Community Acquired Pneumonia

brief overview of community acquired pneumonia

1. COMMUNITY ACQUIRED PNEUMONIA ANKUR GUPTA

2. INTRODUCTION Community-acquired pneumonia (CAP) is a syndrome in which acute infection of the lungs develops in persons who have not been hospitalized recently and have not had regular exposure to the health care system.

3. INTRODUCTION Long recognized as a major cause of death, pneumonia has been studied intensively since the late 1800s. Despite research and the development of antimicrobial agents, pneumonia remains a major cause of complications and death.

4. COMMON CAUSES Infectious Streptococcus pneumoniae , Haemophilus influenzae , Staphylococcus aureus , Influenza virus, Other respiratory viruses Non Infectious Pulmonary edema Lung cancer Acute respiratory distress syndrome

5. LESS COMMON CAUSES Infectious Pseudomonas aeruginosa or other gram-negative rods Pneumocystis jirovecii Moraxella catarrhalis , Mixed microaerophilic and anaerobic oral flora Non infectious Pulmonary infarction

6. UNCOMMON CAUSES Infectious Mycobacterium tuberculosis, nontuberculous mycobacteria, Nocardia species, Legionella species Mycoplasma pneumoniae Chlamydophila pneumoniae Chlamydophila psittaci Coxiella burnetii Histoplasma capsulatum , coccidioides species, Blastomyces dermatitidis , cryptococcus Aspergillus species Non infectious Cryptogenic organizing pneumonia Eosinophilic pneumonia Acute interstitial pneumonia Sarcoidosis Vasculitis ( granulomatosis with polyangiitis ) Pulmonary alveolar proteinosis Drug toxicity Radiation pneumonitis

7. Causes of pneumonia vary according to the patient population host immune status geographic region. No cause is determined in about half of patients with CAP despite intense investigation . Normal flora, especially streptococci from the upper airways, may be responsible for many of these cases

8. Although pneumococcus remains the most commonly identified cause of CAP, the frequency with which it is implicated has declined. In parts of the world where pneumococcal vaccines have been used less often and smoking rates remain high, pneumococcus remains responsible for a higher proportion of cases of CAP

9. Patients with chronic obstructive pulmonary disease ( COPD ) are at increased risk for CAP caused by H. influenzae and Mor. Catarrhalis . P. aeruginosa and other gram negative bacilli also cause CAP in persons who have COPD or bronchiectasis , especially in those taking glucocorticoids . Legionella pneumonia occurs in certain geographic locations and tends to follow specific exposures . Mixed microaerophilic and anaerobic bacteria (so-called oral flora) are often seen on Gram’s staining of sputum, and these organisms may be responsible for cases in which no cause is found. Mandell LA et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007;44:Suppl 2:S27-S72. Falguera M, Carratalà et al. Risk factors and outcome of community-acquired pneumonia due to Gram-negative bacilli. Respirology 2009; 14:105-11.

10. APPROACH TO DIAGNOSIS Sputum Gram stain and cultures – Positive in more than 80% of cases of pneumococcal pneumonia when a good-quality specimen (>10 inflammatory cells per epithelial cell) can be obtained. The yield diminishes with increasing time after antibiotics have been initiated and with decreasing quality of the sputum sample. Nebulization with hypertonic saline (so-called induced sputum) may increase the likelihood of obtaining a valid sample.

11. Blood cultures – Not required in routine outpatient management of CAP. Should be obtained in all hospitalised patients with CAP. Positive in about 20 to 25% of inpatients with pneumococcal pneumonia but in fewer cases of H. influenzae or P. aeruginosa and only rarely in cases caused by Mor. catarrhalis . Positive in only about 25% of cases in which inhalation or aspiration is responsible for the CAP.

12. Pneumococcal antigen detection Not required routinely for the management of CAP. Pneumococcal PCR Not recommended as a routine diagnostic test in patients with CAP. Legionella urinary antigen test Desirable in patients with severe CAP.

13. For influenza, PCR is far more sensitive than rapid antigen tests and has become the standard for diagnosis, BUT, positive results on PCR do not exclude the possibility that bacterial pneumonia is present.

14. MICROBIOLOGICAL INVESTIGATION

15. ROLES OF IMAGING Imaging is indispensable for the management of CAP. Imaging also play a complementary role for the evaluation of treatment effects of antibiotics. Imaging may also be usable for differentiating noninfectious diseases from infectious pneumonia. Chest radiography is usually enough to confirm the diagnosis of pneumonia and to evaluate treatment effects, whereas computed tomography (CT) is required to suggest causative pathogens, to exclude noninfectious pneumonia and to reveal underlying diseases.

16. LUNG ULTRASOUND Sensitivity of 94.0 % and a S pecificity of 96.0% Advantages Radiation-free C an be done at the bedside / on pregnant woman A llows for dynamic evaluations, H as increased accuracy in the detection of consolidation and pleural effusion compared with chest radiograph, T akes less time. Limitations L earning curve, R epeatability , O perator dependency

17. PATTERNS OF IMAGING FINDINGS CAP has classically been divided into three distinctive patterns on imaging examinations, namely Consolidation (alveolar/lobar pneumonia), Peribronchial nodules (bronchopneumonia) Ground-glass opacity. The fourth, a unique uncommon pattern of CAP is random nodules, suggestive of hematogenous pulmonary infection or granulomatous infection.

18. Consolidation predominant pattern (alveolar/ lobar pneumonia) Believed to be formed by the spread of inflammation through pores of Kohn or canals of Lambert at the periphery of the lung. Thus, nonsegmental consolidation in the early stage of disease. Most bacterial pneumonias like Streptococcus and Klebsiella .

19. Streptococcus pneumoniae pneumonia showing alveolar pattern nonsegmental consolidation in the right middle lung field, which is demarcated by the fissure suggestive of upper lobe pneumonia

20. Klebsiella pneumonia Suspected when there is a  cavitatory pneumonia, a bulging fissure sign. Often there can be extensive lobar opacification with air bronchogram .

21. Mycoplasma pneumoniae pneumonia showing alveolar pattern Chest radiograph demonstrates ill-defined consolidation in the right lower lung field (arrow); B: Thin-section CT reveals a non-segmental consolidation with air bronchograms at the dorsal aspect of the right lower lobe.

22. Peribronchial nodules predominant pattern (bronchopneumonia) P redominance of peribronchial nodules including centrilobular nodules with or without peribronchial consolidations. C onsolidations are probably formed by enlargement and coalescence of the peribronchial nodules . may follow a chronic clinical course. Bronchial wall thickening is often associated. Hemophilus influenzae , Mycoplasma pneumoniae,Staphylococccus aureus , Chlamydophila pneumoniae , and viruses, MTB, NTM

23. Staph aureus pneumonia Chest radiograph shows extensive consolidations and peribronchovascular consolidations of the right lung (arrows); B: Thin-section CT reveals extensive consolidation with air bronchograms and cavities in the left upper lobe (black arrows). Note that the bronchi in the consolidation are dilated. Dense centrilobular nodules are seen in the left lower lobe (white arrows).

24. Mycoplasma pneumoniae CXR shows reticulonodular opacities and focal consolidation in the left middle to lower lung field (arrow). The left pulmonary hilum appears enlarged; B: Thin-section CTdemonstrates fluffy centrilobular nodules with surrounding ground-glass opacity in the left lower lobe (arrows). Note that central bronchial wall is thickened (arrow heads).

25. Chlamydophila pneumoniae pneumonia showing infectious bronchiolitis Chest radiograph shows faint reticulonodular opacities in both lower lung fields (arrows); B: Thin-section computed tomography reveals centrilobular nodules (arrows) with bronchiectasis (arrow heads) in the middle lobe and lingula

26. G round-glass opacity predominant pattern GGO may correspond to I ncomplete alveolar filling by inflammatory cells or exudate , P ulmonary edema secondary to infection leaving air in the alveoli, I nterstitial infiltrates of inflammatory cells (interstitial pneumonia). Viruses, Mycoplasma pneumoniae and Pneumocystis jirovecii are the representative pathogens

27. Mycoplasma pneumoniae pneumonia showing groundglass opacity predominant pneumonia Chest radiograph shows patchy ground-glass opacity (GGO) with peribronchial nodules in the right middle lung field (arrow); B: Thin-section computed tomography reveals areas of GGO in the right upper lobe. Note that the GGO are partly demarcated by interlobular septa (arrows).

28. Pneumocystis jirovecii pneumonia Chest radiograph shows bilateral reticulonodular opacities; B: Chest computed tomography with a 5 mm slice thickness demonstrates bilateral ground-glass opacity with reticulations.

29. R andom nodules predominant Probably produced by hematogenous spread of the disease or granulomatous infection. V iral pneumonia ( varicella -zoster ) , M iliary tuberculosis, Granulomatous infection, such as tuberculosis , nontuberculous mycobacterial infection or fungal infection

30. Random nodules predominant pneumonia ( varicella -zoster pneumonia) Thin-section computed tomography demonstrates scattered small solid or ground-glass opacity nodules which are unrelated to centrilobular structures (arrows).

31. Miliary tuberculosis Chest radiograph Diffuse reticulonodular opacities in both lungs; B: Thin-section CT demonstrates diffuse military nodules with a random distribution.

32. Pathogen Specific imaging appearances Streptococcus pneumoniae Alveolar/lobar pneumonia Mycoplasma pneumoniae Bronchopneumonia with bronchial wall thickening affecting central bronchi Chlamydophila pneumoniae Infectious bronchiolitis with bronchial dilatation Legionella pneumophila Sharply marinated peribronchial consolidations within ground-glass opacities varicella -zoster Scattered nodules with a random distribution Staph aureus Patchy unilateral or bilateral consolidation,rapid progression,centrilobular nodules,pneumatocele in children. Cryptococcus neoformans Multiple nodules/masses with or without cavities in the same pulmonary lobe Pneumocystis jirovecii Bilateral patchy ground-glass opacities with a geographic distribution

33. CLINICAL CONDITIONS RELATED TO CAP 1) Aspiration pneumonia – Caused by inhalation of bacteria, food, gastric acid or other materials that provoke pulmonary inflammation or edema. Commonly occurs in patients with deteriorated consciousness, chronic debilitating disease, and hospital settings . Imaging : Patchy ground-glass opacities at dorsal parts of the lung, bronchopneumonia or infectious bronchiolitis .

34. CLINICAL CONDITIONS RELATED TO CAP 2) Sinobronchial syndrome - Chronic and repeated infection of the lower respiratory tract and paranasal sinuses due to altered immune status. Imaging : Chest radiograph - Reticulonodular opacities with lower lung field predominance. CT - Centrilobular or peribronchial nodules with bronchial wall thickening and mucus filled bronchi are seen. There are usually evidences of chronic and repeated infection, such as bronchiectasis , parenchymal distortion or reticular opacities.

35. Sinobronchial syndrome in a man . A: Chest radiograph shows bilateral reticulonodular opacities in both lower lung fields (arrows); B:computed tomography (CT) at the level of maxillary sinus demonstrates opacification of the maxillary sinuses (*) and bone sclerosis of the sinus walls (arrows), suggestive of chronic paranasal sinusitis; C: Thin-section CT reveals bronchial wall thickening with bronchiectasis (arrows) and minimal centrilobular opacities (arrow heads).

36. CLINICAL FEATURES Fever Cough Shortness of breath Pleuritic chest pain Non-specific features in the elderly. May present ‘off legs’ or with confusion, in the absence of fever.

37. CLINICAL FEATURES ASSOCIATED WITH SPECIFIC CAUSES OF CAP 1) Favoring typical bacterial or legionella pneumonia Acute presentation May Present with septic shock Initial upper respiratory illness followed by acute deterioration (suggesting viral infection with bacterial superinfection ) White-cell count, >15,000 or ≤6000 cells per cubic millimeter with increased band forms Dense segmental or lobar consolidation Procalcitonin level, ≥0.25 μg per liter

38. CLINICAL FEATURES ASSOCIATED WITH SPECIFIC CAUSES OF CAP 2) Favoring atypical bacterial ( mycoplasma or chlamydophila ) pneumonia Absence of factors that favor typical bacterial pneumonia Extra pulmonary constitutional symptoms Cough persisting >5 days without acute deterioration Absence of sputum production Normal or minimally elevated white-cell count Procalcitonin level, ≤0.1 μg per liter

39. CLINICAL FEATURES ASSOCIATED WITH SPECIFIC CAUSES OF CAP 3) Favoring nonbacterial (viral) pneumonia Acute presentation Exposure to sick contacts Upper respiratory symptoms at time of presentation Patchy pulmonary infiltrates Normal or minimally elevated white-cell count Procalcitonin level, ≤0.1 μg per liter

40. CLINICAL FEATURES ASSOCIATED WITH SPECIFIC CAUSES OF CAP 4) Favoring influenza pneumonia Absence of factors that favor typical bacterial pneumonia Influenza active in the community Sudden onset of flulike syndrome Positive diagnostic test for influenza virus

41. POOR PROGNOSTIC FACTORS Age (≥65) Coexisting disease-cardiac disease, diabetes, COPD, stroke Respiratory rate ≥ 30/min Confusion Blood pressure Hypoxemia Urea ≥ 7 mmol / l Albumin < 35 g/l White cell count- WCC >20 or < 4* 10 9 /l Radiology – bilateral and multilobar involvement. microbiology

42. SCORING OF DISEASE SEVERITY Scoring systems and assesment tools may predict the severity of disease and help determine whether a patient with CAP requires hospitalization or admission to an intensive care unit (ICU).

43. Severity assessment is a crucial component in the management of patients presenting with CAP to guide physicians in clinical decisions. Severity assessment tools are evolving, but at present have major limitations and should be used with caution and only in conjunction with clinical judgment.

44. ACUTE MANAGEMENT OF CAP

45. EMPIRICAL TREATMENT OF CAP - Outpatient For syndromes suggesting typical bacterial pneumonia : amoxicillin– clavulanate with the addition of azithromycin if legionella species are a consideration; levofloxacin or moxifloxacin may be used instead. For syndromes suggesting influenza pneumonia : oseltamivir with observation for secondary bacterial infection

46. EMPIRICAL TREATMENT OF CAP - Outpatient For syndromes suggesting viral pneumonia other than influenza : symptomatic therapy For syndromes suggesting mycoplasma or chlamydophila pneumonia : azithromycin or doxycycline

47. EMPIRICAL TREATMENT OF CAP - Inpatient For initial empirical therapy : a beta- lactam ( ceftriaxone , cefotaxime , or ceftaroline ) plus azithromycin ; levofloxacin or moxifloxacin may be used instead If influenza is likely : oseltamivir If influenza is complicated by secondary bacterial pneumonia : ceftriaxone or cefotaxime plus either vancomycin or linezolid in addition to oseltamivir

48. EMPIRICAL TREATMENT OF CAP - Inpatient If Staphylococcus aureus is likely : vancomycin or linezolid in addition to the antibacterial regimen If pseudomonas pneumonia is likely: antipseudomonal beta- lactam ( piperacillin–tazobactam , cefepime , meropenem , or imipenem – cilastatin ). plus azithromycin

49. INDICATIONS FOR EMPIRICAL COMBINATION THERAPY IN CAP Presence of Comorbid Medical Conditions Chronic heart, lung, liver or renal disease Diabetes mellitus Alcoholism Malignancies Use of antimicrobials within the previous 3 months Severe CAP With or Without Comorbidities

50. COMPARISON

51. DURATION OF THERAPY A meta-analysis of studies comparing treatment durations of 7 days or less with durations of 8 days or more showed no differences in outcomes.* Pneumonia that is caused by Staph. aureus or gram-negative bacilli tends to be destructive – prolonged therapy is used by majority. Cavitating pneumonia and lung abscesses are usually treated for several weeks. * Li JZ, Winston LG, Moore DH, Bent S. Efficacy of short-course antibiotic regimens for community-acquired pneumonia: a meta-analysis. Am J Med 2007;120: 783-90.

52. REASONS FOR A LACK OF RESPONSE TO TREATMENT OF CAP Correct organism but inappropriate antibiotic choice or dose Resistance of organism to selected antibiotic Wrong dose (e.g., in a patient who is morbidly obese or has fluid overload) Antibiotics not administered Correct organism and correct antibiotic but infection is loculated (e.g., most commonly empyema ) Obstruction (e.g., lung cancer, foreign body)

53. REASONS FOR A LACK OF RESPONSE TO TREATMENT OF CAP Incorrect identification of causative organism No identification of causative organism and empirical therapy directed toward wrong organism Noninfectious cause Drug-induced fever Presence of an unrecognized, concurrent infection

54. NONINFECTIOUS COMPLICATIONS Influenza pneumonia and bacterial pneumonia are each strongly associated with acute cardiac events. Myocardial infarction and new major arrhythmias (most commonly, atrial fibrillation) were each seen in 7 to 10% of CAP patients, worsening of heart failure occurred in nearly 20%, and one or more of these complications occurred in 25% of patients.

55. HIGH RISK GROUPS IN WHOM VACCINATION IS RECOMMENDED

56. FUTURE DIRECTIONS Important unresolved problems remain with respect to CAP. Despite the most diligent efforts, no causative organism is identified in half of patients. It remains to be determined whether the availability of sensitive diagnostic tests such as PCR will increase the use of targeted therapies and reduce dependence on empirical antibiotic therapy. Increasing antibiotic resistance in bacteria may compound the difficulty of selecting an effective regimen. Randomized trials are needed to determine whether the antiinflammatory activity of macrolides or statins is beneficial in treating CAP.

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