Hospitals that make you sick

Fig. 1. Patient location and overlap during the outbreak. (A) Timeline of first positive cultures of the outbreak strain for the 18 affected patients.(B) Patient traces for each of the 18 patients shown in (A). Black lines, first positive culture; blue lines, medical ICU; yellow lines, cohorted areas;other colors represent specific wards at the NIH Clinical Center. (C) Graph of possible transmission links among patients. Patient IDs are within the circles. An arrow is present from one patient to another if the two patients overlapped in the same unit before the potential recipient culturing positive. Red links, the transmission event is predicted by the analysis reported here (see Fig. 3). www.ScienceTranslationalMedicine.org 22 August 2012 Vol 4 Issue 148 148ra116

This week's article was kindly forwarded to me by Melanie. We all heard about the outbreak of the carbapenem-resistant Klebsiella pnueumoniae that killed 11 out of 18 patients at the NIH Health Clinical Center in 2011. Here we have an opportunity to review the detective science behind elucidating the super-bug, tracking it down, and stomping it out of the hospital, pipes?!?!!!! My goodness, this article stirs several questions of pre-medical students: 1.How does whole-genome sequencing work as a detective art? 2. How do you feel about working in hospitals after learning about bugs like this? 3. What will be your stance on antibiotics as a physician? 4. Should more patients be sent home or prevented from entering hospitals knowing the dangers of pathogens such as these?

Please comment on one of the questions I pose above, or comment on whatever strikes you most after reading this Nature Translational Medicine article.

Click here:Article 3_Snitkin et al. Tracking Down Carbapenem-Resistant Klebsiella Pneumoniae

Article 2: Evidence For Haploinsufficiency in Marfan's Syndrome

Radiographs of engineered mice in Marfan Study.

In this week's discussion we will delve into mouse genetics to try to determine the molecular mechanism of Marfan Syndrome. In lecture this week, we learned about different types of dominant mutations. We ased the question, How can a mutated gene be dominant? We also tried to delineate differences between gain of function, dominant negative, and haploinsufficiency mutations. The article here tries to address a conundrum: whether Marfan Syndrome is caused by a dominant negative mutation, or by another mechanism. Click onto link below:

Judge et al., "Evidence for a critical contribution of haploinsufficiency in the complex pathogenesis of Marfan syndrome", Jo Clin Invest, 2004k

I would like for you to think about whether evidence provided in the paper supports the authors' conclusion that Marfan Sydrome is due to haploinsufficiency, and not by a dominant negative mutation. Please come to class organized with notes you have taken that you feel answer this question.

For the blog please answer this question with a post:
Do you feel this study was appropriate for publication in the Journal of Clinical Investigation, or not, and why? (For this, think about quality of data, novelty of work, and overall impact on the field) Try to limit your response to 1/2 a page.

If you have trouble with the above link (which directs you to the paper on BlackBoard) try this one instead:
Judge et al. article