 an infection of the pulmonary parenchyma

 is often misdiagnosed, mistreated, and underestimated

 was typically classified as :
1. Community-Acquired Pneumonia (CAP)
2. Health Care–Associated Pneumonia (HCAP)
 subcategories of HCAP including
 Hospital-acquired pneumonia (HAP)
 Ventilator-associated pneumonia (VAP)
 Factors responsible for infection with multidrug-resistant (MDR) pathogens include :
 development and widespread use of potent oral antibiotics
 earlier transfer of patients out of acute-care hospitals to their homes or various lower-acuity facilities
 increased use of outpatient IV antibiotic therapy
 general aging of the population
 more extensive immunomodulatory therapies
 Table 251-1 Clinical Conditions Associated with and Likely Pathogens in Health Care–
Associated Pneumonia

Pathogen
Condition MRSA Pseudomonas Acinetobacter MDR
aeruginosa spp. Enterobacte riaceae

Hospitalization for ≥48 h X X X X

Hospitalization for ≥2 X X X X
days in prior 3 months

Nursing home or X X X X
extended-care facility
residence
Antibiotic therapy in X X
preceding 3 months
Chronic dialysis X
Home infusion therapy X

Home wound care X

Family member with X X

MDR infection
 Although the new classification system has been helpful in designing empirical antibiotic
strategies, it is not without disadvantages
 For instance »»»»»»»»»»»»»»
not all MDR pathogens are associated with all risk factors »»»»»» each patient must be considered
individually
 For example
 the risk of infection with MDR pathogens for a nursing home resident with dementia who can
dress, ambulate, and eat is quite different from the risk for a patient who is in a chronic
vegetative state with a tracheostomy and a percutaneous feeding tube in place
 In addition, risk factors for MDR infection do not preclude the development of pneumonia
caused by the usual CAP pathogens
 Pneumonia results from the proliferation of microbial pathogens at the alveolar level and the host's response to those pathogens
 Microorganisms gain access to the lower respiratory tract in several ways: »»»»»»»»»»»»»»»»»»
• The most common is by aspiration from the oropharynx
• Many pathogens are inhaled as contaminated droplets
• pneumonia occurs via hematogenous spread
• contiguous extension from an infected pleural or mediastinal space
 Mechanical factors are critically important in host defense: »»»»»»»»»»»»
 hairs and turbinates of the nares catch larger inhaled particles
 branching architecture of the tracheobronchial tree traps particles on the airway lining
 mucociliary clearance and local antibacterial factors either clear or kill the potential pathogen
 gag reflex and the cough mechanism
 normal flora adhering to mucosal cells of the oropharynx
 resident alveolar macrophages
 Only when the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded does clinical pneumonia become
manifest »»»»»»»»»»»» the alveolar macrophages initiate the inflammatory response to bolster lower respiratory tract defenses
 The host inflammatory response, rather than the proliferation of microorganisms, triggers the clinical syndrome of pneumonia
 The release of inflammatory mediators, such as IL-1 and TNF »»»»»»»»»»»» fever
 Chemokines, such as IL-8 and GCSF, stimulate the release of neutrophils and their attraction to the lung »»»»»»»»»»» peripheral
leukocytosis and increased purulent secretions
 Even erythrocytes can cross the alveolar-capillary membrane, with consequent hemoptysis
 The capillary leak results in a radiographic infiltrate and rales detectable on auscultation
 hypoxemia results from alveolar filling
 some bacterial pathogens appear to interfere with the hypoxic vasoconstriction that would normally occur with fluid-filled alveoli, and this
interference can result in severe hypoxemia
 Increased respiratory drive in the SIRS leads to respiratory alkalosis
 Dyspnea due to :
 Decreased compliance due to capillary leak Hypoxemia
 increased respiratory drive increased secretions
 infection-related bronchospasm
 The initial phase »»»»»»»» edema
presence of a proteinaceous exudate—and often of bacteria—in the alveoli
This phase is rarely evident in clinical or autopsy specimens because it is so rapidly followed by a red hepatization
 The second stage »»»»»»»»» red hepatization
presence of erythrocytes in the cellular intraalveolar exudate
neutrophils are also present and are important from the standpoint of host defense
Bacteria are occasionally seen in cultures of alveolar specimens
 The third phase »»»»»»»» gray hepatization
no new erythrocytes are extravasating, and those already present have been lysed and degraded
The neutrophil is the predominant cell
fibrin deposition is abundant
bacteria have disappeared
This phase corresponds with successful containment of the infection and improvement in gas exchange
 The final phase »»»»»»»»» resolution
the macrophage is the dominant cell type in the alveolar space
the debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory response
 This pattern has been described best for pneumococcal pneumonia and may not apply to
pneumonias of all etiologies, especially viral or Pneumocystis pneumonia
 in VAP, respiratory bronchiolitis may precede the development of a radiologically apparent
infiltrate
 Because of the microaspiration mechanism, a bronchopneumonia pattern is most common in
nosocomial pneumonias
 a lobar pattern is more common in bacterial CAP

Despite the radiographic appearance, viral and Pneumocystis pneumonias represent

alveolar rather than interstitial processes.
 The extensive list of potential etiologic agents in CAP includes bacteria, fungi, viruses, and protozoa
 Newly identified pathogens include hantaviruses, metapneumoviruses, the coronavirus (SARS), and community-acquired strains of MRSA
 Most cases of CAP are caused by relatively few pathogens
 Streptococcus pneumoniae is most common
 other organisms must also be considered in light of the patient's risk factors and severity of illness
 it is most useful to think of the potential causes as either "typical" or "atypical" organisms
 Typical bacterial pathogens includes : S. pneumoniae, Haemophilus influenzae, S. aureus , gram-negative bacilli such as Klebsiella
pneumoniae and Pseudomonas aeruginosa
 Atypical organisms include : Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella spp, respiratory viruses such as influenza
viruses, adenoviruses, RSVs
The atypical organisms cannot be cultured on standard media, nor can they be seen on Gram's stain
are intrinsically resistant to all -lactam agents and must be treated with macrolide, fluoroquinolone, tetracycline
 Data suggest that a virus may be responsible in up to 18% of cases of CAP
 In the ~10–15% of CAP cases that are polymicrobial
 a
Influenza A and B viruses, adenoviruses, respiratory syncytial viruses, parainfluenza viruses
 Anaerobes play a significant role only when an episode of aspiration has occurred days to weeks before presentation for pneumonia.
combination of an unprotected airway (alcohol or drug overdose or a seizure disorder) and significant gingivitis constitutes the major risk
factor. Anaerobic pneumonias are often complicated by abscess formation and significant empyemas or parapneumonic effusions
 S. aureus pneumonia is well known to complicate influenza infection. Recently, however, MRSA strains have been reported as primary
causes of CAP. While this entity is still relatively uncommon, clinicians must be aware of its potentially serious consequences, such as
necrotizing pneumonia. Two important developments have led to this problem: the spread of MRSA from the hospital setting to the
community and the emergence of genetically distinct strains of MRSA in the community. These novel CA-MRSA strains have infected
healthy individuals who have had no association with health care
 Unfortunately, despite a careful history and physical examination as well as routine radiographic studies, it is usually impossible to predict
the pathogen in a case of CAP with any degree of certainty; in more than half of cases, a specific etiology is never determined.
Nevertheless, it is important to consider epidemiologic and risk factors that might suggest certain pathogens
Table 251-2 Microbial Causes of Community-Acquired Pneumonia, by Site of Care

Hospitalized Patients
Outpatients Non-ICU ICU
Streptococcus pneumoniae S. pneumoniae S. pneumoniae
Mycoplasma pneumoniae M. pneumoniae Staphylococcus aureus
Haemophilus influenzae Chlamydophila pneumoniae Legionella spp.
C. pneumoniae H. influenzae Gram-negative bacilli
Respiratory virusesa Legionella spp. H. influenzae

Respiratory viruses
 Table 251-3 Epidemiologic Factors Suggesting Possible Causes of Community-Acquired
Pneumonia

Factor Possible Pathogen(s)

Alcoholism Streptococcus pneumoniae, oral anaerobes, Klebsiella
pneumoniae, Acinetobacter spp., Mycobacterium tuberculosis
COPD and/or smoking Haemophilus influenzae, Pseudomonas aeruginosa, Legionella
spp., S. pneumoniae, Moraxella catarrhalis, Chlamydophila
pneumoniae
Structural lung disease (e.g., P. aeruginosa, Burkholderia cepacia, Staphylococcus aureus
bronchiectasis)
Dementia, stroke, decreased Oral anaerobes, gram-negative enteric bacteria
level of consciousness
Lung abscess CA-MRSA, oral anaerobes, endemic fungi, M. tuberculosis,
atypical mycobacteria
Travel to Ohio or St. Histoplasma capsulatum
Lawrence river valleys
Travel to southwestern Hantavirus, Coccidioides spp.
United States
Travel to Southeast Asia Burkholderia pseudomallei, avian influenza virus
Stay in hotel or on cruise Legionella spp.
ship in previous 2 weeks
Local influenza activity Influenza virus, S. pneumoniae, S. aureus
Exposure to bats or birds H. capsulatum
Exposure to birds Chlamydophila psittaci
Exposure to rabbits Francisella tularensis
Exposure to sheep, goats, Coxiella burnetii
parturient cats
 In the US, ~80% of the 4 million CAP cases that occur annually are treated on an outpatient basis
 The incidence rates are highest at the extremes of age

 RF for CAP: alcoholism, asthma, immunosuppress, institutionalization, age of 70Y versus 60–69 Y
 RF for pneumococ: dementia, seizure, heart failure, CVA, alcoholism, smoking, COPD, HIV
 RF for CA-MRSA: Native Americans, homeless youths, men who have sex with men, prison inmates, military recruits,
children in day-care centers, and athletes such as wrestlers
 RF for Enterobacteriaceae: recently hospitalization and/or antibiotic therapy, comorbidities such as alcoholism, heart
failure, renal failure
 RF for P. aeruginosa : as above, severe structural lung disease
 RF for Legionella: diabetes, hematologic malignancy, cancer, severe renal disease, HIV infection, smoking, male
gender, a recent hotel stay or ship cruise
 CAP can vary from indolent to fulminant in presentation and from mild to fatal in severity
 constitutional findings and manifestations limited to the lung and its associated structures
 fever, tachycardia, chills and/or sweats
 cough that is either nonproductive or productive of mucoid, purulent, or blood-tinged sputum
 the patient may be able to speak in full sentences or may be very short of breath
 If the pleura is involved, the patient may experience pleuritic chest pain
 Up to 20% of patients may have GI symptoms such as nausea, vomiting, and/or diarrhea
 Other symptoms may include fatigue, headache, myalgias, and arthralgias
 An increased respiratory rate and use of accessory muscles of respiration are common
 Palpation may reveal increased or decreased tactile fremitus
 Percussion can vary from dull to flat, reflecting underlying consolidated lung and pleural fluid
 Crackles, bronchial breath sounds, and possibly a pleural friction rub may be heard
 Severely ill patients who have septic shock are hypotensive and may have evidence of organ failure
 The clinical presentation may not be so obvious in the elderly
 who may initially display new-onset or worsening confusion and few
other manifestations.
When confronted with possible CAP, the physician must ask two questions:
1) Is this pneumonia? »»»»»»»»»» answered by clinical and radiographic methods
2) what is the etiology? »»»»»»»» requires the aid of laboratory techniques
The differential diagnosis includes:
 infectious
 noninfectious ******* acute bronchitis, acute exa of chronic bronchitis, heart failure, PTE, radiation
 The importance of a careful history cannot be overemphasized »»»»»»»»»»»»»» known
cardiac disease may suggest worsening pulmonary edema
underlying carcinoma may suggest lung injury secondary to radiation
 Epidemiologic clues, such as recent travel to areas with known endemic pathogens
 Unfortunately, the sensitivity and specificity of the findings on physical examination are less than
ideal, averaging 58% and 67%, respectively ***************** C-Xray is often necessary
Radiographic findings serve:
 severity (cavitation or multilobar involvement)
 suggest an etiologic diagnosis *************
 pneumatoceles suggest infection with S. Aureus
 upper-lobe cavitating lesion suggests TB

CT is rarely necessary but may be of value in a patient with suspected

postobstructive pneumonia caused by a tumor or foreign body
 For cases managed on an outpatient basis, the clinical and radiologic assessment is usually all that
is done before treatment is started since most laboratory test results are not available soon enough
to influence initial management
 In certain cases, however (influenza virus infection), the availability of rapid point-of-care
diagnostic tests and access to specific drugs for treatment and prevention can be very important.
 The etiology of pneumonia usually cannot be determined on the basis of clinical presentation
 Except for the 2% of CAP patients who are admitted to the ICU, no data exist to show that treatment directed at a
specific pathogen is statistically superior to empirical therapy.
 The benefits of establishing a microbial etiology can therefore be questioned, particularly in light of the cost of
diagnostic testing.
 a number of reasons can be advanced for attempting an etiologic diagnosis:
 Identification of an unexpected pathogen allows narrowing of the initial empirical regimen, which decreases antibiotic
selection pressure and may lessen the risk of resistance
 Pathogens with important public safety implications, such as TB and influenza virus
 without culture and susceptibility data, trends in resistance cannot be followed accurately
 a sputum sample must have >25 neut and <10 squamous epithelial cells per low-power field
 sensitivity / specificity of the sputum Gram's stain and culture are highly variable »»»»»»»»»

in cases of proven bacteremic pneumococc, the yield of positive cultures from sputum samples is
50%
 Some patients, particularly elderly individuals, may not be able to produce an appropriate
expectorated sputum sample.
 The inability to produce sputum can be a consequence of dehydration, and the correction of
this condition may result in increased sputum production and a more obvious infiltrate on
radiography
 For patients admitted to the ICU and intubated, a deep-suction aspirate or BAL sample
1) The yield from blood cultures, even those obtained before antibiotic therapy, is disappointingly low
 Only ~5–14% of cultures of blood from patients hospitalized with CAP are positive
 the most frequently isolated pathogen is S. Pneumoniae
2) Since recommended empirical regimens all provide pneumococcal coverage, a blood culture positive for this pathogen has little effect
on clinical outcome ************* susceptibility data may allow a switch from a broader-spectrum regimen to penicillin in
appropriate cases
 Because of 1) the low yield and 2) the lack of significant impact on outcome, blood cultures are no longer considered de rigueur for
all hospitalized CAP patients
should have blood cultured : 
 neutropenia secondary to pneumonia
 Asplenia
 complement deficiencies
 chronic liver disease
 severe CAP
 Two commercially available tests detect
a) pneumococcal
b) certain Legionella antigens in urine
 The test for Legionella pneumophila detects only serogroup 1, but this serogroup accounts for
most CAP cases of Legionnaires' disease
 The sensitivity and specificity of the Legionella urine antigen test are as high as 90% and 99%
 The pneumococcal urine antigen test is also quite sensitive and specific 80% and >90%
 false-positive results can be obtained with samples from colonized children,but the test is
reliable
 Both tests can detect antigen even after the initiation of appropriate antibiotic therapy and after
weeks of illness
 Other antigen tests include a rapid test for influenza virus and direct fluorescent antibody tests
for influenza virus and RSV
 the test for RSV is only poorly sensitive
PCR tests are available for a number of pathogens, including :
 L. Pneumophila
 Mycobacteria

a multiplex PCR can detect the nucleic acid of

 Legionella spp.
 M. Pneumoniae
 C. pneumoniae
 A fourfold rise in specific IgM antibody titer between acute- and convalescent-
phase serum samples is generally considered diagnostic of infection with the
pathogen in question

 Recently, however, they have fallen out of favor because of the time required to
obtain a final result for the convalescent-phase sample
 Site of Care
 cost of inpatient management exceeds that of outpatient treatment by a factor of 20
 There are currently two sets of criteria:
 Pneumonia Severity Index (PSI), a prognostic model used to identify patients at low
risk of dying
 the CURB-65 criteria, a severity-of-illness score
 The PSI is less practical in a busy emergency-room setting because of the need to
assess 20 variables
points are given for 20 variables, including:
 Age
 coexisting illness
 abnormal physical
 laboratory findings

On the basis of the resulting score, patients are assigned to one of five classes with the following mortality rates:
 class 1, 0.1% lower admission rates for class 1 and class 2
 class 2, 0.6%
 class 3, 2.8% »»»»»»»»»»»»» those in class 3 should ideally be admitted to an observation unit
 class 4, 8.2%
 class 5, 29.2% classes 4 and 5 should be admitted to the hospital
The CURB-65 criteria include five variables:
1) confusion (C)
2) urea >7 mmol/L (U)
3) respiratory rate 30/min (R)
4) blood pressure, systolic 90 mmHg or diastolic 60 mmHg (B)
5) age 65 years (65)

Patients with a
 score of 0, among whom the 30-day mortality rate is 1.5% »»»»»»»»»»»» can be treated outside the hospital
 score of 2, the 30-day mortality rate is 9.2% »»»»»»»»»»»»» should be admitted to the hospital
 scores of 3, mortality rates are 22% overall »»»»»»»»»»»»» may require admission to an ICU
 CAP due to MRSA may be caused by infection with :
 the classic hospital-acquired strains »»»»»»»»»»»»» classified as HAP in the past, now be classified as HCAP
 the more recently identified, genotypically and phenotypically distinct community-acquired strains

 Methicillin resistance in S. aureus is determined by the mecA gene, which encodes for resistance to all -lactam drugs
 At least five staphylococcal chromosomal cassette mec (SCCmec) types have been described:
 The typical hospital-acquired strain usually has type II or III
 whereas CA-MRSA has a type IV SCCmec element

 CA-MRSA isolates tend to be less resistant than the older hospital-acquired strains and are often susceptible to :
TMP-SMX
Clindamycin in addition to vancomycin and linezolid
Tetracycline
 CA-MRSA strains may also carry genes for superantigens »»»»»»»»»» enterotoxins B and C and Panton-
Valentine leukocidin »»»»»»»»»»»»» a membrane-tropic toxin that can create cytolytic pores in neutrophils, monocytes,
macrophages
 Fluoroquinolone resistance among isolates of E-coli from community appears to be increasing

 Enterobacter spp. are typically resistant to cephalosporins

 the drugs of choice for use against these bacteria are usually
 fluoroquinolones
 Carbapenems
 Similarly, when infections due to bacteria producing extended-spectrum ß-lactamases
(ESBLs) are documented or suspected, a fluoroquinolone or a carbapenem should be used
 these MDR strains are more likely to be involved in HCAP
In general, pneumococcal resistance is acquired :
(1) by direct DNA incorporation and remodeling resulting from contact with closely related oral commensal bacteria
(2) by the process of natural transformation
(3) by mutation of certain genes

Pneumococcal strains are classified as:

 sensitive to penicillin if the minimal inhibitory concentration (MIC) is 0.06 g/Ml
 intermediate if the MIC is 0.1–1.0 g/mL
 resistant if the MIC is 2 g/Ml

 Strains resistant to drugs from ≥3 antimicrobial classes with different mechanisms of action are considered MDR
 Pneumococcal resistance to ß-lactam drugs is due solely to the presence of low-affinity penicillin-binding proteins

 propensity for resistance to penicillin »»»» reduced susceptibility to other drugs( macrolides, tetracyclines, TMP-SMX)
 In the US, 58.9% of penicillin-resistant pneumococcal isolates from blood cultures are also resistant to macrolides
 Penicillin is an appropriate agent for the treatment of pneumococcal infection caused by strains with MICs of 1 g/mL
 For infections caused by pneumococcal strains with penicillin MICs of 2–4 g/mL, the data are conflicting; some studies
suggest no increase in treatment failure with penicillin, while others suggest increased rates of death or complications
 For strains of S. pneumoniae with intermediate levels of resistance, higher doses of the drug should be used

Risk factors for drug-resistant pneumococcal infection include :

 recent antimicrobial therapy
 an age of <2 years or >65 years
 attendance at day-care centers
 recent hospitalization
 HIV infection
Fortunately, resistance to penicillin appears to be reaching a plateau
resistance to macrolides is increasing through several mechanisms, including :
 target-site modification

Target-site modification is caused by ribosomal methylation in 23S rRNA encoded by the ermB gene and results in resistance to
macrolides, lincosamides, and streptogramin B–type antibiotics
This MLSB phenotype is associated with high-level resistance, with typical MICs of 64 g/mL
 the presence of an efflux pump

The efflux mechanism encoded by the mef gene (M phenotype) is usually associated with low-level resistance (MICs, 1–32 g/mL)

o Pneumococcal resistance to fluoroquinolones (e.g., ciprofloxacin and levofloxacin) has been reported
o Changes can occur in one or both target sites (topoisomerases II and IV)
o changes in these two sites usually result from mutations in the gyrA and parC genes, respectively
Outpatients
Previously healthy and no antibiotics in past 3 months:
A macrolide [clarithromycin (500 mg PO bid) or azithromycin (500 mg PO once, then 250 mg od)] or Doxycycline (100 mg PO bid)

Comorbidities or antibiotics in past 3 months: select an alternative from a different class

A respiratory fluoroquinolone [moxifloxacin (400 mg PO od), gemifloxacin (320 mg PO od), levofloxacin (750 mg PO od)]
A β-lactam [preferred: high-dose amoxicillin (1 g tid) or amoxicillin/clavulanate (2 g bid); alternatives:
ceftriaxone (1–2 g IV od), cefpodoxime (200 mg PO bid), cefuroxime (500 mg PO bid)] plus a macrolide

Inpatients, non-ICU
A respiratory fluoroquinolone [moxi (400 mg PO or IV od), gemi (320 mg PO od), levofloxacin (750 mg PO or IV od)]
A β-lactamc [cefotaxime (1–2 g IV q8h), ceftriaxone (1–2 g IV od), ampicillin (1–2 g IV q4–6h), ertapenem (1 g IV od)] plus
a macrolided [oral clarithromycin or azithromycin or IV azithromycin (1 g once, then 500 mg od)]

Inpatients, ICU
β-lactam [cefotaxime (1–2 g IV q8h), ceftriaxone, ampicillin-sulbactam (2 g IV q8h)] plus Azithromycin or a fluoroquinolone
Special concerns

If Pseudomonas is a consideration:
antipneumococcal, antipseudomonal »»»»» β-lactam [piperacillin/tazobactam (4.5 g IV q6h), cefepime (1–2 g IV q12h),
imipenem (500 mg IV q6h), meropenem (1 g IV q8h)] plus ciproflox (400 mg IV q12h) or levofloxacin (750 mg IV od)
The above β-lactams plus an aminoglycoside [amikacin (15 mg/kg od) or tobramycin (1.7 mg/kg od) and azithromycin]
The above β-lactamsf plus an aminoglycoside plus an antipneumococcal fluoroquinolone

If CA-MRSA is a consideration:
Add linezolid (600 mg IV q12h) or vancomycin (1 g IV q12h)
 In these guidelines, coverage is always provided for the pneumococcus and the atypical pathogens
 Atypical pathogen coverage provided by a macrolide or a fluoroquinolone has been associated with a significant reduction in mortality rates
compared with those for -lactam coverage alone.
Telithromycin, a ketolide derived from the macrolide class
 differs from the macrolides in that it binds to bacteria more avidly and at two sites rather than one
 This drug is active against pneumococci resistant to penicillins, macrolides, and fluoroquinolones
 If blood cultures yield S. pneumoniae sensitive to penicillin after 2 days of treatment with a macrolide plus a -lactam or a fluoroquinolone, should
therapy be switched to penicillin?
 Penicillin alone would not be effective in the potential 15% of cases with atypical co-infection
 One compromise would be to continue atypical coverage with either a macrolide or a fluoroquinolone for a few more days and then to complete the
treatment course with penicillin alone

 Management of bacteremic pneumococcal pneumonia is also controversial »»»»»»»»»»» Data from nonrandomized studies suggest that
combination therapy (e.g., with a macrolide and a -lactam) is associated with a lower mortality rate than monotherapy, particularly in severely ill
patients
 The main risk factors for P. aeruginosa infection are structural lung disease (e.g., bronchiectasis) and recent treatment with antibiotics or
glucocorticoids
 Although hospitalized patients have traditionally received initial therapy by the IV route, some drugs
(fluoroquinolones) are very well absorbed and can be given orally from the outset to select patients
 For patients initially treated IV, a switch to oral treatment is appropriate as long as the patient can ingest
and absorb the drugs, is hemodynamically stable, and is showing clinical improvement

The duration of treatment for CAP »»»»»»»»»»»»

 Patients have usually been treated for 10–14 days
 studies with quinolones and telithromycin suggest, a 5-day course is sufficient for uncomplicated CAP
 A longer course is required for patients with:
1) bacteremia 2) metastatic infection 3) infection with a particularly virulent pathogen ( P. aeruginosa
or CA-MRSA) 4) initial treatment was ineffective 5) severe CAP

Patients may be discharged from the hospital once they are clinically stable and have no active medical
problems requiring ongoing hospital care
 Adequate hydration
 oxygen therapy for hypoxemia
 assisted ventilation
 Patients with severe CAP who remain hypotensive despite fluid resuscitation may have adrenal
insufficiency and may respond to glucocorticoid treatment
 Immunomodulatory therapy in the form of drotrecogin alfa (activated) should be considered for CAP
patients with persistent septic shock and APACHE II scores of 25, particularly if the infection is caused
by S. pneumoniae.
who are slow to respond to therapy should be reevaluated at about day 3 (sooner if their condition is
worsening »»»»»»»»»
 a number of possible scenarios should be considered:

(1) Is this a noninfectious condition? (2) If this is an infection, is the correct pathogen being targeted?
(3) Is this a superinfection with a new nosocomial pathogen? (4)The pathogen may be resistant to the
drug (5) a sequestered focus (lung abscess or empyema) may be blocking access of the (6) patient
may be getting either the wrong drug or the correct drug at the wrong dose or frequency of
administration (7) CAP is the correct diagnosis but that a different pathogen (M. tuberculosis or a
fungus) is the cause (8) nosocomial superinfections—both pulmonary and extrapulmonary—are
possible

A number of noninfectious conditions can mimic pneumonia, including:

*pulmonary edema *PTE *lung ca. *radiation *HP *connective tissue disease involving the lungs
 common complications of severe CAP include:
“respiratory failure “shock “multiorgan failure “bleeding diatheses “complicated pleural effusion “exacerbation of
comorbid illnesses “lung abscess “metastatic infection
 Lung abscess may occur in association with aspiration or with infection caused by a single CAP pathogen(CA-MRSA, P.
aeruginosa,(rarely) S. Pneumoniae)
 Aspiration pneumonia is typically a mixed polymicrobial infection involving both aerobes and anaerobes
 In either scenario, drainage should be established

 A significant pleural effusion should be tapped for both diagnostic and therapeutic purposes
 If the fluid has a pH of <7, a glucose level of <2.2 mmol/L, and a LDH concentration of >1000 U/L or if bacteria are seen
or cultured, then the fluid should be drained; a chest tube is usually required.
The prognosis of CAP depends on the:
 patient's age
 Comorbidities
 site of treatment (inpatient or outpatient)

The overall mortality rate for:

 the outpatient group is <1%
 patients requiring hospitalization is 10% »»»»»»»» with ~50% of the deaths
directly attributable to pneumonia
 Fever and leukocytosis usually resolve within 2 and 4 days
 in otherwise healthy patients with CAP, physical findings may persist longer

 Chest radiographic abnormalities are slowest to resolve and may require 4–12 weeks to clear
the speed of clearance depending on :
 the patient's age
 underlying lung disease »»»»»»»»»»

For a patient whose condition is improving and who (if hospitalized) has been discharged,
a follow-up radiograph can be done ~4–6 weeks later
 The main preventive measure is vaccination
 The recommendations of the Advisory Committee on Immunization Practices should be followed for
influenza and pneumococcal vaccines
 In the event of an influenza outbreak, unprotected patients at risk from complications should be
vaccinated immediately and given chemoprophylaxis with either oseltamivir or zanamivir for 2 weeks—
i.e., until vaccine-induced antibody levels are sufficiently high
 Because of an increased risk of pneumococcal infection, even among patients without obstructive lung
disease, smokers should be strongly encouraged to stop smoking