PATHOLOGY OF THE REPIRATORY SYSTEM

Dr. Raghad Hanoon LEC.4

PULMONARY INFECTIONS:
 Pneumonia can be very broadly defined as any infection of the lung
parenchyma; Pneumonias are common cause of death.
 Could be bacterial (90% due to streptococcal pneumoniae), viral and fungal.
Predisposing factors:
1. Defect in immunity:
 Defect in humoral immunity & neutrophils pyogenic infection.
 Defect in cellular immunity Intracellular infections (tuberculosis,
viruses, pneumocystic carinii).
2. Cigarette smoking
 decrease in mucociliary clearance
 Affect pulmonary macrophages activity.
3. Alcohols
 Decrease cough & epiglottis refluxes.
 Increase aspiration
 Decrease neutrophils activity.
4. Head injury & surgery increase aspiration
5. Lung cancers & cystic fibrosis Pulmonary Obstruction increases
risk of pneumonia.
Classification of pneumonia:
1. According to anatomical (and radiographic) patterns
2. According to setting in which the pneumonia is occurred
3. Microbiological classification: it Could be: bacterial, Viral, fungal…
I. According to anatomical (and radiographic) patterns:
1) Bronchopneumonia showing a patchy distribution of inflammation that generally
involves more than one lobe. The initial infection is of the bronchi and bronchioles with
extension into the adjacent alveoli.
2) Lobar pneumonia, which affect the airspaces of part or all of a lobe; these are
homogeneously filled with an exudate that can be visualized on radiographs as a lobar
or segmental consolidation.
 The anatomic distinction between lobar pneumonia and
bronchopneumonia is often become blurred because:
1- many organisms can produce either of the two patterns of distribution
2- Confluent bronchopneumonia can be hard to distinguish radiologically from
lobar pneumonia.

II According to setting in which the pneumonia is occurred:

1. Community acquired bacterial pneumonia: characterized by
  This is the commonest type.
 Often follow viral upper respiratory tract infection.
 Streptococcus pneumoniae, or pneumococcus, is the most common cause of
community-acquired pneumonia.
 Haemophilus influenzae can cause life-threatening lower respiratory tract
infections and meningitis in children and is a common cause of pneumonia in
adults, especially those with COPD
 Moraxella catarrhalis: especially in the elderly; it exacerbates COPD and is a
common cause of pediatric otitis media.
 Staphylococcus aureus pneumonia often complicates viral illnesses and has a
high risk of abscess formation and empyema. Intravenous (IV) drug abusers are
at high risk of staphylococcal pneumonia in association with endocarditis.
 Klebsiella pneumoniae is the most common cause of Gram negative pneumonia;
it affects debilitated individuals, especially chronic alcoholics.
 Pseudomonas aeruginosa is a common cause of nosocomial infections with a
propensity to invade blood vessels and spread systemically; it is also common in
cystic fibrosis and neutropenic patients.
 Legionella pneumophilia: cause severe pneumonia in the immunocompromised
patient (particularly in organ transplant recipients).
 Mycoplasma pneumoniae: common among children and young adults. They
occur sporadically or as local epidemics in closed communities (schools,
military camps, prisons).
 Morphology of bacterial pneumonia
• Depending on bacterial virulence and host resistance, the same organism can
cause bronchopneumonia, lobar pneumonia.
 Bronchopneumonia
• The consolidation is patchy centered around inflamed bronchi that involve more
than one lobe (Multifocal & may be bilateral)
Grossly:
• The lungs exhibit focal areas (patches) of palpable consolidation.
• Lesions are multiple & may be bilateral.
Microscopically:
• There is a neutrophil-rich exudate fills the bronchi, bronchioles, and adjacent
alveolar spaces
 Lobar pneumonia
• Consolidation of a large portion of a lobe or of an entire lobe defines
• There are four stages of evolvement of lobar pneumonia, they are:
1- Congestion stage:
Grossly:
The lung is heavy, boggy, and red.
Microscopically:
Characterized by vascular engorgement, intraalveolar fluid with few neutrophils,
and often the presence of numerous bacteria.
2- Red hepatization:
Grossly:
• Lobe is red, firm, airless, look like a liver.
Microscopically:
• The inflammatory exudate composed of RBC, neutrophils and fibrin fill the
alveolar spaces
3- Gray hepatization:
Characterized by red cell disintegration but persistence of fibrinopurulent exudates.
Grossly:
• Gray –brownish, dry surface & firm.
Microscopically:
• The exudate within alveoli is fibrino-suppurative (WBC, fibrin and lysed RBC).
4- Resolution:
• Characterized by progressive enzymatic digestion of the exudates and
macrophage resorption of the debris, or organized by fibroblasts growing into it.
• Exudate resolution usually restores normal lung structure and function, but
organization with fibrous scarring can occur.
 The anatomic distinction between lobar pneumonia and
bronchopneumonia is often become blurred because:
1. Many organisms can produce either of the two patterns of distribution
2. Confluent bronchopneumonia can be hard to distinguish radiologically from lobar
pneumonia.
• Most important from the clinical standpoint are identification of the
causative agent and determination of the extent of disease.
 Symptoms of pneumonia (in general):
• Abrupt onset of high fever with shaking chills, pleuritic chest pain, cough
with mucopurulent (rusty) sputum. Occasionally hemoptysis.
 Diagnostic tests:
• Sputum examination: for Gram stain (numerous neutrophils contain diplococci).
(nonspecific because due to presence of normal flora)
• Blood culture: More specific, 20-30% is positive in early cases.
• CXR: The whole lobe is radiopaque in lobar pneumonia, whereas there are focal
opacities in bronchopneumonia.
Complications:
• 90% of cases will end up with resolution, otherwise complication includes:
1. Abscess formation because of tissue destruction and necrosis
2. Spread of infection to the pleural cavity empyema (pus inside the pleural
cavity).
3. Bacteremic dissemination cause meningitis, infective endocarditis, arthritis
4. Organization (fibrosis) of the exudate  part of the lobe will turn solid.
2. Community acquired atypical pneumonias:
• The most common causes are influenza types A and B, the respiratory syncytial
viruses, adenovirus, rhinoviruses, rubeola virus, and varicella virus Nearly all of
these agents also cause upper-respiratory tract infections (“common cold”).
  Morphology:
 Grossly:
• Patchy or lobar areas of congestion (red- blue areas) appear without the
consolidation of bacterial pneumonias (hence the term atypical pneumonia).
 Microscopically:
• Interstitial Pneumonia;
The inflammatory reaction is largely confined within the alveolar walls and
connective tissue of lung (interstitial tissue). Alveolar walls widened by edema &
inflammatory infiltrate of lymphocytes, histiocytes, and occasionally plasma cells.
• In contrast to bacterial pneumonias alveolar
spaces are free of cellular exudates. Superimposed bacterial infection, as
expected, results in a mixed histologic picture.
3- Nosocomial Pneumonia (hospital-acquired):
 Defined as "pulmonary infections acquired in the course of a hospital stay".
 They are common in hospitalized persons with severe illness, immune
suppression, or prolonged antibiotic therapy and those on mechanical ventilation
are also susceptible.
 Gram negative rods (Klebsiella spp., Escherichia coli and Pseudomonas spp.)
and Staphylococcus aureus are the most common cause.
4- Aspiration Pneumonia:
 Occurs in markedly debilitated patients or those who aspirate gastric contents
either while unconscious (e.g., after a stroke) or during repeated vomiting.
 The resultant pneumonia is partly chemical, resulting from the extremely irritating
effects of the gastric acid, and partly bacterial.
 This type of pneumonia is often necrotizing with a fulminant clinical course. In
those who survive, abscess formation is a common complication.
5- Necrotizing pneumonia & Lung Abscess
 Necrotizing pneumonia often coexists or evolves into lung abscess, making the
distinction between the two somewhat subjective.
Lung abscess
• Define as necrosis of pulmonary parenchyma and formation of cavity containing
necrotic debris and fluids or pus.
• The formation of multiple small abscesses in lung parenchyma is referred as
necrotizing pneumonia.
Clinically:
• Cough, copious amount of foul smell sputum and fever.
Complications:
• Extension into the pleural cavity (Empyema), hemorrhage, septic embolization,
and secondary amyloidosis.
Pathogenesis:
These microorganisms reach lungs via the followings mechanisms:
1) Aspiration of infected material from carious teeth, infective sinuses or tonsils, this is
occurring during oral surgery & anesthesia, acute alcoholism, coma, in which the
cough reflexes are depressed.
2) Aspiration of gastric contents
3) Complications of necrotizing bacterial pneumonia (staph. aureus, sterpto. Pyogenes,
& pseudomonas).
4) Bronchial obstruction: particularly with bronchogenic cancers; Obstruct the bronchi,
impaired drainage of secretion & increase risk of abscess formation.
5) Septic embolism from infective endocarditis of right side of heart or from septic
thrombophlebitis.
6) Hematogenous spread of bacteria (Staphylococcal Bacteremia).
7) Direct traumatic penetrations of the lungs; spread of infections from a neighboring
organ, such as pleural cavity.
Gross:
• Various size cavities, filled with pus.
• Those occure on right side are mostly due to aspiration (more vertical airway).
• Those follow pneumonia & Bronchiactasis are multiple, basal in locations
Microscopically:
Suppurative inflammation, necrosis &destruction of the lung parenchyma
6- Chronic Pneumonia:
• Localized lesion in an immunocompetent person, with or without regional
lymph node involvement.
• There is typically granulomatous inflammation, which may be due to
bacteria (e.g., M. tuberculosis; discussed in infection) or fungi.
• In the immunocompromised, there is usually systemic dissemination of the
causative organism, accompanied by widespread disease.
Fungal pneumonia:
• Histoplasmosis, Coccidioidomycosis and Blastomycosis
• Mainly caused by Histoplasma capsulatum, Coccidioides immitis and
Blastomyces dermatidis.
• Most are asymptomatic and result in only limited granulomatous disease;
however, immunocompromised can cause fulminant, widespread dissemination.
• Initiated by delayed-type hypersensitivity response to the organism.
• The lesions develop in to small granulomas with giant cells, may develop central
necrosis and later fibrosis and calcification
• Should be differentiated from tuberculosis; by identification of the yeast forms
which are best seen with periodic acid- Schiff or silver stains.
7- Pneumonia in the Immunocompromised Host
• A wide variety of opportunistic microorganisms, many of which rarely cause
infection in normal hosts, but can cause life-threatening pneumonias in the
immunocompromised host.
Examples of pulmonary opportunistic pathogens include;
1. Bacteria (Pseudomonas aeruginosa, Mycobacterium spp., etc)
2. Viruses (cytomegalovirus and herpesvirus )
3. Fungi (Pneumocystis jiroveci, Candida spp., Aspergillus spp.,
and Cryptococcus neoformans).