Blood Stream Infections

Question 1

factors contributing to the increasing incidence of sepsis

Answer 1

increasingly aggressive oncological chemo/radiation, widespread corticosteroid/immunosuppression for transplants, increasing survival of patients predisposed to sepsis, increased use of invasive devices such as prostheses, catheters, etc, and indiscriminate use of antimicrobial drugs that create new bad strains

Question 2

bacteremia

Answer 2

the presence of viable bacteria within the liquid component of the blood

Question 3

septicemia

Answer 3

same as bacteremia, but implies the presentation of clinical manifestations associated with bacteria in the bloostream

Question 4

severe sepsis

Answer 4

sepsis with associated organ dysfunction with one or more of the following: hypotension, confusion, oliguria, hypoxia, metabolic acidosis, disseminated intravascular conjugation, hepatic dysfunction

Question 5

septic shock

Answer 5

sepsis-associated hypotension that is associated with lactic acidosis or organ hypoperfusion and cannor be reversed by the administration of IV fluids

Question 6

SIRS (systemic inflammatory response syndrome)

Answer 6

an inflammatory state of the whole body without a proven source of infection. abnormal generalized inflammatory reaction in organs remote from the initial insult. SIRS + proof of bloodstream infection = sepsis

Question 7

causes of SIRS besides bloodstream infection

Answer 7

severe trauma, complication of surgery, burns, acute pancreatitis, immunodeficiency

Question 8

clinical features of sepsis

Answer 8

symptoms are usually nonspecific and include fever, decreased urination, rapid pulse/breathing, nausea, vomiting, diarrhea, confusion. early recognition of sepsis is critical for effective intervention

Question 9

most common sign of sepsis in elderly

Answer 9

confusion. may just show confusion and nothing else

Question 10

role of TLRs in mediating SIRS

Answer 10

TLR4 is the most critical. engagement of TLR4 leads to release of proinflammatory mediators TNF alpha, IL-1, and IL-6 that can lead to gram-negative shock

Question 11

endotoxic (gram-negative) shock

Answer 11

excessive release of cytokines, often triggered by LPS of gram negative bacteria can lead to diffuse intravascular coagulation, changes in vascular permeability, circulatory collapse, and hemorrhagic necrosis.

Question 12

how does variation in the number of acyl chains in lipid A impact signaling through TLR4?

Answer 12

lipid A with a reduced number of acyl chains can serve as an inhibitor of immune activation induced by gram-negative bacteria. bacteria can change the number of acyl chains in response to the environment

Question 13

inflammation activated coagulation

Answer 13

severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation.

Question 14

DIC (disseminated intravascular coagulation)

Answer 14

condition in which blood clots form throughout the body’s small blood vessels, blocking or reducing blood flow through them

Question 15

activated protein C (APC)

Answer 15

Protein C circulates as an inactive zymogen, but in the presence of thrombin and thrombomodulin, is converted to APC. restores fibrinolytic potential by inhibiting plasminogen activator inhibitor. inhibits production of proinflammatory cytokines by LPS.

Question 16

antithrombin

Answer 16

second naturally occurring endothelial regulator affected during sepsis. Inhibits thrombin production at multiple steps in the coagulation cascade as well as by binding and inhibiting thrombin directly

Question 17

bacteremic patterns

Answer 17

the level of bacteria in the blood rises and falls, meaning blood draws at certain times might not detect it

Question 18

transient bacteremia

Answer 18

from chewing, teeth brushing, manipulation of infected tissue, and surgery involving non-sterile sites. in a patient with good liver and spleen, this is of little consequence

Question 19

intermittent bacteremia

Answer 19

often associated due to an extravascular infection which provides a portal of entry for the bacteria (UTI, abcess). most common bacteremia pattern. seen early in meningitis, pyogenic arthritis, and osteomyelitis

Question 20

continuous bacteremia

Answer 20

bacterial endocarditis and other endovascular infections. seen during early stages of typhoid fever, brucellosis, leptospirosis

Question 21

intravascular vs. extravascular infections

Answer 21

intra are within the cardiovascular system, while extra have bacteria enter the bloodstream through the lymphatic system from another site of infection

Question 22

infective endocarditis

Answer 22

denotes infection of the endocardial surface of the heart and implies the physical presence of microorganisms in the lesion. acute form follows a fulminant course, usually with high fever, systemic toxicity, and leukocytosis. death in several days to

Question 23

pathogenesis of infective endocarditis

Answer 23

1. damage to cardiac endothelium.
2. deposition of platelets and fibrin
3. organisms gain access to bloodstream and stick leading to colonization (biofilm)
4. protective layer of fibrin and platelets form matrix
5. bacterial multiplication
6. vegetation formation

Question 24

mycotic aneurysm

Answer 24

results from damage to the endothelial cells lining the arteries leading to seeding of the organism

Question 25

suppurative thrombophlebitis

Answer 25

results from damage to the endothelial cells lining a vein. results in clot formation and seeding of the clot by organisms. common with IV placement

Question 26

catheter related bloodstream infection (CRBSI)

Answer 26

nearly 70% are due to gram positive organisms, primarily S. aureus and coagulase-negative staphylococci

Question 27

risk factors associated with catheter related bloodstream infections

Answer 27

prolonged catheterization, frequent manipulations, occlusive plastic dressings, contaminated skin solutions, poor aseptic technique, catheter material, location of catheter

Question 28

sources of organisms in CRBSI

Answer 28

insertion site (patient’s own flora), the catheter hub (improper cleaning), hands of health care people, hematogenous seeding of the catheter (transient bacteremia), contamination of the infusate

Question 29

organisms causing CRBSI

Answer 29

common: coagulase negative staph, staph aureus, candida
other: bacillus, corynebacterium JK, acinetobacter, pseudomonas, xanthomonas

Question 30

secondary (extravascular) BSI

Answer 30

1. local site of infection
2. spillage of the organism into the bloodstream
3. lymphatics spread organism
4. potential seeding of secondary organisms

Question 31

organisms associated with neoplastic disease

Answer 31

clostridium septicum, streptococcus gallolyticus, aeromonas hydrophilia, plesiomonas shigelloides, campylobacter

Question 32

diagnosis of BSIs

Answer 32

blood cultures. important in diagnosis for a febrile patient.

Question 33

blood culture collection

Answer 33

adults: direct relationship between blood volume and yield. more blood = better chances of getting bacteria. children: take what oyu can get. higher bacteria load

3 sets in a 24 hour period.

Question 34

what differentiates infectious SIRS from noninfectious SIRS

Answer 34

procalcitonin level is elevated in sepsis.

Question 35

procalcitonin (PCT)

Answer 35

marker of inflamm response and is stimulated by cytokines and bacterial products. evidence suggests that it can be used as a biomarker for bacterial pneumonia and bacterial sepsis. levels go up within 3-6 hours of stimulus, and higher = worse prognosis. levels can be used to indicate appropriate therapy

Question 36

PCT concentrations and sepsis risk

Answer 36

less than 0.5 ng/mL: low risk for progression to severe sepsis/septic shock
between 0.5 and 2 ng/mL: sepsis should be considered
higher than 2 ng/mL: high risk for progression to severe sepsis and/or septic shock