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Micr2000 > Module 3 - Bacteriology > Flashcards

Module 3 - Bacteriology Flashcards

1
Q

How do bacteria spread their antibiotic resistance?

A
  1. Conjugation
  2. Transposition
  3. Integrons
  4. Gene cassettes
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2
Q

What are transposable elements?

A

Transposable elements are DNA sequences that can jump from one position to another or from one DNA molecule to another. Bacteria contain a wide variety of transposable elements. The two major types of transposable elements are insertion sequences (IS) and transposons

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3
Q

Mechanism of Plasmid DNA Transfer by Conjugation

A
  1. Initiation: The F+ (donor) cell forms a pilus to connect with the F- (recipient) cell.
  2. Pilus Retraction: The pilus retracts, pulling the cells close together.
  3. Stabilization and Nicking: The cells stabilize; one strand of the F plasmid is nicked and prepared for transfer.
  4. Strand Transfer: One strand of the F plasmid is transferred to the F- cell while a complementary strand is synthesized in the F+ cell.
  5. Synthesis in Recipient: The recipient cell synthesizes a complementary strand to complete the plasmid.
  6. Completion: The transfer and synthesis are completed, converting the F- cell into an F+ cell, capable of transferring the plasmid to other cells.
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4
Q

What are insertion sequences?

A

Insertion sequences are the smallest and simplest
transposable elements. They are 1-3 kb in length & contain a gene encoding the transposase protein (has endonuclease & integrase activities). The IS element contains an inverted repeat sequence at its ends that is recognized by the transposase.

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5
Q

What are transposons and how are they inserted into conjugative plasmids?

A

Transposons contain one or more genes unrelated to transposition that can be mobilized along with the transposable element. Transposons can insert into the chromosome or plasmids. Insertion of a transposon into a conjugative plasmid can result in highly efficient transfer to recipient cells. Transposable elements are flanked by insertion sequences and often contain multiple antibiotic resistance genes.

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6
Q

What are the two types of mechanisms of transposition?

A

Conservative and Replicative Transposition.

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7
Q

What is conservative transposition and give an example?

A

The transposable element is excised from one location and becomes reinserted at a second location (eg IS1, Tn5). The copy number of a conservative transposon therefore remains one.

Example: IS1
Transposase cuts target DNA (staggered nick), IS integrates, and gaps are filled by DNA polymerase and DNA ligase. Formation of direct repeats (DR) flanking the integrated IS.

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8
Q

What is replicative transposition and give an example?

A

A new copy of the transposon is produced during transposition and inserted at another location (eg Tn3). Thus, one copy of the transposon remains at the original site and another copy is found at a new site (Copy number = 2).

Example: Replicative transposition by TN3
Total size 4957 bp.
Inverted terminal repeats 38 bp each

  1. Transposase binds to IR and initiates transposition
  2. Ligation of Tn3 ends to target ends 3‘ ends prime replication through Tn3
    - A cointegrate is formed between the transposon
    and the target DNA
    - Resolvase binds to ‘res‘ sequences of duplicated transposon and resolves co-integrate at ‘res“ sites by site-specific recombination.
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9
Q

What are mobile antibiotic resistance genes?

A

DNA containing antibiotic resistance genes moves from cell to cell via conjugative plasmids.
The conjugative plasmids acquire the antibiotic resistance gene via transposons.

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10
Q

How do the transposons acquire multiple resistance genes?

A
  • Gene capture and accumulation
  • Insertion sequence (IS) and Integrons
  • Horizontal gene transfer
  • Selective pressure in antibiotic enriched environment
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11
Q

What is an integron?

A

A genetic unit capable of the capture and expression of genes that are contained in mobile elements called gene cassettes.
The integron also provides a promoter, thus 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.

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12
Q

What are the essential features of an integron?

A
  • An attachment site (att), which is recognized by the integrase and acts as the acceptor site for the cassettes.
  • A gene encoding a site specific recombinase (intI; integrase)
  • A promoter that drives expression of the incorporated sequence.
  • Cassettes encoding a gene followed by an integrase specific recombination site “59 base element”
    These cassettes can be excised as circles and move from integron to integron.
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13
Q

What are approaches to reduce the spread of antibiotic resistance?

A
  1. Stop the inappropriate use of antibiotics to reduce the selective pressure for antibiotic resistance.
  2. Remove some antibiotics that are currently ineffective from use.
  3. Introduction of monitoring, isolation and treatment programs to prevent multiply resistant pathogens from establishing and spreading.
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14
Q

What is Staphylococcus aureus?

A

Staphylococcus aureus is a gram + cocci. It is part of the normal skin flora, 40% are asymptomatic carriers. Has yellow colour when grown on growth plate.

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15
Q

What is Methicillin Resistant Staphylococcus aureus (MRSA)?

A

MRSA is resistant to a broad range of penicillin analogues, and is especially common in hospitals. It can be treated by first running antibiotic sensitivity testing to determine optimal therapy options. But, instead of determining antibiotic sensitivity every time doctors over prescribed Vancomycin (second-line antibiotic). Now there is VRSA - very difficult to treat.

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16
Q

What is a virulence factor?

A

A bacterial product or strategy that contributes to virulence or pathogenicity.
- Factors which aid in colonisation of the host e.g. adhesins such as pili (fimbriae), iron binding proteins, invasins.
- Factors that evade the host immune system e.g. surface polysaccharides such as capsule, lipopolysaccharide (LPS).
- Virulence factors that damage the host e.g. exotoxins.

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17
Q

How do we measure virulence?

A

Can be estimated from experimental studies of the LD50 (lethal dose50).
– The dose of an agent that kills 50% of the animals in a test group.
Highly virulent pathogens show little difference in the number of cells required to kill 100% of the population as compared to 50% of population.

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18
Q

What are some virulence factors that promote bacterial colonization of the host?

A
  1. Adhere to host cells and resist physical removal.
    - Pili; adhesins
  2. Invade host cells
    - Invasins
  3. Contact host cells
    - Motility and flagella
  4. Resist phagocytosis and complement
    - Capsule
  5. Evade immune defences
    - Phase variation of surface structures
  6. Compete for nutrients
    - Siderophores
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19
Q

Explain the role of pili in infection.

A

Pili of Uropathogenic E. coli:
adherence to the urinary epithelium
–>
Urinary tract infection

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20
Q

Explain the infection process of virulence factors that adhere to host cells and resist physical movement.

A

Exposure: Host is exposed to pathogens.
Adherence: Pathogens adhere to host skin or mucosa, resisting physical removal.
Invasion: Pathogens invade through the epithelium.
Multiplication: Pathogens multiply, producing virulence factors and toxins.

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21
Q

How do invasins invade host cells?

A

Surface proteins that allow penetration of host cells.

Inside the cytoplasm of the host cell the bacterium:
- access to nutrients.
- protected from complement, antibodies, other defences.
- multiplies causing disease

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22
Q

How does bacterial motility aid in contacting and colonizing host cells?

A
  1. Flushing Defense: Mucosal surfaces of the bladder and intestines flush bacteria away to prevent colonization.
  2. Motility for Contact: Motile bacteria can contact, attach to, and colonize host cells despite this defense.
  3. Colonization in Bladder & Intestines: Many bacteria that colonize these areas are motile.
  4. Movement Through Mucus: Motility helps bacteria move through mucus to reach host cells.
    Example: Helicobacter pylori, which uses motility to colonize the stomach lining.
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23
Q

How do certain bacteria resist phagocytic engulfment by macrophages?

A

Some bacteria, like Streptococcus pneumoniae, evade phagocytosis by producing a capsule, which protects them from being engulfed by macrophages. This allows them to cause infections such as pneumonia, sinusitis, otitis media, and meningitis.

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24
Q

What role do capsules and biofilms play in bacterial infections on medical devices?

A

Capsules and biofilms enable bacteria to adhere to and colonize medical devices, like urinary catheters, making infections harder to treat.

25
Q

How do certain bacteria evade immune defenses?

A

Neisseria gonorrhoeae uses phase and antigenic variation of surface proteins.
N. meningitidis and S. pyogenes have capsules (sialic acid and hyaluronic acid, respectively) that resemble human tissue carbohydrates, avoiding immune detection.

26
Q

How do bacteria compete for nutrients with the host and normal flora?

A

Bacteria compete with host tissue and normal flora for essential nutrients, especially iron.
They produce iron chelators, called siderophores, to capture iron needed for growth.

27
Q

What are the two virulence factors that damage the host?

A
  • Endotoxin
  • Exotoxins
28
Q

What are endotoxins?

A

Endotoxin, specifically the lipid A portion of lipopolysaccharide (LPS), is a structural component of the outer membrane of Gram-negative bacteria. It produces similar symptoms regardless of the organism. Neisseria meningitidis, for example, secretes LPS vesicles in large quantities.

29
Q

What are exotoxins, and how do they affect the host?

A

Produced by: Both Gram-positive and Gram-negative bacteria.

Characteristics: Secreted, soluble toxins, with some genes carried on plasmids.

Types:
- Cytotoxins (kill host cells),
- Neurotoxins (disrupt nerve impulses),
- Enterotoxins (affect GI tract cells).

Disease Mechanism: Exotoxins often cause disease symptoms rather than the bacteria itself.

Immune Response: Requires antitoxin antibodies for neutralization; vaccines may use inactivated toxins (toxoids) for immunity.

30
Q

What are the virulence factors of Staphylococcus aureus?

A

Adhesins: Help bacteria attach to host cells.
Capsule: Protects against immune detection.
Protein A: Acts as an immunological disguise.
Coagulase: Forms blood clots, aiding in immune evasion.
Catalase: Neutralizes hydrogen peroxide from immune cells.
Exotoxins: Includes leukocidin (PVL), hemolysin, TSST, and α-toxin.
Secreted Enzymes: Hyaluronidase, fibrinolysin, and deoxyribonuclease help spread through tissues.

31
Q

What Causes Ulcers?

A

The “excess acid hypothesis” was the prevailing theory
for gastric ulceration within the medical community.
Thought to be related to stress, age, diet (alcohol, spicy
foods), and treated using antacids.

32
Q

What are the key characteristics of Helicobacter pylori?

A

Gram-negative, spiral-shaped, with 4-6 flagella.
Enzyme tests: Urease (+), Catalase (+), Oxidase (+).
Requires pH 7, microaerophilic conditions (2-8% O₂, 10% CO₂), and grows very slowly.
Inhabits the mucosal layer of the human stomach (noninvasive) and is not cleared by the host immune response.

33
Q

How is Helicobacter pylori transmitted?

A

Mode: Person-to-person transmission; humans are the main reservoir.
Prevalence Higher In: Elderly, certain ethnic groups, and crowded households.
Route: Mainly oral-oral, often through gastro-esophageal reflux or belching.
Family Transmission: Family members frequently carry the same strain.

34
Q

What are the virulence factors of Helicobacter pylori?

A

Urease: Neutralizes gastric acid by producing ammonia. Catalyzes the hydrolysis of urea into ammonia (NH₃) and carbon dioxide (CO₂). This reaction leads to an increase in pH around the bacteria, creating a more neutral microenvironment amid the highly acidic gastric juice. Urease gene expression is regulated to be activated under acidic conditions, ensuring that the bacteria can efficiently produce urease when needed.
The Urel protein facilitates the transport of urea into the bacterium, allowing for the continuous production of ammonia as long as urea is available.
Flagella: Allows penetration of the gastric mucous layer.
Adhesins: Enable binding to host cells (BabA and SabA).
Mucinase: Degrades gastric mucus.
CagA: Induces host cells to release pro-inflammatory cytokines.

35
Q

What has genome sequencing revealed about Helicobacter pylori strains?

A

Genome sequencing shows differences in gene content among H. pylori strains, affecting symptom severity (e.g., no symptoms, gastritis, gastric ulcer, or duodenal ulcer).
The cagA pathogenicity island is an example of a genetic variation that influences pathogenicity.
Host factors also play a role in the infection outcome, affecting how H. pylori impacts different individuals.

36
Q

How is CagA delivered into epithelial cells in Helicobacter pylori infection?

A

The cagA pathogenicity island encodes a type IV secretion system (T4SS).
CagA protein is injected into host epithelial cells through this T4SS, where it disrupts cellular signaling and promotes inflammation.

37
Q

How does Helicobacter pylori cause infection and lead to ulcers?

A

Adheres to gastric epithelium and lives within the mucous layer.
Evades host immune defenses, leading to chronic infection.
Secretes urease to produce ammonia, neutralizing gastric acid.
Produces CagA cytotoxin, disrupting intercellular junctions.
Increases mucus layer permeability, allowing gastric acid to penetrate and create ulcers.

38
Q

What are the treatment and prevention options for Helicobacter pylori?

A

Treatment:
- Acid-lowering drugs.
- Combination antibiotics (single antibiotic treatment is ineffective).
Antibiotics Used: Amoxicillin, Tetracycline, Metronidazole (not used during pregnancy).
Prevention: No effective vaccine is available.

39
Q

Is Helicobacter pylori a commensal or a pathogen?

A

Commensal:
- Half the world’s population is infected, but few show symptoms.
- Infection typically begins in childhood and lasts for life.
- Found in ancient mummies, suggesting a long human association.
- May protect against esophageal adenocarcinoma.

Pathogen:
- Causes 90% of duodenal ulcers, 70% of gastric ulcers, and 60% of gastric cancers.
- Strong association with gastric cancer, with some strains being more virulent.
- Risk from infection is 4x greater than the risk of eradicating it.

40
Q

What are Group A streptococci?

A
  • Known as Streptococcus pyogenes, also called the “flesh-eating bacterium.”
  • Bacterial pathogens that colonize the throat and skin in humans.
  • Cause a wide range of endemic human diseases.
  • Appear as Gram-positive cocci and display beta-hemolysis on blood agar.
41
Q

What is the most common disease caused by Streptococcus pyogenes, and how is it commonly treated?

A

The most common disease is pharyngitis, also known as “strep sore throat.”
Treatment: Over-the-counter lozenges like Strepsils are often used to relieve symptoms.

42
Q

What are some localized infections caused by Streptococcus pyogenes?

A

Cellulitis
Impetigo

43
Q

What are some less common invasive infections caused by Streptococcus pyogenes?

A

Bacteremia
Toxic Shock Syndrome
Necrotizing Fasciitis

44
Q

What are post-streptococcal sequelae, and what conditions can they cause?

A

Post-streptococcal sequelae are diseases that develop after repeated Streptococcus pyogenes infections, especially in endemic regions like northern Australia.
- Acute post-streptococcal glomerulonephritis: Leads to kidney failure.
- Acute rheumatic fever: Can result in heart failure.

45
Q

What is immune sequelae, and how can it relate to group A streptococcal infections?

A

Immune sequelae is a pathological condition caused by an inappropriate immune response to an infectious agent.

Example: The immune response to group A streptococci can lead to rheumatic heart disease.

46
Q

How does the immune response to group A streptococcal M protein contribute to rheumatic heart disease?

A

Rheumatic heart disease can be triggered by an immune response against the M protein of group A streptococci.

M protein has anti-phagocytic properties and shares structural similarity with heart myosin (both are coiled-coil alpha helices).

This molecular mimicry may lead to cross-reactive antibodies attacking heart valve tissue, causing autoimmune damage.

47
Q

What is Pulse Field Gel Electrophoresis (PFGE) and how is it used in epidemiological categorization of pathogens?

A

PFGE is a gold-standard technique for DNA fingerprinting in epidemiology.

Process: DNA is extracted from the pathogen strain, digested with restriction enzymes, and then electrophoresed with an alternating current to separate large DNA fragments.

Outcome: The resulting banding pattern allows for comparison with known strains to trace outbreaks back to a single or multiple sources, aiding in epidemiological investigations.

48
Q

What are Koch’s Postulates, and how do they determine if a bacteria causes a specific disease?

A
  1. The bacterium must be present in every case of the disease and absent from healthy animals.
  2. It must be isolated from the diseased host and grown in pure culture.
  3. The disease must be reproduced when the pure culture is introduced to a healthy, susceptible host.
  4. The bacterium must be recoverable from the experimentally infected host, identical to the original.
49
Q

What are some limitations of Koch’s Postulates in establishing causation for certain diseases?

A

Koch’s Postulates may not apply if:
1. The microorganism cannot be grown in pure culture (e.g., Mycobacterium leprae, which causes leprosy).
2. There is no suitable animal model for the infection (e.g., leprosy has no effective animal model).

50
Q

What are Koch’s Molecular Postulates for identifying the gene responsible for a virulence determinant?

A
  1. The gene should be present in strains of bacteria that cause the disease.
  2. The gene should not be present in avirulent strains.
  3. Disrupting the gene should reduce virulence, while complementation (restoring the gene) should restore virulence.
  4. Introduction of the cloned gene into an avirulent strain should confer virulence.
  5. The gene should be expressed in vivo (within the host).
  6. A specific immune response to the gene product should provide protection.
51
Q

What is HtrA

A

Protease involved in folding and maturation of
secreted proteins.

52
Q

What does it mean when HtrA does not restore virulence in a mouse model, even after reinsertion?

A

In this study, disrupting HtrA in the bacterium eliminated its ability to cause disease in mice. Even when HtrA was reinserted, virulence was still not restored. This suggests that either HtrA is not solely responsible for virulence, or other factors or genes are also essential for disease.

53
Q

Why does reinserting htrA not restore virulence in the mouse model?

A

The htrA gene is located near dnaA and dnaN, which are crucial for DNA replication. Any genetic insertion in this area disrupts bacterial viability, a phenomenon known as the “polar effect.” This effect impacts nearby essential genes rather than htrA itself, explaining why virulence isn’t restored after reinsertion.

54
Q

Why does a precise deletion of htrA not affect virulence?

A

When htrA is precisely deleted using a double-crossover recombination event, the virulence in the mouse model remains unaffected. This suggests that the loss of htrA alone does not impair the virulence of the organism, indicating that htrA is not essential for the pathogen’s virulence in this context.

55
Q

What is the role of fibronectin in Group A streptococcal colonization?

A

Fibronectin binds to human cell surfaces via the α5β1 integrin receptor, facilitating bacterial adhesion to host tissues.

56
Q

Name some fibronectin binding proteins identified on the surface of Streptococcus pyogenes.

A

SfbI, SfbII (serum opacity factor), PrtF2, PFBP, FbaA, FbaB, Fbp54, and GAPDH.

57
Q

What did gene knock-out studies reveal about fibronectin binding proteins in S. pyogenes?

A

They are “essential” for colonization in some strains but absent in others, indicating variability in colonization strategies.

58
Q

Why are there so many Fibronectin Binding Proteins?

A

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.

Micr2000 (7 decks)

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