Pathology of Infectious Diseases Flashcards
infection is established if (2 factors)
- virulence factors overcome normal host defenses
OR - host defenses are compromised
infections can get in by various methods, including
-breaching epithelial surfaces
-inhalation
-sexual transmission
-vertical transmission (mother to fetus, birth, postnatal maternal milk)
dissemination of pathogens
-may remain at localized site
OR
-spread to other sites via:
*direct extension (following tissues planes of least resistance)
*lymphatics
*bloodstream
*nerves
*tissue tropism (specific tissue involvement/characteristic disease patterns)
evasion of defenses by pathogens
-antigenic variation (looking different to the immune system: expressing different surface antigens, etc)
-avoiding phagocytosis (capsule, protein A, etc)
-inactivation of complement
-suppressing adaptive immunity
-latency phase genes
damage mechanisms of pathogens
- direct cytotoxicity (infect a cell and kill it or transform it)
- indirect cytotoxicity (release toxins, killing distant cells)
- collateral cytotoxicity (induce host immune responses, causing tissue damage)
endotoxins
LPS in outer membrane of gram - organisms stimulates host immune responses and injury
exotoxins
secreted bacterial proteins that cause cellular injury and disease
spectrum of inflammatory responses to infection
- suppurative acute inflammation
- non-suppurative inflammation
- granulomatous inflammation
- cytopathic / cytoproliferative change
- necrotizing inflammation
- chronic inflammation
suppurative acute inflammation
neutrophilic infiltration
*response to acute infection from extracellular bacteria
*results in formation of EXUDATE (pus = neutrophils + liquefactive necrosis)
non-suppurative inflammation
**NON-neutrophilic infiltrates (eosinophils, lymphocytes, monocytes, etc)
*response to acute infections from viruses, intracellular bacteria, or parasites
granulomatous inflammation
*defined aggregates of macrophages, some combining into multi-nucleated giant cells
*T-cell mediated immune response
*response to SLOWLY DIVIDING organisms (mycobacteria, fungi)
cytopathic / cytoproliferative change
*virus-mediated cellular damage
*ABSENT host inflammatory response
1. polykaryons (cells induced to fuse, forming a blister)
2. inclusion bodies (visible viral replication within cell)
3. neoplastic cellular proliferation (b/c of oncogene expression)
necrotizing inflammation
*toxin-mediated severe tissue damage and cell death
*typically only few inflammatory cells involved
-viruses may cause necrotic inflammation when host cell damage is widespread and severe
what are the most relevant pathogens for necrotizing inflammation
*Clostridium perfringens
*group A strep
chronic inflammation / scarring
*lymphocytes/plasma cells with associated fibrosis
*final common pathway of many infections
*progressive shift in cell type at site of inflammation
*simultaneous destruction and healing