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“The only thing necessary for these diseases to the triumph is for good people and governments to do nothing.”

       
     

Updated U.S. Public Health Service Guidelines for the Management of

Occupational Exposures to HBV, Hepatitis C Virus, and HIV and Recommendations

for Postexposure Prophylaxis: June 2001

Table of Contents

       Summary

       Introduction

            Definitions of Health-Care Workers and Exposure

       Background

            Occupational Transmission of HBV

            Occupational Transmission of Hepatitis C Virus

            Occupational Transmission of HIV

       Recommendations for the Management of HCP Potentially Exposed to HBV, Hepatitis C Virus, or HIV

            Hepatitis B Vaccination

            Treatment of an Exposure Site

            Exposure Report

            Evaluation of the Exposure and the Exposure Source

            Management of Exposures to HBV

            Management of Exposures to Hepatitis C Virus

            Management of Exposures to HIV

            Recommendations for the Selection of Drugs for HIV PEP

            Occupational Exposure Management Resources

       References

       Appendices

            Appendix A

            Appendix B

            Appendix C

       Table 1. Reported instances of failure of combination drug postexposure prophylaxis to prevent

       HIV infection in health-care personnel exposed to HIV-infected blood

       Table 2. Primary side effects associated with antiretroviral agents

       Table 3. Recommended postexposure prophylaxis for exposure to hepatitis B virus

       Table 4. Recommended HIV postexposure prophylaxis for percutaneous injuries

       Table 5. Recommended HIV postexposure prophylaxis for mucous membrane exposures and

       nonintact skin* exposures

 

Reprinted from the MMWR June 29, 2001/ 50(RR-11);1-42

 

The MMWR series of publications is published by the Epidemiology Program Office, Centers for

Disease Control and Prevention (CDC), U.S. Department of Health and Human Services,

Atlanta, GA 30333.

 

Centers for Disease Control and Prevention

Jeffrey P. Koplan, M.D., M.P.H.

Director

The material in this report was prepared for publication

by National Center for Infectious Diseases

James H. Hughes, M.D.

Director

Division of Healthcare Quality Promotion

Julie L. Gerberding, M.D.,

M.P.H.

Director

Division of Viral Hepatitis (Proposed)

Harold S. Margolis, M.D.

Acting Director

Division of AIDS, STD, and TB Laboratory Research

Harold W. Jaffe, M.D.

Director

National Center for HIV, STD, and TB Prevention

Helene D. Gayle, M.D., M.PH.

Director

Division of HIV/AIDS Prevention — Surveillance and

Epidemiology

Robert S. Janssen, M.D.

Director

National Institute for Occupational Safety and Health

Kathleen Rest, Ph.D.

Acting Director

Division of Surveillance, Hazard Evaluations, and Field

Studies

R. Delon Hull, Ph.D.

Acting Director

This report was produced as an MMWR serial

publication in Epidemiology Program Office

Stephen B. Thacker, M.D., M.Sc.

Director

Office of Scientific and Health Communications

John W. Ward, M.D.

Director

Editor, MMWR Series

CDC Surveillance Summaries

Suzanne M. Hewitt, M.P.A.

Managing Editor

 

Patricia A. McGee

Project Editor

 

Lynda G. Cupell and Morie M.

Higgins

Visual Information Specialists

 

Michele D. Renshaw and Erica R.

Shaver

Information Technology

Specialists

The following CDC staff members prepared this report:

 

Elise M. Beltrami, M.D.

Francisco Alvarado-Ramy, M.D.

Sara E. Critchley, R.N.

Adelisa L. Panlilio, M.D., M.P.H.

Denise M. Cardo, M.D.

Division of Healthcare Quality Promotion

National Center for Infectious Diseases

 

William A. Bower, M.D.

Miriam J. Alter, Ph.D.

Division of Viral Hepatitis*

National Center for Infectious Diseases

 

Jonathan E. Kaplan, M.D.

Division of AIDS, STD, and TB Laboratory Research

National Center for Infectious Diseases

and

Division of HIV/AIDS Prevention

National Center for HIV, STD, and TB Prevention

 

Boris Lushniak, M.D., M.P.H.

Division of Surveillance, Hazard Evaluations, and Field Studies

National Institute for Occupational Safety and Health

 

in collaboration with

 

David K. Henderson, M.D.

National Institutes of Health

 

Kimberly A. Struble, Pharm.D.

Food and Drug Administration

 

Abe Macher, M.D.

Health Resources and Services Administration

 

*Proposed.

 Summary

 This report updates and consolidates all previous U.S. Public Health Service

 recommendations for the management of health-care personnel (HCP) who have

 occupational exposure to blood and other body fluids that might contain hepatitis B virus

 (HBV), hepatitis C virus (Hepatitis C Virus), or human immunodeficiency virus (HIV).

 Recommendations for HBV postexposure management include initiation of the hepatitis B

 vaccine series to any susceptible, unvaccinated person who sustains an occupational

 blood or body fluid exposure. Postexposure prophylaxis (PEP) with hepatitis B immune

 globulin (HBIG) and/or hepatitis B vaccine series should be considered for occupational

 exposures after evaluation of the hepatitis B surface antigen status of the source and the

 vaccination and vaccine-response status of the exposed person. Guidance is provided to

 clinicians and exposed HCP for selecting the appropriate HBV PEP.

 

 Immune globulin and antiviral agents (e.g., interferon with or without ribavirin) are not

 recommended for PEP of hepatitis C. For Hepatitis C Virus postexposure management, the Hepatitis C Virus status of the source and the exposed person should be determined, and for HCP exposed to an Hepatitis C Virus positive source, follow-up Hepatitis C Virus testing should be performed to determine if infection develops.

 

 Recommendations for HIV PEP include a basic 4-week regimen of two drugs (zidovudine

 [ZDV] and lamivudine [3TC]; 3TC and stavudine [d4T]; or didanosine [ddI] and d4T)

 for most HIV exposures and an expanded regimen that includes the addition of a third

 drug for HIV exposures that pose an increased risk for transmission. When the source

 person's virus is known or suspected to be resistant to one or more of the drugs

 considered for the PEP regimen, the selection of drugs to which the source person's virus

 is unlikely to be resistant is recommended.

 

 In addition, this report outlines several special circumstances (e.g., delayed exposure

 report, unknown source person, pregnancy in the exposed person, resistance of the source

 virus to antiretroviral agents, or toxicity of the PEP regimen) when consultation with

 local experts and/or the National Clinicians' Post-Exposure Prophylaxis Hotline

 ([PEPline] 1-888-448-4911) is advised.

 

 Occupational exposures should be considered urgent medical concerns to ensure timely

 postexposure management and administration of HBIG, hepatitis B vaccine, and/or HIV

 PEP.

 

 Return to Top

 Introduction

 Avoiding occupational blood exposures is the primary way to prevent transmission of hepatitis B

 virus (HBV), hepatitis C virus (Hepatitis C Virus), and human immunodeficiency virus (HIV) in health-care

 settings (1). However, hepatitis B immunization and postexposure management are integral

 components of a complete program to prevent infection fol-lowing bloodborne pathogen

 exposure and are important elements of workplace safety (2).

 

 The U.S. Public Health Service (PHS) has published previous guidelines for the man-agement of

 HIV exposures that included considerations for postexposure prophylaxis (PEP) (3‚5). Since

 publication of the 1998 HIV exposure guidelines (5), several new antiretroviral agents have been

 approved by the Food and Drug Administration (FDA), and more information is available about

 the use and safety of HIV PEP (6‚11). In addition, questions exist regarding considerations

 about PEP regimens when the source person's virus is known or suspected to be resistant to one

 or more of the antiretroviral agents that might be used for PEP. Concern also has arisen about

 the use of PEP when it is not warranted. Data indicate that some health-care personnel (HCP)

 take a full course of HIV PEP after exposures that do not confer an HIV transmission risk

 (10,11).

 

 In September 1999, a meeting of a PHS interagency working group* and expert consultants

 was convened by CDC. The PHS working group decided to issue updated recommendations

 for the management of occupational exposure to HIV. In addition, the report was to include

 recommendations for the management of occupational HBV and Hepatitis C Virus exposures so that a single

 document could comprehensively address the manage-ment of occupational exposures to

 bloodborne pathogens. This report updates and con-solidates the previous PHS guidelines and

 recommendations for occupational HBV, Hepatitis C Virus, and HIV exposure management for HCP.

 Specific practice recommendations for the management of occupational bloodborne pathogen

 exposures are outlined to assist health-care institutions with the implementation of these PHS

 guidelines (Appendices A and B). As relevant information becomes available, updates of these

 recommendations will be published. Recommendations for nonoccupational (e.g., sexual,

 pediatric, and perinatal) HBV, Hepatitis C Virus, and HIV exposures are not addressed in these guidelines

 and can be found elsewhere (12‚15).

 

 *This interagency working group comprised representatives of CDC, the Food and Drug Administration (FDA), the Health Resources and Services Administration, and the National Institutes of Health. Information included in these recommendations may not represent FDA approval or approved labeling for the particular product or indications in question. Specifically, the terms "safe" and "effective" may not be synonymous with the FDA-defined legal standards for product approval.

 

 Return to Top

 Definitions Of Health-Care Workers And Exposure

 In this report, health-care personnel (HCP) are defined as persons (e.g., employees, students,

 contractors, attending clinicians, public-safety workers , or volunteers) whose activities involve

 contact with patients or with blood or other body fluids from patients in a health-care,

 laboratory, or public-safety setting. The potential exists for blood and body fluid exposure to

 other workers, and the same principles of exposure management could be applied to other

 settings.

 

 An exposure that might place HCP at risk for HBV, Hepatitis C Virus, or HIV infection is defined as a

 percutaneous injury (e.g., a needlestick or cut with a sharp object) or contact of mucous

 membrane or nonintact skin (e.g., exposed skin that is chapped, abraded, or afflicted with

 dermatitis) with blood, tissue, or other body fluids that are potentially infectious (16,17).

 

 In addition to blood and body fluids containing visible blood, semen and vaginal secre-tions also

 are considered potentially infectious. Although semen and vaginal secretions have been

 implicated in the sexual transmission of HBV, Hepatitis C Virus, and HIV, they have not been implicated in

 occupational transmission from patients to HCP. The following fluids also are considered

 potentially infectious: cerebrospinal fluid, synovial fluid, pleural fluid, peritoneal fluid,  pericardial

 fluid, and amniotic fluid. The risk for transmission of HBV, Hepatitis C Virus, and HIV infection from these

 fluids is unknown; the potential risk to HCP from occupational exposures has not been assessed

 by epidemiologic studies in health-care settings. Feces, nasal secretions, saliva, sputum, sweat,

 tears, urine, and vomitus are not considered potentially infectious unless they contain blood. The

 risk for transmission of HBV, Hepatitis C Virus, and HIV infection from these fluids and materials is

 extremely low.

 

 Any direct contact (i.e., contact without barrier protection) to concentrated virus in a research

 laboratory or production facility is considered an exposure that requires clinical evaluation. For

 human bites, the clinical evaluation must include the possibility that both the person bitten and the

 person who inflicted the bite were exposed to bloodborne pathogens. Transmission of HBV or

 HIV infection only rarely has been reported by this route (18‚20) (CDC, unpublished data,

 1998).

 

 

 This section provides the rationale for the postexposure management and prophy-laxis

 recommendations presented in this report. Additional details concerning the risk for occupational

 bloodborne pathogen transmission to HCP and management of occupa-tional bloodborne

 pathogen exposures are available elsewhere (5,12,13,21-24).

 

 Occupational Transmission of HBV

 

 Risk for Occupational Transmission of HBV

 

 HBV infection is a well recognized occupational risk for HCP (25). The risk of HBV infection is

 primarily related to the degree of contact with blood in the work place and also to the hepatitis B

 e antigen (HBeAg) status of the source person. In studies of HCP who sustained injuries from

 needles contaminated with blood containing HBV, the risk of developing clinical hepatitis if the

 blood was both hepatitis B surface antigen (HBsAg)-and HBeAg-positive was 22%‚31%; the

 risk of developing serologic evidence of HBV infection was 37%‚62%. By comparison, the risk

 of developing clinical hepatitis from a needle contaminated with HBsAg-positive,

 HBeAg-negative blood was 1%‚6%, and the risk of developing serologic evidence of HBV

 infection, 23%‚37% (26).

 

 Although percutaneous injuries are among the most efficient modes of HBV trans-mission, these

 exposures probably account for only a minority of HBV infections among HCP. In several

 investigations of nosocomial hepatitis B outbreaks, most infected HCP could not recall an overt

 percutaneous injury (27,28), although in some studies, up to one third of infected HCP recalled

 caring for a patient who was HBsAg-positive (29,30). In addition, HBV has been demonstrated

 to survive in dried blood at room temperature on environmental surfaces for at least 1 week

 (31). Thus, HBV infections that occur in HCP with no history of nonoccupational exposure or

 occupational percutaneous injury might have resulted from direct or indirect blood or body fluid

 exposures that inoculated HBV into cutaneous scratches, abrasions, burns, other lesions, or on

 mucosal surfaces (32‚ 34). The potential for HBV transmission through contact with

 environmental surfaces has been demonstrated in investigations of HBV outbreaks among

 patients and staff of hemodialysis units (35‚37).

 

    

 Blood contains the highest HBV titers of all body fluids and is the most important vehicle of

 transmission in the health-care setting. HBsAg is also found in several other body fluids, including

 breast milk, bile, cerebrospinal fluid, feces, nasopharyngeal washings, saliva, semen, sweat, and

 synovial fluid (38). However, the concentration of HBsAg in body fluids can be 100‚1000ófold

 higher than the concentration of infectious HBV particles. Therefore, most body fluids are not

 efficient vehicles of transmission because they contain low quantities of infectious HBV, despite

 the presence of HBsAg.

 

 In serologic studies conducted in the United States during the 1970s, HCP had a prevalence of

 HBV infection approximately 10 times higher than the general population (39‚42). Because of

 the high risk of HBV infection among HCP, routine preexposure vaccination of HCP against

 hepatitis B and the use of standard precautions to prevent exposure to blood and other

 potentially infectious body fluids have been recommended since the early 1980s (43).

 Regulations issued by the Occupational Safety and Health Administration (OSHA) (2) have

 increased compliance with these recommendations. Since the implementation of these

 recommendations, a sharp decline has occurred in the incidence of HBV infection among HCP.

 

 PEP for HBV

 

 Efficacy of PEP for HBV. The effectiveness of hepatitis B immune globulin (HBIG) and/ or

 hepetitis B vaccine in various postexposure settings has been evaluated by prospec-tive studies.

 For perinatal exposure to an HBsAg-, HBeAg-positive mother, a regimen combining HBIG and

 initiation of the hepatitis B vaccine series at birth is 85%‚95% effective in preventing HBV

 infection (44,45). Regimens involving either multiple doses of HBIG alone or the hepatitis B

 vaccine series alone are 70%‚75% effective in prevent-ing HBV infection (46). In the

 occupational setting, multiple doses of HBIG initiated within 1 week following percutaneous

 exposure to HBsAg-positive blood provides an estimated 75% protection from HBV infection

 (47‚49). Although the postexposure efficacy of the combination of HBIG and the hepatitis B

 vaccine series has not been evaluated in the occupational setting, the increased efficacy of this

 regimen observed in the perinatal setting, compared with HBIG alone, is presumed to apply to

 the occupational setting as well. In addition, because persons requiring PEP in the occupational

 setting are generally at continued risk for HBV exposure, they should receive the hepatitis B

 vaccine series.

 

 Safety of PEP for HBV. Hepatitis B vaccines have been found to be safe when admin-istered

 to infants, children, or adults (12,50). Through the year 2000, approximately 100 million persons

 have received hepatitis B vaccine in the United States. The most com-mon side effects from

 hepatitis B vaccination are pain at the injection site and mild to moderate fever (50‚55). Studies

 indicate that these side effects are reported no more frequently among persons vaccinated than

 among those receiving placebo (51,52). Approximately 45 reports have been received by the

 Vaccine Adverse Event Report-ing System (VAERS) of alopecia (hair loss) in children and

 adults after administration of plasma-derived and recombinant hepatitis B vaccine; four persons

 sustained hair loss following vaccination on more than one occasion (56). Hair loss was

 temporary for approximately two thirds of persons who experienced hair loss. An epidemiologic

 study conducted in the Vaccine Safety Datalink found no statistical association between

 alope-cia and receipt of hepatitis B vaccine in children (CDC, unpublished data, 1998). A low

 rate of anaphylaxis has been observed in vaccine recipients based on reports to VAERS; the

 estimated incidence is 1 in 600,000 vaccine doses distributed. Although none of the persons

 who developed anaphylaxis died, anaphylactic reactions can be life-threaten-ing; therefore,

 further vaccination with hepatitis B vaccine is contraindicated in persons with a history of

 anaphylaxis after a previous dose of vaccine.

 

 Hepatitis B immunization programs conducted on a large scale in Taiwan, Alaska, and New

 Zealand have observed no association between vaccination and the occurrence of serious

 adverse events. Furthermore, in the United States, surveillance of adverse events following

 hepatitis B vaccination has demonstrated no association between hepatitis B vaccine and the

 occurrence of serious adverse events, including Guillain-BarrÈ syn-drome, transverse myelitis,

 multiple sclerosis, optic neuritis, and seizures (57‚59) (CDC, unpublished data, 1991).

 However, several case reports and case series have claimed an association between hepatitis B

 vaccination and such syndromes and diseases as mul-tiple sclerosis, optic neuritis, rheumatoid

 arthritis, and other autoimmune diseases (57,60‚ 66). Most of these reported adverse events

 have occurred in adults, and no report has compared the frequency of the purported

 vaccine-associated syndrome/disease with the frequency in an unvaccinated population. In

 addition, recent case-control studies have demonstrated no association between hepatitis B

 vaccination and development or short-term risk of relapse of multiple sclerosis (67,68), and

 reviews by international panels of experts have concluded that available data do not demonstrate

 a causal asso-ciation between hepatitis B vaccination and demyelinating diseases, including

 multiple sclerosis (69).

 

 HBIG is prepared from human plasma known to contain a high titer of antibody to HBsAg

 (anti-HBs). The plasma from which HBIG is prepared is screened for HBsAg and antibodies to

 HIV and Hepatitis C Virus. The process used to prepare HBIG inactivates and eliminates HIV from the final

 product. Since 1996, the final product has been free of Hepatitis C Virus RNA as determined by the

 polymerase chain reaction (PCR), and, since 1999, all products avail-able in the United States

 have been manufactured by methods that inactivate Hepatitis C Virus and other viruses. No evidence exists

 that HBV, Hepatitis C Virus, or HIV have ever been transmitted by HBIG commercially available in the

 United States (70,71).

 

 Serious adverse effects from HBIG when administered as recommended have been rare. Local

 pain and tenderness at the injection site, urticaria and angioedema might occur; anaphylactic

 reactions, although rare, have been reported following the injection of human immune globulin

 (IG) preparations (72). Persons with a history of anaphylactic reaction to IG should not receive

 HBIG.

 

 PEP for HBV During Pregnancy. No apparent risk exists for adverse effects to devel-oping

 fetuses when hepatitis B vaccine is administered to pregnant women (CDC, unpub-lished data,

 1990). The vaccine contains noninfectious HBsAg particles and should pose no risk to the fetus.

 HBV infection during pregnancy might result in severe disease for the mother and chronic

 infection for the newborn. Therefore, neither pregnancy nor lacta-tion should be considered a

 contraindication to vaccination of women. HBIG is not con-traindicated for pregnant or lactating

 women.

 

 Return to Top

 

 Occupational Transmission of Hepatitis C Virus

 

 Risk for Occupational Transmission of Hepatitis C Virus

 

 Hepatitis C Virus is not transmitted efficiently through occupational exposures to blood. The aver-age

 incidence of anti-Hepatitis C Virus seroconversion after accidental percutaneous exposure from an

 Hepatitis C Virus-positive source is 1.8% (range: 0%‚7%) (73‚76), with one study indicating that

 transmission occurred only from hollow-bore needles compared with other sharps (75).

 Transmission rarely occurs from mucous membrane exposures to blood, and no trans-mission in

 HCP has been documented from intact or nonintact skin exposures to blood (77,78). Data are

 limited on survival of Hepatitis C Virus in the environment. In contrast to HBV, the epidemiologic data for

 Hepatitis C Virus suggest that environmental contamination with blood con-taining Hepatitis C Virus is not a significant

 risk for transmission in the health-care setting (79,80), with the possible exception of the

 hemodialysis setting where Hepatitis C Virus transmission related to environmental contamination and poor

 infection-control practices have been impli-cated (81‚84). The risk for transmission from

 exposure to fluids or tissues other than Hepatitis C Virus-infected blood also has not been quantified but is

 expected to be low.

 

 Postexposure Management for Hepatitis C Virus

 

 In several studies, researchers have attempted to assess the effectiveness of IG following

 possible exposure to non-A, non-B hepatitis. These studies have been difficult to interpret

 because they lack uniformity in diagnostic criteria and study design, and, in all but one study, the

 first dose of IG was administered before potential exposure (48,85,86). In an experiment

 designed to model Hepatitis C Virus transmission by needlestick exposure in the health-care setting, high

 anti-Hepatitis C Virus titer IG administered to chimpanzees 1 hour after exposure to Hepatitis C Virus-positive blood

 did not prevent transmission of infection (87). In 1994, the Advisory Committee on

 Immunization Practices (ACIP) reviewed available data re-garding the prevention of Hepatitis C Virus

 infection with IG and concluded that using IG as PEP for hepatitis C was not supported (88).

 This conclusion was based on the following facts:

 

      No protective antibody response has been identified following Hepatitis C Virus infection.

      Previous studies of IG use to prevent posttransfusion non-A, non-B hepatitis might not be

      relevant in making recommendations regarding PEP for hepatitis C.

      Experimental studies in chimpanzees with IG containing anti-Hepatitis C Virus failed to prevent

      transmission of infection after exposure.

 

 No clinical trials have been conducted to assess postexposure use of antiviral agents (e.g.,

 interferon with or without ribavirin) to prevent Hepatitis C Virus infection, and antivirals are not

 FDA-approved for this indication. Available data suggest that an established infection might need

 to be present before interferon can be an effective treatment. Kinetic studies suggest that the

 effect of interferon on chronic Hepatitis C Virus infection occurs in two phases. During the first phase,

 interferon blocks the production or release of virus from infected cells. In the second phase, virus

 is eradicated from the infected cells (89); in this later phase, higher pretreatment alanine

 aminotransferase (ALT) levels correlate with an increasing decline in infected cells, and the

 rapidity of the decline correlates with viral clearance. In contrast, the effect of antiretrovirals

 when used for PEP after exposure to HIV is based on inhibition of HIV DNA synthesis early in

 the retroviral replicative cycle.

 

 In the absence of PEP for Hepatitis C Virus, recommendations for postexposure management are intended

 to achieve early identification of chronic disease and, if present, referral for evaluation of

 treatment options. However, a theoretical argument is that intervention with antivirals when Hepatitis C Virus

 RNA first becomes detectable might prevent the development of chronic infection. Data from

 studies conducted outside the United States suggest that a short course of interferon started early

 in the course of acute hepatitis C is associated with a higher rate of resolved infection than that

 achieved when therapy is begun after chronic hepatitis C has been well established (90‚92).

 These studies used various treat-ment regimens and included persons with acute disease whose

 peak ALT levels were 500‚1,000 IU/L at the time therapy was initiated (2.6‚4 months after

 exposure).

 

 No studies have evaluated the treatment of acute infection in persons with no evi-dence of liver

 disease (i.e., Hepatitis C Virus RNA-positive <6 months duration with normal ALT lev-els); among patients

 with chronic Hepatitis C Virus infection, the efficacy of antivirals has been demonstrated only among patients

 who also had evidence of chronic liver disease (i.e., abnormal ALT levels). In addition, treatment

 started early in the course of chronic Hepatitis C Virus infection (i.e., 6 months after onset of infection) might

 be as effective as treatment started during acute infection (13). Because 15%‚25% of patients

 with acute Hepatitis C Virus infection spontaneously resolve their infection (93), treatment of these patients

 during the acute phase could expose them unnecessarily to the discomfort and side effects of

 antiviral therapy.

 

 Data upon which to base a recommendation for therapy of acute infection are insuf-ficient

 because a) no data exist regarding the effect of treating patients with acute infec-tion who have

 no evidence of disease, b) treatment started early in the course of chronic infection might be just

 as effective and would eliminate the need to treat persons who will spontaneously resolve their

 infection, and c) the appropriate regimen is unknown.

 

 Return to Top

 

 Occupational Transmission of HIV

 

 Risk for Occupational Transmission of HIV

 

 In prospective studies of HCP, the average risk of HIV transmission after a percutane-ous

 exposure to HIV-infected blood has been estimated to be approximately 0.3% (95% confidence

 interval [CI] = 0.2%‚0.5%) (94) and after a mucous membrane exposure, approximately 0.09%

 (95% CI = 0.006%‚0.5%) (95). Although episodes of HIV transmis-sion after nonintact skin

 exposure have been documented (96), the average risk for transmission by this route has not

 been precisely quantified but is estimated to be less than the risk for mucous membrane

 exposures (97). The risk for transmission after exposure to fluids or tissues other than

 HIV-infected blood also has not been quantified but is probably considerably lower than for

 blood exposures (98).

 

 As of June 2000, CDC had received voluntary reports of 56 U.S. HCP with docu-mented HIV

 seroconversion temporally associated with an occupational HIV exposure. An additional 138

 episodes in HCP are considered possible occupational HIV transmis-sions. These workers had

 a history of occupational exposure to blood, other infectious body fluids, or laboratory solutions

 containing HIV, and no other risk for HIV infection was identified, but HIV seroconversion after

 a specific exposure was not documented (99).

 

 Epidemiologic and laboratory studies suggest that several factors might affect the risk of HIV

 transmission after an occupational exposure. In a retrospective case-control study of HCP who

 had percutaneous exposure to HIV, the risk for HIV infection was found to be increased with

 exposure to a larger quantity of blood from the source person as indicated by a) a device visibly

 contaminated with the patient's blood, b) a procedure that involved a needle being placed

 directly in a vein or artery, or c) a deep injury (100). The risk also was increased for exposure to

 blood from source persons with terminal illness, possibly reflecting either the higher titer of HIV

 in blood late in the course of AIDS or other factors (e.g., the presence of syncytia-inducing

 strains of HIV). A laboratory study that demonstrated that more blood is transferred by deeper

 injuries and hollow-bore needles lends further support for the observed variation in risk related

 to blood quantity (101).

 

 The use of source person viral load as a surrogate measure of viral titer for assessing

 transmission risk has not yet been established. Plasma viral load (e.g., HIV RNA) reflects only

 the level of cell-free virus in the peripheral blood; latently infected cells might trans-mit infection

 in the absence of viremia. Although a lower viral load (e.g., <1,500 RNA copies/mL) or one that

 is below the limits of detection probably indicates a lower titer exposure, it does not rule out the

 possibility of transmission.

 

 Some evidence exists regarding host defenses possibly influencing the risk for HIV infection. A

 study of HIV-exposed but uninfected HCP demonstrated an HIV-specific cyto-toxic

 T-lymphocyte (CTL) response when peripheral blood mononuclear cells were stimu-lated in

 vitro with HIV-specific antigens (102). Similar CTL responses have been observed in other

 groups who experienced repeated HIV exposure without resulting infection (103‚108). Among

 several possible explanations for this observation is that the host immune response sometimes

 might prevent establishment of HIV infection after a per-cutaneous exposure; another is that the

 CTL response simply might be a marker for exposure. In a study of 20 HCP with occupational

 exposure to HIV, a comparison was made of HCP treated with zidovudine (ZDV) PEP and

 those not treated. The findings from this study suggest that ZDV blunted the HIV-specific CTL

 response and that PEP might inhibit early HIV replication (109).