Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Micro/Immuno FINAL > G-pathogens of mucosal surfaces pt.2 > Flashcards

G-pathogens of mucosal surfaces pt.2 Flashcards

1
Q

name some toxin producing bacterial pathogens

A
  • vibrio spp.
  • but primarily v. cholerae
  • enterotoxigenic e. coli ETEC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe the outcomes of infection with toxin-producing bacterial pathogens…

A
  • in small intestine
  • copious amounts of watery stool
  • no blood in stool
  • no leukocytes in stool
  • no tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

all of the vibrio spp. can induce gastroenteritis but specifically what do v. cholerae, v. parahaemolyticus, v. vulnificus, and v. alginolyticus do?

A
  • v. cholerae: diarrhea, “cholera gravis”
  • v. parahaemolytius: diarrhea
  • v. vulnificus: tissues and blood
  • v. alginolyticus: tissues and blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe the structure of v. cholerae.

A
  • curved
  • spiral
  • long flagella
  • highly motile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

there are two main cholera types. name them and describe them.

A
  • El Tor: commonly found in endemic areas, but didn’t cause disease; disappeared after 1960s but reappeared in 1992 because of a mutated O; O139 is a new LPS stereotype and is also encapsulated; about 1 in 20 infected developed cholera
  • Classical: caused disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the virulence factors of v. cholerae?

A
  • flagella
  • pili to adhere to mucosal tissue : shift from saltwater to reduced ion levels found in body leads to expression of pili and to the toxin; pili with adhesin on tip and not always expressed when in environment of low ion levels
  • cholera toxin: phage encoded
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how does vibrio invade and infect?

A
  • once in interior, activates adenylate cyclase
  • which produces cAMP
  • which has a neg feedback look to adenylate cyclase to turn it off
  • toxin activates cAMP & changes it so can’t be affected by healthy cell = neg feedback inhibition
  • therefore, adenylate cyclase changes function of cell: stops absorption of Na+ and secretion of Cl- ions and loss of H2O

*Ctx causes transfer of ADP from NAD to active Gs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how many different strains of e. coli exist and what kind of strain predominates?

A
  • thousands of different strains

- most are commensals but some are pathogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what type(s) of e. coli cause secretory diarrhea?

A

ETEC and EPEC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what type(s) of e. coli are dysentery-like?

A

EHEC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what type(s) of e. coli cause urinary tract infections?

A

UPEC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which type of e. coli is responsible for 30-45% of cases of traveler’s diarrhea (when traveling to Mexico)?

A

ETEC = enterotoxigenic e. coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

does ETEC have a large of small infectious dose?

A

large

not resistant to gastric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is on the fimbriae of ETEC to help the adhere to mucosal tissues?

A

colonization factor antigens (cfa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the two toxins that are responsible for the diseases caused by ETEC?

A
  • heat-labile toxin (LT)

- heat-stable toxin (ST)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does ETEC invade and infect?

A
  • similar to cholera toxin
  • LT also activates adenylate cyclase
  • act on adenylate cyclase to increase cAMP
  • changes adenylate cyclase to impede neg feedback loop
  • loose Cl- and H2O also can’t absorb Na+
  • ST activates GC
  • uses cGMP but same concept
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do you rule out that vibrio cholerae is not the cause of illness?

A
  • must have eaten shellfish
  • thiosulfate-citrate-bile-sucrose (TCBS) agar
  • agglutination test (El Tor strain)
  • serological testing
  • inoculate plates with diluted stool samples
  • not very rich medium, so fastidious G- won’t grow
  • aerobic incubation kills the anaerobes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the best way to treat cholera secretory diarrhea?

A
  • rehydrate as quick as possible (mix of sugar and salt)
  • used “cholera cots” with whole for shit and bucket to catch it
  • reported as alert and playful 2 hrs after rehydration therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what antibiotic treatment is also possible for secretory diarrhea?

A
  • can help shorten duration or reduce the severity
  • tetracyclines for vibrio infections: doxycycline
  • 2nd generation flouroquinolones for ETEC: ciprofloxacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

which e. coli are the “hybrid” misfits?

A
  • enteropathogenic e. coli (EPEC)

- enterohemorrhagic e. coli (EHEC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

where do the “hybrid” misfits colonize?

A

lower small intestine and upper large intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does colonization of the “hybrid” misfits cause?

A

attaching and effacing lesion (reorganization of epi cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how do the “hybrid” misfits affect stool?

A

blood in stool (and possibly urine) with EHEC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

enteropathogenic e. coli is prevalent in which age class of humans?

A
  • newborns

- not good at causing disease in healthy adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

enteropathogenic e. coli (EPEC) causes what and colonizes which area of the GI tract?

A
  • noninflammatory secretory diarrhea

- distal small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

does EPEC require a small or large infectious dose?

A

large and in charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is unique about EPEC?

A

absence of traditional endotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

EPEC/EHEC have a characteristic intimate adherence pattern (attaching and effacing lesion), describe!

A
  • stage 1: bundle forming pili (bfp) assist in adherence from a relative long distance (bundling of pili together to make one structure used for adherence to host epi cell)
  • stage 2: syringe-like secretion system (called type III secretion) injects Tir into host cell
    • Tir is a transmembrane intimate receptor that causes actin polymerization and pushes e. coli up on pedestal
  • stage 3: Tir binds to intim on E. coli resulting in pedestal formation (attaching and effacing region)

** this is what leads to diarrhea

29
Q

what causes diarrhea for EPEC?

A
  • no toxin production
  • malabsorption due to microvilli disruptions
  • disruption of epithelial tight junctions (due to pedestal formation)
30
Q

what are the set of EPEC genes called that produce an attaching effecing region?

A

eae genes

31
Q

does EHEC or EPEC produce a toxin?

A

EHEC: toxin that can lead to hemolytic uremic syndrome (which is much more serious)

32
Q

Which type of e. coli is known as the hamburger pathogen?

A

EHEC (enterohemorrhagic e. coli)

33
Q

what is the O and H antigens associated with EHEC?

A

O157:H7

34
Q

what is the primary reservoir for EHEC?

A

cattle

35
Q

how does EHEC cause gastroenteritis?

A
  • causes an attaching effacing legion
  • produces a Shiga-like toxin that cause hemorrhagic colitis and/or hemolytic uremic syndrome (HUS)
  • HUS: 250-500 deaths each year (children most susceptible)
  • HUS toxin can infect kidneys too
36
Q

how do shiga-like toxins act on mucosal surfaces?

A
  • mucosal surfs are heavily vascularized and they attack the small block vessels of the large intestines
  • this is intensified when inflammatory cytokines are present (macrophages that release IL-1, IL-6, TNF)
37
Q

how is EHEC diagnosed?

A
  • clinical manifestations recognized: frankly bloody stool, edema of ascending colon
  • EHEC cannot ferment sorbitol, usually
  • detection of Shiga-like toxins
38
Q

how is EHEC treated?

A

CONTROVERSIAL:

  • CDC says no antibiotics because can make toxins more potent
  • supportive therapy: rehydrate, usually not necessary
  • dialysis if HUS is pending
39
Q

what species of bacteria infects the urinary tract?

A

Proteus spp. (UHEC)

40
Q

what species of bacteria infects the respiratory tract?

A

klebsiella spp

41
Q

T/F: UTI’s are the most common form of bacterial infection of an organ system (not including the mouth), and the most frequent cause of doctor’s visits by adults (not including trips to the dentist).

A

TRUEEE

42
Q

what is another way of saying inflammation of the bladder?

A

cystitis

43
Q

how does age influence the prevalence of UTI’s in men and women?

A
  • women: incr with age exponentially

- men: when the prostate is active low chance of UTI but equals same chance of women getting it when prostate inactive

44
Q

what is an uncomplicated UTI?

A
  • all normal defense mechanisms are intact
  • no recent hospital admissions
  • disease limited to lower urinary tract
45
Q

what is a complicated UTI?

A
  • some structural abnormality in urinary tract
  • recently admitted to hospital (from catheter)
  • disease most likely will spread to kidneys
46
Q

what are the natural defenses found in the urinary tract?

A
  • complete voidance of bladder
  • peristalsis
  • urerterovesicle valves (unidirectional)
  • mucous layer
  • normal microbiota (eg. Lactobacillus spp.) which colonize urethra and acid kills the pathos
47
Q

what happens when a UTI spreads to kidney?

A

causes pyelonephritis

48
Q

pyelonephritis can be caused by retrograde flow of urine from bladder to kidneys as well as urethral cathers… how does this affect children and pregnancy?

A
  • neurological disorders leading to poor empyting of bladder
  • children: incomplete closing of the ureterovesical valves
  • pregnancy: hormones cause dilation and decrease peristalsis of the ureters
49
Q

describe urinary tract stones?

A
  • some bacteria, like Proteus spp. neutralize pH of urine and cause the formation of “struvite” calculi (insoluble ppt that can damage vesicles)
  • leads to kidney infection
50
Q

how does UPEC (uropathogenic e. coli) adhere to uroepithelial cells?

A

fimbriae:
- acute cystitis: (ie. uncomplicated UTI) associated with fimbrial antigen FimH
- pyelonephritis is assoc. with expression of P fimbriae

51
Q

what does Proteus mirabilis cause?

A
  • uncomplicated UTI’s
  • G- that is heavily flagellated so very motile
  • occurs in uncomplicated and nosocomial infection, abnormal urinary tract structure more likely to have UTI caused by P. mirabilis
  • P. mirabilis UTI tends to more severe than e. coli induced UTI
52
Q

what are the Proteus mirabilis virulence factors?

A
  • flagella
  • an adhesin on the fimbriae is specific for urinary epithelium (exact adhesin is not known)
  • hemolysins (blood in urine)
  • IgA protease (adhesin degrades)
  • urease, an enzyme that raises the pH of urine
  • converts urea to ammonia and carbon dioxide
  • bacteria will grow better in the less acidic environment
  • toxic to renal cells
  • enhances formation of struvite (magnesium ammonium phosphate) urinary stones, which can lead to chronic infection
53
Q

how is Proteus mirabilis diagnosed?

A
  • difficult to positively ID the causative agent of a UTI
  • count bacteria in the urine
  • healthy (asymptommatic) individual bacteriuria greater than or equal to 10^5 CFU/mL
  • individual with dysuria greater than or equal to 10^2 (with pyuria)
  • proteus can be diagnosed by:
  • consistently alkaline urine
  • production of urease
54
Q

how is Proteus mirabilis treated?

A
  • variety of antimicrobials
  • trimethoprim-sulfamethoxazole first choice
  • 3 day therapy for actue cystitis
  • 10-14 day therapy for polynephritis
  • aymptomatic bacteriuria: prego females
55
Q

what shape of colonies does klebsiella form and why?

A

large, mucoid colonies due to large capsule

56
Q

what does klebsiella cause?

A

bacterial pneumoniae

57
Q

what are klebsiella’s virulence factors?

A
  • pili:
  • type 1: important for adherance to urinary tract epithelial cells (urothelium)
  • type 3: important for adherence to respiratory tract epithelial cells
  • enterotoxin similar to ST and LT (of ETEC) so they can induce secretory diarrhea
  • aerobactin: an iron sequestering protein
  • antiphagocytic capsule: thought to be the PRIMARY virulence factor because hard for macrophages to engulf
58
Q

Helicobacter pylori is unlike any other GI bugs we’ve studied thus far… why?

A
  • believed to be transmitted thru oral-to-oral contact (as well as fecal to oral)
  • it is a “slow” bacterium
  • in the GI tract, only found in the mucous overlying mucous secreting cells of the stomach
  • an animal reservoir for H. pylori has not been found

*** among the most prevalent G- GI bugs

59
Q

describe erosive gastritis.

A
  • initially low grade inflammation in stomach

- can go on for years with few symptoms

60
Q

describe a duodenal ulcer.

A
  • erosion disrupts epithelial cells

- gastric acid deteriorates deeper tissues

61
Q

where does MALT lymphoma occur?

A

lower stomach/upper duodenum

62
Q

what is a progressive form of gastric cancer?

A

gastric adenocarcinoma

63
Q

is h. pylori readily killed by gastric acid?

A

YEZ

64
Q

what enzyme is efficiently produced by h. pylori?

A

urease

65
Q

what causes epithelial cells to produce IL-8 in h. pylori infection?

A

inflammatory effector molecules

66
Q

cytotoxin is associated with what disease in h. pylori infection?

A

peptic ulcer disease

  • induces vacuolation and apoptosis of epithelial cells)
  • neutrophils contribute to ulcer formation
67
Q

h. pylori causes the downregulation of what?

A

somatostatin-producing-D-cells

68
Q

what is one method that can diagnose h. pylori?

A

urea breath test for presence of ammonia

69
Q

how is h. pylori infection treated?

A
  • intensely with many side effects
  • first line: proton pump inhibitor, antibiotic cocktail (clarithomycin and metronidazole)
  • second line: proton pump inhibitor, bismuth subsalicylate, tetracycline, metronidazole

Micro/Immuno FINAL (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions