Prevention of Occupationally Acquired Viral Hepatitis in Healthcare Workers
David K. Henderson
Susan E. Beekmann
Viral hepatitis was first recognized as an occupational hazard for healthcare workers nearly half a century ago when a blood bank worker acquired viral hepatitis after sustaining multiple needlesticks (1). Since then, we have witnessed an explosion of knowledge in the fields of both basic virology and healthcare epidemiology. Five primarily hepatotropic viruses (hepatitis A-E, see Hepatitis Viruses, Chapter 46) have been identified and characterized, their modes of occupational transmission have been determined, and strategies for prevention have been developed. This chapter addresses the healthcare-associated epidemiologies of these five agents and does not specifically address the several additional agents that currently contribute to the viral hepatitis alphabet, including the agent called hepatitis French (origin) virus (HFV) (hepatitis F) (2); the bloodborne “GB” agents (GB virus A [GBV-A], GB virus B [GBV-B] and GB virus C, [GBV-C] (3,4) which rarely cause hepatitis; and hepatitis G virus (HGV), a common, easily transmitted bloodborne agent that is closely related to GBV-C, which causes clinically mild, if any, hepatitis (5,6, 7 and 8), and may not, in fact, be hepatotropic (9). Until these “non-A-E hepatitis” viruses, and other putative hepatitis agents (10, 11 and 12) are formally recognized as hepatitis viruses and have their respective epidemiologies delineated, general infection control practices for protecting healthcare workers from enterically transmitted or parenterally transmitted agents, as appropriate, are indicated. This chapter focuses on the etiology of occupationally acquired viral hepatitis, the epidemiology of these viruses in the healthcare setting, and the specific prevention and control strategies for each of the five hepatotropic agents identified above.
ETIOLOGY AND EPIDEMIOLOGY
The risk of occupational transmission of each of the hepatitis viruses differs according to the infective body substance, the modes of transmission, the occupations and work responsibilities of individual healthcare workers, the varying prevalences of infection in the patient population, healthcare workers’ immune statuses, and the individual worker’s compliance with infection control procedures. An overview of the five major hepatitis viruses, risks for occupational transmission in the healthcare setting, modes of occupational transmission, relevant prevention strategies and currently imprecise or unanswered questions is presented in Table 73-1. Factors affecting the risks for occupational transmission for each virus are discussed separately, below, in more detail.
Hepatitis A Virus
Although healthcare workers are generally not considered to be at substantially increased risk for acquiring hepatitis A virus (HAV) infection (13, 14, 15, 16 and 17), occupational transmission of this virus has been well documented and occurs, albeit rarely, under unusual circumstances. Most HAV transmission in healthcare settings occurs from index patients who are asymptomatic, from those in whom the infection is otherwise unsuspected and/or undiagnosed, from patients who are in the prodromal phase of the infection when viral shedding in the stool is maximal, in instances in which when infection control procedures are less than optimal, and/or in settings in which patients are incontinent of feces (18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32 and 33). Occupational HAV transmission occurs primarily
via the fecal-oral route, following direct or indirect contact with the index patient’s fecal material and is generally only recognized when a cluster of cases occurs. Although healthcare workers can acquire HAV from contaminated food or drink (34, 35 and 36), occupational infection usually occurs following direct contact with infectious patients. Neonatal intensive care units may provide a unique setting for healthcare-associated/occupational transmission, because several reported outbreaks, some with widespread secondary transmission, have occurred in this setting (20,22,23,28,31,37,38). Outbreaks in neonatal intensive care units have most frequently followed the rare occurrence of transfusion-acquired infection of a neonate. Unless staff members practice strict hand washing and environmental cleaning, neonatal and pediatric intensive care settings may provide optimal opportunities for fecal contamination of healthcare workers’ hands and environmental surfaces. HAV can survive on workers’ hands and this aspect of HAV epidemiology may contribute to the indirect spread of the virus to other patients and staff members (39).
via the fecal-oral route, following direct or indirect contact with the index patient’s fecal material and is generally only recognized when a cluster of cases occurs. Although healthcare workers can acquire HAV from contaminated food or drink (34, 35 and 36), occupational infection usually occurs following direct contact with infectious patients. Neonatal intensive care units may provide a unique setting for healthcare-associated/occupational transmission, because several reported outbreaks, some with widespread secondary transmission, have occurred in this setting (20,22,23,28,31,37,38). Outbreaks in neonatal intensive care units have most frequently followed the rare occurrence of transfusion-acquired infection of a neonate. Unless staff members practice strict hand washing and environmental cleaning, neonatal and pediatric intensive care settings may provide optimal opportunities for fecal contamination of healthcare workers’ hands and environmental surfaces. HAV can survive on workers’ hands and this aspect of HAV epidemiology may contribute to the indirect spread of the virus to other patients and staff members (39).
TABLE 73-1 Major Hepatitis Viruses and Occupational Transmission to Healthcare Workers | ||||||||||||||||||||||||||||||||||||||||||
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Although occupational HAV infection occurs rarely in US healthcare workers, seroepidemiological studies in other countries suggest that selected healthcare workers may be at increased risk for occupational infection. One study proposed that HAV is an occupational hazard in Germany, ranking third, with respect to morbidity statistics, among infectious occupational diseases, based on frequency of compensation (40). Compared to the general population, medical occupational groups with the highest anti-HAV seroprevalences, in decreasing order, included medical charwomen, foodhandlers, pediatric nurses, other nurses, and physicians. Another study in Belgium found that healthcare workers in a pediatric hospital had a higher seroprevalence of anti-HAV than workers in general hospitals (41), and a study in France reported a higher seroprevalence among nursing staff when compared to nonmedical employees (42). A study of healthcare personnel in Korea found no evidence of occupational infection, an overall prevalence of prior infection in 28.3%, and a substantial increase in seroprevalence associated with increasing age (43). Of interest, lower seroprevalences were identified among physicians between the ages of 25 and 39 (43).
Various studies have investigated risk factors for occupational infection with HAV. Factors that facilitate fecaloral spread enhance transmission. Fecal material from most normal HAV-infected patients is usually easily contained and presents a limited risk to staff members who practice good hand washing and rigorously follow infection control procedures. Conversely, patients who are incontinent of feces and those who have diarrhea present a much
higher risk. Factors associated with occupational infection include an index case with diarrhea or incontinent of feces (19,21,22,24, 25, 26 and 27,29,30,32); an index case hospitalized during the prodromal period of maximal virus fecal excretion (18,19,21,24, 25, 26, 27, 28, 29 and 30,44); adult patients who have poor hygiene (44); and less-than-optimal adherence to recommended infection control procedures, including lack of adherence to Standard and/or Contact Precautions (29,33,38,44). One study identified four additional activities that may have enhanced fecal-oral spread in the occupational setting: sharing food with patients or their families, drinking coffee, sharing cigarettes, and eating in the nurses’ office on an intensive care unit (30). Another study (31) identified risk factors for transmission to staff during an outbreak in a neonatal intensive care unit, including caring for an infant with HAV infection, drinking beverages in the unit, and not wearing gloves when taping an intravenous line. This study also documented prolonged viral excretion in infected neonates; some infected infants excreted virus for 4 to 5 months after infection. This prolonged period of viral excretion in neonates and infants may also contribute to the risk for healthcare-associated transmission. Other studies in neonatal intensive care units found that risk of occupational infection was greater among staff members who did not routinely wash their hands after treating an infected infant (38) and among staff members who cared for the index (i.e., infected) case for longer periods of time (28). Another outbreak investigation in a burn treatment center implicated eating on the hospital ward as the single most important risk factor for HAV infection among staff members (45). Vomitus, bile-stained emesis, or bile-contaminated nasogastric suction material may also serve as a reservoir for HAV transmission (21,25,29,46), since there is evidence that HAV is excreted in bile (47). One study that involved an index patient who had neither diarrhea nor fecal incontinence identified intensive handling of infectious bile, rather than contact with feces, as the most likely mode of transmission (46). Other likely factors contributing to this outbreak included inadequate terminal cleaning of equipment, food consumption in the unit, and inadequate hand-washing practices (46). Recent studies have documented decreasing risks for HAV infection, in great measure due to improving sanitary conditions and aggressive vaccination of populations at risk (43,48,49).
higher risk. Factors associated with occupational infection include an index case with diarrhea or incontinent of feces (19,21,22,24, 25, 26 and 27,29,30,32); an index case hospitalized during the prodromal period of maximal virus fecal excretion (18,19,21,24, 25, 26, 27, 28, 29 and 30,44); adult patients who have poor hygiene (44); and less-than-optimal adherence to recommended infection control procedures, including lack of adherence to Standard and/or Contact Precautions (29,33,38,44). One study identified four additional activities that may have enhanced fecal-oral spread in the occupational setting: sharing food with patients or their families, drinking coffee, sharing cigarettes, and eating in the nurses’ office on an intensive care unit (30). Another study (31) identified risk factors for transmission to staff during an outbreak in a neonatal intensive care unit, including caring for an infant with HAV infection, drinking beverages in the unit, and not wearing gloves when taping an intravenous line. This study also documented prolonged viral excretion in infected neonates; some infected infants excreted virus for 4 to 5 months after infection. This prolonged period of viral excretion in neonates and infants may also contribute to the risk for healthcare-associated transmission. Other studies in neonatal intensive care units found that risk of occupational infection was greater among staff members who did not routinely wash their hands after treating an infected infant (38) and among staff members who cared for the index (i.e., infected) case for longer periods of time (28). Another outbreak investigation in a burn treatment center implicated eating on the hospital ward as the single most important risk factor for HAV infection among staff members (45). Vomitus, bile-stained emesis, or bile-contaminated nasogastric suction material may also serve as a reservoir for HAV transmission (21,25,29,46), since there is evidence that HAV is excreted in bile (47). One study that involved an index patient who had neither diarrhea nor fecal incontinence identified intensive handling of infectious bile, rather than contact with feces, as the most likely mode of transmission (46). Other likely factors contributing to this outbreak included inadequate terminal cleaning of equipment, food consumption in the unit, and inadequate hand-washing practices (46). Recent studies have documented decreasing risks for HAV infection, in great measure due to improving sanitary conditions and aggressive vaccination of populations at risk (43,48,49).
Because most patients are hospitalized for hepatitis A only after they become jaundiced, (and at a time when viral excretion is often substantially reduced from peak excretion during the prodromal stage of infection), these patients are generally considered less infectious. Although fecal excretion of HAV may persist longer in children than in adults, quantitative determinations may be important to determine the risk of exposure to infected pediatric patients (50).
Reported attack rates for occupationally acquired HAV have varied, ranging from a low of 2% of exposed susceptible staff members (29), to 10% (21), 12% (24), 4% to 16% (23), 3% to 30% (28), and 21% to 50% (25). Reasons for the wide variability in attack rates may include differing definitions of occupational exposure to the index case, differing levels of infectivity of source patients, differing intensity of exposures, and the effectiveness and timing of prophylactic immunoglobulin administration.
Hepatitis B Virus
Historically, the highest risk for occupationally acquired hepatitis among healthcare workers has been associated with exposure to hepatitis B virus (HBV); in fact, before the advent of the hepatitis B vaccine, HBV infection was the major occupational risk to healthcare workers (51). In the 1980s, the annual incidence of HBV infection among healthcare workers in the United States was staggering. The Centers for Disease Control and Prevention (CDC) estimated that in the mid-1980s approximately 12,000 HBV infections occurred annually in healthcare workers who had frequent occupational exposure to blood or other potentially infectious materials, with an annual rate of infection between 4.89 and 6.63 per 1,000 exposed susceptible workers (52). Of these 12,000 occupationally infected workers each year, CDC scientists estimated that 3,000 developed symptomatic clinical illnesses, more than 600 were hospitalized, and more than 250 of these healthcare workers died. CDC estimated that between 600 and 1,200 of these healthcare workers became chronic hepatitis B carriers. Since the HBV vaccine was developed and aggressive hepatitis B vaccination of healthcare workers in the United States has been promoted, HBV infections among healthcare providers has decreased dramatically to an estimated 400 annually by 1995 (53).
Numerous studies have documented that healthcare workers exposed to blood are at high risk for acquiring HBV infection. In one of the earliest studies, Williams et al. (54) investigated a large epidemic of hepatitis B infections among hospital personnel and found that clinical hepatitis attack rates and HBV antibody prevalence rates correlated with occupational exposure to blood from patients being treated with hemodialysis. Transmission was thought to occur by both accidental parenteral and so-called inapparent parenteral routes of inoculation of contaminated blood. Pattison et al. (55) studied workers in a large community hospital between 1972 and 1974 and found a significant association between frequency of blood contact and prevalence of HBV, but no association between frequency of patient contact and HBV prevalence. The first nationwide, cross-sectional seroepidemiological survey of occupationally acquired HBV infection among physicians was conducted by Denes et al. (56) in 1975 to 1976. These investigators found that infection rates were higher among those practicing in urban settings, that the risk for infection increased with the number of years in practice, and that infection rates were highest among pathologists and surgeons. Dienstag and Ryan (57) studied workers at a large urban hospital and found that the prevalence of HBV serologic markers increased as a function of contact with blood, years in a healthcare occupation, and age, but not as a function of contact with patients, years of education, previous needlestick, transfusion, or globulin injection. The highest seroprevalences were found among emergency room nurses, pathology staff members, blood bank staff members, laboratory technicians, intravenous teams, and surgical house officers. Similar high-risk occupations (emergency room, medical and surgical intensive care units, and dentistry-oral surgery) were identified by Jovanovich et al. (58) in a study conducted in an urban hospital.
Snydman et al. (59) conducted a multi-institutional seroepidemiological survey of hospital employees in 1980
and 1981 and found that the duration of employment for laboratory workers, surgical staff members, and medical staff members was associated with increased risk for having HBV markers. In this study, the highest gradient of risk in these occupations occurred during the first 5 years of employment. Another large multi-institutional study of nearly 5,700 hospital employees conducted by Hadler et al. (60) controlled for nonoccupational risk factors and confirmed the earlier findings of Dienstag and Ryan that occupational blood exposure, but not patient contact, was associated with risk for prior HBV infection. Hadler and coworkers also found that the frequency of needle accidents during daily work was directly related to HBV seroprevalence. The occupational group with the highest HBV infection rate was clinical laboratory and blood bank technicians, who routinely handled large numbers of blood specimens. In general, these and similar studies in the pre-HBV-vaccine era may be summarized by noting that healthcare workers who have occupational exposure to blood had a prevalence of HBV markers several times both that of workers who did not have blood exposure and that of the general population. This prevalence of HBV infection increased with increasing years of occupational exposure. HBV infection was related to the degree and frequency of blood exposure and not to the degree of patient contact. West reviewed studies evaluating the risk for HBV infection in healthcare providers and found the risk to be approximately four times elevated when compared to the risk for infection in the at-large adult population (61). In West’s review, physicians and dentists were found to be five to 10 times more likely to experience hepatitis B infection and surgeons, dialysis personnel, personnel providing care for developmentally disabled individuals, and clinical laboratorians to be at 10-fold or higher risks for HBV infection (61).
and 1981 and found that the duration of employment for laboratory workers, surgical staff members, and medical staff members was associated with increased risk for having HBV markers. In this study, the highest gradient of risk in these occupations occurred during the first 5 years of employment. Another large multi-institutional study of nearly 5,700 hospital employees conducted by Hadler et al. (60) controlled for nonoccupational risk factors and confirmed the earlier findings of Dienstag and Ryan that occupational blood exposure, but not patient contact, was associated with risk for prior HBV infection. Hadler and coworkers also found that the frequency of needle accidents during daily work was directly related to HBV seroprevalence. The occupational group with the highest HBV infection rate was clinical laboratory and blood bank technicians, who routinely handled large numbers of blood specimens. In general, these and similar studies in the pre-HBV-vaccine era may be summarized by noting that healthcare workers who have occupational exposure to blood had a prevalence of HBV markers several times both that of workers who did not have blood exposure and that of the general population. This prevalence of HBV infection increased with increasing years of occupational exposure. HBV infection was related to the degree and frequency of blood exposure and not to the degree of patient contact. West reviewed studies evaluating the risk for HBV infection in healthcare providers and found the risk to be approximately four times elevated when compared to the risk for infection in the at-large adult population (61). In West’s review, physicians and dentists were found to be five to 10 times more likely to experience hepatitis B infection and surgeons, dialysis personnel, personnel providing care for developmentally disabled individuals, and clinical laboratorians to be at 10-fold or higher risks for HBV infection (61).
The risk of occupational exposure to HBV depends on several other factors besides occupation and frequency of occupational exposures. The prevalence of HBV infection in the patient population also influences the risk for occupational exposure. Because HBV prevalence is generally higher in urban settings, workers in urban hospitals have been found to be at higher risk for HBV infection (56) than are workers in rural hospitals (62). Renal dialysis patients (see also Chapter 63) who require frequent blood transfusions and have suppressed immune responses have long been known to be at high risk, both for acquiring HBV infection and for developing chronic HBV infections. For this reason, staff caring for dialysis patients are at increased risk for occupational HBV infection (61,63,64). Workers in hospitals serving large numbers of other patient population groups at risk for HBV infection, such as intravenous drug users, homosexual men, prison inmates, the developmentally disabled, or immigrants from highly endemic areas, are also at higher risk for occupational exposure and infection with HBV (65). Patients who are asymptomatic HBV carriers are the primary reservoir for HBV infection in the healthcare setting. Broad-scale testing to identify infected patients is neither practical nor cost-effective. In one study, testing patients who reported a history of hepatitis would have detected fewer than 20% of HBV-infected patients (66).
The infectivity of the source material also influences the risk of acquiring HBV infection. Although hepatitis B surface antigen (HBsAg) has been detected in nearly all body fluids, blood is considered the most infectious and is probably responsible for most occupationally acquired infections. The infectivity of blood is generally correlated with the presence of increased circulating viral burdens, HBV DNA polymerase activity, or hepatitis B e antigen (HBeAg) in the blood. The risk for HBV infection after a percutaneous (“needlestick”) exposure to blood from an HBV-infected individual has been estimated to range from 19% to 37% if the donor blood is HBeAg positive (67,68). In the dental setting, saliva, particularly bloody saliva, is also considered to represent a substantial infectious risk.
The type of exposure to blood or other potentially infectious materials also influences the risk of acquiring infection. Percutaneous exposures, such as needlesticks or injuries with contaminated sharp instruments, are associated with the highest risks for occupational infection. Very small inocula of HBsAg-positive blood may produce infection, since the blood of acute or chronic HBV carriers may contain as many as 1013 virus particles of HBV per milliliter of blood (51). Infectivity studies in chimpanzees have demonstrated that serum positive for HBeAg is infectious in dilutions up to 10-8 (69). Despite the fact that percutaneous exposures are the most efficient route of infection, CDC estimates that fewer than 20% of HBV-infected healthcare workers recall an injury/exposure of this type (70). Thus, other, so-called inapparent parenteral exposures account for a substantial fraction of occupational HBV infections. Preexisting cuts, dermatitis, other skin lesions, or mucous membranes may provide portals of entry for HBV infection. Blood-contaminated inanimate objects or environmental surfaces also have been implicated in occupational transmission in certain settings. In one study, sustaining paper cuts while handling laboratory computer cards in a hospital clinical laboratory was associated with an outbreak of HBV infection (71). Before strict infection prevention measures were implemented in hemodialysis centers, environmental contamination with blood that subsequently resulted in contaminated workers’ hands was hypothesized to facilitate HBV transmission (72,73). Contamination of mucous membranes of the eye or mouth, which may occur with accidental splashes or pipetting accidents, also may result in HBV transmission (74).
In the past 25 years, seroprevalence studies in healthcare workers have documented the importance of hepatitis B vaccine in preventing infections. Thomas et al. (75) studied 943 healthcare personnel in an inner city hospital. Their multivariate analysis identified only one risk factor—absence of HBV vaccination—to be independently associated with HBV infection in this population of healthcare workers. Similarly, Panlilio et al. (76) studied 770 surgeons for markers of HBV infection and found two risk factors—not receiving hepatitis B vaccine and practicing surgery for at least 10 years—for HBV infection. Another study in 114 operating room personnel in Pakistan also documented that nonvaccinated workers were more likely to be infected with HBV (76). Supplementing these seroprevalence studies, Lanphear et al. (77) investigated the incidence of clinical HBV infection in hospital workers and found a dramatic decrease associated with increased immunity due to vaccination.
Hepatitis C Virus
Our current understanding of the role of hepatitis C virus (HCV) in occupationally acquired infections is less clear than for HAV and HBV and is complicated by the evolving understanding of the pathogenesis and immunopathogenesis of exposure and infection with this flavivirus (see also Chapter 46). Since the parenteral mode of transmission of HCV has been clearly established as a primary route of infection for transfusion recipients and intravenous substance users, by analogy to HBV, occupational transmission of HCV in the healthcare setting—including transmission from patients to staff, from patient to patient, and from infected providers to their patients—is likely to be linked to apparent and inapparent parenteral exposure to blood. To date, exposure to blood remains the primary vehicle for occupationally acquired HCV infection as is evidenced by the overwhelming majority of the cases of occupational infection that have been described in the literature (78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93 and 94). HCV also has been transmitted by a punch (95). HCV RNA has been detected in saliva (96, 97 and 98), and two cases suggest that transmission of HCV occurred following human bites (99,100). Abe et al. (101) also provided experimental documentation of HCV transmission by saliva. When present in saliva, HCV titers are lower than in blood. The potential infectivity of saliva may have important implications for patient to provider transmission, primarily in the dental healthcare setting. HCV RNA also has been detected in a variety of other body fluids from infected patients, including menstrual fluid (102), semen (98,103,104), urine (98), spinal fluid (105), and ascites (98). The relevance of these latter body substances to the transmission of HCV is unclear. One recent study demonstrated transmission of HCV as a result of a nurse providing care for a patient with severe epistaxis and concluded that the transmission occurred as a result of the exposure of the nurse’s nonintact skin to the patient’s blood (106). In summary, blood is the body substance that presents the most risk for HCV transmission in the healthcare setting. Despite the fact that transmission of HCV resulting from exposures to body fluids other than blood has not yet been documented; presumably because viral titers in these fluids are substantially lower than in blood, other body substances may present measurable risks for occupational infection, particularly if the healthcare worker is exposed by the parenteral route and/or receives a large inoculum.
Parenteral exposures represent the primary mode of occupationally acquired infection, as is evidenced by the overwhelming majority of the cases of occupational infection that have been described in the literature (82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93 and 94). However, two cases of HCV infection have been documented following mucosal exposures to blood (107,108) and one case has been associated with exposure of “nonintact skin” to blood (106). Extensive HCV environmental contamination of instruments and surfaces in hemodialysis (109, 110, 111, 112 and 113) and dental surgery settings (114) can occur, and such HCV environmental contamination has been suggested to play a role in transmission of HCV (115). However, to our knowledge, transmission of a specific HCV strain through environmental contamination has not yet been documented. Transmission resulting from environmental contamination should be an extremely unlikely consequence if proper sterilization and disinfection procedures are practiced and if current standards of infection control, particularly hand hygiene, are followed.
Numerous cases of healthcare-associated transmission from patient to patient (often as a result of cross-contamination from an index case, for example, in hemodialysis, from multidose vials for sequential patients, reuse of spring-loaded finger-stick devices, and contamination of endoscopes and other devices for invasive procedures) have been reported in the literature. The past 5 years have seen a disturbing increase in the detection of such cases (116, 117, 118, 119, 120, 121, 122, 123, 124, 125 and 126). A detailed discussion of this topic is beyond the scope of this chapter (see also Chapter 46).
Recognizing the epidemiological similarities between HCV and HBV, several investigators attempted to assess the risk of occupational infection by testing healthcare workers for the serological prevalence of HCV antibodies, when serologic tests for HCV became available. Interpretation of these studies must take into account both the limitations of the serological assays (127) and the inadequacy of assessing only the humoral immune response as a measure of exposure and HCV infection (128). Many of the published studies employed the first-generation anti-HCV test that detects an antibody directed against a nonstructural HCV protein, anti-c100-3, and that has low sensitivity and specificity for diagnosing HCV infection when compared with second- and third-generation tests. Even later-generation anti-HCV antibody tests still may not detect 100% of infected persons, and tests designed to detect circulating HCV RNA may be necessary to identify some infected individuals. In addition, the anti-HCV tests have a high rate of false positivity in populations with a low prevalence of infection, and supplemental tests for specificity are necessary. The recombinant immunoblot assay (RIBA) or another supplemental HCV neutralization assay should be used to verify repeatedly reactive enzyme immunoassays. Even HCV RNA detection assays are problematic. These tests are subject to false-positive and false-negative results following improper collection, handling, or storage of test samples, and their interpretation is not conclusive: a single negative test may not indicate lack of infection but may be due to fluctuating RNA levels (129) and a single positive test should be repeated to exclude the high likelihood of contamination and a false-positive assay. In summary, the evolving diagnostic technology has complicated comparisons of HCV seroprevalence and incidence among the various published studies. Keeping these limitations in mind, Table 73-2 summarizes published studies of anti-HCV seroprevalence among many diverse types of healthcare workers (75,76,130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144, 145, 146, 147, 148, 149, 150, 151, 152, 153, 154 and 155,156,157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175 and 176).
In addition to the substantial variation in study design, the differences in healthcare worker populations studied, and the differences in the technologies used for detection, other considerations further complicate comparing and interpreting these studies. HCV seroprevalence varies geographically, so similar occupational groups from different locations cannot be compared directly, and local comparison groups are needed for determining if particular healthcare worker groups are at increased risk. Because blood donor seroprevalence data are readily available, blood donors were often used for comparison in these prevalence studies. However, blood donors are not a good comparison group, because they are preselected to avoid a history of
hepatitis as well as a history of risk factors for bloodborne infections (177). Most of these studies were not designed to investigate risk factors for HCV seroprevalence, or had too few HCV-seropositive subjects to do so. Those studies that did identify risk factors for HCV infection found associations with increasing age (141,162), years in healthcare occupations (143,158,162), a history of blood transfusions (140,162), and a history of prior needlestick injuries (140,151). In aggregate, given the limitations of the study designs, testing methodology, and selection bias, these studies suggest that healthcare workers’ risk of HCV infection is only minimally higher than that of volunteer blood donors and appears to be approximately 10-fold lower than the occupational/healthcare-associated risks posed by HBV in the healthcare setting.
hepatitis as well as a history of risk factors for bloodborne infections (177). Most of these studies were not designed to investigate risk factors for HCV seroprevalence, or had too few HCV-seropositive subjects to do so. Those studies that did identify risk factors for HCV infection found associations with increasing age (141,162), years in healthcare occupations (143,158,162), a history of blood transfusions (140,162), and a history of prior needlestick injuries (140,151). In aggregate, given the limitations of the study designs, testing methodology, and selection bias, these studies suggest that healthcare workers’ risk of HCV infection is only minimally higher than that of volunteer blood donors and appears to be approximately 10-fold lower than the occupational/healthcare-associated risks posed by HBV in the healthcare setting.
TABLE 73-2 Seroprevalence Studies of Anti-HCV Among Healthcare Workers | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Table 73-3 summarizes the results of HCV incidence studies conducted in various populations of healthcare workers who had sustained occupational exposures to HCV (86,90,147,149,155,157,162,178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194 and 195). Although most of studies employed anti-HCV antibody testing as the primary detection system for HCV infection, nine of the studies used polymerase chain reaction (PCR) technology to attempt to detect HCV RNA as a marker for infection among individuals who had sustained parenteral exposures to blood from patients known to harbor HCV infection (90,147,180,187,189, 190 and 191,193,195).
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