gram (-) pathogens of mucosal surfaces pt. 1 Flashcards
gram (-) path of mucosal surfaces
Enterobacteriaceae: -e. coli, -salmonella -shigella -klebsiella -proteus Vibrionoaceae: -vibrio
what is inoculum size?
how many bact are needed to cause disease
natural barriers of GI tract
secretory antimicrobial compounds microflora acidity motility mucous layer tight jcns
where are microflora bact and how do they help?
ileum and colon (b/c rest of GI tract is too motile)
outcompetes for food/binding sites
what secretory antimicrobial compounds do we have and what do they do?
lysozyme - cleaves NAM and NAG of bact
lactoferrin - bacteriostatic b/c sequesters iron
cathelicidin - disrupts bact membrates of Gm-and Gm+ and fungi
defensins - create pores in microbes
IgA - makes it hard for microbes to adhere to surfaces
how do bact fight innate barriers?
acid resistance fimbriae/pili cell structures (cationic AA's repel antimicrobial peptides and siderophores sequester iron in low iron environ. ) capsule phagocytic compartment neutralization
how do macrophages help w/ mucosal immunity?
hang out in mucous till activation of pattern recognition receptors (TLR4) initiates inflammatory resp.
downside to macrophage activation?
inflammatory cytokines (TNF alpha) disrupt tight jcns of epithelial cells
adaptive immune resp is generated in the …
lymph nodes
traits and example of invasive pact pathogens
large intestine
sm. bloody stool w/ lymphocytes
tissue ulcerations
ex: salmonella and shigella
types of shigella and how they’re distinguished
dist. by O antigen dysenteriae flexneri boydii sonnei
shigella virulence factors/multiplication
acid resistant so low inoculum size
grow/multiply once in anaerobic env. in colon/ileum
how do shigella cross epithelial membrane?
enter M cells via invasion plasmid antigen (IPA = membrane prot)
ingested by macrophages which start innate imm resp. causing inflammation opening tight jcns
ep cells ingest bact whose proteins lyse the phagosomal vesicle
shigella spread intracellularly by IcsA which help it avoid re-entering lamina propria where immune cells are
which shigella is diff than the others and how?
s. dysenteriae type 1
causes invasive diarrhea (like other types) but also produces shiga toxin which kills intestinal ep and endothelial cells and disrupts Na absorption causing LOTS of watery bloody stool
diseases caused by salmonella
gastroenteritis - self limiting typhoid fever (only caused by s. typhi) - deadly
characteristics of salmonella infection
fecal oral transmission
large inoculum (more acid sensitive than sigella)
acidity of stomach triggers virulence genes
how do samonella enter cell?
induce phagocytosis through inducing cell signaling pathways and causing ruffled cell surface
remain in cell vescicles for hours then get into lamina propria
some are phagocytosed but some escape and cause bacteremia
(typhi stay in phagosomes where they thrive)
traits of s. typhi
enter in lymph
replicate w/in macrophage phagosomes
only in humans
asymptomatic carriers with gall bladder infections
similarities btwn shigella and salmonella
both respond/activate virulence factors due to env. changes (shig= anaerobic env.; salm = low pH)
both are invasive so cause low vol. bloody leukocytic diarrhea
dissimilarities btwn shigella and salmonella
salm has high inoculum size, shig. has low innoculum size
salm. spreads thru bacterimia, shig spreads intracellularly and locally thru IcsA
species that cause severe disease are v. dissimilar (typhi v. dyssenteria)
treatment of invasive enteric path
rehydration
fluoroquinolones
typhiod fever = vaccine, gall bladder removal or fluoroquinilones
