Risk and
Management of Blood-Borne Infections in Health Care Workers
Elise M. Beltrami,1,* Ian T. Williams,2
Craig N. Shapiro,2 and Mary E. Chamberland1
Clinical
Microbiology Reviews, July 2000, p. 385-407, Vol. 13, No. 3
0893-8512/00/$04.00+0
HIV Infections Branch, Hospital Infections Program,1
and Hepatitis Branch, Division of Viral and Rickettsial
Diseases,2 National Center for Infectious Diseases,
Centers for Disease Control and Prevention, Public Health
Service, U.S. Department of Health and Human Services, Atlanta,
Georgia
SUMMARY
Exposure to blood-borne pathogens poses a serious risk to
health care workers (HCWs). We review the risk and management of
human immunodeficiency virus (HIV), hepatitis B virus (HBV),
and hepatitis C virus (HCV) infections in HCWs and
also discuss current methods for preventing exposures
and recommendations for postexposure prophylaxis. In
the health care setting, blood-borne pathogen
transmission occurs predominantly by percutaneous or mucosal
exposure of workers to the blood or body fluids of
infected patients. Prospective studies of HCWs have
estimated that the average risk for HIV transmission
after a percutaneous exposure is approximately 0.3%, the risk
of HBV transmission is 6 to 30%, and the risk of HCV
transmission is approximately 1.8%. To minimize the
risk of blood-borne pathogen transmission from HCWs
to patients, all HCWs should adhere to standard
precautions, including the appropriate use of hand washing,
protective barriers, and care in the use and disposal of
needles and other sharp instruments. Employers should
have in place a system that includes written
protocols for prompt reporting, evaluation,
counseling, treatment, and follow-up of occupational exposures
that may place a worker at risk of blood-borne pathogen
infection. A sustained commitment to the occupational
health of all HCWs will ensure maximum protection for
HCWs and patients and the availability of optimal
medical care for all who need it.
INTRODUCTION
Exposure to blood-borne pathogens poses a serious risk to
health care workers (HCWs). Transmission of at least
20 different pathogens by needlestick and sharps
injuries has been reported (79). Despite improved
methods of preventing exposure, occupational
exposures will continue to occur.
Assessment of the risk of blood-borne pathogen transmission
in the health care setting requires information derived from
various sources, including surveillance data, studies
of the frequency and preventability of blood
contacts, seroprevalence studies among patients and
HCWs, and prospective studies that assess the risk of
seroconversion after an exposure to infected blood. Factors
influencing the risk to an individual HCW over a lifetime
career include the number and types of blood contact
experienced by the worker, the prevalence of
blood-borne pathogen infection among patients treated
by the worker, and the risk of transmission of
infection after a single blood contact.
In this article, we review the risk and management of the
three blood-borne viruses most commonly involved in occupational
transmission: human immunodeficiency virus (HIV),
hepatitis B virus (HBV), and hepatitis C virus (HCV).
We also will discuss current methods of preventing
exposure, including standard precautions and the use
of safety devices in the health care setting, as well
as recommendations for postexposure prophylaxis.
TRANSMISSION OF BLOOD-BORNE
PATHOGENS IN THE HEALTH CARE SETTING
Modes of Blood-Borne Pathogen Transmission
In the health care setting, blood-borne pathogen transmission
occurs predominantly by percutaneous or mucosal exposure of
workers to the blood or body fluids of infected patients.
Occupational exposures that may result in HIV, HBV,
or HCV transmission include needlestick and other
sharps injuries; direct inoculation of virus into
cutaneous scratches, skin lesions, abrasions, or burns; and
inoculation of virus onto mucosal surfaces of the eyes,
nose, or mouth through accidental splashes. HIV, HBV,
and HCV do not spontaneously penetrate intact skin,
and airborne transmission of these viruses does not
occur.
Epidemiology of Blood Contact
To understand the nature, frequency, and prevention of
percutaneous injuries and mucocutaneous blood contacts among
HCWs, prospective observational studies have been
performed in different patient care settings (Table
1). The percentage of procedures with at least one
blood contact of any type ranged from 3% of
procedures performed by invasive radiology personnel in a study
in Dallas, Tex. (130), to 50% of procedures performed by
surgeons in a study in Milwaukee, Wisc. (224). The
percentage of procedures with at least one injury
caused by a sharp instrument also varied widely, from
0.1 to 15%. These differences may be related to variations
in study methods, procedures observed, and precautions
used by the workers performing the procedures.
|
|
|
TABLE 1. Prospective observational
studies of blood contact among HCWs |
|
|
|
|
|
Specialty and authors (reference) |
Yr |
Location(s) |
No. of procedures observed |
No. of procedures with 1
blood contact |
% Procedures with 1
sharps injury |
|
|
|
Surgery |
|
|
|
|
|
|
Tokars et al. (256) |
1990 |
New York, N.Y.; Chicago,
Ill. |
1,382 |
46.6 |
6.9 |
|
Popejoy et al. (220) |
1988 |
Albuquerque, N.Mex. |
684 |
27.8 |
3.1 |
|
Quebbeman et al. (224) |
1990 |
Milwaukee, Wisc. |
234 |
50.4 |
15.4 |
|
Gerberding et al. (116) |
1988 |
San Francisco, Calif. |
1,307 |
6.4 |
1.3 |
|
Panlilio et al. (208) |
1988-1989 |
Atlanta, Ga. |
206 |
30.1 |
4.9 |
|
Obstetrics |
|
|
|
|
|
|
Panlilio et al. (210) |
1989 |
Atlanta, Ga. |
230 |
32.2 |
1.7 |
|
Invasive radiology |
|
|
|
|
|
|
Hansen et al. (130) |
1992 |
Dallas, Tex. |
501 |
3.0 |
0.6 |
|
Emergency room |
|
|
|
|
|
|
Marcus et al. (178) |
1989 |
New York, N.Y.; Chicago,
Ill.; Baltimore, Md. |
9,793 |
3.9 |
0.1 |
|
Dentistry |
|
|
|
|
|
|
Cleveland et al. (77) |
1993 |
New York, N.Y. |
16,340 |
NAa |
0.1 |
|
|
|
a
NA, not available. |
|
Several of these studies assessed specific risk factors for
injury or exposure. For example, of the 99 percutaneous injuries
observed by Tokars et al. during 1,382 operations in five
different surgical specialties (general, orthopedic,
gynecologic, trauma, and cardiac), most (73%) were
related to suturing (256). Rates were highest (10%)
during gynecologic surgeries (256). Panlilio et al.
found in their study of blood contacts during surgery that
risk factors for blood contacts by surgeons included
performing an emergency procedure, patient blood loss
greater than 250 ml, and surgery duration greater
than 1 h (208). In their study of dental procedures,
Cleveland et al. found that most percutaneous
injuries sustained by dental residents occurred extraorally and
were associated with denture impression procedures (77).
Retrospective studies and surveys have also shown high rates
of blood contact among HCWs in different patient care settings.
Tokars et al. found that among 3,420 participants at the
American Academy of Orthopaedic Surgeons annual
meeting, 87.4% of surgeons surveyed reported a
blood-skin contact and 39.2% reported a percutaneous
blood contact in the previous month (258). In a retrospective
survey by O'Briain in 1991 (202), 56% of 36 resident and
staff pathologists reported that they had sustained a
cut or needlestick injury in the preceding year. In
this study, pathologists reported 72 injuries,
corresponding to a rate of one injury for every 37 autopsies
performed and one injury for every 2,629 surgical specimens
handled (202). An anonymous national survey of certified
nurse-midwives by Willy et al. found that 74% had
soiled their hands with blood, 51% had splashed blood
or amniotic fluid in their faces, and 24% had
sustained one or more needlestick injuries in the preceding
6 months (281). Among 550 medical students and residents
in Los Angeles, Calif., who were surveyed anonymously
by O'Neill et al., 71% reported exposures to
patients' blood and body fluids during the preceding
year (204). In a recent study of third- and fourth-year
medical students in San Francisco, Calif., by Osborn et
al., 12% reported an exposure to infectious body
substances over the 7-year study period, from 1990 to
1996 (205). There is evidence among some groups of
HCWs, such as dentists, that rates of exposure are
decreasing over time, temporally associated with increased
awareness and compliance with the practice of standard
precautions (76).
DETECTION AND DIAGNOSIS OF
BLOOD-BORNE PATHOGEN INFECTIONS
An understanding of the detection and diagnosis of HIV, HBV,
and HCV infection is vital for the appropriate management and
care of HCWs exposed to or infected with bloodborne
viruses.
Detection and Diagnosis of HIV Infection
After initial primary infection with HIV, there is a window
period prior to the development of detectable antibody. In
persons with known exposure dates, the estimated
median time from initial infection to the development
of detectable antibody is 2.4 months; 95% of
individuals develop antibodies within 6 months of infection
(34). Among HCWs with a documented seroconversion to HIV,
5% tested negative for HIV antibodies at >6 months
after their occupational exposure but were
seropositive within 12 months (73).
The two antibody tests commonly used to detect HIV
are the enzyme immunoassay (EIA) and the Western
blot. An HIV test result is reported as negative when
the EIA result is negative. The result is reported as
positive when the EIA result is repeatedly reactive and when
the result of a more specific, supplemental confirmatory
test, such as the Western blot, is also positive.
Once an individual develops an antibody response, it
usually remains detectable for life. HIV infection
for longer than 6 months without detectable antibody
is uncommon (73, 226).
Direct virus assays (e.g., PCR for HIV RNA) are sensitive
methods for the detection of HIV infection. However, problems
with laboratory contamination, false-positive rates,
and increased costs limit their routine use. While
PCR for HIV RNA is approved for use in established
HIV infection, its reliability in detecting very
early infection has not been determined (34). At present,
the false-positive and false-negative rates of PCR are too
high to warrant a broader role for it in routine
postexposure management (207).
Detection and Diagnosis of HBV Infection
The incubation period for acute hepatitis B ranges from 45 to
160 days, with an average of 120 days. Exposure to HBV can lead
to an acute infection which may result in a chronic
infection. Acute hepatitis B resembles other forms of
viral hepatitis and cannot be distinguished based on
history, physical examination, or serum biochemical
tests.
The diagnosis of acute HBV infection is confirmed by the
demonstration in serum of hepatitis B surface antigen (HBsAg),
which appears well before onset of symptoms and
before development of antibody to hepatitis B core
antigen (anti-HBc), and immunoglobulin M (IgM)
antibody to HBc, which appear at approximately the same
time as symptoms (143). The presence of IgM anti-HBc
indicates recent HBV infection, usually within the
preceding 4 to 6 months. The presence of hepatitis B
e antigen (HBeAg) in serum correlates with HBV
replication, high titers of HBV, and infectivity. Persons
who are positive for HBeAg typically have 108
to 109 HBV particles per ml of blood (243). In
persons who resolve acute HBV infection, antibody to
HBsAg (anti-HBs) develops and indicates immunity. The
persistence of HBsAg for 6 months after the diagnosis
of acute HBV is indicative of progression to chronic
HBV infection.
HBV serologic markers in different stages of infection and
convalescence are summarized in Table 2. Anti-HBc indicates
prior infection and lasts indefinitely. In persons
who respond to the hepatitis B vaccine, anti-HBs is
the only antibody that is elicited. Persons with
chronic infection who have mutations in the precore
region of the HBV genome that prevent the expression of HBeAg
but allow the expression of infectious virus have been
described (40, 260). High titers of HBsAg can be
observed in these persons even though they are HBeAg
negative. The prevalence of these precore mutations
in persons in the United States is unknown. The prevalence
may be relatively high in certain parts of the world (41,
124, 171, 173, 197).
|
|
|
TABLE 2. HBV serologic markers in
different stages of infection and
convalescence (201a)a
|
|
|
|
|
|
Stage of infection |
HBsAg |
Anti-HBs |
Anti-HBc
|
HBeAg |
Anti-HBe |
|
Totalb |
IgM |
|
|
|
Late incubation period |
+ |
 |
 |
 |
+ or  |
|
|
Acute hepatitis B |
+ |
 |
+ |
+++ |
+ |
|
|
HBsAg carrier |
+ |
(+ rarely) |
+ |
 |
+ or  |
+ or
|
|
Recent (<6 months; resolved
infectionc) |
 |
++ |
++ |
+ |
 |
+ or
|
|
Distant (>6 months;
resolved infectionc) |
 |
++ |
++ |
 |
 |
+ or
|
|
Vaccinated |
 |
++ |
 |
 |
 |
 |
|
|
|
a
+, positive; ++, strongly positive; +++, very
strongly positive; + or ,
variable reaction; ,
negative. |
|
b
The total anti-HBc assay detects both IgM and
IgG antibody. |
|
c
Resolved, the patient no longer has the disease.
|
|
Detection and Diagnosis of HCV Infection
The incubation period for acute HCV infection ranges from
2 to 24 weeks, with an average of 6 to 7 weeks (166, 179; L. B. Seef,
Letter, Ann. Intern. Med. 115:411, 1991). Because
different types of viral hepatitis are indistinguishable
based on clinical symptoms alone, serologic testing
(Table
3) is necessary to establish a specific diagnosis
of hepatitis C (121). Screening EIA and supplemental
immunoblot assays are licensed and commercially
available to detect antibodies to HCV (anti-HCV) (283). Because
the rate of false positivity for the screening EIA is high
in many populations, including HCWs, supplemental
immunoblot assays must be used to judge the validity
of repeatedly reactive EIA results. Anti-HCV may be
detected within 5 to 6 weeks after the onset of
infection and remains detectable long after the primary
infection. In general, the interpretation of serologic
tests for anti-HCV is limited by the following
factors: (i) assays for anti-HCV do not distinguish
between acute, chronic, or past infection; (ii) in
acute infection there may be a prolonged interval between
onset of illness and anti-HCV seroconversion (though most
infected individuals seroconvert within 3 months of
exposure); and (iii) the detection of anti-HCV does
not necessarily indicate active HCV replication (8).
|
|
|
TABLE 3. Tests for HCV infectiona
|
|
|
|
|
|
Test and type |
Description |
Application(s) |
Comments |
|
|
|
Anti-HCV |
EIA and supplemental assay
(i.e., recombinant immunoblot assay [RIBA]) |
Indicates past or present
infection but does not differentiate between
acute, chronic, or resolved infection; all
positive EIA results should be verified by a
supplemental assay |
Sensitivity 97%;
EIA alone has low positive predictive value in
low-prevalence populations |
|
HCV RNA |
|
|
|
|
Qualitative testsb,c |
Reverse transcriptase PCR
(RT-PCR) amplification of HCV RNA by in-house or
commercial assays (e.g., Amplicor HCV) |
Detects presence of
circulating HCV RNA; for monitoring patients on
antiviral therapy |
Detects virus as early as
1-2 weeks after exposure; detection of HCV RNA
during course of infection may be intermittent
(a single negative RT-PCR result is not
conclusive); false-positive and false-negative
results might occur |
|
Quantitative testsb,c |
RT-PCR amplification of HCV
RNA by in-house or commercial assays (e.g.,
Amplicor HCV Monitor); branched-chain DNA assays
(e.g., Quantiplex HCV RNA Assay) |
Determines concentration of
HCV RNA; may be useful for assessing the
likelihood of response to antiviral therapy |
Less sensitive than
qualitative RT-PCR; should not be used to
exclude the diagnosis of HCV infection or to
determine treatment endpoint |
|
Genotypingb,c |
Several methodologies
available (e.g., hybridization, sequencing) |
Groups isolates of HCV
based on genetic differences into six genotypes
and >90 subtypes; with new therapies, length of
treatment may vary based on genotype |
Genotype 1 (subtypes 1a and
1b) most common in United States and associated
with lower response to antiviral therapy |
|
Serotypingb |
EIA based on
immunoreactivity to synthetic peptides (e.g.,
Murex HCV Serotyping 1-6 Assay) |
No clinical utility |
Cannot distinguish between
subtypes; dual infections often observed |
|
|
|
a
Adapted from reference 64a. |
|
b
Currently not FDA approved; lack
standardization. |
|
c
Samples require special handling (e.g., serum
must be separated within 2 to 4 h of collection
and stored frozen [ 20
or 70°C];
samples should be shipped on dry ice). |
|
HCV RNA can be detected in serum or plasma within 1 to
2 weeks of exposure to the virus and several weeks before onset
of alanine aminotransferase (ALT) elevations or the
appearance of anti-HCV (103). In patients with
chronic HCV infection, HCV RNA levels may remain
relatively stable or can fluctuate over 1,000,000-fold.
Fluctuations in HCV RNA may or may not correlate with
elevations in transaminase levels. Rarely, the
detection of HCV RNA may be the only evidence of HCV
infection (14).
PCR techniques to amplify reverse-transcribed cDNA are
currently the most sensitive methods for detecting HCV RNA. Both
qualitative (122) and quantitative (87, 229) methods
can be used to detect HCV RNA. Quantitative assays
are less sensitive than qualitative assays and should
not be used as a primary test to confirm or exclude
the diagnosis of HCV infection (212). Currently, testing
for HCV RNA is available on a research basis and no tests
have been approved by the U.S. Food and Drug
Administration. Because of assay variability, results
of HCV RNA testing should be interpreted cautiously.
There are at least six different genotypes and more than
90 subtypes of HCV (33). About 70% of HCV-infected persons in
the United States are infected with genotype 1;
subtype 1a predominates over subtype 1b. Several
different nucleic acid detection methods are
commercially available to group isolates of HCV based on
genotypes and subtypes (172).
RISK OF OCCUPATIONAL
TRANSMISSION OF HIV FROM PATIENTS TO WORKERS
Risk of HIV Infection Postexposure
Prospective studies of HCWs have estimated that the average
risk for HIV transmission after a percutaneous exposure to
HIV-infected blood is approximately 0.3% (95%
confidence interval = 0.2 to 0.5%) (23) and that
after a mucous membrane exposure it is 0.09% (95%
confidence interval = 0.006 to 0.5%) (147). The risk after
a cutaneous exposure is less but has not been well
quantified since no HCW enrolled in a prospective
study has seroconverted after an isolated skin
exposure. There are insufficient data to quantify the
risk of transmission after occupational exposure to
potentially infectious tissues or fluids other than blood.
However, in a study by Fahey et al., none of
559 participants reporting cutaneous exposures to
blood, sputum, urine, feces, or other body substances
from patients presumed infected with HIV acquired HIV
infection (102). There is also no evidence of a risk
for HIV transmission by the aerosol route. Transmission
of HIV by aerosol would require the generation of
aerosolized particles of blood, the presence of
infective HIV in these aerosolized particles, and the
deposition of a sufficient number of infective
particles in the respiratory tract or on the mucous membranes
of a susceptible host to cause infection. Biological or
epidemiologic evidence that HIV can be transmitted by
aerosols via the respiratory route currently does not
exist (22). Although not specifically designed to
assess the possibility of aerosol transmission of
HIV, the 1991 seroprevalence survey of attendees of the annual
meeting of the American Academy of Orthopaedic Surgeons
addressed this concern indirectly (258). There were
1,201 study participants without nonoccupational risk
factors who had participated in procedures on
patients with HIV infection or AIDS and had never used a "space
suit" or other device to prevent inhalation of aerosols.
Since power instruments are used frequently in
orthopedic procedures, many of these participants may
have been exposed to blood or tissue aerosols
produced by these instruments; all were HIV seronegative
(258).
The risk of HIV transmission after a percutaneous exposure
appears to be influenced by several factors. To assess possible
risk factors, the Centers for Disease Control and
Prevention (CDC), in collaboration with international
public health authorities, conducted a retrospective
case-control study using data reported to national
surveillance systems in the United States, France,
Italy, and the United Kingdom. Based on logistic regression
analysis, factors associated with HIV transmission
after percutaneous exposure included a deep injury, a
device visibly contaminated with the source patient's
blood, procedures involving a needle placed directly
in the patient's vein or artery, and a source patient who died
from AIDS within 60 days of the exposure (39). The
findings of the case-control study suggest that the
risk for HIV infection likely exceeds 0.3% for
percutaneous injuries involving a larger volume of
blood and/or higher titer of HIV in the blood. Several
laboratory studies support these findings. In vitro models
have shown that increasing needle size and
penetration depth are associated with increased blood
transfer volume (182), that hollow-bore needles
transfer greater volumes of blood than solid suture needles,
and that gloves reduce the amount of blood transferred
(26). Studies also have shown that the level of
infectious HIV present in the blood of most patients
with symptomatic AIDS is significantly higher than
the level present in patients with asymptomatic HIV
infection (141). An additional finding of the case-control study
was that postexposure use of zidovudine (ZDV) by HCWs was
associated with a lower risk for HIV transmission
(39). (This issue will be discussed in more detail in
the section Postexposure Chemoprophylaxis for HIV
[below]). It is also possible that host defense mechanisms
influence the risk of HIV transmission. One study
demonstrated an HIV-specific T-helper cellular immune
response when peripheral blood mononuclear cells from
a small number of HCWs exposed to HIV were stimulated
in vitro by HIV. None of the HCWs seroconverted. One
possible explanation for these observations is that host immune
responses prevented establishment of HIV infection after
exposure (75). Similar cytotoxic T-lymphocyte
responses have been observed in other populations
with repeated HIV exposure without resulting
infection (70, 74, 160, 170, 225).
HIV Seroprevalence among Patients
In the United States, HIV seroprevalence rates vary widely by
geographic area and patients' demographic characteristics. The
CDC's Sentinel Hospital Surveillance System tested
195,829 anonymous patient blood samples at
20 hospitals in 15 cities between September 1989 and
October 1991. The HIV seroprevalence at these institutions
ranged from 0.2 to 14.2% and was highest among men aged
25 to 44 years and patients with infectious
conditions (excluding symptomatic HIV infection) and
drug-related conditions (153).
Similarly, seroprevalence data for unselected hospital
admissions and for patients presenting to emergency departments,
operating rooms, and obstetrical units have
demonstrated considerable variation (Table 4). The
lowest seroprevalence rates have been reported in
rural and suburban areas: 0.15% among trauma patients in
Wichita, Kans. (190), and 0.4% among elective surgery
patients in suburban Baltimore, Md. (68). The highest
seroprevalence rates have been reported in urban,
inner-city populations: 5.2 to 6.0% among emergency
department patients in inner-city Baltimore, Md. (157, 191),
and 5.5% among non-obstetric hospitalized patients in
Denver, Colo. (K. Krasinski, W. Borkowski, D. Bebenroth,
and T. Moore, Letter, N. Engl. J. Med. 318:185,
1988).
|
|
|
TABLE 4. HIV seroprevalence in
emergency, hospital, surgery, and
obstetrics patients |
|
|
|
|
|
Authors (reference) |
Yr |
Setting |
Location |
No. of patients tested |
No. of patients HIV positive (%) |
|
|
|
Kelen et al. (158) |
1987 |
Emergency department |
Baltimore, Md. |
2,302 |
119 (5.2) |
|
Kelen et al. (157) |
1988 |
Emergency department |
Baltimore, Md. |
2,544 |
152 (6.0) |
|
Marcus et al. (178) |
1989 |
Emergency department |
Six high-AIDS areas |
20,382 |
a
|
|
Nagachinta et al. (191) |
1990 |
Emergency department |
Los Angeles, Calif. |
1,945 |
40 (2.1) |
|
Mullins and Harrison (190) |
1987-1991 |
Trauma center |
Wichita, Kans. |
2,004 |
3 (0.15) |
|
Gordin et al. (119) |
1987 |
Hospital |
Washington, D.C. |
616 |
23 (3.7) |
|
Trepka et al. (261) |
1993 |
Hospital |
Denver, Colo. |
2,825 |
155 (5.5) |
|
Charache et al. (68) |
1989 |
Elective surgery |
Baltimore, Md. |
4,087 |
18 (0.4) |
|
Montecalvo et al. (187) |
1992 |
Surgery-obstetrics |
Valhalla, N.Y. |
1,056 |
15 (1.4) |
|
Krasinsi et al.b
|
1986-1987 |
Obstetrics |
New York, N.Y. |
1,192 |
28 (2.4) |
|
Donegan et al. (94) |
1987-1990 |
Obstetrics |
Boston, Mass. |
3,845 |
93 (2.4) |
|
|
|
a
4.1 to 8.9 patients per 100 patient visits. |
|
b
K. Krasinski, W. Borkowsky, D. Bebenroth, and
T. Moore, Letter, N. Engl. J. Med. 318:185,
1988. |
|
In a CDC study conducted in six emergency departments in
three urban and three suburban areas of New York, N.Y., Chicago,
Ill., and Baltimore, Md., the overall rate of HIV
infection ranged from about 4 to 9 per 100 patient
visits (178). The study found that many patients' HIV
infections were unrecognized at the time of initial
presentation to the hospital. The percentage of patients
whose HIV infection was unknown to hospital emergency
department workers was about 70% in the three inner
city hospitals and ranged from 40 to 90% in the three
suburban hospitals.
Incidence of Occupationally Acquired HIV Infection
As of 30 June 1999, a total of 191 U.S. workers had been
reported to the CDC's national surveillance system for
occupationally acquired HIV infection (Table
5) (65). Fifty-five HCWs had known occupational
HIV exposures, with a baseline negative HIV test and
subsequent documented seroconversion. Fifty of these
exposures were to HIV-infected blood, one was to visibly bloody
fluid, one was to an unspecified fluid, and three were to
concentrated virus in a laboratory. Of the 55 HCWs,
47 sustained percutaneous exposures, 5 had
mucocutaneous exposures, 2 had both a percutaneous
and a mucocutaneous exposure, and 1 had an unknown route of
exposure. Twenty-five of these HCWs have developed
AIDS.
|
|
|
TABLE 5. HCWs with documented and
possible occupationally acquired HIV infection
reported through June 1999 in the United Statesa
|
|
|
|
|
|
Occupation |
No. of documented cases of occupational
transmission |
No. of possible cases of occupational
transmission |
|
|
|
Dental worker, including
dentist |
|
6 |
|
Embalmer or morgue
technician |
1 |
2 |
|
Emergency medical
technician or paramedic |
|
12 |
|
Health aide or attendant |
1 |
15 |
|
Housekeeper or maintenance
worker |
1 |
12 |
|
Laboratory technician,
clinical |
16 |
16 |
|
Laboratory technician,
nonclinical |
3 |
|
|
Nurse |
23 |
34 |
|
Physician, nonsurgical |
6 |
12 |
|
Physician, surgical |
|
6 |
|
Respiratory therapist |
1 |
2 |
|
Technician, dialysis |
1 |
3 |
|
Technician, surgical |
2 |
2 |
|
Technician or therapist,
other |
|
10 |
|
Other health care
occupations |
|
4 |
|
Total |
55 |
136 |
|
|
|
a
HCWs are defined as those persons, including
students and trainees, who have worked in a
health care, clinical, or HIV laboratory setting
at any time since 1978. Adapted from reference
65. |
|
Of the 191 U.S. workers reported to the CDC's surveillance
system, 136 have been reported as possible cases of
occupationally acquired HIV infection. None of these
HCWs reported behavioral or blood transfusion risk
factors, and all reported occupational exposures to
blood, body fluids, or laboratory specimens containing
HIV. However, the time or source of infection was
undocumented, usually because no baseline serum
sample was available to establish seronegativity at
the time of exposure.
The CDC's surveillance system likely does not reflect the
full extent of occupationally acquired HIV infection because of
underreporting of known infections or underrecognition of
HIV infection. Studies of HCWs in hospital settings
suggest that many percutaneous injuries are not
reported (129, 177). Also, HCWs may not complete
postexposure follow-up serologic testing (D. Cardo
and the Health Care Worker Surveillance Study Group, Abstr.
6th Annu. Meet. Soc. Healthcare Epidemiol. Am., abstr. 67, 1996).
HIV Seroprevalence Surveys among HCWs
HIV seroprevalence surveys provide a way of indirectly
assessing the risk of occupationally acquired HIV infection. The
CDC has conducted two voluntary anonymous
seroprevalence surveys of surgeons in different
specialties. In 1992, a seroprevalence survey was
done among general surgeons, obstetricians, gynecologists,
and orthopedic surgeons practicing in moderate to high
AIDS incidence areas. Of the 770 participating
surgeons, one general surgeon, who reported
nonoccupational risk factors for HIV infection on an
anonymous questionnaire, was HIV positive (209). In 1991, a
seroprevalence survey was done among surgeons attending the
annual meeting of the American Academy of Orthopaedic
Surgeons. Of the 3,420 participants, two surgeons,
both of whom reported nonoccupational risk factors,
were HIV positive (258). Other seroprevalence studies
similarly have shown low rates of HIV seropositivity
among HCWs without nonoccupational risk factors for HIV
infection (Table 6) (20, 66, 71, 80, 82, 107, 117,
118, 123, 163, 215, 264; P. Ebbensen, M. Melbye, F. Scheutz,
A. J. Bodner, and R. J. Bigger, Letter, JAMA 256:2199,
1986; C. Siew, S. E. Gruninger, and S. A. Hojvat,
Letter, N. Engl. J. Med. 318:1400-1401, 1988).
|
|
|
TABLE 6. Published HIV seroprevalence
in selected HCWs |
|
|
|
|
|
Occupation and authors (reference) |
No. of HCWs tested |
No. of HCWs HIV positive |
% Prevalence |
|
|
|
Surgeon |
|
|
|
|
Panlilio et al. (209) |
770 |
1 |
0.13 |
|
Tokars et al. (258) |
3,420 |
2 |
0 |
|
HCW blood donor |
|
|
|
|
Chamberland et al. (66) |
9,449 |
3 |
a
|
|
U.S. Army Reserve
physician, dentist |
|
|
|
|
Cowan et al. (82) |
3,347 |
3 |
Not known |
|
Dentist |
|
|
|
|
Flynn et al. (107) |
89 |
0 |
0 |
|
Klein et al. (163) |
1,132b |
1 |
0.09 |
|
Siew et al.c |
1,195 |
0 |
0 |
|
Gruninger et al. (123) |
1,165 |
1 |
0.09 |
|
Gruninger et al. (123) |
1,433b |
0 |
0 |
|
Gruninger et al. (123) |
1,429b |
0 |
0 |
|
Ebbesen et al.d |
961 |
0 |
0 |
|
Hemodialysis staff |
|
|
|
|
Assogba et al. (20) |
40 |
0 |
0 |
|
Chirgwin et al. (71) |
25 |
0 |
0 |
|
Comodo et al. (80) |
84 |
0 |
0 |
|
Goldman et al. (118) |
49 |
0 |
0 |
|
Peterman et al. (215) |
161 |
2 |
1.2 |
|
Mortician, embalmer |
|
|
|
|
Gershon et al. (117) |
130 |
1 |
0.8 |
|
Turner et al. (264) |
129b |
0 |
0 |
|
|
|
a
One HCW lost to follow-up. |
|
b
Persons with nonoccupational risk excluded. |
|
c
C. Siew, S. E. Gruninger, and S. A. Hojvat,
Letter, N. Engl. J. Med. 318:1400-1401,
1988. |
|
d
P. Ebbesen, M. Melbye, F. Scheutz, A. J. Bodner,
and R. J. Bigger, Letter, JAMA 256:2199,
1986. |
|
One limitation of seroprevalence studies is that the extent
of occupational and nonoccupational exposure to HIV among tested
workers is usually unknown. Also, the rates may be
underestimates if individuals deferred testing
because they knew they were or suspected they might
be HIV positive. Nonetheless, these seroprevalence
surveys indicate that there was not a high rate of undetected
HIV infection among the HCWs studied, many of whom had
substantial opportunity for occupational
exposures.
RISK OF OCCUPATIONAL
TRANSMISSION OF HBV FROM PATIENTS TO WORKERS
Risk of HBV Infection Postexposure
The probability of HBV transmission after an occupational
exposure is dependent upon the concentration of infectious
virions in the implicated body fluid, the volume of
infective material transferred, and the route of
inoculation (e.g., percutaneous or
mucosal).
HBV is present in high titers in blood and serous fluids,
ranging from a few virions to 109 virions per ml
(142). The virus is present in moderate titers in
saliva, semen, and vaginal secretions (154). The titer in
semen and saliva is generally 1,000 to 10,000 times lower
than the corresponding titer in serum (44, 269).
Other body fluids such as urine and feces contain
very low levels of HBV unless contaminated with blood
(91, 106, 149).
One of the most common modes of HBV transmission in the
health care setting is an unintentional injury of an HCW from a
needle contaminated with HBsAg-positive blood from an
infected patient (5). The average volume of blood
inoculated during a needlestick injury with a
22-gauge needle is approximately 1 µl (V. M. Napoli
and J. E. McGowan, Letter, J. Infect. Dis. 155:828,
1987), a quantity sufficient to contain up to
100 infectious doses of HBV (243). The risk of
transmission after a needlestick exposure to a
nonimmune person is at least 30% if the source patient is
HBeAg positive but is less than 6% if the patient is HBeAg
negative (17, 120, 277). Blood from patients with
HBsAg titers below the threshold of detection using
routine serologic tests is rarely infectious (4).
While overt percutaneous injuries are efficient modes
of HBV transmission, other less-obvious exposures may also
lead to occupationally acquired HBV infection. In a case
series of HBV-infected HCWs, fewer than 10% recalled
a specific percutaneous injury, while 29 to 38%
recalled caring for an HBsAg-positive patient within
6 months prior to their onset of illness (35;
A. K. R. Chaudhuri and E. A. C. Follet, Letter, Br. Med. J. |