Lomentospora prolificans
a) Microscopic morphology of the colony (lactophenol cotton blue, magnification x400)
Lomentospora prolificans_2
b) Direct microscopic examination of a nasal swab with 20% KOH at ×400 magnification reveals hyaline hyphae and fungal spores

(Photos: M. Drogari-Apiranthitou, Infectious Diseases Research Laboratory/4th Department of Internal Medicine, National and Kapodistrian University of Athens)

4. Lomentospora prolificans

Lomentospora prolificans (formerly Scedosporium prolificans or S. inflatum) is found in hydrocarbon-contaminated soils (oil-soaked soils), sewage, manure, and decaying organic material, mainly in dry and warm climates. It has been primarily identified in Australia, the southern United States, and Spain, particularly in areas with significant human activity.

It primarily affects immunocompromised individuals, such as those who have undergone solid organ transplantation, and especially patients following hematopoietic cell transplantation (HCT). It can infect the skin, sinuses, lungs, or the central nervous system. In cases of brain abscesses, delayed treatment is associated with mortality rates exceeding 75%. Phylogenetically, it differs from Scedosporium species and has been reclassified under its original genus, Lomentospora.

Diagnosis, as in other hyalohyphomycoses, is based on direct microscopy, culture, and histopathology. In contrast to Scedosporium, L. prolificans is unable to grow in the presence of cycloheximide. Blood cultures are positive in over 50% of cases. Colonies are olive-grey to black. Microscopically, the fungus is identified by its flask-shaped conidiophores with a swollen base, from which conidia arise either individually or in clusters. However, species identification should be confirmed by sequencing the internal transcribed spacer (ITS) gene region. MALDI-TOF mass spectrometry is increasingly used as a rapid and accurate identification method for Scedosporium/L. prolificans species.

Treatment is challenging due to the organism’s broad resistance to antifungal agents, with mortality reaching up to 95% in severely immunocompromised patients. Voriconazole demonstrates the strongest in vitro activity and may be more effective when combined with colistin, terbinafine, or caspofungin. Combinations of azoles with terbinafine, or sequential administration, also appear to be effective. The emergence of olorofim as a novel antifungal offers a promising alternative, with low MICs demonstrated in a murine experimental model. Management of L. prolificans infection focuses on restoring immune function, surgical debridement of infected tissues, and the use of voriconazole combined with terbinafine as first-line therapy.

In the present case, the patient received antifungal treatment with voriconazole. Despite a high MIC (8 mg/l), cultures soon became negative. However, the patient ultimately succumbed due to the rapid progression of her underlying disease.

[Case editor: M. Drogari-Apiranthitou, Research Laboratory of Infectious Diseases, 4th Dept of Internal Medicine, National and Kapodistrian University of Athens]

 

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