Acremonium kiliense: Reappraisal of Its Clinical Significance

Abstract

A case of Acremonium kiliense peritonitis is described. Diagnosis was established by repeated isolation of the fungus from peritoneal dialysate and by its identification on the basis of morphological characteristics and sequencing of internal transcribed spacer (ITS) regions of ribosomal DNA (rDNA). This report and available literature suggest that A. kiliense may have a greater clinical significance than hitherto recognized. CASE REPORTA 75-year-old Jordanian man with a long history of diabetes mellitus and hypertension developed end-stage kidney disease requiring continuous ambulatory peritoneal dialysis (CAPD). His course of CAPD was largely uneventful except for a single episode of bacterial peritonitis, for which he was hospitalized and treated with parenteral antibiotics, with an excellent response. In January 2010, he became febrile, with clinical evidence of peritonitis, and was admitted to the hospital. The peritoneal fluid was turbid, with a white blood cell (WBC) count of 2.1 ϫ 10 9 /liter. On initial microscopic examination, the presence of fungal elements in the peritoneal dialysate was missed. The peritoneal fluid sample was inoculated into aerobic Bactec blood culture bottles, which yielded a growth after 59 h of incubation. The Gram-stained smear from blood culture bottles showed branched hyphal elements. On Sabouraud dextrose agar (SDA; Oxoid Ltd., Basingstoke, England), the specimen yielded slimy colonies with a pinkish appearance ( Fig. 1). Microscopic examination of the primary culture (isolate Kw441-2010) showed hyaline hyphae, with scanty sporulation. A provisional identification of Acremonium/Fusarium species was made, and the growth was subcultured on Sabouraud dextrose agar and oatmeal agar (OMA; oatmeal [30 g], agar [20 g], distilled water [1 liter]) for further identification and antifungal susceptibility testing. Subsequent cultures of the peritoneal fluid yielded the same fungus on three occasions. A serum sample was obtained for the detection of galactomannan (Platelia Aspergillus enzyme immunoassay [EIA] kit; BioRad, Marnes-la-Coquette, France) and (1-3)-␤-D-glucan (Fungitell; Associates of Cape Cod); the latter test was positive (253 pg/ml). An Etest performed on RPMI 1640 medium supplemented with 2% glucose revealed that the isolate was resistant to amphotericin B and caspofungin but susceptible to voriconazole and posaconazole, with MIC values of Ͼ32 g/ml, Ͼ32 g/ml, 0.064 g/ml, and 0.75 g/ml, respectively. The patient was started on voriconazole, with a loading dose of 400 mg, followed by a maintenance dose of 200 mg, given every 12 h via the oral route. Although the patient showed clinical improvement after 2 weeks of voriconazole therapy, the peritoneal dialysate remained turbid (WBC counts, 2.0 ϫ 10 9 / liter). Abdominal ultrasound examination did not reveal any evidence of intraperitoneal adhesions or organ invasion. Since the response to treatment was not adequate, the Tenckhoff catheter was removed and the patient was temporarily switched to hemodialysis. After 1 week of a...

In Vitro Evaluation of Antifungal Drug Combinations against Sarocladium (Acremonium) kiliense, an Opportunistic Emergent Fungus Resistant to Antifungal Therapies

“…However, the presence of underlying immunological disorders can predispose to the development of a usually fatal systemic infection (3). The optimal treatment for these infections is unknown; however, amphotericin B (AMB) seems to be the most efficacious drug, although therapeutic failure has also been reported (3,4). In addition, this drug shows important side effects that are commonly incompatible with use by patients in poor health.…”

Evaluation of the Efficacies of Amphotericin B, Posaconazole, Voriconazole, and Anidulafungin in a Murine Disseminated Infection by the Emerging Opportunistic Fungus Sarocladium (Acremonium) kiliense

“…Recently, based on molecular studies, this fungus has been transferred to the genus Sarocladium as Sarocladium kiliense (1). This species is the most clinically relevant of the genus and apparently also the most virulent (4,19,20). Considering that the morphological identification of these fungi is difficult, it is likely that some clinical isolates of this species have been misidentified as Acremonium strictum, another clinically important species of Acremonium (19).…”

“…A cremonium kiliense is a saprobic fungus with a worldwide distribution which has been reported in recent years as an emerging opportunistic pathogen able to cause a wide range of human infections (1)(2)(3)(4). Localized infections, such as mycetoma, keratitis, or onychomycosis, are acquired mainly by immunocompetent patients through trauma (5)(6)(7)(8)(9)(10)(11).…”

Purpureocillium lilacinum as a Cause of Cavitary Pulmonary Disease: a New Clinical Presentation and Observations on Atypical Morphologic Characteristics of the Isolate

“…The Etest (bioMérieux, Marcy l'Etoile, France) was employed to determine MICs of five antifungal agents as described previously (17). Briefly, the test was performed on RPMI 1640 me-dium supplemented with 2% glucose, and the pH was adjusted to 7.0 with 0.165 M morpholinepropanesulfonic acid buffer.…”

“…The divergent domains (D1/D2) of the 28S rRNA gene were amplified with the NL-1 and NL-4 primers, the internal transcribed spacer (ITS) region (ITS1, 5.8S rRNA, and ITS2) of ribosomal DNA (rDNA) was amplified with the ITS1 and ITS4 primers (3), and the variable region of the ␤-tubulin (benA) gene was amplified by using the BTUBF (5=-TGGTAACCAAATC GGTGCTGCTT-3=) and BTUBR (5=-GCACCCTCAGTGTAGT GACCCT-3=) primers, while the variable region of the calmodulin gene was amplified by using the Cmd5 (5=-GTCTCCGAGTACA AGGAGGC-3=) and Cmd6 (5=-TCGCCGATRGAGGTCATRAC GTG-3=) primers, and the amplicons were sequenced as described previously (3,16,17). The sequencing primers included BTUFS1 (5=-TAACCAAATCGGTGCTGCTTTCTG-3=) and BTURS (5=-C CTCAGTGTAGTGACCCTTGGC-3=) for the ␤-tubulin amplicon and CMDFS (5=-TCCGAGTACAAGGAGGCCTTC-3=) and CMDRS (5=-GATAGAGGTCATRACGTGRCGCA-3=) for the calmodulin gene fragment.…”