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Infection And Immunity > Causes Of Infection > Flashcards

Causes Of Infection Flashcards

1
Q

What is this?
Smaller than cellular organisms
Metabollically inert
Simple structure
Needs host cell to replicate
1/100th size of bacteria
Infects animals plants and bacteriophages

A

Virus

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2
Q

Components of a virus

A

CAPSD IS PROTEIN COAT
GENES (DNA OR RNA)
Cell wall
Sheath
Core
Some have lipid envelope derived from host cell

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3
Q

What is this?
Have genetic material no organelles

Rely on host organelles or systems to reproduce

Use surface proteins to bind to a cell and put their genetic material in it

A

Virus replication

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4
Q

can lay dormant for decades, emerging to cause shingles

A

Chickenpox

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5
Q

infects hosts for days, causing a cold

A

Rhinovirus

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6
Q

causes chronic
liver infection over years

A

Hepatitis C VIRUS

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7
Q

Unicellular organisms
Cell membrane
Cell wall
No nucleus
• Genetic material is DNA but not bounded by a membrane
Reproduce asexually
Some move using flagella and attach via fimbriae

A

Bacteria

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8
Q

stain pink
stain purple

A

Gram -ve
Gram +ve

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9
Q

Meningococcal sepsis
Bacterial endocarditis
Cellulitis
Streptococcal throat infection

A

Bacterial diseases

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10
Q

Eukaryotes
Cell membrane
cell wall
nucleus
cytoplasmic structures
Reproduce sexually and asexually

A

Fungi

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11
Q

Mild infections-
• thrush
•athletes foot
• ringworm

• Severe infections –In the Immunocompromised
• Cryptococcal meningitis in HIV patients
• Invasive candida in ICU –Or Immune competent

A

Fungal infections

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12
Q

Ectoparasites
– live outside body
• Fleas
• Ticks

Endoparasites
– Iive inside body
• Worms

Epiparasites
– a parasite which lives on another parasite
• Malaria (mosquito)

A

Parasites

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13
Q

Giardia
Cause bloody diarrhoea

Caught from drinking infected water

May be seen in stool under a light microsope

Cyst form aids survival + spread

A

Parasitic diseases

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14
Q

One of the biggest killers worldwide

• Complex life cycle

• Reproduce in female anopheles mosquito

A

Malaria

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15
Q

Cestodes (tapeworms)
Segmented, flat

Trematodes (flukes)
Unsegmented, flat

Nematodes (round worms)
Cylindrical, have digestive tract with lips, teeth and anus

A

Worm helminths

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16
Q

Tapeworms – Fish, pork, beef tapeworms

• Cause
– Malabsorption
– Malnutrition in chronic disease
– Cysts in muscle or brain

A

Cestodes

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17
Q

Round worms
Biggest

Cause diarrhoea and malabsorption

A

Nematodes

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18
Q

Flukes
-lung flukes
-liver flukes
- pancreatic
-intestinal
-blood= schistosoma

A

Trematodes

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19
Q

Smallest infective agents known

Proteinaceous Infectious particles

Lack nucleic acid - not a ‘living organism’

Proteins fold abnormally and accumulate

mainly in neural tissue

They are very difficult to destroy

• Concerns over cleaning surgical instruments

A

Prions

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20
Q

CJD- fatal, degenerative neurological disease – Affects 1 in a million people each year – Transmitted through contaminated human growth hormone, surgical instruments and corneal grafts

• Variant CJD- typically occurs in young adults

• BSE- occurs in cattle

• Scrapie- occurs in sheep

• Kuru- similar to vCJD
– occurred in Papua New Guinea in 1950s
– thought to be spread by cannibalism

A

Prions diseases

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21
Q

Nutrients - carbon, hydrogen, oxygen, nitrogen

Synthesise of new molecules

Energy

A

Growth requirements

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22
Q

Break down molecules to produce energy. (lerger substrates, smaller products)

A

Catabolic metabolism

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23
Q

Use energy to combine small molecules into macromolecules (energy+ source of elements especially carbon)

A

Anabolic pathway

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24
Q

Phototrophs: uses sunlight energy to produce its energy
(photophosphoryla tion)

• Chemotrophs: extract energy from chemical bonds mainly by oxidation of electron donor compounds.

A

Source of energy

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25
Q

• Organic compunds (organotrophs)
e.g. Sugar, fat…etc

• Inorganic molecules:
(lithotrophs) • e.g. Ferrous iron ferric

iron
• Amonia nitrite

A

Source of electron donor

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26
Q

Autotrophs:
produce complex organic compounds from simple inorganic ones

• Heterotrophs: consume organic molecules as a source of carbon.

A

Source of carbon

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27
Q

availability of the main building blocks (protien, DNA, RNA, cell membrane….etc)

A

Growth and reproduction

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28
Q

fatty acids, amino acids, nucleic acids, carbohydrates…

A

Are precursors

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29
Q

vitamins.

A

Act as catalyst in the synthesis process

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30
Q

Consumed in the food

A

If organism can’t make those precursors carbs,nucleic acids amino acids fatty acids

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31
Q

No energy needed driven by concentration gradient

A

Passive diffusion

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32
Q

Need energy
Needs receptors and works against conc gradient

A

Active transport

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33
Q

Less energy
involved phosphorylation of molecule

A

Group translocation

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34
Q

Temp
Water,ph, osmolarity, oxygen, pressure. Light, physical space availablity

A

Physical requirements

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35
Q

Temperature affect protein structure and fluidity of the cytoplasm and the cytoplasmic membrane.

A

Temp

36
Q

lowest temperature that a given organism can carry out its metabolic activities

A

Minimum growth temp

37
Q

temperature at which metabolic activity is at its peak and thus growth rate is the highest.

A

Optimum Growth

38
Q

Essential for life

Bacteria usually require at least Aw= 0.8 (G-ve requires higher 0.97), and fungi at least 0.7 (water Aw= 1).

A

Water

39
Q

vapour pressure of a sample divided by that of pure water at the same temperature.

A

Water activity

40
Q

reflects high concentrations of solutes (hypertonic solution).

A

Low AW water effect

41
Q

PH effect: High or low PH inhibit microbial growth except for few!
Acidic conditions are body defense mechanism
e.g. stomach and vagina (via fermentation by normal flora)
Acidophiles can tolerate acidic conditions. Some are obligate acidophiles

Alkalinophile lives in alkaline media like soil and alkaline water (e.g. Vibrio cholerae).

A

Ph effect

42
Q

requires O2 for energy production (respiration)

A

Obligate aerobes

43
Q

do not use O2 for energy production

A

Anaerobes

44
Q

can survive with or without O2

A

Facultative anaerobes

45
Q

can tolerate oxygen levels from 2-10% (limited ability to detoxify hydrogen peroxide and superoxide radicals)

A

Microaerophiles

46
Q

Anaerobes but have some enzymes that detoxify oxygen’s poisonous forms.

A

Aerotolerant

47
Q

Skin
Mucus membrane
Stomach
Commensal microflora
Immune system: innate learnt
Behavioural: good hygiene

A

Defence mechanism

48
Q

immune cell non-reactivity to antigens.

A

Self tolerance

49
Q

Tolerance to innate antigens

A

Self tolerance

50
Q

Antigens encountered within hours after birth

A

Neonatal tolerance

51
Q

Acquired tolerance

A

Self tolerance with self recognition is key in maturation of both Tand B cells

52
Q

When immunological tolerance breakdown what does it lead to

A

Autoimmune disease

53
Q

What is this: T cells have to recognise s LF MHCs (self recognition) and display S T

A

Self tolerance

54
Q

Loss of B CELLS leads to A I D

A

Auto Immune Disease

55
Q

Pre T cells develop in the THymus via P S

A

Positive Selection

56
Q

Self tolerance happens by the opposite of positive selection

A

Negative selection

57
Q

Of the T cells produced what percentage become fully mature immunocompetent cells

A

1-5

58
Q

deletion of self reactive T cells happen if they leave the thymus and meet what? What type of protein does it meet

A

Contact unrecognised self protein

59
Q

B cells also develop what? S TOL

A

Self tolerance

60
Q

Non reactivity to an antigen that should cause immune response is what

A

Acquired tolerance

61
Q

What are these examples of? Failure of immune system to destroy sperm and fertilised eggs

A

Acquired tolerance

62
Q

Which type of tolerance can be linked to inflammatory bowel disease

A

Oral

63
Q

IgE-mediated, immediate type hypersensitivity (IgE-mediated degranulation of mast cells) (e.g. allergic rhinitis, allergic asthma, urticaria)

A

Type 1

64
Q

Cytotoxic reaction (complement lysis/ADCC) (e.g. drug allergy)

A

Type 2

65
Q

Immune complex reaction- complement activation) (e.g. allergic vasculitis)

A

Type 3

66
Q

T-cell mediated, delayed type hypersensitivity (e.g. allergic contact eczema)

A

Type 4

67
Q

Small 15-40,000 Mw proteins

Soluble

Long lasting in environment

Low dose of allergen Mucosal exposure.

Often proteases

Most allergens promote a Th2 immune

A

Properties of antigens

68
Q

Atopic diseases caused by individuals’ tendency to mount over zealous IgE responses

Example - Dust allergens

A

Type 1 IgE mediated

69
Q

Protease allergens can potentially activate PAR receptors

A

Protease mediated type 1 IgE hypersensitivity

70
Q

IgE mediated reaction to inhaled allergens
Upper airways:
rhinitis
• nasal itch;
• Sneeze;
• Rhinorhoea;
• nasal obstruction.

Lower airways:
asthma
• bronchoconstriction
, mucus hypersecretion;
• Wheeze;
• Breathlessness;
• Cough.

A

Asthma/ rhinitis

71
Q

Direct/rapid route in to blood stream (sting, ingestion) Route and dose greatly affect out come

A

Urticaria/ anaphlaxis

72
Q

Cold induced urticaria- triggered by NLP3 mutants

Overly sensitive mechanotransduction induces mast cell degranulation

Vibrational urticaria over activation of the GPCR- EMR2

A

Mast cell role in urticaria

73
Q

mainly kill parasites via reacting towards opsonised parasites.
large amounts of IL5 / IL3 in allergy cause degranulation

A

Eosinophils

74
Q

IgE response evolved to expel/destroy helminth/protozoal pathogens

A

IgE EVOLUTION

75
Q

IgG mediated destruction of blood cells/platelets-autoimmune hemolytic anemia. Hemolytic disease of the newborn Thrombocytopenia. Change in signalling Type IV

A

Non IgE allergic diseases: Type 2

76
Q

Antibodies attach to epitopes on self cells

Induces activation of compliment

Results in vasodilatation and migration of phagocytic cells to the effected tissue.

Promotes activation of membrane attack complex.

Used to refer to antibodies that attacked self blood cells, but now is used to describe antibodies that target other tissues.

A

Type 2

77
Q

Caused by antigen antibody complexes.

Antigen can be self antigens (i.e., nuclear material as in Lupus) or non-self antigens such as bacteria.

Promotes inflammatory response.
Can be either :
Local form Type 3 Hypersensitivity
Systemic form Type 3 Hypersensitivity

A

Type 3

78
Q

individual is immunised against an antigen, subcutaneous injection of a high concentration of that antigen induces an inflammatory response peaking within seven hours at that site.
Example - inhaled spores causing extrinsic allergic alveolitis.

A

Type 3 local

79
Q

Antigen complexes may form systemically - promoting system wide inflammatory responses.

Example – Post infectious glomerulonephritis

  • antibody complexes become stuck in the glomeruli of the kidney inducing an inflammatory response.

Can be caused by any bacterial infection, but most common complication with streptococcal pharyngitis

A

Type 3 systemic

80
Q
  1. Antigen injected into subcutaneous tissue and processed by local antigen presenting cells
  2. A TH1 effector cell recognises antigen and releases cytokines that act on vascular endothelium
  3. Phagocytes to site of antigen injection causes visible lesion is recruited
A

Type 4 delayed hypersensitivity

81
Q
  1. Contact sensitising agent penetrates the skin and bids to self proteins that are taken up by Langerhans cells
  2. Langerhans present self peptides haptenated with the contact sentising agent to TH1 cells which secrete IFN-Y and other cytokines
  3. Activated keratinocytes secrete cytokines like IL 1 AND TNF-A and chemokiens such as CXCL8 CXCL11 and CXCL9
  4. Products of keratinocytes and TH1 CELLS ACTIVATE MACROPHAGES TO SECRETE MEDIATORS OF INFLAMMATION
A

Type 4 hypersensitivity

82
Q

Related to Helper T cells interacting with activated cytotoxic T cells, NK cells or macrophages.

Response is delayed and cannot be transferred in the serum.

Examples BCG – injection of inactivated M.
bovis will cause a localised inflammatory response after 2 days.
Indicates that the individual has already encountered the TB bacillus.
Contact dermatitis Donor organ rejection

A

Type. 4

83
Q

Mediated via lipid soluble urushiol oil haptens binding MHCI

A

Allergic contact dermatitis

84
Q

Binds α-gliadin (derivatised by transglutaminase-enzyme)

A

Coeliac disease

85
Q
  1. Peptides naturally produced from gluten do not bind to MHC class 2 molecules
  2. An enzyme tissues transglutaminase modifies the peptides so they now can bind to the MHC class 2 molecules
  3. The bound peptide activates gluten specific CD4 T cells
  4. Activated T CELL can kill mucosal epithelial cells by binding FAS. They also secrete IFN-y which activates the epithelial cell
A

Cellular destruction in coeliac disease

Infection And Immunity (8 decks)

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