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An Overview of Invasive Candidiasis, Aspergillosis, Cryptococcosis, and Pneumocystis Pneumonia

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An Overview of Invasive Candidiasis, Aspergillosis, Cryptococcosis, and Pneumocystis Pneumonia Review article: Current opinion | Published 22 February 2016, doi:10.4414/smw.2016.14281 Cite this as: Swiss Med Wkly. 2016;146:w14281 Common invasive fungal diseases: an overview of invasive candidiasis, aspergillosis, cryptococcosis, and Pneumocystis pneumonia Yvonne Schmiedel, Stefan Zimmerli Infectious Diseases, Inselspital, Bern, Switzerland Summary benefit from prophylaxis. Ongoing searches for disease- associated genetic polymorphisms may contribute to the Every year, Candida, Aspergillus, Cryptococcus and establishment of individual risk profiles and targeted pro- Pneumocystis infect an estimated two million individuals phylaxis. worldwide. Most are immunocompromised or critically ill. Candida is the most common fungal pathogen of the crit- Key words: invasive fungal diseases; invasive candidiasis; ically ill and of recipients of transplanted abdominal or- aspergillosis; cryptococcosis; Pneumocystis pneumonia gans. In high-risk haemato-oncological patients, in con- trast, the introduction of antifungal prophylaxis with fluc- Introduction onazole and later with mould-active posaconazole has led to a remarkable reduction of invasive candidiasis and is Out of more than 100'000 known fungal species, only about likely to have a similar effect on invasive aspergillosis. In- 300 cause disease in humans [1]. Our body temperature vasive aspergillosis remains the dominant invasive fungal may provide a protective thermal barrier against the ma- disease (IFD) of haemato-oncological patients and solid- jority of species that grow best at ambient temperature [2]. organ transplant recipients and is increasingly found in in- The most common pathogens are Candida, Aspergillus, dividuals with exacerbated chronic obstructive pulmonary Cryptococcus, and Pneumocystis spp. – causing more than disease on corticosteroids. In the developed world, ow- 90% of reported deaths due to fungal disease [3]. The top ing to antiretroviral therapy Pneumocystis pneumonia and ten fungal infections are responsible for at least as many cryptococcosis have become rare in patients with human deaths as tuberculosis or malaria [3–5]. Yet, on a global immunodeficiency virus (HIV) and are mainly found in scale, fungal diseases are neglected. This is reflected by the solid-organ transplant recipients or immunocompromised lack of initiatives by the World Health Organization and the patients. In the developing world, cryptococcosis remains paucity of national surveillance programmes [3]. Although a common and highly lethal disease of HIV positive indi- current trends show an overall increase of invasive fungal viduals. diseases (IFDs), their incidence is likely to be underestim- With invasive candidiasis and invasive aspergillosis, timely ated [6]. diagnosis is the principal challenge. The clinical presenta- IFDs are associated with high morbidity and mortality. tion is nonspecific and current diagnostic tests lack sens- Their diagnosis is challenging and their timely treatment itivity and specificity. The combination of several tests often depends on a high level of clinical suspicion. There- improves sensitivity, but not specificity. Standardised poly- fore, this review aims to give an overview of the current merase chain-reaction-based assays may be promising epidemiology, clinical presentation, diagnosis, and man- tools for more rapid and specific diagnosis of candidiasis agement of the four most common IFDs: invasive candidi- and invasive aspergillosis. Nevertheless, initiation of treat- asis, aspergillosis, cryptococcosis, and Pneumocystis pneu- ment is often based solely on clinical suspicion. Empirical monia. therapy, however, may lead to over-treatment of patients without IFD or it may miss its target in the case of resist- Definitions of invasive fungal disease ance. Despite the success of antifungal prophylaxis in re- ducing the incidence of IFDs in haemato-oncological pa- IFDs are proven by the presence of moulds or yeasts in a tients, there are a considerable number of breakthrough deep tissue biopsy or a culture obtained by a sterile pro- infections demonstrating not only fungal resistance but also cedure [7]. Additional definitions for probable and possible the emergence of rare and often lethal fungal pathogens. IFDs based on host-specific, clinical, and mycological fea- Knowledge of the local epidemiology and antifungal res- tures, which were originally established for haemato-onco- istance is therefore pivotal. Current trial-based guidelines logical research purposes, are now commonly applied in leave major gaps in identifying those most at risk, who may the clinical setting [8]. However, these definitions lack pre- Swiss Medical Weekly · PDF of the online version · www.smw.ch Page 1 of 12 Review article: Current opinion Swiss Med Wkly. 2016;146:w14281 cision and universal applicability to all patients groups – bution of blood-stream isolates of 65% C. albicans, 15% notably the critically ill – and do not include Pneumocystis C. glabrata, 6% C. tropicalis, 5% C. parapsilosis and 2% pneumonia. C. krusei [21]. In contrast to the USA, in Switzerland and Northern Europe no shift to fluconazole-resistant C. krusei Invasive candidiasis and C. glabrata has been observed [27, 38]. In some areas (Southern Europe, the Americas and Asia) C. parapsilosis Candida is the most common cause of IFDs in the deve- is the second most common isolate after C. albicans. The loped world [9]. As a normal commensal of humans, this identification of Candida isolates to the species level is yeast may be found in the oral cavity, the gastrointestinal important because of species-specific antifungal drug res- tract, the female genital tract or on the skin [10]. An es- istance patterns, which have major impact on the choice timated 24–70% of healthy people above one year of age of best treatment. More than 98% of C. albicans isolates are colonised by Candida. Presumably, everyone is tem- are susceptible to fluconazole [39], whereas C. krusei is porarily colonised at least once during their lifetime [11, constitutiively resistant to fluconazole, but susceptible to 12]. Invasive candidiasis originates from the patient’s own newer-generation azoles. Because of its wide array of res- flora: it is introduced into the bloodstream or deep tissue istance mechanisms, C. glabrata poses the greatest treat- following iatrogenic breaks of the skin or mucosal barrier. ment challenge [23, 27]: azole therapy is usually advised Since its introduction in the 1990s, antifungal prophylaxis against because of the capacity of C. glabrata to develop with fluconazole has led to a remarkable reduction of can- or to extend resistance under treatment, and some studies didaemia in haemato-oncological patients [13–16]. Invas- also report rapidly occurring and/or increased resistance to ive candidiasis is predominantly a disease of the critically echinocandins [40–42]. Previous azole exposure increases ill, hospitalised patient. the risk for infection with azole-resistant Candida isolates [43–46]. Epidemiology The incidence rate of invasive candidiasis shows a large Clinical presentation geographical variation. In Europe, invasive candidiasis Signs and symptoms of invasive candidiasis are nonspecif- makes up 2-3% of all nosocomial infections – four times ic. Candidaemia is the most common manifestation, deep- less than in the USA [9, 17–20]. Despite an increased use seated infections with or without concomitant candidaemia of antifungals, the incidence of candidaemia is on the rise. are rarer. Intra-abdominal candidiasis may occur after com- Between 2000 and 2010 its incidence rate in Swiss hos- plicated abdominal surgery or with necrotising pancreatitis; pitals has doubled from 0.49 to 1.01/10 000 patient days simultaneous candidaemia is detected in only 10% of cases [21]. A similar trend was observed in other European sur- [47–49]. Candidaemia may go unnoticed when it produces veillance studies, with an average incidence rate increasing a single febrile peak among many – typically in the crit- to approximately 0.59/10 000 population and 11/10 000 ad- ically ill patient. It may induce sepsis or ultimately septic missions [22–25]. Incidence rates in intensive care unit shock, both indistinguishable from bacterial infection [43]. (ICU) patients are 5–10 times higher than in patients from Signs of intra-abdominal candidiasis include persistent medical or surgical wards [20, 22, 26]. The average 30-day fever and clinical deterioration despite continued antibiotic mortality rate for candidaemia is 43% [27, 28]. This is sub- treatment. Deep-seated organ infections are more common stantially higher than for any other blood stream infection in solid organ transplant recipients, whereas candidaemia [29]. occurs more often in haematological or critically ill pa- The main risk factor and principal portal of entry for can- tients [50]. Candida pneumonia is rare [11, 51]. didaemia is an intravenous (IV) catheter [30]. Candida Candida chorioretinitis, found in approximately 8–16% of biofilms formed on IV catheters are also an important candidaemic patients, may be an easily detectable sign of source of continued infection [31]. Other critical risk recent or ongoing candidaemia. It is usually asymptomatic factors for candidaemia are the use of broad-spectrum anti- unless progression to vitritis and vision-threatening en- biotics, total parenteral nutrition, dialysis, and chemother- dophthalmitis produces blurred vision or floating black apy. Notably, all of these factors are associated with critical spots [52, 53].
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