TY - JOUR AU - Mikulska, Malgorzata AU - Bassetti, Matteo AU - Ratto, Sandra AU - Viscoli, Claudio PY - 2011/01/25 Y2 - 2024/03/28 TI - INVASIVE CANDIDIASIS IN NON-HEMATOLOGICAL PATIENTS. JF - Mediterranean Journal of Hematology and Infectious Diseases JA - Mediterr J Hematol Infect Dis VL - 3 IS - 1 SE - Review Articles DO - 10.4084/mjhid.2011.007 UR - https://www.mjhid.org/mjhid/article/view/2011.007 SP - e2011007 AB - <p class="MsoNormal" style="text-align: justify; margin: 0cm 0cm 0pt;"><span style="font-size: small;"><em><span style="font-family: " lang="EN-GB">Candida</span></em><span style="font-family: " lang="EN-GB"> is one of the most frequent pathogens isolated in bloodstream infections, and is associated with significant morbidity and mortality. In addition to haematological patients, there are several other populations with a substantial risk of developing invasive candidiasis (IC). These include patients undergoing prolonged hospitalisation with the u</span><span style="font-family: " lang="EN-GB">se of broad-spectrum antibiotics, those fitted with intravascular catheters, admitted to both adult and neonate intensive care units (ICU) or gastrointestinal surgery wards and subjects with solid tumours undergoing cytotoxic chemotherapy. As a general rule, every immunocompromised patient might be at risk of </span><em><span style="font-family: " lang="EN-GB">Candida</span></em><span style="font-family: " lang="EN-GB"> infection, including, for example, diabetic patients.</span></span></p><p class="MsoNormal" style="text-align: justify; margin: 0cm 0cm 0pt;"><span style="font-size: small;"><span style="font-family: " lang="EN-GB">The epidemiology of species responsible for IC has been changing, both at local and worldwide level, shifting from <em style="mso-bidi-font-style: normal;">C. albicans</em> to non-albicans species, that can be intrinsically resistant to fluconazole (<em style="mso-bidi-font-style: normal;">C. krusei</em> and, to some extent, <em style="mso-bidi-font-style: normal;">C. glabrata</em>), difficult to eradicate because of biofilm production (<em style="mso-bidi-font-style: normal;">C. parapsilosis</em>) or than might acquire resistance to azole during therapy.</span></span></p><p class="MsoNormal" style="text-align: justify; margin: 0cm 0cm 0pt;"><span style="font-size: small;"><span style="font-family: " lang="EN-GB">Delaying the specific therapy has been shown to increase morbidity and mortality, but traditional microbiological diagnosis is poorly sensitive and slow. Thus, c</span><span style="font-family: " lang="EN-GB">ulture-based treatment may result in therapy started too late. In order to reduce the mortality in IC, several management strategies have been developed: prophylaxis, empirical and pre-emptive therapy. Compared to prophylaxis, the latter approaches allow to reduce the use of antifungals by targeting only patients at very high risk of IC. Non-invasive serological markers and scores based on clinical prediction rules such as the presence of risk factors or <em>Candida </em>colonisation, have been developed with the aim of allowing prompt initiation of treatment. Although the use of these diagnostic tools in pre-emptive strategies is promising, the performance and cost-effectiveness should be tested in large trials. </span></span></p><p class="MsoNormal" style="text-align: justify; margin: 0cm 0cm 0pt;"><span style="font-family: " lang="EN-GB"><span style="font-size: small;">Agents recommended for initial treatment of candidemia in severely ill patients include echinocandins and lipid formulations of amphotericin B, while stable patients without risk factors for azole-resistance might be treated with fluconazole. </span></span></p><span style="font-family: " lang="EN-GB"><br style="page-break-before: always; mso-special-character: line-break;" /></span> ER -