During initial infection, the fungal spores would appear to enter through the unbroken cutaneous surface, and to germinate mostly in and around the hair follicle and sometimes in the shaft of the hair. Species
Favus is the first human fungal disease in which a fungus was definitely identified by J. L. Schönlein in 1839. The discovery was published in a brief note of twenty lines in Müllers Archiv for that year (p. 82). In 1841, the Hungary-born French physician David Gruby independently described the fungus associated favus. The fungus was subsequently named by Robert Remak as Achorion schoenleinii in honor of its discoverer. In 1892, two additional "species" of the fungus were described by Paul Gerson Unna, the Favus griseus, giving rise to greyish-yellow scutula, and the Favus sulphureus celerior, causing sulfur-yellow scutula of a rapid growth. This was in the days before scientists learned to rigorously distinguish microorganism identities from disease identities, and these antique, ambiguous disease-based names no longer have status either in mycology or in dermatology today. Similar looking infections, sometimes diagnosed as favid but more often as atypical inflammatory tinea, may be caused by more common dermatophyte infections, in particular Microsporum gypseum, the most common soil-borne dermatophyte, and Trichophyton quinckeanum. The latter was previously called Trichophyton mentagrophytes var. quinckeanum, the agent of mouse favus infection.
This study suggests that a buccal swab approach can be used to informatively examine mitochondrial dysfunction in children with seizures and may be applicable to screening mitochondrial disease with other clinical presentations.Proceedings of the National Academy of Science of the United States of America published an article investigating the human mitochondrial tRNA (hmt-tRNA) mutations which are associated with mitochondrial myopathies. Since the current understanding of the precise molecular mechanisms of these mutations is limited, there is no efficient method to treat their associated mitochondrial diseases. All pathogenic mutants displayed pleiotropic phenotypes, with the exception of the G34A anticodon mutation, which solely affected aminoacylation. See also
Epilepsy
Mitochondrial disease
Myoclonus
Ragged red fibers

References
External links
MERRF+Syndrome at the US National Library of Medicine Medical Subject Headings (MeSH)
merrf at NIH/UW GeneTests