Enteric Bacteria Flashcards
function of microbiota in health
contribute to host health
- fermentation of carbohydrates
- SCFA production
- promotes Treg development
- converts primary bile acids to secondary
- vitamin B and K synthesis
function of microbiota in presence of pathogen
provide colonization resistance
colonization resistance
- promotes production of antimicrobial peptides, IgA, and GI mucus
- maintains tight junctions between epithelial cells
- niche preemption
niche preemption
“good” bacteria occupies the available space and resources to prevent pathogens from growing and occupying the niche
where is the microbiome located
gut
lungs
skin
vagina
most exist in the lumen and are separated from epithelial cells by a mucus barrier
where are the main microbes located
in the colon and other sites of fermentation (rumen, cecum)
what are the main microbes of the microbiome
bacteroidetes
firmicutes
bacteroidetes
gram negative
anaerobic
rods
firmicutes
gram positive
anaerobic or facultative anaerobes
rods
dysbiosis
microbiota disruption that contributes to disease/signs of disease
caused by disease, poor diet, travel or stress, medications, and weaning
leads to loss of normal microbiome functions
how do antibiotics contribute to dysbiosis
reduces diversity of the gut microbiome
how to prevent dysbiosis
- only use medications when clinically indicated
- reduce stress
- maintain good diet
how to treat dysbiosis
- prebiotics
- probiotics
- fecal microbiota transplant
prebiotics
non digestible carbohydrates that support bacteroidetes and firmicutes
safe but not always efficacious
probiotics
supplying live bacteria to replace lost microbiota
minimally regulated
species differences in probiotic requirements
fecal microbiota transplant
replacing full microbiota with a healthy one from donor
may cause problems in immunocompromised animals
what are the requirements for bacteria to cause disease
- resources (niche)
- ability to avoid or survive the immune system
must be able to overcome colonization resistance
opportunistic pathogens
bacteria that are typically part of the normal microbiota and don’t cause disease in their normal location
ex. klebsiella, enterobacter, proteus, some E. coli
how do opportunistic pathogens cause disease
bloom in normal location then spread to abnormal locations
do NOT use virulence factors
often antibiotic resistant – survive treatment with abx while others get eliminated
what are 3 factors that allow opportunistic pathogens use to overcome host defenses
- pre-existing infection by parasites/viruses
- drugs
- host factors
how does pre-existing infection by parasites/viruses allow opportunistic pathogens to spread
causes immunosuppression and GI damage that leads to altered host immune system
opportunists are then able to take advantage of pre-established dysbiosis
how do host factors allow opportunistic pathogens to spread
increased genetic risk (ex. SCID), stress, and poor nutrition all contribute to pre-established dysbiosis
frank pathogens
bacteria that are able to provide their own resources/niche and ways of avoiding the immune system
NOT present in microbiome normally
how do frank pathogens cause disease
uses VIRULENCE FACTORS
create their own niche by causing GI damage –> inflammation –> bacteria thrives off inflammation
what are 3 factors that allow frank pathogens use to overcome host defenses
- bloom to high levels
- evade host immunity
- damage host cells
how does blooming to high levels allow frank pathogens to spread
overwhelms the host barriers and out-competes other bacteria by rapid replication or slow GI transit time
requires virulence factors to overcome colonization resistance
what are mechanisms that frank pathogens use to evade host immunity
- survive in wide pH range
- motility to invade mucus barrier
- evade IgA binding (ex. antigenic variation)
antigenic variation
changing surface antigen as the bacteria grows to avoid recognition by the immune system
how do frank pathogens cause damage to host cells
- binding to intestinal cells to cause direct damage (no virulence factors required)
- toxin production (binding does not cause damage)
non-invasive vs invasive bacteria
noninvasive: causes attaching and effacing lesions on intestinal cell surface
invasive: attach to cells then go intracellular - requires toxin secretion
how do the toxins produced by frank pathogen cause damage
- form pores - increase host cell permeability
- disrupt adhesion or tight junctions - decreases barrier function
- alter immune response or cell signaling
