Some viruses cause food borne disease, they are-
Hepatitis A virus
Norwalk virus
Rotavirus
In this presented we included some food borne viruses and their history, infectivity, pathogenecity, lab diagnosis and treatment.
2. CONTENT
Introduction
Hepatitis A virus
• Place and history of outbreaks
• Food and pathogenic agent related to infection
• Structure of organism
• Infectivity of disease
• Diagnosis
• Treatment
• Precautions
Norovirus
• Place and history of outbreaks
• Food and pathogenic agent related to infection
• Structure of organism
• Infectivity of disease
• Diagnosis
• Treatment
• Precautions
Reference
3. INTRODUCTION –
Food borne outbreak-
• “When two or more people get the same illness from the same
contaminated food or drink, the event is called a foodborne illness
outbreak.”
• Many outbreaks are local in nature. They are recognized when a group of
people realize that they all become ill after a common meal.
• Illness caused by food contaminant with bacteria, viruses, parasites.
• Viruses cause a wide range of diseases in plants, animals and humans. The
most relevant in foodborne infections are those viruses that infect the cell
lining of the intestinal tract and are dispersed by shedding into the stool or
through emesis. Some of the significant foodborne viruses are-
• Hepatitis A virus
• Norwalk virus
• Rotavirus
4. • Hepatitis A virus was previously classified as Enterovirus . Now it is
assigned to new genus Heparnavirus (Hepatovirus).
• Hepatitis A formerly known as infectious hepatitis or epidemic jaundice
is an acute infectious disease caused by hepatitis A virus.
• Also cause acute liver failure. It does not cause long term infection.
• The disease is benign with complete recovery in several weeks.
• In developing countries with very poor sanitary conditions and hygienic
practices 90% children have been affected with hepatitis A.
5. • Over 30,000 cases of hepatitis A were reported to the CDC in the US
in 1997.
• In Michigan (1997), an outbreak of hepatitis A affected 153 persons.
The outbreak was linked to frozen stawberries.
• Another widespread outbreak in the United States, the 2003 US
hepatitis outbreak, affected at least 640 people (killing four) in
northeastern Ohio and southwestern Pennsylvania in late 2003. The
outbreak was blamed on tainted green onions at a restaurant in
Monaca, Pennsylvania.
• In June 2013, frozen berries sold by US retailer Costco and purchased
by around 240,000 people were the subject of a recall, after at least 158
people were infected with HAV, 69 of whom were hospitalized.
• An outbreak of hepatitis A at tropical smoothie cafe resturants
affected 9 states, 143 people become ill after drinking smoothies
imported from Egypt.
• The most widespread hepatitis A outbreak in the United States
occurred in 2018, in the state of Kentuckyand the total number of
suspected cases was 969 with six deaths.
6. • Types of food implicated in the transmission of Hepatitis A virus
include shellfish, vegetables, fruits, reconstituted frozen orange juice,
ice cream, rice pudding, bread, cookies and other raw unprocessed
food.
• Outbreak associated with water contaminants are rare in areas with a
well maintained water supply and good sanitation, contaminants can
occur with sewage runoff into well, streams, swimming areas.
• From shellfish - HAVs is excreted in the stools and hence it enters
the sewage system. The largest foodborne outbreak of hepatitis A ever
recorded occurred in Shanghai in 1988 where almost 300,000 people
were infected after consuming clams harvested from polluted waters.
• Bivalve molluscs grow in shallow coastal and estuarine waters that are
polluted with sewage in many parts of the world.
• They feed by filtering seawater to obtain nutrients, and, where water is
contaminated, can accumulate by microorganisms, including HAVs,
within their tissues.
7. • Viruses do not replicate in the shellfish but may be concentrated at levels
greater than those in the surrounding water.
• Thorough cooking will inactivate virus, but this renders the shellfish
meat tough and unpalatable.
• These shellfish are frequently consumed raw or are only very lightly
cooked; such cooking may not inactivate microbial contaminants.
From fruits and vegetables –
• Fruit and vegetable crops can be contaminated with viruses in their
growing or harvesting areas from contact with polluted water and from
inadequately or untreated sewage sludge used for irrigation and
fertilization.
• The investigation of an outbreak of hepatitis A in New Zealand
associated with blueberries revealed multiple opportunities for
contamination of the blueberries by pickers.
• Outbreaks of hepatitis A have been associated with green onions in the
United States.
8. • HAVs is a 27 nm to 32 nm spherical particle with icosahedral symmetry
containing a linear single-stranded RNA genome with a size of 7.5 kb and
non-enveloped.
• HAVs can be divided into three parts -
• A 5′ noncoding region (NCR) that comprises approximately 10% of the
genome, is uncapped, and is covalently linked at the 5′ terminus to viral
protein VPg.
• A single open reading frame that appears to encode all of the viral
proteins, with regions designated as P1 for capsid proteins and P2 and P3
for nonstructural proteins.
• A short 3′ NCR terminating in a poly A tail.
9. The regions P1 contains four segments for structural proteins which make
up the capsid protein; 1A-VP4, 1B- VP2, 1C-VP3, 1D-VP1.
P2 comprises of three non-structural proteins; 2A, 2B, 2C which play a
role in viral replication.
P3 makes up four non- structural proteins-
• 3A- anchors the replication complex to cell membrane.
• 3B- it is VPg protein.
• 3C- it is cysteine protease that cleaves the protein from polypeptides.
• 3D- it is RNA dependent RNA Polymerase.
10. • The incubation period is between 2-1o weeks.
• After about 2 weeks of infection, virus is detectable in the liver, blood and
faeces.
• HAVs causes an acute, self-limiting infection that does not progress to
chronic phase.
• Symptoms of Hepatitis A range from mild to severe and can include fever,
loss of appetite, diarrhoea, nausea, abdominal discomfort, dark colored
urine and jaundice.
• Disruption of hepatobilary metabolism results in passage of dark coca cola
like urine, light gray colored stool.
• Appearance of biochemical abnormalities including abnormal elevation of
liver derived enzymes like ALT- alanine aminotransferase, ALP- alkaline
phosphatase, GGTP- gamma glutamyl transpeptidase and increased level
of serum bilirubin.
• The severity of infection is associated with age of patient indicating
individuals over 50 years of age at increased risk.
• Severe complication includes cholestatic hepatitis characterized by
persistent jaundice associated with pruritis, anorexia and weight loss.
11. 1. Viral replication occurs primarily within hepatocytes and the secretion of
virus into bile results in large quantities of virus being shed in the faeces.
2. During the incubation period, viremia is observed at about the same time
that fecal shedding of HAV is occurring.
3. Parenchymal cells undergo ballooning degeneration.
4. These hepatocytes are swollen and have indistinct plasma membranes,
enlarged nuclei, and a featureless cytoplasm, except for some cytoplasmic
remnants condensed around the nuclei.
5. Disruption of bile canaliculi may lead to bile retention after liver cell
enlargement or necrosis.
6. HAVs replication in the liver triggers a substantial immune response,
both humoral and cell mediated.
7. CD8 +, cytotoxic T cells that are capable of lysing autologous HAVs
infected cells , but not of controlling uninfected cells, are present both in
circulation and in the liver at the site of disease.
8. These virus specific T cells also produce interferon gamma and other
cytokines at the site of infection that may be responsible for much of liver
injury.
9.Serum antibody responses are first noted at onset of symptoms and
include virus specific IgM as well as IgG and IgA.
12. 1. Liver function test (LFT):
• Increase in both Alanine aminotransferase (ALT) and Aspartate
aminotransferase enzyme by 4-100 times in Hepatitis patient than
normal.
• A sharp rise of ALT with short duration (4-20 days) is suggestive of HAV
infection.
• Increase serum bilirubin level (5-20 mg/dl)
• Increase serum globulin level
• Decrease in serum albumin level
2. Serology:
• Antibody detection: rapid kit for detection of anti-HAV IgM in serum.
• Antigen detection: detection of hemagglutination antigen or virus
particle in faeces using PCR and nucleic acid hybridizing essay.
3. Virus culture:
• culture of HAV is difficult and takes upto 4 weeks to get result.
• In cell line culture, virus does not replicate well and produces
variability till cytopathetic effects.
13. 4. Molecular diagnosis:
• Through Electron microscopy.
• Reverse-transcriptase (RT)- PCR assays have been developed and can
be used for detecting viral antigen in fecal specimens should early
specimens be available.
14. • Supportive treatment to reduce other non-specific symptoms.
• No antiviral therapy
Vaccine –
• Formalin inactivated HAV vaccine given in two doses- an initial dose
followed by booster dose after 6-12 months.
• Two inactivated whole-virus hepatitis A vaccines are available:
HAVRIX (GlaxoSmithKline) and VAQTA (Merck).
15. • Norovirus are a genetically diverse group of ssRNA, non-enveloped
viruses belonging to the calciviridae family.
• The name derives from the Latin for chalice—calyx—meaning cup-like
and refers to the indentations of the virus surface.
• Norovirus, sometimes referred to as the winter vomiting bug, is the
most common cause of gastroenteritis.
• The virus is usually spread by the fecal–oral route
Each year, on average in the United States, norovirus causes:
900 deaths, mostly among adults aged 65 and older
109,000 hospitalizations
465,000 emergency department visits,
mostly in young children
2,270,000 outpatient clinic visits annually,
mostly in young children
19 to 21 million cases of vomiting and diarrhea illnesses.
16. • The Norovirus was originally named the norwalk agent after Norwalk,
ohio, USA, where an outbreak of acute gastroenteritis occurred among
children at bronsons elementary school in 1968.
• Norovirus is a common cause of epidemics of gastroenteritis on cruise
ships. The CDC through its Vessel Sanitation Program records and
investigates outbreaks of gastrointestinal illness—mostly caused by
norovirus—on cruise ships with both a US and foreign itinerary, there
were 12 in 2015, and 10 from 1 January to 9 May 2016. An outbreak may
affect over 25% of passengers, and a smaller proportion of crew
members.
• Most norovirus outbreaks in the United States happen from November
to April. In years when there is a new strain of the virus, there can be
50% more norovirus illness.
• Norovirus was behind a foodborne outbreak in 2018 caused by eating
take-out food in China, according to a study. The outbreak involved 157
probable cases and 20 people had laboratory-confirmed norovirus
infections in two weeks in March 2018.
17. Norovirus is the leading cause of illness from contaminated food in the united
states.
The virus can easily contaminated food because it is very tiny and spread easily.
It only takes a very small amount of virus to make someone sick.
Foods can get contaminated with norovirus when:
• Infected people who have poop and vomit on their hands touch the food.
• Food is placed on counters or surfaces that have infectious stools or vomit
on them.
• Tiny drope of vomit from an infected person spray through the air and land
on the food.
Foods can also be contaminated at their source. For example-
• Oysters that are harvested from contaminated water.
• Fruit and vegetables that are contaminated in the field.
Norovirus causes about half of all outbreaks of food related illness. Food
workers cause most reported norovirus outbreaks from contaminated food.
18. • The virus is non-enveloped, round, 27-nm particles with a ‘ragged’
outer edge but lacking a definite surface structure.
• It has a buoyant density of 1.33–1.41 g/cm3, an inability to
propagate in vitro.
• Characteristically, Norwalk virus possesses a single capsid protein.
• The genome is a non-segmented, single-stranded, positive polarity
RNA genome.
• Ten prominent spikes and can be seen on the virion by microscopy.
• The structure of the capsid protein is organized into two domains
joined by a flexible hinge.
• The inner shell (S) domain is composed of the N-terminal 225
residues and is involved in the formation of the icosahedral capsid
shell.
• The protruding (P) domain forms prominent structures extending
from the surface of the shell and is formed from the C-terminal
half of the protein.
• The P domain is further organized into two subdomains (P1 and
P2).
19. • Norwalk viruses are now established as the most important cause of
epidemic nonbacterial outbreaks of gastroenteritis worldwide. Outbreaks
occur among children and adults, but rarely among neonates or very young
children.
• The illness in symptomatic cases typically begins after an incubation
period of 24–48 hours.
• The illness is characterized by sudden onset of nausea, vomiting, which can
be projectile and severe.
• Low-grade fever and diarrhea usually occur, the latter being relatively mild.
• In contrast to bacterial gastroenteritis, diarrheal stools do not contain
blood, mucus, or white cells.
• Fecal leukocytes are absent.
• Other symptoms- mild abdominal pain, malaise, and headache.
• Vomiting may arise from a decrease in gastric motility, giving rise to a
reflux action into the stomach.
• Gastric emptying is delayed, and malabsorption of fat, D-xylose, and
lactose has been observed.
20. • The virus enters the body predominantly via the oral route.
• Virions are acid-stable, consistent with an ability to survive passage
through the stomach and replication occurs in the jejunum.
• Damage to the intestinal brush border prevents proper absorption of
water and nutrients and causes watery diarrhea.
• Partial flattening and broadening of villi with disorganization of the
mucosal epithelium.
• Lamina Propria infiltrated with mononuclear cells and vacuolization
of mucosal epithelium.
• Crypt cell hyperplasia is common.
• Dilatation of the rough and smooth ER with an increase in multi
vesicular bodies in mucosal epithelial cells.
• Microvilli were significantly shortened and amorphous electron-dense
was present in the expanded intercellular spaces.
• Shedding of the virus may continue for 2 weeks after symptoms have
ceased
21. • Virus isolation by the transmission of Norwalk virus in chimpanzees,
in which serological responses and excretion of Norwalk virus antigen
in stools were described.
• The use of RT-PCR for detection of the genome in stool or emesis
samples.
• Immuno-electron microscopy can be used to concentrate and identify
the virus from the stool.
• The addition of an antibody directed against the suspected agent
causes the virus to aggregate, thereby facilitating recognition.
• ELISA tests have been developed to detect the virus, viral antigen, and
antibody to the virus.
• Both ELISA and RIA are the sero-diagnostic tests frequently used to
detect specific antibodies.erum.
23. • No specific treatment is available for the Norwalk virus.
• Bismuth subsalicylate may reduce the severity of the gastrointestinal
symptoms.
• No vaccine is available against the virus.
Practice proper hand hygiene-
• Always was your hands carefully with soap and water-
• Especially, after using the toilet and changing diapers, and
• Always before eating, preparing and handling food.
Wash fruits and vegetables and cook seafood throughly-
• Carefully wash fruit and vegetables before preparing and eating them.
Cook oysters and shellfish thoroughly before eating.
When you are sick, do not prepare food for others-
• Food workers should stay home when sick and for at least 48 hours
after symptoms.
Clean and disinfect contaminated surfaces –
• Use a chlorine bleach solution or other disinfectant effective against
norovirus by the environmental protection agency
