MODULE 7: VIRULENCE FACTORS Flashcards
Inhibits migration of WBCs to the site of infection and causes chronic granulomas
Cord factor (trehalose-6’6-dimycolate)
Prevents fusion of phagosome and lysosome allowing MTB to survive and multiply within macrophages
Sulfatides
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
Mycolic acid
Because of MTB’s [?], the immune system may not readily recognize the bacteria or may not be triggered sufficiently to eliminate them
Slow generation time
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
Intracellular growth and granuloma formation
T. pallidum subspecies pallidum has [?] that breaks down the hyaluronic acid in the ground substance of tissue and presumably the invasiveness of the organism.
Invasiveness; hyaluronidase
T. pallidum subsp. pallidum has the ability to [?] mucous membranes and the placenta, disseminate throughout the body, and infect almost any organ system
Invasiveness; cross intact
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.
Evasion of host immune response; host proteins
The cell surface proteins of T. pallidum subspecies pallidum undergoes [?] which contributes to its ability to evade host immune response and establish persistent infection.
Evasion of host immune response; antigenic variation
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.
P1 proteins
excreted by the mycoplasma penetrate into the host cell and cause oxidative
damage of the respiratory epithelium, leading to necrosis.
- Hydrogen peroxide (H2O2)
- Superoxide radicals (O2-) e
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.
H2O2
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.
lipid peroxidation
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.
superoxide radicals (O2-)
plays an important role in the complications affecting organs distant from the respiratory tract in some patients infected with M. pneumoniae
Immunopathologic mechanism