Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbe hazard > Non- bacterial foodbourn illness > Flashcards

Non- bacterial foodbourn illness Flashcards

1
Q

Faecal-Oral Route

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Viruses

Structure/ microscopy/ how many enteric viruses

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hepatitis A virus

family/ structure

A

member of enterovirus group of the Picornaviridae family

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hepatitis A virus

infectious dose / at risk gp

A

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

Common in infants and young children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hepatitis A virus

Incubation period

A

2-6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hepatitis A virus

Symptoms & Duration

A

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

variable (2 weeks – 3 months)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hepatitis A virus

Transmission

A

Faecal-oral route

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hepatitis A virus

Associated foods

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hepatitis A virus

Treatment

A

Supportive care, prevention with immunisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Gastroenteritis viruses

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Gastroenteritis viruses

Incubation period

A

15-50 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Gastroenteritis viruses

Symptoms & Duration

A

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

24-48 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gastroenteritis viruses

Detection

A

immune electron microscopy and various enzyme immunoassays from stool samples

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Gastroenteritis viruses

Transmission

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Rotavirus

family / structure / serological gps

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Rotavirus

at risk gp/ symptoms

A

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

17
Q

Norovirus

family / structure / common cause of

A

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’
18
Q

Norovirus

at risk gp/ symptoms / Infective dose

A

Vomiting common in children and diarrhoea is predominant in adults

Infective dose extremely low

19
Q

Gastroenteritis viruses

spread via/ treatment

A

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

20
Q

What is a prion?

A

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.

21
Q

Prions linked to a group of human diseases

A

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)

22
Q

Prion structure associated with disease

explain

A

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.

23
Q

Foodborne Prion Disease - BSE

link between new human disease
no of reported cases
Incubation period

A

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

24
Q

clinical indications for vCJD or BSE

A

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

25
Q

damage of vCJD or BSE

A

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

26
Q

BSE outbreak

cases reported / control

A

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

27
Q

Detection of BSE

A

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

28
Q

Variant Creutzfeld-Jakob disease (vCJD) at risk gp

A

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

29
Q

(vCJD) symptoms

A

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
30
Q

BSE & vCJD Food Associations

A

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

31
Q

BSE & vCJD Control measures introduced by the British government

A

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

32
Q

The cost of BSE

A

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

Microbe hazard (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions