2. Introduction
Hepatitis is a general term that means inflammation (irritation and swelling)
of the liver
Hepatitis A refers to liver inflammation caused by infection with the hepatitis
A virus (HAV)
HAV has been known as “Infectious Jaundice” since 1912
According to WHO1
, HAV had many names in the past;
•Epidemic hepatitis
•Epidemic jaundice
•Infectious hepatitis
•Catarrhal jaundice
•HA and type A hepatitis
1. ANON. “Hepatitis A.” 2000. Available from: http://www.who.int/csr/disease/hepatitis/HepatitisA_whocdscsredc2000_7.pdf. Accessed February 20, 2008
3. HAV is referred to as one of the oldest diseases known to humankind by the
WHO1
It was recognized as as separate entity from other types of hepatitis during
World war II
It was discovered in 1973 by Steven M. Feinstone as a nonenvoloped,
spherical, positive stranded RNA virus
HAV was an unidentified viral disease prior to this discovery
1. ANON. “Hepatitis A.” 2000. Available from: http://www.who.int/csr/disease/hepatitis/HepatitisA_whocdscsredc2000_7.pdf. Accessed February 20, 2008
4. Virology
Naked RNA virus
Related to enteroviruses, formerly known as Enterovirus 72,
now put in its own family: heptoviridae
One stable serotype only
But seven genotypes exist (four human & three simian) most common being 1A
in Humans
Difficult to grow in cell culture: primary marmoset
cell culture and also in vivo in chimpanzees and
marmosets
Human and vertebrates serve as natural hosts
5. Globally, symptomatic HAV infections are believed to occur in around 1.5 million people a year
In 2010, acute hepatitis A resulted in 102,000 deaths, which is slightly up from 99,000 in 1990*
Hepatitis A is much more common in countries with
underdeveloped sanitation systems and, thus, is a
risk in most of the world
Developed countries have low circulating levels of hepatovirus A while developing
countries have higher levels of circulation.
HAV is a common infection in developing nations of Africa, Asia, and Central and
South America.
Most adolescents and adults in developing countries have already had the disease, thus
are immune.
*Lozano, R (Dec 15, 2012). “Global and regional mortalityfrom 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010”.
Lancet 380 (9859): 2095–128.doi:10.1016/S0140-6736(12)61728-0. PMID 23245604.
6. Transmision
Its communicable (or contagious) disease that spreads from person to person via
“fecal-oral route”
While all other exposure is generally attributable to
contaminated food or water
Food-related outbreaks are usually associated with contamination
of food during preparation by a HAV-infected food handler
Infected individuals are infectious prior to onset of symptoms,
roughly 10 days following infection.
The food handler is generally not ill because the peak time
of infectivity—that is, when the most virus is present in the
stool of an infected individual—occurs two weeks before illness
begins.
7. The virus is resistant to detergent, acid (pH 1), solvents
(e.g., ether, chloroform), drying, and temperatures up to 60°C
It can survive for months in fresh and salt water.
Infection is common in children in developing countries,
reaching 100% incidence, but following infection,
lifelong immunity results
Travelers who visit developing countries remain at risk for infection.
Contaminated food, water (e.g., infected food handlers, raw shellfish)
Close personal contact (e.g., household contact, sex contact, child day care centers)
Blood exposure (rare) (e.g., injecting drug use, transfusion)
Unknown
52%
Intl travel
5%
Household/
sexual
25%
Outbreak
3%
Daycare
15%
9. Clinical manifestations
Apprroximately 70% of hepatitis A infectious children younger than 06 years of age are
asymptomatic
In older children and adults, infection tends to be symptomatic with more than 70% of
those infected developing jaundice
Symptoms typically begin about 28 days after contracting HAV, but can begin as early as
15 days or as late as 50 days after exposure
The symptoms include
Muscle aches
Headache
Anorexia (loss of appetite)
Abdominal discomfort
Fever
Malaise
Usually manifestations resolve in 6 to 8 weeks but it can also take 6 months
10. Diagnosis
Acute infection is diagnosed by the detection of HAV-IgM in serum by (enzyme
immunoassay)EIA.
Past Infection i.e. immunity is determined by the detection of HAV-IgG by EIA.
Cell culture – difficult and take up to 4 weeks, not routinely performed
Direct Detection – Electron microscopy, RT-PCR of faeces. Can detect illness
earlier than serology but rarely performed.
11. Events in hepatitis a virus infection
0 1 2 3 4 5 6 7 8 9 10 11 12 13
Week
Response
Clinical illness
ALT
IgM IgG
HAV in stool
Infection
Viremia
12. CONCENTRATION OF HEPATITIS A VIRUS IN VARIOUS BODY FLUIDS
Source: Viral Hepatitis and Liver Disease 1984;9-22
J Infect Dis 1989;160:887-890
Feces
Serum
Saliva
Urine
100 102 104 106 108 1010
BodyFluids
Infectious Doses per mL
13. Managemant
No specific treatment is known
Appropriate rest (when nescessary)
In the past, however, strict bed rest until complete resolution of all symptoms was
common
An Randomized control trial has shown no difference in the duration of illness with
the institution of a deliberate exercise program. So strict bed rest is controversial
Avoid fatty foods and alcohol (these may be poorly tolerated for some additional
months during the recovery phase and cause minor relapses)
Eat a well-balanced diet, and stay hydrated.
14. In fulminant hepatic failure, management is determined by the complications
that develop and the availability of transplantation.
Similarly, extrahepatic manifestations such as renal failure and pancreatitis
are managed in a routine manner.
The expectation for all patients is for complete recovery without sequelae,
which occurs in the vast majority.
15. In some individuals, the course of hepatitis A is unusually prolonged.
Since prolonged excretion of virus (i.e., viral nucleic acid detected by RT-
PCR) may occur in patients with persistent elevation of alanine
aminotransferase , any patient with prolonged course should be regarded as
potentially infectious.
The occurrence of “cholangiolytic” or cholestatic variants of acute hepatitis
A has been described in 1984 in literature
Severe pruritus, diarrhea, weight loss, and malabsorption may accompany the
cholestasis
16. Complication
Like hepatitis B, delta hepatitis, and hepatitis E, hepatitis A can cause acute
hepatic failure
FHF-Less frequent than acetaminophen toxicity and hepatitis B
The spontaneous recovery rate for patients with fulminant acute hepatitis A
in retrospective U.S. study, which included all age groupss was 35%, whereas
it was 39% in a French pediatric population. Other patients may survive
following liver transplantation*
The risk of fulminant hepatitis is increased in patients with underlying
chronic liver disease who develop acute viral hepatitis (co-infection or
superinfection)
*Debray, D., P. Cullufi, D. Devictor, M. Fabre, and O. Bernard. 1997. Liver failure in children with hepatitis A. Hepatology 26:1018–1022.
22. DURATION OF PROTECTION AFTER HEPATITIS A VACCINATION
Persistence of antibody
At least 5-8 years among adults and children
Efficacy
No cases in vaccinated children at 5-6 years of follow-up
Mathematical models of antibody decline suggest protective antibody levels
persist for at least 20 years
Other mechanisms, such as cellular memory, may contribute
Need for post exposure prophylaxis uncommon. If needed, administer immune
serum globulin within 2 weeks 0.02 ml/Kg IM
23. PREVENTING HEPATITIS A
Hygiene (e.g., hand washing)
Sanitation (e.g., clean water sources)
Hepatitis A vaccine (pre-exposure)
