Hdm Test 3: Gi Infections

Front 1

4 main GI host defenses

Back 1

stomach acid, intestinal motility, resident intestinal flora, innate and adaptive immunity

Front 2

4 main classifications of GI diseases

Back 2

Diarrheal diseases (inflammatory or secretory)
Typhoid fever
peptic ulcer disease
food poisoning

Front 3

2 Modes of inflammatory diarrhea

Back 3

-B invade and replicate in host cells
-B colonize large intestine and produce cytotoxins that provoke inflammation
(blood and pus)

Front 4

Mode of secretory diarrhea

Back 4

(non-invasive)
B colonize intestine and secrete enterotoxins that induce diarrhea
(key is high volume of BM)

Front 5

Main tx of diarrheal patients

Back 5

rehydration (most can be cleared)

Front 6

Cause of typhoid fever

Back 6

Salmonella enterica

Front 7

Start of typhoid fever

Back 7

GI infection, disseminates to other organs

Front 8

Sign of typhoid fever

Back 8

Slowly progressing fever

Front 9

Cause of peptic ulcer disease

Back 9

H. pylori, colonize the stomach mucosa

Front 10

Intoxications caused by ingestion of pre-formed emetic toxin

Back 10

food poisoning

Front 11

Poor canning

Back 11

C. botulinum: Botulism

Front 12

Food poisoning from improperly stored pastries, picnic items

Back 12

Staph aureus (bacteria killed in stomach, toxin is not)

Front 13

Improperly stored soups/stews

Back 13

Bacillus cereus

Front 14

Difference between onset for infection and food poisoning

Back 14

Shorter onset for food poisoning

Front 15

Disease caused by facultative intracellular pathogens; invasion of host cells is key to causing disease

Back 15

Enteroinvasive

Front 16

Disease caused by bacteria that produce enterotoxin; invasion not playing role

Back 16

enterotoxic

Front 17

Disease caused by bacteria that destroy epithelium; invasion does NOT play a role

Back 17

enteropathogenic

Front 18

Ex of enteroinvasive pathogens

Back 18

Salmonella enterica
Shigella
Campylobacter jejuni
Listeria monocytogenes
Enteroinvasive E.coli
(Yersinia enterocolitica)

Front 19

Bacterial penetration of non-professional phagocytes

Back 19

invasion

Front 20

two mechanisms of entry for bacteria

Back 20

zipper and trigger

Front 21

Mechanism used from transmission of effectors for GI enteroinvasive pathogens

Back 21

Type 3 secretion systems

Front 22

Microbio of Salmonella

Back 22

Gram- rods, multiple flagella, lactose-negative

Front 23

Air usage of Salmonella

Back 23

facultative anaerobes

Front 24

Main disease causing Salmonella species

Back 24

Salmonella enterica

Front 25

Symptoms of Typhoid fever

Back 25

Gastroenteritis
Slowly progressing fever
Profuse sweating

Front 26

Transmission of Typhoid fever

Back 26

Humans only (person to person)
Often a carrier (think Typhoid Mary)
Highly virulent

Front 27

Salmonella Typhi pathogenesis

Back 27

High acid tolerance
Invade epithelial cells and M cells (w/T3SS)
Prevents fusion of vacuole to lysosome.
HIGHLY resistant to macrophage killing
Produces a capsule.

Front 28

Tx for Typhoid fever

Back 28

Long-term antibiotic therapy
two vaccines for S. Typhi, no long-term protection

Front 29

Source of non-typhoid Salmonella

Back 29

Zoonotic

Front 30

Which Salmonella has a smaller infective dose?

Back 30

Salmonella typhi

Front 31

Symptoms of non-typhoid Salmonella disease

Back 31

intestinal inflammation, diarrhea, cramping, vomiting, fever

Front 32

Pathogenesis of non-typhoid Salmonella disease

Back 32

Similar to Typhoid Salmonella, but NO CAPSULE-->bacteria thus do not disseminate, self-limiting, Antibiotics not recommended, just rehydration

Front 33

Microbio of Shigella

Back 33

Gram- bacilli, non-motile, cannot ferment lactose

Front 34

3 types of shigella; which causes epidemics?

Back 34

S. sonnei, S. flexneri, S. dysenteriae (epidemics)

Front 35

Transmission of Shigella

Back 35

Low infectious dose, person to person, community outbreaks (schools or nursing homes)

Front 36

Symptoms of Shigellosis (dysentery)

Back 36

Symptoms in 1-7 days
Ranges from mild diarrhea to dysentery
Also, rarely: hemolytic uremic syndrome

Front 37

Tx for Shigellosis

Back 37

rehydration, antibiotics

Front 38

Shigella pathogenesis

Back 38

Invades through M cells;
can move within and between adjacent cells using actin-based motility

Front 39

Shiga toxin produced by what two bacteria?

Back 39

S. dysenteriae and Enterohemorrhagic E. coli

Front 40

Potential mechanisms of Shiga toxin

Back 40

Blocks absorption of glucose, electrolytes, AA from intestinal lumen; cytotoxic for some cells by inhibiting protein synthesis

Front 41

Microbio of Campylobacter jejuni

Back 41

Gram-, curved rods, motile

Front 42

Growth medium for Campylobacter

Back 42

Charcoal

Front 43

Most common bacterial cause of diarrheal disease in US

Back 43

Campylobacter

Front 44

Air requirements for Campylobacter

Back 44

microaerophilic (8-10% O2)

Front 45

Symptoms of Campylobacter infections

Back 45

Inflammatory diarrhea, sometimes bloody, cramps, fever, lasts about a week, self-limiting

Front 46

Infective dose of campylobacter

Back 46

500 CFU, pretty low

Front 47

Tx for campylobacter

Back 47

rehydration/antibiotics (usually just stay home)

Front 48

Campylobacter jejuni virulence factors

Back 48

Flagellar motility
Invasion
Cytolethal distending toxin (large cells)

Front 49

Microbio of Listeria monocytogenes

Back 49

Gram+ bacillus, grows at 4 C

Front 50

Method of movement for Listeria

Back 50

Motile, actin-based motility

Front 51

Bacteria that can contaminate dairy, processed meats; Issue for pregnant women, fetuses, neonates

Back 51

Listeria

Front 52

Symptoms for Listeria in pregnant women

Back 52

Mild, flu-like symptoms (trouble in immunocompromised pts)
Can cause miscarriage
Can cause neonate issues like group B strep
CNS infections include meningitis, encephalitis

Front 53

Enterotoxigenic bacteria have what drive their disease symptoms?

Back 53

Enterotoxins

Front 54

Microbio of Vibrio cholerae

Back 54

Gram-, comma-shaped rod

Front 55

Movement by V. cholerae

Back 55

Polar flagellum, highly motile

Front 56

Reservoir for v. cholerae

Back 56

fresh, marine, and brackish waters (and plankton found within)

Front 57

Transmission of V. cholerae

Back 57

humans, colonize small intestine;
lack of access to clean water is issue

HIGH infectious dose (low during hyperinfectious state)

Front 58

Incubation period of V. cholerae

Back 58

1-3 days, abrupt onset diarrhea (15-20 L/day)

Front 59

Cause of rice water stool

Back 59

Cholera toxin (resulting in loss of fluids/electrolytes, hypokalemia, cardiac arrhythmia)

Front 60

Therapies for Cholera

Back 60

Oral rehydration solution, IV rehydration, antibiotics, vaccine options (can be given IV if can't keep down)

Toxin is the problem, antibiotic limited use.

Front 61

Mortality with and without tx

Back 61

without tx: 50-60%
With tx: <1%

Front 62

Virulence factors of V. Cholerae

Back 62

Motility/chemotaxis
Proteases
Adhesins/Pili
Toxins

Front 63

What type of toxin in the Cholera toxin?

Back 63

A-B (active, binding)

Front 64

How does cholera toxin enter cell?

Back 64

Endocytosis, binding to GM1 ganglioside, A subunit transferred to cytosol

Front 65

How does cholera toxin drive Cl secretion?

Back 65

Cholera toxin ribosylates Gs, which constitutively activates Adenylate cyclase, which provides the cAMP needs to drive the Cl pump. Electrolytes follow this Cl, as does H2O

Front 66

Microbio of C. Difficile

Back 66

Gram+ rod, spore former, can be in human microflora

Front 67

Air needed for C. difficile

Back 67

Obligate anaerobic

Front 68

2 other outcomes of C. difficile

Back 68

Pseudomembranous colitis
Toxic megacolon

Front 69

How does transmission occur between people?

Back 69

Through spore formation

Front 70

Major risk factor for C.difficile

Back 70

Antibiotic therapy for another primary infection (not clear if present before tx or obtained after)

Front 71

toxins from C.difficile

Back 71

Toxin A (TcdA), enterotoxin
Toxin B (TcdB), cytotoxin

Front 72

Results of C.difficile toxins

Back 72

Disrupt cell actin
Cause cell rounding, death, necrosis
Inc colonis permeability
Pronounced inflammatory response, PMNs

Front 73

Tx for C.difficile disease

Back 73

Discontinuation of antibiotic therapy
Vancomycin and metronidazole
Probiotics with Lactobacillus
Fecal bacteriotherapy

Front 74

How do enteropathogenic bacteria provoke disease?

Back 74

Provoke inflammatory response from epithelial cells

Front 75

H. pylori pathogenesis

Back 75

-Flagella help colonize
-Produce urease to convert urea to ammonia and CO2 (reduces acidity, can get pH up to 7.6)
Mucinases and injected effectors damage and induce inflammation

Front 76

tx for H. pylori

Back 76

Combo of antibiotics
PPI
Bismuth subsalicylate

Front 77

Microbio of E.coli

Back 77

Facultative gram- rod, ferments lactose

Front 78

What is a reason that E.coli has such a wide presentation for disease?

Back 78

Propensity for horizontal gene transfer

Front 79

4 types of E.coli

Back 79

Enterotoxigenic EC, Enteroinvasive EC
Enteropathogenic EC, Enterohemorrhagic EC

Front 80

What does ETEC compare to?

Back 80

Cholera (b/c of heat stable toxin and LT toxin)

Front 81

What does EIEC compare to?

Back 81

Shigella, bacteria invade and escape from phagosome

Front 82

What does EPEC compare to?

Back 82

Bacteria adhere and damage epithelium, but don't invade

Front 83

What does EHEC compare to?

Back 83

Shige-like toxin, otherwise attaches to host cells like EPEC
-form pedestals, driving inflammation

Front 84

What do EHEC and EPEC inject into host cells?

Back 84

Tir protein, drive actin polymerization

Front 85

Age groups affected by Hemolytic Uremic syndrome

Back 85

6 mos-4 yrs

Front 86

Results from Hemolytic uremic syndrome

Back 86

Kidney failure (from clotting problems)

Front 87

Transmission of EIEC

Back 87

Person to person (like shigella)

Front 88

Transmission of ETEC

Back 88

Lack of clean water

Front 89

Differentiating between cholerae and ETEC

Back 89

Check for darting motility of V. cholerae