As a result, the probability that pathogens will reach sufficient numbers to cause illness is reduced. Innate immune system
Microorganisms or toxins that successfully enter an organism encounter the cells and mechanisms of the innate immune system. The innate response is usually triggered when microbes are identified by pattern recognition receptors, which recognize components that are conserved among broad groups of microorganisms, or when damaged, injured or stressed cells send out alarm signals, many of which are recognized by the same receptors as those that recognize pathogens. Innate immune defenses are non-specific, meaning these systems respond to pathogens in a generic way. This system does not confer long-lasting immunity against a pathogen. The innate immune system is the dominant system of host defense in most organisms, and the only one in plants. Immune sensing
Cells in the innate immune system use pattern recognition receptors to recognize molecular structures that are produced by pathogens. They are proteins expressed, mainly, by cells of the innate immune system, such as dendritic cells, macrophages, monocytes, neutrophils and epithelial cells to identify two classes of molecules: pathogen-associated molecular patterns (PAMPs), which are associated with microbial pathogens, and damage-associated molecular patterns (DAMPs), which are associated with components of hosts cells that are released during cell damage or cell death.Recognition of extracellular or endosomal PAMPs is mediated by transmembrane proteins known as toll-like receptors (TLRs). TLRs share a typical structural motif, the leucine rich repeats (LRR), which give them a curved shape.
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.