WHO estimates, 450 million

cases of pneumonia are

recorded every year; about
4 million people die from
this illness, accounting for
7% of total mortality (2011)
Pneumonias - consultation
dr. Gergely Peskó

SEMMELWEIS UNIVERSITY
Faculty of Medicine
3rd Department of Internal Medicine
Director: Professor Tamás Masszi
Airway infections

Upper airway infections

Pharyngitis
Otitis media
Sinusitis
Stomatitis
Lower airway infections
Bronchitis
Pneumonia
Lung abscess, empyema
What we are going to focus on?
The three questions needed to be
answered:
Pneumonia: approach to a clinical syndrome • choice of AB therapy
• extent of testing
Community-acquired pneumonia (CAP) • appropriate site of treatment
Healthcare-associated pneumonia (HCAP)???
Hospital-acquired pneumonia (HAP) /not ventilator-
associated/
Ventilator-associated pneumonia (VAP)
Concomitant or post influenza pneumonia
Pneumonia in neutropenic patients

Pneumonia: approach to pathogens

Pneumonia – general overview
Pneumonia is an infection of the pulmonary parenchyma: patogen
proliferaton at the alveolar level + host response
Patogen gains access: small-volume aspiration, droplet inspiration, hematogenous
spread, contiguous extension
Host decense: hairs, turbinates, mucociliar clearance, gag reflex, cough, normal
flora, alveolar macrophages
When the capacity of the alveolar macrophages to ingest or kill the
microorganisms is exceeded does clinical pneumonia become manifest.
Host inflammatory response, rather than proliferation of microorganisms,
triggers the clinical syndrome of pneumonia:
IL-1, TNF-alfa fever; IL-8, GCSF neutrofils, leukocytosis localized
capillary leak, alveolar filling = radiologic infiltrate, typical ascultation,
hypoxemia / confusion/ (some patogen even interfere with hypoxemic
vasoconstriction), sputum, pleuritic chest pain
Increased respiratory drive respiratory alkalosis fatigue
Decreased compliance dyspnea
In the end: partial global respiratory failure
Pneumonia – general overview
About 30% of elderly patients do not show typical signs and symptomes
New lung infiltrates may be difficult to identify in patients with chronic lung
disease
About 17% of patients who are hospitalized for CAP do not have an infection
Pneumonia – general overview

Pneumonia was defined in the 2005 IDSA guideline as “new lung infiltrate plus
clinical evidence that the infiltrate is of an infectious origin, which include
the new onset of fever, purulent sputum, leukocytosis, and decline in
oxygenation.”
Cause of significant morbidity and mortality
Often misdiagnosed, mistreated and underestimated
In addition to a constellation of suggestive clinical features, a demonstrable
infiltrate by chest radiograph or other imaging technique, with or without
supporting microbiological data, is required(?) for the diagnosis of pneumonia
Make a good guess
 Infiltration/consolidation
Alveoli fill with fluid or blood cells (air in bigger local airways ; air in
parenchyma (alveoli) )
In massive infiltration:
Lobar pneumonia Secretion fills even the bronchi
Pulmonary edema air in bigger local airways
Pulmonary hemorrhage air in parenchyma (alveoli) )
NO bronchial breathing, NO increased tactile fremitus
Infiltrating pulmonary tumour
Pulmonary embolism pulmonary infarct

Syndrome Chest Percussion trachea Breath sounds Adventitious Tatile phremitus

name expansion note sounds and TVS-s
Infiltration / Unilaterally dullness midline Bronchial over Late Increased with
consolidation decreased involved area inspiratory bronchophony,
cracles, egophony,
cracles whispered
(pleural rub) pectoriloquy
Bronchi are visible only up to the
fourth order of branching
You can see the trachea, main
stem bronchi and the next order
of bronchi
Distal bronchi are surrounded by
air filled alveoli, there is no
contrast between air filled bronchi
and surrounding air filled alveoli,
thus, the bronchi are not visible
If the alveoli are filled with liquid
density (pneumonia, edema, and
hemorrhage, etc.) there is
contrast with air filled bronchi
and they become visible as
branching tubular structures
through the density.
visible air bronchogram implies
that there is alveolar filling and
the bronchi are patent
Community-aquired pneumonia (CAP)
Individuals of all ages not recently hospitalized and lacking healthcare
associated risk factors:
2005 IDSA – HCAP - NOT WORKING reworked
hospitalization for more than 2 days in an acute care hospital in the last 90 days
residence in a skilled nursing facility
recent intravenous antibiotic therapy, chemotherapy, or wound care in the last 30 days
attending a hospital or hemodialysis clinic
Immunosuppression

The concept of HCAP was introduced by the authors of the 2005 ATS and IDSA’s
guidelines to address the concern of the shifting microbiology of patients
presenting to the hospital with pneumonia. Recent or chronic contact with the
health care system seemed to be a risk factor of infection with MDR pathogens.
HCAP is a poor predictor of multidrug-resistant pathogens. The definition of HCAP
needs further modification.
HCAP guideline compliance did not result in better outcomes.
Community-aquired pneumonia (CAP)

Individuals of all ages not recently hospitalized and

lacking healthcare associated and risk factors and
underlying patient characteristics:
prior intravenous antibiotic use within 90 days or
antibiotic therapy within the last 30 days
hospitalization within 90 days
severity of pneumonia
immunosuppression
poor functional status
Renal replacement therapy
The risk score:
Recent hospitalization for at least 48h-s in the last 90 days – 4 points
Admission from a long term care facility – 3 points
Chronic HD – 2 points
Admitted to ICU within 24h-s of evaluation – 1 point
Community-aquired pneumonia (CAP)

Historically divided into „typical” amd „atypical”

syndromes but there is a significant overelap
Nearly 20% of patients with CAP who have proven
bacterial pneumonia are coinfected with a virus
In the preantibiotic era, Streptococcus pneumoniae
caused 95% of cases of pneumonia
The key to appropriate therapy is adequate coverage of
Streptococcus pneumoniae and the atypical bacterial
pathogens (mycoplasma, chlamydophila, and legionella)
Community-aquired pneumonia (CAP)
Site of care decision
Hospital admission
Objective scores, such as the CURB-65 score or the PSI, can assist
in identifying patients who maybe appropriate for outpatient care,
but the use of such scores must be tempered by the physician’s
determination of additional critical factors, including the ability to
safely and reliably take oral medication and the availability of
outpatient support resources.
ICU admission
patients with septic shock requiring vasopressors or with acute
respiratory failure requiring intubation and mechanical ventilation
admission to an ICU or high-level monitoring unit is recommended
for patients with 3 of the minor criteria for severe CAP
CURB-65
score
Severe CAP
significant percentage of patients with CAP
are transferred to the ICU in the first 24–48
h after hospitalization. Mortality and
morbidity among these patients appears to
be greater than those among patients
admitted directly to the ICU
Additional risk factors: lactic acidosis, low
pH, albumin under 3.5g/dl, Na under
130mmol/L, leukocitosis over 20000/mm3,
pulse over 125/min, over 80 years of age
Community-aquired
pneumonia (CAP)
pathogens
Community-aquired pneumonia (CAP)
pathogens
 Community-aquired pneumonia (CAP)
pathogens
Group I: outpatients, no cardiopulmonary disease, no
modifying factors *, †

*Excludes patients at risk

for HIV
†In roughly 50~90% of the

cases no etiology was

identified
 Community-aquired pneumonia (CAP)
pathogens
Group II: outpatients,
with cardiopulmonary
disease, and/or other
modifying factors *, †

Excludes patients at risk for

HIV
†In roughly 50~90% of the cases

no etiology was identified

Community-aquired
pneumonia (CAP)
pathogens

Group III: inpatients, not in intensive care

unit *, †

*Excludespatients at risk for HIV

†In
roughly one-third to one-half of the cases no etiology
was identified
Community-aquired pneumonia (CAP)
pathogens
Group IV: intensive care unit-
admitted patients *, †

*Excludes patients at risk for HIV

†Inroughly one-third to one-half of the
cases no etiology was identified
Community-aquired pneumonia (CAP)
diagnostic testing
Patients with CAP should be investigated for specific pathogens that would
significantly alter standard (empirical) management decisions, when the
presence of such pathogens is suspected on the basis of clinical and
epidemiologic clues
Routine diagnostic tests to identify an etiologic diagnosis are optional for
outpatients with CAP
In patients requiring hospitalization, clinicians should make a conscientious
effort to determine the causative organism.
Pathogen-directed therapy greatly fosters antibiotic stewardship, decreasing
the cost of care and reducing the risk of complications such as Clostridium
difficile infection.
Gram’s staining and culture of sputum, blood cultures, testing for legionella
and pneumococcal urinary antigens, and multiplex PCR assays for Myc.
pneumoniae, Chl. pneumoniae, and respiratory viruses
Community-aquired pneumonia (CAP)
diagnostic testing
Gram’s staining and culture of sputum are positive in more than 80% of cases of
pneumococcal pneumonia with a good-quality specimen (>10 inflammatory cells
per epithelial cell) before, or within 6 to 12 hours after, the initiation of
antibiotics.
Blood cultures are positive in about 20 to 25% of inpatients with pneumococcal
pneumonia but pretreatment blood cultures yielded positive results for a probable
pathogen in 5%–14% in large series of nonselected patients hospitalized with CAP
Hematogenous Staph. aureus pneumonia, blood cultures are nearly always
positive, but they are positive in only about 25% of cases in which inhalation or
aspiration is responsible for the CAP.
ELISA of urine samples detected pneumococcal cell-wall polysaccharide in 77 to
88% of patients with bacteremic pneumococcal pneumonia and in 64% with
nonbacteremic pneumonia.
ELISA for legionella urinary antigen is positive in about 74% of patients with
pneumonia caused by Legionella pneumophila serotype 1
PCR assays can detect most important respiratory viruses as well as Myc.
pneumoniae and Chl. pneumoniae.
Community-aquired pneumonia (CAP)
treatment
Once the diagnosis of CAP is made, antimicrobial therapy should be started as
soon as possible and at the site where the diagnosis is made.
Outpatients with CAP are generally treated empirically.
Several factors favor the use of a beta-lactam as empirical therapy for CAP in
outpatients:
most clinicians do not know the level of pneumococcal resistance in their
communities, and Str. pneumoniae is more susceptible to penicillins than to
macrolides or doxycycline
it seems inappropriate to treat a patient with a macrolide or doxycycline to which
15 to 30% of strains of Str. pneumoniae are resistant
if a patient does not have a prompt response to a beta-lactam, a macrolide or
doxycycline can be substituted to treat a possible atypical bacterial infection
where isolates produce betalactamase, amoxicillin–clavulanate may be preferable
to amoxicillin or penicillin, especially in patients with underlying lung disease
Community-aquired
pneumonia (CAP)
treatment –
outpatient IDSA
The key to appropriate therapy
is adequate coverage of
Streptococcus pneumoniae and
the atypical bacterial pathogens
(mycoplasma, chlamydophila,
and legionella)
Macrolides, doxycycline, and
fluoroquinolones are the most
appropriate agents for the
atypical bacterial pathogens.
Community-aquired pneumonia (CAP)
treatment – inpatient, non-ICU IDSA
These regimens have been
studied extensively and
generally produce a cure in
about 90% of patients with CAP
of mild or moderate severity
 Community-aquired
pneumonia (CAP)
treatment – inpatient,
ICU IDSA
When influenza is active in the community, patients with CAP
should be treated with oseltamivir even if more than 48 hours
have elapsed since the onset of symptoms
Patients at high risk for Staph. aureus pneumonia (e.g., those
taking glucocorticoids or those with influenza), vancomycin or
linezolid should be added to treat MRSA
Ceftaroline, which is active against Staph. aureus, including
MRSA, as well as Str. pneumoniae and H. influenzae, may
eventually replace ceftriaxone plus vancomycin or linezolid
S. pneumoniae remains the most common cause of severe
community-acquired pneumonia requiring ICU admission
Observational evidence suggests that the macrolide
combination may be associated with better outcomes
explained by nonbactericidal effects, such as
immunomodulation
CAP – risk factors
related to specific
patogens
Community-aquired pneumonia (CAP)
additional therapies
Many, but not all, retrospective studies have shown that the addition
of a macrolide to a beta-lactam antibiotic to treat pneumococcal
pneumonia or all-cause CAP reduces morbidity and mortality,
presumably by inhibiting the inflammatory response
Statins block the synthesis of HMG-CoA reductase, inhibiting the
synthesis of farnesyl pyrophosphate and geranylgeranyl pyrophosphate
(which are needed to activate G proteins), thereby dampening
inflammatory responses. A randomized trial of adjunctive simvastatin
in patients with ventilator-associated pneumonia was stopped early
because no 28-day mortality benefit was seen in those who received
this drug
 Community-aquired pneumonia (CAP)
durations of treatment
Patients with CAP should be treated for a minimum of 5
days, should be afebrile for 48–72 h, and should have no
more than 1 CAP-associated sign of clinical instability
before discontinuation of therapy
The currently recommended duration of antibiotic
therapy for community-acquired pneumonia is 5 to 7 days
(or even shorter). There is no evidence that prolonged
courses lead to better outcomes, especially in
outpatients, or in inpatients who have a prompt response
to therapy, unless they are immunocompromised.
Hematogenous Staph. aureus pneumonia mandates
treatment for at least 4 weeks, but segmental or lobar
pneumonia that is caused by this organism may be treated
for 2 weeks.
Community-aquired pneumonia (CAP)
IV/PO treatment and discharge
Patients should be switched from intravenous to oral
therapy when they are hemodynamically stable and
improving clinically, are able to ingest medications, and
have a normally functioning gastrointestinal tract.
Patients should be discharged as soon as they are
clinically stable, have no other active medical problems,
and have a safe environment for continued care. Inpatient
observation while receiving oral therapy is not necessary!
Community-aquired pneumonia (CAP)
other treatment considerations
Hypotensive, fluid-resuscitated patients with severe CAP
should be screened for occult adrenal insufficiency.
Patients with hypoxemia or respiratory distress should
receive a cautious trial of noninvasive ventilation (NIV)
unless they require immediate intubation because of
severe hypoxemia (arterial oxygen pressure/fraction of
inspired oxygen [PaO2/FiO2] ratio, lower then 150) and
bilateral alveolar infiltrates.
Community-aquired pneumonia (CAP)
non-responding disease

May be additionally
needed:
Cheast CT
Thoracocentesis
Bronchoscopy with
BAL and/or biopsy
Community-aquired pneumonia (CAP)
prevention
Influenza vaccine:
be offered to persons older than 50 years, residents of extended-
care facilities, and patients who have chronic heart and lung
disorders, chronic metabolic diseases (including diabetes
mellitus), renal dysfunction, hemoglobinopathies, or
immunosuppression
Pneumococcus vaccine:
Pneumococcal 13-valent conjugate (PCV13): immune response is
strong, immunememory +, longer immunity, decrease
nasopharyngeal carriage
Pneumococcal polysaccharide (PPSV23): immune response is
strong-intermediate, immunememory -, shorter immunity, no
effect on nasopharyngeal carriage
Community-aquired pneumonia (CAP)
prevention
Immunocompromising conditions that are indications for pneumococcal
vaccination are congenital or acquired immunodeficiency (including B- or
T-lymphocyte deficiency, complement deficiencies, and phagocytic
disorders excluding chronic granulomatous disease), HIV infection, chronic
renal failure, nephrotic syndrome, leukemia, lymphoma, Hodgkin disease,
generalized malignancy, multiple myeloma, solid-organ transplant, and
iatrogenic immunosuppression (including long-term systemic
corticosteroids and radiation therapy).
Anatomical or functional asplenia that are indications for pneumococcal
vaccination are sickle cell disease and other hemoglobinopathies,
congenital or acquired asplenia, splenic dysfunction, and splenectomy.
Administer pneumococcal vaccines at least 2 weeks before
immunosuppressive therapy or an elective splenectomy, and as soon as
possible to adults who are newly diagnosed with asymptomatic or
symptomatic HIV infection.
PCV13 and PPSV23
Hospital-aquired pneumonia (HAP=non-VAP)

HAP is defined as a pneumonia not incubating at the time of hospital

admission and occurring 48 hours or more after admission
VAP is defined as a pneumonia occurring >48 hours after endotracheal
intubation
HAP and VAP continue to be frequent complications of hospital care.
Together, they are among the most common hospital-acquired
infections (HAIs), accounting for 22% of all HAIs in a multistate point-
prevalence survey
all-cause mortality associated with VAP has been reported to range
from 20% to 50%
even in HAP, generally considered to be less severe than VAP, serious
complications occur in approximately 50% of patients, including
respiratory failure, pleural effusions, septic shock, renal failure, and
empyema
 Hospital-aquired pneumonia (HAP) – risk
factors for MDR pathogens
fifteen potential risk factors were included in meta-analysis.
Only one risk factor was significantly associated with MDR HAP:
prior intravenous antibiotic use in the last 90 days
while other risk factors may be relevant, evidence is lacking:
some evidence suggesting that a positive MRSA screen
from nasal or respiratory samples may increase the risk of
MRSA
prior use of antibiotics, mechanical ventilation, and
history of chronic obstructive pulmonary disease have
been identified as potential risk factors for MDR P.
aeruginosa infection
patients with cystic fibrosis and bronchiectasis are more
likely than patients with other pulmonary diseases to be
chronically colonized with P. aeruginosa and are therefore
also likely at increased risk for MDR P. aeruginosa

It includes MRSA and MR Pseudomonas.

HAP - pathogens
Early-onset (<5 days in the hospital, no other risk factors for
MDR)
Strep. pneumoniae
Staph. aureus
H. influenzae
Enteric gram-negative bacilli
Late-onset (>5days in the hospital, risk factors for MDR present)
Staph. aureus (often MRSA)
Gram-negaive enterics (often MDR)
E. coli, Klebsiella pneumoniae, Enterobacter sp., Serratia
marcescens, Pseudomonas aeruginosa, Acinetobacter
beumanii
ESKAPE pathogens in nearly 80% of patients
Hospital-aquired pneumonia (HAP) –
diagnostic measures
patients with suspected HAP (non-VAP) be treated according to the results of
microbiologic studies performed on respiratory samples obtained
noninvasively, rather than being treated empirically
high value on the potential to accurately target antibiotic therapy and then
deescalate antibiotic therapy based upon respiratory and blood culture results
Noninvasive methods to obtain respiratory samples include the following:
spontaneous expectoration
sputum induction
nasotracheal suctioning in a patient who is unable to cooperate to produce a
sputum sample
endotracheal aspiration in a patient with HAP who subsequently requires
mechanical ventilation
Some patients in whom a respiratory sample cannot be obtained noninvasively,
there may be factors which could prompt consideration of obtaining samples
invasively.
 HAP – use of PCT for diagnosis and
initiation of therapy
PCT
PCT is a precursor of calcitonin that is constitutively secreted by C cells of the
thyroid gland and K cells of the lung
In healthy individuals, PCT is normally undetectable (<0.01 ng/mL)
stimulated by endotoxin, PCT is rapidly produced by parenchymal tissue
throughout the body; this PCT production has also been observed in diverse
types of bacterial infections
PCT may increase in response to sterile inflammation or viral infection, but it
is less common

The evidence indicates that serum PCT plus clinical criteria can diagnose
HAP/VAP with a sensitivity and specificity of 67% and 83%.

For patients with suspected HAP/VAP, it is recommended to use clinical criteria

alone, rather than using serum PCT plus clinical criteria, to decide whether or
not to initiate antibiotic therapy. (Same goes for CRP!)
HAP – use of PCT for stoping antibiotic
therapy
For patients with HAP/VAP, using PCT levels plus clinical
criteria to guide the discontinuation of antibiotic therapy
is suggested, rather than clinical criteria alone
A low serum procalcitonin concentration (<0.1 µg per
liter) can help to support a decision to withhold or
discontinue antibiotics

Discontinuing antibiotics on the basis of PCT levels plus

clinical criteria decreases antibiotic exposure compared with
using clinical criteria alone; all other outcomes remain
unchanged
HAP - treatment

Lokal antibiotic resistance is critically important:

all hospitals are to regularly generate and disseminate a
local antibiogram, ideally one that is tailored to their HAP
population
empiric antibiotic regimens are to be based upon the local
distribution of pathogens associated with HAP and their
antimicrobial susceptibilities
HAP – treatment: not at high risk of mortality
and no factors increasing the likelihood of
MRSA
Risk factors for mortality:
need for ventilatory support due to pneumonia
septic shock, (hypotension, rapid progression on CXR)
Indications for MRSA coverage:
include intravenous antibiotic treatment during the
prior 90 days
treatment in a unit where the prevalence of MRSA
among S. aureus isolates is not known or is >20%
Prior detection of MRSA by culture or non-culture
screening may also increase the risk of MRSA
if MRSA coverage is omitted, the antibiotic regimen
should include coverage for MSSA.
These AB-s cover MSSA, pseudomonas and G neg.!
HAP – treatment: not at high risk of
mortality but with factors increasing
the likelihood of MRSA
If patient has factors increasing the likelihood of
gram-negative infection, 2 antipseudomonal agents
are recommended:
If patient has structural lung disease increasing
the risk of gram negative infection (ie,
bronchiectasis or cystic fibrosis), 2
antipseudomonal agents are recommended
A high-quality Gram stain from a respiratory
specimen with numerous and predominant gram-
negative bacilli provides further support for the
diagnosis of a gram-negative pneumonia, including
fermenting and non-glucose-fermenting
microorganisms
Prior intravenous antibiotic use within 90 days
increases the risk of pseudomonas infection.
HAP – treatment: high risk of
mortality or receipt of intravenous
antibiotics during the prior 90 days
PHARMACOKINETIC/PHARMACODYNAMIC
OPTIMIZATION OF ANTIBIOTIC THERAPY:
potential advantages of PK/PD-optimized
dosing (decreased mortality, decreased ICU
length of stay, and increased clinical cure
rate) against the potential downsides (more
burdensome and costly, possibly more
toxicity among patients who require higher
doses due to augmented clearance)
D – means: extended infusions may be

appropriate.
HAP – treatment: MRSA, Pseudomonas
aeruginosa
MRSA HAP/VAP be treated with either vancomycin or linezolid rather
than other antibiotics or antibiotic combinations
HAP/VAP due to P. aeruginosa:
choice of an antibiotic for definitive (not empiric) therapy be
based upon the results of antimicrobial susceptibility testing
aminoglycoside monotherapy is NOT recommended
not in septic shock or at a high risk for death, and for whom the
results of antibiotic susceptibility testing are known, monotherapy
is recommended
in septic shock or at a high risk for death when the results of
antibiotic susceptibility testing are known, combination therapy is
suggested
HAP – treatment: ESBL-producing G neg.
bacteria, Acinetobacter
HAP/VAP due to ESBL-producing gram negative bacilli:
choice of an antibiotic for definitive (not empiric) therapy be based upon
the results of antimicrobial susceptibility testing and patient specific
factors
failed to identify an agent that is clearly preferable to others in the
treatment of HAP/VAP due to ESBL-producing gram-negative bacilli
HAP/VAP caused by Acinetobacter species:
treatment with either a carbapenem or ampicillin/sulbactam if the
isolate is susceptible to these agents
If it is sensitive only to polymyxins, intravenous polymyxin and adjunctive
inhaled colistin is suggested
If it is sensitive only to colistin, adjunctive rifampicin is NOT
recommended
use of tigecycline is NOT recommended
HAP – treatment: carbapenem rezistant
pathogens
In patients with HAP/VAP caused by a carbapenem-
resistant pathogen that is sensitive only to polymyxins,
intravenous polymyxins and adjunctive inhaled colistin are
recommended
HAP – optimal duration and deescalation
of therapy
For patients with HAP, a 7-day course of antimicrobial therapy is
recommended
There exist situations in which a shorter or longer duration of antibiotics may
be indicated, depending upon the rate of improvement of clinical, radiologic,
and laboratory parameters:
Staph. aureus, MRSA and more resistant organisms (Pseudomonas,
Acinetobacter, Stenotrophomonas) may need longer therapy – 14 days?
For patients with HAP/VAP, antibiotic therapy should be de-escalated
rather than fixed
De-escalation refers to changing an empiric broad spectrum antibiotic
regimen to a narrower antibiotic regimen by changing the antimicrobial agent
or changing from combination therapy to monotherapy. In contrast, fixed
antibiotic therapy refers to maintaining a broad-spectrum antibiotic regimen
until therapy is completed.
HAP – good to know
P. aeruginosa pneumonia is characterized by fever, cyanosis,
hypotension, and rapid cavitation (<72 hours) on chest radiography.
Sputum recovered from these cases is typically greenish due to the
pyocyanin pigment that is produced by the organism when it invades
tissue. This is usually accompanied by an almond odor.
Enterobacter species do not typically cause hospital-acquired
pneumonia
S. maltophilia and B. cepacia are common colonizers of respiratory
secretions, but they rarely, if ever, cause nosocomial pneumonia in
otherwise healthy hosts
S. aureus (MSSA/MRSA) commonly colonizes respiratory secretions
(30%-50%) but rarely, if ever, causes necrotizing cavity nosocomial
pneumonia.
Oropharyngeal anaerobes are unimportant from a therapeutic
standpoint.
Viral pneumonia: no clinical algorithm exists
that will distinguish clearly
the cause of pneumonia
100 million in children and 100 million in adults every year
viruses are the putative causative agents in a third of cases of community-
acquired pneumonia, in particular influenza viruses, rhinoviruses, and
coronaviruses
Laboratory diagnosis of viral pneumonia has relied on detection of virus or
viral antigen in upper-respiratory specimens (eg, nasopharyngeal aspirates)
and lowerrespiratory samples (eg, induced sputum)