MODULE 7: VIRULENCE FACTORS Flashcards

1
Q

Inhibits migration of WBCs to the site of infection and causes chronic granulomas

A

Cord factor (trehalose-6’6-dimycolate)

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2
Q

Prevents fusion of phagosome and lysosome allowing MTB to survive and multiply within macrophages

A

Sulfatides

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3
Q

High lipid concentration in cell wall accounts for impermeability and
resistance to antimicrobial agents, resistance to killing by acidic and alkaline
compounds in both the intracellular and extracellular environment, and resistance to osmotic lysis via complement deposition and attack by lysozyme

A

Mycolic acid

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4
Q

Because of MTB’s [?], the immune system may not readily recognize the bacteria or may not be triggered sufficiently to eliminate them

A

Slow generation time

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5
Q

The intracellular location of MTB is an
effective means of evading the immune system. In particular, antibodies and
complement are ineffective. Caseous materials block the penetration of drugs. This is attributed to the necessity for protracted (prolonged) therapy against TB, which usually lasts for 6-9 months

A

Intracellular growth and granuloma formation

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6
Q

T. pallidum subspecies pallidum has [?] that breaks down the hyaluronic acid in the ground substance of tissue and presumably the invasiveness of the organism.

A

Invasiveness; hyaluronidase

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7
Q

T. pallidum subsp. pallidum has the ability to [?] mucous membranes and the placenta, disseminate throughout the body, and infect almost any organ system

A

Invasiveness; cross intact

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8
Q

T. pallidum subsp. pallidum coats itself with [?], hence delaying the antibody-mediated immune response of the host. The effectiveness of humoral response is reduced as the treponemes
are already extravascular once antibodies are produced.

A

Evasion of host immune response; host proteins

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9
Q

The cell surface proteins of T. pallidum subspecies pallidum undergoes [?] which contributes to its ability to evade host immune response and establish persistent infection.

A

Evasion of host immune response; antigenic variation

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10
Q

mediate adherence to respiratory epithelium and cause ciliostasis (inhibition of ciliary action). Adherence is firm enough to prevent the elimination of the parasites by mucous secretions. The intimate association between the adhering mycoplasmas and their host cells provides an environment in which local concentrations of toxic metabolites
are excreted by the parasite.

A

P1 proteins

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11
Q

excreted by the mycoplasma penetrate into the host cell and cause oxidative
damage of the respiratory epithelium, leading to necrosis.

A
  • Hydrogen peroxide (H2O2)

- Superoxide radicals (O2-) e

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12
Q

the end product of respiration in mycoplasmas, has been implicated as a major pathogenic factor responsible for the lysis of erythrocytes by mycoplasmas in vitro.

A

H2O2

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13
Q

For the H2O2 to exert its toxic effect, the must adhere closely enough to the host cell surface to maintain a toxic, steady-state concentration of H2O2 sufficient to cause direct damage, such as [?], to the cell membrane.

A

lipid peroxidation

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14
Q

Moreover, M. pneumoniae inhibits host cell catalase by excreting [?]. This would be expected to further increase the accumulation of H2O2 at the site of parasite-host cell contact.

A

superoxide radicals (O2-)

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15
Q

plays an important role in the complications affecting organs distant from the respiratory tract in some patients infected with M. pneumoniae

A

Immunopathologic mechanism

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16
Q

Because mycoplasmas lack cell walls, [?] between the membranes of the M. pneumoniae and host cells has been suggested. This causes the following events that are expected to cause serious damage to the host cells.

A

fusion

17
Q

play a role in autoimmune reactions; During the course of the infection with M. pneumoniae, some auto-agglutinating
antibodies (cold agglutinins) may be formed against red blood cells. This is responsible for the acute anemia that is triggered by cold

A

Deposition of mycoplasma antigens

18
Q

enables the introduction of the parasite’s hydrolytic enzymes into the host cell

A

Alteration of the composition and permeability of the host cell membrane

19
Q

Borrelia species evades the immune system and avoids destruction by changing their surface antigens during growth (i.e. multiplication). During this time, antigenically altered spirochetes are produced, hence, initial antibodies produced against the spirochetes possessing the [?] are rendered useless

A

“original” antigenic determinants

20
Q

These antigenically altered spirochetes survive, multiply, and cause a second wave of symptoms. Eventually, the immune systems forms new
antibodies, but it is soon faced with another antigenic form. A single
strain has been known to generate [?] distinct serotypes. Complete
recovery can occur once immunity against the variety of antigens produced by the organism develops.

A

24

21
Q

B. burgdorferi surface proteins facilitate persistence of the spirochete by binding the host’s [?] thereby preventing complement deposition on
host cells and promoting suppression of host immune response
including inhibition of mononuclear and natural killer cell function, lymphocyte proliferation, and cytokine production

A

serum factor H

22
Q

B. burgdorferi surface proteins facilitate persistence of the spirochete by binding the host’s [?] thereby preventing complement deposition on
host cells and promoting suppression of host immune response including inhibition of mononuclear and natural killer cell function, lymphocyte proliferation, and cytokine production

A

serum factor H

23
Q

B. burgdorferi surface proteins bind with plasminogen and [?] plasminogen activator. This binding convert plasminogen to plasmin, a potent protease and could facilitate tissue invasion

A

urokinase-type

24
Q

B. burgdorferi surface proteins stimulate [?] that contribute to the arthritis in late stages of Lyme disease

A

inflammation