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AI > Exam 2: Conceptual > Flashcards

Exam 2: Conceptual Flashcards

1
Q

For abx to work it must do the following 4 things

A
  1. enter bacterial cells
  2. reach site of action
  3. bind to target involved in bacterial function
  4. significantly impair function
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2
Q

GP or GN?: Thick peptidoglycan layer

A

Gram positive

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3
Q

GP or GN?: Thin peptidogylacan

A

Gram negative

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4
Q

___ are enzymes in the cell wall that are vital for cell wall synthesis, cell shape, and structural integrity

A

Penicillin binding proteins (PBPs)

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5
Q

___ is the location of beta-lactamases in gram negative bacteria

A

Periplasmic space

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6
Q

Outer membrane of gram negative bacteria contain ___ and ___

A

Lipopolysaccharide (LPS, endotoxin) and porins

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7
Q

The periplasmic space of gram negative bacteria is located between __ and ___

A

Cytoplasmic membrane and outer membrane

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8
Q

GP Aerobic: Cocci: Clusters: Coagulase +

A

Staphylococcus aureus

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9
Q

GP Aerobic: Cocci: Clusters: Coagulase -

A

Other staphylococcus

  • epidermis
  • Hominis
  • Haemolyticus
  • Capitus
  • Saprophyticus
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10
Q

GP Aerobic: Rods

A

Listeria

Nocardia

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11
Q

GP Anaerobic: Cocci

A

Peptostreptococcus

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12
Q

GP Anaerobic: Rods

A

Clostrium spp (Spore forming) – C. diff
Propionibacterium
Actinomyces

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13
Q

GN Aerobic: Cocci

A

Neisseria meningitidis
Neisseria gonorrhoeae
Moraxella catarrhalis

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14
Q

GN Aerobic: Rods: Lactose forming

A

SKEEP

Salmonella spp.
Klebisella pneumoniae 
Escherichia coli
Enterobacter spp.
Proteus mirabilis
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15
Q

GN Aerobic: Rods: Non-lactose forming

A

PAS

Pseudomonas aeruginosa
Acinetobacter baumanni
Stenotrophomonas maltophilia

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16
Q

GN Anaerobic: Rods

A

Bacteroides spp
Prevotella
Fusobacterium

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17
Q

Atypical

A

Chlamydia spp (C. pneumoniae, trachomatis)

Mycoplasma spp (M. pneumoniae, genitalium)

Legionella spp (L. pneumophilia)

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18
Q

Two distinct systems of immunity

A

Innate (nonspecific)

Adaptive (specific)

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19
Q

Systems of immunity: Innate (non-specific)

A

Physical barriers, phagocytes (neutrophils, macrophages), proteins

Strategically predeployed and prepositioned to prevent and/or quickly neutralize infection

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20
Q

Systems of immunity: Adaptive (specific)

A

Evolves and adapts against invading pathogens

Divided into humoral (B lymphocytes) and cellular (T lymphocytes) mediated arms

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21
Q

Systems of immunity: Innate: Exterior defences

A

Skin, mucus, cilia, normal flora, saliva, low pH of stomach, skin, and GU tract

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22
Q

Systems of immunity: Adaptive: Exterior defenses

A

none

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23
Q

Systems of immunity: Innate: Specificity

A

Limited and fixed

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24
Q

Systems of immunity: Innate: Memory

A

None

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25
Q

Systems of immunity: Innate: Time to response

A

Hours

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26
Q

Systems of immunity: Innate: Soluble factors

A

Lysozymes, complement, C-reactive protein, interferons

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27
Q

Systems of immunity: Innate: Cells

A

Neutrophils, monocytes, macrophages, natural killer cells, eosinophils

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28
Q

Systems of immunity: Adaptive: Specificity

A

Extenisve

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29
Q

Systems of immunity: Adaptive: Memory

A

Yes

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30
Q

Systems of immunity: Adaptive: Time to response

A

Days

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31
Q

Systems of immunity: Adaptive: Soluble factors

A

Antibodies, cytokines

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32
Q

Systems of immunity: Adaptive: Cells

A

B lymphocytes

T lymphocytes

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33
Q

Barriers: Skin

A

Physical and immunologic barrier to invasion by microbes

Dryness, salinity, and mild acidity, combined with normal skin flora, help make it an inhospitable environment for invading pathogens

Sebum, a lipid-rich coating that protects and lubricates hair and skin, has antimicrobial properties

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34
Q

Barriers: Mucous Membranes

A

Most pathogens enter through mucosal surfaces of the respiratory, GI, and urogenital tracts

Mucus, formed by highly glycosylated proteins called mucins, which are often specific to the mucosal site, carries immune cells, antimicrobial factors, bacteria, nutrients, and waste

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35
Q

Barriers: Respiratory tract

A

Inhaled microorganisms can cause respiratory disease if they are not eliminated quickly

Trachea, bronchi, and bronchioles are lined with a ciliated epithelial surface that propels mucus upward, leading to the mechanical clearance of any trapped pathogens

This, with the addition of coughing, leads to 90% of deposited material being cleared in less than 1 hour

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36
Q

Barriers: GI Tract

A

Acidic pH of the stomach and the antibacterial effect of the pancreatic enzymes, bile, and intestinal secretions are effective, non-specific, antimicrobial defense factors

GI tract is also coated in mucus that has different properties

Small intestine - mucus limits the number of bacteria that can reach the epithelium and Peyer patches

Large intestine - inner mucus layer relatively free of bacteria, but the outer mucus layer supports a subset of commensal flora

Paneth cells of the small intestine, located in the crypts of Lieberkühn, secrete AMPs such as β-defensins, lysozyme, REGIIIγ, and type II phospholipase A

Most of these AMPs are localized in the mucus layer; thus, in addition to functioning as a physical barrier, mucus limits bacterial penetration by concentrating AMPs near the epithelial surface

Mucus is continuously secreted from goblet cells and Paneth cells and moves distally with peristaltic waves, expelling potential pathogens and requiring bacteria to travel against mucus flow to reach the tissue surface

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37
Q

Barriers: GI Tract: Small intestine

A

Mucus limits the number of bacteria that can reach the epithelium and Peyer patches

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38
Q

Barriers: GI Tract: Large intestine

A

inner mucus layer relatively free of bacteria, but the outer mucus layer supports a subset of commensal flora

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39
Q

Mucus is continuously secreted from __ and ___

A

goblet cells

Paneth cells

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40
Q

Barriers: GU tract

A

Lactobacillus spp. metabolize sugars into lactic acid, lowering the pH of the vagina (restricts growth of invading organisms)

The vaginal flora prevents urogenital diseases, including bacterial vaginosis, yeast infections, UTIs, and HIV

The lower urinary tract is rinsed with urine 4-8 times each day, eliminating potential pathogens– Unless they are capable of firmly attaching to epithelial cells of the urinary tract (e.g., Neisseria gonorrhoeae, certain strains of Escherichia coli )

Urine is bactericidal for some strains of bacteria, mostly because of its pH, although factors such as hypertonicity, urea, and the presence of AMPs play a role

Uromodulin is a glycoprotein produced by the kidneys that protects against kidney stones and binds to E. coli, preventing them from attaching to the cellular lining of the urinary tract

41
Q

Barriers: GU Tract:____ is a glycoprotein produced by the kidneys that protects against kidney stones and binds to E. coli, preventing them from attaching to the cellular lining of the urinary tract

A

Uromodulin

42
Q

Barriers: Eye

A

Constant bathing of the eye by tears is an effective means of protection

Foreign substances are diluted and washed away via the tear ducts into the nasal cavity

43
Q

Cells of Innate Immunity: WBC

A

Major role is defense against invading organisms

Normal range 4500-10,000 cells/mm3

Usually elevated in response to infection

44
Q

Cells of Innate Immunity: Neutrophils

A

70% of WBCs
Enter tissues to phagocytize pathogens
Segs (segmented nucleus) mature neutrophils
Bands (lack segments) immature neutrophils

Left shift (historical term) = bands increased (~5%) during acute infection and shift to the left

45
Q

Cells of innate immunity differential: WBC splits to

A

Granulocytes

Agranulocytes

46
Q

Cells of innate immunity differential: Agranulocytes splits to

A

Lymphocytes

Monocytes

47
Q

Cells of innate immunity differential: Granulocytes splits to

A

Polymorphonuclear granulcytes (PMNs)

48
Q

Cells of innate immunity differential: Polymorphonuclear granulocytes (PMNs) splits to

A

Neutrophils
Basophils
Eosinophils

49
Q

Cellular function of macrophage/monocytes

A

Antigen presenting cell

Surveillance of antigens

50
Q

Cellular function of neutrophils

A

Defense against bacteria and fungus

51
Q

Cellular function of eosinophils

A

Defense against parasites

Response against allergic reactions

52
Q

Cellular function of basophils

A

Allergic response

53
Q

Cellular function of B lymphocyte

A

Antibody production

Antigen presenting cell

54
Q

Cellular function of T lymphocyte

A

Cellular immunity against virus and tumors

Regulation of the immune system

55
Q

Bacterial resistance: Intrinsic

A

some organisms are notorious for intrinsic ability to express multiple types of resistance

Acinetobacter baumanni

Pseuodomonas aeruginosa

56
Q

Bacterial resistance: Acquired

A

some organisms acquire genes, which enable a mechanism of resistance, from another species of bacteria that already had it through transfer of mobile genetic elements

57
Q

Bacterial Resistance : Intrinsic Resistance: Mechanisms

A

Absence of abx target

Bacterial cell impermeability

58
Q

Bacterial resistance: Intrinsic resistance: Examples

A

Vancomycin vs. Gram-negative bacteria
Large molecule – too big to get through porin channel

Cephalosporins vs. enterococci

Beta-lactams vs. mycoplasma
Mycoplasma have no cell wall (no active site)

Aminoglycosides vs. anaerobic bacteria
Actively transported across cytoplasmic membrane into interior of cell
Process is dependent on energy, oxygen, and pH

59
Q

Bacterial resistance: Acquired: Mutation

A

May occur spontaneously in every 106 to 107 bacterial cells

May alter the target site of the antibiotic leading to reduced affinity and decreased activity

60
Q

Bacterial Resistance: Acquired: Genetic exchange

A

Conjugation – direct contact or mating via sex pili (most common)

Transduction – genes are transferred between bacteria by viruses

Transformation – The transfer or uptake of “free floating” DNA from the environment; then DNA is integrated into the host DNA

Plasmids (KNOW THIS)
Self replicating extrachromosomal DNA
Genes encoding for resistance to many antibiotics can exist on one
Conjugative plasmids contain additional genes that can initiate transfer from one bacterium to another

61
Q

Mechanisms of resistance: Streptococcus pneumoniae: Beta-lactams

A

Target site changes PBPs

62
Q

Mechanisms of resistance: Streptococcus pneumoniae: Macrolides

A

Target site changes (methylation of adenine residue in domain V of 23S rRNA)

Efflux (mefE)

63
Q

Mechanisms of resistance: Streptococcus pneumoniae: Fluoroquinolones

A

Target site changes (DNA gyrase (gyrA mutations) and topoisomerase IV (parC mutations)

64
Q

Mechanisms of resistance: Staphylococcus aureus: Penicillin

A

Enzymatic modification (penicillinases)

65
Q

Mechanisms of resistance: Staphylococcus aureus: Methicillin, oxacillin, nafcilin, and cefazolin

A

Target site changes (PBP2a-mecA)

66
Q

Mechanisms of resistance: Staphylococcus aureus: vancomycin (intermediate)

A

Alteration of cell wall precursor targets (thickened cell wall)

67
Q

Mechanisms of resistance: Staphylococcus aureus: Vancomycin (resistant)

A

Alteration of cell wall precursor targets (plasmid-mediated transfer of vanA from VRE)

68
Q

Mechanisms of resistance: Pseudomonas aeruginosa: Beta-lactams

A

Enzymatic modification (AmpC cephalosporinases, extended-spectrum beta-lactamases, etc.)

Active Efflux (MexAB)

Reduced outer membrane permeability (loss of OprD channel)

69
Q

Mechanisms of resistance: Pseudomonas aeruginosa: Aminoglycosides

A

Enzymatic modification (aminoglycoside modifying enzymes)

Efflux (MexXY)

Alteration of ribosomal targets

70
Q

Mechanisms of resistance: Pseudomonas aeruginosa: fluoroquinolones

A

Efflux

Alteration of target enzymes (DNA gyrase mutations)

71
Q

Mechanisms of resistance: Klebsiella pneumoniae: Beta-lactams

A

Enzymatic modification (penicillinases, ESBLs, KPC, NDM-1)

Reduced outer membrane permeability

72
Q

Mechanisms of resistance: Klebsiella pneumoniae: Aminoglycosides

A

Enzymatic modification (aminoglycoside modifying enzymes)

Alteration of ribosomal targets

73
Q

Mechanisms of resistance: Klebsiella pneumoniae: Fluoroquinolones

A

Alteration of target enzymes (DNA gyrase mutations)

Efflux

Protection of target site (plasmid-mediated qnr genes)

74
Q

What do beta-lactamases do

A

Enzymes that hydrolyze beta-lactam ring, inactivating it

75
Q

What are 3 examples of beta-lactamases

A

Extended-spectrum beta-lactamases (ESBLs)

AmpC beta-lactamases

Carbapenemases (ex. KPC)

76
Q

Beta-lactamase inhibitors

A

Beta-lactamase inhibitors structurally similar to beta-lactam antibiotics but generally lack antibacterial activity (exception: sulbactam)

When combined with beta-lactams, they bind beta-lactamases and protect active antibiotic from inactivation

77
Q

Beta-lactamase inhibitors structurally similar to beta-lactam antibiotics but generally lack antibacterial activity (exception:____)

A

sulbactam

78
Q

Term ‘ESBL’ refers to group of beta-lactamases that are able to hydrolyze penicillins and cephalosporins up through the____ generation

A

third

(resistance thru 3rd gen like ceftriaxone)

*Resistance thru ceftriaxone and aztreonam= ESBL

79
Q

Treatment of ESBL

A

Getting more complex

Carbapenems – long-standing drugs of choice

80
Q

ESBL: Comparable outcomes data for older beta-lactam/beta-lactamase inhibitors (piperacillin/tazobactam)

A

Data fairly new; role for ESBL yet to be firmly established

New data for bloodstream infections showed worse outcomes with BLBLI compared to carbapenems

81
Q

ESBL: worse outcomes for ___

A

Cefepime

82
Q

ESBL: Newer inhibitor combinations are newer paradigm as broader spectrum, however mostly being reserved for carbapenem-resistant organisms

A

Ceftazidime/avibactam

Ceftolozane/tazobactam

83
Q

ESBL confers resistance to (3 abx classes)

A

penicillins, cephalosporins, and monobactams

Not carbapenems (still active, TOC) ; cefepime activity is variable

84
Q

AmpC

A

Class C cephalosporinases (AmpC enzymes)

(“SPICE”):
Serratia
Pseudomonas aeruginosa
Indole positive Protea (Proteus vulgaris, Providencia spp.)
Citrobacter freundii
Enterobacter cloacae, Klebsiella aerogenes (previously E. aerogenes)

(“SPACE”): Acinetobacter spp. are capable of similar beta-lactamase production by a similar mechanism and should be treated as above

85
Q

AmpC: Treatment options and what to avoid

A 
Treatment options: 
Carbapenems
Fluoroquinolones
TMP/SMX
Cefepime
Aminoglycosides

Avoid:
Ceftriaxone
Piperacillin-tazobactam

86
Q

ESBL or AmpC?: Ceftriaxone is susceptible

A

AmpC (if ceftrixone is susceptible, def not ESBL)

87
Q

Carbapenemases: 2 types

A

Serine carbapenemases (KPC)

Metallo-beta lactamases (NDM, VIM, IMP)

88
Q

Carbapenemases: 2 types: Serine carbapenemases (KPC)

A

Found worldwide in many Gram-negatives including E. coli, Citrobacter, Enterobacter, Salmonella, Serratia, and Pseudomonas

Transmitted via a plasmid

89
Q

Carbapenemases: 2 types: Metallo-beta lactamases (NDM, VIM, IMP)

A

Confer resistance to all beta lactams except monobactams (aztreonam); however often other mechanisms combined

Found in many Gram-negatives

90
Q

Carbapenemases Potential treatment options

A 
Tigecycline
BL/BLI with activity against KPC
Ceftazidime-avibactam
Meropenem-vaborbactam
Imipenem-relebactam
\+/- aminoglycosides
Polymyxins (colistin, polymyxin B)
Some interesting data for double carbapenem therapy (high-dose, prolonged therapy)
91
Q

Altered target site 4 types

A

PBPs

Altered cell wall precursor targets

Altered DNA gyrase and/or topoisomerase IV

Ribosomal alterations

92
Q

Altered target site is more common in ___ bacterial

A

GP

93
Q

Altered target site: PBPs

A

Alteration in PBP decreased binding affinity of beta-lactam to target

Organisms may exhibit increased MICs but remain susceptible (alteration generally confers full resistance)

Examples
Penicillin and cephalosporin resistance in S. pneumoniae
Methicillin (Oxacillin) resistance in Staphylococci (PBP2a – mecA gene **won’t be asked specifically but know that GP staph strep have alterations of PBPs for beta lactams)

94
Q

Altered target site: Altered cell wall precursor targets

A

Vancomycin inhibits cell wall synthesis by binding to D-alanyl-D-alanine terminus of the peptidoglycan precursor

Glycopeptide resistance in enterococci (vancomycin resistant enterococci; VRE)
Acquired resistance by the VanA/B genes leading to a change in the target site to D-alanyl-D-lactate
Genes can be transferred to other organisms like S. aureus because it is on a plasmid

95
Q

Altered target site: Altered DNA gyrase and/or topoisomerase IV

A

Responsible for resistance to the fluoroquinolones

96
Q

Altered target site: Ribosomal alterations

A

Responsible for resistance to macrolides, azalides, aminoglycosides, tetracyclines, clindamycin

97
Q

Reduced outer membrane permeability

A

In Gram-negatives, passage of hydrophilic antibiotics is dependent on porin channels

Mutations result in loss of specific porins Resistance

Most commonly seen in Enterobacteriaceae and P. aeruginosa
Beta-lactams, including carbapenems (OprD)
Fluoroquinolones

98
Q

Efflux pumps

A

Antibiotic efflux – multidrug resistance efflux pumps
Resistance-nodulation-cell division (RND) family of transporters responsible for significant portion of clinically relevant resistance

Majority of RND efflux systems chromosomally encoded and overexpressed due to mutations in regulator genes

Huge problem among Pseudomonas aeruginosa: at least 7 RND systems identified

Responsible for broad resistance to tetracyclines, fluoroquinolones, aminoglycosides, chloramphenicol, macrolides, azalides, beta-lactams

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