 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
 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
 The ho st in flam m ato ry response, rather than the p ro liferation of
microorganism s, triggers the clin ical syndrom e of pneum onia
 The release of in flam m ato ry m ediato rs, such as IL-1 and TNF
»»»»»»»»»»»» fever
 Chem okin es, such as IL-8 and GCSF, stim ulate the release of
neutrophils and their attraction to the lung »»»»»»»»»»» p eripheral
leukocyto sis and in creased pu ru lent secretion s
 Even er yth rocytes can cro ss the alveolar-capillary m em brane, w ith
consequent h em optysis
 The capillary leak results in a radiog raphic in filtrate and rales
detectable on au scultation
 hypoxem ia results from alveolar filling
 som e b acterial p athogens appear to in terfere w ith the h ypoxic
vasoconstriction that w ould no rm ally o ccur w ith flu id -filled
alveoli, and th is in terference can result in severe h ypoxem ia
 Increased respirato ry d rive in the SIRS leads to respirato ry
alkalo sis
 Dyspnea due to :
 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
 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
 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
 aInfluenza 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
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
Factor
Alcoholism
COPD and/or smoking
Structural lung disease (e.g.,
bronchiectasis)
Dementia, stroke, decreased
level of consciousness
Lung abscess
Travel to Ohio or St.
Lawrence river valleys
Travel to southwestern
United States
Travel to Southeast Asia
Stay in hotel or on cruise
ship in previous 2 weeks
Local influenza activity
Exposure to bats or birds
Exposure to birds
Exposure to rabbits
Exposure to sheep, goats,
parturient cats
Pneumonia
Possible Pathogen(s)
Streptococcus pneumoniae, oral anaerobes, Klebsiella
pneumoniae, Acinetobacter spp., Mycobacterium tuberculosis
Haemophilus influenzae, Pseudomonas aeruginosa, Legionella
spp., S. pneumoniae, Moraxella catarrhalis, Chlamydophila
pneumoniae
P. aeruginosa, Burkholderia cepacia, Staphylococcus aureus
Oral anaerobes, gram-negative enteric bacteria
CA-MRSA, oral anaerobes, endemic fungi, M. tuberculosis,
atypical mycobacteria
Histoplasma capsulatum
Hantavirus, Coccidioides spp.
Burkholderia pseudomallei, avian influenza virus
Legionella spp.
Influenza virus, S. pneumoniae, S. aureus
H. capsulatum
Chlamydophila psittaci
Francisella tularensis
Coxiella burnetii
 In the US, ~80% of the 4 m illion CA P cases that o ccur
annually are treated on an ou tpatient basis
 The in cid ence rates are h ighest at the extrem es of ag e

 RF fo r CA P: alcoholism , asthm a, im m unosuppress,

in stitu tionalization , ag e of 70Y versu s 60–69 Y
 RF fo r pneum ococ: d em entia, seizure, heart failu re,
CVA, alcoholism , sm oking , C OPD, HIV
 RF fo r CA -MRSA: Native Am ericans, hom eless youth s, m en
who have sex with m en, p rison inm ates, m ilitary
recru its, child ren in d ay-care centers, and ath letes
such as wrestlers
 RF fo r Enterobacteriaceae: recently ho spitalization
and/or an tib io tic therapy, com orb id ities such as
 CAP can vary from indolent to fu lm in ant in p resentation
and from m ild to fatal in severity
 constitu tional find ing s and m anifestation s lim ited to
the lung and its associated stru ctu res
 fever, tachycard ia, chills and/or sweats
 cough that is either nonproductive o r p roductive of
mucoid , pu ru lent, o r b lood -tinged sputum
 the patient m ay b e ab le to speak in fu ll sentences o r
may b e very short of b reath
 If the p leura is in volved, the patient m ay experience
pleuritic chest pain
 Up to 20% of patients m ay have GI sym ptom s such as
nausea, vom iting , and/or d iarrhea
 Other sym ptom s m ay in clude fatigue, headache, m yalg ias,
 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 thi s pneumoni a? »»»»»»»»»» answered by clinical and
radiographic met hods
2) what is the eti ol ogy? »»»»»»»» requi res the ai d of laboratory
techni ques
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
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

 Forcases 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
 The etio logy of pneum onia u sually cannot b e d eterm in ed
on the basis of clin ical p resentation
 Except fo r the 2% of CA P patients who are adm itted to
the ICU, no d ata exist to show that treatm ent d irected
at a specific pathogen is statistically superio r to
em pirical therapy.
 The b enefits of establishing a m icrobial etio logy can
therefo re b e questioned, particularly in ligh t of the
cost of d iagnostic testing .

 a n um ber of reasons can b e advanced fo r attem pting an

etio log ic d iagnosis:
 Identification of an unexpected pathogen allo ws
narro wing of the in itial em pirical regim en, which
 a sputum sam ple m ust have >25 n eut and <10 squam ous
epithelial cells p er lo w-power field
 sensitivity / specificity of the sputum Gram 's stain and
cultu re are h igh ly variable »»»»»»»»»
in cases of p roven bacterem ic pneum ococc, the yield of
positive cultu res from sputum sam ples is 50%

 Som e patients, particularly eld erly ind ividuals, m ay

not b e ab le to p roduce an app ropriate expecto rated
sputum sam ple.
 The in ability to p roduce sputum can b e a consequence of
dehydration , and the correction of th is condition m ay
result in in creased sputum p roduction and a m ore
1) The yield from b lood cultu res, even those ob tain ed
befo re an tib io tic therapy, is d isappoin ting ly lo w
 Only ~5–14% of cultu res of b lood from patients
hospitalized with CA P are po sitive
 the m ost frequently iso lated pathogen is S. Pneum oniae
2) Sin ce recommended em pirical regim ens all p rovid e
pneum ococcal coverage, a b lood cultu re po sitive fo r
th is pathogen has little effect on clin ical ou tcom e
************* susceptib ility d ata m ay allo w a switch
from a b roader-spectrum regim en to p enicillin in
appropriate cases
 Because of 1) the lo w yield and 2) the lack of
sign ificant im pact on ou tcom e, b lood cultu res are no
longer consid ered d e rigueur fo r all ho sp italized CA P
patients
 Two commercially available tests detect
a) pneumococcal
b) certain Legionella antigens in urine
 The test for Legionella pneumophil a 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
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
poin ts are g iven fo r 20 variables, in clu ding :
 Age
 coexisting illn ess
 abnorm al physical
 laborato ry fin ding s

On the b asis of the resulting score, p atients are assigned to one of

five classes w ith the fo llow ing m ortality rates:
 class 1, 0.1% low er adm ission rates
fo r class 1 an d class 2
 class 2, 0.6%
 class 3, 2.8% »»»»»»»»»»»»» those in class 3 should ideally
be adm itted to an ob servation un it
 class 4, 8.2%
 class 5, 29.2% classes 4 an d 5 should
be adm itted to the ho spital
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 I CU
 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
 Fluo roquino lone resistance am ong iso lates of E-coli
from community appears to b e in creasing

 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
In general, pneum ococcal resistance is acquired :
(1) by direct DNA incorporation and rem odeling resulting from contact
with closely related oral commensal bacteria
(2) by the process of natural transform ation
(3) by m utation of certain genes

Pneum ococcal strains are classified as:

 sensitive to p enicillin if the m inim al inhibitory concentration
(M IC ) is 0.06 g/M l
 in term ediate if the M IC is 0.1–1.0 g/m L
 resistant if the M IC is 2 g/M l

 Strain s resistant to drugs from ≥3 antim icrobial classes w ith

different m echanism s of action are considered M DR
 Pneum ococcal resistance to ß-lactam drugs is due solely to the
presence of low -affinity penicillin-binding proteins
 Penicillin is an appropriate agent for the treatment of pneumococcal
infection caused by strains with MI Cs of 1 g/mL
 For infections caused by pneumococcal strains with penicillin MI Cs 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
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
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 alw ays provided for the
pneum ococcus and the atypical p athogens
 Atypical pathogen coverage provided by a m acro lide or a
fluo ro quino lone has been associated w ith a significant reduction in
mortality rates com pared w ith those for -lactam coverage alone.
Telith rom ycin , a ketolide derived from the m acrolide class
 differs from the m acrolides in that it binds to bacteria m ore
avidly and at tw o sites rather than one
 This drug is active against pneum ococci resistant to penicillins,
macrolides, and fluoroquinolones

 If blood cultures yield S. pneum oniae sensitive to penicillin after

2 days of treatm ent w ith a m acrolide plus a -lactam or a
fluoroquinolone, should therapy be sw itched to penicillin?
 Penicillin alone w ould not be effective in the potential 15% of
cases w ith atypical co-infection
 One com prom ise w ould be to continue atypical coverage w ith either
a m acrolide or a fluoroquinolone for a few m ore days and then to
 Al though hospi talized patients have tradi tionally recei ved
ini tial therapy by the IV rout e, some dr ugs (fluor oqui nol ones)
are ver y well absor bed and can be gi ven or ally from the out set
to sel ect patients
 For patients ini tially treated IV, a swi tch to or al treatment is
appropriate as long as the patient can ingest and absor b the
dr ugs, is hemodynami cally stabl e, and is showi ng clini cal
improvement

The duration of treatment f or CAP »»»»»»»»»»»»

 Patient s have usually been treated for 10–14 days
 studi es wi th quinolones and telithromycin suggest, a 5-day
cour se is suffici ent for uncomplicated CAP
 A longer cour se is requi red for patients wi th:
1) bacteremi a 2) metastatic inf ection 3) inf ection wi th a
 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
 common complications of severe CAP incl ude:
“respi rator y failure “shock “mul tior gan failure “bl eedi ng
di atheses “complicated pl eur al effusi on “exacerbati on of
comor bi d illnesses “l ung abscess “metastatic inf ection
 Lung abscess may occur in associ ation wi th aspiration or wi th
infection caused by a si ngl e CAP pathogen(CA-MRSA, P.
aeruginosa, (rarel y) S. Pneumoniae)
 Aspi ration pneumoni a is typi cally a mi xed pol ymi crobi al
inf ection invol vi ng bot h aerobes and anaerobes
 In ei ther scenari o, dr ai nage shoul d be established

 A si gni ficant pl eur al effusi on shoul d be tapped for bot h

di agnostic and therapeuti c pur poses
 If the flui d has a pH of <7, a glucose level of <2.2 mmol/L,
The prognosis of CAP depends on the:
 patient's age
 Com orbidities
 site of treatm ent (inpatient or outpatient)

The overall m ortality rate for:

 the outpatient group is <1%
 patients requiring hospitalization is 10%
»»»»»»»» with ~50% of the deaths directly
attributable to pneum onia
 Fever and leukocyto sis 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 d epending on :
 the patient's age
 underlying lung disease »»»»»»»»»»

For a patient whose condition is improving and

who (if hospitalized) has been discharged, a
 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