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Microbiology & Immunology > Bacteria > Flashcards

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
Q

1) What are targets for bacterial killing? 2) What determines effectiveness of microbial killing?

A
  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
Q

Define sterilization. Methods?

A
  • 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
Q

Define disinfection.

A
  • 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
Q

Define antisepsis.

A
  • use of chemical agents on skin or other tissues to remove or inhibit bacterial agents
29
Q

Define pasteurization.

A
  • heat treatment between 62-74 degrees Celcius
  • duration from seconds to minutes
  • kills vegetative bacterial cells w/o altering nature of food
30
Q

With what bacteria do you see infections w/ dramatic purulent exudate?

A

pyogenic bacteria (staphylococci, streptococci, Neisseriae)

31
Q

What is the major immune cell involved in bacterial infections?

A

neutrophils

32
Q

Why is C3b important in bacterial clearance?

A
  • 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
Q

How do neutrophils kill bacteria?

A
  • 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
Q

How can a bacteria evade the innate immune response?

A
  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
Q

What are the ways antibodies can defend against microbes?

A
  • Agglutination
  • Blocking the function of bacterial factors
  • Opsonization
  • Activation of the classical pathway (MAC)
36
Q

How does the classical pathway of complement activation defends against bacterial infections?

A
  • 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
Q

What causes septic shock with gram- bacteria?

A
  • 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
Q

What are the two types of gram- sepsis?

A
  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
Q

What causes septic shock with gram+ bacteria?

A
  • host response to peptidoglycan fragments and teichoic acids (in gram+ cell wall)
  • binds to TLR2
40
Q

What are bacterial defenses against complement-mediated bacteriolysis?

A
  • 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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