Q9.  From me - 10/30 - 2:30 pm.  During Dr. Southwick’s first lecture today he said that you didn’t have to know certain causes of pneumonia.  Dr. Southwick does not have the authority, nor do I believe that it was his intent, to tell you that you do not have to know material that was taught by other faculty (lectures) or through other means (Virtual Lab, BUGS cases, etc.) in this course.  He has control over what is testable from his own lectures and the CMCs.  There are other venues in which you were taught about Klebsiella (e.g., Virtual Lab) and Pseudomonas (Virtual Lab and Dr. Jin’s lecture), among other causes of pneumonia that he did not cover.  You are still responsible for the reasonable expectations from those venues.

Someone asked about the format of the exam.  It will be basically the same format as the second exam from last year.  Mainly MCQs, a few short answer, and one essay based on the respiratory CMC.  There will be quite a few images from lab that you will need to be able to recognize when put in the proper context.  As noted previously, you don’t have to memorize spectra of antibiotics or the toxicities beyond what was discussed in a previous email (which by the way are now located in the email archive of the web page (http://www.mgm.ufl.edu/~gulig/mmid/email/index.html)). 

Let me say one other thing.  I became aware over the weekend that some of you had found the link to the key for the Virtual Lab.  I replaced the file with a notice that was supposed to make some of you wonder if you had gotten yourselves in trouble by trying to find it and look at it.  No, contrary to what the page said, I did not record who accessed the page.  However, I told you several times that the exercise was not going to be strictly graded, and that it was mainly being submitted to get you to thoughtfully go through the exercise (I even encouraged group endeavors).  I can tell you this.  If anyone simply copied the right answers into the result/quiz form and blew off the exercise for expediency, they will not be equipped to answer some questions on the exam which are derived from understanding why/how some tests work or not.  You need to learn that material by going through the exercise and using the Lab Guide as a learning tool in conjunction with Dr. Jin’s lecture.

We have given you the past 5 years of exams.  Please note that the exams have evolved recently with the addition of short answer and CMC essays, so very old exams may not be as useful as recent exams for those things.  Also, Dr. Lawrence gave the diphtheria/whooping cough/strep lecture for the time this year, so his emphasis might be a little different that years past.

Q8.  From me on Oct. 30 - While going over the strep web teaching page yesterday (http://www.snaption.net/med/strep.htm) I discovered an error which you should have caught on your own.  On the final page for diagnosis, the text boxes for "rapid strep tests" and "antibody tests" are reversed.  I have asked the student working with me on this to change "antibody tests" to "serological tests" since the rapid strep tests also involve antibodies, as well as switching the boxes.  But I don't know when he will get my email and be able to make the change. 

Q7.  From me - note - Dr. Lawrence skipped over some important diagnostic information in his lecture today.  Look at page 162 of Schaecter.  You should understand using antibodies in patient sera to DNase B (anti-DNase B) and Streptolysin O (ASO) to document prior GAS infection when you suspect glomerulonephritis or rheumatic fever.  The bacteria might be gone by the time these nonsuppurative sequallae appear, so a negative culture is not definitive.

Q6.  On the BUGS case "Coughing Baby", I am confused about the virulence factors for pertussis.  Question 11 states that the tracheal cytotoxin is not a major virulence factor for pertussis.  Why is this?  Dr. Jin told us some major effects that is has on infected patients, I think my definition of virulence factor may be off.  I also understand that for the vaccine all that is needed is FHA and the pertussis toxin, but even so, why isn't the TCT considered a virulence factor?

A. This is clearly wrong.  Anything that contributes to the steps of pathogenesis is a virulence factor.  TCT destroys the ciliated epithelium.  I will change this right now and point this out to the class.  Do question 11 again.  Thanks for pointing that out.  Note also that I changed question 12 to reflect the current vaccination situation.

Q5.  In Dr. Jin's lecture, he said that urine was a non-sterile site with normal flora; the answer online said pharynx.  Could you clarify the distinctions here?  Does it have something to do with the urine being in the bladder and not mid stream?

Question 15 - Single Best Answer

Normal flora are always found in the: 

A) urine in the bladder

B) spinal fluid

C) blood

D) pharynx

E) lung

F) more than one of the above

A.  You will be taught by Dr. Southwick later that if you were to do a needle aspirate of urine in the bladder (what is on the question) it would be sterile.  How often do we obtain urine by needle aspirate?  Not very often!  Imagine that.  So what do we do?  We get a mid stream catch that passed through the distal uro-genital tract which is definitely not sterile.  Therefore, it will get contaminated on the way out - there's no avoiding that.  Among answers in the question, only the pharynx is always colonized.  Had mid-stream urine been on the question, the correct answer would have been more than one of the above.  That question must have been from a practice test from years past from Dr. Duckworth, because I would not have written a question like that for this year (we actually haven't stressed the bladder urine sterility issue yet, and I checked, it's not in the Schaecter book (I bet it's in ID30).

Q4.  The virtual lab indicates that MacConkey's agar plates contain bile salts and thus they prevent growth of gram positives such as strep and staph.  However, p.23 of Schaechter states that as a result of the dense, hydrophilic peptidoglycan layer, "many gram-positives can withstand certain noxious hydrophobic compounds, including bile salts".  Could you please explain this discrepancy?

A.  You are the first person to point out that issue.  It's great that you found the apparent discrepancy in the text.  Believe it or not, despite my going on and on endlessly, I am often simplifying the world for you!  There are some gram positives that can withstand bile.  Clostridium difficile that you will learn about next exam is one of them, as are the enterococci, as their name implies.  What makes these organisms special?  I don't know.  However, unless we are talking about these particular organisms, it would be best to stay in the simplified world (i.e., among the gram-positives under discussion for the respiratory infections, they don't like MacConkey).  Not every gram negative grows on MacConkey, either (for example, the Neisseria don't).  So the real world is not black and white in either direction.

Q3.  Clarification by me on studying:

OK, I can see that waiting until Monday to make a decision on the issues of clarifying what must be memorized is an undue burden for your studying ahead of time, so I will make some executive decisions today.

A.  Dr. Southwick's antibiotic lecture:

1.  Understand MIC vs. MBC and their significance in practice.  (I have already taught you some of the reasons for varying levels of sensitivity and resistance, both innate and acquired, by bacteria).

2.  Factors that affect levels for treatment (also redundant with my lecture to some extent): absorption, distribution, metabolism in liver, clearance by kidney - and how you would deal with this information should it specifics be provided to you (i.e., don't memorize which ones are kidney vs. liver, but how you would use that information should it be given to you on a question.)

3.  Toxicities - Who's the safest (cephalosporins) and the worst (aminoglycosides), problems with allergies (penicillins in particular), and clindamycin (Clostridium difficile problems in the hospital).

4.  Spectra - OK, we'll give you the data for specifics and then ask you to use the data in a question.  However, that being said, there are some issues of spectrum that you should know based on your understanding of mechanisms of action from me (e.g., metronidazole for obligate anaerobes, vancomycin and bacitracin related to permeability, all peptidoglycan-active antibiotics and Mycoplasmas, etc.).

5.  Understand the flow chart that Dr. Southwick gave you and explained in lecture.

B.  The infectious disease case discussion - there will be no questions specifically from this exercise.

C.  Dr. Ramphal's classification and disease - no questions specifically from this lecture (does not rule out issues that were covered in other lectures, especially Dr. Jin's).

D.  Sepsis - yes, most definitely!

E.  Dr. Southwick's pneumonia and TB lectures - most definitely!

Q2.  In the notes (p.18) it shows the gene itself flips and inverts (and thus turns off) but in the book (p.177) it shows the promoter element flips and inverts but the gene itself stays in its original orientation. Does it happen both ways? Am I reading too much into this?

A.  Either way is OK (glad to see someone is reading the book!).  The main thing for phase variation is ON/OFF or A/B. The basic genetic mechanism is a flip of DNA, whether it's the promoter or the gene is not important.

Q1.  In your notes you write that vancomycin inhibits transpeptidation and transport, by recognizing D-Ala-D-Ala.  However on pages 62 and 25 of Schaecter (I know you like us to look it up before asking), it says that vancomycin inhibits incorporations of new disaccharides into the growing murein chain, and doesn't really mention transpeptidation.  So I don't know if this is an inconsistency or I just don't understand how these two explanations go together.  Does vancomycin have both functions (binding D-Ala-D-Ala to inhibit transpeptidation AND disaccharide addition for chain elongation)?

A.  This is an excellent and appropriate question.  Bottom line - vancomycin binds to D-Ala-D-Ala and prevents PBPs from doing their job, hence peptidoglycan fails.  Of lesser importance (i.e., I won't split hairs on an exam) is which of the following are primary, as opposed to secondary, effects.  It likely has effects on several steps: backbone elongation is mentioned, as is transport, and cross-linking.