how viral hepatitis spreads

7/25/2019 How Viral Hepatitis Spreads

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How Viral Hepatitis Spreads

Hepatitis A

Hepatitis A virus is found in the feces of infected persons. It is usually spread from

person to person by ingesting food or water contaminated with fecal matter.

Hepatitis A virus can be transmitted through:

Drinking contaminated water.

Being in close contact with an infected person.

Eating food that was handled by a person with the virus who did not carefully

wash their hands after using the bathroom.

Hepatitis B

!nfortunately hepatitis B often has a stigma attached to it because it can be

contracted through socially unaccepted behavior such as in"ecting illegal drugs or

engaging in unprotected se#.

However many people do not reali$e that most of the time a person infected with

hepatitis B is an innocent victim who has encountered the virus through:

Birth when his or her mother who was infected with hepatitis B passed the

virus on. %&ost common' A transfusion with blood that has not been screened for the hepatitis B virus

%HB('.

Direct contact with blood from an open wound.

)haring contaminated toothbrushes or ra$ors.

Improperly cleaned tattooing needles.

Improperly cleaned medical or dental tools.

It is important to note that most people who are infected with hepatitis B have no

symptoms yet they can still transmit the disease and are at risk of developing liver

cancer.


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Hepatitis C

*he mode of transmission for hepatitis + is similar to hepatitis B however there are

a few differences. Hepatitis + virus is spread through:

Blood transfusions and organ transplants that have not been screened for

hepatitis +.

)haring of needles during in"ected drug use.

Birth: a small number infected mother can pass the virus to her baby.

)e#ual contact: very rarely hepatitis + can be spread through se#.

Misconceptions

&any misconceptions e#ist about hepatitis B and + especially regarding the way in

which it spreads. Hepatitis B and + cannotbe transmitted by:

,ood or water %however hepatitis A can be transmitted in this manner'.

+asual contact such as hugging shaking hands or kissing.

)nee$ing or coughing.

Breastfeeding.

What Is Hepatitis?

The Liver

-our liver is the largest organ in your body and plays an essential role in regulating

life processes. It performs many vital functions such as:

+onverting food into chemicals for life and growth

Deto#ifying and removing substances poisonous to the body

&anufacturing important substances needed by the rest of the body

-ou simply cannot live without your liver.

Hepatitis

Hepatitis is inflammation of the liver. It may occur with limited or no

symptoms but sometimes leads to fever and "aundicea yellowish tint to the skin


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eyeballs and urine that is caused by a build/up of bile in the body. *he three main

forms of hepatitiscalled A B and +are all caused by a virus.

According to the +enter for Disease +ontrol viral hepatitis is the leading cause of

liver cancer and the most common reason for liver transplantation. In the !nited

)tates an estimated 0.1 million Americans are living with chronic hepatitis B and 2.1

are living with chronic hepatitis +. &any do not know they are infected. Each year an

estimated 13444 persons become infected with Hepatitis A5 62444 with hepatitis B

and 07444 with hepatitis +.

Acute Viral Hepatitis

Acute viral hepatitis is the inflammation of the liver caused by a hepatitis virus. In

most cases the disease onsets suddenly and lasts only a few weeks. It can causeanything from symptoms of the flu to fatal liver failure. *he symptoms if any

usually develop 8uickly and may include: loss of appetite nausea fever vomiting

and abdominal pain. In most people special treatment is not needed however people

with severe acute hepatitis may re8uire hospitali$ation. 9eople with acute viral

hepatitis usually recover in 6 to weeks and should avoid alcohol until they have

fully recovered.

Chronic Viral Hepatitis

+hronic viral hepatitis is the inflammation of the liver caused by a virus that lasts at

least ; months. ,or most people there are usually no symptoms until serious liver

damage has developed. If symptoms manifest they often include fatigue poor

appetite and abdominal discomfort. +hronic viral hepatitis is most commonly caused

by hepatitis B and hepatitis + virus and can lead to complications such as cirrhosis

liver failure and liver cancer if left unmonitored and


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B or +. Illness from hepatitis A is usually brief and infection with the virus does not

lead to chronic liver disease or liver cancer.

Hepatitis Bis caused by the hepatitis B virus and is usually transmitted through the

blood of another person with hepatitis B or from mother to child during birth. *here

are usually no symptoms until there are serious liver complications. =hen symptoms

do appear they may include high fever "aundice and abdominal pain. !ntreated

chronic hepatitis B can lead to cirrhosis ands own

immune system attacking the liver. *his disease is chronic and usually has very minor

symptoms. =hen symptoms do occur it usually includes fatigue abdominal

discomfort itching "aundice enlarged liver and nausea. If left untreated

automimmune hepatitis can lead to cirrhosis and liver failure.

"on#alcoholic $att Liver Disease

?on/alcoholic fatty liver disease occurs in people with fatty liver who have no history

of alcohol use. )ymptoms may include fatigue pain in the upper right abdomen and

weight loss. In the most severe cases non/alocholic fatty liver disease can progress to

liver failure.

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Discussion

Epidemiology of Hepatitis A Infection

Hepatitis A virus %HA(' is the leading cause of acute viral hepatitis worldwide.

Indeed in some developing areas of the world HA( seropositivity is close

to 044%C . verall hepatitis A infection in the !nited )tates is much lower in

industriali$ed countries&C . Data from 0 to 06 in the ?HA?E) III %?ational

Health and ?utrition E#amination )urvey' revealed particularly high seroprevalence

rates in the !nited )tates among poor immigrant and Fatino populations'C . In more

recent surveillance data the most fre8uent risk for HA( infection was travel outside

the !nited )tates or +anada(C . In the !nited )tates HA( causes appro#imately

63 of all cases of acute viral hepatitis and 01 of all cases of acute liver failure)C .

*he incidence of HA( in the !nited )tates has declined more than 4 since the

availability of the hepatitis A vaccine in 03. In 1404 the +enters for Disease

+ontrol and 9revention %+D+' received 0;74 reported cases of acute symptomatic

hepatitis A infection and this represented the lowest number of cases per year

ever reported*C . *he +D+ estimates that the actual numbers of symptomatic acute

HA( infections and total new infections in 1404 were 7444 and 07444 respectively.

Transmission, and Risk Factors

Hepatitis A virus is primarily transmitted via the fecal/oral route and is most

commonly ac8uired via ingestion of contaminated food or during se#ual activity%C .

,ood can be contaminated at the time of harvesting packaging or meal preparation

and multi/state outbreaks have been associated with ingestion of fresh and fro$en

produce. !ndercooked bivalves have also been implicated in hepatitis A outbreaks.

Although transmission of HA( can occur through serum blood products in the

!nited )tates do not routinely undergo screening for HA( because transfusion/related

hepatitis A infection rarely occurs. *his low transmission rate is attributed to the
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virus> short incubation period and e#clusion of patients with "aundice from blood

donation. (ertical transmission is e#ceedingly rare. In the !nited )tates the leading

three risk factors for hepatitis A infection are %0' se#ual or household contact %1'

international travel and %2' male/male se#ual activity %$i+ure %'&C . In a more recent

population/based surveillance study conducted during 1443 to 1447 the reported risk

factors for HA( ac8uisition were international travel %6.3' contact with a case

%06.' employee or child in a day care center %7.;' e#posure to food or

waterborne common/source outbreak %7.2' illicit drug use %6.2' and men who

have se# with men %2.'(C . Although needle sharing is likely responsible for

transmission in some instances among in"ection drug users poor hygiene with

resultant fecal/oral transmission may play a role in the passage of hepatitis A amongin"ection/drug users,C . +hildren and employees at daycare facilities %and their

contacts' are at higher risk for hepatitis A. ?o risk factor is identified in more than

24 of cases.

Clinical Course

*he incubation phase lasts from 1 to 7 weeks %mean 1/24 days'. 9rodromal

symptoms are non/specific and often include anore#ia fever nausea and malaise

%$i+ure &'. Gaundice typically appears within 0 week after symptom onset and occurs

in 74 to 4 of the adult population but in less than 04 of children younger than ;

years of age. Bilirubinuria may precede "aundice by a few days and dark urine is a

common presenting complaint. Gaundice and hepatomegaly are the most commonly

observed physical e#amination abnormalities%$i+ure ''-C . E#tra/hepatic

manifestations may occur but with less fre8uency than that observed in hepatitis B or

+ %$i+ure ('. *he acute illness can be disabling5 patients missed an average of days

of work in one food/borne outbreak.C and 01 days in another outbreak that involved

homose#ual men%/C . After the onset of "aundice most constitutional symptoms

abate 8uickly although some patients complain of residual fatigue for several weeks.
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Gaundice typically resolves within two weeks%%C . &ost cases of hepatitis A are self/

limited and 3 of people show complete resolution of symptoms by 2 months-C .

Hepatitis A carries no risk for chronic hepatitis. Fess common presentations of

hepatitis A include cholestatic hepatitis relapsing hepatitis and acute hepatic failure.

In recent years fewer than 044 HA(/related deaths per year have been reported*C .

In rare instances hepatitis A infection may trigger autoimmunehepatitis%&C .

Relapsing Hepatitis A

Hepatitis A infection relapses in appro#imately 3 to 04 of cases %range 0.3 to 14'

typically within several weeks after apparent resolution of the original illness%0%'C .

*he severity of the relapse is variable and often resembles the initial presentation with

manifestations that can include "aundice elevated hepatic aminotransferase levels

and fecal shedding of the virus. 9atients with relapse may have a greater risk of

developing either short/term cholestasis%C or immune/related manifestations such

as purpura arthralgias and nephritis%'C . ?evertheless patients with relapsing

hepatitis A infection should generally e#pect a full recovery. A review of several cases

of relapsing hepatitis A suggested steroids may e#pedite recovery%'C . *he e#isting

published case series have involved too few patients to accurately identify risk factors

for relapse. Available data suggest that multiple relapses appear to be highly unusual

but may be more common in children%(C .

Cholestatic Hepatitis A

+holestatic hepatitis A occurs in fewer than 04 of cases and is characteri$ed by

serum bilirubin greater than 04 mg


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cholestatic hepatitis A infection with oral prednisone at 64 mg


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a high mortality rate as only 23 to 64 of patients with acute hepatic failure caused

by HA( infection will recoverspontaneously%-0%.C . )ince more than ;3 of

patients with acute liver failure from hepatitis A will survive after

livertransplantation%(C these patients with acute hepatic failure should receive an

e#pedited evaluation for potential liver transplantation as soon as possible after

presentation.

La"oratory Findings and Diagnosis of Acute HA#

)oon after inoculation HA( is carried via the bloodstream to the liver where it

replicates within hepatocytes. *he virus is shed into the bile ducts and e#creted in the

stool. (iremia and fecal shedding of the virus peak in the two weeks prior to the onset

of clinical symptoms %$i+ure )'. ,ecal shedding of the virus likely continues for at

least a week after symptoms begin and the period of shedding can be longer in

children %in some cases up to several months'%(C . Fow/level viremia may persist for

0/24 days after the onset ofsymptoms%(C . Although 9+ can detect HA( in blood

and stool the techni8ue is time/consuming costly and rarely used outside of the

research setting. Hepatocellular in"ury becomes evident by the marked elevation in

hepatic aminotransferase levels %often greater than 344 units


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*he Ig& levels characteristically peak before 2 months and gradually decline until

they become undetectable. *he Ig levels however remain elevated and confer

lifelong immunity.

!onitoring and Treatment

&ost e#perts would recommend that any patient with moderate to severe acute

hepatitis should have immediate measurement of prothrombin time %9*' with

international normali$ed ratio %I?' and should be evaluated for subtle signs of

encephalopathy including lethargy or irritability%(0%*C . If liver function is normal

or minimally abnormal and there is no evidence for encephalopathy patients and

their family members or caregiver should be counseled to monitor for changes in

sensorium and close clinical follow/up should be arranged. *here is no specific

antiviral therapy for acute hepatitis A infection. &ost patients can be treated

symptomatically as an outpatient with laboratory and clinical follow/up. In general

patients with acute HA( infection who do not develop acute liver failure will have

complete recovery without any permanent se8uelae. ,or patients who present withor

develop more severe disease including 9* I? of 0.3 or greater or significant

symptoms such as nausea and vomiting hospitali$ation is usually re8uired.

Hospitali$ation is mandatory for patients with acute liver failure %9* I? of 0.3 or

greater and encephalopathy'5 in this situation the patient should be admitted to an

intensive care unit %I+!' and contact inititated with a liver transplantation center

since patients with acute liver failure can rapidly deteriorate.

*es ,ungsi Hati pada Jelainan Hepatobilier

Genis Jelainan Bilirubin Aminotransf

erase

Alkaline

phosphatas

e

Albumin 9rothrombin

*ime
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Hemolisis ? K 3 !


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Intra dan e#tra

hepatic

kolestasis

%obstructive

"aundice'

Bilirubin direk dan

indirek mungkin

meningkat

Bilirubinuria

?ormal

sampai

peningkatan

sedang

Garang L344

I!

&eningkat

kebanyakan

L6#

peningkata

n normal.

?ormal

kecuali

kronik

?ormal "ika

ter"adi

prolonged

dikoreksi dengan

vitamin J

parenteral.

9enyakit

infiltratif

%tumor

granulomata

partial bile

duct

obstruction'

Biasanya normal. ?ormal

sampai

sedikit

meningkat.

&eningkat

kebanyakan

L6#

peningkata

n normal.

?ormal ?ormal.

how viral hepatitis spreads

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