Lesson 1 And 2 Flashcards

1
Q

The ability of a microbe to damage a host is
called ?

A

Pathogenicity

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2
Q

The bacterial traits that confer pathogenicity are called ?

A

Virulence factors include Adhesions , capsule and toxins.

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3
Q

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

A

Degree of virulence

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4
Q

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

A

Phase variation

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5
Q

Mobile genetic elements are ?

A

Bacteriophage
Plasmids
Pathogenicity islands

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6
Q

It 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

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7
Q

They are Able to adhere to body
surfaces.

A

Commensal organisms,

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8
Q

The composition of the microbial communities?

A

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

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9
Q

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

A

Normal microflora

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10
Q

The
microflora of the rumen synthesizes what ?

A

vitamin K and some of the vitamin B

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11
Q

This 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

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12
Q

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

A

Exogenous infections

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13
Q

Pathogens may enter a host through ?

A

the skin,
the conjunctiva,
the
umbilicus, or
the teat canal

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14
Q

The main portals of entry are ?

A

the mucosae of the
gastrointestinal,
respiratory and
urogenital tracts

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15
Q

In bacterial infections, the host may be damaged by?

A

By bacterial toxins,
by the
inflammatory response elicited by the bacteria or their toxins or, commonly, by both
toxins and inflammatory reactions

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16
Q

This may also be a
source of tissue damage?

A

The immune responses of the host

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17
Q

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

A
  1. strict (obligate)
    intracellular pathogens $ 2. facultative intracellular pathogens
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18
Q

These are are obligate intracellular pathogens

A

Chlamydiae and
rickettsiae

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19
Q

It enter and replicate in phagocytic cells

A

Mycobacterium species

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20
Q

It invade and replicate in non-phagocytic epithelial cells

A

Brucella species,
Uropathogenic E. coli,
Salmonella species
Listeria monocytogenes

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21
Q

Pathogens use ________ to attach to host tissues and to resist the flushing
action of body fluids

A

Adhesins

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22
Q

It is subject to phase variation in response to
local conditions.

A

The expression of adhesins

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23
Q

It attach to the
epithelial cells of the urinary bladder

A

Type 1 fimbriae of uropathogenic E. coli

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24
Q

It attach to
epithelial cells in the kidney

A

P fimbriae

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25
It is a transcription factor that moves to the cell nucleus where it up-regulates the expression of a number of pro-inflammatory genes.
factor-kappaB (NF-κB)
26
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 interfere with opsonization,
27
Is resistant to phagocytic cells because of its large size.
Biofilm
28
Is composed of polyglutamic acid; it is anti-phagocytic and is regarded as an essential virulence factor.
The capsule of Bacillus anthracis
29
Bacterial toxins have been considered to be of two types:
1. exotoxins 2. endotoxins
30
Produced and secreted by viable bacteria
Exotoxins
31
Are integral constituents of the bacterial cell wall not released until the microorganisms are lysed
Endotoxins
32
Is the lipopolysaccharide (LPS) of the outer leaflet of the outer membrane of Gram-negative bacteria
Endotoxin
33
It is composed of three parts
1. hydrophobic glycolipid (lipid A) 2. hydrophilic polysaccharide composed of a core 3. oligosaccharide and an Opolysaccharide (O antigen)
34
It resides in the lipid A portion.
Toxicity
35
It is released when bacterial cell walls are damaged by the complement system, phagocytes or antimicrobial drugs
Lipopolysaccharide
36
The in vivo effects of endotoxin depend on ?
The amount present in the circulation.
37
High concentrations of circulating endotoxin greatly increase the release of ?
Cytokines
38
It induce fever, activate macrophages and clotting factor XII, and stimulate B cells to divide and produce antibodies.
Released cytokines
39
It stimulate the production of prostaglandins and leukotrienes which are mediators of inflammation
Cytokines
40
It is 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
41
Exotoxins can be produced by either ?
Gram-positive or Gram-negative bacteria
42
They are highly antigenic proteins that can induce the production of protective antitoxins
The toxins
43
It is ingested in contaminated food and produces systemic effects.
Clostridium botulinum toxin,
44
possesses toxic enzymatic activity
A subunit
45
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
46
Both tetanus toxin and botulinum toxin have what ?
A–B subunit structure.
47
Categories of exotoxins
(i) toxins that act on the extracellular matrix; (ii) toxins that act on the plasma membrane of their target cells, (iii) toxins that act inside the cells, where they modify signalling pathways or the activities of the cytoskeleton; (iv) toxins that cause dysfunction of the immune system, so-called superantigens.
48
Are capable of detecting conserved molecular ‘patterns’ that are unique to microorganisms and are not expressed by the hosts?
pattern-recognition receptors (PRRs)
49
These microbial ‘patterns’ are present in commensals and pathogens , they are known as ?
pathogen-associated molecular patterns (PAMPs)
50
Mammals possess a family of transmembrane PRRs, called ?
toll-like receptors (TLRs)
51
Can detect the molecular signatures of microbial pathogens, they orchestrate the innate immune responses, and they help to initiate the adaptive immune response
TRLs
52
If an enteric pathogen sequestered in the gall bladder or in lymph nodes and is not excreted in the faeces, the host is described as
latent carrier
53
If the pathogen is shed in faeces, either continuously or intermittently, the host is considered as?
active carrier
54
It secretes a number of toxins that degrade the epithelial barrier and allow the opportunistic pathogen to enter the subepithelial tissues.
Pseudomonas aeruginosa
55
Two routes by which invasive pathogens can breach the epithelial barrier:
by passage through the intercellular spaces (the paracellular route), or by passage through the epithelial cells (the transcellular route).
56
It is induced by specific ligand–receptor interactions at the cell membrane
The zipper mechanism
57
It is induced by effector molecules delivered into the cell by a type III secretory system.
trigger mechanism
58
It is invariably peracute and fatal
Anthrax in ruminants
59
Bacterial infections can be conveniently categorized as
acute, subacute, chronic or persistent
60
It has usually have a short severe clinical course, often a matter of days
Acute infections
61
Produce clinical effects of less intensity
Subacute infections
62
It tends to occur when the host fails to eliminate the pathogen
Chronic infections
63
It occurs in certain sites such as the uriniferous tubules and the CNS in which the effects of cell-mediated and humoral immunity are minimal. Persistent 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.
Persistence