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Phase 2a - Jemima > MICROBIOLOGY > Flashcards

MICROBIOLOGY Flashcards

1
Q

what is a commensal

A

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

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2
Q

what is an opportunistic pathogen

A

a microbe which can only cause disease if the host defences are compromised

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3
Q

What colour do gram positive bacteria stain

A

Purple

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4
Q

What colour do gram negative bacteria stain

A

Pink

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5
Q

what are the bacterial names for spheres or rods

A

coccus or bacillus

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6
Q

what is the outer membrane of gram positive bacteria like

A

there is a inner membrane, surrounded by a large layer or peptidoglycan which is linked to the phospholipid membrane

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7
Q

what is the outer membrane of gram negative bacteria like

A

There is two phospholipid membranes with a periplasmic space in-between containing a thin peptidoglycan layer

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8
Q

what type of bacteria is lipopolysaccharide found on

A

found on gram negative bacteria

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9
Q

what are the two types of bacterial toxins

A

Endotoxins - Component of the outer membrane of bacteria - LPS on gram negative bacteria
Exotoxins - secreted proteins of gram positive and gram negative bacteria

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10
Q

how does bacteria gain genetic variation

A
  1. Mutation - base substitution, deletion, transfer
  2. Gene transfer - Transformation (plasmid), Transduction (phage), Conjugation
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11
Q

what is the initial classification of bacteria

A

those that bay be cultured on artificial media, and obligate intracellular bacteria

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12
Q

What are bacteria that may be cultured on artificial media split into

A

split into those with a cell and those without a cell wall

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13
Q

what are the bacteria with a cell wall split into

A

those which grow as single cells and those that grow as filaments

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14
Q

what are the bacteria that grow as single cells split into

A

Rods - ZN stain, Gram positive and gram negative
Cocci - Gram positive and gram negative
Spirochaetes

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15
Q

what is the gram stain

A

it is where you apply a primary stain (such as crystal violet) to heat fixed bacteria. You then add iodide which binds to the crystal violet and fixes it to the cell wall. You then decolourise with ethanol or acetone and counterstain with safranin (pink)

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16
Q

what is the coagulase test used for

A

distinguished S. aureus from other staphylococci (clustered gram positive cocci)
- it is coagulase positive
- if negative S. epidermidis (opportunistic factors)

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17
Q

What bacteria would be gram positive cocci growing in
A. Chains
B. Clusters

A

A. Streptococcus
B. Staphylococcus

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18
Q

what test do you do to distinguish between staphylococcus bacteria

A

the coagulase (or DNAse) test
- if positive then its S. aureus

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19
Q

what test is done to distinguish streptococcus bacteria species

A

the haemolysis test

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20
Q

what is seen in the haemolysis test for an alpha haemolytic strep

A

there is partial haemolysis of the blood agar, bacteria uses hydrogen peroxide to oxidise the haemoglobin and the agar appears green

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21
Q

if the haemolysis test shows alpha haemolytic strep what other tests are then done

A

the optochin test
- if the bacteria is sensitive then it is S. Pneymoniae
- if the bacteria is resistant it is Viridans strep

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22
Q

what bacteria are beta haemolytic strep

A

S. Pyogenes

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23
Q

what is seen in the haemolysis test for beta haemolysis strep

A

there is complete lysis of the red blood cells causing the blood agar to appear clear

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24
Q

what does gamma haemolysis for the haemolysis test imply

A

that no haemolysis was seen

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25
Q

what is the oxidase test

A

it tests if a microorganism contains a cytochrome oxidase which implies it is able to use oxygen as the terminal electron acceptor
- aerobic

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26
Q

why do gram positive bacteria stain purple

A

Because they retain the colour of the crystal violet stain because they have a thick peptidoglycan layer in their cell wall.

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27
Q

what are three ways to classify streptococci

A
  1. Haemolysis
  2. Lancefield typing
  3. Biochemical properties
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28
Q

what is Lancefield grouping

A

where you group catalyze negative, coagulase negative bacteria, based on the bacterial carbohydrate cell surface antigens

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29
Q

what are the important gram positive bacteria to remember

A
  1. S. aureus
  2. S. epidermis
  3. S. pyogenes
  4. S. Pneumoniae
  5. Viridans Streptococci
  6. C. Diphtheriae
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30
Q

what is the main treatment for staphylococcus

A

flucloxacillin for 3 months

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31
Q

what is coagulase

A

it is an enzyme produced by bacteria that clots blood plasma

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32
Q

where is the normal habitat for staphylococci

A

the nose and skin

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33
Q

how is staphylococcus aureus spread

A

aerosol and touch

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34
Q

what are the virulence factors of staphylococcus aureus

A

Pore-forming toxins
Proteases
Toxic shock syndrome toxin
Protein A

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35
Q

what two types of infection can S. aureus produce

A
  1. Pyogenic (pus)
  2. Toxin mediated
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36
Q

what are two examples of coagulase negative staphylococci

A
  1. S. epidermidis
  2. S. saprophyticus
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37
Q

what is an example of a gamma haemolysis bacteria

A

S. mutans

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38
Q

what is antigenic sero-grouping used for

A

its used for beta haemolytic strep only and it looks at carbohydrate cell surface antigens. There are groups A-H and K-V.
- Group A - S. pyogenes
- Group B - S. agalactiae

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39
Q

how does the Lancefield microbead agglutination test work

A
  • antibodies made that recognise each group
  • these are tagged to tiny plastic beads
  • added to suspension of bacteria
  • antibodies bind to bacteria and beads clump
  • this is visible to the naked eye
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40
Q

what are the S.pyogenes virulence factors

A

. Exported factors = enzymes: Streptokinase, hyaluronidase C5a peptidase
. Toxins = Streptolysins O&S, Erythrogenic toxin
. Surface factors = capsule, M protein

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41
Q

what are the tissue systems that S. pyogenes can infect

A

Respiratory, Skin and soft tissue
- can also cause scarlet fever and complications

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42
Q

what bacteria causes scarlet fever

A

S. pyogenes

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43
Q

what percentage of the population have S. pneumoniae as a commensal

A

about 30%

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44
Q

what factors can predispose you to catch S. pneumoniae

A
  • impaired mucus trapping
  • hypogammaglobulinemia - low serum immunoglobulin
  • asplenia - absence of a spleen
  • HIV
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45
Q

what are S. pneumoniae virulence factors

A
  1. Capsule
  2. Inflammatory wall constituents
  3. Cytotoxin
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46
Q

what are examples of aerobic gram positive bacilli

A
  1. Listeria monocytogenes
  2. Bacillus anthracis
  3. Corynebacterium diphtheriae
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47
Q

what are examples of anaerobic gram positive bacilli

A

Clostridia
1. C. tetani
2. C. botulinum
3. C. difficile

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48
Q

what are the four major groups of gram negative bacteria

A
  1. Proteobacteria - rod shaped
  2. Bacteroides - rod shaped
  3. Chlamydia - round pleiomorphic
  4. Spirochaetes - spiral/helical
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49
Q

what are the sterile sited of the body (should normally have no bacteria/pathogens)

A
  1. Blood
  2. CSF
  3. Pleural fluid
  4. Peritoneum
  5. Joints
  6. Urinary tract
  7. Lower respiratory tract
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50
Q

what are pathogenicity determinants

A

any product or strategy which contributes to the pathogenicity or virulence

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51
Q

what are pathogenicity determinants of gram negative bacteria

A
  1. colonisation factors: adhesins, invasins, nutrient acquisition, defence against host
  2. Toxins
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52
Q

what is found in blood agar

A

sheep or horse blood

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53
Q

what is chocolate agar

A

blood agar which has been cooked for 5 minutes at 80oC to release some of the nutrients (allows more organisms to grow)

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54
Q

what is the function of CLED agar

A

it is cysteine lactose electrolyte deficient - used for urinary bacteria analysis

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55
Q

what is MacCONKEY agar

A

it contains natural red dye and lactose. Differentiates between lactose fermenting gram negative bacteria (E.Coli turns it pink)
and non lactose fermenters (salmonella, shigella)

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56
Q

what is gonococcus agar used for

A

for Neisseria culture

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57
Q

what is XLD agar used for

A

to differentiate between salmonella and shigella (salmonella red with black centres and shigella red only)

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58
Q

what is sabourard agar used for

A

for fungal culture

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59
Q

what bacteria would you be looking at down the microscope if its was purple and
A. in clusters
B. in chains

A

A. staphylococcus
B. Streptococcus

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60
Q

other than the coagulase test what’s another was to differentiate S. aureus from other staphs

A

culture of blood agar, S. aureus colonies are gold while other staphs are colourless (white)

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61
Q

What are the mycobacteria of medical importance

A
  • M. tuberculosis - tuberculosis
  • M. leprae - leprosy
  • M. avium - disseminated infection in AIDS
  • M. kansasii - chronic lung infection
  • M. marinum - fish tank granuloma
  • M. ulcerans - buruli ulcer
  • rapid growing myobacteria for skin and soft tissue infection
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62
Q

what are the features of mycobacteria

A

they are aerobic, non-spore forming, non motile bacilli

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63
Q

what do mycobacteria show on gram stain

A

weakly positive (or colourless)

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64
Q

can mycobacteria survive in harsh environments

A

yes, they can survive within macrophages even within a low pH environment

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65
Q

what is the reproduction time for mycobacteria

A

slow 0 M tuberculosis generation time is 15-20 hours. This means they are also slow growing and slow at responding to treatment

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66
Q

what stain can be used for mycobacteria which are resistant to gram stain

A

acid fast test - stain used to identify organisms with wax like thick cell walls

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67
Q

how are mycobacteria diagnosed

A

they are diagnosed using nucleic acid amplification such as PCR

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68
Q

are gram positive bacteria mostly cocci or bacilli

A

cocci

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69
Q

are gram negative bacteria mostly cocci or bacilli

A

bacilli

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70
Q

what patients might get opportunistic infections

A

those on immunosuppressant drugs, those with immunocompromise and those with a breakdown of host defences

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71
Q

what are the common spiral bacteria

A

vibrios, spirilla and spirochaetes

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72
Q

what is blood agar used for

A

commonly for streptococcus

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73
Q

what is chocolate agar used for

A

fastidious neisseria

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74
Q

what environment do gram positive bacteria prefer

A

dry, dusty environments. skin colonisers and spread by breathing in shed skin cells

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75
Q

what environment do gram negative bacteria prefer

A

wet, damp environments where the majority prefer to colonise mucous membranes

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76
Q

what is the catalase test used for

A

to differentiate between staphylococcus and streptococcus

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77
Q

what bacteria would it be if it was catalase positive

A

staphylococcus

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78
Q

what is the method for the catalase test

A

apply hydrogen peroxide to a small simple colony and if it bubbles then it is positive

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79
Q

what lancefield group is S. pyogenes

A

group A

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80
Q

how quickly do symptoms appear with CAP

A

they occur after LESS than 48 hours in the hospital

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81
Q

what is the common cause of CAP

A

S. Pneumoniae

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82
Q

what is treatment for CAP

A

amoxicillin first line, co-amoxiclav in unwell

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83
Q

how quickly do symptoms appear with HAP

A

symptoms occur after MORE than 48 hours in the hospital

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84
Q

who are the most likely to get HAP

A

People on ventilators, stroke, long stays, infection contact

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85
Q

what are the most likely causes of HAP

A

E. coli, Klebsiella pneumoniae, Enterobacter spp, pseudomonas aeruginosa, MRSA, streptococci

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86
Q

what is the treatment for HAP

A

guided by microbiology, often IV co-amoxiclav and gentamicin

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87
Q

what are the gram positive rods you need to know

A
  • Anaerobic: Clostridium Spp (difficile and perfingens)
  • aerobic: Bacillus spp and Corynebacterium
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88
Q

what are the medications for C. difficile

A

The 4 C’s
- Clindamycin
- Cephalosporins
- Co - amoxiclav
- Ciprofloxacin

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89
Q

what are symptoms of C. difficile

A

diarrhoea, fever, abdominal pain, Hx of Ab

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90
Q

what is the pathological basis of meningitis

A

there is inflammation of the pia and arachnoid mater - microorganisms infect the CSF

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91
Q

what are symptoms of meningitis

A

stiffness of the neck, photophobia and severe headache.
infective: fever and malaise
Petechial rash associated with meningococcal meningitis

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92
Q

what is the treatment for meningitis

A

Bacterial: start on antibiotics before tests come back
- cephalosporins: IV cefotaxime/IV ceftriaxone
- if over 50 or immunocompromised add IV amoxicillin to cover listeria
- one oral dose of ciprofloxacin
Meningococcal septicemia: immediate IM benzylpenicillin in community and IV cefotaxime in hospital
Viral: supportive treatment

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93
Q

What are the oxidative positive gram negative rods

A

Indole negative: if its motile its pseudomonas aeruginosa
Indole positive: Haemophiles influenzae

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94
Q

what can pseudomonas aeruginosa cause

A

CF lung infection
Diabetic foot
burn infections
UTI

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95
Q

what can haemophilus influenzae cause

A

septic arthritis
CODP exacerbations
pneumonia

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96
Q

what are the oxidase negative gram negative rods

A

Bordetella pertussis (whooping cough)
Enterobacteria - non lactose fermenting and lactose fermenting

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97
Q

what are the non lactose fermenting enterobacteria

A
  1. proteus mirabilis - UTI
  2. Shigella spp - gastroenteritis
  3. salmonella spp
  4. S. typhi - typhoid fever
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98
Q

what are some lactose fermenting enterobacteria

A
  1. indole positive E. coli - UTI, gastroenteritis, abdominal infection
  2. Indole negative Klebsiella pneumoniae - UTI, abdominal infections, CF lungs
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99
Q

how can a UTI occur

A

certain bacteria and yeasts can enter the renal tract via the renal artery. Infection can also gain access via the urethra, with incompetence of the cysto-ureteric valves allows organisms to enter the upper urinary tract. organisms can then ascend the urethras to the kidneys

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100
Q

what are the symptoms of lower UTI

A

dysuria, urgency, frequency, cloudy or foul urine, haematuria, suprapubic tenderness

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101
Q

what are the symptoms of upper UTI

A

fever, confusion, loin tenderness

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102
Q

what are the common microorganisms that cause UTI

A

Klebsiella, E. coli, Enterococcus, proteus, S. saprophyticus

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103
Q

what is the most common cause of UTIs

A

85 - 90% of cases are E. coli

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104
Q

what is the treatment for UTIs

A

Oral nitrofurantoin or trimethoprim
in pregnancy give cefalexin

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105
Q

what are characteristics of viruses

A

Non - cellular structure
Consist of an outer protein coat and a strand of nucleic acid (DNA or RNA)
come in a variety of shapes
do not carry out metabolic reactions on their own

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106
Q

what is the process of viral replication

A
  1. viral attachment: viral and cell receptors
  2. cell entry; only central viral core carrying the nucleic acid and some associated proteins enter the host cell
  3. Interaction with host cells: use cell materials (enzymes, amino acids, nucleotides) for their replication
  4. Replication: may localize in nucleus, cytoplasm or both
    Assembly: occurs in nucleus, in cytoplasm or at cell membrane
  5. Release: bursting open of cell, or by leaking from the cell over a period of time
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107
Q

how do viruses cause disease

A
  1. damage by direct destruction of host cells
  2. damage by modification of host cell structure or function
  3. damage involving over reactivity of the host cell as a response to infection
  4. damage through cell proliferation and cell immortalization
  5. evasion of both extracellular and intracellular host defences
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108
Q

what is the infectivity of a pathogen

A

the ability to become established in a host, can involve adherence and immune escape

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109
Q

what is a pathogens virulence

A

the ability to cause disease once established

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110
Q

what is required for a virus to infect someone

A

1, a rapid cell entry
2. correct receptors
3. evasion of immune cells
the ability to replicate and pass on

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111
Q

what is antigenic drift

A

spontaneous mutations, occur gradually giving minor changes in surface proteins such as haemaglutinin and neuraminidase in influenza. Epidemics

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112
Q

what is antigenic shift

A

sudden emergence of new subtype different to that of preceding virus. Pandemics

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113
Q

what are different ways bacteria can invade a host

A

respiratory tract
gastrointestinal tract
genitourinary tract
skin break

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114
Q

what immune responses are mounted against protozoan infection

A

depends on where the infection is
in blood there will be humoral immunity
in the tissues it will be cell mediated immunity

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115
Q

how is malaria spread

A

by the female anopheles mosquito bite

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116
Q

how do protozoa evade the immune system

A
  1. surface antigen variation - different genes which can be switched on or off and mean that surface antigens can change
  2. intracellular phase
  3. outer coat sloughing - removed and replaced with a new one
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117
Q

what are features of helminth infection

A
  1. they dont multiply in humans
  2. they are not intracellular
  3. few parasites carried
  4. poor immune response - immune evasion
  5. immune response not sufficient to kill
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118
Q

how to worms evade the immune response

A

decreased antigen expression by adults and they have a host derived glycolipid/glycoprotein coat

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119
Q

what is passive immunisation

A

where a preformed antibody is transferred
- transplacental
- colostrum
- injecting preformed antibody

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120
Q

what are the 5 major groups of protozoa

A

flagellates, amoebae, sporozoans, ciliates, microsporidia

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121
Q

what are features of flagellates

A

they have flagellum as the main way to move about, they usually reproduce by binary fission and they are found in intestine (can be elsewhere)

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122
Q

what are the features of amoeba

A

they move by means of flowing cytoplasm and production of pseudopodia

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123
Q

what are features of sporozoans

A

they have no locomotory extensions and are the most intracellular parasite. they reproduce by multiple fission

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124
Q

what is the most common sporozoan protozoa

A

malaria

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125
Q

what are features of ciliate protozoa

A

they have cilia that rhythmically beat at some stage so they can move. they have two types of nuclei, macro and micronucleus

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126
Q

what are features of microsporidia

A

they produce resistant spores, they have a unique polar filament which is coiled inside a spore

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127
Q

what are the 5 species of malaria

A

P. falciparum
P. orale
P. vivax
p. malariae
p. knowlesi

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128
Q

what is the most common type of malaria infection and the most deadly

A

P. falciparum

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129
Q

what are the clinical features of malaria

A

Very varied
Fever !!!!!!!!!!!!!!!!!!!!!!!!!
Other common;
Chills and sweats
Headache
Myalgia
Fatigue
Nausea and vomiting
Diarrhoea
These acute symptoms common to all 4 species

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130
Q

what is the lifecycle of malaria

A
  1. mosquito has blood meal and takes in gametocytes of malaria (in gut of the mosquito)
  2. sporozoites are released an migrates to salivary glands to mosquito
  3. in its saliva it injects sporozoites into human host
  4. migrates to liver cell and proliferates
  5. bursts and ruptures into blood stream
  6. in the blood stage the new trophocytes are made - infection of RBC, proliferating, bursting out
  7. some become gametocytes to be taken up by another mosquito
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131
Q

what are symptoms of tuberculosis

A

night sweats, cough, hemoptysis, weight loss and malaise

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132
Q

what are treatments for tuberculosis

A

isoniazid, ethambutamol, rifampicin and pyrazinamide

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133
Q

what is the side effect of isoniazid

A

numb or tingly extremities

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134
Q

what is a side effect of ethambutamol

A

ocular side effects

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135
Q

what is a side effect of rifampicin

A

orange or red urine

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136
Q

what is a side effect of pyrazinamide

A

arthralgia

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137
Q

what types of bacteria CANT you use gram stain on

A

Mycobacteria, actinomycetes and parasite cryptosporidium as they have waxy lipid cell walls

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138
Q

what stain is used on bacteria that you cant gram stain

A

the Ziehl-Neelson stain
- heating the sample with strong dye (carbol fuchsin)

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139
Q

what are the two forms of fungi

A

yeast - single cells that divide by budding
moulds - multicellular hyphae or spores

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140
Q

what is the fungal cell wall made of

A

chitin and glucan

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141
Q

what is the treatment for fungal infection

A

antifungals - they tend to target the cell wall or the plasma membrane but they dont work incredibly well
- generally quite difficult to treat

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142
Q

what are features of fungus Candida albicans

A

it is the most pathogenic Candida spp
- vaginal and oral infections and cause sepsis (candidiasis)
- can also cause line or catheter infections
- can kill rapidly

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143
Q

What are the features of fungus Aspergillus fumigatus

A

it is the most pathogenic Asp. spp.
- predominantly causes lung infections and allergic disease
- poor prognosis but it kills slowly

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144
Q

what are the three subclasses of antibiotics

A
  1. Cell wall synthesis
  2. Nucleic acid synthesis
  3. Protein synthesis
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145
Q

what are the different antibiotics which affect cell wall synthesis

A
  1. Beta lactams - penicillins, cephalosporins, carbapenems, monobactams
  2. Vancomycin
  3. Bacitracin
  4. cell membrane - polymyxins
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146
Q

what are the different antibiotics which affect nucleic acid synthesis

A
  1. folate synthesis - sulfonamides, trimethoprim
  2. DNA gyrase - quinolones
  3. RNA polymerase - rifampin
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147
Q

What are different antibiotics which affect protein synthesis

A
  1. 30S subunit affecting - tetracyclines, aminoglycosides
  2. 50S subunit affecting - macrolides, clindamycin, linezolid, chloramphenicol, streptogramins
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148
Q

what is the cell wall affecting antibiotic mechanism of action

A

beta lactams bind covalently and irreversibly to the penicillin binding proteins. The cell lysis is disrupted and lysis occurs. this results in bacterial death

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149
Q

what is the most common cell wall affecting antibiotics

A

beta lactams

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150
Q

are gram negative or positive bacteria more susceptible to beta lactams

A

gram positive bacteria as they have thick walls making them more vulnerable

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151
Q

how do nucleic acid synthesis affecting antibiotics work

A

they prevent production of folic acid synthesis - cant make thymidine or purines
they affect the enzymes that are required for DNA replication

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152
Q

when are macrolides used (antibiotics affecting protein synthesis)

A

they will be used in respiratory infection, and when people are allergic to penicillin

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153
Q

what are the different antibiotic resistance mechanisms

A
  1. efflux pumps
  2. inactivating enzymes
  3. alternative enzymes used
  4. decreased uptake
  5. target alterations - changes in gene/protein shape
154
Q

what are the three specific examples of antibiotic resistance

A
  1. Beta lactamase producing bacteria = resistant to penicillin derived Ab
  2. MRSA carries mecA which is a unique transpeptidase that is not inhibited by beta lactams.
  3. Efflux pumps
155
Q

what is the minimum inhibitory concentration

A

the minimum antibiotic that will inhibit bacterial growth

156
Q

what can be given for a toxin producing bacteria

A

you can use protein inhibitory antibiotics

157
Q

how do you determine the minimum inhibitory concentration

A

Multiple tubes which contain the bacteria, tubes that have solution that promote growing and into these you add in different amounts of antibiotic
- from this you can work out at what concentration of antibiotic the bacteria cant grow

158
Q

what two things are important for a drug to work

A
  • concentration of the drug in use
  • time
159
Q

What is time dependent killing

A

key parameter is the time that serum concentrations remain above the MIC during dosing

160
Q

what drugs use time dependent killing

A
  • beta lactams
  • clindamycin
  • macrolides
  • oxazolidinones
161
Q

what is concentration dependent killing

A

the key parameter is how high the concentration is above the MIC

162
Q

what drugs use concentration dependent killing

A
  • aminoglycosides
  • quinolones
163
Q

whats important when considering distribution to the site of infection

A

some sites of infection dont have a blood supply
- pus doesnt have a blood supply and so it can go to the outside and will have to diffuse in
- heart valves

164
Q

how do bacteria develop intrinsic resistance

A

this is where the bacteria is naturally resistant to something, all subpopulations are affected equally

165
Q

how can bacteria acquire mutations

A
  • spontaneous gene mutation - single point mutations
  • conjugation
  • transformation - free DNA taken up and integrated
  • transduction - viruses (bacteriophage) move genes from one bacteria to another
166
Q

what are the two resistance gram positive bacteria to be aware of

A

MRSA - mecA gene which confers resistance to beta lactams
VRE - plasmid mediated acquisition of gene preventing vancomycin binding

167
Q

what are the 5 known hepatitis viruses that infect the liver

A
  1. Hepatitis A - RNA
  2. Hepatitis B - DNA
  3. Hepatitis C - RNA
  4. Hepatitis D - RNA
  5. Hepatitis E - RNA
168
Q

how is hepatitis A and E spread

A

fecal - oral transmission

169
Q

How is hepatitis B, C and D spread

A

blood to blood transmission

170
Q

what is acute viral hepatitis

A

when there is viral hepatitis which ends with complete resolution

171
Q

what is chronic viral hepatitis

A

prolonged course of active disease or silent asymptomatic infection

172
Q

what hepatitis viruses can cause chronic infection

A

HBV, HCV, HDV

173
Q

what are features of acute viral hepatitis

A
  • fatigue, fever, muscle or joint ache, cough, runny nose
  • 1-2 weeks in you will develop jaundice bilirubin levels
  • hepatic cell death
  • liver function decreases (seen on LFT)
  • can cause ALT and AST to elevate very high
174
Q

what are the symptoms of Hep A

A

incubation 3 to 4 weeks
- fever, anorexia, nausea, vomiting and jaundice
- dark urine, pale feces, elevated transaminase levels
- most cases resolve in 2-4 weeks

175
Q

how do you diagnose Hep A

A
  • Liver function tests: high AST and ALT levels
  • serology: detection of anti- HAV IgM and will remain positive for 3-6 months
176
Q

What are the three main antigens for HBV

A
  1. HBsAg - surface antigen
  2. HBcAg - Core antigen
  3. HbeAg -e antigen - indicator of transmissibility
177
Q

what are the 3 clinical stages of HBV

A
  1. acute hepatitis
  2. fulminant hepatitis - severe acute hepatitis, rapid liver destruction
  3. chronic hepatitis: asymptomatic carrier, chronic-persistent hepatitis and chronic active hepatitis
178
Q

what does it mean if patient has HBsAg present

A

means that there is a LIVE virus and infection, either acute, chronic or carrier

179
Q

what does the presence of high HBeAg suggest

A

high infectivity and active disease

180
Q

what are the possible complications of Hep B

A
  • HDV co-infection
  • Hepatocellular carcinoma
  • end stage liver disease/cirrhosis
181
Q

how long is the incubation period of hepatitis C

A

6-12 weeks

182
Q

what is the clinical features of Hep C

A
  • often asymptomatic
  • symptoms; malaise, nausea, upper right quadrant pain, fever, anorexia, nausea, vomiting and jaundice
  • chronic carrier state occurs more often with HCV than HBV
  • significant autoimmune reactions: vasculitis, arthralgias, purpura, glomerulonephritis
183
Q

how is infection with HCV diagnosed

A

antiHCV antibodies

184
Q

how is a positive HCV result confirmed

A

measured with HCV viral RNA

185
Q

how do you treat HCV

A

peginterferon alfa decreases patients who become carriers
- Patients with chronic infection are advised to reduce alcohol consumption, and this is monitored with alpha fetoprotein levels
- most common HCV treatment is direct acting antivirals

186
Q

what are the features of HDV

A
  • it cant replicate by itself because it doesnt have the gene for its envelope protein, it can only replicate when the person is also infected with HBV
187
Q

what is the difference between acute and chronic diarrhoea

A
  • acute lasts less than two weeks
  • chronic - persists more than four weeks
188
Q

what is acute diarrhoea categorised as

A
  1. noninflammatory (watery and non bloody)
  2. inflammatory (bloody); dysentery
189
Q

what are risk factors for developing diarrhoea

A
  • patients taking PPI
  • recent travel to developing countries
  • antibiotic treatment
  • immunosuppressed patients
190
Q

what diarrhoea causing pathogens secrete exotoxins

A

staphylococcus aureus, bacillus cereus and clostridium perfringens

191
Q

what pathogens cause non inflammatory acute diarrhoea by enterotoxin production

A

Enterotoxigenic Escherichia coli (ETEC)
Vibrio cholerae

192
Q

what are pathogens that cause acute inflammatory diarrhoea

A
  • Salmonella
  • Shigella
  • Campylobacter
  • shiga toxin producing E. coli
  • C. difficile
193
Q

what bacteria can cause pseudomembranous colitis through antibiotic use

A

C. difficile

194
Q

what does vomiting and diarrhoea indicate

A

suggests infection with S. aureus food poisoning or viral gastroenteritis

195
Q

what bacteria cause acute non inflammatory diarrhoea

A
  • staphylococcus aureus
  • bacillus cereus
  • ETEC
  • listeria monocytogenes
  • vibrio cholerae
  • norovirus
  • giardia lamblia
196
Q

where are the most common sites for cellulitis to occur

A

legs, face and arms

197
Q

what are risk factors for developing cellulitis

A

skin wounds, diabetes, bits, elderly, swollen legs, immunosuppression

198
Q

what are the causative organisms of cellulitis

A
  • beta hemolytic streptococci are common (S. pyogenes and streptococcus agalactiae)
  • staphylococcus aureus
199
Q

how does cellulitis present

A
  • symptoms spread quickly
  • erythema
  • pain, swelling and warm to the touch
  • associated wound such as an ulcer, bite or injection
  • can have fever malaise and systemic signs
200
Q

what is treatment for cellulitis

A
  • elevate and mobilize limb
  • washout wounds
  • empiric treatment with IV flucloxacillin or clindamycin
  • vancomycin, teicoplanin, linezolid or daptomycin are indicated for MRSA cellulitis
201
Q

what is necrotizing fasciitis

A

it is a necrotizing infection of the deep structures of the skin including the underlying fascia

202
Q

what are the causes of necrotizing fasciitis

A

break in the skin allows passage of the organism to deeper structures. Infection of the fascial layer results in thrombosis of the vascular supply and adjacent nerves. this manifests as necrosis and anaesthesia of more superficial layers

203
Q

what pathogens can cause necrotizing fasciitis

A
  • type 1: due to both aerobic and anaerobic organisms
  • type 2: Usually due to streptococcus pyogenes. Others: V. vulnificus clostridium perfringens
204
Q

how does necrotizing fasciitis present

A
  • erythema, warmth and tenderness; pain out of proportion with findings
  • skin changes often spread and progress quickly
  • skin hypoperfusion, grey-blue colouring, loss of sensation
  • signs and symptoms of systemic infection
  • Fournier’s gangrene if male
205
Q

how is necrotizing fasciitis diagnosed

A

using surgery, confirmed by exploration and debridement
- microbiology; gram stain and culture

206
Q

how do you treat necrotizing fasciitis

A

emergency surgery
empirical therapy: broad- piperacillin-tazobactam plus clindamycin
S. pyogenes causative; penicillin and clindamycin

207
Q

what pathogens can cause appendicitis

A
  1. normal colonic gut flora
  2. Escherichia coli
  3. Peptostreptococcus
  4. Bacteroides fragilis
  5. pseudomonas
208
Q

how is appendicitis treated

A

surgery
management with antibiotics - metronidazole and cefoxitin

209
Q

what is diverticulitis

A

it is inflammation of the diverticula (sac like protrusion of the colonic wall usually around the sigmoid colon)

210
Q

what is acute diverticulitis

A

it is uncomplicated and common in the elderly and those with extensive disease

211
Q

what is complicated diverticulitis

A

it is acute diverticulitis with one of the following:
1. abscess
2. colovesical or colovaginal fistula
3. perforation
4. obstruction

212
Q

what pathogens can cause diverticulitis

A

bowel flora
- B. fragilis and E. coli are typically involved

213
Q

how does diverticulitis present

A

dull aching pain in the lower left quadrant
low grade fever with nausea and vomiting
diarrhoea or constipation may be present
- if there has been perforation then there will be diffuse abdominal pain and shock

214
Q

how do you treat diverticulitis

A

uncomplicated - co-amoxiclav, ciprofloxacin plus metronidazole
complicated; piperacillin-tazobactam

215
Q

what is osteomyelitis

A

it is a bone or bone marrow infection with can occur in both adults and children. it can be acute or chronic

216
Q

what pathogens can cause osteomyelitis

A
  • most commonly caused by staphylococcus aureus
  • IVD users; pseudomonas, E. coli
  • Sickle cell patients; Salmonella
  • hip of knee prosthesis: staphylococcus epidermis
217
Q

how does osteomyelitis present

A
  • pain around the infected region
  • swelling, tenderness, warmth and erythema
  • can be associated with systemic signs such as fever or tiredness
  • chronic can have sinus tracts or within ulcers
218
Q

how is osteomyelitis diagnosed

A

blood tests; raised white blood cell count and inflammatory markers
CT or MRI
X-ray after two weeks
bone or percutaneous biopsy

219
Q

how do you treat osteomyelitis

A

surgery with antibiotics
- flucloxacillin and fusidic acid
- vancomycin and cefotaxime

220
Q

what is septic arthritis

A

an infection of the joints
- organisms reach joint via blood

221
Q

what are risk factors of septic arthritis

A

old age, diabetes mellitus, rheumatoid arthritis, prosthetic joint, recent joint surgery, skin infections or ulcers, intra-articular corticosteroid infection, injection drug use, alcoholism

222
Q

what pathogens can cause septic arthritis

A
  • most common cause is staphylococcus aureus
  • young sexually active adults - Neisseria gonorrhoeae
  • prosthetic hip or knee joints - s. epidermis
  • IVD users; P. Aeruginosa
223
Q

how does septic arthritis present

A

acute onset of an inflamed joint
fever is often present
- joint is red, warm, swollen, painful

224
Q

how do you diagnose septic arthritis

A
  • raised WBC and inflammatory markers
  • ultrasound
    CT/MRI
225
Q

what is the treatment for septic arthritis

A

drainage of the joint urgently and removal or prosthetic if it is infected
- flucloxacillin or vancomycin
- vancomycin in staph aureus
- ceftriaxone in N. gonorrhoeae

226
Q

what is the most common bacterial STI

227
Q

what is the pathogen that causes chlamydia

A

chlamydia trachomatis

228
Q

what is the presentation of chlamydia in men

A

urethritis
testicular pain
- 50% of cases are asymptomatic

229
Q

what is the presentation of chlamydia in women

A

vaginal discharge
post coital bleeding
intermenstrual bleeding
lower abdominal or pelvic pain
- 80% of cases asymptomatic

230
Q

what are complications of chlamydia

A

Pelvic inflammatory disease
infertility
reactive arthritis
epididymo-orchitis

231
Q

how id chlamydia diagnosed

A

NAAT - vaginal swabs, urethral swabs and first catch urine samples

232
Q

how do you treat chlamydia

A

avoid sexual intercourse until treatment finished
screening for other STIs
antibiotics - doxycycline or azithromycin
alternatives: erythromycin or ofloxacin
in pregnancy doxycycline is contraindicated
- contact trace

233
Q

what is the pathogen that causes Gonorrhoea

A

Neisseria gonorrhoea

234
Q

how does ghonorrhoea present

A
  • asymptomatic
    in men: urethritis, purulent discharge and dysuria
    in women: pelvic pain, vaginal discharge, itch, dysuria
235
Q

how do you diagnose gonorrhoea

A

NAAT; first line screen
microscopy showing gram negative diplococci

236
Q

what type of bacteria is Neisseria gonorrhoea

A

Gram negative diplococci

237
Q

what is the treatment for gonorrhoea

A

antibiotics: ceftriaxone single dose plus azithromycin single dose

238
Q

what pathogens cause viral meningitis

A
  • enteroviruses (echoviruses, coxsackieviruses, polioviruses)
  • herpes simplex virus
239
Q

how does viral meningitis present

A

influenza like illness followed by meningism (stiff neck, headache, photophobia)
fever and non specific signs may also be present

240
Q

how do you diagnose viral meningitis

A

lumbar puncture: CSF microscopy, PCR
- viral culture can be taken

241
Q

what treatment is given for viral meningitis

A

no specific antiviral therapy
Supportive: analgesics, antipyretics, hydration
Acyclovir for herpes simplex virus

242
Q

what bacteria causes bacterial meningitis

A
  • Neisseria meningitidis
  • Haemophilus influenzae
    streptococcus pneumoniae - most common in young and old
243
Q

how is neisseria meningitidis spread

A

spread by the respiratory route or via bloodstream

244
Q

how does bacterial meningitis present

A
  • usually rapid onset, headache, fever, meningism
  • cerebral dysfunction
  • seizures
  • focal neurological deficits (cranial palsies)
  • papilledema
  • non blanching rash
245
Q

how do you treat bacterial meningitis

A
  • blood culture performed urgently
  • lumbar puncture unless contraindicated (low glucose and increased protein
  • physical examination
246
Q

what is the treatment for bacterial meningitis

A

benzylpenicillin or cefotaxime/ceftriaxone
- vancomycin if resistant strep. is suspected
- steroids

247
Q

what condition gives you protection against malaria

A

sickle cell trait (HbS) is protective

248
Q

what pathogens cause malaria

A
  1. P. falciparum: 80% of cases, highest mortality
  2. P. vivax
  3. P. ovale
  4. P. malariae
  5. P. knowlesi
249
Q

how does malaria spread

A

humans acquire malaria from sporozoites transmitted by the bite of the female anopheles mosquito.
sporozoites travel through the bloodstream and hepatocytes
they mature into tissue schizonts which rupture and release merozoites into the bloodstream
they invade RBC and release more merozoites
some divide into sporozoites which can then be taken up by mosquito

250
Q

how does malaria present

A
  • fever and sweats; cyclical or continuous with spikes
  • anemia; erythrocyte hemolysis
  • hepatosplenomegaly
  • complications; cerebral malaria, jaundice, kidney injury, acidosis
251
Q

how do you diagnose malaria

A
  • thick and thin blood smears; Field’s or Giemsa stain
  • lab findings; haemolytic anemia, thrombocytopenia, uremia, hyperbilirubinemia, abnormal LFTs, coagulopathy
252
Q

what is the treatment for malaria

A
  • quinoline derivatives (chloroquine, quinine)
  • antifolates and ribosomal inhibitors - tetracycline, doxycycline
253
Q

what is the cause of tuberculosis

A

mycobacterium tuberculosis

254
Q

what is the pathogenesis of primary TB

A
  • inhalation of M. tuberculosis results in mild reaction in lung
  • alveolar macrophages phagocytose the pathogen
  • some bacilli survive and multiply within the macrophages and are carried to the hilar lymph nodes
  • the local lesion and lymph nodes are called the primary complex
  • immune cells form a granuloma lesion
  • in many individuals immune system kills the bacteria and the lesion becomes fibrotic and calcified
  • in a small number of cases the TB isnt killed and is dormant
  • in some patients TB spreads and invades the blood to other organisms - miliary TB
255
Q

what is the pathogenesis of secondary TB

A
  1. dormant TB reactivates often in those immunocompromised
  2. a patient may become re-infected after further exposure
256
Q

how does tuberculosis present

A

fever, night sweats
pleuritic chest pain and dyspnea
cough
fatigue, arthralgia, weight loss

257
Q

how do you diagnose TB

A

sputum smear microscopy - acid fast bacilli
mycobacterial culture
chest x-ray and ultrasound
elevated ESR, SCR, anemia
tuberculin skin test shows latent TB

258
Q

what is the treatment for tuberculosis

A
  • for drug susceptible pulmonary TB; 2 month initiation phase with rifampicin, isoniazid, pyrazinamide, ethambutol, followed by 4 months of rifampicin and isoniazid
259
Q

what are the 4 classifications of pneumonia

A
  1. community acquired pneumonia
  2. hospital acquired pneumonia
  3. pneumonia in immunocompromised individuals
  4. aspiration pneumonia
260
Q

what are the risk factors for community acquired pneumonia

A
  • extremes of age
  • smoking
  • COPD
  • diabetes
  • cardiovascular disease
  • severe recurrent illness
  • recent anesthetic or intubation
  • immunosuppression
261
Q

what pathogens cause CAP

A
  • mycoplasma pneumoniae
  • H. influenza
  • strep. pneumoniae
  • pneumocystis jiroveci in HIV/AIDS patients
  • respiratory syncytial virus in young children
262
Q

how does CAP present

A

sudden onset of chills, fever, cough, sputum, pleuritic chest pain, fatigue, anorexia and sweats. Tachypnoea, tachycardia and postural blood pressure may drop
- elderly may present as confused, with abdominal pain and nausea

263
Q

how do you diagnose CAP

A
  • sputum specimens for culture and microscopy
  • blood cultures
  • urine antigen detection for pneumococcal and legionella
  • PCR for viral, mycoplasma, chlamydia and Coxiella infections
  • bronchoalveolar lavage
  • chest X-ray
  • severity score of results
264
Q

how do you treat CAP

A
  • IV fluids and oxygen
  • amoxicillin for non severe
  • clarithromycin plus co-amoxiclav for severe
  • once organism is identified you can give specific treatment
265
Q

how do you treat S. pneumoniae CAP

A

amoxicillin or benzylpenicillin

266
Q

how do you treat M. pneumoniae CAP

A

erythromycin or clarithromycin

267
Q

how do you treat C. pneumoniae CAP

A

erythromycin or clarithromycin

268
Q

how do you treat C. psittaci CAP

A

doxycycline

269
Q

how do you treat C. burnetti CAP

A

doxycycline

270
Q

how do you treat Legionella spp. CAP

A

clarithromycin (and rifampicin)

271
Q

what is an antimicrobial agent

A

a substance with inhibitory properties against microorganisms, but with minimal effect on mammalian cells

272
Q

what is an empirical therapy

A

it refers to the antimicrobial regimen used when a clinical diagnosis of infection has been made and delay in initiating therapy to await microbiological results would be inappropriate

273
Q

what is pathogen susceptibility

A

the level of vulnerability of a microorganism to an antimicrobial

274
Q

what are examples of beta lactams

A

penicillin, cephalosporins, monobactams, carbapenems

275
Q

when are carbapenems used

A

they have broad spectrum activity and are generally used for treatment of severe infections of for infection caused by multiply resistant bacteria

276
Q

what are glycopeptides

A

they are bactericidal for gram positive bacteria and have no activity against gram negative.
- vancomycin and teicoplanin

277
Q

what is the mode of action of aminoglycosides

A

they inhibit protein synthesis via 30s ribosome inhibition

278
Q

what problems can aminoglycosides cause

A

hypersensitivity, ototoxicity and nephrotoxicity

279
Q

what are some side effects of vancomycin

A

can occasionally cause nephrotoxicity and ototoxicity
rapid infusion can cause erythematous rash

280
Q

what is the action of tetracyclines

A

they inhibit the 30s ribosome subunit
- treat infections caused by Mycoplasma spp., rickettsia spp. coxiella burnetiid and chlamydia trachomatis

281
Q

what are side effects of tetracycline

A

gastrointestinal intolerance

282
Q

what is the mechanism of action for macrolides

A

they inhibit protein synthesis of the 50s subunit
- used for strep and staph soft tissue infections and resp infections including those caused by mycoplasma pneumoniae

283
Q

what are examples of macrolides

A

clarithromycin, azithromycin and erythromycin

284
Q

what is clindamycin useful against

285
Q

what is the mechanism of action of clindamycin

A

it inhibits the 50s ribosome subunit
- associated with pseudomembranous colitis

286
Q

what is fusidic acid used for

A

active against staphylococci (combine with flucloxacillin for serious staph infections0
- Inhibits protein synthesis

287
Q

what are quinolones used for

A

inhibition of nucleic acid synthesis and function
- e.g ciprofloxacin, ofloxacin, norfloxacin

288
Q

what are side effects of quinolones

A

gastrointestinal disturbances - photosensitivity, rashes, neurological disturbances

289
Q

what is trimethoprim used for

A
  • UTIs
    inhibits folic acid synthesis
290
Q

what is metronidazole used for

A

anaerobic infections - dysregulates DNA synthesis

291
Q

what is nitrofurantoin used for

A

uncomplicated UTIs

292
Q

what are the stages of the viral life cycle

A
  1. attachment
  2. entry
  3. genome release
  4. transcription
  5. translation
  6. genome replication
  7. assembly
  8. exit
293
Q

what are the different ways viruses cause disease

A
  1. direct destruction of host cells
  2. modification of host cells
  3. over reactivity of immune system
  4. damage through cell proliferation
  5. evasion of host defences
294
Q

give an example of a virus that causes direct destruction of host cells

A

Polio virus causes host cell lysis and death after viral replication
the lysis of neuron cells leads to paralysis
HIV lyses CD4 t cells

295
Q

give an example of a virus that causes modification of its host cell

A

rotavirus atrophies villi and flattens epithelial cells which means sugars cant be absorbed and hyperosmotic state leads to diarrhoea

296
Q

give an example where a virus causes over reactivity of the immune system

A

the immune system response to HBV during chronic infection results in low level liver cell destruction leading to cirrhosis

297
Q

give an example where a virus causes damage through cell proliferation

A

human papillomavirus integrated into cervical epithelial cells, expresses oncoproteins which can lead to the over proliferation of cells and cervical cancer

298
Q

give an example where a virus evades host defences and causes disease

A

varicella zoster virus can lay dormant after chicken pox and can reactivate later as shingles

299
Q

what are the different ways to diagnose viral infection

A

PCR, serology, histopathology
- less used is viral culture, light microscopy and electron microscopy

300
Q

what type of virus is HIV

A

retrovirus

301
Q

what type of cell does HIV infect

A

it infects CD4 T cells and macrophages
- transmits in bodily fluids

302
Q

what is the treatment for HIV

A

Highly acting anti-retroviral therapies (HAART)

303
Q

what are protozoa

A

microscopic unicellular eukaryotes

304
Q

how are protozoa classified

A

classified on movement:
ameoboids, ciliates, sporozoan, flagellates

305
Q

what type of malaria can go dormant in the liver causing relapse

A

P. vivax
P. ovale

306
Q

what are the four major groups of gram negative bacteria

A
  1. proteobacteria - all are rod shaped
  2. bacteroids - rods shaped
  3. chlamydia - round pleiomorphic
  4. spirochaetes - spiral/helical
307
Q

what are the direct ways one can diagnose bacterial infection

A
  • gram stain
  • acid fast stains
  • wet film
  • KOH (fungi)
  • india ink
308
Q

what are cultures you can do to diagnose bacterial infection

A
  • solid media
  • liquid culture
  • blood culture
309
Q

what is the difference between yeast and mould

A

yeasts are small single cell organisms that divide by budding
moulds form multicellular hyphae and spores

310
Q

what are dimorphic fungi

A

where some fungi exist as both yeasts and moulds switching between the two when conditions suit them

311
Q

how do you treat fungal disease

A

more difficult to treat fungi because they are eukaryotic cells
- the aim of antimicrobial therapy is to achieve inhibitory levels of agent at the sit of infection without host cell toxicity

312
Q

what are the different classes of vaccine

A

inactivated - killed
attenuated
toxoid vaccines
proteins - components of pathogen

313
Q

what are the key components of infection prevention and control

A
  • infection prevention and control team
  • ward teams
  • microbiology/virology labs
  • trust management
  • estates
  • domestic services
  • pharmacy
314
Q

what are the different infection control policies

A

MRSA policy
Tuberculosis policy
medical equipment management manual
single use items
outbreak control plan

315
Q

when do you need to wash your hands in a hospital

A
  • before and after handling patients/ clients
  • after handling any item that is soiled
  • after using the toilet
  • before and after an aseptic procedure
  • after removing protective clothing including gloves
316
Q

when should use alcohol gel

A
  • following hand washing, prior to a ward based invasive procedure
  • following hand washing, when caring for a patient with barrier precautions
317
Q

when would you were PPE

A

must be worn by all staff, whatever their role or grade, when there is a risk of contamination to the person or their clothing

318
Q

what is an endogenous infection

A

infection of a patient by their own flora
- important in hospitalised patients, especially in those with invasive devices or surgical patients

319
Q

how do you prevent endogenous hospital acquired infection

A

good nutrition and hydration
antisepsis/skin prep where indicated
control the underlying disease - drain pus, remove lines and catheters as soon as clinically possible, reduce antibiotic pressure as much as clinically possible

320
Q

what are the different ways HIV can be transmitted

A

blood, sexual and vertical

321
Q

what is the 90/90/90 rule

A

global target
- 90% of people living with HIV being diagnosed
- 90% diagnosed on ART (antiretroviral therapy)
- 90% viral suppression for those on ART

322
Q

what is the benefits of knowing HIV status

A
  • access to appropriate treatment and care
    -reduction in morbidity and mortality
  • reduction in vertical transmission
  • reduction of sexual transmission
  • public health
  • cost effective - saving on social care, lost working days, benefits claims, costs associated with onward transmission
323
Q

what are symptoms of HIV

A
  • acute glandular fever rah
  • glandular fever
  • indicators of immune dysfunction
  • unexplained weight loss or night sweats
  • recurrent bacterial infections including pneumococcal pneumonia
324
Q

what HIV receptors are needed for infection

A

HIV infects CD4 expressing cells (gp120 interacts). it also needs the accessory receptors CCR5 and CXCR4

325
Q

what are the two markers that are used to monitor HIV infections

A
  1. CD4 cell count
  2. HIV viral load
326
Q

what is the most common opportunistic infection in HIV

A

pneumocystis pneumonia (PCP)

327
Q

good HIV drug adherence and avoidance drug interactions are key to what?

A
  • suppression of HIV replication
  • Avoidance of drug resistance
328
Q

who is the most at risk of HIV

A
  1. men who have sex with men
  2. heterosexual women
  3. injecting drug users
  4. commercial sex workers
  5. heterosexual men
329
Q

what type of organisms would you stain with Ziehl Neelsen stain and why

A

Mycobacteria such as TB
because they dont stain with gram stain

330
Q

what are the different appearances of coccus bacteria

A

diplococcus - pair
chain of cocci
clusters of cocci

331
Q

what are the different appearances of bacillus bacteria

A

chains of rods
curved rods
spiral rods

332
Q

what are the steps of a gram stain

A

come in and stain
- crystal violet
- iodine
- acetate/alcohol
- safranine counterstain

333
Q

how do you perform a gram stain

A

apply crystal violet to heat fixed bacteria. treat with iodine. decolourise the sample and then counterstain

334
Q

between what temperatures and what pH range can bacteria grow

A

between -80 and 80
between 4 to 9

335
Q

what are the three phases of bacterial growth

A
  1. lag phase
  2. exponential phase
  3. stationary phase
336
Q

give an example of slow growing and fast growing bacteria

A

slow - TB doubling time is 2 weeks
fast - E.coli and S. aureus doubling time of 20-30 minutes

337
Q

what are two functions of pili

A
  1. adhere to cell surfaces
  2. plasmid exchange
338
Q

what is a nosocomial infection

A

a hospital acquired disease

339
Q

give an example of a gram negative diplococci

A

neisseria
N. meningitidis and N. gonorrhoeae

340
Q

how would you describe the arrangement of staphylococci

A

clusters of cocci

341
Q

how would you describe the arrangement of streptococci

A

chains of cocci

342
Q

what test can be done to distinguish between different streptococci

A

blood agar haemolysis

343
Q

Name 2 gram negative bacilli that will give a positive result with MacConkey agar.

A
  1. E.Coli.
  2. Klebsiella pneumoniae
344
Q

What gram negative bacteria are non-lactose fermenting and what colour would they appear on MacConkey agar?

A

Appear white.
Shigella
Salmonella
Pseudomonas
Proteus

345
Q

Give examples of some conditions that S.aureus can cause

A

Pyogenic - wound infections
Impetigo
septicaemia
osteomyelitis
pneumonia
endocarditis

346
Q

How can you distinguish between gram negative bacilli (salmonella, shigella and e.coli)?

A

Use MacConkey agar and use serology to detect the presence of the H antigen

347
Q

Describe the process by which enterotoxigenic e.coli (ETEC) causes traveller’s diarrhoea?

A

Heat labile ETEC toxin modifies Gs protein, it is in a ‘locked on’ state. Adenylate cyclase is activated and there is increased production of cAMP. This leads to increased secretion of Cl- into the intestinal lumen, H2O follows this down an osmotic gradient and this subsequently results in traveller’s diarrhoea.

348
Q

What are the symptoms of enteropathogenic e.coli infection?

A

Chronic watery diarrhoea

349
Q

What are the symptoms of enterohaemorrhagic e.coli infection?

A

Bloody diarrhoea.

350
Q

what are the four species of shigella of medical importance

A

S.dysenteriae
S.flexneri
S.boydii
S.sonnei

351
Q

What is the action of shigella in the intestine?

A

In the intestine it induces self uptake and leads to macrophage apoptosis. Cytokines are released and neutrophils are attracted = inflammation. Shigella spread to adjacent cells.

352
Q

what bacteria is responsible for salmonellosis

A

S. enterica

353
Q

what are the three conditions caused by salmonellosis

A
  1. gastroenteritis
  2. enteric fever
  3. bacteraemia
354
Q

Describe the pathogenesis of gastro-enteritis.

A
  1. Endocytosis.
  2. Chemokine release.
  3. Neutrophil recruitment and migration.
  4. Neutrophil induced tissue injury.
  5. Fluid and electrolyte loss -> diarrhoea
355
Q

Describe the pathogenesis of enteric fever.

A
  1. Endocytosis.
  2. Migration to the basolateral membrane.
  3. Survival in macrophage -> systemic spread.
356
Q

What are the 2 developmental stages of chlamydia’s unique growth cycle?

A
  1. Elementary bodies (infective).
  2. Reticulate bodies (intracellular multiplication).
    - Reticulate bodies are converted back into elementary bodies and are released. The cycle continues.
357
Q

Name the spirochaete that is responsible for causing lyme disease

A

Borrelia .burgdorferi.

358
Q

name the spirochaete that is responsible for causing syphilis

A

T. pallidum

359
Q

what are the three stages of syphilis

A
  1. Primary stage: localised infection.
  2. Secondary stage: systemic - skin, lymph nodes etc.
  3. Tertiary stage: CV syphilis and neuro syphilis.
360
Q

what are three common fungal infections

A
  1. Nappy rash
  2. Tinea pedis
  3. Onychomycosis (fungal nail infection)
361
Q

antifungal treatments: how does amphotericin work

A

targets ergosterol in the plasma membrane and causes pore formation and therefore cell death

362
Q

antifungal treatment: how does azoles work

A

affect the ergosterol synthetic pathway

363
Q

what are 4 disadvantages of azoles

A
  1. High first pass metabolism, bioavailability = 45%.
  2. ADR’s, can cause hepatitis.
  3. Drug interactions due to CYP450.
  4. Resistance can develop e.g. in candida.
364
Q

what are virulence factors of S. pyogenes

A

Streptokinase

Streptolysin O and S

Erythrogenic Toxin

M Toxin

365
Q

which group of streptococci can cause infective endocarditis

A

alpha haemolytic strep

366
Q

why do bacteria produce coagulase

A

defence mechanism to clot areas of plasma around them and thereby resisting phagocytosis

367
Q

name 4 sanctuary sites for HIV

A
  1. Genital tract
  2. GI tract
  3. CNS
  4. Bone marrow
368
Q

what is a clinically important gram negative bacteria

A

ESBL - extended spectrum b lactamase
- mutation at active site

369
Q

If a HIV test comes back as negative in a high risk individual why should a second HIV test be done?

A

A second test should be done after the window period: the window period is the time between exposure to HIV infection and the point when the test will give an accurate result. During this time a person can be infected with HIV and be very infectious but still test HIV negative.

370
Q

what is the CD4+ count of someone diagnosed with having AIDS

371
Q

Name 3 respiratory diseases associated with HIV.

A
  1. Bacterial (pneumococcal) pneumonia.
  2. TB.
  3. Pneumocystis pneumonia (PCP).
372
Q

Name 3 CNS diseases associated with HIV.

A
  1. Mass lesions e.g. primary CNS lymphoma, cerebral toxoplasmosis.
  2. Meningitis e.g. pneumococcal, cryptococcal.
  3. Opthalmic lesions e.g. CMV, toxoplasmosis, choroidal tuberculosis etc.
373
Q

Chains of purple cocci are seen on a gram film. They show alpha haemolysis when grown on blood agar. They don’t grow near the optochin disc. What bacteria is likely to have caused this?

A

Streptococcus pneumonia.

374
Q

Give 3 defining features of systemic inflammatory response syndrome (SIRS)

A
  • Temperature >38℃ or <36 ℃.
  • Heart rate >90.
  • White cell count >12.
  • Hyperglycaemia.
375
Q

Name 6 vaccine preventable diseases that are notifiable.

A
  1. Diptheria.
  2. Measles.
  3. Mumps.
  4. Rubella.
  5. Tetanus.
  6. Whooping cough.
376
Q

Name 5 diseases that are notifiable.

A
  1. Anthrax.
  2. Cholera.
  3. Rabies.
  4. Smallpox.
  5. Yellow fever.
  6. Acute encephalitis.
  7. Botulism.
  8. Enteric fever.
  9. Leprosy.
  10. Malaria
377
Q

What is primary vaccine failure?

A

When a person doesn’t develop immunity.

378
Q

what are disadvantages of polysaccharide vaccines and how can they be improved

A

protection is not long lasting and the response in children is poor
improved by conjugation to help improve immunogenicity

379
Q

Name 5 AIDS defining conditions.

A
  1. Oesophageal candidiasis.
  2. TB.
  3. PCP (pneumocystis jirovecii pneumonia).
  4. Recurrent bacterial pneumonia.
  5. Kaposi’s carcinoma.
  6. Hodgkins and Non-Hodgkin’s lymphoma.
  7. HIV dementia.
380
Q

What does C.botulinum do to the body?

A

Botulinum toxin blocks ACh release at the NMJ and therefore causes paralysis spreading from head to body.
(inverse of C.tetani)

381
Q

Why should you not give a pregnant women trimethoprim?

A

Because it will inhibit folate acid synthesis which is required for neural tube closure and therefore could cause the child to have spina bifida or anencephaly

382
Q

What qualities of P.falciparum make it more serious?

A

obstructs microcirculation to make complex malaria
Causes in situ rosetting of RBCs causing obstruction of vessels

Phase 2a - Jemima (11 decks)

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