COMMUNITY- ACQUIRED PNEUMONIA

An infection of the lower respiratory tract in an individual who has not been recently
hospitalized
CAUSES
The single leading cause of community-acquired pneumonia is Streptococcus pneumoniae.
Common organisms are S. pneumoniae, Haemophilus influenzae, Staphylococcus
aureus, Peptostretococcus,Fusobacterium,Bacteroides,Prevotella, Mycoplasma
Parainfluenza Influenza
PATHOPHYSIOLOGY
■Decreased mucociliary clearance of airway (eg, cystic fibrosis, smoking, COPD, elderly) 

host defenses.
■Relative/absolute immunosuppression (eg, chronic disease, HIV)   susceptibility to
bacterial infection.
■ Hematogenous spread of organism to lung
■ Patients at risk for the above pathophysiologic process are most likely to get pneumonia.
SYMPTOMS/EXAM
Fever, dyspnea, or cough productive of purulent or bloody sputum are most common.
Pleuritic chest pain, tachypnea, and abnormal breath sounds
In the elderly, the presenting complaint may be vague and nonspecific, eg, altered mental
status, poor appetite, or a fall.
DIFFERENTIAL
Hospital-acquired pneumonia: Occurs after at least 5 days of inpatient care and frequently
caused by Pseudomonas, Enterobacter, Legionella, or S. aureus. Also consider pulmonary
embolism, bronchiectasis, bronchitis, CHF.
DIAGNOSIS
Suspect based on clinical presentation
It is not possible to differentiate atypical from typical infections based on clinical criteria.
CXR
Radiographic findings cannot accurately predict the microbial cause, but lobar infiltrates are
more likely due to typical bacterial pathogens and interstitial infiltrates due to atypical
pathogens.
The initial CXR may be negative in patients with significant dehydration.
Microbiological diagnosis is reserved for more seriously ill admitted patients:
Blood cultures: Low yield overall but accurately identifies organism when positive
Sputum Gram stain and culture. Diagnostic sample must have <10 epithelial cells and >25
WBC/hpf. See Table 10.9 for Gram stains of common organisms that cause pneumonia.
Specific culture and antigen testing if Legionella suspected
Pleural fluid evaluation, if present.
 TREATMENT
■The Pneumonia Patient Outcomes Research Team (PORT) score can help guide decisions regarding the

need for hospitalization in immuno- competent adults

PATIENT CHARACTERISTIC POINTS ASSIGNEDa

Demographic factor

THORAC IC AN D RESPI
Age: men Number of years

DISORDE RS
Age: women Number of years minus 10

RATORY
Nursing home resident 10
Comorbid illnesses
Neoplastic diseaseb 30
Liver diseasec 20
CHFd 10
Cerebrovascular diseasee 10
Renal diseasef 10
Physical examination finding
Altered mental statusg 20
Respiratory rate 30 breaths/min 20
Systolic BP 90 mmHg 20
Temperature 35°C or 40°C 15
Pulse 125 bpm 10
Laboratory or radiographic finding
Arterial pH 7.35 30
BUN 30 mg/dL 20
Sodium 130 meq/L 20
Glucose 250 mg/dL 10
Hematocrit 30% 10
Arterial Po2 60 mmHg 10
Pleural effusion 10
 Risk Stratification Based on PORT Score

MORTALITY AT RECOMMENDED SITE OF CARE

NUMBER OF POINTS RISK
CLAS 30 DAYS (%)
S
Absence of predictors I 0.1–0.4 Outpatient

THORAC IC AN DPI RATORY

 70 II 0.6–0.7 Outpatient

DISORDE RS
71–90 III 0.9–2.8 Outpatient or brief inpatient

91–130 IV 8.2–9.3 Inpatient

 130 V 27.0–31.1 Inpatient

Healthy adults: Macrolide (azithromycin or clarithromycin) or doxy- cycline.
Adults with comorbidity (or recent antibiotic use): Antipneumococcal fluoroquinolone or
combination of macrolide (azithromycin or clar- ithromycin) + a -lactam against S.
pneumoniae (high-dose amoxicillin
or amoxicillin-clavulanate or cefpodoxime or cefuroxime).
Inpatient empiric therapy not admitted to the ICU
Ceftriaxone or cefotaxime IV + azithromycin or antipneumococcal
fluoroquinolone
Inpatient empiric therapy admitted to the ICU
Patients are more likely to have risk factors for resistant pathogens, including community-
associated MRSA and Legionella spp, therefore intravenous combination therapy with a
potent antipneumococcal
-lactam (ceftriaxone or cefotaxime) + either azithromycin or a respira-
tory fluoroquinolone (levofloxacin or moxifloxacin).
Special considerations
Suspected Pseudomonas: Add combination therapy with both an anti-
pseudomonal -lactam antibiotic and fluoroquinolone such as piperacillin- tazobactam,
imipenem, meropenem, cefepime, ceftazidime + ciprofloxacin, or levofloxacin. For -lactam
allergic patients, options include: aztreonam + levofloxacin or moxifloxacin plus an
aminoglycoside.
Suspected Legionella spp: Add fluoroquinolone or azithromycin. Suspected MRSA: Add
vancomycin or linezolid.
Suspected aspiration pneumonia: Add piperacillin-tazobactam or clindamycin.
Tuberculosis
Approximately one-third of the world’s population is infected with TB; how- ever, only about
10% of infected hosts develop active disease.
CAUSES
Mycobacterium tuberculosis, a slow-growing aerobic rod Transmitted human-to-
human via respiratory droplets
Humans are the only natural reservoir and usually must be in confined environments over
extended periods of time to transmit the disease.
PATHOPHYSIOLOGY
Primary infection in immunocompetent host  small number of organisms contained in
granulomas or spread through the body  latent (dormant) infection .
■ Host becomes immunocompromised (eg, HIV, malignancy, immunosuppressant
medications)  reactivation of latent disease and symptoms.
■ Hematogenous spread during primary or reactivation  miliary TB.
SYMPTOMS/EXAM
■ Primary TB

■ Usually asymptomatic, but a small number of cases may develop progressive primary

infection.
■ Latent TB
■ No symptoms of active disease,

■ Active TB/reactivation disease

■ Pulmonary TB: Persistent cough, malaise, night sweats, fever, weight loss, and

hemoptysis
■ Extrapulmonary TB: Sites include lymph node (most common), pleura, genitourinary

tract, bones and joints, pericardium, and meninges

DIAGNOSIS
CXR
Primary TB: May be completely normal or reveal nonspecific infiltrate
in any region of the lung. This infiltrate in association with regional lymphadenopathy is termed
the Ghon complex. PPD(purified protein derivative) will be positive.
Reactivation TB: Upper lobe infiltrates with or without cavitation
Sputum smears are stained for acid-fast bacilli.
Cultures of sputum, blood, or tissue are the gold standard for diagnosing active infection but
may take weeks to grow.
PPD test is the gold standard for diagnosing latent infection. Positive test is based on the degree
of induration(hardening of soft tissues) in a given patient risk group.
Low-risk individuals (eg, aged 4 years, without any risk factors): 15 mm Average risk
individuals: 10 mm
High risk patients 5 mm
Many foreign-born patients may have been immunized with BCG, the therapeutic effectiveness of
which is unclear. Therefore, the CDC recommends that history of such is ignored when
TREATMENT
Latent TB (newly +PPD): 6–9 months of INH(isoniazid)
Active TB: Initial therapy with four drugs is now recommended until a multi–drug-
resistant strain can be ruled out by culture. There are six first- line drugs now commonly
employed: INH, rifampin, pyrazinamide, ethambutol, rifabutin, and rifapentine. The drugs are
selected for treatment based on local practice, patterns of resistance, and patient tolerance.
Baseline labs, particularly liver function tests, are indicated before use of these drugs.
Corticosteroids: For TB meningitis and pericarditis
COMPLICATIONS
Hyponatremia, anemia, elevated LFTs, thrombocytosis Pneumothorax empyema
Adverse drug reactions, eg, hepatitis, secondary to INH
Inadequate therapeutic effect of warfarin, steroids, OCPs(oral contraceptive pills), oral
hypoglycemics, digoxin, anticonvulsants, and methadone secondary to treatment with INH