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Microbiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What are the main virulence factors of N. meningitidis

A
  1. Fimbrae, to attach to nasopharynx
  2. capsule, antiphagocytic and different serotypes
  3. IgA protease, to destroy IgA of course
  4. LPS blebs, systemic inflammation if in blood
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2
Q

How is N. meningitidis spread

A

Via respiratory droplets among individuals with prolonged contact

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3
Q

What are the natural carriers of N. meningitidis

A

Only humans

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4
Q

What is the asymptomatic carrier rate of N. meningitidis

A

~10% of individuals

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5
Q

Who is most susceptible to N. meningitidis

A

Babies, elderly, late teens, and those who live in crowded conditions

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6
Q

Which of the virulence factors do all invasive strains of N. meningitidis have

A

Anti-phagocytic capsule

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7
Q

What makes an individual susceptible to N. meningitidis

A

Lack opsinizing antibodies to the particular strain, and further compromised by respiratory damage (smoking, infection)

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8
Q

What diseases can N. meningitidis cause, and which is the most severe

A

meningitis (10% fatality) and meningococcal sepsis (40% fatality)

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9
Q

How does meningococcal sepsis cause damage

A

Bacteria blebs off outer membrane which activates monocytes to produce large quantities of cytokines. This causes systemic inflammation, with decreased blood pressure, disseminated intravascular coagulation, etc “septic shock”

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10
Q

What is meningitis

A

N. meningitides make their way to the brain and set up home there, where their endotoxin triggers a massive immune response with local and systemic inflammation

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11
Q

What are the methods for prevention of meningococcal disease

A

antimicrobial prophylaxis of persons in close contact with a carrier, and vaccination

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12
Q

What are some viruses that cause lymphocytic meningitis

A

coxsackie and polio

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13
Q

What are the main causes of acute purulent meningitis in neonates

A

Strep. pneumoniae, H. influenza

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14
Q

What are the main causes of acute purulent meningitis in children

A

H. influenza, N. meningitidis, Strep pneumoniae

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15
Q

What are the main causes of acute purulent meningitis in adults

A

N. meningitidis, strep. pneumoniae

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16
Q

What are the main causes of acute purulent meningitis in elderly

A

Strep. pneumoniae

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17
Q

Viruses and bacteria can both cause meningitis and encephalitis, which is more common and which is more deadly

A

Viral is more common, bacterial is more deadly

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18
Q

Where is Neisseria normally found

A

It is a normal, hardy, oral species

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19
Q

Are the pathogenic Neisseria bugs hardy?

A

nope! very fragile actually and drying kills it

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20
Q

Is Neisseria gam positive or negative

A

Negative, it’s got LPS

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21
Q

What is the appearance of Nesseria under the microscope

A

Pairs, “the official bacteria of starbucks” because it looks like a coffee bean

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22
Q

What are the main virulence factors of N. gonorrhoeae

A
  1. Fimbrae (attachment and escape phagocytosis) 2. Ag-variation of pili structure (gene conversion and phase variation) 3. Surface receptors for host protein (camo) 4. IgA protease 5. LPS 6. Penicillin resistance (beta-lactimase) 7. Intracellular (hide)
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23
Q

Why does N. gonorrhoeae remain a local infection

A

It doesn’t have a capsule

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24
Q

What is the natural reservoir for N. gonorrhoeae

A

humans, particularly the asymptomatically infected person (usually a woman)

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25
Q

What could happen if a N. gonorrhoeae infection is left untreated

A

10-20% of untreated women develop pelvic inflammatory disease, which can result in scarring, sterility, and ectopic pregnancy

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26
Q

What risk do newborns have in contracting a N. gonorrhoeae infection

A

They can get gonorrhoeae in their eyes via the whole birthing process, so they are often treated with antimicrobial drops in their eyes

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27
Q

Why is there no vaccine for N. gonorrhoeae

A

Because it has so many variable surface antigens (epitopes)

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28
Q

Can you get N. Gonorrhoeae from a toilet seat

A

extremely unlikely since it is a very fragile bug; needs mucosal contact

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29
Q

What are the top 4 STI’s in the US

A
  1. HPV 2. Chlamydia 3. Trichamoniasis 4. Gonorrheae
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30
Q

Where does N. Gonorrhoeae live and replicate

A

In mucosal cells, usually in the genital tract, occasionally oral or eyes (newborns). They also pass through to the lamina propria

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31
Q

Can you be reinfected with N. Gonorrhoeae

A

Absolutely. The antigenic variation and phase variation means that we have poor immunity to them

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32
Q

What type of infection does N. Gonorrhoeae cause

A

A local, pyogenic infection. Thanks, LPS!

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33
Q

What type of cells are killed by N. Gonorrhoeae

A

ciliated columnar cells = ulcerant

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34
Q

Can you ever get rid of N. Gonorrhoeae infection without antibiotic treatment

A

Yes, it often ‘self cures’ in 2-3 weeks.

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35
Q

What does rickettsia, chlamydia, and mycoplasma have in common

A

They are all very small, gram negative coccobacilli and all steal from their host

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36
Q

What type of environment does N. Gonorrhoeae like

A

Microaerophilic

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37
Q

What do rickettsia and chlamydia steal from their host

A

They are intracellular obligate parasites that steal ATP and amino acids

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38
Q

What does mycoplasma steal from its host

A

It is an extracellular parasite that steals host cholesterol and lipids to strengthen its cell membrane.

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39
Q

What type of infection does Rickettsia cause

A

Systemic infections by infecting endothelial cells, with capillary blockage and fever caused by LPS

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40
Q

What type of infection does chlamydia cause

A

local infection IN mucosal epithelium

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41
Q

What type of infection does mycoplasma cause

A

Local infection ON mucosal epithelium, and releases a super-ag that is the main cause of epithelial damage

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42
Q

What is the cell wall situation with rickettsia, chlamydia, and mycoplasma

A

Rickettsia has a cell wall and LPS, chlamydia has LPS but no cell wall, and mycoplasma has no LPS and no cell wall

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43
Q

What diseases do rickettsia cause

A

Spotted fever, Typhus, Q fever (systemic LPS)

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44
Q

What diseases does chlamydia cause

A

eye infection (not so much in the US), STI chlamydia

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45
Q

What diseases does mycoplasma cause

A

pneumonia and urethritis

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46
Q

What is the main reservoir for Rickettsia

A

animals and arthropods

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47
Q

What is the main vector for Rickettsia

A

arthropods

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48
Q

What is the reservoir for R. prowazekii

A

Human

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49
Q

What disease does R. prowazekii cause

A

Epidemic typhus, which spreads human to human in crowded, poor sanitary conditions by body lice.

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50
Q

What is endemic (murine) Typhus

A

A common but mild disease caused by rickettsia typhi with urban rodents as its main reservoir

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51
Q

What are the three majors species of Chlamydia

A

C. trachomatis, pneumoniae, psittaci

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52
Q

What disease does C. trachomatis cause

A

STI, and another strain causes trachoma

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53
Q

Which species of Chlamydia is best adapted to humans as the host

A

C. trachomatis. C. psittaci is a bird bacteria, and C. pneumonia is very mild

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54
Q

How are C. trachomatis eye infection strains spread

A

From eye-to-eye by tears, hands and flies, repeat infection leads to permanent inflammation and in-turning of the eyelids resulting in blindness

55
Q

How does chlamydia STI compare to gonorrhoeae STI

A

4x more chlamydia STI than gonorrhoeae, both untreated lead to PID, and chlamydia is not treated with penicillin because it has no cell wall

56
Q

What is the main disease that Mycoplasma pneumonia causes

A

walking pneumonia. Other species cause mild UTI and genital diseases

57
Q

What type of environment does Mycoplasma like

A

Common inhabitants of mucosa; they are facultative

58
Q

What is the main pathology of mycoplasma

A

It produces a toxin which decreases ciliary action and epithelial sloughing leading to poor mucus clearance

59
Q

What type of bacteria is Corynebacterium

A

Gram positive, non-spore-forming rod (bacilli)

60
Q

Where is Corynebacterium found

A

It is ubiquitous in plants and animals

61
Q

Where does Corynebacterium colonize humans

A

Skin, URT, and GI. All can be opportunists

62
Q

What makes Corynebacterium diphtheriae pathogenic

A

It is infected by a virus that carries the genetic information for an AB exotoxin

63
Q

What type of infection is diphtheria

A

Local infection, systemic disease

64
Q

What is a main sign of a C. diphtherium infection

A

The production of a psuedo-membrane of a thick, proteinaceous matrix, that causes bleeding when dislodged

65
Q

What does the AB exotoxin in C. diphtheriae do

A

It causes a major decrease in protein synthesis and primarily affects heart tissue, causing permanent heart damage and/or death

66
Q

What is a toxoid

A

a toxin that has been modified so that it is no longer pathogenic, but is still immunogenic

67
Q

What is an anti-toxin

A

something (antibody) that neutralizes a toxin

68
Q

What type of bacteria form spores

A

Some gram positive, but never gram negative, bacteria like Clostridium and Bacillus

69
Q

What is a spore

A

Dehydrated, multi-shelled structure that allows the bacterium to exist in ‘suspended animation’ for an incredible period of time

70
Q

How does a spore keep a bacterium alive for so long

A

The structure of a spore protects the DNA from desiccation, heat, radiation, enzymes, and chemicals

71
Q

What type of bacteria are Clostridium

A

Gram positive, obligate anaerobic bacilli capable of forming spores

72
Q

What Clostridium species are human pathogens

A

C. tetani, botulinum, perfringens, difficile

73
Q

What is the main pathology of Clostridium tentani

A

It produces an AB exotoxin that blocks inhibitory neuron release of glycine causing spasmodic paralysis

74
Q

What is the main pathology of Clostridium botulinum

A

It produces an AB exotoxin that blocks the release of acetyl choline causing flaccid paralysis

75
Q

What is the lethal dose of C. tetani or botulinum

A

roughly 0.1 microgram

76
Q

How does one get a C. tetani infection

A

a dirty wound. Spores get way into a wound, where there are nice anaerobic necrotic conditions which prompt it to germinate

77
Q

How does one get a C. botulinum infection

A

By eating food that was improperly canned and thus allowed C. botulinum to germinate, or it will also germinate in the gut of an infant.

78
Q

How does C. Perfringens cause gas gangrene

A

Spores get into a deep wound, germinate, and then produce massive amounts of cytolytic exotoxins and digestive factors

79
Q

How does C. perfringens cause food poisoning

A

Not a true food poisoning, one eats food (typically meat) that has been left out for too long. In the small intestine, they release a toxin that causes cramping and diarrhea

80
Q

How does C. difficile cause pseudomembrane colitis

A

After receiving antibiotic therapy, the C. difficile overgrows and produces 2 exotoxins. It forms a pseudomembrane that blocks the colons function

81
Q

How serious is C. difficile infection

A

it has a 10-15% mortality, partially because many people who get it are already sick. But deaths have 2x in the past 10 years thanks to a particularly virulent strain

82
Q

What type of bacterium is Bacillus anthracis

A

gram positive, spore forming, facultative bacillus

83
Q

What are the main sites of infection for Bacillus anthracis

A

Cutaneous, pulmonary, gastrointestinal

84
Q

What is the main pathology of Bacillus anthracis

A

Macrophage taxis, Edema AB exotoxin, Lethal AB exotoxin

85
Q

What is the mortality rate of anthrax

A

cutaneous: 20% GI: 50% Pulmonary: 90% mortality

86
Q

Who is most at risk for a Bacillus anthracis infection

A

Primarily grazing animals, and those who handle them

87
Q

What type of bacterium is Mycobacterium tuberculosis

A

Acid-fast, aerobic slender rod

88
Q

What is the main virulence factor of Mycobacterium tuberculosis

A

Lipid rich wall/coat that is resistant to disinfectants, detergents, common abx, and traditional stains

89
Q

What is the typical treatment for a Mycobacterium infection

A

Because the body can’t rid itself of Mycobacterium by itself, a long, multi-drug course of antibiotics is necessary

90
Q

What cell does Mycobacterium tuberculosis typically infect

A

Macrophages; it evades phagocytosis with its waxy coat

91
Q

What is the main reservoir for Mycobacterium

A

humans

92
Q

What are the disease stages of M. tuberculosis infection

A

Latent infection, in which you are infected but not infectious, and active disease in which you are infected and infectious

93
Q

What are problems with getting rid of a M. tuberculosis infection

A

Compliancy is traditionally poor, and so multi-drug resistant strains have been bred.

94
Q

Who normally develops active tuberculosis disease

A

Those with a compromised immune system

95
Q

What tissue does Mycobacterium leprae normally infect

A

Schwann cells in the periphery and cool parts of the body

96
Q

What slows the progression of a Mycobacterium Leprae infection

A

Launching a Th1 response (tuberculoid, humoral) to isolate the bacteria in granulosas

97
Q

Why doesn’t a Th2 response work well against Mycobacterium leprae or tuberculosis

A

Because antibodies and c’ are ineffective against it, and CD8 doesn’t help either

98
Q

What is the main transmission route for M. tuberculosis

A

Respiratory from person to person, M. bovis can spread from cows or dust to a person

99
Q

How hardy is M. tuberculosis

A

It is resistant to chemicals and drying (5% phenol for 24 hrs) and heat sensitive (30 minutes at 62 C) this is the basis for pasteurization and sterilization protocols

100
Q

How long does it take M. tuberculosis to double

A

10-20hrs (sloooooow)

101
Q

How many people have died from TB in the last century

A

1.5 billion! that’s 5% of all deaths

102
Q

Who is at risk for TB

A

Alcoholics, crowding, poverty, homeless, prisons, drug abuse, HIV, Immune therapy, health workers

103
Q

What are the classic signs of tuberculosis disease

A

chronic, bloody, productive cough, fever and night sweats, weight loss

104
Q

What diagnostic techniques are used to confirm M. tuberculosis infection

A

PPD skin test or TST(cheap), lung X-ray, Sputum smear stain and culture, PCR (expensive machine)

105
Q

Why doesn’t the USA routinely recommend TB vaccination

A

Because TB is rare in the US, and then the PPD skin test would be worthless. Cost vs Risk

106
Q

What is DOT

A

Directly Observed Therapy. This was designed to improve compliance with abx courses

107
Q

What is the most popular TB vaccine

A

BCG: Attenuated M. Bovis, designed to stimulate CD4 cells, is 80% effective

108
Q

What is the difference between parasitism and saphrophytism

A

A parasite’s host is live, a saprophyte’s host is dead

109
Q

What is the different between commensalism and mutualism

A

Mutualism both parties benefit, commensalism only one benefits while the other is neutral

110
Q

What type of organism is Candida

A

It is a fungus, eukaryotic mono cellular

111
Q

What makes fungal infections tricky to treat

A

They are eukaryotes, like us, so they have very mechanisms drugs can target without damaging the patient

112
Q

What are the sterols used in cell walls

A

Yeasts use: ergosterol and zymosterol. Animals use: cholesterol

113
Q

What is the main virulent factor of fungi

A

C3b protease; enzyme that destroys proteins, like Ab and C’

114
Q

What is candida’s cell wall made of

A

Beta 1-4 N-AGM (chitin)

115
Q

What are the 7 fungal pathologies

A
  1. mycotoxicoses 2. hypersensitivities 3. superficial mycoses 4. cutaneous mycoses 5. subcutaneous mycoses 6. systemic mycoses 7. opportunistic mycoses
116
Q

What causes mycotoxicoses

A

a variety of toxins, all gained by eating mushrooms and result in liver damage. Rare

117
Q

What are fungal Hypersensitivities

A

Hay fever and asthma are IgE response to fungi, contact dermatitis to fungal products. Common

118
Q

Where are superficial mycoses

A

in the outermost skin layers, hair. No immune response. Common

119
Q

What cause cutaneous mycoses

A

Dermatophytes cause skin and nail infections. common

120
Q

What causes subcutaneous mycoses

A

Fungi/spores that get into a wound. Serious. Rare

121
Q

Who is susceptible to opportunistic mycoses

A

Young, old, immunocompromised individuals, oral appliance (dentures), IV catheter

122
Q

What are the common opportunistic mycoses species

A

from common to rare: candida, cryptococcus, aspergillosis, pneumocystis

123
Q

What is systemic mycoses

A

Typically a lung infection from a HUGE dose that overwhelms host immunity. Clinically similar to TB. Rare-ish

124
Q

What is the most common fungal opportunist and what diseases does it cause

A

Candida albicans causes thrush and yeast infections

125
Q

How many forms can candida take

A

3: single cell, non-seperated single cells “pseudohyphae”, true hyphae

126
Q

What prompts candida to switch forms

A

pH. it is yeast in acidic environments and switches to hyphae in basic environments

127
Q

What is the most pathological form of candida

A

hyphae form. it secretes ammonia and may help it “jailbreak”

128
Q

What is the best immune response to candidiasis

A

Th1 response; Ab’s, C’ are of no value because it has protease

129
Q

What is the pseudomembrane in candidiasis composed of

A

Dead PMNs, live PMNs, fibrin, and fungal cells. It is easily wiped off

130
Q

What is a common treatment for thrush

A

Painting it with crystal violet or gentian violet

131
Q

What does skin do in a fungal infection

A

It often hyper-proliferates to increase protective keratin layer and to hopefully slough off the fungal colonization

132
Q

What causes rocky mountain spotted fever

A

Rickettsia rickettsii. This is the most frequent and severe rickettsial disease in the US. Spread by ticks

133
Q

What causes scrub typhus

A

Orientia tsutsugamuchi

Microbiology (4 decks)

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