Infections I: Aetiology, Symptoms & Transmission of Infection

Question 1

Define: Infection

Answer 1

The colonisation of a host organism by a pathogenic organism

Question 2

List the 6 stages of infectious disease

Answer 2

1. Acquisition
2. Colonisation
3. Penetration
4. Spread
5. Damage
6. Resolution

Question 3

What is the acquisition stage known as if it is an exogenous infection?

Answer 3

Transmission

Question 4

How can exogenous microbes be transmitted?

Answer 4

Direct contact e.g. STIs
Inhalation/droplet infection e.g. common cold
Ingestion/faecal-oral route e.g. gastroenteritis
Trauma/inoculation e.g. malaria
Trans-placenta e.g. congenital toxoplasmosis

Question 5

List 3 factors that the success of colonisation depends on

Answer 5

1. pH
2. Temperature
3. Competing endogenous organisms

Question 6

List 2 mechanisms that some organisms have evolved to help colonisation

Answer 6

1. Mucolytic enzymes = penetrate mucous layers

2. Adhesins = help stick to colonisation site

Question 7

Define: Biofilms

Answer 7

Complex colonies of bacteria
Cells stick together and adhere to a surface (slimy protective outer layer)
More difficult to treat than isolated bacteria

Question 8

What must an organism do in order to invade/penetrate?

Answer 8

Breach the surface barrier

e.g. skin, mucous membrane

Question 9

What in the upper respiratory tract protect against particulate exposure?

Answer 9

Muco-ciliary clearance

Cough reflex

Question 10

What defends the GI tract from penetration

Answer 10

Stomach acid

However organisms can damage the mucosal surface by releasing toxins or getting taken into cells

Question 11

List the 3 ways an invading organism can spread

Answer 11

Along tissue planes
By extension of colony into surrounding area
Via vasculature/lymph (= effective rapid spread)

Question 12

What are the 3 lines of defence against an invading organism?

Answer 12

1st  = intact skin and mucous membranes
2nd = phagocytosis
3rd = inflammation

Question 13

How do intact skin and mucous membranes act as defences against invading organisms?

Answer 13

Mucous traps bugs
Sweat (pH)
Secretions e.g. stomach acid, lysosomes in tears

Question 14

How does phagocytosis act as a defence against invading organisms?

Answer 14

Phagocytic cells in blood (monocytes, neutrophils), tissues and lungs (macrophages) engulf and destroy micro-organism

Question 15

How does inflammation act as a defence against invading organisms?

Answer 15

As well as phagocytic cell increase as local site, body tries to limit spead by e.g. forming clot

Question 16

How is damage caused by an invading organism?

Answer 16

Mechanical damage from bulk effects e.g. biofilm obstructing a hollow organ
Toxins
Altered function of host cell
Host response

Question 17

How do toxins from an invading micro-organism cause damage?

Answer 17

Exotoxins = produced inside bacteria and diffuse out, very toxic
Endotoxins = LPS-protein complexes, mainly in cell wall, G-ve bacteria, less toxic

Question 18

How does the altered function of a host cell cause damage?

Answer 18

Can affect functioning of cell, tissue or organ

Can be as the body tries to combat infection e.g. c.dif causes diarrhoea

Question 19

How does host response cause damage?

Answer 19

Usually inflammatory then immune response

Can get swelling, pus, scarring, necrosis

Question 20

Describe the ‘vicious cycle’ of inflammation

Answer 20

1. Tissue infected by bacteria and toxins
2. Inflammation of tissue
3. Immune system chemicals attack tissue to contain infection
4. More tissue damage as collateral effect
5. More immune system chemicals released
   6 More inflammation
   etc etc

Question 21

What is the resolution stage of infection?

Answer 21

Subsiding of pathologic (disease) state = reduction of inflammation

Question 22

Define: Pathogen

Answer 22

An organism capable of causing disease

Question 23

Define: Virulence

Answer 23

Degree of pathogenicity of an organism = ability to cause disease

Question 24

Define: Attenuation

Answer 24

A reduction in the virulence of a pathogen

avirulent if gone

Question 25

Define: Exaltation

Answer 25

An increase in virulence

Question 26

What is microbial virulence controlled by?

Answer 26

Controlled genetically

e.g. genes encoding toxins

Question 27

In what ways do the expression of virulence factors respond to the environment?

Answer 27

Switching virulence on/off allows bacteria to avoid mechanical, non-specific and immune defences
Some species can also form spores

Question 28

Define: Chemotherapy

Answer 28

The use of synthetic chemicals to destroy infective agents

Question 29

Define: Chemotherapeutic agents

Answer 29

Chemicals intended to be toxic for the pathogenic organisms but safe for the host

Question 30

Define: Microbe

Answer 30

General term used to describe bacteria, viruses and fungi

Question 31

Define: Parasite

Answer 31

General term used to describe protozoa and helminths

Question 32

What does the selective toxicity of chemotherapy for bacteria depend on?

Answer 32

It depends on exploiting the biochemical differences between pathogen and host

Question 33

What are the targets of chemotherapy for bacteria?

Answer 33

3 general classes of biochemical reaction (I, II, III)

Question 34

Describe the 3 classes of biochemical reaction which are the targets of chemotherapy for bacteria

Answer 34

Class I = reactions which utilise glucose & other carbon sources to produce ATP and simple carbon compounds
Class II = pathways utilising energy and class I compounds to make small molecules (e.g. amino acids, nucleotides)
Class III = pathways that convert small molecules into macromolecules (e.g. proteins, nucleic acids, peptidoglycan)

Question 35

Why are Class II reactions better targets for chemotherapy then Class I reactions?

Answer 35

Class II:
Folate synthesis in bacteria is inhibited by sulphonamides
Folate utilisation is inhibited by folate antagonists e.g. trimethoprim

Question 36

Why are Class III reactions important targets for chemotherapy?

Answer 36

Bacterial protein synthesis selectively inhibited by antibiotics that:
Prevent the binding of tRNA = tetracyclines
Promote misreading of mRNA = aminoglycosides
Inhibit transpeptidation = chloramphenicol
Inhibit translocation of tRNA = erythromycin