microorganisms in disease and infection Flashcards

1
Q

define pathogenicity

A

the capacity of a micro-organism to cause an infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the main characteristics which an organism must show to be pathogenic

A

transmissibility
establisment in or on a host
Harmful effects
Persistence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the stages in the chain of infection

A

pathogenic organism- in adequate numbers.
reservoir or source that allows the organism to survive and multiply.
mode of exit from the source
mode of transmission from the source to the host
Portal of entry through which the pathogen can enter the host
Suceptible host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

define virulence

A

the degree to which a microorganism is able to cause disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the main routes of transmission for infection

A

faecal oral
blood borne
respiratory
direct contact- hand to hand to mucous membrane.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

define LD50- Lethal dose

A

lethal dose- dose of organism which causes death in 50% of the exposed population.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

define ID50- Infection dose

A

ID50-dose or organism which causes infection in 50% of the organism exposed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how do pathogens colonise ( attachment to to what on surface of host cell)

A

Ligands in the organism binds to receptors on the surface of the host cell
Complementary ligand- receptor interaction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

define infectivity

A

The ability of a microorganism to become established in/on a host.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Examples of ligand receptor interactions

A

E. coli P fimbriae: glycolipids on human uroepithelial cells

S. pyogenes protein-F: fibronectin (Large multifunctional glycoprotein)

Influenza haemagglutinin: respiratory epithelial sialic acid receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the virulence mechanisms

A

adhesion, toxic affect, tissue damage, interference with host defence mechanisms, facilitation of invasion
modulation of host cytokine response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is a important toxin produced by the gram -ve bacterial cell wall and name infections where endotoxins are used

A

endotoxin
E.coli
Neisseria meningitidis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

In which layer of the gram -ve bacterial wall in endotoxin an active part of

A

active component of the liposaccaride membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

when is an endotoxin released

A

released from damaged or dead cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is a lipopolysaccharide made from

A

Lipid A, polysaccaride and a specific O antigen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the host response to an endotoxin

A

uncontrollable T lymphocyte response- cytokine release, shock and cardiac and renal failure.
uncontrollable clotting cascade activation- DIC, depletion of clotting factors and a tendency to bleed.
uncontrollable complement activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what effects do the neisseria meningitidis endotoxin have on the host

A

mediated increase in vascular permeability causes loss of protein, fluid and plasma into the tissues, with pathological compensatory vasoconstriction.
peripheral necrosis.

18
Q

Are exotoxin produced by living or dead bacteria

A

living

19
Q

Are endotoxin produced by living or dead bacteria

A

dead

20
Q

how does the Boutulism exotoxin work (where does it work)

A

affects the presynaptic membrane so that the neurotransmitter cannot be relased.

21
Q

How does the preformed botulism toxin colonise the host.

A
Ingestion of pre-formed toxin
Contaminated food
Infection of dirty wounds
May be trivial wounds
Gastrointestinal colonisation (infants)
22
Q

what is the clinical presentation of botulism

A

diplopia, dysphagia, dysarthria, dry mouth, death, rigid paralysis (respiratory failure)

23
Q

How does clostridium tetani colonise the host

A

infects wounds

24
Q

what is the toxin in tetanus called

A

tetanospasim.

25
Q

How does the tetanospasim (tetanous toxin work)

A

binds to nerve synapses

inhibited release of inhibitory neurotransmitter in the central nervous system.

26
Q

what are the main clinical presentations of tetanus

A

Jaw spasm
rigid paralysis
opisthotonos (body thrown into shapes which depends on muscle strength)
death caused by respiratory paralysis

27
Q

what is the treatment for tetanus

A

metronidazole and tetanus antitoxin.

28
Q

what effect do the strep pyogenes virulence factors have

A

promote connective tissue breakdown and invasion.

29
Q

what infections can strep pyogenes cause

A

streptococcal sore throat
Erysipelas- skin infection
Necrotizing fascilitis.
Scarlet fever- streptococcus (sore throat caused by erthyrogenin toxin.)

30
Q

what is the function of Hyaluronidase and streptokinase virulence factor of S pyogenes

A

Break down connective tissue components – facilitate tissue invasion

31
Q

what is the function of C5a peptidase virulence factor of S pyogenes

A

inactivates complement component C5a

32
Q

what is the function of streptolysisn O and H virulence factors of S pyogenes

A

Lyses RBC, WBC and platelets.

33
Q

what is the function of the Erythrogenic toxin (phage-encoded) virulence factor of S pyogenes

A

rash and scarlet fever.

34
Q

what is the function of the toxic shock syndrome toxin virulence factor of S pyogenes

A

Streptococcal toxic shock syndrome is superficially similar to a syndrome of endotoxin release

35
Q

what are the symptoms of infection of S pyogenes

A

mild- red and swelling around cheeks

severe- necrosis, necrotizing fascialis

36
Q

how does S pyogenes inhibit phagocytosis

A

M Protein binds fibrinogen and masks bacterial surface, blocking complement binding and opsonisation.

37
Q

how does S pneumonia inhibit phagocytosis

A

Polysaccharide capsule inhibits opsonisation and therefore phagocytosis

38
Q

which organisms are intracellular. This means they invade cells of host to clear, so you must kill your own cells to get rid of it.

A

Mycobacterium tuberculosis
Salmonella typhi
Listeria monocytogenes

39
Q

are viruses intracellular or extracellular organisms

A

intracellular,

40
Q

what is the composition of a virus

A

Genome - RNA or DNA
Capsid - protein
(Envelope – lipid bilayer)