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pathophysiology > yersinia and strep > Flashcards

yersinia and strep Flashcards

1
Q

Yersinia types

A

Y. enterocolitica

Y. pestis

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2
Q

Bacteria in Yersinia genus

A

gram-negative bacilli

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3
Q

Yersinia bacteria are

A

facultative anaerobes

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4
Q

Y. enterocolitica main idea

A

causes food poisoning and mimics appendicitis

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5
Q

Y. pestis main idea

A

causes plague

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6
Q

Yersinia is able to divide quickly

A

at temps as low at -2 degrees C

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7
Q

Yersinia is able to contaminate

A

contaminate refrigerated samples

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8
Q

Yersinia bacteria are also…..

A

zoonotic

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9
Q

zoonotic

A

normal hosts are other animals

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10
Q

examples of host of Yersinia

A

RATS, rabbits, prairie dogs, squirrels, chipmunks

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11
Q

Yersinia loves

A

iron

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12
Q

since yersinia loves iron it’s classified as

A

siderophilic

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13
Q

who are most succptible to Yersinia infections

A

people with hemochromatosis

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14
Q

hemochromatosis

A

high iron levels

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15
Q

what is the most common contaminant of blood transfusions

A

Y. enterocolitica

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16
Q

how many samples of blood are contaminated with Y. enterocolitica

A

1 in 1 million

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17
Q

people who receive a blood sample contaminated with Y. enterocolitica

A

quickly enter septic shock, mortality rate over 50%

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18
Q

Because Y. enterocolitica is gram-negative,

A

it has endotoxin (LPS)

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19
Q

prescence of LPS from Y. enterocolitica in the bloodstream causes

A

widespread inflammation, strong immune reaction

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20
Q

symptoms of blood transfusion with Y. enterocolitica

A

hypotension, fever, shivering

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21
Q

symptoms of blood transfusion with Y. enterocolitica set in

A

within 3 hours of transfusion

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22
Q

why is food contaminated with Y. enterocolitica

A

because of urine or feces of rats

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23
Q

once food contaminated with Y. enterocolitica is eaten

A

bacteria get eaten by macrophages, but cannot be destroyed

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24
Q

when Y. enterocolitica can’t be destroyed by macrophages

A

macrophages unknowingly carry bacteria to Peyer’s patches of the small intestine

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25
Q

Peyer’s patches

A

lymph-like regions of the small intestine.

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26
Q

digested material passes through the Peyer’s patches

A

passes through them and must pass through many macrophages and dendritic cells.

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27
Q

Peyer’s patches are like

A

surveillance system for food and drink… or a breeding ground for Y. enterocolitica

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28
Q

when macrophages carry Y. enterocolitica to Peyer’s patches

A

Bacteria grow and “arm” themselves, then eventually pop out, ready for a bigger war

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29
Q

when macrophages carry Y. enterocolitica to Peyer’s patches ……….. and arm and grow and attack

A

causes swelling and inflammation that mimics that of appendicitis

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30
Q

Y. enterocolitica colonies produce

A

yst toxin

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31
Q

what does yst toxin do

A

binds to receptors on cells in the GI tract

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32
Q

when yst toxin binds to receptors on cells in the GI tract

A

causes intestines to secrete more cGMP

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33
Q

cGMP

A

cyclic guanosine monophosphate

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34
Q

when intestines to secrete more cGMP

A

channels that absorb water from the small intestine slam shut

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35
Q

Result of intestines to secrete more cGMP and channels that are responsible for absorbing water from the small intestine slam shut

A

extra water in the GI tract, which leads to diarrhea

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36
Q

what accompanies diarrhea when channels that absorb water from the small intestine slam shut

A

abdominal pain, fever and sometimes…vomiting

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37
Q

Y. enterocolitica food poisoning is also sometimes associated with

A

erythema nodosum

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38
Q

erythema nodosum comes from

A

an exaggerated and delayed immune response to a Yersinia antigen

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39
Q

erythema nodosum

A

splotchy patches usually confined to fatty tissue in the legs

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40
Q

Yersinia pestis has identified

A

as the causative agent of the european plague outbreaks

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41
Q

outbreak of Yersinia pestis often called

A

bubonic plague

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42
Q

3 ways Y. pestis an infect

A
  • bubonic plaque
  • pneumonic plague
  • septicemic plague
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43
Q

bubonic plague

A

Flea bite or other vector bite permits bacterial entry to the body

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44
Q

bubonic plague death rate w/ o treatment

A

75%

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45
Q

pneumonic plague

A

bacteria are inhaled through droplets and enter lungs

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46
Q

pneumonic plague mortality rate without treatment

A

99%

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47
Q

septicemic plague

A

Y. pestis bacteria enter bloodstream, usually through open wound

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48
Q

septicemic plague mortality rate w/o treatment

A

99%

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49
Q

Y. pestis forms a ____ in the _______

A

forms a biofilm in the gut of the oriental rat flea

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50
Q

when Y. pestis forms a biofilm in the gut of the oriental rat flea

A

causes a small amount of bacteria to be regurgitated with each bite

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51
Q

Aside from biofilm formation Y. pestis does not

A

does not harm the flea

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52
Q

1894

A

outbreak of plague struck southern China

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53
Q

who cam to investigate outbreak of the plague in china

A

Shibasaburo Kitasato from JAPAN

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54
Q

who cam to investigate theh plague inchina 3 days later

A

Alexandre Yersin

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55
Q

what did Kitasato examine

A

the organs and blood of dead bodies and jndentified an unknown microbe

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56
Q

what did Kitasato do with the microbe to test it

A

isolated it, put it in rats, and quickly saw rats die.

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57
Q

what happened to the lymph nodes of rats with the bacteria

A

lymph nodes of the rats were overwhelmed with the same bacteria.

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58
Q

what did kitasato do with the bacteria he teste

A

took slides to london to be published…. but they WERE MESSEY

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59
Q

Kitasato messy slides were

A

contaminated w other bacteria

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60
Q

Yersin got access…

A

to cadavers for his own research&raquo_space;> SHADY

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61
Q

with his cadavers Yersin was able to

A

produce a purer slide 6 days later&raquo_space;> credited with the discovery of the bacillus»»YERSIN-ia.

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62
Q

black plague

A
  • most infamous world crisis of infection

- cutting population of europe in HALF during 1300s

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63
Q

main waves of Y. pestis

A

Justinian plague
Black Death
Third Wave

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64
Q

Justinian plague

A

600s– killed 40% of population of Constantinople

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65
Q

Black death.

A

mid 1300s killed half of europe’s population

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66
Q

Third Wave

A

late 1800s in southern china and india… killed 12 million before vaccine discovered

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67
Q

After a bit, Y. Pestis is able to grab onto _______

A

extracellular collagen with the help of pla protein

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68
Q

pla (PESTIS)

A

plasminogen activator

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69
Q

pla converts

A

host cell plasminogen into plasmin

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70
Q

what does plasmin do

A

break apart fibrin tissues in clots

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71
Q

by breaking up fibrin……. the plague

A

the plague is able to invade into further tissue

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72
Q

when is Yersinia killed by the body

A

phagocytosed by neutrophils

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73
Q

what is usallly NOT recruited to fight Yersinia

A

dendritic cells

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74
Q

Yersinia is NOT KILLED

A

not killed by macrophages

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75
Q

what happens when Yersinia is eaten by macrophage

A

waits inside the phagosome, using it as an “oven” to “cook” many proteins that will help it invade the human» POPS OUT

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76
Q

when Y. pestis pops out of a macrophage

A

shifts gears completely

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77
Q

when Y. pestis pops out of a macrophage and shifts gears it STOPS

A

creating the proteins that protected it from a phagosome

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78
Q

when Y. pestis pops out of a macrophage and shifts gears it STARTS

A

produces different anti-phagocytic proteins so the new bacteria can’t be eaten

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79
Q

what anti-phagocytic proteins does Y.pestis produce after shifting gears

A

yops

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80
Q

yops

A

Yersinia outer proteins

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81
Q

when Y. pestis shifts gears it eneters

A

antiphagocytic mode

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82
Q

when Y. pestis is in antiphagocytic mode

A

multiplies rapidly in the lymph nodes and causes the formation of a bubo or many buboes

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83
Q

buboes

A

hugely inflamed lymph nodes.

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84
Q

once Y. pestis is in the lymph nodes

A

eventually can make it into the blood

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85
Q

once Y. pestis is in the blood

A

secretes endotoxins that lead to the formation of many tiny blood clots

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86
Q

when Y. pestis secretes endotoxins that lead to the formation of many tiny blood clots it is called

A

DIC

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87
Q

DIC

A

disseminated intravascular coagulation

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88
Q

what does DIC do

A
  • cuts off circulation to extremities(further away parts)

- results in acral necrosis

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89
Q

acral necrosis

A

a blackening of tissue especially in fingers and toes.

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90
Q

why is black plague the name

A

acral necrosis

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91
Q

eventually, the tiny blood cots caused by Y. Pestis releasing endotoxins in the blood

A

cut circulation to organs and DEATH

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92
Q

plague is treated with

A

antibiotics… miniscule mortality rate if treated early

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93
Q

RED ALERT PLAGUE

A

Antibiotic-resistant strain of Y. pestis found in Madagascar

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94
Q

Streptococcus bacteria

A

gram-positive cocci

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95
Q

how many species in the Streptococcus genus

A

at least 37

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96
Q

how many species of Streptococcus can be pathogenic in humans

A

5 in immunocompetent humas

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97
Q

ALL STREP BACTERIA

A

obligate parasites of human mucosa

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98
Q

what does it mean to be .a obligate parasites of human mucosa

A

can’t reproduce without finding a host

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99
Q

biggest three species Streptococcus

A

S. pyogenes, S. agalactiae, S. pneumoniae

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100
Q

S. pyogenes gist

A

strep throat and much more

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101
Q

S. agalactiae

A

Infant pneumonia and meningitis

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102
Q

S. penumoniae

A

Pneumonia, ear infection, sinus infection, meningitis

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103
Q

first tests to diminish the many gram-positive cocci

A

coagulase and catalase tests

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104
Q

for species that both turn up _____ on coagulase and catalase tests

A

both turn up negative: series of tests for surface antigens devised

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105
Q

series of tests for surface antigens of gram-positive cocci that is negative on coagulase and catalase tests DEVISED BY

A

Rebecca Lacefield

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106
Q

Rebecca Lancefield breaks bacteria into what groups

A

Lancefield groups

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107
Q

Easier to examine virulence factors of Streptococcus bacteria by

A

examining whole group rather than species by species

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108
Q

what Lancefield groups exist

A

groups A-V

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109
Q

do all strep bacteria fit into one Lancefield group

A

NO

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110
Q

clinically relevant Strep bacteria fall in what Lancefield group

A

group A or B or cannot be grouped

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111
Q

Hemolysis S. pyogenes

A

Beta

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112
Q

Hemolysis S. agalactiae

A

Beta

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113
Q

Hemolysis S. pneumoniae

A

Alpha

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114
Q

Lancefield group S. pyogenes

A

Group A

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115
Q

Lancefield group S. agalactiae

A

Group B

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116
Q

Lancefield group S. pneumoniae

A

NO GROUP

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117
Q

Disease Associated w/ group A strep

A
  • Strep Throat (Pharyngitis)
  • Impetigo
  • Scarlet Fever
  • Cellulitis
  • Pneumonia
  • Streptococcal TSS
  • Necrotizing Fasciitis
  • Rheumatic Fever
  • PANDAS?

BRUH

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118
Q

main virulence factor in group A strep

A

membrane protein M protein

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119
Q

M protein extends

A

from the membrane beyond cell surface

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120
Q

M protein allows

A

S. pyogenes to avoid phagocytosis by neutrophils and macrophages

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121
Q

M protein ALSOOOO

A

stops antibody binding

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122
Q

M protein binds to

A

human fibrinogen, giving it a camouflage

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123
Q

when the M protein binds to human fibrinogen…..

A

only a small bit protrudes beyond this

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124
Q

how many unique M protein structures have been observed

A

over 100

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125
Q

to beat strep (M proteins)

A

body has to produce antibodies that bind to a particular strain of M protein’s tip

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126
Q

many different M protein structures is an example of……

A

ANTIGENIC VARIATION

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127
Q

rheumatic fever

A

severe condition associated w/ S. pyogenes infections

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128
Q

Rhematic fever usually develops how long after the initial infection

A

2-4 weels

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129
Q

Regions of the M protein have……………

A

amino acid sequence very similar to cardiac myosin

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130
Q

because regions of M protein have amino acid sequence very similar to cardiac myosin

A

antibodies fighting the infection can wrongly recognize heart muscle as bad guy

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131
Q

Role of M protein in rheumatic fever first 2

A
  • colonization of throat» severe inflammation

- M protein enters bloodstream and elicits antibody response

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132
Q

Role of M protein in rheumatic fever after elicitign antibody response

A
  • antibodies-cross react with heart tissue

- autoimmune response damages heart valves

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133
Q

more virulence factors in group A Strep

A
  • M-like protein
  • Hyaluronidase
  • MSCRAMMs
  • SPEs
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134
Q

M-like protein

A

surface protein that grabs Fc region of random antibodies and holds them

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135
Q

purpose of M-like protein

A

camouflage

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136
Q

Hyaluronidase

A

breaks down hyaluronic acid,&raquo_space; increase spread of bacteria through body

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137
Q

MSCRAMMs

A

Promote attachment to epithelium

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138
Q

SPEs

A

Streptococcal pyrogenic exotoxins

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139
Q

SPEs are different ….

A

Different strains release different exotoxins

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140
Q

ranges of SPEs

A

SpeA to SpeJ

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141
Q

the TYPES OF SPEs we need to know

A

SpeA

SpeB

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142
Q

SpeA

A

in the blood can lead to STSS (Streptococcal toxic shock syndrome)

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143
Q

STSS

A

Streptococcal toxic shock syndrome

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144
Q

SpeA is a ….

A

SUPERANTIGEN

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145
Q

SpeB

A

cuts many proteins like fibronectin

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146
Q

fibronectin

A

extracellular protein that connects collagens

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147
Q

result of SpeB cutting fibronectin

A

This leads to breakdown of skin in the area

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148
Q

result of SpeB cutting fibronectin&raquo_space;> but the infection is superficial»>

A

redness

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149
Q

result of SpeB cutting fibronectin&raquo_space;> but the infection is DEEP&raquo_space;>

A

Necrotizing fasciitis

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150
Q

Necrotizing fasciitis

A

s an infection of the fascia, a deeper skin layer

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151
Q

if in Necrotizing fasciitis, the infection spreads through this layer ….

A

BAD THINGS HAPPEN

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152
Q

what is the main species of Group B strep

A

S. agalactiae

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153
Q

the bacteria of group B strep

A

do not typically infect humans

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154
Q

the bacteria of group B strep are a member of

A

the normal flora in about 20% of female vaginas.

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155
Q

do group B strep cause infection in the vagina…

A

NO, but is a risk of inhalation of a new born during child birth

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156
Q

because infants ______ inhalation of group B strep (S. agalactiae) can cause

A

have a weak immune system…. can lead to pneumonia and or meningitis

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157
Q

because of the risks of group B strep to infants preg woman should

A

be testes and be administered antibiotics before birth

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158
Q

S. pneumoniae is commonly found

A

in the pharynx of humans, is harmless there

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159
Q

S. pneumoniae can do bad things when

A

go other places

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160
Q

S. pneumoniae can cause…… BRUH

A

ear infection
sinus infection
pneumonia
brain infection

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161
Q

brain infection is ie

A

MENINgitis

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162
Q

usually the places that S. pneumoniae infects are

A

protected by cilia

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163
Q

S. pneumoniae infections are often a result of

A

previous infection that impedes cilia function

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164
Q

what are infectious diseases caused by

A

viruses, bacteria, fungi , parasites

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165
Q

most bacteria is not is not dangerous

A

yes

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166
Q

clinically significant

A

bacteria that are linked to disease

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167
Q

like other species, how are bacteria named

A

by binomial nomenclature

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168
Q

what is binomial nomenclature

A

two words: genus and species

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169
Q

typically many species for

A

for one genus

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170
Q

binomial nomenclature should always be

A

italicized in print

underlined in writing

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171
Q

first letter of genus in binomial nomenclature

A

capitalized

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172
Q

species name in binomial nomenclature

A

entirely lower case

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173
Q

there are often many species

A

in a genus

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174
Q

members of a species can _____ through

A

vary a lo through horizontal gene transfer

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175
Q

what is the genetic material of bacteria

A

one large circular chromosome… called plasmid

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176
Q

why are bacteria much harder to classify tan more complex species

A

horizontal gene transfer

177
Q

horizontal gene transfer

A

passing of DNA into bacteria

178
Q

three main ways of horizontal gene transfer

A

transformation
transduction
conjugation

179
Q

transformation

A

“naked” DNA is absorbed by bacterium and worked into its DNA

180
Q

transduction

A

DNA is injected by a bacteriophage

181
Q

bacteriophage

A

bacteria-infecting virus

182
Q

conjugation

A

DNA is spread from bacterium to bacterium through(cell to cell contact) sex pilus

183
Q

horizontal gene transfers caused there to be many

A

many strains of any species

184
Q

different strains of a species can be very unique…..

A

VERY unique

185
Q

in most cases of bacteria; inheriting just one gene will a grant a bacterium….

A
  • resistance to certain antibiotics
  • the ability to synthesize a new nutrient
  • or the ability cling to a new surface
186
Q

metric by which bacteria are classified

A
  • color
  • morphology
  • flagellation
  • staining
  • growth on various agars
  • oxygen dependence
  • other habitat preferences
  • spore formation
187
Q

how do we classify bacteria w color

A

bacteria secrete pigments or colored particles, they are sometimes fluorescent

188
Q

colors can also be used to identify

189
Q

classifying using morphology

A

classified with their shape

190
Q

(rounds) a circle

191
Q

two round circles

A

diplococci

192
Q

pill shape

A

coccobacilli

193
Q

rod-shaped

194
Q

two other shapes

A

curved and spiral

195
Q

in many cases the name of the genus comes from the

A

shape of the bacterium

196
Q

curved bacteria often called

197
Q

many bacteria have flagellation…

A

to help them move

198
Q

flagellation comes in what forms

A

monotrichous
lophotrichous
amphitrichous
peritrichous

199
Q

monotrichous

A

just one flagellum

200
Q

lophotrichous

A

just one “tuft” of flagella

201
Q

amphitrichous

A

having flagella on both sides

202
Q

peritrichous

A

surrounded by flagella

203
Q

flagella are made of what

204
Q

classifying with stain

A

results of gram stain

205
Q

on a gram stain purple

A

is a positive result

206
Q

what bacteria usually have a purple stain

A

bacteria have thick layers (usually 30-40 layers) of peptidoglycan

207
Q

on a gram stain pink

A

is a negative result

208
Q

what bacteria usually has a pink stain

A

bacteria usually have much thinner layers of peptidoglycan, as thin as 1-2layers

209
Q

some bacteria don’t stain with a gram stain

A

especially ones that grow in eukaryotic cells

210
Q

bacteria are grown in cultures on

211
Q

agar

A

gel-like substance

212
Q

agars can be packed with

A

various substances like antibiotics, nutrients, blood

213
Q

classifying with agars

A

depending on how they grow on those plates

214
Q

example of a special type of medium (agar)

A

blood agar

215
Q

blood agar

A

bacteria are plated with blood to see what happens

216
Q

things that can happen with blood agar

A

gamma hemolysis
alpha hemolysis
beta hemolysis

217
Q

gamma hemolysis

A

means that bacteria do not break blood

218
Q

alpha hemolysis

A

means that the bacteria partially break blood

219
Q

beta hemolysis

A

means that the bacteria fully break blood

220
Q

blood agar can be very

A

important diagnostic tool… especially for Streptococcus species

221
Q

oxygen is required

A

for human cells, not all bacteria

222
Q

when can oxygen be bad

A

when it forms toxic compounds such as peroxides or superoxides

223
Q

classifying with oxygen dependence

A

classified by their relationship

with oxygen

224
Q

types of relationships with oxygen for bacteria

A

obligate anaerobes
obligate aerobes
facultative anaerobes
aerotolerant bacteria

225
Q

obligate anaerobes

A

bacteria that can only survive if oxygen is absent

226
Q

obligate aerobes

A

bacteria that can only survive if oxygen is present

227
Q

ex obligate anaerobes

A

Clostridium ( cause of gangrene )

228
Q

ex obligate aerobes

A

Pseudomonas

229
Q

facultative anaerobes

A

bacteria that prefer to use oxygen-based respiration but can also survive in oxygen-free homes

230
Q

ex of facultative anaerobes

A

Staphylococcus, Streptococcus)

231
Q

aerotolerant bacteria

A

bacteria that do not use oxygen-based respiration but can survive if oxygen is present

232
Q

classifying with other preferred living conditions

A

based on preferred living arrangements

233
Q

different preferences for bacteria living conditions (temp)

A

thermophiles
psychrophiles
mesophiles

234
Q

thermophiles

A

like it hot

235
Q

psychrophiles

A

like it cold

236
Q

mesophiles

237
Q

different preferences for bacteria living conditions (acidity)

A

acidophiles
alkaliphiles
neutrophiles

238
Q

acidophiles

A

like it acidic

239
Q

alkaliphiles

A

like it basic

240
Q

neutrophiles

A

like it neutral

241
Q

body temp

A

37 degrees C

242
Q

blood pH

243
Q

classifying with spore formation

A

spores or no spores

244
Q

special survival mechanism of some bacteria

A

ability to form endospore

245
Q

bacterial cells that can form an endospore

A

divide and then wrap the important stuff inside a thick double-layered cell wall and lay dormant until conditions turn more favorable

246
Q

bacteria that can form an endospore are immune to

A

to many things like extreme temperature and can wait years before reactivating

247
Q

obligatory steps for infectious “bugs”

A
  • entry or attachment to the body
  • evasion of the immune system
  • shedding from/exiting the host
  • causing damage or disease-associated processes in the host*
248
Q

bacterial parts that allow obligatory steps for infectious bugs are called

A

virulence factors

249
Q

many bacteria enter the body through

A

cuts in the skin

250
Q

for bacteria that do not enter through cuts in the skin

A

they need to pass through a mucus layer

251
Q

two ways bacteria can pass through a mucus layer (Entry to the Body)

A

sigA proteases

mucinases

252
Q

the protection of mucus membranes across the body s mediated by

A

antibody secretory IgA (sigA)

253
Q

sigA is found

A

in extremely high concentrations in the airway and GI tract

254
Q

why would bacteria release sigA proteases

A

destroys human IgA antibodies

255
Q

destruction of human IgA antibodies causes what

A

neutralizes host defense in those areas, allows bacteria to live there

256
Q

mucinases

A

enzymes that degrade the proteins inside mucus

257
Q

mucinases allow what for bacteria

A

allows them to settle on or under mucus membranes

258
Q

many bacteria have what for attachment to body

A

pilli

fimbriae

259
Q

singular of pilli

260
Q

singular of fimbriae

261
Q

fimbria and pilus can be used interchangeably

A

yes, for some pilus is only for conjugation

262
Q

pili and fimbriae are what on most bacteria

A

peritrichous

263
Q

peritrichous

A

projections all over its surface

264
Q

pili act as

A

feelers for bacteria

265
Q

when pili feel a desired surface

A

shorten and pull the bacterium in

266
Q

pili are more prevalent in what

A

gram-negative bacteria

267
Q

adhesive proteins that stick to other proteins

268
Q

membranes of many microbes have

A

special type of adhesins

269
Q

what are the special adhesins that the membranes of many microbes have

270
Q

MSCRAMMs

A 
Microbial 
Surface 
Components 
Recognizing 
Adhesive 
Matrix 
Molecules
271
Q

roles of MSCRAMMs

A

target host cells and allow for tight connections between them and bacteria

272
Q

human cells are coated in what proteins for MSCRAMMS to targe

A
  • transport
  • receptor
  • adhesion
  • glycoproteins
273
Q

role of transport proteins

A

move things in or out of cells

274
Q

characteristics of transport proteins

A
  • opened and closed

- very selective

275
Q

role of receptor proteins

A

help the inside and outside of the cell communicate

276
Q

which proteins usually work together in human cells

A

transport and receptor

277
Q

example of adhesion proteins in human cells

278
Q

role of adhesion proteins

A

help stick cells in place

279
Q

characteristics of adhesion proteins

A
  • grab onto collagen in the extracellular space

- grab onto other integrins on other cells to hold hands

280
Q

role of glycoproteins

A

stick carbon chains into the extracellular space, forming a glycocalyx around a cell (CELL ID)

281
Q

different MSCRAMMs target

A

different types of host membrane proteins

282
Q

bacteria also have their own

A

OWN GLYCOCALYX

283
Q

integrin proteins connect cell to

A

to extracellular collagen

284
Q

different bacteria attack the body by

A

colonizing different surfaces

285
Q

bacteria choosing to live on outer epithelial layer

A

try to outcompete normal flora, but it is hard

286
Q

bacteria choosing to live into deeper extracellular space

A

burrow way through epithelial layer to get there

287
Q

bactiera choosing to live inside …

A

inside the host cell

288
Q

place the bacteria chooses to live…

A

-deeper extracellular space
-inside the host cell
outer epithelial layer
-eaten by phagocyte

289
Q

bacteria deliberately eaten by phagocyte

A

so they can reproduce inside a phagosome or phagolysosome.

290
Q

after reproducing inside a phagocyte or phagolysosome a bacteria can

A

pop out or keep living there

291
Q

depending on how deep into skin a pathogen gets

A

the manifestation of infection varies

292
Q

where does Y. pestis grow

A

inside white blood cells

293
Q

some bacteria come with a very THICK

A

thick glycocalyx.. called slime layer

294
Q

inside the slime layer there is

A

thinner layer of proetins called the S layer

295
Q

proteins of S layer

A

highly variable between species

296
Q

the slime layer and S layer provide the bacteria with

A

partial defense from phagocytes and covers some of the bacteria’s PAMPs

297
Q

example of bacteria w/ slime layer

A

streptococcus pneumoniae

298
Q

what caues gonorrhoea

A

Neisseria gonorrhoeae

299
Q

pili are what in Neisseria gonorrhoeae

A

the immunodominant structure

300
Q

pili being the immunodominant structure in Neisseria gonorrhoeae means

A

predominantly N. gonorrhoeae’s pili that are recognized by antibodies.

301
Q

different strands of N. gonnorhoeae

A

different structures of pilli; over1 million different pilus structures

302
Q

N. gonnorhoeae having so many different plius structures causes

A

memory B cells to be useless against it, makes people prone to reinfection

303
Q

the N. gonorrhoeae phenomenon is a tactic many other bacteria and virus use called

A

antigenic variation

304
Q

bacteria that live inside a host cell need to

A

need to find a way to escape

305
Q

some ways of exiting the host leave the host cell intact,

A

some do not

306
Q

1 st way of exiting the host

A

-settle inside vacuole and drive vacuole out

307
Q

2nd way of exiting the host

A

hijack cellular machine designed to secrete proteins through exocytosis

308
Q

3rd way of exiting the host

A

pop a big hole in the cell’s membrane, causing it to die

309
Q

bacteria often cause collateral

A

damage to surrounding tissues

310
Q

humans cells towards____ have ____

A

towards mucosal linings have hyaluronic acid in their membrane as a mortar

311
Q

hyaluronic acid is very

A

large molecule (molecular weight in millions), largely unknown functions

312
Q

large molecule (molecular weight in millions), largely unknown functions

A

largely unknown

313
Q

some pathogenic bacteria secrete what to break down hyaluronic acid

A

hyaluronidase

314
Q

why do bacteria secrete hyaluronidase

A

to break down hyaluronic acid to use its carbons for own processes

315
Q

result of bacteria using hyaluronidase to break down hyaluronic acid

A

damage to cell membranes, cellular death

316
Q

iron is

A

essential nutrient for bacteria, difficult to come across

317
Q

iron is necessary to build

A

peroxidases and operate an electron transport chain

318
Q

electron transport chains are

A

important for ATP production in bacteria

319
Q

easiest place for bacterial colony to find iron in the human body

A

hemoglobin found in blood

320
Q

because iron is found in the blood, bacteria secrete

A

hemolytic enzymes called hemolysins

321
Q

why do bacteria secrete hemolysins

A

to steal the body’s iron from hemoglobin

322
Q

bacteria can also cause damage through

323
Q

two types of toxins that bacteria have

A

endotoxins, exotoxins

324
Q

endotoxin

A

refers to LPS in the membrane of gram-negative bacteria

325
Q

LPS

A

lipopolysaccharides

326
Q

why is LPS dangerous to humans - reason 1

A

-cause vast increase in secretion of cytokines cause inflammation and swelling

327
Q

why is LPS dangerous to humans - reason 2

A

-leads to release of histamines…. causing vasodilation

328
Q

why is LPS dangerous to humans - reason 3

A

-leads to activation of coagulation cascade

329
Q

coagulation cascade

A

cascade that leads to the formation of thrombi (blood clots

330
Q

LPS puts people at risk for

A

septic shock, heart attack, and stroke.

331
Q

exotoxins

A

diverse class of toxins, all proteins created by a bacterium

332
Q

1st thing that exotoxins can do

A

are secreted and act on surrounding issue

333
Q

examples of exotoxins that act on surrounding tissue

A

hyaluronidase and hemolysin

334
Q

2nd thing that exotoxins can do

A

enter cells and ribosylate host proteins

335
Q

how does an exotoxin ribosylate a host protein

A

add ADP+ ribose… turns proteins on or off… often off

336
Q

3rd thing that exotoxins can do

A

break turn certain proteins such as sigA

337
Q

4th thing that exotoxins can do

A

other mechanisms

338
Q

in the case of exotoxins, symptoms..

A

not cause y bacterium themselves but by the exotoxins secreted

339
Q

staphylococcus genus are

A

gram-positive cocci

340
Q

how long can Staphylococcus survive at 60 degree

A

about a half-hour

341
Q

how long can Staphylococcus survive at 4 degrees

342
Q

3 importantS Staphylococcus species

A
  • Staphylococcus aureus
  • Staphylococcus epidermidis
  • Staphylococcus saprophyticus
343
Q

each of the important species of staph are

A

normal flora, disease occured when misplaced or when a bad strain is aqquired

344
Q

hemolysis S. aureus

345
Q

hemolysis S. epidermidis

346
Q

hemolysis S. saprophyticus

347
Q

coagulas S. aureus

348
Q

coagulase S. epidermidis

349
Q

coagulase S. saprophyticus

350
Q

color S. aureus

A

gold/yellow

351
Q

color S. epidermidis

352
Q

color S. saprophyticus

A

white/yellow

353
Q

novobiocin

A

antibiotic

354
Q

is S. aureus resistant to novbiocin

355
Q

is S. epidermidis resitant to novobiocin

356
Q

is S. saprophyticus resistant to novobiocin

357
Q

novobiocin

A

is an antibiotic

358
Q

in human blood, what waits for a signal to come from damaged tissue

A

prothrombin

359
Q

when prothrombin gets a signal from damaged tissue… it is converted to

360
Q

what does thrombin do

A

convert fibrinogen into fibrin

361
Q

what does fibrin do

A

weaves into a mesh, an integral part of clot formation

362
Q

who secretes coagulase

A

S. aureus (few other non-staph bacteria)

363
Q

when S. aureus and (few other non-staph bacteria) secrete coagulase

A

it mimics the damaged signal, but instead causes prothrombin to be converted into a special form

364
Q

when when S. aureus and (few other non-staph bacteria) secrete coagulase it causes prothrombin to be converted into what special form

A

staphylothrombin

365
Q

staphylothrombin function

A

converts fibrinogen to fibrin that coats the staph bacteria, protecting it from the immune system

366
Q

in phagocytosis, dendritic cells and macrophages

A

hold out digested guts (antigens) for other immune cells to see

367
Q

dendritic cells and macrophages holding out macrophages is a

A

delicate process- only a small subset of T cells actually res

368
Q

why is dendritic cells and macrophages holding out macrophages is a delicate process

A
  • only a small subset of T cells actually respond to an antigen, even if bad
369
Q

what percentage of T cells actually respond to an antigen

370
Q

superantigens are different than normal antigens because

A

they stimulate a large amount of T cells in an area

371
Q

what percentage of T cells do superantigens stimulate

A

20% or more

372
Q

superantigens stimulating a large amount of T cells is called

A

polyclonal T cell activation

373
Q

polyclonal T cell activation leads to

A

excessive cytokine release

374
Q

excessive cytokine release of polyclonal T cell activation can lead to

A

fatal shock or organ failure

375
Q

some strains of what create a superantigen

376
Q

superantigen created by strains of S. aureus

377
Q

SEB

A

Staphylococcal enterotoxin B

378
Q

another word for SEB, depending on wher it acts

379
Q

TSST

A

toxic shock syndrome toxin

380
Q

TSST / SEB is

A

a single protein created by 30-50% of strains of S. aureus

381
Q

if an SEB-secreting strain of S. aureus makes is way to _____

A

to intestines, the superantigen causes widespread inflammation

382
Q

result of SEB-secreting strain of S. aureus in intestines

A
  • projectile vomiting
  • abdominal pain
  • sometimes diarrhea
383
Q

S. aureus and its superantigen iin the intestines are a type of

A

food poisoning that is rapid onset

384
Q

how long after eating food w/ S. aureus do you show symptoms of food poisoning

385
Q

is staph the only caue of food poisoning

A

no, but is a common one

386
Q

other staph associated enterotoxins :

A

SEA - SEE, SEE - SEI, and SER - SET have been named

387
Q

which is the only staph-associated superantigen

388
Q

first example of S. aureus and its superantigen

A

Laredo TX, 1968

389
Q

Laredo TX, 1968

A

1364 elementary school children fell ill, chicken salad off-sit, not refrigerated, shipped to district

390
Q

example 2 of S. aureus and its superantigen

A

Spring 1989» canned mushrooms

391
Q

when SEB enters the blood stream

A

leads to toxic shock syndrome

392
Q

toxic shock syndrome primarily associated with what 3 things

A
  • extended use of hyperabsorbent tampons
  • cosmetic surgeries
  • uncleaned abrasions(rare)
393
Q

what cosmetic surgeries usually lead to toxic shock syndrome

A

material packed into the nose

394
Q

in each case of toxic shcok syndrome

A

S. aureus secretes SEB/TSS into the bloodstream

395
Q

the result of of toxic syndrome is

A

bad.. defined by 5 plus of characteristics

396
Q

what characteristics does toxic shock syndrome show - First 3

A
  • body temperature over 102 degrees F
  • blood pressure below 90 mmHg
  • Macular Erythroderma
397
Q

what characteristics does toxic shock syndrome show - Second 3 `

A
  • desquamation
  • involvement/failure of at least organ systems
  • no positive blood results for other likely suspects
398
Q

desquamation during toxic shock syndrome is

A

within 7-14 days, especially on palms and soles of feet

399
Q

Macular Erythrodema

A

sunburn appearance

400
Q

in adition to carrying superantigens, certain strains of S. aureus can carry

A

exfoliatins

401
Q

what two exfoliatins can S. aureus carry

A

exfoliative toxin A and exfoliative toxin B

402
Q

each of the exfoliative toxins targets

A

targets and cleaves protein dsg-1

403
Q

dsg-1

A

desmoglein-1

404
Q

where is desmoglein-1 found

A

only in the desmosomes of human skin

405
Q

desmosomes

A

structure that holds cells together

406
Q

staph (S. aureus) is more commonly the cause of

A

pyogenic infections

407
Q

pyogenic infections

A

buildups of pus to fight the bacteria.

408
Q

pus usually comes….

A

as a byproduct of the war between phagocytes and pathogens: the phagocytes eat so much that they eventually “pop”.

409
Q

what makes more pus

A

bacteria also secrete substances to kill phagocytes before they start eating

410
Q

forms that pus buildup can take

A
  • Impetigo
  • Folliculitis
  • Carbuncle
  • Furuncle
411
Q

Impetigo

A

superficial infection

412
Q

Folliculitis

A

infection of hair follicle

413
Q

Carbuncle

414
Q

Furuncle

415
Q

treatment of staph infections;

A

antibiotics , but staph infections evolving to counteract

416
Q

MRSA

A

Methicillin-resistant Staphylococcus aureus

417
Q

MRSA actually

A

resists many different types of antibiotics not just methicillin

418
Q

now in order to treat MRSA doctors

A

give stronger antibiotic vancomyscin

419
Q

in other regions where vancomycin was the first choice antibiotic

A

VRSA emerged

420
Q

VRSA

A

vancomycin-resistant S. aureus

421
Q

from horizontal gene transfer of S. aureus there is now

A

MVRSA&raquo_space;> SUPERBUG

422
Q

S. epidermidis is

A

not very scary, not have many virulence factors like S. aureus

423
Q

scary feature of S. epidermidis

A

form biofilms on plastic surfaces

424
Q

S. epidermidis forming biofilms on plastic surfaces

A

make it incredibly difficult for antibiotics to penetrate

425
Q

the result of a biofilm forming is often

A

follow-up surgery to remove the plastic

426
Q

biofilms of S. epidermidis often form on

A
  • catheters
  • replacement heart valves
  • prosthetic joints
427
Q

biofilms forming on catheters

A

response for over 50% of catheter infections

428
Q

biofilms forming on replacement heart valves

A

leads to endocarditis

429
Q

endocarditis

A

inflammation of heart inner lining

430
Q

what staph species sometimes occupies the normal flora of the body

A

S. saprophyticus

431
Q

when S. saprophyticus gets inside the urinary tract of a woman

A

(usually through sex) causes a urinary tract infection

432
Q

symptoms of urinary tract infection

A
  • burning sensation while urinating
  • need to urinate often
  • cloudy urine
433
Q

urinary tract infections usually onsets

A

24-48 hours after sexual activity

434
Q

urinary tract infections are often called

A

honeymoon cystitis

435
Q

the proteins are degraded by exfoliative toxins are

A

in the junction between the stratum granulosum and the stratum spinosum of the epidermis

436
Q

degradation of desmosomes between the stratum granulosum and the stratum spinosum leads to what

437
Q

SSSS

A

Staphylococcal scalded skin syndrome

438
Q

symptoms of SSSS

A

skin blisters within 24-48 hours of onset, common in young children

pathophysiology (24 decks)

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