gram (-) pathogens of mucosal surfaces pt. 1 Flashcards

1
Q

gram (-) path of mucosal surfaces

A
Enterobacteriaceae:
-e. coli,
-salmonella
-shigella
-klebsiella
-proteus
Vibrionoaceae:
-vibrio
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2
Q

what is inoculum size?

A

how many bact are needed to cause disease

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3
Q

natural barriers of GI tract

A
secretory antimicrobial compounds
microflora
acidity
motility 
mucous layer
tight jcns
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4
Q

where are microflora bact and how do they help?

A

ileum and colon (b/c rest of GI tract is too motile)

outcompetes for food/binding sites

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5
Q

what secretory antimicrobial compounds do we have and what do they do?

A

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

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6
Q

how do bact fight innate barriers?

A
acid resistance
fimbriae/pili
cell structures (cationic AA's repel antimicrobial peptides and siderophores sequester iron in low iron environ. )
capsule
phagocytic compartment neutralization
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7
Q

how do macrophages help w/ mucosal immunity?

A

hang out in mucous till activation of pattern recognition receptors (TLR4) initiates inflammatory resp.

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8
Q

downside to macrophage activation?

A

inflammatory cytokines (TNF alpha) disrupt tight jcns of epithelial cells

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9
Q

adaptive immune resp is generated in the …

A

lymph nodes

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10
Q

traits and example of invasive pact pathogens

A

large intestine
sm. bloody stool w/ lymphocytes
tissue ulcerations
ex: salmonella and shigella

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11
Q

types of shigella and how they’re distinguished

A
dist. by O antigen
dysenteriae
flexneri
boydii
sonnei
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12
Q

shigella virulence factors/multiplication

A

acid resistant so low inoculum size

grow/multiply once in anaerobic env. in colon/ileum

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13
Q

how do shigella cross epithelial membrane?

A

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

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14
Q

which shigella is diff than the others and how?

A

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

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15
Q

diseases caused by salmonella

A
gastroenteritis - self limiting
typhoid fever (only caused by s. typhi) - deadly
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16
Q

characteristics of salmonella infection

A

fecal oral transmission
large inoculum (more acid sensitive than sigella)
acidity of stomach triggers virulence genes

17
Q

how do samonella enter cell?

A

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)

18
Q

traits of s. typhi

A

enter in lymph
replicate w/in macrophage phagosomes
only in humans
asymptomatic carriers with gall bladder infections

19
Q

similarities btwn shigella and salmonella

A

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

20
Q

dissimilarities btwn shigella and salmonella

A

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)

21
Q

treatment of invasive enteric path

A

rehydration
fluoroquinolones
typhiod fever = vaccine, gall bladder removal or fluoroquinilones