Resistant Fugal infections

Let us talk on Fungal (DERMATOPHYTES) infection of female body :

Fungus what we need to know ?? Ponit 1: CLASSIFICATION OF DERMATOPHYTES

A)Anthropophilic : Person  to person  transmission  by fomites and by direct contact.

B)  Zoophilic : Animal   to human transmission by direct contact  or by fomites.

C) Geophilic : Originating  in soil.

The importance    of this is that zoophilic species would mount a severe inflammatory reaction    whereas   the anthrophilic species ( which is transmitted by person  to person )  transmission  by fomites and by direct contact)  would mount a milder reaction and thus would   lead to a more persistent  infection However these groups  are not    sharply  demarcated as geophilic species may infect animals. In vivo dermatophytes   grow only on or within   keratinized structures and as such involve the following 

Epidermal dermatopytosis; ) A)  Tinea   capitis(over head)   dermatophytic  folliculitis   B) Tinea facie(face), C) tinea    corporis (body –say abdomen ,back side)  D) tinea cruris  -femoral-thigh areas E) tinea manum( fingers)  F) tinea Pedis(legs lowermost part)  G) Tinea unguium i.e. nails beds--special mention in the sense that Dermatophytoses of nail apparatus( Tinea unguium  )  . Spl points are  onychomycosis is a more inclusive  term including   nail infections caused by  dermatophytes  and also yeasts  and molds which may mimick Fungal infection . H)  Majocchi  granuloma nea  barbae(cheek of males) .

 How fungus does enters in human body?? Where is gate pass –It is keratinases enzyme which allow to eneter in the body be it head(capitis),Cheek of males Tinea facie(face), or say nails (Tinea unguium i.e. nails beds)   !!!  Pathogenesis  of human fungal infections:-The     pathogenesis of dermatophytosis has    three main  aspects which  determine   its course. This includes the Factor I :-host response  Factor 2 How epidermis behaves the  barrier   function of skin and Factor  3:- aggressiveness the fungi .  There is usually no drug resistance in case of most fungal infection and antifungal agents . The    frequent cases of relapse which are mistaken for resistance are due to   the ambient local factors. Clinical resistance is a wrong term as in vitro resistance    is rare    is probably due to the interplay of the fungal species and the host immune response. Thus it is meaningless to prolong the duration of antifungals  or even combine and add   oral azoles to the therapy as that is not a solution when microbiological resistance  is not an issue as is the case.

Steps on pathogenesis:-What is keratinases synthesized by Fungi-so that fungi are able to penetrate the epidermis and can get attached.

Dermatophytes synthesize    keratinases that digest keratin and sustain existence  of fungi in keratinized structures ..Dermatophytes that initiate   little inituial inflammatory response are better able   to establish chronic infection .Organisms  such as  Microsporum canis cause an acute   infection associated   with a brisk inflammatory     response and thus elad to spontaneous resolution. In some individuals    infection   seems  to involve the dermis    as in kerion and Majocchi   granuloma however it should be noted   that it is the inflammation which is extending  to the dermis and not the infection  as the fungus is present  only in stratum corneum  fully keratinized hair    shaft  nail plate    or keratinized  nail  bed .

To remember that “Mannans  in the cell walls of dermatophytes  “-à have  1)  immune inhibitory    effects. In T rubrum the mannans may also decrease   2) epidermal proliferation thereby decreasing the likelihood of the fungus being   sloughed off prior to invasion. This mechanism is though   to contribute   to the chronicity of infections caused by T rubrum.

Why fungal infn is hard to treat and achieve cure?? Poinits to  remember by the clinicians :-Local  factors  that favor dermatophyte  infection include sweating  occlusion   occupational exposure  geographic  location high  humidity     . In India a common cause for   persistence is the type of clothing We have   moved from cotton to denim the latter    being     a preferred cloth of the Western world   suited for their   cold climate. In our climate this prevents evaporation of sweat and thus    does not let the skin breathe. In our  practice almost  all such patients have   recurrences. Another observation is that the use of   leather shoes predisposes to tinea   Pedis. I have    rarely seen a villager who   usually works   barefoot having tinea Pedis though the well heeled usually      have tinea Pedis and commonly  onychomycosis both   being causes of relapse.

host factors The severity  of clinical  disease is also  affected by several  host factors. Sebum has an inhibitory  effect on dermatophytes and the degree of disease activity may be related to the number    and activity   of sebaceous glands  in a particular body    region. Breaks in the skin barrier or macerated skin encourage     dermatophyte invasion and increased   susceptibility   may be inherited or related    to the competency  of the  immune  system. Once  deramtophytes   have invaded and begun to proliferate in the skin several mechanisms  aid in   limiting the infection to keratinized  tissue. These include the preference of dermatophytes for the cooler  temperature at the skin  surface   serum factors that inhibit  dermatophyte  growth    and the host  immune system.

Cell mediated  immunity and antimicrobial activity  of polymorphonuclear leukocytes restrict  dermatophyte   pathogenicity. Host factors    that  facilitate   dermatophyte   infections include   atopy  topical and systemic   glucocorticoids  ichthyosis collagen   vascular disease.

Thus the clinical  presentation of dermatophytoses  depends   on several   factors. Site of  infection immunologic response of the host and  species   of fungus. An overview  of the treatment  is detailed