WEEK 1: Food poisoning and food safety

Question 1

Define Foodborne illness.

How are they transmitted?

Answer 1

Infections or illness initiated by the consumption of contaminated food (or water).

Transmission via consumption of food (or water) contaminated with pathogenic bacteria, viruses or parasites (&/or their natural toxins) or chemicals.

Question 2

Outline Common clinical symptoms of foodborne illness.

Answer 2

Acute gastroenteritis, diarrhea & vomiting

Nausea
Vomiting
Diarrhea
Abdominal cramps
Loss of appetite
Mild fever
Weakness
Headaches
Severe life-threatening symptoms of food poisoning include:

Severe diarrhea lasting for more than two days
High fever
Difficulty in speaking or seeing
Severe dehydration, including dry mouth
Blood in urine

Question 3

Describe the epidemiology of foodborne illness.

Answer 3

Common cause of death in developing countries: 2nd most common cause of morbidity & mortality in young infants.

In most adult cases symptoms are brief but in children potentially more detrimental.

Question 4

Foodborne (& waterborne) illness remain a global public health problem with substantial economic impact.

State the Associated risk factors for foodborne illness.

Answer 4

1. High pop. density; limited access to clean water; frequent flooding
2. Poor sanitation resulting in surface water bodies make communities vulnerable to fecal contamination of food & water supplies.
3. Untreated water may subsequently be used for food preparation &/or drinking

Question 5

Describe the pathogenesis of foodborne illness.

Answer 5

Intestinal epithelial cells connected by tight junctions (TJs). Facilitate in reducing permeability of intestinal lining.

1. Act as physical barrier to pathogens & harmful molecules
2. Involved in absorption of nutrients & water

Infection &/or inflammation of the GIT can result in disruptions of the epithelial cells, leading to

-Significant alterations in acid-base & fluid balances
-Intestinal disease: common clinical signs: gastroenteritis, diarrhea, vomiting

Question 6

Although a range of microbial pathogens can cause foodborne illness, a ‘handful’ cause most cases

Discuss the Etiology of foodborne illnesses.

Answer 6

1. Bacteria
   e.g. Salmonella spp., Campylobacter jejuni, Shigella spp., Listeria monocytogenes, Clostridium botulinum & Clostridium perfringens

2, Viruses
e.g. Norovirus, Hepatitis A & E, Rotavirus (particularly assoc. with gastroenteritis in children)

3. Parasites
   e.g. Cryptosporidium parvum& Giardia intestinalis
4. Chemicals
   e.g. high concentrations of pesticides on foods, algae toxins (built up) in shellfish, fish.
5. Parasites
   e.g. tapeworm, roundworm, Anisaki (parasite that lives in fish & can be acquired by eating raw fish meals e.g. sushi)
   Certain parasites & protozoans live in the gastrointestinal tract
6. Transmission: release of cysts, eggs or larvae in stools then acquired through consumption of contaminated food or water
7. Protozoa
   Rare foodborne illness outbreaks i.e. Cryptosporidium, Giardia & Toxoplasma spp.

Fungi
Some contaminate/ grow in grains & produce toxic metabolites assoc. with human illness incl. gastroenteritis
Some macroscopic fungi e.g. mushrooms are eaten but a few species are poisonous & cause serious illness e.g. Amanita phalloides

Question 7

In Botswana, there have been several foodborne illness outbreaks over the years.
State the main causative agent of foodborne illness in the under 5 in Botswana and its major mode of transmission.
.

Answer 7

Sep.2018 reports: ROTAVIRUS-Associated-diarrhea outbreak in Botswana mainly affecting children ≤5yr

One of modes of transmission- contaminated water

Listeria monocytogenes outbreak from cold meat: was more predominant in South Africa.

Question 8

Describe the transmission of foodborne illnesses.

Answer 8

Fecal-oral route

1. Sanitation hazards: Unhygienic conditions
2. Hazardous events: Animal vectors, water sources
3. Exposure to individuals

Question 9

.Describe 2 ways in which microorganisms can cause foodborne illnesses.

Answer 9

Food borne illness caused by:
Eating food containing sufficient no.s of viable pathogens that can cause infection
BUT:
Some microorganisms do not need to be in high no.s & cause illness at very low colony forming units

Expressed microbial toxins rather than the presence of the ‘viable’ microorgansims

Certain mycotoxins or bacterial toxins can also cause severe illness

Question 10

What are the main causes of foodborne illness due to microbial toxins?

Answer 10

Can be caused by a variety of bacteria & fungi:

Examples

*Staphylococcus aureus

*Clostridium perfringens & Clostridium botulinum

*Bacillus cereus

*Aspergillus species

Question 11

What is a common normal commensal found in the nasopharynx of approximately 30% of the host population?

Q: How is staphylococcal foodborne illness primarily caused?

Q: What is the prevalence of Staphylococcal enterotoxins (SEs) among S. aureus strains?

Q: How many different types of Staphylococcal enterotoxins (SEs) are known, and what are their designations?

Q: What are some characteristics of Staphylococcal enterotoxins (SEs) that contribute to their pathogenicity?

Q: To which family do Staphylococcal enterotoxins (SEs) belong?
A: Staphylococcal enterotoxins (SEs) belong to the family of Pyrogenic toxin superantigens.

Q: Which Staphylococcal enterotoxin (SE) is the most common cause of staphylococcal food poisoning?

Answer 11

A: Staphylococcus aureus.

A: By eating foods contaminated with sufficient amounts of preformed enterotoxins produced by Staphylococcus aureus.

A: Approximately 50% of S. aureus strains express Staphylococcal enterotoxins (SEs).

A: There are around 20 known types of Staphylococcal enterotoxins (SEs), designated from SEA to SEE, and from SEG to SET.

A: Staphylococcal enterotoxins (SEs) are resistant to conditions that typically destroy bacteria, such as heat, low pH, and proteolytic enzymes. They remain active in the digestive tract even after the destruction of viable bacteria. Additionally, they are active in very low quantities, ranging from nano to microgram counts.

A: SEA (Staphylococcal enterotoxin A) is the most common cause of staphylococcal food poisoning.

Question 12

Q: What is the conventional process by which microbial antigens are presented to T cells by antigen-presenting cells (APCs)?

Answer 12

A: Conventional antigen presentation involves the uptake and processing of microbial antigens by antigen-presenting cells (APCs). The antigenic peptides derived from the microbial antigens are then transferred to major histocompatibility complex II (MHCII) molecules on the surface of APCs and presented to T cells.

Question 13

How are MHC/antigen peptide complexes typically recognized by T cells?

Answer 13

A: MHC/antigen peptide complexes are recognized by T cells via the hypervariable loops within the T cell receptor (TCR) α and β chains, leading to a specific interaction between the TCR and the MHC/antigen peptide complex.

Question 14

How do superantigens differ from conventional antigens in their interaction with T cells?

Answer 14

A: Superantigens bypass the highly specific interaction between T cell receptors (TCRs) and major histocompatibility complex II (MHCII)/antigen peptide complexes.

Instead, they directly cross-link the conserved structures of the TCR β chains with those of the MHCII molecules.

This interaction occurs outside of the antigen binding sites of the TCRs and MHCII molecules.

Question 15

Q: What is the consequence of superantigens bypassing the specific interaction between TCRs and MHC/antigen peptide complexes?

Answer 15

A: By bypassing the specific interaction, superantigens can activate a large proportion of T cells that express certain TCR Vβ chains, leading to a massive release of cytokines and causing a strong immune response.

This activation of a large number of T cells is characteristic of superantigen activity and can lead to severe immune system dysregulation.

THE FOLLOWING CAN THEN HAPPEN:

-Cardiovascular system & other organs (e.g. renal, hepatic & gastrointestinal)

-Leading to toxic shock syndrome effect

-S. aureus assoc. gastroenteritis characterized by nausea, vomiting & diarrhea usu. within ≤6hr

Symptoms can be severe but generally self limiting (48hrs

Question 16

Discuss characteristics of Staphylococcus enterotoxins.

Answer 16

-Highly stable & resistant to most proteolytic enzymes i.e. pepsin or trypsin, so after ingestion maintain activity in digestive tract

-Heat resistant & thought to be more heat resistant in foodstuffs than in lab culture medium

Can be inactivated during heat treatments used in sterilization of canned foods when present at low concentrations.

In Botswana Loeto et al (2007) study on 200 food handlers:
57.5% carried S. aureus
30.9% S. aureus isolates from hands, 44.6% from nares & 24.5% from face
21% S. aureus: detected SEA (34.9%) & SED (9.3%)

Question 17

Q: Where are Clostridium perfringens and Clostridium botulinum commonly found?

Answer 17

A: Clostridium perfringens and Clostridium botulinum are commonly found in soil, sewage, and the intestinal tract.

Question 18

Q: What distinctive feature do Clostridium perfringens and Clostridium botulinum possess that aids their survival?

Answer 18

A: They produce endospores, which are highly resistant structures that allow them to survive harsh conditions such as canning and cooking.

Question 19

Q: How is Clostridium perfringens classified into biotypes, and what determines these classifications?

Answer 19

A: Clostridium perfringens is classified into biotypes A through E, depending on the production of one or more of four exotoxins: alpha, beta, epsilon, and iota

Question 20

What percentage of Clostridium perfringens type A strains produce Clostridium perfringens enterotoxin (CPE)?

Answer 20

A: Approximately 1 - 5% of Clostridium perfringens type A strains produce Clostridium perfringens enterotoxin (CPE).

Question 21

: When is Clostridium perfringens enterotoxin (CPE) produced, and what is its significance?

Answer 21

A: Clostridium perfringens enterotoxin (CPE) is produced during sporulation in the large intestine. It is an important cause of foodborne gastrointestinal disease.

Sporulation refers to the formation of spores from vegetative cells during unfavorable environmental conditions.

Question 22

C. perfringens food intoxication

Q: What conditions typically favor the ingestion and survival of Clostridium perfringens, leading to the expression of Clostridium perfringens enterotoxin (CPE)?

Answer 22

A: Clostridium perfringens ingestion and survival are favored by the ingestion of a large dose of bacteria (>10^8), typically found in high protein foods such as meat and poultry cooked in bulk where heat penetration is incomplete. Additionally, environments lacking oxygen, such as jars or cans, can also support the survival of Clostridium perfringens.

Question 23

Q: At what temperature range do surviving endospores of Clostridium perfringens typically germinate in foods?

Answer 23

A: Surviving endospores of Clostridium perfringens can germinate in foods at temperatures around 20-40°C.

Question 24

What happens when ingested endospores of Clostridium perfringens germinate?

Answer 24

A: When ingested endospores of Clostridium perfringens germinate, Clostridium perfringens enterotoxin (CPE) is expressed.

Question 25

Q: What is the cytotoxic target of Clostridium perfringens enterotoxin (CPE), and what is its significance?

Answer 25

A: Clostridium perfringens enterotoxin (CPE) targets enterocytes in the intestinal epithelium.

These enterocytes are joined by intercellular tight junctions (TJs).

The cytotoxic action of CPE on these enterocytes disrupts the integrity of the intestinal epithelium, leading to gastrointestinal symptoms.

Question 26

Describe the pathogenesis of C. perfringens food intoxication.

Answer 26

Ingestion of large dose of bacteria (>108) required

Usually in high protein foods e.g. meat, poultry cooked in bulk where heat penetration incomplete. Or in anoxic environment e.g. jars or cans

Surviving endospores can germinate in foods20-40C

Ingested endospores germinate & C. perfringensenterotoxin (CPE) expressed

CPE is cytotoxic targeting enterocytes in the intestinal epithelium, which are joined by intercellular tight junctions (TJs)

CPE binds to enterocytes & forms small complex, which may act as a pore in membrane

Causing membrane permeability in enterocytes resulting in cell death

It also disrupts the TJ (permeability barrier) structures

Leading to fluid/ electrolyte transport alterations, inducing diarrhea

Also, nausea & intestinal cramps (usually no fever)

Question 27

C. botulinum

Q: What is botulism, and what is its primary cause?

Q: What are some potentially fatal outcomes associated with botulism?

Q: What types of foods are typically associated with botulism outbreaks?

Q: What happens under conditions conducive to botulism in terms of Clostridium botulinum endospores?

Answer 27

A: Botulism is a rare but serious illness primarily caused by eating food contaminated with the botulinum toxin.

A: Death can occur from respiratory failure or cardiac arrest due to the paralyzing effect of the botulinum toxin.

A: Botulism outbreaks are typically associated with foods eaten without cooking, such as canned vegetables (e.g., corn, beans) and vacuum-packed meats.

A: Under conditions conducive to botulism, Clostridium botulinum endospores germinate, and the vegetative cells produce toxin. These vegetative cells can be killed by heat treatment, typically at 80°C for 10 minutes.

Question 28

What is botulinum toxin, and which bacterium produces it?

Q: How is botulinum toxin characterized in terms of potency?

Q: How many types of botulinum toxin are there, and which type is the most potent?

Q: Which types of botulinum toxin are commonly associated with systemic botulism in humans?

Q: What are the effects of botulinum toxin on the human body?

Answer 28

A: Botulinum toxin is a neurotoxin produced by Clostridium botulinum.

A: Botulinum toxin is considered the most potent biological toxin known.

A: There are eight types of botulinum toxin: A, B, C1, C2, D, E, F, and G. Among them, type A is the most potent toxin.

A: Types A, B, and E are commonly associated with systemic botulism in humans.

A: Botulinum toxin causes flaccid paralysis by affecting autonomic nerves that control vital body functions such as respiration and heartbeat.

Question 29

Describe the pathogenesis of C. botulinum & botulism.

Answer 29

Acetylcholine in nerve terminals is packaged in vesicles

Normally vesicle membranes fuse with nerve terminals & release acetylcholine

Botulinum toxin cleaves SNARE proteins, preventing assembly of fusion complex & blocking acetylcholine release

Blockage of neurotransmitter release is irreversible.

Resulting in lack of stimulus to muscle fibers, irreversible relaxation of muscles & flaccid paralysis

Question 30

C. botulinum & botulism

Q: How long does it typically take for botulinum toxin to take effect once ingested?

Q: What is the duration of the effect of botulinum toxin on the body?

Q: What are the recommended treatments for botulism?

Answer 30

A: Botulinum toxin typically requires 24-72 hours to take effect after ingestion, although in rare circumstances, it may take days.

A: The effect of botulinum toxin typically lasts nearly 8-12 weeks.

A: The recommended treatments for botulism include the quick administration of botulinum antitoxin or mechanical ventilation for flaccid respiratory paralysis.

Question 31

Bacillus cereus

Q: What are some characteristics of Bacillus cereus?

Q: What toxins are produced by Bacillus cereus?

Q: What are the effects of the enterotoxins produced by Bacillus cereus?

Q: What additional function does the HBL enterotoxin serve?

Answer 31

A: Bacillus cereus is a Gram-positive rod-shaped bacterium and a spore-forming bacteria.

A: Bacillus cereus produces one emetic toxin (ETE) and three enterotoxins: HBL, Nhe, and EntK.

*HBL (Hemolysin BL), Nhe (Non-hemolytic Enterotoxin),

A: All the enterotoxins produced by Bacillus cereus are cytotoxic, causing the formation of holes or channels in cell membranes.

A: In addition to its cytotoxic effects, the HBL enterotoxin also acts as a hemolysin.

NOTE: The function of a hemolysin, such as the one produced by Bacillus cereus, is to lyse or break down red blood cells (erythrocytes). This can lead to the release of hemoglobin from the cells.

In the context of Bacillus cereus, the hemolysin may contribute to the pathogenicity of the bacterium by causing damage to host cells, disrupting tissues, and aiding in the spread of the infection.

Question 32

Q: What are the two distinct types of illnesses caused by Bacillus cereus, and what are their incubation times?

Q: How does Bacillus cereus cause emetic illness?

Q: What is the cause of long-incubation illness associated with Bacillus cereus?

Answer 32

1. Emetic illness, characterized by a short incubation time of approximately one to six hours.

Diarrheal illness, characterized by a long incubation time of about 10 to 16 hours.

2. A: Bacillus cereus causes emetic illness by producing a preformed, heat-stable emetic toxin (ETE). This toxin leads to symptoms of nausea and vomiting shortly after ingestion of contaminated food.
3. A: Long-incubation illness associated with Bacillus cereus is caused by the production of heat-labile diarrheagenic enterotoxins, such as Nhe (non-hemolytic enterotoxin) and/or HBL (hemolytic enterotoxin). These toxins contribute to the development of symptoms such as diarrhea and abdominal cramps.

Question 33

What is food infection?

Answer 33

Food infection refers to a type of foodborne illness caused by the ingestion of food contaminated with pathogenic microorganisms, such as bacteria, viruses, parasites, or fungi.

In food infection, the microorganisms themselves proliferate within the host’s body after ingestion, leading to symptoms of illness.

This proliferation may occur in the gastrointestinal tract, causing symptoms such as nausea, vomiting, diarrhea, abdominal pain, fever, and sometimes more severe complications.

Question 34

Food infection.

Shigella species

Q: How many species make up the Shigella genus, and what are their serogroups?

Q: What are the primary modes of transmission for Shigella infections?

Q: Why is intermediate bacterial replication not necessary for Shigella transmission?

: How do Shigella bacteria survive transit through the stomach?

Q: What happens once Shigella bacteria reach the colon?

Answer 34

A: The Shigella genus consists of four species: DFBS
S. dysenteriae (serogroup A), S. flexneri (serogroup B), S. boydii (serogroup C), and S. sonnei (serogroup D).

A: Shigella infections can be transmitted via contaminated food and water or through direct person-to-person spread, such as via contaminated fingers.

A: Shigella can be transmitted directly from contaminated fingers because it has a low infectious dose, meaning that only a small number of organisms (10 - 100) are sufficient to cause disease. Therefore, intermediate bacterial replication is not necessary for transmission.

A: Shigella bacteria are less susceptible to stomach acid, allowing them to survive transit through the stomach and pass into the small intestine where they multiply.

A: Once in the colon, large numbers of Shigella bacteria cause symptoms of shigellosis, including severe diarrhea (often bloody), abdominal cramps, fever, and sometimes vomiting.

Question 35

What is Shigella bacterial dysentery?

Q: How does the severity of Shigella infections vary among the different species?

Answer 35

Shigella bacterial dysentery is an invasive infection of the large intestine mucosa caused by Shigella bacteria. It results in inflammation of the intestinal lining, characterized by the presence of pus and blood in diarrheal stool.

*S. sonnei infections are typically the mildest.
*S. flexneri and S. boydii infections are associated with more severe symptoms.
*S. dysenteriae infections are the most severe, causing severe dysentery and potentially deadly epidemics.

Question 36

What toxin does Shigella dysenteriae produce, and what are its characteristics?

Describe the structure of Shiga-toxin (Stx).

Q: What are the effects of Shiga-toxin (Stx) on cells?

Q: Which blood vessels are most affected by Shiga-toxin (Stx), and what are the consequences?

Answer 36

Shigella dysenteriae produces a toxin called “Shiga-toxin” (Stx), which is both cytotoxic and enterotoxic.

A: Shiga-toxin (Stx) is an AB5-toxin consisting of two main components: a pentameric binding moiety (StxB) and an enzymatically active A-moiety (StxA).

A: Shiga-toxin (Stx) inhibits protein synthesis in cells, leading to cell death. It also degrades the vascular endothelium, which can result in hemorrhage and bloody diarrhea.

A: Shiga-toxin (Stx) is most effective against small blood vessels, particularly those in the digestive tract, kidneys, and lungs.

It targets the vascular endothelium of the glomerulus in the kidneys, which can lead to kidney failure and a condition known as hemolytic uremic syndrome (HUS).

Question 37

Describe Mechanism of action of Stx.

Answer 37

Step 1: B subunits bind to globotriaosylceramide (Gb3) receptors on some eukaryotic cells
i.e. mostly endothelial cells, kidney epithelium & some antigen presenting cells (subsets of dendritic cells & B cells)

Step 2: Stx internalized by endocytosis

Step 3: Stx transported to the trans-Golgi network

Step 4: Stx transported to endoplasmic reticulum & the ribosome, binds & inhibits protein synthesis. Causes cell death.

Question 38

Shiga toxin-producing E. coli.

Q: What is Shiga toxin-producing Escherichia coli (STEC), and what toxin do they produce?

Q: What is the most common strain of STEC responsible for infections, and where is it commonly found?

Q: Describe the two main groups of Shiga toxins harbored in STEC and their similarities to the toxin produced by Shigella dysenteriae.

Q: How do infections with STEC typically occur, and what foods are commonly associated with them?

Q: What are the health consequences of STEC infections, particularly related to the verotoxin produced?

Answer 38

A: Shiga toxin-producing Escherichia coli (STEC) are strains of E. coli bacteria that produce “verotoxins,” which are enterotoxins similar to the Shiga toxin produced by Shigella dysenteriae.

A: The most common strain of STEC responsible for infections is E. coli O157:H7, which is a commensal bacterium of healthy cattle, with approximately 90% of STEC infections attributed to this strain.

A: STEC harbors two main groups of Shiga toxins: Stx1, which is 98% homologous to the Shiga toxin produced by Shigella dysenteriae, and Stx2, which is approximately 60% homologous.

: STEC infections typically occur after ingestion of contaminated food or water. Approximately 40% of STEC infections are attributed to consumption of contaminated uncooked or undercooked meat.

A: STEC verotoxin can cause hemorrhagic colitis (bloody diarrhea) and hemolytic uremic syndrome (HUS), which can lead to kidney damage. These consequences are similar to those seen in infections caused by Shigella dysenteriae.

Question 39

Other pathogenic E. coli

What are some characteristics of Enterotoxigenic Escherichia coli (ETEC), and what toxins do they produce?

Describe the characteristics of Enteroinvasive Escherichia coli (EIEC) and its mode of infection.

What distinguishes Enteropathogenic Escherichia coli (EPEC) from other pathogenic E. coli strains?

Answer 39

1. Two heat-labile enterotoxins which cause diarrhea
   Common associated foods: fresh vegetables e.g. lettuce in salads
   Also, common cause of ‘Traveller’s diarrhea’ (source commonly contaminated water)
2. Invasive disease in colon, with watery sometimes bloody diarrhea
   -When taken up by phagocytes, evades lysis & then multiplies in cytoplasm
3. Milder infection: does not produce toxins & nor cause invasive disease.
   -Common in infants

Question 40

Salmonella spp.

Q: What are some of the infections caused by Salmonella spp.?

Q: How can Salmonella serotypes be broadly categorized, and what are examples of each category?

Answer 40

A: Salmonella spp. can cause a broad range of infections, including gastroenteritis, enteric fever (typhoid fever), bacteremia, endovascular infections, osteomyelitis, and abscesses.

A: Salmonella serotypes can be broadly categorized into two groups:

1. Typhoid or enteric fever, which includes S. typhi and S. paratyphi.
   *These serotypes cause systemic illness with little or no diarrhea and are transmitted via consumption of fecally contaminated food or water.
2. Gastroenteritis, which includes S. enteritidis and S. typhimurium.

*These serotypes cause salmonellosis, characterized by symptoms such as diarrhea, abdominal cramps, and fever.

*They are transmitted via improperly handled food contaminated with animal or human fecal material.

Question 41

Salmonellosis.

Q: What is the main cause of gastrointestinal disease in salmonellosis?

Q: How do Salmonella bacteria initially interact with the gastrointestinal tract during infection?

Q: What happens to Salmonella bacteria after attachment to epithelial cells in the gastrointestinal tract?

Answer 41

A: Gastrointestinal disease in salmonellosis is mainly caused by Salmonella enteritidis and Salmonella typhimurium.

A: Salmonella bacteria initially attach to columnar epithelial cells or specialized epithelial cells overlying Peyer’s patches in the colon, known as M (microfold) cells.

A: After attachment, Salmonella bacteria induce bacterial-mediated endocytosis, allowing them to enter host cells. Once inside, they survive and replicate within a modified phagosome called the Salmonella-containing vacuole (SCV).

Question 42

Q: How is gastrointestinal disease typically caused by foodborne Salmonella infection?

Q: What is the typical onset and symptoms of foodborne Salmonella infection?

Q: How does Salmonella colonization occur in the gastrointestinal tract?

Q: What is the usual outcome of foodborne Salmonella infection?

Answer 42

A: Gastrointestinal disease caused by foodborne Salmonella infection usually occurs through the ingestion of contaminated food, especially poultry and dairy products. This contamination is primarily due to serotypes S. enteritidis and S. typhimurium.

A: Foodborne Salmonella infection typically has an onset of symptoms occurring 8 to 48 hours after ingestion of contaminated food. The symptoms often include a sudden onset of headache, chills, vomiting, and diarrhea.

A: Ingestion of food contaminated by “viable” Salmonella species leads to colonization of both the small and large intestines.

A: Foodborne Salmonella infection typically resolves without intervention. However, patients may shed organisms for months or become chronic carriers, potentially contributing to the spread of infection.

Question 43

Salmonella infectious dose

Q: How does the infectious dose of Salmonella affect the likelihood and severity of illness?

Q: Which clinical conditions are associated with a lower infectious dose of Salmonella?

Q: Can asymptomatic excretion of Salmonella occur after ingestion of small inocula?

Q: How long can Salmonella persist in certain food products, and what are some examples?

Answer 43

A: A: Larger inocula (greater than 10^4 bacteria) typically result in higher rates of illness and shorter incubation periods compared to smaller inocula (less than or equal to 10^3 bacteria).

A: A: Clinical conditions associated with reduction in gastric acidity, such as neonates, individuals with achlorhydric states, those who have undergone gastric surgery, or individuals using antacids, may have a lower infectious dose for Salmonella.

A: A: Yes, asymptomatic excretion of Salmonella may occur after ingestion of small inocula, but even very small inocula (5 -100 organisms) can cause disease in susceptible hosts.

A: A: Salmonella species can persist for months in food products such as cheese, frozen meat, or ice cream, increasing the risk of transmission if these foods are consumed without proper cooking or processing.

Question 44

Describe the pathogenesis of Salmonellosis.

Answer 44

Invasion of epithelial cells in terminal portion of the small intestine

Bacteria multiply in the ‘ileocecal region’, causing an inflammatory response

Inflammatory response confines infection to gastrointestinal tract

Released prostaglandins activate cyclic adenosine monophosphate which results in fluid secretion & diarrhea

Question 45

Campylobacter

1. What are the characteristics of Campylobacter jejuni and Campylobacter coli?
2. What is the significance of Campylobacter jejuni and Campylobacter coli in terms of foodborne infections?
3. Which foods are commonly associated with Campylobacter contamination?
4. What happens after ingestion of food contaminated with Campylobacter?

Q: How does the infectious dose of Campylobacter jejuni compare under different conditions?

Answer 45

A: A: Campylobacter jejuni and Campylobacter coli are Gram-negative, curved or spiral-shaped rods that are microaerophilic. They may also produce cytotoxins.

A: A: Campylobacter jejuni and Campylobacter coli are the most common cause of bacterial foodborne infections in the USA.

A: A: Contaminated poultry, with chickens being a natural reservoir, as well as turkey, pork, and raw shellfish, are commonly associated with Campylobacter contamination.

A: A: After ingestion of contaminated food, Campylobacter bacteria multiply in the small intestine, invade the epithelium, and cause inflammation, leading to symptoms of infection.

A: A: Campylobacter jejuni is sensitive to gastric acid, and a high number of bacteria (around 10^4) are typically required for infection. However, lower numbers (e.g., 500) can be sufficient when individuals are taking medication to reduce stomach acidity.

Question 46

Q: What are the symptoms of Campylobacter infection?

Q: How long does Campylobacter infection usually last?

: What is the usual outcome of Campylobacter infection?

Answer 46

A: A: Campylobacter infection typically presents with symptoms such as high fever, headache, malaise, nausea, abdominal cramps, and either watery or bloody diarrhea.

A: A: Campylobacter infection typically subsides within 7-10 days.

A: A: Most individuals experience spontaneous recovery, and the infection resolves completely. However, relapses may occur in approximately 25% of cases.

Question 47

Listeriosis

Q: What is the causative agent of listeriosis?

Q: What are the characteristics of Listeria spp.?

Q: Where is Listeria monocytogenes commonly found?

Answer 47

A: Listeriosis is caused by bacteria belonging to the genus Listeria, with Listeria monocytogenes being the most commonly associated species in human infections.

A: Listeria spp. are Gram-positive, nonsporulating coccobacilli.

A: Listeria monocytogenes is widely found in soil and water.

Question 48

Q: Why is no food source immune from Listeria monocytogenes contamination?

Q: What factors contribute to Listeria monocytogenes being ranked high among microorganisms of concern for the food industry?

Q: Which types of foods are commonly associated with Listeria monocytogenes contamination?

Answer 48

: Listeria monocytogenes can contaminate any food source due to its widespread presence in soil and water.

A: Listeria monocytogenes is ranked high among microorganisms of concern for the food industry due to its ability to tolerate high concentrations of salt, low pH levels, and multiply at refrigeration temperatures.

A: Processed refrigerated ready-to-eat foods such as sausages, polonies, pâtés, smoked fish, and dairy products are commonly associated with Listeria monocytogenes contamination.

Question 49

Q: What is the typical mortality rate associated with Listeria monocytogenes infections, despite early antibiotic treatment?

Q: What are the two main types of Listeria monocytogenes infections?

Q: Describe the common characteristics of Listeria monocytogenes infections.

Q: What are some potential complications associated with neonatal listeriosis?

Answer 49

A: The mortality rate for Listeria monocytogenes infections is approximately 20-30%, even with early antibiotic treatment.

A: The two main types of Listeria monocytogenes infections are neonatal listeriosis and adult listeriosis.

A: Listeria monocytogenes infections typically involve disseminated systemic infection or sepsis, as well as central nervous system (CNS) infection.

A: Neonatal listeriosis may also lead to complications such as hydrocephalus or psychomotor impairment.

Question 50

Discuss L. monocytogenes pathogenesis.

Q: How does Listeria monocytogenes enter host epithelial cells and what are the key virulence factors involved?

Q: Describe the process by which Listeria monocytogenes escapes the phagocytic vacuole and replicates within the host cell.

Q: How does Listeria monocytogenes evade the immune system during its intracellular lifecycle?

Answer 50

A: Listeria monocytogenes enters host epithelial cells by inducing phagocytosis.

Key virulence factors involved in this process include InlA and InlB, which facilitate intracellular survival and cell-to-cell spread.

Additionally, the surface protein ActA is crucial for the formation of “comet tails” composed of host-cell actin polymerization, enabling movement within the cell and pushing through the cell membrane.

A: Listeria monocytogenes temporarily resides within the phagocytic vacuole, where it produces listeriolysin O (also known as cytolysin) to escape into the cytoplasm. Once in the cytoplasm, the bacterium replicates.

A: Listeria monocytogenes evades the immune system by not being exposed to antibodies, complement, or neutrophils.

It achieves this by residing within host cells and escaping from phagosomes, allowing it to replicate and spread without direct confrontation by the immune system.

Additionally, the formation of pseudopods and filopods, as well as the phagocytosis of pseudopods by neighboring cells, contribute to the evasion of immune surveillance.

Question 51

What is food safety?

State the 2 Objectives of food safety.

Answer 51

A: Food safety refers to the practices and conditions that preserve the quality of food to prevent contamination and foodborne illnesses.

Prevent transmission of foodborne pathogens

Maintain good quality of the food

Question 52

Discuss the Four pillars of food safety

Answer 52

Temperature control
Maintain food below or above TC danger zones (5-60C)

2. Cleanliness
   Sanitary conditions where food is stored, processed, prepared & served
   Cleaning with food grade chemical sanitisers
3. Eradication of cross-contamination
   Good cleaning; good sanitation; good manufacturing practices & good handling practices
4. Maintenance of good personal hygiene
   Food handlers to keep body clean, healthy & not pose health risk

Question 53

Monitoring water quality to reduce waterborne & foodborne illness.
Ensuring good drinking water quality is vital to minimise illness. Done at diff. levels
Describe what can be done at the following levels.
1. Domestic: boiling & filtration of water

2. Private/ commercial services
3. National bodies/ authorities

Answer 53

Domestic: boiling & filtration of water

Private/ commercial services

National bodies/ authorities
Sampling water sources, lab testing & assessment of: water sources, efficacy of water treatment processes

Analysis of water quality according to national standards.

Question 54

Q: What are faecal indicator organisms?

Q: Why are faecal indicator organisms routinely monitored in water treatment services?

Answer 54

: Faecal indicator organisms are specific microorganisms used as a marker for faecal contamination, such as E. coli.

A: They are monitored to verify, operationally monitor, and surveil water quality.

Question 55

Q: In which industries are faecal indicator organisms monitored besides water treatment?

Q: What conventional methods are used to test for faecal indicator organisms?

Answer 55

A: They are also monitored in the food and environmental industries.

A: The conventional methods include membrane filtration tests and multiple fermentation tube/most probable number index techniques.

Question 56

Describe the membrane filtration method for faecal indicator organisms.

Answer 56

1. Use of a special filter (with specific pore size) to trap microorganisms
2. Put the filter in nutrient media
3. Incubate for 24-48 hours
4. Growth of typical colonied

Question 57

Discuss ways of Minimizing food contamination insmall scale production

Answer 57

1. Food handlers personal hygiene must be excellent esp. hand washing (soap & warm water) then dried thoroughly
   Before preparing food
   After touching raw meat
   After using toilet
   After touching bins
   After touching animals
2. Food handlers should not work with food if they are sick i.e. diarrhea, uncovered & infected wounds
3. Raw food & cooked foods should be stored in a separate refrigerators. Or raw food stored below cooked food, to avoid blood & fluids dripping onto cooked food
4. Food should be kept covered or stored in airtight containers
5. Storage areas: well lit, clean, dry, cool, well ventilated & protected from pests
6. Separate colour coded chopping boards & utensils should be used for raw, cooked foods & different types of foodstuff
7. Utensils rather than hands should used to handle food
8. Safe rubbish disposal techniques should be practiced, rubbish should not accumulate, to prevent contamination by pests.

Question 58

Discuss ways of Minimizing food contamination inlarge scale production

Answer 58

Good management processes

Good sanitary practices

Rapid movement of food through processing procedures

Application of preservation procedures

Question 59

What is pasteurization?

State the temperatures time for pasteurization.

State the temperature for Ultrahigh-temperature process.

Answer 59

Application of heat for reduction of bacterial load

Pasteurization: process in which liquids are heated at specific T Cs & times e.g. milk, juices
*63C / 30sec or 71C / 15sec
*Does not eradicate but reduces bacterial load

Ultrahigh-temperature process
(138C / 2-4sec) (sterilises)

Question 60

What is canning?

What factors affect temperature time for canning?

Answer 60

Food is sealed in a container & then heated i.e. can, glass jar

TC / time relationships for canning depend on the type of food, pH, size of container, consistency & density of food

If microorganisms remain in can, growth can produce gas, resulting in built up pressure

Question 61

What is fermentation?

State Examples of bacteria used industrially in fermentation.

Answer 61

Fermentation is a metabolic process where microorganisms like bacteria and yeast convert sugars into other chemicals, such as alcohol or acids, in the absence of oxygen.

Can be used as a form of preservation for a variety of foods

Examples of bacteria used industrially in fermentation: lactic acid bacteria, acetic acid bacteria, propionic bacteria

Question 62

Membrane filter used to remove microorganisms
Slows down microbial growth

Name the preservation method.

Answer 62

Filtration

Filtration e.g. water, beer, wine, juices, soft drinks

Low temperature

Question 63

Sterilizes surfaces for food handling

Extend shelf life or sterilize meat, seafoods, fruits & vegetables

Name the preservation method.

Describe its 2 types.

Answer 63

Radiation
Ionizing radiation - gamma rays

Non-ionizing radiation (UV light)

Question 64

Decreases water availability
Name the preservation method.

Answer 64

Lyophilization
(Drying/ freeze drying)

Addition of salt or sugar

Question 65

Discuss ways of Minimizing foodborne illnesses during commercial/ retail food production

Answer 65

Hazard Analysis Critical Control Point (HACCP)
A methodical & preventative system that aids food business operators to assess how they handle food production to ensure it is safe for consumption.

*Monitoring & control of in-processes
*Identification of potential hazards & taking appropriate actions before situations are critical

Biological, chemical & physical hazards in production process

Question 66

State the 7 principles of Hazard Analysis Critical Control Point

Answer 66

1. Conduct a hazard analysis to identify hazards
   biological (e.g. pathogens); chemical (e.g. toxins); physical (e.g. metal fragments)
2. Identify the critical control points (CCPs)
   Points in process at which hazard can be controlled or eliminated
3. Establish critical limits for each CCP.
   Criterion that should be met to ensure food safety (e.g. TC & time to ensure elimination of harmful bacteria)
4. Establish CCP monitoring procedures.
   To determine if CCP is under control
5. Establish corrective actions
   If CCP not within established limits, corrective actions ensure control is regained
6. Establish verification procedures
   Confirms HACCP plan operating effectively
7. Establish record-keeping & documentation procedures