QUESTIONS

1. What four events/things are necessary in order to cause a vegetative lesion to grow?
   
2. What is structural heart lesion has been shown to have a definite association with the development of vegetative endocarditis?
   
3. What valves are generally associated with vegetative endocarditis?  Which valve has the worst prognosis in an endocarditis case?
    
4. Which of the following is not a "usual suspect" bug for vegetative endocarditis?
   
   a) Pasteurell multocida
   
   b) Staph intermedius
   
   c) Aerobacter aerogenes
   
   d) Strep sp.
   
   e)  Corynebacteria sp
   
   f)  Erysipelothrix rhusiopathiae
   
   g)  E coli
    
5. What kind of murmur is usually heard in endocarditis & why?
    
6. When I was a student, PDP1 told us that the pulses on an aortic endocarditis dog not only could be called "bounding" but you could actually stand across the room & see the dog pulsing.  Wow!  What is the mechanism for this?
    
7. Why are ventricular arrhythmias more common than supraventricular arrhythmias in this disease?
    
8. An S3 gallop is often heard over the left ventricle. Why might this be?
    
9. What are the most common biochemical changes seen on a panel in this disease?
    
10. Describe to someone like they're a 4 year old how to run a blood culture.
    
    
    
    
     

ANSWERS

1. First, you need bacteremia (so far, seems straight forward).  Second, you need a pre-existing lesion on the heart.  Third, you need a platelet-fibrin thrombus.  And fourth, you need a high titer of agglutinating antibodies against the organism.
   
   The idea is that you need a bug, a place for it to grow & some stuff to make it stick there.
   
   You should note, though, that some really evil bacteria can make their own heart lesion or create a thrombus (so that all 4 events don't have to occur separately.)
   
   
   
   
    
2. Did I fool you?  Mitral endocardiosis gets all the press for this but there's no proven association that this structural lesion predisposes in any way to endocarditis.  The lesion that HAS been definitely associated is SAS!
   
   
   
   
    
3. Despite the above answer, the mitral valve gets more than its share of endocarditis.  The aortic valve gets the rest AND wins the poor prognosis contest.
   
   Intractable left heart failure generally results 4-12 weeks after the signs of sepsis have been noted.  Mitral endocarditis cases can go even a year before CHF sets in.
   
   So how do we get such bad failure with aortic regurg?  Well, we are volume over-loading the left ventricle.  In diastole, it is supposed to be receiving blood from the Left atrium but the problem is that it is just about sucking the blood it just pumped out of the aorta.  This means it is trying to handle rather an unusual volume of blood.  It eccentrically hypertrophies.  It tries to pump more to meet the demands of the bod for oxygen.  But the more it pumps, the more it regurges.  And after a while, it just can't get any bigger/it gets too tired/ & you get myocardial failure.  Also, in diastole, with all the valves open, isn't the huge diastolic pressure reflected all the way back to the pulmonary veins just like in MR?  And you get pulmonary edema?
   
   
   
   
    
4. The only non-member of the endocarditis club is Pasteurella.  The others are relatively common isolates.
   
   Erysipelothrix rhusiopathiae?!  Doesn't that cause some kind of pig disease?  You know that it does but it also is something like the 5th most common isolate in k9 endocarditis.
   
   Who is Erysipelothrix rhusiopathiae?  It is a rather hardy bug though it cannot survive >35 days in soil.  It causes arthritis in lambs, acute sepsis in turkeys, & erisepeloid in humans.  It is a slender gram + rod and is sensitive to penicillins.  What is it doing in a dog & how did it get there?  I certainly have no idea but this is the same Erysipelothrix of the "diamond-shaped" skin lesions of swine that some of us may yet recall from our school days.
   
   
   
   
    
5. Systolic murmurs are heard in mitral endocarditis.  This is because turbulence occurs when the heart is pumping (when the heart is pumping, blood is regurging).  When the aortic valve is involved the murmur is diastolic.  This means that turbulence occurs during the filling phase.  (Er, Paul, is this right?  Regurg is occuring in diastole?  The heart pumps blood into the aorta & when done, it is ready to fill again.  The problem is that as soon as there's low pressure in the ventricle for filling, there's no competent valve to keep the blood in the aorta from leaking back in.)
   
   
   
   
    
6. Bounding pulses occur when there is a big difference between diastolic & systolic pressure.  OK, in such a case, why is diastolic pressure so small?  Because in diastole all the blood in the aorta is being sucked back into the left ventricle.  No blood in the aorta = no diastolic pressure.
   
   (Just a possibly helpful image I learned  in physics in High School.  When you drink through a straw, you think you are pulling liquid into your mouth, don't you.  But you aren't really.  What you are really doing is creating a low pressure area in your mouth.  Fluid really wants to go to a low pressure area.  When you think of blood shunting L>R, think of the R sucking the blood up from the L.  When you think of a chamber in diastole, the blood is being sucked in.  SLURP.  I think this image is  more powerful than just thinking of the heart filling or the left side pushing blood to the right.)
   
   
   
   
    
7. Every time blood goes squirting through the aortic valve it is dragging little flotsoms & jettsoms of septic emboli. These are happy to get stuck in the myocardium (& even abscess there).  There are more emboli in the ventricle as this is closer to the infected valve.  (Right?)
   
   
   
   
    
8. S3 gallops are associated with dilated left ventricles.  (Exactly what you see in a volume overload such as this)  Paul, what exactly are we hearing the sound from though?
   
   
   
   
    
9. 51% have low albumen
   
   24% have hypoglycemia
   
   48% have elevated ALP
   
   
   
   
    
10. Okay, I am taking this out of a compendium article on blood culturing. They recommend taking a urine culture at the same time & shoot for the hour precedding a fever spike if you can (use ESP for this). Clip & scrub venipuncture site.  Take 3 culture samples within 24 hours (2 = ok for endocarditis - actually since bacteremia is supposedly continuous in endocarditis, Im not sure I understand why one sample isn't adequate). Space cultures at least one hour apart.  Take 10cc from a dog & 5cc from a cat & you must use a broth bottle containing at least 10x the volume of the blood you drew.  If you don't use this much growth medium, you will not counter act the bacteriocidal action of the serum.   Antibiotics will delay but not prevent growth.  (You can also use special antibiotic straining lids to remove antibiotics from the blood sample).
    
    Prognosis is rather stinky in endocarditis.  Plan on 7-10 days of IV antibiotics followed by 6 weeks of PO antibiotics.  Treat well beyond apparent remission & do a blood culture 1-2 months afer d/c of meds.