This post will not cover the clinical course or risk factors. We’ll be going over the direct fluorescence antibody, PCR, as well as the elusive beta-D glucan as well as taking a brief look at the original ways we used to diagnose PJP (or in some places, how they still diagnose it. In the days
This is the cell wall of fungi. It is not inert and, the cell wall undergoes a consistent process of assembly and remodeling during cell growth. Glucan is the most abundant polysaccharide, and it is made up of glucose polymers linked by carbon at the first and third position: Back in the day (roughly the
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
Tamma PD, Conley AT, Cosgrove SE, et al. Association of 30-Day Mortality With Oral Step-Down vs Continued Intravenous Therapy in Patients Hospitalized With Enterobacteriaceae Bacteremia. JAMA Intern Med. 2019;179(3):316–323. doi:10.1001/jamainternmed.2018.6226 This is a multicenter retrospective cohort on patients with monomicrobial Enterobacteriacae blood stream infections (Citrobacter spp, Enterobacter spp, E.coli, Klebsiella spp, Proteus mirabilis, or Serratia marcecens) comparing
This is a confusing bit that no one really seems to understand, because it seems so basic. Bactericidal antibiotics kill bacteria, bacteriostatic doesn’t. Seem simple, but it’s a bit more complicated. First things first: all antibiotics kill. Otherwise, they wouldn’t work. The whole bacteriocidal vs static definition is mostly a microbiogical one rather than a
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
The ACTIVE trial! This is a phase III, RCT, double blind, multicenter, non-inferiority trial comparing isavuconazole vs caspofungin in invasive candidiasis. Folks, in ID, it doesn’t get any better than this (look at all these studies!) Exclusion criteria were Candida in any body part (i.e. osteomyelitis, IE, meningitis), severe immunodeficiency, >48hrs of other antifungal therapy.
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 is a retrospective, observational cohort study from Detroit evaluating the frequency of IV to PO switch and the population for which this is use, as well as to figure out the factors associated with failure. They recruited 492 patients with MRSA bacteremia (basically anyone with the exception of polymicrobial bacteremia and those with wither