Nosocomial Candida infections

The progress in medicine over the last two decades with introduction of new technologies and therapies, which has allowed the survival of more and more patients suffering from serious diseases, has brought about an increase in the number of hospitalised and immunocompromised subjects. These individuals are highly susceptible to nosocomial fungal infections, especially to candidosis. Candida spp. infections range from thrush to invasive diseases such as arthritis, osteomyelitis, endocarditis, endophthalmitis, meningitis, or fungaemia [1, 2]. Nosocomial candidosis may be exogenous or endogenous. Although the finding of Candida on superficial body sites cannot be considered evidence of infection, the adhesion and persistence of yeast on these surfaces is the first step in the development of candidosis. Disseminated candidosis is commonly associated with an inadequate immune response, sometimes with an abnormal production of IgA. This allows the invasion of the mucosal barriers, in proportion to the magnitude of colonisation [3-5]. Genotypical analyses carried out on colonising and infecting strains showed that strains causing infections often originate from a commensal population on the body surface and/or gastrointestinal tract of patients [3, 6]. This is supported by cases of candidaemia that occurred in patients in bone marrow transplant and haematology/oncology units, in positive-pressure or private rooms. In these situations, isolation, the proper employment of hygienic measures by the hospital personnel and the provision of specialized diets minimize the risk of cross-infection from patient to patient [2]. The exogenous acquisition of nosocomial candidosis is proved by several reported outbreaks. These cases seem to be associated with environmental factors, such as the presence of multiple doors into the rooms, the transportation of patients to different units or the contamination of liquid for infusion and biomaterials, but above all with the behaviour of the personnel [2, 3, 6, 7]. Studies carried out using different methods to verify the similarity among strains isolated from the hands of health care workers (HCWs) and strains colonising their patients demonstrated the role of personnel in the spread of infection; C. parapsilosis and C. albicans are the species most frequently isolated from the hands of HCWs [3, 8, 9]. The differentiation between endogenous and exogenous infections is important to determine suitable control measures to prevent further transmission of Candida [2]. Over the last 20 years there has been world-wide increase in mucocutaneous and invasive fungal infections [3]. The 115 hospitals participating in the National Nosocomial Infections Surveillance (NNIS) system reported between 1980 and 1990 an increase in the rate of nosocomial fungal infections from 2.0 to 3.8 per 1,000 discharges [10]. This trend was observed for all clinical manifestations including oropharyngeal infections, surgical site infections, and urinary tract infections, but especially for fungaemia, which rose from 5.4% of all nosocomial bloodstream infections (BSI) in 1980 to 9.9% in 1990 [2, 10]. In addition to the increase in the incidence of endemic nosocomial fungal infections, numerous nosocomial fungal outbreaks were reported [2, 4]. In the European Prevalence of Infection in Intensive Care (EPIC) study, carried out in 1992 on 1,417 intensive care units (ICUs) in 14 European countries, 17.1% were fungal infections. Fungi were the fifth most common cause of nosocomial infections after Enterobacteriaceae, Staphylococcus aureus, Pseudomonas aeruginosa and coagulase-negative staphylococci [4, 12]. The majority of nosocomial fungal infections are reported to be caused by Candida spp. [2, 10]. C. albicans is the single most common species causing infections. The NNIS reported in 1990-1992 C. albicans as ranking seventh among the pathogens isolated from major infection sites (i.e., urinary tract, surgical site, bloodstream and lungs) [2, 13]. C. albicans accounted for 76% of 24,227 cases of candidosis reported in the NNIS hospitals in the period 1980-1990, with an increase in the proportion of nosocomial infections from 2% in 1980 to 5% in 1986-89; in the Netherlands it accounted for 73% of all Candida infections [3, 4, 14]. REVIEW