INTRO-- BACTERIOLOGY Flashcards

(95 cards)

1
Q

The vast majority of resident bacteria are —
history of co-evolution and harmonious co-existence with the host.

A

commensals

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

acquired soon after birth, are able to adhere to body surfaces.

A

COMMENSALS

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

They form stable polymicrobial communities that are present throughout life as

A

‘normal microflora’

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

The composition of the microbial communities tends

A

to be host-specific
and, within hosts,
to be organ- specific.

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

on the skin and in the hollow organs whose surfaces and
cavities are open to the environment.

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

beneficial to the host in many ways

A

stable microflora

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

The digestive system relies on the normal microflora to

A

to degrade ingested material in the rumen of cattle and sheep, in the caecum and colon of horses, and in the colon of pigs.

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

The microflora of the rumen synthesizes

A

vitamin K and some of the vitamin B group,
as does the microflora of the intestine in non-ruminants

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

a primes the immune system, facilitating a more efficient host response to challenge by
bacterial pathogens

A

normal microflora

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

when that equilibrium is
disturbed or when the host is under severe stress, an indigenous member may escape from the restraining influences of the bacterial community and act as an

A

opportunistic pathogen

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

This can occur in the

A

gastrointestinal tract following the
administration of oral antibiotics

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

can exist as a commensal in the rumen but when it transfers to the liver of feedlot cattle it can act as a pathogen that causes hepatic abscesses

A

Fusobacterium necrophorum

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

The ability of a microbe to damage a host is
called

A

pathogenicity

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

the relative capacity of a pathogen to damage a host is the
degree of

A

virulence

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

The bacterial traits that confer pathogenicity are

A

virulence factors

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

virulence factors; these include

A

adhesins, toxins and capsules

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

whose genes are
expressed only when their products are required in a process called

A

phase variation

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

Many of the genes that encode virulence factors are
associated with mobile genetic elements:

A

bacteriophages, plasmids and
pathogenicity islands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

arise when bacteria that live on the skin or mucous membranes as harmless commensals take advantage of impaired antimicrobial defenses of the host and behave as opportunistic pathogens.

A

Endogenous infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

This is likely to happen
when

A

-epithelial barriers are damaged,
-when immunity is weakened by drugs, -radiation or exogenous pathogens,
-when the ecological balance of the resident
-microbial community is disturbed by administration of antibiotics, or
-when the bacteria gain access to sites from which they are usually absent.

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

are driven by microbial genes that express virulence factors and by host genes that are responsible for resistance to pathogens.

A

Subsequent interactions

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

occur after direct or indirect transmission from an infected animal or from the environment

A

Exogenous infections

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

Pathogens that
are able to survive within host cells are grouped into two categories:

A
  • strict (obligate) intracellular pathogens
    -facultative intracellular pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

are obligate intracellular pathogens

A

Chlamydiae and rickettsiae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Among the facultative intracellular pathogens,
Mycobacterium species enter and replicate in phagocytic cells
23
invade and replicate in non-phagocytic epithelial cells
- Brucella species, - Uropathogenic E. coli, - Salmonella species, - Listeria monocytogenes
24
The major virulence factors are
adhesins, capsules and toxins.
25
to attach to host tissues and to resist the flushing action of body fluids
adhesins
26
play a significant role throughout the course of an infection
27
The expression of adhesins is
subject to phase variation in response to local conditions
28
attach to the epithelial cells of the urinary bladder
Type 1 fimbriae of uropathogenic E. coli a
28
attach toepithelial cells in the kidney
P fimbriae
29
Adhesin–receptor interaction of enteropathogens with intestinal epithelium results in activation of signalling pathways that generate the release of n
nuclear factor-kappaB (NF-κB)
30
a transcription factor that moves to the cell nucleus where it up-regulates the expression of a number of pro-inflammatory genes.
Nuclear factor-kappaB (NF-κB),
31
interfere with opsonization, the binding of complement and antibody to the bacterial surface, thus protecting the bacterium from engulfment by phagocytes and from attack by antimicrobial agents.
capsules
32
Encapsulated bacteria are often resistant to phagocytosis.
33
During growth, encapsulated bacteria may stick together, forming a microcolony or a biofilm that is resistant to phagocytic cells because of its large size.
34
Many capsules are composed of
polysaccharides and are hydrophilic
35
; thus, these capsules may help the bacterium to resist desiccation
polysaccharides and are hydrophilic
36
composed of polyglutamic acid;
Bacillus anthracis
37
; it is anti-phagocytic and is regarded as an essential virulence
Polyglutamic acid;
38
Traditionally, bacterial toxins have been considered to be of two types:
exotoxins endotoxins
39
produced and secreted by viable bacteria
exotoxins
40
integral constituents of the bacterial cell wall not released until the microorganisms are lysed.
endotoxins
40
Toxicity resides in the lipid A portion.
41
It is composed of three parts:
- hydrophobic glycolipid (lipid A) - a hydrophilic polysaccharide composed of a core oligosaccharide and an Opolysaccharide (O antigen)
41
is the lipopolysaccharide (LPS) of the outer leaflet of the outer membrane of Gram-negative bacteria.
Endotoxin
42
Is released when bacterial cell walls are damaged by the complement system, phagocytes or antimicrobial drugs
Lipopolysaccharide
42
LPS interacts with cells that have the toll-like receptor 4 (TLR-4):
mononuclear phagocytes neutrophils platelets dendritic cells and B lymphocytes
43
High concentrations of circulating endotoxin greatly increase the release of
cytokines, notably interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α)
44
Released cytokines induce
fever, activate macrophages and clotting factor XII, and stimulate B cells to divide and produce antibodies
45
stimulate the production of prostaglandins and leukotrienes which are mediators of inflammation
Cytokines
46
responsible for the deposition of thrombi in small vessels (disseminated intravascular coagulation) and for a dramatic drop in blood pressure, giving rise to life-threatening endotoxic shock.
LPS
47
ingested in contaminated food and produces systemic effects.
potent exotoxin, such as Clostridium botulinum toxin
47
can be produced by either Gram-positive or Gram-negative bacteria.
Exotoxins
48
are highly antigenic proteins that can induce the production of protective antitoxins.
toxins
49
are produced within the host and they may exert their effects either locally or systemically
exotoxins
50
Exotoxins have a two-subunit structure comprising an A subunit & B
50
that possesses toxic enzymatic activity
A subunit
51
which acts on intracellular targets, does not become active until it is released in the cell.
enzymatic component
51
that is responsible for binding the exotoxin to specific receptors on the host cell membrane and may help in the transfer of the B subunit across the cell membrane.
B subunit
51
determines the host cell specificity of the toxin: if the cell does not have receptors for the B subunit, it is not vulnerable to the toxin.
B subunit
51
Categories of exotoxins:
(i) toxins that act on the extracellular matrix; (ii) toxins that act on the plasma membrane of their target cells, where they interfere with transmembrane signalling pathways or alter membrane permeability; (iii) toxins that act inside the cells, where they modify signalling pathways or the activities of the cytoskeleton; and (iv) toxins that cause dysfunction of the immune system, so-called superantigens.
52
Both tetanus toxin and botulinum toxin have the
A–B subunit structure.
53
toxins that cause dysfunction of the immune system,
superantigens
54
The cells of the innate immune system express various --- capable of detecting conserved molecular ‘patterns’ that are unique to microorganisms and are not expressed by the hosts
pattern-recognition receptors (PRRs
55
Although these microbial ‘patterns’ are present in commensals and pathogens alike, they are known as
pathogen-associated molecular patterns (PAMPs)
56
– rather than ‘molecular patterns’ that are recognized in most instances.
It is molecules – specific, individual molecules
57
that are expressed constitutively in a variety of host immune cells, such as macrophages, dendritic cells, neutrophils, mast cells, B cells, and specific types of T cells.
57
Mammals possess a family of transmembrane PRRs, called
toll-like receptors (TLRs
58
They are expressed also in some non-immune cells, such as epithelial cells, endothelial cells and fibroblasts
toll-like receptors (TLRs)
59
detect the molecular signatures of microbial pathogens, they orchestrate the innate immune responses, and they help to initiate the adaptive immune response
TRLs
60
If an enteric pathogen, such as Salmonella Dublin in cattle or S. Typhi in humans, is sequestered in the gall bladder or in lymph nodes and is not excreted in the faeces, the host is described as a
latent carrier
61
In stressful situations, latent carriers can become active carriers, asymptomatic hosts that contaminate the environment and infect other susceptible animals.
61
if the pathogen is shed in faeces, either continuously or intermittently, the host is considered an a
active carrier
61
In cattle herds, ---- can establish long-term residence in both latent carriers and active carriers.
Salmonella Dublin
62
is common amongst pathogens, there are exceptions
‘restrained virulence'
63
These bacteria produce highly lethal toxins that kill the host, which then becomes an anaerobic substrate in which the bacteria multiply and from which they can be disseminated as spores
Clostridium species
64
Some pathogens are not invasive and do not spread systemically, yet they release toxins and other signals that pose challenges to homeostasis, local or systemic.
64
contaminate a wound in any region of the body, producing a neurotoxin.
Clostridium tetani
64
secretes a number of toxins that degrade the epithelial barrier and allow the opportunistic pathogen to enter the subepithelial tissues.
Pseudomonas aeruginosa
64
There are two routes by which invasive pathogens can breach the epithelial barrier: b
- through the intercellular spaces (the paracellular route), or by - passage through the epithelial cells (the transcellular route).
65
The paracellular route can be taken by bacteria that are able to disrupt the intercellular tight junctions: for example,
-Enteropathogenic E. coli, -Listeria monocytogenes, -Helicobacter pylori, -some Clostridium species and -some Salmonella serovars
66
may pass through the paracellular route when tight junctions are opened by emigrant neutrophils responding to chemotactic stimuli from pathogens present on the epithelial surface.
Shigella species
67
There are two major types of induced uptake
- a ‘zipper’ mechanism and - a ‘trigger’ mechanism
67
induced by specific ligand–receptor interactions at the cell membrane
Zipper mechanism
67
During bacteraemia, bacteria are present transiently in the bloodstream without replicating,
67
induced by effector molecules delivered into the cell by a type III secretory system
trigger mechanism
68
whereas, during septicaemia, pathogenic organisms multiply and persist in the bloodstream, producing systemic disease.
69
Bacterial infections can be conveniently categorized as
acute, subacute, chronic or persistent.
70
usually have a short severe clinical course, often a matter of days, and the invading bacteria are usually cleared from the body by the host’s immune response.
Acute infections
70
produce clinical effects of less intensity
70
tend to occur when the host fails to eliminate the pathogen.
Chronic infections
70
occurs in certain sites such as the uriniferous tubules and the CNS in which the effects of cell-mediated and humoral immunity are minimal.
Persistence
71
shedding may occur from some of these sites as in bovine leptospirosis, in which leptospires may be shed in urine for more than a year.
Persistent