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Phase 2a > ICS Microbiology > Flashcards

ICS 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

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

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3
Q

What is an opportunistic pathogen?

A

Microbe that only causes disease if host defences are compromised

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4
Q

What is virulence?

A

The degree to which a given organism is pathogenic/ any strategy to achieve this

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5
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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6
Q

What are the shape of bacilli?

A

Rods

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7
Q

What are the shape of cocci?

A

Round, circular

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8
Q

What are diplococci?

A

Pairs of cocci

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9
Q

What are the difference between gram positive and gram negative bacteria?

A

Gram positive= Single membrane, large amount of peptidoglycan on outer surface. do not have endotoxin
Gram negative= Double membrane, smaller amount of peptidoglycan between membranes, The outer membrane has lipopolysaccharide which the immune system can react to (Endotoxic shock)

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10
Q

How can you differentiate between gram positive and gram negative bacteria?

A

Gram stain
Apply a primary stain such as crystal violet, add iodine, decolourise and stain with counterstain
Gram positive= Purple
Gram negative= Red/pink

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11
Q

What does gram stain differentiate?

A

Gram positive and gram negative
Gram positive= Purple
Gram negative= Red/pink

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12
Q

What does ziehl-neelsen stain differentiate?

A

Mycobacteria (rods) that don’t take up gram stain
e.g. M. TB, M. Leprae, M. Ulcerans
Acid-fast bacilli: Red
Non acid-fast bacilli: Blue

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13
Q

How do you differentiate acid-fast bacilli from non acid-fast bacilli?

A

Ziehl-Neelsen stain for mycobacteria
Acid-fast bacilli: Red
Non acid-fast bacilli: Blue

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14
Q

Name an anaerobic gram negative cocci

A

Viellonella

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15
Q

Name an aerobic gram negative cocci

A

Neisseria

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16
Q

Name a gram positive aerobic cocci

A

Strep or staph

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17
Q

Name a gram positive anaerobiccocci

A

Peptostreptococcus

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18
Q

Name a gram positive aerobic bacilli

A

Corynebacterium, listeria, or bacillu

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19
Q

Name a gram positive anaerobic bacilli

A

Clostridium or propionibacteria

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20
Q

Name a gram negative aerobic bacilli

A

Vibrio, Escherichia, salmonella, shigella, citrobacter, haemophillius, Helicobacter, campylobacter, pseudomonas

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21
Q

Name a gram negative anaerobic bacilli

A

Bacteroides

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22
Q

How can you differentiate between staphylococci and streptococci?

A

Catalase test

  • Add h2o2 and look for bubbling
  • Staph are catalase positive
  • Strep are catalase negative
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23
Q

How can you differentiate between staph. Aureus and other staph?

A

Coagulase test

  • Staph. aureus= Coagulase positive (clumping)
  • Other staph.= Coagulase negative (no clumping)
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24
Q

How can you differentiate salmonella and shigella?

A

XLD Agar

  • Salmonella- Red/ Pink colonies with some black spots
  • Shigella- Red/ Pink colonies
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25
Q

How can you differentiate lactose fermenting bacteria from non lactose fermenting bacteria?

A

MacConkey Agar

  • Lactose fermenting= Red/pink
  • Non-lactose fermenting= White/transparent
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26
Q

What does MacConkey agar differentiate?

A

Lactose fermenting from non-lactose fermenting bacteria

Only grows gram-negative bacteria

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27
Q

Name a lactose fermenting enterobacteria

A

E. coli,

Klebsiella pneumoniae

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28
Q

Name some non-lactose fermenting enterobacteria

A

Salmonella spp., shigella spp.

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29
Q

What is the optimum temperature of a bacteria?

A

-80 - 80 degrees (or up to 120 for spores)

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30
Q

What is the optimum pH for bacteria?

A

4-9

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31
Q

How do bacteria divide?

A

Binary Fission

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32
Q

What are endotoxins?

A

Component of the outer membrane of gram negative bacteria- lipopolysaccharide
Only produced by bacteria, mainly gram neg bacteria

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33
Q

What are exotoxins?

A

Secreted from gram positive and gram negative bacteria- Proteins
Produced by mainly gram positive bacteria

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34
Q

Can endotoxins or exotoxins be converted to toxoids?

A

Exotoxins

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35
Q

What happens in transcription?

A

RNA polymerase acts on the bacterial chromosome to form mRNA

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36
Q

What genetic variations can occur in bacterial genetics?

A

Mutations can occur on the bacterial chromosome: Base substitution, deletion, insertion. Mutations can cause antibiotics to be ineffective.

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37
Q

What are plasmids?

A

small circular pieces of DNA. Many plasmids carry antibiotic resistance genes.

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38
Q

What is transformation?

A

The genetic alteration of a bacterial cell via the uptake of an exogenous substance e.g. Via plasmid

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39
Q

What is transduction?

A

The process by which foreign DNA is introduced into a bacteria via vector or virus

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40
Q

What is conjugation?

A

The transfer of genetic material between bacterial cells by direct cell-cell contact

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41
Q

How do you perform a haemolysis test?

A

Put streptococcal samples on the blood agar
Alpha haemolysis= An indistinct zone of partial destruction of red blood cells, often accompanied by a greeenish discolouration
beta haemolysis= A clear colourless zone around the colonies (complete lysis)
Gamma haemolysis= No change

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42
Q

Which bacterias are beta haemolytic?

A

Strep. Pyogenes, Strep. Aureus

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43
Q

Which bacterias are alpha haemolytic?

A

Strep pneumonia, strep viridans, oral strep

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44
Q

Which bacterias are gamma haemolytic?

A

Strep. Bovis

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45
Q

How can you differentiate between strep?

A

Haemolytic test

Optochin test

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46
Q

What does the optochin test do?

A

Differentiate between different streptococcus

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47
Q

What does the oxidase test do?

A

Test if the microorganism contains a cytochrome oxidase
Oxidase postive= Blue= Bacteria is aerobic
Oxidase negative= No colour change= Bacteria may be aerobic or anaerobic

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48
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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49
Q

Do strep. or staph. appear as clusters?

A

Staph. appears as clusters

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50
Q

Name a staph. Aureus associated condition

A

Would infections, abscesses, osteomyelitis, scalded skin syndrome, toxic shock syndrome, food poisoning

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51
Q

What virulence factors are produced by staph. aureus?

A

Pore-forming toxins, Proteases

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52
Q

How is staph. Aureus infection normally treated?

A

flucloxacillin

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53
Q

What type of bacteria appears as clusters of cocci?

A

Staphylococcus

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54
Q

What type of bacteria appears as chains of cocci?

A

Streptococcus

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55
Q

What is lancefield grouping?

A

A method of differentiating beta haemolytic bacteria

- An antiserum is added to a suspension of each group= clumping indicated recognition

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56
Q

What are some associated conditions to staph. Aureus?

A

Wound infections, abscesses, Osteomyelitis, scalded skin syndrome, toxic shock syndrome, food poisoning

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57
Q

How can staph. Aureus be treated?

A

Flucloxacillin

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58
Q

What does MRSA stand for?

A

Methicillin resistant staphylococcus aureus

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59
Q

What are some associated conditions to staph. epidermis?

A

Opportunistic infections in prosthetic limbs and catheters

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60
Q

Name an associated condition to staph. Saprophyticus

A

Acute cystitis

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61
Q

How can streptococcus be differentiated?

A

Haemolysis
Lancefield typing
Biochemical properties

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62
Q

What infections are caused by strep. pyogenes?

A

Wound infections such as cellulitis, tonsillitis, pharyngitis, otitis media, scarlet fever

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63
Q

What infections are caused by strep. Pneumoniae?

A

Pneumonia, Otitis media, sinusitis, meningitis

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64
Q

Name some pre-disposing factors for strep. pneumoniae infection

A

Impaired mucous trapping
Hypogammaglobinaemia
Aslenia
Very young

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65
Q

What is the clinical presentation of diptheria

A 
Thin greyish film on tonsils 
High temp
Nausea
Sore throat
Headache
Difficulty swallowing
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66
Q

What infection does corynebacterium diptheriae cause?

A

Diptheria

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67
Q

What is lipopolysaccharide?

A

An endotoxin

Forms the outer leaflet of the outer membrane of gram-negative bacteria

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68
Q

What are the three major components of lipopolysaccharides?

A

Lipid A- The toxic portion of LPS
Core (R) Antigen- Short chain of sugars, some are unique to the LPS
Somatic (O) antigen- A highly antigenic repeating chain of oligosaccharides

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69
Q

What is H antigen?

A

Flagellum

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70
Q

What are the major groups of enterobacteria?

A

E coli
Shigella
Salmonella

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71
Q

Which enterobacterias are motile?

A

E coli
Salmonella
(Shigella is not)

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72
Q

How is E coli differentiated from shigella and salmonella?

A

E coli uses lactose so will show positive on MacConkey-Lactose agar

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73
Q

What infections are caused by pathogenic E coli strains?

A 
Wound infections
UTIs
Gastroenteritis
Travellers diarrhoea 
Bacteraemia 
Meningitis
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74
Q

What infection does shigella infection cause

A

Damage to large intestinal mucosa, causing acute infection of the large intestine, severe bloody diarrhoea and frequent passage of stools (Normally self limiting)

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75
Q

How does shigella infection spread?

A

Person-to-person or via contaminated water or food

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76
Q

What is shiga toxin?

A

A toxin that shigella releases
Disrupts protein synthesis by blocking specific bond formation, resulting in necrosis
This results in kidney failure

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77
Q

Briefly describe gastroenteritis

A
  • Often a salmonella infection
  • Frequent cause of food poisoning from milk/ poultry
  • Neutrophil-induced tissue injury due to inflammatory response
  • Fluid and electrolyte loss resulting in diarrhoea
  • Inflammation/necrosis of gut mucosa
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78
Q

Briefly describe enteric fever

A
  • Typhoid
  • Caused by salmonella
  • Spread faecal-oral
  • Fever, headache, dry cough, splenomegaly, diarrhoea
  • Bacteria may migrate into cell membranes, and spread systemically via lymph nodes
  • Can result in septicaemia and massive fever
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79
Q

Briefly describe Cholera

A
  • Caused by vibrio cholerae
  • Transmitted via faecal-oral route
  • Results in voluminous watery stools
  • Severe dehydration and death
  • Can be 80% treated with oral rehydration
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80
Q

What infections could be caused by pseudomonas aeruginosa?

A

UTIs, Keratitis

Systemic infection in immunocompromised

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81
Q

How can you grow haemophilius influenzae?

A

Chocolate agar (It is fastidious)

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82
Q

What are the two major neisseria bacterias?

A

N. Meningitidis, N. Gonorrhoeae

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83
Q

What infection is caused by bordetella pertussis?

A

Whooping cough

  • Highly contageous
  • Non specific flu-like symptoms followed by paroxymal coughing
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84
Q

What bacteria is the most common cause of food poisioning?

A

Campylobacter

Salmonella is second most common

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85
Q

What diseases can be caused by H. pylori?

A

Gastritis
Peptic ulcer disease
Gastric adenocarcinoma

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86
Q

What bacteria is the most common cause of STD?

A

Chlamydia trachomatis

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87
Q

What are the two developmental stages of chlamydia?

A

Elementary bodys (round, infectious), and reticulate bodies (pleomorphic and non-infectious, but replicate)

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88
Q

List some gram negative bacterias that cause STD

A

Neisseria Gonorrhoeae
Chlamydia trachomatis
Treponema Pallidum (Syphilis)

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89
Q

List some gram negative bacterias that cause UTIs

A

Some E. coli serotypes
Proteus mirabilis
Klebsiella pneumoniae

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90
Q

List some gram negative bacterias that can cause meningitis

A

N. Meningitidis
Some E.coli serotypes
Haemophilius influenzae

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91
Q

List some gram negative bacterias that can cause sepsis

A

N. Meningitidis
E.coli and K. Pneumoniae
Pseudomonas aeruginosa

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92
Q

List some gram negative bacterias that can cause GI infection

A 
Vibro Cholerae (Cholera)
Shigella dysenteriae (Dysentry)
H. Pylori ( Gastritis, peptic ulcers)
S.enterica (food poisoning)
Campylobacter Jejuni (Food poisoning)
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93
Q

Why are fungal infections rare in healthy hosts?

A

They can’t grow at 37 degrees and can’t evade the adaptive/innate immune response

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94
Q

Name a fungal skin infection

A

Athletes foot

Ring worm

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95
Q

List some invasive fungal diseases

A

Candidasis
Aspergillus
Pneumocystitis Pneumonoa
Cryptococcosis

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96
Q

What is 1,3 B-D Glucan?

A

The cell wall component of many fungal cell walls, which is released into serum during invasive infection
Can be detected to see fungal infections

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97
Q

What is onychomycosis?

A

Very common fungal infection of the nail

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98
Q

What is pneumocystis pneumonia?

A

Fungal infection of the lungs

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99
Q

What does flucytosine target?

A

Targets the DNA/RNA synthesis of fungi

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100
Q

What is voriconazole used for?

A

Moulds

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101
Q

What things can we get samples of?

A

Skin swab of infected area
Secretions= Faeces, urine, mucous etc
Blood

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102
Q

List the different types of agar

A 
Blood agar
Chocolate agar
CLED agar
MacConkey agar
Gonococcus agar
XLD agar
Sabouraud's agar
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103
Q

What is chocolate agar?

A

Contains blood agar heated to 80 degrees for 5 minutes to release some nutrients into the agar and make it easier to grow certain organisms that do not grow easily

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104
Q

What is blood agar?

A

Contains sheep/horse blood and provides a good medium for growing many different types of bacteria

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105
Q

What is CLED agar?

A

Cysteine lactose electrolyte deficient agar is a relatively non-inhibitory growth medium often used to differentiate microorganisms in urine. It allows classification of lactose-fermenting (yellow) and non-lactose fermenting (blue) gram negative bacilli,

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106
Q

What is MacConkey Agar?

A

MacConkey agar is agar designed to grow gram negative bacilli and differentiate them. It grows lactose fermentors pink, and non-lactose fermentors yellow/colourless

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107
Q

What is gonococcus agar?

A

Agar that contains growth factors to promote the growth of neisseria gonnhorea and other neisseria spp.

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108
Q

What is XLD agar?

A

Xylose lysine deoxycholate agar is a very selective growth medium used to isolate salmonella spp., and shigella spp. It has a pH indicator. Shigella are red and salmonella are red with black centres.

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109
Q

What is Sabouraud’s agar?

A

User to culture fungi. Inhibition of bacteria is aided by the presence of antibiotics in the agar.

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110
Q

How does staph aureus appear in blood agar?

A

It appears creamy/yellow in blood agar

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111
Q

What type of infection are A, C and G type antigen normally?

A

Tonsillitis and skin infections

Type A is normally strep. pyogenes.

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112
Q

What type of infection are B type antigen normally?

A

Sepsis and meningitis

Type B is normally strep Agalactiae

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113
Q

What areas of the body are sterile?

A 
Blood
Cerebrospinal fluid
Pleural fluid
Peritoneal cavity
Joints
Urinary tract
Lower resp tract
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114
Q

What type of bacterias can use the oxidase test?

A

Non-lactose fermentors

Gram negative bacilli

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115
Q

What disease does m. tuberculosis form?

A

Tuberculosis

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116
Q

List some mycobacteria of medical importance

A 
M. Tuberculosis
M. Leprae
M. Avum complex
M. Kansasii
M. Marinum
M. Ulcerans
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117
Q

What are mycobacteria?

A

Aerobic, non-spore forming, non-motile bacillus, Slow growing
Have resistance to gram stain (should be gram positive) , so need to be stained with acid and alcohol (Acid fast)

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118
Q

What is the issue with mycobacteria being slow growing?

A

It is difficult for antibiotics to target their division phase
It is also hard to culture so harder to diagnose

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119
Q

What are some key cell wall components of mycobacteria?

A

Mycololic acids and liporabinomannan- make up a strong waxy cell wall that is hard for the immune system to target

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120
Q

Why are mycobacteria hard to diagnose and treat?

A

They are slow growing = take weeks to diagnose

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121
Q

What are Koch’s postulates?

A

Bacteria should be found in all people with disease
Bacteria should be isolated from the infected lesions in people with the disease
A pure culture inoculated into a susceptible person should produce symptoms of the disease
The same bacteria should be isolated from the potentially infected individual

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122
Q

How can you identify mycobacteria?

A

Ziehl-neelson stain (appears red/pink)

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123
Q

How can TB be diagnosed?

A

Culture growth (but takes weeks to get a result)
Nucleic acid detection (Rapid diagnosis, highly sensitive)
Tuberculin skin test (can analyse the amount of response to TB)
Interferon gamma release assays= Uses antigens specific to TB to demonstrate exposure

124
Q

How do mycobacteria cause infection?

A
  • It is phagocytosed by macrophages but can withstand this, and escape into the cytosol
  • T cell stimulation
  • Granulomas arise in response to contain the mycobacteria
  • Central tissue may necrose to form a craveating granuloma
  • Granuloma tries to starve the mycobacteria
  • Excessive immune response = hypersensitivity reactions
125
Q

What are the two types of leprosy?

A

Tuberculoid leprosy

Lepromatous leprosy

126
Q

Why is TB infection so dangerous?

A

Associated with excessive tissue hypersensitivity and granuloma

127
Q

What is tuberculoid leprosy?

A
  • Associated with tissue hypersensitivity and granulomata
  • Tissue damage including nerve damage
  • Predominant Th1 biased CD4+ T cell responses
128
Q

What is lepromatous leprosy?

A
  • Lesions full of bacilli but little or poorly formed granulomata
  • Extensive skin lesions
  • Predominant Th2 biased CD4+ T cell responses
129
Q

How is tuberculosis treated?

A

Standard therapy= Isoniazid, rifampicin, pyranzanamide, and ethambutol for 2 months, and isoniazid and rifampicin for a further 4 months
If resistance develops= Fluroquinolones, prothionamide, injectable agents such as streptomycin

130
Q

What are the different stages of tuberculosis?

A

Primary
Latent
Pulmonary
TB spread beyond lungs

131
Q

What is primary tuberculosis?

A
  • Bacilli settle in apex and granuloma forms

- Bacilli taken in lymphatics to hilar lymph nodes

132
Q

What is latent tuberculosis?

A
  • Cell mediated immune response from T cells
  • Primary infection is contained but CMI persists
  • No clinical disease
133
Q

What is pulmonary tuberculosis?

A
  • Cell mediated immune response from T-cells
  • Necrosis in lesions
  • Caseous material coughed up leaving cavity
  • CMI and caseation in lesion results in cavity
134
Q

Where does TB normally spread to beyond the lungs?

A

TB meningitis, Miliary TB, Pleural TB, Bone and Joint TB, Genitourinary TB

135
Q

What is a virus?

A

An infectious, obligate intracellular parasite composing genetic material surrounded by a protein coat and/or a membrane

136
Q

What are the stages of virus replication?

A
  1. Attachment
  2. Cell entry
  3. Interaction with host cells
  4. Replication
  5. Assembly
  6. Release
137
Q

How can viruses cause disease?

A
  • Direct destruction of host cells
  • Modification of host cell structure or function
  • Over-reactivity
  • Cell proliferation and cell immortilisation (Cancer)
  • Evasion of host defenses
138
Q

What are the clinical features of poliovirus?

A
  • It enters the body orally and then invades and replicates in the gut
  • Then travels to the bloodstream and targets the brain
  • Direct brain destruction
  • Can result in paralysis
139
Q

What are the clinical features of rotavirus?

A
  • Shortening and atrophy of the villi in the jejunum
  • Stripping of the microvilli
  • Malabsorptive state
  • Profuse diarrhoea
140
Q

How is hepatitis B virus spread?

A

Blood or sexual contact

141
Q

How does HPV cause cervical cell carcinoma?

A
  • It infects the supra basal layer, where the virus becomes integrated into the host cell chromosome
  • Different proteins are expressed, preventing tumour suppressor genes
142
Q

How can viruses be tested for?

A

PCR (Tests if viral genetic material is present)
Serology (Is there immune memory)
Histopathology (Is there any features of viral infection)

143
Q

How do you get bovine TB?

A

M. Bovis from Cows

144
Q

What is used to culture mycobacteria?

A

Löwenstein–Jensen medium

145
Q

What are the three groups of worms?

A

Nematodes (Roundworms)
Trematodes (Flatworms, flukes)
Cestodes (Tapeworms)

146
Q

What is the pre-patent period?

A

The interval between worm infection and the appearance of eggs in stool

147
Q

What are protozoa?

A

Single-celled eukaryotic organisms with a definite nucleus

148
Q

What are the four types of protozoa?

A

Mastigophora (Flagellates)
Sarcodina (Amoebae)
Apicomplexia (Sporozoans)
Ciliophora (Ciliates)

149
Q

List some common flagellate protozoa

A
  • Giargia lambila
  • Trypanosoma spp.
  • Trichomonas Vaginalis
150
Q

What infection is caused by trypanosoma spp. ?

A

Sleeping sickness

  • Chancre at site of bite
  • Fever, lethargy, myalgia, excessive weight loss, personality change, coma
151
Q

What infection is caused by trichomonas vaginalis?

A

STD= Trichomoniasis

152
Q

How do amoebae protozoa move?

A

Flowing cytoplasm and pseudopodia

153
Q

What infection is caused by entamoeba histolytica?

A

Amoebiasis

  • Foecal oral transmission
  • Bloody diarrhoea
  • Liver abscess
  • Right upper quadrant pain
  • Rural botswana
154
Q

What antibiotic is commonly used to treat protozoa infections?

A

Metronidazole

155
Q

What infection is caused by toxoplasma gondii?

A

Toxoplasmosis

  • Commonly immunosuppressed patients in contact with feline faeces
  • Left sided weakness
  • Headaches and visual disturbances
  • Ring enhancing lesion on CT
156
Q

What species of protozoa cause malaria infection?

A
  • Plasmodia spp.

= P. Falciparum, P. Ovale, P. Vivax, P. Malariae

157
Q

How is malaria infection transmitted?

A

Transmitted by the bite of the female anopheles mosquito

158
Q

What is the developmental cycle of malaria within the vector?

A
  • The female anopheles mosquito becomes infected after taking a blood meal containing infected gametocytes
  • After 7-20 days, the infective sporozoites have migrated into the insects salivary glands
159
Q

What is the liver cycle of malaria within a human?

A
  • Sporozoites are inoculated into a new human host
  • Taken up into the liver
  • They multiply inside hepatocytes as schizonts
  • After afew days, hepatocytes rupture releasing merozoites into the blood
  • P. Vivax and P. Ovale remain dormant in the liver
160
Q

What is the blood cycle of malaria within a human?

A
  • Merozoites are taken up into erythrocytes
  • The erythrocyte ruptures, releasing merozoites to infect further cells
  • Some immature trophozoites differentiate into gametocytes
161
Q

List some clinical features of malaria

A
  • Normal incubation period of 10-21 days
  • Fever
  • Chills and sweats
  • Headache
  • Myalgia
  • Fatigue
  • Hepatosplenomegaly
  • Nausea and vomitting
  • Diarrhoea
  • Anaemia= tiredness, dark urine, jaundice
162
Q

Which plasmodia species(s) gives the most severe strain of malaria?

A

P. Falciparum

163
Q

Which plasmodia species(s) give the most mild strain of malaria?

A

P. Vivax or P. Ovale

164
Q

List some complications of malaria?

A
  • Coma and confusion (Cerebral anaemia)
  • Adult resp distress syndrome
  • Anaemia
  • Jaundice
  • Hepatosplenomegaly
  • Renal failure
  • Shock
165
Q

How does cerebral anaemia occur in malaria?

A
  • Cytoadherance= Infected RBCs display specific membrane proteins to adhere to microvascular endothelium
  • They also adhere to other non-infective RBCs causing “Rosettes”
  • This blocks arteries
166
Q

How is malaria diagnosed?

A

Thick and thin films

  • Thick= Tells if malaria is present and how severe
  • Thin= Identify specific species of plasmodia
167
Q

How is malaria treated?

A
  • Complicated malaria= IV artesunate
  • Uncomplicated= Oral riamet or oral quinine
  • P Vivax and P Ovale= Also give primaquine to prevent dormant stage
168
Q

List some things that give immunity against malaria

A
  • Sickle cell trait
  • Glucose-6-phosphate dehydrogenase deficiency
  • Thalessaemias
169
Q

What are the key attributes of pathogens?

A
  • Infectivity
  • Virulence
  • Invasiveness
170
Q

What are the stages of pathogenesis?

A

Exposure, adhesion, invasion, infection, transmission

171
Q

What are commensal microorganisms?

A

The resident flora and usually nonpathogenic

172
Q

What are opportunistic infections?

A

Infections that only arise if immune status is altered

173
Q

What is a zoonotic disease?

A

A disease that spreads between animals and people

174
Q

List some humoral defenses against pathogens

A
  • IgA= Blocks binding of pathogens
  • IgM= Agglutinates particles making them difficult to enter cells
  • Complement= Opsonisation and cell lysis
  • Antibodies= Neutralise toxins
175
Q

List some examples of viruses that cause direct cell toxicity

A

Influenza virus to respiratory epithelium
Varicella zoster virus to skin cells
Yellow fever virus to liver cells
HIV to CD4 T-cell

176
Q

What are biofilms?

A

Produced by bacteria to help to stick together on a surface and help protect against microbes

177
Q

What do bacterias adhesins do?

A

They help bacteria to bind to mucosal surfaces

178
Q

What is the effect of TNF release in response to infection?

A
  • Inflammatory response leading to some symptoms of infection (pyrexia, nausea, malaise)
179
Q

Which inflammatory mediators cause vasodilation?

A

Prostaglandins
Kinins
Leukotrienes

180
Q

Which inflammatory mediators cause increased vascular permeability?

A

Prostaglandins

Leukotrienes

181
Q

List some beta lactam antibiotics

A
  • Penicillins
  • B-lactamase inhibitors
  • Cephalosporins
  • Carbapenems
  • Monobactams
  • Glycopeptides
182
Q

How do beta lactam antibiotics target bacteria?

A
  • Inhibit cell wall synthesis by targeting peptidoglycan

- Therefore generally kill gram positive bacteria better than gram negative

183
Q

What are antimicrobials?

A

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

184
Q

What are bacterosteric antibiotics?

A

Prevents the growth of bacteria, including those that inhibit protein synthesis, DNA replication or metabolism

185
Q

What are bactericidal antibiotics?

A

Agents that kill the bacteria, kill more than 99% of bacteria in 18-24 hrs, generally inhibit cell wall synthesis

186
Q

What is conc dependent killing?

A

Kills bacteria by having a high concentration above minimal inhibitory concentrations

187
Q

What is time dependent killing?

A

Kills bacteria by sustained killing= how long does the conc stay above the minimal inhibitory conc

188
Q

What is the minimal inhibitory conc?

A

The minimum concentration of antibiotic that is required to kill the bacteria

189
Q

How do bacteria resist antibiotics?

A
  • Target site mutation
  • Destroying or inactivation of antibiotics
  • Prevention of antibiotic entry
  • Pumping out the antibiotic from the cell
190
Q

How does antibiotic resistant develop?

A
  • Intrinsic natural resistance= The antibiotic doesn’t work on that bacteria
  • Acquired resistance= Spontaneous gene mutation or horizontal gene transfer
191
Q

What are some factors to consider when deciding if an antibiotic is safe?

A
  • Intolerance, allergy
  • Side effects
  • Age
  • Renal and liver function
  • Pregnancy and breastfeeding
  • Drug interactions
  • Risk of C. Difficile
192
Q

Name an antibiotic class that targets the bacterial ribosomal 50s subunit and one example

A

Macrolides (Includes clarythromycin and erythromycin)

193
Q

Name an antibiotic class that targets the bacterial ribosomal 30s subunit and give one example

A

Tetracyclines (Tetracycline, doxycycline, lymecycline, minocycline)
Aminoglycoside (Gentamicin)

194
Q

Name an antibiotic class that works by targeting DNA gyrase and give an example

A

Quinolones (Ciprofloxacin, Levofloxacin, Moxifloxacin, Ofloxacin)

195
Q

Name an antibiotic class that works by targeting RNA polymerase and give an example

A

Rifampin

196
Q

Name an antibiotic that works by inhibiting folate synthesis

A

Trimethoprim

Sulfonamides

197
Q

Name some antibiotics that inhibit cell wall synthesis

A

Glycopeptides e.g. Vancomycin
Penicillins e.g. Amoxicillin, flucloxacillin
Cephalosporins
Carbapenems

198
Q

Name some antibiotics which inhibit protein synthesis

A

Chloramphenicol
Macrolides e.g. Erythromycin
Tetracyclines
Aminoglycosides e.g. Gentamycin

199
Q

What would be the treatment of a lower UTI in a non-pregnant female?

A

3 days of oral nitrofurantoin

Could also use 3 days of oral trimethoprim

200
Q

What would be the treatment of cellulitis?

A

Flucluxacillin +/- benzylpenicillin for 10-14 days

201
Q

What would be the treatment of bacterial pneumonia?

A

Amoxicillin/ Co-amoxiclav for 5 days

202
Q

What would be the treatment for strep. Aureus infections?

A

Flucoxacillin

203
Q

What would be the treatment for group A,C,G strep tonsillitis?

A

Oral penicillin V, or IV benzylpenicillin

204
Q

Which antibiotics can result in C. Difficile?

A 
Generally antibiotics that begin with the letter C= 
Ciprofloxacin
Clindamycin
Cephalosporins
Carbapenems
Co-amoxiclav
205
Q

What is the single most effective method of preventing cross infection?

A

Hand hygiene

206
Q

What are the broadest spectrum beta-lactam antibiotics available?

A

Carbapenems

207
Q

What are the 2 main approaches to viral diagnosis?

A
  • Virus detection

- Serology

208
Q

What are the methods of viral serology?

A
  • CFT (Complement fixation test)
  • HA/HAI (Haemagglutination/ haemagglutination inhibtion)
  • ELISA (Enzyme linked immunosrbent assay)
  • RIA (Radioimmunoassay)
  • IF (Immunofluorescence)
209
Q

Briefly explain the polymerase chain reaction

A
  • Enzymes unzip chains of nucleic acid DNA/RNA and then make up complementary copies
  • Primer sequences are added
  • Cycles of heating and cooling
  • New chains are marked with fluorescent material
  • This is repeated many times
210
Q

What are the pros and cons of PCR?

A

+ Sensitive and quick

  • So sensitive that it may give false positives
  • Only detects nucleic acid material complementary to primer sequence (need to know which virus you’re looking for)
211
Q

What is serology?

A

The study or detection of an antibody response in the serum (especially in IgG and IgM)

212
Q

What are black swabs used for?

A

Bacteria detection

213
Q

What are green swabs used for?

A

Viral detection

214
Q

What is shingles?

A
  • Varicella Zoster Virus
  • Causes shingles which can appear on various dermatomes
  • Usually seen at areas associated with tight clothing
215
Q

What is a blue blood bottle used for?

A

Coagulation tests

216
Q

What are yellow blood bottles used for?

A

U&E

Liver function tests

217
Q

What are purple blood bottles used for?

A

Full blood cells

218
Q

What are pink blood bottles used for?

A

Group and Save

Crossmatch

219
Q

How can you detect if a virus is an acute infection?

A

There will be IgM, but not highly specific IgG antigens

220
Q

How can you detect if a virus infection has been present chronically?

A
  • Presence of both IgM and highly specific IgG antigens available
221
Q

How is an ELISA test performed?

A
  • Virus or bacterial antigen is absorbed to wells of a plate and washed
  • Patient serum added in dilutions
  • It is then washed
  • Enzyme substrate is then added
  • Washed
  • If positive, a colour change will occur
222
Q

How long does a blood film take to get results?

A

Hours

223
Q

How long does PCR take to get results?

A

A day

224
Q

What does anti-streptolysin O titre detect?

A

Lancefield group A beta-haemolytic streptococci (Strep. Pyogenes) especially streptolysin O

If positive, visible agglutination occurs

225
Q

What can be tested using a CSF sample?

A
  • Cell count
  • Gram stain for organisms
  • qPCR for virus and bacterial pathogens
  • Protein and glucose
226
Q

How is HIV normally tested for?

A

COBAS Ag/Abs screen

If positive, repeat testing and if that is positive, report as positive

227
Q

Give some signs and symptoms of infectious mononucleosis?

A
  • Central= Fatigue, malaise, loss of appetite, headache
  • Photophobia
  • Tonsils= Reddening, swelling and white patches
  • Resp= Cough
  • Lymph nodes swelling
  • Chills and fever
  • Splenomegaly
228
Q 
Chains of purple cocci are seen on a gram film. They don't grow near the optochin disc 
These are probably..
A) Streptococcus pneumoniae
B) Staphylococcus epidermidis
C) Viridans Streptococci
D) S. pyogenes
E) Neisseria meningitidis
A

Correct answer=A

229
Q 
A pink colony is picked off this MacConkey plate and is found to contain pink staining bacilli with Gram's staining. Which organism is most likely? 
A) Shigella sonnei
B) Listeria monocytogenes
C) Neisseria meningitidis
D) Eschericia coli
E) Streptococcus pyogenes
A

Correct answer= D

230
Q 
Which of the following is Haemophilus influenzae NOT an important cause of? 
A) meningitis in pre-school children
B) Otitis media
C) Pharyngitis
D) Gastroenteritis
E) Exacerbations of COPD
A

Correct answer= D

231
Q

Which of these is NOT a means by which viruses cause disease?
A) direct destruction of host cells
B) cell proliferation and cell immortalisation
C) inducing immune system mediated damage
D) Endotoxin production
E) modification of host cell structure or function

A

Correct answer= D

232
Q

The HIV envelope contains
A) RNA + capsid + DNA polymerase
B) DNA + capsid + RNA reverse transcriptase
C) DNA + p24 + RNA polymerase
D) RNA + capsid + RNA reverse transcriptase
E) RNA + gp120 + RNA polymerase

A

Correct answer = D

233
Q

List some protozoa

A

Giardia Lamblia
Toxoplasma
Falciparum malaria

234
Q

Which micro-organisms resist destaining by acid and alcohol?

A

Mycobacteria

235
Q

Which micro-organisms have a cell wall containing lipoarabinomannan?

A

Mycobacteria

236
Q

Which micro-organisms divide every 30-60 minutes?

A

Bacteria

237
Q

Which micro-organisms usually withstand phagolysomal killing?

A

Mycobacteria

238
Q

Which micro-organisms can cause meningitis?

A

Bacteria

239
Q

How is antimicrobial resistance spread?

A

Plasmid mediated gene transfer

240
Q

A 21 year old complains of myalgia, sore throat and tiredness. He is febrile and has an enlarged spleen. On examination, he has purulent tonsils. What is it likely to be?

A

Glandular fever caused by EBV

241
Q

What causes pneumocystis pneumonia in HIV?

A

P. jirovecci = an opportunistic fungal infection

242
Q

What groups of people are most at risk of HIV?

A

Gay and bisexual men, sex workers, people who inject drugs, black-African men and women, Uncircumised men

243
Q

How can HIV be transmitted?

A

Sexual= World-wide, sexual intercourse accounts for the vast majority of infections
Vertical = Mother to child in utero or through breast feeding
Blood

244
Q

List some HIV preventative measures

A 
Antiretroviral treatment (U=U)
PreP
Circumcision
PEP
STI control
Vaccines
Microbicides
HIV diagnosis / partner notification
Behavioural / condom use
Screen blood products / needle exchange
245
Q

Explain U=U

A

If viral load is treated and lowered meaning that the antiretroviral load is low, then it can’t be transmitted
Undetectable= Untransmittable

246
Q

What is pre-exposure prophylaxes?

A

Taking HIV medication before sex to prevent transmission

About an 86% Risk reduction

247
Q

What is post-exposure phopholyaxes?

A

Antiretroviral therapy after exposure to HIV (must be started within 72 hrs of exposure)

248
Q

List some benefits of knowing HIV status?

A 
Access to appropriate treatment and care
Reduction in morbidity and mortality
Reduction of vertical transmission
Reduction of sexual transmission
Public health
Cost-effective
249
Q

What are the risk factors of HIV?

A

Sexual contact with people from high prevalence groups
Multiple sexual partners
Sexual assault
Vertical transmission

250
Q

What are the components of a viron?

A
  • Lipid envelope
  • Nucleic acid
  • Protein capsid
  • Viron associated polymerase
  • Spike projections
251
Q

What are the steps if HIV replication?

A 
Attachment
Entry
Uncoating
Reverse transcription (error prone so genomic variability)
Genome integration
Transcription of viral RNA
Splicing of mRNA and translation into proteins
Assembly of new virions
Budding
252
Q

What are the types of HIV?

A

M (main), O (outlying) and N (new) groups.

Main group separated into clades A-D, F-H, J-K.

253
Q

Where is clade B HIV most predominant?

A

Europe and USA

254
Q

Where is clade A HIV most predominant?

A

West and central Africa

255
Q

Where is clade C HIV most predominant?

A

Southern Africa

256
Q

Where is HIV-2 found?

A

Mainly West Africa

257
Q

Why does HIV have reverse transcriptase enzyme?

A

To allow viral RNA to be transcribed into DNA and thence incorporated into host cell genome

258
Q

Why is there considerable genetic variation in HIV?

A

Reverse transcriptase enzyme is highly error-prone due to high rate of viral turnover

259
Q

What cell type does HIV target?

A

CD4 T helper cells

260
Q

What does gp120 glycoprotein do on HIV?

A
  • Allows HIV to bind to CD4 receptors

- Allows for HIV entry into cells

261
Q

What does HIV’s integrase enzyme do?

A

Integrate the double stranded HIV viral DNA into the host cells DNA

262
Q

Why does CD4 count lower in HIV?

A

Activated CD4 cells will apoptose via Fas ligand upregulation

263
Q

Why are HIV vaccines difficult to make?

A

There is ongoing virus replication and mutation

Ethical constraints

264
Q

How does HIV develop drug resistance?

A

Non-adherance

Drug-Drug interactions

265
Q

What is aids?

A

Acquired immune deficiency syndrome

- Defined as a CD4 count of less than 200 cells per mm3

266
Q

What is the clinical presentation of acute primary infection of HIV?

A
  • Transient immunosuppression and fall in CD4 count followed by a gradual rise
  • Acute rise in viral load
  • Transient illness 2-6 weeks after exposure with abrupt onset of non specific symptoms (Fever, malaise, pharyngitis, weight loss, rash)
267
Q

What is the clinical presentation of the asymptomatic phase of HIV?

A
  • Progressive loss of CD4 T cells resulting in poor immunity

- Can have generalised lymphadenopathy

268
Q

What is the clinical presentation of the symptomatic phase of HIV?

A
  • Rise in viral load and fall in CD4 count
  • Fever, night sweats, diarrhoea, weight loss
  • Minor opportunistic infections: Oral candida, herpes zoster, PID
  • Resp condition= Dry cough
  • Known as AIDS-related complex (ARC)
269
Q

How long does it normally take for HIV to develop into AIDS?

A

8 years

270
Q

List some AIDS defining conditions

A
  • Infections= Candidiasis oesophageal/ lung, TB, Persistant herpes simplex, Pneumocystitis jiroveci, bacterial pneumonia
  • Neoplasms= Kaposi’s carcinoma, invasive cervical carcinoma
  • Toxoplasmosis
271
Q

What are the two methods of testing for HIV?

A

CD4 T cell count/μl and HIV viral load (RNA copies/ml)

272
Q

When should patients be tested for HIV?

A
  • High protein but low albumin on bloods
  • Non-specific symptoms
  • Recurrent shingles and candidiasis
  • If there is a sharp drop in O2 stats after walking (Pneumocystitis pneumonia)
273
Q

When would IgG antibody p24 be used to test for HIV?

A
  • If it is early on = it is frequently lost as the disease progresses
274
Q

When are genome detection assays used to test for HIV?

A

Used to test for HIV in the babies of HIV positive mothers

275
Q

What are the possible treatments for HIV?

A 
HAART
NRTI
NNRTI
PI
Fusion inhibitors
Integrase inhibitors
276
Q

What is HAART?

A

Highly active antiretroviral therapy

  • Aims to reduce viral load and increase CD4 count
  • Uses 3 drugs to minimise replication and cross resistance
277
Q

How do nucleoside reverse transcriptase inhibitors (NRTIs) help to treat HIV, and give one example

A

Examples: Abacavir, Didanosine, Emtricitabine

They inhibit the synthesis of DNA by reverse transcription and act as DNA chain terminators

278
Q

How do non-nucleoside reverse transcriptase inhibitors (NNRTIs) help to treat HIV, and give one example

A

Examples: Efavirenz, Etravirine, Nevirapine

Bind directly to, and inhibit reverse transcriptase

279
Q

How do protease inhibitors help to treat HIV and give one example

A

Examples: Atazanavir, Darunavir, Indinavir

Act competitively on HIV enzyme involved in production of functional viral proteins and enzymes

280
Q

How do fusion inhibitors help to treat HIV and give one example

A

Example: Enfuvirtide

Inhibits fusion of HIV with target cells

281
Q

How do integrase inhibitors help to treat HIV and give one example

A

Example: Raltegravir

Prevents the insertion of HIV DNA into the human genome

282
Q

What are the sanctuary sites for HIV?

A 
Genital tract
Central nervous system
GI system
Bone marrow
Macrophages & Microglia
283
Q

How can children of HIV infected mothers become infected with HIV?

A

In-utero
Intra-partum
Via breast milk

284
Q

What are the risk factors for mother-to-child transmission of HIV?

A
  • High maternal plasma viral load
  • Viral strain (HIV2 is rarely passed mother to child)
  • Breast feeding
285
Q

What are the clinical features of varicella zoster virus infection?

A

Chickenpox

  • Brief fever, headache and malaise
  • A rash, predominantly on the face, scalp and trunk
  • Macules, then papules, then vesicles
286
Q

What are the clinical features of herpes zoster virus inefction?

A

Shingles

  • Remains in dorsal root ganglia
  • Pain and tingling in a dermatomal distribution
  • Papules and vesicles in same dermatome- commonly lower thoracic and opthalmic division of trigeminal
287
Q

A 6 year old patient is seen with macules on the face and trunk. He has been feeling unwell with a headache and fatigue. What is it likely to be?

A

Chickenpox

varicella zoster virus

288
Q

A 68 year old man is in clinic complaining of a rash along his back. It is papules and vesicles and they are running in a line. What is it likely to be?

A

Shingles

Herpes zoster virus

289
Q

How is infective endocarditis by strep. viridans treated?

A

IV benzylpenicillin for 4-6 weeks +/- synergistic gentamicin for the first 2 weeks

290
Q

How is infective endocarditis by enterococci treated?

A

IV amoxicillin and gentamicin for 4-6 weeks

291
Q

List some lancefield group A conditions?

A

Pharyngitis, cellulitis, erysipelas, necrotising fascitis, septicaemia, rheumatic fever, Acute glomerulonephritis, Scarlet fever

292
Q

List some lancefield group B conditions?

A

Neonatal meningitis and septicaemia

293
Q

List a lancefield group C condition?

A

Pharyngitis, cellulitis

294
Q

List a lancefield group D bacteria

A

Enterococci

295
Q

List a lancefield group G condition?

A

Cellulitis

296
Q

How can you differentiate beta-haemolytic bacteria?

A

Lancefield grouping

297
Q

One way bacteria can be classified as gram positive and gram negative. What do these terms mean?

A

Gram positive bacteria have cell walls composed of thick layers of peptidoglycan. Gram positive cells stain purple when subjected to a Gram stain procedure. Gram negative bacteria have cell walls with a thin layer of peptidoglycan

298
Q

A mother brings her 18 month child to General Practice complaining of having seen small white “threads” in the nappy. What is the likely cause and the most appropriate treatment?

A
  • Threadworms

- Mebendazole

299
Q

What is the commonest condition associated with Mycobacteria? What term is used to describe these bacteria which is relevant to detecting them in the labs?

A
  • Tuberculosis

- Acid fast= Resistant to standard staining and require specific tests

300
Q

What are the five properties of a virus?

A
  • Grow only inside living cells
  • Contain either RNA OR DNA
  • No cell wall, but have an out protein coat
  • Carry enzymes that function inside the cell
  • Protein receptors on surface to allow attachment to host cell
301
Q

What viral vaccine has been introduced to the UK programmme and what cancer is it designed to prevent?

A
  • Human papilloma virus

- Cervical cancer

302
Q

What is the commonest causative organism in fungal nail infection?

A

Trichophyton species

303
Q

A patient presents with fever and recent travel overseas to Africa. What protozoal illness should be top of your differential diagnosis and what is the key diagnostic test?

A
  • Malaria

- Thick and thin blood film

304
Q

Summarise what an antibiotic is and how it works

A

Antibiotics are molecules that work by binding a target site on a bacteria

305
Q

Give four possible clinical situations that might indicate the need of a HIV test

A
  • Prolonged episodes of herpes simplex
  • Persistent frequently recurrent candidiasis
  • Recurrent infections
  • Oral candida
  • Indicators of immune dysfunction
  • Odd looking mouth lesions
  • New onset abnormal skin lesions (Kaposi’s sarcoma)

Phase 2a (31 decks)

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