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Flashcards in Microbiology II Deck (205):
1

What is the gram type and shape of the major flora in the gut?

Gram negative rods

2

What are the 5 F's that infect the gut with the bacilli Enterobacteriaceae?

food
fluids
fingers
flies
feces

(but really it's just feces)

3

What are two pathologically important features of Gram negative rods?

Sharing of virulence factors
(through conjugation, etc)

Antibiotic resistance

4

Where are gram negative rods found?

ubiquitous
dirt, water, GI flora

5

T/F
Gram negative bacteria can cause cancer

True

6

How many species of Enteric Gram negative rods are there?
What is their metabolic category?

over 500
Facultative anaerobes

7

T/F
Enteric Gram negatives are highly fastidious.

False

they are non-fastidious but sensitive to drying

8

All of the Gram- Enterics are have a _______ cycle.

Oro fecal

9

What type of infection is Campylobacter?

Zoonotic

10

Where can Helicobacter live?

Stomach

*causes cancers and ulcers

11

What are the Serotype terms for:
Flagella
Capsules
Endotoxins (LPS)

H-antigens
K-antigens
O-antigens

*these are determined by agglutination

12

What is meant by Antigen Variation?

Bacteria evade adaptive response by changing epitopes

*referring to Gram- Enterics

13

How does Phase Variation in Gram- Enterics protect them from Antibody-mediated death?

They change the expression of major features (Antigens), like capsule and flagella.

14

Name 6 virulence factors for Gram- Enterics.

Adhesive factors
Endocytosis (invade cells)
Macrophage Taxi
Capsules (phagocytic resistance)
Phase variation
Antibiotic Resistance
Toxins

15

T/F
All Gram- Enterics have endotoxin, and some have exotoxin.

True

16

What are the specific adhesion molecules on Fimbrae called?

Adhesins

17

T/F
All Gram- Enterics initiate actin assembly and internalize into attached cells

False

some do

*Bacterial-directed endocytosis

18

Which Gram- Enterics enter mucosal epithelium?
Which of these use macrophage taxis?

E. coli (EIEC)
Shigella

Salmonella
Yersinia
(these two taxi)

19

How do macrophage taxi Gram- Enterics survive?

Block endosome-lysosome function and escape the death chamber

20

E. coli (EPEC variant) does what to intestinal cell walls?

Attaches to brush border and causes malabsorption

21

What 4 things does LPS directly activate?

(this is our innate immune response)

Macrophage
Hageman Factor (coagulation)
Platelets (coagulation)
Complement (mast cell degranulation/pro-inflammatory mediators)

22

TNF-alpha stimulated endothelial cells to produce:

NO

23

Gram - bacteria can, in large numbers, cause sepsis, which entails:

*this is caused especially by what bacteria?

Hypovolemic shock (CV)
Intravascular coagulation (causing internal bleeding)
then,
Multiple organ shutdown
ARDS

*bacteriamia

24

What are the 3 major classes of A-B Exotoxins produces by Gram - Enterics?

2 Robosylation of regulatory proteins (gut)
1 cleave rRNA and block protein synth

25

What is the equation for disease causing potential?

Virulence x Dose / Host resistance

26

Why is Shigella's infectious dose very small?

Very acid resistant

27

How does Shigella infect the colon?

By invading epithelial "M" cells and dividing inside.

28

How does Shigella move laterally once inside these epithelial cells?

Actin-directed pseudopodia

29

What is the result of a local Shigella infection of the colon?

dysentery

30

What type of toxin do some strains of Shigella dysenteriae produce?

Shiga toxin
(A-B cleaves rRNA)

*damages intestinal epithelial cells

31

What can Shiga toxins do if they get into blood?

HUS - Hemolytic Uremic Syndrome
(damage glomerular endothelial cells & renal failure)

32

What encodes a Shiga-like Toxin?

Entero-hemorrhagic E. coli (EHEC)

*similar to S. dysenteriae

33

List Shigella species from most pathogenic to least:

S. dyssenteriae
S. flexneri
S. sonnei

34

The Shigella bacteria cause a _____ LPS caused by invasion of bacteria into the endothelium.

Local

35

What is the immune response to M-cell invasion by Shigella?

Ulcers, which causes dyssenteric symptoms

36

What is stool filled with in dysentery caused by Shigella?

mucus
pus
blood

37

EHEC 0157:H7 has _____ toxin and can act _____.

Shiga-like
Systemically

38

What causes Typhoid Fever?

Salmonella typhi

macrophage taxis rupture and releases lots of bacteria
*systemic

39

Where is Salmonella typhi found in carriers?

Gallbladder (maybe gallstones)
feces

*typhoid Mary

40

How many Salmonella serotypes are there?

over 2000

41

How is Salmonella different from Shigella?

Doesn't tolerate stomach acid as well
*need large dose for infection

42

How do most Salmonella species act in the gut?

Invade epithelial cells and destroy.
Usually isolated infection

43

Why is Salmonella typhi particularly infectious?

Evades macrophage destruction by using taxis

44

What is the definition of bacteremia?

Bacteria in blood

45

List Salmonella species from most to least virulent:

S. typhi
S. typhimurium
S. enterica

46

T/F
Salmonella is acid sensitive

True

47

What type of virulence factors can be transferred to normal Gi flora?
What are 2 types of pathogens that transfer such genes?

adhesions and endotoxins

Shigella and V. cholera

48

Name 4 pathogenic E. coli that have gained virulence factors from Shigella or V. cholera?

(one gained from an unknown source)

ETEC - Enterotoxigenic E. coli
EHEC - Enterohemorrhagic E. coli
EPEC - Enteropathogenic E. coli
EIEC - Enteroinvasive E. coli

49

E. coli outbreak's pts are often hospitalized with what condition?

HUS (hemorrhagic uremic syndrome)

50

What causes most (75%) UTI's?
What allows them to survive in the urinary tract?

E. coli (uropathogenic strains)
Specialized adhesions (fimbrae)

51

At what point can a UTI cause systemic LPS?

Once it reaches the kidney

52

Aside from LPS, what do E. coli strains of UTI's secrete?

Cytolytic exotoxin

53

What is a curved Gram- rod and has enterotoxin causing ribosylation (increases cAMP)?

Vibrio cholerae

54

What zoonotic infection has Shiga-like toxin?

Campylobacter jejuni

55

What causes ulcers and is a spiral Gram- rod?

Helicobacter pylori

56

What causes cystic fibrosis and is a big problem in burn victims and has a poor response to antibiotics?

Pseudomonas aeruginosa

57

What's a key periodontal bug that is Gram- rod anaerobe?

Bacteroides

58

What Gram- rod comes through skin, oral mucosa, and grows in macrophage?

Brucella abortus

59

What fragile Gram- rod with a capsule binds ciliated bronchi and is not enteric?

Bordetella pertusis

60

What Gram- rod causes Plague?

Yersinia pestis

61

Mortality rates:
Bubonic plague
Pneumonic plague

75%
100%

62

T/F
Y. pestis uses macrophage taxis

True

63

What are the toxic agents used by Y. pestis?

LPS
Superantigen

64

What are 2 sources of Passive Immunity?

Mother
Injection of antibody

65

Why is passive immunity temporary?

IgG half life 21 days

66

What is an important mild antibody?

slgA

(blocks colonization of gut viruses and toxins)

*protects from Vibrio cholerae

67

What Gram- curved rod is Non-invasive, and does not fully penetrate enteric endothelium?

Cholera
(Vibrio cholerae)

68

What type of toxin does Cholera release?
What does it do?

A-B exotoxin
pumps salts and water into colon

*rice water stools

69

What is the treatment for Cholera?

Water/electrolyte matching

70

When is the "window of susceptibility" for babies?

3-5 months

71

What are the 2 major pathogenic Neisseria species?

N. meningitidis
N. gonorrhoeae

72

Neisseria meningitidis and gonorrhoeae are both?

Gram- diplococci
aerobic or microaerophilic

73

T/F
Both pathogenic Neisseria species cause purulent infections

True

74

Where is Neisseria meningitidis commonly found in healthy individuals?
What is the medical slang for this species?

nasopharynx
meningococcus

75

What are the 2 diseases caused by Neisseria meningitidis?

meningitis
meningococcemia

76

What are the major virulence factors of N. meningitidis?

Fimbrae (nasopharynx)
Capsule
IgA protease (very clever)

77

What two benefits does N. meningitidis get from having a capsule?

Anti-phagocytic
Antigenic differences between strains

78

How is N. meningitidis spread?
Natural carriers?

respiratory droplets and prolonged contact
humans only

79

What percentage are asymptomatic and carrying N. meningitidis?

10%

80

Who is susceptible to N. meningitidis?

Those lacking opsonizing antibodies to anti-phagocytic capsules

*moves from nasopharynx into blood - bacteremia

81

What can bacteremia from N. menigitidis lead to?

meningococcal sepsis (septic shock)

'blebs' - lots of endotoxin from meningococcal outer membrane > cytokine > systemic inflammation > decrease BP > Disseminated Intravascular Coagulation

82

When are the peaks for death by menigococcal sepsis?

3 months (vast majority of deaths)
20 yrs

83

What is the difference between meningitis and meningococcal septicemia?

Bacteria cross to the brain and local endotoxin causes damage

84

What results in capillary blockage and damage during sepsis?

Disseminated Intravascular Coagulation

85

What are the 3 most serious brain infections in children that cause meningitis?
Are they Gram+/-?

H. influenza G-
N. meningitidis G-
Strep pneumococcus G+

86

T/F
Viral meningitis is much more severe than bacterial.

False

Viral much more common much less severe

87

On gross examination of CSF, what is indication of bacterial meningitis?

Cloudy

88

The 3 species that cause bacterial meningitis in children (H. influenza, N. meningitidis, S. pneumococcus) all have _____ and live _____

capsules
back of throat

89

Where does the human reservoir for N. meningitidis reside?

Carrier rate?

Nasopharynx

10%

90

T/F
N. meningitidis is very hardy.

False

Very fragile, drying kills, hard to grow

91

What are meningits and meningococcemia both caused by?

Systemin LPS

92

Meningococcemia is often accompanied with a.....

rash

93

Both meningitis and meningococcemia are both ultimatley caused by....

Blebbed endotoxin released by N. meningitidis

94

What is the fatality rate for bacterial meningitis?
% with serious outcomes like brain damage?

15%
15%

95

What is the Fatality rate for Meningococcemia?
Serious outcomes like brain damage?

40%
50%

96

Common name for N. meningitidis
Common name for N. gonorrhoeae

meningococcus
gonococcus

97

What are the major virulence factors for N. gonorrhoeae?

Fimbrae attachment to mucosal epithelium*
Gene conversion and Phase Variation
Incorporates host surface receptors
IgA protease*
LPS*
Penicillin resistance

98

Is N. gonorrhoeae encapsulated?

no capsule

99

Why is gonorrhea so difficult to get rid of?

Half women have no symptoms
less that 10% men have no symptoms

100

What is a consequence of untreated gonnorhea?

PID
Pelvic Inflammatory Disease

101

Why are newborns routinely treated with anti-microbial eye ointment?

Prevent gonococcal eye infections
(if bad can lead to blindness)

102

N. gonorrhoeae is very hardy

False

103

Name 3 important Virulence factors for N. gonorrhoeae.

Fimbrae
LPS
IgA protease

104

Inflammation from gonorrhea is local/systemic and leads to _______

Local LPS
Pus (pyogenic)

105

Gonorrhea in women:
% asymptomatic
% untreated

50
10-20

*leads to PID 1 million/yr

106

Where does adhesive scarring occur in PID?

Fallopian tubes

107

Is there a vaccine for gonorrhea?

NO

extreme antigen variation makes it difficult

108

What are the 3 very small Gram- bacteria that cause human disease?

Rickettsia
Chlamydia
Mycoplasma

109

What are Rickettsia and Chlamydia's effects on tissues?

Obligate Intra-cellular (invaders)
Attacks endothelium
Energy parasites (steal ATP)

110

What are Mycoplasma's effects on tissue?

Extra-cellular
Attacks epithelium

111

What toxins does Mycoplasma have?

Super Antigen

and no LPS

112

What are 2 results of a Rickettsia infection?

Spotted Feve
Typhus

113

What are 2 results of a Chlamydia infection?

Eye infection
STD

114

T/F
Rickettsia is an obligate intracellular parasite.

True

115

Why must Rickettsia live inside cells?

Lack enzymes required to produce AA's

116

What is the main reservoir for Rickettsia?

Arthropods

117

What is the mechanism of Rickettsia infection from vector to host?

Infected arthropod defecates while biting, bacteria enter blood

118

What can many of the pathologies associated with Rickettsia be traced to?

LPS flooding bloodstream systemically

119

What is the most common and important Rickettsial disease worldwide?

Typhus

120

What is the only Rickettsial Typhus that can cause explosive epidemics?
How is it spread?

Louse-born

R. prowazekii > lice > clothes

121

What is the most common Rickettsia in the United States?

R. rickettsii, species of bacteria transmitted by ticks causing Rocky Mountain Spotted Fever

122

Organism and Vector causing the following:
Rocky Mountain Spotted Fever
Scrub typhus
Epidemic typhus
Murine typhus

R. rickettsii ticks
O. tsutsugamushi mites
R. prowazekii Louse
R. typhi fleas

*skip scrub/murine

123

What do all the arthropod transmitted Rickettsia's have in common?

small
G-
Obligate intracellular parasites

124

Rickettsia is an obligate _______ bacteria.
Gram?
Shape?

Intracellular
G-
coccobacilli

125

What kind of parasite is the Rickettsia bacteria?

Energy parasite
Steals AA's and ATP

*Chlamydia also does this

126

What does Mycoplasma steal from its host?

lipids and cholesterol to strengthen its membrane

127

Ticks are both the _____ and the ______ for Rickettsia.

reservoir
vector

128

LPS in Rickettsia is systemic and causes what symptoms?

Headache, fever, chill
Rash

129

What are the 3 biotypes in the serological taxonomy of Rickettsia?

Spotted fever group
Scrub typhus group
Typhus group

130

How does Typhus differ from Typhoid?

Typhus - caused by Rickettsia

Typhoid - "typhus like" caused by Salmonella typhi
(typhoid mary)

*typhus/typhoid - think fever/rash

131

What does Rickettsia prowazekii cause?
What is its reservoir?

epidemic typhus in close quarters via lice
humans (and some rodents)

*DDT extremely effective against

132

Describe Chlamydia

Obligate intracellular parasite
no cell wall
two lipid bilayer/LPS
G-
energy parasite

133

What are the 3 major species of Chlamydia that affect humans?

C. trachomatis (STD)
C. pneumoniae (bronchitis & pneumonia)
C. psittaci (pneumonia)

*psittaci is mostly bird pathogen, occasionally human

134

What 2 diseases does Chlamydia trachomatis cause?

STD
blindness (trachoma)

135

What is the primary reservoir for Trachoma?
What is the pathological progression?

children
eyelids turn inward and scar

136

How is Chlamydia symptomatically similar to Gonorrhea?

symptomatic in men
asymptomatic in women

(generally)

*also a cause of PID

137

T/F
Chlamydia and Rickettsia are energy parasites

true

138

T/F
Chlamydia has a peptidoglycan wall and LPS

False

No peptidoglycan, but has LPS

139

What does Chlamydia infect and what type of inflammation does it cause?

Mucosal epithelium
Local (and chronic)

140

Chlamydia pneumonia has an association with atherosclerosis, is community acquired, and is very rare.

False

More than 50% population has serologic evidence of previous infection

141

What is the common route of infection for C. psittaci?

Birds to dust to lung

*generally only affecting immunocompromised

142

T/F
There is a vaccine for C. trachmatis

False

143

What is the most common bacterial STI in the USA?

Chlamydia trachmatis

144

What are the smallest known self-replicating organisms?

Mycoplasma and Ureaplasma

145

Describe Mycoplasma

No LPS
Gm+
Very common
No cell wall
sterols

146

What is the major Mycoplasma pathogen?

M. pneumonia

147

Where does M. pneumonia live?

Surface of respiratory epithelium

*destroys ciliated cells

148

What type of inflammation does M. pneumonia elicit?
How?

Local
super antigen

149

What is "walking pneumonia"?

atypical, mild

150

T/F
Mycoplasma species have been implicated in genitourinary tract diseases, PID, and STI's

True

151

What are Koch's 4 postulates to determine causality of agent?

1. Found in all cases
2. grown
3. cause disease when introduced
4. reisoloation from inoculated host and identified as identical to original causative agent

152

What causes diphtheria and where is it found?

Corynebacterium diphtheriae

skin, upper respiratory, GI

153

What are 3 defining characteristics of C. diphtheriae?

G+
non-spore forming
Rods (bacilli)

154

What kind of toxin does C. diptheriae make and how is it spread?

A-B exotoxin
(inhibits protein synth)

only spreads when lysed by virus
(the infection has an infection)

155

Where does the A-B exotoxin of C. diptheriae preferentially spread systemically?
Where is it locally?

B-subunit binds heart and nerve cells

Throat

156

How is C. diptheriae usually transmitted?

Respiratory droplets of asymptomatic, immune carriers

157

What is the distinctive thick, grayish white exudate caused by C. diphtheriae that adheres firmly to tissue?
What does this cause in advanced cases?

Pseudomembrane
Suffocation

*difficult to dislodge without making underlying tissue bleed

158

How is diphtheria treated?
How avoided?

anti-toxin
toxoid (modified immunogenic toxin)

159

Besides C. diphtheriae, what causes a pseudomembrane to form?

Candidiasis

160

T/F
Diphtheria is non-invasive.

True

*toxin invades

161

Two major ways to die from diphtheria?

Suffocation
Heart

162

Why does Corynebactirum diphtheriae infections increase when vaccination rates go down?

Bacteria is found everywhere

USSR - Russia breakup lag in public health

163

What type of bacteria form spores?

Gram positive (some)
NEVER Gram negative

164

T/F
A minimum amount of metabolism goes on in endospores.

False

NO metabolic processes

165

Structure of endospore:

Dehydrated core with DNA
thick Peptidoglycan
Keratin-like protein

166

What are 2 of the most common and important spore forming bacteria?

Bacillus
Clostridium

167

Describe Clostridium:
metabolism
Gram
Shape
spore forming?
where found

Obligate anaerobe
G+
Bacilli (rods)
spore forming
ubiquitous

168

What are the 4 Clostridium human pathogens?

C. tetani
C. botulinum
C. perfringens
C. difficile

*these are all G+ spore formers and strict anaerobes

169

What is special about the A-B exotoxin secreted by C. tetani and C. botulinum?

They are the most potent toxins known

170

T/F
Botulism causes "true" food poisoning.

True

171

T/F
Perfringens is an infection food poisoning

True

172

What is the worldwide mortality rate for tetanus?
For infants?

20-50%
90%

173

What is the mechanism of the Clostridium tetani toxin?

Blocks neurotransmitter release of Inhibitory Synapses

174

What is the main way we contract C. botulinum?

spores in Food

*infants and honey, home canning ("true")

175

What is the mechanism of the Clostridium botulinum toxin?

Blocks RELEASE of neurotransmitter acetylcholine at the NMJ

*this prevents contraction (flaccid paralysis)

176

T/F
The immune system can respone to C. tetani and C. botulinum.

False

they are so powerful immune system never sees it at lethal dose

177

Why do infants have less tolerance for C. botulinum?

Stomachs higher pH

178

What two pathologies do Clostridium perfringens cause?

Gas gangrene
Food poisoning

179

What type of exotoxin does C. perfringen produce?

mostly Cytolytic

*huge number

180

What is the mode of most C. perfringens food poisoning?

left out meat

181

What Clostridium is associated with broad spectrum antibiotics?

C. difficile

*has 2 exotoxins

182

What is another G+ spore forming pathogen other than Clostridium species?

Bacillus anthracis

*this is a HUGE G+

183

What are the 3 types of pathologies caused by Bacillus anthracis?
Mortality rates?

Cutaneous anthrax (20%)
Pulmonary anthrax (90%)
GI anthrax (50%)

184

What type of toxin is released by Bacillus anthracis?

two potent A-B exotoxins
Edema Toxin
Lethal Toxin

*uses Macrophage taxis

185

What is the Bacillum species that causes true food poisoning, mostly by re-heated fried rice?

Bacillum cereus

186

What are the 2 most important species of Mycobacterium affecting humans?

M. tuberculosis
M. leprae

187

Why is B-cell immunity no good against Mycobacterium?

Because they get INTO cells

188

Describe the pathology/immune response in M. tuberculosis.

Infects macrophage (mostly)
Immunity isolates into lung granulomas

189

Describe the pathology/immune response of M. leprae.

Infects Schwann cells

Immunity only slows disease progression
either Tuberculoid (strong) or Lepromatous (weak)

190

T/F
1/3 of the world is infected with TB

True

191

Where does Mycobacterium tuberculosis usually live?

Man, cows, birds, soil, milk, deer, etc.

192

What is unique about the membrane of M. tuberculosis?

High lipid content
(60% dry weight)

193

T/F
TB grow fast

False

194

T/F
TB is an Obligate Aerobe

True

195

Why is milk pasteurized?

TB is sensitive to heat

196

What are some morphological features of M. tuberculosis?

Poor staining Gram+
lipid rich
Acid Fast

197

What is the infection rate of TB in US and worldwide?

10 million US
2 billion world

198

What does it mean to be Infected Latent?

Infected but not infectious

199

How many die/yr from TB?

1.2 million

200

What are 3 major problems in wiping out TB?

complacency
poor compliance
multi-drug resistance

201

What is THE virulence factor in TB?

Lipid (waxy) membrane

*has Mycolic Acid
(relatively impervious barrier to enzymes, etc)

202

Why are antibodies of no use fighting TB?

It wants to be in macrophage

*only way to deal is put it in Granuloma jail

203

T/F
M. tuberculosis has resistance to enzymes, pH, drying

True

204

How is TB detected in the US?

PPD skin test
IFN-gamma release assay

205

How is the vaccine (BCG) for TB made?

from M. bovis
makes cross reactive immunity
(false + PPD screens)

Decks in Tim's Cards Class (140):