Among critically ill patients, the diagnosis of bloodstream infection poses a major challenge. Current standard bacterial identification based on blood culture platforms is intrinsically time-consuming and slow. The continuous evolvement of molecular techniques has the potential of providing a faster, more sensitive and direct identification of causative pathogens without prior need for cultivation. This may ultimately impact clinical decision-making and antimicrobial treatment. This review summarises the currently available technologies, their strengths and limitations and the obstacles that have to be overcome in order to develop a satisfactory bedside point-of-care diagnostic tool for detection of bloodstream infection.

Mycoplasma pneumoniae (M. pneumoniae) belongs to the class Mollicutes and has been recognized as a common cause of respiratory tract infections (RTIs), including community-acquired pneumonia (CAP), that occur worldwide and in all age groups. In addition, M. pneumoniae can simultaneously or sequentially lead to damage in the nervous system and has been associated with a wide variety of other acute and chronic diseases. During the past 10 years, the proportion of LRTI in children and adults, associated with M. pneumoniae infection has ranged from 0% to more than 50%. This variation is due to the age and the geographic location of the population examined but also due to the diagnostic methods used. The true role of M. pneumoniae in RTIs remains a challenge given the many limitations and lack of standardization of the applied diagnostic tool in most cases, with resultant wide variations in data from different studies. Correct and rapid diagnosis and/or management of M. pneumoniae infections is, however, critical to initiate appropriate antibiotic treatment and is nowadays usually done by PCR and/or serology. Several recent reviews have summarized current methods for the detection and identification of M. pneumoniae. This review will therefore provide a look at the general principles, advantages, diagnostic value, and limitations of the most currently used detection techniques for the etiological diagnosis of a M. pneumoniae infection as they evolve from research to daily practice.

During the past 15 years, many studies have been devoted to the relationship of Chlamydia pneumoniae and atherosclerosis: the serologic link has been investigated, and chlamydial organisms have been detected in lesions by electron microscopy, immunohistochemistry, in vitro cultivation, PCR, or in

Antibiotics are frequently used in intensive care units (ICUs), and their use is associated with the emergence of bacterial resistance to antibiotics. The aim of this study was to investigate the association between the emergence of Pseudomonas aeruginosa resistance and the duration of antibiotic exposure or mode of administration in an ICU unit. A 4-year cohort study of intensive care unit was performed in patients with P. aeruginosa isolates from clinical specimens, initially susceptible to the investigated antibiotics (piperacillin/tazobactam, ceftazidime, ciprofloxacin, meropenem and amikacin). Odds ratios (ORs) with 95% confidence interval (95% CI) of emergence of resistance were calculated using logistic regression analysis for various exposure periods to antibiotics (1–3, 4–7, 8–15 and >15 days) relative to no exposure with adjustment for age, sex, Simplified Acute Physiology Score 3 (SAPS 3) and length of stay. ORs on the emergence of P. aeruginosa resistance were also calculated for the various modes of administration. Included were 187 patients [mean age 61 years, 69% male, mean SAPS 3 score (SD): 59 (12.3)]. None of the antibiotics investigated showed the emergence of resistance within 1–3 days. Significant meropenem resistance emerged within 8–15 days [OR 79.1 (14.9–421.0)] after antibiotic exposure unlike other antibiotics (>15 days). No difference was observed between intermittent and extended administration of meropenem and between beta-lactam mono- or combined therapy. Use of meropenem was associated with the emergence of resistance as soon as 8 days after exposure to the antibiotic.