Bacterial pathogenesis L11 Flashcards
why are commensals important for health and disease?
- prevents pathogen colonisation
- outcompetes nutrient acquisition of pathogens
-production of antimicrobials
-colonisation of newborns acts as powerful stimulus to develop immune system - microbiome educates immune system
- gut-associated commensals provide important nutrients
how can commensals become harmful?
if displaced, in different areas than where they are supposed to be - can cause infections
can convert food into carcinogenic substances
pathogenic meaning
disease causing bacteria, affects all with normal host defences
non-pathogenic meaning
organisms that invade an individual without causing any obvious detectable symptoms
asymptomatic infections meaning
these can only be detected by the presence of organisms or antibodies, no symptoms
latent meaning
organisms that are dormant - only become reactivated when recurrence of symptoms occurs
opportunistic meaning
organisms that can cause disease under certain conditions
infectious dose of pathogen is made up of 3 factors
dose
virulence
host immune response
commensal definition
an organism that is found normally on parts of body that are exposed to or communicate with the external environment like skin or stomach
commensals and immunocompromised patients
many of these commensals can cause disease
when do changes occur in our natural flora -microbiome
microbiome is very dynamic
- change in normal physiology and development - like female genital tract with pregnancy or periods
- when antibiotics select for a resistant flora
- when new organisms may be acquired
harmful effects of antibiotics in gut bacteria
antibiotic use can lead to the ‘good’ sensitive gut bacteria to be killed, causing an overgrowth of resistant bad bacteria and then infection and disease
treatment
- stop prescribing antibiotics
koch’s postulates
this is how to determine that a specific pathogen caused a specific disease
- pathogen must be present in every case of disease
- pathogen must be isolated from diseased host and grown in pure culture
- specific disease must be reproduced from a pure culture into a healthy host
- pathogen must then be recovered from this experimental host
how are pathogens transmitted
oral - oral
feces to oral
blood to blood
sexual contact
food
environment - soil water, air
animals
vectors - ticks, bugs, insects
what are microbial pathogenicity factors
also can be virulence factors
the things that cause disease or help pathogen to invade host or evade immune system
examples
- toxins
- iron uptake
- adhesins
-LPS
-invasions
-capsule
-slime
- enzymes
- plasmids and chromosomal DNA
how does a bacteria go from commensalism to pathogenicity
commensalism = exposure and adherence of bacteria - this is fine, no barrier broken
intermediate - breaking of barrier and further exposure, invasion through epithelium and then crowns and colonised starting to produce virulence factors
pathogenicity = these virulence factors are released causing toxic effects, invasiveness and tissue damage or disease
bacterial adhesins
found on gram -ve bacteria, like flagella
- multi-subunits structures that are mono or poly
helps the movement to specific targets in host
however, are recognised by innate immune system as a PAMP (TLR5)
fimbriae adhesins
these are hairlike structures that interact with eukaryotic cells or surfaces via receptors
these receptors recognise sugars and help ‘stick’
pili adhesins
similar to fimbriae but longer, only one present
conjugation (sex or F-pilus) or receptors for phages
colonisations and adherence
needs to be an entry points - like GI tract, skin breach in order to overcome diverse host defence
colonisation - cell wall associated proteins like capsule or polysaccharide layer
adherence - via adhesins which prevents the bacteria from being moved off, allowing a micro colony to form and important of pathogenicity
commensals to pathogenicity p2
- need to find a place to stay - colonisation and adherence - do this by cell wall associated proteins, pili, fimbriae and flagella
- get something to eat - invasion of and survival in host - do this via degradative enzymes, LPS, toxins
- protecting itself against any adversity - does this by capsules, biofilms, trichroic acids etc
exotoxins
any toxin that is actively secreted by a bacteria in the environment or supernatant - external
endotoxin
like LPS - cell surface bound toxin
enterotoxin
an exotoxin that is effective in gastrointestinal tract
exoenzymes that are used for invading host (invasion factors)
proteases
glycosidases
nucleases
lipases
iron sequestering
as iron is essential nutrient in most bacteria, and limited in host, sequestration is really important
it produces iron binding compounds called siderophores to capture iron in host and bind it to bacterial surface
defensive pathogenicity factors
protection from host defence mechanisms - example - polysaccharide capsule, slime, biofilm
immunogenicity mechanisms - LPS - causes cytokine overstimulation to cause septic shock
Outer membrane proteins - OMPs that inactivate antimicrobial peptides or complement proteins
self protection of capsule in bacteria
prevents against drying out as contains water and phagocytosis
really important for vaccine development
self protection with teichoic acids in bacteria
found gram +Ve bacteria, negatively charged and involved in inflammation, antimicrobial resistants, autolysis
self protection using LPS in bacteria
interacts with immune system and activates inflammatory response - lipid a part
example of how endotoxins cause a fever
as macrophage ingests bacteria and digests it, the endotoxins releases and this causes the macrophage to produce cytokines IL-1 and TNF-A, which go to the brain and cause the body temp to increase, causing a fever
