Bennett & Brachman's Hospital Infections, 5th Edition

4

Personnel Health Services

Elise M. Beltrami

Elizabeth A. Bolyard

Healthcare personnel (HCP) are at risk of exposure to infectious diseases in both the workplace and the community. If they develop an infection, they may pose a risk for transmission of that infectious pathogen to patients, other HCP, members of their households, or other community contacts. In this chapter, the term health care personnel refers to all paid and unpaid persons working in healthcare settings who have the potential for exposure to infectious materials, including body substances and contaminated medical supplies, equipment, environmental surfaces, or air. In general, HCP inside or outside hospitals who have contact with patients, body fluids, or specimens have a higher risk of acquiring or transmitting pathogens than do other HCP who have only brief casual contact with patients and their environment (e.g., beds, furniture, bathrooms, food trays, or medical equipment).

This chapter outlines the infection control elements of a personnel health service and discusses important aspects of selected transmissible diseases excluding hepatitis B virus (HBV) infection, hepatitis C virus infection, and human immunodeficiency virus (HIV) infection, which are discussed in Chapter 42, Bloodborne Pathogen Prevention.

Infection Control Elements of a Personnel Health Service

Whether performed “in house” or contracted out, certain elements are necessary for the appropriate functioning of a personnel health service: (a) coordination with other departments, (b) pre-employment or placement medical evaluations, (c) health and safety education, (d) immunization programs, (e) management of job-related illnesses and exposures to infectious pathogens, including policies for work restrictions for infected or exposed personnel, (f) counseling services for personnel on infection risks related to employment or special conditions, and (g) maintenance and confidentiality of personnel health records.

The organization of a personnel health service can be influenced by the size of the institution, the number of personnel, and the services offered. To ensure that contractual personnel who are not paid by the healthcare facility receive appropriate personnel health services, contractual agreements with their employers should contain provisions consistent with the policies of the facility that uses those employees. Personnel with specialized training and qualifications in occupational health can facilitate the provision of effective services.

Coordination with Other Departments

For infection control objectives to be achieved, the activities of the personnel health service must be coordinated with infection control and other appropriate departmental personnel. This coordination will help ensure adequate surveillance of infections in personnel and provision of preventive services. Coordination of activities also will help to ensure that investigations of exposures and outbreaks are conducted efficiently and preventive measures implemented promptly.

Placement Medical Evaluations

Medical evaluations before employee placement can ensure that personnel are not placed in jobs that would pose

P.46


undue risk of infection to them, other personnel, patients, or visitors. An important component of the placement evaluation is a health inventory. This includes determining immunization status and obtaining histories of any conditions that could predispose personnel to acquiring or transmitting infectious diseases.

A physical examination can be used to screen personnel for conditions that could increase the risk of transmitting pathogens or acquiring work-related diseases and can serve as a baseline for determining whether future diseases are work related. However, the cost effectiveness of routine physical examinations, including laboratory testing (e.g., complete blood cell counts, urinalysis, and chest radiographs) and screening for enteric or other pathogens for infection control purposes, has not been demonstrated. Conversely, screening for some vaccine-preventable diseases, such as HBV, measles, mumps, rubella, or varicella, could be cost effective. In general, the health inventory can be used to guide decisions regarding physical examinations or laboratory tests. However, some local public health ordinances could mandate that certain screening procedures be used. Periodic evaluations may be done as indicated for job reassignment, for ongoing programs (e.g., tuberculosis [TB] screening), or for evaluation of work-related problems.

Personnel Health and Safety Education

Personnel are more likely to comply with an infection control program if they understand its rationale. Thus, personnel education is an important element of an effective infection control program. Clearly written policies, guidelines, and procedures ensure uniformity, efficiency, and effective coordination of activities. However, because the risk of infection varies by job category, infection control education should be tailored accordingly. In addition, some HCP may need specialized education on infection risks related to their employment and on preventive measures that will reduce those risks. Furthermore, educational materials need to be appropriate in content and vocabulary to the educational level, literacy, and language of the employee. The training should comply with existing federal, state, and local regulations regarding requirements for employee education and training. All HCP need to be educated about the organization's infection control policies and procedures.

Immunization Programs

Ensuring that personnel are immune to vaccine-preventable diseases is an essential part of successful personnel health programs. Optimal use of vaccines can prevent transmission of vaccine-preventable diseases and eliminate unnecessary work restriction. Prevention of illness through comprehensive personnel immunization programs is far more cost-effective than case management and outbreak control. In particular, interventions to increase influenza vaccination of HCP have been shown to be effective [1]. Mandatory immunization programs, which include both newly hired and currently employed persons, are more effective than voluntary programs in ensuring that susceptible persons are vaccinated [2].

National guidelines for immunization of and postexposure prophylaxis (PEP) for HCP are provided by the U.S. Public Health Service's Advisory Committee on Immunization Practices (ACIP) [3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18].

Screening tests are available to determine susceptibility to certain vaccine-preventable diseases (e.g., HBV, measles, mumps, rubella, and varicella). Such screening programs should be combined with tracking systems to ensure accurate maintenance of personnel immunization records. Accurate immunization records ensure that susceptible personnel are promptly identified and appropriately vaccinated. For more details about vaccinations for HCP, see Vaccinations in Patients and Healthcare Workers.

Management of Job-Related Illnesses and Exposures

Primary functions of the personnel health service are to arrange for prompt diagnosis and management of job-related illnesses and to provide appropriate PEP after job-related exposures. It is the responsibility of the healthcare organization to implement measures to prevent further transmission of pathogens, which sometimes warrants exclusion of personnel from work or patient contact [19]. Decisions about work restrictions are based on the mode of transmission and the epidemiology of the disease (Table 4-1). The term exclude from duty in this chapter should be interpreted as exclusion from the healthcare facility and from healthcare activities outside the facility. Personnel who are excluded should avoid contact with susceptible persons both in the facility and in the community. Exclusion policies should include a statement of authority defining who may exclude personnel. The policies also need to be designed to encourage personnel to report their illnesses or exposures, not to penalize them with loss of wages, benefits, or job status. Workers' compensation laws do not cover exclusion from duty for exposures to infectious diseases; therefore, policies should include a method for providing wages during the period that HCP are not able to work. In addition, exclusion policies must be enforceable, and all HCP, especially department heads, supervisors, and nurse managers, should know which infections warrant exclusion and where to report the illnesses 24 hours a day, 7 days a week. HCP who have contact with infectious patients outside the healthcare setting also need to be included in the postexposure program and encouraged to report any suspected or known exposures promptly.

P.47

TABLE 4-1
SUMMARY OF SUGGESTED WORK RESTRICTIONS FOR HEALTHCARE PERSONNEL EXPOSED TO OR INFECTED WITH INFECTIOUS DISEASES OF IMPORTANCE IN HEALTHCARE SETTINGS, IN THE ABSENCE OF STATE AND LOCAL REGULATIONS. (MODIFIED FROM BOLYARD EA, TABLAN OC, WILLIAMS WW, et al. GUIDELINE FOR INFECTION CONTROL IN HEALTH CARE PERSONNEL, 1998. INFECT CONTROL HOSP EPIDEMIOL 1998;19:407–63)

Disease/Problem

Work Restriction

Duration

Conjunctivitis

Restrict from patient contact and contact with the patient's environment

Until discharge ceases

Cytomegalovirus infections

No restriction

Diarrheal diseases

Acute stage (diarrhea with other symptoms)

Restrict from patient contact, contact with the patient's environment, or food handling

Until symptoms resolve

Convalescent stage,Salmonella spp.

Restrict from care of high-risk patients

Until symptoms resolve; consult with local and state health authorities regarding need for negative stool cultures

Hepatitis A

Restrict from patient contact, contact with patient's environment, and food handling

Until 7 days after onset of jaundice

Herpes simplex Hands (herpetic whitlow)

Restrict from patient contact and contact with the patient's environment

Until lesions heal

Measles Active

Exclude from duty

Until 7 days after the rash appears

Postexposure (susceptible personnel)

Exclude from duty

From the 5th day after the 1st exposure through the 21$st$ day after last exposure

Meningococcal infections

Exclude from duty

Until 24 hours after start of effective therapy

Mumps Active

Exclude from duty

Until 9 days after onset of parotitis

Postexposure (susceptible personnel)

Exclude from duty

From 12th day after 1st exposure through until 25 days after last exposure or until 9 days after onset of parotitis

Pertussis Active

Exclude from duty

From beginning of catarrhal stage through 3rdweek after onset of paroxysms or until 5 days after start of effective antimicrobial therapy

Postexposure (asymptomatic personnel)

No restriction, prophylaxis recommended

Exclude from duty

Postexposure (symptomatic personnel)

Until 5 days after start of effective antimicrobial therapy

Rubella Active

Exclude from duty

Until 5 days after rash appears

Postexposure (susceptible personnel)

Exclude from duty

From 7th day after 1st exposure through 21st day after last exposure

Staphylococcus aureusinfection

Restrict from contact with patients and patient's environment or food handling

Until lesions have resolved

Active, draining skin lesions

Tuberculosis

Active disease

Exclude from duty

Until proved noninfectious

TST converter

No restriction

Varicella Active

Exclude from duty

Until all lesions dry and crust

Postexposure (susceptible personnel)

Exclude from duty

From 10th day after 1st exposure through 21st day (28th day if VZIG given) after last exposure

Viral respiratory infections, acute febrile

Consider excluding from the care of high risk patients or contact with their environment during community outbreak of RSV and influenza

Until acute symptoms resolve

Zoster

Localized, in healthy person

Cover lesions; restrict from care of high-risk patients

Until all lesions dry and crust

Generalized or localized in immunosuppressed person

Restrict from patient contact

Until all lesions dry and crust

Postexposure (susceptible personnel)

Restrict from patient contact

From 10th day after 1st exposure through 21st day (28th day if VariZIG given) after last exposure or, if varicella occurs, until all lesions dry and crust

P.48

Health Counseling

Access to adequate health counseling for HCP is another crucial element of an effective personnel health service. Health counseling allows personnel to receive individually targeted information regarding (a) the risk and prevention of occupationally acquired infections, (b) the risk of illness or other adverse outcome after exposure, (c) management of exposure, including the risks and benefits of PEP regimens, and (d) the potential consequences of exposure or communicable disease for family members, patients, or other personnel, both inside and outside the healthcare facility.

Maintenance of Records, Data Management, and Confidentiality

Maintenance of records related to medical evaluations, immunizations, exposures, PEP, and screening tests in a retrievable, preferably computerized, database allows efficient monitoring of the health status of HCP. Such record keeping also helps to ensure that the organization will provide consistent and appropriate services to HCP.

Individual records for all HCP should be maintained in accordance with the Occupational Safety and Health Administration (OSHA) medical records standard, which requires the employer to retain records, maintain employee confidentiality, and provide records to employees when they ask to review them [20]. In addition, the OSHA “Occupational Exposure to Bloodborne Pathogens; Final Rule” [21] requires employers, including healthcare facilities, to establish and maintain an accurate, confidential record for each employee with occupational exposure to bloodborne pathogens. The standard also requires that each employer ensure that it maintain employee medical records for at least the duration of the worker's employment plus 30 years.

Occupational health departments need to protect and safeguard protected health information as defined by the Health Insurance Portability and Accountability Act of 1996 (HIPAA) and the American Disabilities Act (ADA) [22]. Information about injuries and communicable diseases may be disclosed to public health authorities for the purpose of preventing or controlling disease, injury, or disability.

Epidemiology and Control of Selected Infections Transmitted Among Hospital Personnel and Patients

The following section provides more detail about selected infectious pathogens and conditions that can be transmitted in the healthcare setting. These pathogens and conditions could require consideration for employee placement or work restrictions. Bloodborne pathogens, including HBV, hepatitis C virus, and HIV, are not included here but are discussed inChapter 42, Bloodborne Pathogen Prevention.

Conjunctivitis

Although conjunctivitis can be caused by a variety of bacteria and viruses, adenovirus has been the primary cause of healthcare-associated outbreaks of conjunctivitis. Healthcare-associated outbreaks have primarily occurred in eye clinics or offices but also have been reported in neonatal intensive care units and long-term care facilities [23,24,25,26,27]. The incubation period ranges from 5 to 12 days, and shedding of virus occurs from late in the incubation period to as long as 14 days after onset of disease [24]. Adenovirus survives for long periods on environmental surfaces; ophthalmologic instruments and equipment can become contaminated and be a source of transmission. Contaminated hands also are a major source of person-to-person transmission of adenovirus, both from patients to HCP and from HCP to patients. Hand hygiene, glove use, and disinfection of instruments can prevent the transmission of adenovirus [23,24]. Infected personnel should not provide patient care for the duration of symptoms after onset of purulent conjunctivitis caused by adenovirus or other pathogens [24,25].

Cytomegalovirus

There are two principal reservoirs of cytomegalovirus (CMV) in healthcare institutions: (a) infants and young children infected with CMV and (b) immunocompromised patients for example, those undergoing solid-organ or bone-marrow transplantation or those with acquired immunodeficiency syndrome (AIDS) [28,29]. However, HCP who provide care to such high-risk patients have a rate of primary CMV infection that is no higher than that among personnel without such patient contact (3% vs. 2%) [30,31,32,33,34].

CMV transmission appears to occur directly either through close, intimate contact with a person excreting CMV or through contact with contaminated secretions or excretions, especially saliva or urine [33,35,36]. Transmission by the hands of HCP or infected persons also has been suggested [29,37]. The incubation period for person-to-person transmission is not known. Although CMV can survive on environmental surfaces and other objects for short periods [38], there is no evidence that the environment plays a role in the transmission of this pathogen [29].

Because infection with CMV during pregnancy may have adverse effects on the fetus, women of childbearing age need to be counseled regarding the risks and prevention of transmission of CMV in both nonoccupational and occupational settings [39]. No studies clearly indicate that sero-negative HCP can be protected from infection by

P.49


transfer to areas with less contact with patients likely to be reservoirs for CMV [28,29,30,34].

Serologic or virologic screening programs to identify CMV-infected patients or sero-negative female personnel of childbearing age are impractical and costly for the following reasons: (a) the virus can be intermittently shed [40], and repeated screening tests could be needed to identify shedders, (b) sero-positivity for CMV does not offer complete protection against maternal re-infection or reactivation and subsequent fetal infection [28], and (c) no currently available vaccines or prophylactic therapy for HCP can provide protection against primary infection.

Work restrictions for personnel who contract CMV illnesses are not necessary. The risk of transmission of CMV can be reduced by careful adherence to hand hygiene and Standard Precautions [28,41].

Diphtheria

Healthcare-associated transmission of diphtheria among patients and personnel has been reported [42,43,44]. HCP are not at substantially higher risk than the general adult population for acquiring diphtheria.

Prevention of diphtheria is best accomplished by maintaining high levels of diphtheria immunity among children and adults [13,45,46]. Immunization with tetanus and diphtheria toxoid (Td) is recommended every 10 years for all adults who have completed the primary immunization series [4,13]. HCP directly exposed to oral secretions of patients infected with Corynebacterium diphtheriae should be evaluated in consultation with local public health authorities.

Gastroenteritis

Gastrointestinal infections may be caused by a variety of agents, including bacteria, viruses, and protozoa. However, only a few agents have been documented in healthcare-associated transmission, such as Salmonella typhimurium, Yersinia enterocolitica, Escherichia coli, and norovirus [47,48,49,50,51,52,53,54,55,56,57,58]. Healthcare-associated transmission of agents that cause gastrointestinal infections usually results from contact with infected individuals [47,53,59], from consumption of contaminated food, water, or other beverages [47,59,60], or from exposure to contaminated objects or environmental surfaces [48,61]. Inadequate HCP hand hygiene [62] and inadequate sterilization or disinfection of patient-care equipment and environmental surfaces increase the likelihood of transmission of agents that cause gastrointestinal infections. Generally, adherence to good hand hygiene by HCP before and after all contacts with patients and food and to either Standard or Contact Precautions [4] will minimize the risk of transmitting enteric pathogens [55,63].

Laboratory personnel who handle infectious materials also may be at risk for occupational acquisition of gastrointestinal infections, most commonly with Salmonella typhi.

Personnel who acquire an acute gastrointestinal illness (defined as vomiting, diarrhea, or both, with or without associated symptoms such as fever, nausea, and abdominal pain) are likely to have high concentrations of the infecting agent in their feces (bacteria, viruses, and parasites) or vomitus (viruses and parasites). It is important to determine the etiology of gastrointestinal illness in HCP who care for patients at high risk for severe disease (e.g., neonates, elderly persons, and immunocompromised patients). The initial evaluation of personnel with gastroenteritis needs to include a thorough history and determination of the need for specific laboratory tests, such as stool or blood cultures, stool staining procedures, or serologic or antigen-antibody tests [54,61,64].

Restriction from patient care and the patient's environment or from food handling is indicated for HCP with diarrhea or acute gastrointestinal symptoms regardless of the causative agent [41,61]. Some local and state agencies have regulations that require work exclusion for HCP, food handlers, or both who have gastrointestinal infections caused by Salmonellaor Shigella spp. These regulations may require such personnel to be restricted from duty until results of at least two consecutive stool cultures obtained at least 24 hours apart are negative.

Hepatitis A

Healthcare-associated hepatitis A occurs infrequently, and transmission to HCP usually occurs when the source-patient has unrecognized hepatitis and is fecally incontinent or has diarrhea [65,66,67,68,69,70,71,72]. Other risk factors for hepatitis A virus (HAV) transmission to personnel include activities that increase the risk of fecal-oral contamination such as (a) eating or drinking in patient-care areas [65,67,69,73], (b) not washing hands after handling an infected infant [67,73,74], and (c) sharing food, beverages, or cigarettes with patients, their families, or other staff members [65,67].

HAV is transmitted primarily by the fecal-oral route. The incubation period for HAV is 15 to 50 days. Fecal excretion of HAV is greatest during the incubation period of disease before the onset of jaundice. Once disease is clinically obvious, the risk of pathogen transmission is decreased. However, some patients admitted to the hospital with HAV, particularly immunocompromised patients, can still be shedding virus because of prolonged or relapsing disease, and such patients are potentially infectious [66]. Fecal shedding of HAV, formerly believed to continue only as long as 2 weeks after onset of dark urine, has been shown to occur as late as 6 months after diagnosis of infection in premature infants [65]. Anicteric infection is typical in young children and infants [75].

HCP can protect themselves and others from infection with HAV by adhering to Standard Precautions [41].

Three inactivated HAV vaccines are now available and provide long-term pre-exposure protection against clinical

P.50


infection with >94% efficacy [75]. Routine administration of HAV vaccine in HCP is not recommended. However, vaccine may be useful for personnel working or living in areas where HAV is highly endemic and is indicated for personnel who handle HAV-infected primates or are exposed to HAV in a research laboratory. The role of HAV vaccine in controlling outbreaks has not been adequately investigated [4]. Immune globulin given within 2 weeks after an HAV exposure is 80% to 90% effective in preventing HAV infection [75] and may be advisable in some outbreak situations [4,75].

Restriction from patient-care areas or food handling is indicated for personnel with HAV infection. They may return to regular duties one week after onset of the illness [4].

Herpes Simplex

Healthcare-associated transmission of herpes simplex virus (HSV) is rare. It has been reported in nurseries [76,77,78] and intensive care units [79,80] where high-risk patients (e.g., neonates, patients with severe malnutrition, patients with severe burns or eczema, and immunocompromised patients) are located. Healthcare-associated transmission of HSV occurs primarily through contact either with primary or recurrent lesions or with virus-containing secretions, such as saliva, vaginal secretions, or amniotic fluid [77,79,81]. Exposed areas of skin are the most likely sites of infection, particularly when minor cuts, abrasions, or other skin lesions are present [80]. The incubation period of HSV is 2–14 days [82]. The duration of viral shedding has not been well defined [83].

HCP can acquire a herpetic infection of the fingers (herpetic whitlow or paronychia) from exposure to contaminated oral secretions [80,81]. Such exposures are a distinct hazard for nurses, anesthesiologists, dentists, respiratory care personnel, and other personnel who have direct (usually hand) contact with either oral lesions or respiratory secretions from patients [80]. Less frequently, HCP may acquire mucocutaneous infection on other body sites from contact with infectious body secretions [84].

HCP with active HSV infection of the hands (herpetic whitlow) can potentially transmit the pathogen to patients with whom they have contact [81]. Transmission of HSV from HCP with orofacial HSV infection to patients also has been infrequently documented [76]; however, the magnitude of this risk is unknown [78,85]. Although asymptomatic HSV-infected persons can shed the virus, they are less infectious than persons with active lesions [83,86].

HCP can protect themselves from acquiring HSV by adhering to Standard Precautions [41]. The risk of transmission of HSV from personnel with orofacial infections to patients can be reduced by performing hand hygiene before all patient care and by the use of appropriate barriers (e.g., a mask or gauze dressing) to prevent hand contact with the lesion.

Because HCP with orofacial lesions could touch their lesions and potentially transmit HSV, they should be evaluated to determine their potential for transmitting HSV to patients at high risk for serious disease (e.g., neonates, patients with severe malnutrition, patients with severe burns or eczema, and immunocompromised patients) and excluded from the care of such patients as indicated. The evaluation also should consider the extent of the lesion and the severity of illness in the patient population that personnel will contact. Personnel with HSV infections of the fingers or hands can more easily transmit HSV and therefore need to be excluded from patient care until their lesions have crusted. In addition, herpetic lesions can be secondarily infected by Staphylococcus or Streptococcus spp., and HCP with such infections should be evaluated to determine whether they need to be excluded from patient contact until the secondary infection has resolved. There have been no reports that personnel with genital HSV infections have transmitted HSV to patients; therefore, work restrictions for personnel with genital herpes are not indicated.

Measles

Healthcare-associated transmission of measles virus has been well described [87,88,89,90,91,92]. Measles is transmitted both by large droplets during close contact between infected and susceptible persons and by the airborne route [93]. Measles is highly transmissible and frequently misdiagnosed during the prodromal stage. The incubation period for measles is 5–21 days. Immunocompetent persons with measles shed the virus from the nasopharynx, beginning with the prodrome until 3 to 4 days after rash onset; immunocompromised persons with measles could shed virus for extended periods [94].

Strategies to prevent healthcare-associated transmission of measles include (a) documentation of measles immunity in HCP, (b) prompt identification and isolation of persons with fever and rash, and (c) adherence to airborne precautions for suspected and proven patients with measles [41].

It is essential that all HCP have documentation of measles immunity regardless of their length of employment or whether they are involved in patient care. Although persons born before 1957 are generally considered to be immune to measles, serologic studies indicate that 5% to 9% of HCP born before 1957 may not be immune [4,95]. Consideration should be given to recommending a dose of measles-mumps-rubella trivalent vaccine (MMR) to personnel born before 1957 who are unvaccinated and who lack (a) a history of previous measles disease, (b) documentation of receipt of one dose of live measles vaccine, or (c) serologic evidence of measles immunity [3]. HCP born during or after 1957 should be considered immune to measles when they have (a) documentation of physician-diagnosed measles, (b) documentation of

P.51


two doses of live measles vaccine on or after their first birthday, or (c) serologic evidence of measles immunity (persons with an “indeterminate” level of immunity on testing should be considered susceptible). Persons born between 1957 and 1984 who received childhood measles immunization and were given only one dose of vaccine during infancy could require a second dose of vaccine [2].

Work restrictions are necessary for HCP who acquire measles; they need to be excluded from duty for 7 days after the rash appears. Likewise, HCP not immune to measles need to be excluded from duty from 5 days after the first exposure to 21 days after the last exposure to measles.

Meningococcal Disease

Healthcare-associated transmission of Neisseria meningitidis is rare. When proper precautions were not used, N. meningitidis has been transmitted from patient to personnel through contact with the respiratory secretions of patients with meningococcemia or meningococcal meningitis or through handling laboratory specimens [96].

  1. meningitidisinfection usually is transmitted by close contact with aerosols or secretions from the human nasopharynx; the incubation period is from 2–10 days, and patients infected with N. meningitidisare rendered noninfectious by 24 hours of effective therapy. HCP who care for patients with suspected N. meningitidis infection can decrease their risk of infection by adhering to Droplet Precautions [41].

PEP is advised for persons who have had intensive, unprotected contact (i.e., without wearing a mask) with infected patients (e.g., mouth-to-mouth resuscitation, endotracheal intubation, endotracheal tube management, or close examination of the oropharynx of patients) [8]. Antimicrobial prophylaxis can eradicate carriage of N. meningitidis and prevent infections in HCP who have unprotected exposure to patients with meningococcal infections [97].

Because secondary episodes of N. meningitidis occur rapidly (within the first week) after exposure to persons with meningococcal disease [98], it is important to begin prophylactic therapy immediately after an intensive, unprotected exposure, often before results of antimicrobial testing are available. Rifampin (600 mg orally every 12 hours for 2 days) is effective in eradicating nasopharyngeal carriage of N. meningitidis [97]. Ciprofloxacin (500 mg orally) and ceftriaxone (250 mg intramuscularly) in single-dose regimens also are effective in reducing nasopharyngeal carriage of N. meningitidis and are reasonable alternatives to the multidose rifampin regimen [8]. These antimicrobials may be useful when infections are caused by rifampin-resistant meningococci or rifampin is contraindicated. Rifampin and ciprofloxacin are not recommended for pregnant women [8,99,100].

The quadrivalent A,C,Y,W-135 polysaccharide vaccine has been used successfully to control community outbreaks caused by serogroup C [8,99], but its use is not recommended for PEP in healthcare settings [8]. Pre-exposure vaccination can be considered for laboratory personnel who routinely handle soluble preparations of N. meningitidis [8,96].

In the absence of exposures to patients with N. meningitidis infection, personnel who are asymptomatic carriers of N. meningitidis need not be identified, treated, or removed from patient-care activities. However, HCP with meningococcal infection need to be excluded from duty until 24 hours after the start of effective therapy.

Mumps

Mumps transmission has occurred in healthcare facilities housing adolescents and young adults [100,101]. Most episodes of mumps in HCP have been community acquired.

Mumps is transmitted by contact with virus-containing respiratory secretions, including saliva; the portals of entry are the nose and mouth. The incubation period varies from 12–25 days and usually is 16–18 days. The virus can be present in saliva for 6–7 days before parotitis and can persist for as long as 9 days after onset of disease. Exposed HCP may be infectious for 12–25 days after their exposure, and many infected persons remain asymptomatic [103]. Droplet Precautions are recommended for patients with mumps; such precautions should be continued for 9 days after the onset of parotitis [41].

An effective vaccination program is the best approach to the prevention of healthcare-associated mumps transmission [6]. Vaccination with mumps virus vaccine is recommended, unless otherwise contraindicated, for all those who are susceptible to mumps [6,104]; combined MMR is the vaccine of choice [105], especially when the recipient also is likely to be susceptible to measles, rubella, or both.

HCP should be considered immune to mumps if they have (a) documentation of physician-diagnosed mumps, (b) documentation of receipt of two doses of live mumps vaccine on or after their first birthday, or (c) serologic evidence of immunity (individuals who have an “indeterminate” antibody level should be considered susceptible) [6,106]. Although most persons born before 1957 are likely to have been infected naturally, they should receive one dose of live mumps vaccine if they do not meet criteria (a) or (c). Persons born after 1957 should have documentation of two doses of live mumps vaccine on or after their first birthday. Outbreaks among highly vaccinated populations have occurred and have been attributed to primary vaccine failure [107].

Work restrictions are necessary for HCP who acquire mumps; such restrictions should be imposed for 9 days after the onset of parotitis. Likewise, susceptible personnel who are exposed to mumps need to be excluded from duty from the 12th day after the first exposure until 25 days after the last exposure [4,102].

P.52

Parvovirus

Transmission of human parvovirus B19 (B19), the cause of erythema infectiosum (fifth disease), to HCP from infected patients appears to be rare but has been reported [108,109,110,111,112]. HCP have acquired infection while working in laboratories or during the care of patients with B19-associated sickle-cell aplastic crises [109,110,111,112,113,114,115].

B19 can be transmitted through contact with infected persons, fomites, or large droplets [116]. The incubation period varies, depending on the clinical manifestation of disease, and ranges from 6–10 days [117]. The period of infectivity also varies, depending on the clinical presentation or stage of disease. Persons with erythema infectiosum are infectious before the appearance of the rash, those with infection and aplastic crises for as long as 7 days after the onset of illness, and persons with chronic infection for years.

Pregnant HCP are at no greater risk of acquiring B19 infection than are nonpregnant HCP; however, if a woman does acquire B19 infection during the first half of pregnancy, the risk of fetal death is increased. Female HCP of childbearing age should be counseled regarding the risk of transmission of B19 and appropriate infection control precautions [41].

Most patients with erythema infectiosum are past their period of infectiousness at the time of clinical illness [115]. However, patients in aplastic crisis from B19 or patients with chronic B19 infection can transmit the virus to susceptible HCP or other patients; therefore, patients with pre-existing anemia who are admitted to the hospital with febrile illness and transient aplastic crises should remain on Droplet Precautions for 7 days, and patients with known or suspected chronic infection with B19 should be placed on Droplet Precautions on admission and for the duration of hospitalization [41,110]. Work restrictions are not necessary for HCP exposed to B19.

Pertussis

Healthcare-associated transmission of Bordetella pertussis has involved both patients and personnel; non-immunized children are at greatest risk [118,119,120,121,122]. B. pertussistransmission occurs by contact with respiratory secretions or large aerosol droplets from the respiratory tracts of infected persons. The incubation period usually is 7–10 days. The period of communicability starts at the onset of the catarrhal stage and extends into the paroxysmal stage up to 3 weeks after onset of symptoms. Pertussis is highly communicable in the catarrhal stage, when the symptoms are nonspecific.

Prevention of transmission of B. pertussis in healthcare settings involves (a) early diagnosis and treatment of patients with clinical infection, (b) implementation of Droplet Precautions for infectious patients [41], (c) exclusion of infectious HCP from work, and (d) administration of PEP to persons exposed to infectious patients [121]. Patients with suspected or confirmed pertussis who are admitted to the hospital need to be placed on Droplet Precautions until they have clinical improvement and have received antimicrobial therapy for at least 5 days.

Because immunity among vaccine recipients wanes 5–10 years after the last vaccine dose, HCP can play an important role in transmitting B. pertussis to susceptible infants. A single dose of Tetanus, diphtheria, and acellular pertussis (Tdap) vaccine is now recommended for persons age 11–64 years [14]. Acellular pertussis vaccine is immunogenic in adults and carries a lower risk of adverse events than does whole-cell vaccine [122,123].

PEP is indicated for exposed HCP who have not received a recent dose of Tdap. A course of azithromycin (one 500 mg single dose on day 1 then 250 mg per day on days 2–5), erythromycin (2 g per day in four divided doses for 14 days), clarithroymcin (1 g per day in two divided doses for 7 days), or trimethoprim-sulfamethoxazole (one tablet twice daily for 14 days) has been used for this purpose [14,124].

Restriction from duty is indicated for HCP with pertussis from the beginning of the catarrhal stage through the third week after onset of paroxysms, or until 5 days after the start of effective antimicrobial therapy. Exposed HCP do not need to be excluded from duty.

Poliomyelitis

Poliovirus is transmitted through contact with feces or urine of infected persons but can be spread by contact with respiratory secretions and, in rare instances, through items contaminated with feces. The incubation period for nonparalytic poliomyelitis is 3–6 days, but usually is 7–21 days for paralytic polio [125]. Communicability is greatest immediately before and after the onset of symptoms when the virus is in the throat and excreted in high concentration in feces. The virus can be recovered from the throat for 1 week and from feces for several weeks to months after onset of symptoms.

Poliomyelitis associated with oral polio vaccine (OPV) can occur in the recipient (7–21 days after vaccine administration) or susceptible contacts of the vaccine recipient (20–29 days after vaccine administration) [126]. Inactivated poliovirus vaccine (IPV) should be used when adult immunization is warranted, including immunization of pregnant or immunocompromised personnel and personnel who may have contact with immunocompromised patients [4,9,16,125].

HCP who have contact with patients who could be excreting wild virus (e.g., imported poliomyelitis patient) and laboratory personnel handling specimens containing poliovirus or performing cultures to amplify virus should receive a complete series of polio vaccine; if previously vaccinated, they could require a booster dose of IPV [16].

P.53

Rabies

Human rabies episodes occur primarily from exposure to rabid animals. Laboratory and animal care personnel who are exposed to infected animals, their tissues, or their excretions are at risk for the disease. Also, rabies transmission to laboratory personnel has been reported in vaccine production and research facilities after exposure to high-titered infectious aerosols [127,128]. Theoretically, rabies can be transmitted to HCP from exposures to saliva from infected patients, but no episodes have been documented after bite or nonbite exposures [129,130].

It also is possible for rabies to be transmitted when other potentially infectious material (e.g., brain tissue or transplanted tissue) comes into contact with non-intact skin or mucous membranes [17,129]. Bites that penetrate the skin, especially bites to the face and hands, pose the greatest risk of transmission of rabies virus from animals to human beings [17]. The incubation period for rabies usually is 1–3 months, but longer periods have been reported.

Except for corneal transplants, exposures inflicted by infected humans could theoretically transmit rabies, but no laboratory-diagnosed instances occurring under such situations have been documented [17]. Two nonlaboratory-confirmed episodes of human-to-human rabies transmission in Ethiopia have been described [17]. The reported route of exposure in both instances was direct salivary contact from another human (a bite and a kiss). Routine delivery of health care to a patient with rabies is not an indication for PEP unless exposure of mucous membranes or non-intact skin to potentially infectious body fluids has occurred.

Exposures to rabies virus can be minimized by adhering to Standard Precautions when caring for persons with suspected or confirmed rabies [41] and by using proper biosafety precautions in laboratories [5]. Pre-exposure vaccination has been recommended for all personnel who (a) work with rabies virus or infected animals or (b) engage in diagnostic, production, or research activities with rabies virus [17,130,131]. Consideration also can be given to providing pre-exposure vaccination to animal handlers when research animals are obtained from the wild rather than from a known supplier that breeds the animals.

Rubella

Healthcare-associated transmission of rubella has occurred from HCP to other susceptible HCP and patients, and from patients to susceptible HCP and other patients [132,133].

Rubella is transmitted by contact with nasopharyngeal droplets from infected persons. The incubation period is variable but can range from 12–23 days; most persons have the rash 14–16 days after exposure. The disease is most contagious when the rash is erupting, but virus may be shed from 1 week before to 5–7 days after the onset of the rash [134]. Rubella in adults is usually a mild disease, lasting only a few days; 30% to 50% of patients may be subclinical or inapparent.

Droplet Precautions are used to prevent transmission of rubella. Infants with congenital rubella can excrete virus for months to years; when caring for such patients, it is advisable to use contact precautions for the first year of life unless nasopharyngeal and urine culture results are negative for rubella virus after 3 months of age [41].

Ensuring immunity among all HCP (male and female) is the most effective way to eliminate healthcare-associated transmission of rubella [3,4,6]. HCP should be considered susceptible to rubella if they lack (a) documentation of one dose of live rubella vaccine on or after their first birthday and (b) laboratory evidence of immunity (persons with indeterminate levels are considered susceptible). A history of previous rubella infection is unreliable and should not be considered indicative of immunity to rubella. Although birth before 1957 is generally considered acceptable evidence of rubella immunity, a dose of MMR has been recommended for those HCP who do not have laboratory evidence of immunity [4]. In addition, birth before 1957 is not considered acceptable evidence of rubella immunity for women of childbearing age; history of vaccination or laboratory evidence of rubella immunity is particularly important for women who may become pregnant [4]. Voluntary immunization programs usually are inadequate to ensure personnel protection [1,135]. Because many health departments mandate rubella immunity for HCP, personnel health programs should consult with their local or state health departments before establishing policies for their facilities.

Work restrictions are necessary for HCP who acquire rubella; ill HCP need to be excluded from duty for 5 days after the rash appears. Likewise, HCP susceptible to rubella require exclusion from duty from the seventh day after the first exposure through the 21st day after the last exposure [136].

Scabies and Pediculosis

Scabies

Scabies is caused by infestation with the mite Sarcoptes scabiei. The conventional (typical) clinical presentation of scabies includes intense pruritus and cutaneous tracks where mites have burrowed into the skin. Crusted or “Norwegian” scabies can develop among immunocompromised and elderly individuals in which their skin may become hyperkeratotic; pruritus may not be present. In conventional scabies, 10–15 mites are present; in crusted scabies, thousands of mites are harbored in the skin, increasing the potential for transmission [137,138].

Healthcare-associated outbreaks of scabies have occurred in a variety of healthcare settings. Healthcare-associated transmission of scabies occurs primarily through prolonged skin-to-skin contact with an infested person who

P.54


has conventional scabies [137,139]. Shorter periods of skin-to-skin contact with persons who have crusted scabies can result in transmission. HCP have acquired scabies while performing patient care duties such as sponge bathing, lifting, or applying body lotions [137,138,140]. Transmission by casual contact (e.g., by holding hands) or through inanimate objects, such as infested bedding, clothes, or other fomites, has been reported infrequently [141].

The use of Contact Precautions when taking care of infested patients before application of scabicides can decrease the risk of transmission to HCP [41,138]. Routine cleaning of the environment of patients with typical scabies, especially bed linens and upholstered furniture, will aid in eliminating the mites. Additional environmental cleaning procedures could be warranted for crusted scabies [137,138,142,143].

Most infested HCP have typical scabies with low mite loads [144]; a single correct application of a scabicide is adequate and immediately decreases the risk of transmission [19]. Several lotions are available to treat scabies. The treatment of choice is the topical use of permethrin (5%). Crotamiton and ivermectin are alternative drugs; ivermectin is taken orally and is effective for treating crusted scabies in immunocompromised persons [145]. There are no controlled evaluations of the efficacy of prophylactic scabicide therapy among HCP, and some experts recommend two applications of scabicide for all infested HCP [138,146,147]. If HCP continue to have symptoms after initial treatment, another application of scabicide could be needed. Persistent symptoms likely represent newly hatched mites rather than new infestation; however, pruritus after scabies infestation and treatment can persist for as long as 2 weeks, even without infestation [19]. In outbreak situations in which transmission continues to occur, prophylaxis can be warranted for both patients and exposed HCP [138,146].

Restrictions from patient care are indicated for HCP infested with scabies until after they receive initial treatment and have been medically evaluated and determined to be free of infestation. They should be advised to report for further evaluation if symptoms do not subside.

Pediculosis

Pediculosis is caused by infestation with any of three species of lice: Pediculus humanus capitus (human head louse), Pediculus humanus corporis (human body louse), or Phthirus pubis (pubic or crab louse). Head lice are transmitted by head-to-head contact or by contact with infested fomites such as hats, combs, or brushes. Healthcare-associated transmission, although not common, has occurred [137].

The recommended treatment of pediculosis includes permethrin cream 1%, pyrethrins with piperonyl butoxide, malathion 0.5%, or ivermectin [145,148]. Resistance to various drugs has been reported. HCP exposed to patients with pediculosis do not require treatment unless they show evidence of infestation.

Restriction from patient care is indicated for personnel with pediculosis until after they receive initial treatment and are found to be free of adult and immature lice. If symptoms do not subside after initial treatment, personnel should be advised to report for further evaluation.

Staphylococcal Infection or Carriage, Including Methicillin-Resistant Staphylococcus aureus

Staphylococcal infection and carriage occur frequently in human beings. In healthcare settings, the most important sources of S. aureus are infected or colonized patients. In recent years, healthcare-associated methicillin-resistant S. aureus (HA-MRSA) has accounted for approximately 80% of all S. aureus isolates reported to the National Nosocomial Infections Surveillance (NNIS) system [149,150]. The epidemiology of MRSA does not appear to differ from that of methicillin-susceptible, penicillin-resistant S. aureus except that outbreaks of MRSA tend to occur more frequently among elderly or immunocompromised patients or among patients with severe underlying conditions [151,152].

Although once found almost exclusively in healthcare settings, strains of S. aureus resistant to beta-lactam antibiotics (i.e., MRSA) are becoming increasingly common as a cause of skin and soft tissue infections in persons with no previous contact with the healthcare system. These strains are sometimes referred to as “community-associated MRSA (CA-MRSA).” There is no difference in recommended infection control measures for prevention of transmission of infection when caring for patients infected with either -MRSA or CA-MRSA.

Healthcare-associated transmission of S. aureus occurs primarily via the hands of HCP, which can become contaminated by contact with the colonized or infected body sites of patients or their surrounding contaminated environment [152,153]. HCP who are infected or colonized with S. aureus also can serve as reservoirs and disseminators of S. aureus[154,155,156,157]. The role of contaminated environmental surfaces in transmission of S. aureus has rarely been well documented [158] and remains controversial, although heavy contamination of fomites could facilitate transmission to patients by hands of HCP [152]. The incubation period for S. aureus infections varies by type of disease [159].

Carriage of S. aureus is most common in the anterior nares, but other sites, such as the hands, axilla, perineum, nasopharynx, or oropharynx, also can be involved [152]. Carriage ofS. aureus in the nares has been shown to correspond to hand carriage [149], and persons with skin lesions caused by it are more likely than asymptomatic nasal carriers to disseminate the organism.

Culture surveys of HCP can detect carriers of S. aureus but do not indicate which carriers are likely to disseminate organisms. Thus, such surveys are not cost effective and can subject HCP with positive culture results to unnecessary

P.55


treatment and removal from duty. Culture surveys could be indicated if, after a thorough epidemiologic investigation, HCP are linked to infections. Such implicated HCP then can be removed from clinical duties until carriage has been eradicated [152,154,160,161,162].

Several antimicrobial regimens have been used successfully to eradicate staphylococcal carriage in HCP. These regimens include orally administered antimicrobial agents (e.g., rifampin, clindamycin, or ciprofloxacin) alone or in combination with another oral (e.g., trimethoprim-sulfamethoxazole) or topical (mupirocin) antimicrobial [163,164]. Resistant S. aureus strains have emerged after the use of these oral or topical antimicrobial agents for eradication of colonization [163,164]. Thus, antimicrobial treatment to eradicate carriage should be limited to HCP who are carriers epidemiologically linked to disease transmission. Healthcare-associated transmission of S. aureus can be prevented by adherence to Standard Precautions and other forms of Transmission-Based Precautions as needed [41].

Restriction from patient-care activities or food handling is indicated for HCP who have draining S. aureus skin lesions until they have received appropriate therapy and the infection has resolved. No work restrictions are necessary for HCP colonized with S. aureus unless they have been epidemiologically implicated in S. aureus transmission within the facility.

Group A Streptococcus Infections

Group A Streptococcus (GAS) has been transmitted from infected patients to HCP after contact with infected secretions [165,166,167], and the infected personnel have subsequently acquired a variety of GAS-related illnesses (e.g., toxic shocklike syndrome, cellulitis, lymphangitis, and pharyngitis). HCP who were GAS carriers have infrequently been linked to sporadic outbreaks of surgical site, postpartum, or burn wound infections [168,169,170,171,172,173,174]. The incubation period is variable for other GAS infections [175].

Culture surveys to detect GAS carriage among HCP are not warranted unless HCP are epidemiologically linked to episodes of healthcare-associated infection (HAI). When thorough epidemiologic investigation has implicated HCP in HAI transmission, cultures can be obtained from skin lesions, pharynx, rectum, and vagina; GAS isolates obtained from HCP and patients can be serotyped to determine strain relatedness. Treatment of HCP carriers needs to be individually determined because (a) experience is limited regarding the treatment of HCP carriers implicated in GAS outbreaks and (b) carriage of GAS by HCP could recur through long periods [167,168,169,171]. Contact is the major mode of transmission of GAS in healthcare settings. Healthcare-associated transmission of GAS to HCP can be prevented by adherence to standard precautions or other Transmission-Based Precautions as needed [41].

Restriction from patient care activities and food handling is indicated for HCP with GAS infections until 24 hours after they have received appropriate therapy. However, no work restrictions are necessary for HCP colonized with GAS unless they have been epidemiologically linked to transmission of infection within the facility.

Tuberculosis

Healthcare-associated transmission of Mycobacterium tuberculosis (MTB) is well documented, but such transmission in the United States is generally low. However, the risk can be increased in healthcare facilities located in communities with (a) high rates of HIV, (b) high numbers of persons from tuberculosis (TB)-endemic countries, and (c) communities with a high prevalence of TB infection) [176,177]. In some areas in the United States, the incidence and prevalence of multidrug-resistant M. tuberculosis (MDR-TB) also have increased, and healthcare-associated MDR-TB outbreaks have occurred [178,179,180,181,182,183,184,185,186].

Transmission of MTB can be minimized by developing and implementing an effective TB control program that is based on a hierarchy of controls: (a) administrative controls, (b) engineering controls, and (c) respiratory protection [177,179,187,188,189,190].

A TB screening program for personnel is an integral part of a healthcare facility's comprehensive TB control program. Baseline tuberculin skin test (TST) testing of all personnel (including personnel with a history of bacille Calmette-Guérin [BCG] vaccination) during their placement evaluation will identify HCP who have been previously infected. For base-line testing, a two-step tuberculin skin test (TST) procedure for personnel without a TST in the past 12 months can be used to minimize the likelihood of confusing reactivity from an old infection (boosting) with reactivity from a recent infection (conversion). Decisions concerning the use of the two-step procedure for baseline testing in a particular facility should be based on the frequency of boosting in that facility. Criteria used for interpretation of a TST reaction can vary depending on (a) the purpose (diagnostic or epidemiologic) of the test, (b) the prevalence of TB in the population being tested, (c) the immune status of the host, and (d) any previous receipt of BCG immunization. At a minimum, annual TST testing is indicated for personnel with the potential for exposure to TB.

It also is important to obtain an initial chest radiograph for HCP with positive TST reactions, documented TST conversions, or pulmonary symptoms suggestive of TB. In addition, HCP who have positive TST reactions but also received adequate preventive treatment do not need repeat chest films unless they have pulmonary symptoms suggestive of TB.

It is important to administer TSTs to personnel as soon as possible after MTB exposures are recognized. Such immediate TST testing establishes a baseline with which

P.56


subsequent TSTs can be compared. A TST performed 8–10 weeks after the last exposure will indicate whether infection has occurred. Persons already known to have reactive TSTs need not be retested. HCP with evidence of new infection (i.e., TST conversions) need to be evaluated for active TB. If active TB is not diagnosed, preventive therapy should be considered [177].

For HCP with positive TST results who were probably exposed to drug-susceptible MTB, preventive therapy with isoniazid is indicated unless there are contraindications to such therapy [177]. Alternative preventive regimens have been proposed for persons who have positive TST-test results after exposure to drug-resistant MTB [190,191].

HCP with active pulmonary or laryngeal TB can be highly infectious; exclusion from duty is indicated until they are noninfectious. Work restrictions are not necessary for HCP receiving preventive treatment for latent TB (i.e., positive TST result without active disease) or for HCP with latent TB who do not accept preventive therapy. However, these HCP should be instructed to seek evaluation promptly if symptoms suggestive of TB develop.

Vaccinia

Through aggressive surveillance for smallpox combined with the effective use of smallpox vaccine (vaccinia virus vaccine), the World Health Organization was able to declare the world free of smallpox in 1980. The smallpox vaccine licensed for use in the United States is derived from infectious vaccinia virus. After vaccination, the virus can be cultured from the vaccination site until the scab has separated from the skin (2–21 days after vaccination); thus, susceptible persons could acquire vaccinia from a recently vaccinated person [192,193,194,195]. Covering the vaccination site and washing hands after contact with the vaccination site (including bandages) will prevent transmission.

Smallpox vaccination (every 10 years) is indicated for personnel who work directly with orthopox viruses (e.g., monkeypox, vaccinia, variola) or in animal care areas where orthopox viruses are studied. In selected instances, vaccination should be considered for HCP who provide care to recipients of recombinant vaccinia vaccine [4,12]. HCP who receive the vaccine may continue to have contact with patients if the vaccination site is covered and hand hygiene is strictly observed [12]. Vaccine is not recommended for HCP with immunosuppression or eczema or for HCP who are pregnant.

Varicella

Healthcare-associated transmission of varicella-zoster virus (VZV) is well recognized [196,197,198,199,200]. Sources for healthcare exposures have included patients, HCP, and visitors (including the children of HCP) with either varicella or herpes zoster.

The incubation period for varicella is usually 14–16 days but can be from 10–21 days after exposure, although the incubation period can be shorter in immunocompromised persons [201]. In persons who receive postexposure VZV immune globulin, the incubation period can be as long as 28 days after exposure. Transmission of infection may occur from 2 days before rash onset and usually as long as 5 days after rash onset [201].

VZV is transmitted by contact with infected lesions and, in hospitals, airborne transmission has occurred from patients with varicella or zoster to susceptible persons who had no direct contact with the infected patient [202,203,204,205,206]. Adherence to Airborne and Contact Precautions when caring for patients with known or suspected VZV infection can reduce the risk of transmission to HCP [41].

It generally is advisable to allow only HCP who are immune to varicella to take care of patients with VZV. Because of the possibility of transmission to and development of severe illness in high-risk patients, HCP with localized zoster should not take care of such patients until all lesions are dry and crusted [7,206]. HCP with localized zoster are not likely to transmit infection to immunocompetent patients if their lesions can be covered. However, some institutions may exclude HCP with zoster from work until their lesions dry and crust.

Serologic tests have been used to assess the accuracy of reported histories of chickenpox [207]. In adults, a history of varicella is highly predictive of serologic immunity (97% to 99% seropositive). Most adults who have negative or uncertain histories of varicella also are seropositive (71% to 93%). In healthcare institutions, serologic screening of HCP who have negative or uncertain histories is likely to be cost effective, depending on the relative costs of the test and vaccine [4,7].

Administration of varicella vaccine is recommended for all susceptible HCP, especially those who will have close contact with persons at high risk for serious complications [4,7,208]. Persistence of immunity to VZV after vaccination of HCP has been demonstrated up to 8.4 years [209].

Transmission of the vaccine virus is rare and has been documented in immunocompetent persons by polymerase chain reaction (PCR) analysis on only three occasions out of 15 million doses of varicella vaccine distributed. All three episodes resulted in mild disease without complications. Secondary transmission has not been documented in the absence of a vesicular rash postvaccination [7].

When unvaccinated susceptible HCP are exposed to varicella, they are potentially infectious 10–21 days after exposure, and exclusion from duty is indicated from the 10th day after the first exposure through the 21st day after the last exposure, or until all lesions are dry and crusted if varicella occurs. If vaccinated HCP are exposed to varicella, they can be serologically tested immediately after exposure to assess the presence of antibody [208]. If they are seronegative, they may be excluded from duty or

P.57


monitored daily for development of symptoms. Exclusion from duty is indicated if symptoms (fever, upper respiratory tract symptoms, or rash) develop.

Vaccination should be considered for exposed unvaccinated HCP without documented immunity [200,208]. Because the efficacy of postexposure vaccination is unknown, however, persons vaccinated after an exposure should be managed as previously recommended for unvaccinated persons.

The routine postexposure use of VZV immune globulin (VariZIG) is not recommended among immunocompetent HCP [7]. VariZIG can be costly, does not necessarily prevent varicella, and can prolong the incubation period by a week or more, thus extending the time that HCP will be restricted from duty. The use of VariZIG can be considered for immunocompromised (e.g., HIV-infected) or pregnant HCP [7,210]. Postexposure use of acyclovir can be effective and less costly than the use of VariZIG in some susceptible persons [210]. Antiviral medications are not recommended for routine PEP [201].

Viral Respiratory Infections, Including Influenza, Respiratory Syncytial Virus, and SARS

Healthcare-associated respiratory infections can be caused by a number of viruses, including adenoviruses, influenza virus, parainfluenza viruses, respiratory syncytial virus (RSV), rhinoviruses, or coronavirus (i.e., SARS) [211]. This section focuses on prevention of influenza, RSV, and SARS.

Influenza

Healthcare-associated transmission of influenza has been reported in acute and long-term care facilities [212,213,214,215]. Transmission has occurred from patients to HCP [213,214], from HCP to patients [216], and among HCP [215,217,218,219].

Influenza is believed to be transmitted 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 and by droplet nuclei or small-particle aerosols [10,220].

The incubation period of influenza usually is 1–5 days, and the period of greatest communicability is during the first 3 days of illness. However, virus can be shed before the onset of symptoms and as long as 7 days after illness onset and can be prolonged in young children and immunocompromised persons [221,222]. Adherence to Droplet Precautions can prevent healthcare-associated transmission of influenza [41].

Facilities that employ HCP are strongly encouraged to provide vaccine to HCP by using approaches that maximize vaccination [1,10,223].

During institutional influenza outbreaks, prophylactic antiviral agents (e.g., osetamivir or zanamivir) can be used in conjunction with influenza vaccine to reduce the severity and duration of illness among unvaccinated HCP. Osetamivir or zanamivir may be administered for 2 weeks after HCP vaccination or, in unvaccinated HCP, for the duration of influenza activity in the community [10,211]. Prophylactic antiviral medications can be offered to unvaccinated HCP who provide care to persons at high risk or to all HCP regardless of their vaccination status if the outbreak is suspected to be caused by a strain of influenza virus that is not well matched to the vaccine.

Respiratory Syncytial Virus

Healthcare-associated transmission of respiratory syncytial virus (RSV) is greatest during the early winter when community RSV outbreaks occur; patients, visitors, and HCP can transmit the virus in the healthcare setting. RSV infection is most common among infants and children, who are likely to experience more severe disease. Healthcare-associated transmission has been reported most frequently among newborn and pediatric patients [224,225], but outbreaks associated with substantial morbidity and mortality have been reported among adults in bone-marrow transplant centers [226], intensive care units [227], and long-term care facilities [228,229].

RSV is present in large numbers in the respiratory secretions of persons symptomatically infected with the virus and can be transmitted directly through large droplets during close contact with such persons or indirectly by hands or fomites that are contaminated with RSV. Hands can become contaminated by handling infected persons' respiratory secretions or contaminated fomites and can transmit RSV by touching the eyes or nose [211]. The incubation period ranges from 2–8 days; 4–6 days is most common. In general, infected persons shed the virus for 3–8 days, but young infants can shed it for as long as 3–4 weeks. Adherence to Contact Precautions effectively prevents healthcare-associated transmission.

SARS

SARS is an emerging respiratory tract infection linked to a novel coronavirus that first appeared in late 2002 in China and spread globally until 2005. In several Asian countries, SARS-coronavirus caused outbreaks in healthcare settings with transmission to large numbers of HCP and patients. Although the most important modes of transmission are by (large) droplet and contact, airborne transmission has not been ruled out. High-risk exposures, such as those associated with aerosolization of respiratory secretions and exposures to “supershedders” have been associated with transmission of the disease to HCP outside the United States [211]. Clinicians evaluating suspected episodes of SARS should use Standard Precautions together with Airborne and Contact Precautions [41,211,230].

Work Restrictions

Because large numbers of HCP can have viral respiratory illnesses during the winter, it might not be possible to restrict

P.58


infected HCP from all patient-care duties. Nevertheless, it could be prudent to restrict HCP with acute viral respiratory infections from the care of high-risk patients during community outbreaks of RSV and influenza [231].

References

  1. Centers for Disease Control and Prevention. Interventions to increase influenza vaccination of health-care workers—California and Minnesota. MMWR Morb Mortal Wkly Rep2005;54:196–199.
  2. Heseltine PNR, Ripper M, Wohlford P. Nosocomial rubella—consequences of an outbreak and efficacy of a mandatory immunization program. Infect Control1985;6:371–374.
  3. Centers for Disease Control and Prevention. General recommendations on immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP) and the American Academy of Family Physicians (AAFP). MMWR Morb Mortal Wkly Rep2002;51(RR-2):1–36.
  4. Centers for Disease Control and Prevention. Immunization of health-care workers: recommendations of the Advisory Committee on Immunization Practices (ACIP) and the Hospital Infection Control Practices Advisory Committee (HICPAC). MMWR Morb Mortal Wkly Rep1997;46(RR-18):1–42.
  5. Centers for Disease Control. Protection against viral hepatitis: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep1990:39(RR-2):1–27.
  6. Centers for Disease Control and Prevention. Measles, mumps, and rubella—vaccine use and strategies for elimination of measles, rubella, and congenital rubella syndrome and control of mumps: recommendations of the Advisory Committee on Immunizations Practices (ACIP). MMWR Morb Mortal Wkly Rep1998;47(RR-7):1–57.
  7. Centers for Disease Control and Prevention. Prevention of varicella: recommendations of the Advisory Committee on Immunizations Practices (ACIP). MMWR Morb Mortal Wkly Rep1996;45(RR-11):1–36.
  8. Centers for Disease Control and Prevention. Prevention and control of meningococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP).MMWR Morb Mortal Wkly Rep2000;49(RR-7):1–10.
  9. Centers for Disease Control and Prevention. Update: vaccine side effects, adverse reactions, contraindications and precautions: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep1996;45(RR-12):1–35.
  10. Centers for Disease Control and Prevention. Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep2006;55(RR-10):1–41.
  11. Centers for Disease Control and Prevention. Vaccinia (smallpox) vaccine: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR Morb Mortal Wkly Rep2001;50(RR-10):1–25.
  12. Centers for Disease Control and Prevention: Recommendations for using smallpox vaccine in a pre-event vaccination program: supplemental recommendations of the Advisory Committee on Immunizations Practices (ACIP) and the Healthcare Infection Control Practices Advisory Committee (HICPAC). MMWR Morb Mortal Wkly Rep2003;52(RR-7):1–16.
  13. Centers for Disease Control. Diphtheria, tetanus, pertussis: recommendations for vaccine use and other preventive measures—recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR Morb Mortal Wkly Rep1991;40(RR-10):1–28.
  14. Centers for Disease Control and Prevention. Recommended antimicrobial agents for treatment and postexposure prophylaxis of pertussis: 2005 CDC guideline. MMWR Morb Mortal Wkly Rep2005:54(RR-14):1–16.
  15. Centers for Disease Control and Prevention. Prevention of pneumococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep1997;46(RR-8):1–24.
  16. Centers for Disease Control and Prevention. Poliomyelitis prevention in the United States: updated recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep2000;49(RR-5):1–22.
  17. Centers for Disease Control. Rabies prevention—United States, 1999: recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR Morb Mortal Wkly Rep1999;49(RR-1):1–21.
  18. Centers for Disease Control and Prevention. Recommendations of the Advisory Committee on Immunization Practices (ACIP): use of vaccines and immune globulins in persons with altered immunocompetence. MMWR Morb Mortal Wkly Rep1993;42(RR-4):1–18.
  19. Herwaldt LA, Pottinger JM, Carter CD, et al. Exposure workups. Infect Control Hosp Epidemiol1997;18:850–871.
  20. US Department of Labor, Occupational Health and Safety Administration. Reporting fatalities and multiple hospitalization incidents to OSHA (www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=1278)
  21. US Department of Labor, Occupational Safety and Health Administration. Bloodborne pathogens. (www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=1005).
  22. Centers for Disease Control and Prevention. HIPAA privacy rule and public health: guidance from the CDC and the U.S. Department of Health and Human Services. MMWR Morb Mortal Wkly Rep2003;52(Suppl.):1–12.
  23. Centers for Disease Control. Epidemic keratoconjunctivitis in an ophthalmology clinic—California. MMWR Morb Mortal Wkly Rep1990;39:598–601.
  24. Ford E, Nelson KE, Warren D. Epidemiology of epidemic keratoconjunctivitis. Epidemiol Rev1987;9:244–261.
  25. Birenbaum E, Linder N, Varsano N, et al. Adenovirus type 8 conjunctivitis outbreak in a neonatal intensive care unit. Arch Dis Child1993;68:610–611.
  26. Warren D, Nelson KE, Farrar JA, et al. A large outbreak of epidemic keratoconjunctivitis: problems in controlling nosocomial spread. J Infect Dis1989;160:938–943.
  27. Jernigan JA, Lowry BS, Hayden FG, et al. Adenovirus type 8 epidemic keratoconjunctivitis in an eye clinic: risk factors and control. J Infect Dis1993;167:1307–1313.
  28. Onorato IM, Morens DM, Martone WJ, Stansfield SK. Epidemiology of cytomegaloviral infections: recommendations for prevention and control. Rev Infect Dis1985;7:479–497.
  29. Demmler GJ, Yow MD, Spector SA, et al. Nosocomial cytomegalovirus infections within two hospitals caring for infants and children. J Infect Dis1987;156:9–16.
  30. Ahlfors K, Ivarsson SA, Johnson T, Renmarker K. Risk of cytomegalovirus infection in nurses and congenital infection in their offspring. Acta Paediatr Scand1981;70:819–823.
  31. Gerberding JL, Bryant-LeBlanc CE, Nelson K, et al. Risk of transmitting the human immunodeficiency virus, cytomegalovirus, and hepatitis B virus to health care workers exposed to patients with AIDS and AIDS-related conditions. J Infect Dis1987;156:1–8.
  32. Blackman JA, Murph JR, Bale JF. Risk of cytomegalovirus infection among educators and health care personnel serving disabled children. Pediatr Infect Dis J1987;6:725–729.
  33. Adler SP. Hospital transmission of cytomegalovirus. Infect Agents Dis1992;1:43–49.
  34. Balcarek KB, Bagley R, Cloud G, Pass RF. Cytomegalovirus infection among employees of a children's hospital: no evidence for increased risk associated with patient care.JAMA1990;263:840–844.
  35. Spector SA. Transmission of cytomegalovirus among infants in hospital documented by restriction-endonuclease-digestion analyses. Lancet1983;2:378–381.
  36. Adler SP. Cytomegalovirus and child day care: evidence for an increased infection rate among day-care workers. N Engl J Med1989;321:1290–1296.
  37. Hutto C, Little EA, Ricks R. Isolation of cytomegalovirus from toys and hands in a day care center. J Infect Dis1986;154:527–530.

P.59

  1. Faix RG. Survival of cytomegalovirus on environmental surfaces. J Pediatr1985;106:649–652.
  2. Finney JW, Miller KM, Adler SP. Changing protective and risky behaviors to prevent child-to-parent transmission of cytomegalovirus. J Appl Behav Anal1993;26:471–472.
  3. American Academy of Pediatrics. Summaries of infectious diseases: cytomegalovirus infection. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006, 273–277.
  4. Garner JS, Hospital Infection Control Practices Advisor Committee. Guideline for isolation precautions in hospitals. Infect Control Hosp Epidemiol1996;17:53–80.
  5. Anderson GS, Penfold JB. An outbreak of diphtheria in a hospital for the mentally subnormal. J Clin Pathol1973;26:606–615.
  6. Gray RD, James SM. Occult diphtheria infection in a hospital for the mentally subnormal. Lancet1973;1:1105–1106.
  7. Palmer SR, Balfour AH, Jephcott AE. Immunisation of adults during an outbreak of diphtheria. BMJ1983;286:624–626.
  8. Centers for Disease Control and Prevention. Update: diphtheria epidemic—new independent states of the former Soviet Union, January 1995–March 1996. MMWR Morb Mortal Wkly Rep1996;45:693–697.
  9. Centers for Disease Control and Prevention. Diphtheria epidemic—new independent states of the former Soviet Union, 1990–1994. MMWR Morb Mortal Wkly Rep1995;44:177–181.
  10. Steere AC, Craven PJ, Hall WJ III, et al. Person-to-person spread of Salmonella typhimuriumafter a hospital common-source outbreak. Lancet 1975;1:319–322.
  11. Toivanen P, Toivanen A, Olkkonen L, Aantaa S. Hospital outbreak of Yersinia enterocoliticainfection. Lancet 1973;1:801–803.
  12. Ratnam S, Mercer E, Picco B, et al. A nosocomial outbreak of diarrheal disease due to Yersinia enterocoliticaserotype 0:5, biotype 1. J Infect Dis 1982;145:242–247.
  13. Kurtz JB, Lee TW, Pickering D. Astrovirus associated gastroenteritis in a children's ward. J Clin Pathol1977;30:948–952.
  14. Dryjanski J, Gold JWM, Ritchie MT, et al. Cryptosporidiosis: case report in a health team worker. Am J Med1986;80:751–752.
  15. Lewis DC, Lightfoot NF, Cubitt WD, Wilson SA. Outbreaks of astrovirus type 1 and rotovirus gastroenteritis in a geriatric in-patient population. J Hosp Infect1989;14:9–14.
  16. Koch KL, Phillips DJ, Aber RC, Current WL. Cryptosporidiosis in hospital personnel: evidence for person-to-person transmission. Ann Intern Med1985;102:593–596.
  17. Pike RM. Laboratory-associated infections: summary and analysis of 3921 cases. Health Lab Sci1976;13:105–114.
  18. Tauxe RV, Hassan LF, Findeisen KO, et al. Salmonellosis in nurses: lack of transmission to patients. J Infect Dis1988;157:370–373.
  19. Carter AO, Borczyk AA, Carlson JAK, et al. A severe outbreak of Escherichia coli O157:H7-associated hemorrhagic colitis in a nursing home. N Engl J Med1987;317:1496–1500.
  20. Zingg W, Colombo C, Jucker T, et al. Impact of an outbreak of norovirus infection on hospital resources. Infect Control Hosp Epidemiol2005;26:263–267.
  21. Mattner F, Mattner L, Borck HU, Gastmeier P. Evaluation of the impact of the source (patient vs. staff)on nosocomial norovirus outbreak severity. Infect Control Hosp Epidemiol2005;26:268–272.
  22. Schroeder SA, Aserkoff B, Brachman PS. Epidemic salmonel-losis in hospitals and institutions: public health importance and outbreak management. N Engl J Med1968;279:674–678.
  23. Khuri-Bulos NA, Abu Khalaf M, Shehabi A, Shami K. Foodhandler-associated Salmonellaoutbreak in a university hospital despite routine surveillance cultures of kitchen employees. Infect Control Hosp Epidemiol 1994;15:311–314.
  24. Centers for Disease Control. Viral agents of gastroenteritis. MMWR Morb Mortal Wkly Rep1990;39(RR-5):1–24.
  25. Doebbeling BN, Stanley GL, Sheetz CT, et al. Comparative efficacy of alternative hand-washing agents in reducing nosocomial infections in intensive care units. N Engl J Med1992;327:88–93.
  26. Centers for Disease Control and Prevention. Guideline for hand hygiene in health-care settings: Recommendations of the Healthcare Infection Control Practices Advisory Committee and the HICPAC/SHEA/APIC/IDSA Hand Hygiene Task Force. MMWR Morb Mortal Wkly Rep2002;51(RR-16):1–45.
  27. Centers for Disease Control. Recommendations for collection of laboratory specimens associated with outbreaks of gastroenteritis. MMWR Morb Mortal Wkly Rep1990;39(RR-14):1–13.
  28. Rosenblum LS, Villarino ME, Nainan OV, et al. Hepatitis A outbreak in a neonatal intensive care unit: risk factors for transmission and evidence of prolonged viral excretion among preterm infants. J Infect Dis1991;164:476–482.
  29. Carl M, Kantor RJ, Webster HM, et al. Excretion of hepatitis A virus in the stools of hospitalized patients. J Med Virol1982;9:125–129.
  30. Drusin LM, Sohmer M, Groshen SL, et al. Nosocomial hepatitis A infection in a paediatric intensive care unit. Arch Dis Child1987;62:690–695.
  31. Baptiste R, Koziol D, Henderson DK. Nosocomial transmission of hepatitis A in an adult population. Infect Control1987;8:364–370.
  32. Azimi PH, Roberto RR, Guralnik J, et al. Transfusion-acquired hepatitis A in a pre-mature infant with secondary nosocomial spread in an intensive care nursery. Am J Dis Child1986;140:23–27.
  33. Skidmore SJ, Gully PR, Middleton JD, et al. An outbreak of hepatitis A on a hospital ward. J Med Virol1985;17:175–177.
  34. Klein BS, Michaels JA, Rytel MW, et al. Nosocomial hepatitis A: a multinursery outbreak in Wisconsin. JAMA1984;252:2716–2721.
  35. Krober MS, Bass JW, Brown JD, et al. Hospital outbreak of hepatitis A: risk factors for spread. Pediatr Infect Dis J1984;3:296–299.
  36. Doebbeling BN, Li N, Wenzel RP. An outbreak of hepatitis A among health care workers: risk factors for transmission. Am J Public Health1993;83:1679–1684.
  37. Watson JC, Fleming DC, Borella AJ, et al. Vertical transmission of hepatitis A resulting in an outbreak in a neonatal intensive care unit. J Infect Dis1993;167:567–571.
  38. Centers for Disease Control and Prevention. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR Morb Mortal Wkly Rep2006;55(RR-7):1–23.
  39. Van Dyke RB, Spector SA. Transmission of herpes simplex virus type 1 to a newborn infant during endotracheal suctioning for meconium aspiration. Pediatr Infect Dis J1984;3:153–156.
  40. Linneman CC, Buchman TG, Light IJ, Ballard JL. Transmission of herpes-simplex virus type 1 in a nursery for the newborn: identification of isolates by D.N.A. “fingerprinting.”Lancet1978;1:964–966.
  41. Kleiman MB, Schreiner RL, Eitzen H, et al. Oral herpesvirus infection in nursery personnel: infection control policy. Pediatrics1982;70:609–612.
  42. Buchman TG, Roizman B, Adams G, Stover BH. Restriction endonuclease fingerprinting of herpes simplex virus DNA: a novel epidemiological tool applied to a nosocomial outbreak. J Infect Dis1978;138:488–498.
  43. Greaves WL, Kaiser AB, Alford RH, Schaffner W. The problem of herpetic whitlow among hospital personnel. Infect Control1980;1:381–385.
  44. Adams G, Stover BH, Keenlyside RA, et al. Nosocomial herpetic infections in a pediatric intensive care unit. Am J Epidemiol1981;113:126–132.
  45. American Academy of Pediatrics. Summaries of infectious diseases: herpes simplex. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006:361–370.
  46. Pereira FA. Herpes simplex: evolving concepts. J Am Acad Dermatol1996;35:503–520.
  47. Perl TM, Haugen TH, Pfaller MA, et al. Transmission of herpes simplex virus type 1 infection in an intensive care unit. Ann Intern Med1992;117:584–586.
  48. Turner R, Shehab Z, Osborne K, Hendley JO. Shedding and survival of herpes simplex virus from “fever blisters.” Pediatrics1982;70:547–549.

P.60

  1. Spruance SL, Overall JC Jr, Kern ER, et al. The natural history of recurrent herpes simplex labialis: implications for antiviral therapy. N Engl J Med1977;297:69–75.
  2. Davis RM, Orenstein WA, Frank JA Jr, et al. Transmission of measles in medical settings, 1980 through 1984. JAMA1986;255:1295–1298.
  3. Atkinson WL, Markowitz LE, Adams NC, Seastrom GR. Transmission of measles in medical settings—United States, 1985–1989. Am J Med1991;91(suppl 3B):320S–324S.
  4. Raad II, Sheretz RJ, Rains CS, et al. The importance of nosocomial transmission of measles in the propagation of a community outbreak. Infect Control Hosp Epidemiol1989;10:161–166.
  5. Istre GR, McKee PA, West GR, O'Mara DJ, Rettig PJ, Stuemky J, et al. Measles spread in hospital settings: an important focus of disease transmission? Pediatrics1987;79:356–358.
  6. Rivera ME, Mason WH, Ross LA, Wright HT Jr. Nosocomial measles infection in a pediatric hospital during a community-wide epidemic. J Pediatr1991;119:183–186.
  7. Rank EL, Brettman L, Katz-Pollack H, et al. Chronology of a hospital-wide measles out-break: lessons learned and shared from an extraordinary week in late March 1989. AJIC Am J Infect Control1992;209:315–318.
  8. Bloch AB, Orenstein WA, Ewing WM. Measles outbreak in a pediatric practice: airborne transmission in an office setting. Pediatrics1985;75:676–683.
  9. American Academy of Pediatrics. Summaries of infectious diseases: measles. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006:441–452.
  10. Braunstein H, Thomas S, Ito R. Immunity to measles in a large population of varying age. Am J Dis Child1990;144:296–298.
  11. Centers for Disease Control. Laboratory-acquired meningococcal disease—United States, 2000. MMWR Morb Mortal Wkly Rep2002;51:141–144.
  12. Broome CV. The carrier state: Neisseria meningitidis. J Antimicrob Chemother1986;18(suppl. A)25–34.
  13. Gehanno JF, Kohen-Couderc L, Lemeland JG, Leroy J. Nosocomial meningococcemia in a physician. Infect Control Hosp Epidemiol1999;20:564–565.
  14. American Academy of Pediatrics. Summaries of infectious diseases: meningococcal disease. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006:452–460.
  15. Riedo FX, Plikaytis BD, Broome CV. Epidemiology and prevention of meningococcal disease. Pediatr Infect Dis J1995;14:643–657.
  16. Wharton M, Cochi SL, Hutcheson RH, Schaffner W. Mumps transmission in hospitals. Arch Intern Med1990;150:47–49.
  17. Fischer PR, Brunetti C, Welch V, Christenson JC. Nosocomial mumps: report of an outbreak and its control. Am J Infect Control1996;24:13–18.
  18. American Academy of Pediatrics. Summaries of infectious diseases: mumps. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006:464–468.
  19. Williams WW, Preblud SR, Reichelderfer PS, Hadler SC. Vaccines of importance in the hospital setting: problems and developments. Infect Dis Clin North Am1989;3:701–22.
  20. Koplan JP, Preblud SR. A benefit-cost analysis of mumps vaccine. Am J Dis Child1982;136:362–364.
  21. Centers for Disease Control and Prevention. Notice to readers: updated recommendations of the Advisory Committee on Immunization Practices (ACIP)for the control and elimination of mumps. MMWR Morb Mortal Wkly Rep2006;55:629–630.
  22. Hersh BS, Fine PEM, Kent WK, et al. Mumps outbreak in a highly vaccinated population. J Pediatr1991;119:187–193.
  23. Shishiba T, Matsunaga Y. An outbreak of erythema infectiosum among hospital staff members including a patient with pleural fluid and pericardial effusion. J Am Acad Dermatol1993;29:265–267.
  24. Seng C, Watkins P, Morse D, et al. Parvovirus B19 outbreak on an adult ward. Epidemiol Infect1994;113:345–353.
  25. Bell LM, Naides J, Stoffman P, et al. Human parvovirus B19 infection among hospital staff members after contact with infected patients. N Engl J Med1989;321:485–491.
  26. Harrison J, Jones DE. Human parvovirus B19 in health care workers. Occup Med1995;45:93–96.
  27. Pillay D, Patou G, Hurt S, Kibbler CC, Griffiths PD. Parvovirus B19 outbreak in a children's ward. Lancet1992;339:107–109.
  28. Evans JP, Rossiter MA, Kumaran TO, et al. Human parvovirus aplasia: case due to cross infection in a ward. BMJ1984;288:681.
  29. Cohen BJ, Courouce AM, Schwartz TF, et al. Laboratory infection with parvovirus B19 [letter]. J Clin Pathol1988;41:1027–1028.
  30. Anderson LJ, Gillespie SM, Török TJ, et al. Risk of infection following exposures to human parvovirus B19. Behring Inst Mitt1990;85:60–63.
  31. Dowell SF, Török TJ, Thorp JA, et al. Parvovirus B19 infection in hospital workers: community or hospital acquisition. J Infect Dis1995;172:1076–1079.
  32. Török TJ. Parvovirus B19 and human disease. Adv Intern Med1992;37:431–455.
  33. Centers for Disease Control and Prevention. Outbreaks of pertussis associated with hospitals—Kentucky, Pennsylvania, and Oregon, 2003. MMWR Morb Mortal Wkly Rep2005;54:67–71.
  34. Weber DJ, Rutala WA. Pertussis: a continuing hazard for healthcare facilities. Infect Control Hosp Epidemiol2001;22:736–740.
  35. Linneman CC Jr, Ramundo N, Perlstein PH, et al. Use of pertussis vaccine in an epidemic involving hospital staff. Lancet1975;2:540–543.
  36. Christie C, Glover AM, Willke MJ, et al. Containment of pertussis in the regional pediatric hospital during the greater Cincinnati epidemic of 1993. Infect Control Hosp Epidemiol1995;16:556–563.
  37. Shefer A, Dales L, Nelson M, et al. Use and safety of acellular pertussis vaccine among adult hospital staff during an outbreak of pertussis. J Infect Dis1995;171:1053–1056.
  38. Orenstein WA. Pertussis in adults: epidemiology, signs, symptoms, and implications for vaccination. Clin Infect Dis1999;28(suppl. 2):S147–S150.
  39. Weber DJ, Rutala WA. Management of healthcare workers exposed to pertussis. Infect Control Hosp Epidemiol1994;15:411–415.
  40. American Academy of Pediatrics. Summaries of infectious diseases: poliovirus infections. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006:542–547.
  41. Centers for Disease Control and Prevention. Paralytic poliomyelitis—United States, 1980–1994. MMWR Morb Mortal Wkly Rep1997;46:79–83.
  42. Winkler WG, Fashinell TR, Leffingwell L, et al. Airborne rabies transmission in a laboratory worker. JAMA1973;226:1219–1221.
  43. Centers for Disease Control. Rabies in a laboratory worker—New York. MMWR Morb Mortal Wkly Rep1977;26:183–184.
  44. Helmick CG, Tauxe RV, Vernon AA. Is there a risk to contacts of patients with rabies? Rev Infect Dis1987;9:511–518.
  45. Centers for Disease Control and Prevention. Investigation of rabies infection in organ donor and transplant recipients—Alabama, Arkansas, Oklahoma, and Texas, 2004.MMWR Morb Mortal Wkly Rep2004;53:1–3.
  46. Centers for Disease Control and Prevention, National Institutes for Health. Biosafety in microbiological and biomedical laboratories. 3rd ed. Atlanta: US Department of Health and Human Services, Public Health Service, 1993.
  47. Greaves WL, Orenstein WA, Stetler HC, et al. Prevention of rubella transmission in medical facilities. JAMA1982;248:861–864.
  48. Strassburg MA, Stephenson TG, Habel LA, Fannin SL. Rubella in hospital employees. Infect Control1984;5:123–126.
  49. American Academy of Pediatrics. Summaries of infectious diseases: rubella. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006:574–579.

P.61

  1. Fraser V, Spitznagel E, Medoff G, Dunagan WC. Results of a rubella screening program for hospital employees: a five-year review (1986–1990) Am J Epidemiol1993;138:756–764.
  2. Centers for Disease Control and Prevention. Control and prevention of rubella: evaluation and management of suspected outbreaks, rubella in pregnant women, and surveillance for congenital rubella syndrome. MMWR Morb Mortal Wkly Rep2001;50(RR-12):1–23.
  3. Lettau LA. Nosocomial transmission and infection control aspects of parasitic and ectoparasitic diseases, part III. Ectoparasites/summary and conclusions. Infect Control Hosp Epidemiol1991;12:179–185.
  4. Juranek DD, Currier RW, Millikan LE. Scabies control in institutions. In: Orkin M, Maiback HI, eds. Cutaneous infestations and insect bites. New York: Dekker, 1985,139–156.
  5. Gooch JJ, Strasius SR, Beamer B, et al. Nosocomial outbreak of scabies. Arch Dermatol1978;114:897–898.
  6. Centers for Disease Control. Scabies in health-care facilities—Iowa. MMWR Morb Mortal Wkly Rep1988;37:178–179.
  7. Thomas MC, Giedinghagen DH, Hoff GL. Brief report: an outbreak of scabies among employees in a hospital-associated commercial laundry. Infect Control1987;8:427–429.
  8. Arlian LG, Estes SA, Vyszenski-Moher DL. Prevalence of Sarcoptes scabeiin the homes and nursing homes of scabietic patients. J Am Acad Dermatol 1988;19:806–811.
  9. Estes SA, Estes J. Therapy of scabies: nursing homes, hospitals, and the homeless. Semin Dermatol1993;12:26–33.
  10. Hopper AH, Salisbury J, Jegadeva AN, et al. Epidemic Norwegian scabies in a geriatric unit. Age and Ageing1990;19:125–127.
  11. Drugs for parasitic infections. Med Lett Drugs TherAugust 2004, p. 9.
  12. Degelau J. Scabies in long-term care facilities. Infect Control Hosp Epidemiol1992;13:421–425.
  13. Obasanjo OO, Wu P, Conlon M, Perl TM. An outbreak of scabies in a teaching hospital: lessons learned. Infect Control Hosp Epidemiol2001;22:13–18.
  14. Juranek DD. Pediculosis capitisin school children: epidemiologic trends, risk factors, and recommendations for control. In: Orkin M, Maiback HI, eds. Cutaneous infestations and insect bites. New York: Dekker, 1985,199–211.
  15. Wenzel RP. Healthcare workers and the incidence of nosocomial infection: can treatment of one influence the other? a brief review. J Chemother1994;6(suppl 4):33–37,39–40.
  16. Panlilio AL, Culver DH, Gaynes RP, et al. Methicillin-resistant Staphylococcus aureusin U.S. hospitals, 1975–1991. Infect Control Hosp Epidemiol 1992;13:582–586.
  17. Boyce JM. Methicillin-resistant Staphylococcus aureus: detection, epidemiology and control measures. Infect Dis Clin North Am1989;3:901–913.
  18. Boyce JM. Methicillin-resistant Staphylococcus aureusin hospitals and long-term care facilities: microbiology, epidemiology, and preventive measures. Infect Control Hosp Epidemiol 1992;13:725–737.
  19. Henderson DK. Managing methicillin-resistant staphylococci: a paradigm for preventing nosocomial transmission of resistant organisms. Am J Med2006;121(6 suppl 1):S45–S53.
  20. Boyce JM, Opal SM, Byone-Potter G, Medeiros AA. Spread of methicillin-resistant Staphylococcus aureusin a hospital after exposure to a health care worker with chronic sinusitis. Clin Infect Dis 1993;17:496–504.
  21. Sherertz RJ, Reagan DR, Hampton KD, et al. A cloud adult: the Staphylococcus aureus-virus interaction revisited. Ann Intern Med1996;124:539–547.
  22. Belani A, Sherertz RJ, Sullivan ML, et al. Outbreak of staphylococcal infection in two hospital nurseries traced to a single nasal carrier. Infect Control1986;7:487–490.
  23. Kreiswirth BN, Kravitz GR, Schlievert PM, Novick RP. Nosocomial transmission of a strain of Staphylococcus aureuscausing toxic shock syndrome. Ann Intern Med1986;105:704–707.
  24. Layton MC, Perez M, Heald P, Patterson JE. An outbreak of mupirocin-resistant Staphylococcus aureuson a dermatology ward associated with an environmental reservoir.Infect Control Hosp Epidemiol 1993;14:369–375.
  25. American Academy of Pediatrics. Summaries of infectious diseases: staphylococcal infections. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006,598–610.
  26. Boyce JM, Landry M, Deetz TR, DuPont HL. Epidemiologic studies of an outbreak of nosocomial methicillin-resistant Staphylococcus aureusinfections. Infect Control1981;2:110–116.
  27. Mulligan ME, Murray-Leisure KA, Ribner BS, et al. Methicillin-resistant Staphylococcus aureus: a consensus review of the microbiology, pathogenesis, and epidemiology with implications for prevention and management. Am J Med1993;94:313–328.
  28. Reboli AC, John JF, Platt CG, Cantley JR. Methicillin-resistant Staphylococcus aureusoutbreak at a Veterans' Affairs medical center: importance of carriage of the organism by hospital personnel. Infect Control Hosp Epidemiol 1990;11:291–296.
  29. Boyce JM. MRSA patients: proven methods to treat colonization and infection. J Hosp Infect2001;48(suppl A):S9–S14.
  30. Kluytmans JA, Wetheim HF. Nasal carriage of Staphylococcus aureusand prevention of nosocomial infections. Infection 2005;33:3–8.
  31. Valenzuela TD, Hooton TM, Kaplan EL, Schlievert PM. Transmission of toxic strep syndrome from an infected child to a firefighter during CPR. Ann Emerg Med1991;20:90–92.
  32. Rammelkamp CH, Mortimer EA, Wolinsky E. Transmission of streptococcal and staphylococcal infection. Ann Intern Med1964;60:753–758.
  33. Weber DJ, Rutala WA, Denny FW Jr. Management of health-care workers with pharyngitis or suspected streptococcal infections. Infect Control Hosp Epidemiol1996;17:753–761.
  34. Mastro TD, Farley TA, Elliott JA, et al. An outbreak of surgical-wound infections due to group A Streptococcuscarried on the scalp. N Engl J Med 1990;323:968–972.
  35. Viglionese A, Nottebart VF, Bodman HA, Platt R. Recurrent group A streptococcal carriage in a health care worker associated with widely separated nosocomial outbreaks.Am J Med1991;91(suppl 3B):329S–333S.
  36. Paul SM, Genese C, Spitalny K. Postoperative group A β-hemolytic Streptococcusoutbreak with the pathogen traced to a member of a healthcare worker's household. Infect Control Hosp Epidemiol 1990;11:643–646.
  37. Berkelman RL, Martin D, Graham DR, et al. Streptococcal wound infections caused by a vaginal carrier. JAMA1982;247:2680–2682.
  38. Schaffner W, Lefkowitz LB Jr, Goodman JS, Koenig MG. Hospital outbreak of infections with group A streptococci traced to an asymptomatic anal carrier. N Engl J Med1969;280:1224–1225.
  39. Richman DD, Breton SJ, Goldmann DA. Scarlet fever and group A streptococcal surgical wound infection traced to an anal carrier. J Pediatr1977;90:387–390.
  40. Centers for Disease Control and Prevention. Nosocomial group A streptococcal infections associated with asymptomatic health-care workers—Maryland and California, 1997.MMWR Morb Mortal Wkly Rep1999;48:163–166.
  41. American Academy of Pediatrics. Summaries of infectious diseases: group A streptococcal infections. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2006:610–620.
  42. Barnes PF, Bloch AB, Davidson PT, Snider DE. Tuberculosis in patients with human immunodeficiency syndrome. N Engl J Med1991;324:1644–1650.
  43. Centers for Disease Control and Prevention. Guidelines for preventing transmission of Mycobacterium tuberculosisin health-care settings, 2005. MMWR Morb Mortal Wkly Rep 2005;54(RR-17):1–141.
  44. Edlin BR, Tokars JI, Grieco MH, et al. An outbreak of multidrug-resistant tuberculosis among hospitalized patients with the acquired immunodeficiency syndrome. N Engl J Med1992;326:1514–1521.
  45. Stroud LA, Tokars JI, Grieco MH, et al. Evaluation of infection control measures in preventing the nosocomial transmission of multidrug-resistant Mycobacterium tuberculosisin a New York City hospital. Infect Control Hosp Epidemiol1995;16:141–147.

P.62

  1. Beck-Sagué CM, Dooley SW, Hutton MD, et al. Hospital outbreak of multidrug-resistant Mycobacterium tuberculosisinfections: factors in transmission to staff and HIV-infected patients. JAMA 1992;268:1280–1286.
  2. Wenger PN, Otten J, Breeden A, Orfas E, et al. Control of nosocomial transmission of multidrug-resistant Mycobacterium tuberculosisamong healthcare workers and HIV-infected patients. Lancet 1995;345:235–240.
  3. Dooley SW, Villarino ME, Lawrence M, et al. Nosocomial transmission of tuberculosis in a hospital unit for HIV-infected patients. JAMA1992;267:2632–2635.
  4. Pearson ML, Jereb JA, Frieden TR, et al. Nosocomial transmission of multidrug-resistant Mycobacterium tuberculosis: a risk to patients and health care workers. Ann Intern Med1992;117:191–196.
  5. Cleveland JL, Kent J, Gooch BF, et al. Multidrug-resistant Mycobacterium tuberculosisin an HIV dental clinic. Infect Control Hosp Epidemiol 1995;16:7–11.
  6. Ridzon R, Kenyon T, Luskin-Hawk R, et al. Nosocomial transmission of human immuno-deficiency virus and subsequent transmission of multidrug-resistant tuberculosis in a healthcare worker. Infect Control Hosp Epidemiol1997;18:422–423.
  7. Jereb JA, Klevens M, Privett TD, et al. Tuberculosis in health care workers at a hospital with an outbreak of multidrug-resistant Mycobacterium tuberculosis. Arch Intern Med1995;155:854–859.
  8. Pugliese G, Tapper ML. Tuberculosis control in health care. Infect Control Hosp Epidemiol1996;17:819–827.
  9. Menzies D, Fanning A, Yuan L, Fitzgerald M. Tuberculosis among health care workers. N Engl J Med1995;332:92–98.
  10. Jarvis WR. Nosocomial transmission of multidrug-resistant Mycobacterium tuberculosis. Am J Infect Control1995;23:146–151.
  11. Maloney SA, Pearson ML, Gordon MT, et al. Efficacy of control measures in preventing nosocomial transmission of multidrug-resistant tuberculosis to patients and health care workers. Ann Intern Med1995;122:90–95.
  12. Centers for Disease Control and Prevention. Management of persons exposed to multidrug-resistant tuberculosis. MMWR Morb Mortal Wkly Rep1992;41(RR-11):59–71.
  13. Lane JM, Ruben FL, Neff JM, Millar JD. Complications of smallpox vaccination, 1968: results of ten statewide surveys. J Infect Dis1970;122:303–309.
  14. Centers for Disease Control. Contact spread of vaccinia from a recently vaccinated Marine—Louisiana. MMWR Morb Mortal Wkly Rep1984;33:37–38.
  15. Centers for Disease Control. Contact spread of vaccinia from a National Guard vaccinee—Wisconsin. MMWR Morb Mortal Wkly Rep1985;34:182–183.
  16. Centers for Disease Control. Vaccinia outbreak—Newfoundland. MMWR Morb Mortal Wkly Rep1981;30:453–455.
  17. Gustafson TL, Shebab A, Brunell PA. Outbreak of varicella in a newborn intensive care nursery. Am J Dis Child1984;138:548–550.
  18. Alter SJ, Hammond JA, McVey CJ, Myers MG. Susceptibility to varicella-zoster virus among adults at high risk for exposure. Infect Control1986;7:448–451.
  19. Krasinski K, Holzman RS, LaCouture R, Florman A. Hospital experience with varicella-zoster virus. Infect Control1986;7:312–316.
  20. Haiduven-Griffiths D, Fecko H. Varicella in hospital personnel: a challenge for the infection control practitioner. Am J Infect Control1987;15:207–211.
  21. Weber DJ, Rutala WA. Varicella immunization of health care workers. In: Panlilio A, Cardo D, eds. Bailliere's clinical infectious diseases: prevention strategies for health care workers. London: Harcourt, 2000:405–419.
  22. American Academy of Pediatrics. Summaries of infectious diseases: varicella-zoster infections. In: Pickering LK, Baker CJ, Long SS, McMillan JA, eds. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006:711–725.
  23. Asano Y, Iwayama S, Miyata T, et al. Spread of varicella in hospitalized children having no direct contact with an indicator zoster case and its prevention by a live vaccine.Biken J1980;23:157–161.
  24. Sawyer MH, Chamberlin CJ, Wu YN, et al. Detection of varicella-zoster virus DNA in air samples from hospital rooms. J Infect Dis1994;169:91–94.
  25. LeClair JM, Zaia JA, Levin MJ, et al. Airborne transmission of chickenpox in a hospital. N Engl J Med1980;302:450–453.
  26. Gustafson TL, Lavely GB, Brawner ER Jr, et al. An outbreak of airborne nosocomial varicella. Pediatrics1982;70:550–556.
  27. Josephson A, Gombert M. Airborne transmission of nosocomial varicella from localized zoster. J Infect Dis1988;158:238–241.
  28. Struewing JP, Hyams KC, Tueller JE, Gray GC. The risk of measles, mumps, and varicella among young adults: a sero-survey of US Navy and Marine Corps recruits. Am J Public Health1993;83:1717–1720.
  29. Centers for Disease Control and Prevention. Prevention of varicella: updated recommendations of the Advisory Committee on Immunization Practices (ACIP) MMWR Morb Mortal Wkly Rep1999;48(RR-6):1–5.
  30. Saiman L, LaRussa P, Steinberg SP, et al. Persistence of immunity to varicella-zoster virus after vaccination of healthcare workers. Infect Control Hosp Epidemiol2001;22:279–283.
  31. Centers for Disease Control and Prevention. Varicella-related deaths among adults—United States, 1997. MMWR Morb Mortal Wkly Rep1997;46:409–412.
  32. Centers for Disease Control and Prevention. Guideline for preventing health-care–associated pneumonia, 2003. MMWR Morb Mortal Wkly Rep2004;53(RR-03):1–36.
  33. Evans ME, Hall KL, Berry SE. Influenza control in acute care hospitals. AJIC Am J Infect Control1997;25:357–362.
  34. Kapila R, Lintz DI, Tecson FT, et al. A nosocomial outbreak of influenza. A. Chest1977;71:576–579.
  35. Van Voris LP, Belshe RB, Shaffer JL. Nosocomial influenza B virus infection in the elderly. Ann Intern Med1982;96:153–158.
  36. Pachucki CT, Walsh Pappas SA, Fuller GF, et al. Influenza A among hospital personnel and patients: implications for recognition, prevention, and control. Arch Intern Med1989;149:77–80.
  37. Centers for Disease Control. Suspected nosocomial influenza cases in an intensive care unit. MMWR Morb Mortal Wkly Rep1988;37:3–4, 9.
  38. Centers for Disease Control and Prevention. Outbreak of influ-enza A in a nursing home—New York, December 1991–January 1992. MMWR Morb Mortal Wkly Rep1992;41:129–131.
  39. Gross PA, Rodstein M, LaMontagne JR, et al. Epidemiology of acute respiratory illness during an influenza outbreak in a nursing home. Arch Intern Med1988;148:559–561.
  40. Cartter ML, Renzullo PO, Helgerson SD, et al. Influenza outbreaks in nursing homes: how effective is influenza vaccine in the institutionalized elderly? Infect Control Hosp Epidemiol1990;11:473–478.
  41. Bean B, Moore BM, Sterner B, et al. Survival of influenza viruses on environmental surfaces. J Infect Dis1982;146:47–51.
  42. Hall CB, Douglas RG. Nosocomial influenza infection as a cause of intercurrent fevers in infants. Pediatrics1975;55:673–677.
  43. Noble GR. Epidemiological and clinical aspects of influenza. In: Beare AS, ed. Applied influenza research. Boca Raton, FL: CRC Press, 1982:11–49.
  44. Adal KA, Flowers RH, Anglim AM, et al. Prevention of nosocomial influenza. Infect Control Hosp Epidemiol1996;17:641–648.
  45. Hall CB. Respiratory syncytial virus: its transmission in the hospital environment. Yale J Biol Med1982;55:219–223.
  46. Snydman DR, Greer C, Meissner HC, McIntosh K. Prevention of nosocomial transmission of respiratory syncytial virus in a newborn nursery. Infect Control Hosp Epidemiol1988;9:105–108.
  47. Harrington RD, Hooton TM, Hackman RC, et al. An outbreak of respiratory syncytial virus in a bone marrow transplant center. J Infect Dis1992;165:987–993.

P.63

  1. Guidry GG, Black-Payne CA, Payne DK, et al. Respiratory syncytial virus infection among intubated adults in a university medical intensive care unit. Chest1991;100:1377–1384.
  2. Falsey AR. Noninfluenza respiratory virus infection in long-term care facilities. Infect Control Hosp Epidemiol1991;12:602–608.
  3. Sorvillo FJ, Huie SF, Strassburg MA, et al. An outbreak of respiratory syncytial virus pneumonia in a nursing home for the elderly. J Infect1984;9:252–256.
  4. Centers for Disease Control and Prevention. Outbreak of severe acute respiratory syndrome—worldwide, 2003. MMWR Morb Mortal Wkly Rep2003;52:241–246.
  5. Valenti WM, Hruska JF, Menegus MA, Freeburn MJ. Nosocomial viral infections: III. Guidelines for prevention and control of exanthematous viruses, gastroenteritis viruses, picornaviruses, and uncommonly seen viruses. Infect Control1980;2:38–49.


If you find an error or have any questions, please email us at admin@doctorlib.org. Thank you!