Pulmonary Infection Pathology Flashcards
Pulmonary
Host Defenses
- Physical barriers
- Nasal turbinates, epiglottis, larynx
- Dichotomously branching conducting airways
- Anatomic barrier
- Mucociliary clearance
- Coughing
- Antibaterial activity of bronchial secretions
- Lysozyme, lactoferrin, sIgA
- Defenses in alveolar spaces
- Surfactant ⇒ antibacterial activity

Pulmonary Infection
Risk factors
- Intubation
- Malnutrition
- Cigarette smoke & other noxious fumes
- Congenital structual defects of cilia
- LOC or anesthesia
- Pulmonary congestion, edema, emphysema
- Immunosuppression
Routes of Infection
- Inhalation of infectious droplets
- Aspiration of oral/gastric contents
- Hematogenous
Pulmonary Consolidation
When alveoli filled with supprative exudates
PNA
Patterns

Lobar PNA
Involves one or more lobes uniformly
Strep. pneumoniae most common cause

Bacterial PNA
Inflammatory Stages
- Congestion
- Red hepatization
- Gray hepatization
- Resolution vs organization

Congestion
Stage 1:

Red Hepatization
Stage 2:

Grey Hepatization
Stage 3:

Resolution
Stage 4:
Exudates resolves or undergoes organization.
Organizing PNA
- Virulent organisms damaged basement membrane
- Activates repair reaction
- Influx of fibroblasts ⇒ collagen secretion
- Exudates become organized

Bronchopneumonia
Lobular, patchy, non-uniform distribution of consolidation
Caused by many pathogens:
- Gram ⊕
- S. aureus, S. pneumoniae, S. pyogenes, H. inluenzae
- Gram ⊖
- P. aeruginosa, Enterobacteriaceae, L. pneumophila
Bronchopneumonia
Gross Appearance
Granular consolidation, often adjacent to major airways.
Seen as pale-colored, firm nodules.

Bronchopneumonia
Microscopic Appearance
Alveoli filled with edema, extravasated RBCs, bacteria, PMN, and alveolar Mφ.
Can see virulent organisms, likely to organize:
S. aureus ⇒ microabscesses, results in permanent lung damage
P. aeruginosa ⇒ vasculitis, necrosis

Aspiration Pneumonia
- Material enters LRT
- Respiratory secretions
- Food or gastric contents from OP
- Acute event associated with sudden death vs a chronic recurrent problem
- Etiology ⇒ mixed enteric and anaerobic organisms
- Gross ⇒ necrosis of RML & RLL
- Micro:
- Foreign material inside of FB giant cells
- Surrounding inflammatory cells
- Tissue may be disgested by process

Bacterial
Interstitial PNA
Few bacteria cause interstitial PNA that looks similar to viral infections:
- Mycoplasma pneumoniae
- Chlamydia trachomatis (in infants)
- Chlamydia pneumoniae
Viral PNA
Three major morphologic manifestations:
- Bronchiolitis
- Interstitial PNA
- PNA associated w/ viral inclusions
Bronchiolitis
Morphological manifestation of viral PNA.
-
Peribronchiolar collections
- Lymphocytes
- Epithelial damage and sloughing
- Squamous metaplasia
- Mucus plugging of bronchioles
- Local hyperinflation and subsequent atelectasis
- Pathogens:
- RSV, parainfluenza, influenza A & B, adenovirus
- Bronchiolitis obliterans ⇒ uncommon complication

Interstitial PNA
Morphologic manifestation of viral PNA.
- Lymphocytes and plasma cells within alveolar walls and around small airways
- ± Hyaline membranes
- Pathogens:
- RSV, influenza

PNA w/ Viral Inclusions
Morphologic manifestation of viral PNA.
Viral infection includes morphological changes within the host cell.
CMV
Pneumonia

Adenovirus
PNA

Measles Virus
PNA
Warthin-Finkeldy Gaint Cells

Herpes
PNA
Ground-glass appearance and nuclear molding.

Fungal PNA
Pneumocystis jirivecii
- Epidemiology
- Colonizes immunocompetent persons
- Causes disease in immunocompromised hosts
- Esp. AIDS pts
- Pathology:
- Mononuclear cell interstitial infiltrate ⇒ interstitial PNA
- Alveoli filled with foamy eosinophilic material ⇒ pathogens
- Trophozoites (replicating form) ⇒ stain w/ Giemsa stain
- Cysts ⇒ stain w/ silver stain
