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. Your Questions answered:
.9
What are the local factors??? :--Local factors that
favor dermatophyte infection include
sweating occlusion occupational exposure geographic
location high humidity .
A problem to
think about intelligence of our ancestors!!!! In India a common cause for persistence is the type of clothing : Cause : A in India Change of clothing
pattern: 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. Cause : B in India
:-use of leather shoes : the other observation is that the use of leather shoes predisposes to tinea Pedis. Tinea Pedis is rarely seen a villager who usually works barefooted . having tinea Pedis though the well heeled
usually have tinea Pedis and commonly onychomycosis both being causes of relapse.
Q. 1: What are dermatophytes?? How one can
classify the CLASSIFICATION OF
DERMATOPHYTES i.e. fungus which have affinity for skin only??
Mode of
transmission :What may be source of
fungus??? Dynamics of spread of Fungus
to a healthy men/ women ??:--1) Anthropophilic
: Person to person transmission
by fomites and by direct contact( so onwards please make a point to
invite to count money as U receive at your chamber to avoid Anthropophilic contaminating of Fungus) .
2) Zoophilic : Animal to human transmission by direct contact or by fomites. FROM PETS TO WOMEN
3) Geophilic
: Originating in soil. Wives of agricultural
men & women who works at feild .
Q. 2 :Which fungi have a protracted course?? The
importance of this is that zoophilic species would mount a severe inflammatory reaction and thus clear
early whereas the anthrophilic species (Person to person
transmission by fomites 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 involves the following
Q. 3:- Sites of Fungal infestations site 1 is
epidermis :--Epidermal fungal
infection ??? dermatopytosis; Tinea facie, tinea corporis
, tinea cruris , tinea manus , tinea
Pedis
Q. 4: Sites
of Fungal infestations :: nail
apparatus :: Are U a surgeon?? :Fungus will love you most :: : Know about Dermatophytoses
of nail apparatus in
details as your fungus is less likely to response to common
agents . Why?? U frequently wash your hands with soap/ alkalis:-
Tinea unguium
Q. 5: Sites
of Fungal infestations: Nail infestations:-Onychomycosis is a more inclusive term
including nail infections caused
by dermatophytes yeasts
and molds.
Q. 6 :- Dermatophytoses
of hair and hair follicle
Tinea capitis dermatophytic
folliculitis Majocchi granuloma
tinea barbae.
Q. 7 :--Pathogenesis of fungal infections : Why & when ???
Ans:-The pathogenesis of dermatophytosis has three main
aspects which determine its course. This includes the A) host
response B) barrier function and C) load of the fungi . 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 anti fungals 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.
Q.8:--Why
all women don’t suffer from Fungal infections of Vulva and adjoining skin?? ::: Steps on pathogenesis of fungal infestations?? Ans: Dermatophytes synthesize keratinases that digest keratin and sustain existence of fungi in keratinized structures ,. Dermatophytes that initiate little
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 lead 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 fuly keratinized hair
shaft nail plate or keratinized nail
bed Mannans in the cell walls of
dermatophytes have immune inhibitory effects. In T rubrum the mannans may also
decrease 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.
Q
How beneficial is sebum???? 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 pathogencity. Host
factors that facilitate
dermatophyte infections include atopy
topical and systemic
glucocorticoids ichthyosis
collagen vascular disease.
What factors control the clinical
presentation of dermatophytoses ?? It depends on several
factors. Site of infection
immunologic response of the host and
species of fungus.
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