1. Pathology of respiratory infections
    • Upper airways: laryngitis, croup
    • Bronchi/bronchioles: Whooping cough
    • Lung tissue:
  2. Pulmonary Defense Mechanisms
    • Upper respiratory tract: nasal filtration
    • Tracheobronchial tree: mucociliary escalator
    • Alveolar region: pulmonary macrophages
    • Immunologic factors: BALT, IgA
    • Biochemical factors: anti-proteases, antioxidants
  3. Upper respiratory tract: nose and mouth nasal filtration
    • removes large inhaled particles, trapped on top
    • As particles descend, they encounter the next defense mecanism
    • The mucosa of the bronchi
    • Smaller particles are picked up by macrophages
  4. Causes of Laryngitis
    • Tobacco smoke
    • Chemical reflux
    • Trauma-singing
    • Allergic
    • Usu part of URI
    • Viral, bacterial
  5. Croup
    • Under heading of childhood laryngoepiglottis – RSV, H. influenza, GAS
    • Seen primarily in infants and small children with a small airway (15%)
    • Croup usually due to parainfluenza virus
  6. Croup symptoms/signs
    • Edema of epiglottis and vocal cords
    • Small child has small airway obstruction
    • Inspirational stridor
    • Barking cough (like a seal)
    • Severe with hypoxia, cyanosis (1-2%)
  7. Acute infectious bronchitis causes
    • Viral infection: Influenza, adenovirus
    • Whooping cough:
    • Bortadella pertussis: Gram negative rod, exotoxins
  8. Pertussis Clinical signs and symptoms
    • Lasts 2-4 weeks
    • Fever, rhinitis, sneezing, prodrome
    • Violent coughing
    • May lead to vomiting, dehydration
  9. Bacterial Pneumonia-Sources
    • Community acquired:
    • S. Pneumoniae, H. influenza
    • Nosocomial:
    • Staph. aureus, Gram negatives
    • Opportunistic:
    • Pseudomonas, Pneumocystitis
    • CMV, adenovirus, herpes
  10. Bacterial Pneumonia-symptoms and physical findings
    • Bacterial invasion of the distal lung parenchyma
    • Pathology = purulent exudate and consilidation (solidification – many poly’s accumulate) of the lung
    • Clinical: fever, shaking chills, productive cough
    • Physical exam:
    • Dullness to percussion
    • Rales, bronchial breath sounds, fremitus, egophony
    • Chest x-ray infiltrates and air bronchograms
  11. Pathogenesis of Bacterial Pneumonia
    • Loss of suppression of cough reflex: Coma, anesthesia, etc.
    • Injury to mucociliary apparatus: one example is a viral
    • Increased secretions: CF
    • Imaired phagocytic activity of alveolar macrophages: alcohol, smoking
    • Immune suppression:
    • Pulmonary edema, CHF
    • Lung injury: COPD, viral pneumonia
    • Age, exposure to cold.
  12. Routes of Bacretial Infection in the lung
    • Airway route of spread:
    • Inhaled aerosols – environment or person
    • Aspirated secretions – conditions that favor colonization with pathogens or conditions that favor episodes of aspiration
    • Hematogenous:
    • Contiguous spread:
  13. Pathology of pneumonia
    • Acute: polys in the alveoli, macrophages later
    • Resolving: Polys gone, many macrophages, Infirtrates are cleared, alveolar walls intact – SEE FLUID AND INFILTRATES
    • Organizing: Granulation tissue in terminal bronchioles/alveoli – can cause fibrosis
    Bronchopneumonia is multifocal vs. lobar, a single or mostly one lobe is consolidated with the rest looking fine.
  15. Pores of Kohn
    In bronchopneumonia the infection can spread in between alveoli through these pores that can also be used in case one part is congested, the ventilation can be re-routed to another, healthy lung
  16. Bronchopneumonia begins where?
    Around a bronchiole – terminal bronchiole and infection can spread from lobule to lobule
  17. Lobar Pneumonia
    • Consolidation of entire lobe
    • Middle aged patients
    • Strep. Pneumoniae
    • Klebsiella
  18. Classic stages of Lobar Pneumonia
    • Congestion
    • Red hepatization – more congestion and some consolidation
    • Gray hepatization – less vascularity, many macrophages
    • Resolution – if patient is treated properly and consolidation goes away
  19. Gram Positive Bacterial Pneumonia: Pneumococcal pnemonia
    • Suppurative infection of lungs caused by Streptococcus pneumoniae
    • Leading cause of community acquired pneumonia
    • Classic organism responsible for lobar pattern of bacterial pneumonia, may also cause focal pneumonia
  20. Groups at high risk for Gram Positive Bacterial Pneumonia: Pneumococcal pneumonia
    • Persons with increased aspiration
    • Impaired humoral immunity
    • Defective macrophage clearance
  21. Complications of Gram Positive Bacterial Pneumonia: Pneumococcal pneumonia
    • Pleural effusion – can be complication of any pneumonia, exudate on the surface
    • Pleuritis
    • Empyema – an abscess within the pleural space – can form a capsule, a fibrous wall around it, may have a necrotic center, air-fluid level may appear on CXR
    • Bacteremia
    • Metastatic infections (meningitis, septic arthritis, endocarditis, purulent pericarditis)
    • Mortality significant, esp. in untreated; increased antibiotic resistance a concern, immunize at risk patients!
  22. Leading cause of community acquired pneumonia
    Gram Positive Bacterial Pneumonia: Pneumococcal pnemonia – streptococcus pneumoniae
  23. Lung Abscess Routes of Infection
    • Aspiration
    • Antecedent pneumonia
    • Bacteremia – infection comes from somewhere else
    • Distal to obstruction – bacterial within lung can’t be cleared
    • Local spread
  24. Pseudomonal Pneumonia
    • Confluent bronchopneumonia due to aspiration
    • Necrotizing pneumonia due to bacteremic spread
    • Nosocomial or opportunistic infection
    • Produces a horrible vasculitis (unlike other pneumonias): necrosis of tissue, areas bcome secondarily infected, etc.
  25. Legionell Pneumonia
    • Causative organisms named after outbreak of pneumonia in 1976 of American legion convention
    • Epidemic and sporadic cases follow inhalation of environmental aerosols (not person to person)
    • 10,000 estimated cases per year in U.S.
    • Systemic symptoms can precede signs of pneumonia
    • Has 25% mortality rate
    • Thrombocytopenia:
    • Renal Failure:
    • Respiratory failure:
    • Pathology – grossly broncopneumonia pattern
  26. Legionella
    • Motile, Gram negative – but only weakly gram-positive – so can’t Dx from it, BUT can use special silver stain – adapted to stain them and confirm (Dieterle silver stain)
    • Lives in aquatic environment: AC’s, hot water heaters, shower heads, warm, stagnant water
    • Organism lives and multiplies in macrophages
  27. Atypical – Interstitial Pneumonia
    • Interstitial inflammation rather than alveolar consolidation
    • Infectious agents difficult to identify with routine stains and cultures
    • Clinical presentation differs from usual pyogenic pneumonias
  28. Major agents causing atypical pneumonia
    • Mycoplasma pneumoniae
    • Viruses
    • Chlamydia
    • Coxiella burnetti
    • Others
  29. Interstitial Pneumonia – Interstitial Inflammation
    • Patchy involvement
    • No pleuritis
    • Septa wide with edema
    • Inflammation usually mononuclear
    • Injury to type 1 cells with hyaline membranes
  30. Mycoplasma Pneumoniae
    • One of 3 pathogens in humans
    • Bacteria-very small, once considered a virus
    • No cell wall – resistant to Penicillin
    • Attach to respiratory mucosa
    • Destroy epithelium
    • Aerosol transmission – bacterial nasal secretions
  31. Mycoplasma Pneumonia – public health
    • Worldwide
    • School child > 5yo
    • Close contact
    • Families, recruits
    • 2mln cases yearly
  32. Mycoplasma Pneumoniae – signs and symptoms
    • Most infections acute, self-limited – 90%
    • Fever, headache, etc
    • “walking pneumonia”
    • Patchy bronchiolitis
    • Interstitial inflammation (Polys, macrophages)
    • Danger of superimposed infection
  33. Influenza pneumoniae
    Acute, interstitial, common
  34. Viral Parainfluenza
    • Leless common
    • Less severe than influenza
    • Upper airway disease
    • Many cytoplasmic inclusions
    • No nuclear inclusions
    • Giant cells
    • Dx key: upper airway disease with giant cells and cytoplasmic inclusions
  35. Viral-parainfluenza pathology
    • Immunosupressed pts, recruits
    • Nechrotizing bronchiolitis
    • Dirty pneumonia: multi-focal, alveolar wall necrosis
    • Diffuse alveolar damage
    • Most important DX criteria: Basophilic inclusions, huge nuclei, full of viral DNA
  36. Viru-Herpes simplex
    • Type 1 and 2 Virus
    • Immunocompromised hosts
    • Typically produces: tracheobronchitis with ulcers
    • Can see nodular alveolar lesions
    • Necrosis of walls, polys
    • Large eosinophilic nuclear inclusions
  37. Virus-CMV
    • Extremes of age
    • Immunocompromised pts
    • Usually not really interstitial
    • Hemorrhagic nodules with necrosis
    • Owl eye nuclear inclusions and cytoplasmic inclusions
  38. Rickettsiae/orientia
    • Sptead by ticks and mites and louse
    • Obligate intracellular, aerobic bacteria: RMSF most common Rickettsial disease in US
    • Rickettsiae are gram negative rods
    • Pleiomorphic, coccobacillary
    • Animal and arthropod reservoirs; usually spread by arthropod vectors
  39. Q Fever
    • Coxiella
    • Reservoir in cattle, sheep
    • Common in herders, farmers
    • Spread by inhalation not ticks
    • 50 cases in U.S. yearly, prob underreported
  40. Coxiella burnetti
    • Gram nigative bacteria
    • Coccobacillary, pleiomorphic
    • Infects macrophages which phagocytize them
  41. Q Fever clinically
    • Two forms: chronic and acute
    • Acute pneumonia – worse
    • Fever, chills, myalgias, headache
    • No rash
    • SBE: Can develop bacterial endocarditis
    • There IS a vaccine!
  42. Pnemocystis Carinii Pneumonia PCP – now called Pneumocystis jiroveci
    • Fungus with trophozoites (2-12um), intracystic
    • Hosts-pts with low cell-mediated immunity
    • Reactivation of latent infection
    • Malnourished infants
    • Hematologic malignancies
    • Immunosuppression
    • AIDS
  43. Pnemocystis Carinii Pneumonia PCP – now called Pneumocystis jiroveci – clinical, Rx and Dx
  44. Clinical: Insiduous onset, fever, nonproductive cough
    • Dx: bronchoalveolar lavage – look for organisms – must be seen for Dx - in sputum
    • Treatment available: – PENTAMIDE
    • Pathology: alveoli filled with frothy, eosinophilic fluid and macrophages, many plasma cells in alveolar walls
    • Also for Dx: can use a GMS silver stain – oval-crescentic GMS+ cysts
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