Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MICR2000 > Bacteriology > Flashcards

Bacteriology Flashcards

1
Q

Antibiotic Resistance

A
  • Conjugation
  • Transposition
  • Integrons
  • Gene cassettes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Conjugative R Plasmid

A
  • Circular
  • Structured
  • Stable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Transposable Elements

A
  • Jump between positions on DNA
  • Insertion sequences (IS)
  • Transposons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Insertion sequences

A
  • Smallest and simplest
  • 1-3 kb
  • Contain transposase protein (endonuclease and integrase activity)
  • Inverted repeat sequence at ends that is recognised by transposase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Transposons

A
  • > 1 genes unrelated to transposition
  • Insert into chromosomes or plasmids
  • Flanked by insertion sequences
  • Often contain MDR genes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Conservative transposition mechanism

A
  • cut + paste
  • transposable element excised from one location
  • Reinsert at second location
  • Copy number of conservative transposon = 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Conservative transposition example

A
  • IS1
  • Transposase cuts target DNA (staggered nick)
  • IS integrates
  • Gaps filled by DNA polymerase and DNA ligase
  • Formation of direct repeats (DR)
  • DR: replications of target sequence, replicated on each side
  • DR flanks IS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Replicative transposition mechanism

A
  • Copy + paste
  • New copy of transposon produced
  • Inserted at another location
  • One copy remains at original site
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Replicative transposition mechanism

A
  • Tn3
  • 4957 bp
  • Inverted terminal repeats: 38 bp
  • Transposase binds to IR
  • Initiates transposition (staggered nick)
  • Ligation of Tn3 ends to target ends
  • 3’ ends prime replication
  • Cointegrate formed between transposon and target DNA
  • One big figure 8
  • Revolvase binds to ‘res’ sequences of duplicated transposon and resolves cointegrate by site-specific recombination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mobile Antibiotic Resistance Genes

A
  • DNA containing antibiotic resistance genes moves from cell to cell via conjugative plasmids
  • Conjugative plasmids acquire gene via transposons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The Integron

A
  • Genetic unit
  • Capture and expression of genes in mobile elements called gene cassettes
  • Also provides a promoter, acting as natural cloning and expression vector for the genes cassettes (primarily antibiotic resistance genes)
  • Usually found within a transposon and serves as the mechanism transposons use to accumulate multiple antibiotic resistance genes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Features of Integron

A
  • Attachment site (att)
  • att recognised by integrase + acts as acceptor site for cassettes
  • Gene encoding site-specific recombinase
  • Promoter that drives expression of incorporated sequence
  • Cassettes encoding a gene followed by integrase-specific recombination site
  • These cassettes can be excised as circles and moved from integron to integron
  • Multiple gene cassettes can insert at att site
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Staphylococcus aureus

A
  • Gram +ve cocci
  • Part of normal skin flora
  • “Golden staph” bc yellow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MRSA

A
  • Resistant to broad range of penicillin-analogues
  • Especially common in hospitals
  • Antibiotic sensitivity testing first –> optimal therapy options
  • Doctors over-prescribe Vancomycin instead –> VRSA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Virulence Factors

A

Bacterial product or strategy that contributes to virulence or pathogenicity

Colonisation of host

  • Adhesins (pili/fimbriae)
  • Iron binding proteins
  • Invasins

Evade host immune system
- Surface polysaccharides (capsule), lipopolysaccharide (LPS)

Damage host
- Exotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Measuring Virulence

A
  • Estimated from experimental studies of LD50
  • Highly virulent pathogens show little difference in number of pathogenic cells required to kill 100% of population vs 50% population
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Virulence Factors

A
  1. Adhere to host cells and resist physical removal
  2. Invade host cells
  3. Contact host cells (motility)
  4. Resist phagocytosis by macrophages and complement
  5. Evade immune defences
  6. Compete for nutrients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Adhere to host cells and resist physical removal

A
  • Pili of uropathogenic E. coli adheres to urinary epithelium –> UTI
  • Pili, adherens
    Adhering to “stick around”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Invade host cells

A
  • Invasins of Shigella species permit entry into epithelial cells of colon
  • Invasins
  • Invasins are surface proteins that allow penetration of host cells
  • Inside cytoplasm: nutrients, protection from complement, antibodies, other defences, multiplication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Contact host cells (motility)

A
  • Helicobacter pylori
  • Motility and flagella
  • Mucosal surfaces of bladder and intestines flush bacteria away to prevent colonisation
  • Motile bacteria: contact, attach, colonise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Resist phagocytosis by macrophages and complement

A
  • Streptococcus pneumoniae evade phagocytosis
  • Pneumonia, sinusitis, otitis media, meningitis
  • Urinary catheter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Evade immune defences

A
  • Neisseria gonorrhoeae: phase and antigenic variation of surface proteins
  • Phase variation of surface structures
    ○ N. meningitidis: capsule made of sialic acid
    ○ S. Pyogenes: capsule made of hyaluronic acid
  • Both resemble carbs found in human tissue
  • Therefore not recognised as foreign by immune system
23
Q

Compete for nutrients

A
  • Siderophores
  • Siderophores
  • Bacteria compete with host tissue and normal flora for limited nutrients
  • Iron is essential for both bacterial and human cell growth
  • Bacteria synthesise iron chelators (siderophores)
24
Q

Endotoxin

A
  • Not secreted
  • Structural component of OM of Gram -ve bacteria
  • Lipid portion of LPS is endotoxin (lipid A)
  • Produces same symptoms, regardless of organism
    Some organisms (Neisseria meningitidis) secrete vesicles of LPS in large quantities
25
Q

Exotoxin

A
  • Actively secreted and soluble
  • Some toxin genes carried on plasmids
  • Often cause of disease, not the bacteria
  • Therefore, killing of bacteria is insufficient; must clear toxin
  • Requires host production of antibodies that neutralise toxin- antitoxin
  • Immunisation against disease caused by toxins use inactivated toxins- toxoids

Damage host cells by inhibiting specific metabolic function:

  • Cytotoxins: kills host cells or inhibit function
  • Neurotoxins: interfere with normal nerve impulse transmission

Enterotoxins: affect epithelial cells of GIT

26
Q

Ulcers

A
  • “Excess acid hypothesis”: prevailing theory for gastric ulceration
  • Thought to be related to stress, age, diet (alcohol, spicy)
  • Treated using antacids
27
Q

Antacids

A
  • Antacid treatments –> less symptoms
  • Stop antacids –> ulcer
  • Antacids = treat symptoms, not cause of ulcers
28
Q

Discovery of H. pylori

A
  • Barry J. Marshall and Robin Warren

Peptic ulcer disease: hypothesis that bacteria cause ulcers

29
Q

Helicobacter pylori

A
  • Gram -ve
  • Spiral shaped
  • Multiple (4-6) flagella
  • Urease (+) Catalase (+) Oxidase (+)
  • Culture (pH 7), microaerophilic (O2 2-8%, CO2 10%)
  • Inhabits mucosal layer of human stomach (noninvasive)
  • Not cleared by hose immune response
30
Q

H. pylori mode of transmission

A
  • Person to person
  • Prevalence increased in elderly, some ethnic groups, domestic crowding (large families)
  • Route of transmission is mainly oral-oral (family often carry same strain)
31
Q

H. pylori Infection

A
  • Adheres to gastric epithelium, lives in mucous gel layer
  • H. pylori lives in close association with gastric epithelial cells
  • pH more neutral in mucus gel layer, and closer to epithelial cells
  • Evades host immune defenses (chronic infection)
  • Secretes urease to produce ammonia (protection from gastric acid)
  • Produce cytokines that disrupt intercellular junctions (CagA): inflammatory response
  • Penetrates intracellular junctions
  • Increases permeability of mucus layer
  • Gastric acid seeps in –> ulcer
32
Q

Urease

A

Urease: structural subunits
Assembly: accessory genes for active urease synthesis
Ure1: acid activated urea transporter (embedded in membrane of bacteria)

  • Urea in gastric juice is transported into periplasm through porin in OM
  • Urea is transported into cytoplasm through Ure1 in IM
  • Urease (cytoplasm) –> convert urea into basic (higher) pH
  • NH3 NH4+ acts as buffer in periplasm
33
Q

Rapid Urease Test

A
  • pH indicator: phenol red

- Reading at 1-24 hours

34
Q

CagA (delivery into epithelial cells)

A
  • cagA pathogenicity island encodes for type IV secretion system
  • CagA is injected into epithelial cells by type IV secretion system
  • Inflammation in host cell –> immune response –> ulcer
35
Q

Treatment and Prevention

A
  • Acid lowering drugs
  • Antibiotics (single-antibiotic treatment is ineffective)
  • Amoxicillin, tetracycline, metronidazole (not for pregnancy)
  • No effective vaccine
36
Q

Group A Streptococci

A
  • Tthroat and skin

- Endemic human diseases

37
Q

Group A Streptococci Diseases

A
  • Pharyngitis (strep sore throat)
  • Localised common infections: cellulitis, impetigo
  • Less common invasive infections: bacteraemia, toxic shock syndrome, necrotising fasciitis
  • Post streptococcal sequelae (diseases that develop upon repeated infection): acute post-streptococcal glomerulonephritis (kidney failure), acute rheumatic fever (hear failure)
  • Immune sequelae (triggered by inappropriate immune response to infectious agent): rheumatic heart disease
    ○ M protein: antiphagocytic activity
    ○ Both M protein and heart myosin are coiled-coil alpha helices
  • Thus, antibodies against heart valve myosin may direct immunity against heart valve material
38
Q

Epidemiological Categorisation of Pathogens

A
  • Pulse field gel electrophoresis (PFGE) –> golden standard
  • DNA isolated, cut with restriction enzyme
  • Run on gel with alternating current to resolve large pieces of DNA
  • Banding patterns can be compared to known strains
39
Q

Prevention of Diseases

A
  • Antibiotic treatment
  • Endemic regions –> prophylactic treatment may be unavailable or “needle avoidance”
  • Aim of vaccine research –> one shot vaccines that prevent infection and do not cause post streptococcal sequelae
40
Q

Koch’s Postulates

A
  • Microorganism may not be able to be grown in pure culture

- There may be no animal model of infection for that microorganism

41
Q

Koch’s Postulates for GAS

A
  1. The bacteria must be present in every case of the disease and absent from healthy animals.
    - Present in healthy individuals.
  2. The bacteria must be isolated from the host with the disease and grown in pure culture.
    - Grow in pure culture + quick tests to differentiate from other Strep
  3. The specific disease must be reproduced when a pure culture of the bacteria is inoculated into a healthy susceptible host.
    - Different strains of GAS cause pharyngitis and necrotizing fasciitis. Bacteria will also be absent in auto-immune sequelae.
  4. The bacteria must be recoverable from the experimentally infected host and shown to be the same as the original.
    - Bacteria can be same species, but belong to different strains
42
Q

Koch’s Molecular Postulates

A
  • Identify gene (or gene product) responsible for virulence determinant
  • Show gene present in strains of bacteria that cause the disease
  • Not present in avirulent strains
  • Disrupting the gene reduces virulence and complementation restores virulence
  • Introduction of cloned gene into avirulent strain confers virulence
  • The gene is expressed in vivo
    Specific immune response to gene protects
43
Q

Case Study in Complementation: HtrA

A
  • HtrA- protease involved in folding and maturation of secreted proteins
  • Lyon and Caparon (2004), hypothesized HtrAis involved in protecting GAS proteins during thermal stress, and is therefore involved in virulence
  • Did not demonstrate Koch’s postulates: giving back gene didn’t bring back virulence
44
Q

Case Study in Complementation: HtrA

A

CHECK NOTES

45
Q

Fibronectin Binding Proteins and Colonisation

A
  • GAS fibronectin binding proteins bind the ECM component fibronectin
  • Fibronectin binds to the human cell surface via the a5b1 integrin receptor
  • Fibronectin is efficiently bound to the surface of S. pyogenes
  • Numerous fibronectin binding proteins (FBP) have been identified on the surface of S. pyogenes
  • Gene knock-out studies have concluded these proteins are “essential” for colonisation in some strains, and absent in other strains.
  • Different FBP combinations can contribute to different Group A Strep strains infecting specific tissues (tissue tropism)
  • Redundancy in FBPs may allow Group A Strep to infect more than one tissue helps to explain the broad spectrum of Group A Strep infections
46
Q

Tuberculosis

A
  • Pulmonary (lungs) and extra-pulmonary (others)
  • Symptoms: chronic cough, fever, night sweats, fatigue, weight loss
  • Global
  • Airborne infection
  • Slow growers
47
Q

Tuberculosis Characteristics

A
  • Rods, variable in size
  • Not motile
  • Acid-fast
  • Fast and slow growers
  • Many saprophytes, several obligate and opportunistic pathogens
  • Resistant to common disinfectants
  • Heat susceptible
48
Q

Mycobacterium tuberculosis

A
  • Single circular chromosome
  • Complex regulatory potential
  • Varied metabolic and respiratory potential:
    ○ Aerobic, microaerophilic, anaerobic
    ○ Most anabolic pathways present
    ○ Specialised pathways allow adaptation to host environment
  • Abundance of genes involved in lipid metabolism
49
Q

Tuberculosis Infection description

A
  • Resides within macrophages (intracellular pathogen)
  • Thick waxy wall
  • Active interference with phagosome maturation and lysosome fusion
  • Genes allow for low pH
  • Genes help detoxify reactive radicals
  • DNA repair mechanisms
  • Mtbin cytosol
  • Adaptable carbon metabolism
  • Iron binding proteins (siderophores)
  • Modulation of cytokine production and antigen presentation
50
Q

Tuberculosis Mechanism

A
  • Inhale into lungs
  • Macrophage engulf (around alveolar walls)
  • Infected macrophage sends out signals
  • Try to contain infection –> develop early cellular infiltrate
  • Monocytes, macrophages, neutrophils
  • Attract T cells
  • Granuloma formation
  • Central necrosis –> high density of bacteria in centre
  • Rupture of bronchiole wall –> access airways
51
Q

Tuberculosis Pathogenesis

A
  • Granuloma: localised imflammatory mononuclear cell infiltrate
  • 5-10% active primary disease, 90-95% latent infection
    Latency: infection without disease but with potential
  • Post-primary (secondary) TB
    5-10% of latent infected
    ○ Reactivation
    ○ Extensive cell death and tissue destruction
    ○ Immunopathology
  • Liquefaction of granulomas (cavitation)
  • Rupture of granulomas, dissemination and transmission of bacteria
52
Q

Tuberculosis Diagnosis

A
  • Skin reactivity to mycobacterial antigens (+ =/= active)
  • Chest X-ray
  • Lab tests
  • Ziehl-Neelsen stain (acid fast?), culture, interferon gamma release assay (IGRA), PCR, molecular epidemiology
53
Q

Drug-resistant Tuberculosis

A
  • MDR TB –> resistant to isoniazid and Rifampin

- Extensively drug resistant (XDR) TB –> + multiple second-line drugs

54
Q

Tuberculosis Prevention

A
  • Albert Calmette and Camille Guerin
  • Bacille Calmette Guérin= BCG
  • Attenuated strain of M. bovis by serial passage in artificial media over 13 years
  • Protected against TB
  • Accepted vaccine for TB
  • Some protection for small children
  • Effectiveness not confirmed in all studies
  • No protection of adults
  • Not used in low endemic areas

MICR2000 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions