Lung Infections

Introduction to Pulmonary Infections

Major cause of morbidity and immediate death

Etiologic agents

bacteria, including mycobacteria
fungi
viruses
mycoplasma

Definitions:

Consolidation: exudative solidification (intra- alveolar process)

Pneumonia: inflammation of alveolar portion of lung; usually used for infectious processes but may also refer to non-infectious processes like aspiration pneumonia, eosinophilic pneumonia, lipoid pneumonia

Pneumonitis: also refers to inflammation of alveolar wall but is more a histologic descriptive clinical term, often indicates a non- infectious process such as radiation pneumonitis, hypersensitivity pneumonitis

Defense Mechanisms

Nasal clearance: particles are removed by sneezing and blowing or are swallowed

Tracheobronchial clearance: Mucociliary action: particles are swallowed or expectorated

Alveolar clearance: alveolar macrophages:

digest particles or carry them to the bronchioles - propelled to oropharynx or
move to interstitial space - lymphatics - lymph nodes - bloodstream - bacteremia

Pathogenesis

Thousands of particles and microorganisms inhaled/day (viruses, bacteria and fungi)

Particles >10µm- deposited in the nose and upper airways; 3 to 10 µm lodge in trachea and bronchi

Particles 0.5 to 3µm (size of most bacteria) reach terminal airways and alveoli

Particles less than 0.5 to 1µm may remain suspended in air and can be exhaled

Lowering of host resistance –chronic diseases –immunologic deficiencies –immunosuppressive therapy –leukopenia

Impairment of local defense mechanisms

Loss or suppression of cough reflex: coma, anesthesia, neuromuscular disorders, drugs Þ aspiration

Injury to mucociliary apparatus: smoking, viral diseases, genetic

Interference with activity of alveolar macrophages: smoking, alcohol, anoxia, oxygen intoxication

Accumulation of secretions - cystic fibrosis, chronic bronchitis, bronchial obstruction

Pulmonary edema and congestion

Nosocomial infections

usually affects patients with chronic diseases – often involves bacteria resistant to antibiotics
results from U spread in weakened patient –invasive procedures –contamination of equipment

Microbial virulence factors

mucoid capsule of pneumococcus inhibits phagocytosis by macrophages

proteolytic enzymes by Staphylococcus aureus Þ necrotizing

Toxins: exo and endotoxins

Host response – products of inflammatory cells cause direct injury (proteases) – recruitment of other cells that cause injury (cytokines)

Routes of infection

Inhalation of infective organism
Aspiration of gastric or oropharyngeal contents
Penetrating injury or instrumentation
Hematogenous spread

Classification of Pneumonia by Morphology

lobar pneumonia – entire lung lobe is involved

Organisms gain entry to distal airspaces rather than by colonizing bronchi. Progresses as follows:

(1) Congestion and edema (many bacteria)
(2) Red hepatization (congestion, red cells, fibrin and few neutrophils)
(3) Gray hepatization (abundant neutrophils and fibrin)
(4) Resolution (proteases and antibiotics - clearing by macrophages)

bronchopneumonia (# 1form of pneumonia )- patchy involvement of small airways and surrounding alveoli

Inflammation starts in small bronchioles Þ Spreads to respiratory bronchioles and surrounding alveoli

Patchy, can become confluent and lobar if virulent organism or no treatment

interstitial pneumonia - inflammation located within alveolar walls (usually non bacterial)

Complications of Pneumonia

Abscess formation (tissue destruction and necrosis)

Organisms : Staph. aureus, anaerobes
Stages:

Acute suppurative stage

Chronic stage: fibrotic wall, organizing pneumonia in adjacent lung Healing: persistent open cavity
collapse and fibrosis

Empyema – spread of infection to the pleural space resulting in purulent pleural exudate.

Pathogenesis – most common: post-pneumonic

associated with lung abscess (anaerobes) –penetrating thoracic injury, including iatrogenic (drain tubes)
lymphatic or hematogenous dissemination –subdiaphragmatic infections (liver abscess)

Pathology

Acute = suppurative stage
Chronic organizing stage
dense fibrosis: compressive atelectasis - decortication may be needed •loculations: difficult to drain

Organization of exudate

Bacteremic dissemination to heart valves, pericardium, brain, kidneys, joints, etc.

Bacterial Pneumonia – Etiology

Aerobic gram positive cocci

pneumococcus Streptococcus pneumoniae •Encapsulated gram +

Most common cause of community-acquired pneumonia
Most often lobar pneumonia - antibiotics change the course
Can also cause nosocomial pneumonia
Bronchopneumonia pattern may occur
Capsule provides protection against phagocytosis

ß-hemolytic streptococcus

Staphylococcus aureus - large gram + cocci in clusters

Virulence factors: coagulase, hemolysins, hyaluronidase
Patterns: bronchopneumonia, frequently necrotizing that may evolve into abscess
Septic infarcts (from infected cardiac valves)
Pneumatocele - small children

Gram negative bacilli: Usually nosocomial; often affect debilitated or immunosuppressed hosts;

Usual pattern: bronchopneumonia that can be necrotizing

Haemophilus influenzae, E. coli,

Pseudomonas aeruginosa Þ necrotizing bronchopneumonia with zones of infarct - like necrosis

Klebsiella: causes lobar pneumonia

Serratia

Legionella pneumophila. •Contaminant of water supplies (air conditioning) Þ Hospital or community-acquired

Patterns: necrotizing bronchopneumonia or lobar pneumonia
Micro: Difficult to see by Gram stain; use Dieterle silver stain or direct immunofluorescence

Bacterial Organisms causing chronic pneumonia

Actinomyces israeli is slow growing anaerobic commensal of oral cavity and tonsils

Identified by gram positive branching filamentous bacteria that form yellow clusters resembling sulfur

Spreads by aspiration Þ Chronic suppurative pneumonia Þ Abscesses and fistulae

Nocardia asteroides: a filamentous gram +bacteria which stains weakly acid-fast + •No sulfur granules

Lung involvement is primary or secondary to blood stream
More common in immunocompromised patients •Chronic suppurative pneumonia with abscesses

Mycobacteria (TB covered elsewhere)

Fungi (OK it is not a bacteria but it can cause chronic pneumonia, you figure out where to put it).

Viral Pneumonia

Etiological agents:

Influenza A, B
Parainfluenza
Respiratory syncytial virus
Adenovirus
Herpes simplex
Varicella-Zoster
Cytomegalovirus
Measles

Etiological agents with inclusion bodies:

Adenovirus – nuclear
CMV – nuclear and cytoplasmic
Herpes/Varicella – nuclear
Measles – nuclear and cytoplasmic
RSV – cytoplasmic (rare)

Etiological agents without inclusion bodies: Influenza, Parainfluenza; Characterized by:

pneumonia with Bronchiolitis, Diffuse alveolar damage, lung hemorrhage and no inclusions.

Micro: histological features seen in viral pneumonia

Bronchiolitis: characterized by cellular inflammation Þ bronchiolitis obliterans (fibrous organization) Þ bronchiectasis; frequently seen in infant and small children.

caused by adenovirus, RSV, influenza, parainfluenza

Interstitial pneumonitis - chronic inflammation within alveolar walls. Caused by - CMV, measles

Diffuse alveolar damage - injury to the alveolar capillary wall unit with pulmonary edema, hyaline membranes and inflammatory cells

caused by CMV, influenza, parainfluenza, herpes, varicella, adenovirus

necrosis and neutrophils present in herpes and adenovirus

Features of some viral infections

Influenza - major cause of viral pneumonia in non- immunocompromised adults
Parainfluenza - cause of subglottic tracheitis (croup) in children
RSV: major cause of serious lower respiratory infections in children < 1 year.
Adenovirus - important cause of lower respiratory infections in infants and young children.
Varicella-Zoster - pneumonia occurs more commonly when adults contract varicella