Respiratory Pathogens 1 Flashcards
what is he degree of pathogenicity of a disease determined y
proteins it expresses and how effectively it cn integrate enviro info
what are some virulence mechanisms
bac adhesion
bac invasion
bac evsion host defnece
bac toxins
what is the cycle of bac infectivity
entry attachment multiplication evasion of host defences cause damage release spread
what are the components of bc adhesion
structure ligand
surface mol
receptors
what are some imp structure ligands
capsule (s progenies)
fimbriae (B pertusis)
cell wall (s aureus)
fibrils (s snguinis)
what are some imp surface mols receptors
keratinocytes laryngeal epi cells epi cells platelets salivary proteins
what can bac adhesion be
superificl/sytemic (metastasis)
extra or intracellular
access via general contact or injection
what are some examples of invasion
organism erodes tooth
organsim persisks in epi
org injected via arthropod
what are some common bac assc with caries and perio disease
caries - s mutans
peio - p gingivalis
lames disease from
borrelia burghdorferi
what does penetration of epithelium lead to
blood vessel end = blood circ
to phagocytic cells = both
lymphatic tissue end = accumulates in lymph nodes
what are some ways a bacteria can evade host defences
immunity at mucosal surfaces destroy immune cells interfere with inflam response evade innate immunity overcome acquires immune response
how can a bacteria have immunity at mucosal surfaces
production of glycosidases and Sialidases
(s cocci and veillonlela)
proteases
binding proteins
why is glycosylation of bac imp
imp for structure and function and resit to proteases
why is silica acid on IgA imp
imp for immunoglobulin function
what do proteases do
cleave hinge region of IgA normally protected by glycosylation
(s sanguines)
what do the binding proteins assc with mucosal surface immunity do
M family proteins
bind Fc region of iG
(s pyogeens and s aureus)
how does a bac interfere with cytokines
bac induce septic an ixic shock
TNF a, interferon and interleukins
myeloid, lymphoid and vasc respond to infection
what are cytokines
group of regulatory proteins key to immune response
what are endotoxins
gm -ve cell wall
LPS outer mem complex
what are LPS components
toxicity - lipid A
immunogenicity - polysacc
what does endotoxins induce
variety of inappropriate inflam responses that impair hosts response to pathogen
what does he outer mem of gm -ve bac consist of
assymetirc mem LPS peptidoglycan lipoproteins bind to receps on macrophages, b cells and other cells = cytokines
what is SIRS
systemic Inflammatory Response Syndrome
what are the ways of inflam cytokines being released
macrophages activated by LPS/endotixn or peptidoglycan
or
t cells activated by exotoxins
how is complement evaded
capsules
- prevent activation of C3 and C3B
- mask bound C3b
how is there evasion of phagocytic killing
PVL - s aureus
intracellular survival – M TB
type 3 secretion systems
how is acquired immune repossess overcome
phase variation and antigenic variation
what is phase variation
switch between on and off forms of a gene
flagellin gene of salmonella
opacity genes of neisseria
what is antigenic variation
allows bac to change sequence of a gene
pilin genes of neisseira
what are the early symptoms of diphtheria
sore throat, low fever, swollen neck glands
what are the late stages of diphtheria
airway obstruction
breathing difficulty
shock
what are outbreaks of diphtheria assc with
unsanitary conditions
immunity gaps
vaccination fail
what is the product of diphtheria
toxin = acute inflammation and formation of pseudomembrane
- dead tissue
- fibrin
- polymorphs
what causes diphtheria
corynebacterium diphtheria
- gm +ve bacilli
- aerobic non motile
- toxin prod
how is diphtheria transmitted
direct contact droplets/skin, or indirect via contaminated object
explain some characteristics of corynebacterium diphtheria
sol 3 domain P's endocytosed proteolytic cleavage catalytic domain translocate domain
what is the treatment of diphtheria
inoculation with antitoxin
penicillin or erythromycin to slim bac
how is diphtheria prevented
active immunisation
diphtheria formal toxin
booster and multiple vaccine
what is whooping cough
highly contagious
life threatening
what causes whooping cough
bordetella pertussis
gm -ve cocci
what are the symptoms of whooping cough
severe cough low/no fever at start choking nocturnal coughing short breath vomit
how does bordetella pertussis enter
via resp tract
attach to ciliated epi
mediated by filamentous hem agglutinin
pert actin
what is pertactin
outer mem protein
promotes attach to tracheal epi cells
what are the toxins assc with bordetetlla pertussis
pertussis toxin
adenylate cyclase
tracheal cytotoxin
what does tracheal cytotoxin do
kills ciliated cells and stimulates their extrusion from the mucosa
what is pathogenesis
growth on ciliate epi and toxin prod
- paralyse cilia tracheal cytotoxin
- stim inflam resp
- kill leucocytes
what does pertussis toxin do
disrupts cell function
increases mucus secretion
incapacitates phagocytes
what is the diagnosis and treatment of whooping cough
cough plate swab pharyngeal walls erythromycin remove mucus Ab therapy for secondary infections
how is whooping cough vaccinate
part of multiple vaccine
kill b pertussis
3 antigenic types
