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Summary Table

Domain	Details
Risk Factors	Prior pneumonia, COPD, asthma, heart failure, diabetes mellitus, cerebrovascular disease/stroke, immunosuppression (cancer, HIV), chronic liver disease, chronic kidney disease, aspiration risk (seizure disorder, dysphagia/reflux), smoking, alcohol use, poor oral hygiene, malnutrition, immunosuppressive therapy, oral steroids, acid-suppressive medications
Etiology	CAP: Streptococcus pneumoniae (most common globally), Klebsiella pneumoniae (most common in Indonesian data), Haemophilus influenzae, atypicals (Mycoplasma, Chlamydia, Legionella). HAP/VAP: Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, Staphylococcus aureus (including MRSA)
Patient Presentation	Acute onset cough, chest pain, dyspnea, purulent sputum, fever >38 degrees C; elderly patients may present atypically with altered mental status, disorientation, or decreased appetite
Classic Physical Exam	Signs of consolidation, bronchial breath sounds, crackles (ronki)
Key Diagnostic Results	Chest radiograph showing infiltrate/opacity/consolidation/air bronchogram; leukocytosis >10,000 or leukopenia <4,500 with left shift; sputum Gram stain and culture (quality specimen: epithelial cells <10/lpf, leukocytes >25/lpf)
Management	CAP outpatient without comorbidity: Amoxicillin, or Doxycycline, or Macrolide. CAP outpatient with comorbidity: Amoxicillin-clavulanate or Cephalosporin PLUS Macrolide or Doxycycline; OR Respiratory fluoroquinolone monotherapy. CAP inpatient nonsevere: Beta-lactam PLUS Macrolide; OR Respiratory fluoroquinolone. CAP inpatient severe: Beta-lactam PLUS Macrolide; OR Beta-lactam PLUS Respiratory fluoroquinolone. HAP/VAP: Empiric regimen based on local antibiogram, MRSA risk, and Pseudomonas risk
Keywords	"Infiltrate on chest X-ray," "community-acquired," "nosocomial," "ventilator-associated," "CURB-65," "PSI," "air bronchogram," "purulent sputum," "empiric antibiotics," "de-escalation"

1. Pathophysiology

Pneumonia is an acute inflammation of the lung parenchyma caused by infectious pathogens including bacteria, viruses, fungi, and parasites, but excluding Mycobacterium tuberculosis. The PNPK Pneumonia Dewasa 2023 focuses on bacterial pneumonia in adults.

The pathogenic mechanism begins when microorganisms breach the host's respiratory defense barriers. Under normal conditions, the upper airway filters, warms, and humidifies inspired air, while mucociliary clearance and cough reflexes remove pathogens. Alveolar macrophages serve as the last line of innate defense. When these mechanisms are overwhelmed or impaired, whether by high pathogen inocula, virulent organisms, or compromised host defenses, bacteria colonize the lower respiratory tract and trigger an inflammatory cascade.

Bacterial adherence to the alveolar epithelium activates resident macrophages, which release cytokines (IL-1, IL-6, TNF-alpha). This recruits neutrophils into the alveolar space, causing the hallmark exudative process: protein-rich fluid, inflammatory cells, and fibrin fill the alveoli. This explains why you see consolidation on imaging: the air-filled alveoli become fluid-filled, producing opacity on chest radiograph and bronchial breath sounds on auscultation. The air bronchogram sign occurs because the airways remain patent while the surrounding parenchyma is consolidated.

The systemic inflammatory response accounts for fever, leukocytosis, and elevated inflammatory markers such as CRP and procalcitonin. The ventilation-perfusion mismatch caused by fluid-filled, non-ventilated alveoli that continue to be perfused explains the hypoxemia and dyspnea seen clinically.

Pneumonia is classified based on where infection is acquired:

Community-Acquired Pneumonia (CAP) is acquired outside the hospital setting. The dominant pathogen globally is S. pneumoniae, though Indonesian data from 2015 show K. pneumoniae (14%) and S. pneumoniae (13%) as the leading isolates from sputum cultures.
Hospital-Acquired Pneumonia (HAP) develops >48 hours after hospital admission, not in incubation at the time of admission. Ventilator-Associated Pneumonia (VAP) develops >48 hours after endotracheal intubation. Both carry a higher burden of Gram-negative and drug-resistant organisms. Data from RSUPN Dr. Cipto Mangunkusumo (2018) showed K. pneumoniae (27.1%), A. baumannii (23.4%), A. lwoffii (7.4%), and P. aeruginosa (6.1%) as the predominant HAP/VAP pathogens.

The concept of aspiration is central to HAP pathogenesis. Over 45% of healthy individuals aspirate oropharyngeal secretions during sleep. In debilitated hospitalized patients, impaired consciousness, suppressed cough reflex, and reduced ciliary function allow colonizing bacteria from the oropharynx to reach the lower airways.

The PNPK Pneumonia Dewasa 2023 notes that the former category of Healthcare-Associated Pneumonia (HCAP) has been removed from guidelines. Prospective studies found that contact with healthcare settings alone does not independently predict multidrug-resistant (MDR) pathogens, so HCAP is no longer a separate clinical entity.

2. Classification and Clinical Manifestation

Typical vs. Atypical

Feature	Typical Pneumonia	Atypical Pneumonia
Onset	Acute	Gradual
Fever	High, with rigors	Lower grade
Cough	Productive	Non-productive (dry)
Sputum	Purulent	Mucoid
Associated symptoms	Rare extrapulmonary symptoms	Headache, myalgia, sore throat, hoarseness, ear pain
Extrapulmonary manifestations	Less common	Common
Gram stain	Gram-positive or Gram-negative cocci/bacilli	Normal flora or non-diagnostic
Radiology	Lobar consolidation	Patchy interstitial infiltrates, or normal
Leukocyte count	Elevated	Normal or low
Liver function abnormality	Rare	Common

Atypical pathogens include Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella spp., Chlamydia psittaci, and Coxiella burnetii. These organisms are intracellular or lack a cell wall, making them inherently resistant to beta-lactams and requiring treatment with macrolides or fluoroquinolones.

By Site of Acquisition

Category	Definition
Community-Acquired Pneumonia (CAP)	Acute parenchymal infection acquired outside the hospital
Hospital-Acquired Pneumonia (HAP)	Pneumonia occurring >48 hours after hospital admission, not incubating at time of admission
Ventilator-Associated Pneumonia (VAP)	Pneumonia occurring >48 hours after endotracheal intubation

Severity Classification: CURB-65

Component	Criterion	Score
C (Confusion)	Abbreviated Mental Test score of 8 or below	1
U (Uremia)	BUN >40 mg/dL	1
R (Respiratory rate)	30 breaths/min or more	1
B (Blood pressure)	Systolic <90 mmHg or Diastolic 60 mmHg or below	1
65 (Age)	65 years or older	1

CURB-65 is interpreted as follows:

CURB-65 Score	Risk	Disposition
0 to 1	Low mortality	Outpatient
2	Moderate mortality	Consider inpatient
3 or more	High mortality; manage as severe pneumonia	Inpatient
4 to 5	Very high mortality	Consider ICU admission

Severity Classification: PSI (Pneumonia Severity Index)

PSI Class	Total Points	Mortality	Disposition
I	Not predicted	0.1%	Outpatient
II	<70	0.6%	Outpatient
III	71 to 90	2.8%	Inpatient or outpatient
IV	91 to 130	8.2%	Inpatient
V	>130	29.2%	Inpatient

The PSI incorporates 20 variables including age, sex, nursing home residence, comorbidities (malignancy +30, liver disease +20, heart failure +10, cerebrovascular disease +10, renal disease +10), physical exam findings, and laboratory values. The PNPK recommends using CURB-65 as the standard, with PSI available for hospitals with more complete facilities.

IDSA/ATS 2007 Criteria for Severe CAP

Severe pneumonia is defined by at least one major criterion or three or more minor criteria.

Minor criteria: respiratory rate 30/min or more, $PaO_2/FiO_2$ ratio 250 or below, multilobar infiltrates, confusion/disorientation, uremia (BUN 20 mg/dL or more), leukopenia (<4,000), thrombocytopenia (<100,000), hypothermia (core temperature <36 degrees C), hypotension requiring aggressive fluid resuscitation.

Major criteria: need for mechanical ventilation, septic shock requiring vasopressors.

3. Diagnostic Workup

Test	Role	Key Findings
Chest radiograph (PA)	Best initial test for all suspected pneumonia	Infiltrate, opacity, consolidation, air bronchogram
CT scan thorax	Most accurate imaging; used when CXR is inconclusive or pneumonia is complex/recurrent	Higher sensitivity for parenchymal disease, complications, alternative diagnoses
Thoracic ultrasound	Adjunct for peripheral lesions and complications	Effusion, empyema, pneumothorax
Sputum Gram stain and culture	Identify causative organism (gold standard for microbiologic diagnosis)	Adequate specimen: epithelial <10/lpf, leukocytes >25/lpf
Blood culture	Detect bacteremia in inpatients, especially severe CAP	Positive in a minority but changes management
Procalcitonin (PCT)	Assess severity, guide antibiotic discontinuation	Elevated in bacterial infection; do not withhold antibiotics based on initial PCT
CRP	Alternative inflammatory marker if PCT unavailable	>100 mg/L associated with worse prognosis and need for mechanical ventilation
Multiplex PCR (syndromic panel)	Rapid pathogen identification (detects 27 pathogens + 7 resistance genes)	Guides early targeted therapy for both bacteria and viruses
Urinary antigen (Pneumococcus)	Not routine; used in severe CAP	Detects S. pneumoniae
Urinary antigen (Legionella)	Not routine; used in severe CAP or epidemiologic suspicion	Detects L. pneumophila serogroup 1
CBC, BMP, liver function, ABG	Severity assessment (PSI scoring), organ dysfunction	Leukocytosis/leukopenia, elevated BUN, hyponatremia, hyperglycemia, low hematocrit, hypoxemia

Chest radiograph is the cornerstone of pneumonia diagnosis. The PNPK Pneumonia Dewasa 2023 states that clinical signs and symptoms alone have low diagnostic accuracy. The diagnosis of pneumonia is confirmed when imaging demonstrates infiltrate, opacity, consolidation, or air bronchogram in combination with acute onset of supportive clinical features: cough, chest pain, dyspnea, purulent sputum, fever >38 degrees C, signs of consolidation on exam, and leukocytosis (>10,000) or leukopenia (<4,500) with a left shift.

If a patient shows clinical improvement within 5 to 7 days, a repeat chest radiograph is not necessary. This is an important testing principle: imaging should be repeated only when clinical improvement is not achieved or when clinical deterioration occurs.

CT scan of the chest (with or without contrast) is the most accurate radiologic test. Indications include: clinical suspicion with non-diagnostic CXR, severe/complex/recurrent pneumonia, immunocompromised patients, failure to respond to adequate therapy, suspicion of an underlying condition (malignancy, TB, interstitial lung disease, lung abscess). Contrast is added when malignancy is suspected.

Sputum culture remains the microbiologic gold standard, but sputum quality must be verified first. A valid specimen contains fewer than 10 epithelial cells and more than 25 leukocytes per low-power field. Invalid specimens include saliva and samples delivered to the laboratory beyond 2 hours without cold chain (2 to 8 degrees C). For outpatients, routine sputum and blood cultures are not recommended. For inpatients, Gram stain and culture should be obtained before starting empiric antibiotics, particularly in severe CAP (especially intubated patients), patients receiving empiric MRSA or Pseudomonas coverage, those with a prior respiratory isolate of MRSA or P. aeruginosa, and those hospitalized and given parenteral antibiotics within the preceding 90 days.

Procalcitonin is not ordered routinely. A normal PCT does not exclude bacterial pneumonia, and antibiotics should not be withheld pending the result. PCT is useful in follow-up: to assess response to treatment and to guide antibiotic discontinuation when clinical signs of systemic inflammation persist. This is a commonly tested concept: the role of PCT is in de-escalation, not in initial decision-making.

CRP above 100 mg/L can help determine prognosis and the need for mechanical ventilation but has low specificity for infection.

For HAP/VAP, the diagnostic criteria (per CDC-Atlanta) require a new or progressive opacity/consolidation/infiltrate on imaging plus at least two of the following: temperature >38 degrees C, purulent secretions, crackles or bronchial breath sounds, leukocytosis (>12,000) or leukopenia (<4,000), worsening oxygenation (SpO2 <94%, increased oxygen requirement, increased ventilator demand) or ABG showing decreased PaO2 ($PaO_2/FiO_2$ <240).

4. Management and Treatment

CAP Outpatient

Patient Profile	Regimen
*No comorbidities, no MRSA/Pseudomonas* risk**	Amoxicillin OR Doxycycline 2x100 mg OR Macrolide (Azithromycin 500 mg day 1, then 250 mg/day; or Clarithromycin 2x500 mg)
With comorbidities (chronic heart, lung, liver, kidney disease; diabetes; malignancy; asplenia)	Amoxicillin-clavulanate 3x500/125 mg (or Cephalosporin: Cefpodoxime 2x200 mg or Cefuroxime 2x500 mg) PLUS Macrolide or Doxycycline OR Respiratory fluoroquinolone monotherapy (Levofloxacin 1x750 mg or Moxifloxacin 1x400 mg)

CAP Inpatient (Nonsevere)

Scenario	Regimen
Standard	Beta-lactam (Ampicillin-sulbactam 4x1.5-3 g, or Cefotaxime 3x1-2 g, or Ceftriaxone 1x1-2 g, or Ceftaroline 2x600 mg) PLUS Macrolide (Azithromycin 1x500 mg or Clarithromycin 2x500 mg) OR Respiratory fluoroquinolone monotherapy
Prior MRSA respiratory isolate	Add Vancomycin (2x15 mg/kg, dose adjusted to trough levels) or Linezolid (2x600 mg); obtain culture/nasal PCR for de-escalation
*Prior P. aeruginosa* respiratory isolate**	Add anti-pseudomonal agent; obtain sputum culture or BAL for de-escalation

CAP Inpatient (Severe, per IDSA/ATS 2007 criteria)

Scenario	Regimen
Standard	Beta-lactam PLUS Macrolide OR Beta-lactam PLUS Respiratory fluoroquinolone
Prior MRSA isolate or MRSA risk with recent hospitalization/parenteral antibiotics within 90 days	Add MRSA coverage (Vancomycin or Linezolid); obtain culture/nasal PCR for de-escalation
*Prior Pseudomonas* isolate or Pseudomonas risk with recent hospitalization/parenteral antibiotics within 90 days**	Add anti-pseudomonal coverage; obtain culture for de-escalation

HAP Empiric Therapy

Risk Profile	Regimen
No high mortality risk, no MRSA risk factors	One of: Cefepime 2 g IV q8h, OR Levofloxacin 750 mg IV daily, OR Imipenem 500 mg IV q6h / Meropenem 1 g IV q8h, OR Piperacillin-tazobactam 4.5 g IV q6h
No high mortality risk, WITH MRSA risk	One of the above PLUS Vancomycin (15 mg/kg IV q8-12h, loading dose 25-30 mg/kg for severe disease) or Linezolid 600 mg IV q12h
High mortality risk (requiring mechanical ventilation for HAP, or septic shock) OR IV antibiotics within 90 days	Two anti-pseudomonal agents from different classes (avoid combining two beta-lactams) PLUS MRSA coverage (Vancomycin or Linezolid)

VAP Empiric Therapy

For VAP, antibiotics must cover S. aureus, P. aeruginosa, and other Gram-negative bacilli. The regimen is built by selecting one agent from each column:

Target Organism	Antibiotic Options (select one)
S. aureus (MRSA)	Vancomycin 15 mg/kg IV q8-12h (loading dose 25-30 mg/kg for severe disease) OR Linezolid 600 mg IV q12h
P. aeruginosa and other Gram-negative bacilli (beta-lactam agent)	Piperacillin-tazobactam 4.5 g IV q6h OR Cefepime 2 g IV q8h OR Ceftazidime 2 g IV q8h OR Imipenem 500 mg IV q6h OR Meropenem 1 g IV q8h OR Aztreonam 2 g IV q8h
P. aeruginosa and other Gram-negative bacilli (non-beta-lactam agent, for dual anti-pseudomonal coverage)	Ciprofloxacin 400 mg IV q8h OR Levofloxacin 750 mg IV q24h OR Amikacin 15-20 mg/kg IV q24h OR Gentamicin 5-7 mg/kg IV q24h OR Tobramycin 5-7 mg/kg IV q24h

Aminoglycosides should be avoided when alternative agents provide adequate Gram-negative coverage, because of poor pulmonary tissue penetration, nephrotoxicity, ototoxicity, and lower clinical response rates shown in meta-analyses.

Timing of Antibiotics

This is a high-yield testing point. For nonsevere pneumonia, antibiotics should be administered within 4 to 8 hours of diagnosis. For severe pneumonia with sepsis, antibiotics must be given within 1 hour of diagnosis.

Switch Therapy (Terapi Sulih)

Parenteral antibiotics can be switched to oral after a minimum of 2 to 3 days (safest at day 3, switching on day 4) if the patient meets all of the following stability criteria: hemodynamically stable, clinical improvement, able to tolerate oral medication, normal gastrointestinal function, temperature <37.8 degrees C, heart rate <100/min, respiratory rate <24/min, systolic BP >90 mmHg, oxygen saturation >90% or PaO2 >60 mmHg.

Switch options include sequential (same drug IV to oral, e.g., Levofloxacin IV to Levofloxacin oral), switch-over (different drug with equivalent potency, e.g., Ceftazidime IV to Ciprofloxacin oral), and step-down (same or different drug with lower potency, e.g., Cefotaxime IV to Amoxicillin oral).

Duration of Therapy

For CAP, antibiotics (IV/oral combined) are generally given for 3 to 5 days if clinical improvement is achieved. Prolongation is considered when: initial therapy is ineffective, extrapulmonary infection exists (meningitis, endocarditis), MDRO is the causative agent, or necrotizing pneumonia/empyema/lung abscess develops.

For HAP/VAP, the standard duration is 7 days. This may be shortened or extended based on clinical response and laboratory parameters. For non-fermenting Gram-negatives (Pseudomonas spp., Acinetobacter spp.) with high relapse rates, up to 14 days may be considered.

MDRO Pneumonia

Resistance Pattern	Definition	Treatment Approach
MDR	Resistant to at least 3 major antibiotic classes	Treat based on susceptibility results
XDR	Resistant to all antibiotics except polymyxin and/or tigecycline	Polymyxin- or tigecycline-based regimen
PDR	Resistant to all antibiotics	Combination of polymyxin + carbapenem (especially meropenem), regardless of in-vitro susceptibility; Polymyxin loading dose 2.5 mg/kg IV over 2 hours, then 1.5 mg/kg q12h

Non-Pharmacologic Management

Outpatient: bed rest, adequate hydration, antipyretics for high fever, mucolytics/expectorants as needed.

Inpatient (general ward): supplemental oxygen, IV fluids for rehydration and electrolyte correction, symptomatic medications.

Inpatient (ICU): oxygen therapy, IV fluids, consider non-invasive ventilation (NIV) first, escalate to invasive mechanical ventilation if NIV fails. For septic shock: fluid resuscitation, vasopressors to maintain MAP of 65 mmHg or above, manage per sepsis protocols.

Rehabilitation

The PNPK includes rehabilitation medicine recommendations: airway clearance techniques (chest physiotherapy, vibration, cough assist devices when peak cough flow <270 L/min), breathing exercises (diaphragmatic breathing, pursed-lip breathing), range-of-motion and postural exercises, early mobilization and ambulation, outpatient aerobic training (3-5 times/week, 30 minutes, moderate intensity), and extremity strengthening.

Prevention

Vaccination is the primary preventive strategy. Influenza vaccine: annual, especially for adults over 50, nursing home residents, those with chronic diseases, immunosuppression, and healthcare workers; given IM, effectiveness 38-65% in healthy adults and 34-73% in elderly. Pneumococcal vaccine: indicated for adults 65 and older, those with chronic diseases, asplenia, or immunosuppression; one dose for adults, effectiveness 43-76%. Additional prevention includes smoking cessation, hand hygiene, masking, standard precautions, effective cough training, and aerobic fitness.

For HAP/VAP prevention: hand hygiene, proper sterilization/disinfection of reusable respiratory equipment, use of sterile water for rinsing respiratory devices, avoid routine ventilator circuit changes (change only when visibly soiled), oral hygiene with tooth brushing, head-of-bed elevation to 30-45 degrees, subglottic secretion drainage, ETT cuff pressure maintained at 20-30 cm H2O, check nasogastric tube position before each feeding, assess gastric residual volume, minimize duration of mechanical ventilation (daily extubation readiness assessment, sedation optimization, early mobilization, early tracheostomy in selected cases, use NIV when possible), and judicious antibiotic use to reduce MDRO emergence.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Pulmonary tuberculosis	Cough, fever, infiltrates on CXR, can present as consolidation	Chronic course (weeks to months), upper lobe predominance, cavitary lesions, positive AFB smear/culture, exposure history; the PNPK explicitly excludes TB from its pneumonia definition
Congestive heart failure (pulmonary edema)	Dyspnea, bilateral opacities on CXR, crackles on exam	Bilateral/symmetric perihilar opacities ("bat-wing"), cardiomegaly, Kerley B lines, elevated BNP, no fever or purulent sputum, history of heart disease, responds to diuretics
Pulmonary embolism	Acute dyspnea, chest pain, tachycardia, hypoxemia	Pleuritic chest pain, often no infiltrate initially, wedge-shaped peripheral opacity (Hampton hump) if infarction, elevated D-dimer, positive CTPA, risk factors for DVT (immobilization, recent surgery, malignancy)
Lung malignancy	Persistent infiltrate, cough, weight loss	Mass or nodule rather than diffuse infiltrate, no acute febrile illness, persistent or enlarging lesion despite antibiotics, CT with contrast shows enhancing mass, may present as post-obstructive pneumonia
ARDS	Bilateral opacities, hypoxemia, respiratory failure	$PaO_2/FiO_2$ ratio of 300 or below, bilateral opacities not fully explained by effusions/atelectasis, no evidence of cardiogenic pulmonary edema, occurs in setting of known trigger (sepsis, aspiration, trauma)
Pulmonary vasculitis (e.g., SLE)	Infiltrates, dyspnea, fever, may mimic pneumonia	Multisystem involvement (skin, joints, kidneys), positive ANA/anti-dsDNA, diffuse alveolar hemorrhage pattern, does not respond to antibiotics
Drug-induced pneumonitis	Infiltrates, dyspnea, cough	Temporal relationship with drug exposure (amiodarone, methotrexate, nitrofurantoin), eosinophilia may be present, improves with drug withdrawal, no infection markers
Nosocomial tracheobronchitis (for HAP/VAP differential)	Purulent secretions, fever, leukocytosis in ventilated patient	No new or progressive infiltrate on imaging; the absence of a radiographic correlate distinguishes tracheobronchitis from VAP

6. Traps and High-Yield Pearls

The most common way students lose points on adult pneumonia questions involves three areas.

First, confusing severity scoring with treatment selection. CURB-65 and PSI determine where the patient is treated (outpatient, ward, ICU), not which antibiotic class to use. A student might see a CURB-65 of 1 and correctly identify outpatient management, but then erroneously select an inpatient IV regimen. Conversely, a CURB-65 of 4 should prompt ICU-level care, not just ward admission.

Second, the timing of antibiotics. The PNPK draws a clear line: nonsevere pneumonia must receive antibiotics within 4 to 8 hours, while severe pneumonia with sepsis demands antibiotics within 1 hour. Vignettes that describe a patient with septic shock and pneumonia are testing whether you will delay antibiotics to wait for culture results (wrong) or start empiric therapy immediately and collect cultures beforehand if possible (correct). Notably, the PNPK also states that procalcitonin should not delay antibiotic initiation. A normal initial PCT does not rule out bacterial pneumonia, and antibiotics should never be withheld pending the result.

Third, the approach to treatment failure. The PNPK emphasizes that the most common cause of treatment failure is host factors, not incorrect antibiotic selection. When a patient does not improve within 72 hours, the framework for evaluation is threefold: patient factors (local obstruction by foreign body or malignancy, empyema, superinfection, fluid overload), drug factors (wrong agent, wrong dose, malabsorption, drug interactions, drug fever), and pathogen factors (resistant organism, atypical pathogen, TB, fungal infection). The reflexive answer of "change the antibiotic" is often the distractor. The correct next step is to reassess the diagnosis, broaden the workup (CT scan, bronchoscopy, repeat cultures), and consider referral to a higher-level facility.

Additional pearls to remember: For HAP/VAP, always avoid aminoglycosides if an alternative beta-lactam or fluoroquinolone provides adequate Gram-negative coverage, due to poor lung penetration and toxicity. The concept of de-escalation is repeatedly emphasized: once culture and sensitivity results are available, narrow the antibiotic spectrum. And the former HCAP category no longer exists in current guidelines; healthcare contact alone does not predict MDR organisms. What does predict MDR risk is IV antibiotic use within the preceding 90 days.

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