#3. tinea capitis scalp skin#

Human neutrophils have been shown to destroy up to 60В % of dermatophyte germlings within 2В h macrophages kill up to 20В % in a similar time. Killing of dermatophytes by both murine and human neutrophils and macrophages can also be demonstrated. The mechanism is thought to underlie the observation that tinea capitis is largely seen in children, as at puberty, the relative composition of different unsaturated fatty acids in sebum is altered. This activity appears to reside in saturated fatty acids with chain lengths of 7, 9, 11 and 13 carbon residues. Other innate inhibitory mechanisms, important in the scalp, include medium chain length fatty acids in sebum which are inhibitory to dermatophyte growth. Microsporum canis infection has also been shown to trigger rapid secretion of IL-1ОІ both in vitro and in vivo, and this is dependent on the activation of inflammasomes, intracellular multiprotein complexes that control the release of Il-1ОІ.

#3. tinea capitis scalp skin#

These peptides are known to have activity against bacteria, viruses and fungi and play a key role in protection against skin infections including dermatophytes as well as Candida albicans. The expression of naturally produced antimicrobial peptides, including human ОІ-defensins (hBDs), cathelicidin LL-37 and dermicidin, provides a major source of innate defence.

Generally, the fungi are prevented from invading human skin in a number of different ways. Other enzymes such as sulphur transporters are also involved. Proteases with keratinase activity from certain dermatophytes are inducible by low-molecular-weight peptides released from the epidermal cells by the action of other fungal proteinases. In Microsporum canis, at least three genes, SUB1, SUB2 and SUB3, have been identified encoding serine proteases associated with infection. Dermatophytes produce a variety of proteolytic enzymes, which work in acid, alkali or neutral environments, and these protease genes are variably expressed with distinct enzyme patterns being found in infections versus cultured conditions. Hair penetration by dermatophytes involves the production of proteases, some of which are inducible in the presence of amino acid residues as well as disruption of intercellular junctions due to hyphal turgor pressure. After apposition to the hair shaft dermatophytes develop modified intercalary cells, known as penetrating organs, around which hair shaft invasion is centred. The process is accompanied by structural changes in the organism such as swelling of arthrospores and the expression of an extracellular fibrillar layer. This has been shown to be a time-dependent process in which the invading arthrospore is attached to an underlying keratinocyte over a 2вЂ“3В h period before germination. After transfer of fungal cells from one host to another, the first phase of epidermal or hair shaft invasion in tinea capitis consists of adhesion between fungal cells and keratinocytes. It is still not clear whether this reflects the level of immunological responsiveness to these infections and the vast majority of those affected have no underlying predisposing illness. In some patients, there is a pronounced inflammatory reaction, a feature often seen in zoophilic infections or those spread from animals to human by contrast in others, particularly those with anthropophilic dermatophytosis spread from human to human, lesions are often non-inflammatory and persistent. There is a spectrum of clinical reactions in tinea capitis that also reflects the pathological changes. However, over the last 10вЂ“20В years, this situation has changed with the spread of organisms, in particular Trichophyton tonsurans, in the Americas, Europe and Africa.

Although prevalent in many countries in the early twentieth century, it was brought under effective control in Europe and North America after the introduction of griseofulvin and concerted public health interventions, whereas it remained endemic in other regions. Its clinical manifestations range from mild scaling with little hair loss to large inflammatory and pustular plaques with extensive alopecia. Tinea capitis is a common infection of the scalp hair caused by dermatophyte fungi and occurring predominantly in children.