HEPATITIS C

Contaminated needles and syringes are most important vehicles of spread, especially among injecting

drug users.

Hepatitis C - an introduction

Hepatitis is a general term meaning inflammation of the liver and can be caused by several mechanisms,

including infectious agents. Viral hepatitis can be caused by a variety of different *viruses such as

hepatitis A, B, C, D and E. Since the development of *jaundice is a characteristic feature of liver disease

and not just viral hepatitis, a correct diagnosis can only be made by testing patients’ *sera for the presence

of sp

The *virus infects liver cells and can cause severe inflammation of the liver with long-term complications.

The onset of disease is usually insidious, with anorexia, vague abdominal discomfort, nausea and

vomiting, fever and fatigue, progressing to *jaundice in about 25% of patients, less frequently than

hepatitis B.

Of those exposed to HCV, about 40% recover fully, but the remainder, whether they have symptoms or

not, become chronic *carriers. Of these, 20% develop *cirrhosis. Of those with *cirrhosis, up to 20%

develop liver cancer.

How is HCV spread?

Hepatitis C *virus is usually spread by sharing infected needles with a *carrier, from receiving infected

blood, and from accidental exposure to infected blood. Some people acquire the infection through

nonparenteral means that have not been fully defined, but include sexual transmission in persons with

high risk behaviours, although transmission of HCV Is less common than that of HBV and HIV.

HCV is not spread by breast feeding, sneezing, coughing, hugging, sharing eating utensils or drinking

glasses, other normal social contact, food or water.

Mother-to-baby transmission is now well documented, but uncommon.39 Needs a high viraemia (>1 log­)

as found in HIV co-infections

A person who has hepatitis C can still get other types of hepatitis, such as hepatitis A or hepatitis B.

HCV positive persons should :

• not donate blood, body organs, tissue, or semen

• not share toothbrushes or razors

• keep cuts and skin lesions covered

The disease

Hepatitis C is a major global public health problem. HCV infection is one of the main causes of *cirrhosis

and HCC. HCV-related end stage liver disease is the leading reason for liver transplantation in the USA.

Acute HCV infection

The incubation period for acute hepatitis C averages 6 to 10 weeks.

Most persons (~80%) who develop acute hepatitis C have no symptoms.

The onset of disease is usually insidious, with anorexia, vague abdominal discomfort, nausea and

vomiting, fever and fatigue, progressing to *jaundice in about 25% of patients, less frequently than

hepatitis B.

Rapid, fulminant liver failure associated with HCV infection is a rare event.

Probably as many as 70%-90% of infected people fail to clear the *virus during the acute phase of the

disease and become chronic *carriers

Severity ranges from inapparent cases in approximately 75% of infections to rare fulminating, fatal

cases.41 Chronic liver disease with fluctuating or persistently elevated liver *enzymes is common,

occurring after >60% of HCV infections in adults.

Of those with chronic liver disease, 5%-20% may develop *cirrhosis.

About 5% of infected persons may die from the consequences of long term infection (liver cancer or

*cirrhosis).

The course of acute hepatitis C is variable, although elevations in *serum *ALT levels, often in a

fluctuating pattern, are its most characteristic feature. Normalization of *ALT levels might occur and

suggests full recovery, but this is frequently followed by *ALT elevations that indicate progression to

chronic disease.

After acute infection, 15%-25% of persons resolve their infection without sequelae.94 Spontaneous

elimination of the *virus is rare.

Chronic HCV infection

Chronic hepatitis can be defined as a continuing disease without improvement for at least six months.

Chronic hepatitis is not a single disease, but rather a complex clinico-pathological syndrome with multiple

causes, varying stages of necro-inflammatory and sclerosing liver damage, different prognoses and

responses to treatment.

Most persons (60%-80%) who have chronic hepatitis C have no symptoms.

Chronic HCV infection develops in 75%-85% of persons, with persistent or fluctuating *ALT elevations

indicating active liver disease developing in 60%-70% of chronically infected persons. No clinical or

*epidemiologic features among patients with acute infection have been found to be predictive of either

persistent infection or chronic liver disease.

An important clinical feature of infection with HCV is the high rate of chronic hepatitis and slowly

progressive lifelong infection, which may lead to *cirrhosis and liver failure in about 10%-20% of persons

with chronic hepatitis C.

HCV-associated *cirrhosis leads to liver failure and death in about 20%-25% of cirrhotic cases. HCVassociated

*cirrhosis now represents a leading indication for liver transplantation

Chronic HCV infection appears to be associated with the development of hepatocellular *carcinoma (HCC)

in 1%-5% of persons with chronic hepatitis C.

Development of HCC is rare in patients with chronic hepatitis C who do not have *cirrhosis.5

Chronic infection is often not symptomatic, until evidence of liver failure becomes clinically apparent. The

rate of progression to *cirrhosis is usually slow, with 20 or more years elapsing between infection and the

development of serious complications.

The period of communicability spans from one or more weeks before onset of the first symptoms and may

persist in most persons indefinitely.

Based on infectivity studies in chimpanzees, the *titre of HCV in the blood appears to be relatively low.

Peaks in *virus concentration appear to correlate with peaks in *ALT activity.

Susceptibility is general. The degree of immunity following infection is not known. Repeated infections with

HCV have been demonstrated in an experimental chimpanzee model.

HCV infection does not cause fulminant hepatic failure, but, occurring in the setting of another chronic

liver disease such as chronic HBV infection, may precipitate liver failure.

An early diagnosis in the course of the disease can:

• increase the chances of successful treatment

• increase impact of essential lifestyle changes

• limit cross-infection

*EIA result Suggested action

anti-HCV positive HCV infection in a patient with a positive EIA test

should be confirmed by a qualitative HCV RNA

assay.

However confirmation may be

unnecessary in a patient who has evidence of

liver disease and obvious risk factors for HCV.

The immunoblot assay is still useful as a

supplemental assay for persons screened in

nonclinical settings and in persons with a positive

EIA who test negative for HCV RNA.

anti-HCV negative A negative EIA test is sufficient to exclude a

diagnosis of chronic HCV infection in immunecompetent

patients, if the test is performed

Transmission

Transmission occurs by percutaneous exposure to contaminated blood and *plasma derivatives.

Contaminated needles and syringes are most important vehicles of spread, especially among injecting

drug users.

Because the *virus possesses a lipid-containing envelope, exposure of *virus to bile and secretion from

the liver through the biliary tract to the gut would result in rapid loss of *virus infectivity.

Transmission by household contact and sexual activity appears to be low.

Uncommon but occasional is the transmission at birth from mother to child. About 5 out of every 100

infants born to HCV infected women become infected at the time of birth. Unfortunately, no treatment can

prevent this from happening. Perinatal transmission explains only a small proportion of chronic HCV

infections. This contrasts with HBV infection, in which most adult chronic *carriers acquired infection in

the newborn period.

The risk of mother to infant transmission of HCV increases dramatically if the mother is co-infected with

HIV possibly due to an increase in HCV *titre as a result of immunosuppression.

The risk of mother-baby transmission correlates with the *titre of maternal HCV *viremia.

For women found to be HCV positive, there are no recommendations against pregnancy or breast-feeding,

nor is a special method recommended to deliver the baby. However, invasive fetal monitoring (eg. using

scalp electrodes) should be avoided.HCV-positive mothers should consider abstaining from breastfeeding

if their nipples are cracked or bleeding.

Vaccines

There is no *vaccine against HCV.

There are major challenges to the future development of a hepatitis C *vaccine. Primary infection of

chimpanzees does not protect against subsequent challenge by either the identical *viral strain or a

heterologous strain. Protective or neutralizing *antibodies have not been found.

Comprehensive strategy to prevent and control hepatitis C *virus (HCV) infection and HCV-related

disease

 Primary prevention activities include

- screening and testing of blood, *plasma, organ, tissue, and semen donors

- *virus inactivation of *plasma-derived products

- adequate sterilization of reusable material such as surgical or dental instruments

- risk-reduction counseling and services

- implementation and maintenance of infection-control practices

- needle and syringe exchange programs

 Secondary prevention activities include

- identification, counseling, and testing of persons at risk

- medical management of infected persons

 Professional and public education

 Surveillance and research to monitor disease trends and effectiveness of prevention activites

Prevention of spread of infection should be the main goal at the current time until cost effective therapies

become available.

Monitoring

It is recommended that progression of liver disease be monitored every 6 months by checking blood

counts and liver *enzymes. In patients with more advanced liver disease, level of a-fetoprotein and

ultrasonography should be added.

Patients with chronic hepatitis C should be examined, questioned about side effects, and have blood

tested for *ALT/*AST every 1 to 4 weeks while on therapy. Evaluation should continue for at least 6

months after stopping therapy to assess whether the response to therapy is sustained.

Early response is assessed at 3 months by evaluating the patient’s *ALT and/or HCV RNA response.

End-of-treatment response is assessed by *ALT and/or HCV RNA estimation when therapy is completed.