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Bacteria Flashcards

1
Q

What distinguishes prokaryotes from eukaryotes?

A
  • no true nucleus/ nuclear membrane
  • single chromosome
  • no membrane bound organelles
  • most membranes lack sterols
  • undergo binary fission, not mitosis
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2
Q

Describe bacterial chromosome.

A
  • hypercoiled in cell w/ no histones
  • usually only one, haploid
  • during replication, enzymes nick and unwind it: gyrase topisomerases
    • good target for antibiotics
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3
Q

Describe plasmids.

A
  • replicate along with host chromosome
  • transmitted between bacteria during conjugation
  • often carry genes that encode resistance to antiobiotics
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4
Q

Describe the prokaryotic ribosome.

A
  • different subunits than in eukaryotic ribosomes
    • 16s rRNA can be targeted by antibiotics
  • trascription & translation occur in unison in cytoplasm
    • translation can actually regulate transcription
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5
Q

Describe the cytoplasm (Inner) Membrane.

A
  • lipid bilayer, but lacks sterols
  • harbors machinery for
    • electron transport system
    • motility
    • ion transport
    • metabolite uptake and release
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6
Q

Describe the bacterial cell wall. How can it be targeted by antibiotics? What are the different shapes?

A
  • Comprised of peptidoglycan (Murein)
    • produced by almost all bacteria
    • repeating disaccharide of n-acetyl muamic acid and n-acetyl glucosamine
      • MurNac and GluNac
      • assembly of disaccharides = transglycosidation
      • cross-linking between opposing MurNac and GluNac via pentapeptides= transpeptidation
        • ilnks between 3rd and 4th AAs
  • Steps in synthesis can provide targets for antibiotics
    • cephalosporins, vancomycin (transglycosidation), bacitracin, penicillin (transpeptidation), MurNac-GluNac (lysozyme)
  • Shapes
    • spherical (cocci)
    • rod (bacillus)
    • spiral
    • no cell wall
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7
Q

What’s the difference in cell envelopes between Gram + and Gram - bacteria?

A
  • Gram +
    • peptidoglycan layer thicker
  • Gram -
    • lipopolysaccharide (LPS) outer membrane layer on top of peptidoglycan
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8
Q

What does LPS/endotoxin do?

A
  • binds TLR 4 on many immune cells
  • triggers the release of inflammatory cytokines
  • results in fever, hypotension, and potentially shock and death (“Septic Shock”)
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9
Q

How do Gram + and Gram - stain?

A
  • Gram + : stain purple (stain crystal violet)
  • Gram - : stain pink (counter stain safranin)
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10
Q

Describe capsules.

A
  • loose carbohydrate or protein layers on outermost surface
  • found on some but not all bacteria
  • offer protection
    • physical barrier
    • inhibit phagocytosis (disrupt complement)
    • evade immune cells thru molecular mimicry to host glycans
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11
Q

Describe spores.

A
  • spores occur under harsh environmental conditions– form of division where spores lie dormant until conditions are more favorable
  • only gram +
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12
Q

Desribe bacterial biofilms.

A
  • structured communnity of bacterial cells enclosed in a self-produced polymeric matrix and ahdere to an inert
  • protected mode of growth that allows survival in hostile environment
    • resistant to host defenses & antibiotics
    • ex. dental plaque
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13
Q

Describe bacterial flagella.

A
  • locomotory organelle
  • can be virulence property- swim towards food, away from poison
  • can be serodeterminants (H-serotype scheme)
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14
Q

Describe bacterial pili.

A
  • hairlike structures on cell surface
  • thinner than flagella
  • important for adhesion and communication during conjugation (sex pili)
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15
Q

At what temperatures do pathogenic bacteria grow?

A
  • 30-42 degreed Celcius
  • higher temp range: pyrogenic (fever causing) bacteria
  • lower temp range: cutaneous bacteria
  • exception: listeria monocytogenes- replciates in refridgerated food!
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16
Q

At what level of moisture do pathogenic bacteria grow?

A
  • require aqueous enivornment
  • some bacteria tolerant of drying (Gram +, survive as fomites)
  • sporeformers are designed for survival outside aqueous environment
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17
Q

What are the aerotolerances of pathogens?

A
  • obligate aerobes
    • require O2 for growth
    • do not ferment substrates
    • use aerobic respiration & oxidative pathways
  • obligate anaerobes
    • O2 is toxic
    • use fermentiative metabloism
    • ex. clostridium botulinum
  • Facultative anaerobes
    • grow in presence of absence of O2
    • use aerobic respiration and fermentation
    • grow faster aerobically tan anaerobically
    • ex. E. Coli
  • Microaerophilic aerobes
    • need O2 but too much can kill
    • use aerobic respiration, not fermentation
  • Aerotolerant anaerobes
    • tolerate small about of O2
    • use fermentation
18
Q

Why is odygen toxic to bacteria?

A
  • singlet oxygen, superoxide free radicals, peroxide anions, and hydroxyl radicals are toxic to bacteria
  • bacteria that can handle oxygen have enzymes to deal with these:
    • superoxide dismutase (SOD)
    • catalase or peroxidase
19
Q

What are Capnophilic organisms?

A
  • Bacteria that need CO2
  • ex. TB, Strep, Gonorrhea
20
Q

What nutrients do bacteria need?

A
  • carbon
  • nitrogen
  • essential amino acids, vitamins
  • others: sulfur, phosphorus, trace elements, iron (body sequesters iron away from bacteria vai hemoglobin, transferrin, lactoferrin)
21
Q

In what ways can bacteria carry out metabolism?

A
  1. Glycolysis
    • Glucose(6Cs) –> Pyruvate (3Cs)
    • occurs aerobically or anaerobically
    • 2 moles of ATP, 2 moles NADH
  2. Fermentation
    • Pyruvate –> short chain FAs, alcohols, and CO
    • occurs anaerobically
  3. Aerobic Pyruvate-Citric Acid Cycle
    • 1 ATP, 3 NADH, 1 FADH2
    • TCA cycle
    • occurs in inner membrane
  4. Anaerobic respiration
    • similar electron transport cascade
    • more efficient than fermentation, less efficient than aerobic respiration
22
Q

How do bacteria replicate?

A

binary fission: usually grow slower in vivo than in vitro

23
Q

Describe a bacterial growth curve.

A

Phases: lag, log, stationary, decline

24
Q

How do we quantitate bacterial growth?

A
  1. culture and count resulting colonies
    • viability counts
  2. measure turbidity of broth culture over time
    • optical density of broth
25
1) What are targets for bacterial killing? 2) What determines effectiveness of microbial killing?
1. targets 1. membrane disruption 2. protein denaturation 3. DNA replication disruption 4. Oxidation 2. exposure to agent (time) + number of organisms + agent efficacy
26
Define sterilization. Methods?
* use of physical or chemical means to destroy all microbial forms (vegtative cells AND spores) * ex. autoclaving (heat) ethylene oxide gas (no heat) ionizing radiation (used for commerical products)
27
Define disinfection.
* use of physical or chemical means to destroy most bacterial cells and spores on surfaces and objects * not for use in sterile regions, such as inner body cavites (surgical sites)
28
Define antisepsis.
* use of chemical agents on skin or other tissues to remove or inhibit bacterial agents
29
Define pasteurization.
* heat treatment between 62-74 degrees Celcius * duration from seconds to minutes * kills vegetative bacterial cells w/o altering nature of food
30
With what bacteria do you see infections w/ dramatic purulent exudate?
pyogenic bacteria (staphylococci, streptococci, *Neisseriae*)
31
What is the major immune cell involved in bacterial infections?
neutrophils
32
Why is C3b important in bacterial clearance?
* opsonizes bacteria for uptake via alternative pathway * important if there is no pre-existing antibody formed for that pathogen * CRITICAL for clearance of Gram+ organisms; can also be used against Gram- organisms
33
How do neutrophils kill bacteria?
* Neutrophils kill by three different defenses * **uptake via complement or antibody opsonins** * opsonization- bacteria are coated by serum opsonins (IgM, IgG or C3b) * **induction of respiratory burst** and degranulation of PMN granules * oxygen dependent: superoxide anion which forms H2O2 with FE3+ oxidation, FE3+ will then form OH and HOCL * oxygen independent: granules contain lysozyme M, lactoferrin and serine proteases * **entrapment** of microbe within **NETs** (neutrophil extracellular traps)
34
How can a bacteria evade the innate immune response?
1. **capsule production**: inhibits deposition of C3b 2. **anti-phagocytic proteins**: reduce C3b opsonization by binding soluble negative regulators of the alternative pathway (Factor H) 3. **neutralize ROS** made by neutrophils in O2-dependent killing (superoxide, HO, HOCl): catalase, peroxidase, superoxide dismutase 4. **evade antimicrobial peptides**: negatively-charged bacterial capsules & LPS bind positively charged antimicrobial peptides and neutralize them 5. **efflux pumps**: trap antibiotics and antimicrobial peptides and expel them from bacterium 6. **evade** **neutrophil extracellular traps** (**NETs**): neutrophil creates a "net" of DNA, ROS, and antimicrobial peptides that can trap bacteria; bacteria evade by detoxifying ROS, neutralizing antimicrobial peptides, and cutting thru DNA with **DNAases **
35
What are the ways antibodies can defend against microbes?
* Agglutination * Blocking the function of bacterial factors * Opsonization * Activation of the classical pathway (MAC)
36
How does the classical pathway of complement activation defends against bacterial infections?
* initiated by antibody bound to target * requires C5-9 components, results in MAC * CRITICAL for gram- clearance, not effective for gram+ * important later in infection unless there is pre-existing antibody that recognizes the pathogen
37
What causes septic shock with gram- bacteria?
* Lipid A endotoxin of LPS on gram- bacteria stimulates macrophages * If overwhelmed with LPS * Lipid A binds TLR 4 * systemic release of TNF-alpha, increased vascular permeability * systemic edema, DIC, organ failure
38
What are the two types of gram- sepsis?
1. continuous septicemia * ​in patients with intravascular infection * blood cultures are positive 2. intermittent septicemia * in patients with infections at distal site * blood cultures are often not positive when collected during times of fever (infection has already started to be cleared by immune system by the time we get fever)
39
What causes septic shock with gram+ bacteria?
* host response to **peptidoglycan fragments** and **teichoic acids** (in gram+ cell wall) * binds to **TLR2**
40
What are bacterial defenses against complement-mediated bacteriolysis?
* molecular mimicry * antigenic variation of target surface structures during infection (thwarts capacity of specific antibodies to fix complement) * surface molecules that bind C4b-binding protein

Microbiology & Immunology (7 decks)

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