به نام خداوند جان و خرد , COMMUNITY-ACQUIRED (REVIEW OF ARTICLE)

استاد راهنما : دکتر سعید رضا جمالی متخصص عفونی

ارائه دهنده : دکتر اردالن زیالبی دستیار پزشکی خانواده AUTHOR INFORMATION

Hariharan Regunath1; Yuji Oba2.1 University of Missouri2 University of MissouriPublication History Last Update: April 26, 2018.Copyright

StatPearls Publishing; 2018 Jan-. INTRODUCTION

Community-acquired pneumonia is a leading cause of hospitalization, mortality and incurs significant health care costs. As disease presentation varies from a mild illness that can be managed as an outpatient to a severe illness requiring treatment in intensive care unit, determining the appropriate level of care is important for improving outcomes in addition to early diagnosis and appropriate and timely treatment. THE PATHOGENS CAUSING (CAP): (1) Typical agents: Staphylococcus pneumoniae, H. influenzae, Moraxella catarrhalis, S. aureus, Group A streptococci, anaerobes, and gram(-) organisms  (2) Atypical agents : Legionella, Mycoplasma, Chlamydia pneumoniae, and C. psittaci. Influenza and noninfluenza respiratory viruses EPIDEMIOLOGY

worldwide incidence of ( cap) varies between 1.5 to 14 cases per 1000 person-years, and is affected by geography, season, and population characteristics. In the USA, the annual incidence is 24.8 cases per 10,000 adults with higher rates as age increases.  Pneumonia is the eighth leading cause of and first among infectious causes of death. The mortality rate is as high as 23% for patients admitted to the ICU.

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All patients with comorbid illness are considered at risk for pneumonia, but specific risk factors exist for specific pathogens including (1) Drug-resistant pneumococci - age greater than 65, exposure to children in day care centers, intake of beta- lactam in previous 90 days, alcoholism, chronic medical conditions, immune-suppression (2) Pseudomonas - bronchiectasis, malnutrition, corticosteroid therapy, antibiotic intake for greater than 7 days in the preceding month. CONTINUE

 Other etiological clues from epidemiology: coccidioidomycosis in the Southwestern United States, blastomycosis or histoplasmosis in the states of the Ohio River valley, bird exposures for Chlamydia psittaci, contact with flea-infested or infected rodent or rabbits during outside activities such as lawn mowing in the Northeast US for tularemia pneumonia. PATHOPHYSIOLOGY Colonization of the pharynx with pathogens, followed by micro-aspiration is the mechanism of entry into the lower . In the interaction between the pathogen and host pulmonary defense, pneumonia results if there is a defect in host defense or it is overcome by high inoculum or virulence of the pathogen. Hematogenous spread and macro-aspiration are other mechanisms. HISTORY AND PHYSICAL Fever, chills, cough productive of purulent sputum, dyspnea, pleuritic chest pain, and weight loss are common symptoms.  The elderly, patients with alcoholism, and those who are immune-compromised can have less evident or systemic symptoms such as weakness, lethargy, altered mental status, dyspepsia or other upper gastrointestinal symptoms, and absence of fever. HISTORY AND PHYSICAL Some manifestations provide etiological clues:  diarrhea, headache and confusion (related to hyponatremia) for Legionella;  otitis media, Stevens-Johnson syndrome, or anemia/jaundice (hemolytic anemia) for Mycoplasma. HISTORY AND PHYSICAL  Pneumonia can result in acute decompensation of underlying chronic illness like congestive heart failure which can confound the initial presentation and result in diagnosis and treatment delays. EVALUATION A CBC with differentials, serum electrolytes, renal and LFT: for confirming evidence of inflammation and assessing severity. A chest x-ray : identify an infiltrate or effusion, which if present, will improve diagnostic accuracy. EVALUATION In hospitalized patients: blood and sputum cultures should be collected, preferably before the initiation of antimicrobial therapy but without delay in treatment. Urine for Legionella and pneumococcal antigens must be considered as they aid in diagnosis when cultures are negative. CONTINUE

In the presence of confounding co-morbidities, such as CHF, serum procalcitonin levels can be used as a biomarker to initiate and guide antimicrobial therapy. Influenza testing is recommended during the winter season. If available, testing for respiratory viruses on nasopharyngeal swabs by molecular methods can be considered. CONTINUE CURB 65: (confusion, urea ≥20 mg/dL, respiratory rate ≥ 30/min, blood pressure systolic < 90 mmHg or diastolic < 60 mmHg) and Pneumonia Severity Index (PSI) are tools for severity assessment to determine the treatment setting, such as outpatient versus inpatient, but accuracy is limited when used alone or in the absence of effective clinical judgment. Serology for tularemia, endemic mycoses or C. psittaci can be sent in the presence of epidemiologic clues. TREATMENT / MANAGEMENT

For outpatients: monotherapy with a macrolide (erythromycin, azithromycin or clarithromycin) or doxycycline is recommended. TREATMENT / MANAGEMENT

In the presence of co-morbid illness: (chronic heart disease excluding hypertension; chronic disease - COPD and asthma; chronic liver disease; chronic alcoholism; diabetes mellitus; smoking; splenectomy; HIV or other immunosuppression)

TREATMENT / MANAGEMENT

fluoroquinolone (high-dose levofloxacin, moxifloxacin, gemifloxacin) or a combination of oral beta-lactam (high dose amoxicillin or amoxicillin-clavulanate, cefuroxime, cefpodoxime) and macrolide is recommended. CONTINUE

For patients with CURB 65 score ≥ 2, inpatient management is recommended.  A respiratory fluoroquinolone monotherapy or combination therapy with beta-lactam (cefotaxime, ceftriaxone, ampicillin- sulbactam or ertapenem) and macrolide are recommended options for no intensive care settings. CONTINUE

Admission to the ICU must be considered in patients with three or more signs of early deterioration: These include respiratory rate > 30, PaO2/FiO2 ≤ 250, multilobar infiltrates, encephalopathy, thrombocytopenia, hypothermia, leucopenia, and hypotension.

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Combination therapy with a beta-lactam and either a macrolide or a respiratory fluoroquinolone is recommended. In patients with possible aspiration, ampicillin-sulbactam or ertapenem can be used. Monotherapy is not recommended.

CONTINUE If risk factors for pseudomonas are present, then: anti-pseudomonal beta-lactam: (piperacillin-tazobactam,cefepime,ceftazidime, meropenem, imipenem) along with either an anti-pseudomonal fluoroquinolone: (ciprofloxacin or levofloxacin) or a combination of aminoglycoside and azithromycin are recommended. Vancomycin or linezolid should be added if community-acquired methicillin- resistant S. aureus is a consideration. CONTINUE

The recommended duration of therapy is 5 to 7 days in patients with a favorable clinical such as the absence of fever for more than 48 to 72 hours, not requiring supplemental oxygen, and resolution of tachycardia, tachypnea, or hypotension. CONTINUE

Prolongation of therapy is indicated in patients with a delayed response, certain bacterial pathogens such as Pseudomonas (14 to 21 days) or S. aureus (7 to 21 days) orS. Legionella pneumonia (14 days), and for complications such as empyema, lung abscess, or necrotizing pneumonia. placement will be needed to drain an empyema, and in cases with multiple loculations, a surgical may be needed.

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 A 14-day therapy with macrolide or doxycycline will treat tularemia pneumonia or psittacosis, and itraconazole is the drug of choice for pneumonia caused by coccidioidomycosis or histoplasmosis.

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A five-day therapy with oseltamivir is recommended for all patients who test positive for influenza virus. For outpatients with delayed presentation (greater than 48 hours from onset of symptoms), there is no benefit, but any hospitalized patients with influenza must be treated with this agent irrespective of time of presentation from the onset of illness. CONTINUE

 A 14-day therapy with macrolide or doxycycline will treat tularemia pneumonia or Intravenous glucocorticoids can be considered in critically ill patients with community-acquired pneumonia without risk factors for adverse outcomes from use of steroids (e.g., influenza infection). PEARLS AND OTHER ISSUES

All adults 65 years and older and those considered at risk for pneumonia must receive the pneumococcal vaccination. There are two vaccines available: PPSV 23 and PCV 13.Current ACIP recommendations for unvaccinated non- immune-compromised individuals aged 19to 64 years old and at risk for pneumonia, first should receive PPSV 23. PEARLS AND OTHER ISSUES

After age 65, a dose of PCV 13 can be given (after at least one year of the first dose of PPSV 23), followed by the second dose of PPSV 23 spaced at least one year from PCV 13, followed by the first dose of PPSV 23 8 weeks or later and second dose PPSV 23 after 5 years.

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 A booster PPSV 23 can be given for a patient 65 years or older after at least 5 years or longer from the second dose of PPSV 23. For all unvaccinated adults 65 years or older, first vaccinate with PCV 13, followed by PPSV 23 at least a year later for patients who are immune competent and at least 8 weeks or more apart for patients who are immune compromised or asplenic.Influenza vaccination is recommended for all adult patients at risk for complications from influenza.

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Inactivated flu shots (trivalent or quadrivalent, egg- based or recombinant) are usually recommended for adults. Live attenuated intranasal vaccine can be given to healthy, non pregnant adults who are less than 49 years old.  It is contraindicated in pregnancy, the immune suppressed or health care workers caring for them, and in those with co morbidities REFERENCES

 1.Jain S, Self WH, Wunderink RG., CDC EPIC Study Team. Community-Acquired Pneumonia Requiring Hospitalization. N. Engl. J. Med. 2015 Dec 10;373(24):2382. [PubMed]  2.Niederman MS. In the Clinic: Community-Acquired Pneumonia. Ann. Intern. Med. 2015 Oct 06;163(7):ITC1-17. [PubMed]  3.File TM, Marrie TJ. Burden of community-acquired pneumonia in North American adults. Postgrad Med. 2010 Mar;122(2):130-41. [PubMed]  4.Prina E, Ranzani OT, Torres A. Community-acquired pneumonia. Lancet. 2015 Sep 12;386(9998):1097-108. [PubMed]  5.Alcón A, Fàbregas N, Torres A. Pathophysiology of pneumonia. Clin. Chest Med. 2005 Mar;26(1):39-46. [PubMed]  6.Lee JS, Giesler DL, Gellad WF, Fine MJ. Antibiotic Therapy for Adults Hospitalized With Community-Acquired Pneumonia: A Systematic Review. JAMA. 2016 Feb 09;315(6):593-602. [PubMed]  7.Siemieniuk RA, Meade MO, Alonso-Coello P, Briel M, Evaniew N, Prasad M, Alexander PE, Fei Y, Vandvik PO, Loeb M, Guyatt GH. Corticosteroid Therapy for Patients Hospitalized With Community-Acquired Pneumonia: A Systematic Review and Meta-analysis. Ann. Intern. Med. 2015 Oct 06;163(7):519-28. [PubMed]  8.Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, Dowell SF, File TM, Musher DM, Niederman MS, Torres A, Whitney CG., Infectious Diseases Society of America. American Thoracic Society. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin. Infect. Dis. 2007 Mar 01;44 Suppl 2:S27-72. [PubMed]

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