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Phase 2 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Define pathogen

A

Organism that causes or is capable of causing disease

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2
Q

Define commensal

A

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

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3
Q

Define opportunist pathogen

A

Microbe that only causes disease if the host defences are compromised

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4
Q

Define virulence/pathogenicity

A

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

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5
Q

Define Asymptomatic carriage

A

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

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6
Q

What is the name given to bacteria that have round morphology

A

Coccus

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7
Q

What is the name given to bacteria that have a rod shaped morphology

A

Bacillus

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8
Q

What does the gram stain determine?

A

If a bacteria has a single membrane or a double membrane

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9
Q

A gram positive bacteria will stain what colour on the gram stain q

A

Purple

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10
Q

A gram negative bacteria will stain what colour on the gram stain

A

pink

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11
Q

What is the term used to describe cocci that grow together

A

Diplococcus

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12
Q

What strain of bacteria can not be differentiated by the gram stain

A

Mycobacteria

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13
Q

What stain can be used to differentiate mycobacteria

A

Ziehl neelsen stain

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14
Q

What does the Ziehl Nielsen stain determine?

A

Whether a bacteria is an acid fast bacilli (Red) or a non-acid fast bacilli (Blue)

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15
Q

What does the catalase test involve

A

Adding H2O2 to bacteria and looking for bubbling which indicates a positive reaction

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16
Q

What is the catalase test used for

A

To differentiate between staphylococci and streptococci

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17
Q

Are staphylococci catalase positive or negative

A

Positive

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18
Q

Are streptococci catalase positive or negative

A

Negative

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19
Q

What is the coagulase test used for

A

Coagulase is an enzyme only produce by Staphylococcus aureus so test distinguishes staphylococcus aureus from other staphylococci

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20
Q

Which bacteria produces a positive result with the coagulase test and why is the result positive

A

Staphylococcus aureus because it is coagulase positive and will produce clumping - a negative result will not produce clumping

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21
Q

Describe the observed result for alpha haemolysis in the haemolysis test

A

An indistinct zone of partial destruction of red blood cells appears around the colony accompanied by a greenish to brownish discolouration of the medium

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22
Q

What bacteria is alpha haemolytic

A

Streptococcus pneumoniae

Streptococcus Intermedius

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23
Q

What is the haemolysis test useful for

A

Classifying streptococci

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24
Q

Describe the observed results for beta haemolysis in the harmolysis test

A

A clear colourless zone appears around the colonies in which red blood cells have undergone complete lysis

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25
Q

Name bacteria that are beta haemolytic

A

Streptococci pyogenes
Streptococci agalactiae
Listeria monocytogenes

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26
Q

What test can be used to further differentiate Beta haemolytic bacteria

A

Lancefield grouping

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27
Q

What are the components of the bacterial wall

A

Capsule - protects the bacteria from the host immune system
Cell wall - made of phospholipid membrane
Do not have a nuclear membrane
Contain one circular chromosome

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28
Q

Describe the cell envelope of a gram positive bacteria

A

Single cytoplasmic membrane
Large amounts of peptidoglycan
No endotoxin

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29
Q

Describe the cell envelope of a gram negative bacteria

A 
Double membrane (inner and outer)
Smaller amount of peptidoglycan 
Outer membrane has Lipopolysaccharide (endotoxin)
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30
Q

Which mucosal surfaces are areas open to bacterial colonisation

A

Nasal cavity
Larynx
Stomach
Colon

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31
Q

Which areas need to be kept sterile from bacterial colonisation

A

Lungs
Gall bladder
Kidneys
Eyes

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32
Q

What is the name given to a bacteria with a curved rod morphology

A

Vibrio

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33
Q

What is the name given to a bacteria with a spiral rod morphology

A

Spirochaete

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34
Q

What environment is required for bacterial growth

A

Temperature between -80 and +80
pH between 4 and 9
Water/desiccation - 2 hours to 3 months

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35
Q

What are the three phases of bacterial growth

A

Lag phase
Exponential stage
Stationary stage

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36
Q

Endotoxin is a component of what

A

The outer lipopolysaccharide membrane of gram negative bacteria

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37
Q

Exotoxin is a component of what

A

Protein Secreted by gram +ve and -ve bacteria that can interfere with the nervous system, de-regulate G proteins and stop macrophage phagocytosis of bacteria

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38
Q

Describe the DNA of a bacteria

A

Single chromosome of double stranded DNA that is converted to RNA polymerase by ribosome and then from mRNA to protein by the ribosome

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39
Q

Due to their rapid rates of multiplication, what sort of mutations would you expect to see in a bacteria?

A

Base substitution
Deletion
Insertion

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40
Q

How is genetic variation produced in bacteria

A

Mutations
gene transfer
Conjugation by the sex pillus

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41
Q

What are the two forms of gene transfer in bacteria

A

Transformation via a plasmid

Transduction via a phage

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42
Q

What is bacterial transformation

A

genetic alteration of a bacterial cell via the uptake of an exogenous substance via a plasmid

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43
Q

What is bacterial transduction

A

Process by which foreign DNA is introduced into a bacteria via vector or virus ie. bacteriophage

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44
Q

What is bacterial conjugation

A

Transfer of genetic material between bacterial cells by direct cell to cell contact ie. via the sex pillus

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45
Q

What is an obligate intracellular bacteria

A

Bacteria that cannot be cultured on an artificial media and needs to be grown on host cells

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46
Q

Give examples of the three genus of obligate intracellular bacteria

A

Rickettsia
Chlamydia
Coxiella

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47
Q

Give examples of bacteria with no cell wall

A

Mollicutes including
Mycoplasma pneumoniae
M. Hominis
Ureaplasma Urealyticum

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48
Q

Name three genus of bacteria that grow as filaments

A

Anctinomyces
Nocardia
Streptomyces

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49
Q

Name the types of bacteria that grow as single cells

A

Rods
Cocci
Spirochaetes

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50
Q

What is an obligate anaerobe?

A

Microbe that can only grow in the absence of oxygen

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51
Q

What are the three main types of gram positive bacteria

A

Staphylococcus
Streptococci
Corynebacterium

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52
Q

Is S.aureus coagulase coagulase positive or negative

A

Coagulase positive

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53
Q

What is the normal habitat for staphylococcus

A

Found in the nose and the skin

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54
Q

How is staphylococcus aureus spread?

A

Aerosol and touch (Coughing and breathing)

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55
Q

What is MRSA

A

Methicillin resistant staphylococcus aureus

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56
Q

What is MRSA resistant to

A

B-lactam
Gentamicin
Erythromycin
Tetracycline

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57
Q

What are the virulence factors of staph aureus

A

Pore-forming toxins (Haemolysin)
Proteases (Exfoliatin)
Toxic shock syndrome toxin (Stimulate cytokine release)
Protein A (Surface protein which binds Ig’s in wrong orientation so cant be recognised by immune system)

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58
Q

What are some S.aureus associated conditions

A 
Wound infections (pyogenic)
Absecesses (Pyogenic)
Impetigo (Pyogenic) 
Pneumonia (Pyogenic)
Osteomyelitis (Pyogenic) 
Scalded skin syndrome (Toxin mediated)
Food poisoning (Toxin mediated) 
Endocarditis (Coagulase negative)
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59
Q

Name 2 types of coagulase negative staphylococci

A

S.Epidermis

S.Saprophyticus

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60
Q

What is Staphylococcus Epidermis

A

Opportunistic infection in prosthetic limb and catheters

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61
Q

Name three ways that streptococci can be classified

A
  1. Haemolysis
  2. Lancefield typing
  3. Biochemical properties
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62
Q

What can be differentiated using lancefield typing

A

A method grouping catalase negative and coagulase negative bacteria based on the bacterial carbohydrate cell surface antigens

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63
Q

What are the two important groups of the lancefield typing

A

Group A - strep. pyogenes

Group B - Strep. agalactiae

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64
Q

What are the some of the infections caused by S.pyogenes

A 
Wound infections - cellulitis 
Tonsilitis 
Pharyngitis 
Otitis Media 
Impetigo 
Scarlet fever 
Rheumatic fever 
Glomerular nephritis
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65
Q

What are the virulence factors of S.pyogenes

A

Hyaluronidase - enables spread
Streptokinase - breaks clots
C5a peptidase - reduces chemotaxis
Streptolysins O and S - bind cholesterol
Erythrogenic toxin
Hyaluronic acid capsule - protection
M surface protein - encourages complement degradation

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66
Q

What infections does streptococci pneumoniae cause

A

Pneumonia
Otitis media
Sinusitis
Meningitis

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67
Q

What are the predisposing factors for streptococci pneumoniae

A 
Impaired mucus trapping 
Hypogammaglobulinaemia 
Asplenia 
Diabetes 
Sickle cell 
Renal disease
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68
Q

What are the virulence factor for streptococci pneumoniae

A
  1. Polysaccharide capsule is antiphagocytic
  2. Teichoic acid in wall binds choline receptors on host cell to enable adhesion
  3. Peptidoglycan in wall causes inflammatory reaction in host
  4. Cytotoxin pneumolysin insets into host cell membrane, creating a pore for the cell to burst open
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69
Q

What are the results of viridians streptococci in the haemolysin test

A

Alpha or non-haemolytic

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70
Q

What does viridians streptococci cause

A

Dental caries and abscesses
Infective endocarditis
Milleri group

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71
Q

What is the common clinical presentation of corynebacterium diphtheriae

A 
Child with sore throat 
Fever and malaise 
Lymphadenopathy in neck 
Rapid breathing 
Greyish membrane on tonsils
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72
Q

How does corynebacterium diphtheriae spread

A

Droplet spread

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73
Q

How is corynebacterium diphtheria spread?

A

Production of a toxin that inhibits protein synthesis

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74
Q

How do you prevent corynebacterium diphtheriae

A

Vaccination with toxoid (inactivated toxin)

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75
Q

What is the major difference between gram-negative and gram positive bacteria

A

Gram negative bacteria has lipopolysaccharide

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76
Q

What does the lipopolysaccharide endotoxin on the outer membrane of gram-negative membrane contain

A

Lipid A - toxic portion
Core R antigen - short sugar chain
Somatic O antigen - highly antigenic repeating chain of oligosaccharides

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77
Q

What are the three different cell surface antigens on enterobacteria

A

K (cell capsule)
H (flagellum)
O (LPS antigen)

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78
Q

What are enterobacteria?

A

Proteobacteria that are rod shaped facultatively anaerobic motile bacteria with flagella

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79
Q

What test is used to differentiated between lactose and non-lactose fermenting enterobacteria?

A

MacConkey Agar - if bacteria can use lactose it generates lactate and lowers pH producing red bumps

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80
Q

What are the three main types of enterobacteria

A

E.coli
Shigella
Salmonella

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81
Q

Which enterobacteria is lactose +ve

A

E.coli

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82
Q

Which enterobacteria Is lactose -ve

A

salmonella and Shigella

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83
Q

Is E.coli commensal and does it have a flagella?

A

Yes and Yes

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84
Q

What are infections caused by pathogenic E.coli

A 
Wound infections 
UTIs
Gastroenteritis 
Travellers diarrhoea 
Bacteraemia (Infection of abdominal organ)
Infant meningitis
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85
Q

What are the virulence factors for E.coli

A
  1. Entero-toxigenic (ETEC)
  2. Entero-pathogenic (EPEC)
  3. Entero-haemorrhagic (EHEC)
  4. Entero-invasive (EIEC)
  5. Entero-aggregative (EAEC)
  6. Uro-pathogenic (UPEC)
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86
Q

How does entero-toxigenic E.coli work and what does It cause

A

Toxin and pilli

Acts in small intestine to cause secretory diarrhoea

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87
Q

How does entero-pathogenic E.coli work and what does it cause

A

Pedestal formation

Acts in small intestine to cause chronic watery diarrhoea

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88
Q

How does entero-haemorrhagic E.coli work and what does It cause

A

Pedestal formation and shiga-like toxin

Acts in the large intestine to form bloody diarrhoea

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89
Q

How does entero-invasive E.coli work and what does it cause

A

Invasins –> Inflammation and ulceration

Acts in the large intestine to cause bloody diarrhoea and dysentry

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90
Q

How does entero-aggregative E.coli work and what does it cause

A

Pilli + cytotoxin - shorter villi and mucus production

Acts I the large intestine to produce chronic diarrhoea

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91
Q

How does uro-pathogenic E.coli work and what does It cause

A

Haemolysin producing inflammation

occurs In the urinary tract to produce UTIs

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92
Q

Describe the pathogenicity of entero-toxigenic E.coli

A
  1. Heat labile toxin enters epithelial cell and causes GPCR modification (Gs)
  2. Transfers NAD ribose so GPCR becomes locked on with adenylate cyclase activated
  3. Leads to increased cAMP
  4. cAMP binds PKA which phosphorylates CFTR leading to loss of Cl- into intestinal lumen
  5. This alters osmotic balance so Na+ also leaves followed by water leading to diarrhoea
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93
Q

Describe the pathogenicity of pedestal formation in EPEC and EHEC

A
  1. Pathogen adheres to microvilli with pathogenic ili
  2. T3SS acts like syringe and injects toxin into epithelial cells which rearranges actin and disrupts tight junctions
  3. Microvilli reform in pedestals holding pathogen
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94
Q

What are the four species of shigella

A

S.dysenteriae
S.Flexneri
S.boydii
S.sonnei

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95
Q

How does a shigella infection pass from person to person

A

Person to person contact or via contaminated water or food

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96
Q

Describe the pathogenesis of the shigella

A
  1. Bacteria enter the gut mucosa and invade M cells in the gut associated lymphoid tissue
  2. Bacteria are phagocytose and released during apoptosis resulting in inflammation and cell damage
  3. Shiga toxin damages epithelium which enables the bacteria to infect adjacent cells and polymerise actin to make filaments that it uses to move through the cell
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97
Q

What are the symptoms associated with Shiga toxin

A

Bloody diarrhoea
Small volume stools
pain in straining
Prostrating cramps

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98
Q

What are the complications associated with shiga toxin

A

Targets the kidneys leading to renal failure

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99
Q

What are the two main species of salmonella

A

Salmonella enterica

S.bongori

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100
Q

What is the name of the infection caused by salmonella enterica

A

Salmonellosis

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101
Q

What are the three types of salmonellosis caused by salmonella enterica

A

Gastroenteritis
Enteric fever (Typhoid)
Bacteraemia

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102
Q

Describe the pathogenesis of salmonellosis in gastroenteritis

A
  1. Bacteria mediated endocytosis
  2. Induction of chemokine release
  3. Neutrophil recruitment and migration
  4. Neutrophil induced tissue injury
  5. Fluid and electrolyte loss causing diarrhoea
    Inflammation/necrosis of gut mucosa
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103
Q

Describe the pathogenesis of salmonellosis in enteric fever

A
  1. Bacteria mediated endocytosis
  2. Transcytosis to basolateral membrane
  3. Survival in macrophages
  4. Spreads systemically to the lymph nodes and enters the bloodstream and causes septicaemia
  5. Spreads to the gall bladder from the liver where person can be a carrier for 1 year to rest of the their life
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104
Q

Name three other types of enterobacteria

A

Proteus Mirabilis
Klebsiella pneumoniae
Yersinia

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105
Q

What are the properties of proteus mirabilis and what is its virulence factor

A

Opportunistic infection that causes pyelonephritis and septicaemia
Virulence factor = increased urease –> kidney stones

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106
Q

What are the properties of klebsiella pneumoniae

A

Environmental, opportunistic, nosocomial infection in neonates, elderly and immune compromised
Colonises the GIT and oropharynx leading to UTIs, pneumonia, surgical wound infection and sepsis

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107
Q

What is the shape of vibrio cholerae

A

Curved rods with single polar flagellum

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108
Q

What is the pathogenesis of vibrio cholerae

A
  1. Toxin binds ganglioside (Glycolipid receptor)
  2. A subunit ADP ribosylates G protein (Gs) –> Locked ON state
  3. Leads to uncontrolled cAMP production
  4. Protein kinase becomes activated
  5. CFTR activity becomes modified = loss of Cl- and Na+ which subsequent loss of H2O
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109
Q

What are the symptoms of vibrio cholerae

A

Rice water stools (high volume and watery) (No blood or pus)
Can lose 20L fluid per day leading to dehydration and hypovolaemic shock

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110
Q

What is pseudomonas aeruginosa

A

opportunist Free-living aerobe that has a motile single poler flagellum

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111
Q

What acute infections does pseudomonas aeruginosa cause

A

Localised (Burns, surgery UTI and keratitis)
Systemic (Bacteraemic) - sepsis
ICU patients on ventilators leading to nosocomial pneumonia
Chronic infections - cystic fibrosis

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112
Q

What are the virulence factors of pseudomonas aeruginosa

A

Twitching motility
Pili
Multiple toxins inhibit protein synthesis
Interference with cell signalling (Exoenzyme S and U)
Cell death and damage (Exotoxin A, elastase and phospholipase)

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113
Q

What is haemophilia influenza

A

Exclusively human parasite opportunistic infection carried mainly by nasopharyngeal
Mainly seen in young children and adult smokers

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114
Q

What conditions are associated with haemophilia infleunzae

A 
Meningitis 
Bronchopneumonia 
Sinusitis 
Epiglottis 
Bacteraemia 
Otitis media 
Pneumonia in CF, COPD and HIV patients
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115
Q

What are the virulence factors of haemophilia influenza

A

Pili (adherence)
Invasive strains have a penetrating capsule that can penetrate the nasopharyngeal epithelium and are resistant to phagocytosis and the complement system

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116
Q

What disease does legionella pneumophila cause

A

Legionnaires disease in immunocompromised

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117
Q

Where might one obtain an legionala pneumophila infection

A

Aquatic environment, air conditioning, water towers, shower heads, humidifiers

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118
Q

What is the pathogenesis of Legionella pneumophila

A
  1. Pathogen infects alveolar macrophages so it can avoid destruction and replicate
  2. Release pro-inflammatory signals causing neutrophil influx into the lungs
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119
Q

What disease does bordetella pertussis cause?

A

Pertussis (Whooping cough)

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120
Q

How is bordetella transmitted>

A

Aerosol transmission

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121
Q

What are the virulence factors of bordetella pertussis?

A
  1. Pertussis toxin

2. Adenylate cyclase haemolysin toxin

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122
Q

What is the pathogenesis of the pertussis toxin?

A
  1. S1 subunit ADP ribosylates G protein (Gi) causing it to be locked in an off state
  2. Switching off of Gi prevents the inhibition of adenylate cyclase
  3. Increased cAMP production
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123
Q

What is the pathogenesis of the adenylate cyclase haemolysin toxin

A

Increases cAMP levels in the affected cell which suppresses the innate immune function such as phagocytosis

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124
Q

Describe the characteristics of neisseria bacteria

A

Non flagellated
Gram negative
Diplococci
Fastidious

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125
Q

What are the two main species neisseria bacteria?

A

N.Meningitidis

N.Gonorrhoea

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126
Q

How is N.menigitidis spread and where does it enter the body?

A

Person to person areosol transmission

Enters at the nasopharyngeal epithelium

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127
Q

What are the conditions caused by N.meningitidis

A

Meningitis
Septicaemia
Low level bacteraemia

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128
Q

What are the virulence factors of N.meningitidis

A

Anti-phagocytic capsule
Pili (colonisation)
LPS results in cytokine cascade and inflammatory response which can lead to sepsis

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129
Q

How is N.gonorrhoea spread

A

Person to person contact

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130
Q

What conditions can be caused by N.gonorrhoea

A

Salpingitis
Proctitis
Gingvitis
Pharyngitis

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131
Q

What is the pathogenesis of N.gonorrhoea

A

Sexual transmission

rectal, vaginal and oral inflammation

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132
Q

What are the virulence factors of N.gonorrhoea

A

Twitching motility

LPS –> Inflammation

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133
Q

What are the two main types of campylobacter

A

Jejuni and coli

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134
Q

Describe the characteristics of campylobacter

A

Spiral rods with unipolar or bipolar flagella

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135
Q

What are the two most common causes of a campylobacter infection

A

Undercooked poultry

Unpasteurised milk

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136
Q

What are the symptoms of a campylobacter infection

A

Mild to severe diarrhoea often with blood - usually self-limiting within a week

Campylobacter usually shed in the faeces for around 3 weeks

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137
Q

What are the virulence factors of campylobacter infection

A

Invasins invade the ideal and colonic epithelial cells resulting in acute inflammation

Cytolethal distending toxin arrests cell cycle meaning target cells swell and lyse

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138
Q

What conditions are caused by helicobacter pylori

A

Gastritis
Peptic ulcer disease
Gastric adenocarcinoma

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139
Q

What is the virulence factor of helicobacter pylori

A

Urease hydrolyses urea to generate ammonia to act as a buffer to gastric acid

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140
Q

What are the two main chlamydiae

A

Chlamydia and chlamidophyl

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141
Q

What are the characteristics of chlamydiae

A

Very small and non-motile

Obligate intracellular parasites that cannot be cultured in media

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142
Q

What are the two stages in the development of chlamydia

A
  1. Elementary bodies

2. Reticulate bodies

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143
Q

Describe what happens during the elementary body stage of chlamydia development

A

Infectious stage where the chlamydia enters the cell through endocytosis and inhibits phagosome-lysosome function but Is dormant

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144
Q

Describe what happens during the reticulate body stage of chlamydia development

A

Replicative but not infectious stage where the bacteria acquires nutrients from the host cell and is metabolically active

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145
Q

What are the 4 main types of chlamydia

A
  1. C. trachomatis = STD
  2. C.Pneumoniae = respiratory tract
  3. Atypical community acquired pneumonia pathogen
  4. C. psittaci
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146
Q

What are the three biovars of C.trachomatis

A
  1. Trachoma biovar (blindness)
  2. Genital tract biovar (STD - infects epithelial cells of mucous membranes of urethra and vagina)
  3. Lymph granuloma venereum biovar (Invasive urogenital or anorectal infection)
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147
Q

What are the three main types of spirochetes

A
  1. Borrelia burgdoferi –> Lyme disease
  2. Leptospira –> Zoonosis
  3. Trepinema Pallidum –> Syphilis
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148
Q

What are the three stages of a syphilis infection

A
  1. Primary - localised infection
  2. Secondary - systemic infection (Skin, lymph and vessels)
  3. Tertiary = granuloma of the soft tissue - cardio and neuro syphilis
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149
Q

Which gram -ve bacteria would you most commonly find in the respiratory tract

A 
Bordetella pertussis 
Haemophilus influenzae 
Pseudomonas aeruginosa
Legionella pneumophila 
Chlamydia pneumoniae
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150
Q

Which gram -ve bacteria would you most commonly find in the urinary tract

A

E.coli
Klebsiella pneumoniae
Proteus mirabilis

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151
Q

Which gram -ve bacteria would you most commonly find in the GIT

A 
Vibrio cholera 
Shigella dysenteria 
Some E.coli 
Campylobacter jejuni 
Helicobacter pylori
S. Enterica and S. typhimurium
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152
Q

Describe the structure of fungi

A

Eukaryotic with a nuclear membrane
Chitinous cell wall
Heterotrophic so get nutrients from what they are living on
Move through growth or spore formation

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153
Q

What is a yeast

A

Small single celled organism that divides by budding (Asexual reproduction)

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154
Q

What is a mould

A

Multicellular hyphae with reproduction by spores

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155
Q

Why do very few fungi actually infect humans

A

Have an inability to grow at 37 degrees

Fungi cannot evade the adaptive/innate immune response

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156
Q

What fungal diseases might you see in an immunocompromised host?

A

Candida line infections
Pneumocystis
Invasive aspergillosis

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157
Q

What fungal diseases might you see in a post-surgical patient

A

Intra-abdominal infections

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158
Q

What fungal diseases might you see in a healthy individual

A

Fungal asthma

Travel associated fungal infections (Dimorphic fungi)

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159
Q

What are the three main genera of fungi

A

Ascomycota
Basidiomycota
Mucormycota

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160
Q

Give some examples of ascomycota

A 
Aspergillus
Pneumocystis 
Candida 
Fusarium 
Scedosporium
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161
Q

Give some examples of basidiomycota

A

Cryptococcus

Trichosporon

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162
Q

Give an example of mucormycota

A

Zygomycetes

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163
Q

What is the aim of selective toxicity antimicrobial drug therapy

A

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

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164
Q

What qualities are required in selecting an antimicrobial target

A
  1. Target doesn’t exist in humans
  2. Target is significantly different to human analogue
  3. Drug is concentrated in organism cell with respect to humans
  4. Increased permeability to the compound
  5. Modification of the compound in the organism or human cellular compartment
  6. Human cells are rescued from toxicity by alternative metabolic pathways
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165
Q

Instead of cholesterol, the major component of a fungal plasma membrane Is what?

A

Ergosterol

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166
Q

Flucytosine targets what

A

Fungal DNA synthesis

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167
Q

Echinocandins target what?

A

Cell wall

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168
Q

Amphotericin, azole and terbinafine target what?

A

Ergosterol plasma membrane and causes pore formation leading to cell death

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169
Q

What molecules exist in fungal cells that do not exist in human cells that make them good antimicrobial targets

A

Ergosterol
Mannoproteins
Glucan
Chitin

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170
Q

Amphotericin is what class of antimicrobial

A

Polyene

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171
Q

What is the mechanism of action of amphotericin

A

forms pores in the ergosterol component of the plasma membrane - fungicidal

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172
Q

What are some of the side effects of amphotericin

A

Nephrotoxicity

Distal renal tubule acidosis

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173
Q

Terbinafine is what class of antimicrobial

A

Allylamine

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174
Q

What is the mechanism of action of terbinafine

A

Fungicidal -causes reversible inhibition of squalene epoxidase which is required for the growth of the fungi

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175
Q

What is the mechanism of action of azoles

A

Dose dependent inhibitors of 14a-sterol demethylase which is an important intermediate in the ergosterol production pathway

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176
Q

Clotrimazole and ketoconazole are used against what

A

Candida

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177
Q

Fluconazole is used against what

A

Cryptococcus

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178
Q

Itraconazole is used against what

A

Aspergillus and fusarium

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179
Q

Voriconazole is used against what

A

Moulds! mainly invasive aspergillus

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180
Q

Posaconazole and isavuconazole are used against what?

A

Zygomycetes

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181
Q

What is the mechanism of action of echinocandins

A

Inhibit 1,3 B glucan synthesis

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182
Q

What are the echinocandins used against

A

Yeast and moulds

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183
Q

What are three methods of diagnosing fungal disease

A

Microscopy and histology
Culture
Molecular methods and serology

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184
Q

What is onychomycosis?

A

Fungal infection of the nail

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185
Q

What are the treatment options for onychomycosis

A

Topical amorolfine

Systemic itraconazole or terbinafine

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186
Q

what is the most common causative fungi of onychomycosis

A

Trichrophyton rubrum

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187
Q

Name the sorts of individuals that may be susceptible to infection with pneumocystis

A

Moderate to severe immunocompromised patients ie. HIV, steroids and transplant

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188
Q

What is the major difficulty with pneumocystis

A

Unable to culture it

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189
Q

What is the treatment for pneumocystis

A

Co-trimoxazole

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190
Q

Which gram -ve bacteria would you most commonly find to cause meningitis

A

Neisseria meningitidis
Some E.coli
Haemophilus influenza

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191
Q

Which gram -ve bacteria would you most commonly find in to cause sepsis

A

Neisseria meningitidis
E.coli and K. pneumonia
Pseudomonas aeruginosa

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192
Q

Which gram -ve bacteria would you most commonly find as STDs

A

Neisseria gonorrhoea
Chlamydia trachomatis
Treponema pallidum

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193
Q

Which gram -ve bacteria would you most commonly find in wound infections

A

E.coli
Bacteroides fragilis
Pseudomonas aeruginosa

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194
Q

What Is the morphology of proteobacteria

A

All rod shaped bacilli except neisseria (Diplococci) or campylobacter/helicbacter which are spiral

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195
Q

What is the morphology of bacteroides

A

Rod shaped bacilli

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196
Q

What is the morphology of chlamydia

A

Round (elementary bodies)

Pleimorphic (Reticulate bodies)

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197
Q

What is the morphology of spirochetes

A

Spiral/helical

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198
Q

Define a virus

A

An infectious obligate intracellular parasite comprising genetic material surrounded by a protein coat and or a membrane

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199
Q

What is the name given to a virus when it is not inside a cell and what does it consist of

A 
Virion 
Genetic material (DNA and RNA)
Protein Coat (Capsid)
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200
Q

What are the different shapes of virus nucleocapsid (Protein coat of virus and genetic material)

A

Helical
Iscosahedral
Complex

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201
Q

Give an example of a virus with a helical nucleocapsid

A

Influenza

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202
Q

Give an example of a virus with a icosahedral nucleocapsid

A

Adenovirus

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203
Q

What is the size range of human viruses

A

20-260nm in diameter

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204
Q

Do viruses have a cell wall

A

No

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205
Q

Do viruses have organelles

A

No

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206
Q

Are viruses dependent on the host cell

A

No

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207
Q

Are viruses living

A

No

They do not feed or respire and cannot reproduce independently

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208
Q

What are the 5 main stages of virus replication

A
  1. Attachment
    - Attach to specific receptor
  2. Cell entry
    - Virion uncoats outside the cell and only the core contains nucleic acids and replication enzymes are freed into host cell cytoplasm
  3. Host cell interaction and replication
    - Migration of genome to cell nucleus where transcription to mRNA using host materials occurs
    - mRNA translated to produce structural proteins and viral genome
  4. Assembly of virion
    - Occurs in different locations depending on the virus
  5. Release of new virus particles
    - Either bursts out leading to cell death or undergoes a budding/exocytosis process
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209
Q

assembly of the herpes virion occurs where in the cell

A

Nucleus

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210
Q

Assembly of the poliovirus virion occurs where in the cell

A

Cytoplasm

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211
Q

Assembly of the influenza virus occurs where in the cell

A

Cell membrane

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212
Q

Name a disease that bursts out of the host cell causing cell death

A

Rhinovirus

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213
Q

Name a disease that releases new disease particles by budding/exocytosis

A

HIV or influenza

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214
Q

Name the 5 mechanism through which a virus can cause disease

A
  1. Direct destruction of host cells
  2. Modification of the host cell
  3. Over-reactivity of the immune system
  4. Damage through cell proliferation
  5. Evasion of host defences
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215
Q

Name a virus that causes direct destruction of host cells

A

Poliovirus causes host cell lysis and death after viral replication period of 4 hours

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216
Q

Name a virus that modifies the host cell

A

Rotavirus - atrophies villi and flattens epithelial cells which decreases the small intestine surface area so nutrients aren’t absorbed leading to. a hyperosmotic state and profuse diarrhoea

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217
Q

Name a virus that causes over-reactivity of the immune system

A

Hep B and C

HIV

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218
Q

Name a virus that causes damage through cell proliferation

A

Human papilloma virus ie. cervical cancer

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219
Q

Which virus evades host defences through latency

A

Herpesviridae - after primary disease the virus is not detectable but the viral DNA lies latent and can be reactivated at times of Lower immune control
Hep B and C
Measles virus

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220
Q

Which virus evades host defence via cell to cell spread

A

Measles and HIV
Cell to cell spread avoids random release into the environment, increased the speed of spread and avoids the immune system

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221
Q

Which virus evades the host defence through antigenic variability

A

Influenza, HIV and Rhinovirus

- have ability to change the surface antigens in order to evade the hosts immune system

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222
Q

Which virus evades the host defence through prevention of host cell apoptosis

A

Herpesviridae
- in response to viral infection, cells undergo apoptosis which reduces further viral spread - preventing host cell apoptosis allows virus to continue to replicate so more virus is produced

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223
Q

Which virus evades host defence by interfering with host cell antigen processing pathways

A

Herpesviridae
Measles
HIV

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224
Q

Why do viruses vary in the range of clinical syndromes they can cause

A

Different host cells and tissues they can infect

Different method of interaction with the host cell

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225
Q

What are protozoa

A

Single cell eukaryotes

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226
Q

What are the 5 types of protozoa

A 
Flagellates (Flagella)
Sporozoans (Non-motile)
Amoebae (Pseudopodia)
Ciliates (Cilia)
Microsporidia
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227
Q

Name 4 types of flagellate

A

Trypanosoma (Sleeping sickness)
Trichromonas vaginalis (STI)
Leishmania Spp
Giardia lamblia

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228
Q

Name 3 types of sporozoans

A

Plasmodium (Malaria)
Toxoplasma gondii (Toxoplasmosis)
Cryptosporoidium

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229
Q

Name a type of Amoebae

A

Entamoeba histolytica

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230
Q

Name a type of ciliate

A

Balatidium coli

231
Q

What are the two species of African trypanosomiasis

A

Trypanosoma brucei gambiense (Central/West Africa)

Trypanosoma brucei rhodesiense (East Africa)

232
Q

How is the African trypanosomiasis transmitted

A

By the bite of the Tsetse fly

233
Q

What are the symptoms associated with African trypanosomiasis

A

Flu like symptoms followed by CNS involvement (Sleepiness, extreme fatigue, chancre, confusion, and personality changes) leading to coma and death

234
Q

How do we diagnose African trypanosomiasis

A

Visualise trypomastigotes on microscopy of blood or CSF

235
Q

What is American Trypanosomiasis known as

A

Chagas disease

236
Q

What is the cause of American trypanosomiasis

A

Trypanosoma Cruzi

237
Q

Where is American trypanosomiasis found mainly

A

Central and South America

238
Q

How is American trypanosomiasis transmitted

A

Triatomine bug

239
Q

What are the symptoms of American trypanosomiasis

A

Acute flu like syndrome (Romana’s sign)
Cardiomyopathy
Megaoesophagus
Megacolon

240
Q

Leishmaniasis is spread by what

A

Bite of the sandfly

241
Q

Where is leishmaniasis found

A

Disease of poverty in Africa, Asia and South America

242
Q

How is leishmaniasis found

A

Diagnosed through biopsy and serology

243
Q

What are the three clinical manifestations of Leishmaniasis

A

Cutaneous
Mucocutaneous
Visceral (Kala Azar)

244
Q

What are the cutaneous manifestations of Leishmaniasis

A

Ulcers on the exposed parts of the body including face, arms and legs

Creates issues with social rejection and scarring

245
Q

What are the mucocutaneous manifestations of Leishmaniasis

A

Lesions that cause destruction to the mucous membranes of the nose, mouth and throat

Can lead to pneumonias and sepsis

246
Q

What are the visceral manifestations of Leishmaniasis

A

Affects the internal organs and is characterised by irregular bouts of fever, weigh loss, swelling of the spleen and liver and anaemia

Has an incredibly high fatality rate if not treated

247
Q

What are the symptoms of trichomonas vaginalis in women

A

Dysuria
Yellow frothy discharge
Abdominal pain
Vulvar and cervical lesions

248
Q

What are the symptoms of trichromonas vaginalis

A

Urethritis
Epididymitis
Prostatitis
Can be asymptomatic in males though

249
Q

What is the treatment for trichromonas vaginalis

A

Metronidazole

250
Q

Giardiassis is caused by what

A

Giardia lamblia

251
Q

How is giardiassis spread

A

Faeco-oral spread

252
Q

What are the symptoms of giardiassis

A 
Diarrhoea 
Cramps 
Bloating 
Flatulence 
Recent travel 
Childcare
253
Q

How might we identify giardiassis

A

Trophozoites/cysts seen in the stool

254
Q

What is the treatment for giardiassis

A

Treat with metronidazole and tinidazole

255
Q

What is amoebiasis caused by

A

Entaemoeba histolytica

256
Q

Where are entamoeba histolytic commonly found

A

In the gut

257
Q

How is entamoeba histolytica spread>

A

Faeco-orally
Ingestion of mature cysts faeceally contaminated water and food - cysts travel from the small intestine where they release trophozoites which travel to the large intestine where they invade the intestinal wall

258
Q

What are the symptoms of entamoeba histolytica

A

Dysentry
Colitis
Liver and lung abscesses
Trophozoites/cysts seen in stool

259
Q

How do you treat entamoeba histolytica

A

Metronidazole

260
Q

Which protozoa cause cryptosporidosis

A

Cryptosporidium

261
Q

How is cryptosporidium spread

A

Waterborne - transmitted via contaminated food/water - ingestion of cysts

262
Q

What are the symptoms of cryptosporidosis

A 
Diarrhoea (watery with no blood)
Vomiting 
Fever 
Weight loss 
Oocytes seen in the stool
263
Q

How do we diagnose cryptosporidosis

A

Acid-fast staining

Immunofluorescent

264
Q

How do we treat cryptosporidosis

A

Treat with hydration and replacement of electrolytes

265
Q

What is the cause of toxoplasmosis

A

Toxoplasma gondii

266
Q

How is toxoplasmosis spread

A

Ingestion of contaminated food (Meat and shellfish) and water/feline faeces

267
Q

Toxoplasmosis can cause

A

Disseminated disease
Toxoplasma encephalitis
Chorioretinitis

268
Q

What are the effects of toxoplasmosis

A

Severe consequences in pregnancy and immunodeficient patients

269
Q

How can we identify toxoplasmosis

A

Produces ring enhancing lesions on the brain CT

270
Q

Why is the prevalence of malaria increasing

A
  1. Increasing resistance of parasite to antimalarials
  2. Increasing resistance of mosquito to insecticides
  3. Ecological and climate change
  4. Increased travel to endemic areas
271
Q

What are the 5 malaria causing plasmodium

A 
Falciparum 
Ovale 
Vivax 
Malariae 
Knowlesi (Very rare)
272
Q

What is the vector of malaria

A

Female anopheles mosquito around stagnant water

273
Q

What is the life cycle of malaria

A

3-4 weeks

274
Q

How do you diagnose malaria

A

Using a blood film and microscopy to identify trophozoite

275
Q

Describe the life cycle of the mosquito

A
  1. Exo-erythrocytic
    - Mosquito injects plasmodium (Sporozoites) into human from salivary gland
    - Sporozoites travel in blood to liver hepatocytes
    - Sporozoites replicate asexually in hepatocytes to form merozoites which replicate to form Schizont
    - Schizont ruptures and merozoites enter bloodstream and infect RBCs

Plasmodium ovale and vivax can lie dormant in the hepatocytes and reactivate later (Hypnozoite stage)

  1. Endo-Erythrocytic cycle
    - Merozoites infect RBC and mature to trophozoites which forms a Schizont which ruptures and releases merozoites (Causes clinical manifestations)
    - Some trophozoites become male and female gametocytes which are ingested by another unaffected mosquito during a meal
  2. Mosquito Stage
    - Male and female gametocytes fuse to form a zygote which forms and ookinete and oocyst which ruptures and releases sporozoite which collects in the salivary gland
276
Q

What are the clinical features of malaria

A

Fever, chills, sweats, headaches, myalgia, fatigue, nausea, diarrhoea, vomiting and abdominal pain

277
Q

What are the signs of malaria

A 
Anaemia 
Jaundice 
Hepatosplenomegaly 
Haemoglobinuria 
Monocytosis and lymphopenia 
Thrombocytopenia
278
Q

Describe the pathology of malaria

A
  1. Spleen kills damaged RBCs with macrophages phagocytosing infected RBCs
  2. This can cause ANAEMIA and pro-inflammatory cytokine release (TNFa and IL-1B)
  3. Macrophages release interferon gamma which affects blood vessels as parasites causes RBCs to express a surface protein and interferon gamma causes expression of adhesion molecules on endothelial cells
  4. if infected RBC adheres to adhesion molecule it triggers coagulation and forms a ROSETTE causing tissue inflammation and obstruction leading to tissue hypoxia
279
Q

How do you diagnose malaria

A

Anaemia
Hyperbilirubinaemia
Blood films
Light microscopy

280
Q

What are the affects of malaria in the brain

A

Rosettes blocks the brain circulation leading to tissue hypoxia

Vascular occlusion and hypoglycaemia leads to raised intra-cranial pressure, seizures, coma, drowsiness and death =
CEREBRAL MALARIA

281
Q

What are the affects of malaria on the lungs

A

Vascular occlusion, anaemia, lactic acidosis and increased vascular permeability lead to shortness of breath, hypoxia and pulmonary oedema =

ACUTE RESPIRATORY DISTRESS SYNDROME

282
Q

What are the affects of malaria on the kidneys

A

Vascular occlusion, dehydration leads to decreased blood pressure, haemoglobinuria, proteinuria, fatigue =

RENAL FAILURE and METABOLIC ACIDOSIS

283
Q

Malaria induced thrombocytopenia causes what

A

Activation of coagulation cascade leads to disseminated intravascular coagulation, anaemia and bleeding

284
Q

What are the clinical features of malaria in adults

A 
Coma 
ARDs
Hypoglycaemia 
Renal failure 
Shock
285
Q

What are the clinical features of malaria in children

A

Tachypnoea
Acidosis
Anaemia
Hypoglycaemia

286
Q

Which malaria plasmodium causes complicated malaria

A

Plasmodium falciparum

287
Q

What is the treatment for complicated falciparum malaria

A

IV artesunate (Quinine and doxycycline)

288
Q

What is the treatment for normal falciparum malaria

A

Oral riamet or oral quinine and doxycycline

289
Q

What is the treatment for non-falciparum malaria

A

Oral chloroquine

290
Q

What is the treatment for vivax and ovale malaria

A

Primaquine for hypnozoite clearance to eliminate them from the liver

291
Q

What treatment might be given to an individual suffering cerebral malaria induced seizures

A

Anti-epileptics

292
Q

What treatment might be given to someone with malaria induced ARDs

A

Oxygen
Diuretics
Ventilation

293
Q

What treatment might be given to someone with malaria induced renal failure

A

Fluids and dialysis

294
Q

What treatment might be given to someone with malaria induced sepsis

A

Broad spectrum antibiotics

295
Q

What is the treatment is given to someone with malaria induced anaemia

A

Blood products

296
Q

What are the key attributes of a pathogen

A
  1. Infectivity = ability of to become established in host which involves adherence and immune escape
  2. Virulence = ability to cause disease once established
  3. Invasiveness = capacity to penetrate mucosal surfaces to reach normal sterile sites
297
Q

What does a primary pathogen do?

A

Causes disease in a proportion of exposed individuals irrespective of immunological status

298
Q

Define microbiome

A

Describes the totality of micro-organisms, their genetic elements and their environmental interactions in an environment

299
Q

What does a viral infection require to be effective?

A

Need rapid cell entrance to avoid the immune response as free virus in the blood stream is easily neutralised

300
Q

What is the humoral response to a viral infection

A

IgA blocks viral binding so cant gain entry or inject genetic material into cells

IgM aids agglutination

Complement causes opsonisation, cell lysis and neutralise toxins

301
Q

What is the cell mediated response to a viral infection

A

Interferon = prevents infection of non-infected cell through production of anti-viral protein DAI

Cytotoxic T lymphocytes directly kill infected cells

Natural Killer cells and macrophages activate the antibody dependent cell destruction

302
Q

What are the virulence factors of viral infection

A

Direct cell cytotoxicity

303
Q

Give some examples of viral infection direct cell cytotoxicity

A 
Resp epithelium (Influenza)
Skin (Shingles and varicella zoster virus)
T cells (HIV)
Yellow fever (liver cells)
304
Q

Give some examples of how viral infections evade the host defence

A

Adenovirus and EBV block DAI

HSV binds to C3b and inhibits classic and alternate complement

Rhinovirus, HIV and Influenza cause antigenic variation

HIV, MMR and EBV cause immune suppression

305
Q

What are the two forms of antigenic variation

A

Antigenic Drift - spontaneous mutations occurs gradually producing changes in haemagglutinin and neuramidase (Epidemic)

Antigenic Shift - sudden emergence of new subtype different to that of the preceding virus (Pandemic)

306
Q

Where does a bacterial infection enter the host

A

GIT, GUT or wound

307
Q

What is the response to low number of virulence factors

A

Phagocytes

308
Q

What is the response to high number of factors

A

Cell mediated immunity

309
Q

What is the response to extracellular bacteria

A

antibody response

310
Q

What is the response to intracellular bacteria

A

Cellular response

311
Q

What factors are important for colonisation

A

Adhesins and biofilms

312
Q

How do bacteria compete with host cells

A

Sequestering nutrients
using novel metabolic pathways
Out competing other micro-organisms

313
Q

What do adhesins do and what are some examples

A

Help bacteria bind to mucosal surfaces

  • Fimbriae and pili filamentous proteins
  • Non fibril proteins
  • lipids
  • glycosaminoglycans
  • Lectins of viruses and parasites
314
Q

Whats a biofilm

A

bacteria can stick to a surface by secreting an extracellular polymeric substance of protein,polysaccharides and DNA

Helps protect against antimicrobials

315
Q

What is the immune response to bacterial infection

A

Antibodies to neutralise toxins, block host cell attachment (IgA)

complement to cell lyse, opsonisation and proliferation prevention

316
Q

How does Neisseria gonorrhoea evade the host defence

A

Secretes proteases that lyse IgA

317
Q

How does B pertussis evade the host defence

A

Secretes adhesion molecules

318
Q

How does S.pneumoniae evade the host defence

A

Polysaccharide capsule that prevents phagocytosis

319
Q

How does streptococci pyogenes evade the host defence

A

Release M protein that inhibits phagocytosis

320
Q

How does staphylococci evade the host defence

A

Produces coagulase that form fibrin close around organism thus protecting it

321
Q

How does pseudomonas evade host defence

A

Secrete elastase that inhibit C3a and C5a which normally attract neutrophils to site of inflammation

322
Q

How does mycobacterium evade the host defence

A

Escape from phagolysosome and live in cytoplasm

323
Q

Protozoa in the blood triggers what

A

Humoral immunity

324
Q

Protozoa in the tissue triggers what

A

Cell mediated immunity

325
Q

How does protozoa evade defence

A

Surface antigen variability
Intracellular phase
Shed outer coat

326
Q

Do worms multiple in humans

A

NO - form eggs

327
Q

Is the immune response sufficient to kill worms

A

No

328
Q

What is the immune response to killing worms

A

IgG and IgE produced
IL5- eosinophil production
IL3- Mast cell growth
Eosinophilic basic protein toxic to worms

329
Q

How do worms evade host defences

A

Adult worms demonstrate decreased antigen expression

Glycolipid coat is host derived utilising host self-antigens so not perceived as foreign to the immune system

330
Q

Describe results of inflammation

A 
Up regulation of adhesion molecules 
Chemotaxis 
Degranulation 
Vascular permeability 
Vasodilation
331
Q

Define antibiotic

A

Molecule that binds to bacteria target site and affects reactions critical to bacterial survival

332
Q

What are the different types of antimicrobials

A 
Antifungals 
Antibacterials 
Antihelminthic 
Antiprotozoal 
Antivirals
333
Q

What do we use antibiotics for

A

Treatment
Prophylaxis
Prevention of post surgical infection

334
Q

Name different types of beta-lactam

A 
Penicillins 
Cephalosporins 
Carbapenems 
Glycopeptides 
Vancomycin
Monobactams
335
Q

What is the mode of action of beta lactams

A

Bind to peptidoglycan penicillin binding proteins which inhibits cell wall synthesis

336
Q

What is the mode of action of metronidazole and rifampicin

A

Interfere with nucleic acid synthesis or function

337
Q

What is the mode of action of fluroquinolones

A

Inhibit DNA gyrase (Essential for bacterial DNA replication)

338
Q

What is mode of action of aminoglycosides, tetracyclines, macrolides and chloramphenicol

A

Inhibit ribosomal activity and protein synthesis

339
Q

What is the mode of action of sulphonamides and trimethoprim

A

Inhibit folate synthesis - required for bacteria to grow since folic acid cannot cross the bacteria cell wall

340
Q

What are the two different types of antibiotics

A

Bacteriostatic

Bactericidal

341
Q

How do bacteriostatic bacteria work

A

Inhibit bacterial growth but don’t necessarily kill - inhibits protein synthesis, DNA replication and metabolism

342
Q

How do bactericidal bacteria work

A

Kill bacteria

Inhibit cell wall synthesis

343
Q

When are bactericidal bacteria useful

A

Poor tissue penetration (Endocarditis)
Difficult to treat infections (TB)
Need to eradicate the infection quickly (Meningitis)

344
Q

What are the two major determinant of anti-bacterial effects

A

Concentration of antibiotic

Time the antibiotic remains on these sites

345
Q

What is concentration dependent killing and give an example

A

Knock out punch - eradicate pathogenic bacteria by acheiving high concentrations at site of binding

How high the concentration is above the lowest minimal inhibitory concentration

Aminoglycosides and Quinolones use this mechanism

346
Q

What is time dependent killing and give some examples

A

Sustained killing

Time that the serum concentration remains above the lowest minimal inhibitory concentration during the dosing interval

Beta-lactams, clindamycin, macrolides, oxazolidinones

347
Q

What considerations need to made to safely prescribe antibiotics to a patient

A 
Intolerance, allergy and anaphylaxis 
Side effects
Age 
Renal and liver function 
Pregnancy and breast feeding 
Drug interactions 
Risk of clostridium difficile
348
Q

How do bacteria resist antibiotics

A
  1. Change antibiotic target or mask it
  2. Destroy antibiotic
  3. Prevent antibiotic access
  4. Remove antibiotic from bacteria
349
Q

How do bacteria change antibiotic targets

A

change the molecular configuration of antibiotic site or mask it
- Flucloxacillin no longer able to bind PBP of staphylococci (MRSA)

350
Q

How do bacteria destroy antibiotics

A

Beta lactam ring of penicillins and cephalosporins can be hydrolysed by bacteria enzyme beta lactamase which means they are unable to bind penicillin binding proteins and inhibit cell wall synthesis

351
Q

How do bacteria prevent antibiotic entry

A

Bacteria modify its bacterial membrane porin channel size, numbers or selectivity

352
Q

How do bacteria remove antibiotic from bacterium

A

Proteins in the bacterial membrane can export or efflux so antibiotic pumped out the bacteria resulting in reduced levels so effect of antibiotic on bacteria is reduced

353
Q

What are the two ways that bacterial antibiotic resistance develop

A

Intrinsic natural resistance
Acquired resistance (2 types)
- Spontaneous gene mutation
- Horizontal gene transfer

354
Q

Describe intrinsic natural resistance and give examples

A

All subpopulation of species will be equally resistant

Aerobic bacteria are unable to reduce metronidazole to its active form so antibiotic is harmless

Anaerobic bacteria lack oxidative metabolism required to uptake aminoglycosides

Vancomycin is not taken up by gram negative bacteria because it is too large to penetrate the outer membrane

355
Q

Describe acquired bacterial antibiotic resistance

A

A bacterium that was previously susceptible obtains the ability to resist the activity of a particular antibiotic

356
Q

Describe the different types of spontaneous gene mutations that can cause bacterial resistance

A

New nucleotide base pair
Change in AA sequence
Change to enzyme or cell structure
Reduced affinity or activity of antibiotic

357
Q

What are the three different methods of horizontal gene transfer that can cause antibiotic resistance

A
  1. Conjugation = sharing extra chromosomal DNA plasmids (bacterial sex)
  2. Transduction = insertion of DNA by bacteriophage
  3. Transformation = Picking up naked DNA
358
Q

Name two different gram positive antibiotic resistant bacteria

A

Methicillin resistant staphylococcus Aureus (MRSA)

Vancomycin resistant enterococci

359
Q

Name three different gram negative antibiotic resistant bacteria

A

B-lactamases
Extended Spectrum Beta Lactamase
AmpC
Carbapenems resistant enterobacteria

360
Q

When are cephalosporins used

A

Penicillin allergies
Resistant bugs
Bacteria in hard to reach places (meningitis)

361
Q

What antibiotics are used for gram positive bacteria

A

Beta lactams to target peptidoglycan

362
Q

Skin infections caused by staphylococcus aureus and Group A, C and G strep need what antibiotic

A

Flucoxacillin

363
Q

Chest infections caused by streptococcus are treated by what antibiotic

A

PO amoxicillin

IV Benzylpenicillin

364
Q

Throat infections caused by group A, C and G streptococcus are caused by

A

PO penicillin V

IV Benzylpenicillin

365
Q

Why are beta lactams less effective for gram negative bacteria

A

Gram negative have a thinner cell wall so therefore require a different weapon

366
Q

Urine infections are caused by what bacteria

A

Escherichia coli
Klebsiella Sp
Proteus Sp

367
Q

Gallbladder infections are caused by

A

Escherichia coli
Klebsiella Sp
Proteus Sp

368
Q

Abdominal infections are caused by

A

Escherichia coli
Klebsiella Sp
Proteus Sp

369
Q

Infectious diarrhoea is caused by

A

Shigella and salmonella

370
Q

Vancomycin and teicoplanin are what type of antibiotic

A

Glycopeptides

371
Q

When are glycopeptides required

A

Only gram + ve bacteria
MRSA
Penicillin allergies

372
Q

What modes of action do antibiotics have

A 
Inhibitors of cell wall synthesis 
Inhibitors of protein synthesis 
Inhibitors of nucleic acid synthesis 
Anti-metabolites 
Inhibitors of membrane function
373
Q

Clarithromycin and erythromycin are what sort of antibiotic

A

Macrolides

374
Q

When would you use a macrolide antibiotics

A

Gram +ve (S.aureus, B-haemolytic strep, atypical pneumonia)
Penicillin allergies
MRSA

375
Q

Give an example of a lincosamide antibiotic

A

Clindamycin

376
Q

When would you use a lincosamide antibiotic

A 
Gram +ve 
Anaerobic cellulitis 
Penicillin Allergy 
Necrotising Fasciitis 
MRSA
377
Q

Give an example of a tetracycline antibiotic

A

Doxycycline

378
Q

When might you give a tetracycline antibiotic

A

Cellulitis
Broad spectrum mainly used for gram +ve
Penicillin allergy
Chest infection (Pneumonia)

379
Q

Give an example of a quinolone antibiotic

A

Ciprofloxacin

380
Q

When might one give a quinolone antibiotic

A 
Gram -ve specific 
Affects DNA synthesis 
UTIs 
Gall bladder 
Abdominal infections
381
Q

Give one example of an aminoglycoside antibiotic

A

Gentamicin

382
Q

When might one give an amino glycoside antibiotic

A

Gram -ve bacteria and staphs

used in UTIs and infective endocarditis

383
Q

When might you give trimethoprim

A

Gram -ve bacteria
Folate antagonist
UTIs
Broad spectrum

384
Q

When might you give nitrofurantoin

A

Gram -ve and gram +ve

Used as frontline for UTIs

385
Q

What are the mycobacteria of medical importance

A 
M.Tuberculosis 
M.Leprae (Leprosy)
M.Avium Complex (MAC) -disseminated infections in AIDs
M.Kansasii (Chronic lung infection)
M.Marinum (Fish tank granuloma)
M.Ulcerans (Buruli ulcer)
386
Q

Describe the microbiology of mycobacteria

A 
Aerobic
Non-motile 
Non-spore forming 
Slow growing
Survive in macrophages even in low pH
387
Q

What does the cell wall of mycobacteria contain

A

Mycolic acids
Lipoarabinomannan
Make up a strong waxy cell wall that is hard for the immune system to target/damage

388
Q

Why are mycobacteria resistant to the gram stain

A

High lipid content within the cell wall makes mycobacteria resistant to the gram stain

389
Q

What stain is used for Acid fast bacilli/rods

A

Ziehl-Neelsen stain

390
Q

Describe the immunology of mycobacterial disease

A
  1. Mycobacteria are phagocytosed and placed in a phagolysosome
  2. Bacteria are adapted to intracellular environment and withstand phagolysosomal killings and escape to the cytosol
  3. Host aims to kill the mycobacterium using microbial molecules
  4. Acidification aids digestion by degradation by proteases of the mycobacteria which results in generation of antigens for presentation of T cells
  5. CD4-T cells generate interferon gamma which activates intracellular killing by macrophages
  6. IL-12 release by macrophages further stimulates generation of T helper cells and interferon gamma release
391
Q

What increases susceptibility to mycobacterial infection

A

Genetic defects in interferon gamma or IL-12 receptors or elements of their signalling pathways

392
Q

What are granulomas

A

Lesions that arise in a response that tries to contain mycobacteria

393
Q

How do granulomas form in the case of mycobacteria

A
  1. Highly stimulated macrophages become epithelioid cells
  2. Some macrophages fuse with each other to form giant multinucleated cells (Langahans giant cells)
  3. T Collins including CD8 T cells infiltrate mycobacterial lesion
  4. Fibroblasts laid down around granuloma wall off
  5. Central tissues may necrose an form a caseating granuloma
394
Q

describe tuberculoid leprosy

A

TH1 response (IFN and TNF) –> Tissue hypersensitivity + granulomas = tissue damage

395
Q

Describe Lepramatous leprosy

A

TH2 response (IL 4,5,10) –> Lesions full of bacilli + No granuloma –> Skin lesions

396
Q

What are the treatments for mycobacterium

A

Isoniazid
Rifampicin
Pyrazinamide
Ethambutol

397
Q

What is the name of the skin test for tuberculosis

A

Tuberculin Skin Test (Mantoux test)

398
Q

What occurs in primary tuberculosis

A

Bacilli settle in apex and granulomas forms

Bacilli taken in lymphatics to hilarious lymph nodes

in apex of lungs there is more air and less blood supply so fewer defending white cells to fight off infection

Granuloma + Lymphatics + Lymph nodes = primary complex

399
Q

What occurs in latent tuberculosis

A

Cell mediated immune response from T cells

Primary infection is contained by CMI persists

No clinical disease

Detectable CMI to TB n tuberculin skin test

400
Q

What occurs in pulmonary tuberculosis

A

Occurs immediately following primary disease or after latent reactivation

Necrosis in the lesion

TB may spread in lung causing other lesions

401
Q

Where can TB spread beyond the lungs

A 
TB meningitis 
Miliary TB (widespread dissemination an tiny spotted lesions all over the lungs)
Pleural TB 
Bone and Joint TB
Genitourinary TB
402
Q

What type of organism would you stain with ziehl Nielsen

A

Mycobacteria ie. TB

403
Q

How do you apply the gram stain

A

Apply crystal violet to heat fixed bacteria
Treat with iodine
Decolourise the sample and counterstain

404
Q

Give an example of a slow growing bacteria

A

TB

405
Q

Give an example of a fast growing bacteria

A

E.coli and S.aureus

406
Q

Give two functions of pilli

A
  1. Help adhere to cell surfaces

2. Plasmid exchange

407
Q

What is the primary function of flagella

A

Locomotion

408
Q

What is the primary function of the polysaccharide capsule

A

Protection - prevents MAC or opsonisation molecules attacking

409
Q

What types of bacteria release endotoxin

A

Gram -ve

410
Q

What types of bacteria release exotoxin

A

Gram -ve and gram +ve

411
Q

What are exotoxins made from

A

Proteins

412
Q

How would you describe the arrangement of staphylococci

A

Clusters of cocci

413
Q

How would describe the arrangement of streptococci

A

Chains of cocci

414
Q

what test can be done to distinguish between different streptococci

A

Blood agar haemolysis

415
Q

What further test can be done for streptococci in the B-haemolysis group

A

Serogrouping - detecting the surface antigens ie. Lancefield grouping

416
Q

What would you see on the agar plate in gamma haemolysis and give an example of bacteria in this group

A

gamme haemolysis when there is no haemolysis

ie. Streptococcus Bovis falls in this group

417
Q

What kind of bacteria is MacConkey agar used with

A

Gram negative bacilli

418
Q

What is MacConkey agar

A

Contains bile salts, lactose and pH indicator - if an organism ferments lactose, lactic acid will be produced and the agar will appear a red/pink colour

419
Q

Name two gram negative bacilli that will produce a positive result with MacConkey agar

A

E.coli

Klebsiella Pneumoniae

420
Q

Where in the body might you find staphylococci

A

Nose and skin

421
Q

How is staphylococcus aureus spread

A

Aerosol and touch

422
Q

How is C.diptheriae spread

A

Droplet spread

423
Q

Does shigella have a H antigen

A

Shigella is non motile and doesn’t have flagellum - therefore doesn’t have a H antigen

424
Q

Does shigella produce a positive result with MacConkey agar

A

No - shigella does not ferment lactose and gives a negative result

425
Q

Does salmonella have a H antigen

A

Salmonella is motile and has a flagellum - therefore does not give a H antigen

426
Q

Does Salmonella give a positive result with MacConkey agar

A

No - does not ferment the lactose so gives a negative result

427
Q

Does E.coli have a H antigen

A

E.coli Is motile nd has a flagellum so it does have a H antigen

428
Q

Does E.coli give a positive result with MacConkey agar

A

Yes E.coli ferments lactose and so a red/pink colour would be seen giving a positive result

429
Q

How can you distinguish between gram negative bacilli

A

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

430
Q

Shigella is acid tolerant - why is this advantageous for the shigella

A

Means shigella can pass through the stomach without being destroyed by low gastric pH - can then move into the intestine

431
Q

How would you grow haemophilus influenzae

A

On chocolate agar as it requires haem and NAD

432
Q

Who might be susceptible to infection by legionella

A

Immunocompromised patients

433
Q

Describe the pathogenesis of N.meningitidis

A

crosses nasopharyngeal epithelium and enters the blood stream, can cause asymptomatic bacteraemia or septicaemia - if crosses the BBB can cause meningitis

434
Q

Describe bacterioides

A

opportunistic, obligate anaerobes

435
Q

Can you grow chlamydia on agar

A

No because it is an obligate intracellular parasite

436
Q

How can you detect chlamydia

A

Serum antibodies and PCR

437
Q

Describe the flagellum of a spirochete

A

Have an endoflagellum that lies between the inner and outer membrane

438
Q

Name the spirochaete that is responsible for causing lyme disease

A

B. Burgdoferi

439
Q

Name the spirochaete that is responsible for causing syphilis

A

T.pallidum

440
Q

What are dimorphic fungi

A

Fungi that can exist both as yeast and as mould - they are yeast in tissues but mould in vitro

441
Q

Give an example of a dimorphic fungi

A

Coccidioides Immitis

442
Q

Name three common fungal infections

A

Nappy rash
Tinea Pedis
Onychomycosis

443
Q

name a drug that is used in the treatment of onychomycosis

A

Terbinafine - good at reaching poorly perfused areas

444
Q

What can antifungal treatments target

A
  1. Fungal cell wall which contains polyssacharides and chitin
  2. Ergosterol containing plasma membrane
445
Q

Give 4 disadvantages of azoles

A
  1. High first pass metabolism
  2. ADRs - cause hepatitis
  3. Drug interactions due to CYP450
  4. Resistance can develop ie. in candida
446
Q

What is candida

A

A yeast that grows in warm moist areas and has high levels of B-D-glucan

447
Q

What test can be done to identify fungal antigens

A

B-D-glucan test

448
Q

Give an example of a mould

A

Aspergillus fumigatus

Aspergillus Niger

449
Q

What are moulds composed of

A

Branched filamentous filaments called hyphae

450
Q

Why is it hard to use therapeutic antibodies against mycobacteria

A

Mycobacteria grow very slowly and so treatment with antibodies is difficult and it is hard to culture them

451
Q

How can you detect whether an individual has had previous exposure to Tb

A
  1. Tuberculin skin test (Mantoux)

2. Interferon gamma release assay

452
Q

Name 6 sterile sites in the body

A 
Urinary tract 
CSF
Pleural fluid 
Peritoneal cavity 
Blood 
Lower respiratory tract
453
Q

Where in the body would you find normal flora (Commensals)

A 
Mouth 
Skin 
Vagina 
Urethra 
Large intestine
454
Q

Which lance field groups are associated with tonsillitis and skin infection

A

A, C and G

455
Q

Which lance field groups are associated with neonatal sepsis and meningitis

A

B

456
Q

Which lance field groups are associated with UTIs

A

D

457
Q

What is the oxidase test

A

Detects the presence of cytochrome oxidase in bacteria - positive test is indicated by the disk turning blue

458
Q

Which group of streptococci can cause infective endocarditis

A

Alpha haemolytic streptococci

459
Q

How can you differentiate streptococci pneumoniae from other streptococci

A

Optochin test - Pneumococci are sensitive so clear area would be seen

460
Q

What is the function of bile salts in MacConkey agar

A

inhibit the gram positive bacteria growth

461
Q

What is CLED agar used for

A

It is used to differentiate micro-organisms in urine and can classify lactose fermenters and non-lactose fermenters

462
Q

What is XLD agar used for

A

selective growth medium used to isolate salmonella and shigella

463
Q

Why do bacteria produce coagulase

A

used it as a defence mechanism by clotting the areas of plasma around them thereby resisting phagocytosis

464
Q

What two species of plasmodia genus lie dormant and cause late relapse of malaria

A

P.ovale and P.vivax

465
Q

malaria diagnosis - what can thick and thin films tell you

A

Thick films - sensitive but low resolution - tell if you have malaria

Thin films - tell you the malaria species and the parasite count

466
Q

What genetic consditions can give immunity to malaria

A

Someone with sickle cell anaemia and thalassaemias

467
Q

What part of the virus will enter the host cell

A

Only the viral core carrying nucleic acids will enter the host cell cytoplasm

468
Q

How do viruses interact with host cells

A

Viruses used the cell materials for their replication and they evade host defence mechanisms

469
Q

How can viruses by released from a cell

A
  1. Bursting open = lysis

2. Leaking from the cell over a period of time = exocytosis

470
Q

What are the 5 was a virus can ever host defences

A
  1. Virus persistence or latency
  2. Down regulation of interferons
  3. Virus variability due to gene reassortment or mutation
  4. Prevention of host cell Apoptosis
  5. Viral modulation of host defences
471
Q

Where on the bacteria would penicillin bind

A

Bacteria cell wall

472
Q

What is MIC

A

Minimum inhibitory concentration - lowest concentration of a chemical that prevents bacterial growth

473
Q

Does the lowest MIC mean the best antibiotic

A

No - other considerations are important such as number of binding sites occupied and how long they are occupied for

474
Q

What does a drug need to do to ensure it inhibits metabolic processes

A
  1. Occupy and adequate number of binding sites

2. Occupy these binding sites for a sufficient period of time

475
Q

Amoxiciilin can be given to people infected with which bacteria

A

H.influenzae, enterococci, e.coli, shigella, streptococci etc.

476
Q

A person presents with cellulitis. What antibiotic might you give them?

A

Flucloxacillin - s.pyogenes and staph.aureus are often a cause of cellulitis.

477
Q

What are Carbapenemase producing enterobacteriaceae (CPEs)?

A

Gram negative bacteria that are resistant to broad spectrum antibiotics (carbapenems).

478
Q

What is carbapenemase?

A

An enzyme that hydrolyses carbapenems and confers antibiotic resistance.

479
Q

True or False. Mycobacteria can withstand phagolysosome killing.

A

True. The bacterium has adapted to the intracellular environment can can withstand phagolysosome killing and escape to the cytosol.

480
Q

Is pneumonia caused by pneumocystis jirovecii bacterial or fungal?

A

Fungal!

481
Q

Infection control. What are the five moments of hand hygiene?

A
  1. Before patient contact.
  2. Before aseptic procedure.
  3. After bodily fluid exposure.
  4. After touching a patient.
  5. After touching patient surroundings.
482
Q

Name 6 vaccine preventable diseases that are notifiable.

A
  1. Diptheria.
  2. Measles.
  3. Mumps.
  4. Rubella.
  5. Tetanus.
  6. Whooping cough.
483
Q

What are the disadvantages of polysaccharide vaccines?

A

Protection is not long lasting and the response in children is poor.

484
Q

How can polysaccharide vaccines be improved?

A

Conjugation can help improve immunogenicity.

485
Q

How do live attenuated vaccines work?

A

The organism replicates in the host triggering an immune response. It is important to be aware of the risk of disease in immunocompromised individuals.

486
Q

What antibiotic can be used to kill bacterioides?

A

Bacterioides are gram negative anaerobic bacilli. Metronidazole is the treatment of choice against anaerobes.

487
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. These are probably

  1. Streptococcus pneumoniae
  2. Staphylococcus epidermidis
  3. Viridans Streptococci
  4. Group A streptococci (S. pyogenes)
  5. Neisseria meningitidis
A

Streptococcus Pneumoniae

488
Q

Which of these is a gram negative bacillus that ferments lactose?

  1. Shigella sonnei
  2. Listeria monocytogenes
  3. Neisseria meningitidis
  4. Eschericia coli
  5. Streptococcus pyogenes
A

Eschericia Coli

489
Q

Which is incorrect? Haemophilus influenzae is an important cause of

  1. meningitis in pre-school children
  2. Otitis media
  3. Pharyngitis
  4. Gastroenteritis
  5. Exacerbations of Chronic Obstructive Pulmonary Disease (COPD)
A

Gastroenteritis

490
Q 
Which is a normally sterile site?
The pharynx
The urethra
Cerebrospinal fluid
The lung
Skin
A

CSF

491
Q

Which of these is NOT a means by which viruses cause disease?

  1. direct destruction of host cells
  2. cell proliferation and cell immortalisation
  3. inducing immune system mediated damage
  4. Endotoxin production
  5. modification of host cell structure or function
A

Endotoxin Production

492
Q

When diagnosing viral infections which is not true?

  1. The sample must come from a sterile site
  2. Electron microscopy is rarely used
  3. Use a green swab not a black swab
  4. PCR results take 1-2 days
  5. A detectable IgM in serum may be diagnostic
A

The sample must come from a sterile site

493
Q

Which is most accurate?The HIV virus envelope contains
1. RNA + capsid + DNA polymerase

  1. DNA + capsid + Reverse transcriptase
  2. DNA + p24 + protease
  3. RNA + capsid + reverse transcriptase
A

RNA + Capsid + reverse transcriptase

494
Q

Which pair is correct?
1. Pityriasis versicolor = bacterium

  1. Ringworm = helminth
  2. Aspergillus fumigatus = mycobacterium
  3. Falciparum malariae = fungal
  4. Giardia lamblia = protozoal
A

Giardia lamblia = Protozoal

495
Q

Mycobacteria. Which is not a feature?
1. Resistance to destaining by acid and alcohol

  1. Cell wall contains lipoarabinomannan
  2. They only divide every 20 hours
  3. They cannot withstand phagolysosomal killing
  4. May cause meningitis
A

They cannot withstand phagolysosomal killing

496
Q

Regarding antimicrobial resistance, which is true?
1. it is spread by plasmid mediate gene transfer

  1. spontaneous gene mutations do not occur
  2. MRSA refers to vancomycin resistant S. aureus
  3. Only Mereopenem is effective against all gram negative bacteria
A

MRSA refers to vancomycin resistant S. aureus

497
Q

Antimicrobials. Which paring is incorrect
1. S. pyogenes : can use penicillin

  1. Meropenem : a carbapenem
  2. Glycopeptides : use for MRSA
  3. Co-amoxiclav : contains a Beta-lactamase inhibitor
  4. Cefuroxime : a macrolide
A

Cefuroxime : a macrolide

498
Q

A 21 year old complains of myalgia, sore throat and tiredness. He is febrile and has an enlarged spleen. Which is the best answer?
1. He has sepsis and needs broad spectrum antimicrobial therapy with cefotaxime

  1. A charcoal throat swab will confirm the diagnosis
    Finding atypical lymphocytes on a blood film and a positive EBV IgM in serum would be consistent
  2. PCR on a viral throat swab will confirm the diagnosis
  3. This is a viral upper respiratory tract infection and doesn’t warrant investigation or antimicrobial therapy
A

Finding atypical lymphocytes on a blood film and a positive EBV IgM in serum would be consistent

499
Q

A 34 year old gay man who has had prolonged diarrhoea now presents short of breath with a dry cough and hypoxia. Which is most accurate?

  1. This is bacterial pneumonia caused by pneumocysitis jirovecii.
  2. It is too early for a 4th generation HIV test to be positive
  3. The CD4 T cell count will be between 500 and 750
  4. Even if the HIV test is negative this man has AIDS
  5. With appropriate therapy he has a good prognosis
A

With appropriate therapy he has a good prognosis

500
Q

Which of these does NOT feature in the definition of Sepsis?
1. Temperature >38.3oC or <36oC

  1. Heart rate >90
  2. Systolic blood pressure >130
  3. White Cell count >12
  4. Hypoxia
A

Systolic blood pressure >130

501
Q

What are retroviruses?

A

Enveloped viruses

502
Q

Describe the genetic component of a retrovirus

A

Viral genetic material is RNA which is copied into DNA by reverse transcriptase and incorporated into the host cell to allow gene transcription

503
Q

What is the origin of HIV 1 lentivirus

A

Originates from the simian immunodeficiency viruses chimpanzees

504
Q

What is the origin of HIV2 lentivirus

A

Simian immunodeficiency virus sooty mangabey

505
Q

Describe the structure of HIV

A

Enveloped with GP120 and GP41
Matrix with P17 protein
Protein capsid with p24 protein housing the core enzymes
Viral RNA, reverse transcriptase and integrase

506
Q

What does HIV result in?

A

The death of CD4+ T lymphocytes - replication of the virus within the CD4 T cells leads to their death

507
Q

Describe the pathophysiology of HIV

A
  1. Attachment and entry - gp120 attaches to CD4 receptor and CCR5 co-receptor
  2. Uncoating - Viral capsid enters cell and nucleic acids and enzymes released
  3. Reverse transcriptase - converts RNA to double stranded DNA
  4. Integration - viral integrase integrates viral DNA into host DNA
  5. Transcription - when the cell divides, the viral DNA is transcribed and proteins are produced
  6. Virion assembly - viral RNA and proteins are reassembled to form a new virus
  7. Budding - immature virus leaves the cell through exocytosis and breaks free to undergo more maturation
508
Q

What are the main CD4 T cells affected

A

Memory CD45RO are infected preferentially early on

Naive CD45R cells infected later on

509
Q

What are the main CD4 T cells affected

A

Memory CD45RO are infected preferentially early on

Naive CD45R cells infected later on

510
Q

Describe how the HIV infection works

A
  1. Virus enters the body through mucosa and becomes established in mucosal macrophages or dendritic cells and spreads to other cells
  2. HIV APC’s migrate to the lymph nodes and present to T cells - T cell infection
  3. Infected T cells enter bloodstream = exponential T cell infection rise = viremia
511
Q

What are the mucosal surfaces that viruses infect

A

Vagina/rectal and intestinal

512
Q

Describe the humoral HIV immune response

A

Low numbers of neutralising antibodies due to viral genetic variability

513
Q

Describe the cell mediated HIV immune response

A

CD8 Cytotoxic T lymphocytes cause early reduction in HIV numbers but the immune response is incomplete due to virus escape due to mutations

CD4 lymphocyte numbers are reduced due to the HIV infection - no proliferation

514
Q

What characterises the HIV infection

A

A progressive decline in the number and function of CD4T lymphocytes leading to a susceptibility of disease

515
Q

Name the mechanisms by which CD4 lymphocytes are depleted by the HIV infection

A
  1. CD4 cell death - direct cytotoxicity and premature apoptosis
  2. Decreased T cell production due to infected bone marrow progenitors
  3. Activation induced death
  4. Redistribution
  5. Bystander killing
516
Q

Describe the mechanisms of HIV immune dysfunction

A
  1. CD4 depletion mechanisms
  2. Excessive and innapropriate activation of immune system
  3. Decreased proliferation in response to antigens
  4. Increased activation of CD8 lymphocytes but decreased cytolytic function
  5. Increased B cell activation and decreased proliferation resulting in increased non-specific antibody production but decreased specific antibody production
  6. Decreased function of NK, macrophage and neutrophils
517
Q

Where are the HIV reservoir sites

A

Genital/GIT
CNS
Bone
Macrophages and microglia

518
Q

What is the UNAIDs 90/90/90 principle

A

90% of people with HIV should be diagnosed

90% of diagnosed patients should be on ART

90% of patients on ART should have viral suppressants by 2020

519
Q

Define a late diagnosis of HIV

A

CD4 count below 350 = 10 fold increased in the risk of death in the first year of diagnosis

520
Q

Which groups of people are most likely to be diagnosed late with HIV

A

Women
Older age groups (50+)
Black African ethnicity

521
Q

How Is HIV transmitted

A

Blood
Sexually
Vertically (Mother to child)

522
Q

How can we prevent HIV

A 
Circumcision 
Pre/post-exposure prophylaxis of HIV 
Behaviour (Sex ed, safe sex)
Antiretroviral treatment 
STI control 
Vaccines 
Microbicides 
HIV diagnosis/partner notification 
Screen blood products 
Needle exchange
523
Q

What is the U=U campaign

A

Undetectable = untrabnsmittable
signifies that those who receive effective antiviral therapy and have achieved and maintained an undetectable viral load cannot transmit the virus to a sexual partner

524
Q

What are the effects of the U=U campaign

A

Remove the fear of sexual transmission
Dismantle HIV stigma
Encourage people with HIV to start and stay on treatment
Encourage people to get tested

525
Q

What are the benefits of knowing your HIV status

A 
Access to care 
Reduce vertical transmission 
Reduce sexual transmission
Public health 
Reduction in morbidity and mortality  
Cost effect ie. 
 - Saving on social care
 - prevent lost working days 
- Prevent benefit claims 
- Prevent costs associated with further onward transmission
526
Q

Who gets screened for HIV

A

Clinician triggered tests (Symptoms)
High risk groups
Patient requests
Antenatal screening

527
Q

What are the risk factor for HIV

A

Sexual contact with high risk groups ie. Iv drug users
Multiple sexual partners
Rape in high risk areas
Mother to child transmission

528
Q

What are the general symptoms of HIV

A 
Lymphadenopathy 
Acute rash 
Immune dysfunction 
Glandular fever 
Prolonged episodes of herpes 
Persistent recurrent candidiasis 
unexplained weight loss or night sweats 
Persistent diarrhoea
Increasing shortness of breath and dry cough 
Recurrent bacterial infections (Pneumoccocal pneumonia)
529
Q

How do you test someone for HIV

A
  1. Venous blood sample - detectable 4 weeks after infection

2. HIV point of care tests - pinprick of blood

530
Q

What are the advantages of point of care testing

A

Outreach into community settings
Increase patient choice
Increased access to testing and case detection
Earlier diagnosis in non-healthcare seeking individualls
Reduce risk of complications
Reduce transmission

531
Q

Why do doctors not test for hIV

A
  1. Don’t think of HIV
  2. Underestimate the risk of HIV in their patients
  3. Failure to recognise HIV as modifiable prognostic indicator
  4. Misconception they need pre-test counselling
  5. Misunderstanding of the implications for insurance
  6. Fear of offending the patient
532
Q

Describe what happens to the CD4 count in stages during a HIV infection

A

Acute primary infection = transient immunosuppression where there is a fall then a rise in CD4

Asymptomatic phase where there is progressive loss of CD4+ T cells = poor immunity

Early symptomatic phase - manifestations of clinical features

AIDS

533
Q

Define AIDS

A

CD4 T cell count <200 leading to immune deficiency symptoms and opportunistic infections

Normally takes 5-10 years to reach AIDs status and faster/elderly children with high viral loads

534
Q

Patient with a fever, rash and non-specific symptoms should be test for what?

A

HIV

535
Q

What are the primary HIV infection symptoms

A 
2-4 weeks between infection and symptoms 
Abrupt onset of non-specific symptoms 
Weight loss
Lethargy 
Fever 
Rash
536
Q

A patient with recurrent shingles and candidiasis should be tested for what condition

A

HIV

537
Q

What conditions occur in association or are more frequent with HIV

A

Oral/vaginal candidiasis
Oral hairy leukoplakia
Varicella zooster virus

538
Q

Name some AIDs respiratory conditions

A

Pneumocystis pneumonia
Bacterial pneumonia (Pneumoccocal, H.influenza, S.aureus)
TB
Fungal infections - candidiasis, pneumocystis jiroveci pneumonia (PCP)

539
Q

Name some AIDS CNS conditions

A

CNS lesions = cerebral toxoplasmosis, tuberculoma (Space occupying lesion), primary CNS lesion

Ophthalmic lesions = cytomegalovirus retinitis, choroidal tuberculosis, toxoplasmosis chorioretinitis

Meningitis = cryptococcal, tuberculous, pneumococcal

540
Q

Name some neoplasms associated with AIDS

A

Lymphoma - CD4 count under 100 = non-hodgkins lymphoma or primary CNS lymphoma

Kaposis sarcoma

Cervical Neoplasia

541
Q

What are the treatment options for HIV

A

Reverse transcriptase inhibitors
Protease inhibitors - cant repackage new virus
Fusion inhibitors
HAART

542
Q

Which individuals are most at risk of HIV

A 
Men how have sex with men 
Heterosexual women 
Injecting drug users 
Commercial sex workers 
Heterosexual men 
Truck drivers 
Migrant workers
543
Q

Which age group is most affected by HIV

A

15-24 year olds

544
Q

What are the difficulties in delivering ART in developing countries

A 
Awareness 
Procurment/delivery 
Clinical services (Staff, clinics, testing)
Cost/choice of drugs 
Adherence 
Efficacy 
Co-morbidities
545
Q

What virus can cause shingles

A

Varicella zooster virus

546
Q

Where might one see a shingles rash

A

May appear on the dermatomes but associated with area of tight clothing

547
Q

What laboratory tests may be used to detect viral pathogens

A

PCR

548
Q

Give some signs and symptoms of infective mononucleosis (Glandular fever)

A
  1. reddening, swelling and white patches on tonsils
  2. Swollen lymph nodes
  3. Spleen enlargement
  4. Chills and fever
  5. Cough
  6. Sore throat
  7. Fatigue, malaise, loss of appetite and headache
549
Q

What is the management/treatment of glandular fever

A

Supportive therapy and advise patient to avoid contact sport for 6 weeks in order to avoid splenic rupture

550
Q

What can qPCR detect

A

Presence/absence of DNA/RNA

Can quantify the level of virus in a tissue

551
Q

What are the consequences of infleunza A infection

A

Increased risk of ARDs and secondary bacterial pneumonia - patient will be highly infective

552
Q

What are the markers for HIV in the blood

A

Antigens
Antibodies
HIV RNA

553
Q

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

A

Second test after the window period - window period is time between exposure to HIV infection and the point when the test will give and accurate result - during this time a person can be infected with hIV and be very infectious but still test HIV negative

554
Q

HIV RNA can be detected using RT-PCR - what is this useful for

A

It can quantify the amount of HIV RNA in the blood and so can indicate disease progression and how well the individual is responding to ART

555
Q

What are the three stages of the HIV epidemic

A
  1. Nascent <5% prevalence in risk groups
  2. Concentrated >5% prevalence in one or more risk groups
  3. Generalised >5% prevalence in the general population
556
Q

How does circumcision reduce the sexual transmission of HIV

A

Change in the mucosa - HIV is less able to penetrate due to an increase in keratinisation

557
Q

What are the 4 main phases in the natural history of HIV

A
  1. Acute primary infection
  2. Asymptomatic phase
  3. Early symptomatic HIV
  4. AIDS
558
Q

What are the two markers that are used for monitoring HIV

A
  1. CD4+ count

2. HIV RNA copies (Viral load)

559
Q

What is HIV seroconversion

A

A period of time during which HIV antibodies develop and become detectable - usually takes place within a few weeks of initial infection

560
Q

What are the characteristic signs of pneumocystis pneumonia

A

Decreased CD4+ count
Decreased O2 sats on exertion
Decreased exercise tolerance

561
Q

What is HAART and what does it aim to do?

A

Anti-viral treatment where 3 drugs are taken together - aim is to reduce viral load and increase CD4+ count

562
Q

Chicken pox is caused by what virus

A

Varicella zoster virus

563
Q

What is the primary infection with varicella zoster virus

A

chicken pox

564
Q

What is the second infection with varicella zoster virus

A

Shingles

565
Q

How does the varicella zoster virus enter the body

A

Mucous membranes or if you touch a lesion

566
Q

How long is the symptomatic incubation period for varicella zoster virus

A

7-21 days

567
Q

What are the high risk groups for varicella zoster infection

A 
immunocompromised 
Adults 
Infants 
pregnancy 
Smokers
568
Q

Describe the stages of lesion formation process in chickenpox

A 
Macule (Flat, can see but cant feel)
Papule (See and feel)
Vesicle (Fluid filled)
Pustule (WBC filled)
Crust
569
Q

What are the complications of varicella zoster viral infection

A 
Dehydration 
Haemorrhagic change 
Cerebellar ataxia 
Encephalitis 
Chicken pox pneumonitis 
Skin and soft tissue infections 
Varicella pneumonia
570
Q

Where does the chicken pox virus lie dormant

A

dorsal root or cerebral ganglion for years

571
Q

Describe the pathophysiology of shingles

A

Primary infection moves down sensory neurones - lies dormant in dorsal root
Reduced immune system - localised reactivation affects the dermatome

572
Q

What does parvovirus do

A

Attaches to immature red precursor cells which prevents their maturation and increases the risk of the individual developing anaemia

573
Q

What treatment is used for herpes

A

Acyclovir

Phase 2 (16 decks)

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