Ofelia C. Tablan

Guideline for infection control in health care personnel, 1998

I. Infection control issues for health care personnel: An overview A. EXECUTIVE SUMMARY 291 B. INTRODUCTION 292 C. INFECTION CONTROL OBJECTIVES FOR A PERSONNEL HEALTH SERVICE 292 D. ELEMENTS OF A PERSONNEL HEALTH SERVICE FOR INFECTION CONTROL 293 1. Coordination with other departments 293 2. Medical evaluations 293 3. Personnel health and safety education 293 4. Immunization programs 296 5. Management of job-related illnesses and exposures 298 6. Health counseling 301 7. Maintenance of records, data management, and confidentiality 301 E. EPIDEMIOLOGY AND CONTROL OF SELECTED INFECTIONS TRANSMITTED AMONG HEALTH CARE PERSONNEL AND PATIENTS 302 1. Bloodborne pathogens 302 Affiliations: National Center for Infectious Diseases, National Immunization Program, National Institute of Occupational Safety and Health.

Guideline for Infection Control in Healthcare Personnel, 1998

This guideline updates and replaces the previous edition of the Centers for Disease Control and Prevention (CDC) “Guideline for Infection Control in Hospital Personnel,” published in 1983. The revised guideline, designed to provide methods for reducing the transmission of infections from patients to healthcare personnel and from personnel to patients, also provides an overview of the evidence for recommendations considered prudent by consensus of the Hospital Infection Control Practices Advisory Committee members. A working draft of this guideline was also reviewed by experts in infection control, occupational health, and infectious diseases; however, all recommendations contained in the guideline may not reflect the opinion of all reviewers.

Construction activity: an independent risk factor for invasive aspergillosis and zygomycosis in patients with hematologic malignancy.

Between November 1982 and July 1984, five patients at a 110-bed pediatric hospital were diagnosed with invasive filamentous fungal infection; three had invasive aspergillosis (IA) and two had invasive zygomycosis (IZ). All five had underlying hematologic malignancy (HM). In a case-control study, these five HM patients (cases) were compared to 10 autopsied HM patients without evidence of aspergillosis or zygomycosis (controls). Cases and controls did not differ in underlying disease or in the degree of immunosuppression, as measured by duration of granulocytopenia and number of platelet transfusions. However, case-patients were more likely than controls to have been hospitalized during the construction of a hospital addition (p less than 0.02, Fishers exact test [FET]). Four (80%) of five HM patients autopsied during the period of construction had IA or IZ compared with one (5%) of 21 autopsied before construction began (p = 0.001, FET). These findings suggest that, in a population of comparably immunosuppressed patients, construction activity may represent an independent risk factor for IA or IZ. Hospitals caring for such patients should take precautions which minimize exposure of these patients to construction or renovation activity.

Acquisition of Pseudomonas cepacia at summer camps for patients with cystic fibrosis

To assess the risk of acquisition of Pseudomonas cepacia by person-to-person transmission at cystic fibrosis summer camps, we conducted in 1990 a study at three camps attended by patients with cystic fibrosis who had P. cepacia infection and patients without P. cepacia infection but who were considered susceptible to infection. We obtained sputum or throat cultures from campers on their arrival at, weekly during, at the end of, and 14 to 30 days after camp. We compared the incidence of sputum conversion of patients at camp with that of patients outside camp by culturing specimens from noncamper control subjects with cystic fibrosis who were known not to be infected < or = 2 weeks before and 4 to 6 weeks after camp. We also determined the risk factors for P. cepacia acquisition by determining the relative risk of acquisition between campers who were exposed versus campers who were not exposed to campers known to be infected or to potential environmental sources of P. cepacia at camp. The ribotype of P. cepacia isolates from campers with sputum conversion was compared with that of isolates from other campers and from an environmental source. The cumulative incidence of sputum conversion during the study period was 6.1% (11/181) among campers compared with no incidence (0/92) among noncampers (p = 0.02, Fisher Exact Test). The incidence of sputum conversion at camp varied according to the prevalence of campers with known infection (p < 0.001, chi-square test for trend). The rate of sputum conversion was higher in the camp with longer duration (relative risk = 12.0; 95% confidence interval = 2.7 to 53.5). Ribotyping showed that P. cepacia isolates from all 11 campers with sputum conversion were identical or similar (1 to 2 band difference) to isolates of other P. cepacia-infected campers including co-converters. These results suggest that P. cepacia can be acquired by patients with cystic fibrosis who are attending summer camp for such patients, possibly through person-to-person transmission, and that the risk increases with the prevalence of P. cepacia-infected campers and the duration of camp.

The epidemiology of nosocomial epidemic Pseudomonas cepacia infections

Pseudomonas cepacia has occasionally been identified as an epidemic and endemic nosocomial pathogen. In outbreaks, usually one clinical site predominates but many may be involved. Detailed investigations have usually implicated a contaminated liquid reservoir or moist environmental surface as the source. Liquid sources have included a number of different classes of antiseptics and disinfectants such as quaternary ammonium chlorides, biguanides, hexachlorophene, and iodophors. Environmental and patient isolates have had multiply resistant antimicrobial susceptibility patterns. The clinical distinction between colonization and infection may be difficult and may challenge the skills of the clinician. Expenditure of resources needed to solve epidemics is justified in view of the potential virulence of this organism and the high likelihood that an unrecognized but easily eliminated liquid environmental reservoir may be the source.

Infection Control in Pulmonary Function Laboratories

The role of the pulmonary function (PF) laboratory and PF testing equipment in the transmission of infections has not been established. Although microorganisms have been cultured from parts of in-use pulmonary function testing equipment, a relationship between equipment contamination and transmission of infection or colonization has not been documented. Nosocomial outbreaks of respiratory infections, eg, influenza, tuberculosis, and legionellosis have been described, but transmission of the microorganisms has not been shown to be more likely in the PF laboratory or with PF testing equipment than in other areas in the hospital or with other hospital equipment. Unlike nebulizers, which have been implicated in epidemic and endemic nosocomial gram-negative bacterial infections, PF machines do not generate aerosols. PF testing equipment is thus built without provision for easy machine disassembly and disinfection, except for parts that routinely come in contact with mucous membranes or secretions (eg, mouthpieces, valves, and some tubings).

Nosocomially Acquired Pseudomonas cepacia Infection in Patients with Cystic Fibrosis

Pseudomonas cepacia is a significant respiratory pathogen in patients with cystic fibrosis (CF).‘-‘j Since the first reports of its increasing prevalence and association with rapid pulmonary function decline and unexpected deaths,‘JJ many studies have been conducted in attempts to elucidate its epidemiology in CF patients.s,“14 Surveillance in more than 100 United States CF centers has shown that, since 1986, when center laboratories started routinely using P cepaciaselective media for cultures of sputum specimens from patients with CF,‘O annual incidence and prevalence of PC infection or colonization have plateaued at 1% and 3.5% respectively. The impact of P cepacia has varied from center to center, however. Yearly center incidence and prevalence range from 0% to 7% and 0% to 27% respectively, with most P cepacia -colonized patients being concentrated in a few large CF centers. l5 In many respects, the epidemiology of P cepacia in CF patients appears to resemble that of P aeruginosa, an organism that has long been prevalent in the respiratory flora of patients with CE”J7 Both microorganisms have a predilection for CF patients with severe pulmonary impairment, and both can cause chronic respiratory-tract colonization that is difficult to eradicate and is associated with intermittent exacerbations of bronchitis or pneumonia.“JjsgJT Both have been associated with decreased survival and deterioration of pulmonary function in colonized patients, although a cause-and-effect relationship has not been firmly established with either organism.2v3,gJi-Z” In addition, both P cepacia and P aeruginosa have similar habitats: They can be found in soil and water; their hospital reservoirs are moist environments.“3-27 Several features distinguish P cepacia infection from P aeruginosa infection of the CF patient’s respiratory tract. First, although the virulence and pathogenic properties of P cepacia are still poorly understood,6,12J8-33 P cepacia septicemia and/or necrotizing pneumonia, accompanied by rapid pulmonary-function deterioration and culminating in death, have been documented in patients with mild or moderate CF: whereas reports of similar episodes attributable to P aeruginosa have been lacking in the literature.1JL-34 Second, most isolates of P cepacia are resistant to currently available antipseudomonas antimicrobials and present a major therapeutic challenge.3”37 Thus, many consider P cepacia infection of CF patients more serious than that due to P aeruginosa. Data suggesting patient acquisition of P cepacia in the hospital make prevention of the nosocomial transmission of P cepacia important.ZJ~gJs~40~41 The three possible modes by which P cepacia can colonize or infect the respiratory tract of CF patients in the hospital are: 1) from environmental reservoir to patient, 2) from person to person, and 3) by autoinfection of the respiratory tract with a strain that has colonized another body site. Autoinfection of the respiratory tract with bacteria following colonization of other body sites such as the gastrointestinal tract or oropharynx has been