Hdm Week 16

Front 1

typhoid is a _______________ infection

Back 1

systemic;

starts at the GI, spread to other areas

Front 2

ALL enteroinvasive bact. are;

Back 2

obligate intracellular pathogens

Front 3

what kind of pathogen uses the zipper OR trigger mechanism of entry?

Back 3

entero*invasive*

Front 4

oocysts ~~

Back 4

Cryptosporidosis

Front 5

parentarel =

Back 5

through other than the mouth

Front 6

hepatitis: ALL 5 types infect:

Back 6

hepatocytes

Front 7

only patients already infected with Hep B can get:

Back 7

Hep D

Front 8

4 symptoms of hepatitis:

Back 8

1. fatigue

2. nausea

3. fever

4. coke-urine

Front 9

specific diagnosis of hepatitis infection requires:

Back 9

serologic testing

Front 10

4 serum liver markers of hepatitis =

Back 10

1. ALT

2. AST

3. bilirubin

4. alkaline phosphatase

Front 11

Hep A and E are shed from the liver in:

Back 11

bile

Front 12

A and E virions are:

(2)

Back 12

1. non-enveloped

2. stable in the environment

Front 13

Hep B, C, and D are NOT stable in:

Back 13

the environment

Front 14

"chronic" hepatitis ~~

Back 14

longer than 6 months

Front 15

Hepatitis A features:

(3)

Back 15

1. no envelope

2. (+) RNA

3. picornavirus family

Front 16

Hep A is REALLY stable against:

(2)

Back 16

1. high Temp

2. low pH

Front 17

***Hep A hijacks:***

Back 17

**envelope from host** while inside the body

Front 18

vaccine against Hep A is a:

Back 18

whole virus vaccine

Front 19

distinguishing features of Hep A infection:

(3)

Back 19

1. transferred by fecal-oral transmission

2. relapsing hepatitis is common

3. fulminant hepatitis is not uncommon

Front 20

**even after 2 weeks of infection with Hep A,**

Back 20

giving a pt Hep A vaccine will prevent the disease

Front 21

features of Hep C:

(2)

Back 21

1. (+) RNA

2. enveloped

Front 22

life cycle of Hep C: RNA into cytoplasm =>

Back 22

replication assembly line => membranous web (vesicles) => replication

=> extracellular release OR spread to adjacent cell

Front 23

Hep C usurps:

Back 23

MANY host factors in order to replicate

Front 24

***in order to spread extracellularly, Hep C takes over:***

Back 24

VLDL

=> circulates within apolipoproteins

Front 25

Hep C's diversity/variability of surface proteins =>

Back 25

chronic infections

Front 26

***___% of peope will be persistently infected with Hep C until treated***

Back 26

70%

Front 27

a person persistently infected with Hep C will be aymptomatic until:

Back 27

he starts noticing symptoms of liver cirrhosis

Front 28

Hep C is able to suppress:

Back 28

the II signaling pathways that sense viral RNA

Front 29

immunity against Hep C is:

Back 29

questionable

Front 30

Hep C infection is diagnosed by:

(2)

Back 30

1. Hep C AB's

2. RNA PCR

Front 31

treatment of Hep C =

Back 31

Direct-Acting Antivirals

- MUST be used in *combos* to avoid R

Front 32

Hep B = DNA virus that:

Back 32

replicates through an RNA intermediate

Front 33

**Hep B uses ____ to replicate**

Back 33

RT

DNA to RNA back to DNA via RT

Front 34

**Inhibition of RT will suppress Hep B, but will not:**

Back 34

produce immunity, since the cccDNA is still found as a plasmid in the nucleus

Front 35

___% of people with Hep B are *asymptomatic*

Back 35

50%

Front 36

**almost all adults infected with Hep B:**

Back 36

clear the infection

Front 37

**infants and immunocompromised have a high risk of:

Back 37

NOT clearing a Hep B infection and thus becoming life-long carriers

Front 38

co-infection of Hep B with Hep D greatly increases:

Back 38

the risk of mortality

Front 39

markers of Hep B infection, **acute OR chronic:**

(2)

Back 39

HBsAg + = infectious

HBeAg + = highly infectious

Front 40

IgM HBc AB + =

Back 40

*acute* Hep B infection

Front 41

HBs AB + =

Back 41

full immunity

Front 42

transmission of Hep B comes via:

(4)

Back 42

1. mother to fetus at birth

2. b/w young children

3. sexual (common and efficient)

4. shared needle (parentenal)

Front 43

treatment of Hep B:

Back 43

RT >> interferon

- goal is *suppression* of the disease, to prevent cirrhosis, liver failure, and HCC

Front 44

first-line oral antiviral for Hep B =

Back 44

tenofavir

Front 45

second-line antiviral for Hep B =

Back 45

adefovir

Front 46

Hep B vaccine is:

Back 46

great

- first cancer vaccine, because it challenges HCC

Front 47

Strongyloides is NOT:

Back 47

a hookworm

Front 48

When you see metronidazol, think:

(3)

Back 48

1. anaerobics

2. parasites

3. bact. causes of vaginosis

Front 49

most common STI in the US =

Back 49

Chlamydia

Front 50

except for syphilis, women tend to:

Back 50

have STI's more

Front 51

exposure to STI does NOT mean:

Back 51

infection of STI

Front 52

"natural history" of the infection =

Back 52

how you got expose, then infected; what stage of the infection you're in, etc.

Front 53

3 reasons why adolescent women tend to have greater rates of STI's:

Back 53

1. fewer Lactobacilli => higher vaginal pH

2. thinner genital tract mucus

3. cervical ectopy

Front 54

cervical ectopy =

Back 54

squamo-columnar epithelium of the cervix (aka endocervix) extends down into the vagina

=> easier for pathogens to attach

- adults have just squamous epithelium there

Front 55

ectopy = part of body is in:

Back 55

abnormal position

Front 56

first-line defense against STI pathogens =

(2)

Back 56

1. genital epithelium

2. mucous

Front 57

second line of defense against STI pathogens =

Back 57

II

- which includes TLR's and antimicrobial peptides

Front 58

third line of defense against STI pathogens =

Back 58

AI

Front 59

AI defense against STI pathogens includes:

(3)

Back 59

1. IgA in cervix and urethra

2. IgG in vaginal/semen secretions

3. T cells (most abundant in the lower genital tract)

Front 60

**risk factors for STI's**

(2)

Back 60

1. multiple partners

2. ...at the SAME TIME

Front 61

vaccines against STI's are:

Back 61

RARE

- only 2

Front 62

the only 2 vaccines against STI's =

Back 62

1. HPV vaccine

2. Hep B vaccine

Front 63

3 major bacterial ST pathogens =

Back 63

1. Chlamydia

2. N. gonorrhea

3. Treponema pallidum (syphilis)

Front 64

major protozoan that causes STI's =

Back 64

Trichomonas vaginallis

(trichomoniasis)

Front 65

**many STI's cause NO:

Back 65

(or mild) signs/symptoms

Front 66

genital herpes are often:

Back 66

recurrent

Front 67

some ST pathogens gain access to the body via the mucosal surfaces, but:

Back 67

DON'T affect the mucosa

- others DO cause mucosal disease

Front 68

***4 common features of ST pathogens:***

Back 68

1. **NOT found free in the environment**

2. **humans are the ONLY reservoir**

3. commonly asymp, b/c microbes are NOT eliminated by the IS

4. no vaccines (except HPV and Hep B)

Front 69

women are often:

Back 69

asymptomatic with STI's

Front 70

2 adverse effects of STI on a woman's reproductive health:

Back 70

1. ascending infection (damage due to host response)

2. bad pregnancy outcomes

Front 71

3 results of infections that STI's cause women:

Back 71

1. PID

2. infertility

3. ectopic pregnancy

Front 72

bad pregnancy outcomes due to STI include:

(3)

Back 72

1. preterm birth

2. low birth weight

3. infections of infant during vaginal birth

Front 73

asymptomatic does NOT mean:

Back 73

inconsequential

Front 74

synergy of STI's and HIV: STI's increase:

Back 74

the risk of acquisition/transmission of HIV

Front 75

how do STI's increase the risk of acquisition/transmission of HIV?

(2)

Back 75

1. breaking mechanical barriers to HIV

2. increasing inflammation => brings HIV-susceptible cells to sight of HIV

Front 76

active STI ~~ more likely to:

Back 76

have/get HIV

Front 77

microscopy ~~

(2)

Back 77

1. low sensitivity

2. high specificity

Front 78

culture ~~ high:

Back 78

specificity

Front 79

**we CANNOT culture:**

Back 79

T. pallidum bact.

Front 80

virus cultures take more:

Back 80

time/effort/money

Front 81

**not all STI's produce:**

Back 81

an AB response

Front 82

serology detects:

Back 82

AB's in the serum

- indicative of past infection

Front 83

serology is sometimes able to distinguish between:

Back 83

acute and chronic infections

Front 84

**syphilis infection produces 2 kinds of AB's:**

Back 84

1. AB's the recognize cardiolipin on *host* membranes

2. AB's that T. pallidum antigens

Front 85

AB's that recognize host cardiolipin are detected by:

Back 85

**non-treponemal tests**

Front 86

2 names of non-treponemal tests:

Back 86

RPR, VDRL

Front 87

non-treponemal tests have high sensitivity but modest specificity; =>=>

Back 87

**screening tests**

- need to be confirmed by trep tests

Front 88

(other conditions, including pregnancy and rheumatoid arthritis, also make:

Back 88

AB's against host cardiolipin

=> have to confirm that it's syphilis)

Front 89

AB's against T. pallidum antigens are detected by:

Back 89

**treponemal tests**

- TPPA, TPHA

Front 90

**treponemal AB's stick around; =>

Back 90

treponemal tests remain positive even after treatment**

(non-trep AB's do NOT => non-trep tests are negative after treatment)

Front 91

2 test approaches for syphilis:

Back 91

1. old-school

2. new approach

Front 92

old-school approach to test for syphilis:

(2)

Back 92

1. use non-trep first

2. if positive, confirm with treponemal test

Front 93

interpreting the old-school test results:

(3)

Back 93

1. if non-trep is negative, pt does NOT have syphilis

2. if positive / trep-negative, pt. does NOT have syphilis

3. if pos / pos, pt. HAS syphilis

Front 94

what is the new-school approach to treating syphilis?

(2)

Back 94

1. use new, fast Tp

2. if pos, use non-trep

Front 95

new-school approach: what does it mean if the Tp is positive, but the non-trep is negative?

(3 possible meanings)

Back 95

1. pt could have had treated or untreated syphilis in the past

2. pt has early, primary syphilis

3. Tp was a false positive.

Front 96

NAAT is a great:

Back 96

non-invasive way of testing for STI's

Front 97

syphilis: men have it more, and it's:

Back 97

rising

Front 98

syphilis has lethal synergy with HIV:

(4)

Back 98

1. syphilis destroys epithelial barrier via genital ulcers

2. recruits HIV-susceptible cells into its lesions

3. patients with early syphilis have high HIV loads

4. risk of neurosyphilis is 3-5x greater in pts with HIV

Front 99

stages of syphilis: incubation period (3 weeks) =>

Back 99

primary syphilis => secondary => latent period => tertiary

Front 100

neurosyphilis =

Back 100

T. pallidum is IN the CNS

Front 101

neurosyphilis can occur at ANY:

Back 101

stage of syphilis

Front 102

later forms of neurosyphilis affect:

Back 102

the actual brain and SC

Front 103

primary syphilis:

(3)

Back 103

1. ~ painless ulcer

2. ...in anogenital region and mucous membranes
(including lips, tongue, cheeks, fingers)

3. ...that heals in a few weeks

Front 104

secondary syphilis ~~

Back 104

spread of spirochetes

Front 105

secondary syphilis strikes a few weeks after:

Back 105

the disappearance of the ulcer

Front 106

secondary syphilis ~ systemic symptoms:

(4)

Back 106

1. malaise

2. fever/head

3. sore throat

4. hepatitis

Front 107

***indicative symptoms of secondary syphilis = ***

(2)

Back 107

maculopapular rash and condyloma lata

Front 108

maculopapular =

Back 108

red and raised

Front 109

condyloma lata =

Back 109

genital warts

Front 110

**secondary syphilis will resolve in:**

Back 110

an immunocompetent person

Front 111

latent syphilis:

(2)

Back 111

1. asymp

2. either early or late

Front 112

early latent syphilis ~~

(<1 year)

Back 112

**infectious**

Front 113

late latent syphilis ~~

(2)

Back 113

1. non-infectious (except mother to child)

2. longer course of treatment

Front 114

diagnosis of latent syphilis is made ONLY:

Back 114

with blood test

Front 115

tertiary syphilis occurs:

Back 115

10-30 years after initial infection

Front 116

without therapy, latent syphilis becomes some form of tertiary syphilis in:

Back 116

1/3 of patients

Front 117

tertiary syphilis can result in:

(3)

Back 117

1. neurosyphilis

2. cv problems

3. gummatous cyphilis

Front 118

gummatous syphilis =

Back 118

nasty ulcers on the skin

Front 119

50% of pregnancies of women infected with syphilis =>

Back 119

miscarriage

Front 120

40-70% of infants born to women with syphilis have:

Back 120

congenital syphilis

Front 121

congenital syphilis ~~

Back 121

characteristic bone/eye/ear/brain damage

- including Hutchinson's incisors (moon-shaped bites)

Front 122

syphilis is caused by:

Back 122

Treponema pallidum

Front 123

Treponema palladum:

(3)

Back 123

1. spirochete

2. **outer membrane lacks LPS**

3. **very few exposed proteins**

Front 124

Treponema pallidum CANNOT grow in:

Back 124

culture

Front 125

pathology of T. palladum:

(2)

Back 125

1. spirochetes attach *anywhere* - can infect many tissues

2. active motility is essential for invasion and dissemination

Front 126

no LPS of spirochetes =>

Back 126

TLR4 is NOT activated

Front 127

b/c very few spirochetes' proteins are not exposed on the surface, spirochetes can:

Back 127

escape immediate detection

Front 128

**spirochetes do NOT release:**

Back 128

toxins

Front 129

early syphilic lesions ~

(2)

Back 129

CD4+, CD8+ cells

=> activated macrophages infiltrate the lesion

Front 130

**AB's against T. palladum can opsonize and neutralize, but CANNOT:

Back 130

prevent future infections of syphilis

Front 131

treatment of syphilis:

(3)

Back 131

1. 1 dose of penicillin cures primary OR secondary infections

2. use Z-pak if can't tolerate penicillin

3. R to Z-pak is rising

Front 132

Trichomona vaginallis infects:

Back 132

both males and females

Front 133

Trichomona is found ONLY in:

Back 133

the human genital tract

- no other reservoir

Front 134

Trichomoniasis is the most common:

Back 134

non-viral STI

Front 135

in women, prevalence of Trichomoniasis increases with:

Back 135

age

Front 136

Trichomona is a:

Back 136

protozoan parasite

Front 137

Trichomoniasis is associated with:

Back 137

HIV and other STI's

Front 138

Trichomona vaginalis lacks mit. and instead has:

Back 138

hydrogenosomes

Front 139

treatment of of Trichomoniasis reduces:

Back 139

**HIV RNA in vaginal fluid**

Front 140

**Trichomoniasis has STRONG synergy with:**

Back 140

HIV

Front 141

clinical presentation of Trichomoniasis in women:

(3)

Back 141

1. common site of infection = vagina, urethra, endocervix

2. frothy vaginal discharge, strawberry cervix

3. odor, itching, dysuria

Front 142

dysuria =

Back 142

painful or difficult urination

Front 143

clinical presentation of Trichomoniasis in men:

(4)

Back 143

1. watery discharge

2. urethritis

3. dysuria

4. though it's commonly asymp

Front 144

73% of women are symptomatic with:

Back 144

Trichomoniasis

- 77% of men are ASYMP

Front 145

immune response to Trichomoniasis:

(2)

Back 145

1. NO protection from re-infection

2. inflammation is associated with influx of neutrophils

Front 146

diagnostics of Trichomoniasis:

(4)

Back 146

1. wet mount microscopy -

2. culture

3. rapid antigen

4. NAAT's

Front 147

wet mount microscopy requires:

(2)

Back 147

1. vaginal swab/male urine sediment

2. must be performed within 15 minutes

Front 148

wet mount for Trichomoniasis is NOT:

Back 148

a great diagnostic

Front 149

treatment of Trichomoniasis =

(2)

Back 149

metronidazole,

tinidazole

Front 150

metronidazole and tinidazole are activated within:

Back 150

hydrogenosomes

=> toxic nitro-radicals that target parasite DNA and prot's

Front 151

R of Trichomona to metronidazole:

Back 151

increasing

Front 152

N. gonorrhea is also called:

Back 152

gonococcus / GC

Front 153

gonorrhea is also called:

(2)

Back 153

the clap,

the drip

Front 154

gonorrhea is MOSTLY _____________ but can have a:

Back 154

asymptomatic;

broad spectrum of clinical presentations

Front 155

***there is no such thing as a ____________________ of gonorrhea***

Back 155

chronic carrier

- if you have it, you're ALWAYS infected, b/c it's a frank pathogen

Front 156

uncomplicated gonorrheal infections take of the form of ____________________ in men

Back 156

urethritis

Front 157

UGI's take the form of ____________________ in women

(2)

Back 157

1. cervical inf's

2. urethral inf's

Front 158

cervicitis ~

Back 158

pus of neutrophils

Front 159

UGI's can also be:

(2)

Back 159

1. oropharyngeal infections (in both men and women)

2. rectal infections (esp. with MSM)

Front 160

pharyngitis ~

Back 160

inflamed throat

Front 161

**watch out when testing throat for UGI, because the throat sometimes contains:**

Back 161

N. minigicoccus as normal flora

- **identical** to N. gonorrhea in gram stain

Front 162

symptoms of UGI (urethritis) in men:

(3)

Back 162

1. abrupt onset

2. dysuria

3. profuse, purulent discharge

Front 163

apart from male urethritis, all other UGI's are:

Back 163

often asymptomatic and hard to differentiate from other STI's

Front 164

gonoccocal conjuctivitis:

(2)

Back 164

1. rare in adults

2. acquired by newborns during passage through infected birth canal

Front 165

2 kinds of complicated gonorrheal infections (CGI's):

Back 165

1. PID

2. GCI

Front 166

PID stands for:

Back 166

pelvic inflammatory disease

Front 167

PID =

(3)

Back 167

endometritis, salpingitis, pelvic peritonitis, and inflammation of other parts of the female repro system

Front 168

PID features:

(2)

Back 168

1. occurs within a few days of menses

2. **occurs in 10-20% of women with cervititis**

Front 169

DGI stands for:

Back 169

disseminated gonococcal infection

Front 170

DGI occurs when:

Back 170

GC enters bloodstream => skin and joints => rashes and arthritis

- rare

Front 171

N. gonorrhea are GN _____________

Back 171

*diplococci*

Front 172

N. gonorrhea are really good at:

Back 172

taking up DNA => variation/R

Front 173

N. gonorrhea are R to:

(2)

Back 173

1. neutrophils' ROS

2. regular bacteriocidal effects of human serum

Front 174

what are the 2 pathogenic Neisseria?

Back 174

1. N. gonorrhea

2. N. meningococcus

Front 175

N. gonorrhea - no capsule =

Back 175

rare that it would disseminate

Front 176

N. gonorrhea do NOT have:

Back 176

a capsule

- N. meningicocci DO

Front 177

***3 virulence factors of N. gonorrhea:***

Back 177

1. adherence

2. antigenic variation

3. antibiotic R

Front 178

adherence of N. gonorrhea:

(2)

Back 178

1. pili for initial, long-range attachment

2. opacity prot's for tighter adhesion

Front 179

also on N. gonorrhea surface:

Back 179

LOS

(~LPS)

Front 180

the following 3 factors of N. gonorrhea can undergo antigenic variation:

Back 180

1. LOS

2. opacity prot's

3. pili

Front 181

N. gonorrhea antigenic variation is:

(2)

Back 181

1. spontaneous

2. frequent

Front 182

N. gonorrhea grows R to a drugs every:

Back 182

20 years

Front 183

only effective drug for N. gonorrhea on the market today =

Back 183

ceftriaxone

Front 184

Chlamydia spp are obligate:

Back 184

**intracellular** bact

Front 185

3 Chlamydia spp pathogenic to humans:

Back 185

1. C. trachomatis

2. C. pneumoniae

3. C. psittaci

Front 186

C. psittaci infects:

Back 186

parrots

- inhaling parrots feces dust will infect humans

Front 187

who gets infected more with Chlamydia?

Back 187

women

Front 188

trend of Chlamydia:

Back 188

**rising steadily**

Front 189

different strains of Chlamydia are differentiated by:

Back 189

different surface proteins

=> ocular, genital, lymphogranuloma (genital warts) types

Front 190

C. trachomatis genital infections are often:

Back 190

completely asymp

Front 191

if C. trachomatis genital infections are symptomatic, they cause (3) in men:

Back 191

1. non-gonococcal urethritis

2. epididymitis

3. proctitis

Front 192

if C. trachomatis genital infections are symptomatic in women, they cause:

(3)

Back 192

1. cervicitis

2. urethritis

3. PID

Front 193

symptoms of Chlamydia trachomatis infections are similar to:

Back 193

gonorrheal infections

Front 194

Chlamydial infections ~~

(2)

Back 194

1. mild local infections

2. severe PID

- it's the inverse in gonorrhea

Front 195

complications of C. trachomatis genital infections for both men and women =

Back 195

arthritis

Front 196

compared to gonorrheal discharge, Chlamydial discharge is:

(2)

Back 196

more clear, watery

Front 197

Chlamydial life cycle is unique:

(5 steps)

Back 197

1. EB's attach to epithelium

2. convert to RB's inside the cell

3. inclusion grows as RB's multiply

4. reconverted to EB's

5. released to infect other cells

Front 198

EB's =

(3)

Back 198

elementary bodies

1. extracellular form of Chlamydia

2. **infectious**

3. metabolically inactive

Front 199

RB's =

(3)

Back 199

reticulo-bodies

1. intracellular

2. non-infectious

3. metabolically active (divide/multiply)

Front 200

for energy, RB's use:

Back 200

ATP from the host cell's mit

Front 201

inclusion =

Back 201

membrane that RB's divide and grow in

- recruits host mit to itself

Front 202

Chlamydia bacteriology:

(4)

Back 202

1. GN

2. has LPS and MOMP on the surface

3. small genome

4. energy parasite

Front 203

MOMP of Chlamydia =

Back 203

major outer memb prot

Front 204

pathogenesis of Chlamydia - infected epithelail cells release:

Back 204

pro-inflammatory cytokines

=> PMN's, NK's, phag, APC's

=> continual chronic inflammation

=> necrosis, scarring

Front 205

diagnosis of BOTH gonorrhea and chlamydia: gold standard =

Back 205

NAAT

- high sensitivity, specificity

Front 206

NAAT's are still positive within:

Back 206

10-14 days after treatment

Front 207

bacterial vaginosis can be caused by:

Back 207

LOTS of different organisms

Front 208

bacterial vaginosis is *common* - it occurs most with:

Back 208

the sexually active, but also with those who are not active

Front 209

bacterial vaginosis =

Back 209

the alteration of normal vaginal flora, which is replaced with anaerobes

Front 210

what is the normal vaginal flora?

Back 210

Lactobacilli spp

Front 211

*BV* flora ~~

Back 211

absence of Lactobacilli and presence of large numbers of GN/GV coccobacilli

- called clue cells

Front 212

Lactobacilli produce the protective:

Back 212

H2O2

Front 213

2 pathogens associated with BV:

Back 213

1. Garderella vaginalis

2. Mobiluncus spp

- NOT ALWAYS present
- could be secondary invaders instead of primary cause

Front 214

signs/symptoms of BV:

(3)

Back 214

1. discharge (normal or white)

2. elevated vaginal pH

3. strong odor

Front 215

diagnosis of BV: any 3 of the following:

(4)

Back 215

1. clue cells

2. pH >4.5

3. homogenous, adherent discharge

4. whiff test

Front 216

whiff test =

Back 216

add drop of KOH, should be a fishy smell

Front 217

adverse consequences of BV: associated with increased risk of:

(3)

Back 217

1. acquisition/transmission of HIV

2. other STI's

3. developing PID (if infected with GC/Chlamydia)

Front 218

in pregnant women, BV ~~

Back 218

2x inc. risk for pregnancy problems

Front 219

treatment of BV =

(3)

Back 219

1. metronidazole

2. clindamycin

3. try to prevent relapse (which is common)

Front 220

**treatment of BV does NOT:**

Back 220

*reverse* adverse pregnancy risk

Front 221

VVC stands for:

Back 221

vulvovaginal candidiasis

Front 222

VVC =

Back 222

vaginal yeast infection

Front 223

VVC occurs when:

Back 223

protective Lactobacilli are eliminated *by antbibiotics*

=> **Candida spp overgrow**

Front 224

Candida species can be part of:

Back 224

normal vaginal flora

Front 225

prevalence of VVC is high in:

(3)

Back 225

1. pregnant

2. uncontrolled diabetes

3. immunocompromised

Front 226

80-90% of VVC is caused by:

Back 226

Candida albicans

Front 227

signs/symptoms of VVC =

(3)

Back 227

1. *itching*

2. chunky discharge
- rare, but classic if present

3. penile erythema in partner

Front 228

filamentous form of C. albicans ~~

Back 228

active form of disease

Front 229

VVC does NOT depend on:

Back 229

organism burden

- but rather to an allergic rxn despite low burden

Front 230

best diagnostic of VVC =

Back 230

**wet mount**

Front 231

treatment of VVC:

(2)

Back 231

1. short course of anti-fungals for uncomplicated cases

2. longer-term anti-fungals for complicated VVC's

Front 232

"complicated VVC's" ~~

Back 232

underlying conditions, recurrence, immunocompromised

Front 233

lower UTI is also called:

Back 233

cystitis

Front 234

cystitis =

Back 234

bladder infection

Front 235

symptoms of cystitis =

(5)

Back 235

1. inc. freq

2. dysuria

3. strongury

4. hematuria

5. changes in smell of urine

Front 236

strongury =

Back 236

slow, painful urination

Front 237

hematuria =

Back 237

RBC's in urine

Front 238

upper UTI is also called:

Back 238

pyelonephritis

Front 239

symptoms of pyelonephritis =

(4)

Back 239

1. fever

2. rigors

3. vomiting

4. loin pain

Front 240

onset of pyelonephritis is:

Back 240

rapid

Front 241

pyelonephritis can be prevented by:

Back 241

treating cystitis

Front 242

defenses against UTI's:

(5)

Back 242

1. defensins (local antimicrobials)

2. Lactobacilli

3. mucin layer to block adherence

4. lysozymes

5. Tamm-Horsfall Prot

Front 243

***what do Tamm-Horsful Prot's do?***

Back 243

bind to UPEC that express *Type 1 pili*

=> inhibits UPEC's

Front 244

susceptibility to UTI's is:

Back 244

50x greater in women than in men

- shorter urethra

- pregnancy, spermacide, and normal intercourse also inc. risk for women

Front 245

recurrent UTI's ~~

Back 245

blockage, *greater density of UPEC r's*

Front 246

**a bladder infection in men is almost ALWAYS:**

Back 246

indicative of a *different* condition

(not UTI)

Front 247

causes of UTI's:

(2)

Back 247

1. UPEC (80%)

2. Staph saprophyticus

Front 248

we're not sure if Staph saprophyticus causes:

Back 248

**upper** UTI's

Front 249

pathogenesis of UTI's: pathogen starts in:

Back 249

intestines => urethra => bladder

=> form biofilm on inner surface of the bladder => pods that bulge out

Front 250

what causes the symptoms of UTI's?

Back 250

TLR4-dependent host inflammatory response

Front 251

**what is the key to UPEC virulence?**

Back 251

adherence

Front 252

UPEC's Type 1 pili are necessary for causing:

Back 252

cystitis

- bring them from intestines all the way up through bladder

Front 253

what kind of pili are necessary for UPEC to cause pyelonephritis?

Back 253

Pap pili

- necessary to attach to kidney epithelial cells

Front 254

UPEC adherence is directly proportional to:

Back 254

severity of infeciton, chance of recurrence

Front 255

biofilms form ________ a catheter

Back 255

inside

Front 256

diagnosis of UTI's: gold standard =

Back 256

*quantitative* urine culture

- measures number of colony-forming bact.

(or urine dipstick)

Front 257

treatment of UTI's:

(2)

Back 257

1. short course for e/o

2. proceed to long course if pt doesn't respond

Front 258

**caveat with treating UTI's:**

Back 258

**watch out for yeast infections following UTI antibiotics**

Front 259

asymp UTI is NOT:

Back 259

treated

Front 260

asymptomatic UTI's are not treated, EXCEPT in the case of:

(2)

Back 260

1. pregnant women

2. those about to undergo surgery

Front 261

cranberry juice may:

Back 261

prevent UTI's,

but hard to say if if cures them

Front 262

defining property of all herpes viruses =

Back 262

**latency**

Front 263

**major differences between HSV and VZV = **

Back 263

HSV ~~ local inf,

VZV ~~ dissemination to the LN's => skin

Front 264

VZV stands for:

Back 264

varicella zoster virus

Front 265

features of Herpes viruses:

(3)

Back 265

1. DNA

2. capsid

3. lipid membrane derived from host

Front 266

Herpes viruses are classified in 3 families; HSV1, HSV2, and VZV are all:

Back 266

alphaherpes viruses

Front 267

**3 features of alphherpes diseases:**

Back 267

1. acute infection

2. latency in distinct locations

3. reactivated inf's

Front 268

acute herpes infections range from:

Back 268

sub-clinical to mildly severe

Front 269

both primary and reactivated inf's of Herpes virus are more severe in:

Back 269

the immunocompromised

Front 270

pathogenesis of herpes virus comes in 2 forms:

Back 270

1. direct cell killing

2. immune-mediated disease

Front 271

immune-mediated disease as a result of herpes infection comes in the the form of:

(2)

Back 271

1. sepsis

2. corneal scarring

Front 272

corneal scarring is a result of:

Back 272

repeated attacks against reactivating herpes virus in the eye

Front 273

herpes infections are NOT:

Back 273

seasonal

Front 274

the vast majority of primary HSV1 and VZV infections occur in:

Back 274

adolescents

Front 275

how is HSV (both types) transmitted?

(3)

Back 275

1. saliva

2. lesions

3. sexual activity

Front 276

how is VZV transmitted?

Back 276

respiratory droplets

Front 277

what region does HSV1 tend to infect?

Back 277

the orofacial area

Front 278

what region does HSV2 tend to infect?

Back 278

the genital area

Front 279

lots of people get infected with HSV and:

Back 279

NEVER experience symptoms

- 75% of people are seropositive for HSV1

Front 280

**life cycle of herpes viruses:**

(3)

Back 280

1. DNA replicated in the nucleus

2. virions mature in the cytpoplasm

3. retrograde to neurons to become latent

Front 281

when a herpes virus becomes latent, its DNA:

Back 281

turns from linear to circular, hiding itself as an episome in the neuron nucleus

Front 282

what is the site of HSV1 latency?

Back 282

the Trigeminal Ganglia

Front 283

what is the site of HSV2 latency?

Back 283

sacral ganglia (S2-S5)

Front 284

what is the site of VZV latency?

(2)

Back 284

1. ALL DRG's

2. TG

Front 285

herpes: primary infection =>

Back 285

retrograde to neurons => latency => reactivation

=> 1. retrograde to CNS (rare) => encephalitis
2. anterograde to eye/mouth/genital (HSV) or skin(VZV)

Front 286

symptoms of HSV1 infection:

(4)

Back 286

1. gingivostomatitis

2. pharyngitis

3. flu-like symptoms

4. herpetic whitlow on skin

Front 287

symptoms of HSV infections resolve in:

Back 287

1-2 weeks

Front 288

symptoms of HSV2 infection:

(1)

Back 288

genital sores

Front 289

reactivated HSV infections =>

(4)

Back 289

1. cold sores

2. genital herpes

3. keratitis (=> corneal scarring)

4. *asymptomatic shedding*

Front 290

keratitis =

Back 290

inflammation of the eye

Front 291

asymptomatic shedding of HSV =

Back 291

a significant source of transmission

Front 292

primary infection of VZV =

Back 292

chicken pox

=> itching, *non-uniform lesions*

Front 293

complications from primary VZV infections:

(2)

Back 293

1. rare in children

2. severe in adults

Front 294

quality of immunity to chicken pox after infection:

Back 294

long-lasting

Front 295

VZV spreads via:

Back 295

coughing droplets,

since it disseminates to the lungs

Front 296

reactivated VZV infection =

Back 296

Shingles

Front 297

shingles =

Back 297

rash in *dermatomes*

Front 298

common complication of shingles =

Back 298

post-herpetic neuralgia

Front 299

neuralgia =

Back 299

pain along a nerve

Front 300

host responses to herpes infection:

(4)

Back 300

1. epigenetic/histone silencing of viral DNA

2. interferons => anti-viral state

3. PKR => inhibition of cell prot synth.

4. pro-inflammatory cytokines

Front 301

adaptive immune response to herpes infection:

(4)

Back 301

1. chemokines => T cells to site of inflammation

2. phag. by immature monocytes

3. killing by NK's via IL12

4. AB production

Front 302

one way that herpes combats the host is by:

Back 302

spreading cell-to-cell to evade AB's

Front 303

diagnosing HSV infectoin:

(2)

Back 303

1. look for CPE in affected tissue

2. ELISA

Front 304

**treatment of HSV/VZV:**

Back 304

1. acyclovir (ACV)

2. related nucleoside analogs

3. forcarnet

Front 305

**how does ACV treat a herpes infection?**

Back 305

P'n by viral thymidine kinase => enters nucleus => incorporated into viral DNA during elongation

=> missing 3' OH = can't form a phosphodiester bond => no elongation

Front 306

how does foscarnet work?

Back 306

it's a pyrophosphate analog that

binds directly to the herpes virus DNA Polym, inactivating it

Front 307

Resistance to ACV is achieved by:

Back 307

**absence of reduction of viral thymidine kinase**

=> DNA elongation proceeds

Front 308

R to ACV occurs almost exclusively in:

Back 308

severely immunocompromised pts

Front 309

if viral thymidine kinase is reduced (rather than absent), it can be overcome by:

Back 309

a higher dose of ACV

Front 310

HIV falls under the ____________ family

Back 310

lentivirus

Front 311

lentiviruses can infect:

Back 311

non-dividing cells

Front 312

HIV comes in 2 forms; of the two, HIV1 is far more:

Back 312

pathogenic

- very diverse/variable too

Front 313

HIV features:

(4)

Back 313

1. ss RNA

2. enveloped

3. nucleocapsid too

4. 2 copies of genome

Front 314

***critical factors of HIV virulence:***

(2)

Back 314

1. RT, integrase, protease

2. gp120, gp41

Front 315

what is gp120 necessary for?

Back 315

***binding of CD4 receptor***

and secondary receptor too

Front 316

what is gp41 necessary for?

Back 316

fusion of the HIV mlcl with the host cell

Front 317

**HIV: 3 kinds of transmission:**

Back 317

1. sexual

2. mother to child

3. parenteral

Front 318

3 kinds of mother-to-child HIV transmissions:

Back 318

1. in utero

2. peripartum (around time of birth)

3. breast feeding

Front 319

3 parenteral transmission of HIV:

Back 319

1. IVDU

2. needle stick

3. blood transfusion

Front 320

**life cycle of HIV:**

(5)

Back 320

1. entry via gp120, gp41

2. reverse transcription

3. integration of HIV DNA into human chromosome

4. protease cleavage to release

5. maturation once it's budded off

Front 321

***HIV binds specifically to:***

Back 321

CD4 receptors

- and then to either CCR5 or CXCR4 receptor

Front 322

HIV replication/transcription ~~

Back 322

TONS of mutations and recombinations

=> huge diversity

Front 323

(HIV tends to enter dividing cells =>

Back 323

host machinery is co-opted immediately, to replicate the virus)

Front 324

***acute HIV infections: virus enters => ***

Back 324

encounters susceptible cells (either dc's or CD4+'s)

=> travels to the gut (no matter route of transmission)

=> depletes CD4+/CCR5+ cells in the gut

=> spreads to other tissues (LN's, blood, CNS)

Front 325

**the majority of CD4+/CCR5+ cells reside in:***

Back 325

the gut

Front 326

the initial AB response to HIV is:

Back 326

weak and ineffective

Front 327

host response to HIV =

(4)

Back 327

innate defensins, II, HIV-specific AB's, T cells

Front 328

latency of HIV: during an acute infection, HIV can persist in some:

Back 328

CD4+ cells

=> if these cells divide, you now have more copies of HIV, in the very cells that are supposed to eliminate

Front 329

why is there no cure for HIV?

(3)

Back 329

1. rapid rates of mutations

2. HIV infects the cells that are responsible for eliminating it

3. latency means we can't kill it off

Front 330

the rates of HIV disease progression vary widely; the average is:

Back 330

10 years

- depends a lot on both viral AND host factors

Front 331

**only ONE chromosome encodes all of the host response factors to HIV:**

Back 331

chrom. 6

Front 332

initially, HIV uses ________; then, it mutates to use ________

Back 332

CCR5;

CXCR4

Front 333

what 2 factors determine the potential to develop AIDS?

Back 333

1. HIV load

2. CD4+ count <200

Front 334

HIV is diagnosed with:

Back 334

ELISA

Front 335

ELISA is VERY:

Back 335

sensitive AND specific for HIV

Front 336

**a positive ELISA test must be confirmed with:**

(3 options)

Back 336

1. Western blot

2. RNA PCR

3. DNA PCR

Front 337

target testing ~~

Back 337

testing a specific hiigh-risk group

Front 338

signs/symptoms of acute HIV infection =

(2)

Back 338

1. flu-like symptoms

2. PE flags

Front 339

7 PE flags for HIV:

Back 339

1. oral thrush

2. Karposi's sarcoma on the heel

3. leukoplakia

4. shingles

5. chelitis

6. seborrheic dermatitis

7. severe HSV inf

Front 340

infections associated with HIV (if CD4+ >200):

(3)

Back 340

1. STI's

2. TB

3. strep pneumoniae

Front 341

TB is HIV patients: the lower the CD4+ count,

Back 341

the LESS typical TB looks

- doesn't form granulomas

- PPD's are often false neg's

- but response to TB therapy is the same

Front 342

with AIDS, secondary infections tend to be:

Back 342

bugs of LOWER pathogenic potential

Front 343

***most common opportunistic infection in AIDS patients = ***

Back 343

PCP

Front 344

PCP stands for:

Back 344

pneumocystis jiroveci pneumonia

(fungus)

Front 345

nearly ALL AIDS pts have:

Back 345

PCP

Front 346

hallmark of PCP =

Back 346

SOB/desat

Front 347

cryptococcus infection following AIDS =>

Back 347

meningitis

Front 348

3 other opportunistic infections following AIDS:

Back 348

1. CMV reactivation

2. Myco TB

3. Myco avium

Front 349

lots of cancers occur as a results of HIV infection; common one =

Back 349

Kaporsi's sarcoma

Front 350

KS is caused by:

Back 350

HHV-8

Front 351

AIDS-related cancers of the CNS:

93)

Back 351

1. toxoplasmosis

2. primary CNS lymphoma

3. PML

Front 352

PML (a leukemia) is caused by:

Back 352

the JC virus

Front 353

goal of HIV therapy =

Back 353

suppress replication

Front 354

if HIV isn't replicating, it can't:

Back 354

mutate

Front 355

HIV mutates at a rate of:

Back 355

2000 x's a day

Front 356

***HAART =

Back 356

combo antiviral therapy

Front 357

combos of drugs for HIV are necessary for:

Back 357

survival

(except for the very few)

Front 358

these days, HAART comes in the form of:

Back 358

3 meds in one pill, once daily

Front 359

HIV therapy DOES:

Back 359

increase CD4+ cells

- initially a rapid increase, then a gradual one

Front 360

5 targets of inhibition when treating HIV:

Back 360

1. attachment (via gp120, gp40)

2. fusion

3. RT

4. integrase

5. protease

Front 361

RT, integrase, and protease are all:

Back 361

excellent targets, b/c humans don't have them

Front 362

inflammatory reconstitution syndrome =

Back 362

systemic, prolonged fever due to reawakened host response to pathogens

Front 363

latency of HIV =

Back 363

we can't cure it

- stop therapy => HIV comes out of hiding and replicates again

Front 364

R IS an issue in:

Back 364

HIV meds

Front 365

HPV features:

(3)

Back 365

1. DNA in circular episome

2. common in mammals

3. cause warts

Front 366

the HPV replication cycle is closely associated with:

Back 366

the differentiation state of the epithelial cell

Front 367

HPV infection: microwound =>

Back 367

access to basal epithelial cells

=> infection of basal cells

=> expression of viral DNA as cells differentiate

=> replication

=> release at the top (stratum corneum)

Front 368

which HPV prot's are responsible for viral DNA replication?

Back 368

E1/E2 heterodimer

Front 369

what does HPV's E2/E2 homodimer do?

Back 369

suppresses HPV's E6 and E7 expression

Front 370

2 different warts that HPV causes:

Back 370

1. condylomas

2. skin warts (on hands and feet)

Front 371

condylomas are _______ warts; they appear in:

(2)

Back 371

**mucosal** warts

==> genitals, oropharynx

Front 372

HPV warts tend to resolve:

Back 372

quickly

Front 373

in order for HPV to infect, there MUST be a:

Back 373

break in the skin

Front 374

it's VERy common to have had:

Back 374

HPV

Front 375

in RARE cases, HPV can cause:

(2)

Back 375

1. cervical cancer

2. oral squamous cell carcinoma

Front 376

cervical cancer ~~

(2)

Back 376

1. discharge and abnormal vaginal bleeding

2. dysplasia (enlargement) or neoplasia

Front 377

cervical cancer is usually a:

Back 377

squamous-cell carcinoma

- sometimes adenocarcinoma (of glands)

Front 378

***first step to cancer from HPV infection =

Back 378

***integration of HPV episome into host genome***

Front 379

**what happens with integration of HPV episome into host genome?**

Back 379

**E2/E2 gets disrupted => E6, E7 NOT suppressed

Front 380

***what happens when E6 and E7 are NOT suppressed?***

(2)

Back 380

1. host cells continue to divide

2. apoptosis does NOT occur

Front 381

only the "high-risk" serotypes fail to suppress E6, E7; that's why:

Back 381

cancer from HPV infection is rare

Front 382

diagnosis of HPV =

(2)

Back 382

1. genital warts

2. cervical changes from pap smear

Front 383

vaccines for HPV =

(2)

Back 383

1. Gardasil

2. Cervarix

Front 384

treatment of HPV infection =

Back 384

removal of warts

Front 385

WBC’s in the stool ~~

Back 385

**inflammatory diarrhea**

Front 386

only Shigella dysentariae releases:

Back 386

Shiga toxin

Front 387

syphilis damages cells ==>

Back 387

cardiolipin

Front 388

lytic infection = normal inf =

Back 388

virus replicates a lot, eventually lysing the cell in release

Front 389

clinical symptoms of lytic infections are the result of:

(2)

Back 389

1. tissue damage due to viral replication

2. immune response to infection

Front 390

lytic infections tend to last:

Back 390

2-14 days

Front 391

**chronic infections ** =

Back 391

continual infection = long lytic infections

- viruses are released from cells, but cells DON'T lyse

Front 392

**chronic infections are a subset of lytic infections; main difference between the two = **

Back 392

time to clear

- lytic ~ <2 weeks

- chronic ~ wks/mths/years

Front 393

2 types of chronic infection:

Back 393

1. focal

2. diffuse

Front 394

focal chronic infection =

(3)

Back 394

1. carrier cells produce virus

2. infect neighboring cells

3. die, but neighboring cells continue the cycle

Front 395

diffuse chronic infection =

(2)

Back 395

1. viruses replicate in infected cells that also replicate

2. cells shed viruses for their lifetime

Front 396

Hep C ~~

Back 396

persistent (chronic) viral infection

- eventually leads to cirrhosis

Front 397

***latency =

Back 397

presence of viral nucleic acids in the absence of infectious virus

Front 398

**difference between chronic and latent infections:**

Back 398

chronic infections produce infectious viruses;

latent infections DON'T

Front 399

3 phases of latency:

Back 399

1. getting in

2. maintenance (staying in)

3. reactivation (getting out)

Front 400

establishment of latency (getting in) ~~

Back 400

virus stops expressing proteins

Front 401

**while BOTH RNA and DNA viruses can become latent, the viral genome in *either case* is maintained as:**

Back 401

DNA

Front 402

provirus =

Back 402

latent DNA *integrated* into host genome

e.g. HIV

Front 403

episomal latency =

Back 403

latent viral DNA is maintained extra-chromosomally

- e.g. herpes

Front 404

latently-infected cells tend to:

(2)

Back 404

1. proliferate less

2. have less metabolic demand

Front 405

latency last for:

Back 405

months to years

- long

Front 406

reactivation of latent virus occurs in response to:

Back 406

1. stimuli for host cell to diff/prolif

2. cell stress that would cause cell death - get out of there

Front 407

diagnosis of latent viral infection has to be via:

Back 407

PCR of the viral genome

- searching for antigen or infectious virus is either misleading or pointless

Front 408

latent infections CAN cause diseases, in the form of:

(2)

Back 408

1. cancer

2. lympho-proliferative disorders (too many WBC's)

Front 409

latent EBV =>

Back 409

cancer

Front 410

latent herpes =>

Back 410

KS

Front 411

latent viruses are transmissible via:

Back 411

transplants

- latently-infected cells get transferred to recipient

Front 412

best example of a latent virus that reactivates after a transplant:

Back 412

HCMV

- delayed onset is worse than onset within a year

Front 413

a cure for latent viruses should focus on those patients in whom:

Back 413

the latency keeps springing up into active infection

- leave the others alone

Front 414

one method of treating HIV latency =

Back 414

forcing it to reactive,

=> hit it with antivirals to prevent integration/replication

=> progressive rounds of treatment to eliminate latent reservoir

Front 415

leading disease due to nosocomial infection =

Back 415

pneumonia

Front 416

placement of catheter outside of the OR =>

Back 416

increased risk of nosocomial infection

Front 417

HAP =

Back 417

hospital-acquired pneumonia

Front 418

VAP =

Back 418

ventilator-associated pneumonia

Front 419

HCAP =

Back 419

health care-associated pneumonia

- contracted in the outpatient/home-care setting

Front 420

ranking of most risk for MDR and m/m:

Back 420

HAP/VAP > HCAP > CAP

Front 421

aspiration = huge risk for:

Back 421

nosocomial penumonia

Front 422

VAP prevention bundle:

(4)

Back 422

1. 30-45 degress

2. consider extubating ASAP

3. prevent peptic ulcer disease/ reflux

4. prevent DVT

Front 423

bloodstream infections: major risk =

Back 423

use of intravascular devices

e.g. central line

Front 424

3 major organisms that exhibit R in hospitals:

Back 424

1. Staph aureus

2. VRE

3. C. diff

Front 425

Staph aureus ~~

(3)

Back 425

BSI's, pneumonia, surgical infections

Front 426

Staph aureus is implicated in:

Back 426

nearly every nosocomial infection

Front 427

risk factors for developing Staph aureus R:

(3)

Back 427

1. ab use

2. prolonged stay

3. proximity to patients with MRSA

Front 428

Staph aureus are actually:

Back 428

normal flora of the nasopharynx

Front 429

both Staph aureus and VRE are transmitted via:

Back 429

hands/surfaces

Front 430

VRE =

Back 430

vancomycin-R enterococci

Front 431

VRE aren't:

Back 431

normal flora

Front 432

C. diff =

Back 432

normal flora of GI tract

Front 433

to which bact. does Toxin A and Toxin B belong to?

Back 433

Clostridium difficile