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Immuno mikro eng > Bacterial Structure and Metabolism > Flashcards

Bacterial Structure and Metabolism Flashcards

1
Q

What are the three ways by which we classify bacteria?

A
  1. Cell wall: gram + or -
  2. Shape: rod, cocci, or spirilla
  3. Clustering pattern: pairs, tetrads, clusters, chains
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2
Q

What are the gram stain procedures?

A
  1. Air dry and heat fix bacteria to slide
  2. Add crystal violet
  3. Add iodine as mordant to hold CV into gram + cell wall
  4. Add acetone
  5. Add safranin as counterstain
  6. Visualize with 1000x objective
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3
Q

What do acid-fast bacterial contain in their cell walls? How do they stain via gram stain?

A

Long chain fatty acids (mycolic acids)

They stain poorly via gram stain

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4
Q

What do gram negative cell walls contain which gram + cell walls do not?

A

An outer membrane which contains LPS, and the intervening periplasmic space

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5
Q

What is the purpose of peptidoglycan?

A

Give bacterial cell shape and resistance to osmotic changes

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6
Q

What are the sugars of peptidoglycan?

A

Disaccharide linked

  1. N-acetylglucosamine (NAG)
  2. N-acetylmuramic acid (NAM)
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7
Q

How are sugar chains crosslinked in gram positive and gram negative bacteria?

A

Gram positive - pentaglycine linkage between D-alanine and lysine
Gram negative - Direct linkage between D-alanine and DAP (more compressed)

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8
Q

What component of the gram positive cell wall is analogous to LPS in the gram negative cell wall? Why do you say this?

A

Techoic acid / lipotechoic acids
They are associated with inflammatory response to some gram positive infections

Similar to how LPS causes a toxic shock syndrome due to immune inflammatory response in septicemia

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9
Q

What is the purpose of mycolic acid in acid-fast bacteria? What is the other substance present in the cell wall?

A

Resistance to phagocytosis and drying
(reason why mycobacteria form granulomas)

Other substance: lipoarabinomannan

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10
Q

Is there more sugar chains in a gram + peptidoglycan cell wall, or gram negative?

A

Neither, the only difference is the peptide linkages between sugar chains which make gram positive bacteria peptidoglycan much more spread out (thick)

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11
Q

What is LPS comprised of, and what is the bioactive moiety of the compound inducing a massive immune response? What is its function?

A
  1. Lipid A (Fatty acid moiety)
  2. Core sugars
  3. Repeating sugar residues (O antigens)

Lipid A is bioactive part

Functions in Salmonella typhi as a long O-antigen to resist complement-mediated killing (virulence factor)

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12
Q

What is the periplasmic space and what is its clinical significance?

A

Space between inner and outer membranes (including peptidoglycan) found only in gram negative bacteria

It is the place where toxins and antibiotic degradation factors are assembled

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13
Q

Where does generation of energy occur in the prokaryotic cell?

A

ATP synthase can be found on the inner cell membrane of both gram + and gram - bacteria

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14
Q

Where is the capsule located in bacteria, what is it made of, and what is its function?

A

Outside peptidoglycan in gram +, outside outer cell membrane in gram -, composed of high MW polysaccharides or amino acids

Function: protects cell from complement-mediated killing (virulence factor)

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15
Q

What are most pili made of, and what is on their tips? How does the tip often evade immune response?

A

Subunits called pilin. Tipped with adhesins which function to mediate adhesion to host tissues. This can have antigenic variation which helps them evade immune response.

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16
Q

What are two common types of pili?

A
  1. Common: mediate adhesion

2. Sex pilus: join conjugating bacteria

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17
Q

What are two medically significance genuses of spore-forming bacteria?

A
  1. Bacillus (anthracis)

2. Clostridium (tetani, botulinum, dificile)

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18
Q

Which of the three types of secretion is sec-dependent and how does it recognize proteins?

A

Type 2 secretion: recognizes proteins with a signal sequence

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19
Q

What is the only type of secretion which occurs in gram + bacteria? What is its mechanism in gram +

A

Type 2 secretion, sec-dependent, shoots toxin right into the environment since there is no periplasm

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20
Q

What is the mechanism of Type 1 secretion?

Give one example toxin secreted this way

A

No signal sequence on toxin, ABC transporter (ATP-binding cassette) bypasses the periplasm and uses a pore to shoot the toxin directly into the environment

(i.e. E. coli hemolysin / alpha toxin)

21
Q

What is the mechanism of type 2 secretion in gram negative bacteria?

A

Signal sequence brings toxin into periplasm, where it is clipped off and the toxin is assembled. Toxin is then exported through the outer membrane (peptidoglycan is porous)

22
Q

What is Type 3 secretion? What is one bacteria that utilizes this?

A

It is “contact-dependent” - injects proteins directly into eukaryotic cells via ATPase a “syringe-like” structure

Example: Yersinia pestis

23
Q

What other substrates can anaerobic bacteria use other than oxygen?

A

As terminal electron acceptor

Nitrate, fumarate, sulfate

24
Q

What is a falcultative aerobic microbe?

A

Uses O2 for electron transport when present, otherwise grows via fermentation only

25
Q

What is the purpose of catalase?

A

Enzyme which breaks down toxic O2 formed during respiration

26
Q

What is capnophilic vs microaerophilic bacteria?

A

Capnophilic: requires CO2 at level exceeding ambient air (like strictly anaerobic bacteria)
Microaerophilic: Grows best in micro-oxic zones

27
Q

What is the difference of nuclei / ribosomes between prokaryotic / eukaryotic organisms?

A

Nuclei are bounded by nuclei membrane in eukaryotes, prokaryotes have no nuclear membrane

Eukaryotes: 80S ribosome (40+60)
Prokaryotes: 70S ribosome (30+50)

In prokaryotes, mRNA transcription happens right at transcription site
In eukaryotes, mRNA must be moved out of the nucleus before transcription

28
Q

What are filamentous fungi and what are they composed of? What do they spawn from?

A

They are multicellular fungi, composed of hyphae (making up mycelia), and spawn from spores (conidia)

They can exist unicellularly as yeasts in host, but be filamentous in environment

29
Q

What is one important vector for injecting pathogens into humans?

A

Arthropods like tics and mosquitos

30
Q

What two bacterial genuses bind fibronectin at wound sites?

A

Streptococcus and Staphylococcus

31
Q

What is the primary lung defense against bacteria?

A

Cilia -> if this is overcome, as in immunocompromised or smokers, can cause pneumonia

32
Q

What causes antibiotic-associated enterocolitis?

A

Clostridium difficile

33
Q

What is the easiest route of transmission addressed by public health measures?

A

Fecal-oral transmission

34
Q

What is vertical vs horizontal transmission?

A

Vertical - parent->offspring, via ovum, sperm, placenta, blood, milk
Horizontal - person->person (most common)

35
Q

What is ID50?

A

Dose of pathogen required for 50% of population to get infected

i.e. 10 microbes for Shigella, but 10,000,000 Vibrio cholerae for cholera

36
Q

What is important in determining ID50?

A

Route of infection. Depends on receptors and localized defenses

Most effective: aerosol (i.e. measles)

37
Q

What is the most common example of genetics influence host disease susceptibility?

A

Plasmodium -> cannot infect sickle-cell individuals due to hemoglobin alteration

38
Q

What is functional asplenia? What will these individuals be susceptible to?

A

Individuals who have functionally no spleen, as in reduced function due to sickle cell disease.

They are more susceptible to certain bloodborne pathogens, i.e. Haemophilus influenzae

39
Q

How do S. aureus and S. pyogenes prevent complement-mediated killing?

A

Coat themselves with immunoglobulins

S. aureus can also produce catalase to resist phagoctosis

Both release toxins to kill phagocytes

40
Q

How does T. cruzi escape phagocytosis?

A

Leishmania, escapes the phagolysosome and lives in cytoplasm of macrophage

41
Q

How does M. tuberculosis resist phagocytosis?

A

Prevents phagolysosome fusion

42
Q

What process can lead to cyclical persistent infection, especially via parasites?

A

Antigenic switching or variation, which is done by sequential combination.

This will render vaccine attempts useless. As soon as body mounts a productive immune response, the antigen switches.

43
Q

What is the function of a superantigen?

A

Concealment of true antigens, and induction of tolerance / anergy to evade host immune response

44
Q

What is a bacterial exotoxin vs endotoxin?

A

Exotoxin - hydrolytic enzymes that degrade DNA or connective tissue, promoting spread

Endotoxin - Expressed on cell surface (i.e. LPS)

45
Q

What is a cytolysin?

A

Exotoxin which disrupts mammalian cell membrane and causes cell lysis

46
Q

What are the typical structures of cytotoxins?

A

AB subunit structure.

A = enzyme
B = binding casset

Most will transfer an ADP-ribose via cleavage of NAD
Can inhibit protein synthesis (diphtheria), increase cAMP levels (cholera), or disrupt nerve transmission (tetanus or botulism, synaptobrevin cleavage)

47
Q

What are the symptoms of the toxic shock syndrome exerted by LPS, and what induces similar physiologic responses?

A

Hypotension, fever, and disseminated intravascular coagulation (blood clotting / thromboses) mostly mediated via IL-1 / TNFalpha

Staphylococcal / streptococcal superantigens have a similar effect

48
Q

In the damage-response curve, is it worse when the host response is weak or strong?

A

It is equally bad at both extremes
Weak: microbe takes over and causes huge damage
Strong: Immune system is overactive and causes host death (as in toxic shock syndrome).

Immuno mikro eng (56 decks)

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