Several persons provided information, assistance, and support me during this project. I am grateful to all administrators, nursing directors and staff members at Larkin Community Hospital, Fair Haven Center, Mercy Nursing Home, and Oceanside Extended Care, for their support and assistance in conducting this study. My sincere thanks go to the healthcare workers who completed the questionnaires and to Ms. Marlene Phipps for her support.

Dr. Richard Davis, my practicum chair person, gave me encouragement and insisted on excellence, and I thank him.

I am grateful to Dr. Guy Nehrenz, Chair, Department of Health Science at Nova Southeastern University, for his support and assistance in formulating this study.

Muna Al-Hussami, my wife, gave me encouragement and insisted on excellence, and I thank her. Finally, I dedicate this to my mother Jameelah and my two daughters, Rawan and Razan, who allowed me to share my thoughts on this research.

A fairly common systemic disease, viral hepatitis is marked by hepatic cell destruction, necrosis, and autolysis, leading to anorexia, jaundice, and hepatomegaly (Smith, 2000, p. 453). Hepatitis is defined simply as injury to hepatic cells and infiltration of inflammatory cells into the liver; it is not an uncommon manifestation of a variety of systemic infectious processes. In such instances, histopathologic changes are minimal and liver involvement is usually clinically silent, and thus there is little confusion with viral hepatitis (Beare, 1991, p.487; Beeson, 1979, p. 1657; Kolats, 1994, p. 168; Wilkins, 1978, p. 153).

Hepatitis B, acute inflammatory disease of the liver or a form of viral hepatitis caused by the hepatitis B virus (HBV) (Beare, 1991, p. 486). Acute viral hepatitis is a generalized infection with emphasis on inflammation of the liver. The clinical picture of the infection varies in its presentation from a symptomatic or subclinical infection, mild gastrointestinal symptoms and the anicteric from the disease, acute illness with jaundice, severe prolonged jaundice to acute fulminate hepatitis (Bryan, 1995, p.1114; Weatherall, 1987, p. 339).

There is now compelling evidences of an etiological association between hepatitis B virus and hepatocellular carcinoma, one of the ten most common malignant tumors worldwide (Kawai, 2000, p. 1287; Bryan, 1995, p. 1114; Thomas, 1974, p. 67).

In the past, been called catarrhal jaundice, nonspirochetal infectious jaundice and infectious hepatitis (Goldman, 2000, p. 877; Rakel, 2000, p. 567). It probably is by means a new disease but only for the past twenty or twenty five years has it been properly differentiated from Weil's disease and yellow fever (Rakel, 2000, p. 568).

Hepatitis is an inflammatory state of the liver that may be caused by exposure to toxic chemicals, by autoimmune disease, or by infection (Gladwin, 1996, p. 54; Beeson, 1979, p. 1655). The viral infection most commonly associated with hepatic inflammation includes hepatitis A, B, C, D, and E (Dienstag, 1998, p. 1723). A virus similar in structure to hepatitis C has been designated hepatitis G, but information about this virus and its effects on the liver is limited (Goldman, 2000, p. 878). In 1994 hepatitis F was identified as a cause of fulminate liver failure. This was later found to be a variant subspecies of another virus. Therefore, the F is now omitted in the hepatitis alphabet (Dienstag, 1998, p. 1725; Dolin, 1999, p. 99). The general term viral hepatitis refers to infections caused by at least six different viruses, hepatitis A (infectious or epidemic hepatitis), hepatitis B (serum hepatitis), hepatitis C (non-A, non-B) , and hepatitis D virus (the delta agent). Non-A, non-B hepatitis, which appears to be caused by more than on virus, and an epidemic from non-A hepatitis. Indeed, viral hepatitis has emerged as a major public health problem occurring endemically in all parts of the world (Lemon, 1995, p. 1485; Michael, 1999, p. 14; Thomas, 1974, p. 68; Thorn, 1977, p. 875; Weatherall, 1987, p. 340).

Epidemic jaundice was described by Hippocrates in the 5 ^th century B.C., the first recorded cases of serum hepatitis, hepatitis B, are thought to be those that followed the administration of smallpox vaccine containing human lymph to shipyard workers in Germany in 1883. In the early and middle parts of this century, serum hepatitis was repeatedly observed following the use of contaminated needles and syringes. The role of blood as a vehicle for virus transmission was further emphasized in 1943, when Beeson described jaundice among seven recipients of blood transfusions (Atkinson, 1995, p. 19; Diasio, 1996, p. 1294; Beeson, 1979, p. 1980). Throughout the early part of the 20 ^th century, clusters of cases were reported in venereal disease clinic and diabetic clinic in which reuse of contaminated needles and/or syringes had occurred.

In 1965, medical researcher Baruch Blumberg identified a specific antigen in the serum of an Australian Aborigine who had received numerous blood transfusions. This “Australia Antigen” was later found to be associated with hepatitis B, it is discovery led to rapid advancement in the knowledge of hepatitis B virus. This antigen has now been renamed the hepatitis B surface antigen (HBsAg). This virus as well as the typical serological response pattern of the host, has been extensively studied (Margolis, 1997, p. 387). Australian Antigen, later called hepatitis B surface antigen (HBsAg), was first described in 1965, and Dane Particle was identified in 1970. Identification of serologic makers for hepatitis B virus infection followed, which helped clarify the natural history of the disease (Atkison, 1995, p. 23).

The development of immunologic techniques in the 1960's and 1970's further clarified in the nature of hepatitis and made precise diagnosis possible, the development of immunoassay after the discovery of Australia Antigen(HBsAg) made possible the detection of persons who were antibody positive (Beere, 1991, p. 488; Johns, 1980, p. 256; Last, 1987, p. 198). Study of this virus has been handicapped in that no susceptible experimental animal has been found. Because of this, much of the study has had to be carried out on human volunteers (Beere, 1991, p. 487; WHO, 2001, p. 4; Miller, 1978, p. 211). In the mid 1960's epidemiologists discovered that HBV could be detected in blood by the use of a reactant present in the blood of patients who had received large numbers of transfusions (Arien, 1991, p. 79). Some transfusion units had contained HBV, and the patients had developed antibodies, which could be used to detect the virus in other people's blood. By a strange irony, the blood of people who had already been exposed to the virus and had developed antibodies against it could be used to detect the virus present in donor's blood and prevent its use to infect others (Tyler, 1995, p. 1314; Wallach, 1992, p. 567).

In a relatively short time, sensitive methods were developed to screen donor blood and detect symptomatic carriers of HBV, prior to this discovery, hepatitis following transfusions was very common, particularly with the introduction in the 1950's of surgical procedures such as open heart surgery and kidney transplantation that required large amounts of blood. In some hospitals where these heroic surgical procedures were performed, as many as 50 percent of the patients became infected, and many of them became seriously ill (Arien, 1991, p. 86). Therefore, as soon as it was realized that hepatitis screening would considerably decrease the frequency of post-transfusion hepatitis, many blood banks established testing as a routine procedure, and it soon became a requirement for all hospitals and blood banks (Henderson, 1992, p. 1). The incidence of post-transfusion hepatitis due to HBV has decreased dramatically. Viruses are the cause of some of the earliest disease processes recorded in the medical literature. Though the natural history of viral diseases such as polio, measles, and smallpox had been described for millennia, the first viruses were not identified until the beginning of the 20 ^th century. The knowledge of specific viruses, viral life cycle, and viral/host interaction increased dramatically over the next 50 years, leading to the development of vaccines. More recent techniques such as electron microscopy, electrophoresis, x-ray crystallography, and polymerase chain reaction have permitted in-depth studies of viral structure and more precise identification of viruses causing specific diseases (Tyler, 1995, p. 1327).

Classification of viruses has changed as knowledge of them has increased. Initially, viruses were primarily classified by size, method of transmission, or organ affected in the disease process. More recently, viruses have been classified by the type of nucleic acid in the viral core, the nucleic acid's method of replication, the presence or absence of an envelope, and the symmetry of the viral capsid (protein coat) (Atkinson, 1995, p. 19). The nucleic acid in the viral core can be RNA or DNA and can be either single stranded or double stranded. These nucleic acid strands can be circular or linear. Viruses replicate nucleic acid in one of five different methods. Discussion of these complex methods of replication is beyond the scope of this study, but the method by which a virus replicates contributes to its classification. In the majority of viruses, the nucleic acid is covered with a protein coat called a capsid. Most capsids are either shaped as a helical spiral or as an icosahedral sphere. Some viruses are surrounded by a lipid envelope, an outer layer beyond the capsid. Using this classification system, poliovirus is classified as a single stranded RNA virus with an icosahedral capsid and no lipid envelope. Similarly, the herpes simplex virus is classified as a double stranded DNA virus with an icosahedral capsid and lipid envelope. Viruses are unable to replicate outside the host. Therefore, in order to survive and reproduce, the virus must interact with the host's cells. The first step of this process is attachment, which occurs when proteins on the surface of the virus attach to receptors on the surface of the host cell. Once attachment has been accomplished, the virus penetrates the cell membrane. Within the cell, the virus undergoes a process of “uncoating” as the capsid is removed. After removal of the capsid, replication of the nucleic acid takes place. Next, the nucleic acid of the new viral particles is coated with a capsid. Finally, the new virus leaves the host cell, either through budding or through rupture of the host cell. Viruses can be transmitted through inhalation of respiratory droplets, via direct introduction into the gastrointestinal, genitourinary, respiratory tract, or percutaneously. The virus may cause a localized infection at the area of entrance or may travel through the blood stream, lymphatic, or nerve pathways to the target organ or organs. In response to viral invasion, non-specific defense mechanisms and a specific immune response are activated. Because viruses are intracellular invaders, phagocytosis, the inflammatory response, and antigen/antibody reactions not result in destruction of viral particles but also may injure or destroy host cells.

Viral hepatitis can be classified by mode of transmission, by the type of virus, and by chronicity. Hepatitis A and E are both transmitted by fecal-oral route while hepatitis B, C, D, and G are considered bloodborne pathogens. Hepatitis B is a DNA, while hepatitis C, D, E, and G are RNA viruses. Hepatitis A and E cause acute illness; hepatitis B, C, and D can have both acute and chronic manifestations. Hepatitis G has not yet been demonstrated to cause acute disease, but may be implicated in chronic disease. The hepatitis viruses represent different families of viruses: Hepatitis A is a member of the Picornavirus family; Hepatitis B is a Hepadnavirus; Hepatitis C and G are both Flaviviruses; Hepatitis D is sometimes classified as Hepadnavirus and sometimes as a Satellite virus; and Hepatitis E is the family Calicivirus (Lemon, 1995, p. 1478). The commonality in these viruses is their ability to cause inflammation of the liver. The differences in the individual viruses account for the tremendous variation in outcome of infection, chronicity of the disease, and the ease with which tests to diagnose the virus and vaccine to prevent the virus to develope.

Documents from ancient China describe a contagious jaundice in which the victims experienced symptoms consistent with Hepatitis A and E. In the fifth century BC, epidemics of jaundice occurred in Greece and Rome. Outbreaks of jaundice associated with unsanitary conditions during wartime were reported in Europe during the 17 ^th , 18 ^th , and 19 ^th centuries. Analysis of outbreaks of hepatitis during Word War II supported the theory that some forms of jaundice resulted from unsanitary conditions while others seemed to be related to a shared percutaneous source of infection (contaminated needle or vaccine). Therefore, hepatitis was classified into two categories: infectious hepatitis and serum hepatitis (Kawai, 2000, p. 1296; Schulman, 1992, p. 341). Hepatitis A virus (HAV) was initially identified when viewed in an electron microscope in 1973. Since that time the virus and the bodies response to the virus has been extensively studied. By law, diagnosed cases of HAV must be reported to the local health authorities, who in turn report the incidence to the Center for Disease Control.

Many persons who contract HAV, however, do not have clinical symptoms. Therefore, the Central for Disease Control (CDC) must estimate the actual incidence of HAV infection based upon CDC reports and projections. For the ten-year period 1984 to 1994, the CDC estimates that 125,000 to 200,000 cases occurred within United States each year. The World Health Organization estimates the annual worldwide incidence to be 1.5 million per year (WHO, 2001, p. 3). As indicated above, hepatitis A is transmitted via the fecal-oral route, most commonly from contaminated water or food. After the virus ingested, it is transported from the gut to the liver, where it invades the hepatocytes. The virus uses the hepatocytes for viral replication. The virus is released into the bloodstream and is excreted in the stool. The cellular immune system responds with infiltration of the liver by lymphocytes and cytokines. These lymphocytes are toxic to HAV infected liver cells, thus producing the inflammatory damage to the liver. IgM antibody against HAV is produced, followed by IgG antibody. Levels of IgM antibody decrease to undetectable levels over time, but IgG antibody remains.

Signs and symptoms of hepatitis A can vary from sub-clinical disease to fulminate infection. In symptomatic patients, evidence of infection appears 15 to 50 days after ingestion of the organism. Clinical evidence of the disease include nausea, vomiting, headache, fever, chills, abdominal discomfort, hepatomegaly, and right upper quadrant tenderness. For most patients, symptoms are mild and subside in three to seven days. Others will have more significant disease and will progress to an icteric phase (jaundice). For these patients, recovery typically occurs after about three weeks. Fulminate infection occurs in less than one percent of the cases. Some of these patients may have such severe damage that they require liver transplant. Fatalities from hepatitis A are rare. There is no known chronic carrier state (Tierney, 2000, p. 358). Treatment of HAV is supportive and directed at maintaining adequate nutrition and controlling symptoms. Ingestion of alcohol and/or hepatotoxic medications is avoided. For patients with fulminate hepatic failure resulting from HAV, corticosteroids are sometimes used. However, clinical research has not demonstrated improved outcomes in patients receiving corticosteroids when compared to those who did not receive steroid treatment (Kawai, 2000, p. 1287). As with any other disease, prevention is the most effective strategy. Hepatitis A vaccine is available and is recommended for anyone traveling abroad as well as for health care providers and food handlers in areas in which the endemic rate of HAV is high. Persons in other-risk categories, including homosexual or bisexual men, sewage workers, animal handlers, and individuals with chronic liver disease, should also receive the vaccine (Dienstag, 1998, p. 1723). Individuals receiving the vaccine is protected after approximately two weeks. A booster dose is recommended 6 to 12 months after the initial dose. Lifetime immunity is expected in those who received both doses (Dienstag, 1998, p. 1724).

Sanitation strategies are also important in controlling HAV. If in water, the virus is inactivated by boiling the water for five minutes. HAV is also killed by most household grade disinfectants and all hospital grade disinfectants.

Like Hepatitis A, Hepatitis E virus (HEV) is spread through the fecal-oral route, and like HAV, HEV was also first identified via electron microscope examination of stool of infected patients. HEV has been associated with outbreaks in India, Burma, Pakistan, Russia, China, Northern and Central Africa, Peru, and Mexico. Outbreaks are usually associated with a contaminated water supply. No outbreaks have occurred in the United States or Western Europe, though individual cases have been identified in persons who have recently traveled to areas in which the virus is endemic (Tierney, 2000, p. 357).

HEV most often affects young adults. The incubation period is two to nine weeks, with an average of six weeks. Signs and symptoms are similar to HAV, but with a higher incidence of jaundice, which can be prolonged. The disease is self-limited in the majority of patients. The fatality rate in acute HEV is between 1% and 2% except in pregnant women. During outbreaks, the fatality rate of HEV among pregnant women in their third trimester has reached as high as 26% (Schulman, 1992, p. 342; Springhouse, 2000, p. 178; Tepper, 1997, p. 1735).

In 1977, a new antigen was detected in patients with Hepatitis B. At first it was thought to be a variant of HBV. By 1980, Hepatitis D (HDV) was determined to be a separate virus, but a virus that was dependent upon the presence of HBV in order to replicate (Robinson, 2000, p.

1652; Peter, 1996, p. 165). Hepatitis D Virus is an RNA virus. The core is distinctively different from other viruses. However, due to a defect in replication, HDV is unable to synthesize a viral coat. It must “borrow” a coat from HBV in order to complete the replication process. Therefore, HDV cannot cause infection independently but instead must exist as a co-infection (acquired at the same time as HBV) or a super-infection (HDV acquired in a patient who is chronically infected with HBV). In the United States, the infection primarily occurs as a co-infection among intravenous drug users. In some areas of the world in which chronic HBV infection is endemic (including Mediterranean areas, the Amazon Basin of South America, China, and Southeast Asia), HDV is more commonly a super-infection (Kawai, 2000, p. 1296; Guyton, 1991, p. 543). Patients co-infected with HBV and HDV tend to have a more severe case of acute hepatitis. The mortality rate in co-infection has been reported to be as high as 20%. Super-infection with HDV results in rapid progression of cirrhosis, with liver failure occurring in approximately two years, as opposed to 10-15 years with chronic HBV infection alone (Kawai, 2000, p. 1286).

Prevention of HDV is accomplished through the same means as prevention of hepatitis B. Immunization against hepatitis B is effective prevention of HDV also because if the individual is immune to HBV, he /she cannot become infected with HDV. Avoidance of bloodborne pathogen exposure through observance of standard precautions is primary mechanism of prevention for persons already chronically infected with HBV. After the agents responsible for hepatitis A and hepatitis B were identified and laboratory tests to detect the presence of these agents were available, it became obvious that these two viruses were not the only agents associated with hepatitis. Non-A, Non-B hepatitis became the designation for cases of hepatitisthat followed a course indicative of a viral cause, but did not produce laboratory evidence of HAV or HBV. Two separate syndromes of Non-A, Non-B hepatitis were distinguished; one was present in third-world countries and resulted from ingestion of contaminated water (this is now known as HEV), and one related to blood exposures, particularly transfusions. For over ten years attempts to identify the causative agent for chronic post-transfusion Non-A, Non-B hepatitis were unsuccessful. In 1989, a cooperative effort between the CDC and a private clinical laboratory was successful in discovering the virus-specific antigen for Hepatitis C (HCV) (Foster, 2001, p. 7). Since that time, six distinct genotype of HCV have been identified (Tierney, 2000). Hepatitis C virus is the leading cause of end-stage liver disease, and the leading reason for liver transplantation in the United States. Chronic HCV infection has also been associated with membranoproliferative glomerulonephritis, cryoglobulinemia, and B-cell lymphoma. Co- infection of HCV with HIV occurs in 90% of persons who acquired HIV through intravenous drug use (Dolin, 1999, p. 47; CDC, 2000, p. 14). HCV occurs throughout the world, with endemic rates varying widely. The World Health Organization (WHO) estimates that 10% of the population of the Middle East, Africa, and Eastern Europe are positive for HCV. In the United States, 1.8% of the population (approximately 4 million people) carries the virus. The highest incidence of newly acquired HCV infection occurs in persons 20 to 30 and, at this time, shows no pattern of ethnicity. The demographic data for those currently living with HCV is somewhat different from that of new cases. The highest prevalence of persons living with HCV is among persons 30 to 40, with the rate higher among African American than among Whites and higher among males.

HCV is considered a bloodborne pathogen. The most common source of infection is percutaneous or parenteral exposure through transfusion, use of injectable drugs, and occupational injury of healthcare providers with a contaminated sharp object. The blood supply in the United States has been tested for Hepatitis C since the early 1990s. Therefore, the incidence of HCV transmission from transfusion therapy since 1994 is less than one case per hundred thousand (Bonham, 2000, p. 89). Transmission from mother to infant is uncommon, occurring in less than 5% of pregnancies of HCV positive mothers. Studies of prenatal transmission indicate that HCV transmission does not take place in uterus but instead occurs at the time of delivery. In mothers who are co-infected with both HIV and HCV, the rate of transmission of HCV to the infant is 14% (Baker, 1998, p. 464; Bates, 1995, p. 113).

Transmission of HCV through vaginal intercourse is inefficient, with the transmission rate in long-term mutually monogamous partners who were not using barrier protection reported by various studies as 1% to 21%. HCV is present in menstrual blood; therefore, intercourse during the menstrual period is considered to be higher risk than intercourse when menstrual blood is not present. Studies of transmission among males having sex with males indicates rates of transmission similar to that in heterosexual intercourse, with the highest incidence of infection among those with greater than 50 partners per year (Lemon, 1995, p. 1484; American Health Consultants, 1997, p. 45). Intranasal cocaine use has been associated with HCV transmission, presumably resulting from sharing nasal straws contaminated with blood. Tattooing has been associated with HCV transmission in studies conducted outside the United States (US), but US studies have not demonstrated this association (CDC, 2000, p. 12).

The incubation period for HCV, from exposure to onset of symptoms, is typically six to twelve weeks. HCV antibody is detectable in 80% of cases 15 weeks after exposure and in 97% of cases by six months after exposure. During the acute phase of the illness, 60% to 70% of HCV positive persons will be asymptomatic, approximately 20% of patients will develop mild jaundice, and the remaining persons will have generalized non-specific symptoms such as anorexia, nausea, fatigue, malaise, and abdominal pain (Tierney, 2000, p. 351). After the acute infection, 15% to 20% of patients will demonstrate an absence of HCV RNA in the serum and normalization of liver enzymes, indicating resolution of the infection. In those persons in whom HCV RNA remains detectable, indicating continued presence of the virus, 30% to 40% will maintain normal ALT levels and will show no evidence of chronic liver disease. The remaining 60% to 70% of chronically infected patients will have fluctuating ALT levels; some will develop progressive liver disease. On rare occasions, a patient will demonstrate positive HCV RNA without the presence of HCV antibody. Therefore, in patient who exhibits chronic hepatitis without cause, assessment of HCV RNA may be indicated (Peter, 1996, p. 157; Marx, 2000, p. 8). Chronic HCV infection usually progresses slowly, with cirrhosis developing in 20% of patients over a period of 20 to 30 years. Persons who ingest alcohol or were over age 40 at the onset of infection have a more rapid progression of cirrhosis. Males have a higher incidence of cirrhosis than females. Because acute HCV infection can be asymptomatic, the first indication of the presence of HCV may be elevated liver enzymes on laboratory tests obtained in conjunction with a routine physical examination. In evaluating the cause of liver enzyme elevation, a hepatitis panel is typically ordered. The only FDA approved tests for HCV infection are tests for HCV antibody (anti-HCV). An enzyme assay (EIA) test is typically performed initially as a screening test. The RIBA (recombinant strip immunoblot assay) is a more specific test for anti-HCV and can be used as a confirmatory test to rule out false positive EIA tests. The presence of anti-HCV does not differentiate between acute, chronic, or resolved HCV infection. Testing for the presence of HCV RNA, while not FDA approved for diagnosis, has became an accepted practice. Qualitative HCV RNA testing determines whether or not Hepatitis C viral particles are present in the blood and can therefore differentiate between resolved and continued infection. Quantitative HCV RNA testing evaluates the amount of hepatitis C virus in the blood and can be used to guide therapy. Two methods have been developed for performing quantitative tests: Polymerase chain reaction (PCR) and branched deoxyribonucleic acid signal amplification (BDNA). Because the two methods are performed using different standards, the results obtained cannot be compared with each other. Therefore, for purpose of monitoring therapy, the same of quantitative test should consistently be used (Sebastian, 2001, p. 23; Shaw, 2000, p. 1324; Sherker, 2000, p. 9; Sherman, 2000, p. 8).

Based upon genetic characteristics, six different genotypes and 90 different of HCV virus have been identified. Because the genotypes respond differently to therapy, genotypic testing should be performed for persons with chronic progressive HCV infection who are considering anti-viral therapy.

Clinical management of HCV-positive patients varies according to the severity of liver disease. In patients with no overt evidence of liver disease at the time of HCV diagnosis, liver enzymes should be assessed every six to twelve months. Most authorities agree that it is not advisable to treat persons whose ALT levels persistently remain in normal range (CDC, 1997, P. 19). In patients with fluctuating ALT levels, or those whose ALT levels remain elevated, a liver biopsy to assess the degree of liver damage is indicated. If the biopsy indicates portal or bridging fibrosis includes ascites, variceal hemorrhage, or encephalopathy have sustained too much liver damage to benefit from drug therapy; liver transplant should be considered for these patients.

For several years the medication most commonly prescribed for persons with progressing liver damage from HCV has been interferon alfa-2a or alfa-2b, 3 million units administered subcutaneously three times a week, for six to twelve months. With interferon alone, 50% of patients treated demonstrated decreased inflammation and loss of HCV from the serum during therapy. Persons with genotype 1 are less likely to respond to medication therapy than those infected with other genotypes. Once therapy is stopped, 50% to 70% of responders experience a relapse (Foster, 2001, p. 6).

In patients with progressive chronic HCV or chronic HBV infection who does not respond to pharmacotherapy, liver transplant may be indicated. Replacing the liver, however, does not cure the infection. The transplanted liver will also become infected, and immune suppressive agents facilitate the progression of this infection. Nevertheless, chronic viral hepatitis is the most common diagnosis of persons receiving liver transplants. Because hepatitis C is a bloodborne pathogen, prevention of hepatitis C is similar to prevention of hepatitis B. Observing standard precautions is essential. No vaccine is as yet available for prevention of hepatitis C, nor is gamma globulin effective post-exposure (Rosen, 2000, p. 478).

In 1995, a virus similar to the hepatitis C virus was identified and designated hepatitis G. This discovery was confirmed by another laboratory the following year. The virus is transmitted through blood, either through percutaneous injury or through transfusion. Since its discovery, HGV gas been identified in approximately 2% of banked blood (Sherker, 2000, p. 8).

HGV has never been associated with fulminate hepatitis, and the role of this virus in chronic liver disease is questionable. The virus remains detectable in the blood, with documented cases of seropositive blood up to 16 years after initial exposure. Though the presence of the virus persists, it has not been shown to independently cause liver failure. Whether or not the virus accelerated the course of chronic HCV infection is yet to be determined (Marx, 2000, p. 7; American Health Consultants, 1997, p. 29).

Hepatitis B viral infection in man is unique since concentrations of viral-related antigen in the blood may reach 50 mg per ml. Electron microscopic studies of serum have demonstrated typical morphologic appearance of the virus viral-like particles related to hepatitis B infection. Three types of particles have been observed by this technique. The most numerous are the 22 nanometer (nm) particles which appear as spherical, filamentous or tubular forms (200 nm or longer); these are related to the outer surface or coat (HBsAg) of the hepatitis B virus. Less frequently seen in serum are large 42 nm spherical Dane particles, which are believed to represent the intact hepatitis B virus. These large particles characteristically have an outer coat and an inner spherical core measuring approximately 27 nm in diameter (Goldman, 2000, p. 645; Rakel, 2000, p. 432).

HVB is small, double-shelled virus in the class hepadnaviridae. The virus contains numerous antigenic components, including HBsAg, hepatitis B core antigen (HBcAg), and hepatitis B e antigen (HBeAg). The virus contains partially double-stranded DNA, and a DNA-dependent DNA polymerase enzyme. HBV is relatively resilient and, in some instances, has been shown to remain infectious on environmental surfaces for at least a month at room temperature. Several well-defined antigen-antibody systems are associated with HBV infection. HBsAg, formerly called Australia antigen or hepatitis-associated antigen, is an antigenic determinant found on the surface of the virus. It also makes up subviral 22-nm spherical and tubular particles. HBsAg can be identified in serum 30 to 60 days after exposure to HBV and persists for variable periods (Rakel, 2000, p. 428).

During replication, HBV produces HBsAg in great excess. HBcAg is the nucleocapsid protein core of HBV and is distinct from HBsAg and hepatitis B (HBcAg). HBcAg is not detectable in serum by conventional techniques, but can be detected in liver tissue in persons with acute or chronic HBV infection. HBeAg, a soluble protein, is also contained in the core of HBV. HBeAg is detected in the serum of persons with high virus titers and indicates high infectivity. Antibody to HBsAg (Anti-HBs) develops during convalescence after acute HBV infection or following hepatitis B vaccination. Antibody to HBcAg (Anti-HBc) indicates infection with HBV at an undefined time in the past. IgM class antibody to HBcAg (IgM anti-HBc) indicates recent infection with HBV.

Antibody to HBeAg (Anti-HBe) becomes detectable when HBeAg is lost and is associated with low infectivity of serum (Atkinson, 1995, p. 25). Most HBV infections results from contact with the blood or secretions of HBsAg positive individuals. Abusers may transmit the virus by sharing needles and syringes (Margolis, 1991, p. 88; Tierney, 1994, p. 351). Physicians, dentists, nurses, laboratory personnel, and other health professionals may become infected from contact with blood of HBsAg positive patients (Kawai, 2000, p. 1287).

Contaminated dental instruments or instruments used for ear piercing may also transmit HBV. Since HBV is also present in saliva, vaginal secretions, and seminal fluid, infection may also be spread by close family contracts or sexual contracts (Henley, 1993, p. 739). An HBsAg-positive mother may transmit the virus to her newborn infant, who usually acquires the infection from maternal blood and vaginal secretions at the time of delivery (Robinson, 2000, p. 1671).

Although relatively rare in the United States, hepatitis B is endemic in parts of Asia where hundred of millions of individuals may be infected. HBV is transmitted horizontally by blood and blood products and sexual transmission. It is also transmitted vertically from mother to infant in the prenatal period which is a major mode of transmission in regions where hepatitis B is endemic. The risk of HBV infection is notably high in promiscuous homosexual men but it is also transmitted sexually from men to women and women to men. Transmission is probably prevented by correct use of condoms. Health care workers and patients receiving hemodialysis are also at increased risk of infection (CDC, 2000, p. 13).

Transmission of hepatitis B virus by the parenteral route is well documented. This is a hazard among recipients of transfused blood, pooled plasma, fibrinogen, factor VIII concentrate, and vaccine contaminated with human serum (McMahon, 1995, p. 211). Inoculation with minute amounts of infected blood may transmit hepatitis B virus infection, inadequately sterilized syringes, hypodermic needles, and dental and surgical instruments, tattoo needles, and razors have all been implicated in the transmission of infection (McQuillan, 1999, p. 14).

A high frequency of parenteral drug abuse is a major cause for infection in the young adult population. A majority of patients transfused with HBsAg positive blood either develop HBV infection (either anicteric or icteric) or exhibit a rise in the titer of anti-HBs in their serum.

The frequency of post-transfusion hepatitis B infection is significantly decreased when transfused blood is derived from volunteer rather than paid donors and when HBsAg positive blood is discarded (CDC, 1990, p. 25; Bradbury, 1999, p. 655).

Studies on the infants of mothers who suffered from hepatitis B infection during the last trimester of pregnancy or during the immediate post-partum period have shown a high frequency of neonatal infection. Study on the perinatal transmission of hepatitis B infection in a large population of HBsAg positive maternal carriers suggest that the risk of vertical transmission of HBV infection is greatest when the mother has a high titer of HBsAg, is e-antigen positive, and has transmitted hepatitis to previous children. Maternal carriers who were e-antigen negative with anti-e did not transmit hepatitis B. In view of the high incidence of the hepatitis B carrier state in some African and Asian population, vertical transmission may be of considerable epidemiologic importance (Tierney, 2000, p. 357; CDC, 1991, p. 3).

Perinatal transmission from mother to infant at birth is very efficient. If the mother is positive for both HBsAg and HBeAg, 70% to 90% of infants will become infected, and up to 90% of these infected infants will become HBV carriers. An estimated 25% of these carriers will ultimately die of liver failure secondary to chronic active hepatitis, cirrhosis, or primary hepatocellular carcinoma. The risk of perinatal transmission from a woman who is positive for HBsAg only is estimated to be 20%, with 90% of infected infants becoming carriers (Kawai, 2000, p. 1287). The HBV virus is transmitted by parenteral or mucosal exposure to HBsAg- positive body fluids from persons who are carriers or have acute HBV infection. The highest concentrations of virus are in blood and serous fluids; lower titers are found in other fluids, such as saliva and semen. Saliva can be a vehicle of transmission through bites; however, other types of exposure to saliva, including kissing, are unlikely modes of transmission. There appears to be transmission of HBV via tears, sweat, urine, stool, or droplet nuclei. Direct percutaneous inoculation of HBV by needles during injection drug use is an important mode of transmission. Transmission of HBV may also occur by other percutaneous exposure, including tattooing, ear piercing, and acupuncture, as well as needle-sticks or other injuries from sharp instruments sustained by medical personnel; however, these exposures account for only a small proportion of reported cases in the United States. Breaks in the skin without overt needle puncture, such as fresh cutaneous scratches, abrasions, burns, or other lesions, may also serve as routes for entry (Bonham, 2000, p. 86; CDC, 1992, p. 823).

In United States, the most important route of transmission is by sexual contact, either heterosexual or homosexual, with an infected person. Fecal-oral transmission does not appear to occur. However, transmission among homosexual men occurs possibly via contamination from asymptomatic rectal mucosal lesions at sites of sexual contact. Contamination of mucosal surfaces with infective serum or plasma may occur in mouth pipetting accidents, accidental eye splash, or other direct contact with mucous membranes of the eyes or mouth, such as hand to mouth or hand to eye when contaminated with infective blood serum. Transfer of infective material to skin lesions or mucous membranes via inanimate environmental surfaces may occur by touching surfaces of various types of hospital equipment. Contamination of mucosal surfaces with infective secretions other than serum or plasma could occur with contact involving semen (Briggs, 1994, p. 140).

Hospital personnel, particularly operating room staff, dialysis unit staff, and laboratory technicians, who handle blood, have an increased risk of accidental parenteral exposure to hepatitis B virus. Serologic evidence of previous hepatitis infection was found in 16.8% of health care personnel and in only 8.7% of control group matched for age, sex, and socioeconomic status (Tierney, 2000, p. 340). HBsAg has been detected in mosquitoes and bedbugs collected from West Africa, where there is a high incidence of endemic hepatitis B infection. Although not yet documented, arthropod transmission of hepatitis B virus is possible in tropical areas (Schumacher, 1999, p. 4; Scapa, 1989, p. 402; Sebastian, 2001, p. 23).

Therefore, the outcome of chronic liver disease is often cirrhosis or liver cancer. The clinical course of acute hepatitis B is indistinguishable from that of other types of acute viral hepatitis (Guyton, 1991, p. 541; Bates, 1995, p. 112). The incubation period ranges from 45 to 160 days (average, 120 days). Clinical signs and symptoms occur more often in adults than in infants or children, who usually have an asymptomatic acute course. However, approximately 50% of adults who have acute infections are asymptomatic. When symptoms occur in acute HBV infection, they may occur in the following patterns. Acute viral hepatitis is commonly a mild disease without jaundice, particularly in those with relative immunity from previous infection, or in infants and children. Infection may be followed by a mild illness without clinical evidence of hepatitis, a rise in viral antibody titer or transiently positive test for HBsAg may be the only evidence of infection. In many subjects exposed to either of the viral agents. There is evidence of hepatitis without jaundice-anicteric hepatitis. Icteric hepatitis is usually a short, uncomplicated illness, but sometimes has a prolonged course. Acute exacerbations may follow complete recovery (Thomas, 1994, p. 56).

The symptoms of an icteric hepatitis are similar to those of many other viral infection, the onset of disease may resemble the prodromal period of icteric hepatitis. The diagnosis is suspected only in epidemic situations, in patients exposed to known patients exposed to known infection, or in those who develop tender enlargement of the liver. A diagnosis is confirmed by liver biopsy. There is often slight hyperbilirubinemia with an increase in urinary urobilinogen and bilirubin (Goldman, 2000, p. 642).

The serum enzyme changes are most helpful in diagnosis, serum transaminase and dehydrogenase levels are elevated, and serum alkaline phosphatase and 5-nucleotidase may be slightly increased. On liver biopsy, the hepatic lesion is indistinguishable from that of icteric hepatitis except for the absence of bile stasis. The preicteric phase of nonspecific constitutional and gastrointestinal symptoms varies in duration from a few days to several weeks. These symptoms may mimic those of other viral infections of the respiratory or gastrointestinal tract (Beare, 1991, p. 487).

Fever is usually most pronounced at the onset, and may be accompanied by a shaking chill; it is unusual, however, for shaking chills to be recurrent, although fever may persist until the early icteric phase. Anorexia, weakness, headache, and myalgia are common symptoms. During this phase, the liver may become enlarged and tender and the urine becomes discolored with bilirubin (Wakefield, 1998, p. 637).

Gastrointestinal symptoms which include anorexia, nausea, and vomiting with right upper abdominal discomfort, usually increase during the early period of increasing jaundice, the liver become more enlarged and tender, and the spleen may be palpable (Beare, 1991, p. 485). Fever usually subsides a few days after the onset of jaundice. Within a few days of hospitalization and bed rest, nausea subsides, and the appetite improves in most patients. Typically, the patient is maximally jaundiced within two weeks, and thereafter clinical jaundice and serum bilirubin levels gradually return to normal within six weeks. Hepatic enlargement may subside with symptomatic improvement, but often persists during the icteric period. Liver enlargement usually persists during the period of jaundice, whereas hepatic tenderness is usually observed early in the acute illness (Goldman, 2000, p. 641; Rosen, 2000, p. 478).

Some patients with otherwise typical acute viral hepatitis may remain icteric with hepatic enlargement and abnormalities of liver function for a period of several months. A liver biopsy is indicated in such patients to confirm a diagnosis of chronic persisting hepatitis, the histological feature of typical viral hepatitis in spite of the prolonged clinical course indicate an excellent prognosis for full recovery (Goldman, 2000, p. 640).

HBV infection is a major cause of acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma worldwide. Globally, it is estimated that at least 300 million persons clinically die each year from hepatitis B associated with acute and chronic liver disease (Goldman, 2000, p. 639; Francis, 1995, p. 1242; Margolis, 1991, p. 86). The world can be divided into three areas according to the prevalence of chronic HBV infection. Areas where there is a high prevalence (>8% of the general population is hepatitis B surface antigen HBsAg positive) include China, Southeast Asia, most of Africa and the Middle East, most Pacific Islands, some Caribbean Island and the Amazon River Basin. Areas where there is a moderate prevalence (2% to 7% of the general population is HBsAg positive) include most of Central and South America, the Mediterranean, India, Eastern and Southern Europe, the Soviet Union and Japan. Areas where there is a low prevalence (<2% of the general population is HBsAg positive) include most of the United States, Canada, Western Europe, and Australia (Tierney, 2000, p. 351).

Hepatitis has been reportable in the U.S.A. for many years. Hepatitis B became reportable as a distinct entity during the 1970's, after serologic tests to differentiate different types of hepatitis became widely available (Maynard, 1990, p. 519). Approximately 20,000 cases of hepatitis B are reported annually in the U.S.A.; However, HBV infection is greatly under reported, due primarily to the high proportion of infections that are a non-asymptomatic or non-icteric (Alter, 1990, p. 1219).

More accurate estimates of the magnitude of HBV infection are derived from areas of intensive clinical serologic surveillance for hepatitis. Data from these areas suggest that estimated 200,000-300,000 persons in the United States become infected with HBV each year, and also an estimated one to one and a quarter million persons are chronically infected with it (Atkinson, 1995, p. 22). The estimated incidence of HBV infection rose in the late 1970's through the mid 1980's from approximately 40 cases per 100,000 population in 1970 to the peak of 70 cases per 100,000 population in 1985. Since that time, incidence has gradually decreased to approximately 40 per cases per 100,000 in 1992 (Sherman, 2000, p. 7). Over 80% of acute HBV infections occur among adults. Adolescents account for approximately 8% of infection, and children and perinatal transmissions account for approximately 4% each (Thompson, 1994, p. 56). The most common risk factors for HBV infection in the U.S.A. is sexual contact, either heterosexual (41%) or homosexual (9%), injection drug use accounts for (15%) of cases, 2% of cases occur by household contact with a chronic carrier, and health care workers account for 1% of cases. Approximately 31% of all persons with HBV infection have no known risk factor infection (Atkison, 1995, p. 23). Although HBV infection is uncommon among adults in the general population (the lifetime risk of infection is <20%), it is highly prevalent in certain groups (Thomas, 1994, p. 59).

Risk of infection varies with occupation, life style, or environment. Generally, the highest risk for HBV infection is associated with lifestyle, occupation, or environments in which contact with blood from infected persons is frequent. In addition, the prevalence of HBV markers for acute or chronic infection increases with increasing number of years of high risk behavior. For instance, an estimated 40% of injection drug users become infected with HBV after one year of drug use, while over 80% are infected after 10 years (Atkinson, 1995, p. 18).

The risk of health care workers contraction HBV infection depends on how often they are exposed to blood or blood products through percutaneous and permucosal exposures. Any healthcare or public safety workers may be at risk for HBV exposure depending on the tasks performed. If those tasks involve contact with blood or blood contaminated body fluids, then such workers should be vaccinated. Risk is often highest during training periods. Therefore, it is recommended that vaccination be completed during training in schools of Medicine, Dentistry, Nursing, Laboratory, Technology and other allied health professions (Lanphear, 1994, p. 437; Taras, 1994, p. 122; Thomas, 1992, p. 1).

The role of laboratory tests in establishing a diagnosis has gained increasing importance as newer methods of detection and analysis become available. Each of the type of viral hepatitis described in this learning activity has specific tests for the virus and/or the antibody to the virus. The severity of the impact of these viruses upon the liver is measured by less specific tests of general liver function. Patterns of abnormality in liver function tests rather than specific values of a single test permit the clinician to interpret the functional status of the liver. In addition, it is important to note that diseases that are not hepatic in origin can produce abnormalities in liver function tests. These include but are not limited to hemolytic disease as well as congestive heart failure, sepsis, and other disorders that alter liver perfusion.

Though viral hepatitis can occur without the presence of jaundice, jaundice has historically been considered a diagnostic marker for hepatitis. Jaundice results from elevations in the serum bilirubin. The normal level for total serum bilirubin is less or equal 1.6 mg/dl. In order for clinical jaundice to occur, the total serum bilirubin must exceed 2.5 mg/dl. A total serum bilirubin level less than 10 mg/dl is usually found in viral hepatitis; level higher than this are typically indicative of hepatic carcinoma or biliary obstruction (Wallach, 1992, p. 562).

Elevations in the liver enzymes alanine aminotransferase (ALT), formerly known as serum glutamic pyruvic transaminase or SGPT, and aspartate aminotransferase (AST). Formerly called serum glutamicoxaloacetic transaminase or SGOT occur in response to inflammation of the hepatic cells. The source of this inflammation is most often viral hepatitis or chemical injury.

The chemical injury may be due to drug therapy, alcohol ingestion, poisoning with substances such as acetaminophen or carbon tetrachloride. Elevations in ALT and AST are also associated with centrolobular necrosis due to inadequate perfusion in shock states and in cases of biliary obstruction. The normal range for ALT is 5 to 35 units/l ml; the normal range for AST is 5 to 40 units/l ml. Albumin levels are typically decreased inhepatocellular disease such as hepatitis but are unchanged in uncomplicated obstructive liver disease. Alkaline phosphatase levels remain in normal range in hemolytic disease, are slightly elevated in hepatocellular disease, and are greatly increased in obstructive liver disease (Gladwin, 1995, p. 24).

The diagnosis of HBV infection is generally made on the basis of serology. Virtually all individuals infected with HBV, either acute or chronically, will have detectable serum hepatitis B surface antigen (HBsAg). In acute infection, HBsAg is detectable several weeks after infection and its appearance coincides with the onset of clinical symptoms. HbsAg is also detectable in acute infection which is characterized by a high rate of viral replication. At around the same time, IgM antibodies against core antigen are detectable in serum. Subsequently, IgG antibodies against core are produced. As acute infection resolves, IgG antibodies against core antigen persist and IgM antibodies and HBsAg become undetectable. Subjects who develop an immune response against HBV develop antibodies against HBsAg. Such antibodies are also produced by vaccination.

Most people who have had acute infection that resolves continue to have IgG antibodies against core antigen for life. Some remain immune with antibodies against HBsAg but some lose these antibodies and may be susceptible to future infection (Kawai, 2000, p. 1290). Acutely infected individuals who do not clear HBV continue to have serum HBsAg. In most cases, the chronic infection becomes “non-replicate” and the subjects lose serum HBeAg and develop antibodies against HBeAg. In some cases, “replicate” infection persists along with detectable serum HBeAg. In chronically infected individuals, infection can switch from “non-replicate” to “replicate” and vice-versa. One goal of treatment is to convert patients with chronic hepatitis B from a “replicative” (HBeAg positive) to “non-replicative” (HBeAg negative) state (Foster, 2001, p. 6). HBsAg is the most commonly used test for diagnosing acute HBV infection or detecting carriers. HBsAg can be detected as early as 1-2 weeks and as late as 11-12 weeks after exposure to HBV when sensitive assays are used. The presence of HBsAg indicates that a person is infectious, regardless of whether the infection is acute or chronic (Foster, 2001, p. 6).

Anti-HBc (core antibody) develops in all HBV infections, appears shortly after HBsAg in acute disease, and indicates HBV infection at some undefined time in the past. Anti-HBc only occurs after HBV infection, and does not develop in persons whose immunity to HBV is from vaccine. Anti-HBc generally persists for life and therefore is not a serologic marker for acute infection (Foster, 2001, p. 6; Dolin, 1999, p. 48). IgM anti-HBc appears in persons with acute disease about the time of illness onset and indicates recent infection with HBV. IgM anti-HBc is generally detectable 4 to 6 months after onset of illness and is the best serologic marker of acute HBV infection. A negative test for IgM anti-HBc together with a positive test for HBsAg in a single blood sample identifies a chronic HBV infection. HBeAg is a useful marker associated strongly with the number of infective HBV particles in the serum and a higher risk of infectivity (Dolin, 1999, p. 49). Anti-HBs (surface antibody) are a protective, neutralizing antibody. The presence of anti-HBs following acute HBV infection generally indicates recovery and immunity from reinfection. Anti-HBs can also be acquired as an immune response to hepatitis B vaccine or passively transferred by administration of HBIG. Using radioimmunoassay (EIA), the manufacturer's recommended positive should be considered an appropriate measure of immunity. The level of anti-HBs may also be expressed in milli-international units/ml. Ten milli-international units/ml are considered to indicate a protective level of immunity (Foster, 2001, p 7; Dolin, 1999, p. 49).

In individuals suspected of having chronic hepatitis B, the appropriate screening test is for serum HBsAg. Individuals who may have chronic hepatitis B who should be considered for testing include: those with symptoms of chronic liver disease, those with abnormal laboratory tests suggesting liver disease, individuals from countries where HBV infection is endemic, those with risk factors such as intravenous drug use or unprotected promiscuous sex, children of HBV infected parents or household contacts, health care workers, and patients on hemodialysis.

Individuals with chronic hepatitis B are at increased risk for the developments of hepatocellular carcinoma. Although precise recommendations do not exist, it is reasonable for such individuals to undergo periodic screening for cancer. Screening procedures include measurement of serum alpha-fetoprotein (a tumor marker that is elevated in about 85% of individuals with hepato-cellular carcinoma) and ultrasound examination. The optimal frequency of such screening examinations has not been determined (Dolin, 1999, p. 50).

At the present time, alpha-interferon is the only drugs approved in the United States for the treatment of chronic hepatitis B. Treatment is recommended for individuals who have “replicative disease” (HBeAg positive). About 40% of such individuals will lose serum HBeAg after 16 weeks of treatment with interferon-alpha. Loss of HBeAg is correlated with an improved prognosis. A few treated patients (less than 10%) may even be cured as assessed by the loss of HBsAg (Michael, 1999, p. 432).

Hepatitis B vaccination has been available in the United States since 1981. However, the impact of vaccine on HBV disease has been less than optimal, and the incidence of reported hepatitis B cases is as high now as it was before the vaccine was available (Hanoelman, 1992, p. 265). The apparent lack of impact from the vaccine can be attributed to several factors. First, a large proportion of persons with HBV infection (25% to 35%) deny any risk factors screening approach. Second, the three major risk groups (heterosexuals with contact with infected persons or multiple partners, injection drug users, and homosexually active males) are not reached effectively by targeted programs. Deterrents to immunization of these groups include lack of awareness of the risk of disease and its consequences, lack of public sector programs and vaccine cost. Difficulty in gaining access to these populations is also a problem. Further, there has been limited success in providing vaccine to persons in high-risk groups due to rapid acquisition of infection after beginning high-risk behaviors, low initial vaccine acceptance and low completion rates (Francis, 1995, p. 1243; Waterman, 1994, p. 567).

A comprehensive hepatitis B prevention strategy is now being implemented which includes the following: The risk of health care workers acquired HBV infection depends on the frequency of exposure to blood or blood products and on frequency of needlesticks. These risks vary during the training and working career of each individual but are often highest during the professional training period. For this reason, it is recommended that vaccination be completed during training in schools. The risk of HBV infection for hospital personnel can vary both among hospitals and within hospitals. In developing specific immunization strategies, hospitals should use available published data about the risk of infection and may wish to evaluate their own clinical and institutional experience with hepatitis B. Studies in urban centers have indicated that occupational groups with frequent exposure to blood and/or needles have highest risk of acquiring HBV infection, including (but not limited to) the following groups: medical technologists, operating room staff, phlebotomists and intravenous therapy nurse, surgeons and pathologists, and oncology and dialysis unit staff. Groups shown to be at increased risk in some hospitals include: emergency room staff, nursing personnel, and staff physicians (Margolis, 1997, p. 88). Other healthcare workers based outside hospitals that have frequent contact with blood or blood products are also at increased risk of acquiring HBV infection. These (but are not limited to): dental professionals (dentists, oral surgeon, and dental hygienists), laboratory and blood bank technicians, dialysis center staff, emergency medical technicians, and morticians.

Susceptible clients and staff who work closely with clients of institutions for the mentally retarded should be vaccinated. Risks for staff are comparable to those for healthcare personnel in other high-risk environment. However, the risk in institutional environments is associated, not only with blood exposure, but also with bites and contact with skin lesions and other infective secretions. Susceptible clients and staff who live or work in smaller (group) residential settings with known HBV carriers should also receive hepatitis B vaccine (Lemon, 1995, p. 1481).

Numerous studies have established the high risk of HBV transmission in hemodialysis units. Although recent data have shown not only a decrease in the rate of HBV infection in hemodialysis units but also a lower vaccine efficacy in these patients, vaccination is recommended for susceptible patients. Environmental control measure and regular serologic screening (based on immune status) of patients should be maintained (Lemon, 1995, p. 1485).

Susceptible homosexually active men should be vaccinated regardless of their ages or duration of their homosexual practices. It is important to vaccinate persons as soon as possible after their homosexual activity begins. Homosexually active women are not at increased risk of sexually transmitted HBV infection.

All users of illicit injectable drugs who are susceptible to HBV should be vaccinated as early as possible after their drug use begins. Patients with clotting disorders who receive clotting factor concentrates have an elevated risk of acquiring HBV infection. Vaccination is recommended for these persons and should be initiated at the time their specific clotting disorder is identified. Screening is recommended for patients who have already received multiple infusions of these products.

Household contacts of HBV carriers are at high risk of acquiring HBV infection. Sexual contacts appear to be at greatest risk. When HBV carriers are identified through routine screening of donated blood, diagnostic testing in hospitals, prenatal screening, screening of refugees, or other screening programs, they should be notified of their status and their susceptible household contacts vaccinated. Families accepting orphans or unaccompanied minors from countries of high HBV endemic should have the child screened for HBsAg, and if positive, family members should be vaccinated.

Persons in casual contact with carriers at schools, offices, etc., are at minimal risk of acquiring HBV infection, and vaccine is not routinely recommended for them. However, classroom contacts of deinstitutionalized mentally retarded HBV carriers who behave aggressively or have special medical problems that increase the risk of exposure to their blood or serous secretions may be at risk. In such situations, vaccine may be offered to classroom contacts. Some American populations, such as Alaskan Eskimos, native Pacific Islanders, and immigrants and some refugees from areas with highly endemic disease (particularly eastern Asia and sub-Saharan Africa) have high HBV infection rates. Depending on specific epidemiologic and public health considerations, more extensive vaccination programs should be considered.

The prison environment may provide a favorable setting for the transmission of HBV because of the frequent use of illicit injectable drugs and homosexual practices. Moreover, it provides an access point for vaccination of parenteral drug abusers. Prison officials should consider undertaking screening and vaccination programs directed at those who abuse drugs before or while in prison.

Heterosexually active persons with multiple sexual partners are at increased risk of acquiring HBV infection; risk increases with increasing sexual activity. Vaccination should be considered for persons who present for treatment of sexually transmitted disease and who have histories of sexual activity with multiple partners. Vaccination should be considered for persons who plan to reside more than six months in areas with high levels of endemic HBV and who will have close contact with the local population. Vaccination should also be considered for short-term travelers who are likely to have contact with blood from or sexual contact with residents of areas with high levels of endemic disease. Hepatitis B vaccination of travelers ideally should begin six months before travel in order to complete the full vaccine series; however, a partial series will offer some protection against HBV infection.

A plasma derived vaccine was licensed in the U.S.A. in 1981. It was produced from HBsAg particles purified from the plasma of human carriers. The vaccine was safe and effective, but was not well accepted, possibly because of unbiased fears of transmission of the live HBV and other bloodborne pathogens. This vaccine was removed from U.S.A. market in 1992 (Damme, 1995, p. 27; Waterman, 1994, p. 568). Recombinant vaccine is produced by inserting a plasmid containing the gene for HBsAg, which is harvested and purified. The recombinant vaccine contains over 95% HBsAg protein (5 to 40 meg/ml); yeast-derived proteins may constitute up to 5% of the final product, but no yeast DNA is detectable in the vaccine (Waterman, 1994, p. 568; Wright, 1993, p. 1340).

HBV infection cannot result from use of the recombinant vaccine, since no potentially infectious viral DNA or complete viral particles are produced in the recombinant system. Vaccine HBsAg, is absorbed to aluminum hydroxide, and thimerosal is added as a preservative (Damme, 1995, p. 27). After three intramuscular doses of hepatitis B vaccine, over 90% of healthy adults and over 95% of infants, children and adolescents (from birth to 19 years of age) develop adequate antibody responses. The vaccine is 80% to 100% effective in preventing infection of clinical hepatitis in those who receive the complete course of vaccine. Large vaccine doses (2 to 4 times the normal adult dose) or an increased number of doses are required to induce protective antibody in high proportion of hemodialysis patients and also may be necessary in other immunocompromised persons (Kew, 1995, p. 1065; Wright, 1993, p. 1342). The recommended dosage of vaccine utilized may differ depending on the age of the recipient, certain exposure circumstances, and type of vaccine. Hemodialysis patients should receive a 40 meg/ml dose in a series of three or four doses. One of the vaccines (Recomb-Beeves H) has a special dialysis patient formulation that certain 40 meg (Kew, 1995, p. 1067). The deltoid muscle is the recommended site for hepatitis B vaccination in adults and children, while the anterolateral thigh is recommended for infants and neonates. Immunogenicity of vaccine in