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Tim's Cards > Microbiology II > Flashcards

Microbiology II Flashcards

1
Q

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

A

Gram negative rods

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2
Q

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

A 
food
fluids 
fingers
flies
feces

(but really it’s just feces)

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3
Q

What are two pathologically important features of Gram negative rods?

A

Sharing of virulence factors
(through conjugation, etc)

Antibiotic resistance

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4
Q

Where are gram negative rods found?

A

ubiquitous

dirt, water, GI flora

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5
Q

T/F

Gram negative bacteria can cause cancer

A

True

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6
Q

How many species of Enteric Gram negative rods are there?

What is their metabolic category?

A

over 500

Facultative anaerobes

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7
Q

T/F

Enteric Gram negatives are highly fastidious.

A

False

they are non-fastidious but sensitive to drying

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8
Q

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

A

Oro fecal

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9
Q

What type of infection is Campylobacter?

A

Zoonotic

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10
Q

Where can Helicobacter live?

A

Stomach

*causes cancers and ulcers

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11
Q

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

A

H-antigens
K-antigens
O-antigens

*these are determined by agglutination

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12
Q

What is meant by Antigen Variation?

A

Bacteria evade adaptive response by changing epitopes

*referring to Gram- Enterics

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13
Q

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

A

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

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14
Q

Name 6 virulence factors for Gram- Enterics.

A 
Adhesive factors
Endocytosis (invade cells)
Macrophage Taxi
Capsules (phagocytic resistance) 
Phase variation
Antibiotic Resistance
Toxins
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15
Q

T/F

All Gram- Enterics have endotoxin, and some have exotoxin.

A

True

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16
Q

What are the specific adhesion molecules on Fimbrae called?

A

Adhesins

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17
Q

T/F

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

A

False

some do

*Bacterial-directed endocytosis

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18
Q

Which Gram- Enterics enter mucosal epithelium?

Which of these use macrophage taxis?

A

E. coli (EIEC)
Shigella

Salmonella
Yersinia
(these two taxi)

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19
Q

How do macrophage taxi Gram- Enterics survive?

A

Block endosome-lysosome function and escape the death chamber

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20
Q

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

A

Attaches to brush border and causes malabsorption

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21
Q

What 4 things does LPS directly activate?

this is our innate immune response

A

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

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22
Q

TNF-alpha stimulated endothelial cells to produce:

A

NO

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23
Q

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

*this is caused especially by what bacteria?

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

*bacteriamia

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24
Q

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

A

2 Robosylation of regulatory proteins (gut)

1 cleave rRNA and block protein synth

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25
Q

What is the equation for disease causing potential?

A

Virulence x Dose / Host resistance

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26
Q

Why is Shigella’s infectious dose very small?

A

Very acid resistant

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27
Q

How does Shigella infect the colon?

A

By invading epithelial “M” cells and dividing inside.

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28
Q

How does Shigella move laterally once inside these epithelial cells?

A

Actin-directed pseudopodia

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29
Q

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

A

dysentery

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30
Q

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

A

Shiga toxin
(A-B cleaves rRNA)

*damages intestinal epithelial cells

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31
Q

What can Shiga toxins do if they get into blood?

A

HUS - Hemolytic Uremic Syndrome

damage glomerular endothelial cells & renal failure

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32
Q

What encodes a Shiga-like Toxin?

A

Entero-hemorrhagic E. coli (EHEC)

*similar to S. dysenteriae

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33
Q

List Shigella species from most pathogenic to least:

A

S. dyssenteriae
S. flexneri
S. sonnei

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34
Q

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

A

Local

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35
Q

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

A

Ulcers, which causes dyssenteric symptoms

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36
Q

What is stool filled with in dysentery caused by Shigella?

A

mucus
pus
blood

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37
Q

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

A

Shiga-like

Systemically

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38
Q

What causes Typhoid Fever?

A

Salmonella typhi

macrophage taxis rupture and releases lots of bacteria
*systemic

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39
Q

Where is Salmonella typhi found in carriers?

A

Gallbladder (maybe gallstones)
feces

*typhoid Mary

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40
Q

How many Salmonella serotypes are there?

A

over 2000

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41
Q

How is Salmonella different from Shigella?

A

Doesn’t tolerate stomach acid as well

*need large dose for infection

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42
Q

How do most Salmonella species act in the gut?

A

Invade epithelial cells and destroy.

Usually isolated infection

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43
Q

Why is Salmonella typhi particularly infectious?

A

Evades macrophage destruction by using taxis

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44
Q

What is the definition of bacteremia?

A

Bacteria in blood

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45
Q

List Salmonella species from most to least virulent:

A

S. typhi
S. typhimurium
S. enterica

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46
Q

T/F

Salmonella is acid sensitive

A

True

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47
Q

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

A

adhesions and endotoxins

Shigella and V. cholera

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48
Q

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

(one gained from an unknown source)

A

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

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49
Q

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

A

HUS (hemorrhagic uremic syndrome)

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50
Q

What causes most (75%) UTI’s?

What allows them to survive in the urinary tract?

A 
E. coli (uropathogenic strains)
Specialized adhesions (fimbrae)
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51
Q

At what point can a UTI cause systemic LPS?

A

Once it reaches the kidney

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52
Q

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

A

Cytolytic exotoxin

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53
Q

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

A

Vibrio cholerae

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54
Q

What zoonotic infection has Shiga-like toxin?

A

Campylobacter jejuni

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55
Q

What causes ulcers and is a spiral Gram- rod?

A

Helicobacter pylori

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56
Q

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

A

Pseudomonas aeruginosa

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57
Q

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

A

Bacteroides

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58
Q

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

A

Brucella abortus

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59
Q

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

A

Bordetella pertusis

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60
Q

What Gram- rod causes Plague?

A

Yersinia pestis

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61
Q

Mortality rates:
Bubonic plague
Pneumonic plague

A

75%

100%

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62
Q

T/F

Y. pestis uses macrophage taxis

A

True

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63
Q

What are the toxic agents used by Y. pestis?

A

LPS

Superantigen

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64
Q

What are 2 sources of Passive Immunity?

A

Mother

Injection of antibody

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65
Q

Why is passive immunity temporary?

A

IgG half life 21 days

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66
Q

What is an important mild antibody?

A

slgA

(blocks colonization of gut viruses and toxins)

*protects from Vibrio cholerae

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67
Q

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

A

Cholera

Vibrio cholerae

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68
Q

What type of toxin does Cholera release?

What does it do?

A

A-B exotoxin
pumps salts and water into colon

*rice water stools

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69
Q

What is the treatment for Cholera?

A

Water/electrolyte matching

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70
Q

When is the “window of susceptibility” for babies?

A

3-5 months

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71
Q

What are the 2 major pathogenic Neisseria species?

A

N. meningitidis

N. gonorrhoeae

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72
Q

Neisseria meningitidis and gonorrhoeae are both?

A

Gram- diplococci

aerobic or microaerophilic

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73
Q

T/F

Both pathogenic Neisseria species cause purulent infections

A

True

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74
Q

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

A

nasopharynx

meningococcus

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75
Q

What are the 2 diseases caused by Neisseria meningitidis?

A

meningitis

meningococcemia

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76
Q

What are the major virulence factors of N. meningitidis?

A

Fimbrae (nasopharynx)
Capsule
IgA protease (very clever)

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77
Q

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

A

Anti-phagocytic

Antigenic differences between strains

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78
Q

How is N. meningitidis spread?

Natural carriers?

A

respiratory droplets and prolonged contact

humans only

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79
Q

What percentage are asymptomatic and carrying N. meningitidis?

A

10%

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80
Q

Who is susceptible to N. meningitidis?

A

Those lacking opsonizing antibodies to anti-phagocytic capsules

*moves from nasopharynx into blood - bacteremia

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81
Q

What can bacteremia from N. menigitidis lead to?

A

meningococcal sepsis (septic shock)

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

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82
Q

When are the peaks for death by menigococcal sepsis?

A 
3 months (vast majority of deaths)
20 yrs
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83
Q

What is the difference between meningitis and meningococcal septicemia?

A

Bacteria cross to the brain and local endotoxin causes damage

84
Q

What results in capillary blockage and damage during sepsis?

A

Disseminated Intravascular Coagulation

85
Q

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

A

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

86
Q

T/F

Viral meningitis is much more severe than bacterial.

A

False

Viral much more common much less severe

87
Q

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

A

Cloudy

88
Q

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

A

capsules

back of throat

89
Q

Where does the human reservoir for N. meningitidis reside?

Carrier rate?

A

Nasopharynx

10%

90
Q

T/F

N. meningitidis is very hardy.

A

False

Very fragile, drying kills, hard to grow

91
Q

What are meningits and meningococcemia both caused by?

A

Systemin LPS

92
Q

Meningococcemia is often accompanied with a…..

A

rash

93
Q

Both meningitis and meningococcemia are both ultimatley caused by….

A

Blebbed endotoxin released by N. meningitidis

94
Q

What is the fatality rate for bacterial meningitis?

% with serious outcomes like brain damage?

A

15%

15%

95
Q

What is the Fatality rate for Meningococcemia?

Serious outcomes like brain damage?

A

40%

50%

96
Q

Common name for N. meningitidis

Common name for N. gonorrhoeae

A

meningococcus

gonococcus

97
Q

What are the major virulence factors for N. gonorrhoeae?

A 
Fimbrae attachment to mucosal epithelium*
Gene conversion and Phase Variation
Incorporates host surface receptors 
IgA protease*
LPS*
Penicillin resistance
98
Q

Is N. gonorrhoeae encapsulated?

A

no capsule

99
Q

Why is gonorrhea so difficult to get rid of?

A

Half women have no symptoms

less that 10% men have no symptoms

100
Q

What is a consequence of untreated gonnorhea?

A

PID

Pelvic Inflammatory Disease

101
Q

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

A

Prevent gonococcal eye infections

if bad can lead to blindness

102
Q

N. gonorrhoeae is very hardy

A

False

103
Q

Name 3 important Virulence factors for N. gonorrhoeae.

A

Fimbrae
LPS
IgA protease

104
Q

Inflammation from gonorrhea is local/systemic and leads to _______

A

Local LPS

Pus (pyogenic)

105
Q

Gonorrhea in women:
% asymptomatic
% untreated

A

50
10-20

*leads to PID 1 million/yr

106
Q

Where does adhesive scarring occur in PID?

A

Fallopian tubes

107
Q

Is there a vaccine for gonorrhea?

A

NO

extreme antigen variation makes it difficult

108
Q

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

A

Rickettsia
Chlamydia
Mycoplasma

109
Q

What are Rickettsia and Chlamydia’s effects on tissues?

A 
Obligate Intra-cellular (invaders)
Attacks endothelium
Energy parasites (steal ATP)
110
Q

What are Mycoplasma’s effects on tissue?

A

Extra-cellular

Attacks epithelium

111
Q

What toxins does Mycoplasma have?

A

Super Antigen

and no LPS

112
Q

What are 2 results of a Rickettsia infection?

A

Spotted Feve

Typhus

113
Q

What are 2 results of a Chlamydia infection?

A

Eye infection

STD

114
Q

T/F

Rickettsia is an obligate intracellular parasite.

A

True

115
Q

Why must Rickettsia live inside cells?

A

Lack enzymes required to produce AA’s

116
Q

What is the main reservoir for Rickettsia?

A

Arthropods

117
Q

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

A

Infected arthropod defecates while biting, bacteria enter blood

118
Q

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

A

LPS flooding bloodstream systemically

119
Q

What is the most common and important Rickettsial disease worldwide?

A

Typhus

120
Q

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

A

Louse-born

R. prowazekii > lice > clothes

121
Q

What is the most common Rickettsia in the United States?

A

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

122
Q 
Organism and Vector causing the following:
Rocky Mountain Spotted Fever
Scrub typhus
Epidemic typhus
Murine typhus
A

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

*skip scrub/murine

123
Q

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

A

small
G-
Obligate intracellular parasites

124
Q

Rickettsia is an obligate _______ bacteria.
Gram?
Shape?

A

Intracellular
G-
coccobacilli

125
Q

What kind of parasite is the Rickettsia bacteria?

A

Energy parasite
Steals AA’s and ATP

*Chlamydia also does this

126
Q

What does Mycoplasma steal from its host?

A

lipids and cholesterol to strengthen its membrane

127
Q

Ticks are both the _____ and the ______ for Rickettsia.

A

reservoir

vector

128
Q

LPS in Rickettsia is systemic and causes what symptoms?

A

Headache, fever, chill

Rash

129
Q

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

A

Spotted fever group
Scrub typhus group
Typhus group

130
Q

How does Typhus differ from Typhoid?

A

Typhus - caused by Rickettsia

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

*typhus/typhoid - think fever/rash

131
Q

What does Rickettsia prowazekii cause?

What is its reservoir?

A

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

*DDT extremely effective against

132
Q

Describe Chlamydia

A 
Obligate intracellular parasite
no cell wall
two lipid bilayer/LPS
G-
energy parasite
133
Q

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

A

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

*psittaci is mostly bird pathogen, occasionally human

134
Q

What 2 diseases does Chlamydia trachomatis cause?

A

STD

blindness (trachoma)

135
Q

What is the primary reservoir for Trachoma?

What is the pathological progression?

A

children

eyelids turn inward and scar

136
Q

How is Chlamydia symptomatically similar to Gonorrhea?

A

symptomatic in men
asymptomatic in women

(generally)
* also a cause of PID

137
Q

T/F

Chlamydia and Rickettsia are energy parasites

A

true

138
Q

T/F

Chlamydia has a peptidoglycan wall and LPS

A

False

No peptidoglycan, but has LPS

139
Q

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

A

Mucosal epithelium

Local (and chronic)

140
Q

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

A

False

More than 50% population has serologic evidence of previous infection

141
Q

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

A

Birds to dust to lung

*generally only affecting immunocompromised

142
Q

T/F

There is a vaccine for C. trachmatis

A

False

143
Q

What is the most common bacterial STI in the USA?

A

Chlamydia trachmatis

144
Q

What are the smallest known self-replicating organisms?

A

Mycoplasma and Ureaplasma

145
Q

Describe Mycoplasma

A 
No LPS
Gm+
Very common 
No cell wall
sterols
146
Q

What is the major Mycoplasma pathogen?

A

M. pneumonia

147
Q

Where does M. pneumonia live?

A

Surface of respiratory epithelium

*destroys ciliated cells

148
Q

What type of inflammation does M. pneumonia elicit?

How?

A

Local

super antigen

149
Q

What is “walking pneumonia”?

A

atypical, mild

150
Q

T/F

Mycoplasma species have been implicated in genitourinary tract diseases, PID, and STI’s

A

True

151
Q

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

A
  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
Q

What causes diphtheria and where is it found?

A

Corynebacterium diphtheriae

skin, upper respiratory, GI

153
Q

What are 3 defining characteristics of C. diphtheriae?

A

G+
non-spore forming
Rods (bacilli)

154
Q

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

A

A-B exotoxin
(inhibits protein synth)

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

155
Q

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

A

B-subunit binds heart and nerve cells

Throat

156
Q

How is C. diptheriae usually transmitted?

A

Respiratory droplets of asymptomatic, immune carriers

157
Q

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

A

Pseudomembrane
Suffocation

*difficult to dislodge without making underlying tissue bleed

158
Q

How is diphtheria treated?

How avoided?

A

anti-toxin

toxoid (modified immunogenic toxin)

159
Q

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

A

Candidiasis

160
Q

T/F

Diphtheria is non-invasive.

A

True

*toxin invades

161
Q

Two major ways to die from diphtheria?

A

Suffocation

Heart

162
Q

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

A

Bacteria is found everywhere

USSR - Russia breakup lag in public health

163
Q

What type of bacteria form spores?

A 
Gram positive (some)
NEVER Gram negative
164
Q

T/F

A minimum amount of metabolism goes on in endospores.

A

False

NO metabolic processes

165
Q

Structure of endospore:

A

Dehydrated core with DNA
thick Peptidoglycan
Keratin-like protein

166
Q

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

A

Bacillus

Clostridium

167
Q 
Describe Clostridium:
metabolism
Gram
Shape
spore forming?
where found
A 
Obligate anaerobe
G+
Bacilli (rods)
spore forming 
ubiquitous
168
Q

What are the 4 Clostridium human pathogens?

A

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

*these are all G+ spore formers and strict anaerobes

169
Q

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

A

They are the most potent toxins known

170
Q

T/F

Botulism causes “true” food poisoning.

A

True

171
Q

T/F

Perfringens is an infection food poisoning

A

True

172
Q

What is the worldwide mortality rate for tetanus?

For infants?

A

20-50%

90%

173
Q

What is the mechanism of the Clostridium tetani toxin?

A

Blocks neurotransmitter release of Inhibitory Synapses

174
Q

What is the main way we contract C. botulinum?

A

spores in Food

*infants and honey, home canning (“true”)

175
Q

What is the mechanism of the Clostridium botulinum toxin?

A

Blocks RELEASE of neurotransmitter acetylcholine at the NMJ

*this prevents contraction (flaccid paralysis)

176
Q

T/F

The immune system can respone to C. tetani and C. botulinum.

A

False

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

177
Q

Why do infants have less tolerance for C. botulinum?

A

Stomachs higher pH

178
Q

What two pathologies do Clostridium perfringens cause?

A

Gas gangrene

Food poisoning

179
Q

What type of exotoxin does C. perfringen produce?

A

mostly Cytolytic

*huge number

180
Q

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

A

left out meat

181
Q

What Clostridium is associated with broad spectrum antibiotics?

A

C. difficile

*has 2 exotoxins

182
Q

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

A

Bacillus anthracis

*this is a HUGE G+

183
Q

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

A 
Cutaneous anthrax  (20%)
Pulmonary anthrax  (90%)
GI anthrax  (50%)
184
Q

What type of toxin is released by Bacillus anthracis?

A

two potent A-B exotoxins
Edema Toxin
Lethal Toxin

*uses Macrophage taxis

185
Q

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

A

Bacillum cereus

186
Q

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

A

M. tuberculosis

M. leprae

187
Q

Why is B-cell immunity no good against Mycobacterium?

A

Because they get INTO cells

188
Q

Describe the pathology/immune response in M. tuberculosis.

A 
Infects macrophage (mostly)
Immunity isolates into lung granulomas
189
Q

Describe the pathology/immune response of M. leprae.

A

Infects Schwann cells

Immunity only slows disease progression 
either Tuberculoid (strong) or Lepromatous (weak)
190
Q

T/F

1/3 of the world is infected with TB

A

True

191
Q

Where does Mycobacterium tuberculosis usually live?

A

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

192
Q

What is unique about the membrane of M. tuberculosis?

A

High lipid content

60% dry weight

193
Q

T/F

TB grow fast

A

False

194
Q

T/F

TB is an Obligate Aerobe

A

True

195
Q

Why is milk pasteurized?

A

TB is sensitive to heat

196
Q

What are some morphological features of M. tuberculosis?

A

Poor staining Gram+
lipid rich
Acid Fast

197
Q

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

A

10 million US

2 billion world

198
Q

What does it mean to be Infected Latent?

A

Infected but not infectious

199
Q

How many die/yr from TB?

A

1.2 million

200
Q

What are 3 major problems in wiping out TB?

A

complacency
poor compliance
multi-drug resistance

201
Q

What is THE virulence factor in TB?

A

Lipid (waxy) membrane

*has Mycolic Acid
relatively impervious barrier to enzymes, etc

202
Q

Why are antibodies of no use fighting TB?

A

It wants to be in macrophage

*only way to deal is put it in Granuloma jail

203
Q

T/F

M. tuberculosis has resistance to enzymes, pH, drying

A

True

204
Q

How is TB detected in the US?

A

PPD skin test

IFN-gamma release assay

205
Q

How is the vaccine (BCG) for TB made?

A

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

Tim's Cards (140 decks)

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