Non- bacterial foodbourn illness

Question 1

Faecal-Oral Route

Answer 1

• Faecal matter found on over ¼ of our hands
• 14% of bank notes & 10% credit cards
• Average person’s hands carry 3,000 different bacteria

Question 2

Viruses

Structure/ microscopy/ how many enteric viruses

Answer 2

No cellular structure
Possess only one type of nucleic acid (RNA or DNA) wrapped in a protein coat (capsid)
Diameter 25-300 nm

Invisible to conventional light microscopy
Obligate intracellular parasites
>100 human enteric viruses

Question 3

Hepatitis A virus

family/ structure

Answer 3

member of enterovirus group of the Picornaviridae family

Single molecule of RNA surrounded by a small (27 nm diameter) protein capsid

Question 4

Hepatitis A virus

infectious dose / at risk gp

Answer 4

The infectious dose not known but may be as low as 10-100 virus particles - - a mild illness

Common in infants and young children

Question 5

Hepatitis A virus

Incubation period

Answer 5

2-6 weeks

Question 6

Hepatitis A virus

Symptoms & Duration

Answer 6

fever, malaise, nausea, anorexia, and abdominal discomfort, followed in several days by jaundice

variable (2 weeks – 3 months)

Question 7

Hepatitis A virus

Transmission

Answer 7

Faecal-oral route

Question 8

Hepatitis A virus

Associated foods

Answer 8

shellfish, raw produce, contaminated drinking water, milk, fruits

Question 9

Hepatitis A virus

Treatment

Answer 9

Supportive care, prevention with immunisation

Question 10

Gastroenteritis viruses

Answer 10

Viral gastroenteritis is an infection caused by variety of viruses. Often referred to as ‘stomach flu’ (not caused by influenza viruses)

Question 11

Gastroenteritis viruses

Incubation period

Answer 11

15-50 hours

Question 12

Gastroenteritis viruses

Symptoms & Duration

Answer 12

usually mild, nausea, vomiting, diarrhoea, malaise, abdominal pain, headache and fever

24-48 hours

Question 13

Gastroenteritis viruses

Detection

Answer 13

immune electron microscopy and various enzyme immunoassays from stool samples

Question 14

Gastroenteritis viruses

Transmission

Answer 14

faecal-oral route or ingestion of contaminated foods and water. Contamination of ready-to-eat foods by ill handlers

Question 15

Rotavirus

family / structure / serological gps

Answer 15

Reoviridae family of viruses

Genome consisting of 11 double-stranded RNA segments surrounded by distinctive two-layered protein capsid

6 serological groups – 3 infect humans (A,B,C)

Question 16

Rotavirus

at risk gp/ symptoms

Answer 16

Infect lining of the intestine and cause diarrhoea especially in children

~18,000 children are hospitalised annually in England and Wales due to rotavirus-related disease

Question 17

Norovirus

family / structure / common cause of

Answer 17

Most common cause of infectious gastroenteritis in England and Wales

Belong to Caliciviridae family
Small round-structured viruses (SRSV)
25-30 nm diameter
Single strand RNA genome
Historically known as ‘Winter vomiting disease’

Question 18

Norovirus

at risk gp/ symptoms / Infective dose

Answer 18

Vomiting common in children and diarrhoea is predominant in adults

Infective dose extremely low

Question 19

Gastroenteritis viruses

spread via/ treatment

Answer 19

Viruses spread through close contact with infected persons (e.g. sharing food, water, eating utensils)

Vegetables fertilised with human excrement

Consumption of contaminated foods or beverages

Food may be contaminated by food handlers with viral gastroenteritis

Drinking water and shellfish – sewage contamination

Seasonal outbreaks of various viruses

Group settings e.g. day care, nursing, school, cruise ships

Treatment – rehydration

Question 20

What is a prion?

Answer 20

Prions are normal proteins of animal tissues that can misfold and become infectious.

They are not cellular organisms or viruses.

In their normal non-infectious state, these proteins may be involved in cell-to-cell communication.

Question 21

Prions linked to a group of human diseases

Answer 21

Transmissible Spongiform Encephalopathies (TSEs)

• Gerstmann-Straussler-Scheinker syndrome
• Fatal familial insomnia
• Kuru
• Creutzfeldt-Jakob disease (CJD)

The human diseases are very rare; e.g. classical CJD occurs sporadically worldwide (one case per one million people each year)

Question 22

Prion structure associated with disease

explain

Answer 22

Disease linked to change in protein tertiary structure

Normal prion protein, PrPC - characterised
by four a-helices.

Change to the disease-associated form of PrPSc results in the loss of two of the helical structures which are converted to linear structures (b-sheets).

It is this conversion that is associated with prion infectivity.

Question 23

Foodborne Prion Disease - BSE

link between new human disease
no of reported cases
Incubation period

Answer 23

Bovine Spongiform Encephalopathy (BSE) also known as Mad Cow disease

1986 – Epidemic in a neurological disease in UK cattle
1996 – British government annouce link between new human disease – Creutzfeld-Jakob disease (CJD) and ingestion of beef from cows infected with BSE
(as they caused by the same prion)
British beef market fell by 30% in two days

As of 2004 – 153 reported cases of vCJD worldwide – 143 in UK
Incubation period as long as 20 years

Question 24

clinical indications for vCJD or BSE

Answer 24

No early acute clinical indications for vCJD or BSE :
– caused much concern
– cannot measure the size of the potential problem

Question 25

damage of vCJD or BSE

Answer 25

After an extended incubation period of years, these diseases result in irreversible neurodegeneration (loss of brain function)

Question 26

BSE outbreak cases reported / control

Answer 26

Outbreak related to feeding cattle protein rendered from the remains of scrapie-infected sheep Problem compounded by feeding cattle protein rendered from BSE-infected cow carcasses 180,000 cases of BSE reported in Britain Up to 4 million cattle have been culled

Question 27

Detection of BSE

Answer 27

No practical detection methods exist - (reports of blood test for prion diseases August 2005, Texas) Presence of the BSE agent in tissues determined by injecting animals with samples, then observing the mice to see if they die and have characteristic brain tissue changes: - Mouse inoculation studies take a long time (up to 700 days) to detect the agent - A negative result may only mean that there was too little of the infectious agent to cause symptoms, not that the material was completely free of the infectious agent Can stain for presence of abnormal prion in brain tissue but does not allow an accurate assessment of infectivity of the infected material

Question 28

Variant Creutzfeld-Jakob disease (vCJD) at risk gp

Answer 28

affects younger persons (average age 26 years) and has different clinical features from CJD

Question 29

(vCJD) symptoms

Answer 29

Early symptoms - serious psychiatric problems or problems with senses (ears, eyes or smell) Followed weeks or months later by poor muscle coordination, muscle spasms, and mental confusion. Lasts for at least 6 months On average people with vCJD die approximately 13 months after their symptoms begin Brain at autopsy shows clear changes in tissue structure: - many "spongiform," or open spongy-looking areas, - abnormal clumps of prion protein called plaques, - other areas with less prominent accumulations of abnormal prion protein

Question 30

BSE & vCJD Food Associations

Answer 30

Beef and milk have shown no infectivity in test animals The major concern for consumers is: - potential contamination of meat products by BSE contaminated tissues, or - inclusion of BSE contaminated tissues in foods (mechanically rendered meat products) High risk tissues for BSE contamination - the cattle's skull, brain, spinal cord, - distal ileum (part of the small intestine) - eyes, tonsils The direct or indirect intake of high-risk tissues may have been the source of vCJD in the UK

Question 31

BSE & vCJD Control measures introduced by the British government

Answer 31

Aim to minimize the risk of disease transmission among both animals and humans A ban on feeding ruminant protein to ruminants (1988) Removal of some "high risk" materials (such as brain, spinal cord and intestines) from cattle at slaughter (1989 and 1995) A ban on cattle over 30 months of age from being used for food (1996) Lead to a decrease in the number of cattle with BSE incidence from 36,682 cases in 1992 to 1044 in 2002

Question 32

The cost of BSE

Answer 32

The epidemic of BSE in the UK began in 1986 and affected nearly 200,000 cattle (4 million culled) It leaves in its wake a human outbreak of variant Creutzfeldt-Jakob disease - most probably resulting from the consumption of beef products contaminated by central nervous system tissue. Average only 10-15 cases a year since first appearance in 1994 Early predictions of a vCJD epidemic effecting many 1000s of people has not occurred