BK - Gut Ecology Flashcards

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1
Q

Where do biofilms cause the most trouble?

A

Biofilms, slimy communities of bacteria, can wreak havoc in various parts of the body:

Primary sites:

  • Mouth: Dental plaque formation leading to cavities and gum disease.
  • Subcutaneous tissues: Infections around catheters and implanted devices.

Secondary sites:

  • Brain: Can cause meningitis.
  • Kidneys: Can lead to urinary tract infections (UTIs).
  • Spine: Can cause infections between vertebrae.
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2
Q

How does dental plaque wreak havoc? (3)

A

Bacteria: Streptococcus mutans and others ferment sugars, producing acids that erode teeth (cavities)

Biofilm structure: Plaque forms a sticky layer, protecting bacteria from the immune system and making removal difficult

Consequences: Cavities, gum inflammation (gingivitis), and gum tissue destruction (periodontitis).

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3
Q

Biofilms and medical devices (2)

A
  • Catheters and implants can provide a surface for bacteria to adhere and form biofilms.
  • Biofilms on these devices can lead to serious infections that are difficult to treat
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4
Q

What other organs can be affected by biofilm infections? (3)

A
  • Heart valves (endocarditis)
  • Urogenital tract (STIs like gonorrhea, syphilis)
  • Bones (osteomyelitis)
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5
Q

What is the oral microbiome and how can it become imbalanced?

A

The oral microbiome is a complex community of bacteria in the mouth. It can shift from a healthy state to a disease-causing one (dysbiosis)

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6
Q

How does the body defend itself from harmful oral bacteria? (3)

A

The body employs various physical and chemical barriers to maintain oral health:

  • Physical: Keratinized epithelium (skin lining), mucin production (lubricating mucus), and salivary flow (washing away debris).
  • Chemical: Enzymes and antibacterials in saliva, and gingival fluid secretions containing immune components
  • Inflammatory reaction
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7
Q

How do babies acquire their oral flora?

A

Acquisition of the Oral Flora (Early)

  • Acquisition of oral flora depends upon exposure at the time of birth, cesarean or vaginal. Shortly thereafter, caregivers provide the next insult of microorganisms

Acquisition of the Oral Flora (Later)

  • After tooth eruption: organisms favouring hard tissue e.g. Strep. sanguis and Strep. mutans, Actinomyces spp.

Colonisation of crevicular tissues: anaerobic organisms e.g. Prevotella spp.

Loss of teeth: “a 2nd childhood microflora”

Prosthetic appliance: e.g. dentures - similar to enamel plaque, may harbor large numbers of yeast

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8
Q

What is dental caries (cavities) and what factors contribute to it?

A

Cavities are holes in teeth caused by acid erosion

  • High sugar intake and poor oral hygiene are major risk factors.
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9
Q

How does gingivitis differ from periodontitis?

A
  • Gingivitis is gum inflammation caused by plaque buildup and poor hygiene
  • Periodontitis is a more advanced stage with bone loss, often linked to specific bacteria
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10
Q

How do Streptococcus mutans bacteria contribute to cavities? (4)

A

Streptococcus mutans possess several virulence factors that promote cavities:

  • Saccharolytic: Break down sugars into acids (acidogenic).
  • Glucosyltransferases: Produce sticky glucans that form plaque biofilm (glucosyltransferase).
  • Fructosyltransferases: Contribute to plaque formation (fructosyltransferase).
  • Acidogenic: Ferment sugars to lactic, acetic, and formic acids, lowering the pH and eroding tooth enamel (aciduric)
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11
Q

What is the role of Veillonella in the oral cavity? (3)

A
  • Gram-negative anaerobic cocci.
  • Thrives in the acidic environment of caries and is thought to slow the development of dental caries.
  • Converts the lactic acid of other species to less acidic products.
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12
Q

How are Lactobacillus bacteria associated with dental caries? (4)

A
  • Gram-positive facultative anaerobes.
  • Normally symbiotic in humans and found in the gut flora.
  • Some species with increased numbers in plaque associated with carious lesions.
  • “Microbial indicator of disease state” (with S. mutans etc)
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13
Q

What role do Fusospirochetes play in oral health?

A

In cases of bleeding gums, Fusospirochetes can contribute to infection and diseases like:

  • Acute necrotizing ulcerative gingivitis (ANUG) - also referred to as “trench mouth”
  • Vincent’s angina.” It’s caused by a combination of anaerobic bacteria including Prevotella intermedia, Fusobacterium, Treponema, and Borrelia spp
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14
Q

What are the three main bacterial culprits in chronic periodontitis?

A

Treponema denticola

  • Gram-negative anaerobic spirochete.
  • Elevated levels are found in patients with periodontitis.
  • Considered the most important of the three due to its motility and highly proteolytic nature, contributing to tissue destruction.

Porphyromonas gingivalis

  • Gram-negative oral anaerobe strongly associated with chronic adult periodontitis. Produces a number of well-characterized virulence factors.

Aggregatibacter actinomycetemcomitans

  • Gram-negative facultative non-motile rod, association with localized aggressive periodontitis in young adolescents and bone loss.
  • Virulence factors: leukotoxin kills PMNs and moncytes; cytolethal distending toxin; immunosuppression factors that inhibit blastogenesis, antibody production and activate T-suppressor cells
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15
Q

What is the order of colonization in plaque formation? (4)

A
  • Salivary Proteins: Provide an initial adhesive layer on the tooth surface.
  • Pioneer Species: Bacteria like Streptococcus mutans attach to the salivary layer, initiating biofilm formation.
  • Secondary Colonizers: Species like Veillonella join the community, creating a more complex structure.
  • Tertiary Colonizers: Further diversify the biofilm with a wider range of bacterial species.
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16
Q

How do bacteria in plaque measure and respond to their population density? (2)

A

Bacteria use a chemical signaling system called quorum sensing to communicate and coordinate biofilm formation:

  • Intra-species: Gram-positive oral bacteria produce small peptides like competence-stimulating peptides to promote biofilm formation within a single species.
  • Inter-species: Mediated by 4, 5-dihydroxy-2, 3-pentanedione (DPD), also called Autoinducer-2 (Al-2). This molecule stimulates plaque formation and virulence factors in various bacterial species.
17
Q

How can Helicobacter pylori cause stomach ulcers?

A

H. pylori neutralizes stomach acid with an enzyme (urease) and creates ulcers by damaging the stomach lining

18
Q

What else does H.pylori do? (2)

A

Toxin production:

  • Produce toxins such as vaculating cytotoxin A (VacA) that kill cells in the lining of the stomach.
  • Allows bacteria to better access of nutrients as it decreases the competition from stomach lining cells. vacA mutants are less inflammatory/colonisers

Cell Invasion:

  • Invade protective inner lining of the stomach so can be protected from immune system.
  • Kill the cells they invade, creating holes in mucus lining of the stomach, causing the formation of ulcers.
19
Q

How does the early gut microbiome differ depending on feeding method? (2)

A

Breastfed Babies: Become dominated by Bifidobacteria, possibly due to the presence of bifidobacterial growth factors in breast milk.
Formula-fed Babies: Have a more diverse flora with high numbers of:

  • Enterobacteriaceae
  • Enterococci
  • Bifidobacteria
  • Clostridia
  • Bacteroides spp
20
Q

What are some of the major bacterial groups found in a mature gut microbiome and their functions?

A

Dominant Bacteria:

  • Bacteroides (around 30% of all gut bacteria, suggesting its importance).
  • Clostridium
  • Fusobacterium
  • Eubacterium
  • Ruminococcus
  • Peptococcus
  • Peptostreptococcus
  • Bifidobacterium

Less Common:

  • Escherichia
  • Lactobacillus
21
Q

What are some of the benefits gut microbiota provides to the host? (6)

A

Fermentation of Unused Energy Substrates: Breaks down complex carbohydrates that the human digestive system cannot process on its own, providing additional nutrients.

Training the Immune System: Helps develop and modulate the immune system, distinguishing between harmless and harmful microbes.

Preventing Growth of Harmful Bacteria: Creates a competitive environment that inhibits

Regulate the development of the gut

Produce vitamins for the host (biotin and vitamin K)

Produce hormones to direct the host to store fats

22
Q

How does gut microflora play a role in early gut development?

A

Microflora is essential for promoting the early development of the gut’s:

  • Physical components: Gut mucosal structure.
  • Immune system function: Both in its physical makeup and how it functions.
23
Q

How does gut flora help the immune system fight pathogens? (2)

A

Microflora stimulates the gut-associated lymphoid tissue (GALT) to produce antibodies against pathogens. This allows the immune system to:

  • Recognize and fight harmful bacteria.
  • Develop a tolerance for helpful bacterial species encountered in infancy.
24
Q

What are PRRs and how do they help the gut differentiate between bacteria? (2)

A

PRRs are located on immune cells in the gut lining and help differentiate between:

  • Beneficial bacteria: Essential for a healthy gut.
  • Pathogenic bacteria: Harmful and cause disease.
25
Q

What are the different types of PRRs in the gut?

A

1) Toll-like Receptors (TLRs):

  • Found in the intestines and play various roles, including:
  • Repairing tissue damage.
  • Activating immune responses.

2) NOD/CARD:

Cytoplasmic proteins that recognize:

  • Internal or microbial molecules.
  • Cellular stress responses.

Function:

  • Form complexes (oligomers) that activate inflammatory caspases.
    These caspases then:
    Cleave and activate key inflammatory cytokines (signaling molecules).
    Activate the NF-κB signaling pathway, leading to inflammatory molecule production.
26
Q

What is PSA and how does it influence gut health?

A

PSA (Polysaccharide A) is a capsular polysaccharide (sugar on the cell surface) from Bacteroides fragilis, a gut bacterium, that’s crucial for gut health. Here’s how:

Structure: Resembles kiwi fruit hairs, creating a mucous-like barrier.

Function:
Stimulates the immune system in a beneficial way.

27
Q

How did researchers demonstrate the importance of PSA?

A

A study with germ-free mice explored PSA’s role:

Mice were colonized with:

  • Whole B. fragilis bacteria (containing PSA).
  • Purified PSA alone.
  • B. fragilis lacking PSA but with other polysaccharides.

Results:

  • Only wild-type B. fragilis or purified PSA restored CD4 T cell levels (important immune cells).
  • Mice with B. fragilis lacking PSA showed no improvement in CD4 T cell levels.
    *
28
Q

How does PSA promote a balanced immune response?

A

PSA helps maintain a healthy balance between two types of immune cells:

Th1 Cells: Secrete cytokines that activate the cellular immune response (fights infections).

Th2 Cells: Secrete cytokines that activate antibody-producing B-cells.

PSA’s Role:

  • Stimulates IL-10 (an anti-inflammatory cytokine).
  • Suppresses IL-17 (a pro-inflammatory cytokine).
  • This helps maintain a balanced immune response and protects the intestines from excessive inflammation.
29
Q

How does gut microflora prevent harmful bacteria from colonizing?

A

Microflora employs a strategy called “competitive exclusion” or the “barrier effect” to prevent harmful species from establishing themselves:

  • Beneficial bacteria compete for resources and space, making it difficult for pathogens to colonize the gut.