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Phase 2a Lecture Notes > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Pathogen

A

Organism that causes or is capable of causing disease

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2
Q

Commensal

A

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

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3
Q

Opportunist Pathogen

A

Microbe that only causes disease if host defences are compromised

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4
Q

Virulence/Pathogenicity

A

The degree to which a given organism is pathogenic

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5
Q

Asymptomatic carriage

A

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

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6
Q

What is the genus of Staphylococcus aureus

A

Staphylococcus

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7
Q

What is the Species of Staphylococcus aureus

A

Aureus

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8
Q

Coccus

A

bacterial cell that has the shape of a sphere

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9
Q

Rods (bacilli)

A

bacterial cell that has the shape of a rod

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10
Q

Coccus vs Rod

A

Bacteria may be either round (cocci) or rod-shaped (bacilli). Either shape may be gram-positive or gram-negative. A mixture of gram-positive and gram-negative bacteria can occur in the same field.

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11
Q

Cocci morphology

A

Diplococcus- pair of coci
Chain of cocci
Cluster cocci

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12
Q

Rod morphology

A

Chain of rods
Filamentous/branching bacteria
Vibrio- curved rod
Spirochaete- spiral rod

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13
Q

Organelle of bacteria

A

Cell wall, outer membrane, inner membrane, pili, chromosome of circular double stranded DNA, Capsule (not all bacteria)

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14
Q

Gram +ive cell envelope, outermost to innermost

A

Capsule, peptidoglycan, lipoteichoic acid, cytoplasmic membrane

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15
Q

Gram -ive cell envelope, outermost to innermost

A

Capsule, LPS (endotoxin), outer membrane, lipoprotein, peptidoglycan, inner membrane

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16
Q

Lipopolysaccharide (LPS/ENDOTOXIN)

A

Made up of Lipid A, O antigen and terminal sugars, toxin

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17
Q

Gram staining process

A

Crystal violet (both purple), iodine, (both purple), decolourisation (+ive purple, -ive colourless), counter stain (+ive purple, -ive pink)

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18
Q

Gram staining results

A

Positive= purple
Negative= pink
Remember: Positive stain purPle, Negative stain piNk

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19
Q

Bacterial environment for growth

A

Temperature: <-800C to + 80C (1200C for spores)
pH: <4-9
Water/dessication: 2 hours – 3 months (>50 years for spores)
Light: UV

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20
Q

Average bacteria growth rate

A

double every 20 minutes

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21
Q

ENDOTOXIN

A

Component of the outer membrane of bacteria, eg lipopolysaccharide in Gram negative bacteria

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22
Q

EXOTOXIN

A

Secreted proteins of Gram positive and Gram negative bacteria

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23
Q

Endotoxin vs Exotoxin- Composition

A

Composition: Exo=protein Endo=LPS

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24
Q

Endotoxin vs Exotoxin- Action

A

Action: Exo=specific Endo=non-specific

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25
Q

Endotoxin vs Exotoxin- Effect of heat

A

Effect of heat: Exo=labile Endo=stable

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26
Q

Endotoxin vs Exotoxin- Antigenicity

A

Antigenicity (ability of an antigen to induce an immunological response when it is encountered by the human body) Exo=strong Endo=weak

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27
Q

Endotoxin vs Exotoxin- Produced by

A

Produced by: Exo= gram +ive/-ive Endo=LPS- gram -ive

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28
Q

Endotoxin vs Exotoxin- Convertibility

A

Convertibility to toxoid (a toxin treated (usually with formaldehyde) so that it loses its toxicity but retains its antigenicity) Exo= Yes Endo= no

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29
Q

Bacterial genetics - enzyme responsible of transcription

A

RNA polymerase to produce mRNA

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30
Q

Bacterial genetics - translation

A

mRNA translated in to protein by 30s/50s ribosome

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31
Q

Bacterial genetic variation- mutations

A

-base substitutions, deletion, interion

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32
Q

2 types DNA present in bacteria

A

Bacterial chromosome, Plasmid DNA

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33
Q

Bacterial genetic variation- Gene transfer

A

Transformation eg via plasmid
Transduction eg via phage
Conjugation eg via sex pilus

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34
Q

Genetic variation in bacteria

A

Mutation or gene transfer

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35
Q

Initial classification of bacteria

A

Obligate intracellular bacteria or bacteria that may be cultured on artificial media

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36
Q

Example of Obligate intracellular bacteria gensus

A

Rickettsia, Chlamydia, Coxiella

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37
Q

Division of bacteria that may be cultured on artificial media

A

With a cell wall or no cell wall

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38
Q

Example gensus of bacteria that may be cultured on artificial media with no cell wall

A

Mollicutes

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39
Q

Division of bacteria that may be cultured on artificial media with a cell wall

A

Growing as single cells or growing as filaments

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40
Q

Example genus of bacteria that may be cultured on artificial media with a cell wall growing as filaments

A

Actinomyces, nocardia, streptomyces

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41
Q

Division of bacteria that may be cultured on artificial media with a cell wall growing as single cells

A

Rods, cocci, spirochaetes

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42
Q

Example genus of spirochaetes

A

Leptospira, treponema, borrelia

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43
Q

Spirochaetes

A

long and tightly coiled bacteria

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44
Q

Division of cocci

A

Gram positive or negative

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45
Q

Division of gram -ive cocci

A

Anaerobic or aerobic

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46
Q

Example genus of aerobic gram -ive

A

Neisseria

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47
Q

Example genus of anaerobic gram -ive

A

Veillonella

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48
Q

Division of gram +ive cocci

A

Gram positive or negative

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49
Q

Division of aerobic gram +ive cocci

A

Staphylococcus or Streptococcus

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50
Q

Sub-division of Streptococcus

A

Beta-haemolytic, alpha-haemolytic, non-haemolytic, enterococcus

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51
Q

Example genus of anaerobic gram +ive

A

Peptostreptococcus

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52
Q

Staphylococcus

A

Aerobic, gram positive cocci, forms clumps, positive catalase test

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53
Q

Streptococcus

A

Aerobic, gram positive cocci, forms grows in chains, negative catalase test

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54
Q

Streptococcus vs Staphylococcus

A

Both aerobic gram positive cocci. Staphylococci form clumps, whereas Streptococci grow in chains. They can be discriminated by catalase test because Staphylococci have the capability to produce catalase

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55
Q

Division of aerobic gram +ive cocci test

A

Catalsae test, +ive=Staphylococcus -ive=Streptococcus

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56
Q

Division of Rods

A

Ziehl-Neelsen positive stain, gram +ive or gram -ive

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57
Q

Example genus of Ziehl-Neelsen positive stain

A

Mycobacteria

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58
Q

Division of gram positive/gram negative Rods

A

Anaerobic or aerobic

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59
Q

Example genus of anaerobic gram +ive rods

A

Clostridium, Propionibacterium

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60
Q

Example genus of aerobic gram +ive rods

A

Corynebacterium, listeria, bacillus

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61
Q

Example genus of anaerobic gram -ive rods

A

Bacteroides

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62
Q

Example genus of aerobic gram -ive rods

A

Coliforms, vibrio, pseudomonads, parvobacteria

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63
Q

gram positive

A

Gram-positive bacteria lack an outer membrane but are surrounded by layers of peptidoglycan many times thicker than is found in the Gram-negatives

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64
Q

Staphylococci

A

Currently at least 40 species
Coagulase +ve or – ve
S.aureus most important (coag. +ve)
Coagulase -ve species, e.g. S epidermidis important in opportunistic infections
Normal habitat- nose and skin

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65
Q

Coagulase

A

Enzyme produced by bacteria that clots blood plasma. Fibrin clot formation around bacteria may protect from phagocytosis

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66
Q

Staphylococcus aureus spread

A

Spread by aerosol and touch- carriers & shedders

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67
Q

Staphylococcus aureus

A

Virulence factors
Pore-forming toxins (some strains)- a - haemolysin & Panton-Valentine Leucocidin
Proteases - Exfoliatin
Toxic Shock Syndrome toxin (stimulates cytokine release)
Protein A (surface protein which binds Ig’s in wrong orientation)

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68
Q

MRSA (Methicillin-resistant Staphylococcus aureus)

A

resistant to: beta-lactams, gentamicin, erythromycin, tetracycline

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69
Q

Staphylococcus aureus symptoms

A

Pyogenic- wound infection, abscesses, impetigo, septicaemia, osteomyelitis, pneumonia, endocarditis
Toxin mediated- scaled skin syndrome, toxic shock syndrome, food poisoning

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70
Q

Coagulase-negative Staphylococci examples

A

S.epidermidis: -Infections in debilitated, prostheses (opportunistic)
-Main virulence factor - ability to form persistent biofilms
S.saprophyticus- Acute cystitis (haemagglutinin for adhesion, urease)

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71
Q

Haemolysis

A

used to describe the destruction of red blood cells

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72
Q

Beta-Haemolysis

A

complete lysis e.g. S.pyogenes
Haemolysins O & S

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73
Q

Alpha- Haemolysis

A

partial, greening e.g. S.intermedius

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74
Q

Non (gamma)- Haemolysis

A

no lysis e.g. some S.mutans

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75
Q

Sero-grouping

A

Grouping by Carbohydrate cell surface antigens

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76
Q

Lancefield A-H and K-V

A

Antiserum to each group added to a suspension of bacteria
-clumping indicates recognition

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77
Q

Lancefield Group A+B

A

Group A - S.pyogenes; important pathogen
Group B - S.agalactiae neonatal infections

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78
Q

S.pyogenes virulence exported factors

A

Enzymes
Hyaluronidase - spreading
Streptokinase - breaks down clots
C5a peptidase - reduces chemotaxis
Toxins
Streptolysins O&S - binds cholesterol
Erythrogenic toxin - SPeA – exaggerated response

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79
Q

S.pyogenes virulence surface factors

A

Capsule - hyaluronic acid
M protein – surface protein (encourages complement degradation)

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80
Q

Infections caused by S.pyogenes

A

Wound infections&raquo_space; cellulitis, puerperal fever
Tonsillitis & pharyngitis
Otitis media
Impetigo
Scarlet fever
Complications -rheumatic fever
-glomerulonephritis

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81
Q

Virulence (factors)

A

ability of an organism to infect the host and cause a disease. Virulence factors are the molecules that assist the bacterium colonize the host at the cellular level

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82
Q

Gram positive bacilli

A

Listeria monocytogenes, Bacillus anthracis, Corynebacterium diphtheriae

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83
Q

Gram positive bacilli- Clostridia

A

Spore forming , Survive in environment, Produce toxins
C. tetani- Tetanus
C. botulinum - Botulism
C. difficile- antibiotic associated diarrhea
-pseudomembranous colitis

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84
Q

Gram positive vs Gram negative stain

A

+ive- crystal-violet
-ive- fuchsin or safranin counterstain

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85
Q

Pathogenicity determinants

A

Any product or strategy that contributes to pathogenicity/virulence
Colonisation factors: adhesins, invasins, nutrient acquisition, defence against the host
Toxins (effectors): usually secreted proteins -Damage
-Subversion

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86
Q

Types of aerobic gram -ive rodes

A

Coliforms, Vibrio, parvobacteria, pseudomonads

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87
Q

Coliforms

A

Enterobacteriaceae or Enterobacteria
Rod-shaped
Motile (most)
Peritrichous flagella
Facultatively anaerobic
Colonise the intestinal tract- Advantageously or disadvantageously

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88
Q

MacConkey-lactose agar

A

Lactose fermenters – red (pink)
Acid produced by fermentation turns neutral red dye in plate red

89
Q

Xylose Lysine Deoxycholate (XLD)

A

Lactose fermenters turn phenol red in media yellow
Isolates Salmonella and Shigella
Shigella cannot ferment lactose remains red
Salmonella cannot ferment lactose but reduce thiosulphate to produce hydrogen sulphide (black)

90
Q

Cell surface antigens of Gram negative bacteria

A

Amino acid or carbohydrate variation in cell surface structures gives rise to antigenic variation among species AND between isolates (strains) of the same species
Capsule – polysaccharide
LPS – polysaccharide
Flagellum - protein

91
Q

Serovars

A

groups within a single species of microorganisms, such as bacteria or viruses, which share distinctive surface structures

92
Q

gram negative bacteria

A

Gram-negative bacteria are surrounded by a thin peptidoglycan cell wall, which itself is surrounded by an outer membrane containing lipopolysaccharide.

93
Q

Bacteroides

A

Non-motile rods
Commensal flora (large intestine) - most abundant (30-40% of the total)
Opportunistic - tissue injury (surgery, perforated appendix or ulcer)

94
Q

Spirochaetes

A

Long, slender, helical, highly flexible
Most are free-living and non-pathogenic
Pathogenic varieties difficult to culture
Modified outer membrane (“outer sheath”)
Propels bacterium in a corkscrew motion

95
Q

Obligate intracellular bacteria

A

organisms that absolutely require an eukaryotic host to survive and replicate

96
Q

Examples of mycobacterium species

A

M. tuberculosis-TB
M. avium complex (MAC)- disseminated infection in AIDS, chronic lung infection
M. Kansaii- Chronic lung infection

97
Q

Mycobacteria

A

-Slightly curved, beaded bacilli
-High lipid content with mycolic acids in cell wall makes Mycobacteria resistant to Gram stain
-Identified by Ziehl-Neelsen stain

98
Q

Mycobacteria Microbiology

A

Aerobic, simple rod shapes (bacillus), thick cell wall, high molecular weight lipids
Slow growing

99
Q

Challenges from mycobacteria microbiology

A

Thick lipid rich cell makes immune cell killing and penetration of drug challenging
Slow grow- gradual onset of disease, takes much longer to diagnose/treat

100
Q

How does TB infect us?

A

Transmission via air
Primary TB in lung
Latent TB can remain for decades
Can spread beyond lungs

101
Q

Primary Tuberculosis

A

Initial ‘contact’ made by alveolar macrophages
Bacilli taken in lymphatics to hilar lymph nodes

102
Q

Latent Tuberculosis

A

-no clinical disease
-detectable CMI to TB on tuberculin skin test
-Cell mediated immune (CMI) response from T-cells
-Primary infection contained but CMI persists

103
Q

Pulmonary Tuberculosis

A

Could occur immediately following primary infection (post-primary) or month later after reactivation
Granulomas forms around bacilli that have settled in apex
In apex of lung there
Is more air and less
blood supply (fewer defending
white cells to fight)
TB may spread in lung causing other lesions

104
Q

Primary complex- TB

A

=Granuloma + Lymphatics + Lymph nodes

105
Q

Where does TB spreads beyond lungs

A

Bacilli in lungs apex and lymph nodes
TB meningitis, miliary TB, Pleural TB, bone and joint TB, Genito urinary TB,

106
Q

TB: Hallmark granuloma formation

A

If the granuloma works: Mycobacteria shut down metabolically in order to survive – dormancy
But if fails, e.g. in the lung, this can result in the formation of a cavity full of live mycobacteria and eventual disseminated disease (consumption)

107
Q

What does our body do to protect us from TB?

A

Primarily controlled by macrophages
Requires a CD4 T cell response to be controlled
Involves many cells of immunity- formation of granulomas
Granuloma stability controls reactivation of TB

108
Q

Clinical diagnostic methods- TB

A

Slow growth is challenging for diagnosis using microbiology
Nucleic acid detection is more rapid
Can use immune response as a diagnosis test- tuberculin skin test (TST)

109
Q

Tuberculin skin test (Mantoux)

A

The highly immunogenic nature of mycobacterial lipids stimulates T-cell responses in 3-9 weeks after exposure to M. tuberculosis
This reactivity is measured in the tuberculin skin test (TST) an intradermal injection of purified protein derivatives.

110
Q

Available therapies and resistance

A

Long treatment regimes
Multiple avenues to drug resistance
XDR TB problematic to treat
A pressing need for new therapies

111
Q

Resistance mechanisms

A

Drug inactivation, drug titration, alteration of drug target, altered cell envelope

112
Q

How do we study TB?

A

-Animal models a way to understand complex immunology
-Mouse not a natural host of TB
-Fish have their own mycobacterial species that can be used to help investigate host-directed therapies

113
Q

What is a virus

A

An infectious, obligate intracellular parasite
Comprising genetic material
(DNA or RNA) surrounded by aprotein coat and/or a membrane

114
Q

Virus vs bacteria- Cell wall

A

V=no B=yes

115
Q

Virus vs bacteria- Organelles

A

V=no B=yes

116
Q

Virus vs bacteria- DNA and RNA

A

V=no B=yes

117
Q

Virus vs bacteria- Dependent of host cell

A

V=yes B=no

118
Q

Virus vs bacteria- Alive

A

V=no B=yes

119
Q

Different Shapes of viruses

A

Helical, icosahedral, comples

120
Q

Different Structures of viruses

A

Non-enveloped or enveloped

121
Q

Envelope of virus

A

envelope= lipid coat derived from plasma membrane of the host cell

122
Q

Can viruses replicate independently?

A

No, Viruses require a host cell and it’s machinery in order to replicate

123
Q

How do viruses replicate?

A
  1. ATTACHMENT to specific receptor
  2. CELL ENTRY
  3. HOST CELL INTERACTION + REPLICATION
  4. ASSEMBLY OF VIRION
  5. RELEASE OF NEW VIRUS PARTICLES
124
Q

HOST CELL INTERACTION + REPLICATION of viruses

A

-Migration of genome to cell nucleus
-Transcription to mRNA using host materials
Translation of viral mRNA to produce: -structural proteins
-viral geniome
-non-structural proteins

125
Q

Location of assembly of virion

A

Occurs in different locations depending on virus
-Nucleus (e.g. herpes viruses)
-Cytoplasm (e.g. poliovirus)
-At cell membrane (e.g. influenza virus)

126
Q

Release of new virus

A

-bursts out > cell death e.g. rhinovirus
-budding/exocytosis
e.g. HIV, influenza

127
Q

True or false: Viruses are large, and consist of genetic material surrounded by a lipid coat

A

False, Viruses are very small, and consist of genetic material surrounded by a protein coat

128
Q

How do viruses cause disease?

A

a) Direct destruction of host cells
b) Modification of host cell
c) “Over-reactivity” of immune system
d) Damage through cell proliferation
e) Evasion of host defences

129
Q

Viruses causing disease example: Direct destruction of host cells

A

e.g. poliovirus- host cell lysis and death after a viral replication period of 4 hours

130
Q

Viruses causing disease example: Modification of host cell

A

e.g. rotavirus- atrophies villi and flattens epithelial cells

131
Q

Viruses causing disease example: “Over-reactivity” of immune system

A

e.g. hepatitis B, Sars-CoV-2

132
Q

Viruses causing disease example: Damage through cell proliferation

A

e.g human papillomavirus > cervical cancer

133
Q

Viruses causing disease example: Evasion of host defences- Cellular level

A

Cellular level- Latency: e.g. herpesviridae
-Cell-cell spread: e.g. measles, HIV

134
Q

Viruses causing disease example: Evasion of host defences- Molecular level

A

Molecular level- Antigenic variability e.g. influenza, HIV, rhinovirus
-Prevention of host cell apoptosis e.g. herpesviridae
-Downregulation of interferon and other intracellular host defence proteins e.g. many
-Interference with host cell antigen processing pathways e.g. herpesviridae, measles, HIV

135
Q

Recognising how viruses cause disease allows us to?

A

-Understand transmission and natural history
-Know who is most at risk
-Develop treatments and “preventative” drugs

136
Q

Do all viruses cause the same clinical symptoms

A

Viruses vary wildly in therange of clinical syndromes they can cause, due to:
-Different host cells and tissues that they can infect
-Different methods of interaction with the host cell

137
Q

What is meningitis?

A

Meningitis describes inflammation of the meninges (membranes) which cover the brain and spinal cord

138
Q

three layers of meninges

A

dura mater
arachnoid mater
pia mater

139
Q

Causes of meningitis: infection

A

Bacteria e.g. meningococcus, pneumococcus
Viruses e.g. coxsackievirus, echovirus, herpes virus, mumps virus, influenza, HIV etc
Less common infective causes include fungi, protozoa, and other parasites.

140
Q

Causes of meningitis: non-infectious

A

Medications e.g. antibiotics (amoxicillin, trimethoprim/sulfamethoxazole), carbamazepine, lamotrigine, NSAIDs, ranitidine
Cancers e.g. melanoma, lung cancer, breast cancer, lymphoma, leukaemia
Autoimmune disease e.g. Systemic lupus erythematosus (SLE), Behçet’s syndrome.

141
Q

Invasive meningococcal disease

A

Infection with Neisseria meningitidis
Gram-negative diplococci
Carried by 10-24% of the population
Humans are only known reservoir
Transmission by respiratory droplets/ naso-pharyngeal secretions
Incubation period 2-10 days, usually 3-4 days

142
Q

Two main manifestations of invasive meningococcal disease

A

Meningitis: a localised infection of the meninges, with “local” symptoms
Septicaemia : a systemic infection with widespread signs, and generalised organ damage

143
Q

Risk factors for meningitis

A

Extremes of age
Immunocompromised (e.g. HIV) or immunosuppressed (e.g. chemotherapy)
Asplenia/hyposplenia
Cancer – people with leukaemia and lymphoma
Sickle cell disease
Organ dysfunction – e.g. liver or kidney disease
Smokers
Contiguous infection
Living in overcrowded households, college dormitories or military barracks
People who have had contact with a case
Travellers abroad to high risk area - increased risk of encountering the pathogen

144
Q

Meningococcal meningitis symptoms

A

Fever, stiff neck, headache, confusion, increased sensitivity to light, nausea and vomiting

145
Q

Meningococcal meningitis symptoms- Do babies always present with classic symptoms

A

They may be: -slow or inactive
-irritable
-vomiting
-feeding poorly
-or have a bulging anterior fontanelle (the soft spot of the skull)

146
Q

Brudzinski’s neck sign

A

keeps one hand behind the patient’s head and the other on chest in order to prevent the patient from rising. Reflex flexion of the patient’s hips and knees after passive flexion of the neck constitutes a positive Brudzinski sign
+ive sign of meningitis

147
Q

Meningococcal septicaemia symptoms

A

Fever and chills
Fatigue
Vomiting
Cold hands and feet
Severe aches or pain in the muscles, joints, chest, or abdomen
Rapid breathing
Diarrhoea
Non blanching rash (petechiae)
In the later stages, a dark purple rash (purpura)

148
Q

Disseminated Intravascular Coagulation (DIC)

A

Caused by sepsis
the activation of coagulation pathways that results in formation of intravascular thrombi (clots) and depletion of platelets and coagulation factors.
These clots can cause arterial occlusions leading to gangrene of extremities & auto-amputations

149
Q

Auto-amputation

A

spontaneous detachment of an appendage from the body as a result of arterial occlusions

150
Q

Close contacts are identified by;

A
  • People living in the same household as the case
  • Anyone who slept overnight in the same household as the case in previous 7 days
  • Other household members if case stayed overnight elsewhere in previous 7 days
  • Intimate kissing contacts in last 7 days
151
Q

Chemoprophylaxis

A

Antibiotics given to eradicate throat carriage- stops transmission, doesn’t stop infection

152
Q

What are fungi

A

Eukaryotic
Chitinous cell wall
Heterotrophic
“Move” by means of growth or through the generation of spores (conidia), which are carried through air or water

153
Q

Yeast

A

small single celled organisms that divide by budding

154
Q

Mould

A

Moulds form multicellular hyphae and spores

155
Q

Options for selective fungi toxicity

A

DNA/RNA synthesis,
protein synthesis- Similar to mammalian
Cell wall- doesn’t exist in humans
Plasma membrane- human cell membrane contains cholesterol not ergosterol

156
Q

Why does fungi have limited options for selective toxicity?

A

They are eukaryotes and have several similarities to human cells

157
Q

Is ringworm caused by a worms?

A

No, its caused by a fungus

158
Q

Dermatophytes

A

Fungal organisms that require keratin for growth. These fungi can cause superficial infections. Human-human or animal-human transmission

159
Q

Sampling presumed dermatophyte infections

A

-plucked hair
-scalp scraping
-scarping of scaled edge of lesion
-nail clippings

160
Q

Dimorphic fungi

A

Fungi that have a yeast phase (at 37C in organism) and a mould phase (ambient temp).

161
Q

Dimorphic fungi transmission

A

Infection via inhalation of conidia from soil or implantation

162
Q

Coccidioides geography

A

warm, arid conditions in SW USA

163
Q

Coccidioides disease

A

-Asymptomatic/subclinical infection common (2/3)
-Most of rest – community acquired pneumonia 1-3 weeks post-exposure (1/3 of CAP in Ariziona)
-Severe disease > respiratory failure or septic shock in context of high inoculum or cell-mediated immune defect – e.g. HIV
-Late disease – does not correlate with the severity of initial symptoms

164
Q
A
165
Q

Invasive candidiasis

A

A serious Infection caused by a yeast called Candida, can affect the blood, heart, brain, eyes, bones, or other parts of the body.

166
Q

Main causes of invasive candidiasis

A

mostly due to infection of prosthetic devices or intra-abdominal disease

167
Q

Cryptococcus causes

A

Acute or chronic meningitis in patients with reduced cell mediated immunity

168
Q

Differential diagnosis of sub-acute/chronic meningitis- Infective

A

-Tuberculosis
-Cryptococcus
-Dimorphic fungi –Histoplasma, Coccidioides, Blastomyces
-Lyme
-Brucella
-Syphilis

169
Q

Differential diagnosis of sub-acute/chronic meningitis- Non-infective

A

-Sarcoidosis
-Behçets’s
-SLE
-Malignant
-Drug induced

170
Q

Cryptococcus

A

Association with rotting wood and bird guano
Vast majority of human disease caused by C. neoformans (only causes disease in immunocompromised) and C. gattii (more likely in immunocompetent)

171
Q

Invasive aspergillosis

A

associated with profound immunocompromise but is increasingly recognised in patients with severe viral infection

172
Q

Mucoraceous moulds (zygomyctes)

A

-Rare but cause devastatingly rapidly progressive infections that cross tissue planes
-need aggressive antifungal therapy and surgery for optimal outcomes

173
Q

Pneumocystis jirovecii

A

Pneumocystis jirovecii causes a pneumonitis with severe hypoxia in the immunocompromised

174
Q

Antibiotic

A

Antibiotics are molecules that work by binding a target site on a bacteria- the crucial binding site will vary with the antibiotic class

175
Q

Beta lactam antibiotics

A

-disrupt peptidoglycan production
-by binding covalently and irreversibly to the Penicillin Binding Proteins

176
Q

Beta lactam antibiotics- gram +ive or -ive

A

gram-positive usually more susceptible to β-lactams than gram-negative bacteria

177
Q

What causes differences in β-lactam antibiotics

A

Differences in the spectrum and activity of β-lactam antibiotics are due to their relative affinity for different PBPs.

178
Q

Why are beta-lactam antibiotics ineffective in the treatment of intracellular pathogens?

A

Because the penicillins poorly penetrate mammalian cells

179
Q

Beta Lactams- examples

A

Penicillins, Cephalosporins, Carbapenems, Monobactams

180
Q

Beta Lactams-Penicillins

A

Penicillin V
Penicillin G (Benzyl penicillin)
Flucloxacillin
Amoxicillin/Ampicillin
Pipericillin

181
Q

Beta Lactams-Cephalosporins

A

Cefuroxime
Cefotaxime Ceftriaxone

182
Q

Beta Lactams-Carbapenems

A

Meropenem

183
Q

Nucleic acid synthesis

A

group of antibiotics that interfere with DNA synthesis by inhibiting n enzymes involved in DNA replication

184
Q

Metronidazole action

A

Rifampicin- inhibits protein synthesis by interacting with DNA, and causes a loss of helical DNA structure and strand breakage

185
Q

Ciprofloxacin action

A

Quinolones- target by inhibiting the DNA gyrase (catalyses the super-coiling of double-stranded closed-circular DNA)

186
Q

Gentamicin action

A

Aminoglycosides- action involves inhibition of bacterial protein synthesis by binding to 30S ribosomes

187
Q

Doxycycline action

A

Tetracyclines- reversibly binds to the 30S ribosomal subunits, blocking the binding of aminoacyl tRNA to the mRNA and inhibiting bacterial protein synthesis

188
Q

Clindamycin action

A

Lincosamides- binding to the 50s ribosomal subunit of bacteria. This agent disrupts protein synthesis by interfering with the transpeptidation (transfer of AA) reaction, which thereby inhibits peptide chain elongation
TURNS OFF NASTY TOXINS MADE BY Gram positive bugs

189
Q

Clarithromycin action

A

Macrolides- inhibits bacterial protein synthesis by binding to the bacterial 50S ribosomal subunit, interferes with amino acid translocation during the translation and protein assembly process

190
Q

Trimethoprim action

A

Trimethoprim- inhibits folate synthesis- blocks the reduction of dihydrofolate to tetrahydrofolate (active form of folic acid)

191
Q

Co-trimoxazole

A

co-trimoxazole blocks two consecutive steps in folate synthesis process

192
Q

Fungal cell properties vs mammalian cell

A

DNA/RNA synthesis,
protein synthesis- Similar to mammalian
Cell wall- doesn’t exist in humans
Plasma membrane contains ergosterol whereas human cell membranes contain cholesterol

193
Q

Bactericidal Antibiotics

A

The agent kills the bacteria, inhibits cell wall synthesis

194
Q

Bacteriostatic Antibiotics

A

inhibitory to growth- antibiotics that Inhibit protein synthesis, DNA replication or metabolism

195
Q

Minimum inhibitory Concentration (MIC)

A

the lowest concentration of an antibiotic that inhibits the growth of a given strain of bacteria

196
Q

Does the lowest MIC=best antibiotic?

A

No, drug must not only attach to its binding target but also must occupy an adequate number of binding sites for a sufficient period of time

197
Q

Two major determinants of anti bacterial effects

A

Concentration and the Time that the antibiotic remains on these binding sites

198
Q

Time dependent killing

A

t>MIC- time that serum concentrations remain above the MIC during the dosing interval

199
Q

Concentration -Dependent Killing

A

peak concentration/MIC ratio- how high the concentration is above MIC

200
Q

Pharmacokinetic processes for antibiotics

A

-release from dose form
-absorption into blood
-distribution in body
-rate of elimination via metabolism (liver) or excretion (kidney)

201
Q

Target sites of antibiotics

A

Cell wall/membrane synthesis, nucleic acid synthesis (folate synthesis/DNA gyrase/RNA polymerase), protein synthesis (50s/30S subunit)

202
Q

Antibiotic resistant- Change in antibiotic target- Flucloxacillin and MRSA

A

Flucloxacillin (or methicillin) is no longer able to bind penicillin binding protein of Staphylococci – MRSA (methicillin resistant S. aureus)

203
Q

Antibiotic resistant- Change in antibiotic target- vancomycin and VRE

A

Wall components change in enterococci and reduce vancomycin binding – VRE (Vanocmicin resistant Enterococci)

204
Q

Antibiotic resistant- Change in antibiotic target- Rifampicin and MDR-TB

A

Rifampicin activity reduced by changes to RNA polymerase in MTB – MDR-TB (Multi drug resistant TB)

205
Q

Antibiotic resistant- destroy antibiotic- penicillin

A

Beta lactam ring of Penicillin and cephalosporins hydrolysed by bacterial enzyme ‘Beta lactamase’

206
Q

Methods of antibiotic resistance

A

Change in antibiotic target, destroy antibiotic, prevent antibiotic access, remove antibiotic from bacteria

207
Q

Intrinsic resistance

A

All subpopulations of a species will be equally resistant

208
Q

Intrinsic resistance- example

A

-Aerobic bacteria are unable to reduce metronidazole to its active form
-Vancomycin cannot penetrate outer membrane of gram negative bacteria

209
Q

Acquired resistance

A

-A bacterium which was previously susceptible obtains the ability to resist the activity of a particular antibiotic
-Only certain strains or subpopulations of a species will be resistant

210
Q

MRSA (Methicillin resistant Staphylococcus aureus)

A

Resistance to all β-lactam antibiotics in addition to methicillin (= flucloxacillin)
Bacteriophage mediated acquisition of Staphylococcal cassette chromosome mec (SCCmec)
contains resistance gene mecA encodes penicillin-binding protein 2a

211
Q

VRE (vancomycin-resistant enterococci)

A

-Plasmid mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding
-Promoted by cephalosporin use

212
Q

ESBL (extended spectrum beta lactamase)

A

Extended spectrum beta lactamase (ESBL) inhibition
These hydrolyse oxyimino side chains of cephalosporins: cefotaxime,ceftriaxone, andceftazidime and monobactams: aztreonam

213
Q

Carbapenems- Meropenem

A

-in contrast to other b-lactams, are highly resistant to degradation by b-lactamases or cephalosporinases
-often the antimicrobials of last resort to treat infections due to ESBL

214
Q

CRE (Carbapenem Resistant Enterobacteriaceae)

A

Produce carbapenemases so are resistant to carbapenem so treatment options are very few
and very toxic

215
Q

factors to consider when deciding if an antibiotic is safe to prescribe

A

Intolerance, allergy and anaphylaxis
Side effects
Age
Renal and Liver function
Pregnancy and breast feeding
Drug interactions
Risk of Clostridium difficile

216
Q

Benifts of using cephalosporins instead of penicillin’s

A

Good for people with penicillin allergy
Work against some resistant bacteria
Get into different parts of the body e.g. meningitis

217
Q

Gram positive antibiotic choice

A

Thick cell wall therefore need a simple cell wall weapon- think beta-lactams

218
Q

Gram negative antibiotic choice

A

Thin cell wall, therefore need a different weapon

219
Q
A

Phase 2a Lecture Notes (14 decks)

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