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Semester 2 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are stromatolites?

A

3.5 billion years ago -> sediments alternating layers of limestone and bacterial communities formed.

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2
Q

4 theories explaining the origin of life:

A

Chemical origin, RNA world, The apparition of a cellular life, Panspermia

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3
Q

RNA world hypothesis:

A

RNA could have been the first macromolecule encoding complex information.

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4
Q

RNA world hypothesis: Evidence

A

-4 building blocks
- Requires less energy than DNA to form and degrade
-Uracil formed in early biochemical pathways
-Some viruses use ssRNA
-Some RNA molecules have catalytic activities.

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5
Q

What are the activities of ribozymes?

A

-Cleavage/ligation of RNA molecules
-Replication
-Formation of peptide bonds to form RNA

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6
Q

Purpose of compartmentalisation:

A

-Protection from the environment
-Selective Barrier
-Controls concentrations for molecules.

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7
Q

How would compartmentalisation lead to the formation of LUCA?

A

The spontaneous formation of protocells by phospholipids would trap amino acids and nucleic acids being trapped. Either surface or sub surface origin

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8
Q

What is LUCA?

A

The last universal common ancestor

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9
Q

Surface origin of compartmentalisation:

A

Primitive cells formed spontaneously in prebiotic soup.

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10
Q

Sub-Surface origin of compartmentalisation:

A

Life originated in hydrothermal mounds.
H2 and H2S sued as source of electrons to form organic molecules. Redox and pH gradients used a prebiotic proton motive force to move synthesised components up the mound.

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11
Q

Panspermia:

A

Life comes from space -> waves of viruses from space drive evolution

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12
Q

Panspermia:

A

Life comes from space -> waves of viruses from space drive evolution

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13
Q

Microbes -> definition:

A

Generic term including all microorganisms.

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14
Q

Why are bacteria more susceptible to mutation?

A

They are haploid, and-so only have one copy of a gene.

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15
Q

What are the mechanisms by which bacteria transfer and acquire new DNA molecules?

A

Transformation, conjugation, transduction

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16
Q

What is taxonomy?

A

The study of the classification of organisms

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17
Q

What is the order of hierarchy of classification?

A

Domain, Kingdom, Phylum, Class, Order, Family, Genus, Species

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18
Q

Binomial nomenclature:

A

Genus capital letter. species

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19
Q

What are the phenotypic analytical methods used to determine taxonomy?

A

-Morphology/ differential staining
-Metabolic Properties
-Phage typing
-Fatty acid profiles
-Mass spectrometry

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20
Q

Taxonomy: Metabolic Properties Analysis

A

Selective incubation tubes track growth of inoculation and pH using indicators. Results compared to a reference library.

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21
Q

Taxonomy: Phage typing

A

Unknown Bacteria exposed to known phages -> observe which it’s resistant to -> compare to reference library.

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22
Q

Taxonomy: Fatty acid profiles

A

Bacterial culture -> fatty acids extracted -> form methyl esters -> gas chromatography -> mass spec -> compare with database
-Compares membrane composition.

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23
Q

What are the genotypic analytical methods used to determine taxonomy?

A

-DNA/ DNA hybridisation
-Fluorescence In Situ Hybridisation (FISH)
-rDNA (16S) sequencing– Multi Locus Sequence Typing (MLST) / fingerprinting
-Genome sequencing

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24
Q

Taxonomy: DNA/ DNA hybridisation

A

2 genomes -> one labelled -> hydbridised -> amount of duplex genes observed

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25
Q

Taxonomy: Fluorescence in SItu Hybridisation

A

Fluorescent tags/probes attach to DNA -> allows for observation of the presence of specific sequences.
Requires heavy microscope usage.

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26
Q

Taxonomy: rDNA (16S) sequencing

A

Most organisms share rDNA (16S) -> variation can provide information on the closeness of relation between organisms.

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27
Q

Taxonomy: Multi Locus Sequence Typing (MLST) / fingerprinting

A

Establishes a “bar code” for loci of a sequence -> this is then compared to databases.

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28
Q

Taxonomy: Whole genome sequencing

A

-Most powerful technique but requires specialised equipment.

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29
Q

What is phylogeny?

A

The study of the evolutionary history of organisms.

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30
Q

How is phylogeny studied?

A

-Evolutionary relationships are measured by comparing DNA -> “molecular clocks” -> sequences encoding conserved proteins -> random + neutral mutations

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31
Q

What are the two types of cladograms? (Phylogenetic trees)

A

Rooted trees + unrooted tree.

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32
Q

Archaea:

A

-Prokaryotic
-Membrane composed of branched carbon chains
-Methionine start amino acid
-No antibiotic sensitivity
-Lacks rRNA loop
-Lacks common arm of tRNA

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33
Q

Eukarya:

A

-Eukaryotic
-Membrane composed of straight carbon chains
-Methionine start amino acid
-No antibiotic sensitivity
-No rRNA loop
-Common tRNA loop

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34
Q

Bacteria:

A

-Prokaryotic
-Membrane composed of straight carbon chains
-Formylmethionine start amino acid
- antibiotic sensitivity
- rRNA loop
-Common tRNA loop

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35
Q

Key components of a eukaryotic cell:

A

Nucleus, Endoplasmic Reticulum, Golgi complex, Lysosomes, mitochondria, chloroplasts. flagella/cilia

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36
Q

Key components of a prokaryotic cell:

A

Nucleoid, cytoplasm, envelope, appendages

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37
Q

Prokaryote: nucleoid

A

-Single, circular chromosome
-DNA complexed with histone-like proteins
-Genetic material also in plasmids

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38
Q

Prokaryotes: organelles

A

Some prokaryotes contain organelles -> photosynthetic bacteria.

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39
Q

Prokaryotes: Appendages

A

Pilus: extension used for conjunction
Fimbriae: involved in adhesion to surfaces
Flagella: Supramolecular assembly involved in motility (cell can have multiple) (anchored to cytoplasmic membrane) (rotate in response to ATP hydrolysis couple reaction)

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40
Q

What is endosymbiotic origin of eukaryote organelles?

A

-The stable incorporation of endosymbiotic bacteria resulted in the formation of mitochondria and chloroplasts.

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41
Q

When did the nucleus structure develop?

A

Before the acquisition of mitochondria and chloroplasts.

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42
Q

Evidence supporting endosymbiotic theory:

A

Mitochondria and chloroplasts contain their own DNA and ribosomes. They have a inner and outer membrane.

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43
Q

Problem with endosymbiosis theory:

A

Doesn’t account for the similar lipid composition of eukaryote and prokaryotes.

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44
Q

types of unicellular eukaryotes:

A

Fungi, Protozoa, Unicellular algae, slime moles

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45
Q

Which types of unicellular eukaryotes are protists?

A

Unicellular algae, protozoa, and slime molds.

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46
Q

Human impacts of fungi:

A

Ecological Role: Contribute to carbon cycle (decomposers)
Economic Role: 10-30% crops spoiled + key role in biotech
Human Health:>1.5mil deaths assosciated

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47
Q

Common properties of fungi:

A

Morphology: Form multicellular hyphae and are pleiomorphic
Cell Walls: Carbohydrates, chitin, mannans, or glucans
Life Cycle: 2 phases, asexual and sexual reproduction -> form spores -> alternate between diploid/haploid phases

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48
Q

Where does nutrient absorption and growth occur on a hyphae?

A

The tip

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49
Q

What are the 3 types of fungi?

A

Molds, Yeasts, and Basidiomycetes (mushrooms)

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50
Q

Symbiotic relationship between Basidiomycetes and plant roots?

A

Help plants obtain mineral nutrients from the soil in return for sugars produced by photosynthesis.

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51
Q

Human impact of Yeast:

A

Economic: S.cerevisiae used in brewery + bakery
Human Health: Some S.cerevisiae strains are probiotics + used to model cellular processes.
Cryptococcus and candida cause infections

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52
Q

Yeast cell lifecycle:

A

Alternate between haploid gametes and diploid cells. Both can replicate by mitosis.

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53
Q

What are the 3 types of unicellular algae?

A

Primary endosymbiotic algae, secondary endosymbiotic algae (diatoms), Predatory algae (dinoflagellates)

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54
Q

Secondary endosymbiosis:

A

A cell engulfs a primary endosymbiont (cell that has engulfed another cell)

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55
Q

Ecological importance of Algae:

A

-Compoonents of phytoplankton, produce half the atmosphere’s oxygen, key food item in ocean food web and aquaculture (zooplankton eat phytoplankton)

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56
Q

Key properties of algae;

A

-Photosynthetic organisms
-Have chloroplasts like plants but diatoms have a more diverse metabolism.

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57
Q

Primary endosymbiotic algae can be used to model what?

A

Photosynthesis, motility, cell cycle, and oxidative stress

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58
Q

What do primary endosymbiotic algae contain?

A

-Chloroplast (without phycoerythrin)
-Pyrenoid to stock bicarbonate (HCO3-) that can converted to Co2
-a contractile vacuole for osmoregulation
-A hydroxyproline-rich glycoprotein cell wall.

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59
Q

Life cycle of primary endosymbiotic algae:

A

-Mostly found as haploid dividing by binary fission
-Haploid cells from opposite mating types fuse to form a zygote which loses flagella and grows protective coat.
-Zygote undergoes meiosis and regenerates haploid cells.

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60
Q

Example of unicellular primary endosymbiotic algae with a colonial lifestyle:

A

Volvox carteri

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61
Q

Which is more complex: the chloroplast structure in diatoms or plants?

A

The chloroplast structure in diatoms

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62
Q

Name of the cell wall surrounding diatoms?

A

Frustule

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63
Q

What are the three types of Secondary endosymbiotic algae?

A

Coccolithophores, Centric diatoms, and Pennate diatoms

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64
Q

Why do diatoms undergo an unusual form of cell division?

A

Their rigid frustules prevent ordinary division.

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65
Q

Centric Diatoms:

A

Diatoms with a frustule expressing radial symmetry.

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66
Q

Pennate diatoms:

A

Diatoms with a frustule expressing bilateral symmetry.

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67
Q

What are frustules made of?

A

Silica (Crosslinked silicon oxide)

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68
Q

Diatom reproduction:

A

Usual meiosis however:
Initially mitosis takes place and the Frustule is made of two valves and-so during first division one half is inherited and will synthesise a 2nd valve. This is followed by meiosis and and generation of gametes -> conjugation of a zygote -> formation of auxospore.

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69
Q

What is a household use for diatoms?

A

Natural treatment against fleas and red-mites

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70
Q

Coccolithophores:

A

Frustules of calcium carbonates -> growing multiple “scales” -> play key role in carbon cycle.

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71
Q

Why are protozoa classification controversial?

A

Protozoa are difficult so classify

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72
Q

What are the two major groups of Protozoa?

A

Alveolates and other parasitic protozoa.

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73
Q

What are the three types of alveolates?

A

Ciliates (predatory protists), Apicocomplexans (parasites), Dinoflagellates (Predatory algae)

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74
Q

What are the two types of “other parasitic protozoa”?

A

Metamonads (symbionts or parasites) and Trypanosomes (parasites)

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75
Q

Key properties of alveolates:

A

Contain alveoli - (Cytoplasmic fluid sacs unknown role)
Motile organisms - (Cilia)
Mostly aquatic

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76
Q

Ecological importance of Alveolates:

A

-Play a major role in food web (zooplankton)
-Apicomplexans (e.g malaria)
-Dinoflagellates key role in carbon cycle

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77
Q

Protozoa: Ciliate Structure

A

-Contain alveoli
-Cilia + trichocyst (protrusible filamets)
-Contractile vacuole
-Digestive vacuoles
-3 nuclei -(2 micro + 1 macro)
-Oral groove

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78
Q

Function of trichocysts:

A

Protrusible filament bags that “Sting” prey using toxins

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79
Q

Two types of ciliate reproduction:

A

Asexual binary fission or sexual reproduction (conjugation)

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80
Q

Ciliate binary fusion:

A

Micronuclei – diploid – transcriptionally inactive – germline – copy of genome to be passed on – aren’t used for transcription
Macronuclei – result from the duplication of micronuclei -> transcriptionally active – few hundreds-thousands copies of genome.

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81
Q

Ciliate conjugation:

A

Conjugation: requires an established physical contact -> macronuclei disintegrate and micronuclei duplicate -> two rounds of division -> 4 micronuclei -> undergo meiosis and become haploid -> exchange genetic material of the recombinants -> parent cells split -> undergo 3 successive nuclei divisions and then 2 mitotic divisions.

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82
Q

Apicocomplexans: Summary

A

-Spore-forming parasitic protozoans (without flagella, cilia, or pseudopods.
-Contains apicoplast (degenerate chloroplast carrying out fatty acid metabolism
-Obligate endoparasites

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83
Q

Examples of diseases caused by Apicocomplexans:

A

-malaria
-Crytosporidiosis
-Toxoplasmosis

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84
Q

Apicocomplex: life cycle

A

Infection sporozoites -> target cell -> multiply to form a schizont -> ruptures and releases merozoites -> invade cells before differentiate into gametes -> in host/vector gametes fuse to form resistant zygote -> meiosis to produce sporozoites

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85
Q

Dinoflagellates:

A

-Mobile predatory photosynthetic aquatic mixotrophs: use sources of energy that aren’t light or carbon sources
- involved in complex symbiotic or parasitic interactions.

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86
Q

What is meant by mixotroph?

A

mixotroph: use sources of energy that aren’t light or carbon sources

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87
Q

Dinoflagellate: Structure

A

-2 flagella (one wrapped around cell)
- Chloroplast with triple membrane
-“Cell wall” made of cellulose plates (thecae)
-Contain extrusomes

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88
Q

Dinoflagellates: life cycle

A

Very little known
Undergoes binary fission and sexual reproduction
Can form resistant “spore” (hypnozygote cyst)

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89
Q

“Other Parasitic Protozoa”:

A

-Mobile parasites causing common human disease
-Mostly harmful but sometimes symbionts (metamonds)
- Can be transmitted by vectors and direct contact

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90
Q

Three examples of metamondads:

A

Trypanosoma, Mixotricha paradoxa, and Giardia lamblia

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91
Q

Giardia Lamblia:

A

-Metamonad paraiste that causes diarrhea.
-Contains 2 nuclei
-Adheres to epithelial cells using ventral adhesive disk
-Divide by binary fission and form cysts when condition are unfavourable

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92
Q

Mixotricha paradoxa:

A

-Metamonad
-Found in gut of specific termite species
-Symbiont with other bacteria and the termite
-Important for metabolism
-Very large and can be seen with naked eye

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93
Q

Trypanosoma:

A

Parasitic Metamonad
-transmitted by fly vector
-2 successive phases of disease -> fever, headaches, inflammation -> invades CNS -> disrupts sleep

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94
Q

What do slime molds share morphology with?

A

Amoebas

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95
Q

Pseudopod mobility:

A

extensions formed by actin polymerisation/dissassembly which pushes the membrane and cell across a surface. These cna also be used during engulfment.

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96
Q

Are all amoeba shapeless?

A

No, some are shelled

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97
Q

What kind of diseases are amoeba often the cause of?

A

Water-borne diseases.

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98
Q

Example of a cellular sime mold:

A

Dictyostelium discoideum

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99
Q

Example of a plamsodial silme mold:

A

Physarum polycephalum

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100
Q

Dictyostelium discoideum:

A

-Cellular slime mold.
-Grows as an amoeboid unicellular organism that divides by binary fission
-Forms a “slug” through social mobility -> to move to favourable conditions.
-Slug forms fruiting body which releases cysts.

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101
Q

Physarum polycephalum:

A

-Grows and dives by binary fission as an amoeboid single cell.
-Lives as one large singular cell -> smaller amoeba like cells aggregate and fuse cytoplasm to form plasmodium. -> differentiates into fruiting body -> cysts released.
-

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102
Q

What are the two types of slime mold?

A

Plasmodial and cellular

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103
Q

Difference between cellular and plasmodial slime molds:

A

Plasmodial -> cytoplasms of smaller cells fuse to produce plasmodium
Cellular -> cells remain separate and move via social mobility.

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104
Q

What are the major components of viral particles

A

Nucleic acid genome, capsid, facultative lipid membrane.

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105
Q

What are the 5 stages of the viral life cycle?

A

Attachment, Genome injection, Production of nucleic acid and proteins, Maturation (assembly), release

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106
Q

What is the difference between lytic and temperate bacteriophages?

A

Temperate phages can enter the lysogenic cycle and can integrate with the host DNA and remain dormant -> replicating during cell divisions. This DNA can be excised from the host’s genome and initiate the lytic cycle.

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107
Q

What are viruses?

A

Oligatory parasites that hijack host metabolic machineries to replicates.

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108
Q

Size of virusal genome:

A

2-20kb

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109
Q

Viral genome fragmentation:

A

Genome can be split into multiple specialised fragments.

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110
Q

What proteins make up capsids?

A

Capsomers

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111
Q

What are the two types of symmetry capsids can expresss?

A

Icosahedral + helical symetry.

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112
Q

What is the role of the viral envelope?

A

To allow entry into a host cell via fusion/endocytosis

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113
Q

More complex viruses e.g bacteriophages contain multiple what?

A

Capsids -> e.g icosahedral head and helical tail fibres -> aids attachment to a cell by probing cell surface and form interactions -> allows injection of genome.

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114
Q

Example of a complex virus that effects humans?

A

Poxyviridae (small pox)

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115
Q

What does the balitmore classification of viruses consider?

A

-Nature of genome (DNA or RNA)
-The type of RNA/DNA (ds, ss, and polarity)
-The genome replication mechanism

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116
Q

Which groups of viruses are DNA viruses?

A

1,2, and 7

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117
Q

Which groups of viruses are RNA viruses?

A

3,4,5, and 6

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118
Q

Virus class 1,7: Genome replication

A

ds DNA viruses.
Class 1 - classical semi conservative
Class 7 - transcription followd by reverse transcription

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119
Q

Virus class 2: Genome replication

A

ssDNA (+) virus
Classical semiconservative -> discard -ve strand. forms dsDNA intermediate before transcription of -ve strand.

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120
Q

Virus class 3: Genome replication

A

dsRNA virus
Makes ssRNA (+) from dsRNA -> transcribed to give ssRNA(-) which is then translated

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121
Q

Virus class 4:Genome replication

A

ssRNA (+) virus:
makes ssRNA (-) and transcribes from this to give ssRNA(+) genome.

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122
Q

Virus class 5: Genome replication

A

ssRNA (-) virus:
makes ssRNA (+) and transcribes from this to give ssRNA(-) genome.

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123
Q

Virus Class 6:Genome replication

A

ssRNA (+) Retrovirus:
Makes ssRNA (+) genome by transcription of (-) strand of dsDNA (synthesised from rev.transription)

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124
Q

Papilomavirus:

A

dsDNA class 1 virus: HPV16
No envelope.
5.3-8.kb
19 million new cancer cases (2020)
Causes 2% of cancers in UK
90% of cervical, 85-90% of vulvar, 95% vaginal HPV related cancer in women, 90% HPV related anal cancers in men and women.

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125
Q

Adeno-associated virus

A

Harmless ssDNA class 2 virus

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126
Q

Reovirus:

A

dsRNA class 3 virus:
rarely fatal but associated with economic burden.
Rotavirus vaccine protects against 90% of strains.

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127
Q

Foot-and-mouth disease virus:

A

(+) ssRNA class 4 virus:
2001 outbreak -> 2000 cases across UK -> 4-10mil sheep and cattle killed.
-Cost >3bn to public sector and >5bn to private sector.

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128
Q

Influenza virus:

A

(-) ssRNA class 5 virus:
infected 500mil people across the world and killed 3-5% of the world’s population (1918-1920)

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129
Q

HIV:

A

class 6 retrovirus (RNA):
-Associated with cancer
-Causes AIDS - progressive failure of immune system
-Following loss of immunity body becomes susceptible to opportunistic viruses
-78miilion people infected, 39mil have died, 37mil living with HIV

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130
Q

Hepatitis B virus:

A

reverse DNA class 7 virus:
-Causes cirrhosis and liver cancer

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131
Q

What is cirrhosis:

A

Live damage (degeneration) and scarring

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132
Q

Are all viruses enveloped?

A

No.

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133
Q

Advantages of the small size of bacteria:

A

Largers SA:V -> nutrient exchange and grow rate, > Intracellular nutrient conc, rapid evolution due to high selection of mutations.

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134
Q

Bacteria-specific genetic properties: (transcription)

A

-Transcription occurs in cytoplasm.
-1 RNA pol in prokaryotes (3 in eukaryotes)
-No splicing
-Eukaryotes terminate at AAUAAA seq rather than GC dense region.

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135
Q

What are the most common morphology types for bacteria?

A

cocci, rods, curved, spiral, and exotic.

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136
Q

Can morphology change during a bacterial cell cycle?

A

Yes

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137
Q

Phenotypic diversity of bacteria:

A

Size, Pigmentation, Smell

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138
Q

Bacteria smell example:

A

-contribute to human odour -> degradation of apocrine secretion products

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139
Q

Gram stain method:

A

Stained with crystal violet -> this is then fixed to positive bacteria by iodine -> the culture is washed (alcohol) and then a safranin counterstain is used + attaches to gram -ve bacteria.

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140
Q

Gram +ve bacteria;

A

Have no outer membrane and a thick cell wall

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141
Q

Gram -ve bacteria:

A

Have an outer membrane and a thin cell wall.

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142
Q

Do exceptions to gram+ve/-ve staining exist?

A

Yes, e.g mycobacteria

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143
Q

What is the bacteria s-layer?

A

Layer of facultative structures non covalently bound to the cell wall (Gram +) or surface membrane (Gram -). Made from proteinaceous crystalline arrays;

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144
Q

Bacterial capsules:

A

Most made from polysaccharides.
Some are made from amino-acids.
Covalently bound onto the cell wall or outer membrane.
-confer resistance to phagocytes and bacteriophages.

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145
Q

Bacterial exoploysaccharides:

A

homo/heteropolysaccharides. -> non covalently attached to cell surface. -> important for biofilm formations, some are used commercially in toothpaste, ice creams etc.

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146
Q

Key components of gram - membranes:

A

Phospholipids, proteins, lipoproteins, bacterial liposaccharides (LPS).
Outer membrane interacts with peptidoglycan cell wall.
Integrity provided by anchor proteins.

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147
Q

Bacterial anatomy: peptidoglycan (murein)

A

Elastic 3D network part of a subcellular compartment. Dynamically regulates exchange with the environment. Forms cell wall (heterogenous structure like a sponge)
Determines cell shape and acts as a scaffold for polymers and proteins.

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148
Q

Composition of peptidoglycan:

A

Glycan chains alternating N-acetylglucosamine (G) and N-acetylmuramic-acid (M), substituted by short peptides (L- and D-amino acids)

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149
Q

Key components of the cytoplasmic membrane of a bacteria cell:

A

-Phospholipids, hopanoids (equiv. sterols in eukaryotes), proteins (transporters, sensors, etc.)

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150
Q

Role of hopanoids in bacteria cytoplasmic membrane:

A

Modulate membrane fluidity and permeability. (similar to cholesterol)

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151
Q

Bacterial chromosome:

A

-Always made of dsDNA
-Singular circular chromosome
-Variable size 0.5-14.8Mbp
-chromosome organised as a nucleoid -> supercoiled around histone-like proteins

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152
Q

Bacterial Plasmid DNA:

A

-ds DNA, usually circular
-2-600kbp
-can transfer between bacteria
-carry resistance genes
-can have multiple copies within one cell.

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153
Q

Bacterial gene structure:

A

-No introns -> continuous open reading frame -> don’t req. splicing
-Use operons to control transcription

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154
Q

Gene expression of Bacteria: transcription initiation

A

-The RNA polymerase (a2bb’sw) scans
DNA forming a loose complex
- sigma factor binds to a two specific
sequences upstream of start codon
-DNA is unwound, allowing for the formation of an “open complex” -> transcription starts -> sigma factor released.

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155
Q

Gene expression of Bacteria: transcription termination (rho independent)

A

-Palindromic GC-rich region upstream of an AT-rich sequence.
-Once G-C rich region is transcribed -> hairpin structure forms -> causes RNA poly. to fall apart.

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156
Q

Gene expression of Bacteria: transcription termination (rho dependent)

A

-Rho proteins recognise and bind to 72 residues GC-rich
-RNA-dependent ATPase activity of Rho protein -> wraps around downstream RNA -> once reaches the polymerase Rho unwinds the RNA-DNA duplex and releases RNA polymerase.

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157
Q

What is translation in prokaryotes coupled with?

A

Transcription

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158
Q

Bacteria-specific genetic properties: (translation)

A

-Prokaryotes have 70S ribosomes (Eu have 80S), and bind more productively to mRNA in presence of tRNA.
-40S subunit guided by 5’ mRNA cap
-30S subunit recognise Shine-Dalgarno sequence.
(Eukaryotic translation is inhibited by cycloheximide)

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159
Q

What is the shine-Dalgarno sequence?

A

AGGAGG -> only in prokaryotes -> helps ribosome bind to mRNA -> initiate protein synthesis

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160
Q

What are the two types of energy sources for bacteria?

A

Sunlight (photo) or preformed molecules (chemo)

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161
Q

What are the two types of electron sources for bacteria?

A

Organic (organo), inorganic (Litho)

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162
Q

What are the two types of carbon sources for bacteria?

A

Organic compound (Heterotroph), Inorganic compounds (Autotroph)

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163
Q

What are the 5 parameters important for bacterial growth?

A

Temperature, pH, Osmotic temperature, Nutrients, Oxygen requirements

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164
Q

What are the different methods used to measure bacterial growyh?

A
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165
Q

What are the different classes of microorganisms (Classed by temp. required for optimum growth):

A

Psychrophiles, Mesophile, Thermophile, Extreme Thermophile

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166
Q

Psychrophiles: Membranes

A

Microorganisms adapted to cold temperatures -> have a higher content of unsaturated, polyunsaturated, methyl-branched fatty acids -> increase membrane fluidity.

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167
Q

Psychrophiles: Synthesis

A

Synthesise anti-freeze proteins, cryoprotectants, and cold adapted enzymes (more alpha helices + less weak bonds -> more flexible).

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168
Q

Thermophiles: Genome protection

A

-Stabilise DNA using DNA binding proteins.
-Introduce supercoils using reverse DNA gyrases
-High G-C% -> increased res to denaturation

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169
Q

Thermophiles: Membrane

A

Esther-linked phospholipids (less prone to reactions and alterations) and single lipid layer (glycerol tetraethers bind leaflets)

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170
Q

Thermophiles: Synthesis

A

-Production of thermostable proteins, with increase hydrophobic and ionic interactions.
-thermostable chaperonins restore fold to damaged enzymes.

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171
Q

What are the metabolic adaptations of acidophiles?

A

Respiratory chain pumps h+ out of cell. Use H+ symports to let in solutes. K+/H+ antiporters excrete protons.
-Metabolism mostly reliant on proton gradient.

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172
Q

What are the metabolic adaptations of alkaliphiles?

A

Most transport reactions don’t utilise protons but instead use metal ions (sodium)
ATP is synthesised using Na+ rather than protons.
Alkaline environments often have high salt content -> hence intake of salt to maintain osmotic grad.

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173
Q

The classifications of microorganisms (when classified by resistance to osmotic pressure)

A

Nonhalophile, Halotolerant, Halophile, Extreme Halophile

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174
Q

Example of a non-halophile:

A

E.coli

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175
Q

Why do halophiles require salt?

A

Stabilization of the S-layer glyco-protein by Na+ ions
Accumulation of K+ as a compatible solute (>4M in the cell!)
-> Maintain the integrity of the cell surface membrane -> use counter salt to balance wp balance.

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176
Q

How do microorganisms that have adequately adapted respond to osmotic stress?

A

They regulate water movements by passive diffusion and aquaporins.

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177
Q

What are the the toxic forms of oxygen known as?

A

Reactive Oxygen Species

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178
Q

What are the different reactive oxygen species?

A

Superoxide, Hydrogen Peroxide Hydroxyl Radical

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179
Q

What enzyme breaks down hydrogen peroxide?

A

Catalase/peroxidase (breaks down H2O2 into H2O)

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180
Q

What combinations of enzymes can be used to detoxify superoxide:

A

Superoxide dismutase/reductase + catalase

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181
Q

What are the classification of microorganisms (When classified by oxygen requirements):

A

Obligate aerobes, Facultative aerobes, Microaerophiles, Anaerobes aerotolerant, obligate anaerobes.

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182
Q

Obligate aerobes:

A

Use O2 exclusively for respiration
Have catalase and SOD enzymes

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183
Q

Facultative aerobes:

A

Can use O2 to respire.
Have catalase and SOD enzymes

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184
Q

Microaerophiles:

A

Require O2 for respiration

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185
Q

Anaerobes aerotolerant:

A

Do not use O2 for respiration
Only has SOD enzymes

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186
Q

What are the two ways to measure bacterial growth?

A

Direct and indirect measurements.

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187
Q

What are the direct ways to measure bacterial growth?

A

Microscopic counts, Flow cytometry and viable counting.

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188
Q

Microscopic counts:

A

Microscopic counts – count the number of cells and compare to the number in the original suspension. (Petroff-hauser cell counter)

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189
Q

Viable counting:

A

Viable counting - Start with a cell suspension and use serial dilution -> doesn’t demonstrate number of cellular entities but rather identical colonies.

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190
Q

Flow cytometry:

A

Flow cytometry – Capillary with suspension in – laser used to count number of cells by the effect of density on light scattering.

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191
Q

What are the indirect methods of measuring bacterial growth?

A

Optical density, dry weight, and metabolic activity

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192
Q

Optical density (as a means of measuring bacterial growth):

A

-Measures light not scattered by cells
-Optical density values vary by organism
-Doesn’t work with filamentous bacteria
-Requires high cell densities (>10^7 cell/ml)

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193
Q

What are the 4 phase of the bacterial growth curve?

A

Lag phase, log phase, stationary phase, deathn phase.

194
Q

What are the 2 major phyla of archaea:

A

Euryarcheota + Crenarcheaota

195
Q

What microorganism classification are most archaea part of?

A

Extremeophiles

196
Q

Components of Archaeal ultrastructure:

A

S-layer,
Cell wall (pseudomurein),
Unusual cell envelope structures, Cytoplasmic membrane

197
Q

Archaeal Cell wall:

A

-not always present
-Made from pseudomurein (similar to bacterial peptidoglycan)
-Heteropolymer (disaccharide-peptides)
-Resistant to lysozymes and most antibiotics

198
Q

Archaeal Cytoplasmic membrane:

A

-Phospholipids contain no fatty acid -> contain isoprenes
-Phospholipids ether linked (not ester linked)
-More stable -> as present as mixture of mono and bilayers,

199
Q

Notable unusual Archaeal cell envelope structures:

A

Archaellum, cannulae, and hooks

200
Q

Chromosome organisation and replication of Archaeal cells:

A

-Circular chromosome (+plasmids)
-Circular chromosome wrapped around histones
-Has multiple origins of replication
-Encodes polymerases B (Found in eukarya) and D (Specific to Archea)

201
Q

Transcription and RNA processing of Archaeal cells:

A

-> has a single RNA polymerase -> similar to eukaryotic RNA polymerase 2
-DNA has introns
-Genes organised within operons

202
Q

Translation in Archaeal cells:

A

-Coupled to transcription (Like prokaryotes)
-Involves translation factors (like eukarya)
-Ribosomes are 70S (Like prokaryotes)

203
Q

Hyperthermothiles:

A

Two groups: Crenarchaeota and Euyarchaeota
-High growth temp 80-120’c
-Require elemental sulfur for growth
-Often acidophiles

204
Q

Ex. Acidanus infenus:

A

Crenarchaeota (hyperthermophile):
Facultative aerobe
-optimal growth 75’C pH 2.5-3

205
Q

Industry role of sulfate-reducing archaea:

A

They have a negative impact on the oild industry -> increase sulfur emissions, cost of refining oil, and attak metal in well casings and pipelines.

206
Q

Where are halophiles often found?

A

Evaporating ponds, dead sea, great salt lake

207
Q

Methanogens:

A

Type of Euyarcheaota
-Found in anaerobic env.
-Use acetate as electron acceptor in respiration.

208
Q

Chemoorganotrophy:

A

Reduced organic molecules (e.g sugars) are broken down and used as an energy source

209
Q

Chemolithotrophy:

A

Reduced inorganic molecules (geological compounds) are broken down and used as an energy source.

210
Q

Phototrophy:

A

Sunlight is used as an energy source.

211
Q

What are used as electron donors by chemoorganotrophic, chemolithotrophic, and phototrophic microorgansims?

A

Organic molecules, inorganic molecules, and light energy (used to reduce compounds which then act as electron donors)

212
Q

Free energy change of electron movement:

A

Delta Gibbs = -1 x number of e- transferred x Faraday constant x Redox potentail change

213
Q

Metabolic diversity in prokaryotes: electron transfer systems:

A

NADH, NADHPH, and FADH2 electron acceptors/donors -> pump H+ out of cell -> create PMF to drive synthesis of ATP

214
Q

What are teh 3 metabolic types undergone by Chemoorganotrophs?

A

-Oxygenic respiration
-Anaerobic respiration
-Fermentation

215
Q

Chemoorganotrophs: Oxygenic respiration

A

Glycolysis -> link reaction -> TCA cycle -> Electron transfer chain -> ATP synthesis

216
Q

Chemoorganotrophs: Anaerobic respiration

A

-Wide range of inorganic compounds can be used as electron acceptors
-ETC occurs by cytochromes, quinones, and iron-sulfur proteins
-Depending on redox potential of acceptor -> distinct amounts of energy generated.

217
Q

Anoxygenic respiration:

A

Method using oxygen to expolit wide range of ecological niches.

218
Q

Two key types of chemoorganotrophic anaerobic respiration:

A

Denitrification + methanogenesis (can also be used by chemolithotrophs)

219
Q

Difference between anaerobic respiration and fermentation:

A

Anaerobic uses any molecules (Except O2) as terminal electron acceptors via membran bound resp. chain.
-ATP produced by oxidative phos. via PMF

Fermentation uses organic molecules as electron acceptors -> no resp chain -> ATP produced by substrate-level phos. in the cytoplasm.

220
Q

Major Types of lithotrophy:

A

Hydrogenotrophy, (Sulfate reudction + Methanogenesis), Iron oxidation, Ammonia oxidation, Nitrification, Anammox, Sulfide oxidisation and sulfur oxidation.

221
Q

Important properties of chemolithotrophs:

A

-most use CO2 as carbon source to produce organic molecules
-Can also use complex molecules like acetate
-Use NADH to “fix carbon” -> requires H+ to reverse electron flow process.

222
Q

Iron oxidisation: Chemolithotrophy

A

Reduced Fe2+ can be oxidised into Fe3+ at low pH -> can form insoluble Fe3+ ferrix hydroxide at even lower pH.

223
Q

Use of acid-producing microbes in biomining:

A

Acidothibacillus ferroxidans -> oxidise sulfide of Fe and Cu -> oxidisation of Cu+ and acid production dissolves the metal from the rocks.

224
Q

What are the two types of Phototrophy?

A

Oxygenic photosynthesis (cyanobacteria and plants) + Anoxygenic photosynthesis (bacteriorhodopsin, Green sulfur bacteria, purple bacteria)

225
Q

What photosystems are used by oxygenic photosynthesis?

A

PS1 and 2

226
Q

What photosystems are used by anoxygenic photosynthesis?

A

BR, PS1, PS2

227
Q

What is Bacteriorhodopsin?

A

-Abundant light-driven proton pump in archaeal membranes
-Contains a retinal pigment that undergoes conformation (trans->cis) change once excited by light
-The movement of protons generated PMF for ATP synthesis.

228
Q

Mechanism of BR (bacteriorhodopsin):

A

Retinal pigment excited -> (cis -> trans) -> transfeer of proton to Asp85 -> deprotonates retinal pushes against helix F, opening a channel -> induced deprotonation of retinal from Asp96 -> Asp96 is reprotonated -> Asp85 transfer proton outside through H-bonding via water.

229
Q

Do cyanobacteria have chloroplasts?

A

No they are primitive chloroplasts.
-Either no thylakoids or they are organised with wide range of architecture

230
Q

What are the pigments used by cyanobacteria?

A

Chlorophylls, carotenoids, bilins

231
Q

Oxygenic photosynthesis of cyanobacteria:

A

-Both photosytems excited by light -> energy used to strip e- from H2O -> protons pumped outside cell -> PMF ATP synthesis -> NADPH and ATP fix CO2 -> glucogenesis

232
Q

How are electrons excited in photosystem 1? (green sulfur bacteria)

A

Light is captured by antenna complexes (chlorosomes) and photon energy is directed at the PS1 reaction centre.

233
Q

Anoxygenic photosynthesis: (Green sulfur bacteria)

A

PS1 donates e- to ETC -> ETC pumps protons + reduce NADP+ via ferredoxin -> PMF used to generate ATP -> PS1 recieves electrons from sulfur derivatives.

234
Q

How are electrons excited in photosystem 2? (purple sulfur bacteria)

A

Light is captured by antenna complexes (chromatophores) and photon energy is directed to the PS2 reaction centre.

235
Q

Anoxygenic photosynthesis: (Purple bacteria)

A

-PS2 donates electront to cyclic ETC
-ETC proton pumps establish PMF
-NADH cannot be produced -> lack of transporter with reducing potential
-Inorganic compounds used as electron donors to produce NDAPH

236
Q

Mutualism:

A

Both organisms benefit from the interaction

237
Q

Commensalism:

A

The microbes benefit from the interaction but with no impact on the host

238
Q

Parasitism/Predation/Competition

A

The microbes benefits from the interaction at the expense of the host

239
Q

Ectosymbiosis:

A

Symbiont living on the surface of host cells, e.g Mixotricha Paradoxa

240
Q

Endosymbiosis:

A

Symbiont living inside host cells, e.g associations in Hemiptern insects -> bacteriocytes which can aggregate to form bacteriosomes

241
Q

Parasites: intracellular bacteria: example

A

Legionella pneumophila -> found in fresh water -> parasite of amoeba that can also replicate within alveolar macrophages

242
Q

Parasites: bacterial predators: example

A

Bdellovibrio bacteriovorus: attacks gram - bacteria -> invades perisplasm (cell wall) -> feeds on host cell

243
Q

Plant nodulation as an example of symbiosis:

A

Nodulation, legumes, and Rhizobia

244
Q

Rhizobia:

A

-Alphaproteobacteria (gram -) -> soil dwelling bacteria part of the “rhizosphere” -> induce nodulation

245
Q

Nodulation:

A

Rhizobia induce the formation of root nodules that allow plants to fix atmospheric N2

246
Q

Difference between an organelle and an endosymbiont?

A

Organelles are usually widely conserved accross a range of organisms.

247
Q

What are the 3 physical methods that can be used to eradicate bacteria?

A

Heat, Irradiation, Filtration.

248
Q

What is the difference between bactericidal and bacteriostatic agents?

A

Bacteriostatic control prevents further growth in the number of cells and viable cells, whereas bactericidal control maintains the number of cells but DECREASES the viable cell count.

249
Q

Using heat as a physical antimicrobial control:

A

-Autoclave (15min 121’C), dry heat (oven >150’C 2hours), pasteurization (Mild heat/ HTST 72’C 15s/ UHT140’c 2-5s)

250
Q

Using irradiation as a physical antimicrobial control:

A

ionising (food industry + lab equip) and non-ionsing (surface decontamination) (DNA damage, oxidative stress)

251
Q

Using filtration as physical antimicrobial control:

A

Use of specific pore sizes to exclude microorganisms.

252
Q

Thermal death point:

A

Minimal temp. at which all organisms are killed in 10min in a particular liquid

253
Q

Thermal death time:

A

Minimal time required to kill all bacteria in a particular liquid at a given temperature.

254
Q

Sterilants:

A

Completely eliminate or destroy all forms of microorganisms (including spores) - e.g ethylene oxide

255
Q

Disenfectants:

A

Kill microorganisms, but not necessarily endospores -> e.g alcohols (dentatures proteins + is a lipid solvent disrupting cytoplasmic membranes)

256
Q

Antiseptics + germicides:

A

Inhibit growth or kill microorganisms -> e.g handwash

257
Q

The 3 methods for measuring antimicrobial activity:

A

Disc diffusion technique, Minimum inihibtory Concentration (MIC), Minimum bactericidal concentration (MBC)

258
Q

What is the Minimum Bactericidal concentration?

A

The lowest concentration of a drug killing 99.9< of a test organism after overnight incubation

259
Q

What is the Minimum inhibitory concentration?

A

The lowest concentration of a drug inhibitng the visible growth of a test organism after overnight incubation.

260
Q

Disc diffusion technique:

A

Add microbial disks to culture of test organism -> incubate for 24-28 hours -> test organism shows susceptibility to some agents -> areas of inhibition.

261
Q

Phenolic compounds (1867):

A

Aromatic derivatives -> can be used as local anesthetic at low conc. -> antibacterial (but toxic) at high conc. -> disrupts cytoplasmic membranes and denatures proteins.

262
Q

Aldehydes:

A

Alkylating agents: modify proteins and DNA -> causing cell death

263
Q

Quaternary ammonium compounds:

A

Interact with phospholipids of the cytoplasmic membrane (cationic detergents)

264
Q

Halogen releasing agents:

A

2 types: chlorine/iodine-releasing.
Chlorine: Na hypochlorite (bleach) -> forms chlorinates bases in DNA
Iodine: target DNA and proteins.

265
Q

Louis Pasteur (1822-1895)

A

Formally demonstrated the theory of germs

266
Q

Robert Kock (1843-1910):

A

Establihes relationship between microbe and disease

267
Q

Alexander Flemming (1928):

A

Discovered Penicillin produced by fungus.

268
Q

What are the two major therapeutic strategies?

A

Antibiotics and vaccination.

269
Q

What are the 4 major classes of antibiotics based on modes of action?

A

-Drug inactivation
-Target modification
-efflux/impermeability
-Bypass

270
Q

What causes antibiotic resistance?

A

Overuse of antibiotics and misuse in human therapeutics, farming, agriculture + aquaculture

271
Q

What are the properties of the ideal antibiotic?

A

-Display selective toxicity towards bacteria (selective of essential process or inhibit its virulence)
-Stable in host and active at low concentrations
-Cheap

272
Q

beta-lactam: function

A

inhibit peptidoglycan polymerisation mediated by D,D-transpeptidases.
-Resist against penicillin

273
Q

What are beta-lactams?

A

Structural analogs of D-Ala-D-Ala C-terminal residues in the peptide stem. Used by penicillin binding proteins as substrates and inactivate the enzymes irreversibly.

274
Q

Mechanism 1: inactivation by beta-lactamases

A

Nucleophilic attack by catalytic serine -> form a covalent complex penicillin-beta-lactamase -> penicillin hydrolysis.

275
Q

Mechanism 2: Beta-lactam mutation of target enzyme

A

Reduction of PBP affinity for beta-lactams + the overexpression of PBP targeted bt Beta-lactams

276
Q

Mechanism 3: secretion of antibiotics (gram - bacteria)

A

e.g P. aeruginosa
-Overproduction of MexAB-OprM system -> carbapenem resistance
Overproduction of the MexEF-OprN system -> imipenem resistance

277
Q

Mechanism 4: Modification of the synthetica pathway targeted by beta-lactams

A

Modification of pathway causes beta-lactams to become ineffective on target.

278
Q

Difference between parasites and pathogens?

A

Pathogens aren’t visible to naked eye.

279
Q

What type of microorganisms doesn’t adopt pathogenesis?

A

Archaea

280
Q

What “non-living” particles can be pathogenic?

A

Viruses and proteins (prions)

281
Q

Criteria of a successful pathogen:

A

-Gain access to host
-Locate nutritionally compatible niche
-Avoid, subvert, or circumvent hist innate and adaptive immune responses.

282
Q

Innate immune system:

A

Not specific and rapid. Not improved by repeat infection

283
Q

Adaptive immune system:

A

Highly-specific + slower (esp. on first exposure)
Improved by repeat infection (memory)

284
Q

What are the portals of entry for pathogens into a human?

A

Conjunctival route (eyes), Aural route (ears), Oral route, Respiratory route (nose), abrasions, wounds, puncture of skin (by insects), injections, Genital tract, Animal bites, Transcutaneous channel

285
Q

When does infection upon exposure to the pathogen?

A

Once the host has been exposed to the pathogen past a threshold.

286
Q

Modes of pathogenic transmission:

A

Air(droplets), Water, Food, Mechanical/vector

287
Q

Difference between mechanical and vector?

A

A vector will have its biology effected by the disease and integral to the life cycle of the pathogen -> a mechanical (fomite) will not have its biology effected

288
Q

What values determine virulence:

A

Mortality + Morbidity + infectious Dose

289
Q

Morbidity:

A

The number of case of a disease in the population

290
Q

Mortality:

A

The number of deaths from notifiable diseases

291
Q

Why is high virulence not good for pathogens?

A

High mortality rates reduce spread.

292
Q

Infectious Dose:

A

Number of individual particles/cells required for infection

293
Q

What are virulence factors?

A

Factors that enable a pathogen to colonise the host -> however don’t cause the disease.

294
Q

Virulence Factors: Adhesins

A

Find a niche and colonise host

295
Q

Virulence Factors: S-layers

A

Immune evasion/ survival in host

296
Q

Virulence Factors: Digestive enzymes

A

Help find a niche, colonising it, and finding host resources. e.g collegenases to breakdown and reach deep into tissues

297
Q

Virulence Factors: Toxins

A

Reprogram the host biology to benefit the pathogen

298
Q

Virulence Factors: “stealth mode”

A

Absence of outer-surface structures -> immune evasion -> this is an example of reductive evolution.

299
Q

Worldwide how many deaths is pathogenesis responsible for?

A

26%

300
Q

How many deaths were caused by lower respiratory infections in 2019?

A

2.2million deaths

301
Q

How many deaths were caused by Diarrhoeal diseases?

A

1.5 million deaths

302
Q

How many deaths were caused by Tuberculosis?

A

1.2millions

303
Q

How many deaths were caused by HIV/AIDS in 2019?

A

700,000 people

304
Q

Robert Kock:

A

Established link between diseases and microbes.
Pioneered use of pure cultures to understand infectious diseases. (using Bacillus anthracis - Anthrax)

305
Q

What is Koch’s postulates?

A

Host + pathogen = Death

306
Q

What have the main advances in public health been caused by?

A

Improved sanitation (clean drinking water + waste disposal), less overcrowding, better living conditions, and better diet

307
Q

What is immunity?

A

Upon second exposure to the disease’s antigens the subject doesn’t develop the disease.

308
Q

Small pox vaccination example:

A

1717 Lady Montagu -> innoculated people using pus of small pox into open vein
1796: Edward jenner innoculated person with cowpox -> protected them from small pox.

309
Q

What is the term used for when immunity to a pathogen protects the host from a very similar pathogen?

A

Cross-protection

310
Q

Who developed the first “antibiotics” of penicillin?

A

Florey and Chain

311
Q

What process do penicillins target?

A

The cell wall synthesis of the pathogen.

312
Q

What is a symptom?

A

A change in body function that is felt by the patient as a result of disease.

313
Q

What is a syndrome?

A

A specific group of signs and symptoms that accompany a disease.

314
Q

Some diseases are caused by multiple pathogens: example

A

Pneumonia -> can be bacterial, viral, and fungal

315
Q

What is disease state determined by?

A

The reaction to a pathogen rather than the pathogen itself -> the product of a relationship change/conflict between the host and pathogen

316
Q

Why are general antibiotics often administered for diseases?

A

Many different pathogen can be responsible for the disease, and-so general antibiotics will be administered until a pathogen sample is taken,

317
Q

What is our microbiota?

A

The range of microorganisms that may be commensal or symbiotic found in and on us.

318
Q

What effect do our microbiota have on us?

A

-Aid digestion
-Healthy metabolism
-immune function
-mood and behaviour
-obesity, heart disease + diabetes

319
Q

C.difficile:

A

Clostridium difficile -> causes diarrhoea, colonisation and inflammation -> 9% mortality rate

320
Q

Opportunistic pathogens:

A

Microbes that aren’t ordinarily pathogenic but can cause infection or disease in a compromised host.

321
Q

“hospital aquired “ infections:

A

Infections aquired as a result of hospital stays. E.g C.diff and MRSA

322
Q

Vibrio Cholerae:

A

Disease: Cholera
Symptoms: Diarrhoea, pain + vomiting
Virulence: death through dehydration, 1.3-4mill cases + 21-143 thousand deaths
Classification:Gram - bacteria
Major Virulence factors: Cholera toxin
Transmission: Faecal-oral route (via contaminated water)
Treatment: Oral Rehydration + anitbiotics

323
Q

Vibrio cholerae: Broadstreet pump

A

1854 cholerqa outbreak -> first historical case of a disease outbreak being methodically investigated.

324
Q

Principles of epidemiology:

A

-Identify first patient “patient 0”
-Identify people in contact
-Identify the reservoir for the pathogen
Blocking/containing the pathogen

325
Q

Epidemic disease:

A

Disease aquired by many hosts in a given area in a short time

326
Q

Endemic disease:

A

Disease constantly present in a population

327
Q

Pandemic disease:

A

Worldwide epidemic

328
Q

Salmonella enterica serovar Typhi:

A

Disease: Typhoid fever
Symptoms: Rash + others extremely variable
Virulence: 30% mortality rate
Classification: gram -
Major Virulence factors: toxins
Transmission: Faecal-oral route. Human colonised gall bladder
Treatment: Antibiotics or vaccine

329
Q

Polio Virus:

A

Disease:Polio
Symptoms: 95% mild
or irreversible paralysis, muscle weakness + deformities
Virulence: 15% symptomatic cases death occurs when breathing muscles immobilised
Classification: - strand RNA virus
Transmission:Faecal-oral route (via water contamination)
Treatment: Vaccine - (attenuated)

330
Q

Issue with polio vaccine:

A

In extremely rare cases immunocompromised individuals can become “healthy carriers” and spread disease.

331
Q

Yersinia pestis:

A

Disease: Bubonic and Pneumonic plague
Symptoms: Buboes (swollen lymph glands), fever, sepsis, pneumonia
Virulence: Bubonic = 50%
Pneumonic = 90-100% mortality rate
Classification: Gram - bacteria
Major Virulence factors: toxins, V, W, YopB, Yop D (avoid phagocytosis), F1 (makes fleas hungry)
Transmission: Rodents, prairie dogs (rodent fleas) + human respiratory aerosol
Treatment: Antibiotics + vaccine

332
Q

Zoonotic pathogens:

A

Pathogens that affects both animals and humans

333
Q

Why is epizootics important?

A

Epidemics in animals can be warning signs of potential epidemics.

334
Q

2017 Madagascar:

A

Madagascar - Pneumonic plague outbreak -> epizootics used -> reservoir identified -> killed fleas + rodents -> care workes wore PPE + antibiotics -> 8.6% mortality rate

335
Q

Phytophthora infestans:

A

Disease: “potato blight”
Symptoms: white mycelium growth over surface of leaves and tubers
Virulence: near 100% of crops
Classification: Spore forming oomycete (water mold)
Transmission: Spores
Treatment: Fungicides = CuSO4

336
Q

Influenza virus:

A

Disease: Influenza (flu)
Symptoms: Fever etc.
Virulence: 0.01%-50% -> newer strains have higher case fatality rates
Classification: - ssRNA orthomyxoviridae
Transmission: Droplets
Treatment: Antiviral drugs + vaccine

337
Q

What are the key enzymes found on the surface of influenza virus?

A

Hemagglutinin and Neuraminidase.

338
Q

How can new viruses arise?

A

The reassortment of two virus strains within a host cell, e.g bird flu + human flu -> swine flu

339
Q

How many H1N1 death worldwide?

A

50-100million -> maybe more than black death
10-20% mortality rate.

340
Q

Zika virus:

A

Disease: Zika virus disease
Symptoms: mild fever, rash
Virulence: Extremely low (birth defects: microcephaly + Guillain-Barre syndrome)
Classification: + ssRNA virus
Transmission: Vector by Aedes mosquito + STD (by semen)
Treatment:

341
Q

Microcephaly:

A

Skull doesn’t grow correctly -> brain doesn’t correctly develop - Medical conditions + disease

342
Q

Zika Virus Response:

A

Very fast, epidemiological surveillance took place at the same time as containment.
CDC set up Zika Birth defect surveillance -> found small chance of zika effecting birth. (p = 0.009)

343
Q

Ebola Virus:

A

Disease: Ebola Viruse disease + Ebola hemorrhagic fever
Symptoms: fever, headaches, muscle pain, bleeding
Virulence: 40-90% mortality
Classification: - ssRNA filovirus
Transmission: direct contact + maybe sex -> no known reservoir
Treatment: Currently “untreatable”

344
Q

Ebola 70-70-60 rule:

A

60 days: 70% of patients in isolation and “treatment” + 70% “safe” burials

345
Q

What is the biggest challenge in global health?

A

Antimicrobial resistant (AMR) -> could lead to absence of antibiotics in modern medicine -> increasing dangers of infection

346
Q

What 3 things make antimicrobial resistance complex?

A

Antibiotics: each have different target
Bacterial pathogens: Different virulence characteristics and survival strategies
Resistance Mechanisms: Varied and not well understood.

347
Q

What is immunology?

A

The study of the immune system

348
Q

What is the immune system?

A

Integrated system of cells and molecules that defends against disease.

349
Q

Leucocytes part of the innate immune system:

A

Phagocytes, natural killer cells

350
Q

Leucocytes part of the adaptive immune system:

A

B and T lymphocytes

351
Q

Soluble factors involved in the innate immune system:

A

Lysozymes, complement, inferons

352
Q

Soluble factors involved in the adaptive immune system:

A

antibodies

353
Q

What are leucocytes?

A

White blood cells

354
Q

Which stem cell do all blood cells derive from?

A

Haematopoietic stem cell in bone marrow

355
Q

Which stem cell do leukocytes part of the innate immune system derive from?

A

Myeloid stem cell

356
Q

Which stem cell do leukocytes part of the adaptive immune system derive from?

A

lymphoid stem cell

357
Q

External barriers to infection:

A

Keratinised skin, Secretions, Mucous (cilia), low pH of stomach (2.5), Commensals

358
Q

What external secretions help prevent infection?

A

Sebum, fatty acids, lactic acid, and lysozymes.

359
Q

Why is prevention of infection more beneficial than cure of infection?

A

Prevention requires less nutrients and has less impact on the human -> no symptoms of disease -> increased chance at survival

360
Q

Neutrophils:

A

Type of phagocyte.
-Main phagocyte in the blood
-Short-lived, fast-moving
-Lysosomes release H2O2
-Multi-lobed nucleus

361
Q

Mononuclear phagocytes:

A

-Long lived (months)
-Help initiate adaptive responses.
-Monocytes develop into macrophages in tissue.
-Macrophages ingest hundreds of bacteria.

362
Q

What are phagocytes more effective than macrophages at treating?

A

Bacterial and fungal infection.

363
Q

Natural Killer Cells:

A

type of lymphocyte:
-Kill virally infected cell non-specifically
- important in self/non-self recognition
-May kill cancer cells
-Have prominent granules

364
Q

Pathogen recognition by NK cells:

A

Kill targets unless they recognise self-proteins (major histocompatability complex) that are present on all nucleated cells

365
Q

Pathogen recognition by Phagocytes:

A

-Have general pathogen-recognition receptors (PRRs) that recognise microbe-associated molecular patterns (MAMPS) - shared by microbes.

366
Q

Example of Phagocyte recognising pathogen:

A

Toll-like receptor 4 (TLR4) recognises lipopolysaccharide

367
Q

Defensins:

A

Similar to antibodies -> +ve peptides ->synthesised by neutrophils -> disrupt bacterial membranes

368
Q

Interferons:

A

Produced by virally infected cells -> protect uninfected cells -> interfere with viral replication -> activate macrophage + NK cells

369
Q

What is the complement system?

A

~20 proteins in blood, activated enzyme cascade triggered by infection -> trigger bacterial cell lysis
-Can induce inflammation

370
Q

Cytokines:

A

Produced by innate immune system cells -> small secreted proteins that bind to cell and regulate the immune response e.g interleukins
-Act locally
-Act by binding to spec. receptors on target cells

371
Q

Inflammatory Mediators:

A

Cause conditions (and symptoms of allergy) that inhibit/reduce the action of infection. e.g histamine, prostaglandins.

372
Q

What are the symptoms of inflammation?

A

Heat, redness, swelling, pain

373
Q

What induces the release of inflammatory mediators?

A

Infection or damage + the production of cytokines.

374
Q

Inflammation:

A

-Localised response to infection/damage -> dilation of blood vessels -> increased capillary permeability -> phagocytes migrate to effected tissue

375
Q

integrated responses to infection example: fever

A

On infection, macrophages release cytokines e.g interleukin 1. -> acts on hypothalamus -> raises body temp (fever) -> stimulates phagocytosis + B/T lymphocytes + reduces Fe levels of blood

376
Q

Where do B lymphocytes mature?

A

In bone marrow -> develop antibody receptors

377
Q

Where do T lymphocytes mature?

A

The thymus -> develop T cell receptors

378
Q

What component of the adaptive immune system recognises antigens?

A

Specific Receptors on T and B lymphocytes

379
Q

What is the response of B lymphocytes?

A

secretion of antibodies

380
Q

What kind of immunity is the response of B lymphocytes?

A

Humoral

381
Q

What is the response of T lymphocytes?

A

Kill infected host cell, make cytokines

382
Q

What kind of immunity is the response of T lymphocytes?

A

cell-mediated

383
Q

What kind of infections are T lymphocytes effective against?

A

Viral, intracellular bacterial, and intracellular parasitic infections

384
Q

What kind of infections are B lymphocytes effective against?

A

extracellular bacterial, and secondary viral infections

385
Q

Clonal selection hypothesis: Burnett 1958

A

Lyphocytes that recognise “self” (healthy cells) are deleted early in development -> to prevent damage to host’s tissues

386
Q

Primary lymphoid tissue:

A

Where lymphocytes reach maturity and aquire specific receptors

387
Q

Secondary Lymphoid tissue:

A

Where mature lymphocytes are stimulated by antigemn

388
Q

What can B cells differentiate into upon antigen binding induced mitosis?

A

Plasma cells and Memory cells.

389
Q

What occurs at the spleen?

A

Location at which antigens in the blood are filtered out.

390
Q

Anitbody shape:

A

Y shape made of 4 polypeptide chains -> two light chains (25kD) and two heavy chains (50kD)

391
Q

Other name for antibodies:

A

immunoglobulins

392
Q

What joins the chains of antibodies?

A

Disulphide bridges and non-covalent interactions

393
Q

What is the name of the arm regions of the antibody:

A

FAB arms

394
Q

FAB arms:

A

variable regions of the antibody -> specific to different antigens depending on antibody

395
Q

Role of antibodies:

A

Agglutination and regulation and antigen elimination

396
Q

What is antigen elimination?

A

The process of antibodies “marking” infected cells by the FC region binding to FC receptors on NK cells -> leading to lysis of infected cell.

397
Q

What does FAB stand for?

A

Fragment antigen binding (arms of antibody)

398
Q

What does FC stand for?

A

Fragment crystallizable (tail of antibody)

399
Q

What are the 5 classes of immunoglobulins?

A

IgG, IgM, IgA , IgD, IgE

400
Q

IgG:

A

Immunoglobulin -> Gamma heavy chain -> most abundant in serum and tissues -> can cross placenta -> provides newborns with immune memory from mother

401
Q

IgM:

A

Immunoglobulin -> Mu heavy chain -> first antibody produced upon primary inection-> pentamer shape

402
Q

IgA:

A

Immunoglobulin -> Alpha heavy chain -> in serum and secretions -> protects mucosal surfaces (gut infections)-> either monomer or dimer

403
Q

IgD:

A

Immunoglobulin -> heavy delta chain -> unknown function -> might work against respiratory infection

404
Q

IgE:

A

Immunoglobulin -> Epsilon heavy chain -> present at low levels in serum -> protective against extracellular parasites

405
Q

What is Serum?

A

Blood without cells and clotting factors.

406
Q

What are the two different types of immunoglobulin light chains?

A

kappa and lambda -> not class restricted -> promotes diversity.

407
Q

Primary response to infection in terms of antibodies:

A

-Slower recognition and lower production of IgG -> lag of IgG production after IgM

408
Q

Secondary response to infection in terms of antibodies:

A

-Faster recognition and greater production of IgG = production of IgM.

409
Q

Why do maternal antibodies last a long time?

A

Maternal antibodies are IgG -> which have a higher half life -> can alst 6 months

410
Q

Are variable and constant regions of antibodies coded together?

A

No they are coded by separate exons.

411
Q

What mechanism is used by B+T cells to combat the mutation and variation of viruses and pathogens?

A

Variable region exons can recombine and mutate during the differentiation of B+T cells -> leading to increased variation in the variable regions of antibodies.

412
Q

Which antibodies neutralise toxins?

A

IgG and IgA

413
Q

Which antibodies immobilise motile microbes?

A

IgM

414
Q

What do all antibodies do as a result of their specific binding/multivalency:

A

-Prevent binding to, and infection of, host cells.
-Form complexes

415
Q

What are the effector functions of antibodies?

A

Activate complement (IgG, igM)
Bind Fc receptors: phagocytes (IgG, IgM), mast cells(IgM), NK cells (IgG)

416
Q

What are the two methods by which complement can be activated?

A

Activated specifically by antigen/antibody complexes or non-specifically by bacteria

417
Q

What are the main proteins of the classical complement pathway?

A

C1, 4, 2 , 3, 5, 6, 7, 8, 9

418
Q

What property do the main proteins of the classical complement share?

A

They have enzymic (protease) activity + generate fragments with biological activity

419
Q

What occurs during the initiation of the classical pathway of complement activation?

A

1 antigen bound to 2 antibodies. C1 interacts with the 2 Fc regions to activate them. Activation of C1, C4, and C2 -> generates C3 convertase.

420
Q

Which antibody is the most efficient activator of complement?

A

IgM -> because it’s a pentamer with the most Fc tails -> therefore most regions for C1 interaction.

421
Q

Role of C5-C9:

A

Hollow cylinders form “membrane attack complex” -> create pores in bacterial membranes. -> leading to cell lysis

422
Q

Role of C3 convertase:

A

Breakdown of C3 into C3a and C3b.

423
Q

What is the role of C3b?

A

The activation of C5 convertase and opsonisation ->increase binding of phagocytes -> increase rate of phagocytosis.

424
Q

Role of C5a and C3a:

A

recruitment of phagocytes + induce inflammation.
-Act as chemoattractants and anaphylaxans

425
Q

Which type of bacteria aren’t susceptible to the “membrane attack complex”?

A

Gram + (because peptidoglycan shields the cytoplasmic membrane)

426
Q

Which classes of antibodies can also act as opsonins?

A

IgG, IgA

427
Q

What are opsonins?

A

Antibodies that enhance the recognition of microbes by binding to Fc receptors on the phagocyte surface.

428
Q

What do NK cells secrete?

A

Perforin ->target cells undergo apoptosis.

429
Q

What antibody binds to NK cells?

A

IgG

430
Q

What do mast cells protect against?

A

Mediate allergy + defence against large parasites

431
Q

By what mechanism do mast cells cause local inflammation?

A

Degranulation (exocytosis) releases inflammatory mediators.

432
Q

What antibody is present on mast cells?

A

IgE

433
Q

Polyclonal b cell response to antigen:

A

-Lacks fine specificity -> more flexibility
-Antibodies bind to different shapes “epitopes” on the antigen -> produces mixture of antibodies

434
Q

Monoclonal antibodies:

A
  • Have single specifity
    -Derived from single B lymphocytes
435
Q

How are antibodies produced industrially?

A

The fusion of B cells from an immunised animal and a Tumour cell line -> hybrid cell that secretes antibody and divide indefinitely.

436
Q

OKT3:

A

-Specific to CD3 -> used to treat graft rejection

437
Q

Herceptin:

A

-Specific to Her-2 - treats Breast cancer

438
Q

Rituximab:

A

-Specific to CD20 -> treats B cell leukaemia

439
Q

Remicade:

A

-Specific to TNF -> treats Crohn’s diease + rheumatoid arthiritis

440
Q

Tocilizuman:

A

-Specific to interleukin 6 receptor -> treats COVID and arithitis

441
Q

Sotrovimab:

A

-Specific to SARS-COV-2- spike protein -> treats severe covid

442
Q

T helper cells (CD4 +):

A

-Help B cells make antibodies
-Activate macrophages and NK cells
-Help development of cytotoxic T cells

443
Q

T cytotoxic cells (CD8 +):

A

-Recognise and kill infected host cells
-Similar to NK cells however are more specific.

444
Q

T cell receptor structure:

A

-T lymphocyte receptor (TCR) similar to antibody -> has beta and alpha chain, hinge region, disulphide bonds, variable and constant regions.

445
Q

What type of antigens do T cells recognise?

A

“cell-associated”, processed antigens, which have been broken down into smaller peptides

446
Q

Which types of infection are T cells most effective with treating?

A

Viral, intracellular bacteria, and intracellular parasitic infections.

447
Q

What proteins bring foreign proteins to the surface to form an MHC?

A

MHC proteins

448
Q

Variation of MHC proteins:

A

MHC proteins express great variation -> because they’re the most polymorphic proteins in a human

449
Q

MHC 1:

A

Found on all nucleated cells -> (not on RBC’s) -> display antigen to CD8 +ve T cells

450
Q

MHC 2:

A

expressed by macrophages, dendritic cells, and B cells -> displays antigens to CD4 + T cells

451
Q

T cytotoxic cell recognition of antigen:

A

Proteosome breaks down viral proteins -> peptides transported to the ER and bind to MHC1 -> transported to cell surface -> CD8 + T cells recognise peptide bound to MHC -> kill effected cell by induced apoptosis.

452
Q

T Helper Cell recognition:

A

Macrophage/ dendritic cell/ b cell internalises and breaks down foreign material in endosomes -> peptides bind to MHC2 and transported to cell surface -> Activated T helper cell then helps B cells make antibodies, or produce cytokine that activate/regulate of leucocytes

453
Q

What are the main groups of cytokines?

A

interleukins (IL1 -> IL38), interferons (treat viral infections), chemokines (Control cell movement or chemotaxis)

454
Q

Tumour Necrosis Factor (TNF):

A

pro-inflammatory, toxic factor responsible for the symptoms of sepsis. -> Can kill some tumour cells

455
Q

Colony stimulating factors (CSFs):

A

Stimulate the production of leucocyte colonies in bone marrow.

456
Q

Activation of adaptive immunity in the draining lymph node:

A

Tissues are supplied by lymphatic vessels -> drain to lymph nodes containing B and T cells -> dendritic cells will activate naive T cells via MHC expression.

457
Q

Activation of adaptive immunity in the draining lymph node:

A

Tissues are supplied by lymphatic vessels -> drain to lymph nodes containing B and T cells -> dendritic cells will activate naive T cells via MHC expression.

458
Q

Why are the adaptive and innate immune system interlinked?

A

Both have co-evolved.

459
Q

Vaccination:

A

attenuated form of pathogen -> Evokes a primary response -> a booster evokes a secondary response -> forms an immune memory in event of exposure to disease.

460
Q

What are the different types of vaccine:

A

Attenuate strains, Killed pathogen, subunits, Engineered virus, or RNA

461
Q

What is a risk of the use of attenuated viruses in vaccines?

A

They may revert and become pathogenic.

462
Q

What significant diseases are there with no effective vaccine?

A

Malaria, Schistosomiasis, TB, and HIV/AID (although trials)

463
Q

What is the viral HIV receptor that binds to the surface of host cells?

A

GP 120

464
Q

Steps of HIV integration into DNA:

A

GP 120 binds to cell receptors -> viral envelope fuses with plasma membrane -> nucleocapsid enters cytoplasm -> Viral RNA reverse transcribed into ds DNA -> transported to nucleus and integrates in DNA -> forms provirus

465
Q

What cells are GP120 (HIV receptors) specific to?

A

CD4 receptors on T helper cells.

466
Q

Upon initial infection of HIV what occurs?

A

The virus is “cleared”, however the pool/reservoir of infected cells gradually increases due to proviruses not being identified.

467
Q

What in addition to CD4 expression is required for HIV infection of a cell?

A

co-receptor. e.g CCR5 -> required for virus fusion with host cell

468
Q

Effect of HIV infection of monocytes?

A

Monocytes can traverse blood/brain barrier -> impact CNS

469
Q

Effect of HIV infection of dendritic cells:

A

Spread infection to multiple T-cells. Dendritic cells experience a permissive infection and-so act as a reservoir of the virus.

470
Q

Why is there a rise in HIV virus in plasma years after infection?

A

The virus will mutate to avoid immune detection.

471
Q

What leads to AIDS?

A

T helper cell depletion caused by: direct lysis by viral infection, killed by cytotoxic T cells, apoptosis

472
Q

What is the tissue effects by AIDS?

A

Lymphoid tissue

473
Q

What is the Blood count threshold of CD4+ T cells for aids?

A

<200/mm^3

474
Q

Symptoms of AIDS:

A

-Opportunistic infections
-Reactivation of latent viruses
-Rare cancers
-CNS (dementia, paralysis, blindness)

475
Q

Transmission of HIV:

A

-Sexual intercourse 70%
-Blood 28%
-Breast-feeding
-Mother-foetus

476
Q

What are the 3 key ways to deal with aids?

A

Change to behaviour, vaccination, and drug treatment

477
Q

Prevention of HIV infection: Changes in behaviour

A

Blood testing, “safe sex”, decrease i.v drug use treat HIV + pregnant women

478
Q

Drug therapy of HIV/AIDS: problems

A

-Virus has high mutation rate
-Toxicity of drugs
-Viral latency
-Cost

479
Q

Combination therapy:

A

cocktail of drugs directed at different viral targets

480
Q

How many licensed drugs block HIV replication?

A

> 25

481
Q

Future treatments of HIV/AIDS:

A

Stem cell therapy, “Kick and kIll” (reactivation of virus + immunotherapy), “passive immunisation) (monoclonal antibodies), Gene editing with CRISPR/Cas9

Semester 2 (3 decks)

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