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Osha 2a > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is a pathogen?

A

Organism that causes or is capable of causing disease

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2
Q

What is a commensal?

A

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

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3
Q

What is an opportunist pathogen?

A

A microbe that only causes disease if the host defences are compromised

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4
Q

What is asymptomatic carriage?

A

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

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5
Q

How are bacteria named?

A

Genus species

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6
Q

What colour does gram positive bacteria stain?

A

Purple

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7
Q

What colour does gram negative bacteria stain?

A

Pink

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8
Q

Describe the steps to gram staining?

A
  • come in and stain
    1. crystal violet
    2. iodine
    3. Acetate/alcohol
    4. safranin counterstain
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9
Q

When is a Ziehl-Neelsen stain used?

A

On acid fast mycobacteria which have a high lipid and mycolic acid content (so gram staining doesn’t work)

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10
Q

What is the procedure for Ziehl-Neelsen staining?

A
  • cells stained using carbol fuchsin
  • washed using acid alcohol, mycobacteria remain purple
  • slide then stained with methylene blue.
  • purple mycobacteria can be identified
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11
Q

What is blood agar?

A
  • a mix of sheep and horse blood
  • medium for growing a wide range of bacteria
  • non-selective
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12
Q

What is XLD agar?

A
  • very selective growth medium used to isolate salmonella and shigella
  • gut bacteria appear yellow
  • shigella: red
  • salmonella: red with black centres
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13
Q

What is MacConkey agar?

A
  • designed to grow and differentiate gram negative bacilli
  • contains red dye and lactose
  • lactose fermenters: pink
  • non-lactose fermenters: yellow/colourless
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14
Q

What is CLED agar?

A
  • used in urine
  • for gram -ve bacilli
  • lactose fermenting: yellow
  • non-lactose: blue
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15
Q

Which gram negative bacilli are lactose fermenting and which are non-lactose fermenting?

A

lactose fermenting: E.coli
non-lactose fermenting: salmonella, shigella

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16
Q

What is the catalase test?

A
  • differentiates between staphylococcus and streptococcus genus
  • bubbling = positive for staph
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17
Q

What are mycobacteria?

A
  • slightly curved, beaded bacilli
  • aerobic, non-spore forming, non motile bacillus
  • gram positive
  • slow growing
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18
Q

What challenges does TB present?

A
  • Thick, lipid rich cell wall making immune cell killing and drug penetration challenging
  • Slow growth: gradual onset, longer to diagnose, longer to treat. Can be months or years.
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19
Q

What are the 2 different shapes of bacteria?

A

Rods: bacilli (vibrio - curved and spirochaete)
Blobs: cocci (diplococci, chains, clusters)

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20
Q

In what environment can bacteria survive?

A
  • From -80º to +80º
  • pH 4-9
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21
Q

What are spores?

A

Spores are rounded forms of bacterial cells which are highly resistant to heat, chemicals and desiccation

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22
Q

What are endotoxins?

A

a component of the outer membrane of bacteria e.g. lipopolysaccharide in gram negative bacteria
- non-specific action
- stable in heat
- weak antigenicity

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23
Q

What are exotoxins?

A

Secreted proteins of Gram positive and Gram negative bacteria
- labile in heat
- strong antigenicity

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24
Q

What is gram positive bacteria?

A

Has a thick cell wall with a peptidoglycan layer

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25
Q

What is gram negative bacteria?

A

has a thick cell wall with liposaccharide and protein outer membrane

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26
Q

Describe the properties of S. aureus (coagulase, spread)?

A
  • coagulase positive
  • spread by air or touch
  • people are either carriers or shedders
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27
Q

What is coagulase?

A
  • An enzyme produced by bacteria that clots blood plasma.
  • Fibrin clot formation around bacteria may protect from phagocytosis.
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28
Q

GIve examples of coagulase positive vs negative bacteria

A
  • coagulase positive: staph aureus
  • coagulase negative: staph epidermidis and saprophyticus
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29
Q

What virulence factors does S. aureus release that lead to its success?

A
  • Pore-forming toxins (some strains) a - haemolysin and ‘PVL’
  • Proteases
    Exfoliatin
  • Toxic Shock Syndrome toxin (stimulates cytokine release)
  • Protein A (surface protein which binds antibodies in wrong orientation)
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30
Q

What does MRSA stand for and which antibiotics is it resistant to?

A
  • methicillin resistant staphylococcus aureus
  • resistant to gentamicin (methicillin), erythromycin, tetracycline
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31
Q

What are coagulase negative forms of staph and what diseases do they cause?

A
  • S. Epidermidis: opportunistic infections, forms persistent biofilms
  • S. Saprophyticus: causes acute cystitis
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32
Q

What does streptococcus look like and how is it classified?

A
  • Cocci in chains
  • haemolytic, lancefield typing and biochemical properties
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33
Q

What is haemolysis?

A
  • test performed where bacteria is grown on blood agar
  • α: secretes hydrogen peroxide > partial haemolysis and greening
  • β: 2 pore forming toxins > complete lysis, appears yellow/clear
  • gamma: no lysis
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34
Q

How can β haemolytic strep be grouped?

A
  • antigenic sero-grouping
  • antibodies made that recognise each lancefield group (carb group in cell wall)
  • tagged to white latex beads
  • +ve result: antibodies bind bacteria and clump together
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35
Q

What are the most important Lancefield groupings?

A
  • Group A: S.pyogenes
  • Group B: S. agalacticae
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36
Q

How can α haemolytic strep be identified

A
  • optochin test:
  • resistant: viridans strep: no ring around filter paper disc
  • sensitive: S. pneumoniae
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37
Q

What is an antibiotic?

A

Molecules that work by binding a target site on a bacteria - binding at points on the bacterium that are crucial to its survival

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38
Q

What are antimicrobials?

A

Agents that kill infectious pathogens including antifungals, antibacterials, antihelminithics, antiprotozoals and antiviral agents

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39
Q

What are β lactams?

A

Disrupt peptidoglycan production, through covenant bonding to the transpeptidase enzyme activity which interrupts cross linking and cell wall synthesis

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40
Q

What are examples of penicillins?

A
  • Penicillin V
  • Penicillin G
  • Flucloxacillin
  • Amoxicillin
  • Pipericillin
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41
Q

What are examples of cephalosporins?

A
  • Cefuroxime
  • Cefotaxime
  • Ceftriaxone
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42
Q

What are examples of glycopeptides?

A
  • Vancomycin
  • Teicoplanin
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43
Q

What are the layers of gram negative cell wall?

A
  • capsule, lipopolysaccharide (endotoxin), outer membrane, lipoprotein, periplasmic space, peptidoglycan, inner membrane
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44
Q

What are the layers of gram positive cell walls?

A
  • capsule, peptidoglycan, inner membrane
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45
Q

Which antibiotics affect protein synthesis by affecting ribosomes?

A
  • gentamicin (aminoglycoside)
  • doxycycline (tetracycline)
  • clindamycin (lincosamide)
  • clarithromycin (clarithromycin)
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46
Q

What are examples of sulphonamides?

A
  • trimethoprim
  • co-trimoxazole
  • affect folic acid production
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47
Q

Which antibiotics affect nucleic acid synthesis?

A
  • metronidazole
  • ciprofloaxcin
48
Q

How are bacteria pathogenic?

A
  • Direct: destroy phagocytes + cells in which bacteria replicate
  • indirect: inflammation, immune-pathology
  • toxins: endo and exotoxins
49
Q

What are we trying to achieve with antibiotics?

A
  • give time and support for the immune system to deal with an infection
50
Q

What is the action of antibiotics?

A
  • Kill bacteria: inhibit cell wall synthesis (bacteriocidal)
  • stop bacteria growing: inhibit protein synthesis, DNA replication or metabolism (bacteriostatic)
51
Q

How much antibiotic is needed?

A
  • drug must attach to its binding target and occupy an adequate number of binding sites
  • antibiotic should remain at the binding site for a sufficient time period
52
Q

Which drugs have their efficacy determined by time dependent killing?

A

t> minimum inhibitory concentration
- β lactams, clindamycin, macrolides

53
Q

Which drugs have their efficacy determined by concentration dependent killing?

A
  • aminoglycosides
  • quinolones
54
Q

How are fungal cells comparable to human cells?

A
  • DNA/RNA/protein synthesis similar to mammalian cells
  • cell wall doesn’t exist in humans
  • plasma membrane contains ergosterol instead of cholesterol
55
Q

How do bacteria resist antibiotics?

A
  • change molecular configuration of antibiotic target
  • destroy antibiotics using enzymes
  • prevent antibiotic access
  • remove antibiotic from bacteria
56
Q

What is an example of antibiotic destruction?

A
  • β lactam rings of penicillin are hydrolysed by bacterial enzyme β lactamase so it is no longer able to bind to the PBP
57
Q

How can antibiotic access be prevented?

A
  • bacterial membrane porin channel is modified e.g. the size, number, selectivity
58
Q

How can the antibiotic be removed from the bacteria?

A
  • proteins in bacterial membranes act as export/efflux pumps so the level of antibiotic is reduced.
59
Q

What is intrinsic resistance?

A
  • all subpopulations are equally resistant
  • aerobic bacteria can’t reduce metronidazole to its active form
  • vancomycin can’t penetrate the outer membrane of gram negative bacteria
60
Q

What is MRSA?

A
  • bacteriophage mediated
  • resistance gene mecA is transferred
  • encodes penicillin-binding protein 2a
  • causes resistance to all β-lactam antibiotics
61
Q

What factors must be considered when thinking about if an antibiotic is safe to prescribe?

A
  1. Intolerance, allergy and anaphylaxis
  2. Side effects
  3. Age
  4. Renal and Liver function
  5. Pregnancy and breast feeding
  6. Drug interactions
  7. Risk of Clostridium difficile
62
Q

When are cephalosporins useful?

A
  • Good for people with penicillin allergy
  • Work against some resistant bacteria
  • Get into different parts of the body e.g. meningitis
63
Q

What are fungi?

A
  • eukaryotic
  • chitin cell wall
  • heterotrophic
  • move by growth of spores which are carried through air/water
64
Q

What are some examples of fungal disease?

A
  • Tinea pedis (athlete’s foot)
  • onychomycosis (fungal nail infections)
  • life threatening fungal infection is rare in healthy hosts
65
Q

What are yeasts?

A
  • small single celled organisms that divide by budding
  • some fungi switch between yeasts and moulds
66
Q

Why do fungi not tend to affect humans?

A
  • inability to grow at 37 degrees
  • innate and adaptive immune response
67
Q

What methods can be used for fungal diagnostics?

A
  • Radiology: aspergillus and zygomycetes
  • microscopy: aspergillus, zygomycetes and yeasts
  • culture
  • PCR + antigen tests
68
Q

How can fungal disease be treated?

A
  • drugs that target the cell wall or plasma membrane
  • it is difficult to identify molecules with selective toxicity for fungi because they are eukaryotic
69
Q

What is the main form of treatment of fungal disease?

A
  • azoles: broad class of drugs
70
Q

How do moulds form and spread?

A
  • form multicellular hyphae and spores
71
Q

What are the types of gram positive cocci that can be cultured on artificial media?

A

staphylococcus and streptococcus

72
Q

In what form do staph cocci appear and what are the 2 different types of staph?

A
  • appear in clusters
  • coagulase test > +ve = S. aureus and -ve = coagulase negative staph
73
Q

Which sites in the body are sterile?

A
  • blood
  • CSF
  • joints
  • lower resp tract
  • pleural fluid
  • peritoneal cavity
  • bladder
74
Q

Which sites in the body are colonised by flora?

A
  • GI tract
  • skin
  • oral cavity
  • vagina
  • urethra
75
Q

What is a virus?

A
  • An infectious, obligate intracellular parasite
  • Comprises genetic material (DNA/RNA) surrounded by a protein coat/membrane
76
Q

What is the typical size of a human virus?

A

20-60nm

77
Q

How do viruses replicate?

A
  1. Attachment to specific receptor
  2. Cell entry: uncoating of virion within cell and transcription to mRNA using host materials
  3. Host cell interaction and replication: translation of viral mRNA to produce structural proteins, viral genome or non-structural proteins
  4. Assembly of virion: occurs in different locations depending on virus
  5. Release of new virus particles: bursts out > cell death/budding or exocytosis
78
Q

How do viruses cause disease?

A
  1. Direct destruction of host cells
  2. Modification of host cell
  3. Over-reactivity of immune system
  4. Damage through cell proliferation
  5. Evasion of host defences
79
Q

What are protozoa?

A

Unicellular eukaryotes with a nucleus

80
Q

What are the 5 major classifications of protozoa?

A
  1. flagellates
  2. amobae
  3. cilliates
  4. sporozoa
  5. microsporidia
81
Q

What is the host of malaria?

A

Humans and the female anopheles mosquito acts as a vector

82
Q

What are the symptoms of malaria?

A
  • fever
  • chills
  • headache
  • myalgia
  • fatigue
  • diarrhoea and vomiting
83
Q

What is the malaria cycle?

A
  • parasites grow and multiply in liver cells
  • parasites infect red blood cells, grow and cause them to burst.
84
Q

How do we identify risks of infection?

A
  • risk factors
  • screening
  • clinical diagnosis
  • lab diagnosis
85
Q

What are enterobacteriaceae?

A
  • colonisers of large bowel, skin below waist and moist sites
  • most common causes of UTI and intra abdominal infection
86
Q

What is carbapenemase?

A
  • inactivates carbapenem antibiotics
  • previous one of the last resort antibiotics, now commonly used
  • one of the broadest spectrum antibiotics available
87
Q

What is MRSA resistant to?

A
  • flucloxacillin and other β lactam antibiotics
88
Q

When should hands be washed?

A
  • before and after patient contact
  • after handling bodily fluids
  • after using the toilet
  • before and after handling food
  • before and after an aseptic procedure
  • after removing PPE
89
Q

What are the methods of HIV prevention?

A
  • PREP: pre-exposure prophylaxis
  • PEP: post-exposure prophylaxis (started within 72 hrs) not as effective as PREP.
  • U=U: undetectable = untransmissible
90
Q

What are the benefits to testing for HIV?

A
  • Access to appropriate treatment and care
  • Reduction in morbidity and mortality
  • Reduction of vertical transmission
  • Reduction of sexual transmission
  • Public health /partner notification
  • Cost-effective
91
Q

What is involved in the 4th generation HIV test?

A
  • venous blood sample
  • includes p24 antigen and detects vast majority of infections at 4 weeks - repeated at 7 weeks if high index of suspicion
  • high sensitivity and specificity
92
Q

What is involved in a HIV point of care test?

A
  • finger prick
  • immediate result
  • Lower sensitivity and specificity
  • False positive and negative results
  • Longer incubation period
93
Q

How are HIV test results managed?

A
  • Negative test:
    Repeat if within “window period”
  • Positive result or result not clear
    Phone Sexual Health for advice and appointment is arranged within 48 hours
    Explain test “reactive” and needs further investigation
94
Q

What type of virus is HIV?

A
  • retrovirus
  • uses reverse transcriptase to make a DNA copy which is integrated within DNA of affected cell.
95
Q

What is the socio-economic impact of HIV in Africa?

A
  • significant impact on life expectancy
  • loss of economically productive adults
  • inc and distorted spending on healthcare
  • change in social structure: orphans cared for by grandparents
96
Q

How does paediatric HIV infection occur?

A
  • in utero: transplacental, during 3rd trimester
  • intra partum: exposure to maternal blood/genital secretions during delivery
  • breast milk
  • risk is up to 45% of transmission
97
Q

How can HIV transmission be prevented?

A
  • condom use
  • male circumcision
  • treating STIs
  • PreP/TasP/PeP
98
Q

What are the key features of HIV pathogenesis?

A
  • HIV is integrated into DNA of infected CD4- expressing cells
  • HIV infects CD4+, helper T, Treg, T follicular, dendritic cells, macrophages
  • HIV passes directly cell to cell so is inaccessible to antibodies
99
Q

What are the acute non-specific symptoms of HIV?

A
  • fever
  • sore throat
  • myalgia (muscle ache)
  • rash
  • occurs within 2-4 weeks of infection
100
Q

Which bacteria commonly grows in reheated rice and is associated with takeaways?

A
  • Bacillus cereus produces the toxin cereulide which causes vomiting
101
Q

What indicates a bacterial infection?

A
  • high neutrophil count
  • raised CSF protein: dying bacteria + Abs
  • reduced CSF glucose: neutrophils use as energy
102
Q

What is a charcoal swab used for?

A
  • allow for microscopy, culture and sensitivities
  • used with Amies transport medium
  • used for: ear, eye, skin and abscesses, throat, vaginal and wound swabs
  • used for chlamydia
103
Q

Which STIs and GU infections can a charcoal swab confirm?

A
  • bacterial vaginosis
  • candidiasis (thrush)
  • gonorrhoeae
  • trichomonas vaginalis
  • group B strep
104
Q

What type of bacteria is Neisseria gonorrhoeae and how is it treated?

A
  • gram-negative diplococcus
  • ciprofloxacin or azithromycin
105
Q

What bacteria causes syphilis?

A
  • Treponema pallidum
  • spirochete
  • incubation period: 21 days
106
Q

What type of bacteria is Neisseria meningitidis?

A
  • gram negative diplococci
107
Q

What type of bacteria is Strep. pneumoniae?

A
  • gram positive diplococci
  • α haemolytic and optochin sensitive
108
Q

How is S. pneumoniae treated?

A
  • β lactam antibiotics: amoxicillin, cefuroxime and cefotaxime
  • clarithromycin or ciprofloxacin in penicillin allergy
109
Q

What type of bacteria is Haemophilus influenzae?

A
  • gram negative cocobacilli
110
Q

How is H. influenzae treated?

A
  • β lactam antibiotics: co-amoxiclav
  • tetracyclines: doxycycline
  • NOT macrolides (-romycin)
111
Q

What is Klebsiella pneumoniae and where is it found?

A
  • gram negative bacilli
  • found in flora of mouth and intestines
  • homelessness, alcoholics, hospital
112
Q

How is Klebsiella pneumoniae treated?

A
  • β lactams: co-amoxiclav
  • cephalosporins
113
Q

What is Bordatella pertussis and how is it treated?

A
  • gram negative bacillus
  • causes whooping cough
  • diagnosed by culture, PCR, ELISA for IgG against pertussis toxin
114
Q

What is the treatment of Bordatella pertussis?

A
  • clarithromycin
  • vaccinated against as part of dTaP (diphtheria, tetanus and acellular Pertussis)
115
Q

How is Corynebacterium diphtheriae treated?

A
  • anti-toxin
  • erythromycin/clarithromycin

Osha 2a (15 decks)

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