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Flashcards in Antibiotics Deck (67):
1

what is an infection

invasion of the body by various microorganisms: bacteria, fungus, protozoans, viruses, and worms- and the associated reaction of the body to them

2

how are bacterial infections treated

with antibiotics after appropriate diagnosis

3

pathogen identification requires

culturing and other laboratory work...time and money

4

what is empiric therapy

practical and necessary with life threatening cases but also has significant potential problems

5

drug resistance due to

USE and exacerbated by misuse of antibiotics

6

clinical diagnosis include

-symptoms of infection
-physical exam
-patient history

7

clinical lab test include

microbiological diagnosis
-gram stain analysis
-identify the unique peptidoglycan cell wall of bacteria
-differentiates bacteria as: gram +, gram -(+) or gram -, gram-(-)
-antibody screening, others: x-ray

8

what type of wall does gram-(+) bacteria have

-many layers peptidoglycan (90% of wall)
-a polymer composed of polymerized sugar (polysaccharide) and peptide chains connected by amino acid bridges

9

what type of wall does gram-(-) bacteria have

-much thinner peptidoglycan layer (only 20% of the wall); associated with an OM periplasmic space, and lipopolysaccharide layer
-cell wall is not regulatory structure like cell membrane; it is not selectively permeable

10

what are bactericidal antibiotics

destructive to bacteria, concentration-dependent killing or time-dependent killing

11

what are bacteriostatic antibiotics

inhibit the growth or multiplication of bacteria, let the immune system eradicate them

12

what is pharmacokinetics

absorption, distribution, and drug elimination

13

when selecting antibiotics what should you consider

-adverse effects
-drug interaction
-resistance
-post antibiotic effects
-contraindications: not given during pregnancy, to children, elders, or others (liver, kidney, allergy)
-multiple antibiotic therapy:polymicrobial infections, etc
-cost of therapy

14

what bacteria pathogens are susceptible

gram-(+) and gram -(-); cocci, bacilli, clostridium, mycobacterium, bacteroides

15

what Chlamydia pathogens are susceptible

gram-(-), spherical microorganisms

16

what Spirochete pathogens are susceptible

gram-(-), flexible, sprial-shaped

17

what mycoplasma pathogens are susceptible

smallest free-living microorganisms

18

how do bacteria become resistant to antibiotics

1. antibiotic fails to reach its target
2. antibiotic is inactivated
3. target is altered

19

how do antibiotics fails to reach its target

some bacteria have impermeable membrane for the drug (lack of transport system or reduced porins)

20

how are antibiotic is inactive

bacteria produce enzyme destruction (eg. B-lactamases destroy the B-lactam ring of penicillins), or metabolism of the drug

21

how is the target altered

due to down-reguation of porin, and drug mutation of transpeptidase, reduced drug access elimination by energy-depdendent efflux, etc

22

efflux pumping causes

1. resistance to antibiotics by mutation may be transmitted via plasmids or chromosomal DNA
2. alternative pathways...other mechanisms

23

what are the die hard bacteria

Methicillin-resistant staphylococcus aureus
Pseudomonas Aeruginosa
Vancomycin-resistant enterococci
Clostridium
Enterobacteriacea

24

Methicillin-resistant staphylococcus aureus (MRSA) "golden staph" is the major cause of

nosocomial infection
-cause illnesses from minor skin infections to life-threatening pneumonia, meningitis, endocarditis, and septicaemia

25

what type of bacteria is Pseudomonas aeruginosa

gram-(-), aerobic

26

pseudomonas aerguinosa is a major cause of

hospital infections
-prevalent among patients with burn wounds, acute leukemia, IV drug additions

27

what type of bacteria is Vancomycin-Resistant Enterococci

gram-(-) anaerobic

28

what type of bacteria is Clostridium

gram- (+), anaerobic, produces destructive exotoxins

29

what type of baxter is enterobacteriaceae

gram-(-), anaerobic, can cause fatal abscesses and bacteremias

30

what are the bacteria cell wall synthesis inhibitors

1. penicillins "-cillin"
2. cephalosporins "cef~1-4th gen"
3. carbapenems and monobactam
4. others: vancomycin, bacitracin, fosfomycin & cycloserine

31

mechanism of bacteria cell wall synthesis inhibitors

mechanism of protein synthesis in micoorganisms are not identical to those of mammalian cells
-bacteria have 70s ribosomes, whereas mammalian cells have 80s ribosomes
-differences exist in ribosome subunits and in the chemical composition and functional specificities of component nucleic acids and proteins
-such difference form the basis for the selective toxicity of these drugs against microorganisms

32

what are the B-lactam antibiotics

penicillins:
-penicillin G
-penicillin V
-Oxacillin
-Dicloxacillin
-Ampicillin
-Amoxicillin
-Ticarcillin
-Mezlocillin

33

what is the structure of penicillin

-penicillins contain a thiazolidine ring (a) and a B-lactam ring (b)
-A side-chain of penicillin (R) can be added to 6-aminopenicillanic acid with action of amidase to form a different penicillin

34

what is penicillin G

-the only natural penicillin
-used in the form of benzathine, procaine, potassium & sodium salts

35

what is penicillin V

semi-synthetic

36

what are the narrow spectrum penicillins

-oxacillin
-dicloxacillin

37

what are the broad-spectum pencillins

-ampicillin (amino pencillins)
-amoxicillin (amino penicillin)
-ticarcillin (carboxy penicillins)
-mezlocillin (acylureido penicillins)

38

define bactericidial

kill bacteria

39

define bacteriostatic

inhibit microbial growth

40

define beta-lactam antibiotics

drugs with structures containing a beta-lactam ring

41

what is MIC

lowest concentration of antimicrobial drug capable of inhibiting growth of an organism

42

what is penicillin-binding proteins (PBPS)

bacterial cytoplasmatic membrane proteins that act as the initial receptors for penicillins and other beta-lactam antibiotics

43

what is peptidoglycan

chains of polysaccharides and peptides polypeptides that are cross-linked to form the bacteria cell wall

44

what is selective toxicity

more toxicity to the invader than to the host

45

what is transpeptidases

bacterial enzymes involved in the cross-linking of linear peptidoglycan chains, the final step in cell wall synthesis

46

penicillins and cephalosporins are the major antibiotics that inhibit

-bacterial cell wall synthesis
-inhibit the synthesis of peptidoglycan (PG) by inhibiting transpeptidase (transpeptidation)

47

what are the antimicrobials are narrow spectrum

-natural penicillin (G)
-semisynthetic penicillin V
-anti-staphylococcal pencillins:
Isoazolyl penicillins:
Oxacillin
Dicloxacillin

48

what are the antimicrobials that are broad spectrum

amino penicillins (ampicillin, amoxicillin)
Carboxy penicillins (ticarcillin)
Acyleureido penicillins (mezlocillin)

-bactericidal (if bacteria are growing and dividing)
-effective for gram-(+), some gram-(-) and anaerobes

49

what are the clinical uses of antimicrobials

1. septicicemia
2. meningitis
3. hospital-acquired (bacterial) penumonia
4. cellulitis
5. bone and joint infections
6. acute/chronic urinary tract infections

50

how does resistance to antimicrobials occur

1.inactivation by bacterial B-lactamases
2. mutant transpeptidases
3. down-regulation of porins
4. efflux pump

51

inactivation by bacterial B-lactmase is most common in what bacteria

Staphylococcus aureus
Pseudomonas aeruginosa
E.coli
enterobacters

52

what is mutant transpeptidases

alterations in the drug targeted Penicillin binding proteins, reduce the affinity for drug binding in staphylococci, pneumococci and enterococci

53

effects of down-regulation of porins

impairs drug penetration via porins in gram-(-) bacteria

54

pharmacokinetics of antimicrobials

poor oral absorption, except:
Penicillin V - Isoxazolyl penicillins (oxacillin, dicloxacilllin), Amino penicillins (ampicillin, amoxicillin)
-variable distribution throughout the body, do not enter the CNS unless there is inflammation
-not metabolized and generally excreted by the kidney

55

what are the adverse rxns of antimicrobials

-hypersensitivity/allergic rxns (1-5%) may cause anaphylactic shock
-GI distress: nausea, vomiting with oral high doses (not to be mistaken as allergic run)
-Seizures (with high doses)
-Hypokalemia (with high doses)
-superinfections: chronic use may lead to a new/secondary infection, occuring in a patient having a pre-exisitng infection

56

what are the drug interactions with penicillin

-very few; in vitro mixing with aminoglycosides reduces the activity of both

57

what is probenecid

an uricosuric agent which increases excretion of uric acid in hyperuricemia, decreases excretion of penicillins

58

describe the structure of B-lactamase inhibitors

-they have a B-lactam ring (like penicillins & cephalosporins) but lack antimicrobial activity
-bind irreversible to and inhibit bacterial B-lactmases
-neither bactericidal nor bacteriostatic (not antibiotics)

59

see slide 31

see slide 31

60

what is septicemia

commubity and hospital-acquired pneumonia, cellulitis, sinusitis, bone and joint infection

61

how is clavulanate absorbed

after oral administration

62

how is sulbactum & tazobactum administered

IV due to poor oral administration

63

piperacillin increases the half life of

tazobactum

64

describe the structure of cephalosporins

-have a B-lactam ring
-different structures (extra carbon) makes them more resistant to B-lactamases than penicillins
-group R1 and R2 can be substituted to produce a variety of cephalosporins

65

see slide 34: generations of cephalosporins

see slide 34: generations of cephalosporins

66

MAO of cephalosporins

-inhibit cell wall synthesis by inhibiting transpeptidase, this blocking cross-link of peptidoglycan

67

see charts

see charts