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    Guilherme Kazuo Ogawa
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    Article on aspergilosis

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    32 Ansichten14 Seiten

    Aspergilose

    Hochgeladen von

    Guilherme Kazuo Ogawa
    Article on aspergilosis

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    © All Rights Reserved
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    Markieren Sie unangemessene Inhalte
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    Arne ea Definition + Aspegilosis is caused by species ofthe mold Aspergils + Sydomes range from colonization fungus ball due allergic res allergic bone szergilus aspergilo} ulmonaty aspergillosis: zing pneumonia to invasive pulmonary aspergillosis and other invasive Epidemiology +The highest incidence of infection curs in ‘ents undergoing hematopoietic stem call transplantation or soi-organ transplantation (see Table 258-2), + Infection is mor likely in patients entersive nrunosuppesson or in those with malignancy + Improved survival has been no early diagnose and newer ter mortality rates in severely or pesistenty suppressed patents are d Microbiology + Cultue-based diagnosis i useful to establish speci diagnasis + Aspergils species complexes exit distinct antifungal suscepilties so that cultwe-based diagnosis is dincally relevant Se Table 258-1), + Molecular analysis s required to establish species-evel ident, + Increasing rates of antifungal resistance are rotten Somaletngf vals Soa ene of antifungal-resstant species Diagnosis + Proven infec + Biomarkers such 35 galactomsannan,§-0 lan, and polymerase chain reaction assay are useful fo establishing probable ciagnsis. + Serial assessment of biomarkers may be wef for measuring response to therapy. Therapy is established by culture of rap in most patent (ee Table 259), + iposoml amphotericin 8 canbe use primary therapy in patients in whom voricnazole isnot tolerated or Conivandicated becau + Altemative agents for savage therapy include amphotericin B lipid comple, the sha canine raster ncmmanta ‘snidulaungin),posaconaole, or tvaconazole. + Combination therapy is not recommended fr routine use, but some subgroups of patents (eg. those with early diagnosis of infecto based on detect those with fala of primary therapy with a single st) may benef rom such an aporeach of drug intracons Prevention + Antifungal posi voi highsrisk patents + Thersk-benefit ratio of prophylaxis in individual patients at risk shouldbe considered + infection control's importa hospitalized patents, but lng dura (180 days) n high-k hematopoet Call wansplant o sl patients makes commu gan wanspan acquired inf Invasive aspergillosis is & major eause of morbidity and mortality in immunosuppressed patients This infection is caused by Aspergillus, a ‘mold with hyaline hyphae tht isthe etiologic agent in iovasive sper {illosis and a variety of noninvasive or semi-invasive conditions. These syndomes range ffom colonization, such as fungus ball due to Aspe {illus (also known as aspergilloma); allergic esponses to Aspergillus, including allergic bronchopulmonary aspergilosis (ABPA); to semi invasive or invasive infections, from chronic necrotizing pneumonia tw invasive pulmonary aspergiliosis and other invasive syndromes, Aspergillus and the resultant aspergillosis area major focus of clink «al mycology because the number of patient with this diseage ha risen Gramatically and becauce of the morbidity and mortality of thie infec tion. The increased number of Aspergilus infections bas occurred because more patients ar a rsk for this infection, Patients with estab lished invasive aspergillosis have poor outcomes. Successful therapy depends not only on an early diagnosis but also on reveral of under ‘ng immune defects’ Even when therapy & begua promptly, outeomes fre often poor, particularly in patients with diseeminated or central nervous system disease and in those who remain profoundly immu rnosupprested.” New diagnostic approaches and new management lgics have been established.” In this chapter, clinical mycology cpidemiclogy, pathogenesis, clinical presentation, diagnosis, teat ‘ment, and prevention of aspergillosis are described MYCOLOGY. ‘The genus Asperilus was frst recognized in 1729 by Michel, in Hor cence, who noted the resemblance elreen the sporalaing head of an ‘Asperglls species and an aspergilum used to sprinkle holy water’ In 1886, Virchow published the fist complete microscopic descriptions othe organism” Aspergillus flavus eas formally named by Link in 1805" Thom and Church Best claafed the gene sn 1926 with 69 “Aspergillus species sn 11 groups, The term “group” is now more cor realy referred to at “ection but this reporting is not commonplace in clinieal mycology laboratories” Because phenotypic methods and dnsernal ransribed spacer sequencing identify Aspergiue telates veithin a section and not indsvidval species, it hasbeen recommended that ieolates chou be repored ax members ofa “species complex” ‘With the recent use of molecular techniques a characterine pathogenic fang, apergl have now inreated dramatically to include more than 230" species in eight subgenera (Aspergillus, Furigat, Crcumdat {Candi Tevet Nidulnte, Wareupi and Ornat) which are subdivided sno multiple sections and species complexes “Mest species of Aupergilus reproduce asexually but a tleomorph (or sexual form with frsting body) hasbeen identified fo number of species, incding pathogenic species such as Aspergillus nidulans {leomorph, Emerica nidulans), A. astlodans (Burton amstl. a), A dagows (Nevsartorya suagawae), and the moet common pathogen A. fumigatus (Necuartory fomigats) and many others Fen though the correct taxonomic omenclatre would rename these oxganisme using the sexual form, generally the generic name Asperg luthas heen retained to simplify nomenclature repardlet of ther teen morphs (sexual forms), rather than separating the organisms into snlamilar specie hazed on discovery of sexual state. As with other pathogenic ung, the axonomy of Aspergils bas undergone extensive Feclassifaton with utlization of molecular studies, suchas sequen tng of sboomal, tubulin, calmodulin, ot rodlet A genes, which has allowed mote natural subgroupings of ascomyestour fangi ‘With denity established by means of molecular sequencing, the result 2895 allergic bronchopulmonary aspergillosis; anidulafungin; aspergillosis: Aspergillus, caspofungin. echinocandin: galactomannan; itraconazole, ‘mcafungin; posaconazole; voricanazole 2895.e1 sapods sbindsy sz serdey> Infectious Diseases and Their Etiologic Agents Part i 2896 Peer FREQUENCY OF SPECIES Ene ees ted with Invasive Infecti ASPERGILLUS COMPLEX ISOLATED IN cotony microscopic ‘cuntca, Species CLINICAL INFECTION (%4)""°* CHARACTERISTICS’ FEATURES™ SIGNIFICANCE A fumigatus ee sos Smoky gyaten may have Colt unerate smooth to Most common mse gon and faltjarer vere” “eal ehgheed ona Specs, mon pathogenic fevers grows aso 2S ym A fans ee ane ve wolime seen fadate los cohinna, Sits din econ 25824 ad 8) CetcenteorDrate ough produces aftoxn ‘dlophre conta un A fers ee a5 Beige w cinamon bu Colaar bserae: gbtose; —_bcesnay deteced resistant fig 58300 “ral 2.5m cork sbtose "wo ampnotenen Bmore “eeson cnida sng hyonae Hace To nee eles A rizr 00 39 Int wnte opi tarina Radel; one, ick, Unconmon mre gr 739-04 and 8) hone este clinton Data tom elorncer 3 12,20 aod 26 of a familiar species may be reported as an unfamiliar tlemorph, which has led to assigning one name to one fungus to clarify this potential confusion in clinical mycology.” ‘he genus Aspergillus isan anamorphic member (asexual form) of the family Tichocomaceae. The teleomorphs (sexual forms) of Asper- illus species are classed in eight genera in the order Eurotsles in the Phylum Ascomycota." Identification of the genus and of common pathogenic species is usually not dificult, but speces-level identifi Goa of less common members can be laborious and misidentiication of atypical or zryptic’ members of sections—such as poorly sporulat- ing form:—ie common,” The most commen species causing invasive infection is Aspergillus fumigatus, the most common pathogen in the section Fumigath, which historically has made up a vast majority of invasive isolates: A. flavus Aspergilustereus; and, less commonly for invasive infection, Arpergi- lus niger’ Recent studies have shown emergence of less common species, including A.terzus and unusual, less pathogenic species asthe ‘etiologic agents of invasive infection, including many ‘eryptic species" (hat are identifiable only by molecular studies." With more pro- longed and. profound smmunosuppression—along with molecular ‘dentscation of cryptic epecies within a species complex, the list of fare species causing invasive infection continues to increase, ineluding A. alabamensis, A. alliaceus (teleomoxph, Petromyces alliceus), A favenaceuns, A, caesiellus, A. candidus, A, carneus, A. chevalier (leo morph, Eurotium chevalier, A. clavatus, A. calidoustus, A. flavipes, A. fumigataginss. A. glaucus, A. granulosus, A. insuetus, A. Kevei, A Tentulus, A. nidulans Emericela nidulans), A. novefumigatu, A. ochra- us, A oryzae, A. puniceus, A, pseudodeflectus, A restricts, a. sydowi Emericella quadrlineata (apamorph, A. terazonus), A. tamari, A tanner, A. udagava (Neosartorya udagawae), A. tubingensis, A. ves color, A. viridinutans, A. vitus (eleomorph, Ewrotium amstelodami), A. ‘went, Neosartorya pseudofichers, and many others, although the suthenticity ofa least some ofthese has been questioned and peshape ‘misidentified prior to molecular studies" Pathogenic Apegillus species are easily cultured from pathologic samples and grow rapidly (in 24 to 72 hours) on a variety of media, Blood culture are uncommonly postive and wrually reflect contami nation rather than invasive disease,” A distinguishing characteristic of pathogenic Aspergilur species is thet ably to grow at 37°C. A. fumlg- ftus able to grow at 50°C, a feature than addition to morphology, tan also be used to identify this epecies and can help distinguish Fumigutus {rom eryplic Aspergiliue specice inthe A. fumigatus complex." Most species initially appear as emall, uy white colo- rics on culture plates within 48 hours, Presumpive identification of an Aspergillus species complex is usually accomplished by sppearance ofthe fungus on gross and microscopic inspection ofthe colony whieh ‘provides typical sporulation, although specific species-level identifi ‘Gon requires molecslar confirmation so tha laboratories shosld report isolates identied phenotypically asa “species complex” “Microscopic features and colony morphology for tae most common clinical isolates, A. fumigatus, A. flavus, A. terreus, and A. niger are described in Table 2591 and shown in Figures 259.1 (0-259, FIGURE 259-1 Aspergillus fumigatus. A, Cray-creen colony mor pirogy on potato flakes aga, B, Unie ateconidgphore wth columnar oni (20). (Courtesy Dr Deanna Sutton) Species-level identification of Aspergillus hae hecome increasingly ‘important because of differences sn anungal drug susceptibility.” "A, fumigatus ie the most frequent species in invasive infection, 6 aagross Determine ot eum I say. itns I total aE 500 Id. consider kn Testor measure Ee Acer Conse retest ith ease ‘iocesaton and perm other Sagrestic ‘Therapy for Exacerbations of ABPA. Cericoserids 05:2 mahgiéy acl Recommended fer ease (ednsene equvslerttmoxmum—evacwston nal patents exept So mais Tor 2 wh, tapered ‘hse win contcateoi tency ora ‘rsitunga therapy Gvacenaele—er ‘ter ale nth Asner Seysiorcoszae posscoacok| 1 total aE 20050 tL. repeat if Slow coricostri respense or Tovey, taconaole 3 rahoisy pt doo maha "ees Fecesary (orconazle or escoracle ray ce eecive Siren traconazab fi nt ‘enensieh toses) + manor her ‘Reet test duron 3-8 mo No evence for efficacy n 857A ‘ot may eset natn ‘enol 9 seach for source of ernie mols eps Adjunctive nea: hale orsonerasy erent ‘ata om referees 78 102 ord 10H for asthma in thote who had previously failed therapy with itraconazole." Other Allergic Manifestations Asperglls isan occasional cause of allergic fungal sinusitis, although most cases in the United States are due to dask-walled molds." This ‘entity occurs inpatient with aistory of chronic allergic rhinitis often ‘with hyperplastic nasal mucosa forming nasal polyps. A mass ol insps- ‘ated meus forms in sinus cavity with Aspergilus hyphae and Charcot Leyden crystals, The sinus mucosa is hyperplastic but not invaded." ‘Management is directed al aerating the sins and ensuring that tue invasion is not present, The benefit of Weating with ether intanasal corticosteroids or systemie antifungal agents has not been shown. Saprophytic Colonization and Superficial Aspergillosis Fungus Balls due to Aspergillus A pulmonary fungus ball due to Aspergilus—or aspergilioma—is « Solid mass of hyphae growing in a previously existing pulmonary Infectious Diseases and Their Etiologic Agents Part i 2902 8 FIGURE 259-8 Computed tomography of chest. A, “Halo” sion of low attenuation surrounding a nodular ung lesion detected in early pul- monary aspergoss. B, “Arcrescerc” sign m a rodalar lung iilate 36956 (Courtesy Dr Reginalé Greene) nodular lesions may cavitate (oewally in temporal astociaion with recovery of neutrophil), forming an “st-erescent sign (see Fig. 259- SB). These radiographic features are characteristic of invasive pulmo- rary aspergillosis, but similar findings can also oceur with other angioinvasive organisms, including Mucovales, Fusarium, and Scedo~ sporium, as well as bacterial pathogens ‘Tracheobronchitis Aspergls in the sways can range in significance from colonization, wich is common in lung transplantation, to uleerative tacheebron: iis "The syndrome of dspergillu tracheabronchitietypially occurs inpatients undergoing lung transplantation and in patients with AIDS. and is characterized by extensive preudomembranaus of ulcerative lesions due to Aspergillus" Tn patients undergoing lng transplanta tion, the infection often occurs atthe suture line ofthe lung transplant and can lead to debiscence of the anastomotic site, Symptoms oft cheobronchitis are nonspecific and include dyspnea with ascocisted pulmonary function abnormalities, cough, chest pain fever, or hemop: {ysis Symptoms may be mild and ean be confused with other cauze, including graft tection, Results of plan radiographs may be norma so that clinical suspicion is needed to establish the diagnosis, which is accomplished by bronchoscopy with biopry to document tise iv sion. A prolonged course of a systemic antifungal agent is ervally requited for treatment, although aerosols of liposomal formulations of ‘amphotericin B have been used for prophylaxis or localized dieeare Sinusitis Aspergillus infection ofthe sinsses and nasal cavities in immunocom ‘promised patients manifests ar acute invasive thinosinusitis oft association with invasive pulmonary aspergillosis.” The clini: ‘manifestations are not specific to Aspergillus and include fever, cough, epistaxis, sinus discharge, and headaches. Clinical signs are also non. ‘liagnostic, but findings of an ulcerative nasal lesion with an eschar oF ronsensitve area may be a clue to a fungal diagnosis,” Presence of epistaxis or unexplained fever in a high-risk patient may warrant endoscopy and biopsy of a nasal mucosal lesion. In paients with pro {gressive infection, the disease spreads to contiguous Paranasl sinuses, palate, obit or brain. The mortality in invasive cases is igh, ranging from 20% in patients with leukemia in remission to up to 100% in palients with relapsed leukemia or those undergoing IISCT’ Plain FIGURE 259-9 Computed tomography of sinuses showing sinus ‘wall thickening radiographs are not diagnostic and do not distinguish fungal causes from other eauss of sinusitis. Sinus CT scans ae useful for establish ing extent of infection and determining local tissue invasion (lig 259-5) Routine surveillance cultures of the nose have been advocated, That these lack specificity and sensitivity. Cultures from sinus aspirates ae useful to demonstrate the presence of Asperglus, but a biopsy with tiseue invasion e needed for the diagnos" Therapy for these infec tons is often dificult and requites long-term administration of ant fungal medications” The role of surgery is controversial, ESicacy of antifungal prophylaxis has not been demonstrated, but attempts at reduction of environmental exposures im high-risk patents may be beneficial” Disseminated Infection Progressive invasive pulmonary aspergillosis often results in disemt rated invasive aspergillosis, & complication associated with an ‘extremely high mortality” In patients with severe and ongoing imm- rosuppression, disseminated infection can occur with mortality rates Ihitorically greater than 90%.” Even with advances in antfungel therapy, mortality rates in disseminated disease oceureed i approx: ‘mately 50% in the TRANSNET study. Other Invasive Syndromes Cerebral Aspergillosis Cerebral aspergillosis is associated with the highest mortality of favac sive aspergillosis syndromes, with mortality ates of more than 90% in most series" The ineidence of cerebral aspergillosis is dificult to delermine because the diagnosis is often unsuspected, but it as been ‘estimated to occur in 10% to 20% of al cases of invasive aspergillosis, ‘usualy in patients with persistent immunosuppression and dissemi nated disease In one series of patients undergoing HSCT, Aspergi- ines found in 58% of simple cerebral may occur an extended time ait te always associated with extensive immunosuppresson, such as therapy for graftversushost disease!” Concomitant pulmonary infection i usually but not always present!” Isolated cerebral aspergillosis can ‘occu in immunocompetent patients or inthe setting of injection drug ‘sein which case i may be associated with a slighty better prognosis FIGURE 259-10 Brain abscess of invasive aspergillosis with ring ‘enhancement and extensive edema. provided the diagnosis is made and surgical drainage or removal is performed.” Aspergillus meningitis i rare, The clinical presentation of cerebral aspergillosis is nonspecific and is characterized by focal neurologic sigs, alteration in mental tatu, and headaches."" On CT of the brain the appearance is nonspecific and is similar to that of other {infectious causes of brain abscess with ring enhancement af the abscess slong with euzrounding edema (Fig. 259-10) and may be hem thagle."* Magnetic resonance maging (MRI) may reveal additional lesions, but the fndinge ae sill nonspecific. Conirmation ofthe diag ‘nosis requizes biopsy, but the diagnosis is often presumed. In patients without a dear diagnosis, biopey is recommended because the difer ential diagnosis is extensive, including other fungt and an extensive array of opportunistic diseases. Until recently, the outcome of this Infection has been almost universally fatal although voriconazole has been associated with favorable responses in approximately 30% of patients Bone Aspergillosis Acpergillas osteomyelitis isan uncommon finding of invasive asperil: joss. Vertebral osteomyelitis can result fom local extension of an Anpergills empyema. Aspergillus osteomyelitis can also be seen as 4 ‘complication of disseminated infection or as a primary infection in certain risk groups such as chronie grantlomatous disease or in intra ‘venous drug use, Vertebral osteomyelitis i the most common site for hematogenous spread to bone, usually involving the lambar region. “The lesions can be seen on plain radiographs (Pig. 259-11) a8 well as ‘on aCT or MRI, which can be ureful to stage the infection and to guide needle biopsy of the lesion. Favorable responses with voriconazole in ‘Acpergills osteomayelit of the spine exceeded 60% in one review, although the need for long-term therapy and surgical intervention in ‘medically nonresponsive patients ie noted. Infection of an interver. {eral disk is arate complication of hematogenous spread or surgery fon the disk, Cutaneous Infection Skin involvement by Aspergillus can either represent disseminated hematogenous infection of local inoculation of infection that may arise round an intravenous catheter insertion site or the surrounding areas ‘overedby adhesive dressings” Whereas most lesions occur in patiente ‘with neutropensa ori other immunocompromised patients, Aspergl lus can aleo invade patients with burns or surgical wounds, Clinically, the lesion isan area of rapidly increasing erythema with a necrotic, often ulcerated, center (Fig. 259-12). The lesions resemble pyoderma gangrenostim, Pathological, invasion of blood vessels and cutaneous ‘lcefation occurs, Cataneote disease can also be a manifestation of widespread disseminated disease, and in that selling askin biopsy can be relatively easy method to obtain tissue to establish the diagnosis of invasive aspergillosis. 2903 FIGURE 259-11 Radiograph of spine showing bone destruction associated with spinal aspergillosis. FIGURE 258-12. Necrotic skin I Other Sites Invasive aspergillosishas also been reported in anecdotal cases to cause {nfetion in virtually al body sites, including the heart, kidney, esopha gus, intestine, and others. Aspergilus endocarditis can occur in ether ‘ative or prosthetic heat valves, " Diagnosis is difficult beeause blood cultures usually remain ncgative even with extensive diteate.™ Even with surgical intervention, long-term survival is limited, although favorable outcomes with newer agents, particularly voriconazole, have been reported.” Aspergillus pericarditis also associated with dis seminated infection but can occur because of local extension of inva sive pulmonary aspergillosis and can be complicated with cardiac tamponade, Some. of these uncommon syndromes appear more ‘common in certain epidemiologic setings. Renal infection occurs in patients with AIDS of witha history of injection drug use DIAGNOSIS AND ANTIFUNGAL RESISTANCE ‘A proven diagnosis of invasive aspergillosis requires a tissue biopsy showing invasion with byphae and a positive culture for Agperglie. sapads sn6inésy @g2 sade 2904 ‘he diagnocie can also be established with positive cultures from a normaly sterile ste such a8 a needle biopsy oF cerebrospinal sid (CSE), although blood cultures are rary positive.” Tissue biopsies may not be possible because of potential risks, although Aspergillus Ihyphae are easly seen with common fungal stsine such az Gomori methenamine aver or periodic acid-Sebill, Aspergillus hyphae aze hyaline, septate, uniform in diameter, acute-angle branched, and 3 to 6 um in width ® Although these features usually distinguish Aspergi lus fom agents of mucormycosis, they are not distinguishable from & number of other opportunistic molds, including Fusariuns, Seedospo rum (Pseudalescheria),Paccilomyces, and others, s0 thal a positive calure is needed to confirm the diagnos" Galsures for Aspergillus in respiratory samples in high-risk patients, ‘particularly i obtained via bronchial alveolar lavage ean support the Aliagaosi of probable invasive aspergillosis" Aspergillus can also be callured from adult patient in whom no clinical ines is apparent to that positive cultures in patients with alow risk for invasive epergil- losis should be interpreted with ution.” Radiographic findings can alzo be used in the diagnosis and man- agement of invasive pulmonary aspergillosis. Pain chest radiographs ate of limited diagnostic utility because they are insensitive and find are nonspecific" A “halo” of low attenuation surrounding a ‘nodular lesion isan early nding in invasive pulmonary aspergillosis and has been red as a marker for initiating early antifungal therapy!" Uhe volume oflesions may increase over the first 7 days of infection, even when therapy is successful, so tha early radiologic progression should be interpreted cautiously.”' The CT findings of sve pulmonary aspergillosis have been validated in high-risk. new- twopenic, and bone marrow transplant recipients, but in other patients, Infectious Diseases and Their Etiologic Agents including solid-organ transplant recipients, the CT findings are not as Useful Non-culture-hased methods have been weed to establish a rapid Aiagnosis of invasive aspergillosis Antibody detection is of limited lulity because immunocuppressed hosts fal to mount an antibody response even with invasive infection." Detection of galactomannaa, by enzyme immunoassay hae contributed substantially o the digg. nosis of invasive aspergillosis This assay has been validated in a varie of patent groups. Studice have suggested a senility as high 8 89% and a specificity of 924 in high tsk HSCT patents." Other studies have found the assy tobe less sensitive (40% to 30%), relect- ing the impact of prior antifungal therapy in tedueing the level of circulating galactomannan, a limited number of samples per patient, fextent of infection, and other variables" This has resulted in re fommendations fora lower extol fora postive tet rerul, especial Ihigh-risk patients wath greater probability af infection." A meta analysis using an optical density index cutoff of greater than or equal 0 05 showed a sensitivity of 78% and a specsiety of 81%." Fase Positive results have been reported, including in some neonate, which may be due to dietary intake or the presence af cross-reacting antigens with bacteria such as Bifidobacterium, and in patients receiv ing therapy with piperailinitazebactam—which nove appears to be ‘uncommon—and other antibiotic." Galactomannan detection also has been used for other body fluids such as CSE and in bron: ‘hoalveolar lavage fluid." Galactomannan results from bronchoal- veolar lavage uid testing demonstrate sensitivity that is greater than. that seen in serum testing and may be less affected by antifungal therapy” A negative test result may be useful in ruling out 4 diagnosis of invasive pulmonary aspergillosis." Some colonized ppalients such as thore with chronic obstructive pulmonary diteate or those undergoing lung transplantation may have a positive galscto- mannan result and not have evidence of invasive infection "Ser ‘esesements of galactomannan may offer prognostic value in outcomes of infection, Other potential markers also include the nonspecific fungal marker f--glucan.”™ Several reports demonstrate the potential for using polymerase chain reaction assay ae an catly diagnostic marker for invasive apergil- losis, which may be more sensitive than other methods!" ‘ese asays are not standardized and remain investigational, although hie approach sing ¢erum/blood or other body duds, swch ae bron choalveolar lavage fui, i promising for improving the diagnosis of invasive aspergillosis." Susceptibility testing for Aspergillus has been standardized, but correlation with clinical responses has aot been well established. ‘Antifungal esstance to itraconazole has heen reported that developed aller exposure to antifungal therapy and is associated with point muta lions in the

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