Final; Toxin-Producing Pathogens of Mucosal Surfaces Flashcards Preview

SP14 Microbiology > Final; Toxin-Producing Pathogens of Mucosal Surfaces > Flashcards

Flashcards in Final; Toxin-Producing Pathogens of Mucosal Surfaces Deck (68):
1

What are the symptoms of a toxin producing bacterial invasion

copious amounts of watery stool
no blood in stool
no leukocytes in stool
no tissue damage

2

Where in the intestine are the toxin producing bacteria

small intestine

3

What are the species of vibrio

V. cholerae; cholera
V. parahaemolyticus; dirrhea
V. vulcificus; tissues and blood
V. alginolyticus; tissues and blood

4

True or False
V. cholera are highly motile

True

5

What are the two typs of cholera

nonpathogenic and pathogenic

6

What is the strain of cholera that emerged in 1992

a "new" El Tor

7

What is specific about the new El Tor strain

mutated O antigen
new LPS serotype
now encapsulated
affected all age groups

8

What are three virulence factors of V. cholerae

flagella
pili to adhere to mucosal tissues
cholera toxin; phage encoded

9

What causes the expression of pili and toxin in V. cholerae

a shift from saltwater to reduced ion levels found in the body

10

What does the cholera toxin do to the cells

it enters through epithelial cells
activated adenylate cyclase
forming cAMP
which turn off adenylate cyclase
but the toxin produces negative feedback causing cAMP to build up
lots of cAMP causes the cell to stop absorbing Na and secreting Cl drawing the water to the intestinal lumen
watery stool

11

How many different strains of E.coli are there

thousands; but many are commensal

12

These strains of E.coli cause secretory diarrhea

ETEC (enterotoxigenic E.coli)
EPEC (enteropathogenic E.coli)

13

This strain of E. coli cause dystenery-like symptoms

EHEC (enterohemorrhagic E.coli)

14

This strain of E.coli causes urinary tract infections

UPEC (uropathogenic E.coli)

15

This is responsible for 30-45% of cases of traveler's diarrhea (when traveling to Mexico)

ETEC

16

ETEC requires what kind of infectious dose

large

17

What helps ETEC adhere to mucosal tissues

colonization factor antigens (cfa) on fimbrae

18

What toxins does ETEC produce

heat-labile toxin (LT)
heat-stable toxin (ST)

19

What are the similarities and differences of the ETEC colonization of cells to cholera

same pathway with adenylate cyclase but uses cGMP and guanulate cyclase

20

What is the first step in diagnosing secretory diarrhea agents

rule out V. cholera with tests like;
inoculation of plates
tiosulfate-citrate-bile-sucrose agar
aerobic incubation kills anaerobes

21

What are the treatments for secretory diarrhea

oral rehydration; mix or sugar and salt
antibiotics can help shorten the duration/severity

22

What are considered the hybrid "misfits" where they do not fall into either the toxin producing or invasive pathogens

EPEC
EHEC

23

What does colonization of the hybrids do

causes attaching and effacing lesion; reorganization of epithelial cells

24

What is special about the stool following a EHEC infection

blood in still (and possible the urine)

25

This infection is prevalent in newborns

EPEC

26

What type of diarrhea does EPEC cause

noninflammatory secretory diarrhea

27

Where in the small intestine does EPEC infect

distal small intestine

28

Does EPEC require a small or large infectious dose

large

29

What is characteristic of the exotoxins of EPEC

there is an absence of traditional exotoxins

30

What type of lesion does EPEC cause

characteristic intimate adherence pattern (an attaching and effacing lesion)

31

What is the first stage of intimate adherence by EPEC and EHEC

bundle-forming pili (bfp) assist in adherence from relative long distance; like a "syringe"

32

What is the second stage of intimate adherence by EPEC and EHEC

syringe-like secretion system (called type III secretion) injects Tir (translocated intimin receptor) into host cell

33

What is the third stage of intimate adherence by EPEC and EHEC

Tir bind to intimin on E.coli resulting in pedestal (receptor) formation

34

What is the overall goal of intimate adherence

to inject the receptor into host cell and the host cell expresses the receptor binding the E.coli to the cell

35

What causes diarrhea due to EPEC

no toxin but malabsoprtion due to microvili disruptions and of epithelial tight junctions

36

EHEC has a set of genes which does what

EPEC genes (eae genes) which produces an attaching effacing lesion and a toxin that can lead to uremic syndrome

37

What is the notorious E.coli of EHEC

O157:H7; primary reservoir is cattle

38

O157:H7 causes what

attaching effacing lesion (gastroenteritis)
produces a shiga-like toxin causing hemorrhagic colitis and hemolytic uremic syndrome

39

Shiga-like toxins attack where

heavily vascularized mucosal surfaces like small intestine

40

How would you diagnose EHEC

clinical manifestations easily recognized; bloodily stool and edema of ascending colon
EHEC cannot ferment sorbitol
detection of shiga-like toxins

41

Why would you not use antibiotics to treat EHEC

It makes the toxin more potent by killing the microbes which will release more toxins like LPS and stimulating inflammation

42

What treatment would you use to treat EHEC

supportive therapy; rehydration if necessary
dialysis of HUS pending

43

This is the most common form of bacterial infection of an organ system (not including the mouth) and it is also the most frequent cause of physician visits by adults

urinary tract infection

44

What is cystitis

inflammation of the bladder

45

When do males usually get UTIs

When the prostate in inactive; early and later in life

46

What is an uncomplicated UTI

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

47

What is a complicated UTI

some structural abnormality in urinary tract (immunosuppressive, etc.)
recently admitted to hospital
disease most likely will spread to kidneys

48

What are the natural defenses found in the urinary tract

complete voidance of bladder
peristalsis
ureterovesicle valves
mucous layer
normal microbiota (Lactobacillus spp.)
pH

49

UTI can spread to the kidney and cause what

pyelonephritis
retorgrade flow of urine from bladder to kidney
can be caused by urethral catheters

50

What bacteria cause urinary tract stones

Proteus spp. it neutralizes pH and causes formation of "struvite" calculi

51

How does UPEC adhere to uroepithelial cells

through fimbriae
acute cystitis and pyelonephritis are associated with fimbriae expression

52

UPEC is able to produce what special substances

aerobactin
hemolysin, which lyses host cells

53

This occurs in uncomplicated and nonsocial infection, abnormal urinary tract structure more likely to have UTI caused by this

Proteus mirabilis

54

Which UTI is more severe, one caused by E. coli or one caused by P. mirabilis

P. mirabilis

55

What are the virulence factors of P.mirabilis

flagella
adhesion of frimbriae
hemolysis
IgA protease
Urease; raising pH of urine

56

Is it easy or hard to positively ID the causative agent of a UTI

difficult
must count the bacteria in the urine ≥ 10^5 CFU/ml = normal

57

P. mirabilis can be diagnosed by what

consistently alkaline urine
blood/pus in urine

58

What are the treatment options for UTIs

antimicrobials; trimethoprim-sulfamethoxazole

59

This pathogen exhibits large mucoid colonies due to large capsule and causes pneumonia

klebsiella

60

What are the virulence factors of Klebsiella

pili
enterotoxin similar to ST or LT (secretory diarrhea)
aerobactin; an iron sequestering protein
antiphagocytic capsule**

61

What are the different types of pili

type 1; important for UT epithelial
type 3; important for respiratory tract epithelial

62

This is among the most prevalent gram-negative GI bugs and is mostly transmitted through oral to oral (and fecal to oral)

helicobacter pylori

63

Where is H. pylori only found

in the mucous overlying the mucous secreting cells of the stomach

64

True or False;
H. pylori can lead to many different diseases

True; including gastric adenocarcinoma

65

How does H. pylori survive in the stomach

produces urease
inflammatory effector molecules; cause epithelial cells to produce IL-8
cytotoxin is associated with peptic ulcer disease
down regulation of somatostatin-producing D cells
but is killed by gastric acid

66

How would you diagnose an H. pylori infection

mucosal biospies
urea breath test
serology

67

Why does H. pylori cause carcinogenesis

H. pylori down regulates somatostatin
somatostatin inhibits gastrin
when down regulated it allows gastrin to be produced which causes epithelial cells to proliferate
if there is a mutation, then problems arise

68

What are some treatments of H. pylori infection

first line; proton pump inhibitor and antibiotic cocktail
second line; proton pump inhibitor, bismuth subsalicylate, tetracycline and metronidazole