Blood Stream Infections Flashcards
factors contributing to the increasing incidence of sepsis
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
bacteremia
the presence of viable bacteria within the liquid component of the blood
septicemia
same as bacteremia, but implies the presentation of clinical manifestations associated with bacteria in the bloostream
severe sepsis
sepsis with associated organ dysfunction with one or more of the following: hypotension, confusion, oliguria, hypoxia, metabolic acidosis, disseminated intravascular conjugation, hepatic dysfunction
septic shock
sepsis-associated hypotension that is associated with lactic acidosis or organ hypoperfusion and cannor be reversed by the administration of IV fluids
SIRS (systemic inflammatory response syndrome)
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
causes of SIRS besides bloodstream infection
severe trauma, complication of surgery, burns, acute pancreatitis, immunodeficiency
clinical features of sepsis
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
most common sign of sepsis in elderly
confusion. may just show confusion and nothing else
role of TLRs in mediating SIRS
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
endotoxic (gram-negative) shock
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.
how does variation in the number of acyl chains in lipid A impact signaling through TLR4?
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
inflammation activated coagulation
severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation.
DIC (disseminated intravascular coagulation)
condition in which blood clots form throughout the body’s small blood vessels, blocking or reducing blood flow through them
activated protein C (APC)
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.
antithrombin
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
bacteremic patterns
the level of bacteria in the blood rises and falls, meaning blood draws at certain times might not detect it
transient bacteremia
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
intermittent bacteremia
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
continuous bacteremia
bacterial endocarditis and other endovascular infections. seen during early stages of typhoid fever, brucellosis, leptospirosis
intravascular vs. extravascular infections
intra are within the cardiovascular system, while extra have bacteria enter the bloodstream through the lymphatic system from another site of infection
infective endocarditis
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
pathogenesis of infective endocarditis
- damage to cardiac endothelium.
- deposition of platelets and fibrin
- organisms gain access to bloodstream and stick leading to colonization (biofilm)
- protective layer of fibrin and platelets form matrix
- bacterial multiplication
- vegetation formation
mycotic aneurysm
results from damage to the endothelial cells lining the arteries leading to seeding of the organism
