University:
West Coast University
Course:
PHAR 837 | IPC Infectious Diseases I
Academic year:

2024
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60

Pages:

63
Author:

Asal A.

•1 LOWER RESPIRATORY TRACT INFECTIONS Su Lee, Pharm.D., M.S., BCIDP, BCPS Recommended Reading: • Metlay JP et al., Diagnosis and Treatment of Adults with Community-Acquired Pneumonia (CAP): An Official Clinical Practice Guideline of the American Thoracic Society (ATS) and Infectious Diseases Society of America (IDSA), Am J Respir Crit Care Med, 2019; 200(7):e4567 • Kalil AC, et al., Management of Adults with Hospital- Acquired and Ventilator-Associated Pneumonia (HAP/VAP): 2016 Clinical Practice Guidelines by IDSA and ATS, CID 2016:1-51 •3 Upper & Lower Respiratory Track Infections • Upper Respiratory Infections • Otitis Media • Rhinosinusitis • Pharyngitis nonparent PENG • Lower Respiratory Infections • Bronchitis • Bronchiolitis (common in infants) • Pneumonia • Influenza → Viral Infections of 839 • Tuberculosis→ Tb Lecture of 839 •4 intraabdominal age Pneumonia : Epidemiology • The most common cause of severe sepsis and infectious cause of death in children and adults in the United States • Inflammation of the lung parenchyma (portion of lungs involved in gas transfer including alveoli or alveolar ducts, generally excluding the bronchi) • Does not follow seasonal patterns and does not discriminate based on age Incidence Mortality Rate Yearly Cost Hospital Community Acquired pneumonia Nosocomial Pneumonia 12/1000 5-15/1000 > 10 % 27-50% $ 9-10 Billion $40,000/Patient •5 Pathophysiology • The lower respiratory tract(LRT) should be sterile • Invasion generally occurs by one of three routes -Inhalation of aerosolized particles -Aspiration of oropharyngeal secretions -Translocation (hematogenous spread) • LRT infections Develops -Defense mechanisms are impaired -Host is overcome by inoculum -Virulent Organism •6 Lung Defense Mechanisms/Impairment • Aerodynamics (particle size) • Upper airway defenses • Anatomical defect ifdoahaveextremelydrymouth moreinfection • nasal polyps, nasal deformities, local tumor • Nasopharyngeal filtration • Mucosal adherence • Respiratory failure, starvation, cystic fibrosis • Bacterial interference • Antibiotic exposure • Saliva • Epiglottis & Cough reflexes • Impaired consciousness, stroke, seizures, drugs, alcohol • Muco-cilliary Clearance • Cystic fibrosis, ciliary dyskinesia, elderly, smoking, alcoholism, respiratory viral infections, narcotics, obstruction • Cellular defenses : PMNs, Macrophages, Lymphocytes • Hypogammaglobinemia • Smoking, hypoxia, alcohol, viral infections • Humoral defenses : Complement, IgG, IgM, IgA • Lymphatic drainage: Sarcoidosis, immunosuppressive agents, steroids, AIDS •8 Pneumonia: Classifications by Type • Community Acquired Pneumonia (CAP) • Aspiration pneumonia • Nosocomial Pneumonia: Pneumonia S/S occurred • Hospital Acquired Pneumonia (HAP) : 48 hours or more after admission • Ventilator Associated Pneumonia (VAP) : 48 hours or more after endotracheal intubation •9 Antimicrobials for empiric therapy of CAP, effective against Major Treatable Bacterial CAP Pathogens • Typical CAP pathogens • Other pathogens • Streptococcus pneumoniae • Viruses • Haemophillus influenzae • Fungi • Moraxella catarrhalis • Less Common Pathogens • Staphylococcus aureus • Atypical CAP pathogens (lack of a cell wall) • N. meningitidis, S. pyogenes, • M. tuberculosis • Legionella spp. • Chlamydia psittaci • Mycoplasma pneumoniae • Coxiella burnetii, B. anthracis • Chlamydophilia(=Chlamydia) pneumoniae • Y.pestis, F. tularensis • Am J Med 106:385,1999 •10 Nochits coughHer jIfPneumonia CAP-Atypical (milder symptoms than typical pneumonia, includes upper air way symptoms, myalgias, fever without chills, headache and unproductive couth) • Usually, a bilateral lobar pneumonia • Legionella spp. • Mycoplasma pneumonia • Chlamydophila(=Chlamydia) pneumoniae • Treatment options • Macrolides • Tetracyclines • Respiratory fluoroquinolones https://www.cdc.gov/pneumonia/atypical/index.html, retrieved on 9/29/21 •11 Pneumonia: Aspiration Pneumonia is pneumonia • Aspiration -Implies gross aspiration of oropharyngeal contents and gastric contents in the patients including : • Alcoholics • in post CVA patients • Sedated patients -Organisms • Peptostreptococcus, Fusobacteria, Bacteroides, Peptococcus and polymicrobial infections including gram negative bacilli and facultative anaerobes as well as Streptococcus and Staphylococcus - 2019 CAP guidelines • Suggest not routinely adding anaerobic coverage of suspected aspiration pneumonia unless lung abscess or empyema is suspected. •12 HAP / VAP : Pathogens • Mostly caused by bacterial pathogens • Rarely fungal or viral in immuno-competent hosts • Common bacterial pathogens include • Gram-positive organisms (Staph aureus, 46%) • More common in patients with diabetes, head trauma, and ICU patients • Gram-negative bacilli • P. aeruginosa (25%), E.coli, Klebsiella pneumoniae, and Acinetobacter spp. • Anaerobes • Increased risk with aspiration, but rare in VAP •13 Bacterial Resistance in Pneumonia • Penicillin Resistant S. pneumoniae (PRSP) • Macrolide Resistant S. pneumoniae (20-40%) • Ampicillin Resistance H. influenzae • Beta-lactamase producing M. catarrhalis • MRSA & CA-MRSA • Multiple Drug-Resistant G(-) • Pseudomonas aeruginosa, Stenotrophomonas maltophilia, Acinetobacter spp, • E.coli, Klebsiella pneumoniae (ESBL) •14 Pneumonia: Signs and Symptoms • Abrupt onset of fever, chills, dyspnea and productive cough • Pleuretic chest pain (inflammation of the lining of the pleural cavity) • Tachypnea and tachycardia • Diminished breath sounds on auscultation • Inspiratory crackles • Low O2 saturation (hypoxia) • Leukocytosis with a predominance of PMN cells • Hemoptysis due to destruction of blood vessels •15 Pneumonia : Diagnosis • Clinical Findings • Fever (> 38°C), purulent sputum, leukocytosis, decline in oxygenation(<95%), worsen respiratory status (Cough, SOB ), and chest pain • Unexplained hemodynamic instability (hypotension) or deterioration of blood gases during mechanical ventilation •16 Pneumonia : Diagnosis • Chest X-ray (ambulatory setting no CXR) • New or progressive infiltrate (congestion, and/or pleural effusion) • Multi-lobal involvement indicates severe disease •17 Pneumonia : Diagnosis • Cultures -Sputum culture • • • • For Severe CAP and those empirically treated for MRSA or Pseudomonas aeruginosa (to de-escalate) For Non-severe CAP with h/o hospitalization and parenteral Abx use in 90 days Colonization vs. pathogen; results less reliable < 10 epithelial cells & > 25 PMN’s per field -Lower respiratory tract culture • Quantitative Broncho-Alveolar Lavage (QBAL) -Invasive culture; results more reliable • Endotracheal aspiration -Noninvasive sampling -Blood culture • For Severe CAP and those empirically treated for MRSA or Pseudomonas aeruginosa (to de-escalate) • For Non-severe CAP with h/o hospitalization and parenteral Abx use in 90 days -Nasal MRSA screening test (PCR, or culture) if negative, D/C MRSA agents (de-escalate) te pisconfine •19 Pneumonia : Diagnosis -Urine Antigen Tests in severe CAP • S. pneumoniae and Legionella -Antibody Test (IgM current vs. IgG past) or molecular test • Mycoplasma pneumoniae or Chlamydophila pneumoniae -Rapid influenza molecular assay in season (nucleic acid amplification test) if positive, 2019 CAP guidelines recommend to use antibacterial therapy + oseltamivir -Testing for COVID-19 is recommended for all patient during the COVID-19 pandemic •20 IDSA/ATS CAP severity criteria • Severe CAP: Validated definition includes either one major criterion or three or more minor criteria • Major criteria • Septic shock with need for vasopressors • Respiratory failure requiring mechanical ventilation • Minor criteria • Respiratory rate ≥ 30 breaths/min • PaO2/FiO2 ratio ≤ 250 • Multi-lobar infiltrates • Confusion/disorientation • Uremia (BUN ≥ 20 mg/dL) • Leukopenia (WBC < 4K due to infection alone) • Thrombocytopenia (PLT < 100K) • Hypothermia (core temp < 36 c) • Hypotension requiring aggressive fluid resuscitation •21 Validated Clinical Prediction Rule for Prognosis Pneumonia Severity Index (PSI) better than CURB-65 • https://img.grepmed.com/uploads/1028/pneumoniaseverityindex-stratification-management-pneumonia-criteria-original.png, retrieved on 9/7/20 •23 Goals of Therapy for Pneumonia • Eradication of the offending organism through selection of the appropriate antibiotic(s) and subsequent complete clinical cure • Minimization of the unintended consequences of therapy including toxicities and selection for secondary infections such as C. diff or MDR pathogens Risk Factors for MRSA or P. aeruginosa • Patients • Were previously infected with MRSA or P. aeruginosa, especially those with prior respiratory tract infection N antibiotics in the last 90 days • Were hospitalized and/or received parenteral •24 Egon •25 Hupertentionis NOIor mobilities •26 Empiric therapy of CAP : Out Pt (PO) • Outpatient without comorbidity EM A Erythromycin agrithromycin Azithromycinfidaxomain M Telithromycin • amoxicillin, doxycycline, or macrolide (if local pneumococcal resistance is < 25%) • Outpatient with comorbidities (chronic heart, lung, liver or renal disease; DM alcoholism; malignancy; or asplenia) Azithromycin • B-lactam PLUS Macrolide or doxycycline or • Amoxicillin/clavulanate, Cefpodoxime, or cefuroxime • Monotherapy with Respiratory Fluoroquinolones • Moxifloxacin, levofloxacin, or gemifloxacin Metlay JP et al. CAP guidelines, AM J Respir Crit Care Med, 2019; 200(7):e45-67 •27 Hospital †Ampicillin + Sulbactam 1.5-3 g q6h, cefotaxime 1-2 q 8 h, ceftriaxone 1-2 g qday, or ceftaroline 600 mg q 12 h and azithromycin 500 mg qday or clarithromycin 500 mg BID ‡Levofloxacin 750 mg qday or moxifloxacin 400 mg qday •28 •29 • Non-severe Inpatient -B-Lactam PLUS Macrolide w ceftriaxone, cefotaxime, ceftaroline • Unasyn, -OR Respiratory fluoroquinolones -If prior respiratory isolation of MRSA or Pseudomonas aeruginosa (PSA) : add coverage and obtain cultures/nasal PCR to allow de-escalation -If hospitalization and parenteral Abx use within 90 days: Withhold MRSA/PSA and obtain cultures/nasal PCR. If positive, add the coverage. •30 • Severe Inpatient orTetracycline lyfe • Unasyn, ceftriaxone, cefotaxime, ceftaroline -B-Lactam PLUS Macrolide or Doty -B-lactam PLUS respiratory fluoroquinolones -If prior respiratory isolation of MRSA or Pseudomonas aeruginosa (PSA) or recent hospitalization and parenteral antibiotics and locally validated risk factors : add coverage and obtain cultures/nasal PCR to allow de-escalation It Is •31 Empiric MRSA/PSA Coverage • MRSA • Vancomycin 15 mg/kg IV q 12 h • Linezolid 600 mg q 12 h • Pseudomonas aeruginosa • Pip/Taz 4.5 g q 6 h or extended infusion (loading 4.5g x 1 dose, and 3.375g over 4 hours q8h) • Ceftazidime 2 g q 8 h • Cefepime 2 g q 8 h • Imipenem 500 mg q 6 h • Meropenem 1 g q 8 h • Aztreonam 2 g q 8 h •33 CAP Treatment Recommendations • CAP prevention (quality standards) -Vaccination status : evaluated at admission -Influenza vaccination : Offered at discharge or outpatient in fall and winter -Pneumococcal vaccination : Persons ≥ 65 YO, risk patients -Smoking cessation • Duration of Therapy at least 5 days • MRSA and PSA at least 7 days (Legionella 7-10 days) • Afebrile for 48-72 hrs and stable, consider discontinuing therapy •34 MRSA Pneumonia agents • Vancomycin IV • Possible issues with lung penetration, slow kill rate (but still bactericidal), failure to shut down toxin projection • Linezolid IV/PO (Zyvox) : excellent lung penetration, bacteriostatic, weak MAOI-serotonin syndrome with SSRI, duration dependent thrombocytopenia, anti-toxin effect • No daptomycin CAP Summary • Common Pathogens: S. pneumo, H. inf, M. cat, S. aureus, Atypicals • Based on PSI>>CURB-65 • Severe CAP criteria : 1 major or 3 minor • Major: Ventilator or Septic shock • Minor; multifocal, RR≥30, PaO2/FIO2, confusion, BUN≥20, WBC<4K, PLT<100K, hypothermia, HOTN requiring fluid • Risk factors for MRSA or PSA • Previous cultured, hospitalization and/or IV Abx within 90 days • Treatment • Outpatient without co-morbidity: Amoxicillin, Doxy, Macrolides (if S. pneumo R < 25%) • Outpatient with co-morbidity(chronic heart, lung, liver, kidney; DM, alcoholism; CA; asplenia): {B-lactam PO (Augmentin, cefpodoxime, cefuroxime) + Macrolides or Doxy}, or Resp. FQs mono Tx • Inpatient non-severe: {B-lactam IV (Unasyn, ceftriaxone, cefotaxime, ceftaroline) + Macrolides} or Resp. FQs mono • If previous MRSA or PSA cultured, add the coverage (MRSA-Vanco IV, Linezolid, PSA-AP B-lactams) and stream down based on nasal screening or C/S • Inpatient severe: B-lactam IV + Macrolides or (B-lactam IV + Resp. FQ) • If previous cultured, or hospitalization and/or IV Abx within 90 days, add the coverage and stream down based on nasal screening or C/S • Duration of tx: at least 5 days •37 Major Pathogens isolated from the Patients with Ventilator Associated Pneumonia: Tracheal Aspirate and/or BAL Fluid cultures and Corresponding Mortality Rates Pathogens : 398 ICU patients from 20 ICUs in US Prevalence Mortality MRSA 59(14.8) 19(32.2) P. aeruginosa 57(14.3) 16(28.6) Other Staphylococcus spp. 35(8.8) 8(22.9) Klebsiella pneumoniae 13(3.3) 3(23.1) Enterobacter spp. 13(3.3) 1(7.7) E.coli 12(3.0) 3(25) Acinetobacter 8(2.0) 4(50.0) No major organism identified 146(36.7) 29(19.0) Neither BAL nor Tracheal culture performed 25(6.3) 9(36.0) BAL or tracheal culture identified as “none” 30(7.5) 8(26.7) Values given as No.(%). Percentage reflect patients in organism category only Chest 2006;129;1210-1218 •38 Risk for MDR Pathogens (2016 HAP/VAP Guidelines) d I on'tthinkitilbe intheexamI • MDR-VAP • Prior IV antibiotic use within 90 days • Septic shock at time of VAP • ARDS preceding VAP • Five or more days of hospitalization prior to the occurrence of VAP • Acute renal replacement therapy prior to VAP onset • MDR-HAP • Prior IV antibiotic use within 90 days • Risk factor for mortality • Ventilator support • Septic shock Septic Shock: sepsis with hypotension despite adequate fluid resuscitation with perfusion abnormalities •39 HAP / VAP : Goals of Treatment • Prevent nosocomial pneumonia by modifying risk factors and decreasing length of ventilator use and hospital stay • Improve oxygen exchange • Clinical cure and microbiologic clearing • Avoid inappropriate (under or over) treatment to decrease mortality, superinfections and resistance •40 Empiric therapy of VAP t ventnor 2016 IDSA/ATS Guidelines Eton A. Anti-MRSA Agents B. Anti-Pseudomonal B-Lactams C. Anti-pseudomonal Non-B-lactams Vancomycin 15 mg/kg IV q 8-12 hrs (Consider a loading dose of 25-30 mg/kg) Piperacillin-Tazobactam 4.5 G IV Q6hrs Or Cefepime 2 G IV Q8h Ceftazidime 2 G IV Q8h Or Imipenem 500 mg IV Q6h Meropenem 1 G IV Q8h Or Aztreonam 2 G IV q8h Cipro 400 mg IV Q8h Levo 750 mg IV Q 24h Or Amikacin 15-20 mg/kg IV Q24h Tobramycin or Gentamicin 5-7 mg/kg IV Q 24h Or Colistin Polymyxin B Or Linezolid 600 mg IV q12h •41 Empiric therapy of HAP/VAP 2016 IDSA/ATS Guidelines • A+B+C • 1. MRSA drugs only in patients with any of the following • A risk factor for antimicrobial resistance (prior IV Abx within 90 days, previous MRSA infections) • In a units where > 20% of MRSA or unknown prevalence • where MRSA < 10 %, use MSSA covering drugs : Nowhere !!! • 2. Recommend two Antipseudomonal antibiotics from different classes for the following cases -Risk factors for antimicrobial resistance ( structural lung diseases such as bronchiectasis or COPD, smoking) -Where > 10% of gram-negative isolates are resistant to an agent being considered for monotherapy, or ICU without antibiogram • 3. If B-lactam resistant rate against pseudomonas or other G(-) ≤ 10 %, consider monotherapy • 4. In VAP, try to avoid aminoglycosides or polymyxins if alternative agents are available •42 in Pacific http://resistancemap.cddep.org/resmap/c/us/united%20states accessed 6/30/2016 S. aureus P. aeruginosa Antibiotics 2012 Resistance (%) Number of isolates Daptomycin 0 689 Fluoroquinolone s 43 848 Linezolid 0 792 Oxacillin (MRSA) 38 1000 Rifampicin 2 830 Vancomycin 0 961 Antibiotics 2012 Resistance (%) Number of isolates Amikacin 1 119 Aminoglycosides 7 123 Carbapenems 20 124 Ceftazidime 14 117 Fluoroquinolones 26 124 Piperacillintazobactam 21 106 •43 Empiric therapy of HAP (non-VAP) 2016 IDSA/ATS Guidelines • Neither risk factor for mortality nor MRSA<10% • Monotherapy of BL or Levofloxacin (MSSA + Pseudomonas) • Pip/Taz, Cefepime, meropenem, or LevofloxacinOs MISA *NO MSSA Antipseudomonal Agents: Ceftazidime, Aztreonam, Ciprofloxacin • Risk factors of MRSA without mortality risk • A (Vancomycin or Linezolid) + B (AP-BL) • High risk of mortality or IV Antibiotics last 90 days • A + B + C (APFQ or AGs) •44 HAP/VAP • Doripenem : Not approved for VAP due to worse mortality • Telavancin : increased mortality in renal impaired patients • Zerbaxa, Avycaz, Recarbrio, Fetroja, Xacduro : just approved for HAP/VAP • Inhaled Antimicrobials • Improved clinical outcome (cure rate) but no mortality benefit • TOBI (tobramycin IH) • Colistin (=Polymyxin E) • IDSA is 2ougally • Vanco vs. linezolid • No preference considering patient factors : clinical trial compared with vancomycin trough 12.5 mg/L vs. Linezolid • Consider patient factors : SSRI, thrombocytopenia, or ARF 24004 Cavani •45 Empiric therapy of HAP/VAP 2016 IDSA/ATS Guidelines • Pseudomonas HAP/VAP with Septic Shock • Suggest using Combination of B+ C • Recommend against aminoglycoside monotherapy • Duration of Therapy : 7 days • De-escalate antibiotic therapy after C/S • Procalcitonin (PCT)* level + clinical criteria • Precursor of calcitonin, secreted by C cells of thyroid gland and K cells of lung (Baseline chronic diseases have high PCT)- Caution in patients with immuno-suppression (including HIV), CF, pancreatitis, trauma, pregnancy, high volume transfusion, malaria Schuetz P et al. Clin Chem Lab Med 2019; 57(9):1308-1318 • When stimulated by endotoxin, PCT is rapidly produced by parenchymal tissue throughout the body, which related to diverse bacterial infections • to guide the discontinuation of antibiotic therapy when < 0.25 or > 80% decrease from baseline • Undetectable in normal ( < 0.1), virus suppress PCT • PCT-guided stewardship should not be applied to patients with chronic infections (e.g. abscess, osteomyelitis, endocarditis) or renal failure Schuetz P et al. •46 • Ceftolozane/Tazobactam(Zerbaxa®) : cIAI, cUTI, HABP/VABP • Activity against many MDR Gram-negative bacilli • Most ESBL and AmpC producers (Enterobacteriaceae Class A, C) • Many carbapenem-resistant MDR-P. aeruginosa • No activity against carbapenemase producers • Limited gram-positive activity, including no Staphylococcal activity nor B. fragilis • MDR- Pseudomonas • 1 G TOL/0.5g TAZ(cUTI, cIAI), 2g TOL/1g TAZ q 8 h (HAP/VAP) • Ceftazidime/Avibactam (Avycaz®) : cIAI, cUTI, HABP/VABP • Enterobacteriacea Class A, C, D (ESBL, KPC, AmpC) • MDR- Pseudomonas • 2g CAZ + 0.5 g IV every 8 h infused over 2h • Imipenem/Relebactam (Recarbrio ) : cIAIs, cUTIs, HABP/VABP • Enterobacteriacea Class A, C (ESBL, KPC, AmpC) • MDR-Pseudomonas • 1g IMI-C + 0.25g REL infused over 30 min • Cefiderocol (Fetroja®) : cUTI, HABP/VABP • Enterobacteriacea Class A, B, C, D • MDR- Pseudomonas • Carbapenem Resistant Acinetobacter • 2g q 8 h infused over 3 hours • Sulbactam/Durloabactam (Xacduro ): HABP/VABP • MDR-Acinetobacter baumannii • 1g of sulbactam + 1 g of durlobactam infused over 3 hours (Q6H) •47 Optimizing Tx • Get in quick with appropriate empiric antibiotics • Hit hard with definitive therapy once pathogen is identified and dose appropriately • Get out ASAP limiting collateral damage • 5 days of therapy for CAP vs. 14 days therapy with conventional dosing • 7 days of therapy for HAP, VAP vs. 14 days therapy • Streamline therapy per culture results HAP/VAP 48hrBeforhospitalizationOR • HAP/VAP: definition tubing • MRSA (risk) + AP B-Lactam + AP non B-Lactam (high risk for mortality as septic shock/ventilator) • MRSA screening negative: D/C MRSA drugs • MRSA cultured: D/C Gram-negative covering drugs, stream down based on the sensitivity or continue MRSA drugs • Certain gram (-)bacteria non-ESBL, non-pseudomonas: D/C MRSA drugs, D/C AP B-Lactam, D/C AP non-BLactam, and stream down based on the sensitivity to narrower spectrum • Pseudomonas cultured: D/C MRSA drugs, stream down based on sensitivity data or you can continue AP BLactam • ESBL positive Enterobacteriaceae cultured: D/C appropriately and starts a carbapenem • Duration of Tx: 7 days • D/C antimicrobials : afebrile (vitals normal) for 48-72 hrs, CXR improved or normalized (no filtration or congestion), WBC normalized, Oximetry >94% in room air, and PCT < 0.25 or >80% decrease from the baseline •51 Acute Bronchitis • Common in adults and children • Usually of viral origin for primary acute bronchitis but secondary infection is often bacterial • May be part of the clinical manifestations of other diseases such as influenza • Most commonly caused by respiratory viruses and is most always self-limiting, resolving within 1-3 weeks. Therapy targets associated symptoms such as lethargy, malaise, or fever and may include fluids for rehydration. Routine use of antibiotics should be avoided and medication to suppress cough is rarely indicated •52 Acute Bronchitis • App. 10% of ambulatory care visits in the US or 100 million visits per year • Most commonly in late fall and winter when transmission of respiratory viruses’ peak • Factors that can precipitate an attack -Cold -Damp climates -Presence of irritants (e.g. pollution or smoke) WWE •53 Acute Bronchitis Viral causes (85-95%) of acute bronchitis -Influenza A and B virus, COVID-19 : will be discussed at Influenza and Coronavirus infections in PHAR 839 -Respiratory syncytial virus (RSV) -parainfluenza virus -Common cold viruses -Rhinovirus, coronavirus -Adenovirus Bacterial causes (much less, app. 6%) of acute bronchitis -Bordetella pertussis-whooping cough -Atypicals including Mycoplasma pneumoniae, Chlamydia pneumoniae -Streptococcus pneumoniae, H. Influenzae, M. cat •54 Acute Bronchitis: Clinical Features • Cough persists for 1-3 wks (median duration of 18 days) • May associated with purulent (not predictive of bacterial infection or response to antibiotics) or non-purulent sputum production • Persistent cough • bronchial hyper-responsiveness: resolving in 6 wks • Chest wall or substernal musculoskeletal pain • Paroxysms of cough by an inspiratory whoop or post-tussive emesis suggest pertussis, particularly during known outbreaks • Runny nose • Sore throat, malaise, headache • Fever or other systemic symptoms are rare, but fever+cough+sputum production = influenza (839) or pneumonia (discussed earlier) •55 Acute Bronchitis Diagnosis • Clinical diagnosis • acute onset but persistent cough (1-3 wks) without pneumonia S/S (eg, fever, tachypnea, rales, signs of parenchymal consolidation) nor COPD • Based on history and physical examination • Chest radiograph • Either normal or nonspecific subtle changes with thickening of bronchial walls • To exclude pneumonia • Abnormal vital signs (PR> 100, RR> 24, Temp> 100.4 F, or O2 saturation < 95%) • Signs of consolidation on chest examination (rales, egophony, or tactile fremitus) • Mental status or behavioral changes in patients > 75 YO • Microbiologic testing: not recommended as no change in management • Suspicion for influenza: acute onset fever and cough, for hospitalized patients at high risk for complications, and health care workers • Testing for COVID-19 is recommended for all patients during the COVID-19 pandemic • Procalcitonin: Do not routinely use, only for uncertain cases • Differential Dx: PNA, COVID-19, GERD, asthma, ACE inhibitor, heart failure, PE, Lung CA •-File TM, Acute bronchitis in adults, uptodate, retrieved on 9/29/21 •56 Treatment • Patient education (Reduce inappropriate antimicrobial use) • Self-limiting 1-3 wks, Abx use is not recommended for routine use • Pts who request Abx: discuss disadvantages, increased risk of ADR, alter microbiomes, CDI(C. diff infection), drug allergies, no help in recovery • 50-90% of patients still got Abx: serious AB overuse! • Symptom control • For cough • Nonpharmacologic therapy: throat lozenges, hot tea, honey, and/or smoking cessation or avoidance of secondhand smoke • Eliminating environmental cough triggers (dust), providing vaporized air treatments (air humidifier), Bed rest and fluids •57 Acute Bronchitis: Treatment • Antipyretics and analgesics for symptoms of lethargy, fever, and malaise (e.g., Acetaminophen, • • • • ibuprofen, aspirin-no children < 19 YO Reye’s syndrome) Cough suppressants, Antitussive (e.g., codeine, dextromethorphan): uncertain benefit in uncomplicated acute bronchitis (caution : in bronchitis as ability to mobilize secretions are likely already diminished) Antihistamines : may prolong recovery due to drying mucosal secretions Expectorants (eg, guaifenesin) : efficacy is questionable, but maybe used to increase expectoration, Extended-release tablets 600–1200 mg PO Q 12 H as needed, immediate-release tablets 200–400 mg PO Q 4 H as needed, or liquid 200–400 mg PO Q 4 H as needed may be recommended. Do not take more than 2400 mg in a 24-hour period. Bronchodilators only for patients with wheezing or airflow obstruction •58 •59 •60 •61 Acute Bronchitis: Antimicrobials • Antibiotics are not indicated for uncomplicated acute bronchitis • Routine use of antibiotics should be discouraged as most cases are of viral etiology, most of the symptoms resolve on their own in 1-3 wks • Cough lasts for longer than 3 weeks, it will need to be re-evaluated • Influenza: most pts with influenza do not require therapy. Treatment is reserved for hospitalized pts or those at high risk for complications, neuraminidase inhibitors (Influenza in PHAR 839) • Pertussis: Antibiotic tx is recommended for pts with cough 3 wks, pregnant female with cough 6 wks, and to limit spread. Macrolides are first-line therapy • Bacterial infection should be suspected when • Fever is persistent, or/and severe respiratory symptoms for more than 5-7 days • Predisposed patients (eg, elderly/frail, COPD, and immune compromised) • Treatment for acute bronchitis d/t Mycoplasma pneumoniae or Chlamydia pneumoniae is not recommended, no benefit • Generally, treatment is directed towards common respiratory pathogens • S.pneumoniae, H.influenzae, Mycoplasma • Usually, antimicrobial therapy will be like that for CAP •63 Chronic Bronchitis • Primarily effects adults • Between 10% and 25% of the adult population (>40yo) • Smoking plays a major role in chronic bronchitis • Smokers have chronic bronchial inflammation • Smokers also have an elevated number of alveolar macrophages • Smoking cessation should be a goal of treatment • Causes • Inhalation of noxious agents • Smoking • Occupational dusts, fumes, and environmental pollution • Host factors: genetic factors • Bacterial/Viral infections • Hall mark • Chronic cough • Excessive production, and expectoration of sputum with a persistent presence of microorganisms in the patient’s sputum •64 Chronic Bronchitis Pathogenesis • Chronic inhalation of irritants thicken • • • • bronchial walls The number of mucous producing goblet cells is drastically increased Hypertrophy of mucous glands occurs Hyper-production of mucous leads to mucous plugging of smaller airways Inflammatory infiltration occurs and residual scarring of small bronchi results as well as weakening of the bronchial walls Treatment • To mobilize and enhance sputum expectoration • chest physiotherapy • humidification of inspired air • oxygen if needed • aerosolized bronchodilators in select patients with demonstrated benefit • possibly antibiotics •65 Chronic Bronchitis Clinical Presentation • Cough accompanied by purulent sputum • • • • • production, bad breath and bad taste Cyanosis, rales, rhonchi and expiratory wheezing, hyper-resonance on percussion Radiograph shows antero-posterior diameter increase of the thoracic cage -Barrel chest Depressed diaphragm with limited mobility Abnormal PFTs A patient who coughs up sputum on “most days” for at least 3 consecutive months each year for 2 consecutive years presumptively has chronic bronchitis •66 Chronic Bronchitis: Diagnosis Microbiologic Evaluation of Secretions • An early morning sample is preferred for testing Goals of Therapy • Reduce the number of exacerbations • Cellular constituents -PMN granulocytes : continued bronchial irritation -Eosinophil : allergic component • Gram staining and culture -Mixture of G (+) and G (-) organisms typically from oropharyngeal flora and tracheal colonization -Typical the common respiratory pathogens (CAP bacteria) • S. pneumoniae, H. influenzae, M. cat • Less common pathogens • Enterobacterales (Klebsiella, Serratia), Pseudomonas • Reduce the severity of chronic symptoms •67 Chronic Bronchitis: Treatment • Smoking cessation • Fluids, humidified air, postural drainage • Bronchodilators • Antimicrobials : controversial -Studies are conflicting as to whether antimicrobials are clinically effective despite the regimen used GOLD guidelines: o Long-term azithromycin and erythromycin therapy reduces exacerbations over one year (Evidence A) o Treatment with azithromycin is associated with an increased incidence of bacterial resistance (Evidence A) and hearing test impairments (Evidence B) • Although controversial, it is recommended to start therapy with 1st line agents in patients with less severe infections •68 Chronic Bronchitis: Antimicrobials for 5 days Preferred Antibiotics • Ampicillin; Amoxicillin; Amoxicillin-clavulanate • Fluoroquinolones (Levofloxacin, moxifloxacin) • Tetracyclines (Doxy, Mino, Tetra) • TMP/SMX Alternative Drugs • Macrolide (Azithro, Erythro, Clarithro) • Cephalexin •69 •70 •71 Summary Bronchitis • Acute Bronchitis • Virus: self-limiting, viral etiology • Abx if fever or/and respiratory S/S persist 5-7 days, or Cough persist > 3 weeks • Abx like CAP • Chronic Bronchitis • COPD: Abx decrease COPD exacerbation, but increase resistance/hearing test impairment • Preferred: Aminopenicillins, Resp. FQs, TCs, Bactrim • Alternatives: Macrolide, Cephalexin Pneumonia • Community acquired pneumonia (typical pathogens vs. atypical pathogens) • Hospital/ventilator associated pneumonia (MRSA, Pseudomonas)

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