17: Fusobacterium, Neisseria, Veillonella, & Aggregatibacter Flashcards

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1
Q

Neisseria gonorrhoeae
-gram +/-
-shape
-Identification of agar

A

-gram -
-diplococci
-all (+) catalase, glucose, oxidase

transmitted via sexual transmission and birth canal

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2
Q

Neisseria gonorrhoeae
virulence factors

A

-Pilli (fimbriae)
-Immunglobulin A (IgA) proteases
-B-lactamase
-tracheal cytotoxin damages the fallopian tube, leading to scarring and sterility

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3
Q

Neisseria gonorrhoeae pathogenesis

A

Once it infects mucosal surfaces, N. gonorrhoeae can cause:
-Urethritis
-Cervicitis
-Ophthalmia neonatorum
-tracheal cytotoxin this cytotoxin damages the fallopian tube, leading to scarring and sterility
Although the name suggests an effect on the trachea, TCT also affects other mucosal surfaces, including the fallopian tubes in women.

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4
Q

Neisseria meningitidis
-gram +/-
-shape
-surface antigens
-niche
-Lab identification

A

-gram -
-diplococci
-surface antigens= A,B,C,Y and W135 types
-throat and nasopharynx
-all (+) Oxidase, catalase, glucose, maltose

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5
Q

Neisseria meningitidis virulence factors

A

-pilli
-capsule
-porins porA and porB
-iron sequestration
-LOS endotoxin
-immunoglobulin A1 protease
-intracellular growth/surviving phagocytosis

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6
Q

What triggers the systemic inflammatory response in meningococcal septicemia?

A

The release of bacterial endotoxins, particularly lipooligosaccharides (LOS), leads to a cytokine storm and widespread inflammation.

disseminated intravascular coagulation, necrosis and infarction of organs, hemorrhage into internal organs, hypocalcemia and post-recovery bone abnormalities

potential dental defects
-discoloration
-defective enamel
-premature loss of teeth
-malocclusion/crowding
-ectopic eruption
-fail to erupt

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7
Q

Fusobacterium nucleatum
-where is it found
-gram +/-
-shape
-w/ or w/o O2

A

found in the healthy gingival crevice and periodontal pockets
gram -
cigar-shaped bacilli
-anaerobes

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8
Q

Adhesion A (FadA)

A

FadA is a significant virulence factor in Fusobacterium nucleatum that facilitates adhesion to host cells.

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9
Q

Necrotizing ulcerative gingivitis caused by

A

Necrotizing ulcerative gingivitis (NUG) is a severe form of gum disease caused by
-F.nucleatum
-Prevotella intermediate
-oral spirochetes

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10
Q

Necrotizing ulcerative gingivitis clinical manifestation

A

It is a type of necrotizing periodontal disease caused by F.nucleatum

characterized by
-painful, inflamed (swollen and red), and ulcerated gingival tissues **Punched out” crater-like depressions at the tip of the inter-dental papilla
-grayish pseudomembrane covering depressions
-metallic taste, thick saliva

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11
Q

Veillonella
-gram +/-
-shape
-w/or w/o O2
-late/early colonizer
-production
-found in

A

Gram -
Cocci
Anaerobic
Early colonizer
Lactic acid - acetic acid and propionic
-found in dental plaque

These bacteria are known for their ability to metabolize lactate, which is produced by other bacteria, especially during carbohydrate fermentation. By consuming lactate, Veillonella can reduce the acidity in the oral environment, potentially lowering the risk of dental caries (tooth decay).

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12
Q

Aggregatibacter actinomycetemcomitans
-gram +/-
-w/ or w/o O2
-early or late colonizer
-found in
-plays a significant role in

A

Gram -
Anaerobic
Late
Found in human subgingival sites
plays a significant role in periodontal diseases, particularly aggressive periodontitis.

It is part of the HACEK group of bacteria, which are often associated with endocarditis but are most notable for their involvement in oral and systemic infections

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13
Q

Virulence factors for Aggregatibacter actinomycetemcomitans

A

Virulence factors: contribute to its pathogenicity
leukotoxins
Cytolethal distending toxin (CDT)
Epitheliotoxin bone resorption
lipopolysaccharides (LPS)
Fimbriae (adhesion)

CDT is unique because it causes host cells to distend (swell) and eventually undergo cell cycle arrest, followed by apoptosis (programmed cell death).

Epitheliotoxin-induced bone resorption refers to a process where bacterial toxins target epithelial cells, leading to inflammation and the subsequent breakdown of bone tissue. This process is particularly relevant in periodontal diseases, where toxins produced by pathogenic bacteria in the oral cavity not only damage the soft tissues (gums) but also contribute to the destruction of the underlying bone

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14
Q

Which bacteria is known to cause localized aggressive periodontitis in adolescents and destructive periodontal disease in adults?

A

Aggregatibacter actinomycetemcomitans

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15
Q

Which serotype of Aggregatibacter actinomycetemcomitans is more common in aggressive periodontitis?

A

Serotype B

More aggressive than serotype A-E

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16
Q

Which bacteria is an opportunistic pathogen having an inflammatory mechanism leading to bone loss in periodontitis

A

Aggregatibacter actinomycetemcomitans

17
Q

Which bacteria contains Leukotoxins as a virulence factor?

A

Aggregatibacter actinomycetemcomitans

Leukotoxin: A toxin that forms large pores that can destroy human immune cells particularly neutrophils. This impairs the host’s immune response and helps the bacteria evade immune defense.

18
Q

What type of secretion system is produced by leukotoxin and what is its role?

A

The type 1 secretion system (T1SS) is the mechanism by which leukotoxin, produced by Aggregatibacter actinomycetemcomitans, is transported out of the bacterial cell into the surrounding environment or directly into host cells (to the outer membrane of the bacteria)

19
Q

Which bacteria contains Cytolethal distending toxin as a virulence factor?

A

Aggregatibacter Actinomycetemcomitans

CDT is unique because it causes host cells to distend (swell) and eventually undergo cell cycle arrest of T cells,macrophages, Hepatitis-2 cells and epithelial cells, followed by apoptosis (programmed cell death) of T cells, non-proliferating and proliferating macrophages

20
Q

Which bacteria contains Cytolethal distending toxin as a virulence factor?

A

Aggregatibacter Actinomycetemcomitans

CDT is unique because it causes host cells to distend (swell) and eventually undergo cell cycle arrest of T cells,macrophages, Hepatitis-2 cells and epithelial cells, followed by apoptosis (programmed cell death) of T cells, non-proliferating and proliferating macrophages

21
Q

How many subunits does Cytolethal distending toxin have? And what are their roles?

A

CDT is a tripartite toxin composed of three subunits:

CdtA: The binding subunit, which helps attach the toxin to the host cell surface.
CdtB: The enzymatic subunit, which acts as a DNase (deoxyribonuclease). It is the active component that enters the host cell and damages DNA.
CdtC: Another binding subunit that helps facilitate the entry of the toxin into host cells.

22
Q

What type of cells are arrested by Cytolethal distending toxin?? And which are the cells that after being arrested will the Cytolethal distending toxin induce apoptosis?

A

Arrest the cell cycle of T cell, macrophages, Hep-2 cells, and many epithelial cells

Induce apoptosis in T cells, and macrophages (proliferating and non-proliferating)

23
Q

Chaperonin 60 is found in what bacteria and what is its role?

A

Aggregatibacter actinomycetemcomitans
Is considered a potent bone-degrading molecule because it acts as an osteoclasts ‘growth factor”

24
Q

Biofilm formation is mediated by what? and is associated with what bacteria?

A

Poly-N-acetylglucosamine is a surface polysaccharide that mediates biofilm formation, intracellular adhesion, and detergent resistance.

Aggregatibacter actinomycetemcomitans: associated with periodontal disease

25
Q

What mediates aggregation and colonization to the gingival crevice epithelium by Aggregatibacter actinomycetemcomitans?

A

Surface antigens like vesicles
These vesicles may contain Poly-N-acetylglucosamine

26
Q

What types of collagen does poly-N-acetylglucosamine bind to

A

binds to collagen types I, II, III, and V, but not type IV.

27
Q

What extracellular matrix protein does poly-N-acetylglucosamine bind to?

A

binds to fibronectin but not to fibrinogen.

28
Q

OMP34

A

outer membrane protein 34
and an immunomodulatory virulence factor of Aggregatibacter actinomycetemcomitans.

helping the bacterium evade the host immune response.

29
Q

Which virulence factor of A. Actinomycetemcomitans acts as an immunomodulatory?

A

OMP34

30
Q

Which virulence factor of A. Actinomycetemcomitans acts as an immunomodulatory?

A

OMP34

helping the bacterium evade the host immune response.

31
Q

What type of protein is Omp34 similar to in Escherichia coli?

A

Omp34 is similar to OmpA, which also serves as an Fc binding protein

32
Q

What is the significance of Omp34’s ability to bind the Fc region of antibodies?

A

This binding hinders antibody-mediated immune responses, preventing effective opsonization and clearance of the bacteria.

33
Q

What is the significance of Omp34’s ability to bind the Fc region of antibodies?

A

This binding hinders antibody-mediated immune responses, preventing effective opsonization and clearance of the bacteria.

34
Q

How does Omp34 interact with the IL-10 receptor?

A

Omp34 binds to the IL-10 receptor, interfering with IL-10 signaling and promoting a more favorable environment for bacterial survival. Interfering with chemotaxis = preventing immune cells from reaching the site of infection and facilitating bacterial colonization.

35
Q

Extra oral infections caused by actinomycetemcomitans

A

Brain meninges
Septicemia
UTI
Osteomyelitis
Endocarditis and abscesses