Tonsillitis: Pathogenesis and clinical findings
Authors:
Taylor Krawec Amanda Marchak Reviewers: Nicola Adderley, Jim Rogers Emily J. Doucette, Danielle Nelson* James D. Kellner* * MD at time of publication
Pathogen infiltrates tonsillar epithelium
Microfold cells recognize pathogen & activate immune response
Virus (most common)
Group A Streptococci (GAS) (most common bacteria)
Group B, C & G Strep,
Fusobacterium necrophorum
Age 5-15 (tonsils have ↑ role in immune function at this age)
Tonsillitis
Inflammation of the tonsils
Infectious agent exposure
Susceptible host Pathogen colonizes the oropharynx
Acute suppurative disease
Immune cells release proinflammatory cytokines & antibodies
Inflammatory mediators ↑ vascular permeability of tonsils
Leakage of protein & fluid into surrounding tissue
Regional nodes receive ↑ lymph
Enlarged anterior cervical nodes
Sinusitis**
Pharyngitis**
Local spread of pathogen
Acute otitis media**
Pneumonia**
Cervical lymphadenitis
Bacteria spread from
tonsils into lymphatic system & bloodstream
Bacteremia
F. necrophorum
invades lateral pharyngeal space & soft tissue in neck
Thrombosis forms in peritonsillar vein
Thrombosis extends into internal jugular vein
Lemierre’s syndrome
Systemic inflammatory cytokines disrupt hypothalamic regulation
Fever
Additional immune cells are recruited to facilitate immune response
Macrophages phagocytize pathogen
Bacteria invade distant tissue & elicit local inflammatory response
Hepatitis Osteomyelitis
Infective endocarditis
Bacteria illicit systemic response
Sepsis
Tonsillar tissue become swollen & irritated
Tonsillar hypertrophy
Localized collection of pus forms
Immune cells cause inadvertent cellular injury & hemolysis
Palatal petechiae
Meningitis
Products of immune response & cellular debris are deposited into tonsillar tissue
Peritonsillar or Tonsillar retropharyngeal abscess** exudate
** See corresponding Calgary Guide slide
Toxin-mediated disease
Bacteria release exotoxins into bloodstream
Inflammatory mediators & cytokines are overactivated (cytokine storm)
Skin has local inflammatory response
Toxic shock syndrome**
Scarlet fever**
Post-infectious disease
Antibodies to GAS cross react with host tissue
Acute rheumatic fever** Post-strep glomerulonephritis
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published Nov 5, 2018; updated Mar 14, 2025 on www.thecalgaryguide.com