Microbial Bloodstream Infections Flashcards
Are there normally microbes in the bloodstream
NO, it is normally sterile
How can microbes enter the bloodstream
Damage to the host epithelial barriers (via surgery, catheter use, other trauma), or compromise of host defenses promotes the movement of normal microbiota or pathogens across epithelial surfaces which allow bacterial transmigration into the bloodstream.
How does arthropod. vector transmission work
Can transmit microbes as they feed on blood from the host
Arthropods may include: mosquitoes, fleas, sand flies, mites, lice, ticks
Bacteria transmitted often become intracellular pathogens
Injection of drug use transmission
nfections in drug users may be acquired from:
contaminated drugs or drug paraphernalia (e.g. use of shared needles;transfer of blood–malaria, HIV…)
drug preparation using contaminated liquids (e.g. contaminated water with microbes like Pseudomonas aeruginosa)
transmission of the individual’s commensal flora (e.g. introduction of skin microbiota- Staphylococcus aureus, including MRSA)
How. can dental and medical procedures lead to infection
Dental procedures (e.g. tooth cleaning) which dislodge oral biofilms; can include commensal oral bacteria (e.g. Streptococcus viridans species)
Medical procedures
Artificial joints, prosthetic valves which provide surfaces on which bacteria can collect and grow; bacteria can be released periodically or continuously
Catheter insertion which can move bacteria into bloodstream
Surgical treatment of infected wounds, pressure sores, abscesses which disrupts infected siteand promotes bacterial transfer into the bloodstream
Skin wound infection complications
Any compromise to skin integrity promotes potential for microbial contamination
Attention to wound-care necessary; failure to do so may lead to infection
Main components of the immune system to avoid bloodstream infections
In combating bloodstream pathogens, the immune system relies heavily on the spleen (filters blood by removing pathogens coated with antibody and damaged cells), liver (Kupffer cells (liver macrophages), hepatocytes recognize microbial and damaged products in the blood that travels through the liver and degrade them), and pathogen-specific adaptive immunity
Bacterial mechanisms for evasion of host immunity
Capsule presence: encapsulated bacteria are more resistant to phagocytosis
Inhibition of complement activation via capsules, proteinases, chemical inactivation, binding to proteins that regulate complement activation, inhibition of lytic pathway
Antigenic variation: alteration of bacterial antigen to avoid recognition by antigen-specific antibodies
Scavenging of reactive oxygen species (ROS): bacterial use of ROS (e.g. catalase; ROS produced by host immune response) to “protect” it from damage
Types of BSIs
Primary: infection generally due to contaminated intravascular catheters; unrelated to infection at another site
Secondary: localized infection (e.g. skin, urinary, respiratory, GI tract…) that spreads systemically; systemic infection associated with infection at another site
What is SIRS
(Dont need to memorize)
What is bacteremia
presence of viable bacteria in the blood stream, generally transient (present for limited time and does not reestablish) and asymptomatic
Typically, causes no symptoms when present in low numbers →cleared by host immune system
If bacteria are present in high numbers and are unable to be cleared by the host immune system(due to weakened defenses)→ may lead to sepsis
What is septicemia
presence and multiplication of bacteria in the blood leading to infection
if untreated, can lead to sepsis
What is sepsis
life-threatening systemic inflammation resulting from a dysregulated host response to infection which promotes organ dysfunction; confusion can occur as it worsens
the causative infection may be a primary blood stream infection or may result from infection at any body site
How do bacteria in the blood promote sepsis
*bacterial toxins induce inflammation and release of lots of inflammatory cytokines which promote vasodilation and blood clotting (within organ blood vessels)
Gram (-) bacterial infections tend to result in a worse prognosis and faster progression (due to the release of LPS/ endotoxin into the bloodstream…can lead to endotoxic shock and death in a short amount of time)
What is septic shock
symptoms of sepsis along with severe abnormalities of circulation and/or cellular metabolism; associated with a higher risk of mortality (than sepsis alone)
persistent hypotension (despite fluid resuscitation)vasopressors are needed to:
maintain mean arterial pressure (MAP) ≥ 65 mm Hg
maintain serum lactate level ≥ 18 mg/dL (2 mmol/L)
organ dysfunction progresses to organ failure
Common G(-) causative bacterial pathogens of sepsis
Often associated with Gram-negative bacteremia (immune response triggered by G (-) production of endotoxin)
e.g. common G (-) blood contaminants: Acinetobacter, Klebsiella, Escherichia coli
Common G(+) causative bacterial pathogens of sepsis
Can also be associated with Gram-positive bacteremia (immune response triggered by lipoteichoic acid, peptidoglycan, extracellular products (e.g. toxins))
e.g. common G (+) blood contaminants: Staphylococcus epidermidis, Staphylococcus aureus; presence on skin facilitates transfer into bloodstream
Risk factors for BSI
Age: infections more frequent in elderly (decreased immune responses, impaired integument…) and neonates (underdeveloped immunity)
Hospitalization: increased risk due to hospital-associated drug-resistant infections; Enhanced risk in surgery, transplantation, catheter use…
Metabolic and nutritional deficiencies (e.g. malnourished, diabetic)
Neutropenia: reduced neutrophilsimpaired immune response
Immunosuppression
What increases risks for sepsis
IV drug use, artificial joint prostheses, valve abnormalities, chronic disorders (e.g. diabetes, cirrhosis…), pregnancy, and persistent infection
How is BSI diagnosed
Patient symptoms that suggest BSI warrant confirmation by blood culture
Positive cultures are further analyzed by Gram staining and other staining techniques
Agar plates inoculated and incubated for identification of colonies
Most common bacteria present: E. coli, Followed by Staphylococcus aureus (2nd), Streptococcus pneumoniae (3rd)
MRIs, CT scans to determine source of infection and prevent downstream reseeding
Histopathology may be helpful in early diagnosis of fungemia
TX for sepsis
Antibiotics (immediately due to serious nature of infection)
IV fluids (to increase fluid volume and BP)
O2 administration (ventilator used if needed)
Identification and removal of source of infection (drainage of abscesses, if present; removal of catheters, tubes, or any other device identified as the source; surgery can be performed to remove infected/dead tissue)
Medications to increase BP (e.g. vasopressin, norepinephrine…) if needed)
What is a CLABSI
CENTRAL-LINE ASSOCIATED BLOODSTREAM INFECTION (CLABSI)
Entrance of microbes into the bloodstream through the central line; develop within 48 hrs of placement (not related to infection at another site)
Sterile insertion protocol must be utilized to prevent/minimize infection
Stringent infection control practices must be adhered to each time the line is checked or the associated dressing is changed
Infection is generally indicated by fever, redness and pain around the central line
TX and prevention of CLABSI
Treatment
Removal of central line
Use of IV antibiotics
Fluid administration, O2 therapy (if required)
Prevention
Follow recommended insertion practices (e.g. hand hygiene, drying of skin prep before insertion, sterile barrier precautions (e.g. gloves, gown, cap, mask, drape)
Follow recommended maintenance procedures once line is in place
Removal when not needed
What is infective endocarditis
Infectious inflammation of the endocardium which affects the valves of the heart
Bacteria that are introduced into the bloodstream may adhere to the valves of the heart (via surface adhesins), proliferate and form vegetations (bacteria surrounded by platelet/fibrin lesion), and promote endocardial inflammation
Valves that are damaged, abnormal, or prosthetic are more susceptible to adhesion and colonization
Common agents of infective endocarditis
Bacteria that colonize these valves often produce biofilms
Staphylococcus aureus (most common- particularly in acute)…Recall that S. aureus is a common inhabitant of normal skin flora
Streptococcus viridans group (most common-particularly in subacute)…Recall that viridans (S. sanguis, mitis, mutans…) are normal oral cavity flora
Other microbes include: BACTERIA - Enterococcus faecalis, HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella)
FUNGI-Candida albicans (common in IV drug users)
Risk factors for infective endocarditis
IV drug abuse
Immunosuppression
Prosthetic valves
Birth defects of the heart (including valves), or major blood vessels (particularly a defect that allows blood to leak from one part of the heart to another)
Heart valve damage (due to rheumatic fever)
Degeneration of the heart valves that occurs with aging
TX for infective endocarditis
Antibiotics or other antimicrobial therapy (depending on the microbe(s) present)
Surgery (on infected valve)
Dental treatment (if determined to be the source)
Catheter removal (if applicable)
**Without treatment, endocarditis is generally fatal
