Microbial Bloodstream Infections Flashcards

1
Q

Are there normally microbes in the bloodstream

A

NO, it is normally sterile

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2
Q

How can microbes enter the bloodstream

A

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.

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3
Q

How does arthropod. vector transmission work

A

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

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4
Q

Injection of drug use transmission

A

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)

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5
Q

How. can dental and medical procedures lead to infection

A

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

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6
Q

Skin wound infection complications

A

Any compromise to skin integrity promotes potential for microbial contamination

Attention to wound-care necessary; failure to do so may lead to infection

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7
Q

Main components of the immune system to avoid bloodstream infections

A

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

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8
Q

Bacterial mechanisms for evasion of host immunity

A

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

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9
Q

Types of BSIs

A

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

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10
Q

What is SIRS

A

(Dont need to memorize)

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11
Q

What is bacteremia

A

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

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12
Q

What is septicemia

A

presence and multiplication of bacteria in the blood leading to infection

if untreated, can lead to sepsis

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13
Q

What is sepsis

A

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

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14
Q

How do bacteria in the blood promote sepsis

A

*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)

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15
Q

What is septic shock

A

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

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16
Q

Common G(-) causative bacterial pathogens of sepsis

A

Often associated with Gram-negative bacteremia (immune response triggered by G (-) production of endotoxin)

e.g. common G (-) blood contaminants: Acinetobacter, Klebsiella, Escherichia coli

17
Q

Common G(+) causative bacterial pathogens of sepsis

A

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

18
Q

Risk factors for BSI

A

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 neutrophilsimpaired immune response

Immunosuppression

19
Q

What increases risks for sepsis

A

IV drug use, artificial joint prostheses, valve abnormalities, chronic disorders (e.g. diabetes, cirrhosis…), pregnancy, and persistent infection

20
Q

How is BSI diagnosed

A

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

21
Q

TX for sepsis

A

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)

22
Q

What is a CLABSI

A

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

23
Q

TX and prevention of CLABSI

A

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

24
Q

What is infective endocarditis

A

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

25
Q

Common agents of infective endocarditis

A

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)

26
Q

Risk factors for infective endocarditis

A

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

27
Q

TX for infective endocarditis

A

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