Bacteria Lectures Flashcards

1
Q

phase variation

A

Control of transcription by DNA rearrangement
eg: reversible switching in the synthesis of two alternative flagellar antigens alternation between several antigenic forms of pili expressed on the cell

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2
Q

transposon

A

discrete segment of DNA which is capable of moving itself (or a copy of itself) from one chromosomal location to a new location within the cell

may transpose and become stabley and permanently integrated into the bacterial chromosome.

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3
Q

Insertion Sequences

A

(IS elements) are transposons that simply
encode transposase. Play a role in genome evolution by inactivating genes into which they transpose, or turning on expression of adjacent genes.

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4
Q

Complex transposons

A

carry additional genes such as those encoding

antibiotic resistance, toxins, adhesins and other virulence factors.

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5
Q

F plasmid

A

prototype self-transmissible plasmid

Autonomous replication of the plasmid DNA

ii. Synthesis of sex pili (F pili) which are essential for mediating pair formation between donor and recipient cells
iii. Conjugative transfer of F DNA to recipient (F-) cells
iv. Ability to integrate into the bacterial chromosome

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6
Q

Conjugative transposons

A

mobile elements which mediate conjugation

between pairs of cells, in which the transferred DNA is the conjugative transposon itself

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7
Q

Lipopolysaccharides (LPS) of gram negative bacteria

A

LPS is an example of a pathogen-associated molecular pattern (PAMP) that is recognized by the innate immune system and elicits host responses by a pathway

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8
Q

Toxins that stimulate cytokine production

A
superantigens are the most potent known T 
cell activators. They act by binding both to major histocompatibility (MHC) class II molecules on antigen-presenting cells and to specific Vβ chains on T cells at a site that is different from the antigen-binding site,
and they activate much larger numbers of T cells than any specific antigen does. Superantigens stimulate excessive production of cytokines (including interleukin-2, interferon gamma, and others), thereby causing pathologic effects.
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9
Q

Shiga toxins of Shigella dysenteriae and E. coli, and the plant toxin ricin

A

inhibit protein synthesis

inactivating the ribosomes

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10
Q

Diphtheria toxin and Pseudomonas aeruginosa exotoxin A

A

inhibit protein synthesis

inactivate elongation factor 2 (EF-2)

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11
Q

Toxins that modify intracellular signaling pathways.

A

Pertussis toxin
Heat-labile enterotoxins of Vibrio cholerae and Escherichia
Anthrax
coli

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12
Q

Toxins that inhibit release of neurotransmitters

A

Botulinum toxin

Tetanus toxin

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13
Q

Toxins with intracellular targets must cross the plasma membrane before they can exert their toxic effects.

A

They typically use normal membrane constituents as receptors.
usually enter target cells by endocytosis

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14
Q

β-lactam resistance

A

β-lactam antibiotics act by irreversibly binding to and inactivating the transpeptidase reaction of penicillin-binding proteins, thereby inhibiting peptide cross-linking and peptidoglycan synthesis

β-lactamases are enzymes that inactivate β-lactam antibiotics by splitting the amide bond of the β-lactam ring, and thereby protect the activity of penicillin binding proteins.

ESBLs (extended spectrum beta-lactamases): can even attack up to 3rd gen cephalosporins

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15
Q

ampC-encoded β-lactamase

A

Enterobacter, Pseudomonas,
not inhibited by betalactamase inhibitors
The mutational events that lead to permanent high-level expression of ampC can occur during therapy!

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16
Q

Carbapenemases

A

Klebsiella pneumoniae

hydrolyzes all carbapenems and all other β-lactams

17
Q

Altered penicillin-binding proteins (PBPs)

A

When present in S. aureus, it is classified as “methicillin-resistant” S. aureus, otherwise known as MRSA.

Mosaic PBPs : Seen mainly in Streptococcus pneumoniae and Neisseria gonorrhoeae.

18
Q

Vancomycin resistance

A

vancomycin prohibits incorporation of the precursor molecule into the pedtidoglycan. This disrupts cell
wall synthesis and leads to cell death.

Vancomycin-resistant enterococci (VRE) - modify target

Staphylococcus: reduced susceptibility to vancomycin

a) Cell walls contain markedly thickened layers of peptidoglycan
b) There is LESS cross-linking of the peptides. This leaves free amino acid chains in the cell wall that still contain the D-alanine – D-alanine terminus, where vancomycin can bind.

19
Q

Quinolone resistance

A

target the essential bacterial enzymes DNA gyrase and DNA topoisomerase IV: DNA replication

Quinolone resistance occurs due to one or more nucleotide mutations that result in amino
acid substitutions in a region of GyrA of DNA gyrase, or ParC of topoisomerase IV called the
quinolone-resistance-determining region (QRDR)

reducing the affinity of the enzyme-DNA complex for the quinolone

20
Q

Resistance to Macrolides

A

prevents peptide chain elongation.

Modifying the target: Methylation of the ribosome

D test: Isolates harboring either efflux-mediated resistance or inducible ribosomal methylation will
test the same: resistant to macrolides and sensitive to clindamycin
Either the bacterium has an inducible erm methylase system or a macrolide efflux pump system. In
the first case, one would be wary of using clindamycin, because if a mutation occurs in the bacterial
population while treating with clindamycin, that would cause constitutive expression of erm and
resistance to clindamycin. In the second scenario with the efflux pump, clindamycin use should be ok,
as efflux will only act on the macrolide.

If the bacteria in question possesses the inducible erm system, erythromycin will induce resistance to clindamycin and the zone of clearing for clindamycin will be blunted, forming a D-shape of colony growth.

Bottom line is that for organisms harboring erm that
test sensitive to clindamycin, you shouldn’t use EITHER macrolides or clindamycin. If the organism
harbors an efflux pump to macrolides, you shouldn’t use macrolides, but clindamycin is fine.

21
Q

Select the antibacterial agent that rapidly accumulates in bladder and urine

A

Nitrofurantoin (Macrobid)

22
Q

bone

A

Clindamycin

23
Q

pulmonary cells

A

Macrolides

24
Q

into gingival crevicular fluid and sebum (periodontitis and acne)

A

Tetracyclines

25
Q

bind cells of the inner ear and renal brush border  ototoxicity and nephrotoxicity

A

Aminoglycosides

26
Q

bind Ca++ in developing bone and teeth  abnormal bone growth and tooth discoloration

A

Tetracyclines

27
Q

causes colitis and pseudomembranes

A

Clindamycin (Cleocin)

Toxigenic Clostridium difficile selected out during treatment (superinfection, 0.1-10%)