ^[11] Lecture slides: GC 015. Imaging of the head and neck.pdf, p.39 (Inflammatory/infectious, neoplastic, congenital neck masses) ^[12] Senior notes: Block A - Generalised Lymphadenopathy, p.2–3 (DDx of atypical lymphocytosis / IM-like syndrome) ^[13] Senior notes: Ryan Ho Urogenital, p.66 (PSGN) ^[14] Senior notes: Ryan Ho Rheumatology, p.157 (Erythema nodosum — streptococcal pharyngitis as a cause) ^[15] Senior notes: Ryan Ho Urogenital, p.59 (IgA nephropathy — synpharyngitic haematuria)

Diagnostic Criteria, Algorithm and Investigations for Pharyngitis and Tonsillitis

The vast majority of pharyngitis is viral and self-limiting. The entire diagnostic framework for acute pharyngitis therefore revolves around one pivotal question:

Does this patient have Group A Streptococcal (GAS) pharyngitis?

Why? Because GAS is the only common cause where antibiotic treatment materially changes outcomes — specifically by preventing acute rheumatic fever (ARF). Every other common cause is either viral (self-limiting, antibiotics harmful) or a rare/serious diagnosis requiring a different workup entirely.

Why We Don't Just Treat Everyone With Antibiotics

Empiric treatment is NOT recommended as the best diagnostic accuracy achievable based on clinical symptoms alone is only 50% ^[2]. Overtreatment drives antibiotic resistance, adverse drug reactions (including C. difficile colitis and anaphylaxis), and medicalises a self-limiting illness. Conversely, undertreating genuine GAS misses the window to prevent ARF. Hence the need for a structured approach.

10.2 Centor / Modified Centor (McIsaac) Criteria

Centor criteria: now predominantly used to rule out GAS pharyngitis in those likely to be viral ^[1]^[2].

Historically, the Centor score was developed to identify patients very likely to have GAS who could be treated empirically. However, no clinical scoring system has been demonstrated to be specific enough to eliminate the need for diagnostic testing ^[2]. The modern use of Centor/McIsaac is therefore as a screening tool to decide who needs testing (not who needs treatment).

Centor Criteria	Points
Absence of cough (Cough)	1
Tonsillar exudates (Exudate)	1
Tender anterior cervical adenopathy (Node)	1
History of fever (Temperature)	1

Mnemonic: CENT — Cough (absent), Exudate, Node, Temperature

Modified Centor (McIsaac) criteria add age adjustment ^[1]^[2]:

Age Modifier	Points
Age < 15 years	+1
Age 15–44 years	0
Age > 44 years	−1

Modified Centor Score	Estimated Risk of GAS	Recommended Action
−1 to 1	< 10%	No antibiotics or throat culture necessary ^[1]^[2]
2 to 3	15–32%	Antibiotics if throat culture/RADT positive ^[1]^[2]
4 to 5	~56%	Treat empirically with an antibiotic (or test-and-treat) ^[1]^[2]

Updated Guideline Nuance (2024–2026)

In recent guidelines, antibiotics are given only after a rapid test/throat culture is positive. This avoids inappropriate use of antibiotics ^[2]. Even at a score of 4–5, many guidelines (including AHA/IDSA) now recommend confirming with RADT or culture before treating, except in endemic settings with high ARF prevalence. For HKUMed exams, know both the "empirical at 4–5" and the "test-first" approaches.

10.3 Diagnostic Tests for GAS Pharyngitis

Diagnostic testing: geared towards identifying GAS pharyngitis (associated with complications) ^[1].

Used for those without features suggestive of viral illness — i.e., if the patient has obvious viral features (cough, rhinorrhoea, conjunctivitis, hoarseness), GAS is unlikely and testing is generally not needed ^[1]^[2].

Specimen should be obtained by swabbing both tonsils and posterior pharynx ^[16]. Avoid tongue, buccal mucosa and hard palate as they are not satisfactory sites ^[16].

Why? GAS colonises the tonsillar crypts and posterior pharyngeal wall. Swabbing the wrong site (e.g., running the swab over the tongue or cheek) contaminates the sample with normal oral flora and dilutes the GAS yield, leading to false negatives.

Technique: Use a firm-tipped swab; ask patient to say "ahh" (depresses tongue); use a tongue depressor; swab both tonsillar fossae and the posterior pharyngeal wall with a vigorous rubbing motion; avoid touching any other mucosal surface.

Feature	Detail
Mechanism	Detects GAS-specific carbohydrate antigen (Lancefield group A polysaccharide) directly from the throat swab using immunochromatographic or latex agglutination methods
Advantages	Specificity ≥ 95%; rapid turnaround time (5–10 minutes) → allows timely administration of antibiotics ^[2]
Disadvantages	Sensitivity 70–90% (vs 90–95% for culture) → a negative RADT should be backed up by culture ^[2]; cannot distinguish between active illness and carrier state ^[2]
Clinical implication	A positive RADT is sufficient to initiate treatment (high specificity = few false positives). A negative RADT in a patient with a moderate-to-high Centor score should prompt a backup throat culture to catch false negatives (especially in children, where the stakes of missing GAS are highest due to ARF risk)

Carrier State Caveat

10–25% of the population carry GAS asymptomatically → a positive RADT + pharyngitis ≠ GAS pharyngitis ^[2]. A patient may have viral pharyngitis coincidentally with GAS carriage. This is why clinical context (Centor criteria) matters — testing should only be performed on patients with a reasonable pre-test probability.

Feature	Detail
Mechanism	Inoculation of swab onto blood agar plate; GAS produces beta-haemolytic colonies (clear zone of haemolysis) after 24–48 hours; confirmed by bacitracin sensitivity or Lancefield grouping
Advantages	Gold standard with very high sensitivity (90–95%); also identifies other pathogens (e.g., group C/G streptococcus, A. haemolyticum, C. diphtheriae) ^[2]
Disadvantages	Requires up to 3 days for results ^[2] — delays treatment decisions
When to use	As backup for negative RADT in children/adolescents (< 18 years); or when RADT is unavailable; or when non-GAS bacterial pathogens are suspected

Test	Role
PCR (molecular testing)	Highest sensitivity; seldom used in routine practice due to cost; useful in research or outbreak settings ^[2]
Serology (ASLO, anti-DNase B)	Not helpful for acute diagnosis as it takes > 2 weeks to rise ^[2]; used retrospectively to confirm preceding GAS infection in suspected ARF or PSGN
Anti-streptolysin O (ASLO)	Antibody against streptolysin O; rises 1–3 weeks after GAS infection, peaks at 3–5 weeks; confirms recent strep infection ^[17]^[18]; may be negative in some strains (especially skin infections)
Streptozyme test	Measures 5 different antibodies against streptococcal antigens, including ASLO ^[13]; more sensitive than ASLO alone for confirming recent GAS infection

10.4 Investigations for Specific Diagnoses Beyond GAS

When the clinical picture suggests a cause other than straightforward viral or GAS pharyngitis, targeted investigations are needed:

Investigation	Key Findings	Interpretation
CBC with differential	Atypical lymphocytes (large, activated T cells with "ballerina skirt" cytoplasm); may have relative/absolute lymphocytosis; ± mild thrombocytopenia	Atypical lymphocytes are characteristic but not pathognomonic — also seen in CMV, HIV, toxoplasmosis, drug reactions
Monospot (heterophile antibody test)	Detects IgM antibodies that agglutinate sheep/horse RBCs (Paul-Bunnell test)	Sensitivity ~85% in adolescents/adults but may be negative in first week and in children < 4 years; false negatives early in disease
EBV-specific serology	VCA IgM (+), VCA IgG (+/−), EBNA IgG (−) = acute primary EBV	Gold standard for confirming EBV; EBNA IgG appears weeks-months later (its presence excludes acute primary infection)
Liver function tests	↑transaminases (ALT, AST) in ~80–90%	Subclinical hepatitis is very common in IM
Blood film	Atypical lymphocytes; must not confuse with blasts (ALL)	Always have experienced haematologist review if uncertain ^[12]

Investigation	Key Findings	Interpretation
Clinical diagnosis	Unilateral peritonsillar swelling, uvula deviation, trismus, muffled voice ^[5]	Diagnosis is primarily clinical; imaging for uncertain cases
Needle aspiration	Pus aspirated from peritonsillar space	Both diagnostic AND therapeutic; aspirated pus sent for C/ST
CT neck with contrast	Ring-enhancing collection in peritonsillar space; may show extension to parapharyngeal/retropharyngeal space	Reserved for atypical presentations, suspected complications, or failed initial aspiration
Intraoral ultrasound	Hypoechoic/anechoic collection adjacent to tonsil	Increasingly used as point-of-care; helps differentiate abscess from peritonsillar cellulitis (which does not require drainage)

Investigation	Key Findings	Interpretation
Throat swab for C. diphtheriae culture	Grows on tellurite agar (grey-black colonies) or Löffler's medium	Must specifically request on the lab form; routine throat culture will not detect it
Elek test	Tests for toxin production by the isolate	Not all C. diphtheriae produce toxin; only toxigenic strains cause systemic disease
ECG	ST-T wave changes, heart block, arrhythmias	Evidence of myocarditis from diphtheria toxin

Investigation	Key Findings
Pharyngeal swab for N. gonorrhoeae NAAT	Standard culture may miss pharyngeal gonococcal infection; NAAT is more sensitive
Syphilis serology (VDRL/RPR, TPHA/FTA-Abs)	Secondary syphilis with mucous patches
HIV Ag/Ab combo (4th gen)	Acute retroviral syndrome — pharyngitis + rash + lymphadenopathy; also check HIV RNA viral load if acute seroconversion suspected (Ag/Ab may still be negative in window period)

When evaluating for PSGN or ARF following pharyngitis:

Investigation	Expected Findings	Why
ASLO titre	Raised	Confirms recent streptococcal infection; may be negative in some strains ^[17]^[18]
Throat swab	Only positive in ~25% by the time complications appear ^[13]	GAS may already be cleared by the immune system
Total haemolytic complement activity and C3	Reduced in PSGN ^[17]	Immune complex-mediated complement consumption
Urinalysis	Haematuria (RBC casts = glomerular origin), proteinuria, sterile pyuria	Nephritic sediment in PSGN
RFT (Cr, urea)	Variable ↓GFR	Documents degree of renal impairment

Persistently Low C3

Persistently low C3 for > 8 weeks raises the possibility of lupus nephritis or membranoproliferative glomerulonephritis (complement-mediated MPGN) ^[17]. In PSGN, complement normalises within 6–8 weeks. If it doesn't, reconsider the diagnosis.

Investigation	Purpose
Flexible nasolaryngoscopy (FNL)	Visualise nasopharynx, oropharynx, hypopharynx, larynx; essential for any persistent/unilateral sore throat
Biopsy (incisional or punch)	Histological diagnosis of SCC, lymphoma, or other malignancy
CT/MRI neck	Staging, assess depth of invasion, lymph node involvement
EBV serology / plasma EBV DNA	NPC is strongly EBV-associated; plasma EBV DNA used for screening and monitoring in endemic populations (HK)
PET-CT	Staging for lymphoma or advanced SCC
FNA / excisional biopsy of cervical LN	If malignant adenopathy suspected; FNAC provides cytological information only; excisional biopsy needed for lymphoma architecture ^[6]

Clinical Scenario	First-Line Investigation	Backup / Second-Line	Key Pitfall
Acute pharyngitis, Centor ≥ 2	RADT	Throat culture if RADT negative (especially children)	Positive RADT in a carrier ≠ GAS pharyngitis
Suspected EBV (IM)	CBC + differential, Monospot	EBV-specific serology, LFTs	Monospot may be negative in first week and in children < 4
Suspected peritonsillar abscess	Clinical diagnosis	Needle aspiration (Dx + Tx), CT neck if uncertain	Peritonsillar cellulitis vs abscess — US or aspiration to differentiate
Persistent sore throat > 3 weeks	Flexible nasolaryngoscopy	CT/MRI neck, biopsy, EBV DNA	Must exclude NPC, oropharyngeal SCC, lymphoma
Post-streptococcal complications	ASLO, complement (C3), urinalysis, RFT	Throat swab (low yield), streptozyme test	ASLO may be negative; persistently low C3 > 8 weeks → think lupus/MPGN
Suspected diphtheria	Throat swab for C. diphtheriae on tellurite/Löffler media	Elek test for toxin, ECG	Must specifically request diphtheria culture — not detected on routine culture
Suspected STI pharyngitis	Pharyngeal NAAT for gonorrhoea, syphilis serology, HIV Ag/Ab	HIV RNA viral load if window period suspected	Gonococcal pharyngitis often asymptomatic — always ask about sexual history

Physical examination findings to systematically look for when evaluating pharyngitis ^[16]:

Scarlatiniform rash (sandpaper texture, Pastia lines, circumoral pallor)
Enlarged + erythematous + exudative tonsils
Inflamed uvula
Palatal petechiae
Tender cervical lymphadenopathy

These findings, while suggestive of GAS, are not diagnostic on their own — they inform the Centor score and guide the decision to test.

Additional examination points:

Symmetry of tonsils: Unilateral enlargement → think quinsy or malignancy
Uvula position: Deviation → peritonsillar abscess
Trismus: Inability to fully open mouth → deep space infection
Splenomegaly: Palpate for EBV/IM
Skin: Rash pattern helps narrow aetiology (scarlatiniform → GAS; maculopapular after amoxicillin → EBV; palms/soles → syphilis; "slapped cheek" → parvovirus)
Oral mucosa: Vesicles (HSV vs. herpangina — anterior vs. posterior distribution), Koplik spots (measles), thrush (candida/immunodeficiency)

It is equally important to know when not to test:

Children < 3 years: GAS pharyngitis is uncommon in this age group; ARF is exceedingly rare. Testing leads to detection of the carrier state and unnecessary antibiotics.
Obvious viral syndrome: Cough, rhinorrhoea, conjunctivitis, hoarseness, oral ulcers → viral; testing adds no value.
Post-treatment "test of cure": Generally NOT recommended after completing antibiotics, because positive results often represent the carrier state rather than treatment failure (exception: recurrent symptomatic episodes or history of ARF).
Asymptomatic contacts: Routine screening of household contacts is not recommended unless in a high-risk setting (e.g., known ARF in the community).

High Yield Summary — Diagnosis of Pharyngitis and Tonsillitis

Centor criteria (CENT): Cough absent, Exudate, Node (anterior cervical), Temperature → guides who to test, not who to treat.
Modified Centor (McIsaac): Add +1 if age < 15, subtract 1 if age > 44.
Score 0–1: No testing, no antibiotics. Score 2–3: Test (RADT ± culture). Score 4–5: Test-and-treat or empirical antibiotics.
RADT: Specificity ≥ 95% (positive result is reliable); sensitivity 70–90% (negative result needs backup culture in children).
Throat culture: Gold standard, sensitivity 90–95%, but takes up to 3 days.
10–25% of population carry GAS asymptomatically — positive test + pharyngitis does not always mean GAS pharyngitis.
Empiric treatment NOT recommended — clinical symptoms alone achieve only ~50% accuracy.
ASLO / anti-DNase B: Not useful acutely (takes > 2 weeks to rise); used retrospectively for ARF/PSGN.
Persistently low C3 > 8 weeks after suspected PSGN → think lupus nephritis or MPGN.
Red flags requiring urgent workup: stridor/drooling (epiglottitis), trismus/uvula deviation (quinsy), unilateral mass/persistent > 3 weeks (malignancy), agranulocytosis.
Swab technique: Both tonsils and posterior pharynx; avoid tongue, buccal mucosa, hard palate.

Active Recall - Diagnosis and Investigations for Pharyngitis and Tonsillitis

References

^[1] Senior notes: Ryan Ho Respiratory, p.51 (Section 3.1.1.2 Bacterial Pharyngitis — Centor criteria, diagnostic testing) ^[2] Senior notes: Adrian Lui Pediatrics Notes, p.157 (Centor criteria, RADT, throat culture, carrier state, empiric treatment caveat) ^[5] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf, p.43 (Peritonsillar abscess / Quinsy) ^[6] Senior notes: Ryan Ho Fundamentals, p.395 (Lymphadenopathy approach — FNAC vs excisional biopsy) ^[8] Lecture slides: GC 021. Upper respiratory tract infections.pdf, p.25 (Sore throat — viral > 90%, emergency/serious/pitfalls, exudates viral or bacterial) ^[12] Senior notes: Block A - Generalised Lymphadenopathy, p.2–3 (DDx of atypical lymphocytosis, ALL mimicking atypical lymphocytes) ^[13] Senior notes: Ryan Ho Urogenital, p.66 (PSGN — streptozyme test, throat swab only 25% positive) ^[16] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.130 (Diagnostic criteria for GAS pharyngitis, swab technique, physical examination) ^[17] Senior notes: Block A - Glomerular and Tubulo-interstitial Diseases and AKI, p.19 (PSGN investigations — C3, ASLO, persistently low C3) ^[18] Senior notes: Ryan Ho Fundamentals, p.360; Ryan Ho Urogenital, p.63 (Nephritic syndrome workup — ASLO, complement, throat swab)

Management of Pharyngitis and Tonsillitis

Management of pharyngitis/tonsillitis is guided by three overarching principles:

Most cases are viral and self-limiting → supportive care only; antibiotics are harmful (adverse effects, resistance, cost).
Confirmed GAS pharyngitis is the primary indication for antibiotics → to prevent acute rheumatic fever (ARF), reduce symptoms, and limit transmission.
Complications (suppurative and non-suppurative) require specific management → peritonsillar abscess needs drainage; airway compromise needs emergency airway management; recurrent tonsillitis may need tonsillectomy.

Regardless of aetiology, every patient with pharyngitis/tonsillitis benefits from:

Measure	Rationale	Details
Analgesics / antipyretics	Pharyngeal inflammation → pain via prostaglandin-mediated sensitisation of nociceptors; fever from hypothalamic PGE2	Paracetamol (1g QDS adults, 15mg/kg/dose QDS children) or ibuprofen (400mg TDS adults) — both reduce pain and fever; ibuprofen has additional anti-inflammatory action
Adequate oral hydration	Fever → insensible fluid loss; odynophagia → reduced oral intake → dehydration risk (especially children)	Encourage small frequent sips; cool/cold fluids may soothe; IV fluids if unable to swallow
Rest	Cytokine-driven sickness behaviour; rest supports immune function	Advise time off school/work for 1–2 days; return when afebrile
Topical sore-throat remedies	Local anaesthetic effect on pharyngeal mucosa	Benzydamine spray/gargle (anti-inflammatory + local anaesthetic); warm salt-water gargles; lozenges with lignocaine
Avoid irritants	Mucosal drying and irritation exacerbate symptoms	No smoking; avoid dry air; humidified air may help

Aspirin Warning in Children

Never give aspirin to children or adolescents < 16 years with viral illness due to the risk of Reye syndrome (acute hepatic encephalopathy). Use paracetamol or ibuprofen instead.

11.4 Antibiotic Treatment of GAS Pharyngitis

Even without treatment, GAS pharyngitis is self-limiting by itself, but treatment can help ^[1]:

↓ Symptoms + hasten recovery: symptoms generally improve within 48–72h with appropriate antibiotics ^[1]
Prevent complications: ARF prophylaxis generally useful within ≤ 9 days of onset (but less clear for other complications) ^[1]
↓ Transmission: Patients are considered non-contagious after 24 hours of effective antibiotic therapy (important for school/work return)
↓ Suppurative complications: Peritonsillar abscess, retropharyngeal abscess, cervical lymphadenitis, otitis media, sinusitis

The 9-Day Window

Antibiotics prevent ARF if started within 9 days of symptom onset. This means there is no need to rush treatment before test results return — you have time to confirm the diagnosis with RADT/culture (which takes hours to 2–3 days) and still be within the prevention window. This is the key rationale for the "test-and-treat" approach.

Drug	Regimen	Why This Drug
Penicillin V (phenoxymethylpenicillin)	500mg BD (adults) or 250mg BD–TDS (children) × 10 days	GAS has never developed resistance to penicillin — a remarkable and unique property; narrow spectrum → minimal disruption to normal flora; cheap; safe; well-established efficacy for ARF prevention
Amoxicillin	500mg BD (adults) or 50mg/kg/day divided BD (children) × 10 days	If patient cannot swallow pills → better palatability ^[1] (amoxicillin suspension tastes better than penicillin V suspension); broader spectrum than penicillin V but equally effective against GAS
IM Benzathine penicillin G	Single dose: 1.2 million units IM (adults); 600,000 units IM (children < 27kg)	If patient unlikely to adhere to 10-day regimen ^[19]; single-dose ensures complete treatment; painful injection is the main disadvantage

Why 10 days? Shorter courses (e.g., 5 days) have been studied but do not reliably eradicate GAS from the pharynx and may not prevent ARF. The 10-day course is the established standard based on the landmark ARF prevention trials. Think of it this way: GAS can hide within tonsillar crypt biofilms, and it takes a full 10 days of sustained bactericidal antibiotic levels to fully eradicate it.

Primary prevention of recurrent rheumatic fever (in GAS pharyngitis phase): 10-day oral penicillin (or cephalosporin) ^[19]

The approach depends on the type of allergy:

Allergy Type	Drug Choice	Rationale
Non-anaphylactic penicillin allergy (e.g., rash only)	1st-generation cephalosporin, e.g., cefalexin 500mg BD × 10 days	Cross-reactivity between penicillins and 1st-gen cephalosporins is very low (< 2%); cephalosporins are safe in patients with non-severe penicillin allergy
Anaphylactic penicillin allergy (urticaria, angioedema, anaphylaxis)	Azithromycin 500mg Day 1, then 250mg Days 2–5 (total 5 days) OR Clindamycin 300mg TDS × 10 days	Avoid ALL beta-lactams; azithromycin is convenient (short course, OD dosing); clindamycin has excellent GAS activity
Erythromycin	Oral erythromycin 10 days	If penicillin allergy — but problematic in HK since macrolide resistance is 40–50% ^[19]

Macrolide Resistance in Hong Kong

Erythromycin resistance in GAS is 40–50% in Hong Kong ^[19]. This is a critical local consideration — erythromycin should NOT be the default alternative in HK. Prefer cefalexin (if non-anaphylactic allergy) or clindamycin (if anaphylactic allergy) over erythromycin/azithromycin in this locality unless susceptibility is confirmed.

If symptoms persist or recur after completing a full course:

Reassess diagnosis: Was it truly GAS? (Consider EBV, carrier state with viral pharyngitis, other causes)
Assess adherence: Did the patient complete 10 full days?
Second-line options: Amoxicillin-clavulanate (covers beta-lactamase-producing oral co-pathogens that may "shield" GAS), clindamycin, or IM benzathine penicillin

11.5 Management of Specific Conditions

Aspect	Management	Why
Supportive care	Paracetamol/ibuprofen, fluids, rest	Self-limiting viral illness; no antiviral is effective
AVOID amoxicillin/ampicillin	Do NOT prescribe aminopenicillins	~90% develop widespread maculopapular rash (immune-mediated, not true allergy) — can be distressing and misinterpreted as penicillin allergy
Avoid contact sports	For at least 3–4 weeks (some guidelines say until splenomegaly resolves)	Risk of splenic rupture (spleen is enlarged and fragile from lymphoid hyperplasia)
Corticosteroids	Only if severe complications: airway compromise from tonsillar enlargement, haemolytic anaemia, thrombocytopenia, hepatitis	Routine use NOT recommended; steroids suppress immune response and may prolong viral shedding
Monitoring	LFTs, CBC; watch for complications (splenic rupture, airway obstruction, haemolytic anaemia, Guillain-Barré)	Most resolve in 2–4 weeks; fatigue may persist for months

Peritonsillar abscess: collection of pus between tonsillar capsule and superior constrictor ^[5].

Treatment Step	Details	Rationale
IV antibiotics	Amoxicillin-clavulanate (or clindamycin if penicillin-allergic); add metronidazole if anaerobic coverage needed	Polymicrobial infection (GAS + oral anaerobes); antibiotics alone are insufficient for established abscess
Drainage	Needle aspiration (first-line, can be done bedside under local anaesthesia) or incision and drainage (I+D)	Abscess = walled-off pus → antibiotics alone cannot penetrate; must drain the collection
ENT referral	Urgent if airway concern; elective for interval tonsillectomy consideration	Risk of airway obstruction; recurrence rate ~10–15%
Interval tonsillectomy	Consider if recurrent quinsy or recurrent tonsillitis	Removes the nidus of infection
Emergency	If airway obstruction ^[5] → secure airway first (see below)	Tonsillar swelling can compromise the oropharyngeal airway

Mural causes of upper airway obstruction include infections: tonsillitis, peritonsillar/retropharyngeal abscess, epiglottitis, croup ^[20].

Management follows the critical care airway algorithm ^[20]^[21]:

Visual inspection of airway + suction of debris ^[21]
Airway manoeuvres: head tilt-chin lift or jaw thrust ^[21]
Ventilation: BVM with reservoir + 15L/min high-flow O2 ± airway adjuncts ^[21]
ETT intubation with rapid-sequence induction (RSI) if above measures fail ^[21]
If failed intubation → needle cricothyrotomy as last resort ^[21]
Specific treatment for inflammatory swelling: nebulised adrenaline in O2 (5mL 1:1000), IV dexamethasone 8mg ^[21]

Treatment	Details
Diphtheria antitoxin (DAT)	Must be given IMMEDIATELY on clinical suspicion — do not wait for culture confirmation; neutralises circulating toxin (does not reverse toxin already bound to tissue)
Antibiotics	Penicillin G or erythromycin × 14 days — eradicates the organism and reduces toxin production
Supportive care	Cardiac monitoring (for myocarditis), airway management
Isolation + notification	Diphtheria is a notifiable disease; contacts require prophylactic antibiotics and booster vaccination

11.6 Prevention of Rheumatic Fever — Primary and Secondary

This is one of 3 conditions to know how to prevent ^[19] and is extremely high yield:

The goal is to eradicate GAS from the pharynx before the immune system mounts the cross-reactive response that causes ARF.

Primary prevention (in GAS pharyngitis phase): 10-day oral penicillin (or cephalosporin) ^[19]

Alternatives: Oral erythromycin 10 days → if penicillin allergy (but problematic in HK, since resistance is 40–50%) ^[19]

Intramuscular benzathine penicillin 1 dose → if patient unlikely to adhere to 10-day regimen ^[19]

Once a patient has had ARF, they are at much higher risk of recurrent ARF with each subsequent GAS infection. Continuous antibiotic prophylaxis is essential:

Secondary prevention (known rheumatic fever, prevent recurrent GAS infections): ^[19]

10-day oral penicillin to eradicate carriage, followed by monthly IM benzathine penicillin thereafter ^[19]

Regimen	Details
Monthly IM benzathine penicillin	1.2 MU every 3–4 weeks; most reliable method (ensures compliance)
Oral penicillin V	Twice daily → for those who don't want injections, but obviously compliance is an issue ^[19]
Oral erythromycin	Twice daily; for penicillin-allergic patients (but macrolide resistance is a concern in HK)

Duration of secondary prophylaxis (per AHA/WHO guidelines):

Scenario	Duration
ARF without carditis	Minimum 5 years or until age 21 (whichever is longer)
ARF with carditis but no residual valve disease	Minimum 10 years or until age 21 (whichever is longer)
ARF with carditis and residual valve disease	Minimum 10 years or until age 40 (whichever is longer); some guidelines recommend lifelong

11.7 Tonsillectomy — Surgical Management

Indication	Criteria / Details
Recurrent tonsillitis	Paradise criteria: ≥ 7 episodes in 1 year, ≥ 5 episodes/year for 2 consecutive years, or ≥ 3 episodes/year for 3 consecutive years; each episode must be documented with fever > 38.3°C, tonsillar exudate, positive GAS culture, or cervical adenopathy
Recurrent acute pharyngitis	Severe episodes that significantly impair quality of life / school attendance / work productivity despite adequate medical therapy
Chronic tonsillitis	Persistent sore throat, halitosis, tonsilloliths (calcified debris in crypts) not responding to medical management
Obstructive sleep apnoea (OSA)	Enlarged tonsils causing upper airway obstruction, sleeping disorder and cardiopulmonary complication ^[22] — this is the most common indication in children
Peritonsillar abscess unresponsive to medical treatment and drainage	Absolute indication ^[22]; also consider interval tonsillectomy after successful drainage to prevent recurrence
Biopsy required to define tissue pathology	Absolute indication ^[22]; suspected malignancy (lymphoma, SCC) with unilateral tonsillar enlargement

Contraindication	Reason
Bleeding disorder	Risk of uncontrolled haemorrhage (tonsil bed is highly vascular — tonsillar branch of facial artery)
Anaesthetic risk	Risk of GA due to respiratory, cardiac or neurological problems ^[22]
Atlantoaxial instability	Risk of injury from head extension during surgery, especially in patients with rheumatoid arthritis (RA) and Down's syndrome ^[22] — the neck must be extended during intubation and surgery, which can cause spinal cord compression if the C1-C2 joint is unstable
Active acute infection	Relative contraindication; increased bleeding and oedema; postpone until acute episode resolves (usually wait 4–6 weeks)
Cleft palate (unrepaired)	Tonsillectomy may worsen velopharyngeal insufficiency → nasal regurgitation and hypernasal speech

Timing	Complication	Details
Intraoperative	Haemorrhage	Injury to tonsillar branch of facial artery or paratonsillar venous plexus
Early (0–24h)	Primary haemorrhage	Occurs in ~2%; requires return to theatre for haemostasis
Delayed (5–10 days)	Secondary (reactionary) haemorrhage	Occurs when the eschar (scab) over the tonsillar fossa sloughs off; can be life-threatening; ~3% incidence
Early	Pain / odynophagia	Expected; treat with regular paracetamol ± ibuprofen; adequate oral intake is important to prevent dehydration
Early	Referred otalgia	Via CN IX; expected and self-limiting
Rare	Velopharyngeal insufficiency	Hypernasal speech, nasal regurgitation; more common if pre-existing palatal abnormality
Rare	Atlantoaxial subluxation (Grisel syndrome)	Post-inflammatory ligamentous laxity → C1-C2 instability; presents with torticollis post-tonsillectomy

Scenario	First-Line	Alternative	Duration	Key Notes
GAS pharyngitis	Penicillin V 500mg BD	Amoxicillin 500mg BD (palatability)	10 days	GAS has NEVER developed penicillin resistance
GAS, non-anaphylactic PCN allergy	Cefalexin 500mg BD	—	10 days	Cross-reactivity < 2%
GAS, anaphylactic PCN allergy	Azithromycin 500mg D1, 250mg D2-5	Clindamycin 300mg TDS × 10d	5 days (azithro) / 10 days (clinda)	Erythromycin resistance 40–50% in HK ^[19]
GAS, poor compliance	IM benzathine penicillin G 1.2MU single dose	—	Single dose	Painful but guarantees compliance
Peritonsillar abscess	IV amoxicillin-clavulanate ± metronidazole	IV clindamycin	Until drainage + clinical improvement, then step down to PO	MUST also drain the abscess
ARF secondary prophylaxis	IM benzathine penicillin G monthly	Oral penicillin V BD / oral erythromycin BD	Years to lifelong (see duration table above)	Most important long-term management

Scenario	Why No Antibiotics
Viral pharyngitis	Self-limiting; antibiotics have no benefit; increase resistance, cost, and adverse effects
Centor score 0–1	Risk of GAS < 10%; probability too low to justify antibiotics or testing
Negative RADT + negative culture	GAS excluded; treat symptomatically
EBV / infectious mononucleosis	Viral; antibiotics have no benefit; amoxicillin causes rash and may be misdiagnosed as drug allergy
Asymptomatic GAS carrier	10–25% of population carry GAS ^[2]; carriage does not cause ARF and does not require treatment (exception: close contact of someone with ARF)
"Test of cure" positive	Positive RADT/culture after completing treatment usually represents the carrier state, not treatment failure, unless patient is again symptomatic

Point	What to Tell the Patient
Expected course	Viral: 5–7 days to resolve. GAS on antibiotics: improvement within 48–72 hours
When to return	If symptoms worsen, difficulty breathing/swallowing, drooling, unable to open mouth (trismus), persistent fever > 48–72h on antibiotics, rash
Antibiotics	Must complete full 10-day course even if feeling better (to eradicate GAS and prevent ARF)
Contagion	Non-contagious after 24 hours of effective antibiotics; remain home until then
EBV	Avoid contact sports for 3–4 weeks; no sharing of drinks; report any sudden abdominal pain (splenic rupture)

High Yield Summary — Management of Pharyngitis and Tonsillitis

Most pharyngitis is viral → supportive care only (analgesia, hydration, rest). NO antibiotics.
Confirmed GAS → penicillin V or amoxicillin × 10 days — GAS has never developed penicillin resistance.
IM benzathine penicillin G single dose if compliance is uncertain ^[19].
Penicillin allergy → 1st-gen cephalosporin (non-anaphylactic) or azithromycin/clindamycin (anaphylactic) — avoid erythromycin in HK (40–50% resistance).
Antibiotic goals: ↓ symptoms, prevent ARF (within 9-day window), ↓ transmission, prevent suppurative complications ^[1].
EBV/IM → supportive care, AVOID amoxicillin, avoid contact sports (splenic rupture risk).
Peritonsillar abscess → IV antibiotics + drainage (needle aspiration or I+D) ± interval tonsillectomy.
Airway compromise → emergency airway management (head tilt-chin lift, BVM, nebulised adrenaline, IV dexamethasone, intubation, needle cricothyrotomy).
Tonsillectomy indications: recurrent tonsillitis (Paradise criteria), OSA, quinsy unresponsive to drainage, biopsy for suspected malignancy ^[22].
Tonsillectomy contraindications: bleeding disorder, anaesthetic risk, atlantoaxial instability (RA, Down's syndrome) ^[22].
ARF secondary prophylaxis: monthly IM benzathine penicillin for years to lifelong ^[19].
Safety netting: Return if trismus, drooling, worsening dysphagia, persistent fever on antibiotics, or sudden abdominal pain (EBV → splenic rupture).

Active Recall - Management of Pharyngitis and Tonsillitis

References

^[1] Senior notes: Ryan Ho Respiratory, p.51–52 (Section 3.1.1.2 Bacterial Pharyngitis — Abx treatment, goals, complications) ^[2] Senior notes: Adrian Lui Pediatrics Notes, p.157 (Centor criteria, RADT, carrier state) ^[5] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf, p.43 (Peritonsillar abscess / Quinsy) ^[19] Senior notes: Gen Clerk Anaes + Microbiology Summary, p.13–14 (Primary and secondary prevention of rheumatic fever; penicillin prophylaxis; erythromycin resistance in HK) ^[20] Senior notes: Ryan Ho Critical Care, p.6 (Upper airway obstruction causes — tonsillitis, peritonsillar/retropharyngeal abscess, epiglottitis, croup) ^[21] Senior notes: Ryan Ho Critical Care, p.7 and p.13 (Airway management algorithm; emergency Mx of upper airway obstruction; nebulised adrenaline and IV dexamethasone) ^[22] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.133 (Tonsillectomy — indications, absolute indications, contraindications)

Complications of Pharyngitis and Tonsillitis

The complications of pharyngitis/tonsillitis divide cleanly into two categories based on mechanism — suppurative (direct spread of infection with pus formation) and non-suppurative (immune-mediated damage occurring days to weeks after the infection). This classification is critical because it determines the timeline, the target organ, and the management approach.

Suppurative complications include sinusitis, otitis media and peritonsillar abscess ^[23]^[24].

Non-suppurative complications include acute rheumatic fever, scarlet fever and glomerulonephritis ^[23]^[24].

Category	Mechanism	Timeline	Prevention
Suppurative	Direct extension / haematogenous spread of organisms	During or immediately after the acute infection	Antibiotics reduce risk but do not eliminate it
Non-suppurative	Immune-mediated (molecular mimicry, immune complex deposition, superantigen)	Days to weeks after the infection	Antibiotics prevent ARF (within 9 days); unclear for others

12.2 Suppurative Complications

Suppurative complications result from direct spread of bacteria (predominantly GAS and oral anaerobes) from the pharynx/tonsils into adjacent anatomical spaces or via the Eustachian tube/ostiomeatal complex.

Collection of pus between tonsillar capsule and superior constrictor ^[5].

Feature	Detail	Pathophysiological Basis
Mechanism	Infection penetrates the tonsillar capsule → pus accumulates in the potential space between the capsule and the superior constrictor muscle	The tonsillar capsule is a thin fascia; infection of the Weber glands (mucous glands in the superior tonsillar pole) is thought to be the initial event
Symptoms	Similar to tonsillitis but usually more severe; muffled voice; airway obstruction ^[5]	"Hot potato" voice is due to oedema of the soft palate and limited palatal movement; airway obstruction from mass effect displacing the tonsil medially
Signs	Unilateral peritonsillar swelling; deviation of uvula; trismus ^[5]	Uvula deviates to the contralateral side due to mass effect; trismus occurs because the inflammatory process involves the medial pterygoid muscle, which lies lateral to the superior constrictor
Microbiology	Polymicrobial: GAS + oral anaerobes (Fusobacterium, Prevotella, Peptostreptococcus)	Tonsillar crypts harbour a mixed flora; the anaerobic environment within an abscess cavity favours anaerobe growth
Management	IV antibiotics (amoxicillin-clavulanate ± metronidazole) + drainage (needle aspiration or I+D)	Antibiotics alone cannot penetrate a walled-off abscess; must drain to cure
Complications of quinsy	Parapharyngeal abscess → retropharyngeal abscess → mediastinitis (via danger space); airway compromise; Lemierre syndrome; carotid artery erosion (extremely rare)	Infection tracks through fascial planes; the danger space communicates directly with the posterior mediastinum

Peritonsillar abscess is listed as a "serious" cause of sore throat ^[8] and appears in the CFB ENT lecture ^[5] as a core topic.

Feature	Parapharyngeal Abscess	Retropharyngeal Abscess
Location	Lateral to superior constrictor, between it and the medial pterygoid	Between posterior pharyngeal wall (buccopharyngeal fascia) and prevertebral fascia
Spread from	Peritonsillar abscess, dental infection, parotitis	Suppurative retropharyngeal lymph nodes (mainly children < 4 years — these nodes atrophy later); extension from parapharyngeal space
Clinical features	High fever, neck swelling, torticollis, medial displacement of tonsil/pharyngeal wall, trismus	High fever, neck stiffness/extension, dysphagia, drooling, stridor, "hot potato" voice; risk of airway obstruction ^[1]
Key danger	Proximity to carotid sheath → carotid artery erosion, IJV thrombophlebitis (Lemierre syndrome)	Extension into danger space → mediastinitis (mortality 40–50% even with treatment)
Diagnosis	CT neck with contrast (ring-enhancing collection)	CT neck with contrast; lateral neck X-ray may show prevertebral soft tissue widening
Management	IV antibiotics + surgical drainage (often external approach)	IV antibiotics + surgical drainage (transoral or external) + airway management

Otitis media due to extension of organisms via Eustachian tube into middle ear (especially in children) ^[1]^[2]^[23].

Why children? The paediatric Eustachian tube is shorter, more horizontal, and more compliant → organisms from the nasopharynx/pharynx travel more easily into the middle ear. Infection also causes mucosal oedema that obstructs the tube, trapping fluid and bacteria.
Pathogens: GAS, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis (secondary bacterial infection following viral URTI is very common).
Clinical features: Ear pain (otalgia), fever, irritability (young children), otorrhoea (if TM perforates), bulging erythematous tympanic membrane.

Sinusitis due to extension up ostiomeatal complex ^[1]^[2]^[23].

Mechanism: Viral pharyngitis causes oedema of the nasal mucosa → obstruction of the ostiomeatal complex (the narrow drainage pathway of the maxillary, anterior ethmoid, and frontal sinuses) → mucus stasis → secondary bacterial superinfection.
Distinguishing from viral URTI: Symptoms that persist > 10 days, or worsen after initial improvement ("double sickening"), or are severely disproportionate (high fever > 39°C + purulent discharge for ≥ 3 consecutive days).

Complication	Pathophysiology	Notes
Tonsillopharyngeal cellulitis/abscess	Direct spread of infection within pharyngeal tissues without walling off (cellulitis) or with abscess formation	Precursor to peritonsillar abscess
Skin and soft tissue infections (impetigo, erysipelas, cellulitis, necrotising fasciitis, pyomyositis) ^[1]^[2]	Haematogenous spread or autoinoculation of GAS from pharynx to skin	Necrotising fasciitis occurs following a breach in the skin and also in association with transmission of GAS from an individual with acute pharyngitis ^[23]; rapidly progressive, limb/life-threatening
Septicaemia	Streptococcal bacteraemia is a rare suppurative complication of streptococcal tonsillopharyngitis ^[23]	Can lead to metastatic infection (septic arthritis, osteomyelitis, meningitis)
Lemierre syndrome	Fusobacterium necrophorum pharyngitis → septic thrombophlebitis of IJV → septic emboli to lungs ± other organs	Rare but devastating; suspect in adolescent/young adult with pharyngitis → lateral neck tenderness → respiratory symptoms
Mastoiditis	Extension from middle ear (AOM → acute mastoiditis) via direct extension through the aditus ad antrum	Post-auricular swelling, tenderness, protruding ear; can lead to intracranial complications (epidural/brain abscess, lateral sinus thrombosis)

12.3 Non-Suppurative Complications

These are immune-mediated sequelae and are the main reason we treat GAS pharyngitis with antibiotics. They do not occur from direct bacterial invasion of the target organ.

12.3.1 Acute Rheumatic Fever (ARF)

Acute rheumatic fever is a non-suppurative sequela that occurs 2–4 weeks following Group A Streptococcus (GAS) pharyngitis ^[23]^[24].

Streptococcal pharyngitis is the ONLY streptococcal infection that is clearly associated with ARF ^[23]^[24].

Streptococcal impetigo or pyoderma have NOT been proven to lead to ARF, but impetigo is associated with post-streptococcal glomerulonephritis (PSGN) ^[23]^[24].

Viral pharyngitis and pharyngitis caused by other bacteria do NOT result in ARF ^[24].

The mechanism ^[4]^[24]:

Activation of innate and adaptive immune system following GAS pharyngeal infection ^[24]
Activation of autoreactive B and T cells by GAS antigens ^[24]
Antibodies directed at GAS antigens (Streptococcal M protein) cross-react with host antigens ^[24] — specifically cardiac myosin, laminin, vimentin, and tropomyosin in the heart; N-acetyl-beta-D-glucosamine in cardiac valves; neuronal tissue (basal ganglia) for Sydenham's chorea
Result: inflammation in endocardium, myocardium and pericardium ^[4] — characteristically, rheumatic heart disease is the only disease that affects all three layers of the heart (pancarditis) ^[4]

Most commonly occurs age 5–15
ARF following untreated GAS pharyngitis = 3%
ARF following asymptomatic (subclinical) GAS pharyngitis = 33% — this means that a third of ARF cases occur after unrecognised pharyngitis, which is why secondary prophylaxis (not just primary prevention) is essential

Diagnosis requires: 2 Major criteria, OR 1 Major + 2 Minor criteria ^[23].

Evidence of a preceding GAS infection is helpful but not necessary to make the diagnosis of ARF ^[23].

Major Criteria (Mnemonic: JONES)	Details	Pathophysiology
J — Joints (Arthritis)	Earliest symptom; classically migratory polyarthritis affecting several joints in quick succession; knees, ankles, elbows and wrists most commonly affected ^[23]	Cross-reactive antibodies + T cells target joint synovium; characteristically migrates because each joint flare self-limits as immune complexes are cleared, then new joints become involved
O — O-shaped heart (Carditis/Valvulitis)	Pancarditis involving pericardium, epicardium ^[23]; mitral valve most commonly affected but can also affect tricuspid and aortic valve ^[23]; murmurs: transient MR/AR murmur, MDM at apex (Carey-Coombs murmur) ^[4]	Cross-reactive anti-M antibodies target cardiac myosin and valvular endocardium → valvulitis (MR > AR) + myocarditis + pericarditis
N — Nodules (subcutaneous)	Located over bony prominences or near tendons, usually symmetrical; elbows most commonly involved ^[23]	Granulomatous inflammation around collagen fibres; similar to Aschoff nodules in the heart
E — Erythema marginatum	Temporary red or pink non-pruritic rash involving trunk and limbs but NOT the face ^[23]; pink ring lesions ( < 5%) ^[4]	Immune complex deposition in dermal vessels
S — Sydenham's chorea	Hypotonia; involuntary brief random irregular movements of limbs; "milkmaid sign" (variable grip pressure); emotional lability with outbursts of inappropriate behaviours ^[23]	Cross-reactive antibodies target basal ganglia neurons (caudate and subthalamic nuclei); may appear months after pharyngitis (delayed onset)

Remark: Joint (arthritis or arthralgia) and cardiac (carditis or prolonged PR interval) can only be counted once as either a major OR minor criterion ^[23].

Minor Criteria	Details
Arthralgia	Joint pain without objective swelling (only if arthritis is not used as a major criterion)
Prolonged PR interval	First-degree AV block on ECG (only if carditis is not used as a major criterion)
Fever	Temperature ≥ 38.5°C
Elevated acute phase reactants	↑ESR and CRP ^[23]

Rheumatic heart disease is caused by inflammation and scarring of cardiac valves after one or more episodes of rheumatic fever resulting from an abnormal immune response to GAS infection ^[24].

Most common and severe sequelae of acute rheumatic fever ^[24]
Most common cause of acquired valvular disease (globally) ^[24]
Develops 10–20 years after the original illness ^[24]
Occurs in ≥ 1/2 of all ARF patients, but typically takes 10–30 years to become manifest ^[4]
Pathogenesis: repeated ARF attacks → progressive fibrosis → fusion/distortion of cusps ^[4]
Valve involvement: MV alone > AV+MV > AV alone > TV (rare) ^[4]
Pathology: MS > MR+MS > MR ^[4]
Course: asymptomatic at early stages, may only be detected through auscultation of murmur or by echocardiography; symptomatic at late stages when significant VHD develops → heart failure, arrhythmia ^[24]
The mitral stenosis of RHD is the only native valvular disease that requires warfarin (cannot use NOAC/DOAC) ^[25] — because the thrombus forms in the dilated left atrial appendage under low-flow conditions, and NOACs have not been proven effective in this setting

Post-streptococcal glomerulonephritis: ranges from asymptomatic haematuria to nephritic syndrome; generally self-limiting; occurs 2 weeks after initial pharyngitis ^[1]^[2].

Post-streptococcal rheumatic fever = develops 2–4 weeks after GAS pharyngitis. Post-streptococcal glomerulonephritis = develops 1–3 weeks after GAS pharyngitis ^[24].

Feature	Detail	Pathophysiology
Mechanism	Immune complex deposition in glomeruli + complement activation → glomerular inflammation	GAS antigens → antibody production → circulating immune complexes deposit in subepithelial glomerular basement membrane → complement fixation (↓C3) → neutrophil recruitment → glomerular injury
Timeline	1–3 weeks after pharyngitis; 3–6 weeks after skin infection ^[13]	Time needed for immune complex formation
Clinical features	Haematuria (30–50% gross, smoky/tea/cola-coloured), generalised oedema (2/3), hypertension (50–90%) ^[13]	Haematuria = glomerular barrier disruption; oedema + HTN = salt and fluid retention from ↓GFR
Investigations	↓C3 (normalises within 6–8 weeks), ↑ASLO, haematuria + proteinuria on urinalysis	↓C3 confirms immune complex-mediated complement consumption
Prognosis	Majority have excellent outcome especially children; diuresis in 1–2 weeks, RFT normalise in 4 weeks ^[13]	Self-limiting because the immune complex deposition is a one-off event (unlike lupus nephritis, which is ongoing)
Key caveat	Persistently low C3 > 8 weeks → suspect lupus nephritis or MPGN ^[17]	PSGN complement normalises; if it doesn't, the diagnosis is wrong
Prevention	Unlike ARF, antibiotic treatment of GAS pharyngitis has NOT been conclusively shown to prevent PSGN	The immune complex deposition may already be initiated by the time of diagnosis; molecular mimicry in ARF is a different mechanism that requires ongoing antigen exposure

ARF vs PSGN — Key Exam Distinctions

Feature	ARF	PSGN
Latency after pharyngitis	2–4 weeks	1–3 weeks
Infection type	Only pharyngitis	Pharyngitis OR skin infection
Mechanism	Molecular mimicry (cross-reactive Ab)	Immune complex deposition
Complement	Normal	↓C3
Prevention by antibiotics	YES (within 9 days)	NOT proven
Prognosis	Can cause permanent valve damage (RHD)	Usually self-limiting
Recurrence prevention	Secondary prophylaxis essential	Not applicable

Scarlet fever (scarlatina): diffuse erythematous eruption with numerous small papular elevations, beginning in groin and armpits; most marked in skin folds and pressure points; linear petechial character at antecubital fossa and axillary folds (Pastia's lines); associated with circumoral pallor and strawberry tongue ^[1]^[2].

Feature	Detail	Pathophysiology
Mechanism	GAS strains producing pyrogenic exotoxins (SpeA, SpeB, SpeC) — these are superantigens that activate massive numbers of T cells non-specifically	Superantigen binds outside the antigen-binding groove of MHC class II → crosslinks with T-cell receptor → polyclonal T-cell activation → massive cytokine release → vasodilation, capillary leak → rash
Rash	Sandpaper-textured erythematous papules; blanching; starts in groin/axillae → generalises within 24h; spares face (circumoral pallor)	Capillary dilatation + perivascular oedema in dermis
Pastia's lines	Linear petechiae in skin folds (antecubital fossa, axillary, inguinal)	Increased capillary fragility in areas of skin fold friction
Strawberry tongue	White coating + red papillae → desquamation → beefy red tongue with prominent papillae	Mucosal inflammation + exotoxin effect on lingual papillae
Desquamation	Fine flaking of skin 1–2 weeks after rash, starting on face, then trunk, then hands/feet (including fingertip peeling)	Accelerated epidermal turnover from inflammatory damage
Timeline	Occurs concurrently with pharyngitis (not delayed like ARF/PSGN)	Toxin-mediated, not immune-complex or molecular mimicry

Streptococcal toxic shock syndrome: hypotension with multi-organ failure (GAS antigen acts as superantigen) ^[1]^[2].

Mechanism: Same superantigen-mediated cytokine storm as scarlet fever, but far more severe → distributive shock, DIC, ARDS, renal failure, hepatic failure.
Mortality: 30–70% even with treatment.
Management: Aggressive fluid resuscitation, IV penicillin + clindamycin (clindamycin inhibits toxin synthesis by blocking ribosomal translation even in stationary-phase bacteria), IVIG (to neutralise circulating superantigens), ICU care.

Paediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcal Infection (PANDAS): symptoms of OCD or tics exacerbated by GAS infection ^[2].

Mechanism: Cross-reactive antibodies against basal ganglia neurons (similar mechanism to Sydenham's chorea but milder and without the frank choreiform movements).
Criteria: Pre-pubertal onset, neuropsychiatric symptoms (OCD, tics), temporal association with GAS infection, episodic course.
Management: Controversial; treat the underlying GAS infection; some advocate antibiotic prophylaxis; cognitive-behavioural therapy for OCD/tics.

Strep pharyngitis → guttate psoriasis, raindrop appearance ^[7].

Mechanism: Molecular mimicry between streptococcal M protein and keratinocyte keratins → T-cell–mediated attack on epidermis → Th1/Th17 cytokine release → keratinocyte hyperproliferation.
Timeline: 1–2 weeks after GAS pharyngitis.
Clinical: Widespread small (0.5–1.5cm) papules with silvery scale over trunk and limbs ("raindrop" pattern); often the first presentation of psoriasis in children/young adults.
Management: Treat the GAS infection; topical steroids, phototherapy; most cases resolve in weeks to months but ~30% progress to chronic plaque psoriasis.

Although not a complication of GAS pharyngitis per se, EBV-IM has its own important complication profile:

Complication	Mechanism	Clinical Significance
Splenic rupture	Splenomegaly from lymphoid hyperplasia → capsular thinning → rupture with minimal trauma	Most feared complication; reason to avoid contact sports for 3–4 weeks; presents with acute abdominal pain + haemodynamic instability
Airway obstruction	Massive tonsillar hypertrophy (bilateral "kissing tonsils") ± oedema	May require corticosteroids, nasopharyngeal airway, or rarely tonsillectomy
Autoimmune haemolytic anaemia	EBV-induced polyclonal B-cell activation → cold agglutinins (anti-i IgM) → complement-mediated RBC lysis	Usually mild and self-limiting; responds to corticosteroids if severe
Thrombocytopenia	Immune-mediated platelet destruction + splenic sequestration	Usually mild; rarely severe enough to cause bleeding
Hepatitis	Direct EBV infection of hepatocytes + immune-mediated damage	Subclinical LFT derangement in 80–90%; frank jaundice in < 5%
Neurological	Guillain-Barré syndrome, encephalitis, facial nerve palsy, aseptic meningitis	Rare but serious
EBV-associated malignancy (long-term)	EBV immortalises B cells → risk of Burkitt lymphoma (endemic type), Hodgkin lymphoma, NPC, post-transplant lymphoproliferative disorder (PTLD)	Long-term association, not an acute complication

Covered briefly in the management section, but worth reiterating here for completeness ^[22]^[26]:

Timing	Complication	Mechanism / Detail
Immediate post-operative	Nausea and vomiting	Result from general anaesthesia or post-operative medications such as narcotics or antibiotics ^[26]
	Primary haemorrhage ( < 24 hours)	Intraoperative or early post-operative bleeding from tonsillar vessels; requires re-exploration
	Surgical trauma: uvular oedema, tongue numbness, TMJ dislocation ^[26]	Presence of malocclusion or inability to close mouth (TMJ dislocation) ^[26]; tongue numbness from pressure on lingual nerve by tongue depressor
Early post-operative	Secondary haemorrhage ( > 24 hours, commonly 5th–14th day)	Time period when tonsillar bed eschar separates, exposing small vessels to local trauma ^[26]; the scab sloughs off → bleeding from the raw tonsillar bed
	Aspiration pneumonia	Aspiration of blood or secretions may cause post-operative pneumonia ^[26]
	Post-obstructive pulmonary oedema	Sudden relief of respiratory obstruction from enlarged tonsils results in loss of positive end-expiratory pressure (PEEP) → transudation of fluid into interstitial and alveolar spaces and respiratory compromise ^[26] — this is the same mechanism as negative-pressure pulmonary oedema
	Post-operative tonsillar bed infection	Can extend to paravertebral space → Grisel syndrome may occur as a result of extension of infection through tissue adjacent to the tonsillar region to the paravertebral space, causing atlantoaxial instability ^[26]
Late post-operative	Recurrence of tonsillitis, otitis media, change of voice	Eustachian tube dysfunction from oedema (otitis media) ^[26]; different resonance mechanisms (voice change) ^[26]; recurrence is rare if tonsils fully removed

Complication	Type	Timing After Pharyngitis	Mechanism	Key Clinical Feature
Peritonsillar abscess	Suppurative	During / immediately after	Direct spread through tonsillar capsule	Trismus, uvula deviation, muffled voice
Retropharyngeal abscess	Suppurative	During / immediately after	Extension via retropharyngeal LN or parapharyngeal space	Neck stiffness, stridor, drooling
AOM	Suppurative	During	Extension via Eustachian tube	Ear pain, bulging TM
Sinusitis	Suppurative	During	Extension via ostiomeatal complex	Facial pain, purulent discharge > 10d
Necrotising fasciitis	Suppurative	During	Haematogenous / autoinoculation	Rapidly progressive pain, erythema, necrosis
Lemierre syndrome	Suppurative	Days to weeks	F. necrophorum IJV thrombophlebitis	Neck swelling, septic pulmonary emboli
ARF	Non-suppurative	2–4 weeks	Molecular mimicry (anti-M Ab)	Migratory polyarthritis, pancarditis, chorea
RHD	Non-suppurative	10–20 years	Repeated ARF → valve fibrosis	Mitral stenosis, heart failure
PSGN	Non-suppurative	1–3 weeks	Immune complex deposition	Haematuria, oedema, HTN, ↓C3
Scarlet fever	Non-suppurative (toxin)	Concurrent	Pyrogenic exotoxin superantigen	Sandpaper rash, Pastia's lines, strawberry tongue
STSS	Non-suppurative (toxin)	Concurrent	Superantigen → cytokine storm	Hypotension, multi-organ failure
PANDAS	Non-suppurative	Days to weeks	Cross-reactive Ab vs basal ganglia	OCD, tics
Guttate psoriasis	Non-suppurative	1–2 weeks	Molecular mimicry (M protein vs keratin)	Raindrop papules with scale

High Yield Summary — Complications of Pharyngitis and Tonsillitis

Suppurative complications arise from direct spread: peritonsillar abscess (quinsy), parapharyngeal/retropharyngeal abscess, AOM (via Eustachian tube), sinusitis (via ostiomeatal complex), necrotising fasciitis, septicaemia, Lemierre syndrome.
Non-suppurative complications are immune-mediated: ARF (molecular mimicry, 2–4 weeks), PSGN (immune complexes, 1–3 weeks), scarlet fever (superantigen toxin, concurrent), STSS, PANDAS, guttate psoriasis.
Only pharyngeal GAS infection causes ARF; skin GAS infection does NOT cause ARF but CAN cause PSGN ^[23]^[24].
ARF can be prevented by antibiotics within 9 days; PSGN prevention by antibiotics is NOT proven.
Rheumatic heart disease is the most common and severe sequela of ARF; develops 10–20 years later; MV most commonly affected; MS is the most common pathology ^[4]^[24].
Jones criteria for ARF (JONES): Joints (migratory polyarthritis), O-shaped heart (pancarditis), Nodules (subcutaneous), Erythema marginatum, Sydenham's chorea. Need 2 Major or 1 Major + 2 Minor + evidence of preceding GAS.
Peritonsillar abscess = trismus + uvula deviation + muffled voice; requires drainage + IV antibiotics.
Secondary tonsillectomy haemorrhage (day 5–14) is the most common serious post-tonsillectomy complication, occurring when the eschar separates.
Post-obstructive pulmonary oedema after tonsillectomy results from sudden loss of intrinsic PEEP when chronic upper airway obstruction is relieved.
Grisel syndrome = post-tonsillectomy atlantoaxial instability from infection extending to the paravertebral space.

Active Recall - Complications of Pharyngitis and Tonsillitis

References

^[1] Senior notes: Ryan Ho Respiratory, p.49, 51–52 (Section 3.1.1 URTI complications; 3.1.1.2 Bacterial Pharyngitis — suppurative and non-suppurative complications) ^[2] Senior notes: Adrian Lui Pediatrics Notes, p.158 (GAS pharyngitis complications table) ^[4] Senior notes: Ryan Ho Cardiology, p.146 (ARF pathophysiology, pancarditis, chronic RHD, valve involvement) ^[5] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf, p.43 (Peritonsillar abscess / Quinsy) ^[7] Senior notes: Block A - Dermatology PBL 1.pdf, p.17 (Strep pharyngitis → guttate psoriasis) ^[8] Lecture slides: GC 021. Upper respiratory tract infections.pdf, p.25 (Sore throat — serious causes include abscess/quinsy) ^[13] Senior notes: Ryan Ho Urogenital, p.66 (PSGN — clinical features, timeline, prognosis) ^[17] Senior notes: Block A - Glomerular and Tubulo-interstitial Diseases and AKI, p.19 (PSGN — persistently low C3) ^[19] Senior notes: Gen Clerk Anaes + Microbiology Summary, p.13 (ARF primary and secondary prevention) ^[22] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.133 (Tonsillectomy indications and contraindications) ^[23] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.126, 129 (GAS complications — suppurative and non-suppurative; Jones criteria; necrotising fasciitis; septicaemia) ^[24] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai), p.444 and MBBS Final MB (Pediatrics) (Felix PY Lai), p.303 (ARF/RHD overview, pathogenesis, epidemiology Rule of 3) ^[25] Senior notes: Block A - Three Cases of Dyspnea, p.3 (Mitral stenosis in RHD — warfarin not NOAC) ^[26] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai), p.134 (Tonsillectomy complications — immediate, early, late)

High Yield Summary

Most pharyngitis is viral — antibiotics are NOT indicated unless GAS is confirmed or strongly suspected.
GAS pharyngitis is the most important bacterial cause because of the risk of acute rheumatic fever (preventable with antibiotics within 9 days).
Centor criteria (CENT): Cough absent, Exudate, Nodes (anterior cervical), Temperature (fever) — each scores 1 point; used to guide need for testing/empirical treatment.
Viral clues: Cough, rhinorrhoea, conjunctivitis, hoarseness, oral ulcers.
GAS clues: Sudden onset, exudate, tender anterior cervical lymphadenopathy, fever, absence of cough, scarlatiniform rash, age 5–15.
EBV clues: Severe exudative tonsillitis + posterior cervical lymphadenopathy + splenomegaly + atypical lymphocytes; avoid amoxicillin (causes rash).
Peritonsillar abscess (quinsy): Unilateral peritonsillar swelling, uvula deviation, trismus, muffled voice — a surgical emergency requiring drainage.
Diphtheria: Grey pseudomembrane + bull neck + myocarditis/neuropathy — consider in unvaccinated patients.
In Hong Kong: Always consider NPC in adults with persistent unilateral sore throat + cervical lymphadenopathy.
Molecular mimicry explains ARF: GAS M protein cross-reacts with cardiac proteins → pancarditis.
Referred otalgia in pharyngitis is via CN IX (glossopharyngeal nerve).
Coloured nasal discharge ≠ need for antibiotics — it reflects PMN enzymatic activity, not bacterial infection.

High Yield Summary — Differential Diagnosis of Pharyngitis and Tonsillitis

> 90% of acute sore throat is due to viral URIs — the default diagnosis is viral unless proven otherwise.
Centor criteria (CENT) guide the need for GAS testing/empirical antibiotics, but exudates can mean viral or bacterial — never treat based on exudate alone.
Red-flag / "don't miss" diagnoses: acute epiglottitis (drooling, stridor), peritonsillar abscess (trismus, uvula deviation), deep neck space abscess, lymphoma (unilateral tonsillar mass), NPC (Southern Chinese, unilateral ear/nose symptoms), diphtheria (pseudomembrane), Lemierre syndrome (post-pharyngitis IJV thrombophlebitis), agranulocytosis (ulceration without pus).
EBV-IM is a classic pitfall — posterior cervical LN, splenomegaly, atypical lymphocytes, amoxicillin rash.
Synpharyngitic haematuria (concurrent with pharyngitis) = IgA nephropathy; post-pharyngitic haematuria (1–3 weeks later) = PSGN.
Unilateral tonsillar enlargement in an adult = malignancy until proven otherwise (lymphoma, SCC, minor salivary gland tumour).
GAS pharyngitis is usually NOT accompanied by nasal symptoms — the best single clinical clue to distinguish from viral URTI.
Persistent sore throat > 3 weeks: must exclude malignancy (NPC, oropharyngeal SCC, lymphoma), TB, HIV, foreign body.

High Yield Summary — Diagnosis of Pharyngitis and Tonsillitis

Centor criteria (CENT): Cough absent, Exudate, Node (anterior cervical), Temperature → guides who to test, not who to treat.
Modified Centor (McIsaac): Add +1 if age < 15, subtract 1 if age > 44.
Score 0–1: No testing, no antibiotics. Score 2–3: Test (RADT ± culture). Score 4–5: Test-and-treat or empirical antibiotics.
RADT: Specificity ≥ 95% (positive result is reliable); sensitivity 70–90% (negative result needs backup culture in children).
Throat culture: Gold standard, sensitivity 90–95%, but takes up to 3 days.
10–25% of population carry GAS asymptomatically — positive test + pharyngitis does not always mean GAS pharyngitis.
Empiric treatment NOT recommended — clinical symptoms alone achieve only ~50% accuracy.
ASLO / anti-DNase B: Not useful acutely (takes > 2 weeks to rise); used retrospectively for ARF/PSGN.
Persistently low C3 > 8 weeks after suspected PSGN → think lupus nephritis or MPGN.
Red flags requiring urgent workup: stridor/drooling (epiglottitis), trismus/uvula deviation (quinsy), unilateral mass/persistent > 3 weeks (malignancy), agranulocytosis.
Swab technique: Both tonsils and posterior pharynx; avoid tongue, buccal mucosa, hard palate.

High Yield Summary — Management of Pharyngitis and Tonsillitis

Most pharyngitis is viral → supportive care only (analgesia, hydration, rest). NO antibiotics.
Confirmed GAS → penicillin V or amoxicillin × 10 days — GAS has never developed penicillin resistance.
IM benzathine penicillin G single dose if compliance is uncertain ^[19].
Penicillin allergy → 1st-gen cephalosporin (non-anaphylactic) or azithromycin/clindamycin (anaphylactic) — avoid erythromycin in HK (40–50% resistance).
Antibiotic goals: ↓ symptoms, prevent ARF (within 9-day window), ↓ transmission, prevent suppurative complications ^[1].
EBV/IM → supportive care, AVOID amoxicillin, avoid contact sports (splenic rupture risk).
Peritonsillar abscess → IV antibiotics + drainage (needle aspiration or I+D) ± interval tonsillectomy.
Airway compromise → emergency airway management (head tilt-chin lift, BVM, nebulised adrenaline, IV dexamethasone, intubation, needle cricothyrotomy).
Tonsillectomy indications: recurrent tonsillitis (Paradise criteria), OSA, quinsy unresponsive to drainage, biopsy for suspected malignancy ^[22].
Tonsillectomy contraindications: bleeding disorder, anaesthetic risk, atlantoaxial instability (RA, Down's syndrome) ^[22].
ARF secondary prophylaxis: monthly IM benzathine penicillin for years to lifelong ^[19].
Safety netting: Return if trismus, drooling, worsening dysphagia, persistent fever on antibiotics, or sudden abdominal pain (EBV → splenic rupture).

High Yield Summary — Complications of Pharyngitis and Tonsillitis

Suppurative complications arise from direct spread: peritonsillar abscess (quinsy), parapharyngeal/retropharyngeal abscess, AOM (via Eustachian tube), sinusitis (via ostiomeatal complex), necrotising fasciitis, septicaemia, Lemierre syndrome.
Non-suppurative complications are immune-mediated: ARF (molecular mimicry, 2–4 weeks), PSGN (immune complexes, 1–3 weeks), scarlet fever (superantigen toxin, concurrent), STSS, PANDAS, guttate psoriasis.
Only pharyngeal GAS infection causes ARF; skin GAS infection does NOT cause ARF but CAN cause PSGN ^[23]^[24].
ARF can be prevented by antibiotics within 9 days; PSGN prevention by antibiotics is NOT proven.
Rheumatic heart disease is the most common and severe sequela of ARF; develops 10–20 years later; MV most commonly affected; MS is the most common pathology ^[4]^[24].
Jones criteria for ARF (JONES): Joints (migratory polyarthritis), O-shaped heart (pancarditis), Nodules (subcutaneous), Erythema marginatum, Sydenham's chorea. Need 2 Major or 1 Major + 2 Minor + evidence of preceding GAS.
Peritonsillar abscess = trismus + uvula deviation + muffled voice; requires drainage + IV antibiotics.
Secondary tonsillectomy haemorrhage (day 5–14) is the most common serious post-tonsillectomy complication, occurring when the eschar separates.
Post-obstructive pulmonary oedema after tonsillectomy results from sudden loss of intrinsic PEEP when chronic upper airway obstruction is relieved.
Grisel syndrome = post-tonsillectomy atlantoaxial instability from infection extending to the paravertebral space.

Pharyngitis And Tonsillitis

References

Pharyngitis and Tonsillitis

3. Anatomy and Function

4. Etiology

4.3 Bacterial Pharyngitis/Tonsillitis

5. Pathophysiology

6. Classification

7. Clinical Features

7.4 Specific Clinical Patterns by Etiology

Active Recall - Pharyngitis and Tonsillitis (Definition, Epidemiology, Etiology, Pathophysiology, Clinical Features)

Differential Diagnosis of Pharyngitis and Tonsillitis

9.2 Master Differential Diagnosis Table

9.3 Differential Diagnosis of Specific Clinical Patterns

Active Recall - Differential Diagnosis of Pharyngitis and Tonsillitis

References

Diagnostic Criteria, Algorithm and Investigations for Pharyngitis and Tonsillitis

10.2 Centor / Modified Centor (McIsaac) Criteria

10.3 Diagnostic Tests for GAS Pharyngitis

10.4 Investigations for Specific Diagnoses Beyond GAS

Active Recall - Diagnosis and Investigations for Pharyngitis and Tonsillitis

References

Management of Pharyngitis and Tonsillitis

11.4 Antibiotic Treatment of GAS Pharyngitis

11.5 Management of Specific Conditions

11.6 Prevention of Rheumatic Fever — Primary and Secondary

11.7 Tonsillectomy — Surgical Management

Active Recall - Management of Pharyngitis and Tonsillitis

References

Complications of Pharyngitis and Tonsillitis

12.2 Suppurative Complications

12.3 Non-Suppurative Complications

12.3.1 Acute Rheumatic Fever (ARF)

Active Recall - Complications of Pharyngitis and Tonsillitis

References

On this page

Pharyngitis And Tonsillitis

1. Definition

2. Epidemiology

3. Anatomy and Function

3.1 The Pharynx

3.2 The Palatine Tonsils (Waldeyer's Ring)

3.3 Blood Supply and Innervation

3.4 Surrounding Spaces (Relevant for Complications)

4. Etiology

4.1 Overview of Causes

4.2 Viral Pharyngitis/Tonsillitis (Most Common)

4.3 Bacterial Pharyngitis/Tonsillitis

4.3.1 Group A Streptococcus (GAS) — Streptococcus pyogenes

4.3.2 Other Bacterial Causes

4.3.3 Fungal Pharyngitis

4.4 Non-Infectious Causes of Sore Throat

4.5 Risk Factors

5. Pathophysiology

5.1 Viral Pharyngitis

5.2 GAS (Streptococcal) Pharyngitis

5.3 Pathophysiology of Complications (Brief Overview)

6. Classification

6.1 By Duration

6.2 By Etiology

6.3 By Anatomy

6.4 By Morphology

7. Clinical Features

7.1 Symptoms

7.2 Signs

7.3 Distinguishing Viral from GAS Pharyngitis — Clinical Clues

7.4 Specific Clinical Patterns by Etiology

Infectious Mononucleosis (EBV)

Herpangina (Coxsackievirus A)

Diphtheria

Peritonsillar Abscess (Quinsy) [5]

Streptococcal Pharyngitis Triggering Guttate Psoriasis

8. Summary Table: Clinical Differentiation of Acute Pharyngitis by Etiology

Active Recall - Pharyngitis and Tonsillitis (Definition, Epidemiology, Etiology, Pathophysiology, Clinical Features)

References

9.1 Framework for Thinking About the Differential

9.2 Master Differential Diagnosis Table

A. Infectious Causes of Sore Throat / Pharyngitis / Tonsillitis

B. Non-Infectious Causes of Sore Throat

C. Serious / "Don't Miss" Diagnoses

9.3 Differential Diagnosis of Specific Clinical Patterns

Pattern 1: Sore Throat with Exudative Tonsillitis

Pattern 2: Sore Throat with Vesicles/Ulcers

Pattern 3: Sore Throat with Rash

Pattern 4: Unilateral Tonsillar Enlargement

Pattern 5: Chronic / Persistent Sore Throat ( > 3 weeks)

9.4 Differential Diagnosis of Related URTI Presentations

9.5 Hoarseness as a Related Differential

9.6 Differential Diagnosis of Neck Mass Presenting with Pharyngitis

9.7 Differential Diagnosis Algorithm

9.8 Infectious Mononucleosis — Expanded Differential (High Yield)

9.9 Associations and Sequelae That Enter the DDx Work-Up

Active Recall - Differential Diagnosis of Pharyngitis and Tonsillitis

10.1 The Central Diagnostic Question

10.2 Centor / Modified Centor (McIsaac) Criteria

10.2.1 Purpose and Rationale

10.2.2 The Criteria

10.2.3 Score Interpretation and Action

10.3 Diagnostic Tests for GAS Pharyngitis

10.3.1 Throat Swab Collection — Technique Matters

10.3.2 Rapid Antigen Detection Test (RADT)

10.3.3 Throat Culture (Culture and Sensitivity)

10.3.4 Other Tests

10.4 Investigations for Specific Diagnoses Beyond GAS

10.4.1 Infectious Mononucleosis (EBV)

10.4.2 Peritonsillar Abscess (Quinsy)

10.4.3 Diphtheria

10.4.4 Suspected STI-Related Pharyngitis

10.4.5 Suspected Post-Streptococcal Complications

10.4.6 Suspected Malignancy (Persistent / Unilateral Sore Throat)

10.5 Investigations Summary Table

10.6 Diagnostic Algorithm — Master Flowchart

10.7 Physical Examination Findings to Document

10.8 When NOT to Test for GAS

Active Recall - Diagnosis and Investigations for Pharyngitis and Tonsillitis

11.1 Management Principles — The Big Picture