Mid Test 1

Front 1

e.g. microaerophilic

Back 1

Campylobacter (like a little bit of oxygen) can cause gastric ulcers

Front 2

e.g. facultative anaerobe

Back 2

E. coli (can grow with or without oxygen, found anywhere along flask)

Front 3

Actinomyces +/-

Back 3

+ rods

Front 4

Clostridium +/-

Back 4

+ rods

Front 5

Bacilis +/-

Back 5

+ aerobic

Front 6

Bacteroides +/-

Back 6

- rods (most gram - are rods)

Front 7

lactose fermenters

Back 7

e. coli, klebsiella, enterobacter

(- rods --> facultative anaerobic --> enterobacteriacae)

Front 8

non-lactose fermenters

Back 8

salmonella, shigella

Front 9

Gram - aerobic rods

Back 9

pseudomonas, hemophilus, vibrio

Front 10

Gram - aerobic cocci

Back 10

Neisseria

Front 11

mycoplasma characteristic

Back 11

lack cell wall

Front 12

non-lactose fermenting, oxidase +

Back 12

pseudomonas (blue)

Front 13

non-lactose fermenting, oxidase -

Back 13

shigella, salmonella (no color)

Front 14

glycine pentapeptide bridge

Back 14

gram +

Front 15

transpeptidase (PBP) links:

Back 15

NAMs

doesn't require ATP

Front 16

types of exotoxins

Back 16

1. A-B toxins (cholera, tetanus)
2. Membrane disrupting (hemolysins, alpha toxin)
3. Superantigens (TSS, SPE - strep pyrogenic exotoxin)

Front 17

A-B toxin mechanism

Back 17

cholera - Bs surround A, inject A into cell, upreg. of cAMP, efflux of ions out of channels, --> watery diarrhea

Front 18

LPS = TLR __

Back 18

TLR 4

and CD14 receptor on Mac

Front 19

structure of LPS

Back 19

complex lipid A

Front 20

R --> S strep requires DNA/RNA

Back 20

DNA

Front 21

catalase-negative, beta-hemolytic, bacitracin-sensitive

Back 21

strep pyogenes

Front 22

catalase-negative, alpha-hemolytic, optochin-sensitive

Back 22

strep pneumoniae

Front 23

catalase-positive, coagulase-negative, novobiocin-resistant

Back 23

staph saprophyticus

Front 24

catalase-positive, coagulase-negaive, novobiocin-sensitive

Back 24

staph epidermidis

Front 25

teichoic acid

Back 25

gram +

sepsis syndrome

Front 26

Tx strep pyogenes

Back 26

penicillin (exquisitely sensitive)

Front 27

most common non-supperative complication of strep pyogenes

Back 27

rheumatic fever

(glomerulonephritis is another sequelae -- tea-colored urine)

Front 28

broad based bud

Back 28

blastomyces dermatitidis

Front 29

function of strep pneumoniae that causes the infection

Back 29

cell wall

Front 30

hemolytic uremic syndrome

Back 30

invasive E. coli

Front 31

Shiga toxin interferes with

Back 31

protein synthesis

Shiga toxin can be in E. coli too

Front 32

hemolytic uremic syndrome frequently in

Back 32

children

Front 33

linezolid - static or cidal?

Back 33

static

Front 34

Tx: klebsiella, penicillin allergy

Back 34

Aztreonam

(can't give Vancomycin b/c it's gram negative)

Front 35

painless ulcer, spirochetes; monitor progress of treatment with

Back 35

RPR

Front 36

blue baby, cough, lymphocytosis

Back 36

pertussis

Front 37

after treating with cephalosporin, a new fever days later is most likely from

Back 37

enterococcus

Front 38

most common cause of traveler's diarrhea

Back 38

ETEC

(mechanism similar to cholera toxin)

Front 39

enteric pathogen that mobilizes actin

Back 39

salmonella

Front 40

enteric pathogen that only requires small inoculum

Back 40

shigella

Front 41

spores unique to

Back 41

Gram +

Front 42

anaplasmosis:
1. affects __ cells
2. transmission
3. histological finding

Back 42

neutrophils
Deer tick
morulae

Front 43

treat anaplasmosis with

Back 43

doxycycline

Front 44

fever, high pulse, high RR, normal BP, high white count...no infection identified

Back 44

Systemic Inflammatory Response Syndrome

Front 45

Tx for outpatient MRSA

Back 45

TMP-SMZ

Front 46

tetracycline resistance

Back 46

induction of multi-drug efflux pump
(--> resistance to multiple drugs)

Front 47

transformation

Back 47

lysis of donor (or it secretes DNA) --> free DNA (one segment of 1-2 genes) --> taken up by recipient with one of the strands degraded --> triple strand formation --> crossover followed by degradation of old --> some progeny will be transformant (copied crossover strand) and other non-transformant

*Griffiths-Avery experiment

*competence

*easiest method

Front 48

conjugation

Back 48

R-plasmid in donor (F+) transfers one of the strands to F- recipient through long pilus; each then replicates its strand; recipient is now F+

*usually gram negatives, esp. E. coli
*R factors = "resistance factors"
*tetracycline resistance happens very quickly in E. coli
*F stands for fertility plasmid
*efficient

Front 49

transduction

Back 49

bacteriophage infects host, cell lyses, bacteriophage injects into recipient -- the key is that phage is supposed to be picking up its viral genome that it had the bacterium replicate, but sometimes it accidentally envelopes a bacterial DNA fragment, which it injects into a recipient...that fragment is exchanged with some of the recipient DNA

*proven because DNAases had no effect
*filter prevented contact
*making pore too small for phage blocked transmission
*efficient because virus protects

Front 50

a lot of toxin genes are transmitted b/w organisms via

Back 50

transduction

Front 51

N. gonorrhea pilin variation transferred b/w organisms via

Back 51

transformation

Front 52

bacillus sereus toxin transferred b/w organisms via

Back 52

conjugation

Front 53

where is cholera

Back 53

Zimbabwe

Front 54

common source outbreak epidemic

Back 54

sharp curve, rapidly resolved (broad street pump)

Front 55

propogated epidemic

Back 55

flatter, longer curve; secondary cases; continues until enough of community develops immunity

Front 56

difference between colonization and infection

Back 56

invasion of tissue, stimulation of immune response

Front 57

Tx pseudomonas

Back 57

fluoroquinolones

Front 58

opportunist, osteomyelitis

Back 58

pseudomonas

Front 59

siderophores

Back 59

pigments, iron scaveging

Front 60

pyocyanin

Back 60

anti-oxidant, gives it's blue-green color

Front 61

TLR5

Back 61

flagella

in gut epithelium, TLR5 is basal (intracellular?), because you only want to recognize invasive organisms and not flora

in lung, TLR5 on surface of epithelium because there should never be bacteria there

Front 62

H. pylori virulence mechanism

Back 62

stops making flagella, eludes TLR5

Front 63

Pseudomans ExoU

Back 63

potent phospholipase that destroys tissue

important cause of ventilator-associated pneumonia

Front 64

bacteria coordinate community gene expression through small molecules like

Back 64

HSL (homoserine lactones)
Cyclic di GMP

Front 65

HSL found in

Back 65

Gram negative

secretion allows community coordination, e.g. biofilm in Pseudomonas (on all sorts of foreign materials in body), lung infections

Front 66

GpA strep soft tissue infections may require

Back 66

surgical debridement

s. pyogenes (general) may also benefit from prophylactic Abx, IV antibodies

Front 67

vancomycin does not work against

Back 67

gram negative

prevents cross-linking

Front 68

Rifampin works by

Back 68

inhibiting mRNA synthesis (binds RNA polymerase)

Front 69

Rifampin only used alone for

Back 69

Neisseria meningitidis (prophylaxis)

-ceftriaxone used to treat the infected individual

Front 70

metranidazole for

Back 70

anaerobes
parasites (giardia, gardenerella vaginalis, trichomonas vaginalis)

Front 71

daptomycin does not work against

Back 71

gram negative

(DOES do enterococci)

Front 72

polymixins mechanism

Back 72

bind to LPS on *gram negative*, then act like a detergent

Tx serious, resistant Gram negative

Front 73

prototypical broad spectrum Abx

Back 73

carbapenem

(no enterococci, though)

Front 74

turns urine orange

Back 74

rifampin

Front 75

do not drink alcohol on

Back 75

metronidazole

(-->disulfuram rxn: throbbing, headache, vomitting, flushing)

Front 76

fever, chills, sore throat, myalgias --> abdominal pains, diarrhea, disoriented, drowsy, hypotensive

Back 76

TSS

Front 77

scalded skin syndrome

Back 77

staph

exfoliatin toxins A and B - serine proteases

Front 78

alpha toxin

Back 78

cytotoxic to membranes, forms a pore, responsible for sepsis syndrome

made by staph (maybe others?)

Front 79

most staph aureus infections result from

Back 79

auto-inoculation

Front 80

what kind of toxin in staph food poisoning

Back 80

enterotoxin

heat stable, stimulates vagus nerve (increase peristalsis) and vomiting center

Front 81

staph oxygen classification

Back 81

facultative anaerobe

Front 82

Tx staph epidermidis

Back 82

vancomycin (s. epidermidis is highly resistant to antibiotics)

Front 83

Tx staph saprophyticus

Back 83

penicillin

Front 84

site of colonization - group B strep (S. agalactiae

Back 84

GU tract

--> neonatal infections involving meninges, blood, GU tract

Front 85

enterococci infect:

Back 85

urinary, biliary tract, cardiac valves

(colonize GI as commensal flora)

Front 86

strep pyogenes colonize:

Back 86

oropharynx, rectum

Front 87

s. pyogenes is ___ hemolytic

Back 87

beta (complete)

Front 88

viridans strep is ____ hemolytic

Back 88

alpha (incomplete)

Front 89

enterococci is ____ hemolytic

Back 89

gamma (none)

Front 90

oxygen requirement of streptococci

Back 90

facultative anaerobes

Front 91

enterococcus faecalis can grow in:

Back 91

salt and bile

Front 92

viridans strep can grow in:

Back 92

neither salt nor bile

Front 93

most important virulence determinant of Group A strep

Back 93

(1) M protein is antiphagocytic by inhibiting the *alternate pathway of complement system*

- 80 types (antigenic variation, different types can cause different symptoms; can vary geographically); without M protein, it's *avirulent*
-our antibodies are durable, but are type-specific

(2) also has a big capsule of hyaluronate

(3) pyrogenic exotoxins

-adhere using adhesin proteins F1 and lipoteichoic acid

Front 94

findings not suggestive of Group A strep

Back 94

cough, diarrhea, conjunctivitis

(more viral)

Front 95

Dx of s. pyogenes

Back 95

culture is gold standard

rapid strep antigen test is specific but not sensitive...if negative, confirm with culture

anti-streptolysin O reflects past infection

Front 96

Jones criteria

Back 96

carditis, polyarthritis, chorea, SC nodules, erythema marginatum

(rheumatic fever)

thought to result from cross-reactivity of M protein with myosin

Front 97

Strep TSS

Back 97

pyrogenic exotoxins A-C, superantigen, different from staph b/c of frequent presence of infection (esp. localized)

necrotizing fasciitis linked with specific M types and people who lack antibodies to those

Front 98

rusty-colored sputum

Back 98

s. pneumoniae

Front 99

gram stain of s. pneumoniae

Back 99

gram + lancet-shaped diplococci

Front 100

s. pneumoniae is ___ hemolytic

Back 100

alpha

Front 101

s. pneumoniae is naturally competent, meaning

Back 101

it can uptake naked DNA - virulence/resistance factors

90 different serotypes

Front 102

lipoteichoic acid containing phosphorylcholine C-polysaccharide is unique to

Back 102

s. pneumoniae

adhesins: choline-binding, pneumococcal surface adhesin A

Front 103

risk factors for s. pneumoniae

Back 103

complement deficiency, asplenia, smoking, HIV, COPD, antecedent resp. infection

Front 104

s. pneumoniae pathogenesis

Back 104

nasopharyngeal colonization = 2 phenotypes: opaque and transparent (latter can persist)

capsule is antiphagocytic

**infection follows from aspiration of nasopharyngeal secretions; pneumococci adhere to **type II alveolar cells** and initiate inflammatory response

**CELL WALL IS RESPONSIBLE FOR INFLAMMATORY RESPONSE** as is pneumolysin -- fluid accumulation, IL-1 etc

Front 105

red hepatization, gray hepatization

Back 105

s. pneumoniae

red hepatization - migration of PMNs, leakage of RBCs, TF expression, coagulation

gray hepatization - recruitmen of macrophages, fibrin deposition

Front 106

resolution of s. pneumoniae requires

Back 106

anti-capsular antibodies

Front 107

__ pneumonia is not necrotizing

Back 107

s. pneumoniae

gram - is necrotizing

Front 108

Tx: S. pneumoniae

Back 108

try penicillin, if resistant, then 3rd generation cephalosporin

either way, first 5 days are generally unresponsive -- vaccinate!

Front 109

s. pneumoniae vaccine

Back 109

prevnar - kids - heptavalent (covers 7 types) polysaccarhide protein conjugate, T cell dependent

pneumovax - was another that covered 23 types - used for adults

Front 110

s. pneumoniae can spread to

Back 110

meninges, middle ear, joints

Front 111

scarlet fever

Back 111

s. pyogenes

trunk, neck --> extremities...spares face

Front 112

causes of otitis media in children

Back 112

s. pneumoniae

(followed by hemophilus influenzae, then moraxella)

Front 113

risk factors for IE

Back 113

(1) antecedent valvular damage (rheumatic [old], MVP, degenerative)
(2) transient bacteremia
...plus hemodialysis, IV catheters, HIV

-turbulent blood flow leads to non-bacterial thrombus (platelets), or suture line of prosthetic valve, or normal valve in IDUs + transient bactermia --> adherence, more platelets

prosthetic valve, IDU (normal valves), nosocomial (bacteria in blood from catheters and prosthetics - hard to diagnose b/c maybe quiescent or maybe on Abx)

Front 114

causes of IE

Back 114

1. staph aureus (nosocomial)
2. viridans strep (dental procedure)
3. enterococcus (GI, GU procedures)
4. other staph
5. culture negative (Abx?)
6. strep bovis
7. gram negative (HACEK - oral flora)
8. fungus (candida nosocomial)
9. polymicrobial

mosty gram + disease, esp. staph

Front 115

cause of IE in early post-op period

cause of IE in late post-op period

Back 115

s. aureus

viridans strep

Front 116

in IE, blood cultures should be

Back 116

uniformly positive over time increasing

Front 117

Lumpy-Bumpy

Back 117

IE - glomerulonephritis with deposition of immune complexes + complement; Osler's nodes

Front 118

Immunologic manifestations of IE

Back 118

hyperIgG (rheumatoid factor), hypocomlementemia, immune complexes circulating

may also get sustained bacteremia, bland or septic embolizations

Front 119

bloody sputum

Back 119

infarcted lung tissue, possibly embolus from IE of IDU

may also have cavitating lesions

Front 120

Roth spots

Back 120

subacute IE (in eye)

Osler's nodes, Janeway lesions (macular), splinter hemorrhages

Front 121

subacute IE usually caused by

Back 121

viridans strep (1-2 months of malaise)

staph aureus usually acute

Front 122

Duke criteria

Back 122

Major: NEW murmur, positive culture, positive Echo

Minor: predisposition, fever, vascular phenomena, immunologic phenomena (osler, roth, rheumatoid factor, glomerulonephritis)

definite: 2 major, 1 major + 3 minor, 5 minor

possible: 1 major + 1 minor; 3 minor

Differential: rheumatic fever with carditis; collagen vascular disease, myxoma, left atrial thrombus, neoplasms

Front 123

Tx IE

Back 123

4-6 weeks of synergistic antibiotics (after multiple sets of blood cultures)

urgent for acute

Front 124

High risk (prophylaxis for dental procedures, NOT GI or GU procedures) and medium risk groups for IE

Back 124

High risk:
1. prosthetic valve
2. congenital heart disease
3. previous IE
4. heart transplant with valvulopathy

Moderate risk:
1. rheumatic valve (valvular dysfucntion)
2. MVP **with** regurg

Negligent risk:
1. rheumatic fever w/o dysfunction
2. MVP w/o regurg

Front 125

lower UTI

Back 125

cystitis
urethritis
prostatitis

dysuria, incr. frequency or urgency, hemorrhagic in 10%, bladder fullness, discomfort

Front 126

complicated UTI

Back 126

men, pregnant women, structural abnormalities, catheter, renal stones

cystitis of long duration, hemorrhagic cystitis

Front 127

uncomplicated UTI

Back 127

cystitis of short duration, no structural or neurological abnormalities

Front 128

upper UTI Sx

Back 128

fever with hypotension

vomiting, nausea, CVA tenderness
dysuria, freq., urgency, sweating, dehydration

vaginal discharge should necessitate pelvic exam (PID?)

Front 129

risk of renal abscess in UTI

Back 129

diabetics, urinary tract abnormalities

Front 130

urine dipstick tests

Back 130

leukocyte esterase

nitrate --> nitrite (not sensitive, but specific for certain bacteria that do this

Front 131

indications for urine culture

Back 131

pyelonephritis

pregnant women, children, men

structural abnormalities of urinary tract

treatment failure

Front 132

indications for imaging (CT, IVP, ultrasound)

Back 132

children (look for structure)
unresponsive bacteremic pyelonephritis
neurogenic bladder

men - do ultrasound and prostate exam

Front 133

complicated UTI pathogen

Back 133

e. coli
enterococcus
pseudomonas
s. epidermidis

Front 134

catheter-associated UTI pathogen

Back 134

1. candida
2. e. coli

Front 135

reasons men get UTIs

Back 135

insertive anal sex (age 16-35)
sex with female who has UTI
anatomical
uncircumcised
prostate hypertrophy (age 36-65)
obstruction
catheterization

*most common in older men b/c of urinary catheter

Front 136

reasons for bladder infection in women 36-65

Back 136

gyn. surgery, bladder prolapse

Front 137

routes for UTI pathogenesis

Back 137

hematogenous (staph in blood infects renal parenchyma --> pyelonephritis)

ascending route

Front 138

host factors predisposing for UTI

Back 138

renal stones
DM, transplant PT
neurogenic bladder
incomplete voiding
extrarenal obstruction

Front 139

97% of women with recurrent pyelonephritis have:

Back 139

P1 blood group (have galactose disaccharide on RBC surface that P fimbriae bind)

P fimbriae block phagocytosis; upregulation of P fimbriae is triggered by temperature, [glucose], [AAs]

Front 140

virulence factors in UTI

Back 140

fimbriae
flagella
hemolysin
aerobactin (siderophore)

Front 141

factors inhibiting adhesion in UTI

Back 141

bladder mucopolysaccharide
IgA

(also, high urea and low pH, micturition)

Front 142

complications of acute prostatitis from UTI

Back 142

epididymitis, prostatic abscess, chronic prostatitis (rate)
can also be bacteremia from vigorous prostate massage or spontaneous

Dx: tender prostate + UTI

Front 143

Tx: acute prostatitis

Back 143

broad spectrum gram negative until cultures come back

longer course of treatment

Front 144

Tx UTI

Back 144

3-day TMP-SMX

10-14 for complicated (maybe fluoroquinolones oral/IV)

even longer for prostatitis

Front 145

Treat which patients with asymptomatic bacteriuria

Back 145

pregnant women
neurological or structural abnormalities
**patients undergoing urological surgery

Front 146

Sepsis = __ + __

Back 146

infection + SIRS (systemic inflammatory response syndrome...2 criteria)

Front 147

SIRS criteria

Back 147

fever (>100.4 or <96.8)
HR >90
RR >20
WBC >12K

Front 148

Severe sepsis =

Back 148

sepsis + organ dysfunction (hypoperfusion)

Front 149

septic shock =

Back 149

severe sepsis + hypotension despite resuscitation

Front 150

organisms causing sepsis

Back 150

**most common are gram +

staph, strep, pseudomonas, neisseria meningitidis, mycobacterium, ricketssia, candida, histoplasma, aspergillus

could also be from toxin

Front 151

TLR2

Back 151

peptidoglycan - gram positive

Front 152

life-threatening sepsis linked to incr/decr protein C

Back 152

decreased

also increased coagulation, push toward inflammation

Front 153

TAF1 and PAI inhibit:

Back 153

fibrinolysis

(protein C inhibits these inhibitors)

Front 154

signs of early shock (BP, temp, pulse, skin, mental status, urine output, labs)

Back 154

slightly hypotensive
temp. can be in any direction
bounding pulse
warm dry skin
altered mental status
oliguria
alkalosis

Front 155

signs of late shock (BP, temp, pulse, skin, mental status, urine output, labs)

Back 155

severely hypotensive
temp in either direction
thready pulse
cold/clammy skin
AMS
anuria
acidosis

Front 156

epidemiology of sepsis

Back 156

20-50% mortality
mortality rate is less, but more total deaths, higher proportion stay in hospital
2nd leading cause of death in non-coronary ICUs
10th leading cause of death overall
more common in men and minorities

Front 157

therapies for sepsis

Back 157

works:
fluids
protein C

sepsis bundle: lactate, blood culture prior to abx, abx within 3 hours, pressor if MAP > 65

doesn't work:
steroids (unless stress)
insulin (unless high glucose)
vasopressin
controlling glucose tightly (made it worse)

Front 158

always STD test for

Back 158

syphilis and HIV

screen asymptomatic people with risk factors

Front 159

neisseria gonorrhea classification

Back 159

aerobic, non-motile, non-spore forming

gram negative diplococci kidney bean shaped

Front 160

n. gonorrhea biochem

Back 160

Thayer Martin medium
oxidase +
complex media
CO2 enriched atmosphere
ferments glucose

Front 161

n. gonorrhea ferments

Back 161

glucose only

Front 162

n. meningitidis ferments

Back 162

glucose and maltose

Front 163

gonorrhea transmitted by infected __ surfaces

Back 163

urethral, cervical, rectal, pharyngeal

culture urethral, cervical, pharyngeal, rectal specimen on Thayer-Martin media

**nucleic acid amplification test

Front 164

gonorrhea virulence and immune evasion:

Back 164

pilin (inhibits phagocytosis)
porin (resists degranulation, lysosome fusion, block complement)
OpA (cell-cell communication, tight binding)

antigenic variation (Opa, pilin), phase variation (Opa, pilin), IgA protease, LOS, transferrin binding proteins (compete with humans rather than make siderophores), eta lactamase

Front 165

Dx gonorrhea

Back 165

Gram stain specific and sensitive in symptomatic men

Front 166

gonorrhea incubation

sx in women

Back 166

2-5 days

like UTI + vaginal discharge, vag. bleeding

Front 167

other manifestations of gonorrhea

Back 167

epididymitis, prostatitis, Bartholin glands abscess, pharyngeal infection (kinda like strep), proctitis

Front 168

disseminated gonorrhea

Back 168

1-3% of patients, associated with female sex and menstruation, complement deficiency

Sx: fever, skin lesions, tenosynovitis, migratory polyarthralgias, oligoarthritis

Front 169

Tx gonorrhea

Back 169

3rd generation cephalosporins (single injection) + presumptive Tx for chlamydia (1 day azithromycin or 7 day tetracycline)

for PID, cover GC, chlamydia, GNRs, anaerobes, and strep -- treat longer

Front 170

chlamydia serovar A-C

Back 170

conjunctivitis, could lead to blindness

Front 171

chlamydia more common in M/F

Back 171

females

3-5% outpatient clinic (asymptomatic)
15-20% STD clinic (asymptomatic usually)

25% of men asymptomatic
80% of women with cervicitis have normal cervical exam

Front 172

chlamydia incubation period

Back 172

7-21 days

Front 173

other manifestations of chlamydia

Back 173

epididymitis, prostatitis, PID, proctitis, Reiter's

urethritis in women (not mentioned for gonorrhea), Bartholinitis, LGV

most common cause of NGU in men (non-gonococcal urethritis)

Front 174

Reiter's

Back 174

conjunctivitis, arthritis, urethritis -- sometimes ulcerative lesions on skin

men with chlamydia

Front 175

Dx chlamydia

Back 175

Nucleic acid amplification test
-urethral/cervical samples, urine, vaginal swabs

cultures not routinely done unless sexual abuse suspected

serology for LGV

Front 176

cervical motion tenderness

Back 176

PID

also discharge, burning sensation, abdominal tenderness, cervical discharge

Front 177

LGV sx

Back 177

primary - painless genital lesion
secondary - adenopathy (buboes), fever, headache, myalgias
late (months to years) - chronic hard inguinal masses, lymphatic obstruction, urethral strictures

Front 178

Tx LGV

Back 178

tetracycline or erythromycin 21 days

Front 179

Herpes stages

Back 179

primary (21 days if untreated...2 days lesions come, shedding and sx stop after 2 weeks) - cervicitis, balanitis, urethritis, fever, malaise, itching, discharge, dysuria

recurrence - 70% (milder, shorter, unilateral)

Front 180

Tzanck preparation

Back 180

unreliable herpes thing

Front 181

Dx herpes

Back 181

viral culture - better earlier
in situ, PCR
serology

Front 182

Haemophilus ducreyi classification

Back 182

gram neg. coccobacilli

ragged edges, painful
usually single lesion

**buboes, chancroid ulcer and lymphadenitis

Africa

Front 183

Dx chancroid

Back 183

culture or visualization on an aspirate

Front 184

Tx chancroid

Back 184

macrolide, cephalosporin, or quinolone

Front 185

calymmatobacterium granulomatis

Back 185

granuloma inguinale - Donovan bodies (dark stain in smear)

painless, no regional lymphadenopathy

gram negative bacilli

Papua New Guinea, India, Africa, S. America

Front 186

Tx calymmatobacterium granulomatis

Back 186

doxycycline 21 days

or macrolide/quinolone/TMP-SMZ

Front 187

yaw

Back 187

treponema pertenue

Front 188

highest incidence of syphilis

Back 188

MSM, black, HIV+

25% of people co-infected with HIV (syphilis increases risk)

Front 189

time course of primary syphilis

Back 189

21 day median incubation

clean-based ulcer heals in 3-6 weeks, but spirochete disseminates

Front 190

secondary syphilis

Back 190

chancre resolved
*rash - palms and soles
condyloma lata
mucous patches
alopecia
eye thing

T cells response
dendritic cells express the CCR5 receptor for HIV (HIV likes to infect them)
antibodies detectable

Front 191

tertiary syphilis

Back 191

gummatous (pox)
cardio
CNS

Front 192

Dx syphilis

Back 192

darkfield specific but not sensitive
fluorescence not used b/c expensive
gold standard is inoculation of rabbits, but not routinely done

(1) nontreponemal - very sensitive but not specific
1. RPR
2. VDRL (CSF - specific, not sensitive)
3. Ab to cardiolipin (titer)

(2) treponemal
1. FTA-ABS (positive or negative)
2. MHA (microhemaglutination)

Front 193

Tx for syphilis

Back 193

early syphilis - 1 IM penicillin

late syphilis - 3x IM penicillin (one per week for 3 weeks)

if allergy, try to desensitive, or else try doxy, macrolide, ceftriaxone

Front 194

Jarisch-Herxheimer rxn

Back 194

treatment of syphilis - first 24 hours -- usually patients in early syphilis;

fever, headache, myalgias - give antipyretics

Front 195

response to syphilis Tx should look like

Back 195

at least 4x decrease in 6 months, 8x decrease by 12 months

maybe 4x decrease by 12 months if early latent

if not, suspect HIV

Front 196

examine CSF for neurosyphilis if:

Back 196

HIV with late syphilis or syphilis of unknown duration
ophthalmic signs
treatment failure
evidence of active late syphilis

do titer of that, and cell count

Front 197

stages of neurosyphilis

Back 197

early: asymptomatic meningitis
early symptomatic (weeks to years): ocular, stroke, symptomatic meningitis
late symptomatic (years to decades): dementia, personality change, tabes dorsalis (locomotor ataxia)

Front 198

tabes dorsalis

Back 198

neurosyphilis

ataxia, lancinating pain
Argyll-Robertson pupil
-contracts not to light but accomodation
-dilates to painful stimuli

Front 199

Tx syphilis

Back 199

IV penicillin 2 weeks
LP 3-6 months after tx, then every 6 months after that
VDRL should be non-reactive after 2 years
failure to respond - re-treat

Front 200

pregnancy and syphilis

Back 200

routinely screen pregnant women -- when present, can lead to perinatal daeth 40% of time (also low birth weight, congenital abnormalities, prematurity, active syphilis in neonate)

Front 201

pathogens for neonatal meningitis

prevention?

Back 201

GpB strep agalactiae
Listeria monocytogenes (gram + rod)
enterococci
e. coli K1 specifically
salmonella

(fecal flora or GU flora - birth - baby aspirates)

early onset - sepsis - pneumonia
late onset - sepsis - meningitis

identify colonized mothers (80% are screened), give *ampicillin*
-also preterm and multiple births are at risk

Front 202

Tx for GbS

Back 202

baby has poor host defense, bacteria replicates - treat for 3 weeks or it tends to relapse

Front 203

Listeria monocytogenes

Back 203

gram + rod, motile
unpasteurized cheese, unwashed produce

flu-like illness in mom...not that rare

Front 204

s. pneumoniae virulence factors in meningitis

Back 204

pneumolysin - stimulates neuronal apoptosis
release of NO - tissue damage
platelet activating factor (clotting, lack of perfusion)
acidosis
elastase
reactive oxygen species
cell wall fragments --> inflammation (meningitis)
sialidase - acts as an adhesin

Front 205

pathophys of meningitis

Back 205

inflammation, edema opens up BBB --> CSF protein (loss of tight junctions)

increase ICP --> loss of perfusion, maybe stroke-like picture

derangement of BBB --> hypoglycemia

SIADH - syndrome of inappropriate ADH secretion

Front 206

principles of meningitis treatment

Back 206

steroids (especially in S. pneumoniae)
-->
Abx (has to cross BBB)

manage ICP
manage septic shock
prophylax in school

Front 207

worst meningitis prognosis

Back 207

s. pneumoniae (sooo much inflammation)

high incidence in South

Front 208

treatment for S. pneumoniae meningitis

Back 208

penicillin in 20x MIC

prevent with vaccine

Front 209

epidemiology of H. influenzae B meningitis

Back 209

gone in vaccinated kids (universally vaccinated...pretty much eradicated) - capsule allows efficient phagocytosis

sporadic cases in adults who lack the Ab

Front 210

pathogenicity/virulence of n. meningitidis

Back 210

colonizes nasopharynx, taken up by epithelial cells - receptor-mediated endocytosis (LPS)

**encapsulated**, binds factor H, inhibits lysis

carriage in population - disease in those who lack the antibody

fulminant SEPSIS

Front 211

susceptibility to neisseria meningitidis

Back 211

complement deficiency

Front 212

n. meningitidis B not covered by vaccine because

Back 212

sialic acid epitopes look like self...responsible for sporadic cases

Front 213

normally have n. meningitidis immunity by:

Back 213

cross-reactive carbs (n. lactamica

Front 214

n. meningitidis prophylaxis

new vaccine

Back 214

rifampin, cipro, ceftriaxone

menactra - same + travelers + complement deficiency + HIV+ adults

Front 215

outcome of meningitis survivors

Back 215

1/3 have real cognitive deficits, doesn't matter if they took steroids

hearing loss #1
epilepsy
hydrocephalus
ADD

Front 216

if not bacterial meningitis, what test can you do?

Back 216

india ink - cryptococcus
antibody - western blot
viral culture
PCR
mycobacterium

Front 217

imaging in meningitis

Back 217

CT - ICP, infarct, ventricle size

MRI - diagnostic, followup

Front 218

lower respiratory tract

Back 218

bronchi, lungs

Front 219

#1 cause of pneumonia

Back 219

s. pneumoniae

(in kids, viral is important)
(gram negatives important in alcoholics, immuno-compromised)

Front 220

how do you get pneumonia

Back 220

microaspiration
hematogenous spread (esp. pneumococci)
contiguous spread (i.e. from lymphnode, not so common)
macroaspiration (alcoholic, babies)

Front 221

risk factors for pneumonia

Back 221

smoking, alcoholism, toxic inhalations, travel, asthma

CF, COPD, kartagener's

chemotherapy, HIV, malnutrition, transplant

Front 222

Typical pneumonia features and pathogens

Back 222

rapid onset of fever, cough

s. pneumoniae, h. influenzae, staph aureus, GAS, moraxella

Front 223

atypical pneumonia features and pathogens

Back 223

weeks to months percolating along

legionella, mycoplasma, chlamydia pneumonia, c. psittaci

Front 224

typical organisms for birth-3 wks. pneumonia

Back 224

GpB strep, Listeria monocytogenes, cytomegalovirus, HSV

Front 225

pneumonia in 3 wks.-3 mos.

Back 225

chlamydia, RSV, PIV

s. pneumoniae, pertussis, staph aureus

Front 226

pneumonia in 3 mo. - 5 yrs

Back 226

VIRUSES!

RSV, PIV, adenovirus, rhinovirus

strep pneumoniae, hemophilus, mycobacterium, mycoplasma

Front 227

pneumonia in 5-15 yrs

Back 227

atypicals

mycoplasma, chlamydia, TB, s. pneumoniae

Front 228

pathogens for inpatient ICU

Back 228

s. pneumoniae (but that one is in all categories)

staph aureus is becoming a pneumonia problem

(the atypicals are usually outpatient)

Front 229

Sx of pneumoniae

Back 229

dyspnea, fever, cough, chills, chest pain, myalgia, headache

Front 230

multilobar, abscesses on CXR

Back 230

s. aureus

Front 231

diffuse interstitial CXR

Back 231

mycoplasma

Front 232

virulence factors for s. pneumoniae

Back 232

phosphorylcholine - adherence, PAF
IgA protease
capsule
pneumolysin
adhesins
lipoteichoic acid initiates complement pathway, NO (tissue damage) -- it's hosts inflammatory response that causes problem

Front 233

Dx s. pneumoniae

Back 233

blood culture (6-10% CAP are bacteremic)
urine antigen test
sputum culture

*susceptibility test is key! 60% are penicillin resistant

Front 234

Tx s. pneumoniae

Back 234

beta lactam

cephalosporins, vancomycin, macrolides, linezolid

Front 235

typical presentation of mycoplasma

complications

Back 235

college student, studying, mild respiratory symptoms

"walking pneumonia"
**lacks seasonal pattern**

complications:otitis media, erythema multiforme, hemolytic anemia, myocarditis, pericarditis, neuro

**so if you see pneumonia with weird manifestations, think mycoplasma**

Front 236

features of mycoplasma
and Dx

Back 236

NO cell wall

membrane has sterols
remains extracellular
TLR2 important for binding to epithelium
P1 attachment to sialic acid receptors of resp. epithelium
causes destruction of cilia --> mechanical irritation, persistent cough
**acts as superantigen** for PMNs and macs to release cytokines

**cultures rarely done**
IgG serology instead
bedside tests - cold agglutinin

Front 237

Tx mycoplasma

Back 237

macrolides or fluoroquinolones

Front 238

erythema multiforme

Back 238

mycoplasma

Front 239

types of chlamydial pneumonia

infect how

Back 239

trachomatis, psittaci, pneumoniae

non-ciliated columnar cells; multiply in macrophages

Front 240

Dx chlamydial pneumonia

Back 240

serology -
treat empirically in meantime

Front 241

chlamydia trachomatis pneumonia
presentation:
findings:
Tx:

Back 241

1-3 mo. old infant, staccato cough, rapid RR, NO FEVER
-CXR shows diffuse infiltrates (hilar)
-Tx: erythromycin

*c. pneumoniae is similar but in school age children or elderly

both outpatient usually

Front 242

c. psittaci presentation

Back 242

pneumonia, fever, rash, **neurological** (nerve palsy, seizures, hepatitis, pericarditis)

hazy CXR

outpatient usually

Tx: tetracycline, erythromycin

Front 243

legionella pneumonia epi features

gram?

Back 243

usually serious, requiring hospitalization - multilobar
only 2-6% of CAPs though

immunocompromised, hospitalized

legionella penumophila (1, 4, 6) and micdadei

gram negative bacilli - fastidious (special media)

Front 244

legionella pathogenesis

Back 244

pili and flagella, IC multiplication, evade phago-lysosome fusion

hemolysin, a lot of proteases, ribonucleases --> microabscesses

**T-cell mediated immunity, which is why you see it in immunocompromised or people on steroids

Front 245

legionella presentation

Back 245

incubates 10 days
starts as flu-like, super high fever (105), rigors, cough

CNS (confused plumber), diarrhea, nausea manifestions

high white count, abnormal liver

high mortality 15-20% - ICU

Front 246

Legionella Dx, Tx, prevention

Back 246

culture on special media
urine antigen (only tests one strain)
serology, but takes a while
thus treat empirically

Tx: Macrolide or levofloxacin

prevention: hyperchlorination, superheating, copper-silver ionization

Front 247

presentation for pertussis

Back 247

whooping cough, clear lung exam, leukocytosis with **lymphocytes** unlike with pneumococcus

can also cause encephalopathy

Front 248

three stages of pertussis

Back 248

catarrhal (lot of organisms)
paroxysmal (coughing and coughing)
convalescent (still coughing, but organisms down)

Front 249

Gram of bordatella

types

spread

bacteremia?

Back 249

gram negative coccobacilli

pertussis, parapertussis, bronchiseptica

respiratory droplets

NO bacteremia, unlike pneumococcal

Front 250

pertussis toxins

Back 250

toxins cause **local tissue damage** in respiratory epithelium

pertussis toxin - A/B subunit, works through G-protein to increase cAMP and cause respiratory secretions, sloughing (paroxysmal)

adenylyl cyclase toxin and hemolysin - inhibits WBC chemotaxis, phagocytosis

heat-labile toxin - local tissue destruction

tracheal cytotoxin - destroys ciliated cells, NO kills epithelial cells

Front 251

Bordet-Gengou media

Back 251

pertussis

(blood, charcoal, starch)

Front 252

Dx pertussis

Back 252

special media - Bordet-Genou
nasopharyngeal culture

serology testing is kinda iffy in kids who got the vaccine

PCR testing is becoming standard of care

Front 253

Tx pertussis

Back 253

decrease symptoms and transmission - better if early

macrolide (TMP-SMX is alternative)

give abx prophylaxis to those close by

Front 254

empiric therapy for pneumonia

Back 254

beta-lactam + macrolide

Front 255

Tx for vector-borne

Back 255

doxycycline

(kids with lyme, give amoxicillin)
IV ceftriaxone for the secondary pathology of Lyme

Front 256

RMSF

1. organism
2. vector
3. geography
4. timeline
5. gram stain
6. virulence
7. the bite
8. seasonal
9. who?
10. cause of lethality
11. lab values
12. risk of severe disease
13. Dx

Back 256

1. rickettsia ricketsii
2. hard tick (ixodidae) - dog tick or wood tick
3. southeast, carolinas
4. 5 days - fever, chills, headache, myalgias
10 days - palms/soles petechial rash --> centripetal
5. gram negative bacilli (doesn't stain well)
6. small peptidoglycan, weak LPS
7. most see the tick but don't feel the bite...needs to feed for hours
8. spring and summer
9. kids playing with dogs
10. microvascular injury (incr. vasc. permeability) --> multiorgan failure (CNS, renal, hepatic, pulmonary, gangrene --> amputation)

OmpA/B, phospholipase mediate adherence; escapes phagosome (phospholipase lyse the phagosome membrane), replication in cytosol by binary fission
11. hyponatremia, thrombocytopenia, elevated liver enzymes
12. older, male, black, alcoholism, G6PD deficiency
13. clinical suspicion -- important b/c the IHC on a skin biopsy takes time, also with PCR or IFA serology -- deadly if not treated!!!

Front 257

activates host cell actin, pushing it to surface--> extracellular release, cell-cell spread

damages cell membranes with free radicals, proteases, phospholipases

Back 257

R. ricketsii

Front 258

Rickettsial pox
1. where
2. pathogen
3. vector
4. clinical presentation
5. if not treated
6. Dx

Back 258

1. poor housing, NYC
2. rickettsia akari
3. mite (reservoir: mouse)
4. black eschar (resembles anthrax); 10 days - flu-like sx, diffuse rash resembling chicken pox
5. will resolve on own
6. clinical, or IHC

Front 259

Epidemic typhus
1. association
2. pathogen
3. vector
4. inoculation
5. time course
6. pathogenesis
7. main targets
8. mortality

Back 259

1. crowding, war
2. rickettsia prowazekii
3. body louse (reservoir: humans)
4. after louse bite, you scratch its feces into the bite site
5. 7 days after bite, fever, myalgias, headache, cough, delirium (typhos means HAZY)...centrifugal RASH that spares palms, soles, face
6. lyses cells
7. brain and lung
8. 5-40% depending on how well host is

Front 260

Brill-Zinsser disease

Back 260

reactivation of typhus (less severe); holocaust survivors

Front 261

human granulocytic anaplasmosis HGA (type of ehrlichiosis)
1. pathogen
2. typical patient
3. geography
4. feature
5. gram
6. labs
7. Sx
8. when?
9. vector
10. mortality
11. pathogenesis (no LPS or peptidoglycan)
12. Dx

Back 261

1. anaplasma phagocytophilium
2. gardener/golfer
3. NE, mid-atlantic, upper midwest, pacific NW
4. morulae (live and multiple in phagosome) -- in NEUTROPHILS
5. gram negative coccoid, obligate intracellular
6. leukopenia, thrombocytopenia, elevated liver enzymes
7. can be asymptomatic OR fever, headache, myalgias, arthralgias, malaise, nausea - like rickettsial minus rash
8. spring, summer
9. hard ticks (black-legged/deer tick - east, WESTERN black-legged tick) - reservoir is small mammals like mice
10. up to 3% - can also lead to opportunistic infections because it affects granulocytes
11. prevents lysosome fusion (no LPS or peptidoglycan); disrupts leukocytes' function; AnkA
12. clinical suspicion, PCR acutely, serology is more accurate...looking for morulae is low-yield

Front 262

Human monocytic ehrlichiosis (HME)
1. pathogen
2. geography
3. feature
4. vector/reservoir
5. mortality
6. Sx
7. pathogenesis

Back 262

1. ehrlichia chaffeensis
2. south, southeast; golf-communities with wildlife
3. morulae (monocytes)
4. lone star tick (white-tailed deer reservoir)
5. up to 3% of cases
6. like rickettsial minus rash OR can be asymptomatic
7. prevents lysosome fusion

Front 263

Lyme disease
1. pathogen
2. epidemiology
3. geography
4. transmission
5. reservoir
6. when?
7. Sx progression
8. pathogenesis
9. Dx

Back 263

1. Borrelia burgdorferi (gram neg spirochete)
2. most common vector-borne illness
3. primarily NE
4. tick feeding 24+ hours (i. scapularis tick which is very very small unlike others)
5. small mammal (mouse) for nymph which infects...the adults which don't infect are on deer...can get co-infected with HGA and Lyme)
6. summer almost exclusively
7. early: erythema migrans, possible fever, flu-symptoms
early neuro disease: CN palsy, meningitis, radiculopathy
cardiac disease: heart block
late disease: CNS, arthritis (esp. knee), PNS
8. OspC variant determines dissemination; hematogenous spread facilitated by OspA (binds plasminogen)
DpbA/B bind to decorin on collagen in ECM of joints, heart, CNS
other surface proteins bind fibronectin
9. clinical if erythema migrans; if not, antibodies or CSF

Front 264

post-lyme disease syndrome

Back 264

chronic symptoms after treatment

don't recommend more tx

Front 265

common causes of bacterial diarrhea

Back 265

1. campylobacter
2. salmonella
3. shigella

Front 266

diarrhea that can be person to person b/c of small inoculum

Back 266

shigella
salmonella TYPHI
EHEC
campylobacter jejuni

Front 267

types of toxins in diarrhea, who has them

Back 267

1. enterotoxin - leads to watery diarrhea via efflux from cell (cholera, ETEC, perfringes)
2. cytotoxin - inflammatory diarrhea (shiga toxin: EHEC, shigella)
3. neurotoxin - CNS or PNS, increases peristalsis, causes vomiting (s. aureus, bacillus cereus)
-the staph neurotoxin does both
-bacillus has 2 neurotoxins: emetic (1-6 hours), diarrheal (10-12 hours)

Front 268

shiga toxin mechanism

Back 268

B binds to host cell, transfer of A

A disrupts binding of tRNA to 60S ribosome --> destruction of intestinal cells, decreased absorption from gut

Front 269

Diarrheal tissue invasion associated with

Back 269

salmonella pathogenicity islands - invade gut via M cells by injecting secreted invasion protein --> phagocytosis and ruffling
--replicates in phagosome (tolerant to acids), spreads to adjacent epithelial cells and lymphoid tissue

Front 270

location of 1. watery diarrhea
2. dysentery (cytotoxin)
3. enteric fever (systemic infection)

Back 270

1. proximal small bowel
2. colon or distal small bowel
3. distal small bowel

Front 271

pathogens of dysentery

Back 271

shigella
campylobacter
EIEC
EHEC
C. diff
salmonella NON-TYPHOIDAL

Front 272

pathogens of watery diarrhea

Back 272

cholera
ETEC
c. perfringes
bacillus cereus
s. aureus

Front 273

pathogens of enteric fever

Back 273

salmonella typhi
yersinia enterocolitica

Front 274

Tx cholera

Back 274

doxycycline, rehydration

(75% asx, symptoms last 3 days...no tenesmus, strain, or abdominal pain or fever)

Front 275

daycare

vomiting, diarrhea, fever, lethargy, tachycardia, tachypnea, mild dehydration

Back 275

shigella

Front 276

shigella dysenteriae 1 produces:
transmission:
member of:
Sx timeline:
course in body:
secondary manifestations:

Back 276

shiga toxin
person-to-person (easily)
enterobacteriaceae (gram neg. rod)
first few days: cramping, watery diarrhea, fever
later: tenesmus, dysentery
lasts 7 days, shedding for 1-4 weeks
moves through mucosa only...from small to large bowel
HUS (hemolytic uremic syndrome) - hemolytic anemia with fragmented RBCs, acute renal injury, thrombocytopenia

Front 277

HUS associated with

Back 277

shigella dysenteriae
EHEC (HUC in kids, hemorrhagic colitis)
STEC (HUC in kids, hemorrhagic colitis)

Front 278

e coli resembling shigella dysentery

Back 278

EIEC

Front 279

children's diarrhea (e. coli)

Back 279

EPEC (nursery)
EAEC (also traveler's diarrhea)

Front 280

traveler's diarrhea

Back 280

ETEC
(or EAEC)

Front 281

e. coli in cattle and spinach

Back 281

EHEC (hemorrhagic colitis)

Front 282

salmon pink rash, splenomegaly, fever

Back 282

salmonella typhi

fever begins 5-21 days after ingestion; persists 4-8 weeks if untreated
-death in 1-30%, intestinal perforation, abscesses, endocarditis

Front 283

salmonella serotypes

Back 283

2500

s. typhi and s. paratyphi are strictly human pathogens

non-typhoidal colonizes nearly all animals, so causes infection through contaminated food

Front 284

features of non-typhoidal salmonella

Back 284

(1) gastroenteritis
nausea/vomiting/diarrhea 6-48 hours post
fever, cramping
self-limited in 3-7 days

(2) bacteremia
occurs more rapidly than typhoid
lacks rose spots
often in AIDS patients

(3) tissue invasion/localized infection
cholecystitis, osteomyelitis, septic arthritis

Front 285

Dx diarrhea

Back 285

fecal leukocytes
bacterial culture
toxin
ova and parasites

Front 286

shiga-like toxin

Back 286

EHEC

Front 287

Tx diarrhea

Back 287

many bugs are self-limiting, so rehydration will go a long way

Abx for: ETEC, shigella, campylobacter, salmonella
-doxycycline for cholera

AVOID Abx for EHEC b/c it might elaborate more shiga-like toxin

Front 288

peptostreptococcus

Back 288

gram + in skin

Front 289

synthesizes vitamin K, deconjugates bil acids

Back 289

bacteroides fragilis

Front 290

because anaerobes are less virulent...

Back 290

infections are generally polymicrobial

*usually endogenous flora

Front 291

anaerobe that forms spores

Back 291

clostridium

Front 292

anaerobe with capsule

Back 292

B. fragilis

Front 293

veillonella

Back 293

gram negative cocci

Front 294

normal oral flora; isolated in human bites

Back 294

veillonella

Front 295

peptostreptococcus seen in these infections

Back 295

bone and joint, esp. prosthetic (p. magnus)

female genital tract, intra-abdominal infections

Front 296

proprionibacterium

Back 296

acne, opportunistic infections of prosthetic devices

colonizes skin, oropharynx, GU tract

gram + rod

Front 297

actinomyces transmission

Back 297

only endogenous, no person-person

Front 298

Tx actinomyces

Back 298

prolonged penicillin and debridement

Front 299

infections from lactobacillus

Back 299

bacteremia

endocarditis

Front 300

c. perfringens features

Tx

Back 300

gas gangrene (myonecrosis) - could happen during surgery
-cellulitis, fasciitis
alpha-toxin destroys membranes
food poisoning 8-24 hours after ingesting meat; self-limited

Tx penicillin + clindamycin
debridement, hyperbaric chamber

Front 301

clostridium perfringens found in

Back 301

soil and water contaminated with feces
GI tract of humans and animals

Type A - most human infections

Front 302

pathogenesis of c. perfringens

Back 302

alpha toxin --> lyses erythrocytes and endothelial cells --> vascular permeability and hemolysis

beta toxin --> necrosis

enterotoxin --> membrane permeability of sm. intestine

Front 303

Tx C. diff

Back 303

metronidazole

relapse in 20-30%

Front 304

C. diff toxins

Sx

Back 304

enterotoxin (A) - hemorrhagic necrosis
cytotoxin (B)

mild or bloody diarrhea

only 5% of us are colonized with C. dfif in GI tract

Front 305

Types of tetanus

Back 305

1. generalized (lock jaw, hyperthermia, sweating, risus sardonicus, opisthotonos)
2. cephalic (cranial nerves)
3. localized (to site of injury)
4. neonatal (infected umbilical stump)

Front 306

Tx tetanus

Back 306

tetanus Ig
metronidazole or penicillin
debridement

Front 307

floppy baby

Back 307

c. botulinum

listless, sluggish pupils, no reflexes, poor oral intake

Front 308

clostridium botulinum found

Back 308

soil and water; homemade preserves (food-borne), syrups or honey (infant) with botulinum spores; also dust

symptoms in 2 days

wound botulism (skin popping)

asymptomatic adult carriage

toxin A,B,E, and F = human disease

Front 309

Tx c. botulinum

Back 309

metronidazole or penicillin
supportive care
botulinum Ig, or equine Ig

Front 310

Dx c. botulinum

Back 310

symmetric cranial nerve palsies (4 Ds)
symmetric flaccid paralysis
mentation intact

toxin or organism in stool or serum (mouse bioassay)

electromyography

Front 311

most common intestinal bacterium

80% of peritonitis, intra-abdominal abscesses

Back 311

bacteroides (also in vagina)

Front 312

clinical disease of gram negative anaerobic bacilli

Back 312

*periodontal
*chronic sinus infections
brain abscess
intra-abdominal
gynecological
*diabetic and decubitus ulcers

Front 313

pathogenesis of bacteroides

Back 313

capsule polysaccharide (adhesion, abscess formation, phago. evasion)
superoxide dismutase
synergy with aerobes
**(LPS not a major virulence factor)**

the abscess part is highly associated with anaerobes

Front 314

superficial fungal infections

Back 314

dermatophytes (not dangerous) - keratinase; cause inflammation below

Dermatophytes:
tinea corporis - ring worm
tinea pedis - tinea pedis
tinea unguum - ring worm of nails
tinea capitis - ring worm of scalp
tinea cruris - jock itch

malassezia furfur:
tinea versicolor
(lipiphilic; fungemia with lipid infusion)

Front 315

Subcutaneous fungal infections (dimorph)

Back 315

--sporotrichosis (sporothrix schenkii) - foreign body (splinter/thorn/nail) --> local, can spread to adj bones and joints **e.g. mycetoma of feet**; spread via lymphatics -- inoculated into SC tissue -- **dimorphic** pyogenic granulomatous rxn **ulcerating nodules along hard cord**

Front 316

True pathogens - dimorphs - systemic

Back 316

histoplasma capsulatum
coccidioides immitis
blastomyces dermatiditis

Front 317

Histo:
1. geography
2. niche
3. dissemination
4. patho
5. cavitation?

Back 317

1. ohio, mississippi valleys, carribean
2. guano, chicken coops
3. hematogenous, via macrophages
4. mold transforms into yeast in lung
5. can cavitate, can reactivate

Front 318

spherules

Back 318

coccidioides immitis

Front 319

coccidioides immitis
1. geography
2. morphology
3. clinical

Back 319

1. SW, Mexico, Central/South america
2. spores transform into spherules (pomegranate-like) in lung
3. acute self-limited flu-like (valley fever)
acute or chronic lung disease
dissemination (black, pregnant, immunocompromised)
---localizing in skin, bone, CNS

Front 320

blastomyces dermatiditis
1. habitat
2. patho
3. test
4. clinical

Back 320

1. midatlantic (general east of mississippi), peanut farms, beaver dams, organic debris rather than soil
2. transforms into yeast in lung
3. unlike others, no good skin reactivty test (no good antigen marker)
4. cavitary; disseminates to skin, bone, urinary tract in men (prostatitis, cystitis, osteomyelitis)
**can resemble skin cancer...likes to move out to cooler temperatures

Front 321

cryptococcus neoformans
1. patho
2. source
3. clinical
4. test

Back 321

1. thick gooey capsule causes problems; inhalation of yeast leads to transient colonization OR acute/chronic lung disease OR CNS invasion
2. pigeon droppings, eucalyptus trees
3. pneumonia, meningoencephalitis, fever, headache, stiff neck, hydrocephalus
4. serum or CSF antigen assay diagnostic in >95% of cases...good antigen b/c of big capsule!

Front 322

opportunist fungi

Back 322

1. cryptococcus - YEAST
2. candida albicans - YEAST
3. aspergillus fumigatus - MOLD
4. mucorales genera, rhizopus, mucor - MOLD

Front 323

candida albicans
1. source
2. patho
3. morphology
4. test
5. Tx
6. case

Back 323

1. normal flora mouth, GI, GU
2. colonized areas: change in environment (wet skin, antibiotics, birth control, catheter), leads to overgrowth
non-colonized areas: change in immunity (immaturity, HIV) leads to invasion
3. yeast with pseudo-hyphae - protects against phagocytosis
4. only yeast that can take up gram stain
5. take away the thing that's causing it
6. dishwasher, diaper rash

Front 324

pathogenesis of invasive candida

Back 324

1. elimination of normal flora
2. breach in anatomic integrity (often biofilm on catheter)
3. defective PMN function

**has a lot of -ases; can adhere to plastic

**usually in critically ill patients with multiple risks (hospitalized, neutropenic, on antibiotics, many catheters)

**fever, leukocytosis, organ dysfunction

**microabscesses in heart, lung, kidney, liver, skin, eye

**candida endocarditis

Front 325

aspergillus fumigatus
1. source
2. clinical

Back 325

1. inhalation of spores - mold without a yeast phase
2. a. can elicit allergy (allergic bronchopulmonary aspergillosis...resembles asthma)
b. grow in pre-existing cavity (aspergilloma)
c. invade vasculature - disseminate with local and distant disease (in very sick) (invasive aspergillosis with pneumonia)

**neutrophils prime defenders

**it loves blood vessels, so you can get pulmonary, brain, renal infarcts

Front 326

Dx aspergillosis

Back 326

biopsy needed

Front 327

Mucormycosis
1. source
2. susceptibility
3. clinical
4. mortality

Back 327

1. everywhere - literally - carpet, chair, etc
2. it loves sugar and acidic solutions, so diabetics, metabolic acidosis, iron overload, PMN dysfunction --> fulminant like a mac truck
3. pneumonia progressing to infarct; sinusitis progressing to brain infarct
4. 50% with meds (importance of host defenses)

Front 328

most acute and fulminant fungal infection

Back 328

mucor

Front 329

mold/yeast?

dermatophytes
furfur

Back 329

dermatophytes - mold
furfur - yeast

Front 330

fungal infections that rely more heavily on PMNs vs lymphocytes

Back 330

lymphocytes: dimorphs, crypto, candida

PMNs: candida, aspergillus, mucor

Front 331

classes of anti-fungals

cidal or static?

Back 331

1. polyenes (membrane synthesis) - cidal
2. azoles (membrane synthesis) - static
3. echinocandins (wall synthesis) - cidal

Front 332

amphotericin B

Back 332

polyene - lipiphilic, hydrophobic, hydrophilic, amphipathic, amphoteric - macrolides and polyenes

forms channels - cations and macromolecules leak out, cell dies

**bind to sterols, so they can be toxic to us too

**IV admin is gold standard of antifungal drug (can have an oral suspension for oral thrush of candida)
**very uncomfortable to receive - fever, chills, nausea, vomiting, diarrhea (symptomatic premedication

Front 333

resistance to amphotericin B

Back 333

dermatophytes (less sterol)

(inducible resistance rare)

Front 334

Nystatin

Back 334

topical polyene used Tx candida

Front 335

cumulative amphotericin B toxicity

Back 335

renal cells lyse with cumulative effective; elevated creatinine; low K+, Mg++

normocytic anemia

Front 336

less toxic amphotericin B

Back 336

encased in liposomes or otherwise highly lipid associated, colloidal dispersion - equal efficacy, $$$

Front 337

azoles

Tx

mechanism

Back 337

1. fluconazole** oral, low toxicity, IV available; crypto, cocci, candidiasis
2. itraconazole - dimorphs, dermatophytes; high adipose levels
3. voriconazole - oral and IV; **visual toxicity** - aspergillus, resistant candida

inhibit cytochrome p450 sterol synthesis, toxic byproduct, sabotage membrane integrity

**toxicity is interfering with our sterol synthesis; inhibit our p450 metabolism

Front 338

azole resistance

Back 338

nonalbicans candida

inducible rare, but alter p450 or decrease membrane permeability

Front 339

echinocandins

Tx for

Back 339

caspofungin - IV - generally well tolerated

for tough aspergillosis

Front 340

fluorocytosine

Tx for

Back 340

5-FC

inhibits DNA synthesis

rapid evolution of resistance precludes monotherapy

*effective synergy for crypto
*toxicity - bone marrow suppression, gastritis

Front 341

Tx mucosal candida

Back 341

pretty much anything

Front 342

Tx dermatophytes

Back 342

topical, systemic azole (systemic for nails)

Front 343

Tx histo/blasto/coccid

Back 343

amphotericin B
itraconazole close 2nd

Front 344

Tx crypto

Back 344

ampho
fluconazole
itraconazole
synergy with 5-FC

Front 345

Tx aspergillus

Back 345

ampho
voriconazole
caspofungin

Front 346

Tx systemic candidiasis

Back 346

ampho
fluconazole
voriconazole
caspfungin

Front 347

co-resistance

Back 347

several resistance mechanisms in same organism

Front 348

integrons

Back 348

mobile genetic elements present in both gram + and gram - that mediate both co-resistance and co-selection

Front 349

co-selection

Back 349

the selection of multiple antibiotic resistance genes when one resistance mechanism is selected (usually both have same promoter)

hotspots

Front 350

penicillin resistance in S. pneumoniae

Back 350

alteration of PBP, altered cell wall

Front 351

origin of enterococcal resistance of vancomycin

Back 351

animal feed had glycopeptide avoparcin

Front 352

origin of MRSA resistance

Back 352

pig farmer

Front 353

how long to develop immune response to TB

Back 353

6-12 weeks (slow replication) - positive PPD at this time

proliferation of CD4 cells allows rxn to PPD; release IFN-gamma; macs release TNF-alpha

**TNF-alpha REQUIRED for granuloma formation

**patients with no CD4 cells don't go through this process

Front 354

small antigen load + hypersensitivity -->

large antigen load + hypersensitivity -->

small or large antigen load and no hypersensitivity (AIDS) -->

Back 354

epithelioid (stimulated mac) cells and giant cells

necrosis and caseation

no granuloma and huge #s of bacilli

Front 355

primary infection with resolution: __%

Back 355

85%

ghon complex - hilar node calcification

also enlargement of nodes

progressive primary disease in children -- dissemination, CNS involvement

cavitary is most infectious...highest number of bugs

Front 356

reactivation in __% of TB

Back 356

10-15% (85% of which are in lungs)

caseating necrosis, cavity formation

Front 357

Potts disease

Back 357

spinal manifestation of TB

Front 358

Dx reactivated TB

Back 358

fever, fatigue, night sweats, weight loss; productive or dry cough

Front 359

miliary pattern TB seen in

Back 359

children
immunocompromised

(need to biopsy)

Front 360

INH works by

Back 360

inhibiting synthesis of mycolic acids

Front 361

INH toxicity

Back 361

hepatic (4% >65), neuropathy (pyridoxine - vitamin B6)

Front 362

RMP mechanism

Back 362

inhibits RNA polymerase

Front 363

RMP toxicity

Back 363

GI upset, jaundice, skin rash

**induces p450 system, DDI

highly protein bound

Front 364

PZA use

Back 364

patient must be weighed

not in pregnant

unknown mechanism...need slightly acidic pH

Front 365

PZA toxicity

Back 365

gouty arthritis rarely
increase in transaminases (hepatic)

Front 366

ethambutol use

Back 366

bacteriostatic

weigh patient, adjust dose for **renal insufficiency**

Front 367

ethambutol toxicity

Back 367

Ishihara test for visual deficits (starts as blurry vision, then colorblindness (retrobulbar neuritis)
problem in renal insufficiency

Front 368

MDR TB Tx

toxicity

Back 368

Injectable (streptomycin) + 3 oral (quinolone, cycloserine, others)

cycloserine--> convulsion, psychotic depression
ethionamide --> hepatic
streptomycin --> CN VIII toxicity (capreomycin less toxic but 15x more $$$)

Front 369

XDR =

Back 369

resistant to INH, RMP, quinolone, one of injectables