Micro Exam 3

Front 1

most common cause of ascending UTI

Back 1

E. Coli

Front 2

enterobacteria associated w/ urinary stones

Back 2

proteus mirabelis (produces potent urease to produce ammonia and make urine alkaline)

Front 3

gram + causes of UTI

Back 3

staph saprophyticus, staph epidermis, and enterococcus

Front 4

causes UTI in young sexually active women

Back 4

staph saprophyticus

Front 5

causes UTI in hospitalized pts

Back 5

Staph. epidermis and Enterococcus

Front 6

viral UTI common?

Back 6

no

Front 7

viral UTI causes?

Back 7

human polyomavirus, adenovirus, hantavirus

Front 8

How does humanpolyoma infect?

Back 8

enters via respiratory tract and spreads to tubular epithel cells in kidneys and ureters. establishes latency

Front 9

35% of healthy individs have infx with ____________ but it remains latent

Back 9

polyomavirus

Front 10

fungal causes of UTI

Back 10

candida and histoplasma capsulatum

Front 11

parasitic causes of UTI

Back 11

Trichomonas vaginalis, Schistosoma haematobium

Front 12

which causes urethitis in males/vaginitis in females

Back 12

T. vaginalis

Front 13

which causes allergic response to worm’s egg leading to scarring in area where bladder/ureters meet and ureters get blocked- results in bladder inflammation

Back 13

S. haematobium

Front 14

mechanical factors that predispose to UTI

Back 14

1. shorter female urethra
2. sexual intercourse
3. uncircumcised boys

Front 15

obstructions to complete bladder emptying

Back 15

1.residual urine
2. loss of neurologic control
3. vesicoureteral reflux
4. diabetes mellitus
5. catheterization

Front 16

causes of loss of neurological control:

Back 16

spina bifida, paraplegia, multiple sclerosis

Front 17

who is vesicoureteral reflux common with

Back 17

children w/ anatomic abnormalities of the urinary tract

Front 18

diabetes mellitus may lead to...

Back 18

pyelonephritis

Front 19

where do most urinary tract pathogens originate

Back 19

fecal flora

Front 20

which can colonize/infect the urinary tract

Back 20

aerobic and facultative species such as E. coli

Front 21

what structural feature helps E. coli adhere to epithelium

Back 21

fimbriae

Front 22

what does E. coli produce that causes kidney damage

Back 22

hemolysin

Front 23

is healthy urinary tract resistant to bacterial colonization?

Back 23

yes- eliminates microorganisms rapidly/efficiently

Front 24

how

Back 24

via pH, chemical content, and flushing mechanism

Front 25

3 clinical features of acute lower UTIs (bladder infxs)

Back 25

dysuria, urgency, frequency

Front 26

urine sample shows:

Back 26

cloudiness due to pyuria and bacteriuria, hematuria

Front 27

what may result from an ascending infx?

Back 27

acute bacterial prostatis

Front 28

sx?

Back 28

fever, low back pain, dysuria, and frequency

Front 29

upper UTI spreads to

Back 29

kids

Front 30

what is pyelonephritis

Back 30

kidney infx

Front 31

sn/sx

Back 31

lower UTI sx of dysuria, urgency, frequency but also FEVER

Front 32

common cause of upper UTIs

Back 32

staphylococci

Front 33

what can repeated episodes lead to

Back 33

loss of fx of renal tissue, and HTN

Front 34

how is infx distinguished

Back 34

quantitative culture methods

Front 35

definition of bacteriuria

Back 35

over 10^5 organisms/mL

Front 36

T/F usually are several bacterial species

Back 36

F- only one

Front 37

do a significant proportion of lower UTI pt's have recurrent infxs?

Back 37

yes- either by same organism or by different one

Front 38

does upper or lower cause renal abcesses

Back 38

upper

Front 39

methods of urine collection

Back 39

1. sterile container by pt
2. "bag urine" for babies/infants
3. catheter- collected from tube with syringe and needle

Front 40

Tx of UTI

Back 40

antibiotics- ie augmentin

Front 41

prevention of UTI

Back 41

empty bladder often (esp after intercourse), prophylactic anti-biotic use, good catheter care

Front 42

host factors that influence risk of acquiring an STD

Back 42

genital lesions or ulcers, uncircumcised men, multiple infx

Front 43

What causes syphilis

Back 43

the spirochete Treponema pallidum

Front 44

how does it enter body

Back 44

minute abrasions on skin or mucous m'branes

Front 45

why does transmission require close contact

Back 45

b/c doesn't survive well out side body, sensitive to drying, heating, disinfectants

Front 46

spread?

Back 46

horizontally thru sexual contact or vertically via transplacental infx of fetus

Front 47

5 stages of syphilis pathogenesis?

Back 47

1. initial contact 2. primary syphilis 3. secondary 4. latent 5. tertiary

Front 48

what occurs w/ initial contact

Back 48

2-10 wks: treponemes multiply at infx site, develop a primary painless chancre

Front 49

primary?

Back 49

1-3 months; treponemes proliferate, enlarged inguinal nodes and spontaneous healing

Front 50

secondary?

Back 50

2-6 weeks: treponeme multiplication,flu-like illness, headache, fever, mucocutaneous rash and spontaneous healing, lesions in lymph nodes, liver, joints, muscles, skin and mucous m'branes

Front 51

latent

Back 51

3-30 years: treponemes are dormant in liver or spleen, no sign of illness

Front 52

tertiary

Back 52

re-awakening, multiplication, dissemination, and invasion of trepes; neurosyphilis (general paralysis), and cardiosyphilis (aortic lesions, heart failure; progressive and destructive

Front 53

does T. pallidum respond to vigorous immune response

Back 53

no

Front 54

how does it evade recognition and elimination by the host

Back 54

maintains a cell surface rich in lipid that is antigenically unreactive

Front 55

when is congenital syphilis acquired

Back 55

first 3 mos of pregnancy

Front 56

results in:

Back 56

1. serious infx--> intrauterine death
2. congenital abnormalities
3. silent infx (at 2 y.o)

Front 57

tx

Back 57

penicillin

Front 58

prevention

Back 58

early diagnosis (for 2ndary and tert), early screening and penicillin treatment (congenital)

Front 59

what causes gonorrhea

Back 59

gram pos diplococcus Neisseria gonorrheae

Front 60

resevoir:

Back 60

humans

Front 61

transmission:

Back 61

sexual contact or vertically from mother to baby during childbirth (ophthalmia neonatorum)

Front 62

does it survive outside the body?

Back 62

no- sensitive to drying

Front 63

men or women more?

Back 63

women

Front 64

sx?

Back 64

asymptomatic

Front 65

4 special mechanisms of N. gonorrhea to allow mucosal attachment:

Back 65

1. fimbriae (attachment and antigenic diversity
2. LPS (endotoxin activity)
3. IgA protease (destroys IgA1)
4. capsule (resists phagocytosis)

Front 66

how do they infect?

Back 66

invade non-ciliated epithelial cells that internalize the bacteria, allowing them to multiply in intracellular vacuoles protected from phagos and Abs

Front 67

how does it damage host

Back 67

by inflammatory response elicited by organism

Front 68

sn/sx in males

Back 68

discharge/pain
-complications rare

Front 69

sn/sx in females

Back 69

discharge- no pain, assymptomatic therefore don't seek treatment

Front 70

female complications of gonor:

Back 70

PID, chronic pelvic pain, infertility

Front 71

ophthalmia neonatorum:

Back 71

gon in infants, characterized by sticky discharge

Front 72

other parts infected by gon:

Back 72

throat, rectum (purulent discharge)

Front 73

Tx

Back 73

penicillin, ceftriazone, ciprofloxacin, spectinomycin

Front 74

prevention

Back 74

condoms

Front 75

Cause of chlamydial infxs:

Back 75

Chlamydia trachomatis serotypes D-K

Front 76

2 forms:

Back 76

elementary body (EB):extracellular survival

reticulate body (RB): intracellular multiplication

Front 77

how does it invade/infect?

Back 77

-enter host thru small mucosal abrasions
-bind specific receptors on host and enter by endocytosis
-lysosome fusion is inhibited and EB begins development
-after 9-10 hrs become active RBs
-new EBs produced

Front 78

pathogenesis in men:

Back 78

urethritis, epidymitis, proctitis, conjunctivitis

Front 79

pathogenesis in women:

Back 79

urethritis, cervicitis, salpingitis, conjunctivitis

Front 80

tx

Back 80

doxycycline, tetracycline (beta lactam antibios dont work); tx for babies is erythromycin

Front 81

causes of inguinal lymphadenopathy:

Back 81

genital infxs, LGV, chancroid, donovanosis

Front 82

cause of LGV:

Back 82

C. trachomatis serotypes L1, L2, and L3

Front 83

pathogenesis of LGV:

Back 83

-after 1-4 wks primary lesion develops at site of inoculation
-fever/headache accompany
-lesion heals rapidly and draining lymph nodes are infected causing inguinal buboes

Front 84

complications

Back 84

proctitis, fever, hepatitis, pneumonitis, meningo-encephalitis

Front 85

tx:

Back 85

tetracycline/doxycycline

Front 86

cause of chancroid (soft chancre):

Back 86

H. ducreyi

Front 87

characteristics:

Back 87

painful genital ulcer and local lymphadenitis

Front 88

tx:

Back 88

erythromycin, caftraixone, otrimoxazole

Front 89

cause of donovanosis:

Back 89

Calymmatobacterium granulomatis

Front 90

characteristics:

Back 90

genital nodules that erode to form granulomatous ulcers; bleed readily on contact

Front 91

tx:

Back 91

tetracycline

Front 92

which is most common form of genital ulcers in africa and asia

Back 92

chancroid

Front 93

which is common in caribbean, new guinea, india, and central australia

Back 93

donovanosis

Front 94

What causes mycoplasmas and non-gonococcal urethritis?

Back 94

mycoplasma hominis and ureaplasma urealyticum

Front 95

where do they colonize?

Back 95

genital tracts of healthy sexually active people

Front 96

what are they also associated with

Back 96

PID, postabortal and postpartum fevers

Front 97

tx

Back 97

tetracycline

Front 98

what are other causes of vaginitis and urethritis

Back 98

candida albicans, trichomonas vaginalis, gardnerella vaginalis

Front 99

characteristics of candida

Back 99

-irritant vaginitis
-cheesy discharge
-UTI with it maybe

Front 100

Tx

Back 100

fluconazole or nystatin

Front 101

chars of trichomonas infx

Back 101

-protozoan parasite inhabits vagina/urethra
-transmit during sex
-women: copious foul-smelling discharge, increased pH with actively motile trophozoites
-men: assymptomatic

Front 102

tx

Back 102

metronidazole

Front 103

what causes bacterial vaginosis

Back 103

gardnerella vaginalis plus anaerobic infx of bacteroides that disrupt normal acidity of vagina

Front 104

sx in women:

Back 104

-excessive fish-odored discharge
-pH >4.5
-clue cells (vaginal epithelial cells coated w/ bacteria)

Front 105

tx

Back 105

metronidazole

Front 106

cause of genital herpes

Back 106

HSV2

Front 107

when is primary lesion seen

Back 107

3-7 days after infx

Front 108

sn/sx

Back 108

-vesicles that form shallow ulcers
-local lymph nodes swollen
-fever
-headache
-malaise

Front 109

pathogenicity:

Back 109

healing up to 2 weeks, but virus travels up sensory nerve and establishes latent infx in dorsal root ganglion neurons where it can reactivate and cause a recurrent lesion

Front 110

spread from mom to infant?

Back 110

yes, during delivery and can give rise to disseminated herpes or encephalitis

Front 111

tx

Back 111

acyclovir

Front 112

cause of genital warts

Back 112

HPV- papillomavirus 6,11,12,16,18,and 31

Front 113

where/when do warts appear

Back 113

on penis, vulva, and perianal regions after 1-6 mos incubation

Front 114

cervical lesion description:

Back 114

a flat area of dysplasia visible by colposcopy as a white plaque after local application of 5% acetic acid

Front 115

which are associated with cervical cancer

Back 115

16 and 18

Front 116

tx

Back 116

podophyllin

Front 117

HIV infects which cells

Back 117

TH, monocytes and dendritics

Front 118

pathogenesis

Back 118

-CH4 mc binds GP120 protein
-virus specific CD8+ Tc cells are formed and reduce viremia
-neutralizing antibodies appear
-immune system starts suffering and CD4+ T cells decrease
-delayed type hypersensitivity is absent, NK cell activity and Tc cell activity is dec'd and polyclonal activation of B cell is reduced

Front 119

mechanisms of immunosuppression:

Back 119

1. Th cells are directly killed by virus
2. Th cells undergo apoptosis
3. Th cells are attacked by Tc cells
4. T cell replenishment is impaired by thymus/lymph node damage and stem cell infx
5. defects in antigen presentation (infx of dendritics)
6. antigenic variation in hypervariable region of gp120

Front 120

how does viral invasion of CNS occur

Back 120

independently of AIDS

Front 121

which are the infected cells in CNS

Back 121

microglia or infiltrating macrophages which express CD4

Front 122

this is seen in about 21% of homosexual/bisexual males and is associated with human herpes virus 8 (HHV8)

Back 122

kaposis sarcoma

Front 123

what is a major source of transmitted virus

Back 123

peripheral blood mononuclear cells

Front 124

what are sn of initial infx

Back 124

mild mononucleosis type illness including fever and malaise

Front 125

are antibodies detectable right away

Back 125

no- may take many months; also many mos for t-cells to form

Front 126

what happens to viral replication after initial infx

Back 126

it's reduced and individual remains well

Front 127

sn/sx in later years

Back 127

weight loss, fever, persistent lymphadenopathy, oral candidiasis, diarrhea, ARC-AIDS related complex

Front 128

what occurs with ARC

Back 128

-less than 10% may be well
-may develop AIDS (opportunistic infxs_
-may develop subacute encephalitis and dementia

Front 129

AIDS dementia=

Back 129

opportunistic CNS infxs like HSV, CMV, and toxoplasmosis

Front 130

lab tests for HIV

Back 130

-ELISA
-western blot, radioimmunoassay, or immunofluorescence testing to confirm

Front 131

odds of getting HIV after needle stick

Back 131

<1%

Front 132

what types of HIV vaccinations are being developed

Back 132

various subunit envelope glycoproteins and a whole virus vaccine

Front 133

whats the problem?

Back 133

a vaccine that will induce abs against gp120 may combine w/ the virus w/o neutralizing it.....it then attaches to the Fc receptors on monocytes and the whole complex is ingested and monocyte is now infected

Front 134

tx

Back 134

-AZT
-PIs
-individual tx of opportunistic infxs

Front 135

cause of pubic or crab lice

Back 135

phthirus pubis

Front 136

pathogenesis

Back 136

-clings tight to hairs, takes up to 10 blood feedings/day causing itching
-eggs attached to hairs, lice are visible at base of hair
-infestation is common

Front 137

tx

Back 137

application of malathion

Front 138

cause of genital scabies

Back 138

Sarcoptes scabei

Front 139

characteristics:

Back 139

local lesions on genitalia, can spread as STD; pts may have scabies elswhere on body

Front 140

tx

Back 140

10% benzyl benzoate or 1% benzene hexachloride

Front 141

whats the most common outcome of GI tract infxs

Back 141

diarrhea

Front 142

gastroenteritis:

Back 142

nausea, vomiting, diarrhea, abdominal discomfort

Front 143

diarrhea:

Back 143

abnormal fecal discharge- frequent fluid stool; disease of sm intestine

Front 144

dysentery:

Back 144

inflammatory disorder of GI tract associated w/ blood and pus in feces; accompanied by fever, pain, abdominal cramps; disease of lg intestine

Front 145

enterocolitis:

Back 145

inflammation involving mucosa of both small and large intestine

Front 146

Bacterial causes of diarrhea:

Back 146

E. coli, Salmonella, campylobacter jejuni, helicobacter pylori, vibrio cholerae, shigella dysenteriae, shigella sonei, vibrio parahemolyticus, yersinia enterolytica, c. perfringens, b. cereus, staph aureus, c. botulism

Front 147

What are the 4 types of E. coli:

Back 147

1. Enterotoxigenic (ETEC)
2. Enteroinvasive (EIEC)
3. Enterohemoerrhagic (EHEC)
4. Enteropathogenic (EPEC)

Front 148

which is the most imp bacterial cause of diarrhea in children in developing countries and the most common cause of travelers diarrhea

Back 148

ETEC

Front 149

most important in developed countries but outbreaks an sporadic cases occur worldwide:

Back 149

EHEC

Front 150

important cause of diarrhea in areas of poor hygiene, usually food borne infxs:

Back 150

EIEC

Front 151

spread via water contaminated by human or animal sewage:

Back 151

ETEC

Front 152

causes sporadic cases of infx in babies and young children:

Back 152

EPEC

Front 153

caused by verotoxin-producing serotype 0157 that has direct affect on intestinal epithelium:

Back 153

EHEC

Front 154

produces powerful enterotoxins (LT and ST):

Back 154

ETEC

Front 155

which of these toxins is heat labile

Back 155

LT

Front 156

heat stable

Back 156

ST

Front 157

has a mechanism of adhesion to enterocytes that appears to destroy microvilli

Back 157

EIEC

Front 158

caused by food and unpasteurized milk:

Back 158

EHEC

Front 159

Tx

Back 159

specific antibios not indicated; fluid replacement if necessary

Front 160

prevention:

Back 160

clean water, adequate sewage disposal, food/milk pasteurization

Front 161

what is the most common case of food-associated diarrhea in developed countries

Back 161

salmonellae

Front 162

salmonella and e. coli are both:

Back 162

enterobacteria

Front 163

salmonella transmission:

Back 163

animal resevoir- transmitted via contaminated poultry and dairy

Front 164

frequent waterborne transmission?

Back 164

no

Front 165

where do they invade?

Back 165

epithelial cells of terminal portion of small intestine

Front 166

which species are responsible

Back 166

s. enteritidis, s. cholera suis

Front 167

tx:

Back 167

usually self-limiting (vomiting rare); fluid/electrolyte replacement if necessary

Front 168

which bacteria are S-shaped curved rods

Back 168

campylobacter

Front 169

how acquired?

Back 169

via contaminated milk, poultry, H20

Front 170

tx:

Back 170

erythromycin for severe cases

Front 171

which bacteria is associated with over 90% of duodenal ulcers and 70-80% of gastric ulcers

Back 171

helicobacter pylori

Front 172

what does it produce that helps it survive acid environments

Back 172

urease

Front 173

tx:

Back 173

proton pump inhibitor with 2 antibiotics; eradication heals ulcers

Front 174

acute infx of GI tract caused by comma-shaped gram-negative bacteria

Back 174

cholera

Front 175

species?

Back 175

vibrio cholerae

Front 176

reservoir and spread?

Back 176

-a free living inhabitant of fresh water
-assymptomatic humans major resevoir
-spread via contaminated food (fresh water shellfish)

Front 177

sn/sx

Back 177

severy watery diarrhea, marked dehydration, loss of carbonates and loss of potassium ions, shock resulting in cardiac failure

Front 178

tx:

Back 178

rapid fluid/electrolyte replacement; abs not necessary

Front 179

prevention:

Back 179

clean drinking water supply/ adequate sewage disposal

Front 180

which condition is also known as bacillary dissentery?

Back 180

shigellosis

Front 181

its most severe form is characterized by:

Back 181

-invasion of the mucosa of lg intestine
-inflammation of intestines
-blood/pus in diarrhea
-lower abdomen cramps

Front 182

which species causes mild infxs?

Back 182

shigella sonnei

Front 183

severe?

Back 183

shigella dysenteriae

Front 184

spread?

Back 184

poor sanitation and personal hygiene

Front 185

a halophilic organism that contaminates seafood and fish; causes diarrhea if eaten uncooked:

Back 185

Vibrio parahemolyticus

Front 186

primarily a pediatric disease:

Back 186

shigellosis

Front 187

rice water stool:

Back 187

cholera

Front 188

causes infx in colder parts of the world:

Back 188

Yersinia enterolytica

Front 189

Tx includes omeprazole with amoxicillin and metronidazole:

Back 189

H. pylori

Front 190

enterotoxin producing type A strain and beta-toxin producing type C strains:

Back 190

C. perfringens

Front 191

which are more common and caused by spores that contaminate food?

Back 191

A strains

Front 192

characteristics of type c strains:

Back 192

-acute necrotizing disease of sm. intestine
-more rare
-abdominal pain/diarrhea

Front 193

prevention?

Back 193

thoroughly re-heating food

Front 194

which disease has a long standing history of epidemics and pandemics

Back 194

cholera

Front 195

most common cause of diarrhea:

Back 195

Campylobacter jejuni

Front 196

clinically, which other bacteria is indistinguishable from c. jejuni?

Back 196

salmonella

Front 197

caused by eating contaminated meat in people who are unaccustomed to high protein diets:

Back 197

C. perfringens

Front 198

why?

Back 198

lack sufficient intestinal trypsin to destroy the toxin

Front 199

a heat stable enterotoxin thats resistant to degradation by enzymes in stomach/ sm. intestine:

Back 199

staph aureus

Front 200

spores and vegetative cells contaminate food:

Back 200

B. cereus

Front 201

2 forms of B. cereus:

Back 201

1. ingestion of enterotoxin in food (rice and potatoes)
2. production of enterotoxin in gut

Front 202

which causes rapid onset vomiting and which causes diarrhea?

Back 202

vomiting= ingestion
diarrhea= production in gut

Front 203

found in rabbits, pigs, sheep, cattle, horses, domestic pets:

Back 203

yersinia enterolytica

Front 204

an acute but self-limiting diarrhea that's resolved without tx:

Back 204

salmonella

Front 205

diarrhea not a feature, vomiting occurs 3-6 hrs after consumption and recovery w/in 24 hrs:

Back 205

staph aureus

Front 206

spores are found widespread in the environment and can be isolated from soil samples, animals, and fish:

Back 206

clostridium botulinum

Front 207

is botulin an exotoxin or endotoxin?

Back 207

exotoxin

Front 208

how does it invade?

Back 208

toxins are ingested in food (canned or reheated) or are produced in the gut after ingesting the organisms

Front 209

pathogenesis:

Back 209

-toxins are absorbed by the blood stream
-reach peripheral nerve synapses and block neurotransmission
-leads to flaccid paralysis, progressive muscle weakness, and respiratory distress

Front 210

3 types:

Back 210

1. foodborne (toxin released in food, then ingested)
2. infant (organism ingested)
3. woulnd (organism implanted in wound)

Front 211

tx

Back 211

antibacterial agents not helpful; polyvalent antitoxin recommmended

Front 212

Causes antibiotic associated diarrhea- broad spectrum antibios that inhibit normal flora:

Back 212

Clostridium difficile

Front 213

pathogenesis:

Back 213

produces 2 exotoxins that produce diarrhea and lead to colitis

Front 214

tx:

Back 214

if severe, anti-anaerobic agents (metronidazole)

Front 215

how is viral diarrhea distinguised from bacterial?

Back 215

clinically indistinguishable

Front 216

transmission:

Back 216

fecal-oral route

Front 217

viruses:

Back 217

Rotavirus and Calcivirus

Front 218

which includes the Norwalk virus?

Back 218

Calcivirus

Front 219

sn/sx

Back 219

fever, chills, headaceh, nausea, vomiting, diarrhea

Front 220

transmission:

Back 220

eating sewage contaminated shellfish or mussels

Front 221

Who does rotavirus mostly infect

Back 221

children under 2

Front 222

incubation period:

Back 222

1-4 days

Front 223

where does viral replication occur?

Back 223

intestinal epithelial cells

Front 224

sn/sx

Back 224

acute onset of projectile vomiting and diarrhea

Front 225

tx:

Back 225

rehydration/salt replacement; no anti-virals

Front 226

Protozoa that cause diarrhea:

Back 226

Entamoeba histolytica, Giardia lamblia, and Cryptosporidium parvum

Front 227

how does infx occur with E. histolytica

Back 227

food/drink is contaminated with cysts that pass thru the stomach and excyst in the sm. intestine where they multiply

Front 228

sn/sx

Back 228

-small ulcers in mucosa that lead to mild diarrhea
-more sever leads to amebic dysentery

Front 229

chars. of amebic dysentery:

Back 229

mucus, pus and blood in stool

Front 230

difference between amebic dysentery and bacillary dysentery:

Back 230

amebic can perforate small intestine (peritonitis) and invade extra-intestinally when trophozoites spread via blood to the liver and form an abcess

Front 231

tx:

Back 231

metronidazole

Front 232

Which protozoa causes infx when cysts are swallowed in contaminated drinking water from rivers/streams?

Back 232

Giardia lamblia

Front 233

animal host?

Back 233

beaver

Front 234

characteristics:

Back 234

-assymptomatic infxs (mild)
-self-limiting diarrhea 7-10 days
-immunocompromised may develop chronic infx

Front 235

tx:

Back 235

metronidazole

Front 236

prevention:

Back 236

chlorination and water filtration

Front 237

Pathogenesis of Cryptosporidium parvum:

Back 237

-fecally contaminated material is ingested
-cysts release infective trophozoites which invade epithelial cells in sm. intestine
-parasite found in many animals

Front 238

sn/sx

Back 238

ranges from moderate diarrhea to severe lasting 20 days in immunocompromised

Front 239

cryptosporidiosis:

Back 239

common infx in AIDS; diarrhea can be irreversible and life threatening

Front 240

tx:

Back 240

spiramycin (immunocompromised only)

Front 241

which protozoa is common in subtropical and tropical countries

Back 241

Entamoeba histolytica

Front 242

What are the most important intestinal worms?

Back 242

soil transmitted nematodes

Front 243

2 groups of them:

Back 243

1. Ascaris lumbricoides/Trichuris trichiura
2. Anchylostoma duodenale/Necator americanus/Strongyloides stercoralis

Front 244

large roundworm:

Back 244

ascaris lumbridcoides

Front 245

whipworm:

Back 245

Trichuris trichiura

Front 246

hookworm:

Back 246

Necator americanus

Front 247

which occur by swallowing infective eggs which hatch in intestine and release larvae

Back 247

Ascaris and Trichuris

Front 248

which can cause abdominal pain and nausea

Back 248

Ascaris

Front 249

what happens if there's large numbers of ascaris

Back 249

can cause intestinal blockage and perforations of wall

Front 250

What can Tricuris infx lead to?

Back 250

chronic diarrhea and impaired nutrition/retarded growth (since children mostly affected)

Front 251

How do Ancylostoma, Necator, and Stronglyoides infect?

Back 251

-active skin penetration by infective larvae
-then migration via blood to lungs
-then swallowed where, in intestine, adult worms attach to intestinal mucosa where they rupture capillaries and suck blood

Front 252

Hookworm disease can lead to:

Back 252

iron deficiency anemia due to blood feeding

Front 253

Strongyloidiasis:

Back 253

profuse diarrhea with dehydration and electrolyte imbalance; fatal if immunosuppressed

Front 254

pinworm:

Back 254

Enterobium vermicularis

Front 255

What is the most common intestinal nematode in developed countries?

Back 255

pinworm (Enterobius)

Front 256

how do they infect?

Back 256

females live in the lg. bowel and release infective eggs in the perianal skin

Front 257

sn/sx

Back 257

itching and mild diarrhea

Front 258

transmission

Back 258

contaminated fingers

Front 259

tx

Back 259

anti-heminitic drugs;
piperazine for Ascaris hookworms and pinworms

Front 260

what are the systemic infxs initiated at intestinal tract?

Back 260

typhoid fever, paratyphoid fever (enteric fevers), listeriosis, and hepatitis

Front 261

What causes the enteric fevers?

Back 261

Salmonella typhi and S. paratyphi types A and C

Front 262

transmission:

Back 262

contaminated food/water; spread person to person and they can cary it for months or years

Front 263

pathogenesis:

Back 263

-after ingestion they penetrate the gut mucosa and reach intestinal lymph nodes
-survive and multiply within macrophages
-released into bloodstream and seed other organs (spleen, bone marrow, liver, Peyer's patch)
-gallbladder infected via blood or liver (carrier)

Front 264

incubation period:

Back 264

10-14 days

Front 265

sn/sx

Back 265

fever, aches, repiratory problems, resembles flu-like illness, diarrhea, or constipation, transient rose spots in the upper abdomen (may disappear)

Front 266

complications:

Back 266

-GI lesions that hemorrhage and perforate
-myocarditis, bone marrow damage
-meningitis, osteomyelitis, or endocarditis due to multiplication on other body sites

Front 267

what are chronic carriers?

Back 267

1-3% of pt's who excrete S. typhi in feces or urine for up to 1 yr. after infx

Front 268

Tx:

Back 268

chloramphenicol, ampicillin, ciprofloxacin

Front 269

prevention:

Back 269

good hygiene, exclude carriers from food handling, gallbladder removal in carriers

Front 270

vaccination:

Back 270

killed vaccine of S. typhi and S. paratyphi recommended for travelers

Front 271

Who is listeriosis associated with

Back 271

pregnancy (risk or abortion or stillbirth)and reduced immunity

Front 272

Cause (species):

Back 272

Listeria monocytogenes

Front 273

transmission:

Back 273

uncooked foods= pate, milk, soft cheese, coleslaw

Front 274

Hepatitis=

Back 274

inflammation and damage to the liver

Front 275

causes:

Back 275

Virus (A, E, B, C) or bacteria (less common)

Front 276

sn/sx

Back 276

malaise, anorexia, nausea or if severe acute liver failure (rare)

Front 277

can liver be repaired?

Back 277

yes, regeneration of liver cells is rapid

Front 278

if infx persists, what can result?

Back 278

cirrhosis

Front 279

what type of virus is Hep A (HAV)

Back 279

enterovirus

Front 280

transmission:

Back 280

fecal-oral route (excreted in lg. amounts in feces)

Front 281

incubation period:

Back 281

2-4 weeks

Front 282

pathogenesis:

Back 282

after infection, it enters blood from unknown sites in the GI tract where it can replicate and then infect liver cells

Front 283

what is a sign in adults?

Back 283

jaundice

Front 284

vaccine?

Back 284

yes

Front 285

Hep E spread?

Back 285

fecal oral

Front 286

where common?

Back 286

undeveloped countries and India (waterborne)

Front 287

incubation period:

Back 287

6-8 weeks

Front 288

mild or severe?

Back 288

usually mild, but severe in pregnant women (high mortality)

Front 289

Hep B (HBV) transmission:

Back 289

in blood: between IV users, male homosexuals, or heterosexuals with ulcers, mother/child, earpiercing, actupuncture

Front 290

pathogenesis:

Back 290

enters body and replicates in the lymphoid tissue then reaches the blood and then liver. Then, immune-mediated attack of infected liver cells by T-cells, leading to inflammation and necrosis. IR slowly works and virus replication stops

Front 291

Do all individuals eliminate it?

Back 291

10% don't and become carriers; blood remains infectious for life but liver damage is mild

Front 292

Predisposition to becoming a carrier:

Back 292

-immunodeficiency
-age (infants)
-males more than females

Front 293

complications of HBV

Back 293

-cirrhosis
-hepatocellular carcinoma

Front 294

How likely are hep B carriers to develop liver cancer

Back 294

200 times more likely than non carriers

Front 295

detection:

Back 295

HBsAg (antigen) remains in carriers and is detected

Front 296

Tx:

Back 296

interferon alpha, vaccine

Front 297

What is Hep C most common with

Back 297

transfusion

Front 298

spread?

Back 298

same as HBV-blood

Front 299

differences betw. C and B:

Back 299

-more aggressive
-higher degree of carriers
-also causes liver cancer
-same transmission

Front 300

disease progression:

Back 300

50% get chronic active hepatits and 20% get cirrhosis

Front 301

tx:

Back 301

interferon alpha and ribavirin; no vaccine

Front 302

Congenital infxs:

Back 302

congenital rubella, CMV, syphillis, toxoplasmosis, HIV, listeriosis

Front 303

when is fetus susceptible to rubella?

Back 303

in 1st 3 mos. of pregnancy

Front 304

abnormalities:

Back 304

development of heart, brain, eyes, ears; low birth weight and eye and heart lesions

Front 305

25% develop what

Back 305

IDDM

Front 306

where does virus replicate

Back 306

pancreas

Front 307

prevention:

Back 307

totally- vaccine before pregnancy

Front 308

how many fetuses are infected after primary maternal infx with CMV?

Back 308

40%; 5% show signs at birth

Front 309

abnormalities:

Back 309

mental retardation, spasticity, eye abnormalities, hearing defects, hepatosplenomegaly, anemia

Front 310

vaccine:

Back 310

in clinical trials

Front 311

where's con. syphillis common

Back 311

developing countries

Front 312

abnormalities:

Back 312

rhinitis, skin/mucosal lesions, hepatosplenomegaly, and bone, teeth, and cartilage abnormal

Front 313

prevention:

Back 313

treat mom before 4th month

Front 314

cause of toxoplasmosis:

Back 314

Toxoplasmosis gondii

Front 315

abnormalities:

Back 315

microcephaly, convulsions, chorioretinitis, hepatosplenomegaly, jaundice, mental retardation, defective vision

Front 316

prevention:

Back 316

women avoid contact w/ cat feces or lightly cooked meat

Front 317

HIV abnormalities:

Back 317

poor weight gain, sepsis, developmental delays, oral thrush, pneumonitis, diarrhea, AIDS

Front 318

prevention:

Back 318

mom take AZT

Front 319

Listeriosis sn/sx in mother:

Back 319

flu-like sx or asymptomatic

Front 320

abnormalities:

Back 320

abortion, premature delivery, neonata septicemia and neurological damage

Front 321

tx:

Back 321

penicillin, ampicillin

Front 322

vaccine:

Back 322

no

Front 323

What are the main routes of infx in the CNS?

Back 323

blood vessels and nerves that transverse the walls of the skull and vertebral column

Front 324

what type of invasion is most common

Back 324

bloodborne

Front 325

encephalitis:

Back 325

invasion across the blood-brain barrier

Front 326

meningitis:

Back 326

invasion across the blood-cerebrospinal fluid

Front 327

is invasion via peripheral nerves common?

Back 327

no

Front 328

how does body respond to invading viruses in CNS?

Back 328

increased lymphocytes (mostly T cells) and monocytes in CSF

Front 329

response to pyogenic bacterial invasion:

Back 329

rapid increase in PMNs

Front 330

clear CSF, "aseptic":

Back 330

viral

Front 331

turbid CSF, "septic":

Back 331

pyogenic bacteria

Front 332

which is more severe

Back 332

bacterial

Front 333

which is more common

Back 333

viral

Front 334

bacterial agents:

Back 334

Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae

Front 335

cause of meningococcal meningitis:

Back 335

Neisseria meningitidis

Front 336

transmission:

Back 336

person to person by droplets

Front 337

who's mostly infected:

Back 337

children whove lost abs acquired by their mother, adolescents who've not previously encountered the infecting serotype

Front 338

blood/meninges invasion rare?

Back 338

yes, and poorly understood

Front 339

incubation period:

Back 339

1-3 days

Front 340

sn/sx:

Back 340

sore throat, headaceh, drowsiness, fever, irritability, neck stiffness, hemorrhagic skin rash with petechiae (Due to septicemia)

Front 341

severe complications:

Back 341

35%; intravascular coagulation, shock, renal failure, bleeding into the brain and adrenal glands

Front 342

Mortality:

Back 342

100% if untreated, 10% if treated; serious/lasting complications not common

Front 343

Tx

Back 343

penicillin, ampicillin ASAP! if suspected

Front 344

Prophylaxis:

Back 344

chemoprophylaxis of rifampicin for close contacts for 2-3 days to clear carriage of bacteria in nasopharynx

Front 345

who does haemophilus meningitis infect?

Back 345

infants from 3-4 mo to 2-3 y.o.

Front 346

incubation period:

Back 346

5-6 days

Front 347

mortality:

Back 347

less frequently fatal but 10% higher incidence of lasting complications

Front 348

complications:

Back 348

hearing loss, delayed language development, mental retardation, seizures

Front 349

vaccine:

Back 349

yes- children 6 mos. and older

Front 350

prophylaxis:

Back 350

rifampicin to close contacts

Front 351

cause of pneumococcal meningitis:

Back 351

Streptococcus pneumoniae

Front 352

where is it carried?

Back 352

in the throats of healthy people

Front 353

mortality:

Back 353

20-30% in treated cases

Front 354

complications:

Back 354

sequela such as deafness in 15-20% of treated cases

Front 355

Tx:

Back 355

penicillin

Front 356

vaccine:

Back 356

polyvalent (23 serotype) vaccine

Front 357

which is an important cause of miningitis in immunocompromised adults, esp, renal transplant and cancer pts.

Back 357

Listeria mnoncytogenes

Front 358

Tx:

Back 358

ampicillin and gentamicin

Front 359

causes of neonatal meningitis:

Back 359

E. coli and group B hemolytic streptococci

Front 360

mortality:

Back 360

fatal in 35%

Front 361

complications:

Back 361

permanent neurological sequela such as cerebral or cranial nerve palsy, epilepsy, mental retardation, or hydrocephalus

Front 362

why is clinical diagnosis of neonatal meningitis rare?

Back 362

b/c common sn/sx of fever, poor feeding, vomiting, respiratory distress, or diarrhea

Front 363

tx:

Back 363

gentamicin and ampicillin

Front 364

Tuberculous meningitis:

Back 364

-associated w/ acute miliary TB
-gradual onset of malaise, apathy, and anorexia and proceeds to photophobia, neck stiffness, and altered consciousness

Front 365

Tx:

Back 365

isoniazin, rifampicin, and pyraminamide
- BCG vaccine and isoniazind prophylaxis

Front 366

Fungal meningitis:

Back 366

-Cryptococcus neoformans
-Coccidioides immitis
-invade blood from primary infx in lungs then infect brain

Front 367

C. neoformans:

Back 367

-AIDS pts (depressed T cell immunity)

Front 368

C. immitis:

Back 368

southwest US, Mexico, S. America

Front 369

Tx:

Back 369

amphotericin B

Front 370

Protozoan meningitis:

Back 370

-Naegleria and Harmanella
-multiply in stagnant water in warm countries
-high mortality

Front 371

pathogenesis:

Back 371

inhaled or swallowed and reach meninges via the olfactory tract

Front 372

Most common type of meningitis:

Back 372

viral

Front 373

sn/sx

Back 373

-headache, fever, general illness but less neck stiffness

Front 374

viral causes:

Back 374

HSV, mumps, poliovirus, coxsackievirus, echovirus, Japanese encephalitis virus, Eastern/western equine encephalatis virus, and HIV

Front 375

recovery from viral?

Back 375

no antivirals (except HSV) but usually complete recovery

Front 376

Primary cause of encephalitis:

Back 376

viruses: HSV, poliovirus, mumps, rabies

Front 377

sn/sx

Back 377

cerebral dysfunction: abnormal behavior, seizures, altered consciousness, nausea, vomiting, fever

Front 378

most common severe sporadic encephalitis:

Back 378

HSV, 2 forms:
1. primary and generalized in infancy
2. adults due to reactivation in trigeminal ganglie

Front 379

Tx

Back 379

acyclovir

Front 380

Poliovirus sn/sx

Back 380

1-4 days of fever initially, sore throat, malaise, meningeal sn/sx, paralysis, motor neuron problems

Front 381

common?

Back 381

used to be- CNS disease in less than 1% of those infected now

Front 382

vaccine?

Back 382

yes= completely preventable with it

Front 383

common cause of mild encephalitis:

Back 383

mumps virus- assymptomatic

Front 384

transmission of rabies encephalitis:

Back 384

saliva of infected dogs, foxes, jackals, wolves, skunks, raccoons, and vampire bats and transmitted via a bite or salivary contamination of a wound/abrasion

Front 385

pathogenesis:

Back 385

virus travels up peripheral nerves to CNS; once in brain it spreads cell to cell until many neurons are infected; invades limbic system

Front 386

incubation:

Back 386

4-13 weeks (the further the bite from the CNS, the longer the period)

Front 387

sn/sx

Back 387

sore throat, headache, fever, discomfort at site of bite, muscle spasms, convulsions, diff swallowing, hydrophobia

Front 388

immediate preventative action:

Back 388

1. clean wound
2. confirm if animal is infected (if dog appears healthy after 10 day, infx is unlikely)
3. adiminister human rabies Immunoglobulin (passive immunization)
4. if risk is definite, active immunization with killed virus

Front 389

Causes of togavirus meningitis and encephalitis:

Back 389

arthropod-borne togaviruses

Front 390

which are transmitted via the mosquito Culex tarsalis?

Back 390

western equine encephalomyelitis and St. Louis encephalitis virus

Front 391

What is transmitted via other Culex species?

Back 391

west nile enephalitis virus

Front 392

where is japanese encephalitis virus prevalent?

Back 392

india - 50% mortality; vaccine available

Front 393

Retrovirus meningits and encephalitis:

Back 393

-HIV invades CNS after initial infx
-later, subacute encephalitis may develop, associated w/ dementia

Front 394

cause of brain abcesses:

Back 394

-follow surgery/trauma, chronic osteomyelitis, septic embolism, or chronic cerebral anoxia
-various bacteria of oropharynx origin
-rare b/c of antibiotics

Front 395

Tx:

Back 395

surgical drainage and antibios

Front 396

Scrape-Type Agent features:

Back 396

-slow replication occurs by the conversion of host prion protein into abnormal form
-not a virus
-prion protein is host encoded but slightly altered
-resistant to heat, chemicals and irradiation
-no test tube cultivation
-spongiform appearance
-little or no inflammatory response
-infectious agent restricted to CNS and lymphoid tissues
-No tx, no vaccine, lethal
-originated in sheep/goats in Europe 200-300 yrs ago

Front 397

CJD transmission:

Back 397

-eating bovine spongiform encephalopathy (BSE) contaminated food
-person to person by:
1. neurological steriotactic electrodes
2. corneal grafts
3. injections of growth hormone

Front 398

genetic disposition:

Back 398

10% of CJD occurs in families where affected people have mutation in the gene encoding for the prion protein; easily and spontaneously converted to pathogenic form

Front 399

a fatal neurologic disease with cerebellar signs exclusive to Fore tribes in Papua New Guinea

Back 399

Kuru

Front 400

transmission

Back 400

person to person via cannibalism

Front 401

incubation period:

Back 401

4-20 years

Front 402

Tetanus and botulism affects on CNS:

Back 402

toxins have effect, but bacteria themselves dont invade

Front 403

cause of tetanus:

Back 403

Clostridium tetani

Front 404

pathogenesis:

Back 404

-spores are in soil and animal feces
-spores enter wound and if tissue is necrotized it allows anaerobic growth of the organism
-toxin is carried in peripheral nerve axons and in the blood to CNS where it binds to neurons and blocks release of inhibatory mediators in the synapses causes overactivity of the motor neurons leading to spastic paralysis

Front 405

sn/sx

Back 405

after 3-21 days: exaggerated reflexes, muscle rigidity, uncontrolled muscle spasms, lockjaw, neck stiffness, dysphagia; spasms can lead to injury/respiratory failure

Front 406

immunization:

Back 406

toxoid, lasts 10 years; tetanus immunoglobulin in severe cases

Front 407

pathogenesis of botulism:

Back 407

-spores in soil contaminate veggies, meat, and fish
-can survive in improperly canned food
-ingested then enters blood where it acts on peripheral nerve synapses by blocking acetylcholine

Front 408

sn/sx

Back 408

after 2-72 hrs., descending weakness, flaccid paralysis, dysphagia, vomiting, vertigo, respiratory muscle failure

Front 409

tx:

Back 409

antibodies against toxins

Front 410

Most commmon cause of skin infections such as boils, abcesses, or postoperative wound infxs:

Back 410

Staph aureus

Front 411

how acquired?

Back 411

either from self-innoculation froma carrier state (nose) or from contact with another person

Front 412

This begins w/in 2-4 days of innoculation as a superficial infection of a follicle (foliculitis)

Back 412

boil

Front 413

this typically contains abundant yellow creamy pus formed by organisms and dead WBCs:

Back 413

abcess

Front 414

what can inward drainage of an abcess lead to?

Back 414

peritonits, empyema, or meningitis

Front 415

Tx

Back 415

drainage, antibiotics if severe/fever: enzyme stable penicillins (cloaxicillin and flucoloxacillin)

Front 416

What causes staphylococcal scalded skin syndrome, seen in infants and older children

Back 416

Staph aureus that produces exfoliatin or scalded skin syndrom toxin

Front 417

pathogenesis:

Back 417

minor lesion initally but toxin causes destruction of intercellular connections and separates epidermis from dermis

Front 418

sn/sx

Back 418

-large blisters with clear fluid
-entire skin lost
-irritable, uncomfortable
-rarely severely ill

Front 419

Tx:

Back 419

fluid replacement and cloxacillin

Front 420

What causes TSS?

Back 420

TSS-toxin prodcucing Staph aureus

Front 421

sn/sx

Back 421

skin manifestations, rash followed by desquamation of skin in soles and palms

Front 422

cause of streptococcal skin infxs:

Back 422

Strep. pyogenes (diff strain than sore throat)

Front 423

This occurs independently of upper respiratory tract infx and is limited to the epidermis

Back 423

streptococcal impetigo

Front 424

sn/sx

Back 424

crusted yellow papules that develop 24-48 hrs. after infx

Front 425

This may infect deeper in the dermis causing erysipelas and involves blocking of dermal lymphatics

Back 425

strep pyogenes

Front 426

sn/sx

Back 426

well defined spreading erythromatous inflammation on face, legs or feet; fever, pain

Front 427

tx:

Back 427

penicillin per os or IM

Front 428

If infx with strep pyogenes is deeper than erysipelas, it may infect subcutaneous fat causing:

Back 428

Cellulitis

Front 429

sn/sx

Back 429

hot red swollen lesion, regional lymph nodes enlarged; malaise, fever, chills

Front 430

cause of cellulitis:

Back 430

staph aureus or strep pyogenes

Front 431

where does anaerobic cellulits develop

Back 431

in areas of traumatized or devitalized tissue:
surgical or trauma wounds, diabetic pts are prone

Front 432

sn/sx (anaerobic cellulitis)

Back 432

foul smelling discharge, swelling and gas in tissues

Front 433

tx:

Back 433

antibiotics, surgical debridement

Front 434

This resembles bacterial gangrene but is more acute and highly toxic causing widespread necrosis:

Back 434

Necrotizing fascitis (flesh eating bacteria)

Front 435

Tx

Back 435

radical excision, local and systemic antibios

Front 436

cause of gas gangrene:

Back 436

clostridium perfringens

Front 437

pathogenesis:

Back 437

-organisms invade deep muscle and cause necrosis and produce gas bubbles
-in poor circulation areas
-proceeds rapidly
-lecithinase (alpha toxin) hydrolyzes lipids in cells membranes resulting in cell lysis and death
-dead tissue further allows multiplication and more toxin

Front 438

if toxin gets in blood stream?

Back 438

massive hemolysis, renal failure , death

Front 439

tx:

Back 439

excision, amputation, anit-alpha toxin, hyperbaric oxygen chamber, penicillin, metronidazole

Front 440

Pathogenesis of Proprionibacterium acnes:

Back 440

increase in androgenic hormones leads to in'd sebum production and blockage of ducts leads to sac where they can multiply

Front 441

what causes inflammation:

Back 441

p. acnes acts on sebum to form fatty acids and acts with polymorphs

Front 442

comedones (black heads):

Back 442

greasy plugs composed of keratin, sebum and bacteria capped by melanin

Front 443

tx

Back 443

tetracycline, erythromycin, vitamin A derivates (isoretinoin)

Front 444

cause of leprosy:

Back 444

mycobacterium leprae

Front 445

are there more organisms in nasal secretion or skin lesions

Back 445

nasal secretions

Front 446

transmission:

Back 446

possibly arthropod vecotors; not highly contagious- need prolonged exposure

Front 447

where concentrated on the body?

Back 447

in the skin and superficial nerves (within macrophages and Schwann cells of peripheral nerves)b/c grow under 37 degrees

Front 448

2 manifestations (partly genetically determined):

Back 448

1. Tuberculoid (TT)- blotchy red lesions with anesthetic areas of face, trunk, and extremeties- good prognosis
2. lepromatous (LL)- due to weak CMI- extensive skin involvement- loss of eyebrows, thickening nostrils, ears, and cheeks, typical lion-like appearance

Front 449

tx:

Back 449

LL- triple therapy- dapsone, rifampicin, clofazimine for 2 years
TT- dapsone and rifampcin for 6 mos.
-dapsone prophylaxis for close contacts

Front 450

what are the most common infxs in humans

Back 450

dermatophytes- superficial mycoses (tinea or ringworm)

Front 451

what are they

Back 451

keratin-loving fungi that invade, skin, hair, and nails

Front 452

capitis-

Back 452

affects hair and scalp

Front 453

corporis-

Back 453

affects body

Front 454

pedis-

Back 454

feet

Front 455

sx

Back 455

thickening, dry , scaly skin, cracks between toes, hair loss

Front 456

tx:

Back 456

topical antifungals (miconazole) and ketatolytic agents (salicylic acid, benzoic acid); or griseofulyin orally

Front 457

response time:

Back 457

scalp -6-12 weeks
fingernails- up to 6 mos.
toenails- one year or more

Front 458

When can candida colonize skin

Back 458

when damaged b/c its moist

Front 459

viral mucotaneous lesions:

Back 459

Papillomavirus, HSV, VZV, Varicella, Zoster, or HHV

Front 460

what does papilloma cause

Back 460

skin warts

Front 461

of the 70 types, which infgect genitals:

Back 461

6, 11, 16, 18, and 32

Front 462

sn/sx

Back 462

cauliflower like

Front 463

what do HPV1 and 4 cause

Back 463

plantar warts: flat

Front 464

what causes common warts

Back 464

HPV 2, 3, 10

Front 465

pathogenesis

Back 465

-after entering body via surface abrasions, virus infects cells in basal layers of skin or mucosa
-no spread to deep tissue
-infected cells are stimulated to divide, after 6 months start protruding
-wart regresses and teh viral DNA remains latent in basal cell layer
-immune compromised reactives

Front 466

tx

Back 466

apply karyolytic agents- salicyclic acid, freezing, liquid nitrogen

Front 467

HSV-1 pathogenesis:

Back 467

-basic lesion is intraepithelial vescicle where virus sheds
-virus rich vesicles ulcerate and become coated with whitish gray liquid, then scab over and heal in a week
-virus enters sensory nerve endings in the lesion and goes to tirgeminal ganglia and initiate latent infx
-virus remains for life and can cause cold sore

Front 468

transmission:

Back 468

from saliva or cold sores

Front 469

primary infx can occur in:

Back 469

1. eye- conjunctivitis
2. finger
3. other skin sites (rubbing)
4. genital tract

Front 470

reactivation provoked by:

Back 470

1. common cold, pneumonia
2. direct sunlight
3. stress
4. menstruation
5. immunocompromised

Front 471

txL:

Back 471

acyclovir

Front 472

what does VZV cause

Back 472

chicken pox (varicella) and zoster (shingles

Front 473

what group does VZV belong to

Back 473

herpesvirus

Front 474

transmission:

Back 474

inhalation from respiratory secretions and saliva or by direct contact of lesions

Front 475

Primary infx with VZV causes:

Back 475

chicken pox

Front 476

reactivation causes:

Back 476

shingles

Front 477

pathogenesis of varicella:

Back 477

-after primary infx virus passes across surface epithelium in respiratory tract to lymphoid tissues
-no sx or lesions yet
-replicates and seeds to epithelial celss and produces varicella vesicles
-vesicles appear as crops, develop into pustules and scab over, scarring

Front 478

adult complications:

Back 478

interstitial pneumonia, CNS involvement

Front 479

where is latent infx with zoster established?

Back 479

dorsal root ganglia

Front 480

sn/sx

Back 480

erythromatous rash in thoracic region, severe pain

Front 481

predispostion to zoster if:

Back 481

-increasing age
-leukemia, lymphoma, AIDS, renal transplant (ImunoComp)
-fractures/tumors

Front 482

tx:

Back 482

famciclovir

Front 483

vaccine:

Back 483

live attenuated

Front 484

HHV 6 sn/sx

Back 484

-affects most before age 5
-roseola infantum rash
-2 weeks incubation, then fever and rash

Front 485

how many serotypes of mumps exist

Back 485

1

Front 486

spread?

Back 486

intimate contact-airborne droplets, salivary secretions and possibly urine

Front 487

pathogenesis:

Back 487

-enters respiratory tract, spreads systemically to lymphoid tissues
-after 7-10 days enters the blood and localizes in salivary and other glands
-cells lining ducts degenerate causing inflammation, lymphocyte infiltration, and edema resulting in disease
-

Front 488

sn/sx

Back 488

painful tender and swollen parotid gland: classic 30-40% of cases

Front 489

recovery:

Back 489

1 week, life long resistance

Front 490

tx

Back 490

none, live attenuated vaccine

Front 491

how many serotypes of rubella?

Back 491

1

Front 492

transmission:

Back 492

droplet infx

Front 493

more or less contagious than measles

Back 493

less

Front 494

pathogenesis:

Back 494

-enters respiratory tract and grows in local lymphoid tissue
-spreads to spleen and lymph nodes elswhere
-after 1 week, multiplication in placenta, joints, and kidneys

Front 495

sn/sx

Back 495

after 14-21 days, milde disease, fever, malaise, and maculopapular rash lasting 3 days

Front 496

tx

Back 496

live attenuated vaccine

Front 497

what is the lgst human herpes virus

Back 497

CMV

Front 498

how many serotypes

Back 498

1

Front 499

transmission

Back 499

saliva "salivary gland virus", urine, semen, cervical secretions, blood transfusions, organ transplant

Front 500

pathogenesis

Back 500

-starts as silent infx in URT, then spreads locally to lymphoid tissues and systmeically in circulaing monocytes and lymphocytes
-then localizes in epithelial cells of salivary glands and kidney tubules and in the cervix, epididymis and testes where virus sheds

Front 501

sn/sx

Back 501

assymptomatic; mabye fever in young adults

Front 502

may lead to:

Back 502

1. fetal malformations
2. interstitial pneumonia

Front 503

tx

Back 503

ganciclovir; no vaccine

Front 504

EBV transmission

Back 504

saliva, kissing

Front 505

pathogenesis:

Back 505

-replicates in B lymphocytes binding to Cd3 receptors
-T lymphos respond to infected B's
-remains latent in some B's

Front 506

what are sn/sx attributed to?

Back 506

immunologic response--cytokines released

Front 507

sn/sx

Back 507

-infants/children: none or weak
- mono, fever, sore throat, petechiae on hard palate, lymphadenopathy, splenomegaly, anorexia, lethargia

Front 508

Immunodeficiency can lead to:

Back 508

reactivation with no symptoms

Front 509

tx;

Back 509

no antivirals; acyclovir useful; no vaccine

Front 510

EBV is closely related to

Back 510

Burkitts lymphoma; co-carcinogen is marlaria (weakens t cells)

Front 511

where is it restricted to

Back 511

Africa and papua new guinea

Front 512

Smallpox (variola) caused by:

Back 512

poxvirus

Front 513

spread

Back 513

person to person via contact with skin lesions and via respiratory tract

Front 514

sn/sx

Back 514

generalized rash

Front 515

global eradication of smallpox in 1980 b/c :

Back 515

1. no subclinical infxs
2. no carriers
3. no animal resevoir
4. effective vaccine available (live attenuated vaccinia)

Front 516

what are the arbovirus infxs

Back 516

yellow fever and dengue fever

Front 517

how are they transmitted

Back 517

arthropod borne- via ticks, mosquitoes, and sandflies

Front 518

arbovirus pathogenesis in vector:

Back 518

enters the arthropod as it takes a bloodmeal from infeced animal, passes to the gut and reaches salivary gland where it multiplies and can now transmit (1-2 weeks)

Front 519

Who spreads urban yellow fever

Back 519

person to person by Aedes aegypti

Front 520

jungle yellow fever:

Back 520

monkey to human by Haemoagogus

Front 521

where?

Back 521

Africa, central/south america, and caribean

Front 522

pathogenesis:

Back 522

-virus enters blood vessel
-spreads to vascular epithelium and liver
-2-6 days incubation

Front 523

sn/sx

Back 523

fever, headache, muscle ache; severe- shock, severe liver damage

Front 524

tx

Back 524

prevention via live attenuated vaccine; vector control w/ insecticides, repellants

Front 525

Where does dengue fever occur

Back 525

SE asia, pacific area, india, and caribbean

Front 526

principal vector

Back 526

A. aegypti

Front 527

pathogenesis:

Back 527

-virus replicates in monocytes and in vascular epithelium
-incubation 4-8 days
-increased cytokine release into circulation

Front 528

sn/sx

Back 528

malaise, fever, nausea, vomiting, maculopapular rash

Front 529

SEVERE:

Back 529

dengue hemorrhagic fever syndrome- children endemic 10% mortality

Front 530

what does incre'd cytokine release cause

Back 530

vascular damage, shock, hemorhging into GI tract and skin

Front 531

tx:

Back 531

none