infections 1

Question 1

what is the definition of infections

Answer 1

The invasion and multiplication of a pathogenic organism in a host organism

Question 2

what are the 6 stages of infectious disease?

Answer 2

Acquisition

Colonisation

Penetration

Spread

Damage

Resolution

Question 3

what is endogenous infections?

Answer 3

organisms present in/on the body (e.g. bacteria, fungi – some examples are shown on the right)

Question 4

what is exogenous infection?

Answer 4

exogenous microbes that are not part of our typical body flora

Question 5

what are example bacterias present in oral cavity, nasopharynx , skin , GI tract, Vagina?

Answer 5

Oral cavity
Streptococcus spp
Actinomyces

Nasopharynx
Streptococcal spp
Neisseria spp
Corynebacteria spp

Skin
Staphylococcal spp
Streptococcal spp
Corynebacteria spp
Some fungal species

GI tract
Enterobacteriaceae
Enterococci spp
Clostridium spp
Bacteroides spp
Candida spp

Vagina
Lactobacillus spp

Question 6

1st line- Intact skin & mucous membranes

what is the bodys defence?

Answer 6

Sweat (pH), mucous traps bugs, antibacterial secretions e.g. stomach acid, lysozyme in tears

Question 7

2nd line
Phagocytosis & inflammation
What is the bodys defence to this?

Answer 7

Phagocytic cells in blood (monocytes, neutrophils), tissues and lungs (macrophages) engulf & destroy microorganisms

Along with phagocytic cell increase at local site, body tries to limit spread of the organism e.g. by forming clot

Question 8

what are some exogenous infection transmission?

Answer 8

Direct contact
e.g. STIs

Inhalation / droplet infection
e.g. common cold

Ingestion / faecal-oral route
e.g. gastroenteritis

Trauma / inoculation
e.g. tetanus, malaria, infected atopic dermatitis

Trans-placenta
e.g. congenital toxoplasmosis

Question 9

Explain the stage colonization

Answer 9

Organism must survive and multiply in the environment
pH, temperature, competing endogenous organisms

Some have evolved mechanisms to help colonisation
Mucolytic enzymes to penetrate mucous layers
Adhesins to help stick to colonisation site

Once established in a site (internal or external), organism has colonised but may not necessarily go on to invade & damage host tissue

Question 10

what are the features of Bacteria seldom lone cells

Answer 10

Bacteria seldom lone cells - usually form complex colonies termed “biofilms”
Have co-operation of organisms, often have slimy protective outer layer
More difficult to treat than isolated bacteria in a culture / spread plate

Question 11

what is penetration

Answer 11

To invade, organism must breach the surface barrier (skin, mucous membrane..)

Question 12

can skin avoid penetration and how?

Answer 12

Skin: most bacteria can’t penetrate intact skin

Question 13

how can upper respiratory tract avoid penetration

Answer 13

Upper respiratory tract: muco-cilliary clearance and cough reflex protect against particulate exposure
Influenza “sticks”
Droplets <5μm can reach alveoli and establish infection

Question 14

how does gastrointestinal tract prevent penetration?

Answer 14

Gastrointestinal tract: stomach acid defence but:
Organisms can damage mucosal surface by releasing toxins e.g. causing dysentery
Or get taken into cells - e.g. Salmonella typhi taken in by M cells in Peyer’s patches

Question 15

invading organisms can spread where?

Answer 15

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

Question 16

what are some damages which can take place?

Answer 16

Mechanical damage from bulk effects
Toxins
Altered function of host cell
Host response

Question 17

what is mechanical damage from bulk effect?

Answer 17

e.g. Bacteria/biofilm can obstruct a hollow organ, e.g. cystic fibrosis

Question 18

what are exotoxins

Answer 18

Exotoxins produced inside bacteria (G+/-ve) and diffuse out, usually proteins
Very toxic e.g. Clostridium tetani neurotoxin → tetanus
Strongly antigenic

Question 19

what is endotoxins

Answer 19

Endotoxins are LPS-protein complexes
Mainly in cell wall G-ve bacteria (shed)
Typically less specific toxic reactions
Weakly antigenic, often cause fever
e.g. meningococcal disease and sepsis
from Neisseria

Question 20

what does altered function of host cell mean?

Answer 20

Can affect functioning of cell, tissue or organ - Common with viruses
Can be as the body tries to combat infection - e.g. increased bowel motility in diarrhoea

Question 21

what does host response mean?

Answer 21

Host response
Host damage through response to infection

Can have chronic inflammation and immune response

Can get swelling, pus, scarring, necrosis

Question 22

what are the stages of resolution?

Answer 22

Recovery: organism cleared from body, no lasting effects

Latent infection: Initial symptoms resolve but infection not cleared and can re-occur. Often occurs with viruses – Herpes, CMV, EBV (more in Part 3)

Clinical latency: can have a period of no symptoms but the infection course is continuing. Examples include – HIV, syphilis (more in Part 3) or also during the initial incubation period

Chronic infection: some infection may never clear (HIV, chronic hepatitis), or can take long time to clear. Some may be cleared by have long-term effects.

May recover (clear infection) but have long-lived effects due to damage from infection. Example – from inflammation or leading to autoimmune disorders

Question 23

Pathogen:

Answer 23

an organism capable of causing disease

Question 24

Virulence:

Answer 24

degree of pathogenicity of an organism (ability to cause disease)

Question 25

Attenuation:

Answer 25

a reduction in the virulence of a pathogen (if gone = avirulent)

Question 26

Exaltation:

Answer 26

an increase in virulence

Question 27

Chemotherapeutic agents –

Answer 27

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

Question 28

Parasite

Answer 28

– general term used to describe protozoa and helminths

Question 29

what are the three classes of biochemical reaction:

Answer 29

Three general classes of biochemical reaction are potential targets for chemotherapy of bacteria:

Class I: reactions that utilise glucose and other carbon sources are used to produce ATP and simple carbon compounds

Class II: pathways utilising energy and class I compounds to make small molecules (e.g. amino acids and nucleotides)

Class III: pathways that convert small molecules into macromolecules such as proteins, nucleic acids and peptidoglycan

Class I reactions are poor targets.
Class II reactions are better targets:
folate synthesis is inhibited by sulfonamides and trimethoprim (bacteria), pyrimethamine (malarial parasite), methotrexate (cancer cells)
Class III reactions are important targets:
bacterial peptidoglycan synthesis selectively inhibited by β-lactam antibiotics
bacterial protein synthesis selectively inhibited by antibiotics that: prevent binding of tRNA (e.g. tetracyclines), promote misreading of mRNA (e.g. aminoglycosides), inhibit transpeptidation (e.g. chloramphenicol) or inhibit translocation of tRNA from A site to P site (e.g. erythromycin)
nucleic acid synthesis inhibition (e.g. chain termination such as by antiviral aciclovir) or by inhibiting DNA gyrase (e.g. the ciprofloxacin)