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Mic > LRTI URTI and ANTIBIOTICS > Flashcards

LRTI URTI and ANTIBIOTICS Flashcards

1
Q

Synthetic vs Semi-synthetic antibiotics

A

semi-Synthetic antibiotics are altered versions of naturally occurring antibiotics with altered pharmacological properties. Eg reduced toxicity

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2
Q

Bacteriostatic vs Bacteriocidal

A

Static = stops division. Cidal = kills bacteria (classification is based on killing 99.9% of bacteria)

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3
Q

What are tetracyclines, list 2. Why are they not favoured over B-lactam antibiotics for example?

A

4 ringed antibiotics - Minocyclin and doxycycline. They have a short half life and need to be taken 4 times per day.

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4
Q

How does penicillin work

A

Blocks transpeptidase - leads to loss of cell wall and the bacterium’s ability to maintain hydrostasis. The bacterium becomes hypERtonic and is osmotically lysed.

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5
Q

What is the strucutre of Penam

A
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6
Q

Name 3 natural antibiotics

A

Penacillan G

Cephalosporin C

Clavulanic acid

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7
Q

Benefits and drawbacks of Penacillan G

A

Non toxic - can be used in high doses even in children

Acid labile so needs to be given intramuscularly

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8
Q

What bacteria are the Penicillins effective against/not effective against?

A

Used against Gram + Cocci and Rods, and Gram - cocci (gonococci, meningocococcal mengitis)

Not effective against Pseudamonas aeruginosa - they have thick cell walls and chromosomally encoded beta-lactamase expressed in significant amounts

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9
Q

Methicilin
Flucloxacillin
Dicloxacillin

MRSA

A

It is effective against Pen G resistnat staphylococci. Nephrotoxic - given via IV.

Diclocacillin used more (less nephrotoxicity) or flucoxacillin (some hepatotoxicity) are used - can be given orally.

MRSA are resistant to every penicillin including methicillin

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10
Q

Ampicillin and Amoxycillin

A

Same thing basically

Broad spectrum antibiotics - active on GN bacteria (as well as GP)
H. Influenzae and E. Coli

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11
Q

Carbenicillin

A

Effective against gram negative rods (Pseudamonas aeruginosa) which is intrinsically resistant to ampicillan and penicillan etc)

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12
Q

What do Penicillans, Ampicillan, Methicilin, Flucoxacilin and Carbenicillin all have in common?

A

Beta lactams

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13
Q

Clavulanic acid

A

Beta lactam derived from streptomyces = not a penicilin

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14
Q

Fill in the following table

% resistance to plasmid mediated B-lactamase

Staphylococci

E. coli

Haemophilus spp.

N. gonorrhoeae

A

Staphylococci 80-90%

E. coli ≥50

Haemophilus spp. ≤50

N. gonorrhoeae ≤50

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15
Q

Which of the follow two species will clavulanic acid work against: Pseudomonas aeruginosa or Escherichia coli? Why?

A

Works against P. aeruginosa because Pseudomonas species have genome encoded beta-lactamase but E. coli uses a plasmid encoded beta-lactamase. Clavulanic acid works only against plasmid encoded beta-lactamases.

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16
Q

genii of Gram negative rods

A

Escherichia, Pseudomonas, Klebsiella, Vibrio (as in Virbio cholerae), Salmonella, Yersinia

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17
Q

How do aminoglycosides and tetracyclines work?

A

they target the ribosomes and inhibit protein synthesis. Aminoglycosides interfere at the C-site on ribosome.

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18
Q

What is the action of sulphonomides

A

Inhibit the synthesis of folic acid. Many bacteria synthesize this (it is essential for there growth). Non toxic to humans as we are not able to synthesize rather it is an essential nutrient.

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19
Q

Draw the structure of peptidoglycan:

A

Alternating chains of N-acetylglucosamine and N-acetylmuramic acid. M attached to L-Ala, D-Glu, L-Lys, D-Ala. Pentaglycines linking L-Lys and D-Ala.

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20
Q

How does vancomycin work?

A

Binds to terminal D-Ala D-Ala and stops pentapeptide-tetrapeptide linkage in peptidoglycan cell wall synthesis.

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21
Q

Which does Vancomycin not work against: Gram (-) or (+), and why?

A

Does not work against Gram (-) because it is too large and too charged to pass through the outer cell membrane.

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22
Q

Explain the basis of Vancomycin resistant enterococci?

Why are they worrying?

A

Enterococci uses a sugar residue instead of D-Ala D-Ala: L-Lys - D-Ala - D-lac

Don’t want it to confer vancomycin resistance to MRSA

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23
Q

VISA

A

Vancomycin intermediate Staph aureus - has a thicker cell wall to reduce permeability of vancomycin. The problem is that we can’t increase vancomycin doses too much because of side effects.

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24
Q

What is new/different about MRSA

A

They have altered penicillin binding proteins (i.e. transpeptidases) which penicillans cannot bind to.

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25
Q

What is the basis of resistance to aminoglycosides?

A

Enzymatic modification, ribosomal modification, outer wall modification

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26
Q

List three aminoglycosides.

A

Gentomycin, tobramicin, amikacin

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27
Q

How do bacteria defend against antibiotics?

A
  1. Reduced entry into cell
  2. Increased efflux from cell - pumps
  3. Ribosomal mutation - drug no longer effective
  4. Failure to activate prodrug (metronidazole - bacteria rid themselves of the enzyme which activates the drug).
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28
Q

3 intrinsic resistances to antibiotics

A
  1. Pseudamonas aeruginosa - B lactamase
  2. Mycoplasma spp. No cell wall
  3. GN bacteria - resistant to vancomycin (cannot get through outer membrane of cell)
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29
Q

What are the three mechanisms of hotizontal gene transfer?

A
  1. Transformation
  2. Phage-mediated transduction
  3. Plasmid mediated conjugation
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30
Q

Describe the process of Transfromation

A

A donor bacteria may lyse, fragments are thus released into the surrounding environement. A competent cell (i.e. one with homologies to the original bacteria) will take up the DNA and undergo homologous recombination.

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31
Q

Describe the process of phage mediated transduction

A

A bacteriaphage may infect a cell, this bacterial cell will then go on to replicate the phage. The new phages will be released into the environment. In the process of phage production it is possible that a rare abnormal phage will be produced which carries some sort of mutation which will confer resistance to the bacteria. The rare phage may then go on to infect a new bacterial cell - the genetic material obtained from the phage then undergoes recombination and may confer some sort of resistance.

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32
Q

what is plasmid mediated conjugation?

A

This is perhaps the most dangerous thing form of acquired resistance. Two bacteria (totally unrelated) will form a cytoplasmic bridge, the plasmid will then replicate and the copy will transfer to the attached bacteria. The cells will then seperate and the bacteria will not be able to trancribe the genes in the plasmid.

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33
Q

Name some naturally competent bacteria

A

H. Influenzae
Pnuomococci (strep pneumonia)

Gonococci (Neisseria gonorrhoeae)

Staph epidermis (it is a low grade pathogen with loads of resistance genes) - it can transfer to staph aureus (high grade pathogen)

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34
Q

Where can we find the most intriniscally resistant bacteria

A

The normal human flore has the most intrinsically resistant microbiota

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35
Q

what is lysogenic conversion?

A

When a bacteria is lysogenized (infected with a phage) the phage can insert its genes leading to bacteria which may give rise to a different phenotype.

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36
Q

Name the phases that a phage can be in after infecting a bacteriawhen the :

A
  1. Temperate phage (lysogenic cycle) - this is where the phage is not replicating and not doing damage to the bacteria (bacteria can divide and give phage DNA to daughter cells)
  2. Virulent phage (lytic cycle)

When the phage is replicating directly

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37
Q

Name a situation in which a bacterial infection should not be treated with antibiotics?
What is the toxin produced?

A

If a phage has infected a bacteria and is in the lysogenic cycle stress to the bacteria may trigger the lytic cycle resulting in the upregulation of phage genes and the overproduction of toxin. This is the case with diarrhoea cased by E.Coli - (i.e. it will cause serious damage)

Shiga Toxin

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38
Q

What are the 4 resistances that are typically seen on a multi-resistant plasmid?

A

Ampicillin gene - B-lactamase
Tetracycline gene - Efflux pump (TetM gene)

Kanamycin - Phosphorylase

Chloramphenicol - chloramphenicol acetyl transferase

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39
Q

What is a multiresistant plasmid?

A

Antibiotic resistance is encoded on cassettes, these cassettes can become integrated into a single plasmid.

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40
Q

What is so dangerous about plasmid mediated conjugation?

A

bacteria can transfer plasmids between non-homologous, genetically unrelated bacteria.

Thus a bacteria can go from being totally susceptible to fully resistant in 1 generation

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41
Q

List 5 considerations in administering an antibiotic

A
  1. Clinical diagnosis (i.e. LRTI/URTI)
  2. Microbiological diagnosis (type of bacteria)
  3. In vitro susceptibility (to antibiotics)
  4. Host factors (allergies, pregnant, immunocompromised)
  5. Properties of antibiotic
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42
Q

When they first discovered Streptomycin they believed Salmonella was extremely susceptible to it. But in practice, when they treated patients with Typhoid fever with Streptomycin, it did not work. Why?

A

Salmonella is a facultative intracellular parasite and is thus intrinsically resistant to streptomycin.

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43
Q

What is MIC?

A

MIC = minimum inhibitory concentration

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44
Q

How do we determine MIC?

A

MIC determined by progressive concentration halving. The point at which the bacterial growth is inhibited (indicated by non opacity) is the approximate MIC (the MIC lies between the opaque and clear tubes.)

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45
Q

How does an e-strip work?

A

Don’t know it is patented (haha) but can read off the MIC off the strip

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46
Q

what are the considerations in best guess/empirical therapy?

A
  1. Is antimicrobial treatment necessary
  2. Is it safe/reasonable to wait before treating?
  3. Are diagnostic samples required?
  4. What is the likely agent and what is its likely antimicrobial susceotibility?
  5. Is there evidence that treatment will benefit the patient?
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47
Q

What are the specific considerations regarding which antimicrobial to use?

A
  1. Spectrum
  2. Clinical efficiency
  3. Route of administration
  4. Pharmacokinetics/dynamics - half life, clearance, duration of action, MOA etc
  5. Availability
  6. Cost
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48
Q

What is the only known fungus susceptible to antibiotics?

A

Pneumocystis jirovecii.

49
Q

List either two specific drugs or two classes of drugs that are used in combination therapy for endocarditis. Why?

A

Beta-lactam and aminoglycoside, eg Pen G and streptomycin - form a strong synergy against streptococci, which can cause endocarditis.

50
Q

Would you prescribe antibiotics for a sore throat based on best guess practice? Why?

A

No - sore throat is probably viral.

51
Q

What is co-trimoxazole?

A

Trimethoprim + amoxyzole

Amoxyzole is a sulphonamide

They both interfere with folic acid synthesis

52
Q

What is Jawetz’s law?

A

Stat + stat = additive or indifferent

Stat + cidal = antagonistic

Cidal + cidal = synergistic

53
Q

What are the areas of the RT with no bacteria?

A

nasal, paranasla sinuses, middle ear and area below the epiglotis

54
Q

How are bacteria removed from areas below the epiglottis?

A

Cought it mucous and then either driven down the stomach or coughed up

55
Q

What are 4 microbiota niches in the URT

A

Nasal washings, Saliva, Tooth surfaces, Gingival scrapings

56
Q

List some common pathogenic residents of the URT (in more than 50% of people)

A

Viridans streptococci (alpha-heamolytic, causes infective endocarditis)

Neisserie Spp (gram negative)

Corynebacterium spp (diptheria)

Gram negative anearobes

H. Influenzae (not typable)

Candida albicans (fungus)

Strep pneumoniae (15-85% of pop)

57
Q

Name 2 occasional (1-10% prevalence) pathogenic respiratory microbiota of the URT in health people:

A

Strep pyogenes (group A strep) - increases durign outbreak

Meningococci

58
Q

Name 3 uncommon (<1% prevalence) pathogenic respiratory microbiota of the URT in health people:

A

Enterobacateria

Pseudomonas

C. Diptheria (only has human carriers - most carried are non toxogenic)

59
Q

What are the residents of the lung in a latent state?

A

Pneumocystis jeroveci (this is a fungus and is one of the aids defining illness (i.e. it only becomes active when a person is immunocompromised)

M. Tuberculosis about 1/3 of total world population have latent TB, <1% relapse (but higher in HIV)

60
Q

What are the residents of the lymph nodes?

A

CMV (Cytomegalovirus)
HSV (Herpes simplex virus)
EBV ( Epstein-Barr virus)

All of these can become resident infections (in CNS nerves) and will cuase a blister when the immune system is suppressed

61
Q

Name the inflammations from top to bottom of the RT

A

Rhinitis (sinusitis)

Pharyngitis

Laryngitis

Tracheitis

Bronchitis

Briochiolitis

Pneumonia

62
Q

Which parts of the RT are affected by the following?

Rhinovirus

Parainfluenzavirus

H. Influenzae

Influenza virus

Pertussis

RSV

A

Rhinovirus - Rhinitis and Pharyngitis

Parainfluenzavirus - Rhinitis, Pharyngitis, Laryngitis (can infect lower down but not common)

H. Influenzae - Rhinitis, Laryngitis, Tracheitis, Bronchitis and Bronchiolitis

Influenza virus - Everywhere with a preference for bronchioles and Bornchi

Pertussis - Laryngitis and below (though not so much pneumonia)

RSV - Rhinitis and Bronchitis - Pneumonia

63
Q

What is the most common cause of the common cold?

Why can you be infected so many times with the same pathogen?

A

Rhinovirus

Over 100 serotypes though the same serotype can infect again - thought to be because it is superficial infection

64
Q
A
65
Q

What are 2 causes of a cold during summer?

A

Enterovirus and Coronavirus

66
Q

How is entervirus spread?

A

Fecal oral route

67
Q

What is a suggested reason as to why one is more likely to contract strep pneumonia in cold weather?

A

Cold weather is thought to suppress the cough reflex

68
Q

Name 5 agents which can cause the common cold?

A

rhinovirus, parainfluenza virus, RSV, enterovirus, coron avirus, human metapneumovirus (HMPV)

69
Q

Name 3 agents which can cause pharyngitis/tonsillitis with nasal involvement

A

Adenovirus, enterovirus, parainfluenza

70
Q

What are the symptoms of pharyngitis/tonsillitis?

A

Sore throat and runny nose

Nasal involvement makes it more likely to be viral in origin

71
Q

Name 4 viral agents which can cause pharyngitis/tonsillitis with no nasal involvement

A

Adenovirus, influenza, enterovirus, reovirus

72
Q

Name 3 bacterial which can cause pharyngitis/tonsillitis with no nasal involvement

A

Strep pyogenes

group C and G strep

73
Q

What strep a infects the pharynx/tonsils and how is it treated?

A

Strep pyogenese - can cause serious complications and thus treated with antibiotics

74
Q

When is a rash likely to be present if a child has an URTI

A

If there is a rash it is more liklely to be bacterial. Though epstein barr will also form a rash when treated with ampicillin/amoxicillin

75
Q

What percentage of pharyngitis/tonsillitis with no nasal involvement is bacterial?

A

10-20%

76
Q

What are two causes of secondary sinusitis?

A

H. Influanzae and Strep Pneumoniae

77
Q

What causes primary sinusitis?

A

It is viral (usually part of the presentation of a common cold)

78
Q

Why are children more prone to ottitus media?

A

Children have shorter, more horiziontal and wider eustachian tubes which makes them more susceptible to ottitus media. When they swallow food can enter into the tubes which become non sterile.

79
Q

Which community in aus is most at risk for otitis media?

A

The indigienous population and those in poorer populations

  • they get acute OM which causes chronic OM leading to thick gluey secretions accumulating in the middle ear (this can cause hearing and subsequent learning and behavioural difficulties).
80
Q

What is the most common cause of OM?

A

Pneumococci

81
Q

What are some less common causes of OM?

A

H. Influenzae and Mraxella catarrhalis (GNC)

82
Q

What are the causitive agents of epiglottitis?

A

H. Influenzae type B

83
Q

Why is eppigoltitus rare in first world countries

A

There is a vaccine against HIB (conjugate vaccine)

84
Q

What is the prognosis of epiglotitits and why?

A

Can be very poor, can cause spasms of the epiglottis also inflammation and oedema leading to blockage and occlusion of airway.

85
Q

What is another name for croup? and what is its prognosis?

A

Laryngotracheo-bronchitis - good prog

86
Q

Describe the pathogenesis of the common cold?

A
  1. Virus adheres to nasla epithelial cell
  2. Virus absorbtion
  3. Viral replication
  4. Clear fluid escaping from damaged cells
  5. Host defence system activated with the invasion of phagocytes
  6. Commensal bacteria start comming in and might produce pus
  7. phagocytes come in and kill bacteria

By knocking out cells and cillia the viral infection can generate a secondary bacterial infection (it is known that other viral factors also contribute to its development)

87
Q

Treatment and diagnosis for a common cold?

A

None

88
Q

Should a doctor order tests for pharyngitis/tonsillitus?

A

Yes if possible (can be bacterial or viral), it is generally not a condition which demands immediate treatment so can wait to see if it is bacterial.

Should loop for strep group A

89
Q

How do you treat pharyngitis/tonsilitus?

A

If bacterial then give antibiotics

It can progress to a peritonsular abscess (quincy) and cause acute rheumatic fever - treating early will prevent rare outcomes (cellulitus). Group A 100% susceptible to penicillin

unfounded beleif that treating with antibiotics will preent acute rheumatic fever.

90
Q

Do we treat OM?

A

Yes if bacterial and severe

91
Q

Do we need a patholgical diagnosis of OM?

A

If less than 2 y.o or prolonged or severe

92
Q

Do we need a path diagnosis for sinusitis and is it treated?

A

Not usually necessary, can be done by surgeons directly through the skin (not through nose - will just grow microbiota)

If bacterial and severe can treat

93
Q

Should one take a sample to diagnose epiglottitis?

A

yes if possible, if it is a systemic infection can take blood

should NOT touch epiglottis - can cause sudden death by suffocation

94
Q

How do we treat severe croup?

A

Inhaled steroids

95
Q

Is there a treatment for bronchitis?

A

No - it is usually associated with a viralURTI

96
Q

Do you produce sputum with bronchitis?

A

No -usually viral

97
Q

Who usually has chronic bronchitis?

A

Smokers

98
Q

what causes an exacerbation of chronic bronchitis?

A

Bacterial: Pneumococci and H. Influenzae

99
Q

What is the cuase of bronchiolitis?

A

It is a viral infection caused by RSV (especially when epidemic)

100
Q

What are the signs of an acute exacerbation of chronic bronchitis and why does it occur?

A

As a result of COPD lungs are compromised susceptible to infection.

There is usually a marked increase in sputum, respiratory distress and fever. Tends to get wors with each infection.

101
Q

Presentation of bronchiolitis?

A

It presenta a lot like asthma - expiratory wheeze and a narrowing of the small airways due to inflammation (the bronchioles are not supported by cartilage and thus more prone to collapse)

102
Q

Why is RSV more severe during early childhood/infancy?

A

Babies are born with maternal antibodies to RSV, when the baby is infected an Ag-Ab complex is formed which aggravates inflammation causing bronchiolitis - attracts complement.

Thus more severe in first year of life

103
Q

What is the most common cause of bacterial pneumonia?

A

Pneumococci (strep pneumoniea) - 70-80% of cases in the community and 50% in hospital.

Usually own microbiota which enters into the alveoili

104
Q
A
105
Q

Besides pneumococi what are some other causes of pneumonia?

A

H. Influenza (not type B)

Staph (esp in hospital)

TB, legionella, Klebs

Clamia citici (comes from birds)

106
Q

How does bacterial pneumonia usually present?

A

Lobar pneumonia

acute onset

consolidated mass

usually in the alveoli

107
Q

What is atypical pneumonia and what causes it?

A

It is termed a walking pmneumonia - it has a diffuse pathology

  • it is a bronchopneumonia (spread by the airways), it affects the interstitial space
108
Q

what are some of the causes of atypical pneumonia?

A

Mycoplasma pneumonia (this is a bacteria without a cell wall and not fized shape - hard to fight with antibiotics)

RSV, Adenovirus

Chlamydia tracomatous (especially in neonates, baby asprates during brith it is a obligate intracellular pathogen and also an important source of eye infection)

109
Q

What are some other causes of pneumonia?

A

Fungi

Histoplasma

Aspergillus

Pneumocystis jerovicii - AIDS defining illness

110
Q

What cuases a lung abscess

A

Mixed anearobes of the URT - Staf or Klebs

111
Q

What is empyema and what causes it?

A

It is a collection of pus in a body cavity, it is caused by staph aureus resuting from a penetrating injury or staph bacteraemia

112
Q

What are 7 ways to get a speciment sample:

A
  1. Properly collected sputum - deep cough
  2. Transtracheal aspirate (tracheostomy and endotracheal tube)(
  3. Aspiration via tracheostomy
  4. Aspiration via bronchoscope
  5. Pleural tap (if effusion)
  6. Lung biopsy - by needle
  7. Blood culture and serology
113
Q

Treatment of pneumococcus

A

penicillin or cephalosporins

114
Q

Treatment for klebsiella?

A

Gentamicin works better than penicillins

115
Q

Treatment for Mycoplasma and legionella?

A

Can’t use beta lactams

Mycoplasma has no cell wall

116
Q

What is MERS and SARS-CoV

A

Middle East respiratory syndrome coronavirus (MERS-CoV),

Severe acute respiratory syndrome coronavirus

117
Q

What does spp stand for?

A

species

118
Q

What is the best guess treatment for community aquired pneumonia?

A

Pen G/amoxicillin (covers pneumococci)

Doxycycline/macrolide (these are bacteriostatic and cover atypical legionella and mycoplasma)

  • once the bacteria has been obtained select the appropriate treatment
119
Q

What are some vaccines which prevent pneumonia?

A
  1. Influenza vaccine
  2. Pneumococcal vaccines 23-valent polysaccharide (for older people and those at risk i.e. immunocompromised
  3. there is also a 13 valent conjugate which is given to children
  4. specialised vaccines for those at risk - eg anthrax or human plague vaccine (soldiers), q fever vaccine

Mic (1 decks)

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