2-Host Defense Flashcards
general principles
-host defense = innate + adaptive immunity
-5 types of microbes
-to cause disase must effectively evade host immune resp
types of microbes
- extracellular bacteria
- intracellular bacteria
- fungi
- viruses
- parasites
distinct effector mechanisms
for optimal response by microbe
1. antibody vs intracell bacteria would be ineffective
2. CTL resp vs extracell bacteria useless
extracellular bacteria
staphylococcus + streptococcus + neisseria + escherichia coli + clostridium
will cause tissue damage so inflamm and toxins released
host immune resp to kill bacteria and neutralize toxins
innate immunity vs extracellular
- phagocytosis most effective, first line defense
- alternative complement pathway bc bacterial cell wall can activate
adaptive vs extracellular
-best approach is antibody production via humoral immunity
-IgG opsonizes + toxin specific antibodies neutralize
-IgM/IgG act classical complement to lyse
evasion of immunity
polysaccharide capsules resist phagocytosis and inhib alternative pathway complement
also genetic variation of surface antigens
septic shock
gram neg and some gram pos bacteria induce macrophages to release tumor necrosis factor (TNF) and IL-1
superantigens
bind class II MHC on APCs and to Valpha/beta chains on T cells = T cell activation
-so many activated that large # cytokines = septic shock like condition
disease causing antibodies
- rheumatic fever- induced by streptococcal Mm protein during pharyngeal infection binds sarcolemma proteins in heart = carditis
- poststreptococcal glomerulonephritis- infection with streptococci = antibodies form immune complex with bacterial antigens > lodge in kidney = nephritis
listeria monocytogenes and
mycobacteria
-survive/multiply in macrophages
-inaccessible to circulating antibodies
-allow to thrive in phagocytic cells
myco will inhibt fusion of phagosomes/lysosomes and may savenge ROS to prevent killing bacteria
listeria will disrupt phagosome so bacteria escapes into cytosol then CTLs generated
innate vs intracellular
ineffective bc bacteria not killed when ingested
-NK cells act by IL-12 > prod interferon gamma to act macros but only some killed
need adaptive for full eradication
adaptive vs intracellular
DTH like type IV reaction
-TH1 act > release interferon gamma > act macros
-macros will surround microbes to form granuloma to prevent spread
viruses
general
obligate intracelllular microbes that priate host cell machinery
can lyse host cells = cytopathic effect
innate vs virus
best defense = type 1 IFN = alpha and beta interferons
-upreg expression of class I MHC on host cells
-act NK cells to lyse early in infection
-block virus protein syn
NK cells and viruses
viruses downreg class I MHC so NK cells are released from inhibition by absence of I MHC
enhanced by interferons
adaptive vs viruses
IF antibodies present = humoral imm to prevent virus from binding target host, opsonize virus, act complement
NO antibodies = CTLs principal immune component, virus processed on class I MHC so CTLs effective
viral evasion of immunity
- HIV makes point mutations so antigenic variability, infects CD4 T cells
- influenza - reassortants make antigenic alteration
also prevent class I MHC xpr of viral peptides so not lysed by CTLs
deleterious effects viruses
- hep B virus infection induce CTL resp that destroys liver, if immunodeficient then no liver damage
- molecular mimicry- immune resp vs virus cross reacts with host tissue
fungal disease
general
inc # of opportunistic fungal infections
AIDS, cancer (chemotherapy), transplants (immunosuppressants) high risk
immunity to fungi involves humoral and cell mediated
innate vs fungi
neutrophils main mediators so phagocytosis
neutropenic indivs highly susceptible to fungal infections
adaptive vs fungi
TH1 most important
-cryptococcus neoformans eliminated by CTLs
-intracellular fungus > granuloma formation
parasites
general
protozoa and helminths/worms
complex life cycle so involved intermediate host like mosquitoes, ticks
innate vs parasites
not very effective
-macros phagocytize protozoa but many orgs resistant to killing
outer layer of helminths act alternative complement but resistant to the effects
-resistant to neutrophils and macros bc thick teguments
parasite evasion of immunity
-concealed by intestinal lumen or cysts
-coat with host proteins so not id as foreign
-outer surface inhibits complement
-extracell enz cleave membrane bound antibody
-vary suface antigens
-shed antigens spontaneously or after being bound by antibodys
