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Immuno final > gram - pathogens of mucosal surfaces pt. 2 > Flashcards

gram - pathogens of mucosal surfaces pt. 2 Flashcards

1
Q

invasive bacterial pathogens

A

salmonella

shigella

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2
Q

toxin producing bacterial pathogens

A

vibrio

entertoxigenic e coli (ETEC)

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3
Q

hybrid pathogens (btwn invasive and toxin producing)

A

enterohemorrhagic e coli (EHEC)

enteropathogenic E coli (EPEC)

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4
Q

traits of invasive bacterial pathogens

A

invade lg intestine
sm vol of bloody stool
leukocytes in stool
tissue ulcerations

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5
Q

traits of toxin producing bact

A

invade sm intestines

copious amounts of watery stool w/ no blood leukocytes or tissue damage

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6
Q

traits of hybrid bacterial path

A

invade lower sm or upper lg intestines
colonization causes attaching and effacing intimate adherence pattern (attaching and effacing lesion)
lesions causing blood stool (and urine w/ EHEC)

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7
Q

types of vibrio

A

cholerae - diarrhea
parahaemolyticus - diarrhea
vulnificus - tissues and blood
alginolyticus - tissues and blood

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8
Q

virulence factors of v. cholerae

A

flagella
pili to adhere to mucosal tissue (activated by reduced ion levels caused by shift from saltwater to body
cholera toxin - phage encoded

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9
Q

how does heat labile toxin differ from heat stable toxin?

A

heat labile activates AC causing an inc. in cAMP

heat stable toxin activates GC which causes and inc. in cGMP

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10
Q

traits of ETEC

A

responsable for traveler’s diarrhea
lg infectious does
colonization factor antigens on fimbrae help adhere to mucosal tissue
produces heat-labile toxin and heat-stable toxin

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11
Q

how do you treat toxin prod bact path

A

oral rehydration

antibiotics tetracyclines or fluoroquinolones

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12
Q

traits of EPEC

A 
prevalent in newborns 
noninflammatory diarrhea
distal sm intestine
lg infectious dose
no traditional exotoxins
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13
Q

steps of intimate adherence by EPEC and EHEC

A

1 bundle forming pili assist in adherence
2 type III secretion system injects Tir into host cell
3 Tir binds to intimin on E coli resulting in pedestal formation

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14
Q

how does EPEC cause diarrhea

A

no toxin, so malabsorption due to microvilli disruptions or epithelial tight junctions

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15
Q

how does EHEC cause diarrhea?

A

same way as EPEC (b/c has set of its genes) plus it makes a toxin that leads to hemolytic uremic syndrome

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16
Q

EHEC traits

A

e coli O157H7 is most common
reservoir = cattle
makes effacing lesion
produces shiga-like toxin

17
Q

diagnosis of EHEC

A

bloody stool and edema of ascending colon
also shigalike toxins present
no sorbitol fermentation

18
Q

treatment of EHEC

A

no antibiotics
rehydration
dialysis if hemolytic uremic syndrome

19
Q

what’s cystitis?

A

inflammation of bladder

20
Q

traits of uncomplicated UTI

A

mainly caused by e coli
normal defense mech are intact
no recent hospital admissions
limited to lower urinary tract

21
Q

traits of complicated UTI

A

mainly caused by klebsiella, p. aeruginosa and serratia
structural abnomality in urinary tract
recently in hospital
spread to kidneys

22
Q

natural defenses of urinary tract

A 
voidance of bladder
peristalsis
ureterovesicle valves
mucous layer
microflora
pH
23
Q

traits of uropathogenic E coli (UPEC)

A

adhere to uroepithelial cells through fimbriae (can case acute cystitis, and pyelonephritis)
production of aerobactin and hemolysin (assoc w/ pyelonephritis)
genetically linked to recurrent disease

24
Q

traits of proteus mirabilis

A

can cause uncomplicated UTI that’s more severe than w/ e coli

25
Q

proteus virulence factors

A 
flagella
adhesin on fimbriae specific for urinary ep
hemolysins
IgA protease
urease (raises pH of urine)
26
Q

diagnosis of UTI

A

hard to tell which bact

alkaline urine/urease production = proteus

27
Q

treatment of UTI

A

antimicrobials esp trimethoprim sulfamethoxazole

28
Q

klebsiella virulence factors

A

pili (type 1 = urinary tract and type 3 = repiratory tract)
enterotoxine similar to ST and LT (induces diarrhea)
aerobactin (iron sequestering prot)
large antiphagocytic capsule

29
Q

traits of helicobacter pylori

A 
most prevalent gram (-) GI bug
oral to oral transmission
slow bact
only in mucous overlying mucous secreting cells of stomach
no animal reservoir
30
Q

virulence factors of helicobacter pylori

A

produces urease to inc pH
inflammatory effector molecules cause IL-8 production
cytotoxin
down regulate somatostatin producing D cells which causes inc. gastrin production (causes cell mutation and ulcers)

31
Q

treatment for helicobacter pylori

A

intense w/ many side effects

first line and second line ea. have a proton pump inhibitor and antibiotic cocktail

Immuno final (13 decks)

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