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Y1 - Microbio Exam 2 > 17_Anaerobes 1&2 > Flashcards

17_Anaerobes 1&2 Flashcards

1
Q

aerobes:

define; and part of glycolysis cycle

A
  • can use O2 as terminal electron acceptor; generates more ATP than through glycolysis alone
    • (Respiration: TCA cycle)
  • TCA cycle - CO2 –> PMF –> ATP (respiration)
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2
Q

anaerobes:

define; key piece in the cycle

A
  • do NOT use O2 as terminal electron acceptor
    • fermentation (and/or anaerobic respiration)
    • fail to grow in 10% by definition
  • NO O2; anaerobic respiration
    • reduced pyruvate endproducts (FERMENTATION)
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3
Q

define:

  1. strict (obligate) anaerobes
  2. aerotolerant anaerobes
  3. facultative anaerobes
A
  1. strict (obligate) anaerobes: KILLED by O2
  2. aerotolerant anaerobes: can withstand O2
  3. facultative anaerobes: can grow with or without O2
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4
Q

define the following:

  1. microaerophilic bacteria
  2. obligate aerobes
  3. facultative aerobes
A
  1. microaerophilic bacteria: prefer reduced O2 for growth
  2. obligate aerobes: must have O2
  3. facultative aerobes: uses O2 when available, otherwise fermentation or anaerobic respiration
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5
Q

key difference between anaerobes and aerobes?

A

aerobes: uses O2 as terminal electron acceptor

anaerobes: do NOT use O2 as terminal electron acceptor; fermentation (and/or anaerobic respiration); fail to grow in 10% O2

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6
Q

Overview of where opportunistic anaerobes are found in normal flora?

A
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7
Q

anaerobic infections from non-spore formers

  1. key characteristic
  2. predisposing factors
A
  1. key characteristic: non-spore formers are frequently polymicrobial (aerobes consume oxygen and create a niche for the anaerobes)
  2. predisposing factors:
    • trauma
    • ischemia:
      • diabetes and peripheral vascular disease
      • decubitus ulcers (bedsore/ pressure ulcer)
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8
Q

polymicrobial infections:

  1. common locations & manifestation
  2. etiological agent
  3. abscess may contain…
A
  1. common locations: intestine, mouth, urogenital, skin
    • frequent manifestation is abscess
  2. Possibly more than one etiological agent; mixed infections are also termed polymicrobial infections
  3. Abscess may have:
    • Bacteriodes (gram negative rod)
    • + Fusobacterium (gram negative rod)
    • + Peptostreptococcus (gram positive cocci)
    • + facultative organisms such as E. coli or E. faecalis
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9
Q

what is the most common microbe in anaerobic infections?

A

Bacteroides group;

caused by endogenous organisms, particularly below the diaphragm

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10
Q

Bacteroides fragilis:

  1. characteristics
  2. location
  3. incidence
A
  1. gram negative rod with capsule
  2. dommensal of human intestine;
  3. found in 70% of bacteroides infections
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11
Q

Bacteroides

key virulence factors

A
  • *Capsule: it is anti-phagocytic
    • unlike other bacterial capsules, it has active pathogenic properties
    • stimulates T-cells and seems to contribute to induction of abscesses
  • enzymes including:
    • hyaluronidase, collagenase, heparinase, fibrinolysin
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12
Q

how are bacteroides treated?

A
  1. debridement and drainage of purulent material +
  2. antibiotics: may have to use 2 or more for infection to resolve if it is a polymicrobic infection
    • metronidazole
    • carbapenems
    • chloramphenicol
    • beta-lactam plus beta-lactamase inhibitor
    • clindamycin
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13
Q

name the 4 spore-forming pathogenic anaerobes

and which diseases they cause

A
  • Clostridium tetani: –> tetanus (lock-jaw)
  • Clostridium botulinum: –> botulism; infant botulism; wound botulism
  • Clostridium perfringens: –> gas gangrene; food poisoning
  • Clostridium difficile: –> antibiotic-assoc. diarrhea; pseudomembranous colitis
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14
Q

key characteristics of spores

A
  • Resistant to heat and disinfectants
    • can survive boiling or UV radiation–> must be autoclaved
    • can survive chloroform and ethanol
    • only slowly killed by bleach
  • persists for years
  • spores germinate to produce vegetative cells that are sensitive to heat and disinfectants
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15
Q

steps in spore formation

A
  1. cel division - axial filament formation
  2. septum formation and forespore development
  3. engulfment of forespore
  4. cortex formation
  5. coat synthesis
  6. complementation of coat synthesis, increase in refractility and heat resistance
  7. lysis of sporangium, spore liberation
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16
Q

clostridium tetani: characteristics

  1. structure
  2. found where?
  3. how enter body?
  4. incubation?
A
  1. gram positive rod; strict anaerobe
  2. spores are found in soil, esp if rich in manure
    • also found in GI tract and feces of animals& humans
  3. enters body through wound contaminated with soil;
    • rusty nail is prototypic;
    • puncture wound predisposes to anaerobiasis
  4. incubation period is 8 days or longer
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17
Q

most common source of C. tetani is a rusty nail.

what are other causes?

A
  • umbilical cord infxn from nonsterile dressings or soil contamination in developing countries
  • abortion: using nonsterile instruments
  • black tar heroin: subcutaneous injection of contaminated heroin
18
Q

characteristic symptoms of C. tetani?

A
  • trismus (lock-jaw): due to masseter muscles in jaw being unable to relax
  • risus sardonicus: grim smile
  • contractions of the back muscles (Opisthotonus)
19
Q

Tetanus toxin:

  1. production
  2. structure
  3. encoded on
A
  1. *Toxin is produced during spore germination and released by cell lysis
  2. structure is single 150kDa protein w/ disulfide bridge w/ an active and binding (A and B) parts of the molecule, linked by disulfide bridge
  3. Encoded on a plasmid
20
Q

*Tetanus toxin:

mechanism of action

A
  • Tetanus toxin is a neurotoxin; also called tetanospasmin or tetanus nerotoxin
  • Toxin is endocytosed into neuron in an endosome, travels by retrograde axonal transport to the brain; organisms stay localized at the site of the wound
  • Disulfide bond is reduced, and the A fragment acquires zinc endopeptidase activity –> degrades protein synaptobrevin, (a SNARE protein) needed for release of inhibitory neurotransmitters (glycine adn gaba) from pre-synaptic vesicles
21
Q

effect of Tetanus toxin on presynaptic vesicles?

A

tetanus and botulinum neurotoxins cleave the v-SNARE and/or the t-SNARE –>

preventing the docking and fusion of neurotransmitter-containing vesicles

22
Q

Tetanus vaccine:

  1. hx
  2. composition
  3. administered at which ages
A
  1. 1924: First production of tetanus toxoid.
  2. Tetanus toxoid (T) is dilute formaldehyde treated tetanus toxin which undergoes a conformational change that inactivates the binding capacity of the toxin, but preserves enough of the 3D conformation of the molecule so that antibodies raised to the toxoid bind to the toxin.
  3. Given to infants at 2, 4, 6 and 18 months, and a booster at
    4-6 years.
    • Usually given in a single injection with diphtheria toxoid (D) and acellular pertussis (aP)=DTaP.
    • Booster at 11-12 years and then every 10 years.
23
Q

Wound treatment to Prevent Tetanus

A

treatment:

  • In previously unvaccinated person with a wound
    likely to be infected with C. tetani, give tetanus antitoxin = Tetanus Immune Globulin (TIG).    TIG is a pool of human antibodies in volunteers immunized with the toxoid. In the past antibodies raised in horses were used.Horse serum can cause serum sickness.
  • If person previously had the complete vaccination schedule then only a booster of tetanus toxoid is needed.
24
Q

Regarding the tetanus vaccination;

why can you wait and give booster after exposure to the organism?

A
  • Because it takes time for the spores to germinate. Toxin is only produced by spore germination
    • The memory response is quicker than the primary immune response, so once a person has had a full series of shots, boosting after exposure will raise sufficient antibodies before toxin is produced
25
Q

If a patient has not completed the adsorbed tetanus toxoid doses,

what would you provide w/ a clean minor wound?

what about all other wounds?

A
  • clean wound: just Tdap if they completed series previously
  • all other wounds: both TIG and Tdap
26
Q

Clostridium botulinum:

  1. structure
  2. location
  3. disease
  4. inactivation
A
  1. structure:
    • gram positive, spore-forming rod
  2. location
    • found in soil and lake sediments
    • spores germinade in anaerobic conditions, usually in food (e.g. home-canned food, or Vichyssoise- cold soup)
  3. disease
    • an intoxication due to ingestion of the preformed toxin; toxin is absorbed from gut to blood
  4. inactivation
    • toxin is inactivated by boiling for 10 minutes
    • boiling does not kill spores; need pressure cooker or autoclave
27
Q

Food-borne Botulism:

symptoms

A
  • onset 12-36 hrs after ingesting contaminated food
  • Difficulty swallowing, nausea, dry mouth, sometimes diarrhea
  • Bilat blurred vision; pupillary dilation
  • Descending paralysis; drooping eyelids, slurred speech, breathing difficulty, then flaccid paralysis of limbs
28
Q

compare infant botulism (73% of cases in 2016)

and wound botulism (12% of cases in 2016)

(14% were food-borne)

A

Infant (floppy baby syndrome) <1 yr of age;

  • spores injested on weaning or w/ dietary supplement (esp honey)
  • germinates in intestine –> toxin is produced
  • sxs: constipation, flaccid paralysis, muscle weakness, swallowing and resp weakness

Wound

  • wound contaminated by soil; recent assoc. w/ injection of black tar heroin
  • in 2017-2018, 9 cases in San Diego, CA; 1 death
  • Use of Botox for treatment of muscle spasms and for cosmetic effects; toxin can spread –> causing drooping in other areas of face
29
Q

Botulinum Toxin:

  1. antigenic types
  2. binding
  3. actions
A
  1. antigenic types:
    • multiple antigenic types designated A thru G
    • A, B, E, and rarely F cause disease in humans
  2. binds to ganglioside receptors on cholinergic nerves
    • translocates into cytoplasm (via pore formation)
    • has zinc metalloprotease activity to target a neuronal SNARE protein (synaptobrevin)
  3. actions
    1. Blocks acetylcholine release at peripheral synapses
      (NOT CNS like tetanus toxin)
    2. Blocks neurotransmission that would normally excite motor neurons, so muscles become flaccid.
30
Q

how do the effects of tetanus and botulin compare?

similar? different?

A
  • 35% homology between the 2 toxins
  • Tetanus –> unrelieved muscle contraction due to absence of inhibitory neurotransmitters
  • Botulism –> muscle relaxation due to blockage of ACh release –> flaccid muscles
31
Q

botulism:

therapy

A
  • mechanical ventilation
  • human anti-toxin for infant botulism
  • no antibiotics avail, except for wound botulism
32
Q

diseases caused by

Clostridium perfringens

A
  1. gas gangrene
  2. food poisoning
33
Q

Gas gangrene:

  1. cause,
  2. symptoms
A
  1. caused by C. perfringens; can be carried in the GI tract or spores found in soil
    • follows injury involving muscle lacerations
    • rapidly progressing
  2. Sxs: necrosis, edema, pain, hemolysis, foul odor, greenish gray tissue color –> hemolytic anemia, renal failure, or shock
    • Production of CO2 and H2 (gas of gas gangrene)
34
Q

although there are mutliple toxins implicated in gas gangrene, which are the major ones?

A
  • Alpha-toxin: a lethal, hemolytic toxin
    • causes intravascular hemolysis <–by disrupting membranes of erythrocytes, leukocytes, muscle cells, kidney toxicity
      • has phopholipase C/lecithinase activity that hydrolyses lecithin and sphingomyelin
  • Theta-toxin: (perfringolysin O)
    • a pore-forming toxin; alters capillary permeability;
    • toxic to heart muscle
35
Q

How to treat Gas gangrene?

A
  1. tissue debridement
  2. amputation
  3. massive doses of penicillin + Abx that will target facultative Gram-neg organisms that may co-infect wound
  4. hyperbaric oxygen
36
Q

C. perfringens, Type A: food poisoning

  1. source
  2. mechanism
A
  • source: unrefridgerated meat dishes (beef, stew, poultry, gravy)
  • mechanism:
    1. ingest spores –> germinate in small intestine
    2. organism elaborates an enterotoxin (a 35 kDa protein)
    3. diarrhea, cramps, nausea; no fever or vomiting
      • onset 8-24 after ingestion; self-limiting and resolves in 24 hrs
    4. toxin acts in the ileum
    5. breaks tight junctions b/w intestinal epithelial cells by binding claudin proteins that mediate junction formation;
    6. polymerizes into hexamers; can induce pore in epithelial cell
37
Q

Clostridium difficile (C. diff)

  1. other names
  2. structure
  3. infections
A
  1. other names: antibiotic associated diarrhea, & pseudomembranous colitis
  2. structure: gram positive spore-forming bacillus
    • 2-5% of peopel carry it in their GI tract
  3. infections:
    • most are endogenous,
    • exogenous acquisition can occur in antibiotic treated patients in a hospital setting;
    • some infections now appear community acquired
38
Q

C. difficile:

epidemiology/symptoms

A
  • US: ~500,000 cases/year, and 15,000 deaths;
    • *most common cause of healthcare assoc. infections in the US
  • Sxs:
    • Colitis: watery diarrhea, pain, cramping, foul odor
    • Pseudomembrane colitis or fulminant colitis (more serious stages)
39
Q

C. difficile: pathogenesis

A
  1. Two distinct large toxins, Toxin A and Toxin B:
    • Toxin A is 308 kDa and is considered an enterotoxin.
    • Toxin B is 120 kDa and is considered a cytotoxin
    • Both toxins are glucosyltransferases that inactivate the Rho family of GTPases.
  2. Pseudomembrane is composed of inflammatory cells, fibrin and necrotic cells.
40
Q

C. difficile

treatment of disease

A
  • Tx w/ antibiotic (10 day course of vancomycin or fidaxomicin)
  • Fecal microbiota transplants (FMT) containing normal GI flora have been successful in aborting symptoms

Y1 - Microbio Exam 2 (18 decks)

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