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Disease And Defense > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Gram + or - and Type - Staph Aureus

A

Gram + Cocci in clusters

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2
Q

Characteristics of Staph Aureus

A

Beta-hemolytic, Catalase +, coagulase +, Faculative anaerobe

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3
Q

Catalase + means?

A

organisms that can degrad hydrogen peroxide into H20 and O2 before it becomes harmful

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4
Q

Catalase + organisms

A

Staph, E Coli, Pseudomonas Aeruginosa,

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5
Q

O2 dependency for Staph Aureus

A

Faculative Anaerobe

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6
Q

Virulence Factors of Staph Aureus

A

Protein A, Coagulase, hydorlinases

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7
Q

What does Protein A do?

A

binds to Fc-IgG to inhibit complment activation and phagocytosis - characteristic of Staph Aureus

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8
Q

What does Coagulase do?

A

promotes fibrin formation around the organism - Staph aureus

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9
Q

Inflammatory Disease due to direct invasion of Staph Aureus

A

Cutaneous infection with abscesses, Pneumonia, septic arthritis, osteomyelitis, rapid onset bacterial endocarditis

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10
Q

Exotoxin mediated manifestations of Staph Aureus

A

Scalded Skin Syndrome, Toxic Shock Syndrome, Staph Food poisoning

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11
Q

Toxic Shock Syndrome

A

TSST-1 binds to MHC Class II to cause T-cell activation. Characteristic of Fever, diarrhea, rash, hypotension, desquamation of palms and soles, multiple organ failure

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12
Q

Staph Aureus Food poisoning

A

due to enterotoxin - rapid onset for preformed toxin that is associated with V and non-bloody diarrhea

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13
Q

Staph Epidermis - Gram Stain

A

Gram + cocci in clusters

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14
Q

Staph Epidermis - characteristic in lab

A

Catalase +, Coagulate -, urease +, faculatative anaerobe

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15
Q

Virulence Factor of Staph Epidermis

A

Protective polysacchatide intracellular adhesion that adheres to prosthetic devices.

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16
Q

Clinical Manifestations of Staph Epidermis

A

Infections associated with foreign bodes - artificial joints, catheters, endocarditis of heart valves. Biofilms

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17
Q

Staph Saprophyticus - gram

A

Gram + cocci in clusters

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18
Q

Staph Saprophyticus - lab characteristics

A

Catalase +, coagulate -, urease +, faculative anaerboe, Gamma hemolytic

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19
Q

Clinical manifestations of staph- saprophytic

A

UTIs in sexually active females (#2)

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20
Q

how to distinguish Staph infections in the lab

A

1) Staph Aureus is beta hemolytic, coagulate +
2) Staph Epidermis is Coagulate -
3) Staph Saprophyticus is coagulate - and Gamma hemolytic

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21
Q

Streptococcus pyrogens - gram

A

Gram + cocci in chains

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22
Q

Strep Pyrogens - lab characteristics

A

Beta hemolytic, Streptolycin O, Streptolysin S, Catalase negative, microaerophilic, encapsulated, inhibited by bacitracin

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23
Q

Encapsulated - Strep pyrogens

A

by hyaluronic acid (from CT in the body)

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24
Q

Virulence factors in Strep pyrogens

A

M Protein, Streptolysin O, Capsule, Streptokinase, DNAse

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25
Q

M protein

A

Virulence factor for Strep Pyrogens
anti-oponization, anti-phagocytic, antigenic and illicuts a strong humoral response by host!

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26
Q

Pyrogenic Effects of Strep Pyrogens

A

Pharyngitis, Impetigo, Cellulitis, Erysipela

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27
Q

Toxogenic conditions with Strep Pyrogens

A

Scarlet Fever, Toxic-shock like syndrome, Necrotizing fassciitis

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28
Q

Scarlet Fever

A

associated with Strep Pyrogens - strawberry tongue, pharyngitis, diffuse rash that spares the face

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29
Q

Post-Strep Associations

A

Glomerulonephritis and Rheumatic Fever

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30
Q

Glomerulonephritis

A

Type III immune response to strep Pyrogens, results in dark brown urine, facial edema - 2 weeks after strep infection. Can be post pharyngitis OR impetigo

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31
Q

Rhematic Fever

A

Type II immune response to strep pyrogens, M Factor illicuts autoAb via molecular mimicry to myocin in heart valves (mitral). Due to pharyngitis, but not skin manifestations of strep

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32
Q

Signs of Rheumatic Fever

A

JONES
JONES
J: polyarthritis of joints
O -

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33
Q

does early treatment of Strep Pyrogens with penicillin prevent Rheumatic fever, Glomerulnephriis, or both?

A

Only Rheumatic Fever

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34
Q

Strep Pneumonia - Gram

A

Gram + diplococci

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35
Q

Strep Pneumonia - lab characteritics

A

Optochin and Bile senstive
Alpha hemolytic
Catalase -
Faculative anaerobe

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36
Q

Virulence Factor of Strep Pneumonia

A
  • Polysaccharide capsule that prevent complement and phagocytosis
    IgA protease - prevents colonization and invasion of mucosa
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37
Q

Clinical Manifestations of Strep Pneumonia

A

MOPS: meningitis, otitis media, pneumonia of lower lobe, sinusitis or sepsis

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38
Q

Vaccines for Strep Pneumonia

A

Pneumovax for adults and Prevnar for kids

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39
Q

Pneumovax vs. Prevnar

A

both for Strep Pneumonia. Pneumovax is 23 valent IgM; Prevnar is 7 talent conguate to make IgG. Adult version is against active disease, Kid version is to reduce carriage and disease.

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40
Q

Viridan Streptococci - gram

A

Gram + cocci in chains

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41
Q

Viridans Strep. Laboratory Characteristics

A

Optochin and bile resistant, alpha hemolytic, catalase negative, facultative anaerboe

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42
Q

Virulence factor of viridans strep.

A

Synthesis of dextran from glucose to adhere to fibrin.

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43
Q

Clinical Manifestation sof Viridans Streptococci

A

Dental caries —> access blood strem and effect previously damaged valvues to cause endocarditis in mitral values. Or can also cause liver and brain abcesses

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44
Q

Dextran

A

produced in Viridans Strep to creaste a sticky surface that can adhere to teeth, oral tissue, fibrin/platelet aggregate deposits on heart valves.

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45
Q

Enterococcus Faecalis/Enterococcus Faecium - gram

A

Strep Type D - gram + cocci in chains

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46
Q

Enterococcus Faecalis/Enterococcus Faecium - lab characteristics

A

Bile resistant, alpha, beta, and gamma hemolyti, grows well on NaCl (6.5%), catalase - and facultative anaerobe.

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47
Q

Virulence Factor fo enterococcus

A

extracellular dextran helps bind to heart valves

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48
Q

Clinical Manifestations of Enterococcus

A

UTI, surgical wound, biliary tract infections, subacute endocarditis following Gu/GI procedures

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49
Q

Resistance in Enterococcus

A

resistant to penicillin and Vanc

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50
Q

what lab findings help distinguish between strep types?

A

1) Strep Pyrogens - sensitive to bacitracin and encapsulated
2) Strep Pneumo - senstive to optochin and bile
3)Viridan - resistant to optochin and bile
4) Enterococcus - grow on sodium choloride.

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51
Q

Clostridium Difficile - gram

A

Gram + spore forming rods

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52
Q

C. Diff - laboratory characteristics

A

Obligate anaerobe. Must be measured by ELISA or PCR of TOXIN in stool (not bacteria)

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53
Q

C. Diff Virulence Factors

A

Exotoxin A and B

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54
Q

C. Diff Exotoxin A

A

binds to the brush border of the SI to cause inflammation, cell death, and water diarrhea

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55
Q

C. Diff Exotoxin B

A

Disrupts cytoskeleton integrity of depolymerizing actin, leading to enterocyte death and necrosis —> gray psuedomembrane colitis.

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56
Q

Treatment of C. Diff

A

oral vancomycin *NOT IV or metronidozole

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57
Q

Clostridium Tetani - gram

A

Gram + spore forming rods

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58
Q

Costridium Tentani - metabolsim

A

obligate anaerobe

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59
Q

Virulence Factors for C. Tetani

A

Tetanospasmin

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60
Q

Tetanospasmin

A

endotoxin for C. Tetani that when punctured into wound, travels retrograde to CNS to cleave SNARE to block the release of GABA and glycine from Renshaw cells of spinal cord

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61
Q

Renshaw Cells

A

inhibitory interneurons that normally release gaba and glycine in spinal cord - inhibited by tetanospasmin toxin in C. Tetani

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62
Q

Clinical manifestations of C. Tetani

A

Spastic paralysis - rigidity, respiratory paralysis with Risus sardonicus, Trismus, opsothotonus

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63
Q

Risus sardonicus

A

raised eyebrow and open grin

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64
Q

Trismus

A

Lock jaw

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65
Q

Opsothotonus

A

exaggerated back arching

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66
Q

Prevention of Tetanus

A

Toxoid vaccine to generate ab to toxin not organism.

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67
Q

Treatment of tetanus

A

anti-toxin with or without vaccine booster and diazepam.

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68
Q

C. Botulinum - gram

A

Gram + spore forming rods

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69
Q

C. Botulinum - metabolism

A

obligate anaerobe

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70
Q

Where is C. Boltulinum found?

A

soil, smoked fish,, canned food, honey

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71
Q

Mechanism of C. Botulinum

A

Preformed heat labile toxin is absorbed into gut and travels to Peripheral Nervous system (only) to inhibits SNARE release of ACh at NMJ

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72
Q

C. Botulinum clinical manifestations - adults

A

Flaccid descending paralysis through ingestion of preformed toxin —> absent muscle contraction, diplosis, ptosis.

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73
Q

C. Botulinum clinical manifestations - children

A

Floppy baby due to lack of robust gut flora following ingestion of spores in Honey. (NOT preformed toxin).

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74
Q

Clostridium Perfringes - gram

A

Gram + spore forming rods

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75
Q

C. Perfringes - metabolism

A

obligate anaerobes

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76
Q

C. Perfringes - virulence

A

Lechincinase or Alpha toxin

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77
Q

Lechincinase

A

alpha toxin of C. Perfringes that damages cell membranes of lipoproteins and cause RBC hemolysis.

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78
Q

Where is C. Perfringes found?

A

mostly in soil - motocycle accidents and military combat

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79
Q

Clinical manifestations ofC. Perfringes

A

Gas Gangrene (Closridial myonecrosis) and Clostridial food poisoning

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80
Q

Gas Gangrene

A

C. Perfringes - gas is produced under skin to cause crepitace and crackling due to alpha toxin —> leads to crushing type injury, cellulitis, compromised blood flow and hypoxia

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81
Q

Clostridial Food Poisoning

A

enterotoxin as bacterial sporulate in gut (not preformed), slow onset of development of toxin that disrupts tight junctions in ilium —> dysreguation of fluid transport.

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82
Q

E. Coli - gram

A

Gram - rods

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83
Q

E. Coli - Lab characteristics

A

Catalase +, beta hemoytic, Oxidase -, lactose fermentor, faculative anaerobe

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84
Q

Virulence Factors for E. coli

A

K capsule, Fimbriae, LT, ST and shiga-Like Toxins

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85
Q

K capsule

A

a virulence factor in E. coli that causes pneumonia and neonatal meningitis

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86
Q

Fimbriae in E. coli

A

Pilli necessary to colonize in UTI (#1)

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87
Q

LT

A

Heat Labile Enterotoxin of E coli - increases cAMP

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88
Q

ST

A

Heat Stabile Enterotoxin of E. coli - increases cGMP

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89
Q

Shiga-Like Toxin

A

inhibits 60S ribosome

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90
Q

ETEC

A

Enterotoxigenic E coli - non-invasive LT and ST toxins from water lead to watery diarrhea

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91
Q

EHEC

A

Enterohemorrhagic E Coli - Shiga like toxin causes hemorrhagic collitis and hemolytic c uremic syndrome. Due to uncooked meats. Leads to bloody diarrhea - but not fever.

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92
Q

Hemolytic Uremic Syndrome

A

Anemia, Thrombocytopenia, acute renal failure due to damage to endothelial cells in glomerulus where platelets adhere and clump to lyse RBCs.

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93
Q

What strain of E. coli ferments sorbitol?

A

all except EHEC

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94
Q

EIEC

A

Enteroinvasive E coli: bloody diarrhea with fever and pus to to shiga like toxin

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95
Q

Main clinical manifestations of E. Coli infections

A

Diarrhea , LPS acquired sepsis, septic shock, neonatal meningitis, UTI (#1), abdominal infections, hosptial acquired pneumonia

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96
Q

Pseudomonas Aeruginosa - gram

A

Gram - rods

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97
Q

Pseudomonas - Lab characteristics

A

Oxidase +, catalse +, non-lactose fermenter, oglibate aerobe, encapsulated

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98
Q

Pseudomonas Aeruginosa - virulence

A

Exotoxin A

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99
Q

PA exotoxin a

A

blocks EF-2 by fibosylation to inhibit protein synthesis.

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100
Q

Clinical manifestations of Pseudomonas Aeruginosa

A

Nosocomial pneumonia (#1, also in CF), Osteomyelitis, BURNS, UTI, purpuric pustula folliculitid, ecthyma grangrenosum, PSEUDDO - pneumonia, sepsis, otitis externa, UTI, drug use, diabetes, osteomyelitis

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101
Q

Osteomyelitis in Psuedomonas A. infection

A

mostly with IV drug users, diabetics, children

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102
Q

Neisseria Gonorrhoeae - gram

A

Gram - diplococci

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103
Q

Neisseria Gonorrhea - lab characteristics

A

Ferments glucose, but not maltose. Facultative anaerobe and intracellular (invades PMNs),

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104
Q

N. Gonorrhea - virulence Factors

A

LPS, Pilus - adherence, IgA protease for mucosal membrane adherence

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105
Q

N. Gonorrhea - clinical manifestations

A

Urititis, prostatis, orchtis, cervical conorrhea, pelvic inflammaotry disease, Polyarthritis of knee (asymettric)

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106
Q

Charactericis dischange of gonorrhea compared to chlamydia

A

G: white, purulent
C: watery

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107
Q

Congenital Infection of Gonorrhea vs. Chlamydia

A

G: neonatal conjutivitis (early onset)
C: 1-2 weeks post birth (conjunctivitis)

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108
Q

Fitz Hue Curtis

A

when gonorrhea infection spreads to peritoneum and adheres to the liver.

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109
Q

Bacteroides Fragilis - gram

A

Gram - rods

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110
Q

Virulence Factor of Bacteroides Fagilis

A

Tissue destructive enzymes, anti-phagocytic capsule, superoxide dismutase, LPS

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111
Q

Bacteroides fragilis - clinical manifestations

A

Peritonal infections

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112
Q

Chlamydia Trachomatis - gram

A

Gram -, but difficultt o stain due to lacking peptidoglycan layer

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113
Q

Chlamydia - lab characteristics

A

Oblicate intracellular (cannot make own ATP), facultative anaerobe

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114
Q

Chlamydia - virulence factors

A

resistant to lysozyes, non motile, non pilli, no exotoxins released

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115
Q

Chlamydia cell cycle

A

Elementary bodies are small dense infectious bodies that enter the cell.
Reticular body - dividing elementary bodies via binary fission (only in cells with ATP), where it i extruded back out in elementary form. This exhibits tropism.

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116
Q

Chlamydia A-C

A

Causes Trachoma - blindness by corneal scarring. (C with your eyes).

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117
Q

Chlamydia D-K

A

STI, often associated with N. Gonorrhea. Can be asymptomatic of urethritis, cervitis, PID. Active infection can lead to secondary neonatal conjunctitis and pneumonia - staccato funds

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118
Q

L1-3 Chlamydia

A

leads to lymphogranuloma venerium - infection of inguinal nodes with genital ulcers

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119
Q

Reiter’s Syndrome

A

Uvitis, urethritis, reactive arthritis of SI and Knee joints - due to chlamydia

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120
Q

Mycoplasma Pneumoniae - Gram

A

No gram staining due to lack of cell wall

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121
Q

Mycoplasma - Lab Characteristics

A

Membrane with cholesterol/sterols for stabilization, rod-shaped with tip point,

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122
Q

Detection of Mycoplasma

A

1) cold aggultinin 2) PCR

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123
Q

Virulence Factor of Mycoplasma

A

1) H202 to damage respiratory tract, 2) pilli

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124
Q

Clincial Manifestations of Mycoplasma

A

walking pneumonia - generally insidious with nonproductive cough.

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125
Q

what types of antibiotics are bactericidal?

A

Cell wall/membrane, DNA function and synthesis

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126
Q

What types (more specific) of antibiotics are bactericidal?

A

Penicillins, vancomycin, Cephalosporin, Fluoroquinolones, Nitrofuratoin, metronidazole, and Amingoglycosides***

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127
Q

what types of antibiotics are bacteriostatic?

A

Inhibitors of protein synthesis and metabolic pathways

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128
Q

What types (specific) of antibiotics are bacteriostatic?

A

Macrolides, tetracyclines, clindamycin, sulfonamides (NOT amincoglycosides)

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129
Q

Cell wall Inhibitor Antibiotics

A

Penicillins, Vancomycin, Cephalosporins

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130
Q

Protein Synthesis inhibitors - antibiotics

A

Macrolides - Azithromycin, Clarithromycin, Erythromycin; Tetracycline - Doxycycline, tetracycline; Clindamycin; Aminoglycosides - tobramycin, gentamicin;

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131
Q

DNA Function inhibitors - antibiotics

A

Fluroquinolones - ciproflaxin, levofloxican, Moxifloxican; nitrofuranoin, metronidazole (flagyl), sulfonamides - sulfamethoxazole-trimethoprim(TMP-SMX)

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132
Q

Mechanism of Action - Penicillin

A

Stage 3 (cross linking) of cell wall synthesis inhibition - binds to PBP to inhibit transpeptidase enzymes of peptidoglycan and activates autolytic enzymes

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133
Q

Bacterio-cidal vs static - Penicillin

A

Bacteriocidal

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134
Q

Vancomycin Mechanism of Action

A

Inhibits Stage 2 of cell wall synthesis

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135
Q

Bacterio-cidal vs static Vancomycin

A

Bacteriocidal

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136
Q

Cephalosporin - Mechanism of Action

A

Inhibits stage 3 of cell wall synthesis

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137
Q

Bacterio-cidal vs static - Cephalosporin

A

Bacteriocidal

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138
Q

Pharmacokinetics - Penicillin

A

Most are acid liable - preventing good oral absorption except with altered R group, Poor tissue penetration except for inflamed tissues; Renel and breast milk excretion.

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139
Q

Adverse Reactions - Penicillin

A

Hypersensitivity - IgE mediated with possibility of anaphylaxis; most common is a maculopapular rash that is generally mild. (rare: encephalopathy, seizures)

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140
Q

Pencillin G vs V

A

G: poor oral absoprtion - limited to IV use in hosptial
V: Acid resistant prototype with better oral absorbance, however less efficacy.
Both are narrow spectrum only and penicillinase sensitive

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141
Q

Penicillinase Resistant Penicillins

A

Dicloxacillin (oral), naficillin (IM/IV)
NOT suseptible to Penicillinase (Beta-lactamase)

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142
Q

Extended Spectrum Pencillins

A

Extended spectrum due to hydrophilicity - albe to penetrate porins of Gram (-) organisms.
susceptible to penicillinase
Ampicillin, Amoxicillin, Piperacillin

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143
Q

Ampicillin vs. Amoxicillin

A

Both are extended Spectrum penicillins
both are acid resistant, with Amoxicillin has better oral bioavailability.
Both can be given when Beta-Lactamase Inhibitors (Clavulanic Acid)
Risk of rash, diarrhea, superinfection

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144
Q

Piperacillin

A

Extended Spectrum Penicillin
anti-psuedomonal given IV only - effective against B Fragilis and Pseudomonas

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145
Q

Beta-Lactamase Inhibitors

A

Clavulanic Acid and Tazobactam
Resembles Beta-Lactam with not antibiotic activity- irreversible inhibitor of Beta-lactamase
used in combination with ampicillinase sensitive penicillins

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146
Q

Augmentin

A

Clavulanic Acid + Amoxicillin (oral)

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147
Q

Timentin

A

Clavulanic Acid + amoxicillin (IV)

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148
Q

Unasyn

A

Sulbacam + ampicillin (parenteral)

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149
Q

Zosyn

A

Toxabactam + piperacillin (parenteral)

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150
Q

Vancomycin - Pharmokinetics

A

Poor oral absorption - IV usually (except for GI use), Renal Excretion

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151
Q

Adverse Reactions - Vancomycin

A

Infusion related - Red Man: Chills, fever, rash, ototoxicity, renal toxicity

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152
Q

Cephalosporin - Pharmacokinetics

A

All orally avaliabiliy, good tissue penetration (PLACENTA), except brain and CSF. Ceftriaxone (3rd gen) penetrates into CSF.
Renal Excretion

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153
Q

what Cephalosporin penetrates into CSF?

A

Ceftriaxone (3rd)

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154
Q

Adverse Rxns - Cephalosporins

A

Hypersensitivity - not severe like penicillin; but avoid for people with immediate sensitivity to penicillin
Superinfection Risks
nephrotoxicity

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155
Q

Macrolides - Mechanism of Action

A

inhibits elongation of protein synthesis by blocking 50S and translocation of tRNA.

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156
Q

Bacterio-cidal vs static Macrolides

A

Bacteristatic

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157
Q

Tetracyclines - mechanism of action

A

Inhibits initiation of protein sytenshsi, by binding to 30S on A site to prevent ammoniacal tRA into mRNA.

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158
Q

Bacterio-cidal vs static tetracycline

A

Bacteriostatic

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159
Q

Clindamycin - mechanism of action

A

prevents elongation of peptide chain by binding to 50S and preventing translocation

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160
Q

Clindamycin - Bacterio-cidal vs static

A

Bacteriostatic

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161
Q

Aminoglycosides - mechanism

A

Binds irreversibly to 30S and blocks initiation, distorts codong reading frame, blocks translocation (breaks up polysome). blocks initiation! Requires O2 to be transported into bacteria

162
Q

Bacterio-cidal vs static Aminoglycosides

A

Bactericidal!!

163
Q

Types of Aminoglycosides

A

Tobramycin and Gentamicin

164
Q

Types of tetracyclines

A

deoxycline, tetracycline

165
Q

phamacokinetics of macrolides

A

Most are absorbed in GI and widely distributed except in train and CSF. Does cross placent and reaches fetus. ALL are excreted in breast milk, but usually okay. Depending on type of macrolide - liver and renal metabolism and excretion.

166
Q

Excretion of macrolide

A

Bile excretion and liver metabolism: Azithromycin and Erythromycin; Renal in clarithromycin.

167
Q

Absorption of macrolides

A

All in stomach. Azithromycin must be in empty stomach, Clarithromycin without regard to meals - food may improve absorption; Erythromycin - varies depending on salt form.

168
Q

Free base erythromycin

A

destroyed by stomach acid - must have enteric coating

169
Q

Stearate, esoolate, ethyl succinate erythromycin

A

acid resistant and well absorbed.

170
Q

Estolate erythromycin

A

more bioavaliable in kids.

171
Q

Special distibution of macrolides

A

Az/and clarithromycin concentrate in skin, lung, tonsils, cervix, sputum (pulmonary) and in macrophages.

172
Q

Which macrolide are excreted in bile/metabolized in liver?

A

Azithromycin and erythromycin

173
Q

Which macrolide is renaly excreted?

A

clarithromycin

174
Q

adverse reactions of macrolides

A

GI distrubances - N, V, D (Erythromycin)
Hepatotoxicity
Prolonged QT interval leading to ventricular arrhythmia.
Drug interactions

175
Q

Drug interactions in macrolides

A

Erythromycin and Clarithromyin both inhibit P450 to increase plasma toxicity (not azithromycin) - warfarin, cyclosporin, benzodiazepines

176
Q

Pharmacokinetics of Tetracyclines

A

Oral absorption of variable bioavailability. Absorption is impaired by milk, aluminum, calcium, magnesium, iron, salts. Variable degree of tissue penetration - does go into placenta/fetal. Selective accumulation in gingival fluid, subum, bone and teeth; elimination: Doxycline: non-renal, in liver and excreted in bile. Long half life or 16-18 hours. Tetracycline: really eliminated - short acting

177
Q

Elimination of doxycycline vs. tetracycline

A

deoxycycline is concentrated in liver and excreted in bile, long acting 16-18 hours; Tetracycline is renal excretion short acting of 6-8 hours.

178
Q

Adverse Reactions to Tetracyclines

A

Selective accumulation in teeth and bone - depression of growth and discoloration - avoid during pregnancy and children

179
Q

Drug interactions with tetracyclines

A

Antacids/Fe: decrease bioavalibility
Phenytoin/barbituates/barbamezepine: increase metabolism
Oral anticoagulants: increased anticoagulation effect

180
Q

What is the best treatment of community acquired pneumonia?

A

Doxycycline

181
Q

Clinamycin - pharmacokinetics

A

90% bioavailable orally, penetrates into most tissue, especially bone!, not into CSF, metabolized in liver and excreted in bile and breast milk.

182
Q

Adverse Reactions to Clindamycin

A

Psuedomembranous Colitis, N, D, skin rashes, liver dysfunction, neutropenia, C. DIFF infections

183
Q

Aminoglycosides pharmacokinetics

A

No oral admin, only IV or IM, Limited distribution to extracellular fluid and accumulates in renal cortex and inner ear. Excluded from CNS and eye. Excretion: kidney with 2-3 hour half life; but once daily dosing due to post-antibiotic effect. AVOID in late pregnancy.

184
Q

Adverse Reactions to Aminoglycosides

A

Very toxic! irreversible 8th cranial nerve damage - auditory, vestibular; renal toxicity; contact dermatits, rashes, BM depression, nuero-muscular block to cause respiratory arrest; Drug-Drug interactions

185
Q

drug interaction with Aminoglycosides

A

Synergy: beta lactams and aminoglycosides to cause increased entry
Inhibitory: irreverible binding to penicillin can be inactivating

186
Q

Fluorquinolones types

A

Ciproflaxin, levfloxican, Moxiflocian

187
Q

Fluroquinolones - mechanism

A

Inhibition of bacterial DNA gyros and topoisomerase IV to inhibit DNA function.

188
Q

Fluoroquinolones - Bacterio-cidal vs static

A

bacteriacidal!

189
Q

Nitrofurantoin - mechanism

A

prodrug that is reduced by bacterial enzymes to intermediates that cause DNA Damage.

190
Q

Bacterio-cidal vs static - nitrofuranotin

A

Bacteriacidal

191
Q

Metronidazole - mechanism

A

Prodrug that is transformed into nitro radical anion in protozoa and anaerobic bacteria. Anion kills by inducing DNA ds breaks and inhibiting replication

192
Q

Metronidazole - Bacterio-cidal vs static

A

bacteriocidal

193
Q

Sulfonamides

A

folic acid is required for synthesis of thymidine and purines. These are analogs of PAPA that inhibit dihydropteroate synthase. Selectively toxic because humans can get folic acid from diet.

194
Q

sulfonamides Bacterio-cidal vs static

A

bacteriostatic

195
Q

pharmacokinetics - fluroquinolones

A

Good oral avaliabiliby, but also can be parenteral; good tissue penetration and high urinary levels. Large Vd; renal excretion

196
Q

Fluroquinolones - adverse reactions

A

GI: N, V, D, C.Diff; CNS: dizzy, headache, insomnia. Black box warning - increased risk of tendon rupture and arthropathies. Avoid in pregnancy or kids under 18; QT prolongation. Drug interactions

197
Q

Drug interactions of fluroquinolones

A

Theophylline and caffeine - increase toxicity; antacids: reduce oral absoprtion; Cipro is a P450 inhibitor

198
Q

Pharmacokinetics - nitrofurantoin

A

rapid and complete GI absorption, concentrated in renal tubules - not systemic. Excreted in urine.

199
Q

Adverse rxns in Nitrofurantoin

A

GI tract: N, V, D; hypersensitivity - HA, hepatocellular damage, neuropaties.

200
Q

Metronidazole - pharmacokinetics

A

Oral, good distribution into CSF and bone; metabolized in liver; do not breast feed while on drug.

201
Q

Metronidazole - adverse rxns

A

N, headache, dry mouth, metallic taste, exacerbates candida infections, Antabuse-Like effect with alcohol, Durg interactions

202
Q

Antabuse like effect

A

due to metronidzaole with alcohol - causes GI upset and headache

203
Q

Drug interactions of metronicazole

A

inhibits CYP450

204
Q

Phamacokinetics of sulfonamides

A

Weak acid, absorbed in stomach, but best on empty stomach. Wide distribution into pleural, ocular, synovial fluid, CSF, crosses placental and fetus, but predisposes neonates to kernicterus. Metabolism: N-acetylation to inactive form and excreted in breast milk and urine.

205
Q

Adverse rxns Sulfonamides

A

Sensitization - up to stevens johnsons; renal damage, HA, GI, Drug intreaction

206
Q

Drug interaction of sulfonamides

A

displaces bilirubin form albumin to increase risk of kernicterus in brain - brain damage in neonates and infants.

207
Q

what are bacteriacidal antibiotics favored?

A

Severe, quick infections in immunocompromised patients.

208
Q

Penicillin vs. cephalosporin

A

ceph: broader spectrum with gram (-), less suseptible to penicillinase and cross-reactivity.

209
Q

Hepatic Elimination drugs

A

DQ CRIME: Doxycycline, Quinolones (cipro is renal CYP450 inhibit), Clindamycin, Rifampin (induces CYP450 toxicity), Isoniazid, Metronidazole (with alcohol- antabuse rxn), erythrmoycin like (clar and frith) inhibit P450

210
Q

Beneficial Selective accumulation of antibiotics

A

Clindamycin in bone - to treat osteomyelitis
Macrolides: pulmonary to treat URI and pneumonia
tatracycline in gingiva and sebum to treat periodontal and acne.

211
Q

Toxic selective accumulation of antibiotics

A

Aminoglycosides - in inner ear and renal brush border
tetracyclines in bone and teeth to halt growth and cause discoloration.

212
Q

LPS

A

lipopolysaccharides - gram negative endotoxin, a PAMP that recognized by innate immune system. at low doses activates macrophages, B-cells, and alternative complement —> fever, acute phase rxns, inflammation; with high doses leads to shock and DIC.

213
Q

Types of toxins that facilitate spread of microbes through tissue by breaking down ECM, degrading debris…

A

Hyaluonidase, collagenase, elastase, deoxyribounclease, streptokinase.

214
Q

Hemolysin

A

toxin that damages cellular membrane to kill target cells.

215
Q

Cytolysins

A

toxin that inserts into cell membrane to assemble multimeric protein that forms pore to cause cell lysis.

216
Q

Lecithinase

A

toxin that degrades membrane components

217
Q

Pyrogenic endotoxins

A

stimulate the production of cytokines; Scarlatinal and TSST-1 are examples that are super antigens that are T-cell activators that bind to MHC II to activate cytokine cascade (IL2 and IFNgamma).

218
Q

what toxins inhibit protein synthesis

A

Diptheria, Pseudomonas Aeruginosa endotoxin, Shiga Toxin,

219
Q

Pseudomonas Aeruginosa Exotoxin A Inactivated elongation factor

A

ADP ribosyltrasnferase that transfers ADP ribose from NDA to diphthamide on EF-2 to inactive it into the cytoplasm of liver cells.

220
Q

Diptheria toxin

A

an ADP riboxyltransferase toxin that inhibits protein synthesis in the heart, kidney and nuerons

221
Q

Shiga Toxin

A

of Shigella and E coli, toxin that inhibits protein synthesis by RNA N-glycosides that remove adenosine from 28S RNA to make 60S ribosome inactive.

222
Q

How do toxins inhibit protein synthesis?

A

1) ADP ribosyltrasnferase to make inactive Translation machinery 2) make ribosomes inactive

223
Q

how do toxins modify intracellular signaling pathways?

A

Increase cAMP, cGMP, cleave MAPKK protiens, alter actin

224
Q

Heat Labile enterotoxins

A

in V. Cholerae and E coli - AND ribosyltranferase to increase cAMP to cause increase chloride secretion (and water) (changes intracellular signaling)

225
Q

heat Stable enterotoxin

A

in E coli, activate gaunylate cyclase to increase cGAMP and change intracellular signaling

226
Q

Pertussis toxin

A

anADP Ribosyltransferase to increase cAMP

227
Q

Anthrax Edema Factor

A

adenylate cyclase to increase cAMP

228
Q

Anthrax lethal factor

A

endopeptides that cleaves MAPKK to inactive signaling

229
Q

Clostridium Difficile Toxin B

A

glucosyl transferase that alters actin cytoskeleton by transferring glucose from UDP glue to Rho GTPase to inactivate - change intracellular patwhay

230
Q

Botulinum toxin

A

toxin that inhibits release of NT by acting like a n endopeptidase that inactive SNARE proteins to inhibit ACh release

231
Q

Tetanus Toxin

A

toxin that inhibits release of NT by acting like a n endopeptidase that inactive SNARE proteins to inhibit Glycine and Gaba release

232
Q

how do toxins enter the cells?

A

those that cross PM must have two domains - Active and binding. They use receptors on normal membranes to confer specific in location. and they enter cells through endocytosis where toxin is translated in cytosol

233
Q

Prophylaxis/treatment of toxin mediated diseases

A

1) Antitoxin, 2) toxoid 3) passive immunization 4) active immunization

234
Q

Antitoxin

A

antibodies bind to toxin to neutralize. Does not prevent infection or reverse the effects

235
Q

Toxoids

A

derivative of toxin that retain immunogenicity but lack toxicity.

236
Q

Passive immunization

A

admin antibody to patient to provide immediate, but temporary protection from infectious agent.

237
Q

Active immunization

A

admin toxoid to elicit anti-toxic antibodies - 1) primary series and period boosters are required to achieve and maintain protection 2) active immunity persists due to immunologic memory.

238
Q

Immunotoxin

A

hybrid molecules, toxin fragments that lack rector binding domain and are linked to a ligand with a receptor binding domain that binds to a receptor on a different from the native toxin receptor;. These can be used to kill tumor cells or in autoimmune treatment

239
Q

Intrinsic vs. Acquired Resistance

A

intrinsic is natural properties of bacteria that make them resistant to antibiotics; acquired are genetic mutations, acquisition of new gene spread by mobile genetic elements.

240
Q

Mechanisms of resistance

A

inactivate/modify drug; alter drug target; reduce ability to get to target

241
Q

Porins

A

are on the outer membrane of gram - bacteria that are hydrophilic channels that are used for selective uptake of nutrients and hydrophilic antibiotics.

242
Q

Efflux Pumps

A

pumps that pump from the cytoplasm to the extracellular space on both Gram + and -; used to pump antibiotics out of the cells

243
Q

Peptidoglycan linkage

A

GlNAc-MurNAc

244
Q

Peptidoglycan

A

precursors assemble in cyto and are transported to cell surface, where PBP cross links by transpeptidase or gransglycosylatse. Crucial for cell growth, separation, and sporuation.

245
Q

what is important for cross linking in peptidoglycan?

A

D-Ala-D-Ala terminal peptides.

246
Q

Action of Beta Lactamase

A

split amide bond in beta-lactam rin to make inactive. Very specific beta lactam rings!

247
Q

Narrow Spectrum Beta lactamases

A

hydrolyze penicillin antibiotices but not cephalosporins of carbapenems. Exist on Gram + and -, transferred via plasmid or transposon.

248
Q

bla

A

narrow spectrum beta lactase for Staph

249
Q

TEM-1

A

narrow spectrum beta-lactamase for H influenza and E. coli

250
Q

SHV-1

A

narrow spectrum beta-lactamase for Kiebsiella

251
Q

Extended Spectrum Beta-Lactamases

A

Hydrolyze penicillin and MOST cephalosporin antibiodies. Occur only on Gram - Rods. Derived from plasmids, with mutations that have occurred in the narrow spectrum region.

252
Q

CTX-M

A

ES Beta-Lactamase for E. coli

253
Q

SHV-Type

A

ES beta lactamase for Kiebsiella

254
Q

Amp-C Encoded Beta Lactamase

A

hydrolyzes penicillin and 1-3 cephalosporin and is NOT inhibited by beta-lactamase inhbitors! transferred chromosomal and only occurs in Gram - rods like Eneterbaeteria and Pseudomonas. Can be induced or constitutive.

255
Q

Induced vs constitutive AmpC

A

Induced is resistance that is only on some of the time - induced by ampicillin and cefazolin, but constitutive is always on due to mutations!

256
Q

Carbapenemases

A

Beta-lactamases that are active against oxyimo-cephalopsorins, cephamycins and carbapenems. Carbapenems are resistant to ESBL and ampC, so these are very hardy. Plasmid mediated and gram - rods only.

257
Q

KPC

A

hydrolyze carbapenems and all beta lactams

258
Q

NDM-1

A

hydrozlyes all beta lactams except aztreonam

259
Q

Types of Beta-Lactamases

A

1) narrow secptrum 2) extended spectrum 3) amp-C encoded 4) carbapenemases

260
Q

Altered PBPs in B-Lactam resistance

A

Mutation of gene or acquisition of new PBP genes to make the blockage of cross linkage unsuccessful.

261
Q

MecA

A

in Staphylococci encodes for a low affinity PBP2a that is resistant to all Beta-lactam antibiotics except 5th generation cephalosporin. Found on MRSA

262
Q

Mosaic PBP

A

transformation into own genome from another bacteria a lower affinity PBP found in Streptococcus pneumonia and N. Gonorrhoeae. Infers a gradual resistance compared to staph

263
Q

Resistance mechanisms of B-Lactam antibiotics

A

1) Beta lactamase 2) altered PBP

264
Q

Vancomycin mechanism

A

targets peptidoglycan precursor D-Ala-D-Ala peptide chain to disrupt cell wall synthesis

265
Q

Vancomycin resistance

A

1) Modification of target 2) preventing drug-target interaction

266
Q

Modification of target - vancomycin

A

vanA and vanB are transferred via plasmid to substitute termal D-ala for D-lactate on peptidoglycan precursor. Unable to cross link cell wall. Occurs in enterococcus

267
Q

Preventing drug-target int. in Vancomycin

A

the unable to cross link creates thickened layers of peptidoglycan and leaves free d-ala-D-ala. Vancomycin remains bound to cell wall instead of precursor, so it doesn’t have an effect. (staph)

268
Q

VISA

A

vancomyin intermediate suseptibility S. Aureus - most due to prolonged vancomycin use.

269
Q

Quinolone mechanisms

A

target gyrase (GyrA or B) and topoisomerase (ParC and E) to cause DS DNA breaks.

270
Q

Resistance to Quinolones

A

1) modify drug (rare), 2) drug efflux (rare) 3) modifying target (most common)

271
Q

Modifying target - quinolones

A

1-2 NT mutation in GyrA or ParC so it can no longer bind to quinolone to be inhibited.

272
Q

Macrolides - mechanims

A

binds to 23S of 50S bacterial ribosome to prevent peptide elongation.

273
Q

Macrolide resistance

A

rarely drug modification; 1) modifying target 2) increased efflux

274
Q

Modifying target - macrolide

A

erm demethylates 23S so macrolide cannot bind. Transferred via plasmid or transposon and cause resistance to macrolide and clindamycin. Induced and constitutive.

275
Q

Induced vs. constitutive macrolide resistance

A

Induced is resistant to macrolides and sensitive to clindamycin; constitutive is where term is always on so it is resistant to both macrolide and clindamycin

276
Q

Increased Efflux - macrolide

A

passed via chromosomal or plasmids and causes resistance to macrolide and sensitivity to clindamycin. Must use D-test to determine whether due to modification of target or efflux pump

277
Q

D-Test

A

to differentiate between term and efflux pump resistance in macrolides. 1) stream agar plate 2) plate disc with erythromycin near disk with clindamycin. if there is an ERM mutation, you will see an induced resistance to clindamycin and blunting clearing zone. If due to efflux, there will be no blunging zone.

278
Q

Amincoglycosides - Resistance

A

1) modifying drug (classical) 2) modifying target 3) preventing drug-target interaction

279
Q

Modifying drug - aminoglycosides

A

due to plasmic, transposon, chromosme in gram + and -, muletiple modifiers that cause N-acetylation, O nucleotidylation, O phosphorylation.

280
Q

Modifying target - amincoglycosides

A

plasmid to cause methylation of 16s rRNA (site of binding)

281
Q

Preventing drug-target interaction - ahminoglycosides

A

ETC creates electrochemcial gradient for uptake of aminoglycosides. Anaerobic do not have ETC, so they are resistant.

282
Q

what antibiotics target most Gram + cocci?

A

Penicillin V and G, Amox/Amp, cephalosporins, vancomycin, Clindamycin, macroclides, Doxycycline (NOT dicloxcillin, tetracycline, aminglycosides, DNA affectors)

283
Q

what target community acquired penumonia?

A

Doxycycline

284
Q

What antibiotics are good for strep pyro and pneuma?

A

All penicillins, cephalosporins, vancomycin, protein synthesis inhibitors (except aminoglycosides, nitofurantoin, metraonidazole)

285
Q

what antibiotics are good for MSSA?

A

Penicllins that are beta-lactamse resistance - dicloxacillin, Amox w. Calv, pip -taz, cephalosporins, vanc, all protein syntehsis inhibitors, NOT DNA effectors or aminoglycosides

286
Q

what antibiotics are good for MRSA?

A

Doxycycline, TMP-SMX, Clindamycin, vancomycin

287
Q

What antibiotics are good for Gram - cocci?

A

cephtriazone (3rd ceph), and some macrolides and tetracycline

288
Q

what antibiotics are good for most E. coli?

A

Aminoglycosides, Amox, Amox with Clav, pip-tazo, Nitro, ceph, tmp-smx

289
Q

what antibiotics are good for resistant e. coli?

A

aminoglycosides, Cip-levo (only for those with skeletal maturity)

290
Q

what antibiotics are good for pseudomonas?

A

Aminoglycisdes, cip-levo, pip-tax, 3rd ceph

291
Q

what antibiotics are good for most anaerobes?

A

Pip-Tax, Penicillins, Amox, Amox/clav, cephs, tetracycline, Clindamycin, moxifloxican, metronidazole, NOT dicloxacillin, vanc, macrolides, cip/levo, nitrofurantoin

292
Q

what antibiotics are good for C-Diff?

A

metronidozole, vancomycin.

293
Q

what is C-diff caused by?

A

Clindamycin, Fluroquinolones, 2 and 3 gen ceph, amox-clav

294
Q

what antibiotcs are good for bacteroides fragilis?

A

Pip-tax, Amox/clav, clindamycin, metronidazole

295
Q

what antibiotics are good for atypical bacteria?

A

Doxycycline (not in pregnancy or kids), macrolides, fluroquinolones

296
Q

two different ways bacterial evolve?

A

slow incrementa changes to non-pathogenic progenitors by mutations that modify existing genes OR quantum changes by acquisition of NEW genetic material by lateral transfer

297
Q

Regulation of Gene expression in bacteria 2 methods

A

Regulation of transcription by increasing or decreases BP to promoter region OR DNA rearrangement in phase variation

298
Q

Mechanisms of Genetic Variation in bacteria

A

Spontaneous, Recombination, Acquisition of nes DNA segments

299
Q

Spontaneous mutation - genetic variation

A

errors in BP changes, deletions, duplications; typically are deleterious or neutral. Rarely confers selective advantages.

300
Q

Recombination methods

A

1) antigenic variation 2) genetic exchange between related organisms

301
Q

Antigenic recombination

A

Inversion of promoter sites to create selective advantage

302
Q

Acquisition of new DNA segments

A

occurs via lateral transfer from other bacteria or higher organisms - via transposable elements, bacteriophage, plasmids, and pathogenicity islands

303
Q

Transposable Elements

A

segment of DNA contained within bacteria of phage chromosome or within a plasmid that is able to be enzymatically moved.

304
Q

Examples of transposable elements

A

1) transposons, IS elements, composite transposons

305
Q

Transposon

A

must be a part of a self replicating organisms, encodes transposes and becomes integrated into bacterial chromosone.

306
Q

IS

A

insertion sequences that just encode for transpsase

307
Q

Composite transposon

A

carries genes of antibiotic resistance, toxin, adhesion, as well as transposes

308
Q

Bacteriophage

A

virulence genes not normally part of bacterial genome that are expressed in lysogenized strains

309
Q

Acquisition of new plasmids

A

via conjugation and trasduction

310
Q

Pathogenicity Islands

A

insertions of one or more genes that influence pathogenicity - often have been acquired from unrelated organism.

311
Q

T3SS

A

and PI that triggers salmonella invasion and inflammatory response into epithelial cells and translocates 30 effector porteins to host cytoplasm

312
Q

ETEC

A

plasmid encoded enterotoxin that causes travelors diarrhea

313
Q

EPEC

A

plasmid mediated his pathology that causes infant diarrhea in developing countries

314
Q

EIEC

A

plasmid mediated invasion and epithelial destruction

315
Q

Ehec

A

bateriophage! encoded toxin and plasmid encoded virulencef actor that causes hemoragic colitis and hemolytic uremic syndrome

316
Q

EAEC

A

plasmid mediated aherence and pathology

317
Q

mechanisms of exchange between bacteria

A

transformation, transduction, conjugation

318
Q

Transformation

A

genetic transfer of naked DNA (either Ch or plasmid) in gram + and - bacteria; cell must be competent for uptake of DNA; most often occurs between same speciies

319
Q

Transduction

A

mediated transfer via bacteriophages where virus adsorbs bacteria and injects Nucleic acids into cells where it undergoes viral cycle to release virus progeny.

320
Q

Temperate bacteriphage

A

bacteriophage that does not always kil the host - can be in lytic or lysognic

321
Q

Lytic infection

A

entrance of viral chromosome where it is multiplied and viral chrosomes are packaged and released by cell lysis

322
Q

Lysogen formation

A

host is maintained as noninfectious prophage where DNA is inserted into host genome and passively replicated and can either enter lytic state or maintain lysogenic.

323
Q

How does it remain in lysogenic state?

A

repressor proteins, and stress favors lytic cycle

324
Q

Bacterial conversion

A

lysogenic conversion - genes expressed in lysogenic state and transducer and new phenotypic trait is found only in phage genome.

325
Q

Bacterial conjugation

A

genetic transfer dependent on physical contact and mediated by bacterial plasmids (plasmid F); carried selective resistance and virulence.

326
Q

types of bacterial plasmids

A

1) conjugative and non-conjugative and non-mobilized

327
Q

Conjugative plasmids

A

self transmissible that mediate own transfer

328
Q

Non-conjugative plasmid

A

can be mobilized to be passibvly transferred during conjugation by another plasmid in the same cell.

329
Q

Mechanism of conjugation

A

cell comes in contact, single stranded nick in OriT and BP at 5’ end to initiate rolling replication cycle, ssDNA is transfered via sex pili, intregrates into bacterial chormoones

330
Q

OriT

A

origin of transfer, F-DNA plasmid is coupled to this

331
Q

Conjugative transposons

A

transposable elements that mediate conjugation between pairs of cells that often encode antibiotic resistance against tetrcycline.

332
Q

Interspecies conjugation

A

occurs between gram + and Gram -; Gram - to fungi and plants

333
Q

ftsz

A

tubulin equivalent in bacteria - responsible for division

334
Q

MreB/PerM

A

actin in bacteria - polarity and Ch separation

335
Q

Cres

A

intermidate filmanet in bacteria - shape

336
Q

Bond in peptidoglycan

A

GlcNAc-MurNac

337
Q

lysozyme

A

cleaves GlcNAc-MurNac bond

338
Q

Major differences between gram + and -

A

Gram + has high osmotic pressure, lots of cross links, thick cell wall; L-lys - gly(5) - D-ala
Gram - low osmotic pressure, not many crosslinks, think, DAP-D-ala

339
Q

What is characteristic of gram - bacteria

A

Asymmetric lipid bilayer that is barrier to antibics and protective from detergents and toxins

340
Q

Components of asymmetric lipid bilayer

A

1) LPS 2) porins 3) lipoproteins

341
Q

LPS

A

lipopolysaccharids - covalent linkes outer membrane

342
Q

Porin

A

transmembrane channels in gram - that allow

343
Q

Lipoproteins

A

proteins in Gram - wall that anchors outer membrane to peptidoglycan

344
Q

LPS endotoxin

A

Lipid A: toxic component with core polysaccharide; trigger innate immune system to lead to inflammation and endotoxic shock

345
Q

Components of gram +

A

Teichoic acid and Lipoteichoic acid

346
Q

Teichoic acid

A

Polyglycerol and polyribitol backbone that covalently links PG layer and extends outward

347
Q

Lipoteichoic acid

A

FA substition that is embedded in gram + cytoplasmic membrane

348
Q

Function of Gram + cell wall

A

ion homeostasis, adherence for colonization, use TLR to trigger innate immune response and inflammation

349
Q

Capsule

A

polysaccharide coat of bacteria that is anti phaygocytic, a virulence factor. It is antigenic - used as vaccine component

350
Q

Biofilm

A

adherent polysaccharid/glycoprotein that adhere to inert surfaces, host cells, and is protective of phagocytosis and host defence. Limits antibiotics

351
Q

Flagellae

A

used for motility

352
Q

Pertinichous

A

flagella on all sides

353
Q

Flagella moving counterclockwise

A

tumbling

354
Q

flagella moving counterclockwise

A

swimming

355
Q

Pili

A

fine appendages that help adhere to surfacea nd tissues - sex pili are used for conjugation

356
Q

Secretion system

A

delivers proteins to cell surface, assemble organelles, exports to ECM, injects proteins or DNA

357
Q

Binary Fission

A

produces two cells of equal size

358
Q

Phases of bacteria growth

A

lag phase, exp. growth, stationary phase,d eat

359
Q

Lag phase

A

in oculum, induction of growth in new medium

360
Q

Exponential phase

A

logarithmic, increase in cell # and mass

361
Q

Stationary phase

A

essential nutrients are consumed and toxic products accumulate to cause cell death.

362
Q

where does antibiotic resistance work?

A

only on fast growing cells

363
Q

Energy sources of bacteria

A

ATP, PMF (from flagellar rotation), NADPH, ATPase converts ATP,

364
Q

Fermentation vs. Respiration

A

Fermentation anaerobic where you have facultative organic electron donor and acceptor; Respiration uses ATP generation with O2

365
Q

indifferent anaerobe

A

ferments in presence of O2

366
Q

Faculative

A

Respires in O2, ferments in absence of O2

367
Q

Microaerophilic

A

grow sets at low O2, but can grow without O2

368
Q

Sporulation

A

response to advere nutritional conditions that forms spores which are highly resistance and require no metabolism. For prolonged survival in adverse conditions.

369
Q

Germination

A

sporulation back to metabollically active cells when nutritional needs are met

370
Q

Empiric therapy

A

early antibiotic initiation with critically ill patients - broad spectrum considering what organisms are likely and resistant based on clinical context.

371
Q

Definitive therapy

A

narrow spectrum due to microbiology result

372
Q

Antimicrobial suseptibility testing

A

1) broth dilution, Disc diffusion (Kirby Bauer), E test,

373
Q

Broth dilution

A

serial dilution in liquid media to determin MIC

374
Q

MIC.

A

Minimal inhibitory concntration - lowest concentration antibiotic prevents growth

375
Q

Disk Diffusion

A

Kirby Bauer - isolate susension and plate with discs of antibiotics and measure diameter of clearing

376
Q

E -test

A

like KB, but with strip of concentration gradient to determine MIC

377
Q

MBC

A

minimal bactericial concentration - lowest conc ab kills 99.9% of inoculum

378
Q

MIC and MBC - bactericidal

A

MBC = MIC

379
Q

MIC and MBC basteriostatic

A

MBC&raquo_space; MIC

380
Q

Minimun determinant for suseptible oranisms

A

Max CP is greater than MIC

381
Q

Caveats of interpretation of bacteria suseptibility

A

does not account for penetration into tisue, does not account for number of bugs in the infection, does not consider host conditions (pH), does not consider host defense

382
Q

Local Factors of antibiotics

A

Distribution and environment

383
Q

Tx of meningitis

A

must cross BBB, inflammation makes endothelial border leaky to increase CSF concentration; host defesnse mechanism in CNS, must use bactericidal

384
Q

Tx of bone infections

A

has opsonphagocytic removal (bacterial protective) and requires prolonged antibiotic use. Fluroquinolones are good.

385
Q

Endocarditis tx

A

platelets and fibrin create niche to protect bacteria - bactericidal

386
Q

Intracellular niche

A

rifampin, tatrcyclines, erythrmoycin penetrate better than ahminoglycosides and B-lacatms

387
Q

Daptomycin

A

pulmonary surfactant inactives drug - cant tx pneumonia

388
Q

Host factors to Antibiotics

A

1) Hx of adverse rxns
2) renal/liver function
3) age
4) genetic
5) pregnancy
6) Drug interactions
7) immune status

389
Q

Age and antibiotic factors

A

sulfonamides - compete with bilirubin for binding to albumin, increase bilirubin cause kernicterus; tetracycine binds to bone and developing teeth - not recommended for kids

390
Q

Genetic factors for antibiotics

A

G6PD deficiency causes hemolysis with antibiotics ; DM increased risk with fluroquinolones

391
Q

Immune status considerations with Ab

A

if immunocompormised usually affected by uncommon agents, depend only on Ab and require bacteriocidal

392
Q

Selective media

A

permits growth of organisms we wish to recover, but supresses growth of underised. Ie. MacConkey agar with bile salts and dye crystal violet to inhibit all except gram -

393
Q

Differential Media

A

provides selective advantage for growth of one organism over another in polymicrobic specimen. could be chemical *sodium seleniate or temperature

394
Q

MacConkey Agar

A

differential and selective for det and isolation of Gram -; can further separate lactose fermentation - turn red; from those that done remain clear.

395
Q

Lactose fermenters

A

pick on macconkey agar - E. Coli and Klebsiella

396
Q

Lactose non-fermenters

A

stay clear on macConkey agar - salmonella, shigella, pseudomonas

397
Q

Hektoen Eneteric Agar

A

diff and selective for isolation of salmonella and shigella. Contains bile salts to inhibit non-eneric and dytes to inhibit growth of gram +. (high conc of bile salts to kill E. coli)

398
Q

Orange on HE agar

A

fermenters for sucrose, salicin, or lactose - NOT salmonella or Shigella

399
Q

Green blue colonies on HE agar

A

salmonalla or shigella - non fermenters

400
Q

Black coloration of HE agar

A

combination of H2S with ferric ions to isolate salmonellae from shigella.

401
Q

Sheep blood agar

A

common differential, non-selective. supports growth of most bacteria. Good for visualizing hemolysis positive colonies

402
Q

Psuedomonas Isolation Agar

A

selective, formation of blue or blue-green pyocyanin pigments of pseudomonas aeruginoas.

Disease And Defense (7 decks)

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