Pulmonary Infections
Disease
Respiratory Tract
Infections
Overview
- More frequent than
infection in other
organ
- Account for the
largest number of
work days lost in the
general population
- Majority URTIs
caused by viruses
- Lung infections, such
as pneumonia, lung
abscesses and TB
rank among the
major immediate
causes of death
Pneumonia
- Any acute
inflammation of the
lung parenchyma
Etiology:
- Bacteria
- Viruses
- Chemical irritants
Pathogenesis
Respiratory tract
- Inhalation of aerosols – usual mode
- Aspiration of secretions containing pathogenic
organisms that have colonized the oropharynx
- Hematogenous spreadfrom extrapulmonary
Nosocomial infections – hospital acquired
- Acquired resistance to antibiotics
- Invasive procedures and contamination of
instruments, e.g. intubation
- Ventilation
Impairment of defense mechanisms
- Loss or suppression of the cough reflex  aspiration
of gastric contents – coma , anesthesia
- Damage to the mucociliary apparatus
o Smoking, viral infections, genetic (immotile cilia
syndrome), inhalation of hot or corrosive gases
- Interference with alveolar macrophages
o Smoking, alcohol, anoxia, O2 toxicity
- Pulmonary congestion and edema
o CHF
- Accumulation of secretions
o Bronchial obstruction, cystic fibrosis
- Lowered resistance of the host
o Immunodeficiency
o Unusually virulent infections
o Chronic diseases:
 Diabetes, malnourishment, alcoholism
o Leukopenia
o Immunosuppression
Types
- Lobar Pneumonia:
Affects an entire lobe
- Bronchopneumonia: Scattered foci
- Interstitial:
Alveolar interstitium
Course
Most patients recover with antibiotic therapy
< 10% succumb due to:
- A complication
- Meningitis, empyema, endocarditis, pericarditis
- Predisposing condition
- Debility
- Alcoholism
©2010 Mark Tuttle
Clinical
The Pneumonia Syndromes
Community-Acquired Acute Pneumonia
Chronic Pneumonia
- Nocardia
- Actinomyces
- Granulomatous: Mycobacterium
tuberculosis and atypical mycobacteria,
Histoplasma capsulatum, Coccidioides
immitis, Blastomyces dermatitidis
Necrotizing Pneumonia and Lung
Community-Acquired Atypical Pneumonia
Abscess
- Mycoplasma pneumoniae
- Anerobic bacteria (extremely
- Chlamydia spp. (C. pneumoniae, C. psittaci, C.
common), with or without mixed
trachomatis)
aerobic infection
- Coxiella burnetti (Q fever)
- Viruses: respiratory syncytial virus, parainfluenza
- Staphylococcus aureus, Klebsiella
virus (children); influenza A and B (adults);
pneumoniae, Streptococcus pyogenes,
adenovirus (military recruits); SARS (Severe acute
and type 3 pneumococcus (uncommon)
respiratory syndrome) virus
Pneumonia in the Immunocompromised
Nosocomial Pneumonia
- Cytomegalovarus
- Gram-negative rods belonging to
- Pneumocystis carinii
Enterobacteriaceae (Klebsiella spp., Serratia
- Mycobaterium avium-intracullulare
marcescens, Escherichia coli) and Pseudomonas
- Invasive aspergillosis
spp.
- Staphylococcus aureas (usually penicillin-resistant) - Invasive candidiasis
- “Usual” bacterial, viral, and fungal
Aspiration Pneumonia
organisms (listed above)
- Anaerobic oral flora (Bacteriodes, Prevotella,
-
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Legionella pneumophilia
Enterobacteriaceae (Klebsiella pneumoniae) and
Pseudomonas spp.
Fusobacterium, Peptostrepococcus), admixed with
aerobic bacteria (Streptococcus pneumoniae,
Staphylococcus aureus, Haemophilas influenzae, and
Pseudomonas aeroginosa)
Symptoms
- Malaise, fever, productive cough
- Fibrinosuppurative pleuritis – friction rub
- Dyspnea, hypoxia and cyanosis
- X-ray
o Lobar pneumonia – radiopaque lobe
o Bronchopneumonia- focal opacities
Complications
- Abscesses: Localized suppurative necrosis
o Right sided abscesses most often seen in
aspiration pneumoniae
o Type 3 pneumococci or Klebsiella infections
- Pleural Involvement: Empyema
Labs
- Gram stain, culture of sputum
- Rapid urine antigen test Legionella
- Current Jelly Sputum  Klebsiella
- Chest x-ray, CBC
- Blood cultures
- Blood gases if significant hypoxemia
- Bacterial Dissemination
o Heart valves, pericardium, brain,
kidneys, spleen or joints
- Organization
o Converting part of the lung into solid
o Fibrosis, scarring
Disease
Lobar
Pneumonia
Pathogenesis
- Affects a large area or the entire lobe of a lung
- Degree of involvement depends upon:
o Virulence of the organism
 Heavy contamination by virulent organisms
may cause lobar pneumonia in healthy
individuals
o Vulnerability of the host
 Organisms of low virulence may affect
predisposed individuals
- Extensive exudation in the lung allows spread
through the pores of Kohn
- No alveolar injury
- Less common today due to antibiotics
- Stop progression of lung consolidation
Etiology
- Streptococcus pneumoniae in 90-95 %
- Generally types 1, 2, 3 and 7
- Type 3 cause a virulent form of pneumonia
- Other organisms:
o Klebsiella pneumoniae, staphylococci,
streptococci, H. influenzae; gram negative
organisms Pseudomonas and Proteus
Clinical
1. Congestion
First 4 – 12 hrs
- Heavy, wet, red
- Vascular engorgement, intra-alveolar fluid
- Few neutrophils, numerous bacteria
2. Red hepatization
Next 48 hrs
- Firm, red, airless with a liver like consistency
- Massive confluent exudate with red cells,
neutrophils and fibrin
3. Gray hepatization
3 to 8 days
- Grayish brown, dry
- Progressive disintegration of red cells
- Persistence of fibrinopurulent exudate
4. Resolution
7 to 11 days
- Progressive enzymatic digestion
o Granular semi-fluid debris
 ingested by macrophages or coughed up
Labs/Histology
Red Hepatization
Gray Hepatization
Microscopic
Bronchopneumonia
Aspiration
pneumonia
Common organisms:
- Staphylococcus, streptococcus,
Pseudomonas, H. influenzae,
pneumococci, Klebsiella and
other gram negative coliform
bacteria
-
Gross
- Lesions 3-4 cm in diameter, slightly elevated, dry,
granular, gray red to yellow, poorly demarcated, patchy
- Usually an extension of bronchitis of bronchiolitis
- Generally multilobar; frequently bilateral and basal
Microscopic
- Suppurative, neutrophil rich exudate that fills the bronchi,
bronchioles and extends directly into adjacent alveolar
spaces
- Necrosis may be present in more virulent organisms
- Exudate may resolve or organize
- Inhalation of foreign material, usually food, drink, vomit or
Types
secretions
- Partially chemical pneumonitis from irritating gastric acid and partially bacterial
- Aspiration may occur with unconsciousness, repeated
from oral flora
vomiting, and abnormal gag & swallowing reflexes
- Typically >1 organism isolated with aerobes > anaerobes
Disease
Atypical
Pneumonia
(Community
Acquired)
Pathogenesis
- Most common– Mycoplasma pneumonia
- Viruses:
o Immunocompetent individuals -influenza
viruses type A and B, respiratory syncytial
virus, adenovirus, SARS virus, etc.
o Immunocompromised – CMV, herpes
- Chlamydia – Psittacosis (Ornithosis): transmitted
by inhalation of dried excreta of infected birds
- Rickettsia – Q fever due to Coxiella burnetti:
Transmitted by :
o Inhalation of dust particles w/ the organism
o Drinking unpasteurized milk from infected
o Working with infected cattle or sheep
o Unknown
Signs & Symptoms
- Acute Febrile Respiratory disease
- Patchy inflammation of alveolar septa and
interstitium
- No exudate
Serology: cold agglutinis present (mycoplasma)
Complication: cold autoimmune hemolytic anem
Fungal
- Some pathogenic, while others are opportunistic
infections of the - Spectrum of colonization and disease; host
lung
response influenced by immune status
- Characteristic geographic (endemic) regions
Severe Acute
Respiratory
Distress
Syndrome
(SARS)
- First: 2002 in Guandong Province of China
- 2-10 days incubation
- Corona virus
- Often necrotizing pneumonia  fulminant course  frequent death
Clinical
Labs/Histology
- Pneumonia in the immunocompromised
CMV “Owl Eyes”
- Mostly due to opportunistic infections
- Often more than one agent is involved
- Diffuse Infiltrates:
o Cytomegalovirus
o Pneumocystis carinii (esp. in AIDS)
o Drug reaction
- Focal Infiltrates:
o Gram negative rods
o Staphylococcus aureus
Pneumocystis carnii (H&E stain)
o Aspergillus
o Candida
Gross
- Patchy or may involve entire lobes, bilateral or
unilateral
- Red-blue, congested, subcrepitant
- Pleura smooth, pleural involvement infrequent
Microscopic Depends severity
- Interstitial inflammation
- Predominant pattern
- Alveolar septae widened by edema and chronic
inflammatory cells –lymphocytes, macrophages
and occasional plasma cells. Neutrophils may
be present in the acute phase
- Alveoli free of exudate
- Diffuse alveolar damage (DAD)
- Changes similar to ARDS
Pneumocystis Carnii (GMS stain)
- Coccidiodomycosis
- Aspergillus  Aspergilloma
- Cryptococcus neoformans  Immunocompromised hosts
- Mucormycosis (association with diabetes)
- Dry cough
Diagnosis
- Malaise
- PCR
- Myalgias
- Antibodies to virus
- Fever
Morphology
- Diffuse alveolar damage
- Multinucleated giant cells
- Corona viruses can be seen within pneumocytes by EM
Disease
Lung Abscess
Local
suppurative
process in the
lung
characterized by
necrosis of lung
tissue
Pathogenesis
Source: Bacteria
- Anerobic organisms like oral cavity flora ~ 60%
- Aerobic and anaerobic streptococci, S. aureus;
gram negative organisms
Aspiration of infective material
- Most common cause
- Associated with conditions in which cough reflex
is depressed, such as:
o Debilitation
o Alcoholism, acute
o Coma
o Anesthesia
Antecedent primary bacterial infection
- Postpneumonia – S. aureus, K. pneumoniae and
type 3 pneumococcus
- Fungal infections
- Bronchiectasis
Septic embolism
- Systemic veins or from right side of heart
Neoplasia –obstruction ~ 10-15% of cases
Miscellaneous
- Direct penetration of the lung
- Spread from neighboring organ
- Hematogenous seeding
Idiopathic –primary cryptogenic lung abscess
Clinical
Course
- Fever, productive cough- copious amounts of
sputum, generally foul smelling, purulent or
sanguineous
- Clubbing of fingers and toes
- Diagnosis suspected based on clinical signs and
symptoms
- Confirmed by X-ray and bronchoscopy
- Important to rule out cancer present in 10-15%
Resolution: w/antibiotics  no sequelae
Complications
- Extension of infection into the pleural cavity
- Septic emboli  brain abscess or meningitis
Gross:
- Size – variable
- Aspiration more common in right lung,
generally single (more vertical right bronchus)
- Pneumonia or bronchiectasis
 multiple, basal and diffusely scattered
- Septic emboli, hematogenous spread
 multiple and affect any region
- Cavity, filled with suppurative debris
- When communicating with an air space, partly
drained and may show air-fluid level
- Saprophytic infections may be superimposed
resulting in gangrene of the lung
- In chronic infections, fibroblastic proliferation
produces a fibrotic wall
Labs/Histology
Microscopic
- Cardinal histologic change – Suppurative
destruction of the parenchyma within the
central area of cavitation
Disease
Pulmonary
Tuberculosis
Pathogenesis
- Relatively uncommon cause of death in the
United States
- On the rise in the last decade – AIDS
- Emergence of highly drug-resistant strains
- Causative organism – Mycobacterium
tuberculosis
- After HIV, TB is the leading infectious cause of
death in the world.
Clinical
- Three forms:
o Primary pulmonary TB
o Secondary (reactivation) pulmonary TB
o Progressive pulmonary TB
 Cavitary fibrocaseous TB
 Miliary TB
- Tuberculous bronchopneumonia
Labs/Histology
Secondary TB
Gross
- ~ located in apex of one or both lungs
- Usually < 3.0 cm
Microscopic:
- Coalescent caseating granulomas
- Outcome: Heal spontaneously or with
therapy  fibrocalcific nodule
Primary TB - Infection of an individual Progressive pulmonary TB (Cavitary Fibrocaseous)
lacking a previous contact
- Erosion of a lesion into a bronchiole  cavity
- Primary pulmonary focus  Ghon
- Apical cavitary fibrocaseous TB
focus
- Advanced fibrocaseous TB
- Subpleural: just above / below the
Miliary TB
interlobar fissure between the upper - Infection gains access to the bloodstream and
and lower lobes
lymphatics and disseminates
- Primary focus + regional lymph node - Disseminated pulmonary spread: TB gains entry
into the pulmonary arteries
involvement  Ghon complex
Disseminated systemic spread: TB gains entry
- Asymptomatic  fibrosis and
into the pulmonary veins or lymphovascular
calcification
Miliary TB may be seen in either Primary or
- Progression to miliary TB
Secondary tuberculosis
Tuberculous Bronchopneumonia
Secondary TB - Previously sensitized
- In highly susceptible, highly sensitized individuals
- Reactivation – 5-10%
o Apex or posterior segments of the - Rapid spread of infection – “galloping
consumption”; bronchopneumonia or lobar
upper lobe, of one or both lungs
pneumonia
- Reinfection - less common
- Granulomas may not be seen; Acid fast bacilli
present
Miliary TB
Ghon Complex (primary TB)
Granuloma
Acid-fast bacili