Prevention of Occupationally Acquired Human Immunodeficiency Virus Infection in Healthcare Workers
Susan E. Beekmann
David K. Henderson
In October of 2008, scientists from the Centers for Disease Control and Prevention (CDC) estimated that more than 1.1 million people were living with human immunodeficiency virus type 1 (HIV-1) infection in the United States, a prevalence of nearly 450 per 100,000 population (1). Since the beginning of the acquired immunodeficiency syndrome (AIDS) epidemic in 1981 more than 1 million cases of AIDS had occurred in the United States, resulting in more than 560,000 deaths (2). Established risk factors for infection include both homosexual and heterosexual contact, perinatal exposure and parenteral exposure. Parenteral exposure includes such specific risks as sharing needles during intravenous drug use and receiving blood, blood products, or tissues that are contaminated by HIV. Healthcare workers, in addition to these traditional risk behaviors, are at occupational risk for acquiring HIV infection following a parenteral or mucous membrane exposure to blood or blood-containing body fluids from HIV-infected patients.
Exposure to contaminated body fluids from HIV-infected patients and the potential for acquiring occupational HIV infection are issues that usually result in substantial healthcare worker anxiety. Even though the risk for occupational infection with hepatitis B virus (HBV) (see Chapter 73) in the healthcare environment has been documented since 1949 (3) and is associated with significantly more morbidity and mortality in the healthcare setting than is HIV, a clear focus on defining and minimizing healthcare workplace risks was not developed until the HIV epidemic was well underway (4,5). Since the early 1980s, the subject of occupationally acquired HIV infection has received extensive media coverage, both in the lay press and in scientific forums. In this chapter, we attempt to frame these occupational risks in the context of available scientific knowledge in an attempt to provide a somewhat broader perspective regarding the risks for HIV transmission in society.
ETIOLOGY
HIV-1 is the only retrovirus that has been associated with serious occupational morbidity and mortality. Several cases of simian immunodeficiency virus (SIV) seroconversion have been reported (6,7), but this virus has not yet been shown to cause disease in humans, and the SIV-seropositive laboratory workers remain well. Because several other human retroviruses have routes of transmission similar to those of HIV-1 (e.g., HIV-2, human T-cell lymphotrophic virus [HTLV] I (8), and HTLV-II), occupational transmission of these viruses may someday be detected, although no reports of occupational infection with these other agents have been published. Nonetheless, risks of transmission associated with other retroviruses are likely to be extremely low, and current guidelines for prevention of transmission of HIV-1 are thought to be adequate to prevent transmission of all bloodborne viruses, including other retroviruses.
PATHOGENESIS
HIV derives a major survival advantage from its ability to target the immune system by infecting CD4+ T cells and by inducing a specific cytokine milieu. The wide range of immunologic abnormalities in HIV-infected patients results primarily from the impairment of T cell-mediated immunity. The virus produces billions of virions and T-cell turnover is estimated at a billion cells/day, accounting for the very rapid emergence of viral variants and the progressive nature of T-cell depletion. Even during clinical latency, this battle between countless virions and a continuous but slow repopulation with newly produced T-cells results in a highly activated immune system that attempts to control virus replication and renew itself. Several pathologic mechanisms have been suggested as resulting in T-cell loss, including indirect viral killing and activation-induced apoptosis. Highly active antiretroviral regimens can produce sustained reductions of plasma viral RNA to below detectable limits. Even in those with no detectable plasma RNA, viral DNA could be detected in lymph nodes and peripheral blood mononuclear cells (PBMCs) and virus could be grown from peripheral lymphocytes after removal of CD8+ cells and activation (9). These observations that substantial viral replication occurs in lymphatic tissue during the period of clinical latency (10) while viral levels
in peripheral lymphocytes are undetectable or detectable at low levels (11) reinforce the insidious nature of the immunopathogenic effects of this virus. Disease progression is determined by the complicated interplay between viral and host factors, including different genetic polymorphisms of receptors, ligands, and key immune proteins that result in specific modulations of the host response to HIV infection (12). Inoculum size and certain inherent properties of the virus (e.g., syncytium-inducing viral phenotype) appear to confer greater overall HIV pathogenicity and may shorten the time to development of symptomatic HIV infection. In the 24 years since the introduction of zidovudine for the treatment of HIV, 25 drugs in six different classes used in varying combinations have resulted in predicted survival of nearly 40 years after combination antiretroviral therapy is initiated (13). Combination antiretroviral therapy has been clearly linked with reductions in morbidity and mortality, with the most dramatic reductions coinciding with increases in the use of protease inhibitors (14). Despite these therapeutic advances, reservoirs of HIV-1 have been identified that represent major impediments to eradication, including latent CD4+ T cells, hematopoietic stem cells of the monocyte/macrophage lineage, and dendritic cells (15,16). Current antiretroviral therapy effectively suppresses but does not eradicate HIV infection (17). The low rate of occupational infection following parenteral exposures to blood from patients known to be infected (i.e., ˜3/1,000) may relate to the very low inoculum and/or to spontaneous clearance by cellular immune mechanisms. In one study, T-cells from six of eight HIV-exposed, but uninfected healthcare workers produced interleukin-2 when exposed to HIV peptide antigens (18), and in a second study, cytotoxic T-lymphocytic responses to HIV envelope peptides were detected in 7/20 (35%) of healthcare workers who had sustained occupational exposures to HIV-positive blood compare with only 1 of 20 controls (19).
in peripheral lymphocytes are undetectable or detectable at low levels (11) reinforce the insidious nature of the immunopathogenic effects of this virus. Disease progression is determined by the complicated interplay between viral and host factors, including different genetic polymorphisms of receptors, ligands, and key immune proteins that result in specific modulations of the host response to HIV infection (12). Inoculum size and certain inherent properties of the virus (e.g., syncytium-inducing viral phenotype) appear to confer greater overall HIV pathogenicity and may shorten the time to development of symptomatic HIV infection. In the 24 years since the introduction of zidovudine for the treatment of HIV, 25 drugs in six different classes used in varying combinations have resulted in predicted survival of nearly 40 years after combination antiretroviral therapy is initiated (13). Combination antiretroviral therapy has been clearly linked with reductions in morbidity and mortality, with the most dramatic reductions coinciding with increases in the use of protease inhibitors (14). Despite these therapeutic advances, reservoirs of HIV-1 have been identified that represent major impediments to eradication, including latent CD4+ T cells, hematopoietic stem cells of the monocyte/macrophage lineage, and dendritic cells (15,16). Current antiretroviral therapy effectively suppresses but does not eradicate HIV infection (17). The low rate of occupational infection following parenteral exposures to blood from patients known to be infected (i.e., ˜3/1,000) may relate to the very low inoculum and/or to spontaneous clearance by cellular immune mechanisms. In one study, T-cells from six of eight HIV-exposed, but uninfected healthcare workers produced interleukin-2 when exposed to HIV peptide antigens (18), and in a second study, cytotoxic T-lymphocytic responses to HIV envelope peptides were detected in 7/20 (35%) of healthcare workers who had sustained occupational exposures to HIV-positive blood compare with only 1 of 20 controls (19).
Evidence has accumulated that infection of Langerhans cells, which are the dendritic cells of the epidermis, plays a pivotal role in early transmucosal and transepidermal transmission (20). HIV infection of these Langerhans cells is regulated by surface expression of CD4 and HIV coreceptors, specifically CCR5. Langerhans cells, which represent only 2% to 3% of all epidermal cells, become infected very early (within 24 hours of exposure), and within an additional 24 to 48 hours this cell population has migrated from epithelial tissue to lymphoid tissue (21,22). Within 5 days, HIV is detectable in peripheral blood in the SIV model. In addition, a molecule called DC-SIGN functions as an attachment factor and mediates capture of HIV by dendritic cells without infection of these cells (20). HIV captured by dendritic cells maintains infectivity for 25 days in vitro in the absence of replication within dendritic cells, whereas free virus rapidly loses its infectious potential. Langerhans cells are the major epidermal cell type that is involved in transmission of HIV to lymphoid tissue (23). Thus, the ability to block infection of dendritic cells or to block the handoff from dendritic cells bearing HIV on their membranes to susceptible T cells by HIV may importantly impact occupational transmission of HIV (24). Recently, sequencing viruses in heterosexual transmission pairs and in acute HIV infection provided evidence that a single virus (or infected cell) initiated productive infection in close to 80% of the individuals tested, and two to five viruses in the other 20% (25,26). The greatest opportunities for prevention are strategies that target these initially small and genetically homogeneous foci of infection in the first week of infection (27). Additionally, since systemic HIV infection is not thought to occur immediately following exposure, a brief window of opportunity may allow modification of viral replication in the initial target cells or lymph nodes with postexposure antiretroviral treatment.
Once occupational transmission of HIV has occurred, the pathogenesis of infection is not thought to be different from that following other modes of transmission. As occurs with other HIV transmission modalities, some healthcare workers who have acquired occupational HIV infection have progressed quite rapidly to AIDS, while others remain asymptomatic after many years of infection.
DIAGNOSIS AND CLINICAL MANIFESTATIONS
The clinical and laboratory manifestations of HIV infection are generally no different for healthcare workers who acquire occupational infections than they are for persons infected through other routes. Findings that may be useful in establishing the diagnosis of HIV infection of healthcare workers are discussed in detail in the following paragraphs.
HIV-specific antibodies usually appear from 6 weeks to 4 months following exposure. An analysis of 51 seroconversions in healthcare workers determined that the estimated median interval from exposure to seroconversion was 46 days, with a mean interval of 65 days (28). Serodiagnosis consists of screening enzyme-linked immunosorbent assays (ELISAs) followed by a diagnostic Western blot when the ELISA is positive. On evaluation using the Western blot technique, antibodies to the group-specific antigen/core (GAG) proteins (i.e., p18, p24, and/or p55) may be the first to appear, but antibodies to the envelope (ENV) (e.g., gp120, gp160, and gp41) and polymerase (POL) gene products (e.g., p31) develop thereafter, confirming the serodiagnosis of HIV infection. Rapid HIV antibody testing with high sensitivity and specificity (99.6% and 100%, respectively) and 20-minute turnaround time are now widely available with six rapid HIV tests approved by the U.S. Food and Drug Administration (FDA). Rapid testing may facilitate source patient testing and decrease the length of time healthcare workers take postexposure prophylaxis (PEP) pending the source patient HIV test result. Delayed seroconversion has been suggested following sexual exposures (29,30), and the relatively low-inoculum exposures sustained by healthcare workers could result in latent HIV infection and delayed seroconversion. PEP does not appear to prolong time to development of HIV antibodies (31). In 95% of healthcare workers who became infected after occupational exposures, seroconversion occurred within 6 months of the exposures (31) when routine testing has been performed. According to CDC, two cases of delayed seroconversion occurring in healthcare workers have been reported (31). These healthcare workers had both tested seronegative for HIV at least 6 months following exposure, but were seropositive within 12 months after the exposure. One of these delayed seroconversions was associated with
concomitant exposure to hepatitis C virus (HCV), and this individual developed co-infection with hepatitis C that was rapidly fatal (32). CDC models indicate that the upper 95th percentile of the distribution of time between exposure and seroconversion is 190 days, and that 5% of healthcare workers are estimated to seroconvert in <6 months following exposure (33). Acute retroviral syndrome (34, 35 and 36) associated with primary HIV infection has been a relatively common finding among healthcare workers in whom documented occupational HIV infection has occurred. This syndrome usually occurs 4 to 6 weeks after the occupational exposure. The CDC reported that 81% of healthcare workers experienced a syndrome compatible with primary HIV infection in a median of 25 days after exposure (28). This clinical syndrome has been described as resembling acute infectious mononucleosis: fever, rash, malaise, myalgias/arthralgias, headaches, night sweats, pharyngitis, and lymphadenopathy have been documented (34, 35 and 36). Laboratory abnormalities have also been described, including reduced total lymphocyte count, elevated sedimentation rate, and elevated transaminases and alkaline phosphatase levels.
concomitant exposure to hepatitis C virus (HCV), and this individual developed co-infection with hepatitis C that was rapidly fatal (32). CDC models indicate that the upper 95th percentile of the distribution of time between exposure and seroconversion is 190 days, and that 5% of healthcare workers are estimated to seroconvert in <6 months following exposure (33). Acute retroviral syndrome (34, 35 and 36) associated with primary HIV infection has been a relatively common finding among healthcare workers in whom documented occupational HIV infection has occurred. This syndrome usually occurs 4 to 6 weeks after the occupational exposure. The CDC reported that 81% of healthcare workers experienced a syndrome compatible with primary HIV infection in a median of 25 days after exposure (28). This clinical syndrome has been described as resembling acute infectious mononucleosis: fever, rash, malaise, myalgias/arthralgias, headaches, night sweats, pharyngitis, and lymphadenopathy have been documented (34, 35 and 36). Laboratory abnormalities have also been described, including reduced total lymphocyte count, elevated sedimentation rate, and elevated transaminases and alkaline phosphatase levels.
Core (i.e., p24) antigenemia may be detected coincident with the onset of symptoms and usually resolves within several weeks to months, as antibodies to p24 are produced and become detectable in the peripheral circulation (37). One can also detect the presence of virus, either by culture or by polymerase chain reaction (PCR) in cerebrospinal fluid, PBMCs, and plasma before the development of an antibody response in persons who have sustained nonoccupational exposures (35,38, 39 and 40). Plasma HIV RNA levels are highest immediately after acquisition and then rapidly decrease (41). These direct virus assays (including HIV p24 antigen EIA, PCR for HIV RNA, and the branched-chain DNA assay) consistently detect infections 1 to 2 weeks earlier than the most sensitive antibodies, but they still do not become positive until weeks or months postexposure and they may revert to negative following antibody seroconversion (33). Interestingly, no association between plasma HIV RNA levels at the time of seroconversion and subsequent rate of CD4+ cell loss or AIDS progression has been detected (41). The use of PCR to detect circulating viral RNA will likely supplant the use of the p24 antigen test, although the p24 assay turnaround time is much shorter than for the PCR assay in some centers.
Although direct virus assays have been used as ancillary tests in the diagnosis of occupational HIV infection, these tests should not routinely be used to detect infection in exposed healthcare workers (33). These tests may be helpful in defined adjunctive circumstances, such as when the ELISA is positive but the Western blot is indeterminate, or when symptoms are consistent with the acute retroviral syndrome but serologic testing remains negative for more than several weeks. A negative direct virus assay should never be the basis for excluding infection. Although ultrasensitive direct virus assays are available (quantitation of HIV-1 RNA down to 50 copies/mL), the risk for false positive results increases accordingly.
Symptoms consistent with the acute retroviral syndrome signal that HIV antibodies will appear, usually within 1 to 10 weeks (35) if infection has indeed occurred. Healthcare workers who sustain occupational exposures should be educated about the symptoms of the seroconversion illness and should be instructed to seek urgent attention in the employee health clinic if these symptoms appear. In most occupational seroconversions, HIV seropositivity has not been documented as part of the routine serologic follow-up but has been detected after the healthcare worker seeks medical attention for an illness consistent with seroconversion. Nonetheless, the CDC recommends HIV antibody testing at 6 weeks, 3 months, and 6 months following the occupational exposure (42,43). The National Institute of Health (NIH) Clinical Center Occupational Medical Service also elects to check HIV antibody status at 12 months following exposure, although this is not routinely recommended by the CDC because of the rarity of delayed seroconversion events (42,43). Because of the anecdotal experience with delayed HIV seroconversion occurring following concomitant exposures to HIV and HCV, most authorities would recommend extending follow-up to 12 months following simultaneous exposures to hepatitis C and HIV.
EPIDEMIOLOGY
Occupational injuries and exposures to blood and body fluids continue to be commonplace in virtually every healthcare setting. Healthcare workers who sustain these injuries often react immediately with anxiety, fear, and concern over their risk for acquiring HIV. Framing the issue of HIV transmission risk is quite complex. Nonetheless, more than a decade of dealing with HIV infection in the healthcare workplace has led to a fairly extensive database characterizing these occupational risks.
Healthcare workers’ perceptions of risk were initially affected by the news media and publicity regarding cases of occupational infection. The sensationalism that traditionally accompanied HIV-related issues in the media artificially inflated perceptions of occupational risk. We frequently find that both the lay public and, particularly, healthcare workers believe that large numbers of occupational HIV infections have been documented. Depending on the definition of “occupational infection” chosen for the analysis, one can arrive at quite disparate assessments of the number of occupational HIV infections documented in the United States (44). The number of cases of occupational HIV infections in healthcare workers has clearly decreased dramatically over the past decade.
Reports of Occupational Infections
A wide variety of sources have provided information about HIV infection in healthcare workers (44). Several general types of case reports have appeared in the literature, ranging from healthcare workers in whom HIV seroconversions have been documented following an occupational exposure to healthcare workers who are found to be seropositive but in whom the seropositivity cannot be linked to a discrete injury or exposure.
Documented seroconversions are generally defined as cases in which a healthcare worker sustains an injury with a device contaminated with blood from an HIV-seropositive or indeterminate source; the healthcare worker is documented to be HIV-seronegative at the time of the exposure, and then the healthcare worker develops
serologic evidence of HIV infection within the ensuing 6 months. Documented seroconversions are the source of the most detailed and reliable epidemiologic information about occupational infections and are, in fact, the standard against which other types of information about occupational HIV infection can be measured. Through June 30, 2009, 57 cases of occupational seroconversions had been documented either in the medical literature or in individual case reports to the CDC that meet the criteria established for this category of occupational infection (45,46). Of the 57 infected healthcare workers, 48 had percutaneous injuries, 5 had mucocutaneous exposures, 2 had both percutaneous and mucous membrane exposures, and 2 had unknown routes of exposure.
serologic evidence of HIV infection within the ensuing 6 months. Documented seroconversions are the source of the most detailed and reliable epidemiologic information about occupational infections and are, in fact, the standard against which other types of information about occupational HIV infection can be measured. Through June 30, 2009, 57 cases of occupational seroconversions had been documented either in the medical literature or in individual case reports to the CDC that meet the criteria established for this category of occupational infection (45,46). Of the 57 infected healthcare workers, 48 had percutaneous injuries, 5 had mucocutaneous exposures, 2 had both percutaneous and mucous membrane exposures, and 2 had unknown routes of exposure.
In addition to these documented seroconversions, a number of additional cases of HIV infection have been categorized by the CDC as “possible” occupational infections. This “possible occupational infection” category exhibits different demographics from the set of individuals who have documented occupational infections, and likely include individuals who have confounding communitybased risk for infection (44). Since the overwhelming majority of these cases have been reported as anecdotes, these data provide only limited insight into the magnitude of risk for occupational infection (i.e., based on these data, one can state only that healthcare workers are at risk for occupational HIV infection). Some conclusions can be drawn, however, from the cases of documented seroconversions regarding the epidemiology of occupational infection. For example, by examining cases of documented seroconversion for circumstances of occupational exposure, one can gain substantial insight into the types of exposures likely to result in transmission of HIV. Even these relatively small databases provide evidence that the risk associated with mucocutaneous exposures appears to be lower than the risk associated with percutaneous injuries.
Data Describing the Magnitude of Risk of HIV Transmission in the Healthcare Setting
Longitudinal cohort studies of healthcare workers involved in the day-to-day care of HIV-infected patients and in the handling and processing of specimens from such patients provide the best available data regarding the magnitude of risk for transmission in the healthcare setting. A number of prospective studies have followed healthcare workers who have sustained documented exposure to blood or bloodcontaining body fluids from HIV-infected patients. In all of these studies, healthcare workers undergo baseline and follow up HIV serologic testing (at a minimum) any time a healthcare worker sustains a percutaneous exposure to blood from an HIV-infected patient. The average risk of HIV infection following percutaneous exposure to HIV-infected blood has remained at approximately 0.3% (95% confidence interval [CI] = 0.2-0.5%) for a number of years.
Similarly, other prospective studies have examined the risk associated with mucous membrane exposures to blood or body fluids from HIV-infected patients. Although mucous membrane exposures that resulted in HIV transmission have been reported anecdotally (47,48) no seroconversions have occurred following the mucous membrane exposures that were prospectively collected from enrollees in these longitudinal studies.
Factors that Might Influence the Risk of Transmission
Although these data are reasonably specific, and CIs around the calculated risks of transmission are narrow, we still lack sufficient information to predict which injuries will result in transmission of infection. Many of the percutaneous injuries that have been associated with documented seroconversions have been quite deep or extensive or have involved injection of a volume of blood into the healthcare worker, whereas other percutaneous injuries associated with transmission have been relatively minor. Mucous membrane or nonintact skin exposures that resulted in transmission have almost uniformly been quite extensive (e.g., the contact with blood has been for a prolonged period [>15 minutes] or has involved large areas of skin surface). Occasionally, injuries that one might intuitively think would have a higher than average risk for infection have not resulted in infection. For example, a healthcare worker at the Clinical Center, NIH, sustained a severe injury with a bone marrow aspiration needle that had been used on a patient with end-stage HIV disease; the needle actually penetrated through the palm and was visible from the dorsum of the worker’s hand. This exposure did not transmit HIV infection.
The epidemiologic factors contributing to the risk for occupational infection have been explored using the casecontrol method (49). Thirty-three cases of occupational HIV seroconversion following percutaneous exposures to HIV-infected blood and 665 controls who did not seroconvert were studied by Cardo et al. (49) at the CDC. Multivariate logistic regression identified several risk factors associated with HIV transmission after percutaneous exposure: deep injury (odds ratio [OR] 15, 95% CI 6.0-41), visible blood on device (OR 6.2, 95% CI 2.2-21), procedure involving needle in artery or vein (OR 4.3, 95% CI 1.7-12), terminal illness in source patient (OR 5.6, 95% CI 2.0-16), and postexposure use of zidovudine (OR 0.19, 95% CI 0.06-0.52). Increased risk was associated with factors that are indirect measures of the inoculum size (i.e., the quantity of blood transferred in the exposure) or higher viral burden (i.e., source patient in the terminal stage of AIDS). Thus, although the average risk of HIV transmission following a percutaneous exposure is 0.3%, the risk of transmission following exposures involving large quantities of blood or high viral titers may be substantially higher than the average risk. Corroborating evidence for the factors identified by the case-control study was supplied by a laboratory study that demonstrated that more blood is transferred by deeper injuries and hollow-bore needles (50). Mast and Gerberding (51) also determined that glove use reduced the transferred blood volume by nearly 50% in their laboratory model.
Despite our inability to predict with precision which exposures will result in transmission of HIV infection, the documented seroconversions have provided us with specific information about which body fluids have resulted in transmission. Of the 57 documented seroconversions, 49 exposures were to HIV-infected blood, 1 to visibly bloody pleural fluid, 4 to an unspecified fluid, and 3 to a concentrated viral preparation in a laboratory (42). Thus, blood appears to be the major clinical risk associated with transmission. One case report documented transmission of HIV to a laboratory technician from Germany who sustained an
accidental splash of serum from an infected patient to his eye (52). Transmission in this case was likely facilitated by failure to wash the eye and by concomitant conjunctivitis related to a contact lens present in his eye at the time of exposure. Blood, visibly bloody body fluid, and now serum clearly remain the primary risk for occupational transmission of HIV in the healthcare setting (47).
accidental splash of serum from an infected patient to his eye (52). Transmission in this case was likely facilitated by failure to wash the eye and by concomitant conjunctivitis related to a contact lens present in his eye at the time of exposure. Blood, visibly bloody body fluid, and now serum clearly remain the primary risk for occupational transmission of HIV in the healthcare setting (47).
The type and, likely, size of the needle or sharp object involved in the injury also appears to affect the risk of transmission. To date, to our knowledge, no cases of occupational infection have been definitively linked to an exposure resulting from a solid (i.e., suture) needle. Transmission has been associated with several types of hollowbore needles (including injection needles and intravenous catheters) and other sharp objects (including contaminated broken glass, scalpels and an orthopedic pin (47)).
Finally, certain source patient variables, and, perhaps, even several factors relating to the recipient healthcare worker’s status, likely affect transmission. Source patients with terminal HIV disease were found to be associated with higher risks of HIV transmission in the case-control study discussed previously (49). Although data regarding specific measurement of HIV viral burden were not available to the CDC researchers, the increased risk of HIV transmission from source patients who are in the late-stage of HIV infection likely is a surrogate marker for the source patient’s circulating viral burden. Some also have postulated that the recipient healthcare worker’s histocompatibility with the source patient (i.e., human leukocyte antigen [HLA] type, etc.) or any concurrent viral illnesses, such as Epstein Barr virus, cytomegalovirus infection, or infection with human herpesvirus-6 that results in increased CD4 expression, or the presence of chronic inflammation at or around the skin entry site, might also influence the risk of transmission. Despite this educated speculation, the numbers of cases of documented seroconversions with these data available are too few to permit adequate characterization of these risks.
Comparison of the Risk of HIV Transmission to the risk of Transmission of other Bloodborne Pathogens
When assessing the risk of acquiring occupational HIV infection, healthcare workers must be able to place that risk into the broader context of risks associated with other bloodborne pathogens such as hepatitis B and hepatitis C (see Chapter 73). Hepatitis B has long been recognized as a significant cause of healthcare worker morbidity and mortality; healthcare worker risks associated with hepatitis C have been documented and partially characterized in the past decade (53, 54 and 55).
The CDC estimated in 1987 that 12,000 cases of hepatitis B infection per year occurred among healthcare workers in the United States and that 500 healthcare workers were hospitalized each year because of the complications of occupationally acquired hepatitis B (56). Additionally, prior to the full-scale implementation of hepatitis B immunization, approximately 200 workers died each year from occupational hepatitis B or its complications (57). Subsequently, Mahoney et al. (58) found that the calculated number of HBV infections among healthcare workers declined from 17,000 in 1983 to 400 in 1995. This dramatic decline was associated with implementation of Universal Precautions policies, with licensure of recombinant-DNA hepatitis B vaccines, and with the implementation of the Occupational Safety and Health Administration (OSHA) Bloodborne Pathogens Standard (59).
The risk associated with hepatitis C appears to be lower than the risk associated with hepatitis B: healthcare workers with frequent blood contact account for 1% to 2% of reported cases of hepatitis C infection (60), and seroprevalence studies indicate that healthcare workers’ risk of hepatitis C infection is only slightly higher than that of volunteer blood donors. Several small prospective studies have measured the risk of transmission after percutaneous exposure to average 1.9% (see Chapter 73) (61) with a range from approximately 0% (in six studies, summarized in reference (54)) to 22% (62), depending on the size of the population studied and the assays used to test source patients and employees, among other important variables. Lower rates of transmission have been associated with the use of the (much less sensitive) first generation hepatitis C serologic test and with an interesting geographic distribution (see Chapter 73).
PREVENTION AND CONTROL
Despite the fact that several indirect pieces of evidence suggest that the administration of antiretrovirals as PEP may reduce the risk of HIV transmission (46,49,63), because of the toxicity and inconvenience of the agents administered as PEP, the attention of the healthcare community should be focused first on preventing occupational exposures as a means of preventing transmission of HIV. The U.S. Federal government has issued regulations that have just this intent. In 1991, the OSHA issued regulations (59) that were designed to ensure employer compliance with full implementation of Universal Precautions (64). This “Bloodborne Pathogen Standard” also mandates that employers offer hepatitis B immunization to healthcare workers at risk for occupational exposure at no cost to the employee.
Primary Prevention of Exposures in the Healthcare Workplace
In the time that has elapsed since the initial cluster of cases of Pneumocystis jiroveci pneumonia was identified in Los Angeles in the summer of 1981 (65), the CDC issued a series of guidelines with the goal of preventing transmission of HIV infection to healthcare providers (4,42,43,56,64, 66, 67, 68, 69, 70, 71, 72, 73, 74 and 75). The concept of “universal precautions,” or use of blood and body-fluid precautions for the care of all patients was first proposed by the CDC in 1985 (4) and again in 1986 (69). The August 1987 guidelines (frequently referred to as the Universal Precautions guidelines) consolidated and updated all previous CDC recommendations concerning the prevention of occupational infection with HIV (64).
The 1987 Universal Precautions guidelines (summarized in Table 74-1) strongly emphasized the need for every healthcare worker to consider all patients as potentially infected with HIV or other bloodborne pathogens and to adhere to infection-control precautions for minimizing the risk of exposure to blood and body fluids from all patients. These guidelines have been updated by the Hospital Infection Control Practices Advisory Committee (76). Universal Precautions
and body substance isolation (77) are now amalgamated into a single set of guidelines called Standard Precautions (76).
and body substance isolation (77) are now amalgamated into a single set of guidelines called Standard Precautions (76).
TABLE 74-1 Use of the Measures in Standard Precautions to Prevent the Transmission of HIV in Healthcare Settingsa | ||
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Although the use of Universal or Standard Precautions (see Chapter 90) has been advocated as a means to prevent occupational exposures to blood and other body fluids, neither the efficacy nor the cost-effectiveness of these admittedly labor-intensive and costly (78) precautions has been demonstrated definitively. Furthermore, Standard Precautions, with its emphasis on barrier precautions, may not prevent percutaneous injuries, which are the major risk associated with occupational infections, although appropriate handling and disposal of needles and other sharp objects is an integral component of these guidelines.
Studies of the efficacy of Standard Precautions have produced inconsistent results. At least one study has concluded that Universal Precautions training was associated with increased incidence of injuries (79), whereas others have reported stable exposure rates (80). Some studies have shown decreases in recapping or needle-disposal device-related injuries, but stable (or slightly increased) overall injury rates (81, 82, 83, 84 and 85). The studies indicating that implementation of Universal Precautions did not decrease overall injury rates almost uniformly suggest poor healthcare worker adherence to the components of Universal/Standard Precautions or failure to assess adherence to the precautions. Several other groups have reported trends toward fewer needlestick injuries in association with Universal Precautions (78,86). Investigators at the Clinical Center, NIH, reported that implementation of Universal Precautions was associated with a significant decrease in both cutaneous (87) and reported parenteral exposures to blood (88). A review of published percutaneous injury rates per 100 employees found that injury rates following implementation of the Bloodborne Pathogens Standard in 1992 (see paragraph below) were lower than those based on pre-1992 data (89). To the extent that these precautions are actually followed, they will very likely reduce occupational exposures to bloodborne pathogens. Ensuring adherence to the recommended precautions, however, is a challenging matter. Despite these controversies, Universal/Standard Precautions have been widely implemented and are now mandated by the OSHA (59).
This mandate was published by the Department of Labor (59) as the “Occupational Exposure to Bloodborne Pathogens; Final Rule” in the Federal Register in December 1991 (the details of this Final Rule are summarized in Table 74-2). Employers, including hospitals and virtually any setting in which exposure to blood might occur, are now required to have in place an Exposure Control Plan that mandated implementation of Universal Precautions. In addition, a series of other requirements have been imposed, including extensive documentation and record-keeping regarding compliance with these regulations. Other requirements relate to engineering and work practice controls, use of appropriate personal protective equipment, detailed housekeeping standards, and requirements for “biohazard” labeling. Free hepatitis B immunization is now required for all employees with any potential for exposure; healthcare workers who decline vaccination must sign an “informed refusal,” the content of which is specified in the Final Rule. Finally, the OSHA has established an obligatory federal standard of practice
for employers when an employee is involved in an exposure incident; current recommendations of the U.S. Public Health Service must be implemented following an exposure incident.
for employers when an employee is involved in an exposure incident; current recommendations of the U.S. Public Health Service must be implemented following an exposure incident.
TABLE 74-2 Requirements of the OSHA’s Bloodborne Pathogens Standard | |||
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Certain portions of the Final Rule were impatiently awaited by occupational medicine and healthcare epidemiology personnel, in particular the requirement to document compliance with the hepatitis B vaccination. Although the rates of occupational hepatitis B have decreased dramatically with the OSHA Final Rule and use of Universal Precautions (58), absolute protection can only be assured with evidence of serologic immunity. Prior to publication of the OSHA Final Rule, the CDC estimated that only 30% to 40% of healthcare workers had been vaccinated (90,91). In 1995, Agerton et al. (92) concluded that the OSHA Final Rule resulted in a greater awareness in healthcare workers of their risk for hepatitis B and an increase in the number of workers receiving the vaccine; nonetheless, only 51% of eligible workers had completed a vaccination series. Other portions of the Final Rule, such as the “exposure determination” requirement, in which employers must list all job classifications in which some employees have occupational exposure to blood, and then list every task and procedure performed by the employees in those job classifications, are remarkably onerous and have undoubtedly greatly increased the workload of healthcare epidemiology personnel with, in our opinion, little likely benefit to the employee.
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