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Winter course I > Micro > Flashcards

Micro Flashcards

1
Q

What largely affects epidemiology of S. pneumoniae?

A

Co-infection

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2
Q

What age groups have highest incidence and mortality in S. pneumoniae infection?

A

Incidence: young, mortality: elderly

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2
Q

What types of infections does s. Pneumoniae cause?

A

Pneumonia, meningitis and otitis media

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2
Q

What makes some S. pneumoniae so virulent?

A

Capsule: phagocytosis resistance

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2
Q

What determines the composition of a capsule?

A

Serotype

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3
Q

How are capsules produced?

A

Repeating sugar units are produced intracellularly and then flipped outside the membrane.

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4
Q

What determines transformation competence in S. pneumoniae?

A

Environmental signals such as high cell density and stress

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5
Q

How does competence work?

A

It leads to transformation of DNA from neighbouring cells and fratricide

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6
Q

Why is the upper respiratory tract great for transformation competence?

A

Lower temperature and nutrient scarcity

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7
Q

What is pneumolysin

A

A poreforming toxin made by S. Pneumoniae that causes inflammation. It can cause hemolysis even after antibiotic treatment

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8
Q

Why is reduction of capsule important in S. Pneumoniae?

A

Adhesion and colonization

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9
Q

What antibodies are effective against S. Pneumoniae?

A

IgA is cleaved by SP, but IgG can form immune complexes (agglutination)

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10
Q

What’s the biggest problem with capsule vaccines?

A

Serotypes have their own specific structures and thus also their own specific antibodies, hence the word serotype. They also can’t be presented well by APCs so poor T cell immunity. That’s why a carrier protein is added to induce T cell help

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11
Q

What is serotype replacement?

A

Vaccines for pathogens with many serotypes cause some serotypes to die out or slow, so others increase and take their place

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12
Q

What should you make sure of when trying to induce mucosal immunity?

A

Be above tolerance barrier

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13
Q

How does Th17 immunity work?

A

AMPs, IgA production, neutrophil activity

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14
Q

What are outer membrane vesicles?

A

Usually made by gram - bacteria. They are antigen delivery vehicles and adjuvants combined, as they can display PAMPs and attach to pathogens

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15
Q

What is the biggest drawback of outer membrane vehicles?

A

LPS can give a toxic substance and a too strong immune response, so LPS now is detoxified first

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16
Q

How are vaccine antigens selected?

A

You can use programs that can predict conservation, whether it’s surface associated, etc.

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17
Q

What is the life span of a schistosome

A

15 years in the blood vessels

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18
Q

What determines where schistosoma can be endemic?

A

The presence of the specific intermediate host

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19
Q

How do cercariae move to the skin?

A

Chemotaxis to short chain fatty acids that can dissolve into water

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20
Q

How do cercariae get into the skin?

A

Proteases that it produces

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21
Q

How do schistasomas desseminate in the body?

A

The blood vessels

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22
Q

What is the main cause of pathology in schistosomas

A

Granuloma formation around non-secreted eggs trapped in the host tissue, causes liver fibrosis and failure

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23
Q

What type of immune response is induced against schistosomas?

A

Th2 type - IgE, IgG4, eosinophils and mast cells, mucus thickening

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24
Q

What is the hygiene hypothesis?

A

Negative feedback mechanism due to infection with a pathogen (i.e) that induces Th2 response, which suppresses and prevents allergy and asthma, therefore more western countries have the latter

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25
Q

Why are there no blood clots in schistosoma infection?

A

The egg attaches to the vessel through thrombocyte attachment and is engulfed, taking it out.nthey also bind to von Willebrand factor and other clotting factors. There is no adhesion of thrombocytes to eggs, but schistosomas affect thrombin formation in many different ways.

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26
Q

What is the purpose of the double membrane around schistosoma tegument?

A

Protection against lysis through complement pores and turnover of antigens

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27
Q

What are superantigens?

A

When there is a shortcut by T cells to respond to antigens, causing a broad and extreme reaction

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28
Q

What is incidence of S. aureus?

A

High in young children, peak in teenagers, lower as age increases

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29
Q

What is a major risk factor for endogenous S. aureus infection?

A

Nasal carriage

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30
Q

What types of carriers are there for S. aureus?

A

Persistent carriers, intermittent carriers and non-carriers, though intermittent is debated

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31
Q

Is persistent carriage due to host factors or microbe factors?

A

Both

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32
Q

What is noteworthy about the strains of S. aureus in persistent carriers

A

They have the same strain despite exposure with a mix, even after eradication first

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33
Q

What HLA is associated with persistent carriage of S. aureus?

A

HLA-DR3

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34
Q

What characteristic of the immune response is associated with persistence?

A

Local immunity that fails to clear it, caused by SNPs in c reactive protein and IL4 for example

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35
Q

What properties do S. Aureus have to allow for colonization?

A

IL-1 suppression, biofilm formation, clumping factor B

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36
Q

What are candidate targets for decolonization strategies?

A

Clumping factor B, biofilm

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37
Q

What bacteria have an inverse relationship?

A

S. aureus and S. pneumonia

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38
Q

How can local competition be exploited for treatment?

A

High dose of avirulent bacteria can lead to elimination of S. aureus from the nose

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39
Q

What are the patterns of nasal bacteria species richness for S. aureus and S. epidermidis vs others?

A

There is almost no species richness in S. carriers compared to others

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40
Q

What are the the 3 main fungal families that cause human disease?

A

Mucoromycota, ascomycota and basidiomycota

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41
Q

What is amphotericin B

A

The first antifungal discovered. Still low resistance compared to others

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42
Q

What are 4 possible causes of microbial resistance in the clinic?

A

Host immune status, host mutations, presence of catheters and site ofninfection

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43
Q

What is different about antifungal resistance compared to antibacterial resistance?

A

Antifungal resistance can be acquired before infection instead of during treatment, such as due to the use of antifungals in the field

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44
Q

What can cause polyene resistance?

A

Lower ergosterol in the membrane, alteration of fungal cell membrane or cell wall

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45
Q

What do azoles act on?

A

The biosynthesis pathway of ergosterol

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46
Q

What is the principal sterol in fungal cell membranes?

A

Ergosterol

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47
Q

What happens when the azole target is modified?

A

Lower binding due to certain mutations -> resistance

48
Q

What happens when there are multiple target copy numbers of azoles?

A

Resistance

49
Q

What is aneuploidy?

A

An extra chromosome 5 of a fungus

50
Q

What causes overexpression of drug transporters

A

Aneuploidy and induced mutations in chromosome 5

51
Q

What does overexpression of drug transporters lead to?

A

Antifungal resistance

52
Q

Can fungi produce biofilms?

A

Yes

53
Q

When is chitin synthesis upregulated?

A

During stress, to prevent bursting

54
Q

What is ERG11

A

It encodes for an enzyme and is the binding site of azoles

55
Q

Why is it hard to make antifungal drugs?

A

They resemble humans more than bacteria. Making it hard to make a specific drug that is not toxic for humans

56
Q

Why are vaccines hard with fungi?

A

Most infections are in immunocompromised

57
Q

What are the three main targets of antibiotics?

A

Cell wall synthesis, DNA, RNA and protein synthesis, folic acid metabolism

58
Q

What are the broadest antibiotics?

A

Carbapenems, that’s why we try to save them as much as possible

59
Q

What do beta lactams work on and why

A

Gram negative bacteria due to the structures in the cell wall

60
Q

Which group of bacteria have a thick peptidoglycan layer?

A

Gram positive bacteria

61
Q

What are the three stages of peptidoglycan synthesis?

A

Cytoplasmic stage, membrane-associated stage and extracytoplasmic assembly

62
Q

What does bactericidal effect depend on?

A

Lytic enzymes and autolysins when the cell surface stage is disrupted

63
Q

What are peptidoglycans composed of?

A

NAM/NAG sugars, a tetra peptide and bridges that bind the peptides

64
Q

How do beta lactams work?

A

Disrupt Penicillin binding proteins which causes overproduction of autolysins

65
Q

What is primarily needed for beta lactams to work efficiently?

A

Permeability (porins/channels) and high enough speed of diffusion through them

66
Q

What is a second thing that causes resistance of beta lactams?

A

Decreased affinity to PBP due to mutations of PBP

67
Q

What does PBP stand for?

A

Penicillin binding protein

68
Q

What are beta lactamases?

A

Enzymes that break down beta lactams

69
Q

What are the two types of beta lactamases expression patterns?

A

Constitutive and inducible

70
Q

Where is the beta lactam gene located

A

Chromosome or plasmid depending on the bacteria

71
Q

Why is it bad to have beta lactamases genes on plasmids?

A

Transferable

72
Q

What does extended spectrum mean?

A

Broad range of bacteria as targets

73
Q

What is the mechanism of action of aminoglycosides?

A

Binding to the 30S ribosomal unit causing codon misreading and subsequently bacteriocide

74
Q

What is the most important mechanism of resistance to aminoglycosides?

A

Aminoglycoside-modifying enzymes

75
Q

What is the mechanism of action of quinolones?

A

Targets topoisomerases which regulate supercooling and can cut DNA during replication via binding

76
Q

What is the mode of uptake of quinolones?

A

Passive diffusion in the body (it’s very small), active diffusion through the peptidoglycan wall into the cytoplasm.

77
Q

What are the main mechanisms of resistance against quinolones?

A

Mutations in genes of DNA gyrase and topoisomerase, also decreased poring expression, and plasmid mutations

78
Q

Where is risk of acquisition of MDROs highest?

A

Asia (especially southern Asia), (North) Africa, West pacific

79
Q

What are behavioral risk factors of getting an MDRO during travel?

A

Antibiotic use during travel and eating street food, travellers diarrhea, also daily meals at hostels

80
Q

What are the most important measures against MDROs?

A

Surveillance and prevention

81
Q

What are three ESBL enzymes?

A

SHV, TEM, CTX-M

82
Q

What klesbiella clone can possibly spread like crazy?

A

CTX-M

83
Q

Can bacteria be altruistic?

A

Sort of, to prevent the spread of phages

84
Q

What is the relationship between phages and bacteria?

A

Cat and mouse but also mutually beneficial

85
Q

How does the fact that some pseudomonas phages need the efflux pump benefit us?

A

It creates susceptibility to antibiotics due to changing the efflux pump, which plays a big role in antibiotic exposure

86
Q

How can phage treatment be used? Name 2

A

Opsonophagocytosis since a bound phage increases antibody response, crispr cas, and enhancing antibiotic activity against biofilms

87
Q

What two bacteria are the most common causative agents of bacterial meningitis?

A

S. pneumoniae and Neisseria meningitidis

88
Q

What causes Waterhouse-Friderichsen Syndrome?

A

Neisseria meningitidis

89
Q

What is are two important clinical signs of meningitis?

A

Neck stiffness, petechiae

90
Q

What are petechiae specific for?

A

Neisseria meningitidis

91
Q

Where does meningitis occur?

A

In the subarachnoid space

92
Q

What visible characteristic of CSF is a hallmark of meningitis?

A

Purulence

93
Q

What is the pathogenesis of meningitis?

A
  1. Passage through nasopharyngeal mucosa into the bloodstream
  2. Survival in the blood stream, acquisition of iron from transferrin (for replication) and protection using capsule
  3. Crossing of BBB into subarachnoid space due to damaged caused by inflammation
94
Q

What are risk factors for bacterial meningitis cause by N. meningitidis?

A

Smoking, infected hosuehold, nasopharyngela carriage and genetic ploymorphisms (related to inflammatory pathways)

95
Q

What are risk factors for bacterial meningitis cause by S. pneumoniae?

A

Nasopharyngeal carriage, immunocompromised, splenectomy patients, genetic polymorphisms

96
Q

What is behind most complications of bacterial meningitis?

A

Arteritis -> infarction
Purulent CSF and venous thrombosis -> hydrocephalus -> pressure -> low blood flow to cerebellum -> infarction
Septic shock -> low systemic blood pressure -> low blood flow to cerebellum -> infarction and multi-organ failure

97
Q

What are clinical features and tissue damage related to?

A

Violent immune response

98
Q

How is meningitis treated?

A

ASAP. Antibiotics + dexamethasone (anti-inflammatory)

99
Q

How can bacterial meningitis be prevented?

A

Vaccinations

100
Q

What is encephalitis?

A

An acute inflammation of the brain parenchyma that is never sterile

101
Q

What viruses cause viral encephalitis?

A

~100 viruses implicated worldwide, including herpes, entero- and paramyxoviruses. Also zoonotic viruses (arbo, rabies, nipah)

102
Q

What are the two main routes of viral entry into the the CNS?

A

Hematogenous (entero, arbo) and migration via peripheral nerves (herpes, rabies)

103
Q

What are two mechanisms of neurovirulence?

A

Cytopathic effect and immune response (antiviral or exacerbated due to microglial infection)

104
Q

What determined clinical signs of viral encephalitis?

A

Viral tropism

105
Q

What viruses most frequently cause severe encephalitis compared to others?

A

Arboviruses and herpes simplex

106
Q

What is causing an increase in JC virus incidence?

A

Reactivation due to MS treatment

107
Q

What is the incidence of encephalitis in WNV infected individuals?

A

low, mostly related to isolated outbreaks

108
Q

Was is the mortality rate of WNVE cases?

A

9% (up to 35% in elderly)

109
Q

How often do people recover from WNVE?

A

Most people do, but some develop fatigue, myalgia and residual tremors and parkinsomism

110
Q

What happens when WNV enters the parenchyma?

A

Local microglia initiated inflammatory response

111
Q

What herpesviruses are neurotropic?

A

Alphaherpesviruses

112
Q

What is herpes labialis

A

Infection of the mouth area that causes blisters cause by herpes simplex

113
Q

What causes herpetic stromal keratitis?

A

Herpes simplex in the trigerminal ganglion enters the ophthalmic branch

114
Q

How can herpes simplex enter the brain?

A

Through branches of the trigerminal ganglion

115
Q

How often is HSV-1 reactivation the cause of viral encephalitis?

A

11-22%

116
Q

What is the mortality rate of HSE?

A

untreated: 70%, early treated: 30%

117
Q

What is morbidity rate of HSE?

A

> 70% neurological deficits or retinitis

118
Q

What ages are most susceptible to developing HSE?

A

Either really young or really old

119
Q

How can HSE be treated?

A

pre-emptive acyclovir

120
Q
A

Winter course I (3 decks)

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