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3s2: Infection and Immunity > Week 6 > Flashcards

Week 6 Flashcards

1
Q

What is a pathogen?

A

Microorganism that can cause disease (e.g., bacterium, virus, fungi, parasites).

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2
Q

What is pathogenicity?

A

The ability of a pathogen to cause disease (e.g., whether a microorganism is pathogenic)

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3
Q

What is virulence?

A

The degree to which a pathogen can cause disease in an infected host

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4
Q

What is virulence factor?

A

A molecular characteristic that enhances a pathogen’s ability to cause disease in a host (e.g., proteins, toxins)

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5
Q

Which of top ten deaths are caused by infections diseases in 2019 globally?

A

Number 4, 5 and 8
Lower respiratory diseases
Neonatal conditions
Diarrhoeal diseases

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6
Q

Which of top ten deaths are caused by infections diseases in 2019 in low income countries?

A

Number 1, 2, 5, 6, 8 and 9
Neonatal conditions
Lower respiratory conditions
Diarrhoeal conditions
Malaria
Tuberculosis
HIV

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7
Q

Which of top ten deaths are caused by infections diseases in 2019 in HIC?

A

Number 6
Lower respiratory infections

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8
Q

Why are infectious diseases still a leading cause of death?

A

Resurgence of endemic diseases
Growing link between microbes and chronic diseases
Drug-resistant microbes
New/ emerging infections
Lack of vaccination
Healthcare infrastructure, socioeconomic factors
Global warming

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9
Q

What factors contribute to infectious disease in today’s world?

A

Evolution of microbes
Changes in the environment
Breakdown in global public health measures
Human behavior and activities
Globalisation and travel habits

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10
Q

How does evolution of microbes contribute to disease?

A

Pathogens can evolve/ adapt which can result in strains that are more resistant to drugs (e.g. tuberculosis)

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11
Q

How does changes in the environment impact disease?

A

Climate change can alter the distribution of disease vectors (e.g. malaria)

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12
Q

How does breakdown in global public health measures?

A

Impacts on the detection, diagnosis and treatment of infectious diseases

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13
Q

How does human behavior and activities?

A

Vaccine hesitancy, lack of awareness/ adherence to preventative measures (handwashing, wearing face masks)

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14
Q

How does globalisation and travel habits?

A

Increased global travel can facilitate the rapid spread of infectious disease, making it harder to contain outbreaks (e.g.
COVID)

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15
Q

How can we prevent/ combat infectious disease?

A

Disrupt the transmission of pathogens (e.g. intra-species and interspecies)
Remove reservoirs of bacterial pathogens
Prevent infections at common sites of entry (sterile wound sites, catheters, contraception)
Better understand host:pathogen interactions at the molecular level to assist in identifying novel drug targets

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16
Q

What do we mean by “host:pathogen interaction”?

A

Relationships between a host organism (e.g. human, animal, plant) and a pathogen (e.g. bacterium, virus, fungus)

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17
Q

What is microbiota?

A

The collection of microorganisms in a specific environment

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18
Q

What are examples of microbiota around body being dominated by different bacteria?

A

Humans are host to trillions of microorganisms
External auditory canal - 50% Propionibacteriaceae
Umblicus - 99% Corynebacteriaceae
Plantar heel - 80% Staphyloccocaceae

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19
Q

What are commensal microbes?

A

Microbes that inhabit a host as part of the normal flora without usually causing disease are known as commensal microbes

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20
Q

What are opportunistic pathogens?

A

Some microbes may be non-pathogenic until they get an opportunity to cause infection- such as if the host’s defences are compromised e.g. immunodeficiency, break in skin barrier

Some microbes which are a part of the normal flora may also acquire virulence factors that result in pathogenicity e.g. E.coli

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21
Q

What are common sites of host:pathogen interactions in humans?

A

Mucous membranes
Skin
Urinary tract
Lymphatic system
Circulatory system

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22
Q

What are examples of microbes that are common at mucous membrane?

A

Nose, throat, mouth (Porphyromonas gingivalis, Herpes simplex virus)
Gastrointestinal tract (Norovirus, Escherichia coli, Salmonella)
Respiratory tract (Influenza viruses and coronaviruses, Mycobacterium tuberculosis)

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23
Q

What are examples of microbes that are common at skin?

A

Staphylococcus aureus, Candida albicans

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24
Q

What are examples of microbes that are common at urinary tract?

A

Neisseria gonorrhoeae, Chlamydia trachomatis, Escherichia coli

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25
Q

What are examples of lymphatic system that get infected with pathogens?

A

Lymph nodes, tonsils, spleen

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26
Q

What are examples of microbes that are common at circulatory system (septicaemia?

A

Streptococcus pneumonaie, Plasmodium species (malaria)

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27
Q

What defenses do humans have against infection with
pathogens?

A

Eyes - lysozymes
Oral and naval cavities - mucus
Skin - Physical barrier and antimicrobial peptides
Gastrointestinal tract - Mucus, bile and stomach acid
Genitourinary tract - Vaginal lactic acid and washing of urine

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28
Q

Why do infections occur?

A

Pathogens infect their host to gain access to specific ‘niches’ that support their growth (e.g., warmth, nutrients, moisture).

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29
Q

What occurs after pathogen entry?

A

Adhesion, invasion, colonisation and damage

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30
Q

Who was robert koch?

A

German physician and microbiologist
Often referred to as the “father of microbiology”
Awarded a Nobel Prize in Physiology or Medicine in 1905 (for his research on tuberculosis).

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31
Q

What contributes to microbiology dd Robert Koch make?

A

Discovered Bacillus anthracis, Mycobacterium tuberculosis, and Vibrio cholerae as the causative agents of anthrax, tuberculosis and cholera, respectively.
Developed a novel culture system for bacteria (later adapted and termed the ‘Petri dish’ by Koch’s assistant Julius Petri)
Microscopy- oil-immersion lens and condenser
Developed solid culture media for isolating pure cultures (with assistance from Angelina and Walther Hesse)

32
Q

What are Koch’s postulates?

A
  1. The microorganism must be found in diseased but not healthy individuals.
  2. The microorganism must be cultured from the diseased individual.
  3. Inoculation of a healthy individual with the cultured microorganism must recapitulate the disease.
  4. The microorganism must be re-isolated from the inoculated, diseased individual and matched to the original microorganism
33
Q

What are the limitations of Koch postulates?

A

Not all infections result in an active disease state- many infections may be subclinical e.g. Mycobacterium tuberculosis
This postulate may be true of some pathogens, e.g., rabies virus
Only 5-10% of people with M.tuberculosis infection develop symptoms and TB disease

Some pathogens cannot be isolated and grown alone in culture e.g., Plasmodium falciparum

Pathogenicity of pathogens may be limited to certain hosts- e.g. human immunodeficiency virus (HIV) which limits ability to study using animal models

34
Q

What is molecular Koch’s postulates?

A

An extension of Koch’s postulates by Stanley Falkow in 1988 which aim to identify whether a specific gene expressed by a pathogen contributes to the virulence of that pathogen- e.g. a virulence factor

35
Q

How did Falkow outline Molecular Koch’s postulates by phenotypes?

A

The phenotype or property under investigation should be associated with pathogenic members of a genus or
pathogenic strains of a species

36
Q

How did Falkow outline Molecular Koch’s postulates by inactivation of genes?

A

Specific inactivation of the gene(s) associated with the suspected virulence trait should lead to a measurable loss in pathogenicity or virulence, or the gene(s) associated with the suspected virulence trait should be isolated by molecular methods. Specific inactivation or deletion of the gene(s) should lead to loss of function

37
Q

How did Falkow outline Molecular Koch’s postulates reversion or allelic replacement?

A

Reversion or allelic replacement of the mutated gene should lead to restoration of pathogenicity, or the replacement of the modified gene(s) for its allelic counterpart in the strain of origin should lead to loss of function and loss of pathogenicity or loss of virulence

38
Q

How do virulence factors help pathogens?

A

Virulence factors aim to help a pathogen to cause disease by invading the host, cause symptoms of disease, and/or to evade host defences.

39
Q

How do virulence factors vary?

A

Strains of the same microorganism may possess different virulence factors- e.g. the mecA gene acquired by methicillin resistant Staphylococcus aureus (MRSA) bacteria

40
Q

How does conditions impact virulence factors?

A

Pathogens (e.g., bacteria) may only switch on virulence factors under certain conditions
* Salmonella typhimurium switches on type III secretion systems in response to optimal pH
* Pseudomonas- quorum sensing which switches on genes for biofilm production once desired bacterial cell population is reached

41
Q

What are adhesion virulence factors?

A

Adhesins- e.g., spike protein in Coronaviruses, fimbrial adhesins produced by E.coli

42
Q

What are invasion virulence factors?

A

Secretion systems (e.g. type III secretion system in Salmonella)

43
Q

What are immune evasion virulence factors?

A

Antigenic variation (e.g. Influenza)
Capsules (e.g., Neisseria meningitidis)

44
Q

What are nutrient acquistition virulence factors?

A

Siderophores (iron-chelating molecules e.g. staphyloferrin A from S.aureus)
Proteases, lipases

45
Q

What are damage type virulence factors?

A

Exotoxins- e.g., botulinum toxin produced by Clostridium botulinum
Endotoxins- e.g., lipopolysaccharides (LPS) in Gram negative bacteria
Hemolysins
Enzymes- e.g. hyaluronidase

46
Q

How does Clostridium difficile cause disease?

A

C. difficile attachs to gut cells and release toxins
These toxins are glycosylate and inactivate RHO and RAC GTPases disrupting host cell cytoskeleton and tight junction
Interact with immune cells which release inflammmatory molecule and ROS
Distabalise epithelial cell lining leading to excess water loss

47
Q

Why do we need models of infection?

A

Can be used to study host:pathogen interactions
Can be used to screen novel antimicrobial agents or to develop vaccines
Can help to understand how infectious diseases spread

48
Q

Why do we need models of infection for host:pathogen interactions?

A

What virulence factors does a pathogen possess?
What are the effects of pathogenic infection on host cells? (e.g., toxin production).
What cells and mediators are involved in the host immune response?
What is the role of the microbiota in disease?

49
Q

What are immortalised cel lines?

A

Cells that proliferate indefinitely (hence are immortalised)
Viewed as ‘abnormal’ as they evade senescence
Often are derived from a tumour, or are immortalised via use of viruses

50
Q

What are the advantages of immortal cell lines?

A

Easy to culture and maintain
Cheap to initially set up- cultures last a long time!

51
Q

What are the disadvantages of immortal cell lines?

A

They are ‘abnormal’ so are not always biologically relevant.
Long-term cultures may result in change in gene expression

52
Q

What primary cells?

A

E.g. bone marrow derived cells (monocytes → macrophages),
epithelial cells, endothelial cells, fibroblasts, stem cells etc.

53
Q

What are the advantages of primary cells?

A

Isolated directly from patient tissue so is a better representation of the normal function of the cell

54
Q

What are the disadvantages of primary cells?

A

Limited lifespan compared to immortalized lines (typically <10 passages)
Can be difficult/ costly to isolate

55
Q

What are co-culture models?

A

Culture of two or more cell lines (immortalized or primary) to study interaction between cell types and how this may link to infection

56
Q

What are organiods?

A

“Mini-organs”- derived from stem cells or patient tissue that can selforganize and mimic the physiological structure and function of organs

57
Q

What are Organ-on-a-chip models?

A

Micro-physiological systems to mimic the function and structure of organs

58
Q

What are invitromodels?

A

Immortalised cell lines
Primary cells
Co-culture models
Organoids
Organ-on-a-chip models

59
Q

What is the difference beteen invivo and invitro models?

A

More complex than traditional in vitro models
* Number of different cell types
* Circulatory (and lymphatic) systems

60
Q

Why are in vivo models used to study disease?

A

Disease pathogenesis- tissue damage, inflammation etc.
Host immune response to infection
The mechanisms through which pathogens invade, colonise the host
The efficacy of novel antimicrobial agents and vaccines

61
Q

What are non-mammalian in vivo models?

A

Invertebrates (Drosophila melanogaster,
Galleria mellonella)
Nematodes (Caenorhabditis elegans)

62
Q

What are mammalian in vivo models?

A

Mouse (Mus musculus)
Rat (Rattus norvegicus)
Rabbit (Oryctolagus cuniculus)
Non-human primates (Macaca mulatta)

63
Q

Why are Drosophila melanogaster used in infection studies?

A

Easy to maintain, rapid life-cycle, cheap
Can be used to study host:pathogen interactions on whole organism scaledirect infection or ectopic expression of pathogenic proteins
Similarity of innate immune response pathways- e.g., Toll receptors, JAK/STAT signalling, IMD

64
Q

What pathogens have Drosophila melanogaster been used in infection studies?

A

Utilised to study a wide range of pathogens e.g., Zika virus, Pseudomonas aeruginosa, Helicobacter pylori, Bacillus anthracis, Vibrio cholera, Candida albicans, Cryptococcus neoformans

65
Q

What are the drawbacks of Drosophila melanogaster?

A
  • Lacks an adaptive immune response
  • Limited tissue complexity compared to humans
66
Q

Why are Caenorhabditis elegans used as a model organism?

A

Nematode worm- shares many conserved pathways with humans
Cheap and easy to maintain on a large scale
Transparent, so are useful for visualizing fluorescently-tagged cells
Similar innate immune response e.g. MAPK (although lack of some pathways like Tolllike receptors)
Feeds on bacteria in soil → useful in studying host:pathogen interactions in the gut

67
Q

What pathogens have been studied in Caenorhabditis elegans?

A

Susceptible to infection by a number of pathogens relevant to human disease- e.g., Corynebacterium diphtheriae, Candida albicans, Pseudomonas aeruginosa, Staphylococcus aureus

68
Q

What are the drawbacks of Caenorhabditis elegans?

A

Lack of adaptive immune responses
Difficult to assess behavioral abnormalities
Optimal growth is between 20-25oC (not physiologically comparable to humans)

69
Q

What is an overview of Galleria mellonella (wax moth larvae) as a model organism?

A

Cheap and easy to maintain- larvae can be kept in large numbers
Short life-span and can be kept at 37oC
Similar innate immune (cellular and humoral) responses to
mammals (e.g. hemocytes with phagocytic activity)

70
Q

What pathogens have Galleria mellonella (wax moth larvae) been used to study?

A

Susceptible to a number of pathogens e.g., Cryptococcus neoformans, Escherichia coli, Campylobacter jejuni, Vibrio cholereae

71
Q

What are the drawbacks of Galleria mellonella (wax moth larvae) as a model organism?

A

Lack of adaptive immune response
Concerns with standardization of suppliers

72
Q

What is an overview of Danio rerio (Zebrafish) as a model organism?

A

Easy to culture (short life-spans, fairly cheap, wellcharacterised) Fully competent innate immune system and develops an adaptive immune system after 4 weeks
High genomic homology with humans (>80% genes with counterpart in humans)
Embryos and larvae are transparent, which allows easy realtime visualisation of infection (e.g. GFP-labelled strains)

73
Q

What are the drawbacks for using Danio rerio (Zebrafish) as a model organism?

A

Not as relevant to humans as mammalian models e.g. murine
Home Office License required for use of zebrafish >5 days old

74
Q

Why are mouse models used to infection?

A

Share physiological and genetic similarities with humans
Well-characterised model utilised routinely in infection studies Possess both innate and adaptive immune response (in immunocompetent strains)- e.g. Th2 responses
Ease of genetic manipulation (transgenic mice, knockout models)
Xenograft models with human tissue and humanised immune systems being developed

75
Q

What are the drawbacks for using mouse models?

A

Drawbacks:
More costly to maintain than invertebrates etc.
Requires Home Office License and appropriate facility
Ethical considerations (3R’s- replacement, reduction, refinement)

76
Q

What other mammals are used as model organisms?

A

Chicken (Gallus gallus domesticus) - Salmonella, Campylobacter
Rat (Rattus norvegicus) - Candida albicans, Leptospira
Pig (Sus domesticus) - H1N1 (Swine flu), Salmonella
Rhesus macaques (Macaca mulatta) - Coronaviruses, Filoviruses, Helicobacter pylori

77
Q
A

3s2: Infection and Immunity (12 decks)

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