Peer-reviewed veterinary case report
Fluconazole-resistant Cryptococcus infection found in a cat
By Kano, Rui et al.·Published in Mycopathologia·2015·Department of Veterinary Pathobiology, Japan·View original on PubMed →
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Original publication title: First Isolation of Azole-Resistant Cryptococcus neoformans from Feline Cryptococcosis.
- Species:
- cat
Plain-English summary
A cat with cryptococcosis, a fungal infection, was found to have a strain of the fungus that was resistant to fluconazole, a common antifungal medication. Testing showed that while this strain did not respond to fluconazole, it was still treatable with other antifungal drugs like amphotericin B and itraconazole. The researchers discovered that the resistance was due to the fungus producing more of certain proteins rather than a genetic mutation. This means that while fluconazole might not work for this particular case, there are still effective treatment options available.
People also search for: cat cryptococcosis treatment · fluconazole resistance in cats · antifungal medications for cats
Abstract
We report here, to the best of our knowledge, the first description of an in vitro fluconazole (FLZ)-resistant Cryptococcus neoformans var. grubii from a case of feline cryptococcosis. In vitro testing demonstrated that this isolate was resistant to FLZ (minimum inhibitory concentration, MIC, of 128 μg/ml) but remained susceptible to amphotericin B (0.064 µg/ml), itraconazole (0.38 µg/ml), voriconazole (0.023 µg/ml), and posaconazole (0.125 µg/ml). The predicted amino acid sequence of the lanosterol 14-α demethylase (ERG11) protein in the isolate was identical to that of the C. neoformans var. grubii reference strain, indicating that resistance was not mediated by mutation of the target gene's open reading frame. The RT-qPCR analysis for ERG11 and ATP-binding cassette (ABC) transporter-encoding gene (AFR1) indicated that the isolate increased transcription factor function of ERG11 and AFR1 than that of FLZ-susceptive strains. This observation, in combination with the lack of resistance to other azoles (that is, lack of crossresistance), suggests that resistance in our isolate was the result of overexpression of the endogenous ERG11 and ABC transporter.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/26162642/