Viral hepatitis is inflammation of the liver caused by one of the five viruses, hepatitis A, B, C, D, and E. All of these viruses can cause an acute disease with symptomslasting several weeks including yellowingof the skin and eyes (jaundice), dark urine,extreme fatigue, nausea, vomiting, andabdominal pain.
Types of viral hepatitis
Hepatitis A refers to liver inflammation caused by infection with hepatitis A virus (HAV). Although the liver does becomeinflamed and swollen in hepatitis A, itheals completely in most people withoutany long-term damage. Infection withHAV can be spread through the ingestion of food or water, especially whereunsanitary conditions allow water orfood to become contaminated by humanwaste containing hepatitis A (fecal-oralmode of transmission). Infection rates arealso higher in areas where direct fecaloraltransmission is likely to occur, suchas daycare centers, prisons, and mentalinstitutions.
People at increased risk for hepatitis A infection
• Household contacts of people infected with HAV
• Sexual partners of people infected with HAV
• International travelers, especially to developing countries
• Military personnel stationed abroad,especially in developing countries
• Men who have sex with other men
• Users of illegal drugs (injected or non-injected)
• People who may come into contact with HAV at work
Many people with HAV infection have no symptoms at all. Sometimes symptoms are so mild that they go unnoticed. Symptomsof hepatitis A usually develop between2 and 6 weeks after infection. The mostcommon symptoms are as follows:
• Diarrhea, especially in children
• Low-grade fever
• Loss of appetite
• Tiredness, fatigue
• Dark brownish urine
• Pain in the area of liver
Acute hepatitis due to HAV cannot bedistinguished from that due to otherhepatitis viruses both clinically andbiochemically, and serologic tests arenecessary for a virus-specific diagnosis.The specific routine diagnosis of acutehepatitis A is made by finding anti-HAVIgM in the serum of patients. A secondoption is the detection of virus and/orantigen in the feces. Virus and antibodycan be detected by commercially available radioimmunoassay (RIA), enzymeimmunoassay (EIA), or enzyme-linkedimmunosorbent assay (ELISA) kits.
Hepatitis B is caused by infection withhepatitis B virus (HBV). It can spread by sexual contact, the transfer of bloodor serum through shared needles in drugabusers, accidental needle sticks with needles contaminated with infected blood,blood transfusions, hemodialysis, andfrom infected mothers to their newborns.The infection also can be spread bytattooing, body piercing, and sharingrazors and toothbrushes. About 6% to10% of patients with hepatitis B develop chronic HBV infection and can infectothers as long as they remain infected.
Patients with chronic hepatitis B infectionalso are at risk of developing cirrhosis, liverfailure, and liver cancer. This infectionhas 2 phases: acute and chronic. Chronichepatitis B also can lead to a type of livercancer known as hepatocellular carcinoma.
• Men or women who have multiple sex partners, especially if they don’tuse a condom
• Men who have sex with men
• Men or women who have sex with a person infected with HBV
• People with other sexuallytransmitted diseases
• People who inject drugs with shared needles
• People who receive transfusions of blood or blood products
• People who undergo dialysis for kidney disease
• Institutionalized mentally handicapped people and theirattendants and family members
• Health care workers who arestuck with needles or other sharp instruments contaminated with infected blood
• Infants born to infected mothers
Half of all people infected with the HBV have no symptoms. Symptoms maydevelop within 30-180 days of exposure to the virus. The common symptoms aresame as of hepatitis A.
In case of liver failure, following symptomsmay occur:
• Fluid retention causing swelling ofthe belly (ascites) and sometimesthe legs
• Weight gain due to ascites
• Persistent jaundice
• Vomiting with blood in the vomit
• Bleeding from the nose, mouth, or rectum or blood in the stool
• Hepatic encephalopathy
Acute HBV infection is diagnosed by asimple blood test detecting the presence ofhepatitis B surface antigen (HBsAg) andIgM antibody to hepatitis B core antigen(anti-HBcIgM). These antibodies developin the blood in the early stages of infectionat the time symptoms appear. Antibodyto HBsAg (anti-HBs) develops after activeinfection and serves as an indicator ofimmunity.The following antibody variations canoccur, each having a specific implication: Anti-HBs+: indicates individual has beenvaccinated, has received immune globulin,is immune, or is an infant who hasreceived antibodies from its mother.
- Anti-HBc+: indicates past or present infection and lasts indefinitely. Also may be detected in someone who has received immune globulin or an infant who has received antibodies from its mother.
- IgM anti-HBc+: indicates recent infection with HBV, usually within 4-6 months.
- HBeAg+: indicates active viral replication and high infectivity.
- HBsAg+: indicates acute or chronic HBV. Persistence for 6 months after acute infection indicates progression to chronic HBV.
Inflammation of the liver caused by infection with hepatitis C virus (HCV)is referred to as hepatitis C. If theinflammation is not reversed, it becomes chronic, which can be serious or evenfatal. HCV is transmitted mainly bycontact with blood or blood products.
Sharing of contaminated needles amongIV drug users is the most common mode of transmission.
Less common causes of HCV transmissioninclude the following:
• From mother to infant at the time ofchildbirth
• Through sexual intercourse with aninfected person
• Needle sticks with HCV contaminated blood
Although hepatitis C damages the liver, 80% of people with the disease do nothave symptoms. A minority of people havesymptoms during the early acute phase ofthe infection. These symptoms typicallydevelop 5 to 12 weeks after exposureto HCV. The symptoms may last a fewweeks or months. Chronic hepatitis Ccan lead to cirrhosis of the liver in manypeople. Symptoms of cirrhosis include thefollowing:
• Fluid retention causing swelling ofthe belly (ascites), legs, or whole body
• Persistent jaundice
• Disturbances in sleeping
• Itchy skin
• Loss of appetite, weight loss, wasting
• Vomiting with blood in the vomit
• Mental disturbances such asconfusion, lethargy, extremesleepiness, or hallucinations (hepatic encephalopathy)
• Blood transfusion
• Solid organ transplantation from a donor who has hepatitis C
- IV drug use and sharing of contaminated needles
• Long-term kidney dialysis
• Contact with blood in work setting
• Sex with a person who has hepatitis C
• Birth to a hepatitis C infected mother, particularly if she has HIV
• HIV or hepatitis B infection
Diagnosis of hepatitis C depends on demonstration of anti-HCV detectedby an EIA. Anti-HCV is generally notdetectable in patients with initial signsor symptoms of hepatitis C. HepatitisC viremia may be detected by reversetranscription-polymerase chain reaction(RT-PCR) within days after infection.Target amplification techniques using either PCR or transcription-mediatedamplification (TMA) have been developedas qualitative tests for detecting HCVRNA, whereas both target amplification(PCR) and signal amplification techniques(branched DNA) may be used to measureHCV RNA levels.
Hepatitis D virus (HDV), also known as the delta virus or agent, is a small virusthat requires concomitant infection withhepatitis B to survive. HDV cannotsurvive on its own because it requires aprotein that the HBV makes (the envelopeprotein, also called surface antigen) toenable it to infect liver cells. Chronic liverinfection can lead to end-stage liver disease and associated complications. HepatitisD is spread are by shared needles amongdrug abusers, contaminated blood, and bysexual contact, essentially the same ways asfor hepatitis B. Patients who already have chronic hepatitis B infection can acquiredelta virus infection at the same timeas they acquire the hepatitis B infectionor, alternatively, on top of a chronichepatitis B infection. An HDV infection absolutely requires an associated HBVinfection. The outcome of disease largelydepends on whether the two virusesinfect simultaneously (coinfection), orwhether the newly HDV-infected personis a chronically infected HBV carrier(superinfection). Superinfection of HBV and HDV causes a generally severe acutehepatitis with short incubation time thatleads to chronic type D hepatitis in up to80% of cases. Superinfection is associated with fulminant acute hepatitis and severechronic active hepatitis, often progressiveto cirrhosis.
Hepatitis D should be considered in anyindividual who is HBsAg positive or hasevidence of recent HBV infection. Thediagnosis of acute hepatitis D is madeafter evaluation of serologic tests for thevirus. Total anti-HDV is detected bycommercially available RIA or EIA kits.The method of choice for the diagnosis of ongoing HDV infection should be RTPCR,which can detect 10 to 100 copiesof the HDV genome in infected serum.
Acute HBV-HDV coinfection:
• Appearance of HBsAg, HBeAg, and HBV DNA in serum duringincubation
• Appearance of anti-HBc at onset ofclinical disease
• Appearance of IgM anti-HD, HDVRNA, HDAg in serum
• Anti-HDV antibodies develop late inacute phase and usually decline after infection to subdetectable levels
• If HDAg is detectable early duringinfection, it disappears as anti-HDVappears
• All markers of viral replicationdisappear in early convalescence, and both IgM and IgG anti-HD disappear within months to yearsafter recovery
• Usually results in persistent HDV infection
• HDV viremia appears in serumduring preacute phasehigh titers of IgM and IgG anti-
HDV are detectable in acute phase,persisting indefinitely
• Titer of HBsAg declines when HDAgappears in serum
• Progression to chronicity is associatedwith persisting high levels of IgManti-HD and IgG anti-HD
• HDAg and HDV RNA remaindetectable in serum and liver
• Viremia is associated with activeliver disease
Hepatitis E is caused by infection with the hepatitis E virus, a non-enveloped,positive-sense, single-stranded RNA virus.HEV is transmitted via the fecal-oralroute. Hepatitis E is a waterborne disease,and contaminated water or food supplieshave been implicated in major outbreaks.Consumption of fecally contaminated drinking water has given rise to epidemics,and the ingestion of raw or uncookedshellfish has been the source of sporadiccases in endemic areas. The risk factorsfor HEV infection are related poorsanitation in large areas of the world, andHEV shedding in feces. Person-to-persontransmission is uncommon. There is noevidence for sexual transmission or fortransmission by transfusion.
Hepatitis E virus causes acute sporadic and epidemic viral hepatitis. Symptomatic HEV infection is most common in youngadults aged 15-40 years.
• Dark-colored urine
• Pale stools
• Abdominal pain and tenderness
• Nausea and vomiting
Since cases of hepatitis E are not clinicallydistinguishable from other types ofacute viral hepatitis, diagnosis is madeby biochemical assessment of liver function. Acute hepatitis E is diagnosedwhen the presence of IgM anti-HEV isdetected. Hepatitis E should be suspectedin outbreaks of waterborne hepatitisoccurring in developing countries,especially if the disease is more severein pregnant women, or if hepatitis Ahas been excluded. HEV RNA can bedetected in acute phase feces by PCR inapproximately 50% of cases. Immuneelectron microscopy is positive in onlyabout 10% of cases.