microbes and the immune system Flashcards

1
Q

symbiosis

A

= symbiotic relationship involves the association of 2 or more partners

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2
Q

symbiotic relationship

mutualism

A

= both organisms benefit.

bacteria examples:
- colonic bacteria provided with a niche in the host
- Ruminococcus spp. can be found in high numbers in the gut and involved in cellulose breakdown.

fungi examples:
- fungi attach to the roots and allow root extension, in exchange the plant provides sugars to the fungi.

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3
Q

commensalism

A

= one organism benefits and the other neither benefits or is harmed.

example: - Staphylococcus epidermidis utilises dead skin cells without causing harm

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4
Q

parasitism

A

= one organism benefits at the expense of the other
- parasitic microbe lives or multiplies within/on the host, causing damage in the process

example: malaria -> plasmodium falciparum

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5
Q

opportunistic pathogen

A

a pathogen that does not normally cause disease, only causes disease when the host’s defences are compromised

example: cold sores - herpes simplex virus

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6
Q

primary pathogen

A

can cause disease in a host regardless of the host’s immune system state, or barriers.

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7
Q

Koch’s postulates- traditional

A

= koch’s postulates are a set of criteria that establish whether a particular organism is the cause of a particular disease.

traditional states that:
- pathogen must be absent in all healthy individuals but present in all diseased hosts.
- pathogen must be isolated and grown in pure culture
- it must cause the same disease if introduced into a healthy host

limitations:
assumes all organisms can be cultured in a lab
ethical issues infecting healthy hosts ]
doesnt explain disease caused by multiple pathogens or pathogens that can live in healthy hosts

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8
Q

modern Koch’s postulates

A
  • isolation of genetic material enables pathogen identification
  • specific genes correlate with disease
  • used to determine what genes contribute to a pathogen’s ability to cause disease
  • some pathogens can exist in healthy individuals which conflicts the traditional way.
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9
Q

what is pathogenicity, phenotypic switching and virulence?

A

pathogenicity = the ability to cause disease
virulence = the degree of pathogenicity of an organism (infectvity/ intensity)

phenotypic switching = changing appearance depending on the environment it is in, increased invasion as can get passed the defense in alternative form.

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10
Q

identification tools for microbes

A

1.) agar plates (culture method, however is not suitable for all organisms)

2.) molecular techniques (OMICS)
- genomics (can identify genes and organisms from DNA)
- transcriptomics( tells you parts of DNA that have been expressed, to allow protein production from RNA)
- proteomics( what proteins are produced)
- metabolics( metabolites produced by a population living together)

3,) microarray technology ( tells you what genes are expressed within each population using florescence, a general laboratory technique)

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11
Q

viral replication process

A

1.) attatchment of virus to host cell through specific receptors
2. virus enters host cell
3. the viral genome is replicated
4. viral genomes are transcribed and translated by host cells ribosome (gene expression)
5. assembly of viral genomes and proteins
6. release from host cell, to infect new cells.

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12
Q

genetic properties of RNA

A
  • uses uracil instead of thymine
  • nuclear and cytoplasmic
  • OH at 2’ ribose position
  • short term storage
  • small genome size
  • low intrinsic stability ( reactive to neighbouring dipoles)
  • single stranded (either a positive or negative strand)
  • low polymerase fidelity (ability to replicate a template)
  • low error correction
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13
Q

genetic properties of DNA

A
  • uses thymine
  • mainly found in nucleus
  • H at ribose 2’ (no oxygen)
  • long term storage
  • high intrinsic stability (less reactive, cos no O)
  • large genome size
  • high polymerase fidelity
  • high error correction
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14
Q

differences between DNA and RNA viruses in terms of: genome size & organisation; infection cycle; antigenic drift and shift; recombination & mimicry; latency

A

Genome: DNA viruses have larger, stable genomes; RNA viruses have smaller, mutation-prone genomes.

Infection Cycle: DNA viruses often replicate in the nucleus, RNA viruses usually in the cytoplasm.

Antigenic Variation: RNA viruses exhibit frequent antigenic drift and more opportunities for antigenic shift.

Recombination & Mimicry: Both types can recombine and mimic host molecules, but mechanisms differ.

Latency: DNA viruses are more likely to establish long-term latency, while RNA viruses are typically associated with acute infections.

Antigenic shift and drift: RNA viruses are more prone to these changes due to their high mutation rates and segmented genomes.

RNA viruses have faster evolution capacity -> rapid adaptation, they also have greater coding capacity

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15
Q

antigenic shift

A

= a major alteration in antigen sequence by a process of genome reassortment (segmented virus) or inner strain recombination that results in a new strain of the virus. (sudden change in genetic makeup)

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16
Q

antigenic drift

A
  • virus undergoes a gradual change in genetic makeup, causing a different, but somewhat similar genetic makeup to the parent virus.
  • antigens accumulate small mutations, is these are advantageous, will become predominant through selective pressures
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17
Q

segmented virus

A

Viruses that packages all of their genome segments into a single particle. This allows the virus to be infective.

  • they can have multiple segments ( encoded genes are divided across molecules of DNA or RNA)
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18
Q

recombination

A

= allows for major alterations through exchange of genetic material between viruses or with the host
- genetic exchanges between a pair of homologous DNA sequences

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19
Q

viral mimicry

A

= stealing from the host

  • can disable the immune system with decoys which is:
  • favoured by the large size of DNA viral genomes
  • favoured by DNA-DNA host virus recombination
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20
Q

latency

A

=state where a virus remains dormant or inactive within a host cell for an extended period, without actively replicating or causing disease symptoms ( absence of antigens)

  • long lived nature of DNA allows for long lasting infections
  • DNA viruses are more difficult to detect in nucleus -> persistent infections through latency
  • a lack of immune response to infected cells in latent state
  • clinical consequence -> recurrent infections
21
Q

what happens when virus’ undergo mutations

A

= Mutation in viruses (coping errors during replication) - lead to alterations in the virus’ surface proteins or antigens. Our immune system uses these antigens to recognize and fight the virus.

22
Q

what drives bacterial genetic change?

replication

A
  • evolution in bacteria is rapid due to their high replication rates
  • E.coli can double in number every 25 minutes under optimal growth conditions
23
Q

what drives bacterial genetic change?

mutation

A
  • can alter efficacy of antibiotic by altering the target site
  • can alter the receptor recognition of tissue host
  • can alter the recognition by the host for the pathogen
  • can lead to antigenic drift, where minor changes in surface proteins help the virus evade immune recognition.
24
Q

what drives bacterial genetic change?

horizontal gene transfer

A

= accquiring new genetic traits in bacteria through DNA exchange between two bacteria

3 types:

natural transformation = DNA from the environment is taken up and incorporated into the bacterial chromosome by homologous recombination.

Conjugation = genetic exchange between bacteria

Transduction = genetic exchange occurs through predation by bacteriophage. These are small viruses of bacteria that inject DNA into the cells as part of replication cycle.

25
Q

what drives bacterial genetic change?

transformation

A

= occurs in bacteria that are naturally competent. ( able to actively transport environmental DNA fragments across their cell envelope and into their cytoplasm)

  • occurs when DNA is released during bacterial lysis. (when bacteria die and lyse)
  • involves bacteria taking up and incorporating free DNA into their genome from the environment.
  • they do this through homologous recombination.
26
Q

what drives bacterial genetic change

conjugation

A

= bacterial sex (direct exchange of DNA)

  • occurs between two conjugative plasmids which carry the genes for building the pilus structure and ensuring DNA is transfered.

A bacterium with a conjugative plasmid (called F+ bacterium) forms an F pilus on its surface.
The pilus attaches to a bacterium lacking the plasmid (F- bacterium).
The pilus pulls the two bacteria together, creating a mating bridge.
The conjugative plasmid is then transferred through this bridge from the donor to the recipient.

27
Q

what drives bacterial genetic change

transduction

A
  • bacteriophages can adopt to two life cycles:
    1.) lytic cycle = replication of bacterial genome and destruction of bacteria. (attachment, penetration, replication, packaging, and burst out)

2.) lysogenic = integration of the bacteriophage DNA into the bacterial chromosome

28
Q

key difference between lytic and lysogenic cycle

A

Lytic Cycle: bacteria destroys the host immediately.
Lysogenic Cycle: Bacteria integrates into the host and stays dormant, potentially switching to the lytic phase later.

29
Q

pathogenicity islands

A

= large pieces of DNA that encode multiple genes are integrated into the chromosome. These large island regions can encode multiple genes for different structures.

Foreign DNA that’s inserted into bacterial chromosome is identified by their difference in guanine and cytosine content.

30
Q

the two types of communication in bacteria

A

Quorum sensing = results in changes in gene expression as a consequence of signalling at the population level.
- Occurs when bacteria sense their population size and coordinating their behaviour in response
- behaviour changes depend on bacterial cell density
- low density = no transcription of target gene
- high density = transcription occurs

Environmental sensing = results in changes to gene expression within an individual bacterium
- relies on interaction between two proteins in response to particular stimulus.

31
Q
A
31
Q

the two component regulation of environmental sensing

A

component 1 = transmembrane sensor kinase
- sensory domain on outside of cell
- kinase domain protrudes into the cytoplasm
- on detection of a signal -> conformational change in kinase domain -> autophosphorylation.

component 2 = response regulator
- trans phosphorylated by the kinase
- this acts to enhance or repress gene expression of one or more genes.

32
Q

transcriptomics

A

= can use to study the capacity of bacteria to modify gene expression in response to environmental conditions.
this allows us to identify those genes whose expression are essential for growth within a niche.

33
Q

generalized vs specialised transduction

A

Generalized: Random bacterial DNA incorporated into defective phages.
Specialized: Adjacent bacterial DNA excised with phage DNA. ( bacteria can only pick up specific portions of hosts DNA)

34
Q

microbial life strategies to obtain energy and carbon

photoautotrophs

A

Use sunlight and carbon dioxide (CO2) for energy
examples: plants, algae, and cyanobacteria.

35
Q

microbial life strategies to obtain energy and carbon

chemoautotrophs

A

Obtain energy through chemical oxidation and use CO2 as their carbon source, typically found in extremophiles.

36
Q

microbial life strategies to obtain energy and carbon

photoheterotrophs

A

they use sunlight for energy but rely on pre-formed organic compounds for carbon.
Examples are purple and green non-sulphur bacteria

37
Q

microbial life strategies to obtain energy and carbon

chemoheterotrophs

A

Depend on chemical oxidation for energy, obtain their carbon from pre-formed organic compounds.
- animals and humans

38
Q

temperature adaptations of psychophiles, hyperthermophiles and mesophiles

A

Psychrophiles thrive in cold environments, with growth optimal at <15ºC. They adapt by increasing unsaturated fats in their membranes to maintain fluidity.

Hyperthermophiles require high temperatures >70ºC for survival, adapting by increasing saturated fats in their membranes to maintain structural integrity.

Mesophiles grow best at body temperature (37ºC) and are often human pathogens.

39
Q

microbes in the marine environment

A

neritic zone = mild temperatures, low pressure, nutrient rich and home to diverse marine life such as photosynthetic organisms.

oceanic zone = high pressure and deep water environments where chemotrophs thrive.

Ocean plankton, especially species like Prochlorococcus and Synechococcus, are critical for Earth’s oxygen production and carbon fixation.

40
Q

how are microbes used in technology?

A

PCR = Uses Taq polymerase from Thermus aquaticus to amplify DNA, transforming molecular biology.

Restriction Enzymes = Bacterial proteins that cleave DNA at specific sequences, fundamental in recombinant gene technology.

CRISPR-Cas9: A bacterial immune system that can be harnessed for precise gene editing by targeting specific DNA sequences.

41
Q

how are microbes used in medicine?

A

antibiotics = Penicillin, discovered from Penicillium notatum, was the first broad-spectrum antibiotic, inhibiting cell wall synthesis in bacteria.

Recombinant Vaccines: Use microbial methods to express antigens (e.g., hepatitis B surface antigen in yeast) to produce vaccines.

Recombinant Virus Vaccines: For COVID-19, spike protein genes were inserted into harmless viruses to trigger immune responses in the body.

42
Q

microbes and cancer

A

Certain microbes are implicated in cancer development:

Human papillomavirus (HPV): Associated with cervical cancer.

Helicobacter pylori: Linked to gastric cancer.

Schistosoma haematobium: Linked to bladder cancer.

43
Q

biodegradation by microbes

A

= the physical or chemical change of a material by micro-organism(bacteria, fungi)

plastics can impact the microbiome by having toxic effects and providing a platform for colonisation.

44
Q

What role do cryoprotectants and cold/heat shock proteins play in microbial survival?

A

They prevent proteins from denaturing and help maintain proper structure and activity under extreme temperature conditions.

45
Q

describe the methods that have revolutionised the microbiome field

A
  • many bacteria are still not culturable so sequencing is used:
    1.) 16S sequencing = Targets a specific region of rRNA to identify bacteria. cost effective

2.) Whole genome sequencing(WGS) = sequences the entire genome including non coding and coding protein regions. More comprehensive than 16S but high costs.

3.) metagenomics = the study of the structure and function of entire nucleotide sequences

46
Q

describe how communities of micr-organisms colonise us

A
  • by the time we are 3 years old our microbiomes are largely established and remain relatively stable throughout life.
  • our bodies are around 50% bacteria, with different bacterial communities colonisisng different body surfaces.
  • these communities are complex, stable and interdependent.
  • Factors like pet ownership, maternal health, diet and genetics affect microbial colonization.
  • bacteria help in processes like micronutrient synthesis and limit pathogen colonization.
47
Q

how are microbial communities important for ourr health?

A
  • bacteria synthesis essential micronutrients such as vitamin K and biotin.
  • they metabolize plant carbohydrates into short chain fatty acids which provide energy to epithelial cells.
  • short chain fatty acids are produced by bacterial fermentation, including butyrate (has anti-inflammatory effects), acetate and propionate.
  • probiotics have limited evidence of efficacy but are generally safe.
48
Q
A