1. Pulmonary Infections : PNEUMONIAS Dr. Mohammad Abdulhameed Alqudah Assistant Professor Consultant Pathologist

2. Lecture goals Acute Pulmonary infections (Pathology) 1.Define pneumonia and pneumonitis. 2.Clarify pneumonias according to etiology & morphological patterns. 3.Compare bacterial & nonbacterial pneumonias. 4.Outline the events in the resolution of the pneumonic process. 5.List the possible complications of pneumonia. 6.Discuss the causes, morphology and outcome of lung abscess. Chronic Pulmonary infections. (Pathology) 1.Define atypical pneumonia & discuss its etiology & pathology. 2.Be familiar with lung infections in the immunocompromised host.

3. Respiratory tract infections are more frequent than infections of any other organ. They account for the largest number of workdays lost in the general population. The vast majority are upper respiratory tract infections caused by viruses (common cold, pharyngitis). Bacterial, viral, mycoplasmal, and fungal infections of the lung (pneumonia) still account for an enormous amount of morbidity and are responsible for one sixth of all deaths in the United States.

4. Definition of Pneumonia : Pathological : Infection of lung parenchyma distal to the terminal bronchioles. Clinical Constellation of symptoms & signs with at least one opacity on chest x-ray.

5. The clinical presentation may be as an acute, fulminant clinical disease or as a chronic disease with a more protracted course. The histologic spectrum of pneumonia may range from a fibrinopurulent alveolar exudate seen in acute bacterial pneumonias, to mononuclear interstitial infiltrates in viral and other atypical pneumonias, to granulomas and cavitation seen in many of the chronic pneumonias.

6. Acute bacterial pneumonias can manifest as one of two anatomic and radiographic patterns, referred to as bronchopneumonia and lobar pneumonia.

8. Bronchopneumonia implies a patchy distribution of inflammation that generally involves more than one lobe. This pattern results from an initial infection of the bronchi and bronchioles with extension into the adjacent alveoli.

9. Lobar pneumonia the contiguous air spaces of part or all of a lobe are homogeneously filled with an exudate that can be visualized on radiographs as a lobar or segmental consolidation. Streptococcus pneumoniae is responsible for more than 90% of lobar pneumonias.

10. The anatomic distinction between lobar pneumonia and bronchopneumonia can often become blurry, because: 1) Many organisms cause infections that can manifest with either of the two patterns of distribution. 2) Confluent bronchopneumonia can be hard to distinguish radiologically from lobar pneumonia.

11. Therefore, it is best to classify pneumonias either by the specific etiologic agent OR If no pathogen can be isolated, classify them by the clinical setting in which infection occurs.

12. Classification according to clinical setting will considerably narrows the list of suspected pathogens for administering empirical antimicrobial therapy.

13. Factors in Pathogenesis Microbial factors  Capsule (pneumococcus)  IgA protease (pneumococcus, neisseria)  Others – ciliostatic factor…etc Host factors  Impaired host defence  Hypogammaglobulinaemia, phagocytic or ciliary dysfunction, neutropenia, lymphopenia  Anatomical defects  Bronchus obstruction, bronchiectasis  Genetic factors

14. Impairment of defense mechanisms leading to pulmonary infections : 1- Loss or suppression of cough reflex : coma, general anasthesia, neuromuscular disease, drugs. 2- Injury to mucociliary blanket : smoke, viral, alcohol, gases, obstruction, cystic fibrosis. 3- Decrease in macrophage function : alcohol, smoking, phagocyte killing defects.

15. 4- Impaired immune system : chronic diseases, acquired or congenital immune deficiency, aging. 5- Existing pulmonary disease: atelectasis, edema, COPD. 6- Unusually virulent infecting organism

16. Cigarette smoke compromises mucociliary clearance and pulmonary macrophage activity. Alcohol impairs cough and epiglottic reflexes, thereby increasing the risk of aspiration, AND interferes with neutrophil mobilization and chemotaxis.

18. Diagnosis : History Examination : percussion, auscultation. Blood picture: CBC & acute phase reactants. Isolation of microbe :  sputum  blood culture  pleural fluid  serology Chest X ray

19. Morphological patterns of pneumonia LOBAR PNEUMONIA BRONCHO-PNEUMONIA INTERSTITIAL PNEUMONIA MILIARY (usually TB)

20. Lobar Pneumonia

21. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 30 April 2008 02:55 PM) © 2007 Elsevier LOBAR PNEUMONIA

22. Bronchopneumonia

24. Pneumonia can arise in seven distinct clinical settings, and the implicated pathogens are reasonably specific to each category.

25. Classification of pneumonias Community- Acquired Acute Pn. Community- Acquired Atypical Pn. Nosocomial Pneumonia Aspiration Pneumonia Lung Abcess Chronic Pneumonia Pneumonia in the Immunocompromised host

26. Community-Acquired Pneumonia Risk factors:  Dependent on organism.  Alcoholism, asthma, immunosuppression, age >70, smoking, COPD, dementia, seizures, CHF … Aetiology:  Bacteria, fungi, viruses, parasites.  Common – s. pneumoniae, h. influenzae, s. aureus, m. pneumoniae, c. pneumoniae, influenza, adenoviruses, respiratory syncytial virus.

28. Pneumococcal Pneumonia : Pathology : CONSOLIDATION Hardening of lung parenchyma due to presence of exudate in alveolar spaces.  Acute onset of fever, cough, rust coloured sputum & chest pain.  Pathology: Usually LOBAR, but Bronchopneumonia can happen also.

29. There are 4 stages of evolution (lobar):  CONGESTION 1-2 days  RED HEPATIZATION 2-4 days  GREY HEPATIZATION 4-8 days  RESOLUTION 8-9 days

30. 1- Congestion  Heavy red lungs Severe vascular congestion Intra alveolar exudate with neutrophils Watery sputum Bacteria +++

31. 2- Red hepatization  Firm airless, liver-like lung  Fibrinopurulent pleuritis  Intra alveolar exudate : organisms ++ cells: * erythrocytes * neutrophils * fibrin * rusty sputum

32. 3- Grey hepatization : Dry grey brown cut surface ↑ intra alveolar fibrin & macrophages Disintegrating neutrophils & ↓ RBC’s 4- Resolution : Enzymatic digestion of exudate  resorption, phagocytosis, sometimes with residual adhesion

33. Stages of Bacterial Pneumonia

34. Bronchopneumonia  Patchy consolidation involving one or several lobes.  Usually affects lower & posterior portions of lung.  Neutrophilic exudate centred in bronchi & bronchioles with spread to adjacent alveoli.

35. Clinical Manifestations Typical Symptoms :  Fever  Cough  Expectoration of sputum  Pleuritic chest pain  Chills, rigors  SOB

36. Clinical Manifestations Physical signs  Tachypnoea  Single most useful sign for assessing severity: RR >30 bpm  Dullness to percussion.

37. Other common causes of acute pneumonias in the community - H. influenzae and M. catarrhalis (both associated with acute exacerbations of COPD). - S. aureus (usually secondary to viral respiratory infections). - K. Pneumoniae (observed in patients who are chronic alcoholics). - P. aeruginosa (seen in persons with cystic fibrosis, in burn victims, patients with neutropenia). - L. pneumophila, seen particularly in organ transplant recipients.

38. B- Community acquired (Atypical)  A group of pneumonias caused by atypical bacteria or nonbacterial agents:  Mycoplasma Pneumoniae  Viruses - Resp.syncitial virus, measles parainfluenza, adenoviruses, CMV…..  Chlamydia - Psittacosis  Rickettsiae

39. Nearly all of these agents can also cause a primarily upper respiratory tract infection (“common cold”). They can develop pneumonia if not treated properly when they are still in the phase of upper respiratory tract infection (“common cold”).

40. Mycoplasma pneumoniae being the most common. Mycoplasma infections are particularly common among children and young adults. They occur sporadically or as local epidemics in closed communities (schools, military camps, prisons)

41. Pathology Inflammatory process predominantly involving the interstitium  May be patchy or diffuse  Alveolar septa contain infiltrate of lymphocytes, macrophages, plasma cells  Little exudate in alveoli

42. Interstitial Pneumonia

43. - Clinical picture : insidious onset minimal dry cough, minimal expectoration, minimal  WBC’s, NO Consolidation - Radiological picture : Transient ill defined patches, mainly in lower lobes - In case of viruses, viral inclusions are seen. - In mycoplasma: cold agglutinin present.

44. Because the edema and exudation are both in a strategic position to cause an alveolocapillary block, there may be respiratory distress seemingly out of proportion to the physical and radiographic findings.

45. Hospital-Acquired (Nosocomial) Pneumonia Pneumonia occurring at least 48 hrs after admission. Bacterial not viral.  Incidence 6-20x higher among mechanically ventilated patients

47. Pathogenesis Poor infection control measures Prolonged & inappropriate use of antibiotics  spread of antibiotic resistant virulent organisms Endotracheal intubation  Serves as direct bacterial conduit.  Prevents effective coughing.  Damages tracheal epithelium.  Accumulation of oropharyngeal secretions.

48. Aetiology Causative organisms:  Mostly gram-negative bacilli  P. aeruginosa, K. pneumoniae  Gram positive :S. aureus is the most common cause of nosocomial pneumonia in the US

49. Nosocomial Pneumonias : Pseudomonas aeruginosa pneumonia Bronchopneumonia, high mortality. Patients : neutropenic cancer patients, burn patients, ventilator associated… Pathology : abscess formation & empyema with prominent vascular invasion  vasculitis, hemorrhage & necrosis (Necrotizing Pneumonia )

50. CYSTIC FIBROSIS PATIENTS WITH PNEUMONIA ARE PRESUMED TO HAVE PSEUDOMONAS UNTIL PROVEN OTHERWISE.

51. Staphylococcal pneumonia : Severe abscessing broncho - pneumonia with destruction. Risk : children - cystic fibrosis or postviral Adults - COPD, IV drug addicts.

52. Aspiration Pneumonia :  Aspiration from oropharyngeal secretion or acid gastric contents.  Patient : weak, with depressed sensation & control of hypopharynx, repeated vomiting. e.g. post anasthesia & paralysed patient.  Mixed bacterial infection + Acid Chemical damage + consolidation.  Severe Necrotizing Pneumonia

53. Microaspiration, by contrast, occurs in many people, especially those with gastro-esophageal reflux. It may exacerbate other lung diseases but does not lead to pneumonia.

54. Lung abscess Lung abscess refers to a localized area of suppurative necrosis within the pulmonary parenchyma, resulting in the formation of one or more large cavities.

55. Lung Abscess: Pathogenesis : 1- Aspiration of infective material. 2- Aspiration of gastric contents. 2- Post pneumonic. 3- Bronchial obstruction. (tumor) 4- Infection in existing cavities or cysts. 5- Septic embolism. 6- Bacteremic seeding. (In aspiration cases: more in right, single & upper.) (In pnumonia cases: more basal,multiple)

56. Lung Abscess

57. Fate & complications of lung abscess: 1- Healing by fibrosis leaving a sterile cavity. 2- Rupture with partial drainage of material *Radiological picture  Air- Fluid level *Rupture into pleura  Empyema *Rupture into bronchus  Bronchopneumonia 3- Bronchopleural fistula  Pneumothorax 4- Septic emboli. 5- Lung hemorrhage from vessels in fibrous wall

58. Complications of bacterial pneumonias : 1- Pleural effusion 2- Non resolution and organization of exudate  fibrosis 3- Abscess formation 4- Bacteremic dissemination  meningitis, arthritis, infective endocarditis 5- Empyema : accumulation of pus in pleural cavity which is followed by adhesions 6- Atelectasis

59. Empyema

60. Key notes on Acute pneumonias: S. pneumoniae (the pneumococcus) is the most common cause of community- acquired acute pneumonia, and the distribution of inflammation is usually lobar. Morphologically, lobar pneumonias evolve through four stages: congestion, red hepatization, gray hepatization, and resolution. Other common causes of acute pneumonias in the community include H. influenzae and M. catarrhalis (both associated with acute exacerbations of COPD), S. aureus (usually secondary to viral respiratory infections), K. pneumoniae (observed in patients who are chronic alcoholics), P. aeruginosa (seen in persons with cystic fibrosis, in burn victims, and in patients with neutropenia), and L. pneumophila, seen particularly in organ transplant recipients.

61. - In contrast with acute pneumonias, atypical pneumonias are characterized by respiratory distress out of proportion to the clinical and radiologic signs, and by inflammation that is predominantly confined to alveolar septa, with generally clear alveoli. - The most common causes of atypical pneumonias include those caused by M. pneumoniae, viruses including influenza viruses types A and B, human metapneumovirus, C. pneumoniae, and C. burnetii (agent of Q fever).

62. CHRONIC PNEUMONIAS