Kent A. Sepkowitz, MD
http://www.annals.org/cgi/content/full/125/11/917
1 December 1996 | Volume 125 Issue 11 | Pages 917-928
Background: Health care workers are at occupational risk for a vast
array of infections that cause substantial illness and occasional
deaths. Despite this, few studies have examined the incidence,
prevalence, or exposure-associated rates of infection or have considered
infection-specific interventions recommended to maintain worker safety.
Objective: To characterize the type and frequency of infections, the
recommended interventions, and the costs of protecting health care
workers. Part II of this two-part review focuses on infections caused by
bloodborne organisms, organisms spread through the oral-fecal route, and
organisms spread through direct contact. It also reviews established
interventions for controlling transmission.
Data Sources: A MEDLINE search and examination of infectious disease
and infection control journals.
Data Selection: All English-language articles and meeting abstracts
published from January 1983 to February 1996 related to occupationally
acquired infections among health care workers were reviewed. Outbreak-
and non-outbreak-associated incidence and prevalence rates were derived,
as were costs to prevent, control, and treat infections in health care
workers.
Data Synthesis: Occupational transmission to health care workers was
identified for numerous diseases, including infections caused by
bloodborne organisms (human immunodeficiency virus, hepatitis B virus,
hepatitis C virus, Ebola virus), organisms spread through the oral-fecal
route (salmonella, hepatitis A virus), and organisms spread through
direct contact (herpes simplex virus, Sarcoptes scabiei). Most
outbreak-associated attack rates range from 15% to 40%. Occupational
transmission is usually associated with violation of one or more of
three basic principles of infection control: handwashing, vaccination of
health care workers, and prompt placement of infectious patients into
appropriate isolation.
Conclusions: The risk for occupationally acquired infections is an
unavoidable part of daily patient care. Occupationally acquired
infections cause substantial illness and occasional deaths among health
care workers. Further studies are needed to enhance compliance with
established infection control approaches. As health care is being
reformed, the risk for and costs of occupationally acquired infection
must be considered.
More than 10 years have elapsed since the last major consideration of
occupationally acquired infections in health care workers [1, 2]. Since
then, much has changed—new infections have been identified, diagnostic
tests for previously recognized diseases have been improved, the use of
molecular epidemiologic techniques in outbreak investigations has
increasingly become routine, and outpatient and home care have become
more common.
The topic of occupationally acquired airborne infections in health
care workers was addressed in part I of this two-part review [3].
Infections such as occupationally acquired tuberculosis, varicella-zoster,
measles, and respiratory syncytial virus infections were considered, as
were ethical and historical concerns. Part II of this review discusses
infections caused by bloodborne organisms (such as human
immunodeficiency virus [HIV], hepatitis B virus [HBV], hepatitis C virus
[HCV], cytomegalovirus [CMV], and Ebola virus), organisms spread through
the oral-fecal route (such as salmonella and hepatitis A virus [HAV]),
and organisms spread through direct contact (such as herpes simplex
virus and Sarcoptes scabiei). It then summarizes known interventions,
including handwashing, vaccination, and prompt placement of potentially
infectious patients into appropriate isolation. The risks to health care
workers inherent in health care delivery should be considered by
planners of health care for the next century.
Bloodborne Transmission
Bloodborne transmission Table 1 has received increased attention with
the advent of the acquired immunodeficiency syndrome epidemic and, more
recently, the outbreak of Ebola virus infection. Although many
nonmedical occupational groups are at risk for diseases caused by
organisms transmitted through the airborne or oral-fecal route, health
care workers are one of the few groups at risk for the transmission of
bloodborne pathogens. In addition to blood-to-blood transmission, some
of these pathogens may be transmitted in saliva, as occurs with CMV and
B virus infection.
Table 1. Occupationally Acquired Infections Resulting from Bloodborne
Transmission*
| Table 1. Occupationally Acquired
Infections Resulting from Bloodborne Transmission*

|
HIV Infection
The occupational risk for transmission of HIV has been the subject of
numerous thorough reviews [9, 34-40] and is not considered in detail
here. The rate of seroconversion after exposure ranges from 0.1% to 0.4%
[4, 5, 35]. In general, a large inoculum—including that from a source
case with more advanced disease, a stick with a large-bore
blood-containing needle, or a more severe injury—is associated with a
higher rate of transmission [41].
Occupational transmission has been confirmed in 49 health care
workers and may have occurred in 102 others [6] (Table 2). Percutaneous
exposure alone was the source of transmission for most confirmed cases
of infection (42 persons). The optimal management of health care workers
after exposure remains unknown. A recent retrospective, case–control
study examined risks associated with transmission in 31 case-patients
and 679 controls [41]. In this analysis, the use of zidovudine was
associated with a 79% risk reduction, although zidovudine failure has
occurred [42]. Provisional Public Health Service recommendations include
three antiretroviral drugs (zidovudine, lamivudine, and indinavir) for
high-risk exposures [7, 43].
Table 2. Health Care Workers with Documented and Possible Cases of
Occupationally Acquired HIV Infection in the United States, through
1995*
| Table 2. Health Care Workers with
Documented and Possible Cases of Occupationally Acquired HIV
Infection in the United States, through 1995*

|
Hepatitis B
Hepatitis B virus was one of the first bloodborne pathogens to be
recognized as an occupational risk among health care workers [44-46]. An
early review [46] found a preponderance of cases of hepatitis B among
pathologists, laboratory workers, and blood bank workers, alerting
investigators to the risks of exposure to blood. Subsequent studies
confirmed these early observations [47-63]. In general, the
seroprevalence of HBV in health care workers is twofold to fourfold
higher than that of blood donor controls [47, 61]; the highest rates are
seen among dentists [8, 47]; physicians [8, 47, 61, 63]; laboratory
workers [8, 47, 63, 64]; dialysis workers [63]; cleaning service
employees [51, 62]; and nurses [8], including emergency department
nurses [56]. Widespread transmission may occur from a single surgical
procedure [65]. Many infections in health care workers are asymptomatic
[48].
In prevaccine surveys, the annual incidence of hepatitis B was 5 to
10 times higher among physicians and dentists than among blood donors
and more than 10 times higher among surgeons, dialysis workers, persons
caring for the mentally handicapped, and laboratory workers exposed to
blood [47, 61, 66].
The risk for transmission from a single needlestick varies according
to E antigen status: 1% to 6% for E antigen-negative blood compared with
22% to 40% with E antigen-positive blood [8-10, 67]. However,
transmission of E antigen-negative blood has caused fulminant hepatitis
requiring liver transplantation [68]. Hepatitis delta virus has been
transmitted to a surgeon [69]. The quality-adjusted loss in life
expectancy is similar for persons who receive needlesticks involving a
source patient who has HBV infection and for persons who receive
needlesticks involving a source patient with HIV infection [70, 71]. Not
all cases of HBV transmission are explained by needlesticks, suggesting
that other modes of spread may be possible [8, 9, 72].
Infection control interventions, such as the segregation of dialysis
recipients according to surface antigen status [73, 74] and vaccination
[74, 75], have effectively reduced occupational acquisition of HBV.
However, the Centers for Disease Control and Prevention (CDC) calculate
that 6500 to 9000 new HBV infections occurred among health care workers
in 1990 [8]. Given the natural history of HBV infection, 300 to 950 of
these health care workers (5% to 10%) will eventually develop chronic
HBV infection that will lead to death from cirrhosis in 100 to 150
persons and to fatal hepatocellular carcinoma in 25 to 40 persons [8].
Despite this, HBV vaccination of health care workers remains incomplete.
In one study, 23% of health care workers were unvaccinated [52], a rate
similar to that of anesthesiologists in the United Kingdom [76]. A
three-vaccine series is 88% effective [77, 78]; decreased response is
seen among recipients who are older, who smoke, or who are obese [77,
78].
Hepatitis C
The 1990 introduction of a test for HCV infection has dramatically
improved our understanding of disease epidemiology. Because HBV and HCV
have similar modes of transmission, it was assumed that groups of health
care workers at increased risk for hepatitis B also would be at risk for
hepatitis C [19, 52, 60]. This, however, has not proven to be true for
many groups, including dialysis workers [79-82], laboratory workers
[83], persons who work with the mentally impaired [84], and surgical
staff [83]. Indeed, although "occupational exposure" accounts for about
2% of all cases of hepatitis C [19], the seroprevalence of HCV among
health care workers is roughly similar to that of the general population
(about 1%) [83, 85-89]. Dentists do have increased risk [16, 17]: In one
serosurvey [16], significantly more dentists (1.7%) than blood donors
(0.13%) were seropositive for HCV; the highest rate of seroprevalence
was seen among oral surgeons (9%).
Seroconversion occurs in 1.2% to 10% of nonimmune health care workers
who receive needlesticks from a source patient with hepatitis C [11-15].
Variation among control populations [90-92], variation in employee
populations [18, 93, 94], and variation in the sensitivity of tests for
HCV [19] have contributed to the lack of consensus about risk [14, 18,
94]. Optimal management of a needlestick is unknown, but the
administration of immune globulin is not recommended [18, 40].
Cytomegalovirus Infection
The prevalence of CMV infection in the United States varies according
to geography, patient age, and group studied and ranges from 40% to 95%.
The annual community incidence among adults is about 2% [21].
Transmission of CMV may occur through sexual contact or through contact
with infectious blood. Respiratory secretions, saliva, and urine may
also transmit CMV, as shown by increased rates of CMV infection among
day care workers (8% to 10% per year) [95, 96]. Early incidence [97-99]
and prevalence studies [100], as well as meta-analyses [101, 102] and
reviews [103, 104], suggested that pediatric health care workers had
elevated risk, similar to that of day care workers. Subsequent reports
[20, 21, 35, 105, 106], however, have not shown this risk, perhaps
because many recent studies were done in the era of universal
precautions. Similarly, no increase in CMV infection among dialysis
workers [107] or renal transplantation workers [108] has been found.
Studies using molecular epidemiologic techniques have also shown that
health care workers are at low risk for occupational transmission of CMV
[109, 110]. No transmission was documented among 188 health care workers
at a pediatric chronic care or neonatal unit in which many of the
patients were heavy CMV shedders [110]. Molecular analysis of CMV
recovered from one of two nurses who seroconverted showed discordance
with CMV taken from a known occupational contact and concordance with
CMV from a family member with new disease.
Ebola Virus Infection and Other Viral Hemorrhagic Fevers
The recent outbreak of Ebola virus infection in Zaire involved 296
cases and was associated with a 79% mortality rate [22-24]. At least 90
persons (32%) were health care workers [24, 25], a fact that led the CDC
to issue recommendations for the management of persons with suspected
viral hemorrhagic fevers [26]. Among the recommended practices were use
of universal precautions, use of strict barrier protection, restriction
of workers and visitors, and use of negative-pressure ventilation in the
presence of respiratory symptoms.
In a 1979 outbreak of Ebola virus infection in Sudan, persons who
provided nursing care were five times more likely to develop disease
than were those who provided no care [111]. In all, 34 cases of
infection occurred and 22 persons died. Similar outbreaks involving
health care workers have been reported with Crimean hemorrhagic
fever-Congo virus infection in Pakistan, where 10 of 17 exposed workers
developed disease and 2 died [112]; Lassa fever virus infection on an
obstetrics ward, where 7 of 26 exposed workers developed disease and at
least 1 died [113]; and Marburg virus infection [114, 115]. Ribavirin
was effective as therapy for 3 health care workers with Crimean
hemorrhagic fever-Congo virus [116].
B Virus Infection
Fatal, occupationally acquired infection with B virus (Herpesvirus
simiae) was described in 1932, when a physician died of
encephalomyelitis 3 days after being bitten by a clinically well rhesus
monkey [117, 118]. Since that time, more than 24 infections with B virus
have occurred in humans, and 18 persons have died [119]. The peak
incidence of B virus infection occurred in 1957-1958, in conjunction
with the production and testing of poliomyelitis vaccines [119]. In the
1980s, a cluster of four cases (two of which were fatal) occurred in a
research facility in Pensacola, Florida [27], leading to the development
of new recommendations for monkey handlers [28]. Treatment with
acyclovir may be effective [27, 29], but the optimal duration of therapy
is unknown and may extend years.
Other Infections
Creutzfeldt-Jakob disease is a uniformly fatal neurodegenerative
disorder that has been the subject of extensive epidemiologic
investigation [31, 32]. Health care workers are not considered to be a
group at risk [31], but cases have been reported in two neurosurgeons
[31, 32], two histopathology technicians [120, 121], and one pathologist
[122]. In none of these cases could a specific incident that may have
led to transmission be recalled. Recent recommendations stress
sterilization of equipment to minimize the risk [30].
Outbreaks of Epstein-Barr virus infection have seldom been reported.
Transmission of Epstein-Barr virus to 9 of 29 medical staff (31%) in an
obstetrics and gynecology clinic was never explained [123].
Investigators at a hospital that treated hundreds of cases of
nasopharyngeal carcinoma suggested that nosocomial spread was a major
source of Epstein-Barr virus infection among health care workers at
their institution [124]. Occupationally acquired cases of syphilis
[125], malaria [126], and yellow fever [127] have been reported.
Oral-Fecal Transmission
Enteric pathogens spread in various ways, including through the
ingestion of contaminated food; through direct person-to-person contact;
and through contact with infectious waste, usually feces (Table 3).
Insufficient handwashing by health care workers probably contributes
more to the transmission of these pathogens than to the transmission of
bloodborne or airborne pathogens.
Table 3. Occupationally Acquired Infections Resulting from Oral-Fecal
Transmission*

Salmonellosis
The number of cases of salmonellosis has increased steadily since the
1950s, and food-related outbreaks continue to occur. The effect of
contaminated food was vividly shown by a recent outbreak that was traced
to ice cream and that caused more than 200 000 cases of salmonellosis
across 41 states [153]. In general, institutional disease accounts for
10% to 30% of all cases [138, 154, 155]. Hospitals, nursing homes,
psychiatric facilities, pediatric wards, and nurseries are common sites
[138, 154-157].
Massive contamination of mashed potatoes was responsible for a large
outbreak at a hospital in Jordan [128], where 183 of 619 persons (19.6%)
(including 150 hospital employees) developed disease. Investigation
showed that 11 of 61 kitchen workers (18%) were infected with
salmonella; all had been negative on cultures taken 3 months earlier,
suggesting that routine surveillance cultures may not be useful.
Person-to-person transmission of salmonella occurred in a hospital in
Maine [158], where several workers who drank tainted eggnog developed
salmonellosis. As the outbreak progressed, at least eight additional
workers who had not drunk eggnog also developed disease.
Person-to-person spread has been suggested by other studies [159, 160],
including the report of an outbreak that involved fasting patients who
had recently had gastrectomy and infants who were not receiving hospital
food. In a nursing home in Tennessee, 8 of 160 employees (5%) developed
salmonellosis; the highest attack rate was seen in laundry workers
[129]. Several laundry workers had no direct contact with infected
patients, suggesting that transmission occurred through contaminated
linen.
Interrupting an identified outbreak may be difficult. In Cincinnati,
Ohio, 24 of 52 kitchen workers were found to have Salmonella drypool,
which accounted for at least 11 cases of salmonellosis among staff who
ate food that had been prepared at the hospital [161]. The epidemic was
stopped only after 50 of 52 kitchen workers were treated with
trimethoprim-sulfamethoxazole. Because 32% of treated employees
developed reactions to drug treatment, this approach may not be
advisable for routine outbreaks. In one study [162], the cost of
identifying and treating one salmonella-infected health care worker,
including cultures, antibiotic therapy, and lost work time, was $3500.
Hepatitis A
The number of cases of hepatitis A gradually increased in the United
States in the 1980s; incidence peaked in 1989 [163]. Common risk factors
for the acquisition of HAV include contact with an infected person
(26%), employment in or attendance at a day care center (14%), and use
of injection drugs (11%) [163]. The overall prevalence rate of HAV
infection in the United States is about 38%, similar to rates described
in health care workers (35% to 54%) [164-166]. In one report [165], the
rates of antibodies to HAV were significantly higher in nurses older
than 30 years of age than in office workers; in another study, charwomen
had the highest rate [166].
Many outbreaks have been reported in pediatric or neonatal intensive
care units [130, 133-136] and orphanages [167]. A neonate who acquired
HAV through a transfusion spread the organism to 10 of 61 susceptible
nurses (16%) [136]. An infected child who had an immune defect that
resulted in an inability to seroconvert to HAV remained undiagnosed for
a protracted period, leading to transmission of HAV to 15 of 102 staff
[131]. Adults with diarrhea have also transmitted the virus to health
care workers [168, 169].
An outbreak of HAV infection in a burn unit occurred despite the use
of appropriate infection control measures, and HAV was spread to 11 of
59 susceptible nurses (18.6%) [132]. Eating on the hospital ward was the
most important risk factor for infection. Other nosocomial outbreaks
have resulted from the consumption of contaminated food, including
orange juice [170] and sandwiches [171]. One outbreak resulted in 66
cases of clinical or subclinical disease [171].
The intramuscular administration of immune globulin to persons who
have contact with HAV-infected patients has been used effectively for
many years to prevent secondary cases. Defining which, if any, health
care workers should routinely be vaccinated for HAV is currently being
discussed [137, 172].
Shigellosis
Given the small inoculum size required for transmission of shigella
[173], the reason for the relative infrequency of nosocomial shigella
infection has been the subject of speculation but remains obscure [138].
Outbreaks in day care centers have been reported [153, 174]. At a
teaching hospital in Kenya [175], salmonella accounted for 10% and
shigella accounted for 2.5% of 360 cases of nosocomial diarrhea. In
another report [139], 3 of 32 workers in a newborn nursery developed
shigellosis. All were chronic nail-biters. The cost of controlling the
outbreak was $5000.
Cryptosporidiosis
Cryptosporidia have been spread to a medical intern and possibly
other staff [176], a nurse [177], and a laboratory researcher [178].
Proper infection control techniques failed to control an outbreak in
Wales, where 5 of 16 nurses developed disease [140]. This outbreak was
perpetuated by severe environmental contamination; replacement of sinks
and hand basin taps with leg-operated machinery proved to be an
effective intervention. Veterinarians and animal handlers also have an
increased risk for cryptosporidiosis. In one outbreak [141],
cryptosporidiosis developed in 10 of 20 veterinary students who worked
with calves that had died of the disease. This outbreak was similar to
another calf-related outbreak, in which 12 of 18 animal handlers became
infected [142].
Helicobacter pylori Infection
Several recent reports have examined the seroprevalence of antibodies
to Helicobacter pylori among health care workers [143-147]. One found
that seroprevalence was higher among endoscopists (69%) than among
internists (40%) [145]. Two other studies [143, 147] found that about
52% of endoscopists and only about 14% to 21% of blood donors were
seropositive for H. pylori [143, 147]. Dentists have no increased
seroprevalence despite contact with saliva [144]. These findings suggest
that contact with contaminated equipment, rather than routine patient
care or contact with saliva [144], is an important mode of transmission.
Other Infections
Clostridium difficile has emerged as an important cause of
hospital-acquired diarrhea and has been cultured from the hands of 14%
to 59% of asymptomatic health care workers during outbreaks [179, 180].
However, controversy exists about the potential role of C. difficile as
an occupationally acquired organism [181-183]. Possible nosocomial
transmission of fatal C. difficile infection to an otherwise healthy
worker has recently been reported [184]. Several nursing home outbreaks
of infection with the Norwalk virus (a small, round-structure virus)
have resulted in rates of transmission to staff that range from 30% to
50% [148-152]. In one outbreak, "care attendants" had an incidence rate
of 92% [149]. In an outbreak of Escherichia coli O157: H7-associated
hemorrhagic colitis in a nursing home [185], 18 of 137 staff members
(13%) developed symptoms; 5 of the 18 had bloody diarrhea. No health
care worker developed the hemolytic-uremic syndrome. Cholera has spread
to staff [186], but studies done before vaccination found no risk to
personnel on a polio ward [187].
Eating hospital food and drinking hospital beverages expose health
care workers to the same risks faced by patients and visitors, as shown
by hospital food-related outbreaks of salmonellosis [128, 158, 161],
hepatitis A [170, 171], yersiniosis [188], campylobacteriosis [189],
cyclospora infection [190], and typhoid fever [191].
Direct Contact
Infection may spread to health care workers as a result of direct
contact. Outbreaks of scabies, particularly among nurses and laundry
workers, have been reported from several hospitals [192-195]. In one
hospital [193], almost 300 health care workers were affected, including
45 of 200 laundry workers (22.5%), 126 of 1448 nurses (8.7%), and 32 of
87 health care workers (36.8%) who had direct contact with patients. The
outbreak cost about $50 000 for days of work missed and for treatment.
In another outbreak [194], secondary spread to the spouses of health
care workers was seen. A large, sustained outbreak at an extended-care
facility [195] resulted in the infection of 26% of the staff, including
half of all nurses.
Cutaneous herpes (herpetic whitlow) is an occupational hazard for
dentists; anesthesiologists; dialysis technicians; physiotherapists;
physicians; and nurses [196, 197], particularly nurses in intensive care
units [196, 198, 199]. That dermatologists face risk associated with
laser treatment of warts with lasers has been suggested [200, 201],
including a recent study [202] in which molecular epidemiologic
techniques were used. Tinea corporis may spread to staff [203, 204],
further thwarting control efforts.
Specific Groups of Health Care Workers at Risk
Laboratory personnel, veterinarians and animal handlers,
pathologists, surgeons, dentists, anesthesiologists, and laundry workers
are at risk for an array of specific infections (Table 4). In addition,
the concerns of pregnant health care workers are considerable and unique
because certain otherwise mild infections may affect fetal development.
Table 4. Occupationally Acquired Infections Encountered in Specific
Groups of Health Care Workers*

Laboratory-acquired infections have been extensively studied
[205-207]. Collins [205] identified 2168 infections and 48 deaths from
diseases ranging from brucellosis and Q fever (the most common) to
rabies and the plague. The potential danger of working in laboratories
is dramatically illustrated by the fate of Ricketts (for whom Rickettsia
was named), who died of laboratory-acquired rickettsiosis [205].
Neisseria meningitidis has fatally infected laboratory workers [208].
Although many clinical health care workers receive prophylaxis after
exposure to N. meningitidis, studies have not documented the spread of
this organism to health care workers in the clinical setting [209].
Interventions
Despite the seemingly limitless number of infections that health care
workers can acquire on the job, the interventions to prevent
transmission are simple, well known, and effective. Compliance with
three practices—handwashing, vaccination, and appropriate isolation of
infected patients—can control transmission dramatically and
cost-effectively.
Handwashing
Handwashing is the oldest, simplest, and cheapest way to control the
nosocomial spread of infectious organisms. In the 1840s, Semmelweis
introduced the practice of "hygienic hand disinfection" on obstetric
wards in Vienna, decreasing the maternal mortality rate from 13.7% to
1.3% [241-243]. Since that time, handwashing has become routine for all
persons doing any surgical procedures; however, workers involved in
medical care have notoriously low rates of handwashing—usually less than
50% [244-248].
Numerous studies have examined the specific aspects of handwashing,
including type of soap [249, 250], type of sink [251], drying method
[252], and method of scrubbing [243, 253-255]. One study showed that
chlorhexidine was both significantly more effective and more often used
than alcohol and soap [249]. Additional strategies to improve compliance
[244, 247, 251] are necessary because compliance, not brand of soap or
type of sink, remains the major obstacle to preventing transmission. In
addition to preventing patient-to-patient spread, handwashing may
prevent the acquisition by health care workers of such infections as
those caused by rhinovirus, respiratory syncytial virus, HAV,
adenovirus, and salmonella. Emphasis of this might promote compliance
and lead to an overall reduction of transmission.
Vaccination
Recommendations about vaccines are updated frequently [256], but
vaccination of health care workers remains incomplete [257-259]. Indeed,
compliance with HBV vaccination remains appalling: In a recent survey in
an inner-city hospital, 23% of workers were unvaccinated [52]. Health
care workers are often the source of outbreaks of measles and rubella
[257] and, less commonly, HBV infection [260], further emphasizing the
need for improved compliance with vaccination. A demonstration of
evidence of antibodies to vaccine-preventable diseases, including
measles, mumps, rubella, and hepatitis B, is required of employees at
many hospitals. The varicella-zoster virus has recently been recommended
[261], whereas the role of the HAV vaccine is being determined.
Isolation
Appropriate isolation of infected patients is another time-honored
practice [262]. It is the most complicated and potentially expensive of
the three standard interventions. Difficulties arise when trying to
balance the need to protect health care workers against the realities of
cost, as shown by the recent debate surrounding tuberculosis control
[263]. A common sense approach may find an acceptable middle ground
[264, 265]. In general, universal precautions for infections with
bloodborne organisms, respiratory and droplet isolation precautions for
infections with airborne organisms, and contact isolation precautions
(or enteric precautions) for infections caused by organisms spread by
the oral-fecal route are effective and widely used [33]. Updated
guidelines for isolation precautions have recently been published [33].
Conclusions
Public attention has recently focused on the risk to patients posed
by infectious health care workers. Transmission of HIV from an infected
dentist to four patients [266] stirred a national debate in the United
States about mandatory HIV testing of health care workers. Workers have
been the source of many infections other than HIV infections, including
tuberculosis [267], hepatitis B [260], measles, and rubella [257].
Little public concern or awareness, however, has been directed toward
the risk to health care workers of caring for contagious persons,
despite the continuing illness and occasional death that result from
occupationally acquired diseases.
Several recent developments have changed many aspects of occupational
risk. Old diseases that may be spread to health care workers, such as
tuberculosis and diphtheria, have reemerged, forcing the reexamination
of existing infection control policies [268]. New technology has
identified old infections, such as hepatitis C. This, in turn, has been
followed by numerous studies delineating the natural history and
transmission rates of disease, including risk to health care workers
[11-19, 79-94]. Seemingly new diseases with undefined risks, such as HIV
and Ebola virus infection, have become evident, leading to appreciation
of risks to health care workers and recommendations for worker safety
[7, 26].
Recognition and confirmation of outbreaks, as well as improved
understanding of transmission [269, 270], rely increasingly on molecular
epidemiologic techniques. These techniques have been applied to
investigations of many diseases, including CMV infection [109],
adenovirus infection [271, 272], hepatitis B [260], hepatitis C [273],
HIV infection [274], and tuberculosis [275, 276]. Molecular analysis may
identify previously undiscerned outbreaks [275] or rule out others
[276].
The recent trend toward an increase in the use of outpatient care has
also changed the risk for occupationally acquired infection, as well as
the groups of health care workers at risk [64, 277, 278]. In 1867,
Simpson expressed his hope that, given the high concentrations of sick
patients, "hospitals should not become pesthouses, and do more harm than
good" [279]. Since that time, the risk posed to patients and staff by
nosocomial infection has been repeatedly shown. In this regard, the
result of shorter hospitalizations may well be salutary, although the
risk for undetected infection may increase as patients receive more care
away from diagnostic centers.
In summary, daily patient care presents the health care worker with a
real, although small, risk for infection. Indeed, the cost to prevent,
control, and treat occupationally acquired infections is considerable,
in terms of both dollars spent and lives affected. This does not imply
that working with contagious persons is a heroic endeavor. Rather,
incurring the risk for occupationally acquired infection is necessary
for daily health care delivery. Indeed, the willingness of health care
workers to accept this risk is, in many ways, as important to health
care as their professional skills. This should be considered in the
coming years as health care delivery in the United States continues to
be reformed.
Author and Article Information
From Memorial Sloan-Kettering Cancer Center and New York
Hospital-Cornell Medical Center, New York, New York. For the current
author address, see end of text.
Acknowledgment: The author thanks Bruce Artim, JD, for research
assistance.
Requests for Reprints: Kent A. Sepkowitz, MD, Infectious Disease
Service, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, Box
288, New York, NY 10021.
References
1. Patterson WB. Craven DE, Schwartz DA. Nardell EA, Kasmer J, Noble
J. Occupational hazards to hospital personnel. Ann Intern Med. 1985;
102:659-80.
2. Williams WW. CDC guidelines for the prevention and control of
nosocomial infections. Guideline for infection control n hospital
personnel. Am J Infect Control. 1984; 12:34-63.
3. Sepkowitz KA. Occupationally acquired infections in health care
workers. Part I. Ann Intern Med. 1996; 125:826-34.
4. Marcus R. Surveillance of health care workers exposed to blood
from patients infected with the human immunodeficiency virus. N Engl J
Med. 1988; 319:1118-23.
5. Ippolito G, Puro V. De Carli G. The risk of occupational humar
immunodeficiency virus infection in health care workers. Italian
Multicenter Study. The Italian Study Group on Occupational Risk of HIV
Infection. Arch Intern Med. 1993; 153:1451-8.
6. HIV/AIDS Surveillance Report. 1996; 7:21.
7. Update: provisional Public Health Service recommendations for
chemopro-phylaxis after occupational exposure to HIV. MMWR Morb Mortal
Wkly Rep. 1996; 45:468-80.
8. Mast EE, Alter MJ. Prevention of hepatitis B virus infection among
health-care workers. In: Ellis RW, ed. Hepatitis B Vaccines in Clinical
Practice New York: Marcel Dekker; 1993; 295-307.
9. Gerberding JL. Management of occupational exposures to blood-borne
viruses. N Engl J Med. 1995; 332:444-51.
10. Werner BG, Grady GF. Accidental
hepatitis-B-surface-antigen-positive inoculations. Use of e antigen to
estimate infectivity. Ann Intern Med. 1982; 97:367-9.
11. Puro V, Petrosillo N, Ippolito G. Risk of hepatitis C
seroconversion after occupational exposures in health care workers.
Italian Study Group on Occupational Risk of HIV and Other Bloodborne
Infections. Am J Infect Control. 1995; 23:273-7.
12. Kiyosawa K, Sodeyama T, Tanaka E, Nakano Y, Furuta S, Nishioka K,
et al. Hepatitis C in hospital employees with needlestick injuries. Ann
Intern Med. 1991; 115:367-9.
13. Mitsui T, Iwano K, Masuko K, Yamazaki C, Okamoto H, Tsuda F, et
al. Hepatitis C virus infection in medical personnel after needlestick
accident. Hepatology. 1992; 16:1109-14.
14. Puro V. Petrosillo N, Ippolito G, Jagger J. Hepatitis C virus
infection in healthcare workers [Letter]. Infect Control Hosp Epidemiol.
1995; 16:324-5.
15. Marranconi F, Mecenero V, Pellizzer GP, Bettini MC, Conforto M,
Vaglia A. et al. HCV infection after accidental needlestick injury in
healthcare workers [Letter]. Infection. 1992; 20:111.
16. Klein RS, Freeman K, Taylor PE, Stevens CE. Occupational risk for
hepatitis C virus infection among New York City dentists. Lancet. 1991;
338:1539-42.
17. Thomas DL, Gruninger SE, Siew C, Joy ED, Quinn TC. Occupational
risk of hepatitis C infections among dentists and oral surgeons in North
America. Am J Med. 1996; 100:41-5.
18. Alter MJ. Occupational exposure to hepatitis C virus: a dilemma
[Editorial]. Infect Control Hosp Epidemiol. 1994; 15:742-4.
19. Alter MJ. The detection, transmission, and outcome of hepatitis C
virus infection. Infect Agents Dis. 1993; 2:155-66.
20. Dworsky ME, Welch K, Cassady G, Stagno S. Occupational risk for
primary cytomegalovirus infection among pediatric health-care workers. N
Engl J Med. 1983; 309:950-3.
21. Balcarek KB, Bagley R, Cloud GA, Pass RF. Cytomegalovirus
infection among employees of a children's hospital. No evidence for
increased risk associated with patient care. JAMA. 1990; 263:840-4.
22. Muyembe T, Kipasa M. Ebola haemorrhagic fever in Kikwit, Zaire.
International Scientific and Technical Committee and WHO Collaborating
Centre for Haemorrhagic fevers [Letter]. Lancet. 1995; 345:1448.
23. Outbreak of Ebola viral hemorrhagic fever—Zaire, 1995. MMWR Morb
Mortal Wkly Rep. 1995; 44:381-2.
24. Update: outbreak of Ebola viral hemorrhagic fever—Zaire, 1995.
MMWR Morb Mortal Wkly Rep 1995; 44:468-9, 475.
25. Altman LK. Deadly virus still spreads in Zaire: health workers
are mainly affected. The New York Times. 1995; 12 May:A6.
26. Update: management of patients with suspected viral hemorrhagic
fever—United States. MMWR Morb Mortal Wkly Rep. 1995; 44:475-9.
27. Holmes GP. Hilliard JK, Klontz KC, Rupert AH, Schindler CM,
Parrish E, et al. B virus (Herpesvirus simiae) infection in humans:
epidemiologic investigation of a cluster. Ann Intern Med. 1990;
112:833-9.
28. Guidelines for prevention of Herpesvirus simiae (B virus)
infection in monkey handlers. MMWR Morb Mortal Wkly Rep. 1987; 36:680-2,
687-9.
29. Artenstein AW, Hicks CB, Goodwin BS Jr, Hilliard JK. Human
infection with B virus following a needlestick injury. Rev Infect Dis.
1991; 13:288-91.
30. Steelman VM. Creutzfeld-Jakob disease: recommendations for
infection control. Am J Infect Control. 1994; 72:312-8.
31. Schoene WC. Masters CL, Gibbs CJ Jr, Gajdusek DC. Tyler HR, Moore
FD, et al. Transmissible spongiform encephalopathy (Creutzfeidt-Jakob
disease). Atypical clinical and pathological findings. Arch Neurol.
1981; 38:473-7.
32. Brown P, Cathala F, Raubertas RF, Gajdusek DC, Castaigne P. The
epidemiology of Creutzfeldt-Jakob disease: conclusion of a 15-year
investigation in France and review of the world literature. Neurology.
1987; 37:895-904.
33. Garner JS, Hospital Infection Control Advisory Committee.
Guidelines for isolation precautions in hospitals. Am J Infect Control.
1996; 24:24-54.
34. Kuhls TL, Vlker S, Parris NB. Garakian A, Sullivan-Bolyal J,
Cherry JD. Occupational risk of HIV, HBV, and HSV-2 infections in health
care personnel caring for AIDS patients. Am J Public Health. 1987;
77:1306-9.
35. Gerberding JL, Bryant-LeBlanc CE. Nelson K, Moss AR, Osmond D.
Chambers HF, 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 Dis.
1987; 156:1-6.
36. Human immunodeficiency virus (HIV) infection. American College of
Physicians and Infectious Diseases Society of America. Ann Intern Med.
1994; 120:310-9.
37. Gerberding JL, Henderson DK. Management of occupational exposures
to bloodborne pathogens: hepatitis B virus, hepalitis C virus, and human
immunodeficiency virus. Clin Infect Dis. 1992; 14:1179-85.
38. Henderson DK. HIV-1 in the health care setting. In: Mandell GL,
Bennett JE, Doin R, eds. Mandell, Douglas, and Bennett's Principles and
Practice of Infectious Diseases. 4th ed. New York: Churchill
Livingstone: 1994:2632-56.
39. Chamberland ME, Conley LJ, Bush TJ, Ciesielski CA, Hammett TA.
Jaffe HW. Health care workers with AIDS. National surveillance update.
JAMA. 1990; 266:3459-62.
40. Henderson DK. Postexposure prophylaxis for occupational exposures
to hepatitis B, hepatitis C, and human immunodeficiency virus. Surg Clin
North Am. 1995; 75:1175-87.
41. Case-control study of HIV seroconversion in health-care workers
after percutaneous exposure to HIV-infected blood—France, United
Kingdom, and United States, January 1988-August 1994. MMWR Morb Mortal
Wkly Rep. 1995; 44:929-33.
42. Lange JM, Boucher CA, Hollak CE, Wiltink EH, Reiss P, van Royen
EA, et al. Failure of zidovudine prophylaxis after accidental exposure
to HIV-1. N Engl J Med. 1990; 322:1375-7.
43. Gerberding JL. Prophylaxis for occupational exposure to HIV. Ann
Intern Med. 1996; 125:497-501.
44. Leibowitz S, Greenwald L, Cohen I, Litwlns J, Serum hepatitis in
a blood bank worker. JAMA. 1949; 140:1331-3.
45. Kuh C, Ward WE. Occupational virus hepatitis: an apparent hazard
for medical personnel. JAMA. 1950; 143:631-5.
46. Trumbull ML, Greiner DJ. Homologous serum jaundice: an
occupational hazard to medical personne. JAMA. 1951; 145:965-7.
47. West DJ. The risk of hepatitis B infection among health
professionals in the United States: a review. Am J Med Sci. 1984;
287:26-33.
48. Denes AE, Smith JL, Maynard JE, Doto IL, Berquist KR, Finkel AJ.
Hepatitis B infection in physicians. Results of a nationwide
seroepidemiologic survey. JAMA. 1978; 239:210-2.
49. Petrosillo N, Puro V, Ippoolito G, Di Nardo V, Albertoni F,
Chiaretti B, et al. Hepatitis B virus, hepatitis C virus and human
immunodeficiency virus infection in health care workers: a multiple
regression analysis of risk factors. J Hosp Infect. 1995; 30:273-81.
50. Hicks CG, Hargiss CO, Harris JR. Prevalence survey for hepatitis
B in high-risk university hospital employees. Am J Infect Control. 1985;
13:1-6.
51. Janzen J. Tripatzis I, Wagner U. Schlieter M, Muller-Dethard E,
Wolters E. Epidemiology of hepatitis B surface antigen (HBsAg) and
antibody to HBsAg in hospital personnel. J Infect Dis. 1978; 137:261-5.
52. Thomas DL, Factor SH, Kelen GD, Washington AS, Taylor E Jr, Quinn
TC. Viral hepatitis in health care personnel at The Johns Hopkins
Hospital. The seroprevalence of and risk factors for hepatitis B virus
and hepatitis C virus infection. Arch Intern Med. 1993; 153:1705-12.
53. Smith CE. A study of the prevalence of markers of hepatitis B
infection in hospital staff. J Hosp Infect. 1987; 9:39-42.
54. Lewis TL. Alter HJ, Chalmers TC, Holland PV, Purcell RH, Alling
DW, et al. A comparison of the frequency of hepatitis-B antigen and
antibody in hospital and nonhospital personnel. N Engl J Med. 1973;
289:647-51.
55. Segal HE, Irwin GR, Evans LC, Callahan MC. Hepatitis B antigen
and antibody in the United States Army: two-year follow-up of health
care personnel. Mil Med. 1979; 144:792-5.
56. Dienstag JL, Ryan DM. Occupational exposure to hepatitis B virus
in hospital personnel: infection or immunization? Am J Epidemiol. 1982;
115:26-39.
57. Feldman RE, Schiff ER. Hepatitis in dental professionals. JAMA.
1975; 232:1228-30.
58. Hadler SC, Doto IL, Maynard JE, Smith J, Clark B. Mosley J, et
al. Occupational risk of hepatitis B infection in hospital workers.
Infect Control. 1985; 6:24-31.
59. Herruzo-Cabrera R, Malo-Gonzalez L, Calle Puron ME,
Vizcalno-Alcaide MJ, Del Rey-Calero J. Predictive equation for
acquisition of hepatitis B in hospital workers in a general hospital.
Eur J Epidemiol. 1993; 9:442-6.
60. Lettau LA. The A, B, C, D, and E of viral hepatitis: spelling out
the risks for healthcare workers. Infect Control Hosp Epidemiol. 1992;
13:77-81.
61. Gibas A, Blewett DR, Schoenfeld DA, Dienstag JL. Prevalence and
incidence of viral hepatitis in health workers in the prehepatitis B
vaccination era. Am J Epidemiol. 1992; 136:603-10.
62. Weiss Y, Rabinovitch M, Cahaner Y, Noy D, Siegman-Igra Y.
Prevalence of hepatitis B virus markers among hospital personnel in
Israel: correlation with some risk factors. J Hosp Infect. 1994;
26:211-8.
63. Osterholm MT, Garayalde SM. Clinical viral hepatitis B among
Minnesota hospital personnel. Results of a ten-year statewide survey.
JAMA. 1985; 254:3207-12.
64. Reed E, Daya MR, Jui J, Grellman K, Gerber L, Loveless MO.
Occupational infectious disease exposures in EMS personnel. J Emerg Med.
1993; 11:9-16.
65. Shanson DC. Hepatitis B outbreak in operating-theatre and
intensive care staff [Letter]. Lancet. 1980; 2:596.
66. Guillen Solvas J, Luna del Castillo J, Maroto Vela MC, Cueto
Esplnar A, Galvez Vargas R. The risk of infection with hepatitis B virus
in relation to length of hospital employment. J Hosp Infect. 1987;
9:43-7.[Medline]
67. Duthie R, Morgan-Capner P, Wilson M, Hitchen L. Problems in
management of health care workers exposed to HBeAg positive body fluids.
J Hosp Infect. 1994; 26:129-32.
68. Reiss-Levy EA, Wilson CM, Hedges MJ, McCaughan G. Acute fulminant
hepatitis B following a spit in the eye by a hepatitis B e antigen
negative carrier [Letter]. Med J Aust. 1994; 160:524-5.
69. Lettau LA, Alfred HJ, Glew RH, Fields HA, Alter MJ, Meyer R, et
al. Nosocomial transmission of delta hepatitis. Ann Intern Med. 1986;
104:631-5.
70. Owens DK, Nease RF Jr. Occupational exposure to human
immunodeficiency virus and hepatitis B virus: a comparative analysis of
risk. Am J Med. 1992; 92:503-12.
71. Zuckerman AJ. Occupational exposure to hepatitis B virus and
human immunodeficiency virus: a comparative risk analysis. Am J Infect
Control. 1995; 23:286-9.
72. Petersen NJ. An assessment of the airborne route in hepatitis B
transmission. Ann N Y Acad Sci. 1980; 353:157-66.
73. Alter MJ, Favero MS, Maynard JE. Impact of infection control
strategies on the incidence of dialysis-associated hepatitis in the
United States. J Infect Dis. 1986; 153:1149-51.
74. Alter MJ, Hadler SC, Margolls HS, Alexander WJ, Hu PY, Judson FN,
et al. The changing epidemiology of hepatitis B in the United States.
JAMA. 1990; 263:1218-22.
75. Lanphear BP, Linnemann CC Jr, Cannon CG, DeRonde MM. Decline of
clinical hepatitis B in workers at a general hospital: relation to
increasing vaccine-induced immunity. Clin Infect Dis. 1993; 16:10-4.
76. Occupational infection among anaesthetists [Editorial]. Lancet.
1990; 336:1103.
77. Roome AJ, Watsh SJ, Cartter ML, Hadler JL. Hepatitis B vaccine
responsiveness in Connecticut public safety personnel. JAMA. 1993;
270:2931-4.
78. Wood RC, MacDonald KL, White KE, Hedberg CW, Hanson M, Osterholm
MT. Risk factors for lack of detectable antibody following hepatitis B
vaccination of Minnesota health care workers. JAMA. 1993; 270:2935-9.
79. Forseter G. Wormser GP, Adler S, Lebovics E, Calmann M, O'Brien
TA. Hepatitis C in the health care setting. II. Seroprevalence among
hemodialysis staff and patients in suburban New York City. Am J Infect
Control. 1993; 21:5-8.
80. Jankovic N, Cala S, Nadinic B, Varlaj-Knobloch V, Pavlovic D.
Hepatitis C and hepatitis B virus infection in hemodialysis patients and
staff: a two year follow-up. Int J Artif Organs. 1994; 17:137-40.
81. Niu MT, Coleman PJ, Alter MJ. Multicenter study of hepatitis C
virus infection in chronic hemodialysis patients and hemodialysis center
staff members. Am J Kidney Dis. 1993; 22:568-73.
82. Petrosillo N, Puro V, Jagger J, Ippolito G. The risks of
occupational exposure and infection by human immunodeficiency virus,
hepatitis B virus, and hepatitis C virus in the dialysis setting.
Italian Multicenter Study on Nosocomial and Occupational Risk of
Infections in Dialysis. Am J Infect Control. 1995; 23:278-85.
83. Cooper BW, Krusell A, Tilton RC, Goodwin R, Levitz RE.
Seroprevalence of antibodies to hepatitis C virus in nigh-risk hospital
personnel. Infect Control Hosp Epidemiol. 1992; 13:B2-5.
84. Cunningham SJ, Cunningham R, Izmeth MG, Baker B, Hart CA.
Seroprevalence of hepatitis B and C in a Merseyside hospital for the
mentally handicapped. Epidemiol Infect. 1994; 112:195-200.
85. Polywka S, Laufs R. Hepatitis C virus antibodies among different
groups at risk and patients with suspected non-A, non-B hepatitis.
Infection. 1991; 19:81-4.
86. Zuckerman J, Clewley G, Griffiths P, Cockcroft A. Prevalence of
hepatitis C antibodies in clinical health-care workers. Lancet. 1994;
343:1618-20.
87. Polish LB, Tong MJ, Co RL, Coleman PJ, Alter MJ. Risk factors for
hepatitis C virus infection among health care personnel in a community
hospital. Am J Infect Control. 1993; 21:196-200.
88. Campello C, Majori S, Poli A, Pacini P, Nicolardi L, Pini F.
Prevalence of HCV antibodies in health-care workers from northern Italy.
Infection. 1992; 20:224-6.
89. Struve J, Aronsson B, Frenning B, Forsgren M, Weiland O.
Prevalence of antibodies against hepatitis C virus infection among
health care workers in Stockholm. Scand J Gastroenterol. 1994; 29:360-2.
90. De Luca M, Ascione A, Vacca C, Zarone A. Are health-care workers
really at risk of HCV intection? [Letter] Lancet. 1992; 339:1364-5.
91. Herbert AM, Walker DM, Davies KJ, Bagg J. Occupationally acquired
hepatitis C virus infection [Letter]. Lancet. 1992; 339:305.
92. Neal KR, Jones DA, Killey D, James V. Risk factors for hepatitis
C virus infection. A case–control study of blood donors in the Trent
Region (UK). Epidemiol Infect. 1994; 112:595-601.
93. Jochen AB. Occupationally acquired hepatitis C virus infection
[Letter]. Lancet. 1992; 339:304.
94. Lanphear BP, Linnemann CC Jr, Cannon CG, DeRonde MM, Pendy L,
Karley LM. Hepatitis C virus infection in healthcare workers: risk of
exposure and infection. Infect Control Hosp Epidemiol. 1994; 15:745-50.
95. Adler SP. Cytomegalovirus and child day care. Evidence for an
increased infection rate among day-care workers. N Engl J Med. 1989;
321:1290-6.
96. Murph JR, Baron JC, Brown CK, Ebelhack CL, Bale JF Jr. The
occupational risk of cytomegalovirus infection among day-care providers.
JAMA. 1991; 265:603-8.
97. Yeager AS. Longitudinal, serological study of cytomegalovirus
infections in nurses and in personnel without patient contact. J Clin
Microbiol. 1975; 2:448-52.
98. Friedman HM, Lewis MR, Nemerofsky DM, Plotkin SA. Acquisition of
cytomegalovirus infection among female employees at a pediatric
hospital. Pediatr Infect Dis. 1984; 3:233-5.
99. Blackman JA, Murph JR, Bale JF Jr. Risk of cytomegalovirus
infection among educators and health care personnel serving disabled
children. Pediatr Infect Dis J. 1987; 6:725-9.
100. Ahlfors K, Ivarsson SA, Johnsson T. Renmarker K. Risk of
cytomegalovirus infection in nurses and congenital infection in their
offspring. Acta Paediatr Scand. 1981; 70:819-23.
101. Flowers RH 3d, Torner JC, Farr BM, Primary cytomegalovirus
infection in pediatric nurses: a meta-analysis. Infect Control Hosp
Epidemiol. 1988; 9:491-6.
102. Farr B, Torner J. Cytomegalovirus infection among employees of a
children's hospital [Letter]. JAMA. 1990; 264:185.
103. Adler SP. Nosocomial transmission of cytomegalovirus. Pediatr
Infect Dis. 1986; 5:239-46.
104. Brady MT. Cytomegalovirus infections: occupational risk for
health professionals. Am J Infect Control. 1986; 14:197-203.
105. Brady MT, Demmler GJ, Anderson DC. Cytomegalovirus infection in
pediatric house officers: susceptibility to and rate of primary
infection. Infect Control. 1987; 8:329-32.
106. Hatherley LI. Is primary cytomegalovirus infection an
occupational hazard for obstetric nurses? A serological study. Infect
Control. 1986; 7:452-5.
107. Tolkoff-Rubin NA, Rubin RH, Keller EE, Baker GP, Stewart JA,
Hirsch MS. Cytomegalovirus infection in dialysis patients and personnel.
Ann Intern Med. 1978; 89:625-8.
108. Balfour CL, Balfour HH Jr. Cytomegalovirus is not an
occupational risk for nurses in renal transplant and neonatal units.
Results of a prospective surveillance study. JAMA. 1986; 256:1909-14.
109. Pekham CS, Garrett AJ, Chin KS, Preece PM, Nelson DB, Warren DE.
Restriction enzyme analysis of cytomegalovirus DNA to study transmission
of infection. J Clin Pathol. 1986; 39:318-24.
110. Demmler GJ, Yow MD, Spector SA, Reis SG, Brady MT, Anderson DC,
et al. Nosocomial cytomegalovirus infections within two hospitals caring
for infants and children. J Infect Dis. 1987; 156:9-16.
111. Baron RC, McCormick JB, Zubeir OA. Ebola virus disease in
southern Sudan: hospital dissemination and intrafamilial spread. Bull
World Health Organ. 1983; 61:997-1003.
112. Burney MI, Ghafoor A, Saleen M, Webb PA. Casals J. Nosocomial
outbreak of viral hemorrhagic fever caused by Crimean Hemorrhagic
fever—Congo virus in Pakistan, January 1976. Am J Trop Med Hyg. 1980;
29:941-7.
113. Monath TP, Mertens PE, Patton R, Moser CR, Baum JJ, Pinneo L. et
al. A hospital epidemic of Lassa fever in Zorzor, Liberia, March-April
1972. Am J Trop Med Hyg. 1973; 22:773-9.
114. Gear JS, Cassel GA, Gear AJ, Trappler B, Clausen L, Meyers AM,
et al. Outbreak of Marburg virus disease in Johannesburg. Br Med J.
1975; 4:489-93.
115. Smith DH, Johnson BK, Isaacson M, Swanapoel R, Johnson KM,
Killey M, et al. Marburg-virus disease in Kenya. Lancet. 1982; 1:816-20.
116. Fisher-Hoch SP, Khan JA, Rehman S, Mirza S, Khurshld M,
McCormick JB. Crimean Congo-haemorrhagic fever treated with oral
ribavirin. Lancet. 1995; 346:472-5.
117. Gay FP, Holden M. The herpes encephalitis problem. II. J Infect
Dis. 1933; 53:287-303.
118. Sabin AB, Wright WM. Acute ascending myelitis following a monkey
bite, with the isolation of a virus capable of reproducing the disease.
J Exp Med. 1934; 59:115-34.
119. Palmer AE. B virus, Herpesvirus simiae: historical perspective.
J Med Primatol. 1987; 16:99-130.
120. Miller DC. Creutzfeldt-Jakob disease in histopathology
technicians [Letter]. N Engl J Med. 1988; 318:853-64.
121. Sitwell L, Lach B, Atack E, Atack D, Izukawa D.
Creutzfeldt-Jakob disease in histopathology technicians [Letter]. N Engl
J Med. 1988; 318:854.
122. Gorman DG, Benson DF, Vogel DG, Vinters HV. Creutzfeldt-Jakob
disease in a pathologist [Letter]. Neurology. 1992; 42:463.
123. Ginsburg CM, Henle G, Henle W. An outbreak of infectious
mononucleosis among the personnel of an outpatient clinic. Am J
Epidemiol. 1976; 104:571-5.
124. Ho NC, Kwan HC, Poon YF, Tse KC, Ng MH. Epstein-Barr virus
infection in staff treating patients with nasopharyngeal carcinoma
[Letter]. Lancet. 1978; 1:710-1.
125. Meyer GS. Occupational infection in health care. The century-old
lessons from syphilis. Arch Intern Med. 1993; 153:2439-47.
126. Haworth FL, Cook GC. Needlestick malaria [Letter]. Lancet. 1995;
346:1361.
127. Cook GC. Fatal yellow fever contracted at the Hospital for
Tropical Diseases, London, UK, in 1930. Trans R Soc Trop Med Hyg. 1994;
88:712-3.
128. Khuri-Bulos NA, Abu Khalaf M, Shehabi A, Shami K.
Foodhandler-associated Salmonella outbreak in a university hospital
despite routine surveillance cultures of kitchen employees. Infect
Control Hosp Epidemiol. 1994; 15:311-4.
129. Standaert SM, Hutcheson RH, Schaffner W. Nosocomial transmission
of Salmonella gastroenteritis to laundry workers in a nursing home.
Infect Control Hosp Epidemiol. 1994; 15:22-6.
130. Outbreak of viral hepatitis in the staff of a pediatric
ward—California. MMWR Morb Mortal Wkly Rep. 1977; 26:77-8.
131. Burkholder BT, Coronado VG, Brown J, Hutto JH, Shapiro CN,
Robertson B, et al. Nosocomal transmission of hepatitis A in a pedlatric
hospital traced to an anti-hepatitis A virus-negative patient with
immunodeficiency. Pediatr Infect Dis J. 1995; 14:261-6.
132. Doebbeling BN, Li N, Wenzel RP. An outbreak of hepatitis A among
health care workers: risk factors for transmission. Am J Public Health.
1993; 83:1679-84.
133. Klein BS, Michaels JA, Rytel MW, Berg KG, Davis JP. Nosocomial
hepatitis A. A multinursery outbreak in Wisconsin. JAMA. 1984;
252:2716-21.
134. Azimi PH, Roberto RR, Guralnik J, Livermore T, Hoag S, Hagens S,
et al. Transfusion-acquired hepatitis A in a premature infant with
secondary nosocomial spread in an intensive care nursery. Am J Dis
Child. 1986; 140:23-7.
135. Drusin LM, Sohmer M, Groshen SL, Spiritos MD, Senterfit LB,
Christenson WN. Nosocomial hepatitis A infection in a paediatric
intensive care unit. Arch Dis Child. 1987; 62:690-5.
136. Noble RC, Kane MA, Reeves SA. Roeckel I. Posttransfusion
hepatitis A in a neonatal intensive care unit. JAMA. 1984; 252:2711-5.
137. Brewer MA, Edwards KM, Decker MD. Who should receive hepatitis A
vaccine? Pediatr Infect Dis J. 1995; 14:258-60.
138. DuPont HL. Nosocomial salmonellosis and shigellosis [Editorial].
Infect Control Hosp Epidemiol. 1991; 12:707-9.
139. Beers LM, Burke TL, Martin DB. Shigellosis occurring in newborn
nursery staff. Infect Control. 1989; 10:147-9.
140. Casemore DP, Gardner CA, O'Mahony C. Cryptosporidial infection,
with special reference to nosocomial transmission of Cryptosporidium
parvum: a review. Folia Parasitol (Praha). 1994; 41:17-21.
141. Levine JF, Levy MG, Walker RL, Crittenden S. Cryptosporidiosis
in veterinary students. J Am Vet Med Assoc. 1988; 193:1413-4.
142. Current WL, Reese NC, Ernst JV, Bailey WS, Heyman MB. Weinstein
WM. Human cryptosporidiosis in immunocompetent and immunodeficient
persons. Studies of an outbreak and experimental transmission. N Engl J
Med. 1983; 308:1252-7.
143. Mitchell HM, Lee A, Carrick JT. Increased incidence of
Campylobacter pylori infection in gastroenterologists: further evidence
to support person-to-person transmission of C. pylori. Scand J
Gastroenterol. 1989; 24:396-400.
144. Reiff A, Jacobs E, Kist M. Seroepidemiological study of the
immune response to Campylobacter pylori in potential risk groups. Eur J
Clin Microbiol Infect Dis. 1989; 8:592-6.
145. Lin SK, Lambert JR, Schembri MA, Nicholson L, Korman
MG.Helicobacter pylori prevalence in endoscopy and medical staff. J
Gastroenterol Hepatol. 1994; 9:319-24.
146. Rae AJ, Bathe OF, Cleator IG.Helicobacter pylori infection in
gastroenterology personnel [Letter]. J Hosp Infect. 1994; 27:241-2.
147. Chong J, Marshall BJ, Barkin JS, McCallum RW, Reiner DK, Hoffman
SR, et al. Occupational exposure to Helicobacter pylori for the
endoscopy professional: a sera epidemiological study. Am J
Gastroenterol. 1994; 89:1987-92.
148. Riordan T, Wills A. An outbreak of gastroenterits in a
psycho-geriatric hospital associated with a small round structured
virus. J Hosp Infect. 1986; 8:296-9.
149. Reid JA, Breckon D, Hunter PR. Infection of staff during an
outbreak of viral gastroenteritis in an elderly persons' home. J Hosp
Infect. 1990; 16:81-5.
150. Pegues DA, Woernle CH. An outbreak of acute nonbacterial
gastroenteritis in a nursing home. Infect Control Hosp Epidemiol. 1993;
14:87-94.
151. Chadwick PR, McCann R. Transmission of a small round structured
virus by vomiting during a hospital outbreak of gastroenteritis. J Hosp
Infect. 1994; 26:251-9.
152. Stevenson P, McCann R, Duthie R, Glew E, Ganguli L. A hospital
outbreak due to Norwalk virus. J Hosp Infect. 1994; 26:261-72.
153. Summary of notifiable diseases, United States 1994. MMWR Morb
Mortal Wkly Rep. 1995; 43:1-80.
154. Baine WB, Gangarosa EJ, Bennett JV, Barker WH Jr. Institutional
salmonellosis. J Infect Dis. 1973; 128:357-60.
155. Mishu B, Koehler J, Lee LA, Rodrigue D, Brenner FH, Blake P, et
al. Outbreaks of Salmonella enteritidis infection in the United States,
1985-1991. J Infect Dis. 1994; 169:547-52.
156. Schroeder SA, Aserkoff B, Brachman PS. Epidemic salmonellosis in
hospitals and institutions. A five-year review. N Engl J Med. 1968;
279:674-8.
157. Palmer SR, Rowe B. Investigation of outbreaks of salmonella in
hospitals. Br Med J (Clin Res Ed). 1983; 287:891-3.
158. Steere AC, Hall WJ 3d, Wells JG, Craven PJ, Leotsakis N, Farmer
JJ 3d, et al. Person-to-person spread of Salmonella typhimurium after a
hospital common-source outbreak. Lancet. 1975; 1:319-22.
159. Datta N, Pridie RB. An outbreak of infection with Salmonella
typhimurium in a general hospital. Journal of Hygiene (Cambridge). 1960;
58:229-40.
160. Edwards GF, Curran ET, McCartney AC, Paterson KR, Girdwood RW,
Threlfall EJ, et al. Nosocomial salmonellosis. Commun Dis Rep CDR Rev.
1993; 3:R40-2.
161. Linnemann CC Jr, Cannon CG, Staneck JL, McNeely BL. Prolonged
hospital epidemic of salmonellosis: use of trimethoprim-sulfamethoxazole
for control. Infect Control. 1985; 6:221-5.[Medline]
162. Choi M, Yoshikawa TT, Bridge J, Schlaifer A, Osterweil D, Reid
D, et al.Salmonella outbreak in a nursing home. J Am Geriatr Soc. 1990;
38:531-4.
163. Shapiro CN, Coleman PJ, McQuillan GM, Alter MJ, Margolis HS.
Epidemiology of hepatitis A: seroepidemiology and risk groups in the
USA. Vaccine. 1992; 10(Suppl 1):S59-62.
164. Germanaud J, Causse X, Barthez JP. Prevalence of antibodies to
hepatitis A virus in health care workers [Letter]. Eur J Clin Microbiol
Infect Dis. 1993; 12:572-3.
165. Domart M, Milka-Cabanne N, Pouliquen A, Xerri B, Henzel D,
Larouse B, et al. Seroprevalence of hepatitis A among hospital workers
in Paris (implications for HAV vaccination) [Abstract]. In: Program and
Abstracts—35th Interscience Conference on Antimicrobial Agents and
Chemotherapy. 17-20 September 1995, San Francisco, California.
Washington, DC: American Society for Microbiology; 1995:269.
166. Hofmann F, Wehrle G, Berthold H, Koster D. Hepatitis A as an
occupational hazard. Vaccine. 1992; 10(Suppl 1):S82-4.
167. Capps RB, Bennett AM, Stokes J. Endemic infectious hepatitis in
an infants' orphanage. I. Epidemiologic studies in student nurses. Arch
Intern Med. 1952; 89:6-23.
168. Goodman RA, Carder CC, Allen JR, Orenstein WA, Finton RJ.
Nosocomial hepatitis A transmission by an adult patient with diarrhea.
Am J Med. 1982; 73:220-6.
169. Baptiste R, Koziol D, Henderson DK. Nosocomial transmission of
hepatitis A in an adult population. Infect Control. 1987; 8:364-70.
170. Eisenstein AB, Aach RD, Jacobsohn W, Goldman A. An epidemic of
infectious hepatitis in a general hospital. JAMA. 1963; 185:171-4.
171. Meyers JD, Romm FJ, Tihen WS, Bryan JA. Food-borne hepatitis A
in a general hospital. Epidemiologic study of an outbreak attributed to
sandwiches. JAMA. 1975; 231:1049-53.
172. Diekema DJ, Doebbeling BN. Employee health and infection
control. Infect Control Hosp Epidemiol. 1995; 16:292-301.
173. DuPont HL, Levine MM, Hornick RB, Formal SB. Inoculum size in
shigellosis and implications for expected mode of transmission. J Infect
Dis. 1989; 159:1126-8.
174. Mohle-Boetani JC, Stapleton M, Finger R, Bean NH, Poundstone J,
Blake PA, et al. Communitywide shigellosis: control of an outbreak and
risk factors in child day-care centers. Am J Public Health. 1995;
85:812-6.
175. Paton S, Nicolle L, Mwongera M, Kabiru P, Mirza N, Plummer F, et
al.Salmonella and Shigella gastroenteritis at a public teaching hospital
in Nairobi, Kenya. Infect Control Hosp Epidemiol. 1991; 12:710-7.
176. Koch KL, Phillips DJ, Aber RC, Current WL. Cryptosporidiosis in
hospital personnel. Evidence for person-to-person transmission. Ann
Intern Med. 1985; 102:593-6.
177. Dryjanski J, Gold JW, Ritchie MT, Kurtz RC, Lim SL, Armstrong D.
Cryptosporidiosis. Case report in a health team worker. Am J Med. 1986;
80:753-4.
178. Blagburn BL, Current WL. Accidental infection of a researcher
with human Cryptosporidium [Letter]. J Infect Dis. 1983; 148:772-3.
179. McFarland LV, Mulligan ME, Kwok RY, Stamm WE. Nosocomial
acquisition of Clostridium difficile infection. N Engl J Med. 1989;
320:204-10.
180. Samore MH, Venkataraman L, DeGirolami PC, Arbeit RD, Karchmer
AW. Clinical and molecular epidemiology of sporadic and clustered cases
of nosocomial Clostridium difficile diarrhea. Am J Med. 1996; 100:32-40.
181. Cartmill TD, Panigrahi H, Worsley MA, McCann DC, Nice CN, Keith
E. Management and control of a large outbreak of diarrhoea due to
Clostridium difficile. J Hosp Infect. 1994; 27:1-15.
182. Strimling MO, Sacho H, Berkowitz I.Clostridium difficile
infection in health-care workers [Letter]. Lancet. 1989; 2:866-7.
183. Delmee M.Clostridium difficile infection in health-care workers
[Letter]. Lancet. 1989; 2:1095.
184. Mathis S, Venkataraman L, Sheckman P, DeGirolami P, Samore M.
Nosocomial outbreak of unusually severe C. difficile diarrhea with
presumptive transmission to a health care worker. Infect Control Hosp
Epidemiol. 1996; 17:P33(S20).
185. Carter AO, Borczyk AA, Carlson JA, Harvey B, Hockin JC, Karmali
MA, et al. A severe outbreak of Escherichia coli 0157:H7-associated
hemorrhagic colitis in a nursing home. N Engl J Med. 1987; 317:1496-500.
186. Friedlander WJ. On the obligation of physicians to treat AIDS:
is there a historical basis? Rev Infect Dis. 1990; 12:191-203.
187. Wehrle PF. The risk of poliomyelitis infection among exposed
hospital personnel. Pediatrics. 1956; 17:237-46.
188. Cafferkey MT, Sloane A, McCrae S, O'Morain CA.Yersinia
frederiksenii infection and colonization in hospital staff. J Hosp
Infect. 1993; 24:109-15.
189. Murphy O, Gray J, Gordon S, Bint AJ. An outbreak of
campylobacter food poisoning in a health care setting. J Hosp Infect.
1995; 30:225-8.
190. Huang P, Weber JT, Sosin DM, Griffin PM, Long EG, Murphy JJ, et
al. The first reported outbreak of diarrheal illness associated with
Cyclospora in the United States. Ann Intern Med. 1995; 123:409-14.
191. al-Quarawi SN, el Bushra HE, Fontaine RE, Bubshait SA, el
Tantawy NA. Typhoid fever from water desalinized using reverse osmosis.
Epidemiol Infect. 1995; 114:41-50.
192. Thomas MC, Giedinghagen DH, Hoff GL. An outbreak of scabies
among employees in a hospital-associated commercial laundry. Infect
Control. 1987; 8:427-9.
193. Pasternak J, Richtmann R, Ganme PP, Rodrigues EA, Silva FB,
Hirata M, et al. Scabies epidemic: price and prejudice. Infect Control
Hosp Epidemiol. 1994; 15:540-2.
194. Voss A, Wallrauch C. Occupational scabies in healthcare workers
[Letter]. Infect Control Hosp Epidemiol. 1995; 16:4.
195. Jimenez-Lucho VE, Fallon F, Caputo C, Ramsey K. Role of
prolonged surveillance in the eradication of nosocomial scabies in an
extended care Veterans Affairs medical center. Am J Infect Control.
1995; 23:44-9.
196. Greaves WL, Kaiser AB, Alford RH, Schaffner WH. The problem of
herpetic whitlow among hospital personnel. Infect Control. 1980;
1:381-5.
197. Rowe NH, Heine CS, Kowalski CJ. Herpetic whitlow: an
occupational disease of practicing dentists. J Am Dent Assoc. 1982;
105:471-3.
198. Stern H, Elek SD, Millar DM, Anderson HF. Herpetic whitlow: a
form of cross-infection in hospitals. Lancet. 1959; 2:871-4.
199. Adams G, Stover BH, Keenlyside RA, Hooton TM, Buchman TG,
Roizman B, et al. Nosocomial herpetic infections in a pediatric
intensive care unit. Am J Epidemiol. 1981; 113:126-32.
200. Garden JM, O'Banion MK, Shelnitz LS, Pinski KS, Bakus AD,
Reichmann ME, et al. Papillomavirus in the vapor of carbon dioxide
laser-treated verrucae. JAMA. 1988; 259:1199-202.
201. Gloster HM Jr, Roenigk RK. Risk of acquiring human
papillomavirus from the plume produced by the carbon dioxide laser in
the treatment of warts. J Am Acad Dermatol. 1995; 32:436-41.[Medline]
202. Bergbrant IM, Samuelsson L, Olofsson S, Jonassen F, Ricksten A.
Polymerase chain reaction for monitoring human papillomavirus
contamination of medical personnel during treatment of genital warts
with CO2 laser and electrocoagulation. Acta Derm Venereol. 1994;
74:393-5.
203. Arnow PM, Houchins SG, Pugliese G. An outbreak of tinea corporis
in hospital personnel caused by a patients with Trychophyton tonsurans
infection. Pediatr Infect Dis J. 1991; 10:355-9.
204. Calcutt JA, Goucher-Wilson S, Sulis CA. Nosocomial transmission
of tinea corporis on a pediatrics ward at Boston City Hospital. Am J
Infect Control. 1995; 23:122-3.
205. Collins CH. Laboratory-Acquired Infections: History, Incidence,
Causes, and Prevention. 2d ed. Boston: Butterworth-Heinemann; 1988.
206. Pike RM. Laboratory-associated infections: incidence,
fatalities, causes, and prevention. Annu Rev Microbiol. 1979; 33:41-66.
207. Vesley D, Hartmann HM. Laboratory-acquired infections and
injuries in clinical laboratories: a 1986 survey. Am J Public Health.
1988; 78:1213-5.
208. Laboratory-acquired meningococcemia—California and
Massachusetts. MMWR Morb Mortal Wkly Reo. 1991; 40:46-7.
209. Artenstein MS, Ellis RE. The risk of exposure to a patient with
meningococcal meningitis. Mil Med. 1968; 133:474-7.
210. Kiel FW, Khan MY. Brucellosis among hospital employees in Saudi
Arabia. Infect Control Hosp Epidemiol. 1993; 14:268-72.
211. Johnson JE, Kadull PJ. Laboratory-acquired Q fever. A report of
fifty cases. Am J Med. 1966; 41:391-403.
212. Johnson WM. Occupational factors in coccidioidomycosis. J Occup
Med. 1981; 23:367-73.
213. Johnson JE 3d, Kadull PJ. Rocky Mountain spotted fever acquired
in a laboratory. N Engl J Med. 1967; 277:842-7.[Medline]
214. Barry M, Russi M, Armstrong L, Geller D, Tesh R, Dembry L, et
al. Brief report: treatment of a laboratory-acquired Sabia virus
infection. N Engl J Med. 1995; 333:294-6.
215. Roeckel IE, Lyons ET. Cutaneous larva migrans, an occupational
disease. Ann Clin Lab Sci. 1977; 7:405-10.
216. Glickman LT, Cypess RH.Toxocara infection in animal hospital
employees. Am J Public Health. 1977; 67:1193-5.
217. Baum SG, Lewis AM Jr, Rowe WP, Huebner RJ. Epidemic
nonmeningitic lymphocytic-choriomeningitis-virus infection. An outbreak
in a population of laboratory personnel. N Engl J Med. 1966; 274:934-6.
218. Armstrong D, Fortner JG, Rowe WP, Parker JC. Meningitis due to
lymphocytic choriomeningitis virus endemic in a hamster colony. JAMA.
1969; 209:265-7.
219. Vanzee BE, Douglas RG, Betts RF, Bauman AW, Fraser DW, Hinman
AR. Lymphocytic choriomeningitis in university hospital personnel.
Clinical features. Am J Med. 1975; 58:803-9.
220. Richardson JH. Basic considerations in assessing and preventing
occupational infections in personnel working with nonhuman primates. J
Med Primatol. 1987; 16:83-9.
221. Khabbaz RF, Heneine W, George JR, Parekh B, Rowe T, Woods T, et
al. Brief report: infection of a laboratory worker with simian
immunodeficiency virus. N Engl J Med. 1994; 330:172-7.
222. Kennedy FM, Astbury J, Needham JR, Cheasty T. Shigellosis due to
occupational contact with non-human primates. Epidemiol Infect. 1993;
110:247-51.
223. Votra EM, Rutala WA, Sarubbi FA. Recommendations for pregnant
employee interaction with patients having communicable infectious
diseases. Am J Infect Control. 1983; 11:10-9.
224. Valenti WM. Infection control and the pregnant health care
worker. Am J Infect Control. 1986; 14:20-7.
225. Moore RM Jr, Davis YM, Kaczmarek RG. An overview of occupational
hazards among veterinarians, with particular reference to pregnant
women. Am Ind Hyg Assoc J. 1993; 54:113-20.[Medline]
226. Sepkowitz KA. AIDS, tuberculosis, and the health care worker.
Clin Infect Dis. 1995; 20:232-42.
227. Templeton GL, Illing LA, Young L, Cave D, Stead WW, Bates JH.
The risk for transmission of Mycobacterium tuberculosis at the bedside
and during autopsy. Ann Intern Med. 1995; 122:922-5.
228. Claydon SM. The high risk autopsy. Recognition and protection.
Am J Forensic Med Pathol. 1993; 14:253-6.
229. Smith JR, Kitchen VS. Reducing the risk of infection for
obstetricians. Br J Obstet Gynaecol. 1991; 98:124-6.
230. Panlilio AL, Shapiro CN, Schable CA, Mendelson MA, Montecalvo
MA, Kunches LM, et al. Serosurvey of human immunodeficiency virus.
hepatitis B virus, and hepatitis C virus infection among hospital-based
surgeons. Serosurvey Study Group. J Am Coll Surg. 1995; 180:16-24.
231. Lyerly HK. Transmissible agents and the surgeon [Editorial]. J
Am Coll Surg. 1995; 180:91-2.
232. Mastaj LA, Tartakow DJ, Borislow AJ, Fogel MS. Infection control
in the dental practice with emphasis on the orthodontic practice.
Compendium. 1994; 15:74, 76, 78-80.
233. Bleicher JN, Blinn DL, Massop D. Hand infections in dental
personnel. Plast Reconstr Surg. 1987; 80:420-2.
234. Harris RW, Kehrer AF, Isacson P. Relationship of occupations to
risk of clinical mumps in adults. Am J Epidemiol. 1969; 89:264-70.
235. Cleveland JL, Kent J, Gooch BF, Valway SE, Marianos DW, Butler
WR, et al. Multidrug-resistant Mycobacterium tuberculosis in an HIV
dental clinic. Infect Control Hosp Epidemiol. 1995; 16:7-11.
236. Cleveland JL, Gooch BF, Bolyard EA, Simone PM, Mullan RJ,
Marianos DW. TB infection control recommendations from the CDC, 1994:
considerations for dentistry. United States Centers for Disease Control
and Prevention. J Am Dent Assoc. 1995; 126:593-9.
237. du Moulin GC, Hedley-Whyte J. Hospital-associated viral
infection and the anesthesiologist. Anesthesiology. 1983; 59:51-65.
238. Ellis G. Anaesthesia and the common cold. Anaesthesia. 1955;
10:78-9.
239. Smallpox. Br Med J. 1951; 1:288-9.
240. Oliphant JW, Gordon DA, Meis A, Parker RR. Q fever in laundry
workers, presumably transmitted from contaminated clothing. Am J Hyg.
1949; 49:76-82.
241. Semmelweis IP. [The etiology, the concept, and the prophylaxis
of childbed fever]. Wien, Harlebens Verlag, 1861. Medical Classics.
1941; 5:350-773.
242. Rotter ML. Hygienic hand disinfection. Infect Control. 1984;
5:18-22.
243. Newson SW. Pioneers in infection control: Ignaz Philipp
Semmelweis. J Hosp Infect. 1993; 23:175-87.
244. Larson E, Kretzer EK. Compliance with handwashing and barrier
precautions. J Hosp Infect. 1995; 30(Suppl):88-106.
245. Jarvis WR. Handwashing—the Semmelweis lesson forgotten? Lancet.
1994; 344:1311-2.
246. Lund S, Jackson J, Leggett J, Hales L, Dworkin R, Gilbert D.
Reality of glove use and handwashing in a community hospital. Am J
Infect Control. 1994; 22:352-7.
247. Horton R. Handwashing: the fundamental infection control
principle. Br J Nurs. 1995; 4:926-33.
248. Wenzel RP, Pfaller MA. Handwashing: efficacy versus acceptance.
A brief essay. J Hosp Infect. 1991; 18(Suppl B):65-8.
249. Doebbeling BN, Stanley GL, Sheetz CT, Pfaller MA, Houston AK,
Annis L, et al. Comparative efficacy of alternative hand-washing agents
in reducing nosocomial infections in intensive care units. N Engl J Med.
1992; 327:88-97.
250. Larson E, Mayur K, Laughon BA. Influence of two handwashing
frequencies on reduction in colonizing flora with three handwashing
products used by health care personnel. Am J Infect Control. 1988;
17:83-8.
251. Larson E, McGeer A, Quraishi ZA, Krenzischek D, Parsons BJ,
Holdford J, et al. Effect of an automated sink on handwashing practices
and attitudes in high-risk units. Infect Control Hosp Epidemiol. 1991;
12:422-8.
252. Ansari SA, Springthorpe VS, Sattar SA, Tostowaryk W, Wells GA.
Comparison of cloth, paper, and warm air drying in eliminating viruses
and bacteria from washed hands. Am J Infect Control. 1991; 19:243-9.
253. Reybrouck G. Handwashing and hand disinfection. J Hosp Infect.
1986; 8:5-23.
254. Kjolen H, Andersen BM. Handwashing and disinfection of heavily
contaminated hands—effective or ineffective? J Hosp Infect. 1992;
21:61-71.
255. Wurtz R, Moye G, Jovanovic B. Handwashing machines, handwashing
compliance, and potential for cross-contamination. Am J Infect Control.
1994; 22:228-30.
256. General recommendations on immunization. Recommendations of the
Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal
Wkly Rep. 1994; 43(RR-1):1-38.
257. Poland GA, Nichol KL. Medical students as sources of rubella and
measles outbreaks. Arch Intern Med. 1990; 150:44-6.
258. Heimberger T, Chang HG, Shaikh M, Crotty L, Morse D, Birkhead G.
Knowledge and attitudes of healthcare workers about influerza: why are
they not getting vaccinated? Infect Control Hosp Epidemiol. 1995;
16:412-4.
259. Nosocomial rubella infection—North Dakota, Alabama, Ohio. MMWR
Morb Mortal Wkly Rep. 1981; 29:629-31.
260. Harpaz R, Von Seidlen L, Averhoff FM, Tormey MP, Sinha SD,
Kotsopoulou K, et al. Transmission of hepatitis B virus to multiple
patients from a surgeon without evidence of inadequate infection
control. N Engl J Med. 1996; 334:549-54.
261. Prevention of varicella: recommendations of the Advisory
Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep.
1996; 45(RR-11):13-5.
262. Jackson MM, Lynch P. Isolation practices: a historical
perspective. Am J Infect Control. 1985; 13:21-31.
263. Decker MD. Respiratory protection standard: comments on OSHA's
proposed revision. Infect Control Hosp Epidemiol. 1995; 16:365-71.
264. Mosley JW. Virus transmission in health care settings:
precautions, epidemiologic experience, and common sense [Editorial]. Am
J Public Health. 1993; 83:1664-5.
265. Rao GG. Control of outbreaks of viral diarrhoea in hospitals—a
practical approach. J Hosp Infect. 1995; 30:1-6.
266. Ciesielski C, Marianos D, Ou CY, Dumbaugh R, Witte J, Berkelman
R, et al. Transmission of human immunodeficiency virus in a dental
practice. Ann Intern Med. 1992; 116:798-805.
267. Zaza S, Blumberg HM, Beck-Sague C, Haas WH, Woodley CL, Pineda
M, et al. Nosocomial transmission of Mycobacterium tuberculosis: role of
health care workers in outbreak propagation. J Infect Dis. 1995;
172:1542-9.
268. Guidelines for preventing the transmission of Mycobacterium
tuberculosis in health-care facilities, 1994. MMWR Morb Mortal Wkly Rep.
1994; 43(RR-13):1-132.
269. Rota JS, Heath JL, Rota PA, King GE, Celma ML, Carabana J, et
al. Molecular epidemiology of measles virus: identification of pathways
of transmission and implications for measles elimination. J Infect Dis.
1996; 173:32-7.
270. Sawyer MH, Chamberlin CJ, Wu YN, Aintablian N, Wallace MR.
Detection of varicella-zoster virus DNA in air samples from hospital
rooms. J Infect Dis. 1994; 169:91-4.
271. Brummitt CF, Cherrington JM, Katzenstein DA, Juni BA, Van Drunen
N, Edelman C, et al. Nosocomial adenovirus infections: molecular
epidemiology of an outbreak due to adenovirus 3a. J Infect Dis. 1988;
158:423-32.
272. Singh-Naz N, Brown M, Ganeshanathan M. Nosocomial adenovirus
outbreak: molecular epidemiology of an outbreak. Pediatr Infect Dis J.
1993; 12:922-5.
273. Suzuki K, Mizokami M, Lau JY, Mizoguchi N, Kato K, Mizuno Y, et
al. Confirmation of hepatitis C virus transmission through needlestick
accidents by molecular evolutionary analysis. J Infect Dis. 1994;
170:1575-8.
274. Jaffe HW, McCurdy JM, Kalish ML, Liberti T, Metellus G, Bowman
BH, et al. Lack of HIV transmission in the practice of a dentist with
AIDS. Ann Intern Med. 1994; 121:855-9.
275. Genewein A, Telenti A, Bernasconi C, Mordasini C, Weiss S,
Maurer AM, et al. Molecular approach to identifying route of
transmission of tuberculosis in the community. Lancet. 1993; 342:841-4.
276. Bendall RP, Drobniewski FA, Jayasena SD, Nye PM, Uttley AH,
Scott GM. Restriction fragment length polymorphism analysis rules out
cross-infection among renal patients with tuberculosis. J Hosp Intect.
1995; 30:51-5.
277. Goodman RA, Solomon SL. Transmission of infectious diseases in
outpatient health care settings. JAMA. 1991; 265:2377-81.
278. Valenti WM. Infection control, human immunodeficiency virus, and
home health care: II. Risk to the caregiver. Am J Infect Control. 1995;
23:78-81.
279. Selwyn S. Hospital infection: the first 2500 years. J Hosp
Infect. 1991; 18(Suppl A):5-64.