Management of Unique

Pneumonias Seen in the

In t en si ve C are U n it
Brooke K. Decker, MDa,*, LaToya A. Forrester, MPH, CIC
a
,
David K. Henderson, MDa

KEYWORDS
 Pneumonia  Nosocomial  Health care–associated infections  Legionella

KEY POINTS
 Regions, hospitals, and individual hospital floors may have a unique and clinically signif-
icant microbiota; knowledge of this local antibiogram may improve clinical care.
 Empirical therapy should be converted to targeted therapy as soon as possible to limit
potentially harmful exposure to overly broad-spectrum antimicrobials.
 Infection prevention surveillance definitions are designed to be standardized and sensi-
tive, although they may not perfectly overlap with clinical disease.
 Robust, prospective surveillance detects signals early and may lead to identification of
reservoirs of resistant or waterborne pathogens that can be remediated to prevent future
infections.

INTRODUCTION

Severe infections may require intensive care unit (ICU) admission. Even when admitted
for noninfectious reasons, the clinical course of critically ill patients may be compli-
cated by the acquisition of infection. A 2017 prevalence study conducted at 1150 cen-
ters in 88 countries estimated the incidence of suspected or proven infections among
ICU patients to be about 54%.1 In the United States between the years 2006 and 2010,
approximately 19% of adults hospitalized with pneumonia were admitted to the ICU
and 13% required assisted ventilation.2 The Centers for Disease Control and Preven-
tion (CDC) 2020 National and State Healthcare-Associated Infections Progress Report
noted an overall 35% increase in ventilator-associated events (VAE) between 2019
and 2020.3 The marked increase in VAE strongly aligns with the 2019 SARS-CoV-2
pandemic; however, as earlier data suggest, additional factors may contribute to
the development of cases of pneumonia in patients who require ICU-level care.

a
Hospital Epidemiology Service, NIH Clinical Center, 10 Center Drive MSC 1214, Bethesda, MD
20892, USA
* Corresponding author.
E-mail address: [email protected]

Infect Dis Clin N Am 36 (2022) 825–837

https://doi.org/10.1016/j.idc.2022.07.003 id.theclinics.com
0891-5520/22/Published by Elsevier Inc.

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826 Decker et al

This article explores some unusual and complex pneumonias, focusing on hospital-
acquired infections, and highlights certain unusual microorganisms that have unique
clinical significance. In addition, this article addresses diagnostic and treatment con-
siderations in the critically ill patient population. Establishing a conceptual under-
standing of pneumonia and its epidemiology is an important first step in
understanding what makes some ICU-based infections unusual and complex. Pneu-
monia will be defined both clinically and in a standardized surveillance definition.

DEFINITION

Pneumonia is perhaps most simply described as an acute infection of the lungs.4 The
Infectious Disease Society of America (IDSA) and the America Thoracic Society (ATS)
define pneumonia as the presence of both (1) a new lung infiltrate and (2) signs of acute
infection, including fever, purulent sputum, leukocytosis, or hypoxia.5 As is the case
for the term “fever,” pneumonia” is an infectious process that is not homogeneous
but a group of distinct syndromes with separate epidemiologies, pathogenesis, clin-
ical courses, and outcomes. Pneumonia is the most common cause of hospital admis-
sion for US adults, with about 1.5 million adults seeking care for pneumonia every year
and more than 40,000 resulting deaths.6 The World Health Organization noted that
pneumonia accounts for 14% of all deaths of children younger than 5 years, a devas-
tating (pre-SARS-CoV-2) 740,180 deaths in 2019.7 Pneumonia is additionally classi-
fied by the setting in which the infection was most likely acquired (community- vs
health care–associated) as well as causative microorganisms (viral, bacterial, fungal).
Understanding the definitional differences between community-acquired pneumonia
(CAP) and health care–associated pneumonia (HCAP) is necessary both from diag-
nostic and empirical treatment standpoints and also to ensure prompt identification
and remediation of factors associated with in-hospital morbidity and mortality.
Fig. 1 outlines the rubric used to classify patients presenting on admission with a diag-
nosis of pneumonia (CAP) versus those who potentially acquired pneumonia during
hospitalization (HAP). A retired category of pneumonia, HCAP, included exposure to
the health care environment, hypothesizing increased risk for different or resistant or-
ganisms.8 This category was subsequently discontinued, as causative organisms
were closely aligned with CAP, and patient outcomes worsened with broader anti-
biotic treatment prescribed to cover projected (but not demonstrated) resistant path-
ogens.9 A subset of HAP known as ventilator-associated pneumonia (VAP) represents
the most dangerous extreme, affecting the most vulnerable of hospitalized patients.

Fig. 1. Definition of community-acquired versus health care–acquired pneumonia.

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 Management of Unique Pneumonias Seen in the ICU 827

HAP, including VAP, represents the second most common health care–associated
infection in the United States.10 VAP is defined as pneumonia that develops more
than 48 to 72 hours after endotracheal intubation.11 Establishing an impartial definition
for VAP can be challenging because many conditions that develop in critically ill pa-
tients possess similar signs and symptoms. Specifically, ventilated patients often
have infiltrates detected on chest radiology that have noninfectious causes. Without
objective interpretation of radiological evidence of pneumonia (eg, infiltrates vs opac-
ities vs volume overload), creating a standardized surveillance definition is chal-
lenging. Similarly, the creation of interventional strategies such as preventative
bundles depends on an accurate and specific definition. This picture can be further
clouded by the fact that, in addition to being associated with lung infection, purulent
secretions may be secondary to inflammation of the trachea and bronchi. Finally, a
noted increase in white cell count and fever can indicate sepsis not associated with
the respiratory system.12 To provide a more objective approach to the identification
of VAP, in 2013, CDC shifted its surveillance focus from VAP to VAE for adult patients.
The redefined VAE rubric was designed to eliminate the subjective interpretation found
within the original VAP definition by broadening the focus to capture pneumonia as
well as complications associated with mechanical ventilation that are also a source
of considerable morbidity and mortality in ICU patients.13 The new definition elimi-
nated reliance on radiographic evidence and interpretation, and instead the new
VAE algorithm outlines a baseline period of stability or improvement of a patient’s
oxygenation on the ventilator. A sustained increase in fraction of inspired oxygen
(FiO2) or PEEP may indicate a ventilator-associated condition (VAC). At the point of
identification of a VAC, the reviewer looks for the introduction or change in antimicro-
bial therapy, white cell count, or temperature to meet criteria for infection-related
ventilator-associated complications (IVAC). For VAE that meet the criteria for IVAC,
further evaluation to determine if a possible ventilator-associated pneumonia is pre-
sent includes evidence of purulent respiratory secretions or microbiological speci-
mens positive for organisms compatible with lower respiratory infection. Fig. 2
provides a summary of the key components of the VAE algorithm. Although this algo-
rithm is objective and designed such that surveillance and reporting of cases in even a
large medical center can be accomplished by nonclinicians, it is not without pitfalls.
Only about 40% of clinically diagnosed VAPs meet VAE criteria.13 Because of their
complex and more severely ill patient populations, many academic centers and large,
critical access hospitals feel they are treated inequitably by this change in definition.
Moreover, at the time of the implementation of the adult VAE algorithm, insufficient
data were available to develop a pediatric VAE definition. In 2015, CDC developed
and implemented a pediatric VAE definition, based primarily on a study that demon-
strated that events defined by changes in FiO2 and mean airway pressure were asso-
ciated with increases in patient’s length of stay.14
Given the significant morbidity and mortality associated with a pneumonia diagnosis
and the need to reduce or prevent health care–associated infections, clear, objective,
standardized criteria identifying pneumonia trends within a population are necessary.
The clinical definition is subjective and considers all available diagnostic data unique
to that patient. In the United States, pneumonia categorized by surveillance definitions
are tracked via the CDC via the National Healthcare Tracking System (National Health-
care Safety Network [NHSN]) surveillance system. Aggregated data are used to estab-
lish preventative strategies and guidelines for reducing the mortality and morbidity
associated with pneumonia and can be used as a marker of quality and linked to re-
imbursements. At times, discrepancies are identified between the surveillance defini-
tions and the clinical diagnosis agreed on by the clinicians providing care.15 In these

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828 Decker et al

Fig. 2. VAE definition algorithm summary as of January 2022. (Adapted from Centers for
Disease Control and Prevention. National Healthcare Safety Network (NHSN). Ventilator-
associated Events (VAE): Chapter 10: Ventilator-Associated Event (VAE) Protocol – January
2022. Available at https://www.cdc.gov/nhsn/pdfs/pscmanual/10-vae_final.pdf.)

cases, the surveillance definition should not override the clinical judgment associated
with the diagnosis, management, and treatment of a singular patient with pneumonia.
Similarly, clinical judgment should not be used as a justification for underreporting an
infection meeting the NHSN surveillance criteria, as failing to report these infections
violates Medicare laws and regulations.
The causative agents of pneumonia can vary, including environmental and chemical
irritants (air pollution, smoking), aspiration (foreign substances entering the lungs),
device-related (prolonged mechanical ventilation), and, more commonly, by microor-
ganisms. For the context of this article, the authors focus on microorganisms as the
causative agent.

MICROBIAL CAUSES OF PNEUMONIA

Pneumonia can be caused by viruses, bacteria, fungi, and even some parasites. In the
United States, the most common causes of viral pneumonia are influenza, respiratory

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 Management of Unique Pneumonias Seen in the ICU 829

syncytial virus (RSV), and SARS-CoV-2. The most common cause of bacterial pneu-
monia is Streptococcus pneumoniae (pneumococcus).16 In critically ill patients,
more than 50% of health care–acquired pneumonia and ventilator-associated pneu-
monia are caused by multidrug-resistant (MDR) organisms, regardless of duration of
hospitalization, and previous antibiotic use was the most significant risk factor.17
Fungal pneumonias are often associated with severe immunosuppression but occa-
sionally occur in immunocompetent hosts (eg, Histoplasma and Coccidioides
pneumonias).

DIAGNOSTIC TESTING

Empirical antibiotic treatment should not be delayed in patients who have sepsis and
evidence of infection. Early acquisition of diagnostic specimens, including sputum or
lower respiratory tract cultures and blood cultures, should be obtained, ideally, before
antibiotic initiation or changes to ensure optimal sensitivity in all hospitalized patients
with pneumonia. Identifying the cause of pneumonia may help narrow or tailor therapy
to the causative organism, improving outcomes while limiting adverse events and sup-
porting antimicrobial stewardship. Routine culture is effective in identifying the most
common bacterial causes of pneumonia and is the most appropriate first step. Further
diagnostic testing, molecular testing (including multiplex testing platforms), pathogen-
specific tests such as Legionella urinary antigen, and special media requiring respira-
tory cultures (Legionella, mycobacteria, fungal, and so forth) should be obtained in ICU
patients with undifferentiated pneumonia after routine cultures or with risk factors that
make unusual pneumonia more likely. Legionella cultures are recommended for all
hospital-associated pneumonia and all severe pneumonias. Identifying organisms of
public health concern may serve to identify a remediable outbreak and prevent further
cases.5 Some organisms, including resistant organisms, Mycoplasma pneumoniae,
Mycobacterium tuberculosis, and viral respiratory infections are transmitted person
to person. Transmission-based precautions should be implemented with a transmis-
sible diagnosis, preventing exposures to other patients or staff.18 Noninvasive sam-
pling techniques such as endotracheal aspiration as well as more invasive
techniques including bronchoalveolar or gastric lavage and protected or blind bron-
chial sampling can also be considered, especially in hospital-acquired pneumonia,19
but they should be interpreted with caution, considering the risk of upper airway
contamination and uncertain specificity. Moreover, not prematurely assuming the
pathogen growing in culture is the one responsible for the patient’s illness is important,
especially if the pathogen is not a typical cause of respiratory infection, such as
Candida20 or Enterococcus.21 These organisms are more likely to colonize hospital-
ized patient’s respiratory tracts than cause pneumonia, and the search should
continue for a more likely causative organism when they are isolated.
During influenza season it is reasonable to perform viral polymerase chain reaction
(PCR) for influenza; antigen testing for influenza is not recommended in critically ill pa-
tients due to the lower sensitivity of this modality and the potential to miss cases that
might benefit from appropriate therapy such as oseltamivir.22 During the SARS-CoV-2
pandemic, ruling out COVID-19 has been an appropriate first step in the diagnosis of
severe pneumonia. Other appropriate viral testing, including multiplex PCR platforms,
may serve to identify common respiratory pathogens and, even if no treatments are
available, serve to support discontinuation of unnecessary antimicrobial agents. Clini-
cians must be aware of the limitations of the multiplex system being used, as different
panels test for different sets of organisms, and antimicrobial sensitivities to the organ-
isms on the panel also may differ from one panel to the next. Additional pathogen-

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830 Decker et al

specific testing should be tailored to current endemic trends, regional and/or risk
factor–associated pathogens (such as hantavirus, ebolavirus, fungal, and so forth).
A reasonable approach includes starting with the most likely tests and appropriate
empirical treatments and pursuing further and less probable causes if initial studies
are not revealing.

Bacterial Pathogens
Gram-negative pathogens frequently associated with outbreaks include
Carbapenemase-producing Enterobacterales, MDR Pseudomonas, Acinetobacter
baumannii, and Stenotrophomonas; however, more unusual pathogens may be a
more significant concern to a particular hospital or unit. Having a close relationship
with the hospital infection prevention team and openly collaborating and sharing infor-
mation with that team are essential for successful management of these pathogens.
Although infection prevention is responsible for designating what does or does not
meet criteria for ventilator-associated pneumonia, the astute clinician should always
inquire about what pathogens are implicated. Understanding this level of detail will
assist in identifying trends and may provide a more finely tuned assessment of path-
ogens of interest to the practicing clinician.
Carbapenemase-producing Enterobacterales are gram-negative, fermenting bacte-
ria that test resistant to at least one carbapenem antibiotic (ertapenem, meropenem,
doripenem, or imipenem) or produce carbapenemase. Other organisms including
Pseudomonas may also carry carbapenemases, and the organisms can broadly be
called carbapenemase-producing organisms (CPO). Patients admitted to the ICU
may harbor CPO on admission or may acquire CPO due to transmission from health
care worker hands or the environment during their stay. CPO colonization is associ-
ated with increased length of stay and mortality.23 Surveillance screening and molec-
ular diagnostics may assist in identifying CPO colonized patients before a clinical
specimen is detected, which would allow more rapid organism-based isolation pre-
cautions to be instituted.24 For patients with known CPO colonization who develop ev-
idence of infection, empirical therapy should cover colonizing pathogenic organisms,
but if a susceptible pathogen is isolated, deescalation of antibiotics should be prompt,
as overly broad antibiotics can negatively affect mortality.25
Among ICU patients diagnosed with VAP, infection with Stenotrophomonas was
significantly associated with severe critical illness as measured by Sequential Organ
Failure Assessment (SOFA) score greater than 2 and exposure to broad spectrum an-
tibiotics such as carbapenems. Concerningly, effective antibiotic coverage did not
improve mortality, and diagnosis of Stenotrophomonas was associated with greater
60-day mortality in these patients.26

Atypical Pathogens
The term “atypical pneumonia” was first coined in the preantibiotic period in 1938 to
distinguish these milder cases from the more typical and lethal lobar infections.27
Since that time, it has been used to generally refer to pneumonias wherein the imaging
findings are more diffuse, the organisms are not readily identifiable with routine
methods, or those that may require specific treatments.27 The most commonly iden-
tified atypical pneumonia organisms are Legionella, Mycoplasma pneumoniae, and
Chlamydophila pneumoniae.
Of the atypical pneumonias that occur in health care settings, Legionellosis, first
identified as the cause of a 16% fatal pneumonia associated with the 1976 American
Legion Convention in Philadelphia is the most feared atypical pneumonia.28 Water-
borne Legionella bacteria are the cause of outbreaks of severe and mortal illness.

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 Management of Unique Pneumonias Seen in the ICU 831

As a waterborne pathogen, Legionella can be mitigated, but prevention may necessi-

tate large facility expenditures in buildings that have established biofilms and a history
of nosocomial cases. The Veterans Affairs administration implemented a comprehen-
sive Legionella prevention program in 2014 and has demonstrated significant reduc-
tions in both health care–associated Legionella pneumonia29 and water positivity30
after program implementation. The most important way to prevent nosocomial
Legionellosis is to ensure patients are tested for Legionella when hospital-
associated pneumonia is detected, regardless of severity. Identifying cases will lead
to evaluation and remediation of health care sources of Legionella bacteria, potentially
preventing future infections. Current guidelines recommend testing all severe pneu-
monia and all hospital-associated pneumonia for Legionella. Depending on local prev-
alence, it may be appropriate to test other types of CAP for Legionella. Available
laboratory modalities for the detection of Legionella include antigen testing of urine
and PCR or culture of respiratory samples. Understanding the type of testing available
in your hospital laboratory as well as the limitations of this testing technique will help
avoid missing the diagnosis. The most widely available urinary antigen test only de-
tects Serogroup 1, which is the most common cause of human disease; however,
more than 16% of cases are due to other serogroups or species.31 Detection of
hospital-associated Legionella must result in prompt, exhaustive investigation of hos-
pital water sources, preventive strategies implemented, and any potential sources
remediated. The source of community-acquired Legionella pneumonia may be harder
to identify and remediate, but identification and remediation of these sources provides
significant public health benefit.
The most common agent used to treat Legionella is azithromycin, at least in part
because many cases of Legionella are likely undiagnosed and successfully treated
with outpatient community–acquired pneumonia therapy, although the ideal treatment
would be longer than what is currently recommended for undifferentiated CAP. Fluo-
roquinolones and doxycycline are also effective therapies. Treatment of atypical pneu-
monia should not be withheld in the setting of risk factors for torsades de Pointes such
as prolonged heart rate–corrected QT interval. Doxycycline provides adequate
coverage without the same risk as macrolides and fluoroquinolones.32 Additional an-
tibiotics with activity, although rarely used, include clarithromycin and quinupristin/
dalfopristin.33 Although the literature has suggested a potential fluoroquinolone
benefit over other treatments,34 a recent large systematic review showed no differ-
ence between fluoroquinolone or macrolide treatment.35
Mycoplasma pneumonia is a contagious, endemic, and epidemic upper and lower
respiratory infection. M pneumoniae has been incriminated in outbreaks in congregate
settings and in health care workers.36 This organism is not identified on routine sputum
culture, and will be missed if not specifically looked for, but is estimated to cause 20%
to 40% of epidemic bacterial pneumonias. Infections are commonly relatively mild and
self-limited, but Mycoplasma can present as potentially severe and sometimes deadly
pneumonia. Identifying this organism in real time requires molecular testing or special-
ized culture media and incubation times; in addition, specialized culture and serology
can be used to confirm the diagnosis, although answers will often not arrive in time to
assist in clinical decision-making. M pneumoniae is not susceptible to even broad-
spectrum antibiotics typically prescribed for typical bacterial infections, and unless
atypical organisms are specifically targeted with the use of macrolides, fluoroquino-
lones, or tetracyclines, the patient may fail to improve. Without appropriate diagnostic
testing, Mycoplasma-caused pneumonia may be missed altogether. In keeping with
trends in antimicrobial overuse and resistance, macrolide-resistant M pneumoniae
has been increasingly reported in some areas.37

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832 Decker et al

Viral Pathogens
Before the SARS-CoV-2 pandemic, improved detection using multiplex PCR assays
suggested that up to 50% of lower respiratory tract infection requiring ICU care may
have a viral cause.38 During outbreaks such as the SARS-CoV-2 pandemic, or influ-
enza season, specific testing of respiratory or nasopharyngeal specimens for a sus-
pected virus is the most judicious use of testing resources. Clinicians practicing
during the COVID-19 pandemic are unlikely to neglect viral causes of severe pneu-
monia. Before COVID-19, MERS-CoV and SARS-CoV-1 were causes of severe viral
pneumonia associated with more limited spread of novel coronaviruses. In addition
to SARS-CoV-2, influenza is a frequent cause of severe pneumonia occurring
seasonally in the winter months with a higher mortality in the extremes of age, those
with comorbid health conditions, and those who are pregnant. Influenza vaccination
attenuates risk, and a history of vaccine avoidance should increase the pretest sus-
picion of this vaccine-preventable illness.38 Pandemic, novel, or sometimes called
Avian influenzas are a significant concern and may be responsible for a future
pandemic.39 Outside of pandemic spread, less efficient zoonotic transmission may
occur in persons who have risk factors such as those involved in farming or hunt-
ing.40 These novel influenza strains may be detected by PCR and multiplex PCR
testing platforms but may be reported as “Influenza A, untypable.” Awareness of
the PCR platform being used and its limitations are critical to understanding the po-
tential implications of untyped influenzas (if you are accustomed to receiving a type).
If novel influenza is suspected, airborne isolation rather than droplet isolation should
be initiated,18 and further consultation with the state or local health department or, in
some instances, with the CDC may be necessary to obtain further identification. The
rapid identification of influenza and administration of antiviral neuraminidase inhibi-
tor treatment (within 48 hours of symptom onset) have been shown to improve
outcome.41 RSV, Rhinovirus, human metapneumovirus, and parainfluenza virus
are potential causes of severe pneumonia (often in immunologically compromised
patients) that may be detected by multiplex studies. If these organisms are found,
the most helpful intervention may be to discontinue broad spectrum antibiotic ther-
apy in order to reduce the risk of adverse events.25 Adenovirus is another viral cause
of severe respiratory illness that has been implicated in health care outbreaks of se-
vere pneumonia.42 Enterovirus D68 is an epidemic cause of severe pneumonias and
was associated with a 2014 outbreak of severe pneumonia with associated rare
neurologic complications.43 Mimivirus has been isolated from hospitalized patients
with severe and ventilator-associated pneumonias.44 This fascinating, giant virus
is known to inhabit contaminated potable water from which, similar to Legionella,
it infects waterborne environmental acanthamoeba.45 Commercial testing and treat-
ments are not available for Mimivirus. Other pathogens the authors are currently un-
able to detect can cause clinically significant infections and seems highly likely, so
further study is warranted.
Fungal pneumonias are most commonly seen in patients with significant immuno-
suppression, but ICU stay and the relative immunosuppression of critical illness as
well as iatrogenic immunosuppression with steroids given in this context can increase
the risk of fungal infection. Mold infections are a dangerous complication of severe
COVID-19 infection,46 and a similarly increased risk was seen with H1N1 infections.47
Before the COVID-19 pandemic invasive Aspergillus infection complicated the
courses of 0.3% to 5% of ICU patients and 12% of ventilator-associated pneumo-
nias.48 Increased suspicion and targeted testing for mold infection is warranted in
cases of severe viral pneumonia, corticosteroid treatment, and decompensated

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 Management of Unique Pneumonias Seen in the ICU 833

cirrhosis.49 Treatment with azole antifungal agents such as voriconazole or isavucona-

zole is the mainstay of Aspergillus treatment. Liposomal amphotericin may be neces-
sary in settings of endemic mycosis and resistant molds.46

EMPIRICAL TREATMENT

Critically ill patients manifesting evidence of a new infectious process require empirical
antibiotic therapy, targeted to the most likely cause of their infections. The frequency
of different pathogens may vary from institution, by region and seasonally. Consid-
ering such local insights when selecting empirical therapy is critical to success. The
most common pathogens isolated from nosocomial pneumonia in the ICU are
gram-negative aerobes (64%), and the most commonly reported pathogens were
Staphylococcus aureus and Pseudomonas aeruginosa.21,50 Current guidelines would
suggest treatment with a b-lactam antibiotic plus a macrolide (or fluoroquinolone) if the
patient has risk factors for pseudomonas and/or plus vancomycin if the patient has
risk factors for methicillin-resistant Staphylococcus aureus (MRSA) for severe CAP.
Risk factors associated with MRSA or Pseudomonas infection in this setting include
prior isolation of MRSA or Pseudomonas or hospitalization in the last 60 days that
included parenteral antibiotic treatment.5 Pseudomonas infection is seen more likely
in patients who are ventilated.21 In patients for whom the QT elongation risk makes
prescription of macrolides or fluoroquinolones risky, treatment of atypical organisms
can be accomplished with doxycycline instead.32 Empirical treatment of HAP or
VAP should include broad spectrum anti-MRSA (if >10%–20% of unit isolates are
methicillin-resistant) and antipseudomonal coverage. For VAP, a second gram-
negative agent such as a fluoroquinolone or aminoglycoside may be indicated
depending on the patient’s risk factors for drug resistance or if the resistance level
is greater than 10% to the first agent in the local flora (as represented in the hospital
antibiogram).19 In addition to tailoring your empirical regimen to the local antibiogram,
additional consideration of local factors associated with unique pneumonias should
be made, most specifically for Legionella.32 Being aware of any local outbreaks and
including empirical coverage targeting hospital-specific pathogens, especially in the
setting of an outbreak or endemic resistant pathogen, is a critical success factor.9
Empirical treatment provided should be promptly narrowed when culture data support
such narrowing (eg, stopping vancomycin if gram-negative organisms are isolated or if
MRSA swabs are negative),51 discontinuing double-coverage when, or narrowing
broad-spectrum coverage as soon as, an organism is identified to be susceptible to
a narrow spectrum agent.

SUMMARY

ICU patients are frequently infected on presentation and are vulnerable to hospital
acquisition of infections. Regions, hospitals, and individual hospital floors may have
a unique and clinically significant microbiota. Awareness of the local hospital antibio-
gram and situational awareness of epidemic or endemic pathogens should guide
testing and empirical therapy. Empirical therapy should be converted to targeted ther-
apy as soon as possible to limit potentially harmful exposure to overly broad spectrum
antimicrobials. Infection prevention surveillance definitions are designed to be stan-
dardized and sensitive, although they may not perfectly overlap with clinical disease.
Robust, prospective surveillance detects signals early and may lead to identification of
reservoirs of resistant or waterborne pathogens that can be remediated to prevent
future infections.

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834 Decker et al

CLINICS CARE POINTS

 Treatment with atypical pneumonia is important, especially when cultures are unrevealing in
a clinical situation consistent with pneumonia.
 Doxycycline provides adequate coverage for atypical pneumonia, and does not exacerbate
prolonged QTc.
 Once an organism is identified, antibiotic therapy should be rapidly targeted to the
narrowest effected spectrum to reduce the risk of antibiotic-associated adverse events,
including the selection of resistant organisms.

DISCLOSURE

Ms L.A. Forrester, Dr B. Decker, and Dr D.K. Henderson have no commercial or finan-

cial conflicts of interest, and this article was not supported by any funding source.

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