WK 3- Cardiovascular Infections Flashcards Preview

ID > WK 3- Cardiovascular Infections > Flashcards

Flashcards in WK 3- Cardiovascular Infections Deck (44):

What is bacteraemia

the presence of viable bacteria in the blood stream (doesn’t mean there’s an infectious process present)


What is septicaemia

→ the persistence and invasion of pathogenic organisms in the blood (host has not been able to clear bacteria from the bloodstream→ infectious process involving release of toxins from the pathogen)


What is septic shock

the presence of bacteria and their toxins in the blood stream, characterised by decreased blood flow to organs and tissues, hypotension, organ dysfunction and often multiple organ failure


Why do microbes survive well in the blood stream

Contains oxygen, water & nutrients
Has a neutral pH
Has an appropriate temperature


What makes the blood stream unfavourable for microbes

Constantly moving (prevents colonisation)
Antimicrobial defence mechanisms
Blood recirculates through spleen & liver


What are the 4 conditions required/facilitate an infection to occur

1. Organisms must be released in large numbers
2. Anatomical defect facilitating colonisation (eg heart valves)
3. Organisms have protective mechanism/s
4. Impaired host defence


What is a biofilm

Layer of bacteria that attaches to a surface--> can be found on foreign material such as catheters, IV lines, joints


What are the 5 key risk factors that allow infection to develop

1. Disruption or penetration of anatomical barriers -wounds, IV catheters, contaminated IV drugs
2.Devitalised tissue -necrotic tissue has no blood supply→ no immune cells/antibiotics can move to the area
3.Defective granulocyte function -chemotherapy, diabetes (have no MO or neutrophils)
4.Complement defects/deficiency
5. Splenic malfunction/absence- no filtering mechanism available


What is the pathogenesis of septicaemia

-gram negative cell walls have endotoxins (LPS) that are released when the bacteria die→ acts on macrophages to cause them to become activated and begin to release cytokines and trigger the immune response


What is sepsis

sepsis is the result of the immune system fighting septicaemia (toxins in the blood produced by bacteria)


What causes sepsis

Can be through direct introduction of microbes into the bloodstream eg, IV line or through another infection occurring within the body
eg. meningococcemia-> caused by neisseria meningiditis entering the blood stream from the nasopharynx


Why is strep pneumoniae so common in splenectomy patients

Strep pneumoniae is a capsulated pathogen-> the spleen is responsible for clearing pathogens with a capsule as normal cellular immune responses are often ineffective at eliminating it-> without a spleen the body can not clear these organisms, leading to infection


What are some infections that can result in sepsis (by introduction of bacteria into the blood)

pneumonia, UTI, meningitis, bone or joint infection, wound infection, infective carditis, soft tissue/skin infection


What are the 2 phases of sepsis (immune phases)

immune hyperactivation= high immune response dealing with infection
-immune exhaustion= due to state of massive immune hyperactivcation, cell number will become depleted/chemical mediators will decrease→ over time they will come back to normal


What happens if an immunosuppressed patient gets sepsis (what progression/course do they follow)

if a person already has a decreased immune function, they will have lower hyperactivation→ will immediately go into the exhaustion state and succumb to the infection (death)


What are the investigations to test for sepsis

-blood culture (before antibiotics are delivered)→ use a gram stain/catalase, coagulase
-DO NOT DELAY TREATMENT- use broad spectrum antibiotic whilst taking cultures
-collect urine to use for MCS
-imaging can be used to identify primary and secondary foci of infection


What gram negative diplo-cocci most commonly cause bacteremia

Neisseria meningitides→Colonise nasopharyngeal region


What gram negative rods most commonly cause bacteremia

Pseudomonas (opportunistic- everywhere in environment- unlikely to cause disease in a normal healthy host)
-Escherichia coli→ Colonise GI tract
-Klebsiella pneumonia→ Colonise GI tract- not an opportunist but only normally associated in people with slightly compromised immune system- mainly occurs in resp tract in older males (issues with diabetes/alcoholism)- can be aspirated into lungs and move into blood stream


What part of the LPS structure is used for serotyping

the core polysaccharide (sits between the Lipid A and O-polysaccharide


When does Lipid A (LPS) become active- what is it classed as

not biologically active when stuck on membrane, but lipid A is released when the membrane breaks down


How does LPS contribute to sepsis and septic shock

-LPS begins by acting on MO and activates them→ causes release of TNF and IL1→ causing fever
-also acts to use up stored glucose in the body and lessens effectiveness of gluconeogenesis
-acts on IgE to cause release of mediators from granulocytes (like mast cells)→ cause oxidative stress and damage to endothelial cells
-LPS damages endothelial cells and causes vascular permeability→ causes bleeding into skin and hypotension (due to platelets being used up in the vessels- leading to DIC)→ no platelets left to clot blood leaking from vessels into the skin
-decreased blood content leads to shock


How do gram positive bacteria contribute to sepsis

-they release exotoxins which can damage cell membranes
-release super antigens that can create a cytokine storm
-cell membrane has lipotechoic acids that act the same as lipopolysaccharides but to a lesser degree


What are the 2 major groups of gram positive bacteria that contribute to bacteremia

staphylococcus and streptococcus


What is endocarditis

-inflammation of the endocardium→ usually associated with the valves (mitral valve)


What are the 2 types of presentation of endocarditis

1. Sub-acute endocarditis (~60% non/α-haemolytic Streptococcci*) (Q-fever)
-Poorly defined onset→ fever, malaise
-Symptoms lasting weeks/months before pt often seeks treatment
2. Acute endocarditis (~60% S. aureus)
-acute onset of symptoms→ 24-48 hours before presentation
-majority is by staph aureus→ more virulent organism
-symptoms occurring days before presentation


What is the pathogenesis of endocarditis

1. abnormal or damaged heart valve (ie. Membrane may be damaged→ fibrin and platelets move in and attempt to fix lesion)
2. lay down of fibrin/platelets have organisms accompanying it (organisms can attach to the collagen/fibrin)→over time there is adherence of bacteria and productions of vegetation (mixture of fibrin, platelets and bacteria)
3. as there is bacteria hiding under the host proteins, they are hidden from the immune system → this leads to the symptoms


What are the symptoms of endocarditis

majority occur at the mitral valve (left sided endocarditis)→ causes narrowing of the valve (due to bacteria causing stenosis)→ cause murmur (due to stenosis) or regurgitation (as the valve becomes floppy)
-depending on whether there is valve stenosis or regurgitation depicts what murmur is heard


If the patient with endocarditis has bad oral hygiene, what bacteria would be presumed to have caused the endocarditis

oral streptococci (strep viridan group- most common) or staph aureus→ form a plaque layer/biofilm on the teeth (able to do this due to production of dextrose that aids in adherence)--> the plaques are able to break off and move into the blood stream and form a biofilm on the valves


If the patient with endocarditis is an IV drug user, what bacteria would be presumed to have caused the endocarditis

staph aureus, oral strep or gram neg bacteria- organisms that have come from the skin or dirty needles-> cause right sided endocarditis


What is haemolysin

haemolysin= toxin released by organism that destroys RBC→ when organisms are cultured on agar plates with RBC, can see the haemolysis


If the patient with endocarditis has prosthetic valves what bacteria would be presumed to have caused the endocarditis

-prosthetic valves→ if less than 2 months most likely hospital acquired→ coag negative staph (staph epidermidis)
-prosthetic valves→ if greater than 2 months most likely environmental cause--> staph aureus


What are the 3 types of haemolytic strep

-beta= complete haemolysis→as the organism grows it releases exotoxin (haemolysis) causing RBC lysis
-alpha= agar has a green tinge→ due to toxin not being able to completely destroy the RBC→breaks it from haemoglobin to methaemoglobin
-gamma= no haemolysis


What separates the different strains of staphyloccocus

the presence of coagulase


What is coagulase

enzyme secreted that allows for the bacteria to cause coagulation of RBC-> allowing the bacteria to thrive and grow in the clot and avoid immune detection


What type of strep is Viridans streptococci- where is it found and what does it cause

-Normal flora of the oral cavity
-Alpha–haemolytic streptococci
-Transmitted to bloodstream via dental work, poor oral hygiene-> can cause endocarditis


What causes further subdivision of the beta haemolytic species

Lancefield grouping- is a method of grouping catalase-negative, coagulase-negative bacteria
based on the carbohydrate composition of bacterial antigens found on their cell walls.


What are the different groups of strep

A, B, D, Enterococci


What does group A strep cause- what haemolytic class does it belong to

non-invasive pharyngitis, impetigo, rheumatic fever, TSS and necrotising fasciitis


What does group B strep cause- what strep belongs in this group

-S. agalactiae causes neonatal meningitis and septicaemia after transmission from the normal vaginal flora of the mother.


What does group D strep cause-what strep belongs in this group

- Streptococcus bovis
associated with bacteremia, w or w/o endocarditis
-also causes urinary tract infections, meningitis, septic arthritis, and vertebral osteomyelitis.


What are the 2 most prevalent enterocci species in humans

Enterococcus faecalis and Enterococcus faecium


What are the treatments available for RHD

Antibiotic therapy:
-need to treat sepsis/endocarditis rapidly→ but get cultures first
-start with broad spectrum and narrow down when lab results identify cause
-Cardiac surgery on valve:
-Early if infection is uncontrolled and life-threatening
-Late if valve damage is progressive
→ tissue engineered heart valves
Supportive therapy
Prevention: Prophylactic antibiotics for at risk patients


What is the pathophys of RHD

In RF; Ab recognise proteins in the heart valves (bind to endothelium and ab will bind to self antigen and cause complement to come and cause inflammation→ inflammation leads to healing and then scarring)→ when this happens repeatedly, quicker progression to RHD


Why is Pseudomonas a significant cause of nosocomial related infections?

opportunistic pathogen that is unlikely to cause disease in a healthy host
-is present everywhere in the environment
-most likely to cause infections in those who are immunocompromised-> hence
in hospital