Federal Register, Volume 59 Issue 22 (Wednesday, February 2, 1994)

[Federal Register Volume 59, Number 22 (Wednesday, February 2, 1994)]
[Unknown Section]
[Page 0]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 94-2178]

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[Federal Register: February 2, 1994]

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Part II

Department of Health and Human Services

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Centers for Disease Control and Prevention

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Draft Guideline for Prevention of Nosocomial Pneumonia; Notice of
Comment Period
DEPARTMENT OF HEALTH AND HUMAN SERVICES

Centers for Disease Control and Prevention

Draft Guideline for Prevention of Nosocomial Pneumonia: Part 1.
``Issues on Prevention of Nosocomial Pneumonia--1994'' and Part 2.
``Recommendations for Prevention of Nosocomial Pneumonia''; Notice of
Comment Period

AGENCY: Centers for Disease Control and Prevention (CDC), Public Health
Service (PHS), Department of Health and Human Services (DHHS).

ACTION: Notice.

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SUMMARY: This notice is a request for review and comment of the draft
Guideline for Prevention of Nosocomial Pneumonia. The Guideline
consists of two parts entitled ``Issues on Prevention of Nosocomial
Pneumonia--1994,'' and ``Recommendations for Prevention of Nosocomial
Pneumonia,'' prepared by the Hospital Infection Control Practices
Advisory Committee (HICPAC) and the National Center for Infectious
Diseases (NCID), CDC.

DATES: Written comments on the draft document must be received on or
before April 4, 1994.

ADDRESSES: Comments on this document should be submitted in writing to
the CDC, Attention: Pneumonia Guideline Information Center, Mailstop
A07, 1600 Clifton Road, NE., Atlanta, Georgia 30333. To order copies of
the Federal Register containing the document, contact the U.S.
Government Printing Office, Order and Information Desk, Washington, DC
20402-9329, at (202) 783-3238. Specify the date of the issue requested
and stock number 069-001-000-70-0. See page II of the Federal Register
for additional ordering and cost information. In addition, the Federal
Register may be viewed and photocopied at most libraries designated as
U.S. Government Depository Libraries and at many other public and
academic libraries that receive the Federal Register throughout the
country. The order-desk operator can tell you the location of the U.S.
Government Depository Library nearest you.

FOR FURTHER INFORMATION CONTACT: The Pneumonia Guideline Information
Center, (404) 332-2569.

SUPPLEMENTARY INFORMATION: This document updates and replaces the
previously published CDC Guideline for the Prevention of Nosocomial
Pneumonia. Emphasis is placed on bacterial pneumonias, including gram-
negative bacillary pneumonias and Legionnaires' disease; pneumonia due
to Aspergillus spp.; and lower respiratory tract infections caused by
respiratory syncytial and influenza viruses. Part I, ``Issues on
Prevention of Nosocomial Pneumonia--1994,'' was prepared by staff of
NCID, CDC, and provides the background for the HICPAC-consensus
recommendations contained in Part II, ``Recommendations for Prevention
of Nosocomial Pneumonia.''
HICPAC was established in 1991 to provide advice and guidance to
the Secretary, DHHS; the Assistant Secretary for Health; the Director,
CDC; and the Director, NCID, regarding the practice of hospital
infection control and strategies for surveillance, prevention, and
control of nosocomial infections in U.S. hospitals. The committee also
advises the CDC on periodic updating of guidelines and other policy
statements regarding prevention of nosocomial infections.
The Guideline for Prevention of Nosocomial Pneumonia is the first
of a series of CDC guidelines being revised by HICPAC and NCID, CDC.

Dated: January 25, 1994.
Walter R. Dowdle,
Deputy Director, Centers for Disease Control and Prevention (CDC).

GUIDELINE FOR PREVENTION OF NOSOCOMIAL PNEUMONIA

Second Edition

Table of Contents

Executive Summary

Introduction

Part I. Issues on Prevention of Nosocomial Pneumonia--1994

Bacterial Pneumonia

I. Etiologic Agents
II. Diagnosis
III. Epidemiology
IV. Pathogenesis
V. Risk Factors and Control Measures
A. Oropharyngeal, Tracheal, and Gastric Colonization
B. Aspiration of Oropharyngeal and Gastric Flora
C. Mechanically Assisted Ventilation
D. Cross-Colonization Via Hands of Personnel
E. Contamination of Devices Used on the Respiratory Tract
1. Mechanical Ventilators and Anesthesia Machines
2. Humidifiers, Breathing Circuits, and Heat-Moisture Exchangers
3. Large-Volume Nebulizers
4. Small-Volume Medication Nebulizers
5. Suction Catheters, Resuscitation Bags, Oxygen Analyzers, and
Ventilator Spirometers
F. Thoraco-Abdominal Surgical Procedures
G. Other Prophylactic Measures
1. Vaccination of Patients
2. Prophylaxis With Systemic Antimicrobial Agents
3. Kinetic Therapy for the Immobilized State

Legionnaires' Disease

I. Epidemiology
II. Diagnosis
III. Modes of Transmission
IV. Definition of Nosocomial Legionnaires' Disease
V. Prevention and Control Measures
A. Prevention of Legionnaires' Disease in Hospitals With No
Identified Cases (Primary Prevention)
B. Prevention of Legionnaires' Disease in Hospitals With
Identified Cases (Secondary Prevention)

Aspergillosis

I. Epidemiology
II. Pathogenesis
III. Diagnosis
IV. Risk Factors and Control Measures

Viral Pneumonias

RSV Infection

I. Epidemiology
II. Diagnosis
III. Modes of Transmission
IV. Control Measures

Influenza

I. Epidemiology
II. Diagnosis
III. Prevention and Control Measures

Part II. Recommendations for Prevention of Nosocomial Pneumonia

Introduction

Prevention and Control of Bacterial Pneumonia

I. Staff Education and Infection Surveillance
A. Staff Education
B. Surveillance
II. Interruption of Transmission of Microorganisms
A. Sterilization or Disinfection, and Maintenance of Equipment
and Devices
1. General Measures
2. Mechanical Ventilators, Anesthesia Machines and Circle
Systems, and Pulmonary-Function Testing Equipment
3. Ventilator Circuits With Humidifiers
4. Ventilator Circuits With Hygroscopic Condenser-Humidifiers or
Heat-Moisture Exchangers
5. Wall Humidifiers
6. Small-Volume Medication Nebulizers: ``In-Line'' and Hand-Held
Nebulizers
7. Large-volume nebulizers and mist tents
8. Other Devices
B. Interruption of Person-to-Person Transmission of Bacteria
1. Handwashing
2. Barrier Precautions
3. Care of Patients with Tracheostomy
4. Suctioning of Respiratory Tract Secretions
III. Modifying Host Risk for Infection
A. Precautions for Prevention of Endogenous Pneumonia
1. Prevention of Aspiration
2. Prevention of Gastric Colonization
B. Prevention of Postoperative Pneumonia
C. Other Prophylactic Procedures for Pneumonia
1. Vaccination of Patients
2. Systemic Antimicrobial Prophylaxis
3. Use of Rotating ``Kinetic'' Beds

Prevention and Control of Legionnaires' Disease

I. Staff Education and Infection Surveillance
A. Staff Education
B. Surveillance
II. Interruption of Transmission of Legionella spp.
A. Primary Prevention (Preventing Nosocomial Legionnaires'
Disease when No Cases have been Documented)
1. Nebulization and Other Devices
2. Cooling Towers
3. Water-Distribution System
B. Secondary Prevention (Response to Identification of
Laboratory-Confirmed Nosocomial Legionellosis)

Prevention and Control of Nosocomial Pulmonary Aspergillosis

I. Staff Education and Infection Surveillance
A. Staff Education
B. Surveillance
II. Interruption of Transmission of Aspergillus spp. Spores
A. Planning New Specialized-Care Units for High-Risk Patients
B. In Existing Facilities with no Cases of Nosocomial
Aspergillosis
C. When a Case of Nosocomial Aspergillosis Occurs
III. Modifying Host Risk for Infection

Prevention and Control of Respiratory Syncytial Virus (RSV)

I. Staff Education and Infection Surveillance
A. Staff Education
B. Surveillance
II. Interruption of Transmission of RSV
A. Prevention of Person-to-Person Transmission
1. Primary Measures for Contact Isolation
a. Handwashing
b. Gloving
c. Gowning
d. Staffing
e. Limiting Visitors
2. Control of RSV Outbreaks
a. Use of Private Room, Cohorting, and Patient-Screening
b. Personnel Cohorting
c. Postponing Patient Admission
d. Wearing Eye-Nose Goggles

Prevention and Control of Influenza

I. Staff Education and Infection Surveillance
A. Staff Education
B. Surveillance
II. Modifying Host Risk for Infection
A. Vaccination
1. Patients
2. Personnel
B. Use of Antiviral Agents
III. Interruption of (Person-to-Person) Transmission
IV. Control of Influenza Outbreaks
A. Determining the Outbreak Strain
B. Vaccination of Patients and Personnel
C. Amantadine or Rimantadine Administration
D. Interruption of (Person-to-Person) Transmission

Table 1. Microorganisms Isolated from Respiratory Tract Specimens
Obtained by Various Representative Methods from Adult Patients with
a Diagnosis of Nosocomial Pneumonia
Table 2. Controlled Studies on Nosocomial Lower Respiratory Tract
Infections and Other Associated Outcomes of Selective
Decontamination of the Digestive Tract in Adult Patients with
Mechanically Assisted Ventilation
Table 3. Risk Factors and Suggested Infection Control Measures for
Prevention of Nosocomial Pneumonia

Figure 1. Pathogenesis of Nosocomial Bacterial Pneumonia

Appendix A. Semicritical Items Used on the Respiratory Tract
Appendix B. Maintenance Procedures to Decrease Survival and
Multiplication of Legionella spp. in Potable-Water Distribution
Systems
Appendix C. Culturing Environmental Specimens for Legionella spp.
Appendix D. Procedure for Cleaning Cooling Towers and Related
Equipment to Prevent Legionellosis

References

Executive Summary

This document updates and replaces the previously published CDC
Guideline for Prevention of Nosocomial Pneumonia (Infection Control
1982;3:327-33, Resp Care 1983;28:221-32, and Am J Infect Control
1983;11230-9). The revised guideline is designed to reduce the
incidence of nosocomial pneumonia and provides the rationale (in Part
I) for the recommendations (in Part II) considered prudent by consensus
of the members of HICPAC. A working draft of the guideline has been
reviewed by experts in infection control, pulmonology, respiratory
therapy, anesthesiology, internal medicine, and pediatrics. However,
all recommendations in the guideline may not reflect the opinions of
all reviewers.
Pneumonia is the second most common nosocomial infection in the
United States and is associated with substantial morbidity and
mortality. Most patients with nosocomial pneumonia are those with
extremes of age, severe underlying disease, immunosuppression,
depressed sensorium, cardiopulmonary disease, and thoraco-abdominal
surgery. Although patients with mechanically assisted ventilation do
not comprise a major proportion of patients with nosocomial pneumonia,
they have the highest risk of developing the infection.
Most bacterial nosocomial pneumonias occur by aspiration of
bacteria colonizing the oropharynx or upper gastrointestinal tract of
the patient. Intubation and mechanical ventilation greatly increase the
risk of nosocomial bacterial pneumonia because they alter first-line
patient defenses. Pneumonias due to Legionella spp., Aspergillus spp.,
and influenza virus are often caused by inhalation of contaminated
aerosols. Respiratory syncytial virus (RSV) infection usually follows
viral inoculation of the conjunctivae or nasal mucosa by contaminated
hands.
Traditional preventive measures for nosocomial pneumonia include
decreasing aspiration by the patient, preventing cross-contamination or
colonization via hands of personnel, appropriate disinfection or
sterilization of respiratory-therapy devices, use of available vaccines
to protect against particular infections, and education of hospital
staff and patients. New measures under investigation involve reducing
oropharyngeal and gastric colonization by pathogenic microorganisms.

Introduction

The Guideline for Prevention of Nosocomial Pneumonia is intended
for use by personnel who are responsible for surveillance and control
of infections in acute-care hospitals. The guideline may not be
applicable in long-term care facilities because of the unique
characteristics of these settings.
The revised guideline addresses common problems encountered by
infection-control practitioners regarding the prevention and control of
nosocomial pneumonia in U.S. hospitals. Sections on the prevention of
bacterial pneumonia in mechanically ventilated and/or critically ill
patients, care of respiratory-therapy devices, prevention of cross-
contamination, and prevention of viral lower respiratory-tract
infections, such as respiratory syncytial virus (RSV) and influenza
infections, have been expanded and updated. New sections on
Legionnaires' disease and pneumonia due to Aspergillus spp. have been
added. Lower respiratory tract infection due to Mycobacterium
tuberculosis is not addressed in this document; it is covered in
separate guidelines.\1\*
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*Footnotes to appear at end of docket.
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Part I, Issues for Prevention of Nosocomial Pneumonia--1994, can be
an important resource for educating healthcare workers regarding
prevention and control of nosocomial respiratory tract infections.
Because education of healthcare workers is the cornerstone of an
effective infection control program, hospitals should give high
priority to continuing infection control educational programs for these
staff members.

PART I. ISSUES ON PREVENTION OF NOSOCOMIAL PNEUMONIA--1994

BACTERIAL PNEUMONIA

I. Etiologic Agents

The reported distribution of etiologic agents causing nosocomial
pneumonia varies between hospitals because of differences in patient
populations and diagnostic methods employed.^{2-11 In general,
however, bacteria have been the most frequently isolated
pathogens.^{2-7,10,12-14 Schaberg et al. reported that in 1986-1989,
aerobic bacteria comprised at least 73%, and fungi 4%, of isolates from
sputum and tracheal aspirates of cases at the University of Michigan
Hospitals and hospitals participating in the National Nosocomial
Infection Surveillance (NNIS); very few anaerobic bacteria and no
viruses were reported, probably because anaerobic and viral cultures
were not performed routinely in the reporting hospitals (Table
1).^{4 Similarly, cultures of bronchoscopic specimens from
mechanically ventilated patients with pneumonia have rarely yielded
anaerobes.^{6-8,10,12,15,16 Only the report by Bartlett, which was
based mainly on cultures of transtracheal aspirates in patients not
receiving mechanically assisted ventilation, showed a predominance of
anaerobes.^{5
Nosocomial bacterial pneumonias are frequently
polymicrobial,^{5,8,10,12,13,16-20 and gram-negative bacilli are the
usual predominant organisms (Table 1);^{2-7,10,12-14 however,
Staphylococcus aureus (especially methicillin-resistant S.
aureus)^{6,8,11,16,21 and other gram-positive cocci, including
Streptococcus pneumoniae,^{6,8 have recently emerged as significant
isolates;^{15 and Haemophilus influenza has been isolated from
mechanically ventilated patients with pneumonia that occurs within 48-
96 hours after intubation.^{4-6,13,16,22 In NNIS hospitals,
Pseudomonas aeruginosa, Enterobacter sp., Klebsiella pneumoniae,
Escherichia coli, Serratia marcescens, and Proteus spp. comprised 50%
of the isolates from cultures of respiratory tract specimens of
patients for whom nosocomial pneumonia was diagnosed by using clinical
criteria; S. aureus accounted for 16%, and H. influenzae, for 6% (Table
1).^{4 Fagon and co-workers reported that gram-negative bacilli were
present in 75% of quantitative cultures of protected-specimen brushings
(PSB) from patients who had received mechanically assisted ventilation
and acquired nosocomial pneumonia; 40% were polymicrobial.^{6 In the
report by Torres et al., 20% of pathogens recovered from cultures of
PSB, blood, pleural fluid, or percutaneous lung aspirate were gram-
negative bacilli in pure culture, and 17% were polymicrobial; however,
54% of specimens did not yield any microorganism, probably because of
receipt of antibiotics by patients.^{7

II. Diagnosis

The diagnosis of nosocomial bacterial pneumonia has been
difficult.^{8,9,17,23-32 Frequently, the criteria for diagnosis have
been fever, cough, and development of purulent sputum, in combination
with radiologic evidence of a new or progressive pulmonary infiltrate,
a suggestive Gram's stain, and cultures of sputum, tracheal aspirate,
pleural fluid, or blood.^{4,5,23,25,33-36 Although clinical criteria
together with cultures of sputum or tracheal specimens may be sensitive
for bacterial pathogens, they are highly nonspecific, especially in
patients with mechanically assisted ventilation;^{9,10,13-16,19,24-
26,29,31,37-42 on the other hand, cultures of blood or pleural fluid
have very low sensitivity.^{9,19,20,43
Because of these problems, a group of investigators recently
formulated consensus recommendations for standardization of methods to
diagnose pneumonia in clinical research studies of ventilator-
associated pneumonia.^{44-46 These methods involve bronchoscopic
techniques, e.g., quantitative culture of PSB,^{6,8-
10,14,16,27,31,38,41,47,48 BAL,^{8,13,41,47,49-54 and pBAL.^{15
The reported sensitivities and specificities of these methods have
ranged between 70% to 100% and 60% to 100%, respectively, depending on
the tests or diagnostic criteria they were compared with. Because these
techniques are invasive, they may cause complications such as
hypoxemia, bleeding, or arrhythmia.^{9,14,42,44,52,55,56 In
addition, the sensitivity of the PSB procedure may decrease in patients
receiving antibiotic therapy.^{10,14,27 Nonbronchoscopic (NB)
procedures, e.g., NB-pBAL^{13,27,57,58 or NB-PSB,^{14 which
utilize blind catheterization of the distal airways, have been
developed recently; however, they have not been extensively evaluated.
Although the use of bronchoscopic and nonbronchoscopic diagnostic tests
can be a major step in better defining the epidemiology of nosocomial
pneumonia especially in mechanically ventilated patients, further
studies are needed to determine their applicability in daily clinical
practice.

III. Epidemiology

NNIS reports that pneumonias (diagnosed on the basis of the CDC
surveillance definition of nosocomial pneumonia) and surgical-wound
infections account for approximately 15% each of all hospital-
associated infections and are the second most common nosocomial
infections after that of the urinary tract.^{3 In 1984, the overall
incidence of lower respiratory tract infection was 6 per 1,000
discharged patients.^{3 The incidence ranged from 4.2 to 7.7 per
1,000 discharged patients for nonteaching and university-affiliated
hospitals, respectively, probably reflecting institutional differences
in the level of patients' risk for acquiring nosocomial pneumonia.
Nosocomial bacterial pneumonia often has been identified as a
postoperative infection.^{59,60 In the Study of the Efficacy of
Nosocomial Infection Control in the 1970s, 75% of reported cases of
nosocomial bacterial pneumonia occurred in patients who had had a
surgical operation; the risk was 38 times greater for thoracoabdominal
procedures than for those involving other body sites.^{60 More
recent epidemiologic studies, including NNIS studies, have identified
other subsets of patients at high risk of developing nosocomial
bacterial pneumonia: Patients with endotracheal intubation and/or
mechanically assisted ventilation, depressed level of consciousness
(particularly those with closed-head injury), prior episode of a large-
volume aspiration, or underlying chronic lung disease, and patients >70
years of age. Other risk factors include 24-hour ventilator-circuit
changes, fall-winter season, stress-bleeding prophylaxis with
cimetidine with or without antacid, presence of a nasogastric tube,
severe trauma, and recent bronchoscopy.^{7,34,35,61-69
Recently, NNIS stratified the incidence density of nosocomial
pneumonia by patients' use of mechanical ventilator and type of
intensive care unit (ICU). From 1986 to 1990, the median rate of
ventilator-associated pneumonia per 1,000 ventilator-days ranged from
4.7 in pediatric ICUs to 34.4 in burn ICUs.^{63 In contrast, the
median rate of nonventilator-associated pneumonia per 1000 ICU-days
ranged from 0 in pediatric and respiratory ICUs to 3.2 in trauma ICUs.
Nosocomial pneumonia has been associated with high fatality rates.
Crude mortality rates of 20%-50% and attributable mortality rates of
30%-33% have been reported; in one study, pneumonia comprised 60% of
all deaths due to nosocomial infections.^{18,35,70-75 Patients
receiving mechanically assisted ventilation have higher mortality rates
than patients not receiving ventilation support; however, other
factors, such as a patient's underlying disease(s) and organ failure,
are stronger predictors of death in patients with pneumonia.^{34
Pneumonia-associated morbidity has not been evaluated in recent
years. Past studies, however, have shown that pneumonia could prolong
hospitalization by 4-9 days.^{74-77 A conservative estimate of the
direct cost of excess hospital stay due to pneumonia is $1.1 billion a
year for the nation.^{78 Because of its reported frequency,
associated high fatality rate, and attendant costs, nosocomial
pneumonia is a major infection control problem.

IV. Pathogenesis

Bacteria may invade the lower respiratory tract by aspiration of
oropharyngeal organisms, inhalation of aerosols containing bacteria, or
less frequently, by hematogenous spread from a distant body site
(Figure 1). In addition, bacterial translocation from the
gastrointestinal tract has been recently hypothesized as a mechanism
for infection. Of these routes, aspiration is believed to be the most
important for both nosocomial and community-acquired pneumonia.
In radioisotope-tracer studies of healthy adults, 45% were found to
aspirate during sleep.^{79 Persons with abnormal swallowing, such as
those who have depressed consciousness, respiratory tract
instrumentation and/or mechanically assisted ventilation,
gastrointestinal tract instrumentation or diseases, or have just
undergone surgery, are particularly likely to
aspirate.^{7,34,35,60,80
The high incidence of gram-negative bacillary pneumonia in
hospitalized patients appears to be the result of factors that promote
colonization of the pharynx by gram-negative bacilli and the subsequent
entry of these organisms into the lower respiratory tract.^{33,81-84
Whereas aerobic gram-negative bacilli are recovered infrequently or are
found in small numbers in pharyngeal cultures of healthy
persons,^{81,85 colonization dramatically increases in patients with
coma, hypotension, acidosis, azotemia, alcoholism, diabetes mellitus,
leukocytosis, leukopenia, pulmonary disease, nasogastric or
endotracheal tubes in place, and in patients given antimicrobial
agents.^{33,84,86,87
Oropharyngeal or tracheobronchial colonization by gram-negative
bacilli begins with the adherence of the microorganisms to the host's
epithelial cells.^{83,88-90 Adherence may be affected by multiple
factors related to the bacteria (presence of pili, cilia, capsule, or
production of elastase or mucinase), host cell (surface proteins and
polysaccharides), and environment (pH and presence of mucin in
respiratory secretions).^{82,83,88,91-100 The exact interactions
among these factors have not been fully elucidated, but studies
indicate that certain substances, such as fibronectin, can inhibit the
adherence of gram-negative bacilli to host cells.^{91,93,101
Conversely, certain conditions, such as malnutrition, severe illness,
or post-operative state, can increase adherence of gram-negative
bacteria.^{82,91,95,100,102
Besides the oropharynx, the stomach has been postulated to be an
important reservoir of organisms that cause nosocomial
pneumonia.^{34,103-107 The stomach's role may vary depending on the
patient's underlying conditions and on prophylactic or therapeutic
interventions.^{22,104,108-111 In healthy persons, few bacteria
entering the stomach survive in the presence of hydrochloric acid at
pH<2.^{112,113 However, when gastric pH increases from the normal
levels to >4, microorganisms are able to multiply to high
concentrations in the stomach.^{110,112,114-116 This can occur in
patients with advanced age,^{114 achlorhydria,^{112 ileus, or
upper gastrointestinal disease, and in patients receiving enteral
feeding, antacids, or histamine-2 [H-2]
antagonists.^{104,110,111,116-118 The contribution of other factors,
such as duodeno-gastric reflux and the presence of bile, to gastric
colonization in patients with impaired intestinal motility has been
suggested and needs further investigation.^{109
Bacteria can also gain entry into the lower respiratory tract of
hospitalized patients through inhalation of aerosols generated
primarily by contaminated respiratory-therapy or anesthesia-breathing
equipment.^{119-122 Outbreaks related to the use of respiratory-
therapy equipment have been associated with contaminated nebulizers,
which are humidification devices that produce large amounts of aerosol
droplets <4m via ultrasound, spinning disk, or the Venturi
mechanism.^{119,122,123 When the fluid in the reservoir of a
nebulizer becomes contaminated with bacteria, the aerosol produced may
contain high concentrations of bacteria that can be deposited deep in
the patient's lower respiratory tract.^{119,123,124 Because
endotracheal and tracheal tubes provide direct access to the lower
respiratory tract, contaminated aerosol inhalation is particularly
hazardous for intubated patients. In contrast to nebulizers, bubble-
through or wick humidifiers mainly increase the water-vapor (or
molecular-water) content of inspired gases. Although heated bubble-
through humidifiers generate aerosol droplets, they do so in quantities
that may not be clinically significant;^{120,125 wick humidifiers do
not generate aerosols.
Rarely, bacterial pneumonia can result from hematogenous spread of
infection to the lung from another infection site, e.g., pneumonia
resulting from purulent phlebitis or right-sided endocarditis. Another
mechanism, translocation of bacteria via the passage of viable bacteria
from the lumen of the gastrointestinal tract through epithelial mucosa
to the mesenteric lymph nodes and to the lung has been shown in animal
models.^{126 Translocation is postulated to occur in patients with
immunosuppression, cancer or burns;^{126 however data are lacking
regarding this mechanism in humans.^{127

V. Risk Factors and Control Measures

Several large studies have examined potential risk factors for
nosocomial bacterial pneumonia (Table
3).^{7,\\^{34,\\^{35,\\^{128,\\^{129 Although specific
risk factors may differ between study populations, they can be grouped
into the following general categories: (1) Host factors such as
extremes of age and severe underlying conditions, including
immunosuppression; (2) factors, such as admission to the ICU,
underlying chronic lung disease, or coma, that enhance colonization of
the oropharynx and/or stomach by microorganisms; (3) conditions
favoring aspiration or reflux, including endotracheal intubation or
insertion of nasogastric tube; (4) conditions requiring prolonged use
of mechanical ventilatory support with exposure to contaminated
respiratory equipment and/or contact with colonized hands of healthcare
workers; and (5) factors that impede adequate pulmonary toilet, such as
surgical procedures involving the head, neck, thorax, or upper abdomen,
and immobilization due to trauma or illness.^{7,\\^{33-
35,\\^{59,\\^{128

A. Oropharyngeal, Tracheal, and Gastric Colonization

The association between colonization of the
oropharynx,^{81,\\^{130 trachea,^{131 or
stomach^{103,\\^{104,\\^{110,\\^{116 and predisposition to
gram-negative bacillary pneumonia prompted attempts to prevent
infection either by prophylactic local application of antimicrobial
agent(s)^{132,\\^{133 or utilizing the phenomenon of local
bacterial interference.^{134,\\^{135 Although early work
suggested that the former method, aerosolized antimicrobials, could
eradicate common gram-negative pathogens from the upper respiratory
tract,^{131 superinfection occurred in some patients receiving this
therapy.^{132-134,\\^{136,\\^{137 The latter method, bacterial
interference (with alpha-hemolytic streptococci), has been successfully
used by some investigators to prevent oropharyngeal colonization by
aerobic gram-negative bacilli.^{134 However, the efficacy of this
method for use in general has not been evaluated.
The administration of antacids and H2-blockers for prevention of
stress bleeding in critically ill, postoperative, and/or mechanically
ventilated patients has been associated with gastric bacterial
overgrowth in many
studies.^{34,\\^{105,\\^{106,\\^{111,\\^{115,\\^{116,\
\^{138-140 Sucralfate, a cytoprotective agent that has little effect
on gastric pH and may have bactericidal properties of its own, has been
suggested as a potential substitute for antacids and H2-
blockers.^{141-143 The results of clinical trials comparing the risk
of pneumonia in patients receiving sucralfate to that in patients given
antacids and/or H2-blockers have been
variable.^{105,\\^{111,\\^{140,\\^{141,\\^{144,\\^{145
In most randomized trials, ICU patients receiving mechanically
assisted ventilation and antacids with or without H2-b lockers had
increased gastric pH, high bacterial counts in the gastric fluid, and
increased risk of pneumonia compared with patients given
sucralfate.^{105,\\^{111,\\^{140,\\^{141,\\^{144 In one
report with a large number of study patients, the incidence of early-
onset pneumonia (occurring 4 days after intubation) did not
differ between patient groups, but late-onset pneumonia occurred in 5%
of 76 patients who received sucralfate, 16% of 69 given antacids, and
21% of 68 who received an H2-blocker.^{140 On the other hand, a
meta-analysis of data from eight earlier studies did not show a strong
association between nosocomial pneumonia and drugs that raise gastric
pH.^{146 Further comparative studies are underway in which
bronchoscopy with PSB or BAL is utilized for the diagnosis of
pneumonia.
Selective decontamination of the digestive tract (SDD) is another
strategy designed to prevent bacterial colonization and lower
respiratory tract infection in mechanically ventilated
patients.^{147-170 SDD is aimed at preventing oropharyngeal and
gastric colonization with aerobic gram-negative bacilli and Candida
spp., without altering the anaerobic flora (Table 2).^{147-170 A
variety of SDD regimens use a combination of locally administered
nonabsorbable antibiotic agents such as polymyxin, an aminoglycoside
(tobramycin, gentamicin, or, rarely, neomycin), or a quinolone
(norfloxacin or ciprofloxacin), coupled with either amphotericin B or
nystatin. The local antimicrobial preparation is applied as a paste to
the oropharynx and given orally or via the nasogastric tube four times
a day. In addition, in many studies, a systemic (intravenous)
antimicrobial such as cefotaxime or trimethoprim is administered to the
patient.
While most clinical trials,^{147-151,\\^{153-
160,\\^{162,\\^{164,\\^{169 including two meta-
analyses,^{163,\\^{170 of SDD have demonstrated a decrease in the
rates of nosocomial respiratory infections, these trials have been
difficult to assess because they have differed in study design and
population, and many have had short follow-up periods (Table 2). In
most of these studies, the diagnosis of pneumonia was based on clinical
criteria; bronchoscopy with BAL or PSB was used in only a few
studies.^{152,\\^{153,\\^{164,\\^{167,\\^{169
Two recently published large double-blind, placebo-controlled
trials demonstrated no benefit from SDD.^{166,\\^{167 In one, a
large French multicenter study by Gastinne et al, a significant
decrease in incidence of gram-negative bacillary pneumonia was not
accompanied by a decrease in pneumonia from all causes.^{167 In the
other study, by Hammond et al, no differences were noted between
patients randomized to SDD or to placebo; however, both patient groups
received intravenous cefotaxime.^{166
Although an earlier meta-analysis suggested a trend toward
decreased mortality in patients given SDD,^{163 a more recent and
more extensive analysis highlights the equivocal effect of SDD on
patient mortality, as well as the high cost of using SDD to prevent
pneumonia or death (i.e., in order to prevent one case of nosocomial
pneumonia, or one death due to nosocomial pneumonia, 6 [range: 5-9] or
23 [range: 13-39] patients, respectively, would have to be given
SDD.^{170 Furthermore, there are concerns over the development of
antimicrobial resistance and superinfection with gram-positive bacteria
and other antibiotic-resistant nosocomial
pathogens.^{148,\\^{149,\\^{152,\\^{155 Thus, currently
available data do not justify the routine use of SDD for prevention of
nosocomial pneumonia in ICU patients. SDD may be ultimately useful for
specific subsets of ICU patients, such as those with trauma or severe
immunosuppression, e.g., bone-marrow transplant recipients.
A new approach advocated to prevent oropharyngeal colonization in
patients receiving enteral nutrition is to reduce bacterial
colonization of the stomach by acidifying the enteral feed.^{171
Although the absence of bacteria from the stomach has been confirmed in
patients given acidified enteral feeding, the effect on the incidence
of nosocomial pneumonia has not been evaluated.^{171

B. Aspiration of Oropharyngeal and Gastric Flora

Clinically significant aspiration usually occurs in patients who
have one or more of the following conditions: a depressed level of
consciousness, dysphagia due to neurologic or esophageal disorders, an
endotracheal (naso- or oro-tracheal) and nasogastric tube in place, and
receipt of enteral feeding.^{35,\\^{79,\\^{80,\\^{172-176
Placement of nasogastric tube may increase nasopharyngeal colonization,
cause reflux of gastric contents, or allow bacterial migration via the
tube from the stomach to the upper airway.^{173,\\^{176-178 When
enteral feedings are administered, gross contamination of the enteral
solution during preparation^{179-181 and elevated gastric
pH^{67,\\^{182,\\^{183 may lead to gastric colonization with
gram-negative bacilli. In addition, gastric reflux and aspiration may
occur because of increased intragastric volume and
pressure.^{67,\\^{110,\\^{173
Prevention of pneumonia in such patients may be difficult, but
methods that make regurgitation less likely, for example, placing the
patient in a semirecumbent position by elevating the head of the
bed,^{175,\\^{184,\\^{185 administering enteral nutrition
intermittently in small boluses rather than
continuously,^{67,\\^{183 using flexible, small-bore enteral
tubes,^{176,\\^{186 and witholding enteral feeding when the
residual volume in the stomach is large or if bowel sounds are not
heard upon auscultation of the abdomen, may be
beneficial.^{175,\\^{187,\\^{188 On the other hand, placing
the enteral tube below the stomach (e.g. in the jejunum) has yielded
equivocal results.^{189,\\^{190

C. Mechanically Assisted Ventilation and Endotracheal Intubation

Patients receiving continuous, mechanically assisted ventilation
have 6-21 times the risk of developing nosocomial pneumonia compared
with patients not receiving ventilatory
support.^{34,\\^{60,\\^{62,\\^{70 Data from the study by
Fagon and co-workers indicate that the risk of developing ventilator-
associated pneumonia increases by 1% per day.^{6 This increased risk
is partly due to carriage of oropharyngeal organisms upon passage of
the endotracheal tube into the trachea during intubation, as well as to
depressed host defenses secondary to the patient's severe underlying
illness.^{7,\\^{34,\\^{35,\\^{191 In addition, bacteria can
aggregate on the surface of the tube over time and form a glycocalyx
(biofilm) that protects the bacteria from action of antimicrobial
agents or host defenses.^{192 Some investigators believe that these
bacterial aggregates may become dislodged by ventilation flow, tube
manipulation, or suctioning, and subsequently embolize into the lower
respiratory tract and cause focal pneumonia.^{193,\\^{194
Removing tracheal secretions by gentle suctioning and using aseptic
technique to reduce cross-contamination from respiratory therapy
equipment or hands of personnel have been utilized traditionally to
help prevent pneumonia in patients receiving mechanically assisted
ventilation.
The risk of pneumonia is also increased by the direct access of
bacteria to the lower respiratory tract, often because of leakage
around the endotracheal cuff,^{195,\\^{196 which allows pooled
secretions above the cuff to enter the trachea.^{197 In one recent
study, the occurrence of nosocomial pneumonia was delayed and decreased
in intubated patients whose endotracheal tubes had a separate dorsal
lumen that allowed drainage (by suctioning) of secretions in the space
above endotracheal cuff and below the glottis.^{197 However, further
studies are needed to determine the cost-benefit ratio of using this
device.

D. Cross-Colonization Via Hands of Personnel

Pathogens causing nosocomial pneumonia, such as gram-negative
bacilli and Staphylococcus aureus, are ubiquitous in the hospital,
especially in intensive or critical care areas.^{198,\\^{199
Transmission of these microorganisms to patients frequently occurs via
healthcare workers' hands that become contaminated or transiently
colonized with the microorganisms.^{200-205 Procedures such as
tracheal suctioning and manipulation of ventilator circuit or
endotracheal tubes increase the opportunity for cross-contamination.
The risk of cross-contamination can be reduced by using aseptic
technique and sterile or disinfected equipment when appropriate^{62
and eliminating pathogens from the hands of
personnel.^{62,\\^{206-208
In theory, adequate handwashing is an effective way of removing
transient bacteria from the hands,^{207,\\^{208 but personnel
compliance with handwashing has been generally poor, despite the best
efforts at educating healthcare workers.^{209-212 For this reason,
the routine use of gloves has been advocated to help prevent cross-
contamination.^{213,\\^{214 Routine gloving (in addition to
gowning) was associated with a decrease in the incidence of nosocomial
respiratory-syncytial virus (RSV)^{215 and other ICU
infections.^{216 It should be emphasized, however, that nosocomial
pathogens can colonize gloves,^{217 and that outbreaks have been
traced to healthcare workers who did not change gloves after patient
contact.^{218

E. Contamination of Devices Used on the Respiratory Tract

Devices used on the respiratory tract for respiratory therapy
(e.g., nebulizer), diagnostic examination (e.g., bronchoscope or
spirometer), and administration of anesthesia are potential reservoirs
or vehicles for infectious microorganisms.^{62,\\^{219-221 Routes
of transmission may be from device to
patient,^{120,\\^{122,\\^{221-230 from one patient to another,
or from one body site to the lower respiratory tract of the same
patient via hand or device.^{220,\\^{231,\\^{232 Contaminated
nebulizer reservoirs can allow the growth of hydrophilic bacteria that
may be subsequently aerosolized during device
use.^{119,\\^{122,\\^{123,\\^{228 Gram-negative bacilli
such as Pseudomonas spp., Xanthomonas spp., Flavobacterium spp.,
Legionella spp., and nontuberculous mycobacteria can multiply to
substantial concentrations in nebulizer fluid^{227,\\^{233-235
and increase the patient's risk of acquiring pneumonia.^{120-
123,\\^{227,\\^{228,\\^{236,\\^{237
Proper cleaning and sterilization or disinfection of reusable
equipment are important components of a program to reduce infections
associated with respiratory therapy and anesthesia equipment.^{221-
226,238,239 Respiratory therapy devices have been classified as semi-
critical because they come into contact with mucous membranes but do
not ordinarily penetrate body surfaces, and the associated infection
risk following their use in patients is less than that associated with
devices that penetrate normally sterile tissues (See Appendix
A).^{240 There is no evidence that low-level contamination of
respiratory therapy device prior to use by a patient, as may occur
following high-level disinfection of the device, presents a greater
risk of respiratory infection than does sterile equipment. Thus, if
after they are thoroughly cleaned, these devices cannot be sterilized
by steam autoclave or ethylene oxide,^{241 they can be subjected to
high-level disinfection by pasteurization at 75 deg.C for 30
min,^{242-244 or by using liquid chemical disinfectants approved by
the Environmental Protection Agency (EPA) as sterilants/
disinfectants.^{214,245-247 When rinsing is needed after a
respiratory device has been sterilized or disinfected, only sterile
water is used because tap or locally-prepared distilled water may
harbor microorganisms that can cause pneumonia.^{233,234,248-250
1. Mechanical Ventilators and Anesthesia Machines
The internal machinery of mechanical ventilators and anesthesia
machines is not considered an important source of bacterial
contamination of inhaled air.^{251 Thus, routine sterilization or
high-level disinfection of the internal machinery is considered
unnecessary. Using high-efficiency bacterial filters at various
positions in the breathing circuit had been advocated
previously.^{252,253 Filters interposed between the machinery and
the main breathing circuit can eliminate contaminants from the driving
gas and prevent retrograde contamination of the machine by the patient
but may also alter the functional specifications of the breathing
device by impeding high gas flows.^{252,253 In addition, when used
with anesthesia equipment, filters placed between the inspiratory-phase
circuit and the patient have not been shown to prevent
infections.^{254,255 Placement of a filter or condensate trap at the
expiratory-phase tubing of the mechanical-ventilator circuit may help
prevent cross-contamination of the ventilated patient's immediate
environment,^{231,256 but the importance of such filters in
preventing nosocomial pneumonia needs further evaluation.
2. Humidifiers, Breathing Circuits, and Heat-Moisture Exchangers
Most U.S. hospitals currently use ventilators with either bubble-
through or wick humidifiers that produce either
insignificant^{125,257 or no aerosols, respectively, for
humidification. Thus, they do not seem to pose an important risk for
pneumonia in patients. In addition, bubble-through humidifiers are
usually heated to temperatures that reduce or eliminate bacterial
pathogens.^{257,258 Sterile water, however, is still generally used
to fill these humidifiers^{259 because tap or distilled water may
harbor Legionella spp. that are more heat-resistant than other
bacteria.^{236,250
The potential risk for pneumonia in patients using mechanical
ventilators with heated bubble-through humidifiers stems primarily from
the condensate that forms in the inspiratory-phase tubing of the
ventilator circuit as a result of the difference in the temperatures of
the inspiratory-phase gas and ambient air; condensate formation
increases if the tubing is unheated.^{260 The tubing and condensate
can rapidly become contaminated, usually with bacteria that originate
from the patient's oropharynx.^{260 In the study by Craven et al,
33% of inspiratory circuits were colonized with bacteria from patients'
oropharynx within 2 hours and 80% within 24 hours of use.^{260
Spillage of the contaminated condensate into the patient's
tracheobronchial tree, as can occur during procedures in which the
tubing may be moved (e.g., suctioning, adjusting the ventilator
setting, or feeding or caring for the patient), may increase the risk
of pneumonia in the patient.^{260 Thus, in many hospitals,
healthcare workers are trained to prevent such spillage and to drain
the fluid periodically. Microorganisms contaminating ventilator-circuit
condensate can be transmitted to other patients via hands of the
healthcare worker handling the fluid, especially if the healthcare
worker fails to wash his or her hands after handling the condensate.
The role of ventilator-tubing changes in preventing pneumonia in
patients using mechanical ventilators with bubble-through humidifiers
has been investigated. Initial studies of in-use contamination of
mechanical ventilator circuits with humidifiers have shown that neither
the rate of bacterial contamination of inspiratory-phase gas nor the
incidence of pneumonia was significantly increased when tubings were
changed every 24 hours rather than every 8 or 16 hours.^{261 Craven
et al later showed that changing the ventilator circuit every 48 hours
rather than 24 hours did not result in an increase in contamination of
the inspiratory-phase gas or tubing of the ventilator circuits.\262\ In
addition, the incidence of nosocomial pneumonia was not significantly
higher when circuits were changed every 48 hours than when changes were
done every 24 hours.\262\ More recent reports suggest that the risk of
pneumonia may not increase when the interval for circuit change is
prolonged beyond 48 hours. Dreyfuss and others showed that the risk of
pneumonia (8 [29%] of 28) was not significantly higher when the
circuits were never changed for the duration of use by the patient,
than (11 [31%] of 35) when the circuits were changed every 48
hours.\263\
These findings indicate that the recommended daily change in
ventilator circuits may be extended to 48 hours. This change
in recommendation is expected to result in large savings in device use
and personnel time for U.S. hospitals.^{259,262 The maximum time,
however, that a circuit can be safely left unchanged on a patient has
yet to be determined.
Condensate formation in the inspiratory-phase tubing of a
ventilator breathing circuit can be decreased by elevating the
temperature of the inspiratory-phase gas with a heated wire in the
inspiratory-phase tubing. However, in one report, three cases of
endotracheal- or tracheostomy-tube blockage by dried-up patient
secretions were attributed to the decrease in the relative humidity of
inspired gas that results from the elevation of the gas
temperature.\264\ Until further data are available about the frequency
of the occurrence of such cases, users of heated ventilator tubing
should be aware of the advantages and potential complications of using
heated tubing.
Condensate formation can be eliminated by using a heat-moisture
exchanger (HME) or a hygroscopic condenser humidifier (``artificial
nose'').^{265,270 An HME recycles heat and moisture exhaled by the
patient, and eliminates the need for a humidifier. In the absence of a
humidifier, no condensate forms in the inspiratory-phase tubing of the
ventilator circuit. Thus, bacterial colonization of the tubing is
prevented, and the need to routinely change tubings periodically is
obviated. Some models of HMEs are equipped with bacterial filters, but
the advantage of these filters remains unknown. HMEs can increase the
dead space and resistance to breathing, may leak around the
endotracheal tube, and may result in drying of sputum and blockage of
the tracheo-bronchial tree.^{271 Although recently developed HMEs
with humidifiers increase airway humidity without increasing
colonization with bacteria,^{267,272 more studies are needed to
determine whether the incidence of pneumonia is decreased.^{273-276
3. Large-Volume Nebulizers
Nebulizers with large-volume (>500 cc) reservoirs, including those
used in intermittent positive-pressure breathing (IPPB) machines and
ultrasonic or spinning-disk room-air ``humidifiers,'' pose the greatest
risk of pneumonia to patients, probably because of the total amount of
aerosol they generate.^{222,225,227,236,277 These reservoirs can
become contaminated by hands of personnel, unsterile humidification
fluid, or inadequate sterilization or disinfection between uses.\119\
Once introduced into the reservoir, various bacteria, including
Legionella spp., can multiply to sufficiently large numbers within 24
hours to pose a risk of infection in patients who receive inhalation
therapy.^{121,122,227,237,277 Sterilization or high-level
disinfection of these nebulizers can eliminate vegetative bacteria from
their reservoirs and make them safe for patient use.\240\ Unlike
nebulizers attached to IPPB machines, however, room-air ``humidifiers''
have a high cost-benefit ratio: evidence of clinical benefits from
their use in hospitals is lacking, and the potential cost of daily
sterilization or disinfection of, and use of sterile water to fill,
such devices is substantial.
4. Small-Volume Medication Nebulizers
Small-volume medication nebulizers for administration of
bronchodilators, including those that are hand-held and those that are
in the inspiratory circuit of mechanical ventilators, can produce
bacterial aerosols.\228\ Hand-held nebulizers have rarely been
associated with nosocomial pneumonia, and only when contaminated by
medications from multidose vials.\278\ Medication nebulizers inserted
in the ventilator circuit (``in-line'') may become contaminated by
condensate in the inspiratory tubing and increase the patient's risk of
pneumonia because the nebulizer aerosol is directed through the
endotracheal tube and bypasses many of the normal host defenses against
infection.\260\
5. Suction Catheters, Resuscitation Bags, Oxygen Analyzers, and
Ventilator Spirometers
Tracheal suction catheters can introduce microorganisms into a
patient's lower respiratory tract. Preliminary studies suggest that the
risk of pneumonia is not different between patients on whom the single-
use suction method is used and those on whom the newly developed closed
multi-use catheter system is used.\279\ In addition, the advantages of
using one system over the other, in terms of oxygen desaturation in
patients and less environmental contamination, have not been clearly
shown.^{280-282
Resuscitation bags are particularly difficult to clean and dry
between uses; microorganisms in secretions or fluid left in the bag may
be aerosolized and/or sprayed into the lower respiratory tract of the
patient on whom the bag is used; in addition, contaminating
microorganisms may be transmitted from one patient to another via hands
of staff members.^{283-285 Oxygen analyzers and ventilator
spirometers have been associated with outbreaks of gram-negative
respiratory tract colonization and pneumonia resulting from patient-to-
patient transmission of organisms via hands of personnel.^{220,286
These devices require sterilization or high-level disinfection between
uses on different patients. Education of physicians, respiratory
therapists, and nursing staff regarding the associated risks and
appropriate care of these devices is essential.

F. Thoraco-Abdominal Surgical Procedures

Certain patients are at high risk of developing postoperative
pulmonary complications, including pneumonia. These persons include
those who are more than 70 years of age, are obese, or have chronic
obstructive pulmonary disease.^{287-290 Abnormal pulmonary function
tests (especially decreased maximum expiration flow rate), a history of
smoking, the presence of tracheostomy or prolonged intubation, or
protein depletion that can cause respiratory-muscle weakness are also
risk factors.^{59,65,129 Patients who undergo surgery of the head,
neck, thorax, or abdomen may suffer from impairment of normal
swallowing and respiratory clearance mechanisms as a result of
instrumentation of the respiratory tract, anesthesia, or increased use
of narcotics and sedatives;^{288,291,292 patients who undergo upper
abdominal surgery usually suffer from diaphragmatic dysfunction that
results in decreased functional residual capacity of the lungs, closure
of airways, and atelectasis.^{293,294 Interventions aimed at
reducing the postoperative patient's risk of pneumonia have been
developed.\295\ These include deep breathing exercises, chest
physiotherapy, use of incentive spirometry, IPPB, and continuous
positive airway pressure (CPAP) by face mask.^{295-305 Studies
evaluating the relative efficacy of these modalities have shown
variable results, and have been difficult to compare because of
differences in outcome variables assessed, patient populations studied,
and study design.^{295,297,298,304-307 Nevertheless, many studies
have found deep breathing exercises, chest physiotherapy, use of
incentive spirometry, and IPPB as advantageous maneuvers, especially in
patients with preoperative pulmonary
dysfunction.^{298,299,301,302,304-306 In addition, control of pain
that interferes with cough and deep breathing during the immediate
postoperative period has been shown to decrease the incidence of
pulmonary complications after surgery; several methods of controlling
pain have been used; these include intramuscular or intravenous
(including patient-controlled) administration, or regional (e.g.,
epidural) analgesia.^{308-315

G. Other Prophylactic Measures

1. Vaccination of Patients
Although pneumococci are not a major cause of nosocomial pneumonia,
they have been identified as etiologic agents of serious nosocomial
pulmonary infection and bacteremia.^{316-318 The following factors
render patients at high risk of complications from pneumococcal
infections: 65 years of age, chronic cardiovascular or
pulmonary disease, diabetes mellitus, alcoholism, cirrhosis,
cerebrospinal fluid leaks, immunosuppression, functional or anatomic
asplenia, or HIV infection. Pneumococcal vaccine is effective in
preventing pneumococcal disease.^{319,320 Because two-thirds or more
of patients with serious pneumococcal disease have been hospitalized at
least once within 5 years before their pneumococcal illness, offering
pneumococcal vaccine in hospitals, e.g., at the time of patient
discharge, should contribute substantially to preventing the
disease.^{319,321
2. Prophylaxis With Systemic Antimicrobial Agents
Systemic antimicrobial administration has been a prevalent practice
in the prevention of nosocomial infections, including pneumonia,
especially in patients who are weaned off mechanical ventilators,
postoperative, and/or critically ill.^{322 However, the efficacy of
such practice is questionable; and the potential for superinfection,
which may result from any antimicrobial therapy, is a
problem.^{84,322-326
3. Kinetic Therapy for the Immobilized State
Continuous lateral rotational therapy (CLRT) or ``kinetic'' therapy
is a recently introduced maneuver for prevention of pulmonary and other
complications from prolonged immobilization or bed rest, such as in
patients with acute stroke, critical illness, head injury or traction,
blunt chest trauma, and/or mechanically assisted ventilation.^{327-
332 CLRT involves the use of a bed that turns continuously and slowly
(about eight full rotations per hour) along its longitudinal axis.
Among the hypothesized benefits of CLRT are improved drainage of
secretions within the lungs and lower airways, increased tidal volume,
and reduction of venous thrombosis with resultant pulmonary
embolization.^{174,333-335 However, the efficacy of CLRT in
preventing pneumonia needs further evaluation because available studies
yielded variable results.^{327-330 In addition, the studies either
involved small numbers of patients,^{328 lacked adequate
randomization,^{327 had no clear definition of pneumonia,^{327
did not distinguish between community-acquired and nosocomial
pneumonia,^{328,332 or did not adjust for possible confounding
factors such as mechanical ventilation, endotracheal intubation,
nasogastric intubation, and enteral feeding.^{327

LEGIONNAIRES' DISEASE

Legionnaires' disease is a multisystem illness, with pneumonia,
caused by Legionella spp. In contrast, Pontiac fever is a self-limited
influenza-like illness, without pneumonia, that is associated with
Legionella spp.^{336

I. Epidemiology

Since identification of the etiologic agent, numerous outbreaks of
nosocomial Legionnaires' disease have been reported and have provided
the opportunity to study the epidemiology of epidemic legionellosis. In
contrast, the epidemiology of endemic Legionnaires' disease has not
been well elucidated. The overall proportion of nosocomial pneumonias
due to Legionella spp. in North America has not been determined,
although individual hospitals have reported a ranges of 0%-
14%.^{337-339 Because diagnostic tests for Legionella spp. infection
are not routinely performed on all patients with hospital-acquired
pneumonia in most hospitals, this range probably underestimates the
incidence of Legionnaires' disease.
Legionella spp. are commonly found in a variety of natural and man-
made aquatic environments^{340,341 and may enter hospital water
systems in low or undetectable numbers.^{342,343 Cooling towers,
evaporative condensers, heated potable-water-distribution systems
within hospitals, and locally produced distilled water can provide a
suitable environment for legionellae to multiply. Factors known to
enhance colonization and amplification of legionellae in man-made water
environments include temperatures of 25-42 deg.C,^{344-349
stagnation,^{350 scale and sediment,^{346 and the presence of
certain free-living aquatic amoebae that are capable of supporting
intracellular growth of legionellae.^{351,352
A person's risk of acquiring legionellosis following exposure to
contaminated water depends on a number of factors, including the type
and intensity of exposure and the exposed person's health
status.^{353-355 Persons with severe immunosuppression or chronic
underlying illnesses, such as hematologic malignancy or end-stage renal
disease, are at markedly increased risk for legionellosis.^{355-358
Persons in the later stages of acquired immunodeficiency syndrome are
also probably at increased risk of legionellosis, but data are limited
because of infrequent testing of patients. Persons with diabetes
mellitus, chronic lung disease, or non-hematologic malignancy, those
who smoke cigarettes, and the elderly are at moderately increased
risk.^{336 Nosocomial Legionnaires' disease has also been reported
among patients at children's hospitals.^{359,360
Underlying disease and advanced age are not only risk factors for
acquiring Legionnaires' disease but also for dying from the illness. In
a multivariate analysis of 3,524 cases reported to CDC from 1980
through 1989, immunosuppression, advanced age, end-stage renal disease,
cancer, and nosocomial acquisition of disease were each independently
associated with a fatal outcome.^{355 The mortality rate among 803
persons with nosocomially acquired cases was 40% compared with 20%
among 2,721 persons with community-acquired cases,^{355 probably
reflecting increased severity of underlying disease in hospitalized
patients.

II. Diagnosis

The clinical spectrum of disease due to Legionella spp. is broad
and ranges from asymptomatic infection to rapidly progressive
pneumonia. Legionnaires' disease cannot be distinguished clinically or
radiographically from pneumonia caused by other agents,\361\,\362\ and
evidence of infection with other respiratory pathogens does not rule
out the possibility of concomitant Legionella spp. infection.^{363-
365
The diagnosis of legionellosis may be confirmed by any one of the
following: Culture isolation of Legionella from respiratory secretions
or tissues, or microscopic visualization of the bacterium in
respiratory secretions or tissue by immunofluorescent microscopy; and,
for legionellosis due to L. pneumophila serogroup 1, detection of L.
pneumophila serogroup-1 antigens in urine by radioimmunoassay, or
observation of a four-fold rise in L. pneumophila serogroup-1 antibody
titer to 1:128 in paired acute and convalescent serum
specimens by use of an indirect immunofluorescent antibody test
(IFA).\366\ A single elevated antibody titer does not confirm a case of
Legionnaires' disease because IFA titers 1:256 are found in
1-16% of healthy adults.^{364,367-370
Because the above tests complement each other, performing each test
when Legionnaires' disease is suspected increases the probability of
confirming the diagnosis.\371\ However, because none of the laboratory
tests is 100% sensitive, the diagnosis of legionellosis is not ruled
out even if one or more of the tests are negative.^{371,372 Of the
available tests, the most specific is culture isolation of Legionella
sp. from any respiratory tract specimen.^{373,374

III. Modes of Transmission

Inhalation of aerosols of water contaminated with Legionella sp. is
believed to be the primary mechanism of entry of these organisms into a
patient's respiratory tract.\336\ In several hospital outbreaks,
patients were considered to be infected through exposure to
contaminated aerosols generated by cooling towers, showers, faucets,
respiratory therapy equipment, and room-air humidifiers.^{227,375-
382 In several studies, aspiration of contaminated potable water has
been proposed as the mode of transmission to certain patients.^{383-
385 Person-to-person transmission, however, has not been observed.

IV. Definition of Nosocomial Legionnaires' Disease

The incubation period for Legionnaires' disease is generally 2-10
days; thus, for epidemiologic purposes, in this document and in the
accompanying recommendations by the HICPAC, laboratory-confirmed
legionellosis that occurs in a patient who has spent 10 days
continuously in the hospital prior to onset of illness is considered
definite nosocomial Legionnaires' disease, and laboratory-confirmed
infection that occurs 2-10 days after hospitalization is possible
nosocomial infection.

V. Prevention and Control Measures

A. Prevention of Legionnaires' Disease in Hospitals With No Identified
Cases (Primary Prevention)

Prevention strategies in healthcare facilities with no cases of
nosocomial legionellosis have varied by institution, depending on the
immunologic status of the patients, the design and construction of the
facility, resources available for implementation of prevention
strategies, and state and local regulations.
There are at least two schools of thought regarding the most
appropriate and cost-effective approach to prevent nosocomial
legionellosis, especially in hospitals where no cases or only sporadic
cases of the illness are detected. However, a study comparing the cost-
benefit ratios of these strategies has not been done.
The first approach is based on periodic, routine culturing of water
samples from the hospital's potable water system, for Legionella
spp.^{387 When a positive culture is obtained, the hospital's
potable water system is decontaminated and diagnostic laboratory tests
for legionellosis are made available to clinicians in the hospital's
microbiology department, so that active surveillance for cases can be
instituted.^{388 This approach is based on the premise that no cases
of nosocomial legionellosis can occur in the absence of Legionella spp.
from the potable water system, and, conversely, once Legionella spp.
are cultured from the water, cases of nosocomial legionellosis may
occur.^{383,389 Proponents of this strategy indicate that when
physicians are informed that the potable water system of the hospital
is culture-positive for Legionella spp., they are more inclined to
conduct the necessary tests for legionellosis.^{388 A potential
advantage of this approach is the lower cost of culturing a limited
number of water samples, if the testing is done infrequently, compared
with the cost of routine laboratory diagnostic testing for
legionellosis in all patients with nosocomial pneumonia in hospitals
that have had no cases of nosocomial legionellosis.
The main argument against this approach is that in the absence of
cases, the relationship between the results of water cultures and the
risk of legionellosis remains undefined. The bacterium has been
frequently present in hospital water systems,^{390 often without
being associated with known cases of disease.^{250,338,391,392 In a
study of 84 hospitals in Quebec, 68% were found to be colonized with
Legionella spp., and 26% were colonized at >30% of sites sampled;
however, cases of Legionnaires' disease were rarely reported from these
hospitals.^{250 Similarly, at one hospital where active surveillance
for legionellosis and environmental culturing for Legionella spp. were
done, no cases of legionellosis occurred in a urology ward during a
3.5-month period when 70% of water samples from the ward were culture-
positive for L. pneumophila serogroup 1.^{338 Interpretation of the
results of routine culturing of water may be confounded by variable
culture results among sites sampled within a single water system and by
fluctuations in the concentration of Legionella spp. in the same
site.^{393,394 In addition, the risk of illness following exposure
to a given source may be influenced by a number of factors other than
the presence or concentration of organisms; these include the degree to
which contaminated water is aerosolized into respirable droplets, the
proximity of the infectious aerosol to potential host, the
susceptibility of the host, and the virulence properties of the
contaminating strain.^{395-397 Thus, data are insufficient to assign
a level of risk of disease even on the basis of the number of colony-
forming units detected in samples from the hospital environment. By
routinely culturing water samples, many hospitals will have to be
committed to water-decontamination programs to eradicate Legionella
spp. Because of this problem, routine monitoring of water from the
hospital's potable water system and from aerosol-producing devices is
not widely recommended.^{398
The second approach to prevent and control nosocomial legionellosis
is by: (a) Maintaining a high index of suspicion for legionellosis and
appropriately using diagnostic tests for legionellosis in patients with
nosocomial pneumonia who are at high risk of developing the disease and
dying from the infection,^{338,399 (b) initiating an investigation
for a hospital source of Legionella spp. upon identification of one
laboratory-confirmed case of definite or two laboratory-confirmed cases
of possible nosocomial Legionnaires' disease, and (c) routinely
maintaining cooling towers and using only sterile water for filling and
terminal rinsing of nebulization devices.
In hospitals with no identified cases of legionellosis, further
study is needed of the cost-benefit ratio of control measures aimed at
creating an environment that is not conducive to survival or
multiplication of Legionella spp., e.g., routine maintenance of potable
water at 50 deg.C or <20 deg.C at the tap or chlorination of
heated water to achieve 1-2 mg/L free residual chlorine at the
tap.^{338,383,393,400-403

B. Prevention of Legionnaires' Disease in Hospitals With Identified
Cases (Secondary Prevention)

The indications for a full-scale environmental investigation to
search for and subsequently decontaminate identified sources of
Legionella spp. in hospital environments remain to be elucidated, and
probably vary from hospital to hospital. In institutions where as few
as 1-3 nosocomial cases are identified over a period of up to several
months, intensified surveillance for Legionnaires' disease has
frequently detected numerous additional cases.^{357,376,380,401 This
suggests the need for a low threshold for initiating an investigation
following the identification of nosocomial, laboratory-confirmed cases
of legionellosis. However, when developing a strategy to respond to
such an identification, infection-control personnel should consider the
level of risk of nosocomial acquisition of, and mortality from,
Legionella spp. infection at their particular hospital.
An epidemiologic investigation of the source of Legionella spp.
involves several important steps, including retrospective review of
microbiologic and medical records, active surveillance to identify all
recent or ongoing cases of legionellosis, identification of risk
factors (including environmental exposures for infection, such as
showering or use of respiratory-therapy equipment), collection of water
samples from environmental sources implicated by the epidemiologic
investigation and from other potential sources of aerosolized water,
and subtype-matching between legionellae isolated from patients and
environmental samples.^{382,404-406 The latter step can be crucial
in supporting epidemiologic evidence of a link between human illness
and a specific source.^{407
In hospitals where the heated-water system has been identified as
the source of the organism, the system has been decontaminated by pulse
(one-time) thermal disinfection or superheating (i.e., flushing for at
least 5 minutes each distal outlet of the hot-water system with water
at 65 deg.C) and hyperchlorination (flushing all outlets of
the hot-water system with water containing 10 mg/L free
residual chlorine).^{403,408-410 Following either of these
procedures, most hospitals maintain heated-water at 50 deg.C
or <20 deg.C at the tap or chlorinate heated water to achieve 1-2 mg/L
free residual chlorine at the tap.^{338,383,393,400-403 Additional
measures, such as physical cleaning or replacement of hot-water storage
tanks, water-heaters, faucets, and showerheads, may be required because
scale and sediment that provide organisms protection from the biocidal
effects of heat and chlorine, may accumulate in them.^{346,403
Alternative methods for control and eradication of legionellae in water
systems, such as treatment of water with ozone, ultraviolet light, or
heavy metal ions, have limited the growth of legionellae under
laboratory,^{344,411,412 or, in the case of ultraviolet light,
operating conditions.^{413 However, further data are needed
regarding the efficacy of these methods when used in hospital water
systems^{414 before they can be considered standard. In hospitals
where the cooling towers are contaminated, measures for decontamination
have been previously published.^{415
For highly immunocompromised patients, other preventive measures
have been used. At one hospital, immunosuppressed patients were
restricted from taking showers, and, for these patients, only sterile
water was used for drinking or flushing nasogastric tubes;^{384 In
another hospital, a combined approach, consisting of continuous
heating, particulate filtration, ultraviolet treatment, and monthly
pulse hyperchlorination of the water supply of the bone-marrow
transplant unit, was used to decrease the incidence of Legionnaires'
disease.^{413
In view of the high cost of an environmental investigation and of
instituting control measures to eradicate Legionella spp. from sources
in the hospital^{416,417 and the differential risk, based on host
factors, for acquiring nosocomial legionellosis and of having severe
and fatal infection with the microorganism, the decision to search for
and the choice of procedures to eradicate hospital environmental
sources of Legionella spp. should take into account the type of patient
population served by the hospital.

ASPERGILLOSIS

I. Epidemiology

Aspergillus spp. are ubiquitous fungi, commonly occurring in soil,
water, and decaying vegetation. Aspergillus spp. have been cultured
from unfiltered air, ventilation systems, contaminated dust dislodged
during hospital renovation and construction, horizontal surfaces, food,
and ornamental plants.^{418
A. fumigatus and A. flavus are the most frequently isolated
Aspergillus spp. in patients with proven aspergillosis.^{419
Nosocomial aspergillosis has been recognized increasingly as a cause of
severe illness and mortality in highly immunocompromised patients,
e.g., patients undergoing chemotherapy and/or organ transplantation,
including bone-marrow transplantation for hematologic and other
malignant neoplasms.^{420-423
The most important nosocomial infection due to Aspergillus spp. is
pneumonia.^{424 Hospital outbreaks of pulmonary aspergillosis have
occurred mainly in granulocytopenic patients, especially in bone-marrow
transplant units.^{424-430 Although invasive aspergillosis has been
reported in recipients of solid-organ transplants (e.g., heart or
kidney),^{431-435 the incidence of Aspergillus spp. infections in
these patients has been lower than in recipients of bone-marrow
transplants, probably because of the recent decrease in the use of
corticosteroids and the introduction of cyclosporine.^{433,436 In
solid-organ transplant recipients, the efficacy of infection control
measures, such as provision of protected environments and prophylaxis
with antifungal agents, in preventing aspergillosis has not been well
evaluated.^{433,434,437-439 In one study of heart-transplant
recipients, protective isolation of patients alone failed to prevent
fungal infections.^{440
The reported attributable mortality from invasive pulmonary
aspergillosis has varied, depending on the patient population studied.
Rates have been as high as 95% in recipients of allogeneic bone-marrow
transplants and patients with aplastic anemia, compared with rates of
13-80% in leukemic patients.^{441-443

II. Pathogenesis

In contrast to most bacterial pneumonias, the primary route of
acquiring Aspergillus sp. infection is by inhalation of the fungal
spores. In severely immunocompromised patients, primary Aspergillus
spp. pneumonia results from local lung tissue invasion.^{419,444,445
Subsequently, the fungus may disseminate via the bloodstream to involve
multiple other deep organs.^{419,445,446 A role for nasopharyngeal
colonization with Aspergillus spp., as an intermediate step before
invasive pulmonary disease, has been proposed, but remains to be
elucidated.^{438,447,448 On the other hand, colonization of the
lower respiratory tract by Aspergillus spp., especially in patients
with preexisting lung disease such as chronic obstructive lung disease,
cystic fibrosis, or inactive tuberculosis, has predisposed patients to
invasive pulmonary and/or disseminated infection.^{419,445,449

III. Diagnosis

Diagnosing pneumonia due to Aspergillus spp. is often difficult
without performing invasive procedures. Bronchoalveolar lavage has been
a useful screening test,^{450-452 but lung biopsy is still
considered the most reliable technique.^{453 Histopathologic
demonstration of tissue invasion by fungal hyphae has been required in
addition to isolation of Aspergillus spp. from respiratory tract
secretions because the latter, by itself, may indicate
colonization.^{454 However, when Aspergillus spp. is grown from the
sputum of a febrile, granulocytopenic patient with a new pulmonary
infiltrate, it is highly likely that the patient has pulmonary
aspergillosis.^{447,455 Routine blood cultures are remarkably
insensitive for detecting Aspergillus spp.,^{456 and systemic
antibody responses in immunocompromised patients are likely to be
unreliable indicators of infection.^{457-459 Antigen-based serologic
assays are now being developed in an attempt to allow for the rapid and
specific diagnosis of Aspergillus spp. infections; however, their
clinical usefulness is presently undefined.^{460,461

IV. Risk Factors and Control Measures

The major risk factor for invasive aspergillosis is severe and
prolonged granulocytopenia, both disease- and therapy-induced.^{462
Since bone-marrow transplant recipients experience the most severe
degree of granulocytopenia, they probably constitute the population at
highest risk of developing invasive aspergillosis.^{442,463 The
tendency of bone-marrow transplant recipients to develop severe
granulocytopenia (<1,000 polymorphonuclears/l) is associated
with the type of graft they receive. While both autologous and
allogeneic bone-marrow transplant recipients are severely
granulocytopenic for up to 4 weeks after the transplant procedure,
allogeneic-transplant recipients may, in addition, develop acute or
chronic graft-versus-host disease. The latter may occur up to several
months after the procedure, and the disease and/or its therapy (often
with high doses of corticosteroids, cyclosporine, and other
immunosuppressive agents) may result in severe granulocytopenia.
Consequently, in developing strategies to prevent invasive Aspergillus
spp. infection in bone-marrow-transplant patients, infection control
personnel should consider exposures of the patient to the fungus not
only during the patient's immediate posttransplantation period, but
also other exposures (e.g., at home or in an ambulatory-care setting)
subsequent to the immediate posttransplant period, when the patient
(especially allogeneic-transplant recipients) may again manifest severe
granulocytopenia. To help address this problem, various studies are now
in progress to evaluate newer methods of enhancing host resistance to
invasive fungal (and other) infections, and of eliminating or
suppressing respiratory fungal colonization of the upper respiratory
tract. These methods include, respectively, the use of granulocyte-
colony-stimulating factors and intranasal application of amphotericin
B, or oral or systemic antifungal drug prophylaxis.^{418,464-467 For
solid-organ transplant recipients, risk factors for invasive
aspergillosis have not been as extensively studied. In one study of
liver-transplant recipients, risk factors for invasive infection with
Aspergillus sp. identified by univariate analysis included preoperative
and postoperative receipt of steroids and antimicrobial agents, and
prolonged duration of transplant surgery.^{468
The presence of aspergilli in the hospital environment is the major
extrinsic risk factor for the occurrence of opportunistic invasive
Aspergillus sp. infection.^{437,469 Environmental disturbances due
to construction and/or renovation activities in and around hospitals
markedly raise the airborne Aspergillus spp. spore counts in such
hospitals and have been associated with nosocomial
aspergillosis.^{426,428,429,470-473 In addition, aspergillosis in
high-risk immunosuppressed patients has been associated with other
hospital environmental reservoirs, including bird droppings in air
ducts supplying high-risk patient areas,^{474 and contaminated
fireproofing material or damp wood.^{428,475
A single case of nosocomial Aspergillus spp. pneumonia is often
difficult to link to a specific environmental exposure. However,
additional cases may remain undetected without an active search that
includes an intensive retrospective review of microbiologic,
histopathologic, and postmortem records; notification of clinicians
caring for high-risk patients; and establishment of a system for
prospective surveillance for additional cases. When additional cases
are detected, the likelihood is increased that a hospital environmental
source of Aspergillus spp. can be identified.^{426,428,470-475
Previous investigations have shown the importance of construction
activities and/or fungal ``contamination'' of hospital air-handling
systems as major sources for outbreaks.^{424,426,428,470-474 New
molecular typing techniques, namely karyotyping^{476 and DNA
endonuclease profiling (now available for A. fumigatus),^{477 may
significantly aid in identifying the source of an outbreak.
Outbreaks of invasive aspergillosis reinforce the importance of
maintaining an environment as free of Aspergillus spp. spores as
possible for patients with severe granulocytopenia. To achieve this
goal, specialized services in many large hospitals, in particular bone-
marrow transplant services, have installed ``protected environments''
for the care of their high-risk, severely granulocytopenic patients,
and increased their vigilance during hospital construction and routine
maintenance of hospital air-filtration and ventilation systems, to
prevent exposing high-risk patients to bursts of fungal
spores.^{426,428,470-474,478-483
While the exact configuration and specifications of the protected
environments may vary between hospitals, these patient-care areas are
built to minimize fungal spore counts in air by maintaining (a) high-
efficiency filtration of incoming air as it enters the room (i.e., at
point of use) with HEPA filters that are 99.97% efficient in filtering
0.3-sized particles, (b) directed room airflow--from intake on
one side of the room, across the patient, and out through the exhaust
on the opposite side of the room, (c) positive room-air pressure
relative to the corridor, (d) well-sealed rooms, and (e) high rates of
room-air changes (range: 15 to >400 per hour).^{424,479-481,483-485
The oldest and most studied protected environment is a room with
laminar airflow, consisting of a bank of HEPA filters along an entire
wall through which air is pumped by blowers into the room at a uniform
velocity (30-90 feet/minute), forcing the air to move in a laminar, or
at least unidirectional, pattern.^{486 The air usually exits at the
opposite end of the room, and ultra-high (100-400 per hour) air-change
rates are achieved.^{424 The net effects are: essentially sterile
air in the room, minimal air turbulence, minimal opportunity for
microorganism build-up, and a consistently clean environment.^{424
The efficacy of a laminar-airflow system in decreasing or
eliminating the risk of nosocomial aspergillosis in high-risk patients
has been demonstrated.^{424,479,484,485 However, such a system is
costly to install and maintain.^{469 Less expensive alternative
systems with lower air-change rates (10-15 per hour) have been utilized
in some centers.^{480,481,487 However, studies comparing the
efficacy of these alternative systems with laminar-airflow rooms in
eliminating Aspergillus spp. spores and preventing nosocomial
aspergillosis are limited. One institution employing cross-flow
ventilation, point-of-use high-efficiency filters, and 15 air changes
per hour reported that cases of nosocomial aspergillosis in patients
housed in these rooms have occurred, albeit at a low rate
(3.4%).^{481,487 The infections, however, were due to A. flavus--a
species that was never cultured from the room air, suggesting that the
patients were probably exposed to fungal spores when they were allowed
outside their rooms.^{481
Copper-8-quinolinolate has been used on environmental surfaces
contaminated with Aspergillus spp. to control a reported
outbreak,^{488 and incorporated in fireproofing material of a newly
constructed hospital^{481 to help decrease the environmental spore
burden, but its general applicability is yet to be established.

VIRAL PNEUMONIAS

Viruses can be an important and often unappreciated cause of
nosocomial pneumonia.^{489,490 In one prospective study of endemic
nosocomial infections, approximately 20% of patients with pneumonia had
viral infections.^{490} Although early diagnosis and treatment of
viral infections have become possible in recent years,^{491-494 many
hospitalized patients remain at high risk for developing severe and
sometimes fatal viral infections.^{489,495-502 Based on these data
and on well-documented outbreaks with nosocomial viral
transmission,^{503-506 measures to prevent viral transmission
should be instituted.
Nosocomial respiratory viral infections (1) usually follow
community outbreaks that occur during a particular period every
year,^{505,507-510 (2) confer only short-term immunity,^{511 (3)
affect healthy and ill persons,^{497,498,504,512-514 and (4) have
exogenous sources. A number of viruses, including adenoviruses,
influenza virus, measles virus, parainfluenza viruses, respiratory
syncytial virus (RSV), rhinoviruses, and varicella-zoster virus can
cause nosocomial pneumonia;^{498,505,506,515-521 however,
adenoviruses, influenza or parainfluenza viruses, and RSV have been
reported to account for most (70%) of nosocomial pneumonias due to
viruses.^{522,523
Because influenza and RSV infections account for a substantial
portion of morbidity and mortality due to viral pneumonia and have been
well studied epidemiologically, this section focuses on the principles
and approaches to control these infections. However, because the modes
of transmission of RSV (i.e., by large droplets or by contact with
contaminated hands or other fomites) are the same as those of
parainfluenza viruses and similar to those of adenoviruses and
rhinoviruses (i.e., mainly by large droplets or contact with
contaminated hands or other fomites, but also possibly by aerosol
inhalation), infection-control measures recommended for RSV infection
are applicable to infections caused by the other three
viruses.^{524-529 Prevention of nosocomial infections due to measles
and varicella-zoster is addressed in another document.^{213

RSV INFECTION

I. Epidemiology

RSV infection is most common during infancy and early childhood,
but may also occur in adults.^{134,512,515,530,531 Infection usually
causes mild or moderately severe upper respiratory illness. However,
life-threatening pneumonia or bronchiolitis has been reported in
children with chronic cardiac and pulmonary disease, immunocompromised
patients, and the elderly.^{497,499,514,515,532,533
Recent surveillance of 10 U.S. hospital laboratories performing
cultures for RSV suggests that community outbreaks occur yearly between
December and March, last from 3-5 months, and are associated with
increased hospitalization and deaths among infants and young
children.^{534 During community outbreaks of RSV, children admitted
to the hospital with respiratory symptoms often serve as reservoirs for
RSV.^{503,505

II. Diagnosis

The clinical characteristics of RSV infection, especially in
neonates, are often indistinguishable from those of other viral
respiratory tract infections.^{515,516 Culture of RSV from
respiratory secretions remains the ``gold standard'' for diagnosis.
Although rapid antigen-detection kits utilizing direct
immunofluorescence or enzyme-linked immunosorbent assay are available
and can provide results within hours, the benefit of using these tests
to identify infected and susceptible patients depends on the
sensitivity and specificity of the test. The reported sensitivity and
specificity of RSV enzyme immunoassays vary between 80% and 95%, and
may even be lower in actual practice.^{535-538 In general, once
laboratory-confirmed cases of RSV infection are identified in a
hospital, a presumptive diagnosis of RSV infection in subsequent cases
with manifestations suggestive of RSV infection may be acceptable for
infection control purposes.

III. Modes of Transmission

RSV is present in large numbers in the respiratory secretions of
symptomatic persons infected with the virus and can be transmitted
directly via large droplets during close contact with such persons, or
indirectly via RSV-contaminated hands or fomites.^{503,524,525 The
portal of entry is usually the conjunctiva or the nasal mucosa.^{526
Inoculation by RSV-contaminated hands is the usual way of depositing
the virus onto the eyes or nose.^{503,524-526 Hands can become
contaminated through handling of infected persons' respiratory
secretions or contaminated fomites.^{524,525
In nosocomial RSV outbreaks in which the viral isolates were typed,
more than one strain of RSV has often been identified,^{504,513,539
suggesting multiple sources of the virus. Potential sources include
patients, hospital staff, and visitors. Because infected infants shed
large amounts of virus in their respiratory secretions and easily
contaminate their immediate surroundings, they are a major reservoir
for RSV.^{540 Hospital staff may become infected after exposure in
the community^{541 or in the hospital, and in turn, infect patients,
other health-care workers, or hospital visitors.^{516,542

IV. Control Measures

Various combinations of control measures ranging from the simple to
the complex have been effective, to some degree or other, in preventing
and controlling nosocomial RSV infection.^{215,542-549 Successful
programs have had two elements in common: implementation of contact-
isolation precautions, and compliance with these precautions by
healthcare personnel. In theory, strict handwashing should prevent most
nosocomial RSV infections. However, health-care workers' handwashing
practices have always been poor, even in institutions with good
educational programs.^{210,211 Thus, other preventive measures are
usually relied upon to prevent RSV infection.
The basic precautions that have been associated with decreased
incidence of nosocomial RSV infections are gloving and gowning.^{215
Gloving has helped decrease transmission probably because gloves remind
patient-care personnel to comply with handwashing and other
precautions, and deter persons from touching their eyes or noses. The
benefits from gloving, however, are offset if gloves are not changed
between patients or after contact with contaminated fomites, and if
hands are not adequately washed after glove removal.^{218 Gowning,
in combination with gloving, during contact with RSV-infected infants
or their immediate environment has been used successfully to prevent
infection.^{215 In addition, the use of eye-nose goggles rather than
masks has protected healthcare workers from infection; however, eye-
nose goggles are not widely available and are inconvenient to
wear.^{546,550
Additional measures may be indicated to control ongoing nosocomial
transmission of RSV or to prevent transmission to patients at high risk
for serious complications of infections, such as those with compromised
cardiac, pulmonary, or immune systems. The following additional control
measures have been used in various combinations: (1) Use of private
rooms for infected patients OR cohorting of infected patients, with or
without pre-admission screening by rapid laboratory diagnostic tests,
(2) cohorting of personnel, (3) exclusion of healthcare workers who
have symptoms of upper respiratory tract infection from the care of
uninfected patients at high risk of severe or fatal RSV infection,
e.g., infants, (4) limiting visitors, and (5) postponing admission of
patients at high risk of complications from RSV
infection.^{213,543,545,547,549 Although the exact role of each of
these measures has not been fully elucidated, their use for control of
outbreaks seems prudent.

INFLUENZA

I. Epidemiology

Pneumonia in patients with influenza may be due to the influenza
virus itself, secondary bacterial infection, or a combination of
both.^{551-553 Influenza-associated pneumonia can occur in any
person, but is more common in the very young or old and in persons in
any age group with immunosuppression or certain chronic medical
conditions such as severe underlying heart or lung
disease.^{531,554-556
Influenza typically occurs annually in the winter between December
and April; peak activity in a community usually lasts from 6 to 8 weeks
during this period.^{557,558 During influenza epidemics in the
community, nosocomial outbreaks may occur and are characterized by
abrupt onset and rapid transmission.^{559-561 Most reported
institutional outbreaks of influenza have occurred in nursing homes;
however, hospital outbreaks have been reported on pediatric and
chronic-care wards, as well as on medical and neonatal intensive care
units.^{506,562-565
Influenza is believed to be spread from person to person by direct
deposition of virus-laden large droplets onto the mucosal surfaces of
the upper respiratory tract of an individual during close contact with
an infected person, as well as by droplet nuclei or small-particle
aerosols.^{566-569 The extent to which transmission may occur by
virus-contaminated hands or fomites is unknown; however, it is not the
primary mode of spread.^{570
The most important reservoirs of influenza virus are infected
persons, and the period of greatest communicability is during the first
3 days of illness; however, the virus can be shed before onset of
symptoms, and up to 7 or more days after illness onset.^{506,557,571

II. Diagnosis

Influenza is clinically indistinguishable from other febrile
respiratory illnesses, but during outbreaks with laboratory-confirmed
cases, a presumptive diagnosis of the infection can be made in cases
with similar manifestations.^{572 In the past, diagnosis of
influenza was made by virus isolation from nasopharyngeal secretions or
by serologic conversion, but recently developed rapid diagnostic tests
that are similar to culture in sensitivity and specificity allow early
diagnosis and treatment of cases and provide a basis for prompt
initiation of antiviral prophylaxis as part of outbreak
control.^{573-578

III. Prevention and Control Measures

Vaccination of persons at high risk for complications of influenza
is currently the most effective measure for reducing the impact of
influenza, and should be done before the influenza season each year.
Such persons include those 65 years of age; those in long-
term-care units; those with chronic disorders of the pulmonary or
cardiovascular systems, those with diabetes mellitus, renal
dysfunction, hemoglobinopathies, musculo-skeletal disorders, or
immunosuppression; and children 6 months-18 years of age who are
receiving long-term aspirin therapy.^{564,579-581 When high
vaccination rates are achieved in closed or semi-closed settings, the
risk of outbreaks is reduced because of induction of herd
immunity.^{582,583
When an institutional outbreak is due to influenza A, antiviral
agents may be used both for treatment of ill persons and as prophylaxis
for others.^{584 Two related antiviral agents, amantadine
hydrochloride and rimantadine hydrochloride, are effective against
influenza-A, but not influenza-B, virus.^{493,585-587 These agents
can be used (1) for short-term prophylaxis after late vaccination of
high-risk persons; (2) as prophylaxis for persons for whom vaccination
is contraindicated; (3) as prophylaxis for immunocompromised persons
who may not produce protective levels of antibody in response to
vaccination; (4) for prophylaxis for unvaccinated healthcare workers
who provide care to high-risk patients, either for the duration of
influenza activity in the community or until immunity develops after
vaccination; and (5) when vaccine strains do not closely match the
epidemic viral strain.^{584
Amantadine has been available in the United States for many years;
rimantadine has just recently been approved for use. Both drugs protect
against all naturally-occurring strains of type A influenza virus;
thus, antigenic changes in the virus that may reduce vaccine efficacy
do not alter the effectiveness of amantadine or rimantadine. Both are
70-90% effective in preventing illness if taken before exposure to
influenza A virus.^{585,588 In addition, they lessen the severity
and duration of illness due to influenza A when administered within 24-
48 hours after onset of symptoms.^{589,590 Amantadine can limit
nosocomial spread of influenza A if it is administered to all or most
patients at the time influenza is recognized in a
facility.^{562,591,592
Side effects from amantadine are more common than those from
rimantadine; they include mild and transitory nervousness, insomnia,
impaired concentration, mood changes, light-headedness, anorexia, and
nausea. These symptoms have been reported in 5-10% of healthy young
adults receiving 200 mg of the drug per day.^{493,585 In the
elderly, the symptoms may be more severe; in addition, dizziness and
ataxia are more common in this age group.^{593,594 Thus, it is
recommended that for persons 65 years of age and/or those
who have renal insufficiency, amantadine dosage should be reduced to
100 mg per day. Further reductions are recommended on the
basis of the patient's creatinine clearance.^{595,596 However,
because recommended dosages based on creatinine clearance may provide
only a rough estimate of the optimal dose for a given patient,^{597
such persons should be carefully observed so that adverse reactions can
be recognized promptly and the dose further reduced or the drug
discontinued, if necessary.
Emergence of amantadine- and rimantadine-resistant strains of
influenza A virus has been observed in persons who receive these drugs
for treatment of the infection.^{598,599 Because of the potential
risk of transmission of resistant viral strains to close contacts of
persons receiving amantadine or rimantadine for treatment,^{599,600
to the extent possible, infected persons taking either drug should
avoid contact with others during treatment and for 2 days after
discontinuing treatment.^{600,601 This is particularly important if
the contacts are uninfected persons taking amantadine or rimantadine
for prophylaxis.^{600,602
Vaccination of high-risk patients and of hospital personnel before
the influenza season is the primary focus of efforts to prevent and
control nosocomial influenza.^{581,584,603 The decision to use
amantadine or rimantadine as an adjunct to vaccination in the
prevention and control of nosocomial influenza is based in part on
results of virologic and epidemiologic surveillance in the hospital and
the community. When outbreaks of influenza A occur in a hospital, and
antiviral prophylaxis of high-risk persons and treatment of cases is
undertaken, administration of amantadine or rimantadine is begun as
early in the outbreak as possible to reduce
transmission.^{562,584,591,602
Measures other than vaccination and chemoprophylaxis with
amantadine or rimantadine have been recommended for control of
nosocomial influenza outbreaks. Because influenza can be transmitted
during contact with an infected person, contact-isolation precautions,
such as placing a patient symptomatic with influenza in a private room,
cohorting of patients with influenza, and masking upon entering a room
with persons with influenza have been recommended.^{213 Handwashing,
gloving, and gowning by healthcare workers during the period of viral
shedding by patients have also been recommended, but the exact role of
these measures in preventing influenza transmission remains to be
elucidated.^{213,561,604 Although influenza can be transmitted via
the airborne route, the efficacy of placing infected persons in rooms
with negative pressure in relation to their immediate environment has
not been assessed. In addition, this measure may be impractical during
institutional outbreaks that occur in the midst of a community epidemic
of influenza because many newly admitted patients and healthcare
workers may be infected with the virus; thus, the hospital would face
the logistical problem of accommodating all ill persons in rooms with
special ventilation. Although controlled studies are not available to
measure their effectiveness, the following additional measures have
been recommended for consideration, particularly during severe
outbreaks: (1) Curtailment or elimination of elective admissions, both
medical and surgical; (2) restriction of cardiovascular and pulmonary
surgery; (3) restriction of hospital visitors, especially those with
acute respiratory illnesses; and (4) work restriction for healthcare
workers with acute respiratory illness.^{604

PART II. RECOMMENDATIONS FOR PREVENTION OF NOSOCOMIAL PNEUMONIA

Introduction

The recommendations are presented according to the etiology of the
infection, in the following order: bacterial pneumonia, including
Legionnaires' disease; fungal pneumonia (aspergillosis); and virus-
associated pneumonia (RSV and influenza infections). Each topic is
subdivided according to the following general approaches for nosocomial
infection control, as applicable to the infection:
1. Staff education and infection surveillance;
2. Interruption of transmission of microorganisms by eradicating
infecting; microorganisms from their epidemiologically important
reservoirs, and/or preventing person-to-person transmission; and
3. Modifying host risk for infection.
As in previous CDC guidelines, each recommendation is categorized
on the basis of existing scientific evidence, theoretical rationale,
applicability, and economic impact.^{213,214,605-609 However, the
previous CDC system of categorizing recommendations has been modified
as follows:
CATEGORY IA--Strongly recommended for all hospitals and strongly
supported by well-designed experimental or epidemiologic studies.
CATEGORY IB-- Strongly recommended for all hospitals and viewed as
effective by experts in the field and a consensus of HICPAC based on
strong rationale and suggestive evidence, even though definitive
scientific studies may not have been done.
CATEGORY II--Suggested for implementation in many hospitals.
Recommendations may be supported by suggestive clinical or
epidemiologic studies, a strong theoretical rationale, or definitive
studies applicable to some but not all hospitals.
NO RECOMMENDATION; UNRESOLVED ISSUE. Practices for which
insufficient evidence or consensus regarding efficacy exists.

Prevention and Control of Bacterial Pneumonia

I. Staff Education and Infection Surveillance

A. Staff Education

Educate healthcare workers regarding nosocomial bacterial
pneumonias and infection control procedures to prevent their
occurrence.^{610-613
CATEGORY IA

B. Surveillance

1. Conduct surveillance for bacterial pneumonia in ICU patients at
high-risk for nosocomial bacterial pneumonia (e.g., patients with
mechanically assisted ventilation, selected postoperative patients) to
determine trends and identify potential
problems.^{7,34,35,59,60,614-616 Include data regarding the
causative microorganisms and their antimicrobial susceptibility
patterns.^{2-4 Express data as rates (e.g., number of infected
patients or infections per 100 ICU days or per 1,000 ventilator-days)
to facilitate intra- and inter-hospital comparisons.^{63,617-619
CATEGORY IA
2. Do not routinely perform surveillance cultures of patients or of
equipment or devices used for respiratory therapy, pulmonary-function
testing, or delivery of inhalation anesthesia.^{62,620,621
CATEGORY IA

II. INTERRUPTION OF TRANSMISSION OF MICROORGANISMS

A. Sterilization or Disinfection, and Maintenance of Equipment and
Devices

1. General Measures
a. Thoroughly clean all equipment and devices to be sterilized or
disinfected. Decontaminate equipment or device before or during
cleaning if it is contaminated with blood and/or marked
``contaminated'' and received from patients who are on certain types of
isolation.^{245,246,622
CATEGORY IA
b. Sterilize semicritical equipment or devices, i.e., items that
touch mucous membranes (See device list, Appendix A). If sterilization
is not feasible, use high-level disinfection either by wet heat
pasteurization (76 deg.C for 30 minutes), or by using liquid
disinfectants approved as sterilants or disinfectants by the
Environmental Protection Agency.^{240,242,244,246,623 Follow
disinfection with appropriate rinsing, drying, and packaging, taking
care not to contaminate the items in the process.
CATEGORY IB
c. Use sterile (not distilled, nonsterile), pyrogen-free water for
rinsing reusable equipment and devices after they have been chemically
disinfected.^{227,233,234,248
CATEGORY IB
d. Do not reprocess an equipment or device that is manufactured for
single use only, unless data show that reprocessing the equipment or
device poses no threat to the patient, is cost-effective, and does not
change the structural integrity or function of the equipment or
device.^{624,625
CATEGORY IB
2. Mechanical Ventilators, Anesthesia Machines and Circle Systems, and
Pulmonary-Function Testing Equipment
a. Do not routinely sterilize or disinfect the internal machinery
of mechanical ventilators or anesthesia-breathing machines and their
circle systems.^{626,627
CATEGORY IA
b. Do not routinely sterilize or disinfect the internal machinery
of pulmonary-function testing machines between uses on different
patients.^{628,629
CATEGORY II
3. Ventilator Circuits with Humidifiers
a. Do not routinely change more frequently than every 48 hours the
breathing circuit, including tubing and exhalation valve, and the
attached bubbling or wick humidifier of a ventilator that is in use on
an individual patient.^{34,257,262
CATEGORY IA
b. NO RECOMMENDATION for the maximum length of time after which the
breathing circuit and the attached bubbling or wick humidifier of a
ventilator in use on a patient should be changed.^{263
UNRESOLVED ISSUE
c. Sterilize reusable breathing circuits and bubbling or wick
humidifiers, or subject them to high-level disinfection between their
uses on different patients.^{240,242,244,246
CATEGORY IB
d. Periodically drain and discard any condensate that collects in
the tubing of a mechanical ventilator or anesthesia machine, taking
precautions not to allow condensate to drain toward the patient. Wash
hands after performing the procedure or handling the fluid.^{256,260
CATEGORY IB
e. NO RECOMMENDATION for placing a filter or trap at the distal end
of the expiratory-phase tubing of the breathing circuit to collect
condensate.^{231,256
UNRESOLVED ISSUE
f. Do not place bacterial filters between the humidifier reservoir
and the inspiratory-phase tubing of the breathing circuit of a
mechanical ventilator, or in the circuit of an anesthesia
machine.^{254,627,630
CATEGORY IB
g. Humidifier fluids.
(1) Use sterile water to fill bubbling humidifiers.125,233,234,260
CATEGORY II
(2) Use sterile, distilled, or tap water to fill wick
humidifiers.^{233,234,260
CATEGORY II
(3) NO RECOMMENDATION for preferential use of a closed, continuous-
feed humidification system.
UNRESOLVED ISSUE
4. Ventilator Circuits With Hygroscopic Condenser-Humidifiers or Heat-
Moisture Exchangers
a. NO RECOMMENDATION for preferential use of hygroscopic condenser-
humidifier or heat-moisture exchanger rather than a heated humidifier
to prevent nosocomial pneumonia.^{272-276
UNRESOLVED ISSUE
b. Change the hygroscopic condenser-humidifier or heat-moisture
exchanger when evidence of gross contamination or mechanical
dysfunction of the device is present.^{272
CATEGORY IB
c. Do not routinely change the breathing circuit attached to a
hygroscopic condenser-humidifier or heat-moisture exchanger while it is
in use on a patient.^{272,275
CATEGORY IB
5. Wall Humidifiers
a. Follow manufacturers' instructions for use and maintenance of
disposable wall oxygen humidifiers unless data show that the
modification in their use or maintenance poses no threat to the patient
and is cost effective.^{631-635
CATEGORY IB
b. Between patients, change the reservoir, tubing (including any
nasal prongs), and any mask used to deliver oxygen from a wall outlet.
CATEGORY IB
6. Small-Volume Medication Nebulizers: ``In-Line'' and Hand-Held
Nebulizers
a. Between treatments on the same patient, disinfect or rinse with
sterile water and air-dry small-volume medication
nebulizers.^{228,378
CATEGORY IB
b. Replace nebulizers between patients with those that have
undergone sterilization or high-level disinfection.^{119,121,122,248
CATEGORY IB
c. Use only sterile fluids for nebulization, and dispense these
fluids aseptically.^{223,227,233,234,248,278,378
CATEGORY IA
d. If multi-dose medication vials are used, handle, dispense, and
store them according to directions on the vial label or package
insert.^{278,636,637
CATEGORY IB
7. Large-Volume Nebulizers and Mist Tents
a. Do not use large-volume room-air humidifiers that create
aerosols (e.g., by venturi principle, ultrasound, or spinning disk) and
thus are really nebulizers, unless they can be sterilized or subjected
to high level disinfection at least daily and filled only with sterile
water.^{224,225,227,236,277,638
CATEGORY IA
b. Sterilize large-volume nebulizers that are used for inhalation
therapy, e.g., for tracheostomized patients, or subject them to high-
level disinfection between patients and after every 24 hours of use on
the same patient.^{119,121,122
CATEGORY IB
c. Use mist-tent nebulizers and reservoirs that have undergone
sterilization or high-level disinfection, and replace them between
patients and after every 24 hours of use on the same patient.\639\
CATEGORY IB
8. Other Devices
a. Between patients, sterilize or use high-level disinfection on
respirometers, oxygen sensors, and other respiratory devices used on
multiple patients.^{220,286
CATEGORY IB
b. Sterilize or use high-level disinfection on hand-powered
resuscitation bags (for example, Ambu bags) between
patients.^{239,283-285
CATEGORY IA
c. Remove faucet aerators.\640\
CATEGORY II

B. Interruption of Person-to-Person Transmission of Bacteria

1. Handwashing
Wash hands after contact with mucous membranes, respiratory
secretions, or objects contaminated with respiratory secretions,
whether or not gloves are worn. Wash hands before and after contact
with a patient who has an endotracheal or tracheostomy tube in place,
and before and after contact with any respiratory device that is used
on the patient, whether or not gloves are
worn.^{201,203,207,208,641,642
CATEGORY IA
2. Barrier Precautions
a. Wear gloves for handling respiratory secretions or objects
contaminated with respiratory secretions of any patient.^{215,216
CATEGORY IA
b. Change gloves and wash hands between patients; after handling
respiratory secretions or objects contaminated with secretions from one
patient and before contact with another patient, object, or
environmental surface; and between contacts with a contaminated body
site and respiratory tract of, or respiratory device on, the same
patient.^{215,217,218
CATEGORY IA
c. Wear a gown when soiling with respiratory secretions from a
patient is anticipated, and change the gown after such contact and
before providing care to another patient.^{215
CATEGORY IB
3. Care of Patients with Tracheostomy
a. Perform tracheostomy under sterile conditions.
CATEGORY IB
b. When changing a tracheostomy tube, use aseptic technique and
replace the tube with one that has undergone sterilization or high-
level disinfection.
CATEGORY IB
4. Suctioning of Respiratory Tract Secretions
a. NO RECOMMENDATION for wearing sterile rather than clean gloves
when suctioning a patient's respiratory secretions.
UNRESOLVED ISSUE
b. If the open suction system is employed, use a sterile single-use
catheter.
CATEGORY II
c. Use only sterile fluid to remove secretions from the suction
catheter.
CATEGORY IB
d. Change suction-collection tubing and canisters between patients.

Category IB

e. NO RECOMMENDATION for using a multi-use closed-system suction
catheter in preference to a single-use open-system catheter.^{279-
282
UNRESOLVED ISSUE
f. NO RECOMMENDATION for routinely using an endotracheal tube with
a dorsal lumen above the endotracheal cuff, to allow drainage (by
suctioning) of tracheal secretions that accumulate in the patient's
subglottic area.^{197
UNRESOLVED ISSUE

III. Modifying Host Risk for Infection

A. Precautions for Prevention of Endogenous Pneumonia

1. Prevention of Aspiration
a. Discontinue enteral-tube feeding and remove devices such as
endotracheal and/or nasogastric or other enteral tubes from patients as
soon as the clinical indications for these are
resolved.^{7,34,35,80,110,173,175,176,192,643
CATEGORY IB
b. If there is no contraindication to the maneuver, elevate at an
angle of 30-45 deg. the head of the bed of a patient who is receiving
mechanically assisted ventilation and has a nasogastric or other
enteral tube in place.^{175,184

CATEGORY IB

c. Routinely verify appropriate placement of the feeding
tube.^{175644-646
CATEGORY IB

d. Routinely assess the patient's intestinal motility, (e.g., by
auscultating for bowel sounds and measuring residual gastric volume or
abdominal girth) and adjust the rate and volume of enteral feeding to
avoid regurgitation.^{175,188,643

CATEGORY IB

e. Use small-bore tubes for enteral
feeding;^{175,176,186,644,647

CATEGORY II

f. Administer enteral feeding intermittently in small quantities,
rather than continuously.^{2T167,183,647,648

CATEGORY II

g. NO RECOMMENDATION for preferentially placing the feeding tubes,
e.g., jejunal tubes, distal to the pylorus;^{189,190,649

UNRESOLVED ISSUE

h. NO RECOMMENDATION for using oro-tracheal rather than naso-
tracheal tube.^{650

UNRESOLVED ISSUE

2. Prevention of Gastric Colonization
a. If stress-bleeding prophylaxis is needed for a patient with
mechanically assisted ventilation, use an agent that does not raise the
patient's gastric pH.^{22,34,105,111,115,140-142,144-146
Category II
b. NO RECOMMENDATION for selective decontamination of an ICU
patient's digestive tract with oral and/or intravenous antimicrobials
to prevent gram-negative bacillary (or Candida spp.)
pneumonia.^{147-170
UNRESOLVED ISSUE
c. NO RECOMMENDATION for routine acidification of gastric
feedings.^{171
UNRESOLVED ISSUE

B. Prevention of Postoperative Pneumonia

1. Instruct preoperative patients, especially those at high risk of
developing pneumonia, regarding frequent coughing, taking deep breaths,
and ambulating as soon as medically indicated in the postoperative
period.^{302,304 High-risk patients include those who will receive
anesthesia, especially those who will have an abdominal, thoracic,
head, or neck operation, or who have substantial pulmonary dysfunction,
such as patients with chronic obstructive lung disease, a
musculoskeletal abnormality of the chest, or abnormal pulmonary
function tests.^{287-290,293,294
CATEGORY IB
2. Encourage postoperative patients to cough frequently, take deep
breaths, move about the bed, and ambulate unless it is medically
contraindicated.^{301,302,304
CATEGORY IB
3. Control pain that interferes with coughing and deep breathing
during the immediate postoperative period by using systemic
analgesia,^{309,652 including patient-controlled analgesia,^{310-
312 with as little cough-suppressant effect as possible; appropriate
support for abdominal wounds, such as tightly placing a pillow across
the abdomen; or regional (e.g., epidural) analgesia.^{313-315
CATEGORY IB
4. Use an incentive spirometer or intermittent positive pressure
breathing, perform chest physiotherapy on patients at high risk of
developing postoperative pneumonia.^{295,298,299,302,304,305,307
(See III-B-1 above for definition of high-risk patients.)
CATEGORY II

C. Other Prophylactic Procedures for Pneumonia

1. Vaccination of Patients
Vaccinate patients at high risk for complications of pneumococcal
infections with pneumococcal polysaccharide vaccine. High-risk patients
include persons 65 years old; adults with chronic
cardiovascular or pulmonary disease, diabetes mellitus, alcoholism,
cirrhosis, or cerebrospinal fluid leaks; and children and adults with
immunosuppression, functional or anatomic asplenia, or HIV
infection.^{319-321
CATEGORY IA
2. Systemic Antimicrobial Prophylaxis
Do not routinely administer systemic antimicrobial agents to
prevent nosocomial pneumonia.^{84,191,322-325,653
CATEGORY IA
3. Use of Rotating ``Kinetic'' Beds
NO RECOMMENDATION for the use of continuous lateral rotational
therapy (i.e., placing patients on ``kinetic'' beds that turn on their
longitudinal axes continuously and slowly) for prevention of nosocomial
pneumonia in patients in the ICU, critically ill patients, or patients
immobilized by illness and/or trauma.^{327-332
UNRESOLVED ISSUE

Prevention and Control of Legionnaires' Disease

I. Staff Education and Infection Surveillance

A. Staff Education

Educate (1) physicians and nurses to heighten their suspicion for
cases of nosocomial Legionnaires' disease and to use appropriate
methods for its diagnosis, and (2) patient-care, infection-control, and
engineering personnel about measures to control nosocomial
legionellosis.^{611-613
CATEGORY IA

B. Surveillance

1. Establish mechanism(s) to provide clinicians with appropriate
laboratory tests for the diagnosis of Legionnaires'
disease.^{339,367,368,372,654
CATEGORY IA
2. Conduct active search for cases of nosocomial Legionnaires'
disease, especially in patients who are at high-risk of acquiring the
disease (patients who are immunosuppressed, including organ-transplant
patients, patients with AIDS, and patients receiving systemic steroids;
are 65 years of age; or have chronic underlying disease such
as diabetes mellitus, congestive heart failure, and chronic obstructive
lung disease).^{338,339,353,355-359,365 Refer to the accompanying
background document for definition of nosocomial legionellosis.
CATEGORY II
3. NO RECOMMENDATION for routinely culturing water systems for
Legionella spp.^{250,338,383,387-389,391-393,408,655
UNRESOLVED ISSUE

II. Interruption of Transmission of Legionella SPP.

A. Primary Prevention (Preventing Nosocomial Legionnaires' Disease When
No Cases Have Been Documented)

1. Nebulization and Other Devices
a. Use only sterile (not distilled, nonsterile) water for rinsing
nebulization devices and other respiratory-care equipment after they
have been cleaned and/or disinfected.^{250,656
CATEGORY IB
b. Use only sterile (not distilled, nonsterile) water to fill
reservoirs of devices used for nebulization.^{227,236,250,378,656
CATEGORY IA
c. Do not use large-volume room-air humidifiers that create
aerosols (e.g., by venturi principle, ultrasound, or spinning disk) and
thus are really nebulizers, unless they can be sterilized or subjected
to high-level disinfection daily and filled only with sterile
water.^{236,656
CATEGORY IA
2. Cooling Towers
a. When a new hospital building is constructed, place cooling
tower(s) in such a way that the tower drift is directed away from the
hospital's air-intake system, and design the cooling towers such that
the volume of aerosol drift is minimized.^{375,657
CATEGORY IB
b. For operational cooling towers, install drift eliminators,
regularly use an effective biocide, maintain the tower according to
manufacturers' recommendations, and keep adequate maintenance
records.^{375,415,658
CATEGORY IB
3. Water-Distribution System
a. NO RECOMMENDATION for routinely maintaining potable water at the
outlet at 50 deg.C or <20 deg.C, or chlorinating heated
water to achieve 1-2 mg/L free residual chlorine at the
tap.^{338,383,393,400-403
UNRESOLVED ISSUE
b. NO RECOMMENDATION for treatment of water with ozone, ultraviolet
light, or heavy-metal ions.^{344,411,412,414
UNRESOLVED ISSUE

B. Secondary Prevention (Response to Identification of Laboratory-
Confirmed Nosocomial Legionellosis)

When a single case of laboratory-confirmed, definite nosocomial
Legionnaires' disease is identified, OR if two or more cases of
laboratory-confirmed, possible nosocomial Legionnaires' disease occur
within 6 months of each other (Refer to background document for
definition of definite and possible nosocomial Legionnaires' disease.):
1. Contact the local or state health department or the CDC for
consultation.
CATEGORY IB
2. If a case is identified in a severely immunocompromised patient
such as an organ-transplant recipient, OR if the hospital houses
severely immunocompromised patients, conduct a combined epidemiologic
and environmental investigation (as outlined from II-B-3-b-1 through
II-B-5, below) to determine the source(s) of Legionella sp.
CATEGORY IB
3. If the hospital does not house severely immunocompromised
patients, conduct an epidemiologic investigation via a retrospective
review of microbiologic, serologic, and postmortem data, and an
intensive prospective surveillance for additional cases of nosocomial
Legionnaires' disease.
CATEGORY IB
a. If there is no evidence of continued nosocomial transmission,
continue the intensive prospective surveillance (as in II-B-3, above)
for at least 2 months after surveillance was begun.
CATEGORY II
b. If there is evidence of continued transmission:
(1) Conduct an environmental investigation to determine the
source(s) of Legionella sp. by collecting water samples from potential
sources of aerosolized water, following the methods described in
Appendix C and saving and subtyping isolates of Legionella spp.
obtained from patients and environment.^{227,375-382,404,406
CATEGORY IB
(2) If a source is not identified, continue surveillance for new
cases for at least 2 months, and, depending on the scope of the
outbreak, decide on either deferring decontamination pending
identification of the source(s) of Legionella spp., or proceeding with
decontamination of the hospital's water distribution system, with
special attention to the specific hospital areas involved in the
outbreak.
CATEGORY II
(3) If a source of infection is identified by epidemiologic and
environmental investigation, promptly decontaminate it.^{417
CATEGORY IB
(a) If the heated-water system is implicated:
i. Decontaminate the heated-water system either by superheating
(flushing for at least 5 minutes each distal outlet of the system with
water at 65 deg.C), OR by hyperchlorination (flushing for at
least 5 minutes all outlets of the system with water containing
10 mg/L free residual chlorine).^{403,408-410 Post
warning signs at each outlet being flushed to prevent scald injury to
patients, staff, or visitors.
CATEGORY IB
ii. Depending on local and state regulations regarding potable-
water temperature in public buildings, maintain potable water at the
outlet at 50 deg.C or <20 deg.C, or chlorinate heated water
to achieve 1-2 mg/L free residual chlorine at the tap in hospitals
housing patients who are at high risk of acquiring nosocomial
legionellosis (e.g., immunocompromised patients).^{338,383,393,400-
403 (See appendix B.)
CATEGORY II
iii. NO RECOMMENDATION for treatment of water with ozone,
ultraviolet light, or heavy-metal ions.^{344,411,412,414
UNRESOLVED ISSUE
iv. Clean hot-water storage tanks and water-heaters to remove
accumulated scale and sediment.^{346
CATEGORY IB
v. Restrict immunocompromised patients from taking showers, and use
only sterile water for their oral consumption until Legionella spp.
becomes undetectable by culture in the hospital water.^{384
CATEGORY II
(b) If cooling towers or evaporative condensers are implicated,
decontaminate the cooling-tower system using the protocol outlined in
Appendix D.^{415
CATEGORY IB
(4) Assess the efficacy of implemented measures in reducing or
eliminating Legionella spp. by collecting specimens for culture at 2-
week intervals for 3 months.
CATEGORY II
(a) If Legionella sp. is not detected in cultures during 3 months
of monitoring, collect cultures monthly for another 3 months.
CATEGORY II
(b) If Legionella sp. is detected in one or more cultures, reassess
the implemented control measures, modify them accordingly, and repeat
decontamination procedures. Options for repeat decontamination include
the intensive use of the same technique utilized for initial
decontamination, or a combination of superheating and
hyperchlorination.
CATEGORY II
(5) Keep adequate records of all infection control measures,
including maintenance procedures, and of environmental test results for
cooling towers and potable-water systems.
CATEGORY II

Prevention and Control of Nosocomial Pulmonary Aspergillosis

I. Staff Education and Infection Surveillance

A. Staff Education

Educate healthcare workers regarding nosocomial pulmonary
aspergillosis especially in immunocompromised patients, and about
infection control procedures to decrease its occurrence.^{611-613
CATEGORY IA

B. Surveillance

1. Maintain a high index of suspicion for diagnosis of nosocomial
pulmonary aspergillosis in high-risk patients (i.e., patients with
prolonged, severe granulocytopenia [<1,000 polymorphonuclear cells/
mm^{3 for 2 weeks or <100 polymorphonuclear cells/mm^{3 for 1
week]), such as organ-transplant recipients or patients with
hematologic malignancies who are receiving
chemotherapy.^{435,462,463,659
CATEGORY IB
2. Maintain surveillance for cases of nosocomial pulmonary
aspergillosis by periodically reviewing the hospital's microbiologic,
histopathologic, and postmortem data.
CATEGORY IB
3. NO RECOMMENDATION for routine, periodic culturing of the
nasopharynx of high-risk patients,^{437,438 or devices, air samples,
dust, ventilation ducts, and filters in rooms occupied by high-risk
patients.^{418,428,437,471-473
UNRESOLVED ISSUE

II. Interruption of Transmission of Aspergillus SPP. Spores

A. Planning New Specialized-Care Units for High-Risk Patients

1. When constructing new specialized-care units for high-risk
patients, ensure that patient rooms have adequate capacity to minimize
fungal spore counts via maintenance of (a) high-efficiency air
filtration, (b) directed room airflow, (c) positive air pressure in
patient's room in relation to the corridor, (d) properly sealed room,
and (e) high rates of room-air changes.^{424,479-481,484,488,660,661
CATEGORY IB
a. Air Filtration
Install high efficiency particulate air (HEPA) filters that are
99.97% efficient in filtering 0.3u-sized particles, at the point of
use, i.e. at the room-air intake site.^{424,479-481,484,488,660,661
CATEGORY IB
b. Directed Room Airflow
Place air-intake and exhaust ports such that room air comes in from
one side of the room, flows across the patient's bed, and exits on the
opposite side of the room. In addition, place intake and exhaust ports
such that healthcare personnel entering the room to care for the
patient would stand between the patient and the exhaust
port.^{480,481
CATEGORY IB
c. Well-Sealed Room
Construct windows, doors, and intake and exhaust ports to achieve
complete sealing of the room against air leaks.^{480,481
CATEGORY IB
d. Room-Air Pressure
Ensure that room-air pressure can be maintained continuously above
that of corridor, e.g., as can be demonstrated by performance of the
smoke-tube test, unless there are clinical-care or infection-control
contraindications to do so.^{480,481
CATEGORY IB
(1) To maintain positive room-air pressure in relation to the
corridor, supply room air at a rate that is 10-20% more than the rate
of exhausting air from the room.^{480,481
CATEGORY IB
(2) Construct rooms that have an anteroom with an independent
exhaust for placement of patients at high risk of aspergillosis who
also have an infection (e.g., varicella or infectious tuberculosis)
requiring negative room-air pressure in relation to the
corridor.^{480
CATEGORY IB
e. Room-Air Changes
Maintain room-air changes at 15 per
hour.^{480,486,487
CATEGORY II
2. NO RECOMMENDATION for the preferential installation of a
particular system, such as one with ultra-high (100-400 per hour) air
change rates, e.g., laminar airflow, over other systems that meet the
conditions in II-A-1-a through II-A-1-e above.^{424,479-
481,484,488,660,661
UNRESOLVED ISSUE
3. Formulate hospital policies to minimize exposures of high-risk
patients to potential sources of Aspergillus spp., such as hospital
construction and renovation, cleaning activities, carpets, food, potted
plants, and flower arrangements.^{418,437,662-664
CATEGORY IB
4. NO RECOMMENDATION for prophylactic use of copper-8-quinolinolate
biocide in fireproofing material.^{418,427,481,488
UNRESOLVED ISSUE

B. In Existing Facilities With No Cases of Nosocomial Aspergillosis

1. Place high-risk patients in protected environment that meets the
conditions outlined in Section II-A-1-a through II-A-1-e
above.^{424,437,479,488,660,661,665
CATEGORY IB
2. Routinely inspect air-handling systems in high-risk patient-care
areas, maintain adequate air exchanges and pressure differentials, and
eliminate air leakages. Coordinate repairs of the system with
relocation of high-risk patients to other areas with optimal air-
handling capabilities.^{418,428,437
CATEGORY IB
3. Minimize the time high-risk patients spend outside their rooms
for diagnostic procedures and other activities; and when high-risk
patients leave their rooms, require them to wear well-fitting masks
capable of filtering Aspergillus spp. spores.
CATEGORY IB
4. Regularly clean ceiling tiles, air-duct grates, and other
surfaces in patient rooms to prevent dust accumulation, and maintain
adequate seals on windows to prevent room infiltration by outside air,
especially in areas occupied by patients at high-risk for developing
aspergillosis. Conduct such cleaning when the rooms are not occupied by
patients.^{437
CATEGORY IB
5. Systematically review and coordinate infection-control
strategies with personnel in charge of hospital engineering,
maintenance, central supply and distribution, and catering.^{418,473
CATEGORY IB
6. When planning hospital construction and renovation activities,
assess whether patients at high-risk for aspergillosis are likely to be
exposed to high ambient-air spore counts of Aspergillus spp. from
construction and renovation sites, and develop a plan to prevent such
exposures.^{418,473
CATEGORY IB
7. During construction or renovation activities:
(a) Construct barriers between patient-care and construction areas
to prevent dust from entering patient-care areas; these barriers (e.g.,
plastic or drywall) should be impermeable to Aspergillus
spp.^{418,428,472,473
CATEGORY IB
(b) In construction/renovation areas inside the hospital, create
and maintain negative pressure relative to that in adjacent patient-
care areas if there are no contraindications for such pressure
differential, e.g., there are patients with infectious tuberculosis in
the adjacent patient-care areas.^{418,428,472,473,488
CATEGORY II
(c) Direct pedestrian traffic from construction areas away from
patient-care areas to limit opening and closing of doors (or other
barriers) that may cause dust dispersion, entry of contaminated air, or
tracking of dust into patient areas.^{418,428,472,473
CATEGORY IB
(d) Clean newly constructed areas before allowing patients to enter
the areas.^{418,473
CATEGORY IB
8. Eliminate exposures of patients at high-risk for aspergillosis
to activities, such as floor or carpet vacuuming, that may cause spores
of Aspergillus spp. and other fungi to be aerosolized.^{418,437,473
CATEGORY IB
9. Eliminate exposures of patients at high-risk for aspergillosis
to potential environmental sources of Aspergillus spp., such as
Aspergillus-contaminated food, potted plants, or flower
arrangements.^{418,437,473,662-664
CATEGORY II
10. Prevent birds from gaining access to hospital air-intake
ducts.^{474
CATEGORY IB

C. When a Case of Nosocomial Aspergillosis Occurs

1. Begin a prospective search for additional cases in hospitalized
patients and an intensified retrospective review of the hospital's
microbiologic, histopathologic, and postmortem records.
CATEGORY IB
2. If there is no evidence of continuing transmission, continue
routine maintenance procedures to prevent nosocomial aspergillosis, as
in Section II-B-1 through II-B-10 above.
CATEGORY IB
3. If evidence of continuing Aspergillus spp. infection exists,
conduct an environmental investigation to determine and eliminate the
source.^{424,427,428,472,484,488
CATEGORY IB
a. Collect environmental samples from potential sources of
Aspergillus spp., especially those sources implicated in the
epidemiologic investigation, by using appropriate
methods,^{424,427,428,472,484,488,666 e.g., use of a high-volume air
sampler rather than settle plates.^{424
CATEGORY IB
b. Perform molecular subtyping of Aspergillus spp. obtained from
patients and the environment to establish strain identity.^{476,477
CATEGORY IB
c. If air-handling systems supplying high-risk patient-care areas
are not optimal, consider temporary deployment of portable HEPA filters
until rooms with optimal air-handling systems are available for all
patients at high risk of invasive aspergillosis.^{469
CATEGORY II
d. If an environmental source is identified, perform corrective
measures as needed to eliminate the source from the high-risk patients'
environment.
CATEGORY IB
e. If an environmental source is not identified, review existing
infection-control measures, including engineering aspects, to identify
potential areas that can be corrected or improved.
CATEGORY IB

III. Modifying Host Risk for Infection

A. Administer cytokines, including granulocyte colony-stimulating
factor and granulocyte-macrophage stimulating factor, to increase host
resistance to aspergillosis by decreasing the duration and severity of
chemotherapy-induced granulocytopenia.^{464,465
CATEGORY II
B. NO RECOMMENDATION for administration of intranasal amphotericin
B or oral antifungal agents (including amphotericin B and triazole
compounds) in high-risk patients for prophylaxis against
aspergillosis.^{466,467,667
UNRESOLVED ISSUE

Prevention and Control of Respiratory Syncytial Virus Infection

(The principles and recommendations below are applicable for
prevention and control of nosocomial lower respiratory tract infections
due to adenovirus, parainfluenza virus and rhinovirus.)

I. Staff Education and Infection Surveillance

A. Staff Education

Educate personnel about the epidemiology, modes of transmission and
means of preventing spread of respiratory syncytial virus
(RSV).^{215,611-613
CATEGORY IA

B. Surveillance

1. Establish mechanism(s) by which the appropriate hospital
personnel are promptly alerted to any increase in RSV activity in the
local community.
CATEGORY IB
2. During periods of increased prevalence of RSV in the community
(and during December-March), attempt prompt diagnosis of RSV infection
by using rapid diagnostic techniques as clinically indicated in
pediatric patients, especially infants, and in immunocompromised adults
admitted to the hospital with respiratory illness.^{545,549
CATEGORY IB

II. Interruption of Transmission of RSV

A. Prevention of Person-to-Person Transmission

1. Primary Measures for Contact Isolation
a. Handwashing. Wash hands after contact with a patient, or after
touching respiratory secretions or fomites potentially contaminated
with respiratory secretions, whether or not gloves are
worn.^{207,503,524-526,547
CATEGORY IA
b. Gloving. (1) Wear gloves for handling patients or respiratory
secretions of patients with proven or suspected RSV infection, or
fomites potentially contaminated with patient
secretions.^{215,503,524,525,543,549
CATEGORY IA
(2) Change gloves between patients, or after handling respiratory
secretions or fomites contaminated with secretions from one patient
before contact with another patient.^{215,217 Wash hands after
removing gloves. (See II-A-1-a, above.)
CATEGORY IA
c. Gowning. Wear a gown when soiling with respiratory secretions
from a patient is anticipated, e.g., when handling infants with RSV
infection or other viral respiratory illness, and change the gown after
such contact and before caring for another patient.^{215,542,544,549
CATEGORY IB
d. Staffing. Restrict healthcare workers in the acute stages of an
upper respiratory illness, i.e., those who are sneezing and/or
coughing, from taking care of RSV-uninfected infants and other patients
at high risk for complications from RSV infection, e.g., children with
severe underlying cardio-pulmonary conditions, children receiving
chemotherapy for malignancy, and patients who are otherwise
immunocompromised.^{547,549
CATEGORY IB
e. Limiting Visitors. Do not allow persons with symptoms of
respiratory infection to visit uninfected pediatric, immunosuppressed,
and cardiac patients.^{543
CATEGORY II
2. Control of RSV Outbreaks
a. Use of Private Room, Cohorting, and Patient-Screening
To control ongoing RSV transmission in the hospital, admit young
children with symptoms of viral respiratory illness to single rooms
when possible, OR perform RSV-screening diagnostic tests on young
children upon admission and cohort them according to their RSV-
infection status.^{543,545,547,549
CATEGORY II
b. Personnel Cohorting
During an outbreak of nosocomial RSV, cohort personnel as much as
practical, i.e., restrict personnel who give care to infected patients
from giving care to uninfected patients, and vice-
versa.^{543,547,549
CATEGORY II
c. Postponing Patient Admission
During outbreaks of nosocomial RSV, postpone elective admission of
uninfected patients at high risk of complications from RSV infection.
CATEGORY II
d. Wearing Eye-Nose Goggles
NO RECOMMENDATION for wearing eye-nose goggles for close contact
with an RSV-infected patient.^{546,550
UNRESOLVED ISSUE

Prevention and Control of Influenza

I. Staff Education and Infection Surveillance

A. Staff Education

Educate personnel about the epidemiology, modes of transmission and
means of preventing the spread of influenza.^{611-613,668,669
CATEGORY IA

B. Surveillance

1. Establish mechanism(s) by which the appropriate hospital
personnel are promptly alerted of any increase in influenza activity in
the local community.
CATEGORY IB
2. Arrange for laboratory tests to be available to clinicians, for
use when clinically indicated, to promptly confirm the diagnosis of
influenza and other acute viral respiratory illnesses, especially
during November-April.^{573-578
CATEGORY IB

II. Modifying Host Risk to Infection

A. Vaccination

1. Patients
Offer vaccine to outpatients and inpatients at high risk of
complications from influenza, beginning in September and continuing
until influenza activity has begun to decline.^{581,584,603,670-672
Patients at high risk of complications from influenza include those
65 years of age; in long-term-care units; with chronic
disorders of the pulmonary or cardiovascular systems, diabetes
mellitus, renal dysfunction, hemoglobinopathies, musculo-skeletal
disorders that impede adequate respiration, or immunosuppression; and
children 6 months-18 years of age who are receiving long-term aspirin
therapy.^{581
CATEGORY IA
2. Personnel
Vaccinate healthcare workers before the influenza season each year,
preferably between mid-October and mid-November. Until influenza
activity declines, continue to make vaccine available to newly hired
personnel and to those who initially refuse vaccination. If vaccine
supply is limited, give highest priority to staff caring for patients
at greatest risk of severe complications from influenza infection, as
listed in Section II-A-1 above.^{581
CATEGORY IB

B. Use of Antiviral Agents (See Section IV Below, Control of Influenza
Outbreaks)

III. Interruption of (Person-to-Person) Transmission

A. Keep a patient for whom influenza is suspected or diagnosed in a
private room, or in a room with other patients with proven influenza,
unless there are medical contraindications to do so.
CATEGORY IB
B. As much as feasible, maintain negative air pressure in rooms of
patients for whom influenza is suspected or diagnosed, or place
together persons with influenza-like illness in a hospital area with an
independent air-supply-and-exhaust system.^{566,567,569,673
CATEGORY II
C. Institute masking of individuals who enter the room of a patient
with influenza.^{566,567,673
CATEGORY IB
D. As much as possible during periods of influenza activity in the
community, remove patient-care staff who have symptoms of febrile upper
respiratory tract infection suggestive of influenza from duties that
involve direct patient contact.^{604,674
CATEGORY II
E. When community and/or nosocomial outbreaks are characterized by
high attack rates and severe illness:
1. Restrict hospital visitors who have a febrile respiratory
illness.
CATEGORY IB
2. Curtail or eliminate elective medical and surgical admissions as
necessary.
CATEGORY IB
3. Restrict cardiovascular and pulmonary surgery to only emergency
cases.
CATEGORY IB

IV. Control of Influenza Outbreaks

A. Determining the Outbreak Strain

Early in the outbreak, obtain nasopharyngeal-swab or nasal-wash
specimens from patients with symptoms suggestive of influenza for
influenza virus culture or antigen detection.
CATEGORY IB

B. Vaccination of Patients and Personnel

Administer current influenza vaccine to unvaccinated patients and
staff, especially if the outbreak occurs early in the influenza
season.^{562,581
CATEGORY IB

C. Amantadine or Rimantadine Administration

1. When a nosocomial outbreak of influenza A is suspected or
recognized:
a. Administer amantadine or rimantadine for prophylaxis to all
uninfected patients in the involved unit for whom it is not
contraindicated. Do not delay administration of amantadine or
rimantadine unless the results of diagnostic tests to identify the
infecting strain(s) can be obtained within 12 to 24 hours after
specimen collection.^{584,587
CATEGORY IB
b. Administer amantadine or rimantadine for prophylaxis to
unvaccinated staff members for whom it is not medically
contraindicated, and who are in the involved unit or taking care of
high-risk patients.^{584
CATEGORY II
2. Discontinue amantadine or rimantadine if laboratory tests
confirm or strongly suggest that influenza type A is not the cause of
the outbreak.^{585,602
CATEGORY IA
3. If the cause of the outbreak is confirmed or believed to be
influenza type A AND vaccine has been administered only recently to
susceptible patients and personnel, continue amantadine or rimantadine
prophylaxis until 2 weeks after the vaccination.^{675
CATEGORY IB
4. To the extent possible, do not allow contact between those at
high risk of complications from influenza and patients or staff who are
taking amantadine or rimantadine for treatment of acute respiratory
illness; prevent contact during and for two days after the latter
discontinue treatment.^{586,598-602
CATEGORY IB

D. Interruption of (Person-to-Person) Transmission (See Section III, A-
E Above.)

Table 1.--Microorganisms Isolated From Respiratory Tract Specimens Obtained by Various Representative Methods
From Adult Patients With a Diagnosis of Nosocomial Pneumonia
----------------------------------------------------------------------------------------------------------------
Schaber\4\ Bartlett\5\ Fagon\6\ Torres\7\
----------------------------------------------------------------------------------------------------------------
Hospital Type........... NNIS & UMH^{A........ Veterans........... General............ General.
Patients Studied:
Ventilated or Non- Mixed.............. Mixed.............. Ventilated......... Ventilated.
ventilated.
Number................ N/A^{B............... 159................ 49................. 78.
Number of episodes of N/A................ 159................ 52................. 78.
pneumonia.
Specimen(s) Cultured.... Sputum, Tracheal Transtracheal Protected Specimen Protected Specimen
Aspirate. Aspirate, Pleural Brushing. Brushing, Lung
Fluid, Blood. Aspirate, Pleural
Fluid, Blood.
Culture Results:
No organism isolated.. N/A................ 0.................. 0.................. 54%^{C.
Polymicrobial......... N/A................ 54%^{C............... 40%^{C............... 13%^{C.
Number of isolates.... 15,499............. 314................ 111................ N/A.

Aerobic Bacteria

Gram-Negative Bacilli. 50%^{D............... 46%^{E............... 75%^{E............... 16%^{F.
Pseudomonas aeruginosa 17%^{D............... 9%^{E................ 31%^{E............... 5%^{F.
Enterobacter sp....... 11................. 4.................. 2.................. 0.
Klebsiella sp......... 7.................. 23................. 4.................. 0.
E. coli............... 6.................. 14................. 8.................. 0.
Serratia sp........... 5.................. 0.................. 0.................. 1.
Proteus sp............ 3.................. 11................. 15................. 1.
Citrobacter sp........ 1.................. 0.................. 2.................. 0.
Acinetobacter N/A................ 0.................. 15................. 9.
calcoaceticus.
Others................ N/A................ 0.................. 10................. 0.
Haemophilus influenza... 6%^{D................ 17%^{E............... 10%^{E............... 0%^{F.
Legionella sp......... N/A................ N/A................ 2%^{E................ 2%^{F.
Gram-Positive Cocci..... 17%^{D............... 56%^{E............... 52%^{E............... 4%^{F.
Staphylococcus aureus. 16%^{D............... 25%^{E............... 33%^{E............... 2%^{F.
Streptococcus sp...... 1.................. 31................. 21................. 2.
Others................ 0.................. 0.................. 8.................. 0.
Anaerobes............... N/A................ 35%^{E............... 2%^{E................ 0.
Peptostreptococcus.... N/A................ 14%^{E............... N/A................ 0.
Fusobacterium sp...... N/A................ 10................. N/A................ 0.
Peptococcus sp........ N/A................ 11................. N/A................ 0.
Bacteroides N/A................ 9.................. N/A................ 0.
melaninogenicus.
Bacteroides fragilis.. N/A................ 8.................. N/A................ 0.
Fungi................... 4%^{D................ N/A................ 0.................. 1%^{F.
Aspergillus sp........ N/A................ N/A................ 0.................. 1%^{F.
Candida sp............ 4%^{D................ N/A................ 0.................. 0.
Viruses................. N/A................ N/A................ N/A................ N/A.
----------------------------------------------------------------------------------------------------------------
Legend:

^{ANNIS & UMH=National Nosocomial infection Surveillance System and University of Michigan Hospital.
^{BN/A=Not Applicable: Not tested or Not reported.
^{CPercent episodes.
^{DPercent isolates.
^{EPercent episodes (Percentages not additive due to polymicrobial etiology in some episodes).
^{FPercent patients with pure culture.

Note: Footnotes appear at the end of the document.

Table 2--Controlled Studies on Nosocomial Lower Respiratory Tract Infections and Other Associated Outcomes of Selective Decontamination of the Digestive Tract in Adult Patients With Mechanically Assisted Ventilation
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Lower respiratory tract infection Colonization or infection with Overall mortality in hospital Mean total number of days in ICU^{B
------------------------------------------------------------------ resistant^{A microorganisms -----------------------------------------------------------------------
Author Study patients Infection rate ------------------------------------
Diagnostic method ------------------------------------ SDD^{C (%) Controls (%) SDD^{C Controls
SDD^{C (%) Controls (%) SDD^{C (%) Controls (%)
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Stoutenbeek^{147 (1984)....... Trauma SDD=63; Controls=59.. Clinical & Radiologic;^{D TS^{E 8............... 59.............. ``No increase''. ``No increase''. 3............... 8............... Not reported.... Not reported.
culture.
Unertl^{148 (1987)............ General ICU SDD=19; Clinical & Radiologic;^{D..... 21.............. 70.............. 21^{F............. 20^{F............. 26.............. 30.............. 18^{G............. 23^{G.
Controls=20.
Ledingham^{149 (1988)......... General ICU SDD=163; Clinical & Radiologic;^{D..... 2............... 11.............. ``No increase''. ``No increase''. 24.............. 24.............. Not reported.... Not reported.
Controls=161.
Kerver^{150 (1988)............ Surgical ICU SDD=49; Clinical & Radiologic^{D...... 12.............. 85.............. ``Not recorded'' ``Not recorded'' 29.............. 32.............. 17.............. 20
Controls=47. IR^{H=4........... IR^{H=17..........
Ulrich^{151 (1989)............ General ICU SDD=48; Clinical & Radiologic;^{D TS^{E 15.............. 50.............. GP=78^{I.......... GP=44^{I.......... 31.............. 54.............. 17.............. 13.
Controls=52. culture. GN=3^{J........... GN=2^{J........... IR^{H=0........... IR^{H=15..........
Brun-Buisson^{152 (1989)...... Medical ICU SDD=36; Clinical & Radiologic;^{D TS^{E 20.............. 22.............. 3^{F.............. 16^{F............. 22.............. 24.............. 14.............. 15.
Controls=50. PSB^{K culture. IR^{H=9........... IR^{H=10..........
Godard^{153 (1990)............ General ICU SDD=97; Clinical & Radiologic;^{D TS^{E 2............... 15.............. GN=15^{I.......... GN=15^{I.......... 12.............. 18.............. 11.............. 16.
Controls=84. & PSB^{K culture.
Rodriquez-Roldan^{154 (1990).. General ICU SDD=13; Clinical & Radiologic;^{D TS^{E Pn-0^{L........... Pn=73^{L.......... ``None noticed'' ``None noticed'' 30.............. 33.............. Not reported.... Not reported.
Controls=15. culture. TB=23^{M.......... TB=20^{M.......... IR^{H=0........... IR^{H=13..........
Flaherty^{155 (1990).......... Cardiac Surgery ICU SDD=51; Clinical & Radiologic;^{D..... 2............... 9............... GN=22^{N.......... GN=21^{N.......... 0............... 2............... Not reported.... Not reported.
Controls=56.
McClelland^{156 (1990)........ Renal & Respiratory Failure TS^{E culture................. 7............... 50.............. Not reported.... ``Not reported'' 60.............. 58.............. Not reported.... Not reported.
SDD=15; Controls=12. IR^{H=27.......... IR^{H=8...........
Tetteroo^{157 (1990).......... Esophageal Resection SDD=56; Clinical & Radiologic;^{D 2............... 14.............. 2^{F.............. 4^{F.............. 5............... 4............... 6............... 5.
Controls=56. Culture of Bronchial IR^{H=4........... ir^{H=0...........
Aspirate.
Pugin^{158 (1991)............. Surgical ICU SDD=25; Clinical & Radiologic;^{D TS^{E 16.............. 78.............. ``No New ``No New 28.............. 26.............. 13.............. 15.
Controls=27. culture. antibiotic antibiotic
resistance''. resistance''.
Aerdts^{159 (1991)............ General ICU SDD=17; Controls- Clinical & Radiologic;^{D TS^{E 6............... A=78............ ``Not observed'' ``Not observed'' 12.............. A=22............ 23.............. A=30
A=18^{N Controls-B=21^{O. culture. B=62............ IR^{H=6........... IR^{H=11.......... B=25.
B=10............
IR^{H=0...........
Hartenauer^{160 (1991)........ Surgical ICU ICU-1: SDD=50; Clinical & Radiologic;^{D TS^{E ICU-1; 10....... 46.............. S=34^{Q........... S=33^{Q........... 38.............. 48.............. 12.............. 13.
Controls=61 ICU-2: SDD=49 culture. ICU-2: 10....... 45.............. GN=0^{N........... GN=0^{N........... IR^{H=8........... IR^{H=21.......... 13.............. 17.
Controls=40. S=37^{Q........... S=37^{Q........... 31.............. 43..............
GN=0^{N........... GN=0^{N........... IR^{H=6........... IR^{H=25..........
Fox^{161 (1991)............... Cardiac Bypass SDD=12; TS^{E culture................. 66.............. 50.............. Not reported.... Not reported.... 17.............. 66.............. 12.............. 12.
Controls=12.
Blair^{162 (1991)............. General ICU SDD=126; Clinical & Radiologic;^{D..... 10.............. 35.............. ``No evidence of ``No evidence of 14.............. 19.............. 8............... 8.
Controls=130. increased increased
resistance''. resistance''.
Vandenbroucke-Grauls^{163 ICUs (Pooled data)^{R SDD- Clinical & Radiologic;^{D TS^{E A=7............. A=28............ ``No increase in ``No increase in A=25............ A=26............ Not reported.... Not reported.
(1991). A=488; Controls-A culture. B=8............. B=45............ resistant resistant B=21............ B=26............
(Historical)=540 SDD-B=225; microorganisms microorganisms
Control-B (Random)=266. in 10 of 11 in 10 of 11
studies''. studies''.
Winter^{164 (1992)............ General ICU SDD=91; Control- Clinical & Radiologic;^{D BAL^{S 3............... A=11............ 1-8^{T............ A=1-7^{T.......... 36.............. A=43............ 6............... A=7.
A=84; Controls-B=92. culture. B=23............ B=1-17^{T......... B=43............ B=8.
Ferrer^{165 (1992)............ General ICU SDD+22; Clinical & Radiologic;^{D TS^{E 27.............. 32.............. Not reported^{U... Not reported^{U... 32.............. 23.............. 18.............. 15.
Controls=22. Culture.
Hammond^{166 (1992)........... General ICU SDD=114; Clinical & Radiologic;^{D TS^{E Pn=15^{L.......... Pn=15^{L.......... Not reported^{V... Not reported^{V... 18.............. 17.............. 16.............. 17.
Controls=125. ^{culture. Br=6^{W........... Br=6^{W........... IR^{H=6........... IR^{H=6...........
Gastinne^{167 (1992).......... Medical ICU SDD=220; Clinical & Radiologic;^{D TS^{E 12.............. 15.............. Not reported.... Not reported.... 40.............. 36.............. 18.............. 19.
Controls=225. PSB^{K culture. 34^{X............. 34^{X.............
Cockerill^{168 (1992)......... Surgical and Medical ICUs Clinical & Radiologic;^{D Pn=5^{L........... Pn=16^{L.......... 16.............. 11.............. 15.............. 21.............. 10.............. 12.
SDD=75; Controls=75. TS^{E culture. TB=4^{M........... TB=5^{M...........
Korinek^{169 (1993)........... Neurosurgical ICU SDD=63; Clinical & Radiologic;^{D TS^{E 24.............. 42.............. ``No evidence of ``No evidence of 8............... 7............... 24.............. 29.
Controls=60. & PSB^{K culture. increased increased
resistance''. resistance''.
SDD Trialists^{170 (1993)..... ICUs (Pooled Data)^{R Variable.................... Odds Ratio= Odds Ratio= Not analyzed.... Not analyzed.... 27.............. 27.............. Not analyzed.... Not analyzed.
SDD=2047; Controls=2095. 0.37;^{Y 95% 0.37;^{Y 95% Odds Ratio=0.90; Odds Ratio=0.90;
CI^{Z.0.31-0.43^{. CI^{Z.0.31-0.43^{. 95% CI^{Z:0.79-104 95% CI^{Z:0.79-104
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Legend:

^{AResistant to at least one antimicrobial in the SDD regimen, during the study period.
^{BICU: Intensive care unit.
^{CSDD: Selective digestive tract decontamination.
^{DClinical criteria included temperature >38 deg.C, purulent bronchorrhea, WBC >(12,000-15,000/mm^{3) Radiologic criterion was evidence of new and progressive infiltrate(s).
^{ETS: Tracheal secretions.
^{FPercentage of patients infected or colonized with gram-positive (GP) and/or gram-negative bacillary (GN) organisms at any body site.
^{GMedian.
^{HIR: Infection-related.
^{IPercentage of gram-positive (GP) isolates.
^{JPercentage of gram-negative bacillary (GN) isolates.
^{KPSB: Protected-specimen brushing.
^{LPn: Pneumonia.
^{MTB: Tracheo-bronchial infection.
^{NPercentage of patients with GN infection or colonization.
^{OPatients given penicillin (ampicillin, piperacillin or flucloxacillin) for clinical infection(s).
^{PPatients given cephalosporin (cephadrine, cefuroxime, or cefotaxime) for clinical infection(s).
^{QPercentage of patients with coagulase-negative staphylococcal infection or colonization.
^{RMeta-analysis.
^{SBAL: Broncho-alveolar lavage.
^{TPercentage of isolates.
^{UHowever, MRSA bronchial colonization occurred in 45% of SDD patients and 21% of controls.
^{VHowever, at 4 weeks, 13% and 5%, respectively, of oropharyngeal cultures of SDD and control patients had MRSA, and 41% of SDD and control patients were colonized with enterococci.
^{WBr: Bronchial infraction.
^{XIn ICU.
^{YComputed using data from 3,836 patients and 526 events, 260 in SDD- and 366 in control-patients.
^{ZCI: Confidence interval.

Note: Footnotes appear at the end of the document.

Table 3.--Risk Factors and Suggested Infection Control Measures for Prevention of Nosocomial Pneumonia
----------------------------------------------------------------------------------------------------------------
Infection control measures suggested to prevent nosocomial
Risk factors pneumonia
----------------------------------------------------------------------------------------------------------------
Bacterial Pneumonia:
Host-Related
Age (>65 years)
Underlying illness:
Chronic Obstructive Pulmonary Disease Good chest physiotherapy: incentive spirometry; positive end
(COPD). expiratory pressure or continuous positive airway pressure by face
mask.
Immunosuppression.................... Avoid exposure to potential nosocomial pathogens; decrease duration
of immunosuppression, such as by administration of granulocyte
macrophage colony stimulating factor (GMCSF).
Depressed consciousness.............. Caution on prescribing central nervous system depressants.
Surgery (thoracic/abdominal)......... Chest physiotherapy if with COPD; proper positioning; early
ambulation.
Device-Related........................... Proper cleaning, sterilization or disinfection, and handling of
devices; remove devices as soon as indication for their use
ceases.
Endotracheal intubation and Gentle suctioning of secretions; place patient in semirecumbent
Mechanical ventilation. position, i.e., 30 deg. head-elevation; use nonalkalinizing
gastric cytoprotective agent on patients at risk for stress
bleeding; changing ventilator circuits not more often than every
48 hours; draining and discarding inspiratory-tubing condensate,
or using heat-moisture exchanger if indicated.
Nasogastric-tube (NGT) placement and Use small-bore NGT; routinely verify appropriate tube placement;
Enteral feeding. promptly remove NGT. Avoid large-bolus feeding; drain residual.
Personnel- or Procedure-Related:
Cross-contamination by hands........... Educate and train personnel; adequate handwashing and appropriate
gloving; surveillance for cases of pneumonia, and feedback to
personnel.
Antibiotic administration.............. Prudent antibiotic use, especially on high-risk intensive-care unit
(ICU) patients.
Legionnaires' Disease:
Host-Related
Immunosuppression...................... Decrease duration of immunosuppression, such as by administration
of GMCSF.
Device-Related
Contaminated aerosol from devices...... Sterilize/disinfect aerosol-producing devices before use; use only
sterile water for respiratory humidifying devices; not using cool-
mist room-air ``humidifiers''.
Environment-Related
Aerosols from contaminated water supply Hyperchlorinate or superheat hospital water system; routine
maintenance of water-supply system; consider use of sterile water
for drinking by immunosuppressed patients.
Cooling-tower draft.................... Proper design, placement, and maintenance of cooling towers.
Aspergillosis:
Host-Related
Severe granulocytopenia................ Decrease duration of immunosuppression, such as by administration
of GMCSF; consider placing severely granulocytopenic patients in
protected environment.
Environment-Related
Construction activity.................. Remove granulocytopenic patients from vicinity of construction; if
not already done, placing severely granulocytopenic patients in
protected environment; mask severely granulocytopenic patients
when they leave protected environment.
Other environmental sources of Routine maintenance of hospital air-handling system and rooms of
aspergilli. immunosuppressed patients.
Respiratory Syncytial Virus Infection:
Host-Related
Age (<2 years) Congenital pulmonary/ Consider routine pre-admission screening of high-risk patients for
cardiac disease, Immunosuppression. severe RSV infection, followed by cohorting of patients and
nursing personnel during hospital outbreaks of RSV infection.
Personnel- or Procedure-Related
Cross-contamination by hands........... Personnel education; handwashing; gloving; gowning; during
outbreaks, use private rooms or cohort patients and nursing
personnel, and limit visitors.
Influenza:
Use private room or cohort infected patients.
Host-Related
Age (>65 years) Immunosuppression...... Vaccinate high-risk patients before the influenza season each year;
use amantadine or rimantadine for chemoprophylaxis during an
outbreak.
Personnel-Related
Infected personnel..................... Vaccinate personnel caring for high-risk patients, before the
influenza season each year; use amantadine or rimantadine for
prophylaxis during an outbreak.
----------------------------------------------------------------------------------------------------------------

BILLING CODE 4160-18-P

TN02FE94.004

BILLING CODE 4160-18-C

Appendix A--Semicritical Items Used on the Respiratory Tract

Air-pressure monitors
Anesthesia breathing circuits including:
inspiratory and expiratory tubings
y connectors
right-angle connectors
face mask
reservoir bags
Breathing circuits of mechanical ventilators
Bronchoscopes and their accessories
CO2 analyzers
Endotracheal and endobronchial tubes
Laryngoscope blades
Mouthpieces and tubings of pulmonary-function testing equipment
Oral and nasal airways
Resuscitation bags
Spirometers
Suction catheters

Appendix B--Maintenance Procedures to Decrease Survival and
Multiplication of Legionella SPP. In Potable-Water Distribution Systems

I. Providing water at 50 deg.C at all points in the heated
water system, including the taps

This requires that water in calorifiers (water heaters) be
maintained at 60 deg.C. In the United Kingdom, where
maintenance of water temperatures at 50 deg.C in hospitals
has been mandated, installation of blending or mixing valves at or near
taps to reduce the water temperature to 43 deg.C has been
recommended in certain settings to reduce the risk of scald injury to
patients, visitors, and health care workers.^{400 However,
Legionella spp. can multiply even in short segments of pipe containing
water at this temperature. Increasing the flow rate from the hot-water-
circulation system may help lessen the likelihood of water stagnation
and cooling.^{403,676 Insulation of plumbing to ensure delivery of
cold (<20 deg.C) water to water heaters (and to cold-water outlets) may
diminish the opportunity for bacterial multiplication.\345\ ``Dead
legs'' or capped spurs within the plumbing system provide areas of
stagnation and cooling to <50 deg.C regardless of the circulating-water
temperature; these segments may need to be removed to prevent
colonization.^{677 Rubber fittings within plumbing systems have been
associated with persistent colonization, and replacement of these
fittings may be required for Legionella spp. eradication.^{678

II. Continuous chlorination that maintains concentrations of free
residual chlorine at 1-2 mg/L at the tap

This requires flow-adjusted, continuous injectors of chlorine
throughout the water distribution system. Adverse effects of continuous
chlorination include accelerated corrosion of plumbing resulting in
system leaks and production of potentially carcinogenic
trihalomethanes. However, when levels of free residual chlorine are
below 3 mg/L, trihalomethane levels are kept below the maximum ``safety
level'' recommended by the Environmental Protection
Agency.^{401,679,680

Appendix C--Culturing Environmental Specimens for Legionella SPP

I. Recommended procedure for collecting and processing environmental
specimens for Legionella spp.

A. Collect water (if possible, one-liter samples) in sterile,
screw-top bottles, preferably containing sodium thiosulfate at a
concentration of 0.5 cc of 0.1N solution/liter of sample water. (Sodium
thiosulfate inactivates any residual halogen biocide).
B. Collect culture-swabs of the internal surfaces of faucets,
aerators, and showerheads; in a sterile, screw-top container such as a
50 cc plastic centrifuge tube, submerge each swab in 5-10 cc of sample
water taken from the same device from which the sample was obtained.
C. As soon as possible after collection, water samples and swabs
should be transported to and processed in a laboratory proficient at
culturing water specimens for Legionella spp. Samples may be
transported at room temperature but must be protected from temperature
extremes.
D. Test samples for the presence of Legionella spp. by culture onto
semi-selective media. Use standard laboratory procedures. (Detection of
Legionella spp. antigen by the direct fluorescent antibody technique is
not suitable for environmental samples.^{681-683 In addition, the
use of polymerase chain reaction (PCR) for identification of Legionella
spp. is not recommended until more data on the sensitivity and
specificity of this procedure are available.^{684)

II. Possible samples and sampling sites for Legionella spp. in the
hospital
Water Samples
Potable Water System
Incoming water main
Water softener
Holding tanks/cisterns
Water heater tanks (inflow and outflow sites)
Potable water outlets (faucets or taps, showers) especially outlets
located in or near case-patients' rooms
Cooling Tower/Evaporative Condenser
Make-up water (water added to system to replace water lost by
evaporation, drift, and leakage)
Basin (area under tower for collection of cooled water)
Sump (section of basin from which cooled water returns to heat
source)
Heat source (e.g., chillers)
Other Sources
Humidifiers
Bubblers for oxygen
Water used for respiratory therapy equipment
Decorative fountains
Irrigation equipment
Fire sprinkler system (if recently used)
Whirlpools/spas
Swabs
Potable Water System
Faucets (proximal to aerators)
Faucet aerators
Shower heads
Cooling Towers
Internal components (e.g., splash bars and other fill surfaces)
Areas with visible biofilm accumulation

Appendix D--Procedure for Cleaning Cooling Towers and Related Equipment

(Adapted from the Emergency Protocol in Control of Legionella spp. in
Cooling Towers: Summary Guidelines.^{415)
I. Preparatory to Chemical Disinfection and Mechanical Cleaning
A. Provide protective equipment to workers who would perform the
disinfection, to prevent their exposure to a) chemicals used for
disinfection, and b) aerosolized water containing Legionella spp.
Protective equipment may include full-length protective clothing,
boots, gloves, goggles, and a full- or half-face mask that combines
high efficiency particulate air filter and chemical cartridges to
protect against airborne chlorine levels of up to 10 mg/L.
B. Shut off cooling-tower.
1. If possible, shut off heat source.
2. Shut off fans, if present, on the cooling tower/evaporative
condenser (CT/EC).
3. Shut off the system blowdown (purge) valve. Shut off automated
blowdown controller, if present, and set system controller to manual.
4. Keep make-up water valves open.
5. Close building air-intake vents within at least 30 meters of the
CT/EC until after the cleaning procedure is complete.
6. Continue operating pumps for water circulation through the CT/
EC.
II. Chemical Disinfection
A. Add fast-release, chlorine-containing disinfectant in pellet,
granular, or liquid form, and follow instructions on the product label.
Examples of disinfectants are sodium hypochlorite (NaOCl) or calcium
hypochlorite (Ca(OCl)2, calculated to achieve initial FRC of 50
mg/L, i.e., 3.0 lbs (1.4 kg) industrial grade NaOCl (12-15% available
Cl) per 1,000 gallons of CT/EC water; 10.5 lbs (4.8 kg) domestic grade
NaOCl (3-5% available Cl) per 1,000 gallons of CT/EC water; or 0.6 lb
(0.3 kg) Ca(OCl)2 per 1,000 gallons of CT/EC water. (Other
appropriate compounds may be suggested by a water-treatment
specialist.) If significant biodeposits are present, add more chlorine.
If the water volume in CT/EC is unknown, estimate it (in gallons) to be
10x the recirculation rate in gallons/minute or 30x the refrigeration
capacity in tons.
B. Record type and quality of all chemicals used for disinfection,
exact time when chemicals are added to the system, and time and results
of measurements of free residual chlorine (FRC) and pH.
C. Within 15 minutes of adding disinfectant, add the dispersant by
first dissolving it in water and adding the resulting solution to a
turbulent zone in the water system. Examples of low or non-foaming,
silicate-based dispersants are: automatic-dishwasher compounds, such as
Cascade* or Calgonite* or an equivalent product. (Dispersants are added
at 10-25 lbs. (4.5-11.25 kg) per 1,000 gallons of CT/EC water.)

*Use of product names is for identification only and does not imply
endorsement by the Public Health Service or the U.S. Department of
Health and Human Services.

D. After adding disinfectant and dispersant, continue circulating the
water through the system. Monitor FRC with an FRC-measuring device,
e.g., a swimming pool test kit, and measure pH with a pH meter every 15
minutes for 2 hours. Add chlorine as needed to maintain FRC at
10 mg/L. Adjust pH to 7.5-8.0. The pH may be lowered by
using any acid (e.g., muriatic acid or sulfuric acid used for
maintenance of swimming pools) that is compatible with treatment
chemicals.
E. Two hours after adding disinfectant and dispersant or after FRC
level is stable at 10 mg/L, monitor at 2-hour intervals and
maintain FRC at 10 mg/L for 24 hours.
F. After FRC level is maintained at 10 mg/L for 24 hours,
drain the system. CT/EC water may be drained to the sanitary sewer.
Municipal water and sewerage authorities should be contacted regarding
local regulations. If a sanitary sewer is not available, consult local
or state authorities (e.g. Department of Natural Resources) regarding
disposal of water. If necessary, drain-off may be dechlorinated by
dissipation or chemical neutralization (i.e. with sodium bisulfite).
G. Refill system with water and repeat procedure outlined in steps 2-6.
III. Mechanical Cleaning
A. After water from the second chemical disinfection has been drained,
shut down the CT/EC.
B. Inspect all water contact areas for sediment, sludge, and scale.
Using brushes and/or a low-pressure water hose, thoroughly clean all
CT/EC water contact areas including basin, sump, fill, spray nozzles,
and fittings. Replace components as needed.
C. If possible, clean CT/EC water contact areas within the chillers.
IV. After Mechanical Cleaning
A. Fill system with water, and add chlorine to achieve FRC level of 10
mg/L.
B. Circulate water for one hour, then open blowdown valve and flush the
entire system until it is free of turbidity.
C. Drain system.
D. Open any air intake vents that were closed prior to cleaning.
E. Fill system with water. CT/EC may be put back into service using an
effective water-treatment program.

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