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Hepatitis A

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Rare in the UK, Hepatitis A virus is transmitted when food or water is contaminated by faeces…

Hep A via the faeco-oral route, Hep E from swine flesh as well – and 10% of sausages sold by retail in the UK are contaminated with Hep E… Hepatitis A virus (HAV) causes hepatitis A, a severe food and waterborne disease that is primarily transmitted by the faeco-oral (‘turd to tongue’) route. It is the only notifiable viral foodborne disease. It is a single-stranded RNA virus belonging to the Picornaviridae family and now classified in a distinct genus, Hepatovirus. HAV has a single serotype. Seven genotypes – four of which are found in humans – have been identified. These genotypes can be useful for tracing outbreak sources.

Growth and Survival Inactivation (CCPs and Hurdles) Clinical Notes Reservoirs / Sources

Growth

Hepatitis A virus is culturable in primate cell lines – but wild type strains are difficult to culture and generally do not produce cell changes, and so are not easy to identify by culture alone. It will not grow in food or water.

Survival

HAV is very stable, shows high resistance to chemical and physical agents such as heat, acid and solvents and has been shown to survive in the environment for over 3 months.

Temperature

HAV integrity and infectivity were retained after 60 min incubation at 60°C and the virus was only partially inactivated after 10-12 hours at 56°C. Infectivity was retained after 10 min at 80°C in 1M MgCl2 but for only 5 min in phosphate buffered saline. HAV heat resistance is reported to be greater in foods and shellfish. HAV inoculated into oysters was not fully inactivated after heating in a can for 19 min at 60°C. MAFF recommend a heat treatment of 1.5 min at 90ºC to inactivate HAV in cockles. Under refrigeration and freezing conditions the virus remains intact and infectious for several years.

pH

Stable at acid pH. At pH 1.0 and 25°C, HAV retained high infectivity after 2 hours and was still infectious after 5 hours. So, not killed by stomach acid.

Drying

Infectious for >1 month at 25°C and 42% humidity. Greater resistance to inactivation at low humidity and temperatures.

Sanitisers / Disinfectants

Infectivity is decreased by exposure to 70% alcohol. Resistant to chloroform, Freon, Arklone and 20% ether. Not inactivated by 300mg/l perchloroacetic acid or 1g/l chloramine at 20°C for 15min. HAV is inactivated by chlorine: 99.99% reduction in 6.5 min at pH6 and 49.6 min at pH10 (estimated Ct values under conditions described are 1.8 and 12.3 respectively). Hypochlorite: 3-10mg/l at 20°C for 5 -15min. Iodine: 3 mg/l for 5 min at 20°C Formalin: 1:4000 for 72 hours at 37°C or 3% for 5 min at 25°C.

Radiation

Inactivated by UV irradiation after 1 min exposure to 1.1W or 197μW/cm2 for 4 min. Gamma irradiation has not been found to be effective for inactivation of HAV on fresh fruits and vegetables.

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Incubation

2-6 weeks, average 28 days. Symptoms Initially non-specific symptoms – fever, headache, fatigue, anorexia, nausea and vomiting, then viraemia, jaundice and hepatitis symptoms appear 1-2 weeks later. Virus is present in the blood at weeks 2- 4, and is shed in faeces (>106 particles/g) from the latter 2 weeks of the incubation period for up to 5 weeks. Jaundice is usually evident from weeks 4 to 7, and virus shedding generally continues throughout this period. Overall debility lasting several weeks is common and relapses may occur. Acute hepatitis is usually self-limiting but can occasionally cause fulminant disease that results in death. Estimated hospitalisation rate is 13%.

Condition

HAV infects hepatocytes, causes elevation of liver enzymes and inflammation of the liver. The cytotoxic T cell immune response destroys infected liver cells. Virus particles are released into the bile duct and excreted in faeces. The virus is believed to initially enter the liver via the bloodstream and it is not clear if intestinal replication occurs. The gastrointestinal tract is not a required route for infection.

Toxins

None produced in foods.

At Risk Groups

All age-groups. The disease is milder in young children under 6 years than older children and adults. Case-fatality risk increases with age so risks are higher for unexposed older people.

Long Term Effects

As an illustration overall case fatality rates in the US are 0.3% (0.003 per 100,000) and range between 0.004% for 5-14 years to 2.7% in people > 49 years. HAV has not been associated with chronic liver disease.

Treatment

Rest and an appropriate low-fat diet. Post-exposure prophylaxis may be recommended for certain groups such as day-care centre staff, military and food industry staff. Prevention is possible via HAV vaccination for at-risk groups including overseas travellers and for food handlers when situations warrant it.

Human

Human faeces are the major reservoir. Coprophagy is not recommended.

Animal

HAV infects primates including chimps and some species of monkeys. Non-primates are also infected but disease is milder. Transmission via these hosts is unlikely.

Food

Contaminated bivalve shellfish, salads, fresh fruits and vegetables, water, and any manually prepared food products. HAV survived in cream-filled biscuits for >1 day at 21ºC. Poor hygiene practices and poor sanitation are major risk factors. Pre-symptomatic food handlers excreting HAV pose a risk. Food is rarely available for post hoc analysis because of the long incubation period.

Environment

Survival of HAV in the environment (fresh and seawater, wastewater, marine sediments, soils and shellfish), is prolonged (>12 weeks) at 25°C. Excreta from infected humans may contaminate soil or water. Human faecal pollution from sewage discharges, septic tank leachates and boat discharges has caused contamination of shellfish beds, recreational water, irrigation water and drinking water.

Transmission Routes

The faecal/oral route is the established route of transmission and infection occurs following ingestion of faecally-contaminated food and water. Viral contamination of fresh fruits and salad vegetables through the global marketplace is becoming a significant route of exposure, especially in countries with low levels of hepatitis A. Person to person transmission is also important especially among young children in overcrowded living conditions, day-care centres or institutions. Parenteral transmission occurs in the drug-using population and via contaminated blood products.

Outbreaks

Most cases of disease are outbreak-related. Large outbreaks have been reported in developed countries where there is little immunity. Secondary transmission may account for 20% of cases in an outbreak.

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