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Pase 2a Notes > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Define pathogens

A

Organisms that cause or are capable of causing disease

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2
Q

Define commensal

A

Organism that colonises the host but causes no disease in normal circumstances

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3
Q

Describe opportunist pathogen

A

Microbe that only causes disease if host defences are compromised

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4
Q

What is asymptomatic carriage?

A

When a pathogen is harmlessly carries at a tissue site where it causes no disease

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5
Q

What is virulence / pathogenicity?

A

Degree to which an organism is oathogenic

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6
Q

Rank microbes from largest to smallest

A

Protists
Eukaryotes
Spiral bacteria
Try beacteria
Virus < 1 um

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7
Q

Areas with bacterial colonisation vs sterilisation

A

Bacteria - moist mucosal e.g. groin, skin, gut
Sterile - lungs, blood, heart, kidneys,gallbladder

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8
Q

Gram stain positive vs negative results

A

Gram Positive = purple
Gram Negative = Pink

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9
Q

Classes of bacterial shapes

A

Coccus (circular) - chain, cluster, diplcoccus
Bacillus (rods) - chain, curved
Spirochaetes - spiral rods
Vibrio - curved rod

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10
Q

How is gram negative bacteria different to gram positive?

A

Has 2 membranes - inner and outer separated by lipoproteins, periplasmic space and peptidoglycan

Positive = large area of peptidogylcans links to single membrane by lipoteichoic acid

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11
Q

Typical bacterial cell contains

A

No nucleus- circular, double stranded DNA
Some have capsule
Some have pills of flagella

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12
Q

What is gram stain?

A

Crystal Violet to heat fixed bacteria
Then Iodine which fixes it to cell wall
Decolourise with ethanol / acetone
Counter stain with safranin

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13
Q

Bacterial culture environment

A

Temperature < 80 or 120 for spores
pH 4-9
Light - UV
Without water for 2 hours - 3 months

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14
Q

Phases of bacterial growth

A

Initial lag
Exponential (log)
Stationary (run out of nutrients)
Viability (die once nutrients run out)

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15
Q

2 types of bacterial toxins

A

Endotoxin - component of the outer membrane of bacteria (gram negative) e.g. lipopolysacchrides

Exotoxins- secreted specific, strong proteins of gram positive and negative bacteria can be converted to toxoids

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16
Q

3 methods of gene transfer

A

Transformation e.g. plasmids
Transduction e.g. via phage
Conjugation e.g. via sex pilus

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17
Q

What does the coagulate test identify?

A

Positive = S.aureus from other staphylococci
(Add rabbit p,as a for fibrin)

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18
Q

What are bacteria that CANT be cultured on artificial media called?

A

Obligate Intracellular bacteria
Only grow inside host cells e.g. chlamydia

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19
Q

Bacteria that grow on artificial media with a cell wall called?

A

Grow as a single cell - rods, cocci, spirochaetes
Grow as filaments

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20
Q

Bacteria grown on artificial media without a cell wall called?

A

Mollicutes

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21
Q

A group of bacteria don’t gram stain due to a different cell wall but do stain what?

A

Ziehl-Neelsen stain
E.g. mycobacteria

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22
Q

What does an oxidase test determine?

A

If the micro-organism contains a cytochrome oxidase and can use oxygen as the terminal electron acceptor

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23
Q

3 haemolysis results

A

Alpha - green by production of hydrogen peroxide using haemoglobin

Beta - complete lysis of red blood cells e.g. Streptolysin O

Gamma - implies no haemolysis

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24
Q

Sero grouping to further seperate B-haemolytic strep

A

Antiserum added and clumping indicates recognition

Group A - S.pyogenes
Group B - S.agalactiae

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25
Q

Describe Staphylococcus. Aureus

A

Gold, round gram positive cocci - Coagulase positive

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26
Q

How does Lancfield grouping occur?

A

A method of grouping catalase negative, coagulase negative bacteria based on carbohydrate cell surface antigens

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27
Q

Features of Staphylococci (aerobic gram positive cocci)

A

Spread by aerosols, surface-to-surface contact and cell associated virulence factors

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28
Q

Gram positive virulence factors

A

Pore forming toxins
Proteases
Toxic shock syndrome toxin
Protein A

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29
Q

Gram positive staphylococcus which are coagulase negative

A

S. Epidermis (white and round)

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30
Q

Classifying aerobic gram positive cocci

A

Chains = Streptococcus
- Haemolysis Alpha -> Optochin
Sensitive = S.pneumonia
Resistant = Viridans strep
- Haem Beta -> antigenic groups
- Haem Gamma

Cluster = Staphylococcus
- Coagulase +ve S. aureus
- Coagulase -ve

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31
Q

Examples of gram positive bacilli (rods)

A

Clostridia - spore and toxin forming
C. Tetani
C. Botulinum
C. Diphtheriae

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32
Q

How are gram positive bacteria managed?

A

With antimicrobials and vaccination

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33
Q

4 major groups of gram negative pathogens

A

Proteobacteria - all rod shaped
Bacteroids - rod shaped
Chlamydia - round pleimorphic
Spirochaetes - spiral/helical

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34
Q

2 Pathogenicity factors

A

Colonisation factors - adhesions, invasions, nutrient acquisition, defence

Toxins - secreted proteins for damage, subversion

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35
Q

Gram negative rods classification

A

Anaerobic - Bacteroides
Aerobic
- Coliforms
- Pseudomonads
- Vibrio
- Parvobacteria

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36
Q

Describe coliforms

A

Gran negative rods with flagella for motility and colonises intestinal tract
= Use metabolic processes e.g. fermenting lactose to differentiate

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37
Q

5 agar types

A

Blood - for alpha/ beta strep
Chocolate - for fastidious neisseria
MacConkey - lactose fermenters produce acid (pink)
CLED - stops motility and for lactose (yellow)
Xylose Lysine Deoxycholate agar (XLD agar) - selective isolation of salmonella and shigella (both lactose ferment red, but salmonella turns black)

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38
Q

What is a gram negative rod, short and stubby?

A

E. coli (commensal aids digestion)

Pathogenic when lateral gene transfers form hybrids

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39
Q

Most severe form of shigella

A

S. dysenteriae (bloody diarrhoea)

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40
Q

2 species of salmonella

A

S. bongori - rare

S. enterica- 3 forms of salmonellosis:
1. Gastroenteritis
2. Enteric fever
4. Bacteraemia

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41
Q

What are pseudomonas aeruginosa

A

Rod shaped, free living, motile, opportunistic, resistant to multiple antibiotics
Can cause acute or chronic (CF) infections

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42
Q

Pathogenesis of Vibrio cholera

A

Will bind to intestinal wall and sit there but release toxins

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43
Q

Spiral shaped with tuft of polar flagella

A

Helicobacter pylori

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44
Q

What is Nisseria meningitidis?

A

Gram negative diplococci

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45
Q

What is Bacillus cereus?

A

Gram negative rod

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46
Q

What are bacteria that CANT be cultured on artificial media called?

A

Obligate Intracellular bacteria
Only grow inside host cells e.g. chlamydia

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47
Q

3 examples of parvobacteria

A

Haemophilus influenza - non motile opportunistic capsular infection

Bordetella pertussis - short rods highly aerosol, produces 2 toxins (whooping cough)

Legionella pneumophila - severe inflammation pneumonia in immunocompromised = influx of neutrophils into lungs

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48
Q

Describe bacteroides

A

Non motile strict anaerobic rods
Mostly beneficial in gut but opportunistic with enterobacteria

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49
Q

Gram negative Cocci examples

A

Aerobic Veilonella

Anaerobic Nisseria = non flagellated diplococci
- N. Meningitidis - cytokine cascade = sepsis can kill in 4 hrs
- N. Gonorrhoeae - multi drug resistant STD can lead to infertility and death

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50
Q

Describe spirochaetes

A

Long, helical, highly flexible mostly free living and non-pathogenic
Modified outer sheath, lacks LPS with endoflagella for corckscrew motion

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51
Q

3 examples of spirochaetes

A

Borrelia burgdoferi (lyme’s disease) - bulls eye rash
Leptospira interrogans - rat faeces in water causes multi organ infection
Treponema pallidu (syphillis STD) - has 3 stages

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52
Q

3 main groups of obligate Intracellular bacteria (can’t be artificially cultured)

A

Rickettsia
Chlamydia - detect by serum Ab or PCR
Coxiella

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53
Q

Life cycle of chlamydia

A
  1. Elementary bodies enter through endocytosis but prevents lysosome
  2. Differentiates into reticulate bodies which replicate and acquire host nutrients
  3. Conversion back to EB and cell lysis for release
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54
Q

What accounts for ~10% community acquired pneumonia?

A

Chlamydia Pneumonia

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55
Q

What are mycobacteria?

A

Gram negative single rod cells that identify with Ziehl-Neelson stain

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56
Q

7 mycobacteria of medical importance

A

M. tuberculosis - tuberculosis
M.leprae - leprosy
M.avium - disseminated infection in AIDS, chronic lung infection
M.kansasii - chronic lung infection
M.marinum - fish tank granuloma
M.ulcerans - Burundi ulcer
M.fortutium - skin and soft tissue infections

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57
Q

How many deaths per year by TB?

A

1.5 million

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58
Q

Describe Mycobacterium tuberculosis

A

Slightly curved beaded bacilli, gram negative, red in Ziehl-Neelon stain

Aerobic, non spore forming, non-motile
Survive inside macrophage even in low pH
Slow growth, reproduction or response to treatment

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59
Q

What is Acid fast bacilli?

A

Stain used to identify organisms with wax-like, thick cell walls e.g. mycobacteria which are resistant to germ stain = stains red

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60
Q

Challenges of TB

A

Thick lipid rich wall hard for immune cells to kill and drugs to penetrate
Slow growth=
Takes longer to diagnose and treat

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61
Q

Stages of TB infection

A

Primary in lungs
Latent (decades) - T cell contains primary but cell mediated immune persists
Pulmonary - granulomas form around bacilli in apex of lungs, can cause necrosis, abscess etc

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62
Q

Why does granulomas form in apex of lungs?

A

More air and less blood supply so fewer immune cells

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63
Q

What does our body do to protect us from TB?

A

Mycobacteria are phagocytoses by alveolar macrophages (some may escape to cytosol)
CD4 T-cells generate cytokines
Hallmarks granuloma formation to signal other immune cells (forms cavity for TB reactivation)

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64
Q

Clinical diagnostic methods of TB

A

Nuclei Acid detection - PCR has 88% sensitivity and 98% specificity
Liquid culture - 1-3 weeks
Solid culture - 2-8 weeks
Tuberculin skin test - Tcells after 3-9 weeks

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65
Q

4 types of TB drug resistance

A

Drug inactivation
Drug titration
Alteration of drug target
Altered cell envelope

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66
Q

How do we study TB?

A

Using zebra fish (transparent embryos are genetically maniptable and quick)

To find host-derived therapies (activate the immune system as well as administering antibiotics)

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67
Q

What is Hypoxia Inducible factor?

A

A genetic switch activated during hypoxia is a drug target to trick wbc into an immune response to treat TB

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68
Q

Some common viruses and significant causes

A

CMV, Rubella - Miscarriage
Outbreaks - Measles, Mumps, Covid
Cancer - HIV, HPV, Epstein-Barr
MERS, Ebola
= Morbidity and mortality

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69
Q

What is a virus?

A

An infectious, obligate Intracellular parasite comprising of genetic material (DNA or RNA) surrounded by a protein coat

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70
Q

Why is a virus dependent on a host cell?

A

Does not have membrane or organelles so cannot carry out metabolic reactions

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71
Q

Viruses from largest to smallest

A

Pox virus
Rhabdovirus
Herpes virus
Adenovirus
Parvovirus

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72
Q

Different shapes and structures of virus

A

Helical
Icosahedral
Complex
Non- enveloped or enveloped

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73
Q

How do virus replicate?

A
  1. ATTACHMENT to specific receptors
  2. CELL ENTRY via unloading of virion
  3. INTERACTION + REPLICATION using host materials
  4. ASSEMBLY occurs in nucleus / cytosol or cell membrane
  5. RELEASE via bursting or exocytosis
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74
Q

How do viruses cause disease?

A
  • Direct destruction of host cells
  • Modification of host cell structure or function
  • Over-reactivity of immune system
  • Cell proliferation (inserting viral DNA)
  • Evasion of Extracellular and molecular host defences
75
Q

Examples of how virus evade molecular level host defences

A

Antigenic variability
Prevention of host cell apoptosis
Down regulation of interferon and other defence proteins
Interference with host cell antigen processing pathways

76
Q

4 ways to identify virus

A

PCR (genetic information)
Serology (immune memory)
Histopath (viral infection features)
Culture + electroscopy (Limited as too much time, effort and expense)

77
Q

How does immunity develop?

A

5 types of immunoglobulins:

Active - cell and antibody mediates response when exposed to a pathogen

Passive - Transfer of antibodies from immune individuals but only temporary immunity

78
Q

Types of vaccines

A

Active:
Inactivated
Attenuated
Secreted products
Constituents of cell walls/ subunits
Recombinant components

Passive:
Human normal immunoglobulin injected

79
Q

What is herd immunity?

A

The more people vaccinated, the harder it is for pathogen to spread to immunocompromised

80
Q

2 types of vaccine failure

A

Primary - Person doesn’t develop immunity from vaccine

Secondary - Initial protection wanes over time so needs more doses

81
Q

Where can we find all UK immunisation schedules?

A

Green book

82
Q

Examples of vaccine preventable diseases

A

Diphtheria
Tetanus
Pertussis
Polio
Haemophilus influenza type B
Meningococcal disease

83
Q

What is contact tracing

A

Any close contact needs to be identified to prevent further cases (no need to learn list)

84
Q

How to protect the community from communicable disease?

A

Surveillance for early warning
Investigate severity
Identify and protect close contact
Exclude high risk person
Educate, raise awareness
Multi agency responses

85
Q

3 groups of worms

A

Nematodes (roundworms)
- Intestine, larva, tissue
Trematodes (flatworms)
- Blood, liver, lungs, intestine
Cestodes (tapeworms)
- Can be invasive or non-invasive

86
Q

What is the prepatent period?

A

Interval between infection and appearance of eggs in stool

87
Q

What is meningitis?

A

Inflammation of the meninges (dura, pita, arachnoid)

88
Q

Causes of meningitis

A

Bacteria
Virus
Fungi, Protozoa, or other parasites
Medications
Cancers
Autoimmune diseases

89
Q

What is invasive meningococcal disease?

A

Gram negative diplococci Neisseria meningitidis infection through droplets

90
Q

2 manifestations of invasive meningococcal

A

Meningitis - local
Septicaemia - widespread systemic infection and organ damage

91
Q

Risk factors of of invasive meningococcal

A

Extremes of ages
Smokers
Immunocompromised
Frequent close contact
Travellers to high risk areas
Overcrowded housing or cholla
Winter coughs and colds
Asplenia, cancer, organ dysfunction
Sickle cell, contagious diseases

92
Q

Meningococcal meningitis symptoms

A

Babies - slow, irratible, vomiting, feed poorly, avoid neck stretching

Adults - fever, stiff neck, headache, confusion, vomiting, light sensitivity

93
Q

Meningococcal septicaemia symptoms

A

Fever
Fatigue
Vomiting
Diarrhoea
Cold hands and feet
Severe aches and pain
Rapid breathing
Non blanching rash

94
Q

How to test for meningococcal

A

Blood sample + PCR
CSF for microscopy, culture
Throat swab for culture

95
Q

Should meningitis cases be notified?

A

ALL CASES OF SUSPECTED MENINGITIS ARE NOTFIED IMMEDIATELY

Close contacts identified

96
Q

What is given to eradicate throat carriage (passing it) of meningococcal?

A

Antibiotics
(Prophylaxis for contact)

97
Q

Public health actions of meningococcal

A

Contact school/nursery/uni
If two cases confirmed = cluster
Standard / customised letters
Other support / helpline

98
Q

What is an affordable meningitis vaccine?

A

MenAfriVac (2010)

99
Q

Epidemiology of meningococcal

A

Occurs sporadically in clusters globally
Group B+C common in Europe, America
Group A common in Asia, Africa
Seasonal variations

100
Q

When are meningococcal vaccinations taken?

A

8 weeks
16 weeks
1 year
14 years

(Original sugar vaccine was not effective in kids so conjugated with proteins)

101
Q

Features of fungi

A

Eukaryotic (DNA/RNA , protein synthesis)
Chitinous cell wall
Ergosterol instead of cholesterol in plasma membrane
Heterotrophic
Move by growth, generations of pores carried by air or water

102
Q

2 types of fungi: yeast vs mould

A

Yeast - small single celled that divide by budding

Moulds - form multicellular hyphae and spores

103
Q

What is dimorphic fungi?

A

Fungi exist as both yeast and mould switching when conditioned suit best

104
Q

Why only few fungal infections?

A

Inability to grow at 37 degrees
Innate and adaptive immune system
Common fungi have low morbidity
Invasive fungi easily missed

105
Q

Antifungal drug targets

A

DNA/RNA, protein synthesis
= Flucytosine, Griseofulvin

Plasma membrane (ergestrol)
= Polynesian, Azores, Allylamines

Cell wall (not in humans)
= Echinocandines

106
Q

Describe mucosal candadis (thrush)

A

= common commensal causing significant recurrent morbidity when overgrown

Risk = mucosal disruption, antibacterial, immunosuppressed

Treatment = Topical or oral Azoles

107
Q

What are dermatophytes?

A

Mould causes skin and nail infections
(Human or animal to human transmit)

Treatment = topical, oral azoles, terbinafine

108
Q

Is ringworm a worm?

A

No! It’s a fungi

109
Q

6 Life threatening fungal infections

A

Dimorphic fungi - Mould at warm temp
- Chlamydia via spore inhalation converts to yeast at 37 (true pathogen)

Coccidioides - Rectangles read to release spores in warm arid areas
- mostly asymptomatic, but develop systemic (sepsis) or local (pneumonia) disease

Invasive candidiasis (candida invades blood)

Cryptococcus - common in children but only in immunocompromised

Invasive aspergillus - secondary infection in ITU, commonly elderly
- Fever, respiratory failure
= Voriconazole

Mucoraceous moulds - raid,y progressive infections crossing tissue plains only in immunocompromised

110
Q

Which 3 types of fungi are most commonly seen in Sheffield?

A

Candida, Aspergillus, PCP found in all departments

111
Q

Aim of antimicrobial drug therapy

A

= Achieve inhibitory levels of agent at site of infection without host cell toxicity

112
Q

How does antimicrobial drug therapy work?

A

Identifies molecules with selective toxicity e.g.
- non human targets
- increased permeability to compound
- Modification in organism
- Drug more concentrated in organism
- Human cells rescued from toxicity by alternative metabolic paths

113
Q

Why is fungi challenging to treat?

A

We only have relatively few classes of effective agents

114
Q

What are Protozoa?

A

Single celled eukaryotic

Phagocytose bacteria, algae, micro fungi
Important in parasitic and symbiotic relationships

115
Q

5 major groups of Protozoa

A

Flagellates - have flagella and binary fission to reproduces

Amoebae - move by flowing cytoplasm and production of psudopodia

Sporozoans - all species parasitic, no locomotives and reproduce by multiple fission

Ciliates - cilia beat and 2 types of nuclei - micro/macro

Microsporidia - production of resistant spores with polar filament coiled inside

116
Q

5 Examples of flagellates

A

African trypanomiasis - transmitted by setse fly bite, developing sleepy, flu-like, CNS symptoms and death

American trypanosomiasis - spread by triatomine bug faeces developing acute flu-like symptoms, megacolon, chronic cardiomyopathy etc

Leishmaniasis - spread by sandfly bite
Cutaneous + muscutanoues ulceration = pneumonia, sepsis
Visceral fever, weight loss,
= fatal anaemia, hepato/splenomegaly

Trichomonas vaginalis - STI asymptomatic, dysuria, fishy smell, yellow froth discharge= metronidazole

Giardiasis - faeco-oral spread associated with recent travel. Cramps, bloating, cysts seen in stool
= metronidazole

117
Q

2 examples of sporazoa

A

Cryptosporidiosis - water borne spread
Causes diarrhoea, vomiting, fever, oocytes in stool but sever in immunocompromised

Toxoplasmosis- Ingestion of contaminated causes choriorenitis, disseminated disease

118
Q

1 example of amoebae

A

Amoebiasis - faeco-oral spread
Produces GI - dysentery, colitis
Liver, brain and lung absesses
Cysts in stool
= Metronidazole + amoebicide

119
Q

Travel + Fever = always assume what?

A

MALARIA!!

120
Q

What is malaria?

A

Protozoa infection cause by 5 species of Plasmodia sprazoan:
P. falciparum, orale, vivax, malariae, knowlesi

Transmitted by female anopheles mosquito bite (3-4 weeks life span)
- Infection from another human, for life

121
Q

Malaria symptoms and signs

A

FEVER
chills and sweat
Headache, fatigue
Nausea, vomiting, diarrhoea
Myalgia

Haemolysis causes:
Anaemia
Jaundice
Very dark urine
Hepatosplenomegaly

122
Q

Describe malaria life cycle

A

Sporogenic cycle in mosquito
Infects human causing abdo pain
Exoerythrocytic cycle spread spores
Haemolysis in erythrocytic cycle causes cyclical fever (lies dormant)

123
Q

Why is P. falciparum more complicated?

A

Causes adherence to each other and cells
Obstruction so RBC are not filtered like normal
= Highest mortality rate, harder to manage infections
= vascular occlusion

124
Q

Malaria treatments

A

Complicated = IV artesunate
Uncomplicated - lots of options

125
Q

How can P.ovale and P.vivax cause relapse?

A

Additional stage forms hypnozoites in the liver for years

126
Q

Define infectivity

A

Infectivity - ability to become established in host, can involve adherence and immune escape

127
Q

Define virulence

A

Ability to cause disease once established

128
Q

Define invasiveness

A

Capacity to penetrate mucosal surfaces to reach normally sterile sites

129
Q

Humorous vs cell mediated responses to virus

A

Humoral
- antibody (IgA) blocks binding
- Opsonisation (tags for phagocytosis)
- Complement

Cell mediated
- Antiviral action
- Kill infected cells
- Macrophages
(Peaks 7-10 days then declines)

130
Q

How do virus evade immune system?

A
  1. Interfere with specific or non specific defence
  2. Change coat antigen
    - Antigenic drift where spontaneous mutations give minor change
    - Antigenic shift where sudden emergence of new subtype
131
Q

How do bacteria enter host?

A

Respiratory tract
HI tract
Genitourinary tract
Skin break

132
Q

Low number vs high number of virulence employ which defence mechanisms?

A

Low = phagocytes
High = immune response

133
Q

3 ways of protozoan evasion

A

Surface antigen variation
Intracellular phase
Outer coat sloughing

134
Q

2 ways of worm evasion?

A

Decrease antigen expression by adult
Glycolipid / glycoprotein coat (host derived)

135
Q

5 antiviral drugs

A

Aciclovir + Valaciclovir
Ganiciclovir + Valganiciclovir
Foscarnet
Ribavirin
CoVID antivirals

136
Q

5 immune modulation therapies

A

Lifting immunosuppresion
Specific immunoglobulins
Human NormalImmunoglobulins
Rituximab
CoVID immunomodulators

137
Q

What is Aciclovir?

A

Anti-herpes virus drug with high selective toxicity and few side effects

138
Q

Mechanism of Aciclovir

A
  1. Activated to a monophosphate by viral thymidine kinase only in herpes
  2. Host cell kinases add 2nd and 3rd phosphate group
  3. Aciclovir triphosphate mimic guanine so inhibits herpes DNA polymerases
139
Q

Chicken pox cause and symptoms

A

Varicella-zoster virus is a member of the herpes virus
Signs - lesions in warm areas harden, fill with pus and then crust

140
Q

Shingles pathophysiology

A

Varicella -Zoster virus dormancy in dorsal root or cerebral ganglion

Reactivates and migrates along same sensory nerve = dermatomal shingles

141
Q

When do we use IV Aciclovir?

A

Oral has poor bioavailability so frequent dosing
- Dissemnated herpes (neonates, congenital)
- Herpes in immunocompromised
- Severe shingles / herpes
- Herpes encephalitis

142
Q

What is Valaciclovir and why is t better than Aciclovir?

A

Valine side change of Aciclovir increases 3-5x bioavailability so reduced dosing, less likely to forget.

Also a useful step down from IV therapy

143
Q

What is Ganciclovir?

A

Anti CMV agent = primary use
For treatment and prophylaxis of CMV infection in immunosuppressed or transplant recipients

144
Q

Mechanism of Ganciclovir?

A

Less selective toxicity: Inhibitor of viral DNA polymerase like Aciclovir
(1st phosphorylation by deoxyguanosine kinase in CMV infected cells)

145
Q

What is Valganciclovir?

A

L-valyl ester side chain for better oral absorption and bioavailability

146
Q

GCV adv and Disv

A

Adv
- selective antiviral
- activity and sensitivity amplified

Disv
- haemolytic anaemia
- potential foetal toxicities / low fertility
- resistance due to mutations
- myelosupression = Pancytopenia

147
Q

Cytomegalovirus signs (CMV)

A

Mostly asymptomatic (macular rash, febrile, lethargic poor appetite)
Atypical lymphocytes (RBC stick to wbc)
May stay and reactivate causing
- Pneumonitis, end organ disease
- Ultra-colitis
- Pizza pan retinas
- Internuclear intrusions in kidney

148
Q

What is Foscarnet?

A

= Selectively inhibits phosphate binding on DNA polymerase for all herpes virus

149
Q

Adv and Disv of Foscarnet (phosphonoformic acid)

A

Adv
- Does not require activation
- Retains activity against mutations
- Combination enhances activity

Dis
- Significant renal toxicity
- Acidosis, raised LDH, Alk Phos
- Crystal induced nephropathy
- Electrolyte disturbances leading to seizures

150
Q

What is Rituximab?

A

Monoclonal antibodies that target CD20 molecules for immunisuprresion

151
Q

Rituximab Adv and Disv

A

Adv
- Pre emptive use reduces risk of malignant transformation

Disv
- Risk of reactivation of TB
- Risk of hepatitis B

152
Q

What is Immununoglibulin Post Exposure prophylaxis?

A

Pooled plasma product of people with high antibodies

153
Q

Management of measles exposed

A

Acurate contact tracing
MMR vaccine checks
Prophylaxis for non-immunocompromised
Sero status check for immunosuppressed
Arrange for IVIg

154
Q

What is Ribavirin?

A

Small molecule broad spectrum antiviral
(Guanosine mRNA production interference)
Used for Hep E + Lassa fever

155
Q

Define antibiotic

A

Agents produced by micro-organisms that kill or inhibit the growth of other organisms in high dilution

156
Q

Define antimicrobials

A

Molecules that work by binding at atarget site on a bacterium.
E.g.
- penicillin binding preteins on cell wall
- cell emembrane
- DNA
- ribosomes
- Topoisomeraxe IV or DNA gyrase

157
Q

3 antibiotics classes

A

Cell wall synthesis
- Glycopeotides
- Beta Lactams (work against cell wall peptidoglycans so lysis + bursts)
- Vancomycin
- Bacitracin

Nucleic Acid synthesis
- Folate synthesis (precursor to substrates that generate nucleotides)
- DNA gyrase (stops this unwind DNA)
- RNA polymerase (inhibit e.g. Rifampin)

Protein synthesis
- 305 Subunit
- 505 subunit

158
Q

Beta lactams are more effective on…

A

Gram positive
(Negative have additional lipopolysaccharide layer)

159
Q

3 types of beta lactams

A

Ccephalosporins - more broad than penicillin

Carbapenems - high quality and last resort

Monobactams - very narrow spectrum

160
Q

3 ways bacteria are pathogenic

A

Direct - destroys phagocytes or host
Indirect - inflammation or overimmune
Toxins - Exotoxins/ Endotoxin

161
Q

Bactericidal vs Bacteriostatic Antibiotics

A

1 - Agent kills bacteria quickly (18-24hr)
- Beta lactams inhibit cell wall synthesis
- However bursting releases toxins

2 - Prevents growth and multiply
- Inhibit protein synthesis, DNA replication or metabolism
- Reduces toxin surge

162
Q

How to find Minimum Inhibitory concentration (MIC)?

A

Incubate tubes with different volumes of microbial rich broth and antimicrobial agents

163
Q

Is lowest MIC = best antibiotic and why?

A

NO!
Drug must attach to adequate number of inning sites and remain for enough time for metabolic processes to be sufficiently inhibited

164
Q

2 major determinants of antibacterial effects

A

Time dependent killing
Concentration dependent killing (peak)

165
Q

4 ways antibiotics not work

A
  1. Change, blocks or mutates antibiotic binding site (e.g. MRSA)
  2. Destroy antibiotic via enzymes or proteins (e.g. beta lactamase)
  3. Prevent antibiotic access by modifying membrane porin channel size, number, selectivity
  4. Removes antibiotic from bacteria
166
Q

How do bacteria develop resistance?

A

Intrinsic - naturally resistant
Acquired - Spontaneous gene mutation
- Horizontal gene transfer by conjugation/ transduction/ transformation

167
Q

2 important resistant gram positive bacteria examples

A

MRSA - Methicillin resistant S. Aureus
- Bacteriophage mediated acquisition of chromosome mec (gene mecA)
- encodes penicillin binding protein 2a to all B-lactams as well

VRE - Vancomycin resistant enterococci
- Plasmid mediated acquisition of altered amino acid preventing vancomycin binding
- Promoted by cephalosporin use

168
Q

2 Important resistant gram negative bacteria examples

A

ESBL - Extended Spectrum B-Lactamase inhibition by hydrolysis of side chains
= bind beta lactamase inhibitor to AB

Carbapenam Resistng / Producing Enterobacteriaceae (CRE / CPE) - treatment very few and toxic

169
Q

5 Qs when choosing an antibiotic

A

What kind of bacteria will it cover?
Bioavailability- oral or IV
Is the bacteria resistant?
Allergies?
Is there an infection caused by bacteria?

170
Q

7 Factors to consider when deciding if an antibiotic is safe

A

Intolerance, allergy
Side effects
Age
Renal and liver functions (dose)
Pregnancy and breast feeding
Drug interactions
Risk of C. difficile

171
Q

Common presentations and treatments of gram positive cocci

A

S.aures + Group A,C,G strep
= purple swollen feet
= Fluxocallin

Group A,C,G strep
= Inflammed tonsils
= Penicllin

S.pneumonia
= Cloudy chest X-ray
= Amoxicillin

172
Q

2 scenarios where IV vancomycin and telcoplanin are used

A
  1. Gram positive bacteria resistant to beta lactams
  2. penicillin allergy
173
Q

3 examples of protein synthesis inhibitor antibiotics (gram positive)

A

Clarithromycin and erythromycin- oral
= penicillin allergy / severe pneumonia

Clindamycin - oral
= cellulitis, necrotising fasiculitis

Doxycycline - oral
= cellulitis and pneumonia

174
Q

4 example antibiotics for gram negative

A

Gentamicin - IV
= UTI, infective endocarditis but toxic

Ciprofloxacilllin - oral
= penicillin allergy, UTI, intra-abdominal infections

Trimethhoprim - folate anatagonist
= UTI

Nitrofurantoin
= Lower UTI

175
Q

4 examples of beta lactam antibiotics

A

Cefuroxime
Co-amoxickav
Piperacillin
Meropenem

176
Q

Details of health care act 2006

A

Infection control is every health care worker’s responsibility
Prosectution possible under H&S law

177
Q

How can we identify infection risks?

A

Risk factors - recent travel, previous
Screening
Clinical / Labdiagnosis
Routes and modes of transmission
Patient/Staff/ Environment

178
Q

Things to do everyday to protect patients

A
  • Hand hygiene = most effective way of preventing cross infection
  • Personal Protective equipment
  • Disposal of sharps (never overfill, resheathe, bend etc)
179
Q

What is an endogenous infection and how to prevent it?

A

= Infection of patient by their own flora

  • Good nutrition and hydration
  • Antisepsis/skin prep
  • Control underlying disease (drain pus, remove lines, reduce antibiotics)
180
Q

When to wash hands and use alcohol gel?

A

Hands:
Before and after handling patients
After handling soiled items
After using toilet
Before and after aseptic procedure
After removing PPE

Alcohol gel:
Following hand wash when caring for a patient or ward based invasive

181
Q

5 infection control policies

A

MRSA
Tuberculosis
Medical equipment management manual
Single use items
Outbreak control plan

182
Q

How to differentiate between staph and strep?

A

Catalase test +ve = staph
(Hydrogen peroxide for bubbling)

183
Q

What is the indole test?

A

Ability to decompose aa tryptophan to indole (gram negative rods)

184
Q

What does option in test determine

A

S. Pneumoniae from other alpha haem strep

Pase 2a Notes (6 decks)

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