Recommendations for Hepatitis B Prophylaxis Following Percutaneous or Permucosal Exposure

In document Blue Book (Page 86-97)

Treatment When Source Found To Be:

Source not Tested

HBsAg-positive HBsAg-negative or Unknown

Exposed Person Unvaccinated

No treatment.

If known high-risk source, may treat as if source were HBsAg-positive.

No treatment.

If known high-risk source, may treat as if source were HBsAg-positive.

1. If inadequate, HB vaccine booster dose plus HBIG x1.

Previously Vaccinated Known sero-conversion

Known non sero-conversion

HBIG x 1* and initiate HB vaccine.

Test exposed for anti-HBs 1. If adequate**, no treatment.

2. If inadequate, HB vaccine booster dose.

HBIG x 2 or HBIG x 1 plus 1 dose HB vaccine.

Test exposed for anti-HBs.

1. IG inadequate,

HBIG x1 plus HB vaccine booster dose.

2. If adequate, no treatment.

Initiate HB vaccine.

No treatment.

No treatment.

Test exposed for anti-HBs.

2. If adequate, no treatment.

* Hepatitis B Immunoglobulin (HBIG). Adult dose 400 Units.

** An adequate antibody level is greater than 10 milli International Units per ml, approximately equivalent to 10 sample ratio units (SRU) by radio-immune-assay (RIA) or positive by enzyme-immuno-assay (EIA).

Unknown sero-conversion

Control of Case

Exclusion from school and work until the diagnosis is confirmed. Blood and body fluid precautions should be observed until the disappearance of HBsAg and the appearance of anti-HBs.

Control of Contacts

Household contacts should be tested for anti-HBc and HBsAg and offered vaccination if susceptible.

Sexual contacts should:

• Be offered HBIG (400 IU IM) within 14 days of sexual contact.

• Commence active immunisation at the same time.

Infants born to HBsAg positive mothers should:

• Be given HBIG (100 IU IM) within 12 hours of birth.

• Commence active immunisation within seven days.

This can be given at the same time as HBIG but at a separate site.

Preventive Measures

Pre-exposure vaccination is recommended for:

• Health care workers. Individual risk depends on HBsAg carrier rate in the population served, degree of blood (not patient) exposure, and thoroughness of hygiene measures in dealing with blood.

• Haemodialysis patients and recipients of blood prod-ucts such as factors VIII and IX.

• Residents and staff in institutions for the intellectually disabled.

• Those with multiple sexual contacts.

• Injecting drug users.

• Household and sexual contacts of hepatitis B virus carriers.

• Inmates of long-term correctional facilities.

Paediatric hepatitis B vaccine is given for:

• Infants of HBsAg positive mothers (as discussed above).

• Infants in ethnic groups of high HBsAg endemicity, whether the mother is a carrier or not.

• Children up to 10 years of age in both of the above groups.

WHO recommends that hepatitis B vaccine should be included in all childhood immunisation protocols.

Hepatitis C

Victorian Statutory Re q u i re m e n t

Group B notification.

Infectious Agent

Hepatitis C virus (HCV), a small RNA virus, is closely related to the flaviviruses and animal pestiviruses.

Clinical Features

Most patients with HCV are asymptomatic.

In the acute stage, patients develop elevated serum alanine aminotransferase (ALT) levels.

Up to 25 per cent of patients may develop jaundice.

Symptoms and signs, when they occur, are similar to other forms of hepatitis, but are usually milder than those seen in hepatitis B.

The majority of patients progress to the chronic carrier state that is also, in most cases, asymptomatic. Symp-toms, when they occur, may be non-specific and include fatigue, headaches and nausea.

Public Health Significance and O c c u r re n c e

Hepatitis C occurs worldwide.

The estimated prevalence in the Australian community based on blood donor screening is 0.14 to 0.45 per cent, but the percentage of HCV positive individuals is higher in certain groups, such as injecting drug users. In injecting drug users, seropositivity approaches 100 percent in those injecting for more than eight years.

Infection with HCV results in the chronic carrier state in over 70 per cent of cases.

Approximately 20 to 30 per cent of chronic carriers may progress to liver cirrhosis within a period of about 20 years, and a proportion of those with cirrhosis will de-velop primary liver cancer within a further five to 10 years.

There are at least six major genotypes of HCV and it is thought that some are more pathogenic than others. It is also believed that repeat infection of a HCV carrier with a different strain may exacerbate underlying liver disease.

At present, the main genotypes found in the Australian population are 1 (52 per cent), 3 (41 per cent) and 2 (7 per cent).

Method of Diagnosis

Laboratory diagnosis is based on detection of antibodies directed against the products of expressed clones or peptides of the hepatitis C virus and/or demonstration of HCV RNA by polymerase chain reaction (PCR).

First generation enzyme immunoassay (EIA) became available in Australia in 1990 and since then the second and third generation EIAs have improved sensitivity and specificity.

Supplemental tests are also available in the form of recombinant immunoblot assays (RIBA). Equivocal reactivity by EIA tests and indeterminate reactivity by RIBA testing remains problematic in low-risk groups.

A positive PCR test is a marker for viraemia and infectiv-ity, but a negative PCR does not rule out infection as viraemia may be intermittent.

Current EIA tests cannot distinguish between patients who are currently infectious and those who have recov-ered from infection and developed immunity.

Re s e r voi r


Mode of Transmission

It is primarily transmitted by blood-to-blood contact.

In Australia and other Western countries, sharing inject-ing equipment by drug users is the most common mode of transmission.

Tattooing, earpiercing and body piercing using unsterile equipment are other potential sources.

Health care and laboratory staff handling blood and blood products are at increased risk. The risk of con-tracting hepatitis C from a needle-stick injury from a seropositive source has been estimated at 3 per cent, compared to 0.3 per cent for HIV infection and 30 per cent for hepatitis B infection.

Sexual transmission rates of HCV are very low, but the risk is increased if the HCV positive partner is immuno-compromised as the virus titre may be increased.

Mother-to-baby transmission is also very low but may be increased if the mother is also infected with HIV or has a high titre of HCV in the blood. The risk of transmission through breast milk is considered minimal.

Community or household transmission of HCV is consid-ered rare.

A proportion of HCV individuals do not fall into any known subgroup. It is thought that some may have had exposure to injecting drugs many years ago that they have forgotten or are unwilling to discuss.

Poorly cleaned needles used by medical practitioners in some countries, and cultural practices that involve skin piercing, are other potential sources of infection.

Incubation Period

Ranges from two weeks to six months—most commonly six to nine weeks after which serum ALT levels rise.

Current HCV antibody tests become positive two to three months after exposure.

Period of Communicability

Communicability occurs during the acute clinical stage and indefinitely in the chronic carrier stage.

All HCV positive individuals need to be considered potentially infectious.

Susceptibility and Resistance

Susceptibility is general. The degree of immunity follow-ing infection is unknown.

Control of Case

The patient needs to be considered for possible Inter-feron therapy that is available, for selected patients, under the Highly Specialised Drugs Program of the Commonwealth at certain liver clinics in Melbourne.

Assessment would include examination for signs of liver disease, monitoring of the ALT levels and a PCR test.

Advice should be sought from a liver clinic when neces-sary.

About 50 per cent of patients treated with Interferon respond initially, but about 50 per cent of these relapse after treatment ceases.

Counselling of the patient is a very important part of the management. This counselling should include:

• Likely source of the infection.

• Current knowledge of the natural history.

• Possible symptoms.

• Advice on prevention of further transmission of infec-tion.

• Lifestyle issues, such as immunisation against hepatitis B, minimisation of alcohol intake, cessation of smoking, healthy diet.

The patient should be advised not to:

• Donate blood or body organs.

• Share injecting equipment.

• Share personal items such as toothbrushes or razors.

They should also be advised to:

• Advise any health care providers of their HCV status when undergoing any dental or medical procedure.

• Wipe up any blood spills with household bleach and disposable paper towels.

• Cover any cuts or wounds with a dressing.

• Place blood-stained paper tissues, sanitary towels or dressings in a plastic bag before disposal.

• Use ‘safer sex’ practices. People in long-term stable relationships will need to discuss condom use with their health care provider.

Control of Contacts

There is no vaccine available for hepatitis C.

The role of prophylactic immunoglobulin for contacts has not been established.

Preventive Measures

• Use standard precautions by all health care providers with potential contact with blood or body fluids.

• Use disposable equipment for all skin penetration procedures, or use adequate sterilisation methods when reusable needles are used for any procedure.

Hepatitis D

Victorian Statutory Re q u i re m e n t

Group B notification (as hepatitis non-A, non-B, or associated with hepatitis B).

Infectious Agent

Hepatitis D virus (HDV) is a virus-like particle consisting of a coat of HBsAg and a unique internal antigen (delta antigen). (Replication can only occur in the presence of hepatitis B virus.)

Clinical Features

Two types of infection with hepatitis D occur:

• Co-infection: simultaneous acute infection with HBV and HDV. This usually causes a self-limited hepatitis.

• Superinfection: HDV infection in a HBV carrier. This often causes a fulminant acute hepatitis that progresses to chronic active hepatitis.

Public Health Significance and Oc c u r re n c e

Two general epidemiological patterns are recognised:

• Endemic infection occurs in Italy, the Middle East, some areas of Africa and South America, although the ratio of the two infections varies widely with location.

Transmission occurs primarily within the household setting.

• Non-endemic infection occurs in Australia, North America and Western Europe, where HDV occurs sporadically in the HBsAg population and is largely confined to the risk group of injecting drug users.

Method of Diagnosis

Identification of HDV antigen or anti-HDV in the serum.

Mode of Transmission

The mode of transmission is similar to hepatitis B (see Public Health Significance).

Incubation Period

Not firmly established.

Period of Communicability

Blood is potentially infectious during all stages of active HDV infection.

Control of Case

As for hepatitis B.

Control of Contacts

As for hepatitis B.

Susceptibility and Resistance

All persons who are susceptible to hepatitis B or who are HBV carriers can be infected with HDV.

Among HBV carriers, avoiding exposure to any potential source of HDV is the only effective measure.

Hepatitis E

Victorian Statutory Re q u i re m e n t

Group B notification (as hepatitis non-A non-B).

Infectious Agent

Hepatitis E virus (RNA virus).

Clinical Features

Clinical course is similar to that of hepatitis A.

A high mortality rate (up to 40 per cent) has been de-scribed in pregnant women affected in their third trimes-ter of pregnancy.

Public Health Significance and O c c u r re n c e

Sporadic and epidemic cases have occurred in India, areas of the former Soviet Union, some African countries, Mexico and parts of Asia.

Imported cases have been identified in Australians, and one case in the Northern Territory in a patient who had not been overseas.

Method of Diagnosis

Immune electron microscopy of faeces.

Serological tests, including fluorescent antibody assay and EIR, are available through VIDRL.

R e s e rv o i r

Humans, transmissible to some other primates.

Mode of Transmission

Hepatitis D can be transmitted:

• From contaminated water.

• Person-to-person by the faecal-oral route.

Incubation Period

Two weeks to two months; the mean has varied from 26 to 42 days in different epidemics.

Period of Communicability


Susceptibility and Resistance

Susceptibility unknown.

Control of Case

• Determine occupation of the patient.

• Exclude the patient from food handling until at least one week after the onset of jaundice.

• Educate the patient on the need for strict hygiene practices such as hand washing after toilet and before eating.

Control of Contacts

No specific measures.

The efficacy of immunoglobulin has not been estab-lished.

In document Blue Book (Page 86-97)