Draft Guideline for Prevention of Nosocomial Pneumonia: Part 1. ``Issues on Prevention of Nosocomial Pneumonia1994'' and Part 2. ``Recommendations for Prevention of Nosocomial Pneumonia''; Notice of Comment Period

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

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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\*

---------------------------------------------------------------------------

*Footnotes to appear at end of docket.

---------------------------------------------------------------------------

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-pBAL13,27,57,58 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

pH112,113 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 m 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

stomach103,\\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 preparation179-181 and elevated gastric

pH67,\\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 appropriate62

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 fluid227,\\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

insignificant125,257 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 humidifiers259 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 environments340,341 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 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 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

systems414 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 hospital416,417 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 (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 karyotyping476 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 hospital481 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 community541 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 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 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 [3 for 2 weeks or 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 & UMHA........ Veterans........... General............ General.

Patients Studied:

Ventilated or Non- Mixed.............. Mixed.............. Ventilated......... Ventilated.

ventilated.

Number................ N/AB............... 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 ICUB

------------------------------------------------------------------ resistantA microorganisms -----------------------------------------------------------------------

Author Study patients Infection rate ------------------------------------

Diagnostic method ------------------------------------ SDDC (%) Controls (%) SDDC Controls

SDDC (%) Controls (%) SDDC (%) Controls (%)

----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------

Stoutenbeek147 (1984)....... Trauma SDD=63; Controls=59.. Clinical & Radiologic;D TSE 8............... 59.............. ``No increase''. ``No increase''. 3............... 8............... Not reported.... Not reported.

culture.

Unertl148 (1987)............ General ICU SDD=19; Clinical & Radiologic;D..... 21.............. 70.............. 21F............. 20F............. 26.............. 30.............. 18G............. 23G.

Controls=20.

Ledingham149 (1988)......... General ICU SDD=163; Clinical & Radiologic;D..... 2............... 11.............. ``No increase''. ``No increase''. 24.............. 24.............. Not reported.... Not reported.

Controls=161.

Kerver150 (1988)............ Surgical ICU SDD=49; Clinical & RadiologicD...... 12.............. 85.............. ``Not recorded'' ``Not recorded'' 29.............. 32.............. 17.............. 20

Controls=47. IRH=4........... IRH=17..........

Ulrich151 (1989)............ General ICU SDD=48; Clinical & Radiologic;D TSE 15.............. 50.............. GP=78I.......... GP=44I.......... 31.............. 54.............. 17.............. 13.

Controls=52. culture. GN=3J........... GN=2J........... IRH=0........... IRH=15..........

Brun-Buisson152 (1989)...... Medical ICU SDD=36; Clinical & Radiologic;D TSE 20.............. 22.............. 3F.............. 16F............. 22.............. 24.............. 14.............. 15.

Controls=50. PSBK culture. IRH=9........... IRH=10..........

Godard153 (1990)............ General ICU SDD=97; Clinical & Radiologic;D TSE 2............... 15.............. GN=15I.......... GN=15I.......... 12.............. 18.............. 11.............. 16.

Controls=84. & PSBK culture.

Rodriquez-Roldan154 (1990).. General ICU SDD=13; Clinical & Radiologic;D TSE Pn-0L........... Pn=73L.......... ``None noticed'' ``None noticed'' 30.............. 33.............. Not reported.... Not reported.

Controls=15. culture. TB=23M.......... TB=20M.......... IRH=0........... IRH=13..........

Flaherty155 (1990).......... Cardiac Surgery ICU SDD=51; Clinical & Radiologic;D..... 2............... 9............... GN=22N.......... GN=21N.......... 0............... 2............... Not reported.... Not reported.

Controls=56.

McClelland156 (1990)........ Renal & Respiratory Failure TSE culture................. 7............... 50.............. Not reported.... ``Not reported'' 60.............. 58.............. Not reported.... Not reported.

SDD=15; Controls=12. IRH=27.......... IRH=8...........

Tetteroo157 (1990).......... Esophageal Resection SDD=56; Clinical & Radiologic;D 2............... 14.............. 2F.............. 4F.............. 5............... 4............... 6............... 5.

Controls=56. Culture of Bronchial IRH=4........... irH=0...........

Aspirate.

Pugin158 (1991)............. Surgical ICU SDD=25; Clinical & Radiologic;D TSE 16.............. 78.............. ``No New ``No New 28.............. 26.............. 13.............. 15.

Controls=27. culture. antibiotic antibiotic

resistance''. resistance''.

Aerdts159 (1991)............ General ICU SDD=17; Controls- Clinical & Radiologic;D TSE 6............... A=78............ ``Not observed'' ``Not observed'' 12.............. A=22............ 23.............. A=30

A=18N Controls-B=21O. culture. B=62............ IRH=6........... IRH=11.......... B=25.

B=10............

IRH=0...........

Hartenauer160 (1991)........ Surgical ICU ICU-1: SDD=50; Clinical & Radiologic;D TSE ICU-1; 10....... 46.............. S=34Q........... S=33Q........... 38.............. 48.............. 12.............. 13.

Controls=61 ICU-2: SDD=49 culture. ICU-2: 10....... 45.............. GN=0N........... GN=0N........... IRH=8........... IRH=21.......... 13.............. 17.

Controls=40. S=37Q........... S=37Q........... 31.............. 43..............

GN=0N........... GN=0N........... IRH=6........... IRH=25..........

Fox161 (1991)............... Cardiac Bypass SDD=12; TSE culture................. 66.............. 50.............. Not reported.... Not reported.... 17.............. 66.............. 12.............. 12.

Controls=12.

Blair162 (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-Grauls163 ICUs (Pooled data)R SDD- Clinical & Radiologic;D TSE 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''.

Winter164 (1992)............ General ICU SDD=91; Control- Clinical & Radiologic;D BALS 3............... A=11............ 1-8T............ A=1-7T.......... 36.............. A=43............ 6............... A=7.

A=84; Controls-B=92. culture. B=23............ B=1-17T......... B=43............ B=8.

Ferrer165 (1992)............ General ICU SDD+22; Clinical & Radiologic;D TSE 27.............. 32.............. Not reportedU... Not reportedU... 32.............. 23.............. 18.............. 15.

Controls=22. Culture.

Hammond166 (1992)........... General ICU SDD=114; Clinical & Radiologic;D TSE Pn=15L.......... Pn=15L.......... Not reportedV... Not reportedV... 18.............. 17.............. 16.............. 17.

Controls=125. culture. Br=6W........... Br=6W........... IRH=6........... IRH=6...........

Gastinne167 (1992).......... Medical ICU SDD=220; Clinical & Radiologic;D TSE 12.............. 15.............. Not reported.... Not reported.... 40.............. 36.............. 18.............. 19.

Controls=225. PSBK culture. 34X............. 34X.............

Cockerill168 (1992)......... Surgical and Medical ICUs Clinical & Radiologic;D Pn=5L........... Pn=16L.......... 16.............. 11.............. 15.............. 21.............. 10.............. 12.

SDD=75; Controls=75. TSE culture. TB=4M........... TB=5M...........

Korinek169 (1993)........... Neurosurgical ICU SDD=63; Clinical & Radiologic;D TSE 24.............. 42.............. ``No evidence of ``No evidence of 8............... 7............... 24.............. 29.

Controls=60. & PSBK culture. increased increased

resistance''. resistance''.

SDD Trialists170 (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;

CIZ.0.31-0.43. CIZ.0.31-0.43. 95% CIZ:0.79-104 95% CIZ: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/mm3) 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 pressur

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