Overcoming Host Defence Flashcards
Ability to overcome host D relates to
Virulence
Challenge and infective dose
Host response efficacy
Specific pathogen mechanisms of overcoming host D
Mechanisms of overcoming host d
Rapid repl Low immunogenicity Phagocytosis inhibition IC survival Concealment Antige variation EC products
Rapid replication
Avoid and or overwhelm spec imm resp.
Can allow ‘out running’ of host D or provide too much to deal with
Low imunogenicity mechs
Low antigenicity
Tolerance
Low antigenicity
Expr poorly react antig allow avoidance of inflam opson and spec imm resp
Eg some capsules and LPS O antig fail to act complem or be recog as foreign by phagocytes
Eg Hyaluronic acid capsule strep equi
Low antigenicity hyaluronan eg
Anionic non sulph GAG distrib through CT epi and neural tissue. Major skin comp and cartilage comp
Thick capsule or slime layer made of polysacch (eg hyaluronic acid) expr during infection eg pasteurella multocida
Some bact produce hyaluronidase to break down host hyaluronic acid
Low antigenicity sialic acid eg
Prod by G-ve bact incl E.Coli, neisseria and klebsiella
Neisseria (important cause of sepsis and meningitis) have homopolymeric sialic acid capsule
Grp C caps: alpha 2-9 sialic acid unique bact struct (good vacc)
Grp B caps: alpha 2-8 sialic acid similar ti human so essentially non immunogenic
Tolerance
Imm system doesnt attack antigen
Natural/self tolerance (no imm resp against self antigs)
Acquired/induced tolerance (ext antig tolerance created by imm syst manip eg pregnancy)
Acquired Tolerance cause
De sensitisation of imm cells by spec antigs
Prenatal infection can cause tolerance and persistance
High persistant Ag dose can also cause
Host genetic factors influence dev of tolerance
Phagicytosis inhib
Anti-opsonic act
Inflam inhib
Chemotaxis inhib
Phagocyte killing
Anti opsonic activity: cell surface components
LPS of some G-ve have v long O chain that bind and act complem at remote site to OM so Comp pro can’t insert and cause lysis
M pro of pyogenic strep bind factor H therefore block complem cascade
Pro A of staph a bind Fc region on IgG and present Ab in wrong orientation for Fc recog by phagocytes
Anti opsonic activity: EC components
Staph a prod staphylokinase that act plasminogen to plasmin that degrades compl and IgG
Strep and mycoplasmas prod IgA proteases
Pseudomonas and strep prod EC enz that digest and inact compl
Inflam inhib
Some bact (mycobact infected macrophage) prod anti inflam cytokines eg IL6 - inhib T cell act and strong imm suppressive cytok IL10 and TGF beta
IL10 role in inflam inhib
Inhib macro act and production of reactive O and N intermediates, supress inflam cytok pros abd down reg MHC c2
Chemotaxis inhib
Staph a produce CHIPS that binds transmem rec on phagocytes and blocks recog of chemotactic molecules