Infectious Disease And Therapeutics

Front 1

Infection

Back 1

Invasion of bodily tissues by microorganisms. May or May not generate symptoms. Many cleared by immune system before symptoms show.

Front 2

Colonisation

Back 2

When pathogens are present but not causing any damage

Front 3

2 types of colonisation

Back 3

Transient & permenant

Front 4

What is permenant colonisation

Back 4

When colonisation is permenant, individual becomes carrier of it. E.g typhoid Mary.

Front 5

What are two types of pathogens

Back 5

1) opportunist

2) specialists (oblogate)

Front 6

Specialists (obligate)

Back 6

1. Effect their own entry to host.

2. Have 1 or many hosts.

3. Often tissue specific

E.g vibrio cholerae

Hint 6

3 points

Front 7

Opertunists

Back 7

1. Take advantage of entry opportunities.

2. Do not always have to live as pathogens.

E.g S.aureus (MRSA)

Front 8

How to establish infection?

Back 8

Susceptible host must encounter virulent organism. Organism must gain entry to HOST. It must find a site to MULTIPLY.

Front 9

What is virulence?

Back 9

The ability of an agent to cause disease.

Front 10

What is virulence factor?

Back 10

Characteristic of agent which facilitate the generation of disease.

Hint 10

Generation.

Front 11

Infection risk calculation

Back 11

Dose+time+virulence/host susceptibility

Hint 11

DTV

Front 12

What could be factors of susceptible hosts?

Back 12

Age

Poor nutrients

Injury/wounds

Immunocompromised patients

Genetic

Poor general health

Front 13

Qhat are the stages of infection

Back 13

1. Contact/Exposure

2. Adherence (some infections stop here)

3. Entry

4. Transport around the body (specific organs or generic infection)

E.g shingella

Hint 13

4 steps

Front 14

Explain stages of shigella infection

Back 14

1. Shingella enter epithelial cells.

2. Shigella multiplies in cells.

3. Shingella invade neighbouring epithelial cells thus avoiding immune response.

4. Lumps/abscess form die to epithelial cells killed.

Front 15

What are the 2 host defences?

Back 15

1) Innate immune response

2) immune system

Front 16

What is innate immune response?

Back 16

Physical, anatomical & chemical barriers

Front 17

What are the two types of immune system?

Back 17

1) Specific

2) Non-specific

Front 18

Explain non-specofoc immune system?

Back 18

1. Inflammation response

2. Phagocytic WBCs

3. Interferon

Hint 18

3 points

Front 19

SPECIFIC- ACQUIRED IMMUNITY TYPES

Back 19

1) Naturally acquired = active and passive

2) Artificially acquired = active and passive

Front 20

Naturally acquired

Back 20

Active = Infection contact with pathogens

Passive = Antibodies pass from mum to foetus via PLACENTA

Front 21

Artificially acquired

Back 21

Active = Vaccine_dead/attenuated pathogens.

Passive = injection of immune serum (e.g gamma globulin).

Front 22

What can damage physical defence?

Back 22

Medical operations

Wounds/burns

Animal bites

Front 23

What happens when a disease occurs?

Back 23

Physical defence is damaged so secondary Infection occurs. E.g flu= lung damage = pneumonia.

Front 24

PORTALS OF ENTRY

Back 24

1. Respiratory entry - TB, Diphtheria

2. Alimentary tract - Salmonella, Polio

3. Urino-genital tract - Gonorrhoea, thrush

4. Placenta - Rubella

Front 25

Phagocytosis evasion

Back 25

Bacteria ESCAPES via neutralised vacuoles

Front 26

Direct cell entry

Back 26

Gain entry into nonspecific phagocytic cells use invasins

Front 27

Cell-Cell transport

Back 27

1. Transcytosis - movement through Target cells and release.

2. Movement through CYTOPLASM DUE TO ACTIN POLYMERIZATION.

Front 28

Resistance to phagocytosis

Back 28

Capsule (polysacch and protein)

Fimbriae (pili group a streptococcus)

Surface proteins

Hint 28

3 points

Front 29

Exotoxin

Back 29

Excreted by bacteria when they grow. Can travel around body and can have an impact removed from the site of infection. Associate with spore formation.

Front 30

Enterotoxins

Back 30

Type of exotoxin.

Act on small Intestine, cause fluid secretion. Generate vomit and diarrhoea.

Front 31

Immune modulation

Back 31

Substance that stimulates/stresses immune system response & may help body fight cancer, infections and other diseases.

Monoclonal antibodies, cytokines, vaccines

Front 32

Immune avoidance

Back 32

Strategy used by pathogenic organisms and tumours to evade immune response to maximise probability of transmission of disease.

Front 33

Enzymes virulence factors ImgA

Back 33

Proteases made by pathogens that colonise mucosal surface.

Front 34

AB toxins

Back 34

B = lets toxins IN cell

A = allows toxin to impact.

Enzymic activity not active until it is released by AB complex.

Front 35

Botulinum toxin

Back 35

Cause flacid paralysis by blocking release of ACH so no muscle contraction

Front 36

Tetanus toxin

Back 36

Binds to inhibitory interneurones. Prevents release of glycine. Prevents relaxation of muscle.

Front 37

Diptheria toxins

Back 37

Pseudo membrane forms in back of throat. Inactivates elongation of protein synthesis.

Front 38

Cholera toxins

Back 38

A subunit surrounded by 5 B subunits.

A causes activation of adenylate cyclase

Front 39

Pore-forming toxin

Back 39

Insert pore into host cell membrane. Disrupt membrane function. Produced as subunit that self-assembles as pore on membrane. E.g s.aureus alpha toxin model of pre-forming toxin.

Front 40

SUPERANTIGENS

Back 40

Toxins that act directly on T cells and antigenspresenting cells of immune system. IMPAIRS IMMUNE FUNCTION.

Front 41

Endotoxin

Back 41

1. Part of the outer membrane of CW of GN bacteria.

2. Released from growing bacterial cells that are lysed.

3. Fever

Front 42

What are the impacts of bacterial toxins?

Back 42

1. Functional changes to target cells.

2. Facilitate spread through tissues

3. Damage cell membrane and inhibit protein synthesis.