Reply to “Observations on native valve endocarditis caused by Kocuria kristinae”

Dear Editor,

I am grateful for the comments received by Rahim et al.¹ Our intentions with the letter sent was to point out the pathogenic significance Kocuria kristinae may have on the development of infectious endocarditis,² without any other apparent primary infectious focal point being measured, unlike the cases referenced by Rahim et al. in these cases obvious infectious niches exist (septic arthritis, infected catheter, infections of soft tissues) and appear to be the starting point of the bacteremia which will foster the development of endocarditis. The aim of our letter was to simply reiterate the importance of Kocuria kristinae as a potential pathogen of infectious endocarditis without the need for a clinically apparent primary reservoir. Also that its microbiological determination should be subject to an appropriate clinical interpretation which determines the realisation of the pertinent supplementary techniques.

We insist on several specific aspects: that on occasion this is attributed with a “contaminating” role without pathogenic involvement; that identification should be made not just based on the metabolic study³ of isolation (as in several of the articles referenced by Rahim et al.); that there are no specific sensitivity guidelines (and for this reason it was relativised with Staphylococcus aureus cut-off points).

Our intentions was not to carry out a systematic review of the literature with respect to Kocuria spp and its pathological/microbiological spectrum, but to avoid under-estimations of Kocuria kristinae in isolation and its potential involvement in the development of infectious endocarditis, regardless of whether primary septic systemic outbreaks exist or not.