Truncal acne significantly impairs quality of life yet remains underexplored relative to facial acne, particularly with respect to fungal ecology. The trunk represents a distinct cutaneous niche characterized by thicker epidermis, larger follicular units, and frequent occlusion, and harbors a high abundance of Malassezia species. In this study, we used internal transcribed spacer 2 (ITS2) amplicon sequencing to characterize the truncal mycobiome in patients with acne and in healthy controls and to compare fungal community features across doxycycline exposure groups. Although serial sampling was planned, seven participants contributed a single follow-up sample after doxycycline treatment, and only two participants contributed multiple follow-up samples sufficient for true within-subject longitudinal analyses; therefore, most analyses represent exposure-stratified cross-sectional comparisons rather than confirmed temporal change. At baseline, truncal acne lesions exhibited increased fungal richness and distinct community composition compared with controls. Acne lesions were more frequently enriched for Malassezia globosa, whereas healthy controls were dominated by M. sympodialis. Across doxycycline exposure groups, fungal communities remained Malassezia-dominant with substantial inter-individual variability. Doxycycline exposure was associated with partial and heterogeneous differences in Malassezia species composition without uniform normalization toward control profiles. Because only fungal sequencing was performed, bacterial–fungal interactions were inferred from prior literature and not directly measured. These findings indicate that truncal acne is associated with a distinct fungal community structure and highlight the need for integrated, longitudinal multi-omics studies to clarify treatment-associated microbial dynamics.
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 ATCC 43894 (also known as EDL932) has been widely used as a reference strain for studying the pathophysiology of EHEC. To elucidate the role of a large virulence plasmid pO157 and its relationship with acid resistance, for example, both EHEC ATCC 43894 and its pO157-cured derivative strain 277 were well studied. However, it is unclear whether or not these two strains are isogenic and share the same genetic background. To address this question, we analyzed the whole genome sequences of ATCC 43894 and 277. As expected, three and two closed contigs were identified from ATCC 43894 and 277, respectively; two contigs shared in both strains were a chromosome and a small un-identified plasmid, and one contig found only in ATCC 43894 was pO157. Surprisingly, our pan-genome analyses of the two sequences revealed several genetic variations including frameshift, substitution, and deletion mutations. In particular, the deletion mutation of hdeD and gadE in ATCC 43894 was identified, and further PCR analysis also confirmed their deletion of a 2.5-kb fragment harboring hdeD, gadE, and mdtE in ATCC 43894. Taken together, our findings demonstrate that EHEC ATCC 43894 harbors genetic mutations affecting glutamate-dependent acid resistance system and imply that the pO157-cured EHEC 277 may not be isogenic to ATCC 43894. This is the first report that such genetic differences between both reference strains of EHEC should be considered in future studies on pathogenic E. coli.
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