Where all your ID needs are met! Sort of.
I think I have talked quite a bit about tuberculosis these past few posts. This is because it is difficult to diagnose in certain cases, it can infect virtually any organ, and it can become deadly once it infects any other organ outside of the lungs. Namely the CNS. Tuberculous meningitis is a deadly disease,
I think HIV is a very interesting virus. It has important historical, epidemiological, and societal implications and has had an impact in health care policy. The diagnosis of HIV now is actually relatively straight forward in most centers, but I wanted to take a step back and figure out the reasoning behind the algorithms that
Gram negative bacteremia tends to complicate a variety of infections, including urinary tract infections/pyelonephritis, and intra-abdominal infections. Further, a lot of these patients tend to have severe presentations leading to perhaps overtreatment with IV antibiotic therapy. Until recently, there had been little data to guide uncomplicated gram negative rod bacteremia but there has been a
HIV-associated Immune Reconstitution Inflammatory Syndrome (IRIS) is a known early complication of initiating ART therapy in those who are profoundly immunosuppressed. Here, immune recovery following ART initiation leads to an inflammatory response against an organism leading to a clinical deterioration a few weeks following ART initiation. You can think of it as follows; you have
Procalcitonin is a precursor of the hormone calcitonin and is released into systemic circulation within 4 hours of inoculation of bacterial endotoxin, In general, cytokines enhance procalcitonin release while interferons, which are released in context of viral infections. Because of this, there has been a push towards using PCT to differentiate bacterial from viral infections
This is a complicated issue, but I think it makes antibiotic dosing (especially things like vancomycin and aminoglycoside) more easy to understand. I’ll try to make it as easy and digestible as possible. I’ll discuss mostly pharmacodynamics (i.e how the drug exerts its antimicrobial effect). I discussed MIC testing in a previous post, as well
Thwaites GE, et al. “Adjunctive rifampicin for Staphylococcus aureus bacteraemia (ARREST): a multicentre, randomised, double-blind, placebo-controlled trial”. The Lancet. 2017. 391(10121):668-678. This is a multicenter, randomized, double blind placebo controlled trial on the use of adjunctive rifampin (or if you’re in the UK, rifampicin) for Staph aureus bacteremia. The inclusion criteria was either MSSA/MRSA from at
A pair of Q fever studies: Million, Matthieu, et al. “Thrombosis and Antiphospholipid Antibody Syndrome During Acute Q Fever: a Cross-sectional Study.” Medicine, vol. 96, no. 29, 2017, pp. e7578. This is a cross-sectional study from the French National Referral Center for Q fever that sought to determine whether thrombosis in acute Q fever patients was associated
This one is not groundbreaking but nice to have data supporting our decisions. This was a review of the literature evaluating the efficacy of cefazolin vs anti-staphylococcal penicillin (cloxacillin, nafcillin, flucoxacillin) in staph aureus bacteremia. The primary end point was 90d all cause mortality; secondary end point was 30d all cause mortality, treatment failure/relapse, and
This one out of the one and only Mass Gen. Apparently they have issues with people ordering PCR for Anaplasma when it is not needed (they state 3% of those PCRs ordered ended up being positive). As such, they did a 2 phase study to see if they could use CBC and LFTs to screen
Dr. Germophile 