Micro: Gram Positive Bacilli

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1

what is the main split of gram positive bacteria

cocci and bacilli

2

after breaking into bacilli, what is the next branch

forms spores or doesnt form spores

3

what branches of gram positive bacilli form spores

bacillus and clostridium

4

how are bacillus and clostridium split

bacillus grows in air, clostridium doesn't

5

after distinguishing sporeless bacilli, what is the next split

motility (listeria) or lack of

6

how are sporeless, non motile bacilli split

growth in air or not (propriobacterium)

7

what type of bacilli are sporeless, non motile, and grow in air

corneybacterium and kurthia

8

how are cornyebacterium and kurthia split

cornyebacterium (positive) and kurthia (negative) are split by catalase

9

what are the clinical manifestations of bacillus anthracis

cutaneous anthraw and pulmonary anthrax

10

what is a prominent sign of cutaneous anthrax

malignant pustule: painless black ulcer iwth necrotic eschar and marked local edema

11

what is wooolsorter's disease

pulmonary anthrax

12

what is pulmonary anthrax due to

inhalation of spores

13

what do both pulmonary and cutaneous anthrax lead to

bacteremia that progresses to death

14

how is anthrax used

biologic weapon by aerosolizing spores

15

where does bacillus anthracis live

in the soil where spores can persist for years

animals develop infection and shed organisms and spores onto hair and wool

16

how is bacillus anthracis transmitted

humans come into contact with infected animals, hides, wool, and organisms that enter via skin, mucus membranes, and respiratory tract

17

how long can inhalation anthraw have an incubation period

several weeks

18

what are the virulence factors of bacillus anthracis

polyglutamic acid capsule
anthrax toxin (2 proteins in A-B subunit configuration)

19

what is the binding subunit of anthrax toxin

B subunit, also acts as protective antigen

20

what is the edema factor of anthrax toxin

adenylate cyclase, which increases cAMP

21

what is the role of the protective antigen in anthrax toxin

binds to cell surface receptor and then is cleaved by cellular protease

remaining protective antigen on cell surface binds edema factor or lethal factor that then enter the cell

22

how does the lethal factor act as part of the protective antigen

protease that cleaves a phosphokinase that activates a cell growth pathway, result is inhibition of growth

23

what do edema factor, protective antige, and lethal factor all working together all result in

cell death, increased vascular permeability, and neurotoxicity

24

what was the lab test like in bacillus anthracis

non motile large gram positive bacillus

spore-forming

25

are there serologic tests available for bacillus anthracis

none

26

what are the treatments for bacillus anthracis

quinolones (cipro)
doxycycline
penicllin

27

is there a vaccine for bacillus anthracis

yes

also sterilize dead animals and animal products from endemic areas; wear protective clothing

28

what is the main clinical manifestaton of bacillus cereus

food poisoning

29

what is the incubation period for bacillus cereus

2-16 hours

30

what are the symptoms of b. cereus infection

prominent vomiting and diarrhea

31

where are b. cereus spores

grains of rice

32

can b. cereus spores survive frying

yes

33

what toxins do bacillus cereus make

two enterotoxins

ADP-ribosylator of G protein that stimulates adenylate cyclase and incrased cAMP levels inside enterocytes (like cholera)

super antigen

34

what are the clostridium species

tetani
dificile
botulinum
perfringens

35

what is the main clinical manifestation of c. tetani

tetanus (lockjaw)

36

what are the symptoms of lockjaw

violent muscle spasms with early symptoms of trismus (lockjaw) due to rigid contraction of jaw muscles

hyperreflexia

respiratory failure

37

does c. tetani have a high mortality rate

yes

38

is c. tetani common in the US?

no but most cases are in elderly who have never been vaccinated and who don't keep up with vaccinations

39

what types of people is c. tetani mostly a problem with

underdeveloped country neonates

40

where does c. tetani live

soil, spores are widespread in soil

41

what do the c. tetani spores contaminate

cuts
wounds

42

what does c. tetani produce

tetanospasmin (polypeptide neurotoxin)

43

what is the strucutre of tetanospasmin

polypeptide exotoxin composed of two polypeptide chains held together by disulfide bonds

44

what types of cells make tetanospasmin

vegetative cells growing in anaerobic environment of the wound

45

what does tetaonspasmin toxin bind

peripheral nerves

46

how is tetanospasmin take effect

intraxonnally (retrograde) to CNS where it binds to ganglioside receptors and blocks release of inhibitory NTs (glycine and GABA) at spinal nerves

47

so what is the end result of c. tetani's tetanospasmin

unopposed excitatory neurons results in muscle spasm

48

how would a c. tetani lab be seen

terminal spore, looks like a tennis racket

49

how would you treat c. tetani

penicillin to kill organisms

give hyperimmune human globulin to neutralize unbound toxin

50

is there a vaccine for c. tetani

tetanus toxoid vaccine (formaldehyde treated)

51

how is c. tetani prevented

routine childhood vaccination and every 10 year boosters for adults

treat dirly contaminated wounds with tetanus booster if none in last 5 yeras and hyperimmune globulin if not previously vaccinated

debride devitalized tisssue

52

what are the main manifestations of c. perfringes

food poisoning and gas gangrene

53

what is the incubation period of c. perf food poisoning

8-16 hours

54

how does c. perf food poisoning take effect

abrupt onset profuse diarrhea with little vomiting

55

when does c. perf food poisoning resolve

1-2 days

56

how is c. perf transmitted

organisms and spores in soil, contaminate food

spores survive cooking and if food then reheated at later date, organisms grow to large numbers (especially meat dishes)

57

what type of toxin causes c. perf food poisoning

enterotoxin (protein in the spore coat)

58

when is enterotoxin of c. perf made

produced during sporulation in the gut causes hypersecretion

59

what is the mechanism of c. perf

superantigen like enterotoxin of s. aureus

60

where would c. perf be present normally

colon

61

where is c. perf toxic

small intestine

62

what does c. perf do to flare up

release of inflammatory mediators in gut

63

how would lab detect c. perf

clostridia present in large numbers in cultures of food or feces of patients

64

how is c. perf prevented

refridge and cook adequately

65

how is c. perf treated

symptomatic treatment

66

what are the symptoms of gas gangrene of c. perf

pain and edema at wound site

gas produced and crepitance develops

67

what destroys muscle and tissue in c perf gas gangrene

lecithinase (myonecrosis)

68

what are the later effects of gas gangrene

shock and hemolysis

69

is the mortality high in gas gangrene

yep

70

what percentage of wounds are contaimnated by clostridia in war

25%

71

what are some usual gas gangrene situations

penetrating abdominal wounds and septic abortions

72

where does c. perf live

soil and colon

73

what are the main toxins of gas gangrene

numerous
alpha toxin (lecithinase: damages cell membranes)

74

what is lab diagnosis of gas gangrene like

anerobinc gram positive bacillus
spore forming
cultured anaerobically and identified by sugar fermentation reactions and organic acid production
test for production of lecithinase on egg yolk agar

75

what is the treatment of gas gangrene

penicillin
debride devitalized tissue
hyperbaric oxygen decreases production of alpha toxin

76

how is c. perf prevented

good wound care

77

what is the clincal manifestation of c. dif

antibiotic assd colitis
pseudomembranous colitis

78

what are the symptoms of c dif infection

diarrhea and abdominal pain with preceding history of antibiotic use

79

where is c. dif usually found

colinc flora of asymptomatic individuals in 3%

may be transmitted between patients in hospital on environmental surfaces

80

what is the pathogenesis of c. dif

antibiotics suppress drug sensitive normal colonic flora allowing c. dif to grow, organism multiplies and produces toxin

81

what are the toxins of c. diff

exotoxin A and B

82

what are the actions of exotoxin A and B

damage to mucosa and produces characteristic yellow pseudomembrane visible on inspection of colon

83

what does c. dif do to actin filaments

glucosylate to a G protein involved in actin filament polymerization, which leads to depolymerization of actin and loss of cytoskeletal integrity, apoptosis and cell death

84

what are the lab tests for c. dif

test stool for presence of toxins or PCR for toxin genes

85

why are lab cultures not helpful for c. dif

some don't produce toxin

86

what are some antibiotics useful vs. c. dif

metronidazole, vancomycin

87

what is the clinical manifestation of c. bot

botulism

88

what are the symptoms of c. bot

descending weakness with initial inovlvement of cranial nerves (diplopia, blurry vision, dysphagia) and then repiratory muscle failure

dilated pupils and dry mouth, no fever

89

when do sypmtoms develop with c. bot

18-24 hours after ingestino of contaminated food

90

where are c. bot toxins

organism and spores widespread in soil, contaminate vegetables and meat

if foods vacuum packed without adequate sterilization, spores survive and germinate under anaerobic conditions

91

what are the two clinical forms of the c. bot illness

wound bot
infant bot

92

what happens in would bot

spores contaminate wound, germinate, produce toxin at site

93

what happens in infant bot

ingested organisms grow in bowel and produce toxin (RAW HONEY)

94

how does c. bot exotoxin work

inhibits the release of ACh at myoneural junction causing flaccid paralysis

95

what encodes the polypeptide exotoxin

phage

96

what is the mehcanism of polypeptide exotoxin

protease cleaves proteins involved in ACh release

97

how many different neurotoxins come from c. bot

8

98

which neurotoxins of c. bot normally cause human disease

A, B, E

99

are the neurotxins of c. bot sensitive to heat

heat labile; proper cooking of preserved food can prevent illness

100

which toxins of c. bot are ADP-ribosylating

C2 and C3

101

how would you lab diagnose c. bot

detection of toxin in food or stool

102

is there a c. bot vaccine

NO

103

what is the treatment

equine antitoxin to types A, B, and E

penicilllin for infant and would botulism

supportive measures

discard swollen cans

104

what are the important nonspore forming gram positive bacteria

listeria monocytogenes

cornyebacterium diptheria

105

what is the clinical manifestation of listeria

meningitis and sepsis in newborns and IC adults (transplant patients)

infection during pregnantcy can cause abortion, premature delivery, or sepsis

106

how much later may neonates develop listeria meningitis after delivery

1-4 weeks later

107

where is listeria

organism widespread in animals, plants, soil

may colonize GI tract and female genital tract

108

how is listeria trasnmitted to humans

contact with animals or their feces, or gnestino of unpasteurized milk/cheese or contaminated vegetables

organism crossing placenta or by contact during delivery

109

how do most people get listeria

immunosuppressed: newborn, alcoholic, pregant, cancer

especially with decrased cell mediated immunity as organisms grow intracellularin

110

what are the virulence factors of listeria

internalin
listeriolysin O
actin rockets

111

what is the mechanism of internalin

binds to E-cadherin on cell surface and allows bacteria to enter cells of placenta, meninges, GI tract

112

what is the mechanism of listerolysin O

allows bacteria to escape from phagosome into cytoplasm thereby escaping destruction

113

where does listeria grow

intracellualrly

114

what are the mechanisms of actin rockets

actin polymerization at one pole of organism propels it into the cell membrane allowing it to move from cell to cell

115

what is the primary site of infection for listeria

intestinal epithelium where bacteria invade non-phagocytic cells

116

how is uptake of listeria mediated

binding of listeria internalins to host cell adhesion factors such as E-cadherins

117

what does E-cadherin binding activate

certain Rho-GTPases which subsequently bind and stabilize WASp

WASp then binds Arp2/3 complex and serves as an actin nucleation ponit

subsequent actin polymerizzation extends the cell membrane around the bacterium, eventually engulfing it

118

what is the net effect of intarnalin binding

exploit the junction forming apparatus of the host into internalizing the bacterium

119

can listeria invade phagocytic cells

yes but only needs internalins for invasion of nonphagocytic cells

120

what must bacteria escape from after internalized

vacuole/phagosome before fusion of lysosome

121

what are the main virulence factors that allow the bacterium to escape phagosome

listeriolysin O and phospholipase C B, which disrupt the vacuolar membrane

122

where does listeria proliferate

cytoplasm

123

once in the cytoplasm how does listeria work

ActA proteins associated with old bacterial cell pole are capable of binding the Arp2/3 complex and induce actin nucleation at a specific area of the bacterial cell surface

actin polymerization then propels the bacterium unidirectionally into a neighboring cell, forming a double membrane vacuole from which the bacterium must escape using LLO and PLCB

124

what are the lab tests for listeria

gram positive bacillus
beta-hemolytic on blood agar (listeriolysin O)
motile
sugar fermentation tests

125

what is the treatment for listeria

ampicillin

126

is there a vaccine for listeria

no

127

what is the clinical manifestation of dipthieria

diptheria

128

what is diptheria characterized by

pharyngitis with tough adherent gray pseudomembrane over the tonsils and throat

129

what is the incubation period for diptheria

1-7 days

130

what are the major compliecaiotns of diptheria

extension of inflammatory membrane into larynx and trachea causing airway obstruction
myocarditis (toxin mediated)
recurrent laryngeal nerve palsy, peripheral neuropathies
rare cutaneous diptheria

131

what is the natural host of diptheria

humans only

132

where do diptheria organisms reside

throat, respiratory tract

133

how is diptheria transmitted

coughing and respiratory secretions

134

what are the virulence factors of diptheria

diptheria toxin

135

what does diptheria toxin do

inhibits protein synthesized in eukaryotic cells

136

what are the major parts of the diptheria toxin

subunit B and A

137

what is the role of subunit B

binds to glycoprotein receptors on cell membranes

138

what is the role of subunit A

enzymatic actiity: cleaves nicotinamide from NAD and transfers the remeining ADP-ribose to EF2 (eukaryotic peptidyl tRNA translocase) thereby inactivating it

139

what is the reaction that EF2 catalyzes

NAD+EF2 to ADP-phosphoribose+nicotinamide+H-

140

what is the DNA for the diptheria toxin from

bacteriophage: DNA integrates into bacterial DNA and toxin synthesized

141

are diptheria organisms not infected with a particular bacteriophage pathogenic

nope

142

what are the lab findings for diptheria

gram positive bacillus (club shaped, beaded)
black colonies on tellurite media (Lofflers media

143

is diptheria motile

no

144

does diptheria form spores

no

145

what type of treatment is available for diptheria

equine anti-toxin neutralizes toxin

146

is there immunization for diptheria

toxoid: formaldehyde treated exotoxin

147

does immunizatino against the toxin prevent nasopharyngeal carriage of diptheria

no

148

how often are boosters for diptheria

every 10 yeras

149

what are the organisms that use ADP ribosylation in their toxin

b. cereus enterotoxin
diptheria toxin
p. aeruginosa exotoxin A
cholera toxin
pertussis toxin
E. coli heat-labile enterotoxin

150

what is the target of b. cereus enterotoxin

G protein

151

what is the targed of diptheria toxin and p. aerusginosa exotoxin A

EF2

152

what is the effect of b. cereus toxin

increase cAMP

153

what is the effect of diptheria toxin and p. aeruginosa exotoxin A

inhibits protein synthesis

154

what is the effect of cholera toxin

prevents hydrolyzing GTP to GDP

G protein GTP complex then continually stimulates adenylate cyclase to make cAMP

155

what is the target of pertussis toxin

G protein

156

what is the effect of pertussis toxin

stimulation of adenylate cyclase

157

what is the target of E. coli heat-labile enterotoxin

G protein

158

what is the effect of E. coli heat-labile enterotoxin

prevents hydrolyzing GTP to GDP

G protein GTP complex then continually stimulates adenylate cyclase to make cAMP

159

does diptheria toxin bind to something to enter the cell

no, enters by endocytosis

160

does v. cholerae toxin bind to something to enter the cell

yes, sets off adenylate cyclase actifity and increased cAMP to lose nutrients and cause diarrhea