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Summary This document updates and replaces CDC's previously published "Guideline for Prevention of Nosocomial Pneumonia" (Infect Control 1982;3:327-33, Respir Care 1983;28:221-32, and Am J Infect Control 1983;11:230-44). This revised guideline is designed to reduce the incidence of nosocomial pneumonia and is intended for use by personnel who are responsible for surveillance and control of infections in acute-care hospitals; the information may not be applicable in long-term-care facilities because of the unique characteristics of such settings. This 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 (e.g., respiratory syncytial virus {RSV} and influenza infections) have been expanded and updated. New sections on Legionnaires disease and pneumonia caused by Aspergillus sp. have been included. Lower respiratory tract infection caused by Mycobacterium tuberculosis is not addressed in this document. Part I, "An Overview of the Prevention of Nosocomial Pneumonia, 1994," provides the background information for the consensus recommendations of the Hospital Infection Control Practices Advisory Committee (HICPAC) in Part II, "Recommendations for Prevention of Nosocomial Pneumonia." Pneumonia is the second most common nosocomial infection in the United States and is associated with substantial morbidity and mortality. Most patients who have nosocomial pneumonia are infants, young children, and persons greater than 65 years of age; persons who have severe underlying disease, immunosuppression, depressed sensorium, and/or cardiopulmonary disease; and persons who have had thoracoabdominal surgery. Although patients receiving mechanically assisted ventilation do not represent a major proportion of patients who have nosocomial pneumonia, they are at highest risk for acquiring the infection. Most bacterial nosocomial pneumonias occur by aspiration of bacteria colonizing the oropharynx or upper gastrointestinal tract of the patient. Because intubation and mechanical ventilation alter first-line patient defenses, they greatly increase the risk for nosocomial bacterial pneumonia. Pneumonias caused by Legionella sp., Aspergillus sp., and influenza virus are often caused by inhalation of contaminated aerosols. RSV infection usually occurs after 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 being investigated involve reducing oropharyngeal and gastric colonization by pathogenic microorganisms. Part 1. An Overview of the Prevention of Nosocomial Pneumonia, 1994 INTRODUCTION This document updates and replaces CDC's previously published "Guideline for Prevention of Nosocomial Pneumonia" (Infect Control 1982;3:327-33, Respir Care 1983; 28:221-32, and Am J Infect Control 1983;11:230-44). This revised guideline is designed to reduce the incidence of nosocomial pneumonia and is intended for use by personnel who are responsible for surveillance and control of infections in acute-care hospitals; the information may not be applicable in long-term-care facilities because of the unique characteristics of such settings. This revised guideline addresses common problems encountered by infection-control practitioners regarding the prevention and control of nosocomial pneumonia in U.S. hospitals. Sections concerning 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 (e.g., respiratory syncytial virus {RSV} and influenza infections) have been expanded and updated. New sections on Legionnaires disease and pneumonia caused by Aspergillus sp. have been included. Lower respiratory tract infection caused by Mycobacterium tuberculosis is not addressed in this document; CDC published such recommendations previously (1). Part I, "An Overview of the Prevention of Nosocomial Pneumonia, 1994," provides the background information for the consensus recommendations of the Hospital Infection Control Practices Advisory Committee (HICPAC) in Part II, "Recommendations for Prevention of Nosocomial Pneumonia." HICPAC was established in 1991 to provide advice and guidance to the Secretary and the Assistant Secretary for Health, U.S. Department of Health and Human Services; the Director, CDC; and the Director, National Center for Infectious Diseases (NCID), CDC, regarding the practice of hospital infection control and strategies for surveillance, prevention, and control of nosocomial infections in U.S. hospitals. HICPAC also advises CDC on periodic updating of guidelines and other policy statements regarding prevention of nosocomial infections. This guideline is the first of a series of CDC guidelines being revised by HICPAC and NCID. This guideline can be an important resource for educating health-care workers (HCWs) regarding prevention and control of nosocomial respiratory tract infections. Because education of HCWs is the cornerstone of an effective infection-control program, hospitals should give high priority to continuing infection-control educational programs for these personnel. BACKGROUND Pneumonia is the second most common nosocomial infection in the United States and is associated with substantial morbidity and mortality. Most patients who have nosocomial pneumonia are infants, young children, and persons greater than 65 years of age; persons who have severe underlying disease, immunosuppression, depressed sensorium, and/or cardiopulmonary disease; and persons who have had thoracoabdominal surgery. Although patients receiving mechanically assisted ventilation do not represent a major proportion of patients who have nosocomial pneumonia, they are at highest risk for acquiring the infection. Most bacterial nosocomial pneumonias occur by aspiration of bacteria colonizing the oropharynx or upper gastrointestinal tract of the patient. Because intubation and mechanical ventilation alter first-line patient defenses, they greatly increase the risk for nosocomial bacterial pneumonia. Pneumonias caused by Legionella sp., Aspergillus sp., and influenza virus are often caused by inhalation of contaminated aerosols. RSV infection usually occurs after 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 HCWs, 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 being investigated involve reducing oropharyngeal and gastric colonization by pathogenic microorganisms. BACTERIAL PNEUMONIA
Epidemiology Results of the NNIS indicate that pneumonias (diagnosed on the basis of the CDC surveillance definition of nosocomial pneumonia) account for approximately 15% of all hospital-associated infections and are the second most common type of nosocomial infection after those of the urinary tract (2,61). In 1984, the overall incidence of lower respiratory tract infection was six cases per 1,000 discharged patients (2). The incidence per 1,000 discharged patients ranged from 4.2 cases in nonteaching hospitals to 7.7 in university-affiliated hospitals, 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 (62,63). In the Study of the Efficacy of Nosocomial Infection Control, which was conducted 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 patients who had thoracoabdominal procedures than for those who had procedures involving other body sites (63). More recent epidemiologic studies, including NNIS studies, have identified other subsets of patients at high risk for acquiring nosocomial bacterial pneumonia. Such patients include persons greater than 70 years of age; persons who have endotracheal intubation and/or mechanically assisted ventilation, a depressed level of consciousness (particularly those with closed-head injury), or underlying chronic lung disease; and persons who have previously had an episode of a large-volume aspiration. Other risk factors include 24-hour ventilator-circuit changes, hospitalization during the fall or winter, stress-bleeding prophylaxis with cimetidine (either with or without antacid), administration of antimicrobials, presence of a nasogastric tube, severe trauma, and recent bronchoscopy (6,34,35,64-74). The NNIS has stratified the incidence density of nosocomial pneumonia by patients' use of mechanical ventilation and type of intensive-care unit (ICU). From 1986 through 1990, the median rate of ventilator-associated pneumonia cases per 1,000 ventilator-days ranged from 4.7 cases in pediatric ICUs to 34.4 cases in burn ICUs (66). In comparison, the median rate of nonventilator-associated pneumonia cases per 1,000 ICU-days ranged from zero cases in pediatric and respiratory ICUs to 3.2 cases 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, the number of deaths attributed to pneumonia reflected 60% of all deaths resulting from nosocomial infections (17,35,74-80). Patients receiving mechanically assisted ventilation have higher mortality rates than do patients not receiving ventilation support; however, other factors (e.g., the patient's underlying disease{s} and organ failure) are stronger predictors of death in patients who have pneumonia (34,74). Analyses of pneumonia-associated morbidity have indicated that pneumonia could prolong hospitalization by 4-9 days (79-83); in the United States, a conservative estimate of the direct cost of this prolonged hospitalization is $1.2 billion per year (83). Nosocomial pneumonia is a major infection-control problem because of its reported frequency, associated high fatality rate, and attendant costs. IV. Pathogenesis Bacteria can 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 hypothesized recently 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, 45% of healthy adults were found to aspirate during sleep (84). Persons who swallow abnormally (e.g., those who have depressed consciousness, respiratory tract instrumentation and/or mechanically assisted ventilation, or gastrointestinal tract instrumentation or diseases) or who have just undergone surgery are particularly likely to aspirate (6,34,35,63,85-87). The high incidence of gram-negative bacillary pneumonia in hospitalized patients might result from factors that promote colonization of the pharynx by gram-negative bacilli and the subsequent entry of these organisms into the lower respiratory tract (33,88-91). Although aerobic gram-negative bacilli are recovered infrequently or are found in low numbers in pharyngeal cultures of healthy persons (88,92), the likelihood of colonization substantially increases in comatose patients, in patients treated with antimicrobial agents, and in patients who have hypotension, acidosis, azotemia, alcoholism, diabetes mellitus, leukocytosis, leukopenia, pulmonary disease, or nasogastric or endotracheal tubes in place (33,91,93,94). Oropharyngeal or tracheobronchial colonization by gram-negative bacilli begins with the adherence of the microorganisms to the host's epithelial cells (90,95-97). Adherence may be affected by multiple factors associated with the bacteria (e.g., presence of pili, cilia, capsule, or production of elastase or mucinase), host cell (e.g., surface proteins and polysaccharides), and environment (e.g., pH and presence of mucin in respiratory secretions) (89,90,95,98-107). Although the exact interactions between these factors have not been fully elucidated, studies indicate that certain substances (e.g., fibronectin) can inhibit the adherence of gram-negative bacilli to host cells (98,100,108). Conversely, certain conditions (e.g., malnutrition, severe illness, or postoperative state) can increase adherence of gram-negative bacteria (89,98,102,107,109). The stomach also might be an important reservoir of organisms that cause nosocomial pneumonia (34,110-114). The role of the stomach as such a reservoir might differ depending on the patient's underlying conditions and on prophylactic or therapeutic interventions (22,111,115-118). In healthy persons, few bacteria entering the stomach survive in the presence of hydrochloric acid at pH less than 2 (119,120). However, when gastric pH increases from the normal levels to greater than or equal to 4, microorganisms are able to multiply to high concentrations in the stomach (117,119,121-123). This can occur in elderly patients (121); in patients who have achlorhydria (119), ileus, or upper gastrointestinal disease; and in patients receiving enteral feeding, antacids, or histamine-2 {H-2} antagonists (111,117,118, 123-125). Other factors (e.g., duodeno-gastric reflux and the presence of bile) may contribute to gastric colonization in patients who have impaired intestinal motility; these other factors need further investigation (116). Bacteria also can enter the lower respiratory tract of hospitalized patients through inhalation of aerosols generated primarily by contaminated respiratory-therapy or anesthesia-breathing equipment (126-129). 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 less than 4 um via ultrasound, spinning disk, or the Venturi mechanism (126,129,130). 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 (126,130,131). Contaminated aerosol inhalation is particularly hazardous for intubated patients because endotracheal and tracheal tubes provide direct access to the lower respiratory tract. In contrast to nebulizers, bubble-through or wick humidifiers primarily 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 important (127,132); wick humidifiers do not generate aerosols. Bacterial pneumonia has resulted, in rare instances, 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 viable bacteria from the lumen of the gastrointestinal tract through epithelial mucosa to the mesenteric lymph nodes and to the lung, has been demonstrated in animal models (133). Translocation is postulated to occur in patients with immunosuppression, cancer, or burns (133); however, data are insufficient to describe this mechanism in humans (134). V. Risk Factors and Control Measures Several large studies have examined the potential risk factors for nosocomially acquired bacterial pneumonia (Table_2) (6,34,35,135, 136). Although specific risk factors have differed between study populations, they can be grouped into the following general categories:
LEGIONNAIRES DISEASE
Modes of Transmission Inhalation of aerosols of water contaminated with Legionella sp. might be the primary mechanism by which these organisms enter a patient's respiratory tract (382). 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 (11,241,258, 421-427). In other studies, aspiration of contaminated potable water or pharyngeal colonizers was proposed as the mode of transmission to certain patients (425,428-430). However, person-to-person transmission has not been observed. IV. Definition of Nosocomial Legionnaires Disease The incubation period for Legionnaires disease is usually 2-10 days (431); thus, for the purposes of this document and the accompanying HICPAC recommendations, laboratory-confirmed legionellosis that occurs in a patient who has been hospitalized continuously for greater than or equal to 10 days before the onset of illness is considered a definite case of nosocomial Legionnaires disease, and laboratory-confirmed infection that occurs 2-9 days after hospital admission is a possible case of the disease. V. Prevention and Control Measures
ASPERGILLOSIS
Diagnosis Diagnosing pneumonia caused by Aspergillus sp. is often difficult without performing invasive procedures. Although bronchoalveolar lavage has been a useful screening test (498-500), lung biopsy is still considered the most reliable technique (501). Histopathologic demonstration of tissue invasion by fungal hyphae has been required in addition to isolation of Aspergillus sp. from respiratory tract secretions because the latter, by itself, may indicate colonization (502). However, when Aspergillus sp. is grown from the sputum of a febrile, granulocytopenic patient who has a new pulmonary infiltrate, it is highly likely that the patient has pulmonary aspergillosis (495,503). Routine blood cultures are remarkably insensitive for detecting Aspergillus sp. (504), and systemic antibody responses in immunocompromised patients are probably unreliable indicators of infection (505-507). Antigen-based serologic assays are being developed in an attempt to allow for the rapid and specific diagnosis of Aspergillus sp. infections; however, the clinical usefulness of such assays has not been determined (508,509). IV. Risk Factors and Control Measures The primary risk factor for invasive aspergillosis is severe and prolonged granulocytopenia, both disease- and therapy-induced (510). Because bone-marrow-transplant recipients experience the most severe degree of granulocytopenia, they probably constitute the population at highest risk for developing invasive aspergillosis (490,511). The tendency of bone-marrow-transplant recipients to contract severe granulocytopenia (i.e., less than 1,000 polymorphonuclears/uL) is associated with the type of graft they receive. Although both autologous and allogeneic bone-marrow-transplant recipients are severely granulocytopenic for up to 4 weeks after the transplant procedure, acute or chronic graft-versus-host disease also could develop in allogeneic-transplant recipients. The latter might occur up to several months after the procedure, and the disease and/or its therapy (which often includes high doses of corticosteroids, cyclosporine, and other immunosuppressive agents) might result in severe granulocytopenia. Consequently, in developing strategies to prevent invasive Aspergillus sp. infection in bone-marrow-transplant recipients, infection-control personnel should consider exposures of the patient to the fungus both during and subsequent to the immediate post-transplantation period. After hospital discharge, patients (especially allogeneic-transplant recipients) might continue to manifest severe granulocytopenia and, therefore, are susceptible to fungal exposures at home and in ambulatory-care settings. To help address the problem of invasive aspergillosis in bone-marrow-transplant recipients, various studies are in progress to evaluate newer methods of a) enhancing host resistance to invasive fungal (and other) infections and b) 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 (466,512-515). For solid-organ transplant recipients, risk factors for invasive aspergillosis have not been studied as extensively. In one study of liver-transplant recipients, risk factors for invasive infection with Aspergillus sp. included preoperative and postoperative receipt of steroids and antimicrobial agents and prolonged duration of transplant surgery (516). The presence of aspergilli in the hospital environment is the most important extrinsic risk factor for opportunistic invasive Aspergillus sp. infection (517,518). Environmental disturbances caused by construction and/or renovation activities in and around hospitals markedly increase the airborne Aspergillus sp. spore counts in such hospitals and have been associated with nosocomial aspergillosis (476,478,479,519-522). Aspergillosis in immunosuppressed patients also has been associated with other hospital environmental reservoirs. Such reservoirs include contaminated fireproofing material, damp wood, and bird droppings in air ducts (478,523,524). A single case of nosocomial Aspergillus sp. 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 sp. can be identified (476,478,519-524). Previous investigations have demonstrated the importance of construction activities and/or fungal contamination of hospital air-handling systems as major sources for outbreaks (473,476,478,519-523). New molecular typing techniques (i.e., karyotyping {525} and DNA endonuclease profiling, which is now available for A. fumigatus {526}) may substantially aid in identifying the source of an outbreak. Outbreaks of invasive aspergillosis reinforce the importance of maintaining an environment as free as possible of Aspergillus sp. spores for patients who have severe granulocytopenia. To achieve this goal, specialized services in many large hospitals -- particularly bone-marrow transplant services -- have installed "protected environments" for the care of their high-risk, severely granulocytopenic patients and have 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 (476,478,519-523,527-532). Although the exact configuration and specifications of the protected environments might differ between hospitals, such patient-care areas are built to minimize fungal spore counts in air by maintaining a) filtration of incoming air by using central or point-of-use high- efficiency particulate air (HEPA) filters that are capable of removing 99.97% of particles greater than or equal to 0.3 um in diameter; b) directed room airflow (i.e., 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 greater than 400 per hour), although air-change rates at the higher levels might pose problems of patient comfort (473,528-530,532-534). The oldest and most studied protected environment is a room with laminar airflow. Such an environment consists of a bank of HEPA filters along an entire wall of the room; air is pumped by blowers through these filters and into the room at a uniform velocity (90 plus or minus 20 feet/minute), forcing the air to move in a laminar, or at least unidirectional, pattern (535). The air usually exits at the opposite end of the room, and ultra-high air-change rates (i.e., 100-400 air changes per hour) are achieved (473,527). The net effects are essentially sterile air in the room, minimal air turbulence, minimal opportunity for microorganism build-up, and a consistently clean environment (473). The laminar-airflow system is effective in decreasing or eliminating the risk for nosocomial aspergillosis in high-risk patients (473,528,532,534). However, such a system is costly to install and maintain. Less expensive alternative systems with lower air-change rates (i.e., 10-15 air changes per hour) have been used in some hospitals (529,530,536). However, studies comparing the efficacy of these alternative systems with laminar-airflow rooms in eliminating Aspergillus sp. spores and preventing nosocomial aspergillosis are limited. One hospital that employed cross-flow ventilation, point-of-use HEPA filters, and 15 air changes per hour reported that cases of nosocomial aspergillosis had occurred in patients housed in these rooms, although this rate was low (i.e., 3.4%) (530,536). However, these infections had been caused by A. flavus, a species that was not cultured from the room air, suggesting that the patients were probably exposed to fungal spores when they were allowed outside their rooms (530). Copper-8-quinolinolate was used on environmental surfaces contaminated with Aspergillus sp. to control one reported outbreak of aspergillosis (537), and it has been incorporated in the fireproofing material of a newly constructed hospital to help decrease the environmental spore burden (530); however, its general applicability has not been established. VIRAL PNEUMONIAS Viruses can be an important and often unappreciated cause of nosocomial pneumonia (538-540). In one prospective study of endemic nosocomial infections, approximately 20% of pneumonia cases resulted from viral infections (539). Although the early diagnosis and treatment of viral pneumonia infections have been possible in recent years (541-544), many hospitalized patients remain at high risk for developing severe and sometimes fatal viral pneumonia (538,545-552). These data and reports of well-documented outbreaks involving nosocomial viral transmission (553-556) indicate that measures to prevent viral transmission should be instituted. Nosocomial respiratory viral infections a) usually follow community outbreaks that occur during a particular period every year (555,557-560), b) confer only short-term immunity (561), c) affect both healthy and ill persons (547,548,554,562-564), and d) have exogenous sources. A number of viruses -- including adenoviruses, influenza virus, measles virus, parainfluenza viruses, RSV, rhinoviruses, and varicella-zoster virus -- can cause nosocomial pneumonia (548,555,556,565-571,572); however, adenoviruses, influenza viruses, parainfluenza viruses, and RSV reportedly have accounted for most (70%) nosocomial pneumonias caused by viruses (573). Influenza and RSV infections contribute substantially to the morbidity and mortality associated with viral pneumonia, and the epidemiology of both viral infections has been well researched; for these reasons, this section concerning viral pneumonias focuses on the principles of, and approaches to, the control of these two types of infection. Recommendations for preventing nosocomial pneumonia caused by infection with other viral pathogens were published previously (224). RSV INFECTION
Modes of Transmission RSV is present in large numbers in the respiratory secretions of symptomatic persons infected with the virus, and it can be transmitted directly via large droplets during close contact with such persons or indirectly via RSV-contaminated hands or fomites (553,583,584). The portal of entry is usually the conjunctiva or the nasal mucosa (585). Inoculation by RSV-contaminated hands is the usual way of depositing the virus onto the eyes or nose (553,583-585). Hands can become contaminated by handling either the respiratory secretions of infected persons or contaminated fomites (583,584). In nosocomial RSV outbreaks for which the viral isolates were typed, more than one strain of RSV often was identified (554,563,586), suggesting multiple sources of the virus. Potential sources include patients, HCWs, and visitors. Because infected infants shed large amounts of virus in their respiratory secretions and can easily contaminate their immediate surroundings, they are a major reservoir for RSV (587). HCWs might become infected after exposure in the community (588) or in the hospital and subsequently transmit infection to patients, other HCWs, or visitors (566,589). IV. Control Measures Different combinations of control measures, ranging from the simple to the complex, have been effective in varying degrees in preventing and controlling nosocomial RSV infection (226,589-596). Successful programs have shared two common elements: implementation of contact-isolation precautions and compliance with these precautions by HCWs. In theory, strict compliance with handwashing recommendations could prevent most nosocomial RSV infections; however, studies have indicated that such compliance among HCWs is poor (221,222). Thus, other preventive measures are usually necessary to prevent RSV infection. The wearing of gloves and gowns has been associated with decreased incidence of nosocomial RSV (226). The wearing of gloves has helped decrease transmission of RSV, probably because the gloves remind HCWs to comply with handwashing and other precautions and deter them from touching their eyes or nose. However, the benefits derived from wearing gloves are offset if the gloves are not changed after contact with an infected patient or with contaminated fomites and if hands are not washed adequately after glove removal (229). The wearing of both gloves and gowns during contact with RSV-infected infants or their immediate environment has been successful in preventing infection (226). In addition, the use of eye-nose goggles rather than masks has protected HCWs from infection; however, eye-nose goggles are not widely available and are inconvenient to wear (593,597). Additional measures may be indicated to control ongoing nosocomial transmission of RSV or to prevent transmission to patients at high risk for serious complications resulting from the infection (e.g., patients whose cardiac, pulmonary, or immune systems are compromised). The following additional control measures have been used in various combinations: a) using private rooms for infected patients OR cohorting infected patients, with or without preadmission screening by rapid laboratory diagnostic tests; b) cohorting HCWs; c) excluding HCWs who have symptoms of upper respiratory tract infection from caring for uninfected patients at high risk for severe or fatal RSV infection (e.g., infants); d) limiting visitors; and e) postponing admission of patients at high risk for complications from RSV infection (224,590, 592,594,596). Although the exact role of each of these measures has not been determined, their use for controlling RSV outbreaks seems prudent. INFLUENZA
Prevention and Control of Influenza The most effective measure for reducing the impact of influenza is the vaccination of persons at high risk for complications of the infection before the influenza season begins each year. High-risk persons include persons 6 months-18 years of age who are receiving long-term aspirin therapy and persons who either a) are greater than or equal to 65 years of age; b) are in long-term-care units; or c) have either chronic disorders of the pulmonary or cardiovascular systems, diabetes mellitus, renal dysfunction, hemoglobinopathies, or immunosuppression (611,626-628). Patients who have musculoskeletal disorders that impede adequate respiration also may be at high risk for complications resulting from influenza. When high vaccination rates are achieved in closed or semi-closed settings, the risk for outbreaks is reduced because of induction of herd immunity (629,630). When an institutional outbreak is caused by influenza type A, antiviral agents can be used both for treatment of ill persons and as prophylaxis for others (631). Two related antiviral agents, amantadine hydrochloride and rimantadine hydrochloride, are effective against influenza type A but not against influenza type B (543,632-634). These agents can be used in the following ways to prevent illness caused by influenza A virus: a) as short-term prophylaxis for high-risk persons after late vaccination; b) as prophylaxis for persons for whom vaccination is contraindicated; c) as prophylaxis for immunocompromised persons who might not produce protective levels of antibody in response to vaccination; d) as prophylaxis for unvaccinated HCWs who provide care to patients at high risk for infection, either for the duration of influenza activity in the community or until immunity develops after vaccination; and e) as prophylaxis when vaccine strains do not closely match the epidemic virus strain (631). Amantadine has been available in the United States for many years; rimantadine has been approved for use since 1993. Both drugs protect against all naturally occurring strains of influenza A virus; thus, antigenic changes in the virus that might reduce vaccine efficacy do not alter the effectiveness of amantadine or rimantadine. Both drugs are 70%-90% effective in preventing illness if administered before exposure to influenza A virus (632,635). In addition, they can reduce the severity and duration of illness caused by influenza A virus if administered within 24-48 hours after onset of symptoms (636,637). These drugs can limit nosocomial spread of influenza type A if they are administered to all or most patients when influenza type A illnesses begin in a facility (609,638,639). Compared with rimantadine, amantadine has been associated with a higher incidence of adverse central nervous system (CNS) reactions (e.g., mild and transitory nervousness, insomnia, impaired concentration, mood changes, and lightheadedness). These symptoms have been reported in 5%-10% of healthy young adults receiving 200 mg of amantadine per day (543,632). In the elderly, CNS side effects may be more severe; in addition, dizziness and ataxia occur more frequently among persons in this age group than among younger persons (640,641). Dose reductions of both amantadine and rimantadine are recommended for certain patients, such as persons greater than or equal to 65 years of age and/or those who have renal insufficiency. The drug package inserts for amantadine and rimantadine contain important information regarding administration of these drugs. Guidelines for the use of amantadine and rimantadine and considerations for the selection of these drugs were published previously by the Advisory Committee on Immunization Practices (ACIP) (631). The emergence of amantadine- and rimantadine-resistant strains of influenza A virus has been observed in persons who have received these drugs for treatment of the infection (642,643). Because of the potential risk for transmitting resistant viral strains to contacts of persons receiving amantadine or rimantadine for treatment (643,644), infected persons taking either drug should avoid, as much as possible, contact with others during treatment and for 2 days after discontinuing treatment (644,645). This is particularly important if the contacts are uninfected high-risk persons (644,646). The primary focus of efforts to prevent and control nosocomial influenza is the vaccination of high-risk patients and HCWs before the influenza season begins (628,647,648). The decision to use amantadine or rimantadine as an adjunct to vaccination in the prevention and control of nosocomial influenza is based partially on results of virologic and epidemiologic surveillance in the hospital and the community. When outbreaks of influenza type A occur in a hospital, and antiviral prophylaxis of high-risk persons and/or treatment of cases is undertaken, administration of amantadine or rimantadine should begin as early in the outbreak as possible to reduce transmission (609,638,631). Measures other than vaccination and chemoprophylaxis have been recommended for controlling nosocomial influenza outbreaks. Because influenza can be transmitted during contact with an infected person, the following procedures have been recommended: observing contact- isolation precautions, placing patients who have symptoms of influenza in private rooms, cohorting patients who have influenza-like illness, and wearing a mask when entering a room in which a person who has suspected or confirmed influenza is housed (224). Handwashing and the wearing of gloves and gowns by HCWs during the patient's symptomatic period also have been recommended; however, the exact role of these measures in preventing influenza transmission has not been determined (224,608,649). Although influenza can be transmitted via the airborne route, the efficacy of placing infected persons in rooms that have negative air pressure in relation to their immediate environment has not been assessed. In addition, this measure may be impractical during institutional outbreaks that occur during a community epidemic of influenza because many HCWs and newly admitted patients could be infected with the virus; thus, the hospital would face the logistical problem of accommodating all ill persons in rooms that have special ventilation. Although the effectiveness of the following measures has not been determined, their implementation could be considered during severe outbreaks: a) curtailment or elimination of elective admissions, both medical and surgical; b) restriction of cardiovascular and pulmonary surgery; c) restriction of hospital visitors, especially those who have acute respiratory illnesses; and d) restriction of HCWs who have an acute respiratory illness from the workplace (649). Part II. Recommendations for Preventing Nosocomial Pneumonia INTRODUCTION These recommendations are presented in the following order based on the etiology of the infection: bacterial pneumonia, including Legionnaires disease; fungal pneumonia (i.e., aspergillosis); and virus-associated pneumonia (i.e., RSV and influenza infections). Each topic is subdivided according to the following general approaches for nosocomial infection control:
As in previous CDC guidelines, each recommendation is categorized on the basis of existing scientific evidence, theoretical rationale, applicability, and economic impact (224,225,650-654). 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. These recommendations are 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. These 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; Practices for which insufficient evidence or UNRESOLVED ISSUE consensus regarding efficacy exists. BACTERIAL PNEUMONIA
PREVENTION AND CONTROL OF LEGIONNAIRES DISEASE (b) If cooling towers or evaporative condensers are implicated, decontaminate the cooling-tower system (Appendix D) (463). CATEGORY IB (4) Assess the efficacy of implemented measures in reducing or eliminating Legionella sp. by collecting specimens for culture at 2-week intervals for 3 months. CATEGORY II (a) If Legionella sp. are not detected in cultures during 3 months of monitoring at 2-week intervals, collect cultures monthly for another 3 months. CATEGORY II (b) If Legionella sp. are detected in one or more cultures, reassess the implemented control measures, modify them accordingly, and repeat the decontamination procedures. Options for repeat decontamination include either the intensive use of the same technique used 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 PREVENTION AND CONTROL OF RSV INFECTION PREVENTION AND CONTROL OF INFLUENZA References
The bibliographic citations for references 141-733 can be obtained from CDC's National Center for Infectious Diseases, Hospital Infections Program, Mailstop E-69, 1600 Clifton Road, N.E., Atlanta, GA 30333; telephone: (404) 639-6413; fax: (404) 639-6459; Internet home page: http://www.cdc.gov/ncidod/hip/hip.htm. APPENDIX A Examples of Semicritical Items * Used on the Respiratory Tract
APPENDIX B Maintenance Procedures Used to Decrease Survival and Multiplication of Legionella sp. in Potable-Water Distribution Systems
This requires that water in calorifiers (water heaters) be maintained at greater than or equal to 60 C. In the United Kingdom, where maintenance of water temperatures at greater than or equal to 50 C in hospitals has been mandated, installation of blending or mixing valves at or near taps to reduce the water temperature to less than or equal to 43 C has been recommended in certain settings to reduce the risk for scald injury to patients, visitors, and HCWs (446). However, Legionella sp. can multiply even in short segments of pipe containing water at this temperature. Increasing the flow rate from the hot-water- circulation system may help lessen the likelihood of water stagnation and cooling (449,723). Insulation of plumbing to ensure delivery of cold (less than 20 C) water to water heaters (and to cold-water outlets) may diminish the opportunity for bacterial multiplication (391). Both "dead legs" and "capped spurs" * within the plumbing system provide areas of stagnation and cooling to less than 50 C regardless of the circulating-water temperature; these segments may need to be removed to prevent colonization (724). Rubber fittings within plumbing systems have been associated with persistent colonization, and replacement of these fittings may be required for Legionella sp. eradication (725). II. Continuous chlorination to maintain concentrations of free residual chlorine at 1-2 mg/L at the tap This requires the placement of flow-adjusted, continuous injectors of chlorine throughout the water distribution system. The adverse effects of continuous chlorination include accelerated corrosion of plumbing, which results in system leaks and production of potentially carcinogenic trihalomethanes. However, when levels of free residual chlorine are below 3 mg/L, trihalomethane levels are kept below the maximum safety level recommended by the Environmental Protection Agency (447,726,727).
APPENDIX C Culturing Environmental Specimens for Legionella sp.
Possible samples and sampling sites for Legionella sp. in the hospital (733) Water samples
Swabs
APPENDIX D Procedure for Cleaning Cooling Towers and Related Equipmet *
Chemical disinfection
Mechanical cleaning
After mechanical cleaning
Adapted from information published previously by the Wisconsin Department of Health and Social Services, 1987 (463).
TABLE 1. Microorganisms isolated from respiratory tract specimens obtained by various representative
methods from adult patients who had a diagnosis of nosocomial pneumonia, by epidemiologic investigation
===========================================================================================================
Category Schaberg (3) Bartlett (4) Fagon (5) Torres (6)
-----------------------------------------------------------------------------------------------------------
Hospital type NNIS and UMH * Veterans General General
Patients studied
Ventilated or
nonventilated Mixed Mixed Ventilated Ventilated
No. of patients N/A + 159 49 78
No. of episodes
of pneumonia N/A 159 52 78
Specimen(s) cultured Sputum, tracheal Transtracheal Protected Protected specimen
aspirate, pleural specimen brushing, lung
fluid, blood brushing aspirate, pleural
fluid, blood
Culture results
No organism isolated N/A 0 0 54% @
Polymicrobial N/A 54% @ 40% @ 13% @
No. of isolates 15,499 314 111 N/A
Aerobic bacteria
Gram-negative bacilli 50% & 46% ** 75% ** 16% ++
Pseudomonas aeruginosa 17% & 9% ** 31% ** 5% ++
Enterobacter sp. 11 4 2 0
Klebsiella sp. 7 23 4 0
Escherichia coli 6 14 8 0
Serratia sp. 5 0 0 1
Proteus sp. 3 11 15 1
Citrobacter sp. 1 0 2 0
Acinetobacter
calcoaceticus N/A 0 15 9
Haemophilus influenzae 6% & 17% ** 10% ** 0% ++
Legionella sp. N/A N/A 2% ** 2% ++
Other N/A 0 10 0
Gram-positive cocci 17% & 56% ** 52% ** 4% ++
Staphylococcus aureus 16% & 25% ** 33% ** 2% ++
Streptococcus sp. 1 31 21 2
Other 0 0 8 0
Anaerobes N/A 35% ** 2% ** 0
Peptostreptococcus N/A 14% ** N/A 0
Fusobacterium sp. N/A 10 N/A 0
Peptococcus sp. N/A 11 N/A 0
Bacteroids
melaninogenicus N/A 9 N/A 0
Bacteroids fragilis N/A 8 N/A 0
Fungi 4% & N/A 0 1% ++
Aspergillus sp. N/A N/A 0 1% ++
Candida sp. 4% & N/A 0 0
Viruses N/A N/A N/A N/A
-----------------------------------------------------------------------------------------------------------
* National Nosocomial Infection Surveillance System and University of Michigan Hospitals.
+ Not applicable (i.e., not tested or not supported.)
@ Percentage of episodes.
& Percentage of isolates.
** Percentage of episodes; percentages not additive because of polymicrobial etiology in some episodes.
++ Percentage of patients with pure culture.
===========================================================================================================
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Table 2. Risk factors and suggested infection-control measures for preventing nosocomial pneumonia
========================================================================================================================
Disease/Risk factors Suggested infection-control measures
----------------------------------------------------------------------------------------------------------------------
Bacterial pneumonia
Host-related (persons aged >65 yrs)
Underlying ilness:
-- Chronic obstructive Perform incentive spirometry, positive end-expiratory pressure, or continuous
pulmonary disease positive airway pressure by face mask.
-- Immunosuppression Avoid exposure to potential nosocomial pathogens; decrease duration of
immunosuppression (e.g., by administration of granulocyte macrophage
colony stimulating factor �GMCSF�).
-- Depressed consciousness Administer central nervious system depressants cautiously.
-- Surgery (thoracic/
abdominal) Properly position patients; promote early ambulation; appropriately
control pain.
Device-related Properly clean, sterilize or disinfect, and handle devices; remove
devices as soon as the indication for their use ceases.
Endotracheal intubation and Gently suction secretions; place patient in semirecumbent position
mechanical ventilation (i.e., 30 degrees-45 degrees head elevation); use nonalkalinizing
gastric cytoprotective agent on patients at risk for stress bleeding;
do not routinely change ventilator circuits more often than every 48
hours; drain and discard inspiratory-tubiing condensate, or use heat-
moisture exchanger if indicated.
Nasogastric-tube (NGT) Routinely verify appropriate tube placement; promptly remove NGT when
placement and enteral feeding no longer needed; drain residual; place patient in semirecumbent position
as described as above.
Personnel- or procedure-related
Cross-contamination by hands Educate and train personnel; wash hands adequately and wear gloves
appropriately; conduct surveillance for cases of pneumonia and give
feedback to personnel.
Antibiotic administration Use antibiotics prudently, especially in patients in intensive-care units
who are at high risk.
Legionnaires disease
Host-related
Immunosuppresion Decrease duration of immunosuppression.
Device-related
Contaminated aerosol from Sterilize/disinfect aerosol-producing devices before use; use only
devices sterile water for respiratory humidifying devices; do not use cool-
mist room-air humidifiers without adequate sterilization or disinfection.
Environment-related
Aerosols from contaminated Hyperchlorinate or superheat hospital water system; routinely clean
water supply water-supply system; consider use of sterile water for drinking by
immunosuppressed patientes.
Cooling-tower draft Properly design, place, and maintain cooling towers.
Aspergillosis
Host-related
Severe granulocytopenia Decrease duration of immunosuppresion (e.g., by administration of
GMCSF); place patients who have severe and prolonged granulocytopenia
in a protected environment.
Environment related
Construction activity Remove granulocytopenic patients from vicinity of construction; if not
already done, place severely granulocytopenic patients in a protected
environment; make severely granulocytopenic patients wear a mask when
they leave the protected environment.
Other environmental sources Routinely maintain hospital air-handling systems and rooms of
of aspergilli immunosuppressed patients.
Respiratory syncytial virus
infection (RSV)
Host-related
Persons ages <2 yrs; Consider routine preadmission screening of high-risk patients for
congenital pulmonary/cardiac severe RSV infection, followed by cohorting of patients and nursing
disease; immunosuppression personnel during hospital outbreaks of RSV infection.
Personnel- or procedure-related
Cross-contaminated by hands Educate personnel; wash hands; wear gloves; wear a gown; during
outbreaks, use private rooms or cohort patients and nursing personnel,
and limit visitors.
Influenza
Host-related
Persons ages >65 yrs; Vaccinate patients who are at high risk before the influenza season
immunosuppresion begins each year; use amantadine or rimantadine for chemoprophylaxis
during an outbreak.
Personnel-related
Infected personnel Before the influenza season each year, vaccinate personnel who provide
care for high-risk patients; use amantadine or rimantadine for prohylaxis
and treatment during an outbreak.
----------------------------------------------------------------------------------------------------------------------
========================================================================================================================
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Table 3. Controlled studies on nosocomial lower respiratory tract infections and other associated outcomes of selective decontamination of the digestive tract in adult patients with medchanically assisted ventilation
=========================================================================================================================================================================================================================================
Lower respiratory tract infection Colonization or infection
------------------------------------------------------------ with resistant
Infection rate microorganisms Overall mortality in hospital Mean total no. of days in ICU
--------------------------------- -------------------------------- ------------------------------------ ---------------------------------
Author Study patients Diagnostic method SDD (%) Controls (%) SDD (%) Controls (%) SDD (%) Controls (%) SDD Controls
-----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Stoutenbeek Trauma; Clinical and 8 59 "No increase" 3 8 Not reported
(1984) (155) SDD=63; radiologic; **
Controls=59. TS culture. ++
Unertl (1987) General ICU; Clinical and 21 70 21 @@ 20 @@ 26 30 18 & 23 &
(156) SDD=19; radiologic. **
Controls=20
Kerver (1988) Surgical ICU; Clinical and 21 85 "Not recorded" 29 32 17 20
(157) SDD=49; radiologic. ** IR ***= 4 IR=17
Controls=47.
Ledingham General ICU; Clinical and 2 11 "No increase" 24 24 Not reported
(1988) 158) SDD=163; radiologic. **
Controls=161.
Brun-Buisson Medical ICU; Clinical and 20 22 3 @@ 16 @@ 22 24 14 15
(1989) (159) SDD=36; radiologic; ** TS IR=9 IR=10
Controls=50. and PSB culture ++
Ulrich (1989) General ICU; Clinical and 15 50 GP=78 +++ GP=44 +++ 31 54 17 13
(160) SDD=48; radiologic. ** GN=3 +++ GN=2 +++ IR=0 IR=15
Controls=52.
Flaherty (1990) Cardiac surgery Clinical and 2 9 GN=22 @@ GN=21 @@ 0 2 Not reported
(161) ICU; SDD=51; radiologic. **
Controls=56.
Godard (1990) General ICU; Clinical and 2 15 GN=15 +++ GN=15 +++ 12 18 11 16
(162) SDD=97; radiologic; ** TS
Controls=56. and PSB culture. ++
McClelland Renal and TS culture. ++ 7 50 Not reported 60 58 Not reported
(1990) (163) respiratory IR=27 IR=8
failure; SDD=15;
Controls=12.
Rodriquez- General ICU; Clinical and Pn=0 @@@ Pn=73 @@@ "None noticed" 30 33 Not reported
Roldan (1990) SDD=13; radiologic; ** TS TB=23 @@@ TB=20 @@@ IR=0 IR=13
(164) Controls=15. culture ++
Tetteroo (1990) Esophageal Clinical and 2 14 2 @@ 4 @@ 5 4 6 5
(165) resection; radiologic; **
SDD=56; culture of
Controls=56. bronchial aspirate
Aerdts (1991) General ICU; Clinical and 6 A=78 "None observed" 12 A=22 23 A=30
(166) SDD=17; radiologic; ** TS B=62 IR=6 IR=11 B=25
Controls-A=18; &&& culture. ++ B=10
Controls-B=21. &&& IR=0
Blair (1991) General ICU; Clinical and 10 35 "No evidence of 14 19 8 8
increased resistance"
(167) SDD=126; radiologic. **
Controls=130.
Fox (1991) Cardiac bypass; TS culture. ++ 66 50 Not reported 17 66 12 12
(168) SDD=12;
Controls=12.
Hartenauer Surgical ICU; Clinical and ICU-1:10 46 S=34 @@ S=33 @@ 38 48 12 13
(1991) (169) ICU-1: SDD=50, radiologic; ** TS ICU-2:10 45 GN=0 @@ GN=0 @@ IR=8 IR=21
Controls=61; culture. ++ S=37 @@ S=37 @@ 31 43
ICU-2: SDD=49, GN=0 @@ GN=0 @@ IR=6 IR=25
Controls=40.
Pugin (1991) Surgical ICU; Clinical and 16 78 "No new antibiotic resistance" 28 26 13 15
(170) SDD=25; radiologic; ** TS
Controls=27. culture. ++
Vandenbroucke- ICUs (pooled Clinical and A=7 B=8 A=28 B=45 "No increase in resistant A=25 A=26 Not reported
Grauls (1991) data); **** radiologic; ** TS microorganisms in 10 11 studies" B=21 B=26
(171) SDD-A=488, culture ++
Controls-A
(historical)=540;
SDD-B=225,
Controls-B
(random)=266.
Cockerill (1992) Surgical and Clinical and Pn=5 @@@ Pn=16 @@@ 16 +++ 11 +++ 15 21 10 12
(172) medical ICUs; radiologic; ** TS TB=4 @@@ TB=5 @@@
SDD=75; culture. ++
Controls=75.
Gastinne (1992) Medical ICU; Clinical and 12 15 Not reported 40 36 18 19
(173) SDD=220; radiologic; ** TS +/- 34 ++++ 34 ++++
Controls=225. PSB culture. ++
Hammond (1992) General ICU; Clinical and Pn=15 @@@ Pn=15 @@@ Not reported @@@@ 18 17 16 17
(174) SDD=114; radiologic; ** TS Br=6 @@@ Br=6 @@@ IR=6 IR=6
Controls=125. culture. ++
Rocha (1992) General ICU; Clinical and 26 63 GP=62 +++ GP=38 +++ 21 44 19 18
(175) SDD=47; radiologic; ** TS +/- GN=43 +++ GN=30 +++ IR=2 IR=20
Controls=54. BAL culture. ++
Winter (1992) General ICU; Clinical and 3 A=11 1-8 +++ A=1-7 +++ 36 A=43 6 A=7
(176) SDD=91; radiologic; ** B=23 B=1-17 +++ B=43 B=8
Control-A=84, BAL culture. ++
Control-B=92.
Korinek (1993) Neurosurgical Clinical and 24 42 "No evidence of 8 7 24 29
increased resistance"
(177) ICU; SDD=63; radiologic; ** TS
Controls=60. ans PSB culture
SDD Trialists ICUs (pooled Variable. Odds ratio= 0.37; &&&& Not analyzed 27 29 Not analyzed
(1993) (178) data); **** 95% CI *****= 0.31-0.43
SDD=2,047;
Controls=2,095.
Ferrer (1994) Respiratory ICU; Clinical and 18 24 Not reported +++++ 31 27 Not reported
(179) SDD=39; radiologic; **
Controls=41. TS + PSB or BAL
culture ++ +/-
autopsy histology.
-----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
* Resistant to at least one antimicrobial in the SDD regimen.
+ During the study period.
@ ICU=intensive-care unit.
& SDD=selective digestive-tract decontamination.
** Clinical criteria included temperature >38 C, purulent bronchorrhea, WBC >(12,000-15,000/mm^3). Radiologic
criterion was evidence of new and progressive infiltrate(s).
++ TS=tracheal secretions; PSB=protected-specimen brushing; BAL=bronchoalveolar lavage.
@@ Percentage of patients infected or colonized with gram-positive (GP) and/or gram-negative (GN) bacillary organisms at any body site; GP=percentage of patients infected or colonized with gram-positive organisms at any body
site; S=percentage of patients with coagulase-negative staphylococcal infection or colonization.
&& Median.
*** Infection-related.
+++ Percentage of isolates; GP=percentage of gram-positive isolates; GN=percentage of gram-negative bacillary isolates.
@@@ Pn=pneumonia; TB=tracheobronchial infection; Br=bronchial infection.
&&& Control-A-=patients given penicillin (ampicillin, piperacillin, or flucloxacillin) for clinical infection(s); Control-B=patients given cephalosporin (cephadrine, cefuroxime, or cefotaxime) for clinical infections(s).
**** Meta-analysis.
++++ In ICU.
@@@@ However, at 4 weeks, the oropharyngeal cultures of 13% of SDD patients and 5% of control patients had methicillin-resistant Staphylococcus aureus (MRSA), and 41% of SDD patients and control patients were
colonized with enterococci.
&&&& Computed using data from 3,836 patients and 526 events, 260 in SDD patients and 366 in control patients.
***** CI=confidence interval.
+++++ However, bronchial colonization with MRSA occurred in 45% of SDD patients and 21% of control patients.
=========================================================================================================================================================================================================================================
Return to top. Figure_1 Return to top. Disclaimer All MMWR HTML versions of articles are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the electronic PDF version and/or the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices. **Questions or messages regarding errors in formatting should be addressed to .Page converted: 09/19/98 Which client would the nurse consider to be at the highest risk for developing a nosocomial infection?The incidence of nosocomial infections is greater in the elderly than in any other population groups; the elderly have the highest rates of nosocomial urinary tract infections, infected surgical wounds, and nosocomial pneumonia and bacteremia.
What is the most common way a nosocomial infection is acquired?The most common type of nosocomial infection involves invasive devices and procedures (urinary catheters, central lines, mechanical ventilation, or surgery).
Which of the following has the highest prevalence of nosocomial infections?Among nosocomial infections, surgical site infections were the most common (27.1%), followed by lung infections (22.0%) and urinary tract infections (17.0%).
Which of the following is an example of a nosocomial disease?Some of the common nosocomial infections are urinary tract infections, respiratory pneumonia, surgical site wound infections, bacteremia, gastrointestinal and skin infections.
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