Epiglottitis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Overview

Pathophysiology

Pathogenesis

Acute epiglottitis

Understading the pathogenesis of epiglottitis involves a good knowlegde of the causative organisms. The only known reservoirs for H. influenzae in humans include:

Healthy people are normal carriers of the organism. Pathogenicity of H. influenza is as a result of imbalance between the virulent factors of the organism and the host immune system.

H. influenza type b capsule is antiphagocytic. Serum anit-purified polyribosylribitol phosphate (anti-PRP) antibody is important in the complement dependent phagocytosis and lyses of the bacteria.

The strategies deployed by a microbe to assist its survival and proliferation, may or may not lead to disease process. Epiglottitis caused by H. influenza may therefore be considered as an accidental consequence of the microbial factors that permit its survival.

Acute epiglottis pathogenesis is well exemplified by H. influenzae, with the ability to colonize mucosal surfaces and to spread contiguously or invade epithelial cells, to disseminate within the bloodstream, and to localize to selected tissues among these is the epiglottis. The H. influenza like other infectious agents cause epiglottis mostly via invasion of the bloodstream by the help of its virulence factors. These include:


Necrotizing epiglotitis

The pathogeneiis of necrotizing epiglottitis involves the infection with CMV or EBV usually in immunocompromised people. Affected patients are usually neutropenic and lymphopenic at presentation. CMV and EBV modulate the host's immune defense facilitating immune evasion and thereby predisposing the patient to a superimposed infections. The causative organism of necrotizing epiglottitis is unclear.[1]

References

  1. Tebruegge M, Connell T, Kong K, Marks M, Curtis N (2009). "Necrotizing epiglottitis in an infant: an unusual first presentation of human immunodeficiency virus infection". Pediatr Infect Dis J. 28 (2): 164–6. doi:10.1097/INF.0b013e318187a869. PMID 19106777.