Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bacteriology > Bacterial Pathogenesis > Flashcards

Bacterial Pathogenesis Flashcards

1
Q

What is the difference between an infection and a disease?

A

Infection is the presence of a micro-organism in/on host tissue while disease is the pathological + clinical consequence of an infection

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

What is an opportunistic pathogen compared to a true pathogen?

A

Opportunistic pathogens are usually commensal/environmental while the mere presence of a true pathogen can initiate disease

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

What is the normal function of a commensal bacterium?

A

Metabolism
Immune system development
Colonisation resistance
Protection

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

What are some aseptic sites?

A

Lower resp tract
Upper urogenital tract
Blood, CSF, Synovial fluid
Internal organs and tissues

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

Define pathogenesis

A

Mechanisms by which an infectious agent induces symptoms or pathology

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

What are the different sources of disease?

A

A. Endogenous
B. Animals within a group
-epidemic
-endemic
C. Animals of other species
D. Environment

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

What are direct methods of transmission?

A

Mucosal or droplets: oral, respiratory, urogenital

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

What are methods of indirect tranmission?

A

A. Food and water (fecal oral)
B. Fomites
C. Arthropods - biol and mech
D. Iatrogenic
E. Nosocomial

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

Why are arthropod infections considered invasive/systemic?

A

There is direct entry into the vascular system

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

Why are the Outer Surface Proteins of Borrelia burdorferi important to their pathogenicity?

A

OspA and OspB are the most abundant
Contribue to phase and antigenic variation
Manipulate their expression for survival in different body temps/pH of hosts

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

What allows pathogenic bacteria to overcome normal microflora?

A

Large inoculum
Abx
Host factors - immune suppression, reduced peristalsis
Physical destruction

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

What are some of the mechanisms of persistence in Borrelia burgdorferi?

A

Active immune suppression
-Innate and adaptive: C’ inhibition, induce anti-inflammatory cytokines, tolerization of MAC and lymphocytes, sequester AB
Immune evasion
-Phase and antigenic variation: gene conversion/mutn/recomb, variable Ag expression
-Physical seclusion

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

What are the symptoms of canine lyme disease?

A

Long incubation - arthritis after weeks/months
Rare neurological issues
May cause glomerulonephritis due to immune complexes -> blood in urine

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

Does Coxiella burnetti require ticks as a vector for transmission to humans?

A

No, not tick dependent

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

What disease does Coxiella burnetii cause?

A

Q fever in humans
Ruminant infections usually asymptomatic
Ovine - abortions

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

What is Tularemia?

A

Bacteria septicemia caused by Francisella tularensis - highly virulent, bacterial weapon

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

List some potential sites of entry for bacteria

A
  1. Inhalation - Resp Tracts
  2. Ingestion - GI tract
  3. Coitus - Urogenital
  4. Mucous membranes
  5. Wounds, bites, injections
  6. Transplacental
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Whats the difference between the challenge dose and the infective dose, and when does infection occur?

A

Challenge dose is the number of bacteria that are actually encountered while the infective done is the minimum number of bacteria that are required to initiate infection. When challenge dose >/ inf dose, infection may occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why are flagella important in motility and chemotaxis?

A

Movement to invasion/attachment site or away from negative stimuli, can function as adhesin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does the flagella contribute to entry and establishment of Borrelia burgdorferi?

A

Endoflagella
Spirochete moves as a corkscrew
Hidden from immune recognition
Allows mobility even in viscous environmnet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the steps of actin polymerisation motility of Listeria?

A

Internalized in primary vacuole
Secretion of bacterial escape proteins
Vacuole membrane disrupted
Free cytoplasmic bacteria recruit and polymerize host’s actin
Propel bacteria and allows intrusion into adjacent cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What receptors to fimbriae adhesins tend to bind to?

A

Host glycolipid or glycoproteins such as:
Mannose
Sialic acid
Galactose
Glucosamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What receptors do non-fimrial adhesins tend to bind to?

A

Host glycoproteins or glycan
ECM glycoproteins such as fibronectin, E-cahderin, Integrins
Form cross bridges that confer robust adherence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does invasion refer to?

A

Breach of epithelial barriers
Can be into or between euk, cells.
Utilize invasins and proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are invasins?

A

Pathogen surface factors that drive invasion and can function as adhesins. Can manipulate rearrangement of cell cytoskeleton to promote uptake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Briefly outline salmonella invasion

A

Induce membrane ruffling and consequent pseudopoda uptake of bacteria.
Remain within phagosome and replicate there while cell surface returns to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

List some non-specific host defence mechanisms

A

Physical barriers - skin, mucus +mucociliary elevator, pH, degradative enzymes, dessication
Nutrient sequestering
Commensal microbes
Innate immune response - complement, inflammatory response, PRRs, fever

28
Q

How do pathogens get the nutrients for proliferation?

A

Intracellular path - compete with host for nutrients available to the cell itself
Extracellular - enxzymes to degrade proteins and obtain short peptides for bacterial growth

29
Q

What are some Iron Acquisition mechanisms?

A

Haeme/Tf/Lf binding proteins ->Streptococci, Pasteurella
Binding proteins - siderophores, transport mechanisms for Hg, Heme, etc

30
Q

What proteins are currently being investigated as a vaccine candidate?

A

Iron binding proteins

31
Q

How do pathogens overcome host defences?

A

Rapid replication
Low immunogenicity
Anti-opsonic activity
Intracellular survival
Concealment
Antigenic variation
Extracellular products

32
Q

What are some methods that bacteria use to lower their immunogenicity?

A

Reduce antigenicity with capsules/LPS Oantigen

33
Q

How do polysaccharide capsules reduce the antigenicity of bacteria?

A

Composed of polysaccharides such as Hyaluronic acid + scialic acid present in human and animal tissue that is not recognized as pathogenic
Expressed in infection, used as vx

34
Q

Give an example of a capsule forming bacteria

A

Pasteurella multocida
Has 6 different capsular antigens that contribute to differentiating strains
16 serotypes identified based on LPS

35
Q

What is the potential role of hyaluronidase in pathogenesis?

A

Breaks down Hyaluronic Acid
Contributes to invatsion and dissemination - degrading ground substance in ECM
Tightly regulated - production where capsule loss may be beneficial

36
Q

Give examples of 2 bacteria species that produce hyaluronidase?

A

Pasteurella multiocida
Staphylococcus aureus

37
Q

What is an important bacteria species that forms sialic acid capsules?

A

Neisseria meningitidis -> sepsis and meningitis in humans
Bleb formation of capsule
Group C - unique bacerial sxr that can be a successful vaccine
Group B - homologous to human cell molecules, non immunogenic

38
Q

Define immune tolerance

A

The process in which host immune system does not attack an antigen
Self tolerance
Acquired/Induced tolerance - can be created to external antigens

39
Q

What are some potential problems with immune tolerance?

A

Tolerance of infection in pregnancy
High persistent doses of circulating Ag

40
Q

How does LPS work as an anti-opsonic factor?

A

Binds complement away from cell surface
Sugar side chains not well recognized by complement

41
Q

How do M-like proteins function as anti-opsonic factors?

A

Factor-H (complement blocker) binds to M protein, C3b binds to Factor H and blocks opsonization

42
Q

How does Protein A function as anti-opsonic factors?

A

Non-specifically bind to Fc region of IgG, no recognition by phagocytes

43
Q

How do bacteria survive intracellularly and inhibit inflammation?

A

Stimulate secretion of anti-inflammatory signalling
Block chemotaxis
Kill phagocytes

44
Q

How do extracellular enzymes prevent oposinisation?

A

Break down AB/Complement and prevent opsonization

45
Q

How do mycobacteria inhibit inflammation?

A

Infect macrophages
Produce:
IL-6 -> Inhibit TCell activation
IL-10 -> Immunosuppressant
TGF-B -> antiinflammatory

46
Q

How do bacteria inhibit chemotaxis and give an example

A

Formylated peptides secreted by growing bacteria are highly recognized by PMN
S. aureus produces CHIPS that binds to PMN receptor and blocks major ligand recognition -> no chemotaxis

47
Q

How do bacteria survive intracellularly and inhibit inflammation?

A

Stimulate secretion of anti-inflammatory signalling
Block chemotaxis
Kill phagocytes

48
Q

How do bacteria, such as M. haemolytica and salmonella, kill phagocytes?

A

Toxins + induce apoptosis.
M. haemolytica
Secrete leukotoxin which:
Impairs phagocytosis
As well as:
Reduces lymphocyte proliferation
Cytotoxic
Lyses platelets

49
Q

How do bacteria survive intracellularly?

A

Resist killing and multiply in phagocyte
Inhibit fusion of phagocytic lysosome with the phagosome

50
Q

Give examples of how bacteria inhibit phagosome fusion with phagocytic lysosome

A

M. tuberculosis - cell wall components released that modify lysosomal mem and inhibit fusion
Chlamydia - cell wall component modify phagosome mem
Listeria - escape proteins disrupt phagosome mem

51
Q

How do bacteria conceal themselves from the immune response?

A

Acquisition of host molecules
-ie. Fc bidning protein: binding Fc of IgG so it cannot be recognized
-ie. Fibrinogen binding protein: limit Ab detection
Intracellular locations
‘Privileged’ locations

52
Q

How do bacteria demonstrate antigenic variation?

A

Phase variation
-ie. salmonella flagella subunit
Antigenic drift
-changes in epitopes due to immune selection acting on aa sequences

53
Q

What are some extracellular products bacteria have to overcome host defences?

A

Secreted antigens - bind opsonins/ab and prevent interaction with pathogen
Toxins - compromise host defence
Modulins - modulate host response via cytokines

54
Q

What are 3 types of bacterial toxins?

A

Exotoxins
Endotoxins
Superantigens

55
Q

What are some classes of bacterial exotoxin?

A

Membrane damaging”
-enzymatic
-poreforming
Cellular modification of:
-regulatory proteins
-ion channels
-protein synthesis
-neurotransmitter release

56
Q

Give an example of bacteria with enzymatic lysis

A

C. perfringens alpha toxin
Targets phospholipid bilayer
Hydrolyses cell membrane lipids

Eyrthrocyte lysis important species tropism

57
Q

Give an example of pore formation exotoxin

A

S. aureus alpha toxin forms a pore in the membrane
Disrupts ion balance, lysis

58
Q

What is an example of a cellular modifying toxin?

A

Tend to be A-B toxins
E.Coli
The labile toxin- increase adenylate cyclase activity
Verotoxin or shiga-like toxin - blocks protein synthesis
C. diptheriae
Diptheria toxin - inactivate aa transfer and prevent protein synthesis
C. tetani
Tetanospasmin - block inhibitory trasnmitter release

59
Q

What is an example of bacterial endotoxins?

A

Primarily lipid A component of LPS of Gram-ve bac
interact with humoral and cellular factors and lead to inflammatory mediator release
High levels can lead to significant effects (fever, DIC, shock)

60
Q

How do superantigens confer toxic effects?

A

Non specific Tcell activation by binding to MHC class II mol
Excessive lymphokine production
Eg. Staph Toxic Shock Syndrome Toxin

61
Q

How do fungal exotoxins cause damage?

A

Hepatotoxicity
Mucosal haemorrhage
Immunosuppression
Carcinogenesis

62
Q

What is toxicosis intoxication?

A

Toxin presence can damage host even in absence of pathogen

63
Q

What are the possible outcomes of infection?

A

Acute or chronic disease
-infective agent excreted
-spontaneous recovery
Asymptomatic carriers
-include convalescent carriers
Latency
-dormant phase

64
Q

What influences the outcomes of infection?

A

Immune status
Bacterial factors - virulence
Host factors -stress, age, diet, general health, existing infections, genetic susceptibility
Environmental factor - hygiene, crowding, weather

65
Q

What are the possible ways infection can resolve?

A

Complete recovery
Recovery with persistent damage
Persistence and carriage
Death

66
Q

Why is understanding the pathogenic cycle critical?

A

Disease control:
-management and husbandry
-anti-microbial therapy
-immunotherapy
-preventative vaccines
-quarantine/culling

Bacteriology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions