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

Final; Toxin-Producing Pathogens of Mucosal Surfaces Flashcards

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1
Q

What are the symptoms of a toxin producing bacterial invasion

A

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

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2
Q

Where in the intestine are the toxin producing bacteria

A

small intestine

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3
Q

What are the species of vibrio

A

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

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4
Q

True or False

V. cholera are highly motile

A

True

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5
Q

What are the two typs of cholera

A

nonpathogenic and pathogenic

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6
Q

What is the strain of cholera that emerged in 1992

A

a “new” El Tor

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7
Q

What is specific about the new El Tor strain

A

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

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8
Q

What are three virulence factors of V. cholerae

A

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

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9
Q

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

A

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

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10
Q

What does the cholera toxin do to the cells

A

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

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11
Q

How many different strains of E.coli are there

A

thousands; but many are commensal

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12
Q

These strains of E.coli cause secretory diarrhea

A

ETEC (enterotoxigenic E.coli)

EPEC (enteropathogenic E.coli)

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13
Q

This strain of E. coli cause dystenery-like symptoms

A

EHEC (enterohemorrhagic E.coli)

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14
Q

This strain of E.coli causes urinary tract infections

A

UPEC (uropathogenic E.coli)

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15
Q

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

A

ETEC

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16
Q

ETEC requires what kind of infectious dose

A

large

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17
Q

What helps ETEC adhere to mucosal tissues

A

colonization factor antigens (cfa) on fimbrae

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18
Q

What toxins does ETEC produce

A

heat-labile toxin (LT)

heat-stable toxin (ST)

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19
Q

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

A

same pathway with adenylate cyclase but uses cGMP and guanulate cyclase

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20
Q

What is the first step in diagnosing secretory diarrhea agents

A

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

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21
Q

What are the treatments for secretory diarrhea

A

oral rehydration; mix or sugar and salt

antibiotics can help shorten the duration/severity

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22
Q

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

A

EPEC

EHEC

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23
Q

What does colonization of the hybrids do

A

causes attaching and effacing lesion; reorganization of epithelial cells

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24
Q

What is special about the stool following a EHEC infection

A

blood in still (and possible the urine)

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25
Q

This infection is prevalent in newborns

A

EPEC

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26
Q

What type of diarrhea does EPEC cause

A

noninflammatory secretory diarrhea

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27
Q

Where in the small intestine does EPEC infect

A

distal small intestine

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28
Q

Does EPEC require a small or large infectious dose

A

large

29
Q

What is characteristic of the exotoxins of EPEC

A

there is an absence of traditional exotoxins

30
Q

What type of lesion does EPEC cause

A

characteristic intimate adherence pattern (an attaching and effacing lesion)

31
Q

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

A

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

32
Q

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

A

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

33
Q

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

A

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

34
Q

What is the overall goal of intimate adherence

A

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

35
Q

What causes diarrhea due to EPEC

A

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

36
Q

EHEC has a set of genes which does what

A

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

37
Q

What is the notorious E.coli of EHEC

A

O157:H7; primary reservoir is cattle

38
Q

O157:H7 causes what

A

attaching effacing lesion (gastroenteritis)

produces a shiga-like toxin causing hemorrhagic colitis and hemolytic uremic syndrome

39
Q

Shiga-like toxins attack where

A

heavily vascularized mucosal surfaces like small intestine

40
Q

How would you diagnose EHEC

A

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

41
Q

Why would you not use antibiotics to treat EHEC

A

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

42
Q

What treatment would you use to treat EHEC

A

supportive therapy; rehydration if necessary

dialysis of HUS pending

43
Q

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

A

urinary tract infection

44
Q

What is cystitis

A

inflammation of the bladder

45
Q

When do males usually get UTIs

A

When the prostate in inactive; early and later in life

46
Q

What is an uncomplicated UTI

A

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

47
Q

What is a complicated UTI

A

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

48
Q

What are the natural defenses found in the urinary tract

A 
complete voidance of bladder
peristalsis
ureterovesicle valves
mucous layer
normal microbiota (Lactobacillus spp.)
pH
49
Q

UTI can spread to the kidney and cause what

A

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

50
Q

What bacteria cause urinary tract stones

A

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

51
Q

How does UPEC adhere to uroepithelial cells

A

through fimbriae

acute cystitis and pyelonephritis are associated with fimbriae expression

52
Q

UPEC is able to produce what special substances

A

aerobactin

hemolysin, which lyses host cells

53
Q

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

A

Proteus mirabilis

54
Q

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

A

P. mirabilis

55
Q

What are the virulence factors of P.mirabilis

A 
flagella
adhesion of frimbriae
hemolysis
IgA protease
Urease; raising pH of urine
56
Q

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

A

difficult

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

57
Q

P. mirabilis can be diagnosed by what

A

consistently alkaline urine

blood/pus in urine

58
Q

What are the treatment options for UTIs

A

antimicrobials; trimethoprim-sulfamethoxazole

59
Q

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

A

klebsiella

60
Q

What are the virulence factors of Klebsiella

A

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

61
Q

What are the different types of pili

A

type 1; important for UT epithelial

type 3; important for respiratory tract epithelial

62
Q

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

A

helicobacter pylori

63
Q

Where is H. pylori only found

A

in the mucous overlying the mucous secreting cells of the stomach

64
Q

True or False;

H. pylori can lead to many different diseases

A

True; including gastric adenocarcinoma

65
Q

How does H. pylori survive in the stomach

A

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
Q

How would you diagnose an H. pylori infection

A

mucosal biospies
urea breath test
serology

67
Q

Why does H. pylori cause carcinogenesis

A

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
Q

What are some treatments of H. pylori infection

A

first line; proton pump inhibitor and antibiotic cocktail

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

SP14 Microbiology (31 decks)

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