The trusted source for
healthcare information and
Author: Dawn Demangone, MD, Assistant Professor of Medicine; Director, Emergency Medicine Ultrasound, Temple University Hospital and School of Medicine, Philadelphia, PA.
Peer Reviewer: Susan C. Stone, MD, MPH, FACEP, Assistant Professor, Emergency Medicine, Keck School of Medicine, University of Southern California, Los Angeles.
The emergency physician frequently encounters situations involving aspects of human immunodeficiency virus (HIV) infection. From caring for the advanced HIV-infected patient, to evaluating individuals at risk for acute virus acquisition after exposure, all spectra of infection are encountered. This article briefly will discuss the most recent epidemiologic data regarding HIV infection and review transmission routes before focusing on recognition of acute retroviral syndrome (ARS) and evaluation of the health care professional (HCP) subjected to an occupational exposure to HIV.—The Editor
The most recent worldwide HIV infection statistics presented at the fifth annual International AIDS Conference in Barcelona have surpassed the worst-case scenarios projected a decade ago. As of 2001, 40 million people were living with HIV/AIDS.1 The majority (> 95%) live in developing countries.2 In the absence of effective treatment, most of these 40 million individuals will die within the next 10 years. Through 2001, HIV-related illness had claimed the lives of more than 20 million people worldwide.1
In the United States, more than 40,000 people become newly infected with HIV every year. The majority of new infections occur in men, most commonly acquired through sexual activity.3 Most newly infected women contract the disease in the same manner as men—through sexual contact. While the overall rate of infection in men shows signs of slowing, this is not true for other particular groups. Women, African-Americans, Hispanics and individuals between the ages of 13 and 24 years have increasing infection rates.4 The African-American population accounts for approximately 50% (men) and 64% (women) of new HIV infections, despite representing only 13% of the general U.S. population. Hispanics account for 18% (men) and 20% (women) of new HIV infections, yet make up only 12% of the U.S. population.3 With this knowledge, an opportunity exists to target these high-risk groups with prevention interventions.
With the introduction of effective anti-retroviral treatment regimens, the progression to AIDS and HIV-related deaths has declined. Persons infected with HIV are living longer, and demonstrate delayed progression to AIDS compared to those infected early in the epidemic. Thus, the number of people living with HIV/AIDS in the United States continues to grow.4
As of the year 2000, between 800,000 and 900,000 people were living with HIV infection or AIDS in the United States. Specifically, more than 300,000 of those infected with HIV had progressed to AIDS.3 Adults represent the majority (99%) of those infected. Thus far, more than 450,000 people in the United States have lost their lives to HIV-related illnesses.5 The ethnicity and gender of individuals with AIDS reflect the newly acquired infection distribution; African-Americans and Hispanics are over-represented, and men make up the majority.6
HIV infections may be divided into two main groups: occupational and non-occupational. Non-occupational transmission can include sexual contact, perinatal exposure, transfusions, or non-occupational/non-sexual vectors. The risks of HIV transmission per episode of contact are outlined in Table 1. In the adult and adolescent population of the United States, sexual contact is the most commonly identified route of transmission, accounting for approximately 50% of all reported HIV infections through June 2001.5
The majority of reported pediatric (< 13 years old) HIV infections through June 2001 resulted from perinatal transmission. Most infected mothers reported some high-risk behavior. With the introduction of anti-retroviral therapy use in the pregnant population, the risk of perinatal HIV transmission dramatically declined.4 Other modes of transmission in the pediatric population included the receipt of blood/blood products or human tissue, as in hemophilia, or were not specified.5
Sexual transmission represents the most commonly identified mechanism for HIV infection in adults.5 (See Table 1.) Of note is the absence of the risk associated with oral-genital contact. While it is believed to be less efficient than other sexual activities, oral-genital sexual contact has potential to play a significant role in HIV transmission. Schacker reported that individuals newly infected with HIV participated in oral-genital contact 10 times more frequently than in anal-genital contact prior to becoming infected. Moreover, condoms were used infrequently (3-4%) during oral-genital contact, compared to 42% condom use with anal-genital contact.7 It appears that the public may view oral-genital contact as "lower-risk" behavior based on the increased frequency of participation and poor compliance with condom use. Thus, while the specific risk of HIV transmission through oral-genital contact per incident has not been estimated and may be low, the potential numbers of individuals infected in this manner may be quite high.7
Besides the specific sexual contact, participants may possess factors that can increase the risk of HIV transmission through sexual activity. A known HIV-positive individual with high viral titers, vaginal bleeding/menstruation, or inflammatory or ulcerative genital lesions is more likely to transmit the virus.8,9 An individual who is not circumcised, has ulcerative or inflammatory genital lesions, or has cervical ectopy has a higher risk of acquiring HIV from an infected partner.8
Blood transfusions appear to be the most efficient manner of transmitting HIV—approximately 95% of individuals receiving a single HIV-infected unit will seroconvert.11 The American Red Cross screens all donated blood through self-administered questionnaires and antibody testing. The possibility does exist for an HIV-infected individual who is antibody-negative to donate blood. That risk has been estimated at 1 in 493,000.10 The same group estimated that by adding viral nucleic acid testing to the standard Red Cross blood testing, only 19 additional HIV-infected units would be identified per 12 million units donated annually.10
Non-sexual, non-occupational exposures include percutaneous exposures (sharing needles, tattooing, body piercing, etc.), as well as skin or mucous membrane contact with blood or other body fluids. The risk of needle sharing is estimated at 0.67%, higher than the risk associated with occupational percutaneous exposures.8,9,11-16 Transmission of HIV has been documented through oral mucous membrane contact with blood/body fluids, both occupationally and through kissing.9,17 And, while human bites rarely transmit HIV, such transmission has been documented. One individual seroconverted after sustaining an unintentional bite to his finger, despite beginning post-exposure prophylaxis with azidothymidine (AZT).18
Of special interest to health care workers is the potential for HIV transmission after an occupational exposure. Prophylactic treatment recommendations for occupational exposures will be detailed in the following section of this article. The overall risk of contracting HIV after an occupational percutaneous exposure to a known HIV-positive source patient is < 0.5%. However, certain factors may increase the risk of transmission.9 (See Table 2.) The Centers for Disease Control and Prevention (CDC) reported 57 known cases of occupationally acquired HIV infection in health care workers in the United States through June 2001. The majority (48/57) suffered a percutaneous exposure. Other known exposures included mucocutaneous (5/57) and both percutaneous and mucocutaneous (2/57). An additional 137 HIV-positive health care workers (without other HIV risk factors) reported a history of occupational exposure, although their seroconversion after exposure was not documented. The exact number of these infections that were occupationally acquired is not known.19
Primary HIV Infection
Primary HIV infection refers to the time period between initial HIV acquisition and the appearance of HIV specific antibodies—the "HIV-negative window."20 Reports indicate that this may range from as few as eight days to greater than one year.20,21 However, the majority of those newly infected (> 95%) will demonstrate HIV specific antibodies within six months of exposure.22 Those with primary HIV infection may be completely asymptomatic, or may develop symptoms severe enough to warrant hospitalization.
With acute infection, HIV undergoes massive replication, producing high serologic viral levels.20,23-25 This time period is of significant public health importance, as an increased risk of HIV transmission exists in individuals with high serologic viral levels,8,9 who may or may not be aware of their recent exposure and/or infection. Viral levels peak 21-28 days following exposure, and then begin a rapid decline in response to an apparent activation of the immune system.23,26-27 Further in the course of primary HIV infection, viral levels begin to increase again.23,24 This second inflection point in viral levels, in addition to the initial immune response, appears to hold important predictive information regarding the overall disease course and rate of progression.24,28 Thus, recognition of primary HIV infection may be critical in planning an effective treatment strategy for the infected individual.7,24,26,28
Acute Retroviral Syndrome
When clinical symptoms, particularly fever, are associated with HIV seroconversion, it is designated ARS. Recognition is imperative to the future disease course of the newly HIV infected. Disease progression to AIDS and death due to AIDS occurs more rapidly in symptomatic patients.29 Specifically, one study found that 27% of symptomatic converters vs. 6.5% of asymptomatic converters progressed to AIDS within 48 months of virus acquisition. The same study reported a disparity in death rates due to AIDS-related illnesses as well; 26% of symptomatic converters died within 48 months of viral acquisition compared to only 2.8% of asymptomatic converters.29 Higher viral titers and faster rates of CD4 cell decline are reported in those with ARS than in asymptomatic seroconverters.7 Schacker et al were unable to identify demographic differences between symptomatic and asymptomatic seroconverters.7 It has been theorized that symptomatic HIV seroconversion may represent greater initial disease dissemination or an inadequate host immune response to HIV acquisiton.24 The actual number of symptomatic seroconverters is unclear and difficult to determine, but has been reported between 10% and 90%.7,20,29-33
The first reported case of ARS detailed the symptomatic HIV seroconversion of an occupationally acquired infection in 1984.34 The following year, ARS was described as a mononucleosis-like illness after Cooper reviewed several cases.30 More recently, ARS was defined as a more generalized febrile illness, as it may represent a myriad of symptoms. Typically, onset of ARS occurs between five and 30 days following viral exposure.7,20,26,31 Symptoms may persist 7-28 days, and are followed by a prolonged asymptomatic period.20,23,29-32,35-36 Fever is reported most frequently.7,29-33 Common additional symptoms included fatigue, sore throat, lymphadenopathy, weight loss, myalgias, headache, nausea, vomiting, diarrhea, and rash.7,29-31,33 Symptoms may be of a severity requiring hospitalization in up to 17-42% of symptomatic converters.7,33
Physical findings associated with ARS may include fever, rash, lymphadenopathy, oral manifestations, and postural hypotension.7,20,30,33 Reported temperatures averaged 38.6°C and 38.9°C.7,33 Rash most commonly was described as a maculopapular erythematous truncal rash, but also could involve the face or extremities, with or without urticarial components. Other rashes, specifically ulcers involving the mouth or genitals, also were reported.30,33 Cervical adenopathy was found most commonly, but axillary, inguinal, and epitrochlear locations of lymphadenopathy also were described.33 Exudative pharyngitis or thrush were found in some individuals.7,20,30 The differential diagnosis of acute retroviral illness is extensive, as it may overlap with numerous other infectious diseases. (See Table 3 for a partial list.) Thus, the emergency physician must maintain a high degree of clinical suspicion when evaluating patients at risk for HIV acquisition.
Implications for Acute Retroviral Syndrome Recognition
As noted earlier, individuals experiencing symptomatic HIV seroconversion develop AIDS, and die due to AIDS-related illness, more rapidly than asymptomatic seroconverters.29 Early recognition presents an opportunity to arrange follow-up care and therapy earlier, and potentially improve the disease course, as well as intervene to prevent further transmission. Unfortunately, this opportunity frequently is overlooked. Kinoch de Loes reported 32% of symptomatic patients sought evaluation in an emergency department (ED).33 Another study reported that a significant majority (88%) of patients with ARS sought medical evaluation during their symptomatology; approximately half saw their primary physician, while the other half visited an ED or walk-in type clinic. ARS was considered in only about one-fourth of patients, despite health care professionals’ knowledge of the patients’ high-risk activities.7 These studies suggest that while a significant number of patients seek medical evaluation, the diagnosis of ARS frequently may be unrecognized. As a large number of patients with ARS present to EDs for care, a real opportunity exists for emergency physicians to impact the health and life of the symptomatic, newly HIV-infected individual.
While the emergency physician may not perform the HIV test or begin anti-retroviral therapy, alerting the patient to the possibility of acute HIV infection and advising appropriate follow-up care ultimately may lead to an improved quality and length of life. Early identification of HIV infection can enable early therapy. This potentially can bring important benefits to the patient. Some experts believe early, aggressive therapy can inhibit viral replication during the early stages of infection.27 And, with limited time to mutate and develop anti-retroviral resistance, a perhaps more homogeneous and vulnerable viral load can be targeted.27,37-38
In addition to possibly favorably altering a patient’s HIV disease course, early awareness of infection may contribute to limit further disease transmission. It has been estimated that HIV transmission occurs 4-12 times more frequently during primary infection than later seropositive stages.39-41 A combination of high viral titers characteristic of primary infection, and an individual’s lack of awareness of the newly acquired infection may contribute to the increased transmission rate.39-41 Thus, when considering ARS as part of a patient’s differential diagnosis, the emergency physician has the opportunity to counsel patients to avoid high-risk behavior until the diagnosis is excluded.
Post-Exposure Evaluation and Management
By virtue of their work-related activities, HCPs are at risk for occupationally acquired infectious diseases. The CDC reported more than 11,000 exposures from June 1996 to November 2000. In those exposures with known sources, 6% of sources were HIV-positive, 74% were HIV-negative, and 20% had unknown HIV status.42 In addition to HIV, hepatitis B and C should be considered in any HCP sustaining an exposure. The remainder of this article will focus mainly on HIV transmission.
The overall risk of HIV seroconversion following occupational percutaneous exposure to HIV-positive blood or body fluids is 0.3%, the risk following occupational mucocutaneous exposure is 0.09%.43,44 However, many factors must be considered with each particular contact.
The CDC recommends the primary method to prevent transmission of blood-borne illnesses is to avoid exposure.42 Standard precautions should be employed with any procedure that carries a potential risk of exposure. However, HCPs are not always completely compliant. One study found physicians, nurses, and technicians working in a Level-1 trauma center ED were not knowledgeable of risks for blood-borne pathogens, did not report all exposures, and were not compliant with universal precautions.45 Michaelsen found physician universal precaution compliance rates between 54% and 94%.46 And frighteningly, 44% of physicians admitted to recapping used needles contaminated with blood.46 Kelen et al recommend barrier precautions for all but the most uncomplicated procedures in the ED. They believe face shields should be employed (in addition to other standard precautions) when performing lumbar puncture or examining the bleeding patient, as facial splashes can occur.47
Even when standard precautions are employed, exposures can take place. Latex gloves can leak, exposing skin to blood or body fluids. Hansen et al demonstrated that gloves worn for longer periods, more than one procedure, or during critical care procedures have increased perforation rates.48
Needlesticks are the most commonly reported occupational exposure, accounting for approximately 80% of exposures in one study.49 Exposures can occur any time a needle is used or exposed. However, certain activities appear to carry higher risk of potential exposure. Recapping needles, improper disposal of used needles, and transferring blood/body fluids between different containers are particularly dangerous behaviors.50 Jagger found that 70% of needlestick injuries occurred after use but before disposal of needles, and included recapping needles, contacting exposed needles left on working surfaces, and contacting used needles that had penetrated through their caps.51 Only 17% of needlesticks in their study occurred during actual device use. Additionally, devices requiring disassembly following use increased the risk of exposure.51 Thus, special care should be used when disassembling or disposing of used equipment.
Post-exposure prophylaxis (PEP) may reduce the risk of HIV transmission. Evidence supporting its use has been derived from animal models and retrospective human studies. Cardo et al reported a reduction in occupational exposure HIV transmission of approximately 81% with post-exposure use of zidovudine in their retrospective study.15 The reduction of maternal-fetal HIV transmission with use of anti-retroviral agents may lend further support for its potential efficacy in occupational exposures. When zidovudine was administered to HIV-infected pregnant women during pregnancy, labor and to the infant, Connor et al described a 67% reduction in HIV transmission to the fetus.52 However, PEP failures have been reported. Multiple instances of HIV infection after occupational exposure have been reported despite use of PEP.53-54
Blood-borne disease transmission can occur following percutaneous, mucous membrane, or non-intact skin exposure to a potentially infectious source material.55-56 Blood or visibly bloody fluids obviously carry risk of infection transmission. Other potentially infectious fluids include semen, vaginal secretions, cerebrospinal fluid, pleural fluid, synovial fluid, peritoneal fluid, pericardial fluid, and amniotic fluid.42 Substances generally not considered potentially infectious except when containing blood include feces, nasal secretions, sputum, sweat, tears, urine, vomitus, and saliva.42
After sustaining an exposure, an HCP should report the contact as outlined by institutional protocols. Frequently, occupational health services and/or the ED are involved. Evaluation should occur as soon after the injury as possible. Decisions regarding severity of the exposure and its potential to transmit blood-borne pathogens, as well as whether to begin PEP and which regimen to choose, are included in the evaluation of the exposed HCP by the ED practitioner. Updated guidelines for evaluation and management of the exposed HCP were published by the CDC in June 2001.42 A summary of those recommendations follows.
Detailed information from all HCPs suffering occupational exposure should be obtained and documented. The time and date of the incident should be noted. Specifics regarding the percutaneous exposure should include the procedure being performed at the time of the exposure, the contacted instrument, presence or absence of visible blood/fluid on instrument, depth of injury, and whether fluid was injected. For the mucocutaneous exposure, amount of fluid, duration of contact, and condition of exposed skin should be noted. Information regarding post-exposure care and cleansing of the region also may be included. Details regarding the source patient should be obtained, specifically their hepatitis B, C, and HIV status. All HCPs should be questioned regarding hepatitis B vaccination completion and response. Baseline serologic testing for hepatitis B, C, and HIV should be performed on the exposed HCP. Additional laboratory evaluation, including a baseline complete blood count, chemistry, and liver functions, should be performed when initiating PEP.
The first step in evaluating the occupational exposure is to consider the specific incident. Did percutaneous, mucous membrane, or nonintact skin (abraded, chapped, or affected with dermatitis) contact potentially infectious material? PEP following intact skin contact currently is not recommended.42 The PEP recommendations differ for percutaneous and mucocutaneous exposure, thus this first factor should be determined. (See Table 4.) Laboratory evidence has suggested that percutaneous exposures with either hollow needles and/or deeper injuries demonstrate increased blood inoculums when compared to solid needles and superficial injuries, thus increasing transmission risk.57 Percutaneous injuries should be assessed as either less severe (solid needle and superficial) or more severe (large-bore hollow needle, deep puncture, visible blood on device, or needle in patient’s artery or vein). Mucocutaneous exposures are deemed either small (few drops) or large (major blood splash) volumes.42
Next, factors concerning the source patient should be considered. Of utmost importance is the HIV status of the exposure source. The CDC has outlined four different categories when evaluating the source patient and recommending PEP regimens. If the source is unknown, such as an exposure to a used needle in a needle box, considerations regarding the HIV prevalence in the institution’s patient population should influence the decision regarding PEP. Testing the sharp instrument is not recommended, as the reliability of results is unclear, and other individuals handling the object risk exposure. The CDC recommends expert consultation in this situation, as each case should be considered individually.42 In source patients of unknown HIV status, further information may be obtained by review of the medical chart, prior laboratory studies, or clinical symptoms. HIV testing should be performed after obtaining consent, and in accordance with local and state laws. If the source patient ultimately tests HIV-negative, PEP may be discontinued.42
The known HIV-positive patient may be considered Class 1 or Class 2, distinguished by the viral load and clinical condition. Asymptomatic, HIV-positive patients with low viral loads are considered Class 1. Those HIV-positive patients with symptoms of infection, AIDS, acute seroconversion, or known high viral loads are considered Class 2.42 Please note that viral load provides information regarding cell-free virus present in blood, and not about virus present in cells. Thus, while low or undetectable viral loads likely reflect lower viral exposures, the possibility of HIV transmission still does exist.42 Also, in any exposure involving a known HIV-positive source, the antiretroviral medications used during the disease course are pertinent to consider. Resistance may develop to any antiretroviral medication; thus, treatment history may influence PEP medication choices.58 Transmission of HIV resistant to antiretroviral medication in occupational exposures has been reported despite multi-drug regimen PEP use.42
Based on the above determinations regarding the incident, the CDC has recommended specific regimens, as outlined in Tables 4, 5, and 6. However, there are certain situations in which the CDC recommends expert consultation in choosing PEP medications: greater than 24-hour delay of incident report; exposure to an unknown source; known or suspected pregnancy in the HCP; exposure to a known HIV-positive source patient treated with multiple antiretroviral medications; and in the HCP experiencing PEP medication side effects.42
The potential side effects and toxicities of PEP medications should be considered prior to initiation of therapy, especially in those exposures with very low risk for infection transmission. Almost half of all HCPs taking PEP experience side effects, and about one-third discontinue PEP prior to the recommended four weeks of therapy due to the side effects.42 Common complaints include nausea, headache, malaise, and anorexia.42 In addition, severe toxicities, such as liver failure requiring transplantation, Stevens-Johnson syndrome, and rhabdomyolysis, have been reported in HCPs taking PEP.59
When PEP has been deemed warranted, initiation of therapy should begin as soon after the exposure as possible. The time for delay of therapy that reduces or eliminates PEP benefit is unclear. Animal studies demonstrate significant decreased efficacy when PEP therapy is initiated more than 24-36 hours after an exposure.42 However, in practice, PEP therapy may be initiated even after prolonged intervals from time of exposure when considered high risk for transmission. Therapy with the recommended regimen should continue for four weeks, if tolerated.
When a significant occupational exposure has occurred, the HCP requires specific counseling. Information regarding transmission rates of blood-borne illnesses should be detailed. Exposed HCPs should be informed that limited information exists regarding the efficacy of PEP, and concerns regarding possible antiretroviral resistance lead experts to recommend use of combination regimens. The potential side effects, toxicities, and drug interactions of the prescribed medications should be supplied. Behavioral modification to prevent secondary transmission (e.g., condom use) should be advised. And the HCP must be informed that he or she may decline or stop PEP medication use.42
Thus, evaluation of the HCP subjected to an occupational exposure of HIV is a complex and multi-factorial decision-making process. Specific situations may require expert consultation. Multiple resources exist for guidance in evaluating the occupational exposure. (See Table 7.)
As the HIV epidemic continues, the emergency physician must remain knowledgeable about multiple HIV-related situations. Many individuals suffering clinical symptomatology due to acute HIV infection present to EDs. Recognition of ARS may present an opportunity to positively impact the disease course of the acutely infected individual and prevent further disease transmission. Occupational exposure to HIV is, unfortunately, not an uncommon occurrence. The emergency physician must be familiar with occupational risks of transmission and appropriate use of post-exposure prophylaxis in the exposed HCP.
1. Joint United Nations Programme of HIV/AIDS. UNAIDS Report on the Global HIV/AIDS Epidemic, July 2002. www.unaids.org (accessed 10/31/02).
2. AIDS Virus Education and Research Trust. Worldwide HIV and AIDS Epidemic Statistics. www.avert.org/ (accessed 10/31/02).
3. Centers for Disease Control and Prevention. HIV/AIDS Update. www.cdc.gov/hiv/stats.htm (accessed 10/31/02).
4. Centers for Disease Control and Prevention. Trends in the HIV and AIDS Epidemic 1998. www.cdc.gov/hiv/stats/hasr1002.htm (accessed 10/31/2002).
5. Center for Disease Control and Prevention. HIV AIDS Surveillance Report. www.cdc.gov/hiv/stats/hasr1301.pdf (accessed 10/31/02).
6. AIDS Virus Education and Research Trust. United States HIV and AIDS Statistics Summary. www.avert.org/statsum.htm (accessed 10/31/02).
7. Schacker T, Collier A, Hughes J, et al. Clinical and epidemiologic features of primary HIV infection. Ann Int Med 1996;125:257-264.
8. Dong B. Prophylaxis after nonoccupational exposure to HIV. Am J Health Syst Pharm 1999;56:1011-1016.
9. Ippolito G, Puro V, Heptonstall J, et al. Occupational human immuodeficiency virus infection in health care workers: Worldwide cases through september 1997. Clin Infect Dis 1999;28:365-383.
10. Schreiber GB, Busch MP, Kleinman SH, et al. The risk of transfusion-transmitted viral infections. N Engl J Med 1996;334:1685-1690.
11. Centers for Disease Control and Prevention. Management of possible sexual, injecting drug use, or other nonoccupational exposure to HIV, including considerations related to antiretroviral therapy: Public Health Service statement. MMWR Morb Mortal Wkly Rep 1998;47:1-14.
12. Katz MH, Gerberding J. The care of persons with recent sexual exposure to HIV. Ann Int Med 1998;128:306-312.
13. Katz MH, Gerberding JL. Postexposure treatment of people exposed to human immunodeficiency virus through sexual contact or injection drug use. N Engl J Med 1997;336:1097-1100.
14. Mastro TD, deVincenzi I. Probabilities of sexual HIV-1 transmission. AIDS 1996;10 (Suppl A):S75-80.
15. Cardo DM, Culver DH, Cieselski CA, et al. A case control study of HIV seroconversion in health care workers after percutaneous exposure. N Engl J Med 1997;337:1485-1490.
16. Kaplan EH, Heimer R. A model-based estimate of HIV infectivity via needle-sharing. J Acquir Immun Defic 1992;5:1116-1118.
17. Centers for Disease Control and Prevention. Transmission of HIV possible associated with exposure of mucous membrane to contaminated blood. MMWR Morb Mortal Wkly Rep 1997;46:620-624.
18. Vidmar L. A human bite: Possible mode of HIV-1 transmission. International Conference on AIDS July 7-12, 1996;11:362 (abstract no. Tu.C.2563).
19. Centers for Disease Control and Prevention. Surveillance of Health Care Workers with HIV/AIDS. www.cdc.gov/hiv/pubs/facts/hcwsurv.htm (accessed 10/31/02).
20. Rosenberg E, Cotton D. Primary HIV infection and the acute retroviral syndrome. AIDS Clin Care 1997;9:21-25.
21. Daar ES. Virology and immunology of acute HIV type 1 infection. AIDS Res and Hum Retroviruses 1998;14:S229-S234.
22. Ciesielski C, Metler R. Duration of time between exposure and seroconversion in healthcare workers with occupationally acquired infection with human immunodeficiency virus. Am J Med 1997;102(5B):115-116.
23. Little S, McLean A, Spina CA, et al. Viral dynamics of acute HIV-1 infection. J Exp Med 1999;190:841-850.
24. Schacker T, Hughes J, Shea T, et al. Biological and virologic characteristics of primay HIV infection. Ann Int Med 1998;128:613-620.
25. Jolles S. Primary HIV-1 infection: A new medical emergency? BMJ 1996;12:1243-1244.
26. Schacker T. Primary HIV infection. Postgrad Med 1997;102:143-151.
27. Department of Health and Human Services and Henry J. Kaiser Family Foundation. Guidelines for the use of antiretroviral agents in HIV-infected adults and adolescents. MMWR Morb Mortal Wkly Rep 1998; 47:43-82.
28. Pantaleo G, Demarest J, Schacker T, et al. The qualitative nature of the primary immune response to HIV infection is a prognosticator of disease progression independent of the initial level of plasma viremia. Proc Natl Acad Sci USA 1997;94:254-258.
29. Dorrucci M, Rezza G, Vlahov D, et al. Clinical characteristics and prognostic value of acute retroviral syndrome among injecting drug users. AIDS 1995;9:597-604.
30. Cooper DA. Acute AIDS retrovirus infection. Definition of a clinical illness associated with seroconversion. Lancet 1985;1:537-540.
31. Vanhems P, Allard R, Cooper DA, et al. Acute human immunodeficiency virus type 1 disease as a mononucleosis-like illness: Is the diagnosis too restrictive? Clin Infect Dis 1997;24:965-970.
32. Kopko P, Calhoun L, Petz L, et al. Distinguishing immunosilent AIDS from the acute retroviral syndrome in a frequent blood donor. Transfusion 1999;39:383-386.
33. Kinloch-de Loes S. Symptomatic primary infection due to human immunodeficiency virus type 1: Review of 31 cases. Clin Infect Dis 1993;17:59-65.
34. Anonymous. Needlestick transmission of HTLV-III from a patient infected in Africa. Lancet 1984;2:1376-1377.
35. Joint United Nations Programme of HIV/AIDS. AIDS epidemic update: December 1999. www.unaids.org/publications/documents/epidemiology/index.html (accessed 10/31/2002).
36. Centers for Disease Control and Prevention. Guidelines for treatment of sexually transmitted diseases. MMRW Morb Mortal Wkly Rep 1998; 47:109-111.
37. Perrin L, Markowitz M, Calandra G, et al. An open treatment study of acute HIV infection with zidovudine, lamivudine, and indinavir sulfate. 4th Conference on Retro and Opportunistic Infections, Jan. 22-26, 1997:108 (abstract no. 238).
38. Raines CP. Antiretroviral treatment in HIV infection. Prim Care Pract 2000;4:83-100.
39. Jacquez JA. Role of the primary infection in epidemics of HIV infection in gay cohorts. J Acquir Immun Defic 1994;7:1169-1184.
40. Koopman JS. The role of primary infection in epidemic HIV transmission. International Conference on AIDS, June 6-11, 1993;9:100 (abstract no. WS-C19-5).
41. Koopman JS. The role of early HIV infection in the spread of HIV through populations. J Acquir Immune Defic Syndr Hum Retrovirol 1997;14:249-258.
42. Centers for Disease Control and Prevention. Updated U.S. Public Health Service Guidelines for the Management of Occupational Exposures to HBV, HCV, and HIV and Recommendations for Postexposure Prophylaxis. MMWR Morb Mortal Wkly Rep 2001;50:1-52.
43. Bell DM. Occupational risk of human immunodeficiency virus infection in healthcare workers: An overview. Am J Med 1997;102:9-15.
44. Ippolito G, Puro V, DeCarli G. Italian Study Group on Occupational Risk of HIV Infection. The risk of occupational human immunodeficiency virus in health care workers. Arch Int Med 1993;153:1451-1458.
45. Kim LE, Evanoff BA, Parks RL, et al. Compliance with universal precautions among emergency department personnel: Implications for prevention programs. Am J Infect Control 1999;27:453-455.
46. Michalsen A, Delclos G, Felknor SA, et al. Compliance with universal precautions among physicians. J Occup Env Med 1997;39:130-137.
47. Kelen GD, Hansen KN, Green GB, et al. Determinants of emergency department procedure and condition-specific universal (barrier) precaution requirements for optimal provider protection. Ann Emerg Med 1995;25:743-750.
48. Hansen KN, Korniewicz D, Hexter DA, et al. Loss of glove integrity during emergency department procedures. Ann Emerg Med 1998;31:65-72.
49. Jagger J, Hunt EH, Brand-Elnagger J, et al. Rates of needlestick injury caused by various devices in a university hospital. N Engl J Med 1988;319:284-288
50. Department of Health and Human Services. Preventing needlestick injuries in health care settings. DHHS (NIOSH) Publication 1999. www.cdc.gov (accessed 10/31/02).
51. Jagger J. Reducing occupational exposure to bloodborne pathogens: Where do we stand a decade later? Infect Control Hosp Epidemiol 1996; 17:573-575
52. Connor EM, Sperling RS, Gelber R, et al. Reduction of maternal-infant transmission of human immunodeficiency virus type 1 with zidovudine treatment. N Engl J Med 1994;331:1173-1180.
53. Ippolito G, Puro V, Petrosillo N, et al. Simultaneous infection with HIV and hepatitis C virus following occupational conjunctival blood exposure. JAMA 1998;280:28.
54. Jochimsen EM. Failures of zidovudine posteposure prophylaxis. Am J Med 1997;102:52-55.
55. Centers for Disease Control and Prevention. Recommendations for prevention of HIV transmission in health-care settings. MMWR Morb Mortal Wkly Rep 1987;36 (suppl no. 2S).
56. Centers for Disease Control and Prevention. Update: Universal precautions for prevention of transmission of human immunodeficiency virus, hepatitis B virus, and other bloodborne pathogens in health-care settings. MMWR Morb Mortal Wkly Rep 1988;37:377-82, 387-8.
57. Mast ST, Woolwine JD, Gerberding JL. Efficacy of gloves in reducing blood volumes transferred during simulated needlestick injury. J Infect Dis 1993;168:1582-1592.
58. Hirsch MS, Brun-Vezinet F, D’Aquila RT, et al. Retroviral drug resistance testing in adult HIV-1 infection: Recommendations of an international AIDS Society-USA panel. JAMA 2000;283:2417-2426.
59. Centers for Disease Control and Prevention. Serious adverse events attributed to nevirapine regimens for postexposure prophylaxis after HIV exposures-worldwide, 1997-2000. MMWR Morb Mortal Wkly Rep 2001;49:1153-1156.
After completing the program, participants will be able to:
Physician CME Questions
1. The most common route of newly acquired HIV infection is:
A. occupational exposure.
B. sharing needles.
C. sexual exposure.
D. human bites.
2. In the United States:
A. women represent the most common HIV-infected group.
B. the ethnic distribution of HIV infection mirrors the general population ethnic distribution.
C. the majority of infected children contracted the disease via perinatal transmission.
D. HIV infection rates are greatest in rural areas.
E. All of the above are true.
3. With use of antiretroviral therapy in the United States,
A. the number of people living with AIDS is increasing.
B. the number of HIV-related deaths is decreasing.
C. the rate of perinatal HIV transmission to infants is decreasing.
D. the rate of HIV progression to AIDS is slowing.
E. All of the above are true
4. The exposure route that transmits HIV most effectively is:
C. oral-genital contact.
D. blood transfusions.
5. Early recognition of acute retroviral syndrome:
A. may improve the overall disease course.
B. may prevent further disease transmission.
C. frequently is overlooked.
D. All of the above are true.
6. The majority of HCP occupational exposures involve source patients that are HIV-positive.
7. Which of the following exposures represents the highest risk of HIV transmission?
A. HCP experiences a needlestick after drawing medication into a new syringe.
B. HCP experiences contact with urine on intact skin.
C. HCP experiences a needlestick after drawing an arterial blood gas sample.
D. HCP experiences a splash to eyes with non-bloody vomitus.
8. Generally accepted potentially infectious source materials include all of the following except:
A. visibly bloody sputum.
B. cerebrospinal fluid.
C. synovial fluid.
E. amniotic fluid.
9. Expert consultation for post-exposure prophylaxis should be considered when the HCP:
A. experiences an exposure to an unknown source.
B. reports an occupational exposure 48 hours after incident.
C. is pregnant.
D. is exposed to a known HIV-positive source treated with antiretrovirals.
E. All of the above
10. According to the most recent recommendations from the CDC, which of the following is indicated for the HCP who was splashed in the eyes with a small amount of blood from an AIDS patient?
A. Basic two-drug regimen
B. Expanded three-drug regimen
C. No post-exposure prophylaxis indicated
D. HIV vaccination