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pathophysiology > antibiotics quiz > Flashcards

antibiotics quiz Flashcards

1
Q

the 3 things that target bacteria

A

disinfectant, antiseptic, antibiotic

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2
Q

disinfectant

A

used to sterilize the surface of inanimate objects

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3
Q

disinfectants are typically very

A

very strong, and destroy many features of bacteria

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4
Q

antiseptic

A

used to sterilize body surfaces, these are not as strong as disinfectants

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5
Q

antibiotic

A

used to kill bacteria internally through ingestion or injection

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6
Q

antibiotics are the

A

gentlest, they should not harm human cells

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7
Q

what makes antibiotics good

A

broad-spectrum

minimal side effects

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8
Q

broad-spectrum

A

effective against many different types of bacteria

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9
Q

why is broad-spectrum good

A

many times, growing a culture will take too long

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10
Q

minimal side effects

A

little toxicity or host damage

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11
Q

what makes good antibiotics bad

A

resistance

attack normal flora

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12
Q

why does resistance make good antibiotics bad

A

makes harmful normal flora bacteria grow resistance, could become harmful or trade genes with harmful ones

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13
Q

why does attacking normal flora make good antibiotics bad

A

killing off normal flora can lead to bad things

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14
Q

killing off normal flora can lead to……

A
  • increased risk of yeast infection
  • increased risk of normal flora infection
  • vitamin deficiency
  • GI issues
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15
Q

examples of yeast infections caused by antibiotics attacking normal flora

A

yeast, vaginitis, thrush

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16
Q

examples of normal flora infections caused by antibiotics attacking normal flora

A

CDiff, MRSA/VRSA

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17
Q

examples of vitamin deficiencies caused by antibiotics attacking normal flora

A

B, B12, K

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18
Q

examples of GI issues caused by antibiotics attacking normal flora

A

antibiotic-associated diarrhea.. probiotics

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19
Q

thrush

A

an overgrowth of the fungus Candida albicans on the tongue

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20
Q

thrush causes

A

a white slimy layer on top of tongue

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21
Q

yeast vaginitis

A

an overgrowth of the fungus Candida albicans on the vaginal walls

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22
Q

like in chemotherapy, antibiotics

A

should damage “bad” cells, while doing as little collateral damage as possible

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23
Q

how do antibiotics avoid collateral damage

A
  • peptidoglycan Synthesis
  • protein Synthesis
  • DNA/RNA Synthesis
  • metabolism (bacteria often have different metabolic pathways)
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24
Q

why do we target peptidoglycan synthesis with antibiotics

A

no cell walls in human cells

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25
Q

why do we target protein synthesis with antibiotics

A

ribosome structure is different

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26
Q

why do we target DNA/ RNA synthesis with antibiotics

A

bacteria use different enzymes to facililatet

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27
Q

why do we target metabolism with antibiotics

A

bacteria often have different metabolic pathways

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28
Q

________ are defined by the presence of a

A

beta-lactams are defined by the presence of a beta-lactam ring

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29
Q

how do beta-lactams work

A

they block one of the last steps of the synthesis of peptidoglycan … BETTER ON GRAM POSITIVE

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30
Q

what is one of the last steps of the synthesis of peptidoglycan that is blocked by Beta-lactams

A

when transpeptidases and carboxypeptidases build cross-linkages between peptidoglycan strands

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31
Q

transpeptidases and carboxypeptidases together are known as

A

PBPs

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32
Q

PBPs

A

penicillin-binding proteins

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33
Q

examples of beta-lactams

A
  • penicillin
  • amoxicillin
  • methicillin
  • cephalexin
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34
Q

antibiotic classes that are beta-lactams (by popularity)

A
  • penicillins
  • cephalosporins
  • beta-lactams (increased activity)
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35
Q

antibiotic agents that are beta-lactams (by popularity)

A
  • amoxicillin
  • amoxicillin, clavulanic acid
  • cephalexin
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36
Q

1 antibiotic in india and us

A

Amoxicillin (beta-lactam)

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37
Q

antibiotics can be protein synthesis inhibitors because

A

the ribosomes in animal cells and human cells are different

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38
Q

ribosomes

A

site of protein synthesis

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39
Q

ribosomes are sorted according

A

to the Svedberg rate of sedimentation (S)

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40
Q

what is the Svedberg rate of sedimentation

A

how fast the particle settles to the bottom after centrifuge

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41
Q

for the Svedberg rate of sedimentation for ribosomes

A

the Svedberg rate of 2 subunits of ribosome are added

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42
Q

50s + 30s, 60s + 40s

A

70s , 80s

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43
Q

in bacteria the size of ribosomes are

A

smaller an lighter : 70s

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44
Q

inhumans the size of ribosomes

A

80s

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45
Q

what are the major classes of drugs that take advantage of the different sizes of ribosomes of bacteria and humans

A
  • tetracyclines

- macrolides

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46
Q

Tetracyclines

A

bind and inhibit the 30s subunit of bacterial ribosomes

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47
Q

tetracylines are very common, ecspecially

A

very common, especially doxycycline

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48
Q

tetracyclines always come with

A

with 4 connected rings

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49
Q

Macrolides

A

bind to and inhibit the 50S subunit of bacterial ribosomes

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50
Q

Macrolides are the ______ most-common type of antibiotic prescribed in the US

A

2nd

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51
Q

examples of common macrolides

A
  • erythromycin&raquo_space;> ery-pack

- azithromycin&raquo_space; z-pack

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52
Q

4 th most popular drug in india and example of tetracyclines

A

doxycycline

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53
Q

2 antiboitic class us

A

macrolides

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54
Q

2 antibiotic US

A

azithromycin

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55
Q

5 most popular antibiotic drugs in india

A

macrolides

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56
Q

what antitbiotics stop DNA or RNA synthesis

A

Fluoroquinolones

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57
Q

Fluoroquinolones

A

are a class of antibiotic that target and block the bacterial form of DNA topoisomerase II

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58
Q

DNA topoisomerase II

A

creates small nicks in DNA to relieve torsinal stress

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59
Q

without DNA topoisomerase , bacteri

A

becomes tightly twisted and DNA and RNA synthesis will stop

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60
Q

main fluoroquinolone

A

ciprofloxacin

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61
Q

4th most commone antibiotic class , …

A

fluoroquinolone

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62
Q

3rd most common antibiotic in india, fluoroquinolone

A

contrimoxazole

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63
Q

purines (needed for replication)

A

A and G

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64
Q

to make purines the body needs

A

tetrahydrofolate (THF)

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65
Q

how to make THF

A

the body uses folic acid reductase on folic acid

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66
Q

how is folic acid acquired in humans

A

through diet

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67
Q

bacterial cells getting tetrahydrofolate

A

cannot rely on diet to make THF, instead, make their own

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68
Q

what is used to address THF in bacteria???

A

sulfa drugs

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69
Q

what do sulfa drugs do

A

interfere with an ezyme necessary for bacteria to build THF from precursors

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70
Q

good place to look for more antibiotics

A

bacteria building THF pathway

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71
Q

sulfa drugs always contain

A

sulfur

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72
Q

example of sulfa drug

A

sulfamethoxazole

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73
Q

sulfa drugs interfere in THF pathway from

A

the enzyme that acts on PABA to convert precursor 1 to precursor 2

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74
Q

what is often perscribed w/ sulfa drugs

A

trimethoprim

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75
Q

trimethoprim interferes in the THF pathway from

A

dihydrofolate to tetrahydrofolate

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76
Q

mechanisms of antibiotic resistance

A
  • pushing antibiotics out
  • stopping antibiotic entry
  • target modification
  • inactivation of antibiotic
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77
Q

pushing antibiotics out is achieved by

A

inheriting or overexpressing an efflux pump

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78
Q

efflux pump

A

transmembrane pump that moves the antibiotic out

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79
Q

stopping antibiotic activity is achieved through

A

mutation in the shape of a porin can stop entry of antibiotics, can’t do their job

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80
Q

antibiotics often enter cells through

A

porins

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81
Q

inactivation of antibiotics is achieved through

A

inheriting a gene that codes for an enzyme that cuts the antibiotic

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82
Q

many bacteria have inherited a gene for

A

a beta-lactamase , which cleaves beta-lactam containing compounds

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83
Q

pushing antibiotics out is not usually seen

A

not common with beta-lactams, but often for others

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84
Q

how does bacteria achieve target modification

A

mutation to the structure that an antibiotic attacks

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85
Q

example of target modifications `

A

most MRSA infections as a result of mutant PBP structures

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86
Q

mutant PBP structures means that in MRSA

A

that beta-lactam antibiotics no longer bind to them (and thus, don’t work)

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87
Q

many types of of beta-lactamases

A

YES

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88
Q

Escherichia are gram what?

A

gram-negative

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89
Q

Escherichia shape

A

bacilli

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90
Q

what temp do Escherichia like

A

mesophilic

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91
Q

do Escherichia form spores

A

No

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92
Q

Escherichia relationship with oxygen

A

facultative anaerobes

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93
Q

Escherichia make up what % of human GI flora

A

0.1 %

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94
Q

what is the “claim to fame” of Escherichia

A

conversion of digested K1 into K2

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95
Q

Vitamin K2 is

A

it’s active form in humans

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96
Q

how many species in the Escherichia genus

A

5-6 known

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97
Q

Escherichia can divide in

A

just 20 minutes

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98
Q

a newborn’s intestine will typically be colonized with Escherichia within

A

40 hours of birth

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99
Q

who discovered Escherichia

A

Theodor Escherich in 1886

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100
Q

E. coli is most linked to what categories of disease

A
  • infection of GI tract
  • Urinary Tract Infection
  • Meningitis
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101
Q

E. coli cause infection of the GI tract gist

A

colonization of virulent strain in GI tract can cause bad things

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102
Q

what bad things can colonization of virulent strains of E. coli in GI tract cause

A

diarrhea and dysentery

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103
Q

dysentery

A

diarrhea with blood

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104
Q

E. coli is responsible for how much of UTIs

A

about 85%

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105
Q

how does E. coli cause a UTI

A

passed from the fecal/oral route to the urethra or bladder

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106
Q

E. coli is how much more commen in girls

A

14x … urethra is shorter

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107
Q

Meningitis caused by E. coli is usally only commono in

A

neonates, requires entry into the bloodstream plus the K1 antigen

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108
Q

what does the K1 antigen help E. coli do in meningitis

A

helps it pass through the BBB (brain blood barrier) into the meninges

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109
Q

how does E. coli spread

A

through the fecal-oral route

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110
Q

what does it mean that E. coli spreads through the fecal-oral route

A

feces of fecal matter infected materials must enter the mouth of someone

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111
Q

how does the fecal-oral route usually spread

A

dirty water or inadequate hand-washing after using the bathroom

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112
Q

E. coli spread is closely linked to what food

A

ground beef

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113
Q

most important species of Escherichia is

A

Escherichia coli

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114
Q

E. coli comes in many different

A

serotypes

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115
Q

serotypes

A

different strains catalogued by their surface antigens (think lancefield)

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116
Q

Escherichia coli serotypes are grouped based on what surface antigens

A

Oligosaccharides
Flagellal structure
Capsule

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117
Q

Escherichia coli serotypes are grouped based on what surface antigens KNEUMONIC

A

O- Oligosaccharides
H-Flagellal structure
K - Capsule

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118
Q

Oligosaccharides as a surface antigen of E. coli

A

structure of sugar chains at the outer tip of LPS

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119
Q

how many LPS structures known in E. coli

A

173

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120
Q

how many unique flagellal structures known of E.coli

A

53

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121
Q

Capsule E.coli

A

he structure of the protein on the outermost layer of E. coli

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122
Q

how many unique structure known capsule e. coli

A

60

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123
Q

serotypes of E. coli are another example of

A

antigenic variation

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124
Q

leading disease-causing stereotype of E. coli

A

E. coli O157 : H7

and K antigen does not matter in this case

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125
Q

O antigen is

A

Oligosaccharides, somatic `

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126
Q

E. coli, being negative…. have

A

many fimbriae

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127
Q

most important type of fimbriae that E. coli have

A

type I fimbriae

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128
Q

type 1 fimbriae

A

ecspecially sticky to cells that line the small intestine and/or bladder

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129
Q

type 1 fimbriae allow

A

bacteria to stick to cells that line the small intestine and/or bladder

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130
Q

once E.coli sticks to cells that line the small intestine and/or bladder

A

secrete an exotoxin

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131
Q

which exotoxins would E.coli secrete once attached to cells that line small intestine and or bladder

A

LT, STa, or STb

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132
Q

E.coli secreting exotoxins LT, STa, or STb»» would

A

increase levels of cGMP in the intestine

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133
Q

when levels of cGMP are increased in the intesine by E coli

A
  • stopping water absorption in the intestines,

- leaving more fluid in the intestinal lumen and triggering diarrhea.

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134
Q

one dominant virulence factor of very bad E coli

A

Stx

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135
Q

Stx

A

shiga toxin

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136
Q

Virulent E. coli express that shiga toxins

A

Stx1 or Stx2

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137
Q

Stx2 compared to Stx1

A

400 times as potentt

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138
Q

what an exotoxin agin???

A

secreted proteins

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139
Q

what do Stxs first do when release

A

receptors on human intestinal endothelial cells to enter the cells

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140
Q

the receptors on intestinal endothelial cells that Stxs bind to

A

NOT FOUND IN ANIMALS

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141
Q

since the the receptors on intestinal endothelial cells that Stxs bind to are not found in animals

A

allows virulent strains to grow in animals harmlessly before humans consume them

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142
Q

when shiga toxin enters human intestinal endothelial

A

one part of a shiga toxin binds to and cleaves an important part of ribosomes in those endothelial cells, halts function

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143
Q

if endothelial cells have no functioning ribosomes

A

no proteins»> cell death

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144
Q

what receptors do shiga toxins bind to….maybe

A

GB3

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145
Q

most dangerous E. coli strains like O157 : H7 are called

A

enterohemorrhagic

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146
Q

what does it mean to be enterohemorrhagic

A

disrupt the GI tract and cause hemorrhage (bleeding)

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147
Q

what sometimes causes E. coli to be enterohemorrhagic

A

cell death from Shiga toxin

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148
Q

other times, what causes E. coli to be enterohemorrhagic

A

protein enterohemolysin

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149
Q

enterohemolysin

A

breaks apart blood, only acts in intestines

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150
Q

REALLY BAD E. COLI STRAINS

A

can carry both the genes for a Shiga toxin and enterohemolysin

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151
Q

some E. coli strains re linked to what syndrome

A

hemolytic uremic syndrome

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152
Q

in hemolytic uremic syndrome there is

A

broken down blood (from hemolysins) and/or tissue (from shiga toxins

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153
Q

hemolytic uremic syndrome broken down blood and or tissue leads too

A

mini-clots forming, traveling, and eventually and clogging capillaries

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154
Q

clots from hemolytic uremic syndrome

A

clots spread through the body usually have the biggest impact on kidneys

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155
Q

clots from hemolytic uremic syndrome effect on kidneys

A

begin to fail and die

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156
Q

end result of hemolytic uremic syndrome

A

blood in the urine that onsets 5-10 days after initial E. coli onset

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157
Q

E. coli causes what % of UTIs

A

85%

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158
Q

in UTIs caused by E. coli, bacteria

A

get into the urinary tract

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159
Q

when E. coli enters the urinary tract…

A

problems begin if they hit the bladder

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160
Q

E. coli in the urinary tract can move even

A

further upstream to the ureters or kidneys

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161
Q

symptoms of UTI caused by E. coli

A
  • strong urge to urinate
  • unproductive urination
  • cloudy urine
162
Q

treatment E. coli

A

antibiotics.. but resistance is becoming a problem…

163
Q

myocobacterium genus gram

A

?

164
Q

myocobacterium shape

A

long skinny bacilli

165
Q

myocobacterium relationship with oxygen

A

obligate aerobes

166
Q

myocobacterium spores

A

don’t form them

167
Q

myocobacterium flagella

A

aflagellate

168
Q

myocobacterium temp

A

mesophilic

169
Q

aflagellate

A

no flagella

170
Q

myocobacterium generation time

A

SLOW … hard to culture

171
Q

myocobacterium PARASITE??!!

A

obligate parasites

172
Q

obligate parasites

A

can only grow in humans

173
Q

M. leprae cannot even be cultured unless

A

human macrophages are plated with it

174
Q

since Mycobacterium species are not categorized as gram positive or gram negative

A

called acid-fast

175
Q

acid-fast

A

that all initial dyes are retained instead of washed away

176
Q

acid-fast means gram stain

A

bad idea sis

177
Q

Mycobacteria cell wall

A

thick and waxy, composed of mycolic acid

178
Q

mycolic acid

A

lipid-like compound which holds in dyes

179
Q

mycolic acid is the

A

primary virulence factor of mycobacteria

180
Q

why is Mycolic acid is also the primary virulence factor of Mycobacteria

A

because it stops phagosome/lysosome fusion.

181
Q

most clinically relevant mycobacterium species

A

Mycobacterium tuberculosis

182
Q

Mycobacterium tuberculosis where does it infect

A

many places, most commonly the lungs

183
Q

what percentage of Mycobacterium tuberculosis infections are in the lungs

A

90% ish

184
Q

why are most tuberculosis infections in the lungs

A

bacterial dependence on oxygen

185
Q

how much of population has a tuberculosis infection (TB)

A

1/3

186
Q

tuberculosis infections can be categorized as

A

-latent infection

active infection

187
Q

latent infection of TB is

A

LTBI

188
Q

active infection of TB is

A

ATBI

189
Q

latent tuberculosis infection

A
  • bacteria have colonized but do not cause obvious symptoms

- maybe people never progress beyond this stage.

190
Q

active tuberculosis infection

A

Only about 10% of people with LTBI will develop ATBI (unless HIV-positiv

191
Q

mortality rate if ATBI

A

over 50% if not treated

192
Q

spread of TB is

A

entirely human to human

193
Q

how is TB PASSED

A

aerosols from:

  • speaking
  • singing
  • coughing
  • sneezing
194
Q

one sneeze from TB person

A

40,000 droplets

195
Q

infections dose of TB

A

SMALL»> only 10 bacteria

196
Q

TB is the ___ cause of death

A

2nd, to HIV»> NOW IT 1 DOE

197
Q

how much of US population tests positive

A

5-10%

198
Q

in some Asian and African countries, TB rates can be as high as

A

80%

199
Q

to work at a healthcare facility….. a person in the US must pass

A

PPD test

200
Q

PPD test

A

purified protein derivative test

201
Q

what happens in PPD test

A

mall amounts of M. tuberculosis antigens are injected to see if the body reacts and forms a bump

202
Q

if PPD test is positive

A

you must go through extra testing to ensure you will not pass your TB on to patients`

203
Q

after initial infection of TB symptoms

A

flu-like symptoms

204
Q

f TB progresses to ATBI, the predominant symptoms will be:

A
  • chest pain
  • night sweats/fever
  • persistent (3+ week) and productive cough
  • weight loss
  • loss of appetite
205
Q

where can M. tuberculosis survive

A

inside the phagosome of a macrophage

206
Q

why can M. tuberculosis can survive inside the phagosome of a macrophage

A

mycolic acid coat prevents destruction by lysosom

207
Q

mycolic acid cause the M. tuberculosis in the phagosome to

A

reproduces until it eventually kills the host macrophage.

208
Q

what happens after M. tuberculosis kills the macrophage

A

more macrophages come, consume the dead ones, and fuse their contents together.

209
Q

cycle of M. tuberculosis growth

A

repeats and repeats until formation of Langhans giant cell

210
Q

Langhans giant cell

A

giant, multinucleate cell called a Langhans

211
Q

A Langhans giant cell is a multinucleate cell with a

A

characteristic horseshoe shape

212
Q

after the formation of a Langhans giant cell by M. tuberculosis in macrophages the response is

A

large cellular mass»»> granuloma

213
Q

granuloma (TB)

A

a layer of T cells, B cells, and calcium

214
Q

(TB)when there is granuloma it is

A

is a latent infection (LTBI)

215
Q

in many cases, the granuloma *TB)

A

holds the bacteria for life (YAY)

216
Q

sometimes the granuloma (TB)

A

liquifies and the bacteria escape

217
Q

if the M. tuberculosis stay in the lungs after escaping the granuloma

A

causes ABTI

218
Q

if M. tuberculosis invade bloodstream after escaping granuoma

A

miliary tuberculosis

219
Q

miliary tuberculosis

A

granulomas forming across the body

220
Q

miliary tuberculosis ends in

A

death if untreated

221
Q

tuberculosis treatment

A

antibiotics

222
Q

tuberculosis antibiotic treatment length

A

minimum of six months of multi-antibiotic treatment to clear all granulomas

223
Q

many people with TB in developping countries

A

do not complete their antibiotic courses

224
Q

result of people in developping countries not completing TB treatment

A
  • MDR-TB

- XDR-TB

225
Q

MDR-TB

A

multi-drug resistant TB

226
Q

XDR-TB

A

extensively-drug resistant TB

227
Q

how much to clear regular TB

A

$440

228
Q

treatment for MDR-TB

A

140, 000

229
Q

treatment XDR-TB

A

430,000

230
Q

what causes leprosy

A

Mycobacterium leprae

231
Q

leprosy other name

A

Hansen’s disease

232
Q

leprosy is in BIBLE

A

but is rare, lepers were probs people with bacterial or fungal skin infections

233
Q

leprosy comes from

A

granulomas in the connective tissue below the skin or nerve cells

234
Q

granulomas in the connective tissue below the skin causes

A

boils

235
Q

granulomas in nerve cells

A

neurodegeneration

236
Q

leprosy latency period

A

LONG AF….. long as 20 years

237
Q

about how many people with leprosy develop symptoms

A

5%

238
Q

primary symptoms of leprosy

A

lumps on the skin

239
Q

if leprosy hits active form……

A

sheds original granulosas and colonize Schwann cells

240
Q

which Schwann cells do M. leprae colonize

A

Schwann cells wrapped around axons of neurons

241
Q

resulting damage from leprosy sheding their original granulosas and colonizing Schwann cells wrapped around the axons of neurons

A

resulting damage and inflammation»> irreversible nerve damage»» death

242
Q

M. leprae spreads much better in parts of the body

A

with lower temperatures

243
Q

places where M. leprae spreads good

A

eyebrows, face, fingers, elbows, and scrotum

244
Q

It is thought that M. leprae underwent

A

reverse zoonosis

245
Q

reverse zoonosis M. leprae

A

from humans to armadillos

246
Q

why did leprosy go to armadillos

A

ow body temperature made them excellent reservoirs for leprosy`

247
Q

armadillos

A

now probably pass leprosy back to humans

248
Q

what causes chlamydia

A

chlamydia trachomatis

249
Q

what causes trachoma

A

chlamydia trachomatis

250
Q

what causes Gonorrhea

A

Neisseria gonorrhoeae

251
Q

what causes Syphilis

A

Treponema pallidum

252
Q

gram stain Chlamydia trachomatis

A

negative, no peptidoglycan

253
Q

gram stain Neisseria gonorrhoeae

A

negative

254
Q

gram stain Treponema pallidum

A

negative, no LPS

255
Q

size Chlamydia trachomatis

A

.3 micrometers

256
Q

size Neisseria gonorrhoeae

A

.6-1.0 micrometers

257
Q

size Treponema pallidum

A

5-15 micrometers

258
Q

morphology Chlamydia trachomatis

A

coccoid

259
Q

coccoid

A

elongated sphere

260
Q

morphology Neisseria gonorrhoeae

A

diplococci

261
Q

morphology Treponema pallidum

A

spirochete

262
Q

spirochete

A

spiral

263
Q

what is the most common STD

A

C. trachomatis (chlamydia)

264
Q

how many reported cases of chlamydia reported daily

A

100 million +

265
Q

how many US cases of chlamydia in 2015

A

1.5 million

266
Q

why does chlamydia spread so easily …..

A

75% of infected females
50% of infected men
are……ASYMPTOMATIC BUT CONTAGIOUS

267
Q

why is c. trachomatis an interesting species

A

gram-negative ISH

268
Q

why is C. trachomatis gram-negative ISH

A

no peptidoglycan at all

269
Q

why does it mean if there is no peptidoglycan at all in C. trachomatis

A

peptidoglycan-targeting antibiotics will not work

270
Q

how many serotypes of chlamydia exist

A

at least 15

271
Q

what does it mean if chlamydia has many serotypes

A

you can get it over and over again

272
Q

C. trachomatis can be described as an

A

obligate intracellular parasite

273
Q

why is C. trachomatis an obligate intracellular parasite

A

it can only grow inside human cells because it cannot produce its own ATP

274
Q

what does C. trachomatis usually target

A

epithelial cells in the urinary tract or conjunctiva

275
Q

conjunctiva

A

inner surface of eyelids

276
Q

in infants, when inhaled, C. trachomatis can cause

A

pneumonia

277
Q

does C. trachomatis invade WBCs

A

no

278
Q

two forms C. trachomatis comes in

A
  • reticulate body

- elementary body

279
Q

reticulate body C. trachomatis

A

larger, less dense, divides quickly

280
Q

elementary body C. trachomatis

A

small and dense, acts like an exposure

281
Q

elementary bodies of C. trachomatis are very very

A

very hardy, very small

282
Q

smallest elementary body of C. trachomatis

A

(small as .25 micrometers)

283
Q

like exospores, elementary body of C. trachomatis can

A
  • survive harsh external conditions

- form back into a reticulate body after invading cell

284
Q

in females, C. trachomatis infections begin

A

in the cervix, cause

  • pain
  • fever
  • abnormal menstruation
  • discharge
285
Q

if C. trachomatis goes untreated, (in females)

A

can spread, move far up the reproductive tract and cause inflammation

286
Q

in what percentage of cases do C. trachomatis in females do they move very far up the reproductive tract and cause inflammation

A

40 % of cases

287
Q

when C. trachomatis bacteria moves up the reproductive tract and causes inflammation it is called

A

PID

288
Q

PID

A

pelvic inflammatory disease

289
Q

symptoms of PID vary from

A

none to severe

290
Q

women with extensive PID can develop

A
  • infertility (20%)

- high risk of ectopic pregnancy for life (9%)

291
Q

ectopic pregnancy

A

when a fertilized zygote implants in the fallopian tube instead of the uterus and starts growing there

292
Q

leading cause of maternal death in pregnancy

A

ectopic pregnancy

293
Q

in most cases of chlamydia in men&raquo_space;>.

A

in infects the urethra

294
Q

if chlamydia in men goes untreated…. it can

A

spread to the testes, leading to inflammation

295
Q

if chlamydia in men spreads to the testes it can cause

A
  • random discharge
  • cloudy or painful urination
  • epididymitis
296
Q

epididymitis in men is

A

inflammation of the epididymis, causes sperm damage RARELY»> infertility

297
Q

why are men better at spreading chlamydia

A

it attaches to sperm, C. trachomatis is aflagellate

298
Q

rates of chlamydia are higher

A

much higher in women than men

299
Q

chlamydia infection in conjunctiva can be caused when

A

C. trachomatis travels from the reproductive tract to eye, or eye to eye

300
Q

result of C. trachomatis in the eye

A

swelling of the eyelid called trachoma

301
Q

trachoma from C. trachomatis slowly

A

scratches the cornea of the eye

302
Q

trachoma and it scratching the cornea leads to

A
  • permanent vision problems

- sometimes blindness

303
Q

tracho is the number 1

A

number 1 cause of blindness in the world

304
Q

trachoma is estimated to be responsible for how many cases of blindness worlwide

A

1.3 million and 8 million

305
Q

when does WHO hope to eradicate trachoma

A

by 2020

306
Q

life cycle

A

EB attaches, enters» becomes RB»> binary fission»» reorganize to EBs, lysis and release of EBs» Attachment

307
Q

gonorrhea is commonly called

A
  • the clap

- sometimes gonorrhoea

308
Q

gonorrhea is caused by

A

N. gonorrhoeae

309
Q

Gonorrhea is a close second for

A

most common STD in the world, still 100 million + cases a year

310
Q

Gonorrhea in USA,

A

less common , 400,000 cases a year

311
Q

is gonorrhea spread easily

A

YES

312
Q

how many females infected with gonorrhea are asymptomatic

A

80% asymptomatic

313
Q

how many males infected with gonorrhea are asymptomatic

A

10% asymptomatic

314
Q

what are N. gonorrhoeae’s main for the immune system

A

their pili

315
Q

… N. gonorrhoeae have how many different pili observed indifferent serotypes

A

over 1 million

316
Q

since N. gonorrhoeae have many pili observed in different serotypes

A

you can get reinfected a LOT

317
Q

infection of N. gonorrhoeae is often called

A

gonococcal infection

318
Q

facultative intracellular pathogens are

A

like living inside host epithelial cells, but can survive outside as well

319
Q

does N. gonorrhoeae invade WBCs

A

no (…maybe sometimes)

320
Q

in the first step of invasion, N. gonorrhoeae uses

A

type IV fimbriae to pull bacteria towards epithelial cells

321
Q

N. gonorrhoeae use type IV fimbriae to pull bacteria towards epithelial cells in the

A
  • reproductive tract
  • rectum
  • eyes
  • parts of pharynx
322
Q

in the first step of invasion, N. gonorrhoeae uses _______ to stop

A

uses proteases and mucinases to stop mucus along the cells from breaking them down

323
Q

once N. gonorrhoeae arrive at epithelial cells

A

use endocytosis to pass into epithelial cells

324
Q

once N. gonorrhoeae enters the epithelial cells, some bacteria

A
  • lie dormant and grow

- or pass through the bottom of the epithelial cell deeper into the body

325
Q

what comes to kill N. gonorrhoeae

A

neutrophils, nut most are repelled

326
Q

because neutrophils aren’t working….to kill N gonorrhoeae

A

the body send more to an area, resulting in lots of pus

327
Q

LPS in gonorrhea

A

also causes inflammation

328
Q

N. gonorrhoeae infections very closely

A

resemble C. trachomatis infections

329
Q

symptoms of N. gonorrhoeae and chlamydia (women)

A

are the same, both can cause PID if travel to far in reproductive system

330
Q

PID from both Gonorrhea and chlamydia

A

can lead to infertility or ectopic pregnancy

331
Q

one big difference of symptoms of gonorrhea and chlamydia

A

how fast it is

332
Q

gonorrhea onsets within how many days of sex

A

2-5 DAYS

333
Q

chlamydia infections onsts within how long after sex

A

1-3 WEEKS

334
Q

how to tell chlamydia and gonorrhea apart

A

swap then culture

335
Q

gonorrhea and chlamydia pathologies in males

A

nearly the same , gonorrhea onsets faster

336
Q

gonorrhea symptoms in males

A

almost always shows them

337
Q

most notable symptoms of gonorrhea in males

A

discharge of a mixture of mucus and pus

338
Q

because of its symptoms, gonorrhea in men almost always gets

A

treated before it moves deeper in the tract

339
Q

if gonorrhea in men moves further in the tract

A

can also cause epididymitis

340
Q

very important (gonorrhea?) to distinguish

A

epididymitis from testicular torsion

341
Q

testicular torsion

A

a twisting of the testes leading to immediate ischemia and necrosis thereafte

342
Q

ischemia

A

not enough blood to tissues

343
Q

testicular torsion

A

similar symptoms, but is considered a medical emergency

344
Q

testicular torsion is NOT

A

not bacterial

345
Q

N. gonorrhea in the eye

A
  • symptoms are less severe than chlamydia

- pink eye

346
Q

Gonorrhea that enters the bloodstream

A

latches onto joints and causes gonococcal arthritis

347
Q

gonococcal arthritis

A

most common type in juveniles and young adults,

in 5-10% of gonorrhea infections

348
Q

gonococcal arthritis symptoms

A

include pain and swelling, usually subside once treated w/ antibiotics

349
Q

gonococcal arthritis may require

A

drainage

350
Q

Treponema

A

genus of disease causing bacteria many species

351
Q

most significant species of Treponema

A

Treponema pallidum

352
Q

Treponema pallidum can be broken

A

into 4 subspecies

353
Q

what subspecies of Treponema pallidum causes syphilis

A

T. pallidum, subspecies pallidum

354
Q

other Treponema pallidum subsidies cause

A

rare skin diseases

355
Q

Treponema bacteria are gram and shapes

A

gram-negative (ish)spirochetes, spiral shaped

356
Q

Treponema bacteria are gram-negative ish because

A

they do not have LPS like others

357
Q

T. pallidum cannot be cultured , no obvious

A

without human cells, no obvious virulence factors

358
Q

four stages of syphilis

A
  • primary
  • secondary
  • latent
  • tertiary
359
Q

which stages of syphilis are contagious

A

primary, secondary, tertiary

360
Q

primary syphilis

A

3-5 days after expsosure

361
Q

secondary syphilis

A

6-24 weeks after exposure

362
Q

latent syphilis

A

no outward symptoms for 1-45 years

363
Q

tertiary syphilis

A

Rarely progresses this far

364
Q

tertiary syphilis is less than what % of cases

A

less than 30% and only when it goes untreated w/antibiotics)

365
Q

only symptoms primary syphilis

A

formation of a chancre or multiple chancres

366
Q

chancre (syphilis)

A

painless wart-like lesions where the bacteria are burrowed inside

367
Q

where do chancres occur» ON THE

A

ON THE

  • penis
  • vagina
  • anus
368
Q

where do chancres occur INSIDE THE `

A

INSIDE THE

  • mouth
  • cervix
  • anus
369
Q

chancres are EXTREMELY

A

extremely contagious

370
Q

chancres usually subside

A

within 2 months

371
Q

secondary syphilis comes from when the

A

bacteria enter the blood stream

372
Q

when T. pallidum, subspecies pallidum enters the bloodstream

A

attach throughout the body and cause a variety of symptoms

373
Q

secondary syphilis is difficult to

A

tricky to diagnose because the symptoms are so varied and widespread

374
Q

syphilis is often called

A

the great imitator

375
Q

in latent syphilis the body slowly

A

develops more and more B- and T- cells to fight off T. pallidum

376
Q

eventually, in latent syphillis, the B cells and T cells are

A

ble to keep the infection at bay.

377
Q

during latent syphilis, since the infection has

A

has spread to practically all body structures, it is still present in the body but dormant

378
Q

during latent syphilis, each time the infection “breaks ou”

A

typically tackled quickly and no symptoms develop

379
Q

why is the latent stage of syphilis latent

A

body has the infection under control (although not cleared).

380
Q

many cases of latent stage syphilis

A

do not progress

381
Q

people in latent syphilis

A

not contagious

382
Q

what usually causes a persons immune system to weaken when they have syphilis

A

aging or HIV

383
Q

if a persons immune system with latent syphilis weakens

A

progress into tertiary syphilis

384
Q

tertiary syphilis usually presents as

A

gummata

385
Q

singular gummata

A

gumma

386
Q

what are gummata

A

type of ineffective granuloma formed by the immune system

387
Q

in the tertiary stage, gummata can form almost

A

almost anywhere in the body

-depends on where the bacteria are replicating

388
Q

gummata are VERY

A

very contagious

389
Q

tertiary syphilis often damages the

A

walls of blood vessels, causing aneurysm and eventually hemorrhage

390
Q

aneurysm

A

weakening of vessel

391
Q

hemorrhage

A

rupture of vessel

392
Q

tertiary stage syphilis can damage blood vessels running to

A

the brain or other organs

393
Q

if tertiary syphilis damages blood vessels running to the brain

A

impaired mental function

394
Q

impaired mental function

A

causes organ necrosis

395
Q

most sever and common form of damage to walls from tertiary stage syphilis

A

damage of the wall of the aorta, causes aortic swelling

396
Q

if tertiary syphilis damages of the wall of the aorta, causes aortic swelling

A

eventually lead to aortic rupture

397
Q

tertiary syphilis can cause the aorta to

A

SWELL

398
Q

chladmydia , gonorrhea , syphilis are treated by

A

antibiotics, becoming resistant :(

399
Q

what is T. pallidum becoming resistant to

A

azithromycin

400
Q

what is gonorrhea becoming resistant to

A

cipro

401
Q

chlamydia is becoming resistant to

A

multiple drugs

pathophysiology (24 decks)

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