1. Pulmonary infections (Pneumonia)
Pneumonia can be very broadly defined as any infection in the lung

2. Pulmonary infections
Respiratory tract infections are more frequent than infections of any other organ and account for the largest number of workdays lost in the general population, why?
The epithelium of the lung is exposed to liters of contaminated air
Nasopharyngeal flora are aspirated during sleep
Underlying lung diseases render the lung parenchyma vulnerable to virulent organism.

3. Pulmonary infections
Upper respiratory tract infection are common, caused mainly by viruses (common cold, pharyngitis)
Infection of the lung by virus, mycoplasma, bacteria and fungi account for enormous amount of morbidity and mortality.

4. Pathogenesis of pneumonia
Each day, the respiratory tract is exposed to more
than 10,000 liters of air containing hazardous dust,
Chemicals and microorganisms.
Particle > 10 mm deposited in nose.
Particle 3-10 mm impacted in trachea and bronchi.
Particle 1-3 mm (bacteria) deposited in terminal airways and alveoli.
Smaller particles < 1 mm may remain suspended in air.
Normal lung is free from bacteria.

5. Pathogenesis of pneumonia
Pneumonia can result whenever:
defense mechanisms are impaired
the resistance of the host in general is lowered.

6. Pulmonary host defenses
Upper airways:
Nasopharynx:
Oropharynx
Nasal hair, turbinates, mucociliary apparatus, IgA secretion
Saliva, sloughing of epithelium, local complement production, interference from resident flora

7. Pulmonary host defenses
Upper airways:
Conducting airways (trachea and bronchi):
Cough, epiglottic reflexes, sharp angled branches of the airways, mucociliary apparatus, Immunoglobulin (IgM, IgG, and IgA) secretion

8. Pulmonary host defenses
Upper airways:
Conducting airways (trachea and bronchi):
Lower respiratory tract:
Alveolar lining fluid ( surfactant, immunoglobulin, complement and fibronectin), Cytokines (IL-1, TNF), alveolar macrophages, polymorphonuclear leukocyte, cell mediated immunity

9. Pathogenesis of pneumonia
Impaired defense mechanisms:
Loss or suppression of the cough reflex,
as a result of coma, anesthesia, neuromuscular disorders, drugs, or chest pain.
Injury to the mucociliary apparatus,
by either impairment of ciliary function or destruction of ciliated epithelium e.g. cigarette smoke, inhalation of hot or corrosive gases, viral diseases, or genetic disturbances
Interference with the phagocytic or bactericidal action of alveolar macrophages
by alcohol, tobacco smoke, anoxia, or oxygen intoxication
Pulmonary congestion and edema
Accumulation of secretions
e.g. cystic fibrosis and bronchial obstruction
Defect in innate immunity
Include neutrophil, complement, humoral and cell mediated immune defects

11. Pathogenesis of pneumonia
Defects in innate immunity (including neutrophil and complement defects) and humoral immunodeficiency lead to an increased incidence of infections with pyogenic bacteria.
Cell-mediated immune defects lead to increased infections with intracellular microbes such as mycobacteria ,herpesviruses and Pneumocystis jiroveci.
Several exogenous aspects of lifestyle interfere with host immune defense mechanisms and facilitate infections.
Examples:
cigarette smoke compromises mucociliary clearance and pulmonary macrophage activity
alcohol not only impairs cough and epiglottic reflexes, thereby increasing the risk of aspiration, but also interferes with neutrophil mobilization and chemotaxis.

12. Pathogenesis of pneumonia
General factors that affect resistance:
chronic diseases
immunologic deficiency
treatment with immunosuppressive agents
leukopenia
unusually virulent infections.

13. Pathogenesis of pneumonia
One type of pneumonia sometimes predisposes to another, especially in debilitated patients.
Portal of entry for most pneumonias is the respiratory tract, hematogenous spread from one organ to other organs can occur.
Many patients with chronic diseases acquire terminal pneumonias while hospitalized (nosocomial infection).

14. Pathogenesis of pneumonia
Pneumonia can be acute or chronic
The histologic spectrum may vary from fibrinopurulent alveolar exudate to mononuclear interstitial infiltrates to granulomatous inflammation

15. Bacterial pneumonia
Bacterial invasion of lung parenchyma evoke exudation of fibrinpurulent fluid in the alveoli and solidification.
Classification may be made according to causative agent or gross anatomic distribution of the disease.

16. Anatomic distribution of pneumonia
Bronchopneumonia:
-Represent an extension from preexisting
bronchitis or bronchiolitis.
-Extremely common tends to occur in two
extremes of life.
Lobar pneumonia:
- Acute bacterial infection of a large
portion of a lobe or entire lobe.
-Classic lobar pneumonia is now infrequent.

18. Lobar pneumonia
% are caused by pneumococci
(type 1,3,7 & 2)
- Rare agents: K. pneumoniae
staphylococci - streptococci
H. influenzae - Pseudomonas and Proteus
Bronchopneumonia
– most common agents are:
Streptococcus pneumonea,
Haemophilus Influenza,
Pseudomonas Aeroginosa
coliform bacteria.

19. Overlap of the two patterns often occur.
Identification of clinical pattern is more important.

20. The pneumonia syndromes
Community-Acquired Acute Pneumonia
Community-Acquired Atypical Pneumonia
Nosocomial Pneumonia
Aspiration Pneumonia
Chronic Pneumonia
Pneumonia in the Immunocompromised Host

21. The pneumonia syndromes
Community-Acquired Acute Pneumonia
Community-Acquired Atypical Pneumonia
Nosocomial Pneumonia
Aspiration Pneumonia
Chronic Pneumonia
Pneumonia in the Immunocompromised Host

22. Etiology of pneumonia Community-Acquired Acute Pneumonia
Bacterial
Can follows viral URT infection
Sudden onset of high fever, chills, pleuritic chest pain and productive cough, may be with hemoptysis
Streptococcus pneumoniae is the most common cause of Community-Acquired Acute Pneumonia
Frequently affected pt. are those with:
Underlying chronic disease e.g. DM, COPD, and congestive heart failure
Congenital or acquired immune deficiency
Decreased or absent splenic function
Other causative organisms are:
Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, Legionella pneumophila, Enterobacteriaceae (Klebsiella pneumoniae) and Pseudomonas spp.

23. Staphylococcus aureus
S. aureus is an important cause of secondary bacterial pneumonia in children and healthy adults after viral respiratory illnesses (e.g., measles in children and influenza in both children and adults).
Staphylococcal pneumonia is associated with a high incidence of complications, such as lung abscess and empyema.
Staphylococcal pneumonia occurring in association with right-sided staphylococcal endocarditis is a serious complication of intravenous drug abuse.
It is also an important cause of nosocomial pneumonia

24. Haemophilus influenzaeBoth
encapsulated and unencapsulated forms are important causes of community-acquired pneumonias.
The former can cause a particularly life-threatening form of pneumonia in children, often following a respiratory viral infection.
Adults at risk for developing infections include those with chronic pulmonary diseases such as chronic bronchitis, cystic fibrosis, and bronchiectasis
H. influenzae is the most common bacterial cause of acute exacerbation of COPD.

25. Pseudomonas aeruginosa
it is associated with infections in cystic fibrosis,
P. aeruginosa is most commonly seen in nosocomial
Pseudomonas pneumonia is also common in persons who are neutropenic, usually secondary to chemotherapy; in victims of extensive burns; and in those requiring mechanical ventilation.
P. aeruginosa has a propensity to invade blood vessels at the site of infection with consequent extrapulmonary spread

26. Morphology of pneumonia Community-Acquired Acute Pneumonia
Lobar or bronchopneumonia may occur.
The lower lobes or the right middle lobe are most frequently involved.
Widespread fibrinosuppurative consolidation.

27. Community-Acquired Acute Pneumonia Stages of pneumonia
Congestion – lobes are heavy, red and boggy; histologically, vascular congestion can be seen with proteinaceous fluid, scattered neutrophils and many bacteria in the alveoli.
Red hepatization – alveolar spaces are packed with neutrophils, red cells, and fibrin, pleura – fibrinous or fibrinopurulent exudate.
Gray hepatization – lung is dry, gray and firm and the fibrinous exudate persists within the alveoli.
Resolution – exudates within the alveoli are enzymatically digested.

28. Community-Acquired Acute Pneumonia Morphology of pneumonia
Congestion –
vascular congestion can be seen with proteinaceous fluid,
scattered neutrophils and many bacteria in the alveoli.
Red hepatization –
alveolar spaces are packed with neutrophils, red cells, and fibrin, pleura
fibrinous or fibrinopurulent exudate

29. Community-Acquired Acute Pneumonia
Stages of pneumonia
Gray hepatization –
fibrinous exudate persists within the alveoli.

30. Community-Acquired Acute Pneumonia
Stages of pneumonia
Resolution – exudates within the
alveoli are enzymatically digested.

31. Clinical features
Abrupt onset of high fever, shaking chills, and cough productive of mucopurulent sputum; occasional patients may have hemoptysis.
When fibrinosuppurative pleuritis is present, it is accompanied by pleuritic pain and pleural friction rub

32. Complications of pneumonia
Tissue destruction (abscess).
Empyema.
Organization of alveolar exudate – solid fibrinous tissue.
Bacteremic dissemination may lead to meningitis, arthritis or infective endocarditis.

33. Community-Acquired Acute Pneumonia
Dx & Rx
Examination of Gram-stained sputum smear is helpful in diagnosis
Blood culture is more specific (only +ve in 20% to 30% of pt.)
Pneumococcal pneumonia respond to penicillin Rx

34. Acute Pneumonias
S. pneumoniae (pneumococcus) is the most common cause of community-acquired acute pneumonia
Other common causes of acute pneumonias in the community include:
H. influenzae and Moraxella catarrhalis (both associated with acute exacerbations of COPD)
S. aureus (usually secondary to viral respiratory infections),
K. pneumoniae (observed in chronic alcoholics),
P. aeruginosa (seen in individuals with cystic fibrosis, in burn patients and in neutropenics),
L. pneumophila, seen particularly in individuals who have undergone organ

35. The pneumonia syndromes
Community-Acquired Acute Pneumonia
Community-Acquired Atypical Pneumonia
Nosocomial Pneumonia
Aspiration Pneumonia
Chronic Pneumonia
Pneumonia in the Immunocompromised Host

36. Community-Acquired Atypical Pneumonia: Primary atypical pneumonia
Pt. Usually present with flulike symptoms with pharyngitis evolved into laryngitis, trachiobronchitis and pneumonia with little sputum and no lung consolidation
Mycoplasma pneumoniae, Chlamydia spp. (C. pneumoniae, C. psittaci, C. trachomatis)
Coxiella burnetti (Q fever)
Viruses: respiratory syncytial virus, parainfluenza virus (children); influenza A and B (adults); adenovirus and SARS virus
Mycoplasma pneumoniae is associated with production of IgM antibody ( this react with red cells having I antigen leading to hemagglutination of cooled blood)

37. Community-Acquired Atypical Pneumonia Primary atypical pneumonia
Circumstances that favor extension to lower respiratory tract:
malnutrition
Alcoholism
underlying debilitating disease.

38. Community-Acquired Atypical Pneumonia: Primary atypical pneumonia
Acute febrile respiratory disease characterized by patchy inflammatory infiltration by lymphocyte and plasma cells largely confined to the alveolar septa and pulmonary interstitium- (Interstitial pneumonitis).

39. Community-Acquired Atypical Pneumonia Primary atypical pneumonia
Gross:
Pneumonic involvement may be patchy, or involve whole lobes bilaterally or unilaterally.
Affected areas are red-blue congested.
Micro:
Predominant interstitial inflammatory reaction.
Alveolar septa are widened and edematous with mononuclear inflammatory infiltrate (and neutrophils in acute cases only).
Intra-alveolar proteinaceous material with pink hyaline membrane lining the alveolar walls (diffuse alveolar damage).

40. Community-Acquired Atypical Pneumonia Primary atypical pneumonia
Clinical course:
Extremely variable course.
URTI life-threatening infection.
Commonly:
- bronchopneumonia.
- mycoplasma – lobar pneumonia.
Identification of the organism is difficult.
Treatment: antibiotic.
Prognosis in uncomplicated pt. is good

41. Severe Acute Respiratory Syndrome (SARS)
first appeared in November of 2002 in China
Between fall of 2002 and spring of 2003, there were more than 8,000 cases of SARS, including 774 deaths
SARS begins with a dry cough, malaise, myalgias, fever and chills
A third of patients improve and resolve the infection, but the rest progress to severe respiratory disease with shortness of breath, tachypnea, and pleurisy and nearly 10% of patients die from the illness
Caused by coronaviruses, however the SARS virus differs from previously known coronaviruses in that it infects the lower respiratory tract and spreads throughout the body.

42. Summary
Atypical pneumonias are characterized by respiratory distress out of proportion to the clinical and radiologic signs, and 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 types A and B, C. pneumoniae, and C. burnetti (Q fever).

43. The pneumonia syndromes
Community-Acquired Acute Pneumonia
Community-Acquired Atypical Pneumonia
Nosocomial Pneumonia
Aspiration Pneumonia
Chronic Pneumonia
Pneumonia in the Immunocompromised Host

44. Nosocomial pneumonia Nosocomial Pneumonia:
Hospital acquired Pneumonia
Common in pt. with sever underlying conditions e.g. immunosuppression, prolonged antibiotic therapy, intravascular catheter and pt. with mechanical ventlator
Organism include:
Gram-negative rods belonging to Enterobacteriaceae (Serratia marcescens, Escherichia coli, Klebsiella spp.), Pseudomonas spp. and Staphylococcus aureus (usually penicillin-resistant)

45. The pneumonia syndromes
Community-Acquired Acute Pneumonia
Community-Acquired Atypical Pneumonia
Nosocomial Pneumonia
Aspiration Pneumonia
Chronic Pneumonia
Pneumonia in the Immunocompromised Host

46. Aspiration pneumonia Aspiration Pneumonia
Occur in debilitated patients or those who aspirated gastric contents
Chemical injury due gastric acid and bacterial infection including:
Anaerobic oral flora (Bacteroides, Prevotella, Fusobacterium, Peptostreptococcus), admixed with aerobic bacteria (Streptococcus pneumoniae, Staphylococcus aureus, Haemophilas influenzae, and Pseudomonas aeruginosa)
A necrotizing pneumonia with fulminant clinical course, common complication (abscess) and frequent cause of death.

47. The pneumonia syndromes
Community-Acquired Acute Pneumonia
Community-Acquired Atypical Pneumonia
Nosocomial Pneumonia
Aspiration Pneumonia
Chronic Pneumonia
Pneumonia in the Immunocompromised Host

48. Chronic pneumonia
is most often a localized lesion in an immunocompetent person, with or without regional lymph node involvement.
There is typically granulomatous inflammation,
may be due to bacteria
(e.g., M. tuberculosis) or
fungi
(Histoplasma capsulatum, Coccidioides immitis, Blastomyces )
In the immunocompromised, there is usually systemic dissemination of the causative organism, accompanied by widespread disease.
Tuberculosis is by far the most important entity within the spectrum of chronic pneumonias.

49. The pneumonia syndromes
Community-Acquired Acute Pneumonia
Community-Acquired Atypical Pneumonia
Nosocomial Pneumonia
Aspiration Pneumonia
Chronic Pneumonia
Pneumonia in the Immunocompromised Host

50. Pneumonia in the Immunocompromised Host
Cytomegalovirus
Pneumocystis jiroveci
Mycobacterium avium-intracellulare
Invasive aspergillosis
Invasive candidiasis
"Usual" bacterial, viral, and fungal organisms

51. Pneumocystis Pneumonia
P. jiroveci (formerly known as P. carinii), an opportunistic infectious agent long considered to be a protozoan, is now believed to be more closely related to fungi.
Serologic evidence indicates that virtually all persons are exposed to Pneumocystis during the first few years of life, but in most the infection remains latent.
Reactivation and clinical disease occurs almost exclusively in those who are immunocompromised (AIDS)

52. Pneumocystis Pneumonia
Microscopically, involved areas of the lung demonstrate a characteristic intra-alveolar foamy, pink-staining exudate with H&E stains
Silver stain demonstrates cup-shaped cyst walls within the exudate

53. Pneumocystis Pneumonia
Fever, dry cough, and dyspnea occur in 90% to 95% of patients, who typically demonstrate bilateral perihilar and basilar infiltrates.
Hypoxia is frequent; pulmonary function studies show a restrictive lung defect.
The most sensitive and effective methods of diagnosis:
to identify the organism in bronchoalveolar lavage fluids or in a transbronchial biopsy specimen.
immunofluorescence antibody kits and PCR-based assays have also become available for use on clinical specimens

54. Lung abscess
A localized suppurative process within the pulmonary parenchyma
features: tissue necrosis and marked acute inflammation
Posssile causes: aerobic and anaerobic streptococci, Staphylococcus aureus, and many gram negative organisms
Can follow aspiration ( one abscess of Rt. lung)
occur as complication of pneumonia ( multiple)
Abscess is filled with necrotic suppurative debri

55. Lung abscess Clinical Features
- Prominent cough producing copious amount of foul- smelling purulent sputum
- Change in position evoke paroxysm of cough
- Fever malaise and clubbing of fingers

56. Chest X- ray

57. Chest radiograph of a patient who had foul-smelling and bad-tasting sputum, an almost diagnostic feature of anaerobic lung abscess.

58. Lung abscess

59. Lung abscess Complications
Pleural involvement (empyema) formation resulting from a bronchopleural fistula
massive hemoptysis, spontaneous rupture into uninvolved lung segments
non-resolution of abscess cavity
Bacteremia could result in brain abscess and meningitis
with antibiotic therapy 75% of abscess resolve