Hdm Week 15

Front 1

top 2 childhood death in the world:

Back 1

1. neonatal deaths - 40%

2. diarrheal diseases - 14%

Front 2

what do lysozymes do?

Back 2

break down peptidoglycans (cell walls)

Front 3

**critical aspect of some infections:**

Back 3

it's not just what bact. causes it, it's the *location*

Front 4

3 defenses of the GI tract:

Back 4

1. mucosal epithelial lining

2. mucus/gut motility

3. bile salts

Front 5

mucus and gut motility hinder:

Back 5

bact. adherence

Front 6

what do bile salts do?

Back 6

disrupt lipid membranes

Front 7

dysentery of LI =

Back 7

inflammation of lamina propria

Front 8

3 mechanisms of damage due to infection:

Back 8

1. toxins

2. local inflammation

3. deep tissue invasion

Front 9

enterotoxins =

Back 9

secreted toxins that target enteric cells

Front 10

exotoxin =

Back 10

ANY secreted toxin

Front 11

endotoxin =

Back 11

Lipid A

Front 12

questions to ask when a patient comes to you with an infection:

(6)

Back 12

1. what kind of organism is it?

2. what are the routes of transmission?

3. key virulence factors?

4. host responses?

5. how's it diagnosed?

6. what are features of it that would impact treatment?

Front 13

under what kind of organism, think:

(2)

Back 13

1. what specific type is it?

2. normal flora vs opportunistic vs. pure pathogenic

Front 14

ectopic =

Back 14

in an abnormal location

Front 15

aerotolerant anaerobes:

(2)

Back 15

1. CANNOT use O2

2. but are *unaffected* by its presence

Front 16

facultative anaerobes grow better in:

Back 16

O2

Front 17

microaerophiles can only tolerate O2:

Back 17

a little bit

Front 18

anaerobic bact. are located in:

(3)

Back 18

1. oral cavity

2. intestines

3. genitourinary tract

Front 19

anaerobes can be found within:

Back 19

a fraction of a mm below water's surface

Front 20

microbial synergy =

Back 20

2/3's of **anaerobic** infections are MIXED

- contain both anaerobic AND aerobic bact.

Front 21

BOTH aerobic and anaerobic bact are required to:

Back 21

establish an abscess

Front 22

oral microbiota form:

Back 22

plaques

Front 23

dental plaque-associated biofilms =

Back 23

multi-species, synergistic communities in biofilms

Front 24

supergigival PAB's =

(2)

Back 24

aerobic OR aerotolerant, GP bact.

Front 25

subgingival PAB's =

Back 25

GN anaerobes

Front 26

3 factors that determine growth of PAB's:

Back 26

O2, CO2, and pH

Front 27

order of dental plaque formation:

Back 27

1. primary colonizers/pioneers

2. secondary colonizers/bridges

3. tertiary colonizers

Front 28

primary colonizers/pioneers are usually:

Back 28

facultative anaerobes

Front 29

pioneers' receptors usually recognize:

Back 29

dental pellicle

Front 30

dental pellicle =

Back 30

protein film of enamel

Front 31

primary colonizers/pioneers determine:

Back 31

which bact. attach afterward

Front 32

secondary colonizers/bridges allow:

Back 32

co-adhesion and co-aggregation of different bact.

Front 33

common secondary colonizer =

Back 33

Fusobacterium nucleatum

- a promiscuous co-aggregator

Front 34

together, primary and secondary colonizers create:

Back 34

a chemically-attractive environment for future colonizers

Front 35

primary and secondary colonizers secrete:

Back 35

signals that attract or repel oral bact.,

thus determining composition of PAB's

Front 36

tertiary colonizers are generally:

(2)

Back 36

1. GP bact

2. obligate anaerobes

Front 37

best example of tertiary colonizer =

Back 37

Porphyromonas gingivalis

Front 38

incorporation of tertiary colonizers into PAB's requires:

Back 38

**prior depletion of O2 by primary and secondary colonizers**

Front 39

tertiary colonizers are not real:

Back 39

pathogens

- but they're still inflammatory

Front 40

some tertiary colonizers cause:

Back 40

periodontal disease

Front 41

periodontal disease =

Back 41

disease of gums/bone around teeth

Front 42

4 common periodontal diseases:

Back 42

1. gingivitis

2. chronic periodontitis

3. aggressive periodontitis

4. necrotizing periodontitis

Front 43

gingivitis =

Back 43

swollen gums that bleed easily when probed

Front 44

chronic periodontitis =

Back 44

chronic inflammation of gum tissue

=> bone deterioration in time

Front 45

aggressive periodontitis =

Back 45

rapid bone loss

Front 46

necrotizing periodontitis =

Back 46

massive necrosis of periodontal structures

Front 47

gut anaerobes *also* form:

Back 47

complex multi-species communities

Front 48

highest amount of anaerobic bact is found in:

Back 48

the LI

Front 49

anaerobic bact. are mostly:

Back 49

Firmicutes and Bacteroides

Front 50

opportunistic pathogens =

Back 50

normal bact. in wrong location

Front 51

bacteroides:

(4)

Back 51

1. GN

2. non-spore-forming

3. anaerobic

4. normal flora

Front 52

bacteroides are mostly found in:

(3 total)

Back 52

the intestines,

followed by the oropharynx and the female genital tract

Front 53

special benefits of bacteroids as normal flora:

(3)

Back 53

1. ferment complex carbs

2. recycle bile acid components

3. use nitrogen

Front 54

80% of anaerobic infections contain:

Back 54

**Bacteroid fragilis**

Front 55

disease from Bacteroids requires:

Back 55

synergism between bacteroids and facultative bact.

Front 56

Bacteroid diseases cause:

Back 56

abscesses in various parts of the body

Front 57

actinomycin species:

(4)

Back 57

1. GP

2. anaerobic

3. non-spore-forming

4. hyphae (branching) structure

Front 58

Actinomysins are normal flora of:

Back 58

the oropharynx

Front 59

Actinomysins are also:

Back 59

**opportunistic pathogens**

Front 60

Actinomyces are the most common cause of infection following:

Back 60

dental procedure

Front 61

Actinomyces can cause:

Back 61

actinomycoses (abscesses)

Front 62

Actinomyces also synergize with:

Back 62

facultative anaerobes

Front 63

Clostridia species:

(2)

Back 63

1. GP

2. spore-forming

Front 64

Clostridial spores are everywhere in:

Back 64

the environment

Front 65

Clostridia belong to the phylum:

Back 65

Firmicutes

Front 66

what do CLostridia do?

Back 66

ferments macromlcls

Front 67

what's one cause of bad breath?

Back 67

Clostridia fermenting AA's

Front 68

C. septicum can spread through:

Back 68

the bloodstream

Front 69

C. difficile causes:

Back 69

antimicrobial-associated diarrhea and colitis

Front 70

another name for alpha-toxin =

Back 70

lecithinase

=> tissue degradation

Front 71

alpha-toxin is released by:

(2)

Back 71

1. C. perfringens

2. C. septicum

Front 72

Beta-toxin is a ___________ toxin

Back 72

pore-forming

Front 73

B-toxin is particularly damaging to:

Back 73

endothelial cells

Front 74

B-toxin is released by:

Back 74

C. perfringens

Front 75

**virulent enzymes and metabolites that act extracellularly have the capacity to:**

Back 75

help OTHER, nearby bact to survive

Front 76

actinomycosis =

Back 76

abscess of the jaw

- a chronic infection

Front 77

actinomycosis is caused by:

Back 77

Actinomyces israelli

Front 78

actinomycosisis diagnosed by:

Back 78

sulfer granules

(yellow clumps of the bact.)

Front 79

treatment for actinomycosis =

Back 79

long-term antibiotics course

-up to a year of oral antibiotics

Front 80

aspiration pneumonia is caused by:

Back 80

inhalation of vomit into lung

Front 81

aspiration penumonia begins as:

Back 81

pneumotitis

Front 82

pneumotitis =

Back 82

alveolar inflammation

Front 83

if pneumotitis is untreated for 2 weeks, it becomes:

Back 83

lung abscesses

Front 84

lung abscess ~~

Back 84

fetid breath

Front 85

in severe cases, lung abscess cause:

Back 85

necrotizing pneumonia

Front 86

brain abscesses are caused by:

(2)

Back 86

1. oropharynx bact getting into blood

2. content of lung abscesses getting into bloodstream

- and settling in the small vessels of the brain

Front 87

with brain abscesses, you need to treat:

Back 87

the primary infection, so that it doesn't occur again

Front 88

intra-abdominal infections by anaerobes take the form of:

Back 88

peritonitis

Front 89

peritonitis is the result of:

Back 89

a compromised intestinal barrier

Front 90

chronic wounds: risk factor =

Back 90

vascular disease

Front 91

chronic wounds tend to show up in:

Back 91

the extremities

(due to small vasculature)

- think diabetics' foot infeciton

Front 92

chronic wounds are *also*:

Back 92

mixed infections

Front 93

another name for gas gangrene =

Back 93

Clostridial myonecrosis

Front 94

two types of gas gangrene:

Back 94

1. traumatic

2. spontaneous

Front 95

traumatic gas gangrene is caused by:

Back 95

C. perfringens

Front 96

traumatic gas gangrene results when:

Back 96

there's enough tissue damage for anaerobic growth

Front 97

traumatic gas gangrene is full of:

Back 97

Clostridia contaminating the wound

Front 98

results of traumatic gas gangrene =

(3)

Back 98

1. tissue destruction

2. septic shock

3. gas production

Front 99

treatment of traumatic gas gangrene =

(2)

Back 99

1. remove the tissue

2. antibiotics

Front 100

spontaneous gas gangrene is caused by:

Back 100

C. septicum

Front 101

spontaneous gas gangrene is a result of:

Back 101

breaks in the GI barrier that allow C. septicum to enter the bloodstream

Front 102

after entering the bloodstream, C. septicum invades:

Back 102

muscle tissue at multiple sites

Front 103

results of spontaneous gas gangrene:

(3)

Back 103

1. tissue destruciton

2. septic shock

3. gas production

Front 104

treatment of spontaneous gas gangrene =

(2)

Back 104

1. **aggressive** removal of infected tissue

2. antibiotics

Front 105

early identification of spontaneous gas gangrene is essential: it's mortality rate past a certain point is:

Back 105

100%

Front 106

diagnosing anaerobic infections requires:

Back 106

collecting the specimen properly

- CANNOT collect abscess/tissue/blood aspiration that have touched the mucus membrane

Front 107

treatment of anaerobic infections =

Back 107

1. drainage and debridement

2. antibiotics

Front 108

debridement =

Back 108

removal

Front 109

drainage and debridement of anaerobic infection =

Back 109

removal of necrotic tissue and pus, via wound vac, to allow antibiotics to get in

Front 110

antibiotic therapy against anaerobic infections MUST address:

Back 110

both aerobes AND anaerobes

Front 111

aminoglycosides are ineffective against:

Back 111

anaerobes

Front 112

what animal is a great reservoir for E. coli?

Back 112

cattle

Front 113

4 kinds of GI diseases:

Back 113

1. diarrhea

2. typhoid fever

3. peptic ulcer

4. food poisoning

Front 114

diarrhea comes in 2 forms:

Back 114

1. inflammatory diarrhea

2. secretory diarrhea

Front 115

inflammatory diarrhea is caused by 2 modes:

Back 115

1. bact. invade and replicate within host cells

2. bact. colonize LI and produce cytokines that provoke inflammation

Front 116

**sure-fire diagnosis for inflammatory diarrhea** =

Back 116

blood and pus in the stool

- this won't always be the case with inflammatory diarrhea

Front 117

secretory diarrhea occurs when bact:

Back 117

colonize the intestines and secrete enterotoxins

Front 118

features of secretory diarrhea:

(3)

Back 118

1. *profuse*

2. rice-water

3. non-inflammatory

Front 119

treatment for diarrhea =

Back 119

avoid dehydration, get rehydrated with water/electrolytes

Front 120

typhoid fever symptoms:

(3)

Back 120

1. slow-progressing fever

2. gastroenteritis

3. profuse sweating

Front 121

typhoid fever is caused by:

Back 121

Salmonella enterica serovar Typhi

Front 122

typhoid fever is a systemic infection - it starts as a GI infections, then:

Back 122

spreads to other organs

Front 123

features of typhoid fever:

(4)

Back 123

1. ONLY humans

2. p2p

3. some people can be chronic carriers

4. *highly* virulent

Front 124

peptic ulcers are caused by:

Back 124

H pylori creating a pH-tolerable local environment

Front 125

food poisoning is caused by:

Back 125

ingestion of *pre-formed* emetic toxins

Front 126

features of food poisoning:

(2)

Back 126

1. NO p2p

2. **antibiotics are useless**

Front 127

3 common causes of food poisoning:

Back 127

1. Staph aureus

2. bacillus cereus

3. botullinum

Front 128

***3 classes of enteric pathogens***

Back 128

1. enteroinvasive

2. enterotoxigenic

3. enteropathogenic

Front 129

enteroinvasice pathogens:

(2)

Back 129

1. **invasion**

2. ALL are facultative intracellular pathogens

Front 130

in general, all enteroinvasive bact. cause:

(2)

Back 130

1. *inflammatory* diarrhea

2. severe pain/cramping

Front 131

invasion =

Back 131

survive and replicate inside a phagocyte

Front 132

enteroinvasive pathogens have 2 methods of entry into a host cell:

Back 132

1. zipper mechanism

2. trigger mechanism

Front 133

zipper entry =

Back 133

receptor-mediated endocytosis

Front 134

trigger entry =

Back 134

attachment and T3SS => uptake

Front 135

escape from lysis is achieved by:

(2)

Back 135

modification of vacuole

or

escape into the cytoplasm

Front 136

best examples of enteroinvasive pathogens =

(4)

Back 136

1. Salmonella

2. Shigella

3. Campylobacter jejuni

4. Listeria monocytogenes

Front 137

Salmonella:

(4)

Back 137

1. GN

2. multiple flagella

3. facultative anaerobes

4. lactose negative

Front 138

Salmonella colonize:

Back 138

the GI tract, particularly the lower SI

Front 139

2 species of Salmonella:

Back 139

1. S. enterica - many species

2. S. bongari - nonpathogenic

Front 140

10^5 is considered a:

Back 140

LOW infectious dose

Front 141

Salmonella survives the gastric passage due to:

Back 141

high acid tolerance

Front 142

Salmonella invades:

(2)

Back 142

M cells and epithelial cells

Front 143

which invasion mechanism do Salmonella use?

Back 143

T3SS => trigger

Front 144

Salmonella prevent:

Back 144

fusion of the vacuole with the lysosome

Front 145

Salmonella are HIGHLY resistant to:

Back 145

killing by macrophages

Front 146

Salmonella has a ________ that reduces recognition by the immune system

Back 146

capsule

Front 147

Salmonella diseminates via __________________________ to __________________________

Back 147

the reticulo-endothelial system;

the liver and spleen

Front 148

Salmonella can establish a chronic carrier state by:

Back 148

colonizing the biliary/gall duct and continually sliding into SI => out in stool

Front 149

treatment for Salmonella =

(2)

Back 149

1. long-term antibiotics

2. 2 vaccines for S. Typhi, which work only temporarily

Front 150

features of non-typhoid Salmonella disease:

(4)

Back 150

1. zoonotic

2. large ID

3. **self-limiting*

4. septicemia is RARE

Front 151

symptoms of non-typhoid Salmonella disease:

(3)

Back 151

1. intestinal inflammation

2. d/v

3. fever

Front 152

pathogenesis of non-typhoid Salmonella disease differs from that of typhoid Salmonella in 2 ways:

Back 152

1. NO capsule

2. bact do NOT dessiminate

Front 153

one should not treat non-typhoid Salmonella disease with:

Back 153

antibiotics

- will kill normal flora

Front 154

Shigella species:

(4)

Back 154

1. GN

2. aflagellate

3. lactose negative

4. human ONLY

Front 155

most virulent kind of Shigella =

Back 155

S. dysenteriae

Front 156

Shigellosis (disease):

(3)

Back 156

1. very low ID

2. p2p

3. ~ crowded areas

Front 157

Shigellosis disease is also called:

Back 157

bacilliary dysentery

Front 158

symptoms of Shigellosis appear:

Back 158

within a week

Front 159

symptoms of Shigellosis range from:

Back 159

mild diarrhea to dysentery

Front 160

dysentery symptoms:

(5)

Back 160

1. acute pain/cramps

2. acute fever

3. blood/pus in stool

4. n/v

5. watery diarrhea

Front 161

Shigella invades:

Back 161

M cells

- if it can't, it's avirulent

Front 162

Shigella replicates within:

Back 162

macrophage cytoplasms

Front 163

Shigella is motile via:

Back 163

actin

=> spreads to adjacent epithelial cells

Front 164

***Shigella produces:***

Back 164

Shigella toxins

Front 165

**Shigella toxin:**

(2)

Back 165

1. an enterotoxin

2. blocks absorption of glucose, salts, and AA's from the lumen

Front 166

Shigella toxin is ____________ to some cells:

Back 166

cytotoxic

Front 167

Campylobacter jejuni:

(4)

Back 167

1. GN

2. flagellar motility

3. microaerophilic

4. low ID

Front 168

Campylobacter jejuni is the most:

Back 168

common bact. cause of diarrehal disease in the US

Front 169

C. jejuni causes:

Back 169

inflammatory diarrhea

Front 170

symptoms from C. jejuni last:

Back 170

for one week

Front 171

C. jejuni disease is:

Back 171

self-limiting

- rarely treated with antibiotics

Front 172

virulence factors of C. jejuni:

(3)

Back 172

1. flagella

2. invasion

3. cytolethal distending toxin

Front 173

cytolethal distending toxin:

(2)

Back 173

1. a genotoxin against host cell DNA

2. => cell death

Front 174

Listeria monocytogenes:

(4)

Back 174

1. GP

2. *grows at 4 degrees C*

3. actin motility

4. bunch of animals and humans = reservoir

Front 175

L. monocytogenes contaminates:

Back 175

unpasteurized cheese and processed meats

- but rare as a whole

Front 176

diarrhea as a result of infection with L. monocytogenes is:

Back 176

*uncommon*

Front 177

**highest risk for infection with L. monocytogenes** =

(3)

Back 177

1. pregnant women

2. neonates

3. fetuses

Front 178

enterotoxigenic pathogens express **at least one:**

Back 178

eneterotoxin

Front 179

with enterotoxigenic pathogens, their enterotoxins are:

Back 179

*directly responsible* for disease symptoms

Front 180

enterotoxigenic pathogens do NOT use:

Back 180

invasion

Front 181

2 best examples of enterotoxigenic pathogens:

Back 181

1. Vibrio cholerae

2. Clostridium difficile

Front 182

Vibrio cholerae features:

(2)

Back 182

1. GN

2. flagella => dating motility

Front 183

reservoir of Vibrio cholerae =

Back 183

dirty water

Front 184

Vibrio cholerae infects:

Back 184

humans ONLY

Front 185

upon transmission, Vibrio cholerae:

Back 185

incubate for 1-3 days

Front 186

Vibrio cholerae: after 1-3 days of incubation,

Back 186

*abrupt* onset of (profuse) rice-water diarrhea

Front 187

rice-water diarrhea from Vibrio cholerae infection is caused by:

Back 187

cholera toxin

Front 188

Vibrio cholerae diarrhea =>

Back 188

loss of fluids and electrolytes => cardiac arrythmias, renal failure

Front 189

Vibrio cholerae results in death because of:

Back 189

hipovolemic/hypertensive shock

- within 3 days

Front 190

treatment for Vibrio cholerae:

(2)

Back 190

1. rehydration

2. **antibiotics**

Front 191

mortality from Vibrio cholerae without treatment =

Back 191

50-60%

Front 192

mortality from Vibrio cholerae with treatment =

Back 192

<1%

Front 193

virulence factors of Vibrio cholerae:

(4)

Back 193

1. darting motility

2. proteases

3. TCP

4. cholera toxin

Front 194

TCP =

Back 194

toxin co-regulated pili

Front 195

TCP features:

(3)

Back 195

1. link Vibrio cholerae together

2. necessary for colonization

3. no pili = avirulent

Front 196

cholera toxin:

(2)

Back 196

1. an AB type

2. one A for every 5 B's

Front 197

cholera toxin is released by Vibrio cholerae once:

Back 197

it binds to the intestine

Front 198

how does cholera toxin work?

Back 198

the A subunit binds to Gs and causes **irreversible** activation of adenylate cyclase

Front 199

adenylate cyclase activation =>

Back 199

inc. cAMP => pumping out of water and electrolytes *from the blood into the lumen*

Front 200

Clostridium difficile features:

(4)

Back 200

1. GP

2. obligate anaerobe

3. *spore-forming**

4. can be part of normal flora

Front 201

Clostridium difficile causes:

(3)

Back 201

1. secretory diarrhea

2. pseudomembranous colitis

3. toxic megacolon

Front 202

major risk factor for being infected with Clostridium difficile =

Back 202

antibiotic therapy

- spores activate in when normal flora are removed

Front 203

2 virulence factors of Clostridium difficile:

Back 203

1. Toxin A

2. Toxin B

Front 204

Toxins A and B are both:

Back 204

AB toxins

Front 205

what do Toxins A and B do?

Back 205

disrupt host actin by inactivating Rho

Front 206

Toxins A and B cause necrosis => permeability =>

(3)

Back 206

1. diarrhea

2. pronounced inflammation

3. neutrophil influx

Front 207

enteropathogenic pathogens perturb:

Back 207

the epithelial cell structure => inflammatory response

Front 208

enteropathogenic pathogen use NEITHER:

Back 208

***invasion NOR toxins***

Front 209

symptoms from infection by enteropathogenic pathogens :

Back 209

vary greatly

Front 210

2 best examples of enteropathogenic pathogens:

Back 210

1. Helicobacter pylori

2. E. coli

Front 211

H. pylori: flagellar motility is essential for:

Back 211

colonizing the stomach

- gets it across the mucus

Front 212

H. pylori produce:

Back 212

urease

Front 213

what does urease do?

Back 213

converts urea to ammonia and CO2

=> **decreases acidity**

Front 214

H. pylori replicate in their pH-stable environment; pH can get as high as:

Back 214

7.6

Front 215

H. pylori injects:

Back 215

mucinase and effectors

Front 216

what do mucinase and effectors do?

Back 216

damage epithelail cells and induce inflammation

Front 217

treatment for H. pylori (provided that ulcer is there):

(3)

Back 217

1. combos of antibiotics

2. PPI's

3. pepto bismol

Front 218

E. coli features:

(3)

Back 218

1. GN

2. lactose positive

3. most are normal flora of the colon

Front 219

E. coli have a propensity for:

Back 219

horizontal gene transfer

Front 220

pathogenic E. coli:

(2)

Back 220

1. cause a wide range of diseases

2. often produce toxins

Front 221

4 modes of colonization/infection by E. coli:

Back 221

1. enterotoxigenic

2. enteropathogenic

3. enterohemmorhagic

4. enteroinvasive

Front 222

enterotoxigenic E. coli (ETEC) secrete:

Back 222

ST or LT toxins

Front 223

what are enterotoxigenic E. coli difficult to distinguish from, and why?

Back 223

cholera,

because LT toxins are identical to cholera toxins

*but ETEC lack darting motility*

Front 224

enterotoxigenic E. coli come from:

Back 224

dirty water

- treatment is the same as for cholera

Front 225

enteropathogenic E. coli (EPEC) mode of infection:

Back 225

*adherence,* NOT invasion

(they adhere and damage epithelial cells, causing inflammation)

Front 226

EPEC often contaminate:

Back 226

drinking water,

causing diarrhea

Front 227

EPEC produce:

Back 227

attaching/effacing lesions (pedestals)

=> damage

=> inflammation

Front 228

pedestals are mediated by:

Back 228

T3SS, tirs, and intimins

Front 229

EHEC =

Back 229

EPEC + toxin

Front 230

toxin of EHEC =

Back 230

Shiga or Shiga-like toxin

Front 231

EHEC are highly:

Back 231

virulent

Front 232

primary reservoir of EHEC =

Back 232

cattle GI

Front 233

infection by EHEC =>

(2)

Back 233

1. bloody diarrhea

2. hemmorhagic colitis

Front 234

EIEC are similar to:

Back 234

Shigella

Front 235

how do EIEC work?

Back 235

*invades* colonic epithelial cells and multiplies there

Front 236

EIEC causes:

Back 236

inflammatory diarrhea

Front 237

EIEC does NOT:

Back 237

produce toxins

Front 238

reservoir for EIEC =

Back 238

humans ONLY

Front 239

hemolytic uremic syndrome is caused by:

(2)

Back 239

1. Shigella toxin

2. EHEC toxin

Front 240

HUS usually occurs in:

Back 240

young children

Front 241

HUS occurs as a result of:

Back 241

vascular endothelium damage due to septicemia

Front 242

HUS results in:

Back 242

kidney failure

Front 243

Shigella toxin has no role in:

Back 243

gastritis

Front 244

ingestion of GI virus =>

Back 244

enteric infection

Front 245

freatures of GI viruses:

(3)

Back 245

1. ***lack envelopes***

2. possess sturdy capsids

3. very common infectious agents

Front 246

**envelopes CANNOT:**

Back 246

withstand the GI tract

Front 247

GI viruses are transmitted by:

Back 247

fecal-oral transmission

Front 248

major enteric viruses:

(7)

Back 248

1. rotavirus

2. norovirus

3. astrovirus

4. adenovirus

5. enterovirus

6. Hep A

7. Hep E

Front 249

enteric viruses cause:

Back 249

viral gastroenteritis

Front 250

2 viral gastroenteritis symptoms:

Back 250

1. vomiting

2. watery diarrhea

Front 251

viral gastroenteritis is localized to:

Back 251

the GI

Front 252

one exception to viral gastroenteritis being localized to the GI:

Back 252

enterovirus infection spread to other sites after replication in the GI

Front 253

viral gastroenteritis is NOT:

Back 253

the flu

Front 254

reservoir of enteric viruses =

Back 254

human sewage/waterworks

Front 255

maternal AB's cannot protect neonates from:

Back 255

a localized GI infection by enteric viruses

Front 256

**rotavirus features:**

(4)

Back 256

1. ds

2. ***segmented RNA***

3. 3 capsids

4. reovirus family

Front 257

rotavirus pathogenesis: 2-day incubation =>

Back 257

low-grade fever, emesis

=> 4-8 days of watery diarrhea

Front 258

rotavirus ~ large amounts:

Back 258

of it in stool

=> transmission

Front 259

rotavirus grows in:

Back 259

the villous epithelium

Front 260

one rotavirus enterotoxin =

Back 260

NSP4

Front 261

**rotavirus infection is a huge problem for:**

Back 261

children

=> serious illness/death due to severe dehydration

Front 262

the most severe symptoms of rotavirus infection occur in children aged:

Back 262

6 months to 2 years

Front 263

rotavirus infections tend to spread through:

(3)

Back 263

1. daycares

2. nursing homes

3. hospitals

Front 264

diagnosis of rotavirus infeciton =

Back 264

stool immunoassay or PCR

Front 265

treatment for rotavirus infection =

Back 265

hydration

glove and gown

Front 266

2 vaccines for rotavirus infection:

Back 266

part of routine immunization

work great

Front 267

norovirus features:

(3)

Back 267

1. calicivirus family

2. ss

3. (+) RNA

Front 268

norovirus infection is the top cause of:

Back 268

adult viral gastroenteritis

Front 269

norovirus infection symptoms =

(5)

Back 269

1. n/v

2. cramps

3. diarrhea

4. LG fever

5. myalgia

Front 270

main symptoms of norovirus infection resolve in:

Back 270

2-3 days

Front 271

norovirus infection causes a change in:

Back 271

the villi of the jejunum

Front 272

there are many strain of norovirus, and outbreaks tend to occur in:

Back 272

close quarters

Front 273

treatment for norovirus infection =

Back 273

rehydration

Front 274

diagnosis of norovirus infection =

(2)

Back 274

immunoassay, PCR

Front 275

enterovirus features:

(4)

Back 275

1. picornaviruses

2. icosahedral

3. ss

4. (+) RNA

Front 276

5 different kinds of enterovirus:

Back 276

1. **poliovirus**

2. coxsackie

3. echo

4. entero's

5. parecho

Front 277

**poliovirus infections:

(3)

Back 277

1. most are sub-clinical

2. those that aren't, resolve quickly

3. a small amount cause mild meningitis

Front 278

of the small amount of polio infections that don't resolve quickly, a portion will progress to:

Back 278

*poliomyelitis*

Front 279

poliomyelitis =

Back 279

inflammation of the gray matter of the SC

=> muscle paralysis

Front 280

less than 1% of those with poliomyelitis will progress to:

Back 280

post-polio syndrome, *years* later

Front 281

what's the main symptom of post-polio syndrome?

Back 281

muscle atrophy

=> paralysis

Front 282

vaccine for polio:

Back 282

inactivated polio vaccine (IPV)

Front 283

features of IPV:

(3)

Back 283

1. protects from CNS effects via GREAT IgG response

2. 4 doses in infancy/childhood

3. NO IgA response in the gut or nose

Front 284

wild type polio has been:

Back 284

eradicated in the US

Front 285

features of non-polio enteroviruses:

(4)

Back 285

1. found in various *water supplies*

2. infect all ages

3. ~ summer to fall

4. ~ varying symptoms

Front 286

coxsackie A symptom =

Back 286

HFM disease

Front 287

coxsackie B symptom =

Back 287

***myocarditis***

Front 288

enterovirus 71 symptom =

Back 288

HFM disease

Front 289

diagnosis of non-polio enterovirus infection =

Back 289

enterovirus PCR

Front 290

treatment of non-polio enteroviruses =

Back 290

IVIG's, in some cases

Front 291

there are NO ___________ for non-poli enteroviruses

Back 291

***vaccines, antivirals***

Front 292

features of toxigenic C. difficile:

(3)

Back 292

1. GP

2. ***spore-forming***

3. anaerobic

Front 293

C. difficile can be a part of:

Back 293

**normal flora**

Front 294

C. difficile produces:

Back 294

toxins A and B

Front 295

C. difficile spores are:

Back 295

refractory to disinfectants,

esp. alcohols and ALL antibiotics

Front 296

C. difficile is the most common cause of:

Back 296

diarrheal disease in the industrialized world

Front 297

risk for C. difficile infection =

Back 297

***antibiotics that remove normal flora***

Front 298

C. difficile tends to infect:

Back 298

the elderly

Front 299

why does C. difficile tend to infect the elderly?

(2)

Back 299

1. the normal Bifidobacterium declines with age

2. elderly tend to be on antimicrobials, which clear normal flora (and to which C. difficile is resistant)

=> vacuum

Front 300

3 antimicrobials that correspond to increased risk of C. difficile infection:

Back 300

1. fluoroquinolones

2. cephalosporins

3. clindamycin

Front 301

C. difficile spores are either already present in gut when normal flora are cleared, or are acquired => grow in the vacuum =>

Back 301

produce toxins A and B

=> toxins enter via r'-mediated endocytosis

=> inactivate GTPase

Front 302

what does inactivating a host cell's GTPase cause?

(6)

Back 302

1. apoptosis

2. inc. permeability of colonic epithelium

3. inc. chemokines / inflammatory response

4. inc. neutrophil influx

5. loss of tight junctions (with subsequent nuetrophils into the intestines)

6. pseudomembrane formation

Front 303

symptoms of C. difficile infection range from:

Back 303

mild diarrhea

to

profuse diarrhea, colitis

to

PMC, toxic megacolon

Front 304

mutation of new C. difficile strain produces:

Back 304

20x the amount of toxin

~ N. America, UK

Front 305

diagnosis of C. difficile infection:

Back 305

screen for GDH antigen (glutamate dehydrogenase)

- high sensitivity => **excellent screening test**

Front 306

if the GDH test is positive, use:

Back 306

PCR to confirm presence of C. difficile toxin genes

Front 307

C. difficile infection stick tests:

(2)

Back 307

1. if the stick stands, it's not C. difficile

2. if the stick falls, test for C. diff

Front 308

treatment of C. difficile infections:

(4)

Back 308

1. vancomycin

2. metronidazole

3. fidaxomicin

4. fecal transplant

Front 309

vancomycin as a C. difficile treatment:

(2)

Back 309

1. concern for VRE or VRSA

2. **drug of choice** for treating *recurrence*

Front 310

recurrent infection =

Back 310

new infection from a different strain from the environment

Front 311

relapse =

Back 311

more of the same symptoms, from the original pathogen

Front 312

fidaxomicin =

(2)

Back 312

very effective, very expensive drug for C. difficile

Front 313

fecal microbial transplant =

Back 313

repopulating normal gut flora via family member's stool

Front 314

**when around patients with C. difficile infection, most important thing is to:**

(2)

Back 314

wash hands with soap and water (not alcohol),

glove and gown

Front 315

2 clostridial neurotoxins:

Back 315

1. botulinum

2. tetanus

Front 316

botulinum toxin is produced by:

Back 316

C. botulinum

Front 317

botulinum toxin causes:

Back 317

**flaccid** paralysis

Front 318

the vaccine for botulinum toxin has been:

Back 318

discontinued

Front 319

4 sources of botulinum intoxication:

Back 319

1. honey

2. canned foods

3. tar heroin

4. chemical agent

Front 320

infant botulism is normally seen only in:

(2)

Back 320

Cali and Delaware

Front 321

infant botulism:

(3)

Back 321

1. spores are ingested from soil or honey

2. toxin absorbed from gut into bloodstream

3. constipation, poor suck => floppy baby, pulmonary failure

Front 322

food-borne botulinum intoxication ~

Back 322

improperly-canned foods

Front 323

wound botulism is caused by:

Back 323

subcutaneous injection of drugs

- tar heroine
(skin popping)

or poor botox placement

Front 324

botulinum toxin enters the bloodstream from mucosal surface or wound => A portion enters cells =>

Back 324

=> A portin inactivates ACH vesicles' SNARE's

Front 325

botulinum toxin causes:

Back 325

symmetrical, **descending** flaccid paralysis

- starts at CN's

=> paralysis of respiratory muscles or airway obstruction

Front 326

flaccid paralysis ~~

Back 326

weakened / loss of tone

Front 327

treatment for botulinum toxin =

(2)

Back 327

1. antitoxin, **early**
(otherwise toxin enters cells, becomes irreversible)

2. induced vomiting, early

Front 328

tetanus toxin is produced by:

Back 328

C. tetani

Front 329

vaccines and tetanus toxin:

Back 329

**excellent vaccine has pretty much eliminated tetanus poisoning in the industrial world**

- booster should be given every 10 years, even into adulthood

Front 330

pathogenesis of tetanus toxin:

Back 330

trauma => C. tetani introduced

=> anaerobic environment => production of toxin

=> binds to neurons => inactivates the inhibitor synaptobrevin => hyperexcitability

Front 331

tetanus toxin ultimately causes:

Back 331

**spastic** paralysis

Front 332

tetanus poisoning begins as:

Back 332

weakness, progresses to lockjaw

- death can occur due to respiration

Front 333

treatment of tetanus poisoning:

(2)

Back 333

1. antibiotics ARE useful

2. antitoxin, *early*

Front 334

parasites are creatures that draw nutrients:

Back 334

*directly* from its host

Front 335

3 kinds of protozoa:

Back 335

1. Sporozoans

2. Flagellans

3. Amebae

Front 336

2 kinds of helminths:

Back 336

1. nematodes

2. flatworms

Front 337

2 kinds of flatworms:

Back 337

1. tapeworms

2. flukes

Front 338

some arthropods are also:

Back 338

parasites

Front 339

3 features of protozoa:

Back 339

1. multiply rapidly

2. euk, so NO vaccines

3. potential for latency

Front 340

adult pathogenesis from helminths depends on:

Back 340

burden

Front 341

pathology from helminths is a result of:

Back 341

host immune response

Front 342

with helminths, the infectious form is usually:

Back 342

the larvae

Front 343

myiasis =

Back 343

infestation of human or animal by fly larvae that then feed on the host tissue

Front 344

arthropods are either:

Back 344

1. vectors for other pathogens

2. ectoparasites (some of which are also vectors)

Front 345

ectoparasite =

Back 345

parasite that lives on the surface of an organism

Front 346

2 major forms of protozoa:

Back 346

1. trophozoites

2. cysts

Front 347

trophozoites:

(4)

Back 347

1. motile

2. reproductive

3. destructive

4. in host

Front 348

protozoan cysts:

(4)

Back 348

1. dormant

2. durable

3. "hatch" into trophs

4. in environment

Front 349

5 diseases caused by protozoa:

Back 349

1. Giardiasis

2. Amebiasis

3. Cryptosporidiosis

4. Cyclospora

5. Toxoplasmosis

Front 350

giardiasis is caused by:

Back 350

Giardia lamblia

Front 351

giardiasis is the most common:

Back 351

intestinal parasite infection

Front 352

Giardia trophs have 4:

Back 352

pairs of flagella

Front 353

giardiasis results in:

Back 353

*watery* diarrhea

(NOT inflammatory)

Front 354

it's common for giardiasis to be:

Back 354

recurrent

Front 355

**what kind of stool does giardiasis result in?**

Back 355

**fatty** stool

- steatorrhea

Front 356

giardiasis corresponds to:

Back 356

malabsorption, especially of fat-soluble vitamins

Front 357

how does one get infected with giardiasis?

Back 357

by ingesting contaminated water or food

Front 358

Giardia cysts:

(2)

Back 358

1. R to chlorine

2. small ID

Front 359

giardiasis is transferred:

Back 359

p2p, via fomites

Front 360

reservoirs of Giardia aren't just water/food, but _______________ as well

Back 360

zoonotic

Front 361

Giardia are NON-

Back 361

invasive in the intestine

Front 362

cycle of giardiasis: cysts ingested =>

Back 362

trophs => adhere to intestinal epithelial via adhesive discs => asexual reproduction => diarrhea/malabsorption => cysts in stool (trophs don't survive environment)

Front 363

"asexual reproduction" =

Back 363

binary fission

Front 364

giardiasis is usually:

Back 364

self-limiting

Front 365

treatment for giardiasis:

(3)

Back 365

1. NO vaccine

2. only some acquired immunity

3. remember, self-limiting

Front 366

amebiasis is caused by:

Back 366

Entamoeba histolytica

Front 367

***what kind of pathogen is Entamoeba histolytica?***

Back 367

a PURE pathogen

Front 368

cycle of amebiasis: cysts ingested =>

Back 368

trophs multiply in the intestines => damage => excreted as cysts => contamination of food/water

Front 369

damage caused by amebiasis:

(4)

Back 369

1. degradation of mucin layer by proteases => access to epithelium

2. direct killing of host cells by amebapore prot's

3. ingestion of killed host cells (including macrophages)

4. flask-shaped ulcers

Front 370

**diagnostic of amebiasis =

Back 370

Entamoeba trophs with **ingested RBC's**

Front 371

3 outcomes of amebiasis infection:

Back 371

1. non-invasive infection

2. acute intestinal disease

3. extraintestinal disease

Front 372

non-invasive infection of amebiasis:

(3)

Back 372

1. asymp to low symp

2. cysts are still excreted

3. 90% of infections are these

Front 373

acute intestinal amebiasis infection - trophs cause:

(2)

Back 373

1. ulcer in mucosa

2. bloody stool

Front 374

extraintestinal disease stemming from amebiasis - trophs disseminate to:

(3)

Back 374

liver, lungs, and brain

Front 375

in case of dissemination to liver, amebiasis trophs form:

Back 375

amebic liver abscesses

(there is NO other sign of liver infection)

Front 376

with regard to amebiases, AB's:

Back 376

are NOT protective

Front 377

amebiases trophs kill:

(2)

Back 377

neutrophils and non-activated macrophages

Front 378

the immune response against amebiases can be:

Back 378

dampened by the amoeba, to allow colonization of colon

Front 379

treatment of amebiases:

Back 379

***choice of drug depends on WHERE the pathogen is:***

- intestinal vs. disseminated

- invasive vs. non-invasive

Front 380

Cryptosporidiosis is caused by:

(2)

Back 380

1. C. purvum

2. C. hominis

Front 381

C. purvum affects:

(2)

Back 381

cattle and humans

Front 382

C. hominis affects:

Back 382

ONLY humans

Front 383

Cryptosporidium species are found in:

(6)

Back 383

1. recreational water

2. drinking water

3. food

4. hands

5. daycare

6. cattle

Front 384

Cryptosporidiosis is transferred:

Back 384

p2p

Front 385

Cryptosporidiosis causes:

Back 385

watery diarrhea

Front 386

Cryptosporidiosis is usually:

Back 386

self-limiting

Front 387

with cryptosporidiosis, it's not cysts that are ingested and pooped out, but it's:

Back 387

oocysts

Front 388

Cyclospora =

Back 388

protozoa **similar to** Cryptosporidium

Front 389

Cyclospora are acquired from:

(2)

Back 389

1. contaminated fruits/vegetables

2. tropics

Front 390

Cyclospora cause:

Back 390

self-limiting diarrhea

Front 391

Cyclospora infect ONLY:

Back 391

humans

Front 392

**even though they infect only humans, Cyclospora do NOT participate in:

Back 392

p2p

- cysts don't have time to mature before they're passed out

Front 393

toxoplasmosis is usually acquired by:

Back 393

ingestion

Front 394

even though it's usually acquired by ingestion, toxoplasmosis does NOT cause:

Back 394

intestinal disease

Front 395

toxoplasmosis is found:

Back 395

worldwide

Front 396

4 sources of infection of toxoplasmosis:

Back 396

1. cat feces (soil/litter box)

2. meat that had contacted cat feces

3. congenital transfer

4. blood transfusion

Front 397

toxoplasmosis is a MAJOR problem for:

(2)

Back 397

1. pregnant women

2. the immunocompromised

Front 398

why is toxoplasmosis a major problem for pregnant women?

Back 398

they can transfer the infection to the baby => serious problems

Front 399

why is toxoplasmosis a major problem for the immunocompromised?

Back 399

it can cause lesions in the *brain*

Front 400

90% of people with toxoplasmosis are:

Back 400

asymptomatic

- MANY of us are colonized with it

Front 401

3 kinds of helminths:

Back 401

1. Nematodes/roundworms

2. Cestodes/tapeworms

3. Trematodes/flukes

Front 402

intestinal nematodes are acquired in 3 ways:

Back 402

1. ingestion

2. skin penetration

3. unintended host

Front 403

4 kinds of intestinal nematode:

Back 403

1. pinworms

2. ascaris

3. trichuris

4. trichinella

Front 404

official name of pinworm =

Back 404

Enterobus vermicularis

Front 405

pinworm is the most common:

Back 405

helminth infection

Front 406

**the pinworm egg is:**

Back 406

**immediately** infectious

Front 407

cycle of pinworm: egg is ingested =>

Back 407

larvae in intestine => adult => lays MANY eggs in the perianal region => child scratches subconsciously => hand to mouth

Front 408

symptoms of pinworms:

(2)

Back 408

1. itchy butt

2. potential to transfer worse pathogens to mouth

Front 409

ascaris eggs need to:

Back 409

mature in the soil

Front 410

ascaris cycle: matured eggs ingested:

Back 410

larvae in intestine => *cross into pulm system* => coughed up => swallowed => adult in intestine => eggs in stool

Front 411

ascaris adults can grow to:

Back 411

50 cm

Front 412

in order to be affected by ascaris infection, you need:

Back 412

a BIG burden

- ascaris adults don't actually cause any damage, just irritation

Front 413

trichuris is also called:

Back 413

whipworm

Front 414

trichuris cycle: the *mature* egg is ingested =>

Back 414

larvae in intestine => adults in cecum => immature eggs in stool => 3 weeks to mature

Front 415

what's the definite host of trichuris?

Back 415

humans

Front 416

definite host =

Back 416

organism that supports the adult form

Front 417

symptoms of trichuris infection:

Back 417

range from nothing to diarrhea and ab pain to severe

- depends on burden

Front 418

trichinella comes to humans from 2 cycles:

Back 418

1. domestic cycle

2. sylvatic cycle

Front 419

domestic cycle of trichinella =

Back 419

pigs and mice keep transferring it between themselves

=> we eat infected pork

Front 420

sylvatic cycle of trichinella =

Back 420

wild animals transfer it between themselves


=> we get it through eating game

Front 421

hookworms =

Back 421

intestinal nematodes whose larvae penetrate the skin

Front 422

we are the definite host for:

Back 422

hookworms

Front 423

2 groups of hookworms:

Back 423

1. Nectar amer. and Ancylostoma duodenale

2. Strongyloides spp.

Front 424

both Nectar amer. and Ancylostoma duod. are:

Back 424

blood-feeders

- they repeatedly bite and draw blood to feed off its nutrients

Front 425

concern with Nectar/Ancylostoma infection =

Back 425

anemia

Front 426

instead of teeth, Nectar have:

Back 426

cutting plates

Front 427

Nectar/Ancylostoma cycle - larvae:

Back 427

**either penetrate foot OR are ingested**

=> adults in SI => eggs in stool

Front 428

Strongyloides are ubiquitous in:

Back 428

poorly-developed countries

Front 429

Strongyloides cycle - larvae in environment:

Back 429

penetrate the skin => circulation => lungs => swallowed => adults in SI => eggs in the SI => *hatch*

Front 430

***2 possible routes after Strongyloides eggs hatch in the SI:***

Back 430

1. **larvae** excreted in stool

2. ***larvae penetrate LI => circulation => repeat cycle***
(autoinfection)

Front 431

autoinfection of Strongyloides is a problem for:

Back 431

immunocompromised

Front 432

larvae currens =

Back 432

Strongyloides larvae migrating throughout the body

Front 433

some intestinal nematodes don't mean to infect humans, but:

Back 433

accidentally get into people

- we are NOT the definitive host

Front 434

2 kinds of accidental infecting nematodes:

Back 434

1. cutaneous larva migrans

2. visceral larva migrans

Front 435

cutaneous larva migrans penetrate:

Back 435

the feet, and can't go any further

~~ dog hookworm

Front 436

visceral larva migrans normally infect:

Back 436

cats or dogs

Front 437

visceral larva migrate to:

(3)

Back 437

liver,

eye,

brain (rare)

Front 438

**specific example of visceral larva migrans =

Back 438

Baylisascaris procyonis

Front 439

Baylisascaris procyonis is a _______________ worm

Back 439

raccoon

=> children play in suburbia => infected

Front 440

Baylisascaris procyonis travels to:

Back 440

eye/CNS

Front 441

amisakiasis ~~

Back 441

uncooked fish

Front 442

Cestodes =

Back 442

tapeworms

Front 443

4 kinds of tapeworms:

Back 443

1. Taenia saginata

2. Taenia solium

3. Dwarf tapeworm

4. dog tapeworm

Front 444

T. saginata and T. solium' larvae come from:

Back 444

**pork**

Front 445

T. saginata and T. solium cycle: larvae from pork are ingested =>

Back 445

attach to intestines

=> feed and lay eggs => stool

Front 446

T. saginata and T. solium eggs become __________ in pig muscle

Back 446

cystecerci

Front 447

T. saginata and T. solium cystecerci can form in:

Back 447

the brain

Front 448

humans are the definitive host for these tapeworms:

(3)

Back 448

1. T. saginata

2. T. solium

3. Dwarf tapeworms

Front 449

dwarf tapeworm: official name =

Back 449

Hymenolepsis nana

- very common

Front 450

dog tapeworm: official name =

Back 450

Echinococcus granulosus

Front 451

with the dog tapeworm, humans are:

Back 451

only *intermediate* hosts, **as are grazing animals**

Front 452

Echinococcus cycle - sheep grazes around:

Back 452

dog poo => dog eats sheep => eggs into poo

Front 453

infection with dog tapeworm causes:

Back 453

**hydratid cyst** in people

Front 454

hydratid cysts can show up in:

(2)

Back 454

liver, lungs

- can't be punctured without bad consequences

Front 455

Trematodes:

(3)

Back 455

1. aka flukes

2. human = def. host

3. larvae form in **seafood**