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MICRO 2- BACTERIOLOGY > INTRO-- BACTERIOLOGY > Flashcards

INTRO-- BACTERIOLOGY Flashcards

1
Q

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

A

commensals

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2
Q

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

A

COMMENSALS

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3
Q

They form stable polymicrobial communities that are present throughout life as

A

‘normal microflora’

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4
Q

The composition of the microbial communities tends

A

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

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5
Q

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

A
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6
Q

beneficial to the host in many ways

A

stable microflora

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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.

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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

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9
Q

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

A

normal microflora

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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

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11
Q

This can occur in the

A

gastrointestinal tract following the
administration of oral antibiotics

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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

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13
Q

The ability of a microbe to damage a host is
called

A

pathogenicity

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14
Q

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

A

virulence

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15
Q

The bacterial traits that confer pathogenicity are

A

virulence factors

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16
Q

virulence factors; these include

A

adhesins, toxins and capsules

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17
Q

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

A

phase variation

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17
Q

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

A

bacteriophages, plasmids and
pathogenicity islands.

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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

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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.

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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

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19
Q

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

A

Exogenous infections

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20
Q

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

A
  • strict (obligate) intracellular pathogens
    -facultative intracellular pathogens
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21
Q

are obligate intracellular pathogens

A

Chlamydiae and rickettsiae

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22
Q

Among the facultative intracellular
pathogens,

A

Mycobacterium species enter and replicate in phagocytic cells

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23
Q

invade and replicate in non-phagocytic epithelial cells

A
  • Brucella species,
  • Uropathogenic E. coli,
  • Salmonella species,
  • Listeria monocytogenes
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24
Q

The major virulence factors are

A

adhesins, capsules and toxins.

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25
Q

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

A

adhesins

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26
Q

play a significant role throughout the course of an infection

A
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27
Q

The expression of adhesins is

A

subject to phase variation in response to
local conditions

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28
Q

attach to the epithelial cells of the urinary bladder

A

Type 1 fimbriae of uropathogenic E. coli a

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28
Q

attach toepithelial cells in the kidney

A

P fimbriae

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29
Q

Adhesin–receptor interaction of
enteropathogens with intestinal epithelium results in activation of signalling pathways
that generate the release of n

A

nuclear factor-kappaB (NF-κB)

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30
Q

a transcription factor
that moves to the cell nucleus where it up-regulates the expression of a number of
pro-inflammatory genes.

A

Nuclear factor-kappaB (NF-κB),

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31
Q

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.

A

capsules

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32
Q

Encapsulated bacteria are often resistant to phagocytosis.

A
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33
Q

During growth, encapsulated bacteria may stick together, forming a microcolony or a biofilm that is resistant to phagocytic cells because of its large size.

A
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34
Q

Many capsules are composed of

A

polysaccharides and are hydrophilic

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35
Q

; thus, these capsules
may help the bacterium to resist desiccation

A

polysaccharides and are hydrophilic

36
Q

composed of polyglutamic acid;

A

Bacillus anthracis

37
Q

; it is anti-phagocytic and is regarded as an essential virulence

A

Polyglutamic acid;

38
Q

Traditionally, bacterial toxins have been considered to be of two types:

A

exotoxins
endotoxins

39
Q

produced and secreted by viable bacteria

A

exotoxins

40
Q

integral constituents of the bacterial cell wall not released until the microorganisms are lysed.

A

endotoxins

40
Q

Toxicity resides in the lipid A
portion.

A
41
Q

It is composed of three parts:

A
  • hydrophobic glycolipid (lipid A)
  • a hydrophilic polysaccharide composed of a core oligosaccharide and an Opolysaccharide (O antigen)
41
Q

is the lipopolysaccharide (LPS) of the outer leaflet of the outer membrane of Gram-negative bacteria.

A

Endotoxin

42
Q

Is released when bacterial cell walls are damaged by the complement system, phagocytes or antimicrobial drugs

A

Lipopolysaccharide

42
Q

LPS interacts with cells
that have the toll-like receptor 4 (TLR-4):

A

mononuclear phagocytes
neutrophils
platelets
dendritic cells and
B lymphocytes

43
Q

High concentrations of
circulating endotoxin greatly increase the release of

A

cytokines, notably interleukin-1
(IL-1) and tumor necrosis factor-alpha (TNF-α)

44
Q

Released cytokines induce

A

fever, activate
macrophages and clotting factor XII, and stimulate B cells to divide and produce
antibodies

45
Q

stimulate the production of prostaglandins and leukotrienes
which are mediators of inflammation

A

Cytokines

46
Q

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.

A

LPS

47
Q

ingested in contaminated food and produces systemic effects.

A

potent exotoxin, such as Clostridium botulinum toxin

47
Q

can be produced by either Gram-positive or Gram-negative bacteria.

A

Exotoxins

48
Q

are highly antigenic proteins that can induce the production of protective
antitoxins.

A

toxins

49
Q

are produced within the host and they may exert their effects either locally
or systemically

A

exotoxins

50
Q

Exotoxins have a two-subunit structure comprising an A subunit & B

A
50
Q

that possesses toxic enzymatic activity

A

A subunit

51
Q

which acts on intracellular targets, does not become active until it is
released in the cell.

A

enzymatic component

51
Q

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.

A

B subunit

51
Q

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.

A

B subunit

51
Q

Categories of exotoxins:

A

(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
Q

Both tetanus toxin and botulinum toxin have the

A

A–B subunit structure.

53
Q

toxins that cause dysfunction of the immune system,

A

superantigens

54
Q

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

A

pattern-recognition receptors (PRRs

55
Q

Although these microbial ‘patterns’ are present in commensals and pathogens
alike, they are known as

A

pathogen-associated molecular patterns (PAMPs)

56
Q

– rather than ‘molecular patterns’ that are recognized in most instances.

A

It is molecules – specific, individual molecules

57
Q

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.

A
57
Q

Mammals possess a family of transmembrane PRRs, called

A

toll-like receptors (TLRs

58
Q

They are expressed also in some non-immune cells, such as
epithelial cells, endothelial cells and fibroblasts

A

toll-like
receptors (TLRs)

59
Q

detect the molecular signatures of microbial pathogens, they orchestrate the
innate immune responses, and they help to initiate the adaptive immune response

A

TRLs

60
Q

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

A

latent carrier

61
Q

In stressful situations, latent
carriers can become active carriers, asymptomatic hosts that contaminate the
environment and infect other susceptible animals.

A
61
Q

if the pathogen is shed in faeces, either continuously or
intermittently, the host is considered an a

A

active carrier

61
Q

In cattle herds, —-
can establish long-term residence in both latent carriers and active carriers.

A

Salmonella Dublin

62
Q

is common amongst pathogens, there
are exceptions

A

‘restrained virulence’

63
Q

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

A

Clostridium species

64
Q

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.

A
64
Q

contaminate a wound in any region of the body, producing a neurotoxin.

A

Clostridium tetani

64
Q

secretes a number of toxins that degrade the epithelial barrier and allow the opportunistic
pathogen to enter the subepithelial tissues.

A

Pseudomonas aeruginosa

64
Q

There are two routes by which invasive pathogens can breach the epithelial
barrier: b

A
  • through the intercellular spaces
    (the paracellular route), or by
  • passage through the epithelial cells (the transcellular route).
65
Q

The paracellular route can be taken by bacteria that
are able to disrupt the intercellular tight junctions: for example,

A

-Enteropathogenic E. coli,
-Listeria monocytogenes,
-Helicobacter pylori,
-some Clostridium species and
-some Salmonella serovars

66
Q

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.

A

Shigella species

67
Q

There are two major types of induced uptake

A
  • a ‘zipper’ mechanism and
  • a ‘trigger’ mechanism
67
Q

induced by specific ligand–receptor
interactions at the cell membrane

A

Zipper mechanism

67
Q

During bacteraemia, bacteria are
present transiently in the bloodstream without replicating,

A
67
Q

induced by effector molecules delivered into the cell by a type III secretory system

A

trigger mechanism

68
Q

whereas, during
septicaemia, pathogenic organisms multiply and persist in the bloodstream, producing systemic disease.

A
69
Q

Bacterial infections can be conveniently categorized as

A

acute, subacute, chronic or persistent.

70
Q

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.

A

Acute infections

70
Q

produce clinical effects of less
intensity

A
70
Q

tend to occur when the host fails to eliminate the pathogen.

A

Chronic infections

70
Q

occurs in certain sites such as the uriniferous tubules and the CNS in which the effects of cell-mediated and humoral immunity are minimal.

A

Persistence

71
Q

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.

A

Persistent

MICRO 2- BACTERIOLOGY (7 decks)

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