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Community Acquired Pneumonia (CAP) by

CAP. Community Acquired Pneumonia (CAP) by. Paras Patel MD. Assistant Professor of Internal Medicine, Division of Infectious disease. ETSU. Alphabet Soup for Pneumonia. HAP: Hospital-acquired pneumonia ≥ 48 h from admission VAP: Ventilator-associated pneumonia

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Community Acquired Pneumonia (CAP) by

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  1. CAP Community Acquired Pneumonia (CAP) by Paras Patel MD. Assistant Professor of Internal Medicine, Division of Infectious disease. ETSU

  2. Alphabet Soup for Pneumonia HAP: Hospital-acquired pneumonia ≥ 48 h from admission VAP: Ventilator-associated pneumonia ≥ 48 h from endotracheal intubation HCAP: Healthcare-associated pneumonia Long-term care facility (NH), hemodialysis, outpatient chemo, wound care, etc. CAP: Community-acquired pneumonia Outside of hospital or extended-care facility

  3. Community Acquired Pneumonia • Definition: • … an acute infection of the pulmonary parenchyma that is associated with at least some symptoms of acute infection, accompanied by the presence of an acute infiltrate on a chest radiograph, or auscultatory findings consistent with pneumonia, in a patient not hospitalized or residing in a long term care facility for > 14 days before onset of symptoms. Bartlett. Clin Infect Dis 2000;31:347-82.

  4. Community Acquired Pneumonia • Epidemiology: • 4-5 million cases annually • ~500,000 hospitalizations • ~45,000 deaths • Mortality 2-30% • <1% for those not requiring hospitalization Cdc.gov/data 2007.

  5. Community Acquired Pneumonia • Epidemiology: (contd) • fewest cases in 18-24 yr group • probably highest incidence in <5 and >65 yrs • mortality disproportionately high in >65 yrs

  6. Community Acquired Pneumonia Mortality # in 1000s

  7. Age-specific Rates of Hospital Admission by Pathogen Marsten. Community-based pneumonia incidence study group. Arch Intern Med 1997;157:1709-18

  8. CAP – Pathogenesis Inhalation, aspiration and hematogenous spread are the 3 main mechanisms by which bacteria reaches the lungs

  9. Pathogenesis • Primary inhalation: when organisms bypass normal respiratory defense mechanisms or when the Pt inhales aerobic GN organisms that colonize the upper respiratory tract or respiratory support equipment • Aspiration: occurs when the Pt aspirates colonized upper respiratory tract secretions • Stomach: reservoir of GNR that can ascend, colonizing the respiratory tract. • Hematogenous: originate from a distant source and reach the lungs via the blood stream.

  10. Community Acquired Pneumonia • Risk Factors for pneumonia • age • smoking • asthma • immunosuppression • institutionalization • COPD • PVD • Dementia • HIV/AIDS ID Clinics 1998;12:723. Am J Med 1994;96:313

  11. Community Acquired Pneumonia • Risk Factors in Patients Requiring Hospitalization • older, unemployed • common cold in the previous year • asthma, COPD; steroid or bronchodilator use • Chronic disease • amount of smoking Farr BM. Respir Med 2000;94:954-63

  12. Community Acquired Pneumonia • Risk Factors for Mortality • age • bacteremia (for S. pneumoniae) • extent of radiographic changes • degree of immunosuppression • amount of alcohol

  13. S. pneumoniae: 20-60% H. influenzae: 3-10% Chlamydia pneumoniae: 4-6% Mycoplasma pneumonaie: 1-6% Legionella spp. 2-8% S. aureus: 3-5% Gram negative bacilli: 3-5% Viruses: 2-13% Community Acquired Pneumonia Microbiology 40-60% - NO CAUSE IDENTIFIED 2-5% - TWO OR MORE CAUSES Bartlett. NEJM 1995;333:1618-24

  14. Streptococcus pneumonia (Pneumococcus) • Most common cause of CAP • About 2/3 of CAP are due to S.pneumoniae • These are gram positive diplococci • Typical symptoms (e.g. malaise, shaking chills fever, rusty sputum, pleuritic chest pain, cough) • Lobar infiltrate on CXR • May be Immuno suppressed host • 25% will have bacteremia – serious effects

  15. Pneumonia Atypical Pneumonia • #2 cause (especially in younger population) • Commonly associated with milder Sx’s: subacute onset, non-productive cough, no focal infiltrate on CXR • Mycoplasma: younger Pts, extra-pulm Sx’s (anemia, rashes), headache, sore throat • Chlamydia: year round, URI Sx, sore throat • Legionella: higher mortality rate, water-borne outbreaks, hyponatremia, diarrhea

  16. Viruses and Pneumonia Pneumonia in the normal host Adults or Children Influenza A and B, RSV, Adenovirus, Para Influenza Pneumonia in the immuno-compromised Measles, HSV, CMV, HHV-6, Influenza viruses Can cause a primary viral pneumonia. Cause partial paralysis of “mucociliary escalator” - increased risk of secondary bacterial LRTI. S.aureus pneumonia is a known complication following influenza infection.

  17. Other bacteria • Anaerobes • Aspiration-prone Pt, putrid sputum, dental disease • Gram negative • Klebsiella - alcoholics • Branhamella catarrhalis - sinus disease, otitis, COPD • H. influenza

  18. S. aureus CAP – Dangerous • This CAP is not common; Multi lobar Involvement • Post Influenza complication, Class IV or V • Compromised host, Co-morbidities, Elderly • CA MRSA – A Problem; CA MSSA also occurs • Empyema and Necrosis of lung with cavitations • Multiple Pyemic abscesses, Septic Arthritis • Hypoxemia, Hypoventilation, Hypotension common • Vancomycin, Linezolid are the drugs for MRSA

  19. Diagnosis and Management

  20. Clinical Diagnosis • Suggestive signs and symptoms • CXR or other imaging technique • Microbiologic testing

  21. Signs and Symptoms • Fever or hypothermia • Cough with or without sputum, hemoptysis • Pleuritic chest pain • Myalgia, malaise, fatigue • GI symptoms • Dyspnea • Rales, rhonchi, wheezing • Egophony, bronchial breath sounds • Dullness to percussion • Atypical Sx’s in older patients

  22. Clinical Diagnosis: CXR • Demonstrable infiltrate by CXR or other imaging technique • Establish Dx and presence of complications (pleural effusion, multilobar disease) • May not be possible in some outpatient settings • CXR: classically thought of as the gold standard

  23. Chest Radiograph May show hyper-expansion, atelectasis or infiltrates Normal Pneumonia

  24. Infiltrate Patterns

  25. Clinical Diagnosis: Recommended testing • Outpatient: CXR, sputum Cx and Gram stain not required • Inpatient: CXR, Pox or ABG, chemistry, CBC, two sets of blood Cx’s • If suspect drug-resistant pathogen or organism not covered by usual empiric abx, obtain sputum Cx and Gram stain. • Severe CAP: Legionella urinary antigen, consider bronchoscopy to identify pathogen

  26. Community Acquired Pneumonia Who should be hospitalized?

  27. To Admit or Not?Pneumonia Severity & Deciding Site of Care Using objective criteria to risk stratify & assist in decision re outpatient vs inpatient management PSI CURB-65 Caveats Other reasons to admit apart from risk of death Not validated for ward vs ICU Labs/vitals dynamic

  28. Pneumonia Severity Index

  29. CURB 65 Rule – Management of CAP

  30. Who Should be Hospitalized? Class I and II Usually do not require hospitalization Class III May require brief hospitalization Class IV and V Usually do require hospitalization Severity of CAP with poor prognosis RR > 30; PaO2/FiO2 < 250, or PO2 < 60 on room air Need for mechanical ventilation; Multi lobar involvement Hypotension; Need for vasopressors Oliguria; Altered mental status

  31. CAP – Criteria for ICU Admission Major criteria • Invasive mechanical ventilation required • Septic shock with the need of vasopressors Minor criteria (least 3) • Confusion/disorientation • Blood urea nitrogen ≥ 20 mg% • Respiratory rate ≥ 30 / min; Core temperature < 36ºC • Severe hypotension; PaO2/FiO2 ratio ≤ 250 • Multi-lobar infiltrates • WBC < 4000 cells; Platelets <100,000

  32. Traditional Treatment Paradigm Conservative start with ‘workhorse’ antibiotics Reserve more potent drugs for non-responders

  33. New Treatment Paradigm Hit hard early with appropriate antibiotic(s) Short Rx. Duration; De-escalate where possible

  34. The Effect of the Traditional Approach 45 Inappropriate therapy (%) 50 40 34 30 17 20 10 0 CAP HAP HAP on CAP Kollef, et al. Chest 1999;115:462–474

  35. New data – Don’t Wait for Results ! Mortality (%) n=75 p<0.001 Switching after susceptibility results Adequate treatment within ‘a few hours’ Tumbarello, et al. Antimicrob Agents Chemother 2007;51:1987–1994

  36. Survival (%) Each hour of delay carries 7.6% reduction in survival Delay in treatment (hours) from hypotension onset New data – The Speed of Delay ! (Class 4,5) Kumar, et al. Crit Care Med 2006;34:1589–1596

  37. CAP – Complications Hypotension and septic shock 3-5% Pleural effusion; Clear fluid + pus cells 1% Empyema thoracis pus in the pleural space Lung abscess – destruction of lung . Single (aspiration) anaerobes, Pseudomonas Multiple (metastatic) Staphylococcus aureus Septicemia – Brain abscess, Liver Abscess Multiple Pyemic Abscesses

  38. IDSA: Outpt Management in Previously Healthy Pt • Organisms: S. pneumo, Mycoplasma, viral, Chlamydia pneumo, H. flu • Recommended abx: • Advanced generation macrolide (azithro or clarithro) or doxycycline • If abx within past 3 months: • Respiratory quinolone (moxi-, levo-, gemi-), OR • Advanced macrolide + amoxicillin, OR • Advanced macrolide + amoxicillin-clavulanate

  39. IDSA: Outpt Management in Pt with comorbidities • Comorbidities: cardiopulmonary dz or immunocompromised state • Organisms: S. pneumo, viral, H. flu, aerobic GN rods, S. aureus • Recommended Abx: • Respiratory quinolone, OR advanced macrolide • Recent Abx: • Respiratory quinolone OR • Advanced macrolide + beta-lactam

  40. IDSA: Inpt Management-Medical Ward • Organisms: all of the above plus polymicrobial infections (+/- anaerobes), Legionella • Recommended Parenteral Abx: • Respiratory fluoroquinolone, OR • Advanced macrolide plus a beta-lactam • Recent Abx: • As above. Regimen selected will depend on nature of recent antibiotic therapy.

  41. IDSA: Inpt Management-Severe/ICU • One of two major criteria: • Mechanical ventilation • Septic shock, OR • Two of three minor criteria: • SBP≤90mmHg, • Multilobar disease • PaO2/FIO2 ratio < 250 • Organisms: S. pneumo, Legionella, GN, Mycoplasma, viral, ?Pseudomonas

  42. IDSA: Inpt Management: Severe/ICU • No risk for Pseudomonas • IV beta-lactam plus either • IV macrolide, OR IV fluoroquinolone • Risk for Pseudomonas • Double therapy: selected IV antipseudomonal beta-lactam (cefepine, imipenem, meropenem, piperacillin/tazobactam), plus • IV antipseudomonal quinolone -OR- • Triple therapy: selected IV antipseudomonal beta-lactam plus IV aminoglycoside plus either IV macrolide, OR IV antipseudomonal quinolone

  43. Switch to Oral Therapy • Four criteria: • Improvement in cough and dyspnea • Afebrile on two occasions 8 h apart • WBC decreasing • Functioning GI tract with adequate oral intake • If overall clinical picture is otherwise favorable, can can switch to oral therapy while still febrile.

  44. Duration of Therapy • Minimum of 5 days • Afebrile for at least 48 to 72 h • No > 1 CAP-associated sign of clinical instability • Longer duration of therapy If initial therapy was not active against the identified pathogen or complicated by extra pulmonary infection

  45. Prevention • Smoking cessation • Vaccination per ACIP recommendations • Influenza • Inactivated vaccine for people >50 yo, those at risk for influenza compolications, household contacts of high-risk persons and healthcare workers • Intranasal live, attenuated vaccine: 5-49yo without chronic underlying dz • Pneumococcal • Immunocompetent ≥ 65 yo, chronic illness and immunocompromised ≤ 64 yo

  46. Epidemiology of Pneumococcal Infection in Immunocompromised Adults • Streptococcus pneumoniae remains a leading cause of serious illness, including bacteremia, meningitis, and pneumonia among adults in the United States. • An estimated 4,000 deaths occur annually in USA primarily among adults. • For adults aged 18–64 years with hematologic cancer, the rate of IPD in 2010 was 186 per 100,000, and for persons with human immunodeficiency virus (HIV) the rate was 173 per 100,000 (CDC, unpublished data, 2012). • The disease rates for adults in these groups can be more than 20 times those for adults without high-risk medical conditions.

  47. PCV13 has been used for children since 2010, when it replaced an earlier version targeting seven serotypes (PCV7; Prevnar, Pfizer) that had been in use since 2000. • The routine use of PCV7 in infants and young children resulted in significant reductions in IPD caused by vaccine serotypes in children, and because of indirect effects, also in adults. • Rates of IPD caused by vaccine serotypes in adults aged 18–64 years without HIV decreased from six cases to one case per 100,000 during 2000–2007. • However, even after indirect effects of the pediatric immunization had been realized fully, the incidence of IPD caused by the serotypes included in PCV7 remained high in HIV-infected persons aged 18–64 years at 64 cases per 100,000 persons with acquired immunodeficiency syndrome (AIDS) . • Moreover, 50% of IPD cases among immunocompromised adults in 2010 were caused by serotypes contained in PCV13; an additional 21% were caused by serotypes only contained in PPSV23.

  48. In two randomized, multicenter immunogenicity studies conducted in the United States and Europe, immunocompetent adults aged ≥50 years received a single dose of PCV13 or PPSV23. • In adults aged 60–64 years and aged >70 years, PCV13 elicited opsonophagocytic activity (OPA) geometric mean antibody titers (GMTs) that were comparable with, or higher than, responses elicited by PPSV23. • OPA GMTs elicited by PCV13 in adults aged 50–59 years for all 13 serotypes were comparable with the corresponding GMTs elicited by administration of PCV13 in adults aged 60–64 years.

  49. PCV13 Vaccine in Adults • PCV13 was licensed by the Food and Drug Administration (FDA) for prevention of IPD and otitis media in infants and young children in February 2010, supplanting PCV7 • One dose of PCV13 is recommended by ACIP for children aged 6–18 years with high-risk conditions such as functional or anatomic asplenia, immunocompromising conditions, cochlear implants, or CSF leaks. • In December 2011, FDA licensed PCV13 for prevention of pneumonia and IPD in adults aged ≥50 years . • Approval of PCV13 for adults was based on immunogenicity studies that compared antibody responses to PCV13 with antibody responses to PPSV23

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