The Epidemiology Of Hepatitis B in Canada

Prevalence of Hepatitis B

The precise prevalence of hepatitis B in Canada is unknown. Although some have estimated the prevalence to be about 0.5% Р1.0%, this is, at best, an educated guess. Furthermore, although clinical practice indicates that hepatitis B is not uniformly distributed in the community, the prevalence in different ethnic or occupational, or other risk groups has not been well defined. Specific population groups can be identified, in whom the prevalence is much higher than the national average. Most easily identifiable of these are immigrants from South East Asia and Africa, but other immigrant groups also have a higher than expected prevalence of the hepatitis B carrier. Vietnamese refugees in Montreal, were shown to have a hepatitis B carrier rate of 11.7%.1 Table 1 provides a conservative estimate of the prevalence of hepatitis B in different immigrant groups in Canada. The figures are derived by taking a conservative estimate of the prevalence of hepatitis B in the home countries of the different population groups, and multiplying that rate by the number of immigrants from that part of the world, as estimated by Statistics Canada. Thus, this is likely to be a conservative estimate of the number of hepatitis B carriers in Canada.

Incidence of Hepatitis B Infection

New hepatitis B infections have been reported to the provincial health authorities at the rate of about 3000 cases/year (see Figures 1 A & B). These figures likely represents a large underestimation, since only patients with symptomatic infections would present to a physician for testing in the first place. It has been variously estimated that acute hepatitis case reporting underestimates the incidence of new infections by as much as 50% or more. In Canada, until recently, only acute hepatitis B was notifiable. Thus all positive hepatitis B surface antigen results were reported to the health authorities by the laboratories, but only data on acute hepatitis B were kept. There is no method available to determine the number of new chronic infections.

Transmission of Hepatitis B

Hepatitis B is spread by contact with blood and blood products or body fluids. Common routes of infection are perinatal (or vertical), between young children in endemic communities, parenteral exposure either through intravenous drug use (IVDU) or occupational exposure Transmission by blood transfusion is now rare, whereas before screening of donor blood, it was not uncommon.

The exact mechanism of perinatal transmission is not clear. It is unusual for infants to be infected in utero. Cord blood is usually negative for hepatitis B markers; however, occasionally intrauterine infection does occur. Fetal blood sampling may increase this risk, but amniocentesis does not appear to enhance the risk of intrauterine transmission.3 Infection presumably occurs at or soon after birth. Perhaps birth trauma is important. Perhaps transmission occurs through breast milk, as it is known to carry hepatitis B. Transmission could occur if there was an inapparent breach in the mucosa of the mouth, or during teething.

Perinatal transmission, in the era before vaccination, was a major source of infection in endemic areas. Mothers carrying the hepatitis B e antigen, (i.e. who were carrying actively replicating virus) could transmit disease to their offspring in more than 90% of cases.4-6 Mothers carrying antibodies to the e antigen (anti-Hbe) transmitted disease in about 25% of cases. Vaccination of hepatitis B carrier mothers, which is standard practice in many endemic areas of the world has prevented more than 90% of this transmission.

Horizontal transmission between young children is well documented. Historically, hepatitis B was common in institutions for the care of mentally retarded children. More recently, horizontal transmission has been documented in endemic areas. In Africa, the prevalence of hepatitis B markers increases with age, from age one to five years.7-8¬†In South East Asia, horizontal transmission accounts for up to 33% of all transmission.9¬†Once again, the exact mechanisms are not defined. In Africa, transmission is though to be related to impetigo or scabies in young children who play together. This mechanism may also be present in South East Asia, but transmission in junior school has also been documented. Other possible sources of infection include an infected parent kissing the cut finger or scraped knee of a young child, and sharing of items of personal hygiene between parents and children, (e.g., safety pins which have been in the parent’s mouth inadvertently pricking the infant, etc.).

The extent to which horizontal transmission occurs in Canada is unknown. It is likely that as socioeconomic standards rise, transmission to young children decreases. Good data from elsewhere suggested that most of hepatitis B markers fall in the second and subsequent generations of immigrants. Nonetheless, there is a likelihood that horizontal transmission does occur to some extent. In the US, this has been studied in a Vietnamese refugee community. At age ten, seven percent of the children of non-carrier mothers were themselves carriers.10 These children must have been infected from sources other than their mothers.

Among young adults transmission is most frequently via sexual contacts or IVDU. Indeed, notifications of acute hepatitis B in Canada support this finding (see Figure 2). This data is similar to the findings of the National Health and Nutrition Evaluation Study (NHANES) performed in the US in the 1970’s,11¬†and is the basis for the recommendation that hepatitis B vaccination be given to all pre-adolescents.

Risk of sexual transmission of hepatitis B increases with the number of partners. Several studies have demonstrated in different groups, that the prevalence of hepatitis B markers increase dramatically in subjects who have more than three partners in six months. Similarly, prevalence of hepatitis B markers increases in subjects who have other sexually transmitted diseases (see Table 2)

Identification of Risk Groups

It is clear that hepatitis B is not uniformly distributed. Specific risk groups can be identified, based on the known epidemiological characteristics of the disease. These are listed in Table 3. Some of these risk groups are obvious, such as ethnic origin. Others require careful inquiry on history. Inquiry about intravenous drug use and a sexual history should be part of the initial encounter with all patients. However, these are sensitive subjects, and the patient may not be prepared to reveal such sensitive information at the first meeting. It is therefore worth repeating the inquiry somewhat later, when the relationship between the doctor and patient has been better established.

Identification of a risk factor for infection indicates that the individual either may have been infected previously, or may not have been previously infected, but remains at risk for future infection. Evaluation of these patients therefore, includes testing for previous infection.

From a public health perspective, the question of testing for hepatitis B markers before vaccination depends on the expected prevalence of the hepatitis B carrier state in the target population. Economic analysis has shown that if the prevalence of HBsAg is above two percent, screening for hepatitis B is the preferred strategy. If the prevalence is less than two percent, vaccination without screening is preferred.20 However, this strategy does not identify those who are already infected and are carriers.

In order to test for previous infection and the carrier state there are two possible strategies, and to date, it is not clear which is the most efficient and cost effective. Testing can either be for antibodies to the core antigen (anti-HBc), or for HBsAg and anti-HBs. If anti-HBc is positive then further testing for HBsAg and anti-HBs is required. Patients who are negative for anti-HBc (or both anti- HBs and HBsAg), and who remain at risk for hepatitis B require vaccination (see Figure 3).

Testing of Contacts

Once an acutely or chronically infected individual has been identified, contact tracing and testing has to be undertaken. This is usually carried out by provincial health authorities, although they tend only to deal with acute hepatitis B. For acute hepatitis B, testing of the sexual partner is most important. If the patient is an IVDU, testing of those who shared needles is necessary. This is not always possible, given that the user may have injected in a “shooting gallery” where contacts are usually anonymous. Similarly, in prostitutes and other individuals with multiple sexual partners, tracing may not be possible. One should always bear in mind the possibility of late infection from a family member. This is particularly true when grandparents become infected from a grandchild. This situation is most frequently seen in endemic communities. Usually it is the father’s parents who become infected in the situation where a non-infected man has married an infected woman. The man’s parents are also likely to be uninfected, but the mother’s parents may well have been infected previously. The mother passes the disease to her baby, and the baby in turn infects a previously uninfected grandparent.

If the disease in the index case is chronic, then testing must include the sexual partner(s), and the entire extended family, including siblings, parents and children. In this case the testing protocol is directed at identifying the possible source of the infection, as well as those who may have been infected by the index case.

Patterns of Infection

Whether an individual infected with hepatitis B becomes a carrier or not depends largely on the age at which the infection was acquired. In infants, initial infection is asymptomatic in nearly 100% of cases. More than 90% of infants so infected become chronic carriers.12 The carrier rate in children from ages five to ten is about 40%. The carrier rate in otherwise healthy young adults is controversial. Older estimates suggest that 10% of infected adults become carriers. Newer data suggest that the carrier rate may be less than five percent,13 and possibly less than one percent,14 however, in order adults the carrier rate increases again.

In chronic infections acquired in childhood the disease is usually asymptomatic for many years, despite periods of active hepatitis.15-17 Outcome of disease depends on numerous factors, including gender and ethnic origin. Hepatocellular carcinoma is very common in South East Asian and African male hepatitis B carriers.18-19 It has been estimated that up to 25% of Chinese male hepatitis B carriers who developed the disease in childhood will die of hepatocellular carcinoma. This cancer is less common in women from these areas, and possibly in men from other parts of the world.

Chronic infections acquired in adulthood, in contrast, tend to be more aggressive, frequently causing death from hepatitis and liver failure within seven to ten years.


The epidemiology of hepatitis B in Canada is important in understanding the disease, its risk factors, and who to test for this disease. Populations at greater or lesser risk of hepatitis B can be identified by a number of features, and these factors should be taken into account in assessing patients for this disease.

Hepatitis G

The hepatitis G virus has recently been identified. Existence of this virus was suspected when, after development of an assay for hepatitis C, residual cases of unexplained post transfusion hepatitis, persisted. These were patients with elevation of liver enzymes, some with biopsies which were compatible with viral hepatitis, yet who were negative for anti-bodies to hepatitis C (anti-HCV) and hepatitis CRNA, and no other cause of liver disease could be identified. Using technology initially developed to isolate hepatitis C viral RNA, researchers undertook to determine whether there was viral material present in the serum of such patients. While isolation of hepatitis C RNA, and initial characterization of the virus and disease took about five years, the process for hepatitis G took about one year.

Nucleic acids (genetic material) were extracted from the serum of patients with suspected non- ABC post-transfusion hepatitis. Initially it was not known whether the genetic material was DNA or RNA. A step was included which transformed all RNA to DNA (reverse transcription), and then whatever DNA was present was cloned into vectors which allowed the DNA to be expressed as proteins or peptides. If viral genetic material was present in the original sample, then it could be expected that viral proteins or peptides would be expressed from one or more of the clones produced. To detect these proteins/peptides corresponding to sequences from the putative virus, serum from infected patients, presumed to contain antibodies to at least some of the viral proteins/peptides, was incubated with the proteins/peptides produced from the cloned DNA particles. In this manner an RNA sequence was identified which was of non-human origin. This RNA sequence was then used to clone further RNA sequences, which turned out to be of viral origin. By investigation of several clones the structure of the whole virus was established.

About the same time another group isolated three putative viral strains called GBV 1, 2 and 3 from the serum of a surgeon apparently infected with a non-ABC hepatitis virus. Hepatitis G and GBV 1 and 2 remain undefined.

The new virus, named hepatitis G (hepatitis F is a putative virus found in some patients with fulminant hepatitis), is an RNA virus, a member of the flaviviridae family (as is hepatitis C). The virus has about 25% homology to hepatitis C, but is sufficiently different that it can be classified as a separate virus.

Transmission is via parenteral routes, (e.g., transfusion), but the epidemiology has not yet been worked out. The infection has been identified in patients with community acquired viral hepatitis, and in patients with unexplained liver disease. Cirrhosis has been documented in patients in whom no other cause for liver disease can be found, and it is presumed that hepatitis G can cause such chronic liver disease. At present however, the frequency with which this virus causes cirrhosis has not been established. The rate is likely to be low, since 80% to 90% of cryptogenic cirrhosis has been shown to be due to hepatitis C. A carrier state with normal liver enzymes and normal liver biopsy also exists.

With the currently available information we can say that this virus can cause serious liver disease, but it is likely that cirrhosis will be less frequent than in hepatitis C. Furthermore, hepatitis G is unlikely to account for a large proportion of the burden of liver disease in the community.


1. Chaudhary RK, Nicholls et al. Can Med Assoc J 1981;125:1243-6.

2. Grosheide PM, Quartero HW et al. Prenatal Diagnosis 1994;14(7):553-8.

3. Ko TM, Tseng LH et al. Arch of Gyn Obst 1994;255(1):25-30.

4. Beasley RP, Trepo C, et al. Am J Epid 1977;105:94.

5. Okuda K, Kaniyama 1, et al. N Eng J med 1976;294:746.

6. Stevens CE, Beasley RP et al. N Eng J Med 1975;292:7714.

7. Botha JF, Ritchie MJ et al. Lancet 1984;1(8388):1210-2.

8. Proszesky OW, Szmuness W et al. S African Med J 1983;64:891-3.

9. Beasley RP, Hwang LY et al. J Inf Dis 1982;146:198-204.

10. Franks AL, Berg CJ et al. N Eng J Med 1989;321:1301-5.

11. McQuillan GM, Townsend TR et al. Am J Med 1989; Suppl 3A:55-10S.

12. Stevens CE, Taylor PE et al. JAMA 1987;257:2612-6.

13. Tassopoulos NC, Papaevangelou GJ et al. Gastroenterology 1987;92:1844-50.

14. Seef LB, Beebe GW et al. N Eng J Med 1987;316:965-70.

15. Lok AS, Lai CL. J Hepatol 1990;10:29-34.

16. Lok AS, Lai CL. Hepatology 1988;8:1130-3.

17. Lok AS, Lai CL et al. Gastroenterology 1987;92:1839-43.

18. Beasley RP, Hwang LY et al. Lancet 1981;2:1129-33.

19. McNab GM, Urbanowicz JM et al. BJ Cancer 1976;33:544-8.

20. Mulley AG, Silverstein MD, N Eng J Med 1982;307:644-52.

Sharing is caring!

Leave a Comment