BANTOG, MARIELLE CORAZON NAVARRO, LLOUISE MARYBETH TAJAO, RIZZ A LYN

inflammation of the liver.

Causes: non-infectious agents ionizing radiation chemicals autoimmune responses viruses

Common signs of hepatitis: yellow discoloration of the skin, sclera or dark urine.

FULMINANT HEPATITIS -number of hepatocytes destroyed is so great that too few remain to maintain basic liver function.

Primary viral hepatitis:

HAV HBV HCV HDV HEV HGV

Other viruses that may cause hepatitis: CMV EBV YFV HSV Rubella virus Influenza virus Coxsackie B virus Lassa virus

HEPATITIS A
HEPATITIS B

infectious hepatitis short incubation hepatitis

serum hepatitis long-incubation hepatitis

HEPATITIS C
HEPATITIS D HEPATITIS E *lesions (liver)- IDENTICAL

parenteral, sexual, fecal-oral route

similar to HBV (transmission) Enterically transmitted: fecal-oral or water-borne transmission

 CLASSIC

SIGNS

JAUNDICE & ELEVATED LIVE ENZYMES

Most common form of viral hepatitis infectious hepatitis or short incubation hepatitis
Transmission: fecal-oral route Symptoms (generally self-limited):
fever, malaise, anorexia, nausea, abdominal discomfort, dark urine jaundice

caused by picornavirus, under the new genus Hepatovirus

* HAV non-enveloped RNA virus of the Picornavirus family -excreted in bile and shed in feces

often results from: eating contaminated shellfish or other food & water incubation period: about 1 month does not cause chronic liver disease

responsible for about 40% of all hepatitis cases

high concentration of virus in feces esp. 2 weeks before jaundice

outbreaks a common source (eg. water supply) Incidence: poor hygiene over-crowding

due to immune-mediated damage to the liver

disease in children: milder & usually asymptomatic symptoms usually wanes during icteric phase complete recovery: about 99%

Serology 1. HAV : the agent 2. Anti-HAV : detectable at onset of symptoms; persists throughout life 3. IgM anti-HAV : indicates recent infection; (+) 46 months after infection

HAV Ag Infected individuals shed HAV ag in the feces during the incubation period and early acute stage of the infection. It declines to low levels by the symptoms occur. Anti-HAV Abs IgM anti-HAV - marker of acute Hepatitis A. peak: during first month of the infection decline to undetectable levels within 6-12 months. routinely detected by a solid-phase antibody capture ELISA. IgG anti-HAV result of natural infection or immunization marker of immunity to HAV detected by ELISA.

Methods for detecting HAV infection:

Assay for presence of viral Ag (feces) Amplification of viral RNA by reverse-transcription-polymerase chain reaction (RT-PCR)

TREATMENT, PREVENTION & CONTROL

hygienic measures water chlorination immunization of: Children (1-18 years of age): two or three doses of the vaccine. *Adults need a booster dose six to 12 months following the initial dose of vaccine. *The vaccine is thought to be effective for 1520 years or more

serum hepatitis ;long-incubation hepatitis due to a hepadnavirus 3 Major Routes of Transmission : parenteral, perinatal, sexual associated with primary hepatocellular carcinoma

*HBV- DNA virus from Hepadnaviridae family - primary site of replication: liver - can cause acute and chronic hepatitis - remains viable for longer than 7 days on environment surfaces at room temp.

Primary Hepatocellular Carcinoma

WHO: 80% of all PHC cases are secondary to chronic Hepatitis B infection

HBV: the agent HBsAg: surface antigen HBeAg: indicates viral replication HBcAg: core antigen Anti-HBs: indicates past infection Anti-HBe: suggest presence of HBV Anti-HBc: indicates past infection

median incubation period: 3 mo 5-10% develops chronic hepatitis causally associated with primary hepatocellular carcinoma 3 Major Routes of Transmission : parenteral, perinatal, sexual

3 CLINICAL SYNDROMES

acute infection chronic infection primary hepatocellular carcinoma

only 25% of those infected are clinically apparent characterized by long incubation period & an insidious onset S/S: fever, malaise, anorexia then: nausea, vomiting, abdominal discomfort, chills next: jaundice, dark urine, pale stools 1st sign of recovery: renewed appetite fulminant cases: 1% of icteric cases

occurs in 5-10% of HBV infections (95% of neonates) usually occurs after mild or inapparent illness usually detected by elevated liver enzymes on routine chemistry 10% of chronic cases develops cirrhosis & liver failure

WHO: 80% of all PHC cases are secondary to chronic Hepatitis B infection usually fatal latent period between HBV infection & PHC: 9-35 years

HBsAg hepatitis-associated antigen (HAA) initial serologic marker of acute infection detectable 2-3mos. after infection not infectious however, its presence in serum may indicate presence of hepatitis virus HBsAg positivity reported up to 18 days after Hepatitis B vaccination : clinically insignificant HBcAg Not present in plasma of hepatitis victims/blood donors Present only in nuclei of hepatocytes during HBV acute infection Develops earlier than the surface antigen

HBeAg Detected in the serum of patients with acute or chronic HBV infection Presence of HBeAg in HBsAg carriers - unfavourable prognostic sign -predicts a severe course and chronic liver disease -detected in serum only when surface antigen is present

US: 300,000 infected annually high rates of sero-positives: Italy, Greece, Africa, Southeast Asia chronic carrier: HBsAg positive on 2 occasions at least 6 months apart

screening: agglutination test confirmatory:

ELISA (Ag & Ab detection) PCR (for viral DNA)

Ultrasensitive quantitative real-time PCR technology Quantitative digene hybrid capture assay *Approximately 90% of patients infected with HBV recover within 6 months. Recovery is accompanied by development of the antibody to the HBsAg.

Groups of test recommended for 3 different situations: Acute HBV hepatitis : HBsAg, IgM anti-HBc Chronic HBV hepatitis : HBsAg, IgG anti-HBc, IgG anti-HBs Monitoringg chronic HBV infection : HBs, HBeAg, IgG anti-HBs, IgG anti-HBe, ultrasensitive quantitative PCR

HBsAg

Anti-HBc

IgM anti-HBc

Anti-HBs

Acutely infected
Chronically infected Immune due to natural infection

(+)
(+)

(+)
(+)

(+)
(-)

(-)
(-)

(-)

(+)

(+)

Immune do to hepatitis B vaccination

(-)

(-)

(+)

Susceptible, not infected, not immune

(-)

(-)

(-)

no specific treatment trials: interferon, adenine arabinoside, steroids, azathioprine blood screening vaccination Hepatitis B Immune-globulin

Originally non-A non-B hepatitis Transmission: parenteral, sexual, fecal-oral route high rate of progression to chronic hepatitis, cirrhosis and liver carcinoma

HCV- positive-stranded RNA virus from the genus Hepacivirus

Transmission: parenteral, sexual, fecal-oral route Risk factors: IV drug users, blood recipients Signs and Symptoms: 75% of patients have no symptoms when they first acquire HCV infection only 25% of the acute form may complain of:
fatigue loss of appetite muscle aches fever jaundice (rare)

about 20-30% of patients with chronic infections develop cirrhosis as cirrhosis develops, symptoms increase and may include: weakness
loss of appetite weight loss breast enlargement in men rash on the palms difficulty with the clotting of the blood spider-like blood vessels on the skin

Clinical Syndromes
1. Acute Form: similar to acute Hepatitis A & B but inflammatory response is less and symptoms are milder 2. Chronic Form: more prevalent than HBV, often leads to cirrhosis Anti-HCV is not protective

ELISA (antibody detection) RT-PCR (HCV-RNA)

-detected by a variety of amplification techniques -with acute infection, it is typically present within 2 weeks of infection but falls with development of antibody Anti-HCV detection by enzyme immunoassay (EIA) Quantitative nucleic acid PCR assays for serum HCV RNA

primary test for confirming HCV infection

risk factors: IV drug users, blood recipients suspicion: HBV-negative, post- transfusion epatitis occurs in 5-10% of transfusion recipients

Interferon alfa and ribavirin: the only effective treatment (50% response rate) liver transplant supportive blood screening

Characteristic features: Delta agent: HDAg surrounded by HBsAg envelope *HDV: ssRNA, smallest of known human pathogen responsible for about 40% of fulminant hepatitis dependent on HBV for replication: (can replicate only in HBV-infected cells) subviral satellite for it can only infect in the presence of Hepatitis B virus

Transmission: can be transmitted simultaneously with HBV known as coinfection or superimposed infection in chronic type or Hepatitis B carrier state. Co-infection: occurs when both HDV and HBV are contracted simultaneously Superinfection: occurs when chronic HBV carriers are infected with HDV.
leads to severe acute hepatitis and chronic Hepatitis D infection in 80% of the cases. associated with the fulminant form of viral hepatitis. Fulminant viral hepatitis: most severe form of acute disease

ten times more common in HDV infections than in the other types.

Signs and Symptoms: After an incubation period of 3-7 weeks, nonspecific clinical symptoms, including fatigue, lethargy, nausea, and anorexia, begin and last for about 3-7 days.

Methods of detecting HDV infection ELISA & RIA (Ag /Ab detection) HDV-RNA by PCR Diagnostic Markers HDV:
the agent delta antigen; detectable in early acute infection indicates past or present infection

HD Ag:

Anti-HDV:

Epidemiology agent infects children & adults with underlying HBV infection distribution: worldwide Tx, Prevn, Control Same with HBV