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KLA 604 FOODBORNE PATHOGEN

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SECTION A
Question 1:
a)
In the battle against foodborne disease, one of the most important things to
do is to keep a close look out for any outbreaks of foodborne sickness.
Utilizing this technology will allow for the detection of a foodborne illness
epidemic as well as the coordination of a response to such outbreak.
Campylobacter, Salmonella, Shigella, Escherichia coli that generates shiga
toxin, Listeria monocytogenes, and hepatitis A are all examples of diseases
that may be transmitted via food in Australia. Because of the consistently
rising incidence of these illnesses in Australia and the high mortality rate
associated with them, there is a pressing need for ongoing surveillance in
this country.
Bacteria such as Campylobacter spp., Cryptosporidium spp., Cyclospora
cayetanensis, STEC O157 and STEC non-O157, Listeria monocytogenes,
Salmonella spp., and S. enterica are examples of pathogens that may cause
foodborne illness. In the United States, three of the most prevalent causes of
foodborne disease are always being monitored: S. enterica serotype Typhi,
Shigella spp., and Enterobacter enterocolitica. They are accountable for the
great majority of cases of hospitalisation and fatalities that are caused by
food-borne illnesses. Because of the larger population and higher sickness
rate in the United States, there are more infectious diseases being tracked
there than there are in Australia. This is due to the fact that the United
States has more pathogens.
b)
Both Australia and the United States share seven different pathogens. Due to
the fact that the frequency of foodborne diseases is often overstated by

around 80 percent, it is more appropriate to classify them according to the
rates of mortality and hospitalisation as opposed to categorising them based
on the number of cases per 100,000 people.
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Listeria monocytogenes : despite the fact that Listeria
monocytogenes is a relatively uncommon foodborne pathogen,
those who get it have a 91 percent chance of requiring
hospitalization and a 16 percent chance of dying away.
Shiga-toxin producing E. coli STEC O157: The production of Shiga
toxin by E.coli STEC O157 was associated with a hospitalisation rate
of 0.03 percent and mortality rate of 3.4 percent.
Salmonella (non-typloidal): Only 0.04 percent of people who have
non-typhoidal Salmonella end up in the hospital, but 1.9 percent of
those people end up dying away from infection.
Shigella spp.: There is a wide range of mortality and hospitalization
rates associated with Shigella spp., ranging from 0.008 percent to
0.5 percent.


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Shiga-toxin producing E. coli STEC non-O157 : It is estimated that
0.2 percent of all fatalities are caused by E.coli STEC non-O157,
which is capable of producing Shiga toxin.
Campylobacter spp.: Campylobacter spp. has a mortality rate of
0.05 percent and a rate of hospitalisation of 0.009 percent in the
United States.
Salmonella enteritidis typhi: It patients ìnected with Salmonella
enteritidis typhi, hospitalisation occurs in approximately 10% of
case, although fatalities occur in 0% of cases.

c)
According to the CDC, an incorrect diagnosis of an illness that is transmitted
by food happens in around eighty percent of instances. This helps to explain
why so many individuals who are experiencing diarrhoea do not seek medical
assistance when they should be. The overwhelming majority of patients who
go to the doctor do not produce samples or submit themselves to testing in
order for their ailments to be diagnosed. As a consequence of this, the
underestimating of the prevalence of food-borne diseases is a severe issue
that has to be addressed immediately.
It might be difficult to determine the source of an illness due to the fact that
the onset of foodborne infections can take anywhere from a few hours to
many weeks. As a consequence of this, individuals are unable to determine
what they ate or drank before to experiencing symptoms of illness.
When an individual lives in a nation that has a sophisticated health care
system, the likelihood that someone may get a laboratory diagnostic for a

condition such as diarrhoea is increased. It's possible that this will lead to
varying quantities of data being gathered in various nations for the same
illness.
Due to the fact that foodborne illness surveillance is dependent on the
reporting of cases, hospitalizations, and fatalities, it is possible that an
underestimation of foodborne diseases could lead to an inappropriate
inclusion or exclusion from surveillance, in addition to an inaccurate
evaluation of the disease's severity. This is because an underestimation of
foodborne diseases could lead to a lower number of cases being reported.
Question 3:
Behavior factor
Meals that can be prepared in advance, foods that are already prepared to
eat, commodities that have longer shelf life, and items that need to be
refrigerated are gaining in popularity. Less food processing is something that
consumers want to see. Most of the money spent on food in rich nations goes
towards meals that are cooked away from the house. At the same time, the
number of meals purchased from street vendors by city residents has been
growing over the last several years. As a direct consequence of this, the
frequency of outbreaks of foodborne illness that can be traced back to food
that was cooked outside of the house is increasing all over the globe.
Technological changes


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The advancement of technology in the processing, packing, preserving,
transporting, and storing of food has resulted in the creation of both new
foods and new risks. Because the bacteria now have ample time to

proliferate above 100 CFU/g, Listeria monocytogenes has become more
prevalent in ready-to-eat foods as a consequence of increasing refrigeration.
This is because the bacteria now have the opportunity to develop at a faster
rate. There is a potential for listeriosis to be transmitted by consumption of a
wide variety of ready-to-eat items, such as smoked salmon, cheese,
processed meat, and salad.
Climate impact
Alterations to the climate, such as changes in precipitation, temperature, the
warming of the ocean, and acidity, have an effect on the environment of
bacteria, viruses, fungi, and parasites, which in turn increases the risk of
foodborne disease. There is little question that the incidence of food-borne
illnesses will rise as a result of climate change. The formation of bacteria in
food is encouraged by a high temperature that is maintained for a prolonged
period of time. Another sign pointed to the possibility that changes in the
seasons are connected to an increase in the number of cases of foodborne
contamination and sickness. In addition, during the summer months in
Canada, there is an increase in the number of cases of salmonellosis,
whereas the prevalence of salmonella infections in meat does not change.
This demonstrates that the human exposure component of the rise in
Salmonellosis incidence is responsible for the trend. Additionally, reservoir
populations rise as a result of climate change, leading to an increase in the
total number of disease vectors.
Foodborne diseases continue to challenge public health security
despite improved hygiene, detection technology and in-depth
knowledge of pathogens.
Despite an in-depth knowledge of pathogens, improved hygiene, and
detection technology, foodborne diseases continue to be a burden on public
health for a number of reasons, including those listed below:
- The frequency of pathogens is on the rise. For instance, Salmonella
Typhimurium is replaced by Salmonella Enteriditis, which is linked to

eggs, and the incidence of Trematode infection rises in tropical
countries.
- Mutation and genetic rearrangement are the two mechanisms
responsible for the emergence of new, more lethal disease strains.
- These strains have the potential to acquire resistance to food
processing and preservation techniques as well as antibiotics.
- Pathogens may cause an upsurge in infectious illnesses in new
populations. They are able to grow or change in sensitive
populations.
- A unique pathogen transmission mechanism has been uncovered.
For example, the usage of wood pallets may pose grave threats to


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the safety of our food and medicines. Both almonds and peanuts
contain the bacterium salmonella.
There are several species that are unknown because they have not been
investigated or suspected. Human behaviour, moving demographics, climatic
change, economic hardship, and insufficient public health monitoring are
some of the other factors that contribute to the spread of viruses as
foodborne diseases. These factors could also have an effect on the presence
or recurrence of bacteria that are responsible for food-borne diseases.
In summary, the adaptation and metamorphosis of illnesses result in an
increase in the frequency and severity of the related public health problems.
Climate change, greater globalisation, and changes in human behaviour all
contribute to the genesis of viruses. The emergence of a new disease
transmitted via food. Consequently, foodborne illnesses continue to

represent a concern to public health safety.

SECTION B
Question 4:
a)
The microorganisms that make up this combination are Streptococcus
pyogenes and Bacillus cereus.
It is feasible to test for the presence of S. pyogenes by using blood agar that
contains a proportion of sheep blood. This kind of media is considered to be
selective. The existence of distinct clear zones reveals that beta-haemolysis
on blood agar is produced by bacteria. This may be seen since the clear
zones are present. It is possible to detect S. pyogenes in clinical samples by
using MC&S obtained from a throat swab. RADT is able to identify
carbohydrate antigens that belong to group A.
It is possible to test food for the presence of enterotoxin Nhe or haemolysin
BL by using either a PCR kit or an immunoassay kit. PEMBA, MYPA, and
Chromogenic agar are all viable options for determining the presence of
Bacillus cereus in food and clinical samples, respectively. PEMBA contains
ingredients that are known to suppress the development of bacteria,
including sodium pyruvate, mannitol, and polymyxin B antibiotics. MYPA,
which is used to monitor the activity of lecithinase, contains the ingredients
mannitol, the antibiotic polymyxin B, sodium pyruvate, and egg yolk. B.
cereus will produce blue colonies and a clear zone when grown on
chromogenic agar, but it will produce green or blue colonies with a clear
zone when grown on brilliant agar.
b)
Toxemia may manifest as enterotoxin, which targets the digestive tract, or
neurotoxic, which targets the nervous system. Gram-positive bacteria are the
cause of enterotoxin formation in food and are transmitted by humans.
Enterotoxin is a superantigen that has a high heat tolerance and can

withstand boiling for many minutes. Within a few hours of ingestion, it


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causes severe spells of stomach cramping, nausea, vomiting, and diarrhoea
in addition to these other symptoms. The neurotoxin is produced by the
vegetative cells of the bacteria Clostridium botulinum, Escherichia coli, and
Vibrio cholerae. Neurotoxicity is the consequence of a neurotoxin's toxicity to
the nerve tissue it impacts. In conclusion, gram-positive bacteria produce
toxins in street food, and since the food is not stored on hot surfaces or at
temperatures above 60 degrees Celsius, nor is it refrigerated, it is relatively
easy for people to absorb the toxins.
c)
The food safety problem, which may result in diseases transmitted by food, is
caused by a number of different factors. Buying products of poor quality or
those are beyond their prime and storing them in unsanitary conditions both
have a negative impact on the quality of the meal. The growth of bacteria is
encouraged as a result of this. Food handlers have the potential to be a
cause of food contamination if they practise inadequate hygiene and
manipulate food in an unsafe manner. When preparing different kinds of
food, such as meats and vegetables, the cutting board and knife must be
utilised in a distinct manner each time. In addition, many people may have
trouble re-heating food to the point where it boils before ingesting it, which
may lead to the consumption of unhealthy meals.
d)
Identify hazards: As a rule, street food is not adequately kept, which
increases the risk of contracting a number of illnesses that are transmitted

via food. Cross-contamination might occur in the food industry if employees
did not practise proper hygiene.
Identify critical control points: Because street food is not stored in a
facility that is either refrigerated or heated, germs have the potential to live
for up to four hours after it has been prepared. Because there is a lack of
water and soap in many of the restaurants that serve street food, many of
the employees in these restaurants do not wash their hands after handling
possibly contaminated raw materials or meat.
Establish critical limits: Consumption of the meal must take place either
two hours after it has been cooked or if it has been kept at under 4 or above
60 degrees Celsius. Employees in the food industry are required to wash
their hands with soap and water after processing raw ingredients and meats.
Set corrective actions: After the food has been made, the details of its
preparation together with an estimate of the length of time it cannot be sold
are required to be noted on a page. In the working area, make sure there is a
supply of water and soap for anyone who handle food.
Question 5:
What was the basis of the infection problem associated with this
person?
Mary Mallon works in the kitchen of a New York City restaurant. The typhoid
fever she was sick with was undetectable to the naked eye. Despite her
illness, she continued to work and transmitted it to others by touching her


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infected hands to other people or items. This outbreak of salmonella typhoid
led to the deaths of fifty people, the sickness of one hundred and seventyfive others, and the hospitalisation of about one thousand two hundred

students from schools throughout the state.
What made the infection distinct in terms of the infectious agent
compared to less virulent serotypes of the same species?
This illness is caused by either Salmonella typhi or Salmonella paratyphi. The
presence of the O-antigen "Vi," which improves resistance to host peroxide
and host complement, contributes to the bacteria's more aggressive nature
compared to that of other stains. It helps bacteria hide from antibodymediated opsonization, which is a process that kills germs.
The bacteria produce typhoid toxin, which causes damage to cells and may
lead to prolonged fever and disease in a way that non-typhoid stains cannot.
However, other strains of Salmonella, such as S. bongori, contain just four
pathogenicity islands and lack SPI-2. Salmonella typhi has adequate five
pathogenicity islands for virulence, including SPI-1, SPI-2, SPI-3, SPI-4, and
SPI-5.
In contrast to other stains, they may go through a process called phase
variation, which might change the expression of proteins and provide
tolerance against immune responses.
What specific traits of the infectious agent made the issue possible
in the first place?
This syndrome is characterised by a high prevalence of asymptomatic
infections, and while only 1% to 3% of carriers are able to transmit the
disease to others, this is a crucial factor that causes illness in others.
Salmonella typhi or paratyphi is very harmful since it is immune to the host's
immune response and may thus cause illness. Due to the fact that the
pathogens may be transmitted by faeces and saliva, contaminated foods
have the potential to cause the sickness. Mary is at danger of developing a
disease due to her contact with the faeces of a range of animals, including
cattle, chickens, and other birds. In addition, she spreads the illness to others
since she interacts with a big number of people at her place of work and
because she handles a significant number of food items.
Is it possible that “Typhoid Mary” was badly treated by the public, and

history in general?

I have no doubt in my mind that Mary Mallon is connected in some way to
the recent typhoid epidemic. Mary has been given an unjust reputation by
both those who lived during her time and later historians. The investigation
suggested that Mary was likely to blame for the salmonella typhoid outbreak,
and further evidence confirmed that Mary was aware that she was sick but
continued to go to work despite the fact that she maintained a slovenly level
of hygiene in the workplace. These two pieces of evidence strongly
suggested that Mary was responsible for what had happened. On the other
hand, we are aware that salmonella typhoid is often an asymptomatic
sickness that may spread disease, and that the disease may also be


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transferred between animals and humans. This is something that we must
take into consideration. In addition, the typhoid salmonella virus is
particularly dangerous to humans because of their very high susceptibility.
Question 6:
Define prion disease.
Prion illness is caused by a mutant form of a protein that is normally found in
the body (PrPc). The prion is an infectious protein that has a shape similar to
a sheet. It is also known as the prion protein scrapie related protein (PrP sc). It
is found in the brain and is responsible for the neurodegenerative disease
known as transmissible spongiform encephalopathy, which affects humans,
as well as a variety of other life-threatening neurodegenerative conditions
that affect animals.

The source and transmission of disease
Human-to-human transmission is possible if tainted meat or other products
obtained from cattle are consumed. For example, the use of surgical
equipment that have been contaminated with infectious material may lead to
the spread of disease in people. If a person has the PrP c gene mutation codon
129 homozygous for methionine, they are more likely to acquire this
disorder.
Transmission and proliferation of prions
When prion protein interacts with regular protein, heterodimers are formed
between the two types of proteins. These heterodimers eventually change
into homodimers of aberrant protein and amyloid. Therefore, when regular
PrPc comes into contact with PrPsc, it causes the normal PrPc to convert into
the PrPc form and causes disease.
The accumulation of PrPsc may be harmful to the brain since it can lead to the
production of fibrils and plagues. PrPsc is a hydrophobic, spherical protein that
may cluster with both PrPc and itself. PrPc is attached to the cell membrane
by phosphatidylinositol glycan. As a result of PrP sc's interaction with PrPc, PrPc
is altered to become PrPc that has a sheet. When cells produced new PrP c, a
chain of prion protein was built along anionic glycosaminoglycan on the cell
surface. This was how prions spread from cell to cell. After then, there will be
a break in the chain, and PrPsc will be freed. As a result, neuronal cells import
and store PrPsc.
Prion diseases in human
The bulk of those who die with Kura disease are women, children, and the
elderly, and its incubation period is unusually protracted. Those that
participate in cannibalism are more susceptible to contracting this illness.
Creutzfeldt-Jakob disease is a kind of sporadic human encephalopathy
characterised by memory loss, inability to sleep, progressive weight loss, and
deteriorating muscular coordination. Patients typically perish away after 4.5
months of disease, at which time they have an average onset age of 65

years.
Prion diseases in animals
Animals that are fed meat and bone meal from animals that are infected with
prions are more likely to develop bovine spongiform encephalothapy. It


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results in strange behaviours, such as wobbling and falling, as well as a loss
of weight and mortality within days.
HACCP approach to prevent prion disease.
Identify hazards: Consumption of items generated from animals with
bovine spongiform encephalopathy (BSE), commonly known as creutzfeldtJakob disease, may transmit the prion disease to humans. In addition to
vaccines and growth hormones, other mechanisms of prion transmission
include the contamination of surgical instruments and the injection of growth
hormones. In addition, prions that cause prion disease may be transmitted
by the consumption of gelatine, milk products, and other things containing
gelatine; however, this form of transmission is very rare. If a person's PrP c
gene has two copies of the methionine variation at codon 129, their
likelihood of developing the disease is enhanced.
Consumption of scrapie-infected sheep carcasses or cattle carcasses with an
unknown transmissible spongiform encephalopathy may result in bovine
spongiform encephalopathy (BSE) in cattle. Sheep are susceptible to the
transmissible spongiform encephalopathy known as scrapie. BSE may be
transmitted from a mother sheep to her lambs through both placental
secretions and the placenta itself. Due to their genetic makeup, sheep are
more susceptible to illness than other animals.
Identify critical control points:

In order to protect human health, BSE-infected animals need to be removed
from the food chain. sterilisation of instruments in preparation for surgical
usage Investigate whether or not PrPsc is present in immunizations and in the
growth hormone that is injected. It is prohibited to feed carcasses from cattle
infected with crappie to other cattle, and euthanasia is required for sheep
suffering from prion disease.
Establish critical limits:
Prior to their usage in food production, cattle must undergo monthly BSE
screenings. Surgical instruments are needed to be sterilised both before and
after use. Before being provided to patients, every growth hormone injection
and immunisation must pass prion testing.
Set corrective actions:
Countries have the ability to place import restrictions on live ruminants,
items derived from ruminants, and imports from nations that have animals
afflicted with BSE.
Implementing BSE monitoring and determining whether animals have a high
risk of contracting BSE
A nationwide drive to eradicate scrapie as quickly as possible, including
active testing on live animals and killing of infected animals, animal
identification and tracking, and cleaning up affected areas.
It is optional to participate in the flock certification programme for scrapiefree sheep, which validates the flock's lineage.
Question 7:
a)
Patient A


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Patient Guillain-Barre Syndrome is a consequence of campylobacterosis,
which is often caused by the bacterium Campylobacter jejuni.
Immunotherapy is essential to treat the patient, and the plasma must be
replenished to eradicate potentially harmful antibodies.
The infection that causes illness in males may be transmitted by the
consumption of contaminated food, such as chicken meat or
unpasteurized milk. Additionally, he contracted the sickness by the fecaloral route, which means he acquired it from others by coming into
contact with their hands, which contained the germs, or by touching
surface objects.
Patient B
Clostridium botulinum was the pathogen responsible for the infant
botulism that Patient B developed. Antitoxin administered intravenously
in the form of botulism immune globulin might be used to treat the
patient.
Baby bottles that have been touched by the germs and bacteria that
people carry on their hands have the potential to make newborns ill.
There is a risk that the infant may put his hands in his mouth after
accidently touching bacteria-filled canned items.
b)
Patient A
Campylobacter jejuni may infect humans, chickens, birds, cattle, cats,
dogs, minks, rabbits, and other animals, as well as insects. Often
asymptomatic carriers of the bacteria, animals serve as a reservoir for
the infection.
Within a few hours, a sample is collected from the chicken's faeces and
then examined. There is no excessive oxygenation or chilling of the
specimen. First, the specimen is isolated from the remainder of the
sample using a 0.45-micron filter, and then it is improved using selective
medium. using microscopy to examine for gull-wing appearance in
gramme stain, darting motility in fresh faeces, and faecal leukocytes.

Incubation at 37 or 42 degrees Celsius in an atmosphere containing 5
percent carbon dioxide, such as a candle jar or a gas-producing
apparatus. The C. jejuni hippurate hydrolysis test is positive. On campy
CSM agar, C. jejuni looks black, but on campy CVA agar containing sheep
blood, it becomes red. C. jejuni may be identified by the presence of
oxidase and catalase, the absence of urease, growth in 1 percent glycine,
and nitrate reduction.
Patient B
Therefore, the formation of Clostridium botulinum may be encouraged by
any diet since its sources could produce spores. As a result of the lack of
oxygen in this environment, canned items, such as vegetables and
mushrooms, are particularly susceptible to spoilage. Products made from
poultry, processed meats, and marine goods like smoked and salted
salmon are also susceptible to contamination from the infection.


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For the purpose of testing for Clostridium botulinum, selective media
such as M911 agar and Tryptone-sulfite-cycloserine agar may be used.
The bacteria will degrade, which will lead to precipitation around colonies
on M911 agar and the creation of huge, flat colonies with back centres on
Tryptone-sulfite-cycloserine agar. Both of these results may be seen on
the agar plates.
In order to determine whether or not C. botulinum is present,
immunological tests such as ELISA, which make use of multiplex
antibodies, are carried out. This method is very sensitive, does not cost
too much money, and can be completed in a short amount of time, but it

does not test for toxicity.
Methods based on nucleic acids, such as reverse transcription-PCR (RTPCR) and RNA microarray, are used to investigate C. botulinum. These
methods are not only fast, low-cost, and sensitive, but they also detect
just genes or gene expression without any harm.
The toxicity of C. botulinum may be determined using bioassays
performed on mice; however, these tests are time-consuming and
expensive.

SECTION C
Question 8:
Describe why Listeria monocytogenes is considered a risk for the
food industry even though it is relatively rare.
L. monocytogenes-caused infections have a high death rate, ranging from 20
to 25 percent in adults and 50 percent in newborns. Neonatal patients,
pregnant moms, and the elderly constitute a vulnerable group that must
avoid foods with a high risk of listeria infection. Raw milk, soft cheese, raw
sprouts, deli meats, and rock melon are examples of these foods. The cost of
treating illness in Australia is projected to be between $2 billion and $3
billion. In addition, the cost of keeping food safe from pathogens in Australia
is expected to vary between $0.13 billion and $1.5 billion. This cost
comprises sample testing, equipment design, inspection and packaging of
items, as well as the cleaning and sanitation programme.
L. monocytogenes can survive and thrive at temperatures as low as -80
degrees Celsius, and it is also highly resistant to salt and acid. The bacteria
cannot be controlled since it can survive at temperatures as low as -180
degrees Celsius and grow at temperatures as low as -0.40 degrees Celsius. In
addition, the formation of biofilm by bacteria adds to the difficulty of cleaning
within the food industry.
L. monocytogenes may be found in several settings, such as soil, water,
plant matter, agricultural stuff, fish, amphibians, birds, and other animals.

Describe features and capabilities Listeria monocytogenes
strains possess that makes it a persistent risk in the supply
chain


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Eukaryotic cells may be attached to the surface of L. monocytogenes by the
proteins Ami, LapA, and Lap B. In addition to this, it has FbpA, which has the
ability to attach itself to fibronectin found on host cells, as well as internalin J,
which has the ability to bind to mucin found in the mucus layer.
In particular, it causes internalin A to adhere to and penetrate the cells of the
human gut. Internalin A makes it possible for bacteria to enter host cells by
affixing itself to E-cadherin, a receptor protein found on enterocytes in the
gut. This method is also known as the Zipper mechanism.
By activating Met signalling, initiating the endocytosis process, or binding to
GAGs, which forces Met activation in the absence of internalin B, internalin B
makes it easier for bacteria to enter a wide variety of different cell types.
This is accomplished by internalin B subverting cell junctional endocytosis.
L. monocytogenes produces peptidoglycan deacetylase and peptidoglycan Oacetylase, two enzymes that assist in modifying the bacterial cell wall in
order to circumvent the humoral defences of the host, such as lysozyme.
Internalin C, Internalin K, and Lnt are three more compounds that inhibit the
immune response of the host. Internalin C dampens immune system.
Internalin K blocks the identification of cells necessary for phagocytosis. The
production of interferon by the innate immune system is controlled by Lnt,
which is a transcription factor.
The protein known as listeriolysin O (LLO) provides pathogens with a helping
hand in their escape from the phagosome. Together with phospholipases

(PlcA and PlcB) and the enzyme metalloproteinase (Mpl), which activate PlcB
to facilitate bacterial entrance into the cytoplasm, it performs the role of a
pore-forming toxin.
Within the thick cytoplasm of host cells, the movement of actin, which is
found in host cell, is helped along by a protein on the cell surface called ActA.
The actin tails cause the bacteria to travel in a direction that is determined
by chance, make contact with the cell wall of the host, and then form a
protrusion that moves the cell that is next to them. The process of cell-to-cell
communication triggers an immune reaction, which in turn causes organ
damage.
There is a paucity of knowledge regarding Listeria monocytogenes among
both food manufacturers and consumers. During the food preparation
process, this company is not employing the correct technique in an
acceptable way, which should eradicate any potential pathogens. Listeria
monocytogenes is unlike other bacteria in that it can withstand up to 2.5 M
NaCl, can grow at 10C and live up to 45oC, and can tolerate a pH of 4.2. This
may be unexpected in their situation. In addition, consumers were unable to
properly store or re-heat the food to destroy harmful bacteria.
The bacteria's development of biofilm aids in their resistance to washing and
disinfection and guarantees that they continue to infest food products. In
actuality, 0.3 percent of 272,000 samples had a positive result for the
bacteria.


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The development of pathogenic components, such as those resulting from
mutation, allows bacteria to grow more harmful while escaping the immune

system.
Question 10:
Indicate the names, physical features, and transmission modes of
these viruses
Norovirus: The particles of a norovirus are spherical and they are not
enclosed. Noroviruses have a positive sense and only have one strand of
RNA. It is a member of the family known as Caliciviridae. The size of its
genome is 7.5 kilobase pairs, and the diameter of its particles ranges from
27 to 38 nanometers. Only human beings are susceptible to infection. The
faecal-oral route is the mode of transmission for norovirus, which includes
the consumption of contaminated food and drink, direct contact between
infected individuals, the touching of contaminated surfaces, such as toilets,
and the inhalation of aerosolized particles.
Rotavirus: It is a type III virus with two RNA strands and a spherical, nonencapsulated particle. It is a member of the Reoviridae family. The genome is
18 kbp in size and consists of 11 segments; the diameter of the particle is
between 70 and 80 nm. It starts in insects and eventually spreads to
humans. Rotavirus may be transmitted from person to person through the
faecal-oral route, including consumption of contaminated food and drink,
contact with contaminated surfaces, and even aerosols. It may survive in the
environment for nine to nineteen days and is extremely contagious.
Hepatitis A virus: The Hepatitis A virus is a positive single-stranded RNA
virus that is classified as a category IV virus. Its particles are spherical and
they do not have an envelope. This virus is a member of the Picornaviridae
family. Its genome is 7.5kbp in size and particle size is 27-29nm diameter.
Only human beings are susceptible to infection. The norovirus may be
passed from person to person by excrement to the mouth, as well as through
contaminated food and water, most notably raw or undercooked seafood.
Describe the diseases these viruses cause and any distinctive
properties relevant to human disease
Norovirus-caused gastroenteritis normally lasts for 48 hours and develops

two to three days following introduction to the virus. The digestive tract and
salivary glands are the principal targets. Among the symptoms of this
disorder are vomiting with force, stomach discomfort, nausea, weariness,
loss of taste, muscle aches, weakness, and a low-grade temperature. There
is an association between consuming salads and seafood and contracting
norovirus. This sickness does not elicit a powerful immunological response,
and survivors do not establish long-lasting immunity. Norovirus is recognised
using PCR or RT-PCR kits since it cannot be produced in a culture.
Rotavirus-caused gastroenteritis is often mild and self-limiting, despite
being the greatest cause of infant mortality in developing countries. The
damaged organ is the intestines. This sickness is characterised by nausea,
vomiting, watery diarrhoea, and a low-grade temperature. Rotavirus
genomeNSP4 is capable of cause diarrhoea by means of a mechanism known


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as pushing gut cell Ca2+-dependent transepithelial secretion. The virus is able
to survive pasteurisation and is resistant to disinfectants. Immunization is
the most effective method of rotavirus infection prevention.
The progression of hepatitis caused by the hepatitis A virus may take up to
six weeks, and the sickness can last for eight weeks or even six months. The
severity of the condition's symptoms increases as the sufferer ages. The
organ that will be damaged is the liver. Symptoms of this disorder include
jaundice, fever, watery diarrhoea, vomiting, nausea, and abdominal pain.
The virus is very resistant to chemical disinfectants, although UV light,
chlorine, and other substances may make it harmless. Due to the virus's
reproductive characteristics, it is difficult to culture the virus. A person who

contracts the virus will be immune to it for the remainder of their life.
Vaccination and maintaining high standards of personal and public hygiene
are both effective strategies of preventing and minimising the spread of the
disease.
why food-borne pathogenic viruses are usually not under
surveillance as notifiable pathogens. Also describe means to
mitigate such viral illnesses especially in light of the Covid-19
pandemic.
Vaccines are often effective against the deadly viruses that may be
transferred via food. As a result of the fact that many food-borne pathogenic
viruses cause only mild sickness that clears up in a matter of days, almost all
of these viruses do not cause serious illness in people. Even though
coronavirus has been found in the faeces of infected persons in certain tests,
researchers are still worried that uncontaminated food might become
contaminated and cause the virus to spread to other people. However, there
is no evidence to imply that coronavirus is an infection that is transmitted by
food.
Disinfecting surfaces may help prevent the spread of norovirus. The vast
majority of disinfectants containing chlorine are successful in killing the
virus. Alcohol has the potential to completely eradicate the virus. Twenty
percent of Caucasians are born without a functioning fucosyltransferase
enzyme, which gives them the ability to resist the binding of viruses. The
majority of people have mild symptoms and get well within forty-eight hours.
Vaccinations are the most effective way to prevent rotavirus. Through
immunisation efforts, the frequency of Rotavirus has significantly reduced
across the board, in both industrialised and poor countries alike. Despite the
fact that rotavirus does not affect adults, it is a major contributor to infant
mortality in developing countries. Rotavirus only affects newborns.
The Hepatitis A virus may be contained by the use of vaccines, the
elimination of sewage contamination in areas where shellfish are produced,

and through improved public hygiene in general.
Question 11:
a)


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Diarrhea and a number of other illnesses that are not limited to the digestive
system may be brought on by E. coli. Pathovars and pathotypes of E. coli are
to blame for a broad range of illnesses and deaths across the world. As a
result of this, pathogenic E. coli has been the focus of a significant amount of
research. Research is conducted on a wide variety of topics, including but not
limited to humans, animals, food, and the environment. It is possible for the
same sickness to appear differently in terms of symptoms, start, and
prognosis depending on which pathotypes are currently present in the
intestinal mucosa at any one time. Epidemics are common in industrialised
countries as well as underdeveloped ones, and they may be lethal in any
setting. These illnesses only need to be present in trace amounts for them to
be a danger to the public's health. It's possible that different pathotypes
have varying infectious dosages. There are ways that may be used on both a
national and international scale to identify and monitor E. coli outbreaks.
There is a deficiency of monitoring in many of the world's most
disadvantaged nations. Even while not all pathotypes have the same impact
on public health, they all pose a risk of disease transmission and impede
efforts to improve health outcomes. This is true despite the fact that not all
pathotypes have the same effect. In this article, we take a look at some of
the most recent and significant contributions to our understanding of the
intestinal pathotypes caused by E. coli. It places an emphasis on recent

happenings.
b)
The pathogenicity island of certain bacteria is 35,600 bytes. It's known as the
LOE (LEE). For instance, E. coli strains that are both enterohemorrhagic as
well as pathogenous are included in this list. Because bacteria cling tightly to
enterocytes in affixing lesions, a signalling cascade damages the brush
border and microvilli in effacing lesions, and ions are lost, the two types of
lesions are unique. Frequently, lesions that heal on their own occur. Diarrhea
may be caused by any of these. Intimin and its receptor, the translocated
intimin receptor, are both encoded by one of the type three systems, which
has 41 open reading frames and five major operons (Tir). Transcriptional and
posttranscriptional regulators on and off the pathogenicity island control LEE
expression. Transcriptional feedback inhibition, activation, and repression
have been linked to a number of drugs by scientists. Quorum sensing and
gene transcription and translation are controlled by these molecules. To
understand how this lesion's transcription and expression are controlled, we
conducted a brief overview of the extensive regulatory network involved. It is
this network that regulates gene replication and use.
c)
Escherichia coli is a bacterium that has several pathotypes that are
responsible for a broad variety of diseases. In addition to the fact that


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Escherichia coli is a vital component of the normal intestinal microflora of
animals, including humans, it is also a potent pathogen. Enteric illnesses,
including diarrhoea and dysentery, are caused by at least six main

pathotypes. Extraintestinal infections, such as urinary tract infections and
meningitis, are caused by pathotypes other than those responsible for
intestinal infections.
- E. coli virulence factors are encoded on plasmids, bacteriophages,
transposons, and pathogenicity islands. These genetic components may be
passed across strains, creating new virulence combinations.
- E. coli virulence factors interfere with cell signalling, ion secretion, protein
synthesis, mitosis, and cytoskeletal organisation.
- E. coli pathotypes have a wonderful mosaic genomic structure. K-12 strain
lacks 2,000 genes over 247 islands, like one pathotype. The K-12 pathotype
lacks a similar pattern. Pathogenic E. coli may have less than 0.53 GB K-12
DNA. It's possible.
- Pathogenic E. coli virulence factor-encoding genes are controlled by
pathotype-specific regulators and 'housekeeping' regulators. Pathogenic E.
coli has pathotype-specific regulators. Commensal E. coli lacks pathotypespecific regulators.
E. coli is one of the few microorganisms that has the ability to change its
behaviour in response to a broad range of environmental factors. E. coli is
not only an important component of the normal intestinal microflora of
mammals, such as humans and other animals, but it has also been used
extensively as a cloning host in the field of recombinant DNA technology.
This is due to the fact that E. coli is able to successfully transfer genetic
material from one organism to another. Nevertheless, E. coli is not just a
worker in the laboratory or a harmless resident of the digestive system; it is
also a highly adaptable pathogen that often causes fatalities. There are many
different strains of E. coli, and they are all to blame for the wide variety of
illnesses that affect the intestines and other parts of the body. Virulence
factors, which have an effect on a range of biological processes, are
responsible for the development of many disorders.
d)
In most cases, Escherichia coli may be found living in the digestive systems

of people and other animals. There are several strains of E. coli that are
suitable for human consumption, and some of them may even be beneficial
to the digestive system. If an E. coli strain is pathogenic, for example, it has
the potential to cause diarrhea and perhaps sickness in areas of the body
other than the intestines. Diarrhea-causing E. coli strains may be


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disseminated by any combination of the following three routes of
transmission: direct contact with ill animals or humans; ingestion of
contaminated water or food; or any combination of the two. The E. coli
bacteria are a heterogeneous community consisting of several distinct types
of microorganisms. The many pathotypes of pathogenic E. coli are
categorized under the same umbrella. The term "diarrheagenic E. coli" refers
to a collection of six distinct pathotypes of E. coli that have each been
associated with the sickness. This strain of E. coli is also known as an
enterohemorrhagic E. coli, often abbreviated as EHEC, and a verocytotoxinproducing strain of E. coli, abbreviated as VTEC, EHEC. When an outbreak of
a foodborne illness takes place, the focus of the majority of the media's
attention is directed around a certain pathotype.