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Bacteriology > Bacterial Toxins and Anaerobes > Flashcards

Bacterial Toxins and Anaerobes Flashcards

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1
Q

4 properties of a successful pathogen

A
  1. Gain access into host: correct portal of entry
  2. Colonize host tissue: Attachment to specific host tissue
  3. Resist host-defense mechanism: Non-specific (TLR and cytokines and macrophage) or specific (Aquired T and B cell mediated)
  4. Damage host: Pathogens
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2
Q

two mechanisms of pathogenicity

A
  1. Invasiveness: ability to enter host (and replicate in it)

2. Toxigenicity (ability to produce a toxin)

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3
Q

Where is anaerobic bacteria usually located

A

hundred of species of anaerobes on mucosal surfaces

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4
Q

How many anaerobic species are important in human pathogens

A

only a few

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5
Q

Describe the composition of infection by anaerobes

A

mixed, opportunistic infections. Include either/both aerobic or anaerobic bacteria

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6
Q

Describe how anaerobes are sensitive to O2 intermediates

A
  • they have little superoxide dismutase to remove O2 radicals
  • they have low amounts of catalase to remove H2O2
  • they often lack cytochromes so usually metabolize via fermentation
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7
Q

Site of infections for anaerobic gram negative pathogens

A

colon ( intra-abdominal abscess) mouth and skin

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8
Q

infections by anaerobic gram negative pathogens are often foul smelling-why?

A

due to short chain fatty acids produced during fermentations

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9
Q

anaerobic gram negative pathogens do fermentation metabolism and therefore are often

A

gas producing

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10
Q

Describe the Poly-microbial nature of the anaerobic infection

A

infections often due to the contamination of tissue by

normal flora

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11
Q

How do you isolate isolate anaerobic pathogens

A

culture techniques

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12
Q

anaerobic gram negative pathogens are often void of pathogens

A

aerobic bacteria (anoxic environment)

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13
Q

Common gram negativ anaerobic pathogen

A

Bacteriodes fragilis

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14
Q

Most intra-abdominal infections are due to

A

Bacteriodes fragilis

-common inhbaitant of bowel

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15
Q

Virulence factor for Bacteriodes fragilis

A

-polysaccharide capsule (anti-phagocytic)
-Bacteroides are aerotolerant anaerobes able to tolerate
atmospheric concentrations of oxygen.
-Bacteroides encode two major oxidative stress
response genes, catalase and superoxide dismutase.

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16
Q

•B. fragilis often isolated in mixed bacterial infection with;

A
  • other anaerobes

- with facultative anaerobes (often Peptostreptococcus (gram positive anaerobic cocci) in intra-abdominal abscess

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17
Q

Describe the structure of Bacteriodes fragilis

A

pleomorphic often bacilli

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18
Q

What should you grow bacteria in if you want to see if it is Bacteriodes fragilis

A

bile salts ans gentamicin

most aerobic and anaerobic bacteria are inhibited by bile salts and gentamicinexcept for Bacteriodes fragilis.

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19
Q

While Bacteriodes fragilis are the most intra-abdominal infections, the types of pathogens isolated in other surgical sites differ:

A
  • sites of infection are pathogen-specific

- mixed infections are common

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20
Q

Surgical site infections in cardiac surgery patients

A

gram-positive organisms 48%

gram negative organisms 40%

fungi 12%

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21
Q

Clostridia

A

Anaerobic gram positive, spore forming bacili

obligate anaerobes or aerotolerant

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22
Q

Pathogenesis of clostridia

A

-due invasiveness or an exotoxin

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23
Q

Physiology of clostridia

A

either saccharolytic – sugars
or
proteolytic – amino acid

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24
Q

Where doe sclostridia live

A

soil inhabitant or inhabitant of intestinal tract

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25
Invasive clostridia
histotoxic: C. perfringens produces alpha toxin (pholpholipase) causes tissue damage
26
Toxin producing clostridia: gastrointestinal disease:
C. difficile (Toxin A and Toxin B)
27
Toxin producing clostridia: tetanus:
C. tetani, (tetanus toxin)
28
Toxin producing clostridia : botulism, food poisoning:
C. bolulinum, botulinum toxin
29
Histotoxic clostridia
-invasive and cause extensive destruction of muscle and connective tissue -characterized by the formation of gas. -Invasive C. perfringens (alpha toxin):-cause most clostridial-mediated myonecrosis -pathology: A deep wound to muscle predisposes infection -gas gangrene
30
Steps of infection by C. perfringens (alpha toxin)
- reduction of tissue redox potential leading to host cell death. It turns pyruvate into lactate which decreases the pH - host proteases release the nutrient from the host tissues and the clostridia grow - C. perfringens releases an alpha toxin which is a phospholipase and cases tissue damage
31
C. perfringens toxin
alpha toxin. It is a phospholipase and causes tissue damage
32
What does a C. perfringens infection cause adn how do you treat it
gas gangrene- treatment is antibiotic and often excision with amputation
33
4 types of bacterial infection
1. surface acting toxin 2. pore forming toxin 3. A/B toxin (extreme potency) 4. Type II and IV toxin (injects it toxin and produces 100os of molecules to inject into host and paralyze neutrophils) (Mortal Combat)
34
Each bacterial toxin has what two components
catalytic component and a host cell binding component
35
Catalytic component of bacterial toxin
modifies specific host macromolecules (post-translational modification)
36
Host cell binding component
may be tissue specific (clostridial neurotoxin) or not tissue specific ( diptheria toxin)
37
Diphtheria toxin and Pseudomonas aeruginosa exotoxin A
ADP-ribosylate EF2(elongation factor 2 of the host) : inhibits proteins synthesis
38
Botulinum toxin & Tetanus toxin:
Protease for SNARE proteins: inhibits neurotransmittor vesicle fusion to the cell membrane
39
Large Clostridium difficile toxins:
Glucosylate Rho proteins: inhibits cell motility and | ultrastructure, via active modification
40
Shiga toxin:
- a little unusual bc although it is a protein toxin its targets RNA - Deadenylates a adenine on RNA: inhibits protein synthesis
41
How do we vaccinate for bacteria that produce toxins
lot of times we use an inactive component of their toxin called a toxoid
42
DT/ TT vaccine
formalin inactivated diphtheria/tetanus toxins
43
Conjugate vaccines
Hib polysaccharide conjugated to diphtheria toxoid, making a T cell-dependent immune response (IgM IgG and memory)
44
Antibiotic-associated diarrhea (gastrointestinal colitis) Causative agent: and what toxins does it produce
C. difficile A and B toxins because AB CD Antibiotic therapies may be associated with C. difficile infections where the normal floral are reduced allowing endogenous and ingested C. difficile to expand and produce Toxin A and Toxin B, which contribute to diarrhea and inflammation. C. difficile infection range from asymptomatic to recurrent and life- threatening
45
Pathology of clostridium difficile
C. difficle produces Toxin A and Toxin B which glucosylate Rho GTPases elicit: actin depolymerizationdisrupt gut epithelial cells diarrhea UDP-glucose + Rho  Rho-glucose (inactive) + UDP
46
Whats going on in Canada . with C. difficile
Emergence of a highly toxic strain of C. difficile that is resistant to fluoroquinolones has caused outbreaks in the US and Canada.
47
What produces the most toxic protein for humans
Clostridia
48
C. botulinum symptoms | is there a vaccine
- flaccid paralysis | - no vaccine
49
C. tetani symptoms is there a vaccine
- spastic paralysis (lock jaw) | - licensed vaccine
50
WHy is it difficult to produce a vaccine for Botulinum toxin
there are seven serotypes A,B,C,D,E,F,G defined by antiser neutralization an effective vaccine would have to protect against all seven serotypes and that would be hard to do
51
Mechanism of Action of Clostridium neutotoxins
- proteases - BoNT and TeNT have the same mechanism of action (cleave SNARE proteins) - cleaves SNARE proteins to inhibit synaptic vesicle function - they have the exact same catalytic activity and even cleave at the same site but they have different physiologies bc the SNARE toxin does not define the spasticity of each toxin
52
If the cleavage of the SNARE protein is not responsible for the pathologies what is
- intracellular trafficking - BoNT remains in the periphery (synaptic vesicles) - TeNT (retrograde traffice to CNS)
53
BoNT pathology is caused by
peripheral action at the motor neuron, yielding an inhibition of acetyl choline release at the neuromuscular junction (flaccid paralysis)
54
Tetanus toxin pathology is caused by
retrograde trafficking to inhibitory interneuron, stimulates acetyl choline release at the neuromuscular junction (spastic paralysis)
55
tetanus, C. tetani physiology
• Anaerobe • Proteolytic (peptides & amino acids) • Tetanus toxin responsible for the clinical symptoms of tetanus
56
Determinants of Pathogenicity for C tetani
C. tetani is not invasive, remains at site of infection, | but produces tetanus toxin
57
Intoxication | of C. tetani
– Following injury with a mixed bacterial infection – soil bacteria ferment to reduce redox potential – allows limited growth of C. tetani, sufficient for toxin production
58
How do we prevent tetanus infection
immunization | the preventative vaccine is made from tetanus toxin that was treated with formalin to be tetanus toxoid
59
Preventative vaccine
There is a vaccine to prevent tetanus, diptheria, and pertussis DTaP, Tdap, DT, Td
60
At what age is the DTaP vaccine given and why
5 doses given at 2, 4, 6, and 15-18 months and 4-6 years. It is given at 2 months bc that is when you lose protection from maternal antibodies
61
Therapeutic vaccine
treatment in a suspected case of tetanus
62
Botulism is caused by
Clostridium botulinum
63
Botulism: Clostridium botulinum Pathogenicity
– Botulinum toxin: AB toxin – Zinc Protease (heat labile) – inhibits neurotransmitter release: flaccid paralysis
64
Seven BoNT serotypes (A, B, C, D, E, F, and G)
– Each serotype is defined by the absence of cross neutralization by serotype specific antisera *• For example, anti-BT/A antisera neutralizes only BT/A BoNT serotypes A, B, E, and F most common natural forms for humans -so there is no licensed vaccine bc there are so many serotypes
65
Why is BoNT a potent human therapy for neurological diseases
-depending on the serotype it can last for up to 5 months!!! - not contagious - not trasnmitted from person to person - neuronal specificity
66
BoNTs are clinically useful due to neuron specificity...explain
- Bind receptors on neurons - cleave neuronal SNARE substrates - therefore limited off targets...super specific!!
67
Most common use of BoNT for therapy
for bleopharospasm-absnormal contraction or twitch of eyelid neurons (functional blindness) - BoNT cleaves the SNARE proteins in the spastic nerves relieving spasticity - BoNT has a long half life in nerons (months long therapy per injection0

Bacteriology (15 decks)

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