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Emily Phase 2a > 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 host defences are compromised

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4
Q

Define virulence/pathogenicity

A

The degree to which a given organism is pathogenic/ causes damage to the host

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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 are the shapes of the two main bacteria?

A

Coccus = round
Bacillus = rod

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7
Q

How can we then divide coccus and bacillus bacteria further?

A

Gram positive (purple)
Gram negative (pink)

And then divide both grams into aerobic and anaerobic

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8
Q

What are different shapes of cocci bacteria?

A

Diplococcus = 2
Chain of cocci (streptococcus)
Cluster of cocci (staphylococcus)

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9
Q

What are different shape of rod bacteria?

A

Chain of rods
Curved rod
Spiral rod

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10
Q

What is Gram positive?

A
  • thicker cell wall made of peptidoglycans
  • single inner plasma cell membrane
  • stain purple (retain stain)
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11
Q

What is gram negative bacteria?

A
  • 2 membranes; inner and outer
  • separated by lipoprotein, periplasmic space and peptidoglycan (thinner layer)
  • stain Pink
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12
Q

Which bacteria do not stain with gram stain?

A
  • acid fast bacilli
    e.g. mycobacteria -> TB
  • use Ziehl-Neelsen stain
    (stain red on blue background)
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13
Q

What environment do bacteria require?

A
  1. Temperature = -800C to 80C
  2. pH = 4-9
  3. Water/desiccation = 2hrs - 3 months
  4. Light = UV
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14
Q

What are the 2 types of bacterial toxins?

A

Endotoxin = component of the outer membrane of bacteria released when bacteria is damaged e.g. lipopolysaccharide in gram neg

Exotoxin = specific secreted proteins of gram postive and negative bacteria

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15
Q

What are the characteristics of endotoxins?

A

composition = lipopolysaccharide
action = non-specific
effect of heat = stable
antigenicity = weak
produced by = LPS- Gram negative
Convertibility to toxoid = No
Toxic to host

An outer membrane component released when bacteria are damaged.

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16
Q

What are the characteristics of exotoxins?

A

composition = protein
action = specific
effect of heat = liable
antigenicity = strong (capacity to bind to products that have adaptive immunity- T cell, antibodies)
produced by = Gram negative & positive
Convertibility to toxoid (toxin that has lost its toxicity) = Yes

Secreted from bacteria.

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17
Q

What types of bacterial genetic variation can occur?

A

Mutation
1. base substitution
2. deletion
3. insertion

Gene transfer (pick up genes from environment)
1. transformation e.g. vis plasmid
2. Transduction e.g. via phage
3. Conjugation e.g. via sex pilus

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18
Q

What is the function of pilli?

A

Or fimbiae (bristle like projections)
- adhere to surfaces + deliver toxins to host

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19
Q

What are the two first classifications of bacteria?

A
  1. Obligate intracellular bacteria (bacteria not grown in a lab)
  2. Bacteria that may be cultured on Artificial media
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20
Q

What are 3 species of obligate intracellular bacteria?

A
  1. Rickettsia
  2. Chlamydia
  3. Coxiella
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21
Q

What are mollicutes bacteria?

A

Bacteria grown on an agar plate with no cell wall

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22
Q

What are 3 types of bacteria grown on artificial media as filaments?

A
  1. Actinomyces
  2. Nocardia
  3. Streptomyces
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23
Q

What are 3 types of bacteria that grow as single cells?

A
  1. Rods
  2. Cocci
  3. Spirochaetes - leptospira, treponema, borrelia
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24
Q

What are 2 types of aerobic gram positive cocci bacteria?

A
  1. Staphylococcus
  2. Streptococcus
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25
Q

How would you describe the arrangement of staphylococci?

A

Clusters of cocci

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26
Q

How would you describe the arrangement of streptococci?

A

Chains of cocci

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27
Q

Which parts of the body are exposed to bacteria?

A
  • mouth
  • esophagus
  • stomach
  • intestines
  • bowel
  • vagina & vaginal canal
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28
Q

What parts of the body need to stay sterile?

A
  • blood
  • lungs
  • bile duct
  • kidney
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29
Q

Explain the steps for a gram stain

A
  1. apply a primary stain such crystal violet to heat fixed bacteria
  2. Add iodide which binds to crystal violet and helps fix it to cell wall
  3. Decolourise with ethanol or acetone
  4. counterstain with safranin (pink)

Come In And Stain
Crystal violet
Iodide
Alcohol
Safranin

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30
Q

What does the coagulase test distinguish?

A

Distinguishes S.aureus from other staphylococci
- coagulase positive

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31
Q

What is the oxidase test used for?

A

Tests if micro-organism contains a cytochrome oxidase
- implies organism able to use oxygen as the terminal electron acceptor

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32
Q

How does Haemolysis distinguish bacteria?

A

Some secrete enzyme that break down blood to get more nutrients

Alpha
- partial lysis
- greening

Beta (Better)
- complete lysis
- clear

Gamma
- no lysis

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33
Q

What is the main drug to treat staphylococcus aureus infection?

A

Flucloxacillin

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34
Q

How is staphylococcus aureus spread?

A
  • aerosol
  • touch
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35
Q

What are virulence factors for S.aureus?

A
  • pore forming toxins
  • proteases
  • Toxic shock syndrom toxin
  • protein A (surface protein which binds to antibodies in wrong orientation)
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36
Q

What is MRSA?

A

Methicillin resistant S.aureus
- resistant to major antibiotics
- beta lactams
- gentamicin

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37
Q

What are types of toxin mediated S.aureus infections?

A
  • scalded skin syndrome
  • toxic shock syndrome
  • food poisoning
    causes bodily reaction without infecting
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38
Q

What are 2 types of coagulase-negative staphylococci?

A
  1. S.epidermidis
    - infections are opportunistic
    - able to form persistent biofilms
  2. S.saprophyticus
    - acute cystitis
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39
Q

What are antigenic zero-grouping?

A

Lancefield grouping A-H: a method of grouping catalyse negative, coagulase negative bacteria based on bacterial carbohydrate cell surface antigens

Group A = S.pyogenes
Group B = S.agalactiae

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40
Q

What is the Lancefield microbead agglutination test?

A
  • Antiserum (antibodies) made that recognise each group
  • Tagged to tiny plastic beads
    added to a suspension of bacteria
  • Antibodies bind bacteria and beads clump together
  • Visible to naked eye
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41
Q

What are S.pyogenes virulence factors?

A

Exported factors
Enzymes
- streptokinase
Toxins
- streptolysins
- erythrogenic toxin

Surface factors
- M protein (surface protein)

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42
Q

What is the result for the optochin test?

A
  1. resistant = Viridans group (S.oralis)
  2. sensitive = S.pneumoniae
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43
Q

What are the virulence factors of S.pneumoniae?

A
  1. capsule
  2. inflammatory wall constituents
  3. cytotoxin
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44
Q

What are the characteristics of viridians group streptococci?

A
  • alpha haemolytic
  • optochin resistant
  • cause deep organ abscesses
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45
Q

What are 3 main types of gram positive aerobic bacilli?

A
  1. listeria monocytogenes (soft cheese)
  2. Bacillus anthraces (spore forming)
  3. corynebacterium diphtheria (upper resp infection)
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46
Q

What are 3 main subtypes of clostridia anaerobic gram positive bacilli?

A

Clostridia = spore forming, survive in environment, produce toxins

  1. C.tetani (tetanus)
  2. C.botulinum (botulism - paralysis)
  3. C.difficile (diarrhoea)
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47
Q

What are the 2 types of virulence factors?

A
  1. colonisation factors = adhesions, invasions, nutrient acquisition, defence against the host
  2. toxins = usually secreted proteins (damage, subversion)
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48
Q

What are characteristics of enterobacteria?

A
  • gram negative
  • rods
  • mobile (flagella)
  • some colonise intestinal tract
    (AKA. Phylum Proteobacteria)
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49
Q

Does salmonella or shigella have flagella?

A

Salmonella does making it motile

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50
Q

What are the 4 main shape groups of gram negative bacteria?

A
  1. Proteobacteria = all are rod-shaped except Neisseria + Campylobacter
  2. Bacteroids = rod-shaped
  3. Chlamydia = round, pleomorphic
  4. Spirochaetes = spiral/helical
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51
Q

What are the characteristics of E.coli and what infections it causes?

A

commensals = live in the stomach of healthy people, but when bacteria amount increases when you eat contaminated food they try to look for a new host and release toxins that make you ill

  • Wound infections
  • UTIs
  • Gastroenteritis
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52
Q

What are characteristics of a shigella infection?

A

Gastroenteritis with dysentery (diarrhoea with blood and mucus)

  • acid tolerant
  • person to person spread or contaminated food/water
  • entry through colonic M cells
  • induced uptake
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53
Q

What are the 2 species of salmonella?

A
  1. S.enterica (responsible for salmonellosis)
  2. S. bongori (rare - contact with reptiles)
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54
Q

What 2 main infections does salmonella enterica cause?

A
  1. Gastroenteritis/enterocolitis
    - food poisoning
  2. Enteric fever - typhoid
    - poor drinking water/sanitation
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55
Q

Explain the pathogenesis of salmonellosis?

A
  • invasion of gut epithelium
  • transcytosed to basolateral membrane
  • enters submucosal macrophages
  • intracellular survival/replication
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56
Q

How does gastroenteritis cause illness?

A
  1. Bacterial-mediated endocytosis
  2. Induction of interleukin-8 release
  3. Neutrophil recruitment and migration
  4. Neutrophil-induced tissue injury
  5. Fluid and electrolyte loss - diarrhoea

Inflammation/necrosis of gut mucosa

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57
Q

How does enteric fever cause illness?

A
  1. Bacterial-mediated endocytosis (brought into cell)
  2. Transcytosis (transported across interior of cell) to basolateral membrane
  3. Survival in macrophage - systemic
    spread

Initially, little damage to gut mucosa

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58
Q

Examples of main Gram positive cocci.

A

Staphylococci
Streptococci
Enterococci

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59
Q

Examples of main gram negative cocci.

A

Neisseria
Moraxella
Veillonella

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60
Q

Examples of main gram positive bacilli.

A

Bacillus
Corynebacteria
Diptheriae
Listeria Monocytogenes

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61
Q

Examples of main gram negative bacilli

A

E. coli
Campylobacter
Pseudomonas
Salmonella
Shigella
Proteus

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62
Q

Define serovars.

A

(Or serotypes)
Are strains that have ANTIGENIC properties that differ from other strains of the same species.

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63
Q

Define pathovars.

A

(or Pathotypes)
Are strains that are distinguished by possession of particular PATHOGENIC mechanisms
rather than being based on antigenic differences.

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64
Q

Define biovars.

A

(Or biotypes)
Are variant bacterial strains that differ physiologically or biochemically from other strains in a particular species.

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65
Q

What are the different types of agar?

A
  1. Blood agar
  2. Chocolate agar
  3. CLED agar
  4. MacConkey agar
  5. Gonococcus agar
  6. XLD agar
  7. Sabourard agar
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66
Q

What test could be done to distinguish between different streptococci?

A

Blood agar haemolysis

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67
Q

What further test can be done for the streptococci in the beta haemolysis group?

A

Serogrouping (Lancefield grouping A,B,C,G)
- detecting surface antigens

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68
Q

What kind of bacteria is MacConkey agar used with?

A

Gram Negative bacilli

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69
Q

What does MacConkey agar contain and detect?

A

MacConkey agar 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.

Non- lactose fermenting = white

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70
Q

What are the main examples of mycobacteria?

A

Rods
M. tuberculosis
M.Leprae - leprosy
M. Avium - AIDs
M.Kansasii - chronic lung

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71
Q

What are some characteristics of mycobacteria?

A
  • rods, bacilli
  • Aerobic
  • non-spore forming
  • non-motile
  • slow reproduction
  • slow response to treatment
  • slow growing
  • cell wall contains high molecular weight lipids
  • survive inside macrophages (TB escapes to cytosol to avoid phagosomal killing)
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72
Q

What do you stain mycobacteria with?

A

Resistant to gram stain (wax-like, thick cell walls
- acid fast bacilli

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73
Q

How is TB transmitted?

A

Aerosol
Person to person

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74
Q

How does TB affect the body?

A
  1. Initial contact made by alveolar macrophages
  2. Bacilli taken in lymphatics to hilarious lymph nodes
  3. Leads to cell mediated immune response from T cells
  4. Primary infection contained but CMA persists
    (latent TB - no clinical disease, detectable CMI to TB)
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75
Q

Explain how TB can cause a systemic infection.

A
  1. failure in immunity
  2. granulomas form around bacilli in apex of lungs (more air and less blood supply)
  3. Cause necrosis
  4. Resulting in abscess forming and caseous material coughed up (how its first diagnosed usually)
  5. Lungs can then fill with fluid
  6. Spread to other tissue in the body
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76
Q

How does TB cause formation of granulomas?

A

Macrophage surround bacteria (inside macrophage),
Keeping them walled off due to fibroblasts around the edge

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77
Q

What is blood agar used for and its characteristics?

A

Streptococcus and others
- non-selective

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78
Q

What is chocolate agar used for and its characteristics?

A
  • Fastidious (sensitive)
  • For neisseria
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79
Q

What is MacConkey used for and its characteristics?

A
  • For lactose status
  • enteric gram negatives
  • contains indicator
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80
Q

What is CLED used for and its characteristics?

A
  • Stops motile proteus swarming
  • lactose status
  • urinary gram negatives
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81
Q

What is XLD used for and its characteristics?

A
  • selective (salmonella & shigella)
  • both ferment lactose
  • shigella = red
  • salmonella = red with black dots
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82
Q

Can you grow chlamydia on agar?

A

No, chlamydia is an obligate intracellular parasite

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83
Q

How can you detect chlamydia?

A

Serum antibodies or PCR.

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84
Q

What are the 5 ways viruses can cause disease?

A
  1. Direct destruction of host cells
  2. Modification of host cell
  3. “Over-reactivity” of immune system
  4. Damage through cell proliferation
  5. Evasion of host defences
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85
Q

What is a virus?

A

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

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86
Q

What shapes do viruses come in?

A
  1. helical
  2. Icosahedral
  3. Complex
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87
Q

What are differences between bacteria and viruses?

A

Bacteria
- cell wall
- organelles
- DNA or RNA
- living

Viruses
- none of the things above
- dependent on host cell

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88
Q

Are viruses always enveloped?

A

No
Can be enveloped or non-enveloped

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

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89
Q

How do viruses replicate?

A
  1. Attachment to specific receptor
  2. Cell entry (uncoatinf of vision within cell)
  3. Host cell interaction + replication
    - migration of genome to cell nucleus
    - transcription to mRNA using host materials
    - translation of viral mRNA to produce: structural proteins, viral genome, non-structural proteins (enzymes)
  4. Assembly of viron
  5. Release of new virus particles: burst out or budding/exocytosis
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90
Q

How do viruses caused direct destruction of host cells?

A

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

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91
Q

How do viruses cause disease by modification of host cell? example?

A

atrophies villi and flattens epithelial cells
decreases small intestine surface area
nutrients incl sugar not absorbed
hyperosmotic state
profuse diarrhoea

e.g. rotavirus

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92
Q

What is an example of a virus that causes ‘over-reactivity’ of immune system?

A

e.g. hep B

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93
Q

How do viruses cause damage through cell proliferation? Example?

A

e.g. human papillomavirus -> cervical cancer

  1. Acquisition through contact
  2. Partial viral replication and expression of some HPV proteins
  3. viral DNA integrated into host chromosome
  4. Continuous expression of oncoprotein causing cellular DNA mutations
  5. Dysplasia and neoplasia
  6. Cell proliferation and metastatic spread
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94
Q

What are the different ways viruses evade the host defences?

A
  1. cellular level
    - virus not detectable
    - cell to cell spread (avoids immune system
  2. molecular level
    - antigenic variability e.g. flu
    - prevention of host cell apoptosis
    - down regulation of interferon and other intracellular host defence proteins
    - interference with host cell antigen processing pathways e.g. HIV
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95
Q

Why do viruses vary so much in the clinical syndromes they can cause?

A
  • different host cells and tissues that they can infect
  • different methods of interaction with the host cell
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96
Q

What 2 viruses does varicella zoster virus cause?

A

Primary infection = Chickenpox
Secondary reactivation = Shingles

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97
Q

What are some features of chickenpox?

A
  • common in childhood
  • highly contagious
  • usually benign
  • serious in certain groups e.g. adults, pregnancy, smokers, immunocompromised
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98
Q

What are some features of chickenpox?

A
  • common in childhood
  • highly contagious
  • usually benign
  • period in certain groups e.g. adults, pregnancy, smokers, immunocompromised
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99
Q

What are some complications of chickenpox?

A
  • dehydration
  • haemorrhage change
  • cerebellar ataxia
  • vermicelli pneumonia
  • congenital (foetal) varicella syndrome
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100
Q

How do you confirm the diagnosis for chickenpox?

A
  1. pop lesion with a sterile needle
  2. absorb vesicle contents onto swab
  3. replace swab in cassette and send for PCR
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101
Q

How does viral dormancy occur?

A
  • Virus evades the immune system
  • lies dormant in dorsal root or cerebral ganglion
  • localised reactivation = shingles
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102
Q

Define infectivity.

A

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

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103
Q

Define invasiveness

A

The capacity to penetrate mucosal surfaces to reach normally sterile sites

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104
Q

What are the 4 stages of pathogenesis?

A
  1. exposure (contact, gain entry to host)
  2. adhesion (colonisation)
  3. invasion
  4. infection

cycle is complete when the pathogen exits the host and is transmitted to a new host.

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105
Q

What are commensal microorganisms?

A

The resident flora and usually nonpathogenic
- can cause disease if overgrown
- asymptomatic carriage of potential pathogens

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106
Q

What are the 4 types of pathogens for infections?

A
  1. viruses
  2. bacteria
  3. protozoa (parasitology)
  4. helminths (parasitology)
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107
Q

What are some features of a viral infection?

A
  • need rapid cell entry
  • free virus in blood stream easily neutralised
  • infected cells destroyed
  • elicit humoral (antibody mediated) response and cell mediated response
108
Q

What is the role of IgM in viral infections?

A

Agglutinates particles

109
Q

What is the role of complements in viral infections?

A

Opsonisation and lysis

110
Q

What is the role of antibodies in viral infections?

A
  • block binding
  • block virus host cell fusion
  • are involved in opsonisation
111
Q

What is the cell mediated response in viral infections?

A
  • IFN from Th (CD4+) or Cytotoxic T lymphocytes (CTL)/Tc (CD8+) – has direct antiviral action
  • CTL can kill infected cells
  • NK cells and macrophages are involved in antibody-dependent cellular cytotoxicity(ADCC) killing
  • IFN induces anti viral proteins for bystander cells
112
Q

What is the timeline of viral infections?

A
  1. 3-4 days post infection Cytotoxic T Lymphocyte activity increases
  2. Peaks at 7-10 days then declines
  3. 7-10 days virions eliminated
  4. Parallels development of CTL

CTL eliminate virus infected cells and so eliminates sources of new viral products

113
Q

Which viruses cause direct cell cytotoxicity?

A

Influenza/RSV virus - respiratory epithelium
Varicella Zoster virus - skin cells
Yellow Fever virus - liver cells
HIV – Th cells

114
Q

What are different ways that viruses evade the immune system?

A

Influenza - changes coat antigen
Rhinovirus, HIV, - show antigenic variation
Mumps, measles, EBV, HIV, CMV - cause immune suppression (lymphocytes or macrophages destroyed or altered)
Vaccinia protein - inhibits classical complement pathway

115
Q

Define antigenic drift.

A

spontaneous mutations, occur gradually giving minor changes in HA (haemagglutinin) and NA (neuraminidase). Epidemics.

116
Q

Define antigenic shift.

A

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

117
Q

How does influenza evade the immune system?

A
  • Spherical particles surrounded by lipid bilayer acquired from infected host cell.
  • Glycoprotein projections, haemagglutinin (HA) facilitates attachment (1000 per virion), neuraminidase (NA) facilitates viral budding.
  • 3 virus types, A, B, C.
  • Changes in HA and NA give coat variability.
118
Q

What are the different ways bacteria can enter the host?

A

respiratory tract
gastrointestinal tract
genitourinary tract
skin/mucous membrane break

119
Q

What type of response do extracellular and intracellular bacteria initiate?

A

extracellular = antibody response
intracellular = cellular response

120
Q

What type of response is initiated if low or high numbers of bacteria?

A

low number or virulence = phagocytes active
high numbers or virulence = cellular response

121
Q

What do bacteria do to compete with host cells and colonise flora?

A
  • sequestering nutrients
  • using novel metabolic pathways
  • out-competing other microorganisms
122
Q

What are the different types of bacterial toxins?

A

tissue target
molecular action
biological effect
contribution to disease process

123
Q

What is the role of the two component sensor-kinase system?

A

Sensing changes:
- in competing bacteria
- in cell density
- in nutrient availability
- environmental factors

124
Q

What are adhesins?

A

Help bacteria bind to mucosal surfaces

125
Q

What is regulated in bacteria gene transcription when environmental changes are sensed?

A
  • virulence factors
  • competence to exchange genetic material
  • biofilm formation
  • production of bacteriocins/toxins (to kill other bacteria)
126
Q

What are the types of adhesins?

A
  1. Fimbriae and pili filamentous proteins e.g. Neisseria gonorrhoeae
  2. Non fimbrial proteins e.g. Fibronectin binding protein of Treponema pallidum
  3. Lipid e.g. lipid teichoic acid of Streptococcus pyogenes
  4. Glycosaminoglycans of Chalmydia sp
127
Q

What is the function of biofilms?

A
  • Bacteria can stick together on a surface by secreting an extracellular polymeric substance of protein, polysccharides and DNA
  • bacteria no longer planktonic single bacteria
128
Q

What are the host responses to bacterial infection?

A
  1. IgA - block attachment to host cells
  2. Ab C3b - opsonisation, prevents proliferation
  3. Complement - cell lysis, prevents proliferation
  4. Ab - neutralise toxins
129
Q

What is the benefit of biofilms?

A
  • helps protect against antimicrobials
  • seen in dental plaque, prosthetic materials and in otitis media
130
Q

What is the timeline of a bacterial infection?

A
  1. Sensitisation (1-2 weeks)
  2. Th cell activation (DTH*)
  3. Second contact – effector phase
  4. T(DTH) cells secrete IFN, TNF, IL2
  5. Macrophage recruitment
131
Q

Define delayed-type hypersensitivity.

A

Type IV
- takes a few days to develop (wait for T cells to respond)
- an immune response that occurs through direct action of sensitized Tcellswhen stimulated by contact with antigen

e.g. transplant rejection

132
Q

What happens in a prolonged delayed type hypersensitivity?

A

continuous macrophage activation
granuloma formation (macrophages adhere together - TB)
lytic enzyme release = tissue damage

133
Q

What are ways different bacterial infections evade the immune system?

A

Neisseria, HI- Secrete protease lyses IgA(s)
N.gonorrhoea - Pilli
Antigenic variation
B.pertussis - Secrete adhesion molecules
S.pneumoniae - Polysaccharide capsule (84 serotypes) prevents phagocytosis
Staphylococci - Coagulase, forms fibrin coat round organism
Mycobacterium - Escape from phagolysosome and can live in cytoplasm

134
Q

What are different types of protozoan infection?

A

Malaria
Sleeping sickness
Amoebiasis
Chagas disease
Toxoplasmosis
Leishmaniasis

135
Q

What type of response is initiated in protozoan infection in the blood and tissue stage?

A

Blood stage = humoral immunity (antibodies)
Tissue stage = cell mediated immunity (T cells/macrophages)

136
Q

How does malaria infect the body?

A

triggers anIgE response. IgE elicits an immune response by binding to Fc receptors on mast cells, eosinophils, and basophils, causing degranulation and cytokine release

Excessive production of cytokines (TNF) may cause some of symptoms associated with malaria

Antibody produced against sporozoites – generates a poor response as sporozoites only present in blood for short time

137
Q

What are ways the protozoan evade the immune system?

A
  1. surface antigen variation - trypanosomes
  2. intracellular phase
  3. outer coat sloughing
138
Q

What are features of helminth (worm) infections?

A
  • do not multiply in humans (eggs formed and released)
  • not intracellular
  • few parasites carried
  • poor immune response
  • trigger an IgE response –> causing degranulations dn cytokine release
  • immune response not sufficient to kill
  • eosinophilic basic protein toxic to worms
139
Q

How does worm evasion elicit a hyporesponsiveness?

A
  • Mediated by immunosuppressive T-cell subset, the regulatory T (Treg) cell
  • Decreased antigen expression by adult - shielding
  • Glycolipid/glycoprotein coat (host derived)
    (ie. utilises host self antigens)
140
Q

define immunisation.

A

The process whereby people are protected against illness caused by infection with micro-organisms (formally called pathogens).

141
Q

What are the differences of attenuated and inactivated vaccines?

A

Attenuated
- single dose
- less stable
- humoral and cell mediated response
- reversion may occur (polio)

Inactivated
- multiple boosters
- more stable
- humoral response
- reversion cannot occur

142
Q

What are tumour infiltrating lymphocytes?

A

may contribute to cancer growth and spread and to the immunosuppression associated with malignant disease.

143
Q

What are tumour associated macrophages?

A

are a major component of the infiltrate of most cancers
- can be pro-tumoral or pro-inflammatory

144
Q

What are protozoa?

A
  • one cells animals
  • single cell with nucleus
145
Q

What are the 5 groups of protozoa?

A
  1. Flagellates
  2. Amoebae
  3. Microsporidia
  4. Sporozoa
  5. Cilliates
146
Q

What are the features of flagellates?

A
  • flagellum as main locomotory organelle
  • usually reproduce by binary fission
  • intestinal flagellates or other body sites
147
Q

What are some examples of flagellates?

A
  • American trypanosomiasis
  • Leishmaniasis
  • trichomonad vaginalis
  • giardiasis
148
Q

What are the features of amoeba?

A

Move by means of flowing cytoplasm and production of pseudopodia (arm like projection off the cell)

149
Q

What are the features of protozoans?

A
  • no locomotory extensions
  • all specific parasitic
  • most intracellular parasites
  • reproduce by multiple fission
150
Q

What are the features of cilliates?

A
  • cilia that beat rhythmically at some stage in lifecycle
  • 2 types of nuclei = macro/micronucleus
151
Q

What are the features of microsporidia?

A
  • production of resistant spores
  • unique polar filament, coiled inside spores
  • little know about human disease
152
Q

How is malaria transmitted?

A

By bite of female anopheles mosquito

153
Q

How many species of malaria are there?

A

5 species:
Plasmodium falciparum
Plasmodium ovale
Plasmodium vivax
Plasmodium malariae
Plasmodium knowlesi

154
Q

What are the symptoms for malaria?

A

FEVER
Chills
Headache
Myalgia
Fatigue
Diarrhoea
Vomiting
Abdo pain

155
Q

What are the 4 main signs of malaria?

A
  1. anaemia
  2. jaundice
  3. hepatosplenomegaly (enlargement of spleen and liver)
  4. ‘black water fever’ (RBCs burst in bloodstream)
156
Q

What is the malaria lifecycle?

A
  1. Mosquito bite
  2. Abdo pain - infected liver cell
  3. cyclical fever - in blood
  4. male and female gametocytes produced in RBCs
  5. burst from RBC
  6. Causing anaemia, jaundice and haemoglobinuria
  7. mosquito then feeds on blood of infected individual
  8. parasites form within the mosquito
  9. mosquito then injects saliva with parasite into another person as it sucks blood
157
Q

Which type of malaria causes serious complications?

A

P. falciparum

158
Q

What form of malaria does P.falciparum cause?

A

Obstructed microcirculation
- called ‘complicated malaria’

159
Q

What illnesses can complicated malaria cause?

A
  1. cerebral malaria
  2. ARDS
  3. Renal failure
  4. Bleeding
  5. Shock
  6. sepsis
160
Q

What are the features of cerebral malaria?

A

Complication caused by P.falciform

  1. vascular occlusion
  2. Hypoglycaemia

Causing:
- drowsy
- increased ICP
- seizures
- coma

161
Q

What malaria treatment is there?

A

Complicated
- IV artesunate (IV quinine + doxycycline)

Uncomplicated
- lots of options

162
Q

Which types of malaria can relapse?

A

P.ovale
P.vivax
Form hypnozoites in the liver

163
Q

What are the 3 types of worms?

A
  1. Nematodes (round worms)
    - larva migrans
    - tissue (filaria)
    - intestinal
  2. Trematodes (flatworms, flukes)
    - Blood
    - liver
    - lung
    - intestinal
  3. Cestodes (tape worms)
    - non-invasive
    - invasive
164
Q

When does the pre-patent period occur in worms?

A

Interval between infection and the appearance of eggs in the stool

165
Q

What is an antibiotic?

A

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

166
Q

What are antimicrobials?

A

Moleculs that bind a target on a microorganism (bacteria, fungi, virus, worm, protozoan) to destroy it or prevent further growth

167
Q

What are the 3 main things antibiotics inhibit in bacteria?

A
  1. cell wall synthesis
  2. Nucleic acid synthesis
  3. protein synthesis
168
Q

What type of drugs cause inhibition of cell wall synthesis?

A

Beta lactams
- penicillins
- cephalosporins
- carbapenems
- monobactams

Vancomycin
Bacitracin
Glycopeptides

169
Q

What is the action of beta lactam antibiotics?

A
  1. First diffuse through bacterial cell wall. Gram neg have an additional lipopolysaccharide layer that decreases antibiotic penetration.
  2. Disrupt peptidoglycan production
  3. By binding covalently and irreversibly to the Penicillin Binding Proteins
  4. cell wall is disrupted and lysis occurs
  5. results in a hypo-osmotic or iso-osmotic environment
  6. Active only against rapidly multiplying organisms

(particularly useful for gram positive bacteria with a thicker cell wall - due to thick layer of peptidoglycan)

170
Q

When are beta lactams antibiotics most useful?

A
  • in extracellular pathogens
  • Gram positive bacteria
    (poorly penetrate mammalian cells so ineffective in intracellular pathogens)
171
Q

What are examples of antibiotics that inhibit nucleic acid synthesis?

A
  1. DNA gyrase
    - quinolones
  2. RNA polymerase
    - Rifampin
172
Q

What are examples of antibiotics that inhibit protein synthesis?

A
  • 50s subunit –> macrolides, clindamycin
  • 30s subunit –> tetracyclines, aminoglycosides

Mainly gram positive bacteria

173
Q

What are examples of antiobitcs that inhibit folate synthesis?

A
  • Trimethoprim
  • Co-trimoxazole
174
Q

What is the aim of antibiotics?

A

Give time and support for the immune system to deal with an infection.

175
Q

What are the 5 steps for bacterial agenda?

A
  1. Attach and enter
  2. Local spread
  3. multiply
  4. Evade host defences
  5. shed from body
176
Q

What are the consequences of bacterial infection?

A

Direct
- destroy phagocytes or cells which bacteria replicate

Indirect
- inflammation
- immune pathology e.g. antibodies

Toxins
- exotoxin = protein production
- endotoxin = gram negative

Diarrhoea
- cause reaction in gut to try and clean the bacteria

177
Q

Which antibiotic kills bacteria the quickest?

A

Those that inhibit cell wall synthesis

178
Q

What are the two ways antibiotics work?

A
  1. Kill the bacteria = bacteriocidal antibiotics
  2. Prevent growth of bacteria
    (then immune system does rest of the work)
    = bacteriostatic antibiotics
    e.g. inhibit protein synthesis, DNA replication or metabolism
179
Q

What is minimum inhibitory concentration?

A

MIC = The lowest concentration of an antibiotic that inhibits the growth of a given strain of bacteria.

180
Q

What makes an antibiotic effective?

A
  • the drug must not only attach to its binding target but also must occupy an adequate number of binding sites (need to kill it fully instead of just making some holes) = concentration dependent killing
  • needs to remain at the binding site for a sufficient period of time in order for the metabolic processes of the bacteria to be sufficiently inhibited = time dependent killing

The antibiotic must reach and stay at the site of bacterial infection.

181
Q

What is a key parameter for time dependent killing?

A

Key parameter is the time that serum concentrations remain above the MIC during the dose interval.

182
Q

What is a key parameter of concentration dependent killing?

A

Is how high the concentration is above the MIC

183
Q

What 4 ways can bacteria resist antibiotics?

A
  1. Change antibiotic target
  2. Destroy antibiotic
  3. Prevent antibiotic access
  4. Remove antibiotic from bacteria
184
Q

How do bacteria change antibiotic target?

A

Bacteria change the molecular configuration of antibiotic binding site or mask it

185
Q

What are examples of antibiotic resistance due to change of target?

A

1.Flucloxacillin (or methicillin) is no longer able to bind PBP of Staphylococci – MRSA
2. Wall components change in enterococci and reduce vancomycin binding – VRE
3. Rifampicin activity reduced by changes to RNA polymerase in MTB – MDR-TB

186
Q

What are examples of antibiotic resistance due to destruction of antibiotics?

A
  1. Beta lactam ring of Penicillins and cephalosproins hydrolysed by bacterial enzyme ‘Beta lactamase’ now unable to bind PBP
  2. Staphylococci produce ‘penicillinase’ so penicillin but not flucloxacillin inactivated
  3. Gram negative bacteria phosphorylate and acetylate aminoglycosides (gentamicin)
187
Q

How do bacteria prevent antibiotic access?

A

Modify the bacterial membrane porin channel size, number and selectivity

188
Q

What are examples of antibiotics resistance due to prevention of access?

A
  1. Pseudomonas aeruginosa against imipenem,
  2. Gram negative bacteria against aminoglycosides
189
Q

How do bacteria remove antibiotics? Examples?

A

Proteins in bacterial membranes act as an export of efflux pumps - so level of antibiotic is reduced

E.g. S. aureus or S. pneumoniae resistance to fluoroquinolones

Enterobacteriacae resistance to tetracylines

190
Q

How do bacteria develop resistance?

A
  1. Intrinsic
    - naturally resistant
  2. Acquired
    - spontaneous gene mutation
    - horizontal gene transfer (conjugation, transduction, transformation)
191
Q

What is a major example of bacteria with a intrinsic resistance?

A

Aerobic bacteria are unable to reduce metronidazole to its active form
(all subpopulations of a species will be equally resistant)

192
Q

What is acquired resistance?

A
  • A bacterium which was previously susceptible obtains the ability to resist the activity of a particular antibiotic
  • Only certain strains or subpopulations of a species will be resistant
193
Q

What are the 3 ways horizontal gene transfer occurs?

A
  1. Transduction - insertion of DNA by bacteriophages (MRSA)
  2. Conjugation - sharing of extra-chromosomal DNA plasmids ‘reproduction’ (Beta lactamase)
  3. Transformation - picking up naked DNA (penicillin resistance)
194
Q

What is MRSA?

A

Methicillin resistant S.aureus

195
Q

How does S.Aureus become MRSA?

A
  • Bacteriophages infect bacteria with staphylococcal cassette chromosomes mec
  • this contains resistance to gene mecA
  • encodes penicillin-binding protein 2a (PBP2a)
    (prevents antibiotic binding to these PBP proteins so can’t cause lysis)
  • now resistance to all β-lactam antibiotics in addition to methicillin (= flucloxacillin)
196
Q

What is VRE?

A

Vancomycin resistant enterococci

197
Q

How do enterococci become vancomycin resistant?

A

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

198
Q

What is ESBL?

A

Extended Spectrum Beta Lactamase inhibition

199
Q

How do ESBL cause resistance in bacteria?

A
  • ESBL is the enzyme that makes some strains resistant to beta-lactams antibiotics - beta-lactamase
  • Due to further mutation at active site
  • These hydrolise oxyimino side chains of cephalosporins: cefotaxime,ceftriaxone, andceftazidime and monobactams: aztreonam

(then made beta-lactamase inhibitor antibiotics that inhibit this enzyme)

200
Q

What are carnapenems?

A

Beta-lactam antibiotics highly resistant to Beta-lactamase or cephalosporinases
- last resort as very toxic

e.g. Meropenem

201
Q

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

A

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

202
Q

When are cephalosporin antibiotics useful?

A
  • good for people with penicillin allergy
203
Q

What antibiotic do you use for gram positive bacteria?

A

Thick cell wall therefore need a simple cell wall inhibitor
= beta lactam antibiotics

204
Q

What antibiotic can you use when bacteria are resistant to beta lactase and methicillin?

A

Glycopeptides
e.g. vancomycin and teicoplanin = only given by IV

  • gram positive only
205
Q

What antibiotics do you use for gram negative bacteria?

A

Thin cell wall
- protein synthesis inhibitors (aminoglycosides
- DNA synthesis inhibitors

206
Q

Can you use beta lactam antibiotics for gram negative?

A

Thin cell wall and produce beta lactamase
- so not usually but now made beta lactamase inhibitor antibiotics

207
Q

What type of bacteria does flucloxacillin treat?

A

Beta haemolytic strep
S.aureus

208
Q

What are the ways of identifying risks of infection?

A
  1. Risk factors
  2. Screening
  3. Clinical diagnosis
  4. Lab diagnosis
209
Q

What are CPEs?

A

Carbapenemase producing enterobacteriaceae
- bacteria that now have an enzyme that inactivates carbapenem antibiotics
- used to be the last resort but now very common

210
Q

What is norovirus?

A
  • Very fast spreading virus
  • causes vomiting and diarrhoea
  • healthy people will get over it within a few dyas
  • but if it occurs in hospitals people already have weak immune systems so can die from it
  • short lived immunity
  • relatively resistant to conventional cleaning
211
Q

What is clostridium difficile?

A
  • bacterial spores (live for a long time outside of host)
  • chronic diarrhoea, prolonged hospital stay
  • severe complication = toxic megacolon
212
Q

What are endogenous infections?

A

Infections caused by own bacterial flora
- important in hospitals with invasive devices or surgical patients = break barrier and bacteria can stick to plastic
e.g. from cannula and catheter

213
Q

What are the advantages and disadvantages of PCR vs electron microscopy?

A

PCR
- sensitive
- rapid

Electron microscopy
- can detect any virus, even a novel one
- operator skill dependent

214
Q

Which antibody is the first to develop in a viral infection?

A

IgM

215
Q

What is the screening process for HIV?

A

Negative = lab reports result = still negative = repeat blood test from patient after 6 weeks

Positive = confirm test with a different assay = confirm with a new, second blood sample from the patient

216
Q

What are fungi and how do they move?

A
  • eukaryotic
  • chitinous cell wall
  • heterotrophic
  • ‘move’ by means of growth or through the generation of spores, which are carried through air or water
217
Q

What is the difference between yeast and mould?

A

Yeasts
- small single celled organisms that divide by budding

Mould
- multicellular hyphae and spores

218
Q

What are examples of life threatening fungal diseases?

A
  1. Immunocompromised hosts
    - candida line infections
  2. Post surgical patients
    - intra-abdominal infection
  3. Healthy hosts
    - fungal asthma
    - travel associated fungal infections
    - post influenza aspergillosis
219
Q

What is dimorphic fungi?

A

When fungi exist as both yeasts and moulds switching between the two when conditions suit

220
Q

What are the different methods to diagnose fungal infections?

A
  1. Radiology
  2. Microscopy
  3. culture - subsequent microscopy to ID- tease mounts/selotape
  4. molecular - PCR, antigen tests
221
Q

What are the requirements for an ideal diagnostic test?

A

Non-invasive
Rapid and easy technically
Sensitive and reproducible
Specific – both in terms of pathogen, significance of positive result
Cheap

222
Q

What are the negatives of the different methods for diagnosing fungal infections?

A
  1. Radiology = Insensitive in early stages
  2. Microscopy = Usually insensitive
    Culture = OK for yeasts, poor for moulds
  3. Molecular
    - PCR = mixed results
    - Antigen tests
    Cryptococcal Ag - excellent
    Galactomannan - insensitive
    1,3 Beta-D-glucan – poorly specific
223
Q

What is ‘selective toxicity’ in fungal treatment?

A

Aim to achieve inhibitory levels of agent at the site of infection without host cell toxicity
- pick a target that doesn’t exist in humans
- human cells are recused from toxicity by alternative metabolic pathways

224
Q

Is it more difficult to treat fungal or bacteria infections?

A

Fungal
- they are eukaryotic
- so more similar to human cells

225
Q

What are difference and similarities between human and fungal cells?

A

Similar
- DNA synthesis
- protein synthesis
- plasma membrane

Differences
- fungal have a cell wall
- human cell membrane contains cholesterol not ergosterol

226
Q

What is the main anti fungal drug?

A

Azoles

227
Q

What are the adverse effects of azoles?

A
  • relatively safe
  • alopecia with long term, fluconazole
  • GI symptoms more pronounced
  • visual disturbance
228
Q

What are some examples of azole drug-drug interactions?

A
  • result of cytochrome P450 isoforms
  • Variable depending on relative affinity of drugs for individual enzymes.
  • Fluconazole hydrophilic and principally excreted unchanged – less significant interactions
    (Warfarin, phenytoin, calcineurin inhibitors, anxiolytics)
  • Itraconazole is a potent CYP3A4 inhibitor
    (As above + steroids, statins, rifamycins,PIs)
  • Posaconazole is only a mild CYP3A4 inhibitor.
  • Voriconazole inhibits a number of CYP enzymes
    (Affected drugs similar to itraconazole)
229
Q

What are the features of onychomycosis?

A
  • common
  • caused by dermatophyte moulds
  • microscopy most specific test
  • trichophyto rubrum is most common
230
Q

What is (1–>3)-β-D glucan?

A
  • cell wall component of fungi
  • released into serum during invasive infection
231
Q

What is the pathogenesis of pneumocystis?

A
  • fungal pneumonia infection
  • presents as pneumocystis in people with HIV/AIDs or poor immunity
  • causes difficulty to breath and fever
  • lead to respiratory failure

(most common infection in HIV - big indicator that someone has HIV)

232
Q

How do you treat pneumocystis pneumonia?

A

Fungal but susceptible to some snitbiotics
- co-trimoxazole

233
Q

What is a bad CD4 count?

A

Anything below 200
above 500 = good

234
Q

What 2 blood tests diagnose HIV?

A

CD4 count
Viral loads

235
Q

What is viral suppression for HIV?

A

Viral load is undetectable
- on treatment

236
Q

What is the 90/90/90 UNAIDS goal to eliminate the epidemic?

A

global target of
-90% of people living with HIV being diagnosed
-90% diagnosed on ART (antiretroviral therapy)
-90% viral suppression for those on ART by 2020

237
Q

What are the 3 HIV transmission routes?

A
  1. sexual
  2. vertical = mother to child transmission
  3. blood
238
Q

What are methods of prevention for HIV?

A
  • Male circumcision
  • treatment of STIs
  • female condoms
  • male condoms
  • HIV counselling & testing
  • behavioural change
  • treatment as prevention = if on drugs cannot pass HIV on
  • post exposure prophylaxis = from needle stick injury
  • oral pre-exposure prophylaxis (PreP) = medication before sex
  • microbicides for women and some gay men
  • undetectable = untransmittable
239
Q

What are the benefits of knowing HIV status?

A

Access to appropriate treatment and care
(late diagnosis = below 350)
Reduction in morbidity and mortality
Reduction of vertical transmission
Reduction of sexual transmission
Public health /partner notification
Cost-effective

240
Q

What is prep?

A
  • pre-exposure prophylaxis
  • 2-24hrs before sex and for a few days after
  • highly effective preventative measure for HIV
  • tablet or injectable
    (also Pep, Post the sex)
241
Q

Why do doctors NOT test for HIV?

A

They don’t think of HIV
Underestimate the risk of HIV in their patients
Failure to recognise HIV as a modifiable prognostic indicator
Misconception they need pre-test counselling
Misunderstanding of the implications for insurance, etc
Fear of offending the patient

242
Q

When does HIV screening/ testing occur?

A
  • tests triggered by clinical indicators
  • routine screening in high prevalence locations
  • antenatal screening
  • screening in high risk groups
  • patient initiated requests for testing
243
Q

What are some symptoms of HIV?

A

Generalised lymphadenopathy
Acute generalised rash
Glandular fever/ flu-like illnesses
Seroconversion
Sore throat
Check palms and soles = only also be syphilis

244
Q

What medical condition presentations should make you consider HIV?

A

Common examples:
Multi-dermatomal shingles

Unexplained lymphadenopathy

Unexplained wt loss or diarrhoea, night sweats, PUO

Oral/oesophageal candidiasis or hairy leukoplakia

Flu-like illness, rash, meningitis

Unexplained blood dyscrasias

245
Q

Which screening test is preferred?

A
  • venous blood sample
  • include p24 antigen and detect at 4 weeks
  • high sensitivity and specificity
246
Q

What is a HIV POCT?

A

Point of Care tests
- Finger prick blood
- Immediate result
- Lower sensitivity and specificity
- False positive and negative results
- Longer incubation period

247
Q

What are the advantages of POCT?

A
  • Outreach into community settings/ non-specialist clinics
  • Increased patient choice
  • Increased access to testing and case detection
  • Earlier diagnosis in non-healthcare seeking individuals
248
Q

How does HIV infect a cell?

A
  • HIV is a retrovirus
  • an RNA virus that uses reverse transcriptase
  • to make a DNA copy that becomes integrated into the DNA of the infected cell
249
Q

What is the mechanism of viral replication

A
  1. Attachment - Glycoproteins on the HIV molecule (gP160 made of gP120 and gP 41) allow it to dock and fuse onto the CD4 and CCR5 receptors
  2. Cell entry - The viral capsid the enters the cell and enzymes and nucleic acid are released
  3. Using reverse transcriptase single stranded RNA is converted into double stranded DNA
  4. Viral DNA then is integrated into the cells own DNA by integrase enzyme
  5. When the infected cell divides the viral DNA is read and long chains of viral proteins are made
  6. Assembly the viral protein chains are cleaved and reassembled
  7. Budding here immature virus pushes out of the cell taking with it some cell membrane
  8. Immature virus breaks free to undergo more maturation
  9. Maturation protein chains in the new viral particle are cut by the protease enzyme into individual proteins that combine to form a working virus
250
Q

What are different targets int he cell for antiretroviral therapy?

A
  1. Fusion/entry inhibitors
  2. Reverse transcriptase inhibitors
  3. Protease inhibitors
  4. Integrase inhibitors
251
Q

What makes HIV difficult to treat?

A
  • high replication rate
  • makes a mistake each time it replicates (variants which help to build resistance to drugs)
  • large population sizes
  • 2 strains can then conjugate/combine
252
Q

How is HIV able to cause this damage?

A
  • HIV is integrated into the DNA of infected CD4 expressing cells (T cels, thymus, dendritic cells)
  • Infects a range of CD4 immune cells
  • HIV can pass directly from cell to cell (inaccessible to antibodies)
  • Loss of T cells in lymphoid tissue in the gut, makes gut mucosa leaky allowing passage of bacteria
  • Causes chronic immune activation, exhausting the immune system
253
Q

Why does the immune response to HIV 1 fail to clear the virus?

A
  • HIV infects CD4 T helper cells, making the immune system weaker
  • cytotoxic CD8 T cells vigorously respond but eventually become exhausted
254
Q

Why do most HIV 1 infected people fail to make an effective antibody response?

A
  • HIV 1 envelope spike is heavily glycosylated (with sugars resembling human types) making it difficult for antibodies to bind to the surface
  • envelope proteins can change a lot without affecting virus function
  • avoids antibody recognition
  • HIV 1 nef protein reduces cell surface expression of HLA class I molecules needed for CTL recognition
255
Q

What is the immune response to HIV?

A
  1. Vigorous immune response but no demonstrable protective immunity with rare exceptions
  2. Excessive immune activation which favours viral replication
  3. Immunological dysfunction with involvement of all elements of host defence
  4. Ongoing viral replication with progressive immunological impairment leading to clinical manifestations of immunodeficiency
256
Q

Why is life expectancy still reduced in HIV infected people on cART?

A
  • issues of adherence, side effects and drug resistance
  • increase in non-AIDS (NADIs) defining illness
  • incidence of NADIs related to; size of HIV reservoir, persistent immune activation, CMV co-infection
257
Q

How does male circumcision work to prevent HIV infection?

A
  • inner part of the foreskin contains many langerhans cells which are prime targets for HIV
  • reduces the ability of HIV to penetrate due to keratinisation of the inner part of foreskin
  • contains many bacteria, so infection reduced, so HIV transmission reduced
258
Q

What are the features of acute HIV?

A
  • primary infection
  • seroconversion (the period during which the body starts producing detectable levels of HIV antibodies.)
  • symptoms start within 2-4 weeks of infection
  • similar to glandular fever/flu
259
Q

What presents during the clinical latency period?

A
  • may notice some enlarged lymph nodes
    = persistent generalised lymphadenopathy
  • start getting weird infections: shingles, thrush, oral hairy leukoplakia
260
Q

What are the consequences of late HIV diagnosis?

A
  • increased transmission
  • increased morbidity
  • increased mortality
261
Q

What are some conditions that HIV increases the risk for?

A
  • cancer (cervical, lymphomas - women with HIV will have a smear test every year)
  • TB
  • recurrent pneumonia
  • Kaposi’s sarcoma = skin lesions
  • cryptococcal meningitis
262
Q

What is the treatment of HIV?

A

HAART = Highly Active Anti-Retroviral Therapy

3+ antiretroviral drugs = 2NRTI + other
- act on different points in replication cycle to suppress viral replication

263
Q

How does HIV develop drug resistance?

A
  1. Non adherence
    - missing a dose can cause resistance
  2. Drug-drug interactions
    - some drug decrease drug level e.g. clopidogrel
    - some drugs increase drug levels e.g. steroids
264
Q

When are charcoal and green swabs used?

A

charcoal = For bacterial specimens
green = special viral transport medium

265
Q

What does the HIV virus envelope contain?

A

RNA
Capsid
RNA reverse transcriptase

266
Q

What type of pathogen causes a ringworm infection?

A

Skin fungal infection (NOT a worm)

267
Q

What is the pre-patent period in helminth diseases?

A

Interval between acquiring infection and the appearance of eggs/larvae in the stool

Emily Phase 2a (15 decks)

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