Chapter 29 Viral hepatitis
A clear understanding of viral hepatitis is essential for all dental practitioners, particularly in view of the serious sequelae of the disease and the potential of transmitting the infection in the dental clinic. Hepatitis can be due to a number of causes, such as infections, alcohol abuse, trauma or drug-induced toxicity. However, in global terms, viral infections are by far the single most important agent of hepatitis. These include infections with herpes simplex virus, cytomegalovirus and Epstein–Barr virus, but the vast majority of viral liver diseases are one of the following:
Data from the World Health Organization (WHO) indicate that viral hepatitis B infection alone accounts for more than 1 million deaths worldwide. In terms of morbidity, there are around 350 million hepatitis B chronic carriers and another 100 million chronic carriers of hepatitis C.
The various types of viral hepatitis differ in severity of infection, morbidity, mortality rate, presence or absence of a carrier state and frequency of long-term sequelae such as cirrhosis and cancer. The main differences between the hepatitides caused by these viruses are shown in Table 29.1.
The common symptoms and signs of hepatitis include malaise, jaundice, dark urine and pale, fatty stools. These, together with results of serum and urine biochemistry and specific serology tests, facilitate the diagnosis of viral hepatitis. Investigation typically reveals abnormal liver function with raised levels of serum transaminases and bilirubin, and bilirubinuria. Specific serological tests are now available to detect hepatitis A, B, C, D and E antibodies.
The hepatitis A virus (HAV) is a small (27 nm) RNA virus belonging to the picornavirus group (which also includes poliovirus and coxsackieviruses). The virus is inactivated by ultraviolet light, exposure to water at 100°C for 5 min and by exposure to 2% glutaraldehyde for 15 min.
Hepatitis A commonly occurs in developing parts of the world where sewage disposal measures and food hygiene are unsatisfactory. Only 10–13% of the population in developed countries has been exposed to the virus by the age of 20 years. It is usually contracted by the faecal–oral route from contaminated food and water. Children and young people are most often infected, and for this reason, a history of hepatitis in childhood would, in most instances, be indicative of a hepatitis A infection.
Jaundice is common in adults and rare in young children. There are no chronic sequelae. Some patients continue to excrete HAV in faeces during weeks 1–3 of the illness, and HAV may also be present in saliva (100 particles per millilitre) throughout this period.
Diagnosis is by demonstration of HAV antigen in faeces. Serological tests demonstrate immunoglobulin M (IgM) class anti-HAV antibodies in serum during the acute or early convalescent phase (IgG class antibodies appear later in the disease and confer enduring protection against the disease).
Unlike hepatitis B, there is no carrier state associated with the disease. This, together with its faecal–oral transmission, implies that hepatitis A transmission in the dental clinic is highly unlikely.
Passive immunization by hyperimmune globulin is effective against clinical illness, particularly when administered in the early incubation period. However, the main use of short-term, pre-exposure prophylaxis is for travellers to hepatitis A-endemic areas, such as some parts of the developing world. Several vaccines of inactivated HAV produced in human cell culture are available. Immunization (two doses: initial and a booster 6–12 months after) is safe and effective and recommended for professionals working with institutionalized patients. A combined vaccine for hepatitis A and B is now available.
HAV is not a significant infection risk in dentistry as the route of transmission is faecal–oral. Close contact with saliva may transmit infection as saliva can contain some HAV. Rarely infection has been transmitted by needlestick injury, and there is a report of transmission from a surgeon to a patient. Standard infection control measures are adequate to prevent transmission in dental practice.
Being a hepatotropic virus, HBV will reside and multiply in hepatocytes after entering the body, and cause hepatic injury and inflammation (hepatitis) to varying degrees. When it multiplies in the hepatocytes, for some unknown reason, the virus particles described above are produced in different proportions within the liver cell cytoplasm. As a result of overproduction of these non-infectious spheres and tubules, which are the surface proteins of the virus (hence called hepatitis B surface antigens or HBsAgs), they circulate freely in the serum for prolonged periods after the acute hepatitis episode.
The central core of the HBV consists of a single-stranded DNA, an enzyme (DNA polymerase) and a core antigen (HBcAg). Although this antigen is rarely found in the serum, a breakdown product of HBcAg, termed hepatitis B ‘e’ antigen (HBeAg), may be found in the serum and is a marker of active infection.
The prevalence of hepatitis B varies greatly in different parts of the world: it is higher in African and Asian countries than in the Americas, Australia and western Europe (Fig. 29.2); in urban than in rural areas; and in men than in women. In developed countries, the risk of exposure to hepatitis B is high in certain categories of people, as shown in Table 29.2. Several variants of HBV are now known, and when these involve rearrangement of the surface antigens, existing vaccines may not be protective. This has come to light as a few individuals who had been successfully immunized against HBV but who were at high risk of infection nevertheless contracted hepatitis B. A variant HBV, HBV-2, has been described in West Africa, the Middle East, Spain, France, Taiwan, New Zealand and the USA, and another has been reported from Italy, Greece and the UK. Both variants are able to infect persons immunized against the usual form of HBV.
Selected patient groups
Patients requiring frequent large-volume transfusions of unscreened blood/blood products (e.g. in haemophilia)
Most patients who contract hepatitis B recover within a few weeks without any sequelae (Fig. 29.3). However, serological markers of previous HBV infection are invariably present in these patients for prolonged periods. Such markers take the form of antibodies to various components of the HBV. A minority (2–5%) fail to clear HBV by 6–9 months and consequently develop a chronic carrier state. This state more frequently follows anicteric HBV infection (i.e. infection without jaundice). The converse of this is that a majority of infections that lead to jaundice resolve without a carrier state; hence, a history of jaundice in a patient in most instances indicates little or no risk in terms of hepatitis B transmission.
The chronic carriers of hepatitis B infection fall into two main groups: those with chronic persistent hepatitis (the so-called ‘healthy carrier’ state) and those with chronic active hepatitis (Fig. 29.3). In chronic persistent hepatitis, the patient does not develop liver damage and is generally in good health, although the liver cells persistently produce viral antigen (HBsAg) because of the integration of the viral genome into the DNA of the hepatocytes. The second group of chronic carriers are extremely infectious as they harbour the infective Dane particles in their blood. In addition, they are very susceptible to cirrhosis and hepatocellular carcinoma. Nonetheless, the chronic active hepatitis group represents a small minority of hepatitis B patients. In general, infection with HBV leads to complete recovery in most individuals, while only about 2–5% develop a carrier state. These two disease states elicit characteristic serological profiles in the affected individual during various phases of the disease, as shown in Figures 29.4 and 29.5.
Fig. 29.4 Typical profile of hepatitis B serological markers after recovery from infection. HBsAg, hepatitis B surface antigen; HBeAg, hepatitis B ‘e’ antigen; anti-HBc, antibody to hepatitis B core antigen.
Diagnosis of HBV is complicated by the variety of serological markers and the complex sequelae of the disease itself. Table 29.3 summarizes the significance of the serological markers described below: