What it is:A family of lower airway infections that share a location (below the vocal cords) but almost nothing else: acute bronchitis, an acute exacerbation of chronic bronchitis (AECB), bronchiolitis in infants, and pneumonia (CAP, HAP, VAP, and aspiration). Lumped into one chapter because they're all "cough plus something happening in the lung," but they're treated completely differently.
The core problem:Two questions decide everything. First, is this even bacterial, because most acute bronchitis is viral and antibiotics do nothing but cause harm. Second, if it is bacterial pneumonia, where and how did the patient get it, because the answer to that question tells you which organisms you're up against and whether they're likely to be drug-resistant.
What you do about it:Withhold antibiotics from healthy adults with acute bronchitis. Score pneumonia severity with something objective (CURB-65 or PSI), pick empiric coverage based on setting and resistance risk factors, then narrow the regimen once culture data comes back.
The organizing idea for this whole chapter is the 48-hour clock. Pneumonia onset before 48 hours of hospitalization is CAP. After 48 hours, it's HAP. After 48 hours of endotracheal intubation, it's VAP. That single timestamp is doing enormous work, because it's a proxy for a completely different bug list: CAP is mostly S. pneumoniae, viruses, and atypicals; HAP/VAP is mostly gram-negative rods and S. aureus, and is far more likely to be multidrug-resistant. The clock, not the chest X-ray, is what tells you how wide to swing your empiric antibiotics.
Before picking a drug, sort the patient into a bucket. The bucket determines the pathogen list, and the pathogen list determines the regimen.
| Type | Definition | Key risk factors |
|---|---|---|
| CAP | Onset outside the hospital, or <48 hours after admission | Age >65, diabetes, asplenia, chronic cardiac/pulmonary/renal/liver disease, smoking, alcohol use |
| HAP | Onset >48 hours after hospital admission | Witnessed aspiration, COPD/ARDS/coma, acid suppression (H2RA/PPI), supine positioning, enteral feeding tube, reintubation or tracheostomy, IV antibiotics in prior 90 days (MDR risk) |
| VAP | Onset >48 hours after endotracheal intubation | Same as HAP, plus septic shock, ARDS, acute renal replacement therapy, or ≥5 days of hospitalization preceding the pneumonia (all raise MDR risk) |
Aspiration pneumonia isn't its own bug list, it borrows one.Community-acquired aspiration behaves bacteriologically like CAP; hospital-acquired aspiration behaves like HAP. Anaerobes only enter the picture with specific risk factors (periodontal disease, alcoholism, altered consciousness, esophageal disease), and even then they're a supplement to the CAP/HAP regimen, not a replacement for it.
Bronchitis has its own split that's just as important. Acute bronchitisis a short, usually viral illness in an otherwise normal airway. Chronic bronchitisis a chronic diagnosis (productive cough >3 consecutive months/year for 2 consecutive years, once bronchiectasis and TB are excluded), and what actually brings the patient in is an acute exacerbation of chronic bronchitis (AECB)layered on top of that baseline. Treating an AECB like an episode of acute bronchitis, or vice versa, is a common mix-up. Bronchiolitisis neither of these: it's a distinct viral disease of the small airways that essentially only happens in infants and toddlers.
Infection or irritant exposure (pollution, smoke) inflames the epithelium of the trachea and large bronchi. The mucous membranes become hyperemic and edematous, bronchial secretions increase, and the desquamated epithelial cells mix with thickened mucus to impair mucociliary clearance. Influenza A/B, RSV, and parainfluenza are the dominant causes.Bacteria are a minority player, and when they do appear it's usually the same organisms that cause CAP (S. pneumoniae, H. influenzae) or M. pneumoniae. This is why routine antibiotics don't help: you're treating a virus most of the time.
Years of cigarette smoke, occupational dust and fume exposure, and recurrent infection and inflammation remodel the airway: mucus gland hypertrophy, impaired ciliary function, and a baseline that never fully clears. An AECB happens when that baseline is knocked further off balance, usually by a new viral or bacterial infection. The organisms recovered from sputum during an exacerbation skew toward encapsulated, beta-lactamase-producing gram-negatives and pneumococcus:
| Pathogen | % of cultures |
|---|---|
| H. influenzae | 45% (majority nontypeable; often β-lactamase positive) |
| M. catarrhalis | 30% (β-lactamase positive in 95-100%) |
| S. pneumoniae | 20% (up to 40% intermediate or resistant to penicillin) |
| E. coli, Enterobacter, Klebsiella, P. aeruginosa | 5% |
That β-lactamase burden is exactly why plain amoxicillin is a weaker choice here than amoxicillin-clavulanate or a cephalosporin, and why fluoroquinolones earn their place once P. aeruginosabecomes a concern in patients with frequent, severe exacerbations.
RSV causes up to 75% of cases (parainfluenza, adenovirus, and influenza make up most of the rest). The virus infects and destroys bronchiolar epithelium, triggering edema, mucus hypersecretion, and sloughed cellular debris that plugs the smallest airways. Poiseuille's law is the whole story here:resistance scales with the fourth power of the radius, so in an airway that's already tiny to begin with, a little mucosal swelling causes a huge jump in airway resistance, which is why previously well infants can decompensate quickly. Nearly 50% of infants are affected in year one of life and essentially 100% by age two.
Organisms reach the lower respiratory tract by direct inhalation of infectious droplets, aspiration of oropharyngeal contents, or hematogenous spreadfrom an infection elsewhere. In CAP, the most common bacterial cause by far is S. pneumoniae(up to 35% of cases), with H. influenzaeand the atypicals (M. pneumoniae, C. pneumoniae, Legionella) filling out the list; viruses (rhinovirus, influenza) are actually the single most common cause overall, and dominate even more heavily in young children (up to 80% under age 2).
HAP/VAP looks completely different because the exposure is completely different: a hospitalized, often intubated patient is colonized by hospital flora, not community flora. P. aeruginosaand Acinetobacteraccount for roughly 25-45%of HAP, with Klebsiellaand E. colialso common, and S. aureus(frequently MRSA) is a major player. Intubation itself raises pneumonia risk 6- to 21-fold by bypassing the cough reflex and glottic closure that normally protect the lower airway.
Acid-suppressing drugs (H2RAs, PPIs) raise HAP risk. The mechanism: gastric acid is a chemical barrier that normally kills swallowed organisms. Raise the pH and the stomach becomes a reservoir where bacteria proliferate; supine positioning and enteral tubes then make it easy for that colonized gastric content to be aspirated into the lung. It's not a side effect of the drug class acting on the lung, it's the drug removing a defense two organs away.
Starts like a cold, then cough becomes the hallmarkand outlasts everything else, sometimes for 3 weeks or more. Cough is initially dry, then often turns mucopurulent (mucopurulent sputum does notmean bacterial infection, this is a common trap). Fever, when present, rarely exceeds 39°C (102.2°F) and is most typical with adenovirus, influenza, or M. pneumoniae.
Acute bronchitis should nothave wheezing, shortness of breath, or hypoxemia as prominent features. If those are present, think asthma or bronchiolitis instead, and reconsider the diagnosis.
Baseline is a productive cough, often worst on waking, with tenacious sputum ranging white to yellow-green. An exacerbation is recognized by the Anthonisen criteria: increased dyspnea, increased sputum volume, and increased sputum purulence. Advanced chronic disease can show cyanosis, digital clubbing, a barrel chest, hyperresonance to percussion, and diminished normal breath sounds with prolonged expiration.
Preceded by 1-4 days of upper respiratory symptoms (rhinorrhea, congestion, low-grade fever), then progressing to cough, tachypnea (RR 40-80 in hospitalized infants), wheeze and inspiratory rales, retractions, nasal flaring, and grunting. Vomiting and diarrhea plus poor oral intake from coughing frequently produce dehydration. Mild conjunctivitis occurs in about a third of patients and otitis media in 5-10%.
Different disease, different age group, different bug profile, different treatment. Bronchiolitis is a viral small-airway disease almost exclusively of infants; bronchitis is a large-airway disease seen at any age. Mixing the names up on an exam or a chart is an easy way to pick the wrong management pathway.
| Typical (bacterial) | Atypical (M. pneumoniae, C. pneumoniae) | |
|---|---|---|
| Onset | Abrupt | Gradual |
| Symptoms | Fever, chills, productive cough, rust-colored sputum or hemoptysis, pleuritic chest pain, dyspnea | Milder, plus prominent extrapulmonary/constitutional complaints (headache, myalgia, malaise) |
| Exam | Tachypnea, tachycardia, dullness to percussion, increased tactile fremitus, whispered pectoriloquy, egophony, inspiratory crackles | Often unremarkable relative to symptoms |
| CXR | Dense lobar or segmental infiltrate | Patchy, less dramatic |
| Labs | Leukocytosis with PMN predominance, low oxygen saturation | Often unremarkable |
This split is why empiric CAP regimens almost always cover bothcategories at once (a beta-lactam for typical pathogens plus a macrolide or doxycycline for atypicals) rather than betting on one presentation being reliably distinguishable from the other in practice.
Acute bronchitis, AECB, and bronchiolitis are all diagnosed by history and exam. Sputum culture in acute bronchitis is essentially uselessbecause expectorated samples can't avoid contamination by normal nasopharyngeal flora, and for the vast majority of patients an etiologic diagnosis wouldn't change the (supportive) treatment anyway. RSV PCR is readily available for bronchiolitis but is not recommended routinely, since a positive or negative result doesn't change management for most infants.
Chest radiograph and sputum/blood cultures are the key diagnostic tools for bacterial pneumonia. Blood and noninvasive sputum cultures are recommended for all adults with suspected HAP or VAP(culture data is what lets you de-escalate later). Once pneumonia is suspected, the next step isn't "admit or don't," it's calculating a validated severity score.
| CURB-65 criterion | Threshold (1 point each) |
|---|---|
| Confusion | New disorientation, increased from baseline |
| Urea | BUN >20 mg/dL (7.1 mmol/L) |
| Respiratory rate | ≥30 breaths/min |
| Blood pressure | Systolic <90 mm Hg or diastolic ≤60 mm Hg |
| Age 65 | ≥65 years |
Score <2:outpatient treatment is generally appropriate. Score of 2:admit to a general medical ward. Score ≥3:consider ICU-level care. The Pneumonia Severity Index (PSI)is the tool IDSA guidelines actually prefer, and it's more elaborate (age, comorbidities, exam findings, labs, and imaging all feed into a mortality-risk score), but CURB-65 is the one you can calculate at the bedside in ten seconds, which is why it shows up constantly in practice and on exams.
Goal is comfort, plus treating dehydration or respiratory compromise in the rare severe case. Reassurance, fluids, and antipyretics/analgesics are usually sufficient: acetaminophen 650 mg (adults) or ibuprofen 200-800 mg (adults)every 6-8 hours, weight-based in kids. Avoid aspirin in patients under 19because of the Reye syndrome association with viral illness, use acetaminophen instead. Dextromethorphan covers a bothersome mild cough; more severe cough may warrant codeine in adults, but codeine is no longer recommended in pediatric patients. Inhaled beta-agonists and corticosteroids show no meaningful benefit in otherwise healthy patients.
Antibiotic therapy in acute bronchitis is strongly discouraged. The exception is a patient with persistent fever or respiratory symptoms beyond 5-7 days, where a concurrent bacterial infection becomes plausible; then target likely CAP pathogens (S. pneumoniae, H. influenzae), or azithromycin/a respiratory fluoroquinolone if M. pneumoniaeis suspected clinically or confirmed.
Stable-disease management overlaps heavily with COPD care: reduce exposure to smoking and occupational irritants, pulmonary rehabilitation, chest physiotherapy and humidification for tenacious secretions, and inhaled bronchodilator therapy (short-acting agents as needed, LABA/LAMA regularly, LABA+ICS combinations for more advanced disease). Long-acting theophylline remains a useful, cheap add-on for severe disease. Roflumilast (a PDE-4 inhibitor) is reserved for moderate-to-severe disease with frequent exacerbations.
For an AECB, antibiotics are decided by the Anthonisen criteria: the more of the three cardinal symptoms present (increased dyspnea, increased sputum volume, increased sputum purulence), the stronger the case for antibiotics. The algorithm then splits by severity:
Using the upper limit of the recommended daily dose for 5-7 daystends to extend symptom-free intervals between exacerbations.
In a well infant, this is self-limiting: reassurance, antipyretics, adequate fluids, done. In severe disease the mainstays are oxygen and IV fluids, not drugs. Aerosolized beta-agonists offer little benefit and may even worsen things; systemic corticosteroids are not recommended. The AAP does support nebulized hypertonic (3%) salinefor hospitalized infants. Ribavirin is not used routinely and is reserved for the most severely ill. For high-risk infants (underlying pulmonary or cardiac disease), RSV prophylaxis during RSV season with palivizumab(a monoclonal antibody) is preferred over RSV immune globulin because of easier administration, no administration-related adverse effects, and no interference with routine immunizations.
CURB-65 or PSI decides outpatient vs ward vs ICU.
CAP, HAP, or VAP by the 48-hour clock. This sets the baseline pathogen list.
Prior MRSA or P. aeruginosa, recent IV antibiotics, structural lung disease, local resistance rates.
| Setting | Regimen |
|---|---|
| Outpatient CAP | |
| No comorbidities | Amoxicillin (preferred), OR doxycycline, OR a macrolide (only where pneumococcal macrolide resistance is <25%) |
| Comorbidities (diabetes, chronic heart/lung/liver/renal disease, alcoholism, malignancy, asplenia) or immunosuppression | An antipneumococcal fluoroquinolone (levofloxacin/moxifloxacin) alone, OR a beta-lactam plus a macrolide or doxycycline |
| Inpatient CAP | |
| Nonsevere | Beta-lactam + (macrolide or doxycycline). Add antipneumococcal fluoroquinolone if prior respiratory MRSA hx; add vancomycin/linezolid if prior MRSA (obtain cultures, de-escalate at 48h if negative); add antipseudomonal coverage if prior Pseudomonasor recent hospitalization/IV antibiotics (90 days) |
| Severe | Beta-lactam + (macrolide or antipneumococcal fluoroquinolone), with the same MRSA/Pseudomonasadd-ons as above based on risk factors |
| HAP | |
| Low mortality risk, no MDR factors, local MRSA <20% | Piperacillin-tazobactam, cefepime, levofloxacin, imipenem, OR meropenem |
| Low mortality risk, no MDR factors, local MRSA ≥20% or unknown | Same options + ciprofloxacin/aztreonam choice, PLUS vancomycin or linezolid |
| High mortality risk OR MDR risk factor(s) | Double-coverP. aeruginosawith two agents from different classes, PLUS vancomycin or linezolid |
| VAP | |
| No MDR risk, local resistance both <10% | Piperacillin-tazobactam, cefepime, levofloxacin, imipenem, OR meropenem |
| No MDR risk, local MRSA ≥10%/unknown | Same gram-negative options PLUS vancomycin or linezolid |
| MDR risk factor(s) OR high local resistance | Double-cover P. aeruginosa(2 different classes) PLUS vancomycin or linezolid |
| Aspiration pneumonia | |
| Community-acquired | Treat as CAP above |
| Hospital-acquired | Treat as HAP above |
| Anaerobes suspected (periodontal disease, alcoholism, altered consciousness) | Add clindamycin or metronidazole, or use an agent with intrinsic anaerobic coverage |
Minimum CAP duration is 5 days, though 7-10 days is common in practice. Before stopping, the patient should be afebrile for 48-72 hourswith no more than one sign of clinical instability (tachycardia, tachypnea, hypotension, hypoxia, altered mental status). HAP/VAP duration is 7 days; extending past 10 days hasn't shown clear added benefit and just adds resistance pressure and toxicity. De-escalationfrom broad empiric coverage to a narrower, culture-directed regimen is strongly recommended for HAP/VAP once cultures return negative for MRSA or Pseudomonasand the patient is improving.
| Antibiotic | Usual adult dose |
|---|---|
| Penicillins | |
| Ampicillin ± sulbactam | 2 g IV every 4-6 hours (every 6 hours if ampicillin-sulbactam) |
| Amoxicillin ± clavulanate | 875-2000 mg orally twice daily |
| Piperacillin-tazobactam | 3.375-4.5 g IV every 6-8 hours |
| Cephalosporins / monobactam | |
| Ceftriaxone / cefotaxime | 1-2 g IV daily / 1-2 g IV every 8 hours |
| Ceftazidime / cefepime | 1-2 g IV every 8 hours / 1-2 g IV every 6-8 hours |
| Ceftolozane-tazobactam | 3 g IV every 8 hours |
| Ceftazidime-avibactam | 2.5 g IV every 8 hours |
| Aztreonam | 1-2 g IV every 8 hours |
| Macrolides / azalides | |
| Azithromycin | 500 mg day 1, then 250 mg days 2-5 (IV or oral) |
| Clarithromycin | 0.5-1 g orally once or twice daily |
| Erythromycin | 500 mg IV or orally every 6-8 hours |
| Fluoroquinolones | |
| Moxifloxacin | 400 mg IV or orally daily |
| Levofloxacin | 750 mg IV or orally daily |
| Ciprofloxacin | 400 mg IV every 8 hours / 750 mg orally twice daily |
| Tetracyclines | |
| Doxycycline | 100 mg IV or orally twice daily |
| Carbapenems | |
| Imipenem | 500-1000 mg IV every 6-8 hours |
| Meropenem | 500-2000 mg IV every 6-8 hours |
| Meropenem-vaborbactam | 2 g/2 g IV every 8 hours |
| Aminoglycosides | |
| Gentamicin / tobramycin | 7.5 mg/kg IV daily (each) |
| Amikacin | 15-20 mg/kg IV daily |
| Polymyxins | |
| Colistin | IV: 300 mg × 1, then 150 mg daily; nebulized: 150 mg every 8 hours |
| Polymyxin B | 2-2.5 mg/kg × 1, then 1.25-1.5 mg/kg every 12 hours |
| Other / anti-MRSA | |
| Vancomycin | 15-20 mg/kg IV every 8-12 hours |
| Linezolid | 600 mg IV or orally every 12 hours |
| Clindamycin | 600 mg IV or orally every 8 hours, or 450 mg orally every 6 hours |
| Oral options for AECB specifically | |
| Amoxicillin-clavulanate | 500-875 mg 2-3 times daily |
| Doxycycline | 100 mg twice daily |
| TMP-SMX DS | 1 tablet twice daily |
| Levofloxacin / moxifloxacin | 500-750 mg daily / 400 mg daily |
These are the backbone of nearly every empiric regimen in this chapter because they cover typical CAP pathogens and, at the antipseudomonal end (piperacillin-tazobactam, cefepime, ceftazidime, imipenem, meropenem, aztreonam), the gram-negatives that dominate HAP/VAP.
Ceftriaxone is the only cephalosporin that does not need renal dose adjustment(hepatobiliary elimination). Nafcillin and oxacillin also don't need adjustment. Nearly every other beta-lactam does.
Carbapenem pearl:all carbapenems cover Pseudomonasexcept ertapenem, which is why ertapenem is not on the HAP/VAP lists above despite being a carbapenem.
These cover the "other half" of CAP: M. pneumoniae, C. pneumoniae, and Legionella. That's why a beta-lactam is so often paired with one of these rather than used alone, and why doxycycline or a macrolide can stand on their own in a healthy outpatient with a low pretest probability of resistant pneumococcus.
Never pair clarithromycin or erythromycin with simvastatin or lovastatin(CYP3A4 inhibition raises statin levels and rhabdomyolysis risk). Both also prolong QTc and carry hepatotoxicity risk. Empiric macrolide monotherapy for CAP is only appropriate where local pneumococcal macrolide resistance is <25%,otherwise it's an unreliable single agent.
Renal note:azithromycin and erythromycin need no renal adjustment. Clarithromycin is the odd one out among macrolides and doesrequire adjustment in renal impairment.
Levofloxacin and moxifloxacin cover typical andatypical CAP pathogens well enough to be used as single agents, which is convenient but also means they get overused. Ciprofloxacin lacks reliable pneumococcal activity and isn't a CAP drug, its role here is gram-negative/Pseudomonascoverage in HAP/VAP.
Tendon rupture and peripheral neuropathy (can be irreversible), QT prolongation (worst with moxifloxacin), aortic aneurysm/dissection risk (avoid in patients with known aneurysm or major risk factors: PAD, hypertension, Marfan or Ehlers-Danlos syndrome, elderly), dysglycemia (hypo- or hyperglycemia, occasionally severe), and psychiatric adverse effects that can occur after a single dose. Photosensitivity too. Separate dosing from antacids, and calcium/iron/zinc products by 1-2 hours before or 4 hours after, since divalent/trivalent cations chelate the drug and tank absorption.
Renal shortcut:moxifloxacin is the only fluoroquinolone that does notrequire renal dose adjustment (hepatic elimination), which also means it's a poor choice for a lower urinary tract infection since little reaches the urine unchanged, but it's perfectly fine for pneumonia.
Vancomycin and linezolidare the two options for suspected or confirmed MRSA pneumonia. Vancomycin needs trough or AUC-guided monitoring and renal dose adjustment; linezolid doesn't need renal adjustment but carries its own baggage (thrombocytopenia with courses beyond 2 weeks, serotonin syndrome risk with serotonergic drugs, peripheral/optic neuropathy with prolonged use).
Daptomycin is inactivated by pulmonary surfactant and should never be used for pneumonia, MRSA or otherwise, even though it's a perfectly good MRSA drug everywhere else in the body. This trips people up because daptomycin otherwise looks like a natural vancomycin alternative.
Double-covering Pseudomonasin high-risk HAP/VAP means picking two agents that are active against it from two different classes(for example, an antipseudomonal beta-lactam plus an aminoglycoside or fluoroquinolone), specifically to raise the odds that at least one agent is active while susceptibility data is pending. Delafloxacinis worth knowing as the one fluoroquinolone with activity against both MRSA and Pseudomonasin a single molecule, though it's more often discussed for skin infections than pneumonia specifically.
| Age | Usual pathogens | Empiric therapy |
|---|---|---|
| <1 month | Group B strep, H. influenzae, E. coli, S. aureus, Listeria, CMV/RSV/adenovirus | Ampicillin-sulbactam, a cephalosporin, or a carbapenem (note: cephalosporins don't cover Listeria) |
| 1-3 months | Atypicals (C. pneumoniae, Ureaplasma), CMV, Pneumocystis; also S. pneumoniae, S. aureus | Macrolide/azalide or TMP-SMX; semisynthetic penicillin or cephalosporin for the bacterial possibilities |
| Preschool, viral picture | Rhinovirus, RSV, influenza, parainfluenza, adenovirus | Antimicrobials not routinely required |
| Preschool/school-age, mild-moderate bacterial CAP | S. pneumoniae, M. pneumoniae, other atypicals | Amoxicillin or cephalosporin; macrolide/azalide (or fluoroquinolone in school-age) for atypicals |
| Inpatient, fully immunized | S. pneumoniae, CA-MRSA, atypicals | Ampicillin, penicillin G, or a cephalosporin; add vancomycin/clindamycin for MRSA; add a macrolide/fluoroquinolone/doxycycline for atypical coverage |
Fluoroquinolones are traditionally avoided in children because of concern for cartilage damage in animal models, but they've been used safely for MDR infections in infants and children when the benefit clearly outweighs the theoretical risk. Tetracyclines are avoided under age 8 for permanent tooth discoloration.
Infants with underlying pulmonary or cardiovascular disease benefit from RSV prophylaxis during RSV season. Palivizumab(monoclonal antibody, monthly IM dosing) is preferred over RSV immune globulin for ease of administration, lack of infusion-related adverse effects, and because it doesn't interfere with the infant's other scheduled immunizations.
Periodontal disease, alcoholism, and altered consciousness (sedation, seizure, stroke, intubation) are the classic setups for aspiration. The organism list still follows the CAP/HAP split by setting, anaerobic coverage (clindamycin or metronidazole) is an additionfor suspected anaerobic involvement, not the primary regimen.
| Parameter | When | Watching for |
|---|---|---|
| Fever curve / vitals | Daily until improving | Afebrile 48-72h + ≤1 sign of instability before stopping antibiotics in CAP |
| Clinical response, CAP | First 48-72 hours | Progress expected by day 2, full resolution by day 5-7; if worsening, reassess for wrong bug, wrong drug, empyema, or a noninfectious mimic |
| Clinical response, HAP/VAP | 48-72 hours after starting therapy | Lack of improvement should trigger re-assessment and possible broadening; culture-negative and improving at 48-72h supports de-escalation |
| Vancomycin trough/AUC | Before 3rd-5th dose (steady state) | Sub-therapeutic exposure vs nephrotoxicity |
| Renal function (SCr, CrCl) | Baseline and periodically on renally-cleared agents | Need for dose adjustment (most beta-lactams, vancomycin, aminoglycosides, fluoroquinolones except moxifloxacin) |
| QTc | Baseline if on other QT-prolonging drugs | Macrolides and fluoroquinolones (moxifloxacin especially) add risk |
| CBC / WBC trend | Daily while inpatient | Resolving leukocytosis; new cytopenia with prolonged linezolid |
| Oxygen saturation, work of breathing | Continuous in hospitalized bronchiolitis or severe pneumonia | Need for supplemental O2, escalation of respiratory support |
| AECB symptom-free interval / FEV1 | Follow-up visits | Whether the exacerbation frequency or severity is worsening over time |