Week 11 Flashcards
Does the blood contain a normal biota?
○ No because it’s a closed system. Unless you’re actually puncturing something to get in, there’s no real normal or natural biota in there.
How might organisms get into your bloodstream?
○ Brushing too hard and your gums bleed
○ IVDU
○ Colonization of mucous membranes
○ Hangnail
Infective endocarditis
Endocarditis=Inflammation of the endocardium, specifically mitral and aortic valves
Where is the endocardium in the heart?
□ Inside lining of the heart. Although we primarily see changes in lining of the valves with endocarditis, we can see changes in lining of the heart anywhere. Most frequently in valves d/t stress/turbulence. At any point in the heart when endocardium is exposed to stress/injury/turbulence is where you can have focus of endocarditis.
2 types of infective endocarditis:
Acute or subacute
Acute endocarditis
- cause
- virulence factors
® You can get it from IV Drug Use
® The vegetations can break off. A lot of these organisms are forming colonies (biofilms). This is important as a virulence factor b/c it’s protective against the host defense mechanisms.
- When you talk endocarditis, you think more microbial.
Subacute endocarditis
- what does it affect?
- timeline
- causes
- reason for infection
- signs and sxs
- mimics
- infects already previously damaged valves.
- more slowly than acute endocarditis because you’re dealing with damages over time. Less pronounced.
- damage from Rheumatic fever, Calcified bicuspid aortic valve, Turbulent flow from HTN, Congenital malformations
- Anytime you have irregularities in the valves, that encourages bacteria to come in and attach there.
- Low-grade fever, anorexia, fatigue, abnormal heart beat, anemia, hx of previous valvular issues
- A lot of times mimics MI sx
What is a biofilm?
◊ Biofilms are usually a mixed group of organisms (some fungal, some bacterial, etc), but for endocarditis, fungal cases are rare.
What are different ways that endocarditis can develop?
□ Native valves
□ Prosthetic valves
□ IVDU- Staph aureus
□ Rheumatic heart disease
differential of bacteria for native valve infection
- Strep Mutans– part of viridans streptococci
- Strep bovis
- Strep pyo
- Enterococcus faecalis
- Staph aureus
differential of bacteria for prosthetic valve infection
□ Staph epidermis □ Staph aureus □ Gram negative bacilli □ C. albicans (unit 7--candida, just be aware now) □ Streptococci
differential of bacteria for IV drug use
□ Staph Aureus □ E. faecalis □ Streptococci □ P. aeruginosa □ C. albicans
Streptococcus mutans
- group
- location?
- how do they grow?
- oxidase?
- viridans streptococcus: group of organisms with similar characteristics but same treatment. You can’t truly differentiate them unless you do PCR.
- oral
- green on agar so easy to identify
- oxidase + –> aerobic
Streptococcus bovis
- indicates
- colon CA or IBS
Streptococcus pyogenes
- antigen
- other issues it can cause
- PYR test
- catalase
- there is a group A antigen you can test for
- Glomerulonephritis
- Skin infections that can lead to toxic shock syndrome, can cause scarlet fever, Pharyngitis, Cellulitis, Sinusitis
- positive
- catalase -
Enterococcus faecalis
- what does it cause?
- associated w/
- PYR test
- enterobacteriaceae group
- virulence factor
- lives with
- tx
- VDE strains
- Causes endocarditis and UTI
- hospital-acquired infections
- PYR + (group a strep or coagulase - staph and entero
- Klebsiella, Proteus, Serratia
- Resistance
- eskape pathogens
- Vancomycin- ampicillin or vancomycin with aminoglycosides.
◊ VDE strains: need vancomycin to grow can’t grow without vancomycin would instead use linezolid or daptomycin.
ESKAPE pathogens
◊ E for e.coli or Enterococcus faecium ◊ S for staph aureus ◊ K for Klebsiella pneumoniae ◊ A for Acinetobacter baumannii ◊ P for Pseudomonas aeruginosa ◊ E for enterobacter
Vancomycin MOA
binds to cell wall precursor (things that build the cell wall)–>inhibits cell wall synthesis
Staph epi
- found?
- forms?
- what should you do?
- Lives on the skin; found on catheters
- Form clusters b/c they have adhesin molecules to cluster themselves and to other surfaces
- quickly remove catheter
HACEK organisms
- found with?
- live?
- prosthetic valves
- oral-pharyngeal region)
- Haemophilus, Aggregatibacter (previously Actinobacillus), Cardiobacterium, Eikenella, Kingella.
Rheumatic disease
- what is it?
- damage caused
- what level does it damaged?
- gross features
- clinical features
- Type III hypersensivity
- skin manifestations
- explain progression to chronic rheumatic heart disease
- mitral valve effects and clinical manifestations
- histological findings in acute
- histo findings in chronic
- test for diagnosis
- Prior infection of group a beta hemolytic strep and antibodies made against M protein but then cross react with self cardiac antigens.
- Inflammation causes damage to the tissues, and damage to the endothelium circulating immune complexes, cytokines, and inflammatory cells cause fibrinoid necrosis creating foci of necrosis
- Acute rheumatic fever can damage any of the three levels of the heart: endocardium, myocardium, pericardium
- Vegetations and Subendocardial fibrous plaques
- Fever, Fatigue, Chest pain from pericardial rub, Heart murmurs, Sydenham’s chorea
- This is a type III hypersensitivity.
- subcutaneous nodules, Erythema marginatum
- damage to the heart causes damage to the valves with chronic inflammatory process that is in recurrent episodes; not getting treated and they are getting rheumatic fever over and over
- Mitral stenosis is seen and when there is reduced frequency of rheumatic heart disease,start seeing secondary cause of mitral stenosis–atherosclerosis; • Opening snap with decrescendo murmur, pulmonary hypertension, Left atrial dilation
- leukocytes and other inflammatory cells in the conective tissue with Aschoff nodule/body
- organization, neovascularization, and then fibrosis (collagen deposition)
- Serology for Antibodies against streptomycin O and anti-DNAse B.
Sydenham’s chorea
involuntary movement that tends to occur with rheumatic fever
3 characteristic gross changes seen in chronic rheumatic heart disease
- Commissural fusion of mitral valve
- Leaflet thickening
- Thickening and fusion of the tendinous chords
For the continuous acute attacks, is there instances where we have rheumatic disease and go into states of remission or is it newly infective tissue or continuous attacks?
-This is not an infectious process. It starts with a bug, but continues with the immune system. Those repeated episodes occur in response to seeing the bug again, but perhaps not. There could be other reasons why our body becomes hyper immune reactive.
Types of Hemolysis
• A- partial hemolysis
• B- complete hemolysis
- Gamma- none
Beta hemolytic bugs
- how to differentiate
• Strep Pyogenes and
A galaciae
- bacitracin; S. pyogenes is sensitive. A galaciae is not
