Pulmonary Infections - Pathology Flashcards
Systemic factors that predispose to pneumonia
- immune deficiency or supression
- leukopenia
- chronic illness
Local factors that predispose to pneumonia
- loss of cough reflex/impaired mucociliary apparatus
- interference w/phagocytic or bactericidal action of alveolar MF
- pulmonary congestion/edema
MC cause of community-acquired acute pneumonia
S. pneumoniae
(gram stain for dx; usually lobar)
Which type of pneumonia causes lobar pneumonia?
community-acquired (s. pneumoniae)
Difference between lobar and bronchopneumonia?
broncho: affects alveoli near bronchi
lobar: entire lobe
foci of consolidation (lung exudate) = bronchopneumonia
In lobar pneumonia, what are the four stages of the inflammatory response?
- congestion
- red hepatization
- gray hepatization
- resolution
describe the congestion phase of lobar pneumonia
vascular engorgement, intra-alveolar fluid, neutrophils, bacteria present
Describe the red hepatization phase of lobar pneumonia
- massive exudation with neutrophils
- red cells
- fibrin filling alveolar spaces
lobe appears red, firm, and airless
Describe the gray hepatization phase of lobar pneumonia
- progressive disintegration of red cells
- persistence of a fibrinosuppurative exudate
appears grayish & dry
Describe the resolution phase of lobar pneumonia.
consolidated exudate undergoes enzymatic digestion –> produces granular, semifluid debris that is resorbed, ingested by MF or expectorated
pulmonary architecture restored. some –> organized pneumonia w/fibrous
Dx? Why?
- acute bacterial pneumonia
- large # neutrophils in alveoli
- purulent exudate in alveoli
Difference in xray findings between broncho and lobar pneumonia
- lobar: radiopaque
- broncho: focal opacities
bacterial pneumonia vs. viral pneumonia presentation.
both have fever
bacterial: shaking chills, cough w/mucopurulent sputum
viral: myalgia, headache
(acute/community-acquired)
How long does it take a patient to recover from acute bacterial pneumonia once treated?
2-3 days
(10% of hospitalized pts die)
MC causes of viral pneumonia (5)
- Flu
- rhinoviruses
- RSV
- SARS-CoV-2
- Human metapneumovirus
How does SARS-CoV-2 enter epithelial cells
ACE2 receptor of alveolar epithelial cells
the reason its a lung disease
3 types (morphologies) of viral community-acquired pneumonia
- laryngotracheobronchitis
- bronchiolitis
- interstitial pneumonia
(location based)
Adult pneumonia is typically caused by which viruses?
- flu
- rhinovirus
Pediatric pneumonia is typically caused by which viruses?
RSV
In interstitial pneumonia, alveolar septa become thickened with _______ infiltrate.
mononuclear
What is this? Why?
- intersitital pneumonia
- lymphocytes
- exudate
- hyaline membranes (diffuse alveolar damage –> ARDS)
(this is the usual cause of death in COVID patients)
2 common complications of aspiration pneumonia
necrosis –> lung abscess
high mortality
define lung abscess
- neutrophils
- necrosis
5 Causes of lung abscess
- aspiration
- antecedent pneumonia (necrosis)
- septic emboli (phlebits or endocarditis)
- neoplasia
- penetration injury
Which 3 pathogens are responsible for 60% of lung abscess?
- bacteroides
- fusobacterium
- peptococcus
(usually from aspiration)
lung abscess
neutorphils + exudate
MC signs of lung abscess
copious amt of foul-smelling sputum
CP &. weight loss
4 complications of lung abscess
- empyema
- hemoptysis
- meningitits
- brain abscess
Chronic pneumonia inflammatory reaction involves _________.
granuloma
MC pathogen involved in chronic pneumonia (3)
- M. tuberculosis
- H. capsulatum
- C. immitus
% of TB infection that progresses to primary TB
5
isolated tb
dissemination to one organ
ex: kidneys
What is happening during the 3 weeks of infection with Tb, before cell-mediated immunity begins?
MF take up TB but are not activated –> proliferation –> bacteremia & seeding
Describe the initiation of cell-mediated immunity in tuberculosis infection.
Alveolar MF presents to T-cell via IL-12 & MHC II –> differentiation to TH1 –> activated MF –> TNF, chemokines –> monocyte recruitement & casseous necrosis
very similair to histoplasmosis pathogenesis
ghon complex
yellow = hilar nodes
blue = casseating granuloma in parenchyma
caseating granuloma
yellow = caseating necrosis
blue = langhans giant cell
how are langhans giant cells formed
activation & fusion of activated MF
T-cell mediated response = langhans
What is this? why?
- secondary tb
- cavitation (cassceation coalesce)
acid-fast bacili smear = TB
miliary disseasae
spleen
What is predominate cell type in caseating granulomas?
activated MF
aka epitheliod MF due to increased cytosol which looks like epithelial c
What are the similairities between TB and histoplasmosis (2)?
- primary & secondary disease
- can disseminate to other organs
Dx? Why?
- Histoplasmosis
- “Tree bark” appearance due concentric layers of fibrosis and calcifications
Dx? Why?
- Histoplasmosis
- pair shaped budding yeast w/narrow base
Histoplasmosis is very similair to TB pathogenesis, what is the difference?
mainly that histoplasmosis is a fungi, both are taken in by MF, multiply and lyse MF –> entry into blood –> T cells then activate and recruit MF via INF-g –> caseating granuloma
How is histoplasmosis dx (2)?
- culture yeast
- serologic testing (Ab & Ag)
only 10% of ppl w/San Joaquin Valley Fever develop symptoms. What are the sx (3)?
- lung lesion
- pleuritic pain
- cutaneous lesions
(fever & cough)
Cutaneous involvment in coccidioidomycosis (2)
- erythema nodosum
- erythema multiforme
(only 1% will develop disseminated C. immitis )
Dx? Why?
- bronchopneumona
- spheroles (C. immitus)
will develop caseating granuloma (below)
spheroles containing endospores
Histoplasmosis is endemic to which area?
ohio & mississippi river valleys
