Microsporia

Microsporia, a fungal disease of the hairy part of the head and skin (see Dermatomycetes). In typical cases, the foci on the head appear as limited spots of rounded shape, covered with small whitish scales and short (not higher than 2-3 mm above the level of the skin) hairs of a grayish-white color. Inflammatory phenomena are absent in most cases [see separate table (st. 47-48), fig. 6]. On smooth skin, on the neck, occiput, face, and chest, the lesions usually have a pale-pink color with a light-brown center and a reddish rim with fine scaling. Clearly expressed herpes-like plaques and rings, constituting the so-called microsporia circinata Jadassohni, are also encountered. The causative agent of the disease, Microsporon Audouini, was first discovered by Gruby in 1834. In 1892, Sabouraud finally established the independent nature of the disease. Microsporia differs from the causative agents of trichophytia and scabies not only by the small size of the spores but also by a whole series of cultural and biological features. Relatively rarely affecting adults, microsporia is very contagious for children and often causes large school epidemics in all countries of the world. Infection occurs either from animals (more often from a cat and a dog) or directly from one child to another. According to the latest data (Bruhns and Alexander), microsporia can saprophytize in the surrounding nature and thus serve as an accidental source of infection. But while in Western Europe and in America the main culprits of M. are human-type fungi and above all M. Audouini, in the USSR to this day no epidemic caused by this fungus has been described. Microsporia was first described in Russia by Bogrov (1911). This school epidemic was caused by animal-origin microsporon M. lanosum (M. canis, according to Bodin). This same species of fungus also figures in all later described epidemics of M. According to the materials of the Moscow orphanage and the State Venereal Institute in Moscow, M. Audouini apparently occurs in the USSR very rarely in general. There are essential differences between animal-origin microsporons and human-type ones. The former are easily inoculated on animals and above all on guinea pigs and rabbits (up to 100%); in humans they cause more numerous foci, which often acquire an inflammatory character, up to kerion Celsi, but they pass significantly faster. The Sabouraud culture on sugar agar reaches larger sizes (Micr. vivax, according to Sabouraud) and ages faster (pleomorphism). Micr. Audouini, like the related subspecies (M. depaupertatum Gueguen and others.), on the contrary, grows slowly; in a child they cause more benign lesions, but lasting for years, often until the onset of sexual maturity. The culture is inoculated on guinea pigs extremely rarely, and the process proceeds abortively. The relationship of the fungus with the hair is the same in both cases. The hair is affected from the epidermis. According to Sabouraud, the fungus initially multiplies intensively at the mouth of the follicle and fills the entire follicular opening in the form of a cone. From here, threads of mycelium penetrate into the epidermal cells of the follicle and envelop the hair. Thick threads of mycelium also grow along the hair, branch, and break down into spores. The reproduction of the fungus progresses continuously, so that the spores gradually become denser and take on their characteristic form of a dense mantle consisting of spores, chaotically arranged in contrast to the small-spored trichophytia, which is arranged in the form of a chain. At the root of the hair, the mycelium pierces the cuticle and, growing in the downward direction, form the so-called "Adamson fringe" (frange d'Adamson). The hair bulb remains free of fungi. The overwhelming majority of microsporons that envelop the hair are ectospores, i.e., spores formed by intrapilar mycelium breaking out to the outside through the hair cuticle. Only a small part of the spores consists of septated mycelium. Immunity phenomena in M. were studied experimentally mainly on guinea pigs. It has been proven that an animal that has once undergone M. reacts to a repeated inoculation of both homologous and heterologous strains of the fungus with increased sensitivity, which persists for at least 1.5-2 years. In a primarily inoculated animal, incubation averages 5-6 days, the process proceeds cyclically, acme is observed on the 12th-14th day after infection, spontaneous recovery is at the end of the 3rd or beginning of the 4th week. In the case of repeated inoculation, incubation is significantly shortened; the process in the overwhelming majority of cases proceeds violently and ends already on the 8th-10th day. In children, skin allergy in M. is rare and is disputed by some altogether. It is not in doubt, however, that under certain conditions in humans microsporia can cause a disease of a general nature. This is supported first of all by the so-called microsporides. In 1917, the first description was given of a secondary eruption in the form of small papules covering the whole body in a three-year-old child suffering from M. Clinically, the rash (lichen microsporicus) completely resembles trichophytides and, like the latter, is accompanied by increased temperature, general wasting, and joint pain. Over the past period, microsporides have been observed repeatedly by a number of authors, both Russian (Bobovich, Braude and Per) and foreign (Jessner, Arzt and Funs, etc.). The general nature of M. in humans is also supported by cultures (though single ones) isolated directly from the blood. Prevention, treatment - see Trichophytia.