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Bacteria Flashcards

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Biology 101 flashcards
1
Q

Mycoplasma spp.

A
  • no cell wall (therefore not treatable with penicillin)
  • sterols in plasma membrane
  • smaller than average bacteria (0.15-0.3 um diameter, size of poxvirus)
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2
Q

Spp. lacking cell wall (2)

A
  1. Mycoplasma

2. Ureaplasma

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3
Q

Spp. with flexible cell wall (3)

A
  1. Borrelia
  2. Leptospira
  3. Treponema

“BLT”

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4
Q

Spp. with rigid, filamentous cell wall (3)

A
  1. Actinomyces
  2. Myobacterium
  3. Nocardia
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5
Q

Obligate intracellular pathogens with rigid, simple, cell wall (5)

A
  1. Rickettsiaceae family
  2. Anaplasmataceae family (Ehrlichia/Anaplasma/Neorickettsia/Wolbachia)
  3. Coxiella genus
  4. Chlamydiaceae family (Chlamydia/Chlamydophila)
  5. Mycobacterium leprae
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6
Q

Gram +, cocci spp. (3)

A
  1. Staphylococcus
  2. Streptococcus
  3. Enterococcus
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7
Q

Gram +, rods spp. (6)

A
  1. Bacillus
  2. Clostridium
  3. Corynebacterium
  4. Lactobacilli
  5. Listeria
  6. Propionibacterium
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8
Q

Gram -, cocci spp. (2)

A
  1. Moraxella

2. Neisseria

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9
Q

Gram -, non-enteric rods spp. (8)

A
  1. Bartonella
  2. Bordetella
  3. Brucella
  4. Burkholderia
  5. Francisella
  6. Haemophilus
  7. Legionella
  8. Pseudomonas
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10
Q

Gram -, enteric rods spp. (10)

A
  1. Campylobacter
  2. Enterobacter
  3. Helicobacter
  4. Escherichia
  5. Salmonella
  6. Shigella
  7. Vibrio
  8. Klebsiella
  9. Proteus
  10. Yersinia
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11
Q

Streptococcus pneumoniae

A
  • diplococci arrangement
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12
Q

Streptococcus pyogenes

A
  • gram +
  • streptococcal pharyngitis
  • streptococci arrangement
  • use of an afrimbrial adhesin (lipoteichoic acid)
  • substratum: buccal epithelial cells
  • evades complement/phagocytosis by secreting extraceullular protease (C5a peptidase) -> degrades C5a (inhibits neutrophil chemotaxis)
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13
Q

Staphylococcus spp.

A
  • staphylococcus arrangement
  • highly invasive bacteria
  • evade macrophages and leukocytes -> Panton-Valentine leukocidin (i.e. in meticillin-resistant staph aureus)
  • leukocidins: kill neutrophils and macrophages (alter phospholipid metabolism by ADP-ribosylaiton of a protein controlling phosphatidylinositol -> disruption of cellular activities)
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14
Q

Sarcina spp.

A
  • tetrad arrangement
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15
Q

Coccobacillus

A
  • “cop out” term

- short, fat rods

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16
Q

Pleomorphic

A
  • name for young/old cells, not sure what characteristic shape they have
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17
Q

Acid fast staining spp.

A
  1. Mycobacterium spp.

2. Nocardia spp.

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18
Q

Ziehl-Neelsen Stain

A
  • type of acid fast staining
  • hot method
  • hot basic carbolfuchsin (red stain) -> decolourize (acid-alkali) -> counterstain (methylene blue or malachite green)

acid-fast bacteria: red/pink
non acid-fast bacteria: blue/green

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19
Q

Kinyoun Stain

A
  • type of acid fast staining

- cold method; same as Ziehl-Neelsen, but doesn’t require heating

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20
Q

Fluorochrome Stain

A
  • type of acid fast staining
  • auramine-rhodamine
    fluorescent dyes-> decolourize-> counterstain (potassium permanganate, an oxidizing agent)

stained organisms appear yellow/green against black background

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21
Q

Bacillus anthracis

A
  • anthrax
  • exception: produces polypeptide capsule, not a glycocalyx
  • haematogenous dissemination - disseminate to a different site within the host via blood (in plasma)
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22
Q

Zoonotic pathogens (4)

A
  1. Rickettsiaceae family
  2. Anaplasmataceae family
  3. Coxiella genus (C. burnetti)
  4. Chlamydophila genus (C. psittaci, C. pneumoniae)
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23
Q

Treponema pallidum

A
  • syphillis
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24
Q

Francisella

A
  • tularemia (rabbit fever)
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25
Q

Intracellular facultative bacteria (12)

A 
Brucella spp. 
Bordetella pertussis 
Campylobacter spp. 
(Some) E. coli 
Group B Streptococcus 
Leigonella spp. 
Listeria monocytogenes 
Neisseria gonorrhoeae 
(meningitides) 
Salmonella spp. 
Shigella spp. 
Yersinia spp.
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26
Q

Extracellular bacteria (14)

A 
Bacillus spp. 
Borrelia spp. 
Clostridium spp. 
Corynebacterium diphtheriae 
(Most) E. coli
Group A Streptococcus 
Haemophilus spp. 
Klebsiella spp. 
Helicobacter spp. 
Proteus spp. 
Pseudomonas spp. 
Staphylococcus spp. 
Treponema spp.
Vibrio cholerae
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27
Q

Streptococcus mutans

A
  • tissue tropism/specificity for enaml - causes dental plaque
  • catalase -
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28
Q

Streptococcus salivarius

A
  • tissue tropism/specificity for tongue epithelial cells

- catalase -

29
Q

Helicobacter pylori

A
  • tissue tropism/specificity for gastric mucosa
  • use of an afrimbrial adhesin (LPS or LOS)
  • substratum: gastric epithelial cells
30
Q

Campylobacter spp.

A
  • tissue tropism/specificity for intestinal mucosa
31
Q

Neisseria gonorrhoeae

A
  • tissue tropism/specificity for urethral epithelium

Neisseria spp.

  • have specific surface receptors to “grab” the host’s iron
  • also act as chelators to keep the iron sequestered in the microbe
32
Q

Bordetella pertussis

A
  • tissue tropism/specificity for upper respiratory tract epithelium
  • use of an afrimbrial adhesin (filamentous haemagglutinin, FHA)
  • substratum: epithelial cells of upper respiratory tract
  • **Can give FHA in a vaccine; if given prior to exposure, FHA will bind to receptor sites in the resp tract - actual bacteria cannot attach
33
Q

Staphylococcus aureus

A
  • tissue tropism/specificity for nasal membranes
  • use of an afrimbrial adhesin (lipoteichoic acid)
  • substratum: epithelial cells

Evasion of destruction by phagocyte - replicates and lives in phagocytic cells
- catalase + ; inactivates oxygen radicals and enables bacteria to survive inside phagolysosome

-class I (membrane acting/ superantigen) exotoxin; TSST-1 -> system-wide shock

34
Q

Escherichia coli/ Enterotoxigenic Escherichia coli (ETEC)

A
  • use of an adhesin/ligand: Type I pili (CFA)
  • receptor: GM1 ganglioside (intestinal epithlium)
  • secrete siderophores (low mw compounds that have a high affinity for iron - form a siderophore-iron complex)

Enterotoxigenic E. coli

  • class III (intracellular) exotoxin; LT/ST Enterotoxin - Excessive watery diarrhoea
  • exotoxin structure: A5B - two genes encode A&B subunits; noncovalently associated in stable complex
35
Q

Salmonella typhimurium

A
  • use of an afrimbrial adhesin (LPS or LOS)
  • substratum: macrophages
  • invasion strategy: injected into host cell via membrane ruffling
  • post-invasion, spreads from epithelium to immediate underlying tissue. No further dissemination
36
Q

Candida albicans

A
  • use of an afrimbrial adhesin (mannans)

- substratum: epithelial mucosa

37
Q

Listeria monocytogenes

A
  • facultative intracellular pathogen

invasion strategy: injected into host cell via membrane ruffling
- internalin A on surface of bacterial cell binds to glycoprotein receptors on the host cell surface (i.e. epithelial cadherin, E-cadherin) -> mediates the attachment of Listeria to, and invasion of, hepatocytes, epithelial, and endothelial cells

Evasion of destruction by phagocyte - replicates and lives in phagocytic cells

  • escapes phagolysosome via the action of class II (membrane damaging) exotoxin - Listeriolysin O (aka channel forming toxins - CFTs)
  • forms pores in the phagolysosome
  • also forms pores in cytoplasmic membrane - cytoplasmic contents leak out -> water enters cell (moves down concentration gradient) -> cell lysis
  • haematogenous dissemination; disseminates to a different site within the host via mononuclear cells in the blood
38
Q

Shigella spp.

A
  • post-invasion, restricted at site of entry

infectious dose for shigella dysenteriae: 10 bacteria

39
Q

Hyaluronidase

A
  • dissemination enzyme (facilitate direct dissemination - In surface fluids, by flow of intestinal contents)
  • breaks down hyaluronic acid of connective tissue
40
Q

Streptokinase

A
  • dissemination enzyme (facilitate direct dissemination - In surface fluids, by flow of intestinal contents)
  • breaks down fibrin clots (converts plasminogen -> plasmin)
41
Q

Collaginase

A
  • dissemination enzyme (facilitate direct dissemination - In surface fluids, by flow of intestinal contents)
  • breaks down collagen
42
Q

Mechanisms used by bacteria to evade complement (4)

A
  1. Capsules
  2. Complement-binding proteins
  3. Proteases
  4. Host cell mimicry
43
Q

Mechanisms used by bacteria to evade phagocytic killing (3)

A
  1. Capsules
  2. Type III Secretion systems
  3. Intracellular parasitism
44
Q

Mechanisms used by bacteria to evade antigen processing (1)

A
  1. Interfere with MHC function and antigen processing
45
Q

Mechanisms used by bacteria to evade antibodies (2)

A
  1. Ig-binding/inactivating proteins

2. Antigenic variation

46
Q

Capsule-possessing bacteria/fungi (17)

***evasion of complement

A 
Staphylococcus aureus
Streptococcus pneumoniae 
Streptococcus pyogenes (group A)
Streptococcus agalactiae (group B)
Bacillus anthracis 
Bacillus subtilis 
Neisseria gonorrhoeae 
Neisseria meningitidis 
Haemophilus influenzae 
Escherichia coli
Klebsiella pneumoniae 
Salmonella spp. 
Yersinia pestis 
Campylobacter fetus 
Pseudomonas aeruginosa 
Bacteroides fragilis 
Cryptococcus neoformans (yeast)
47
Q

Chemical composition of capsule

A

***Varies from species to species - allows for serotyping, which is used to generate vaccines

components:

  • polysaccharide
  • polyribose ribitol phosphate
  • hyaluronic acid; “host cell mimicry” - not seen as foreign by host macrophages -> bacteria avoids phagocytosis/opsonization
48
Q

Pseudomonas aeruginosa

A
  • gram -

- evades complement/phagocytosis by secreting extraceullular protease (elastase) -> inactivates C3b, C5a

49
Q

Histoplasma capsulatum

A

Evasion of destruction by phagocyte - replicates and lives in phagocytic cells
- production of surface components that protects the bacterial cell within the phagolysosome

50
Q

Legionella pneumophila

A

Evasion of destruction by phagocyte - replicates and lives in phagocytic cells
- inhibits phagosome-lysosome fusion

51
Q

Biofilm

A
  • collection of microorganisms that are attached to a surface, covered by a microbially-produced exopolymeric substance (EPS) aka the slime layer
  • bacteria growing as biofilms can be significantly more resistant to antimicrobial agents (w/o considering the effects of other resistance mechanisms)
  • can have multiple species living in a single biofilm
52
Q

Klebsiella pneumoniae

A
  • secretes siderophores (low mw compounds that have a high affinity for iron - form a siderophore-iron complex)
53
Q

Biofilm-associated diseases: device-related infections (9)

A
  1. Ventricular derivations
  2. Contact lenses
  3. Endotracheal tubes
  4. Vascular central catheters
  5. Prosthetic cardiac valves, pacemakers and vascular grafts
  6. Peripheral vascular catheters
  7. Tissue fillers, breast implants
  8. Urinary catheters
  9. Orthopedic implants and prosthetic joints
54
Q

Biofilm-associated diseases: tissue infections (10)

A
  1. Chronic otitis media, chronic sinusitis
  2. Chronic tonsilitis, dental plaque, chronic laryngitis
  3. Endocarditis
  4. Lung infection in cystic fibrosis
  5. Kidney stones
  6. Biliary tract infections
  7. Urinary tract infections
  8. Vaginosis
  9. Osteomyelitis
  10. Chronic wounds
55
Q

Gram - bacteria

A
  • inflict damage upon host via TOXIC STRUCTURES (LPS, endotoxin)
  • activates almost every immune mechanism, as well as the clotting pathway, which together make LPS one of the most powerful immune stimuli known
56
Q

Exotoxins

A
  • protein toxins
  • secreted into extracellular environment from live cells
  • effects on the body are specific to the cell type; usually doesn’t cause fever
  • highly potent (small amounts -> toxicity)
  • can be used to make a toxoid
  • gram + and gram - bacteria
57
Q

Endotoxins

A
  • lipopolysaccharide toxins (of cell wall); released via cell lysis
  • only act as toxins under certain circumstances
  • systemic effects, fever, inflammation
  • high doses -> toxicity
  • can’t be used to make a toxoid
  • LPS of gram - bacteria
58
Q

Toxoid

A
  • a bacterial toxin (usually an exotoxin) whose toxicity has been inactivated or suppressed either by chemical (formalin, formaldehyde) or heat treatment
  • immunogenicity is maintained (still antigenic); when used during vaccination, an immune response is mounted and immunological memory is formed against the molecular markers of the toxoid without resulting in toxin-induced illness

-currently: diphtheria toxoid (part of DTaP vaccine), tetanus toxoid

59
Q

Vibrio cholerae

A
  • exotoxin; Cholera toxin - excessive watery diarrhoea
  • toxin structure: A5B - two genes encode A&B subunits; noncovalently associated in stable complex
  • mechanism of action: ADP-ribosylator (toxin removes ADP-ribose group from NAD and transfers it to host cell protein, thereby inactivating it)
  • infectious dose:
    oral: 10^8 bacteria
    oral + bicarbonate: 10^4 bacteria
60
Q

Clostridium botulinum

A
  • exotoxin; Botulism toxin - flaccid muscle paralysis (prevents neurosecretory Ach vesicles from docking/fusing with the nerve synapse plasma membrane of gangliosides, and prevents release of Ach)

Mechanism of action: Zinc metalloendoprotease - two linked fragments, which are proteolytically cleaved

  1. light chain (LC) - enzymatically active, zinc metalloprotease
  2. Heavy chain - binding and translocation
61
Q

Clostridium tetani

A
  • exotoxin; Tetanus Toxin - rigid/spastic muscle paralysis
  • tetanus toxin blocks the release of inhibitory neurotransmitters glycine and gamma-Aminobutyric acid (GABA) at the presynaptic membrane of motor neurons

Mechanism of action: Zinc metalloendoprotease - two linked fragments, which are proteolytically cleaved

  1. light chain (LC) - enzymatically active, zinc metalloprotease
  2. Heavy chain - binding and translocation
  • The rough surface of rusty metal merely provides a prime habitat for C. tetani endospores to reside in, and the nail affords a means to puncture skin and deliver endospores deep within the body at the site of the wound.
62
Q

Clostridium perfringens

A
  • class II (membrane damaging) exotoxin; Lecithinase (alpha toxin/phospholipase C) - type of cytotoxin
  • membrane disruption -> indiscriminate lysis in various target cells
63
Q

Corynebacterium diphtheriae

A
  • class III (intracellular) exotoxin; diptheria toxin - pseudomembrane, systemic effects
  • toxin structure: AB - single gene encodes for single peptide; post-translationally modified to A&B fragments which are covalently linked
  • mechanism of action: ADP-ribosylator (toxin removes ADP-ribose group from NAD and transfers it to host cell protein (elongation factor 2, EF2) thereby inactivating it and halting protein synthesis)
64
Q

Streptococci spp.

A
  • class I (membrane acting/ superantigen) exotoxin; streptococcal pyrogenic exotoxin (SPE) -> rheumatic fever
65
Q

Haemophilus influenzae

A
  • dissemination to a different site within the host via CSF (cross blood-CSF junction via the choroid plexus)
66
Q

Yersinia pestis

A
  • dissemination to a different site within the host via lymphatics/ immune system cells (from tissue fluids -> lymphatic capillaries)
67
Q

Transmission

A

Number of microorganisms shed and the period of time shed for

  • microbial survival/stability in an environment is influenced by:

A) Microbial factors (sensitivity to UV light, ability to resist drying)

B) Extrinsic factors (humidity, temperature, exposure to disinfectants)

68
Q

Infectious dose

A

Via oral route of infection, the number of organisms required for infection to occur

69
Q

Mycobacterium tuberculosis

A

infectious dose: 1-10 bacteria

Microbiology (5 decks)

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