SEARCH RESULTS FOR: tonsillitis

Tonsillitis Pathogenesis and clinical findings

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

Diphtheria

Diphtheria: Pathogenesis and clinical findings Travel to endemic areas Immunity (primarily acquired through vaccination) is incomplete, absent, or waning Poor hygiene environments Exposure to respiratory droplets or direct contact with infected surface Colonization of the pharynx or cutaneous sites with corynebacterium diphtheriae (C. diphtheriae) C. diphtheriae proliferate locally & secrete diphtheria exotoxin Exotoxin enters nearby host cells & inhibits host cell protein synthesis Local epithelial tissue necrosis & activation of inflammatory response Accumulation of dead cells, fibrin, bacteria & inflammatory cells Lymphatic & hematogenous spread of exotoxin to distant tissues (preferentially tissues with ↑ metabolic activity) Author: Julia Fox Reviewers: Steven Quan, Emily J. Doucette, James D. Kellner* *MD at time of publication **See corresponding Calgary Guide slide Cutaneous Diphtheria Cutaneous skin breakdown Vesicle/pustule formation Superficial, non-healing ulcers with grey pseudomembrane Respiratory Diphtheria Presence of inflammatory mediators in the pharynx Mucosal edema & sensitization of nociceptors Dense necrotic pseudomembrane forms & adheres to larynx, pharynx, or tonsils Pseudomembrane dislodgment or extension into the airway Diphtheria antigens drain to cervical lymph nodes Cervical lymphadenitis Pain & inflammatory response at infection site (eg. pharyngitis, tonsillitis, etc.) Diphtheritic membrane (grey mucous membranes) Localized airway obstruction (severe laryngeal cases) Bull neck appearance Systemic Manifestations Protein synthesis inhibition in myocardial cells Protein synthesis inhibition in neurons & Schwann cells Focal myocardiocyte necrosis, inflammation, & fibrosis Demyelination, ↓ myelin regeneration, & axonal injury Myocarditis** Damaged myocardium disrupts conduction pathways & contractility Cranial nerve conduction impaired first (especially CN IX, X, III) due to ↓ length, ↑ metabolic activity & proximity to mucosal infection sites ECG changes (arrhythmias & heart block) Palatal & pharyngeal paralysis Oculomotor palsy Dysphonia, dysphagia, & loss of gag reflex Protein synthesis inhibition in glomeruli & renal tubular epithelial cells Tubular necrosis & interstitial inflammation Renal failure Endothelial injury ↑ glomerular permeability Long peripheral nerve conduction impaired later (2-6 weeks after initial infection) Ascending muscle weakness Paresthesia & numbness Acute tubular necrosis Granular casts in urine Proteinuria Microscopic hematuria Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Dec 18, 2025 on www.thecalgaryguide.com