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CLINICO STUDY O Disser M.D. (DERMA DEP M THE TAMIL EPIDEMIOLOGICAL, MYCOLO OF CHRONIC DERMATOPHYT rtation submitted in partial fulfilment of t Requirements for the degree of ATOLOGY, VENEREOLOGY & BRANCH XX PARTMENT OF DERMATOLOG MADRAS MEDICAL COLLEGE CHENNAI - 600 003 LNADU DR. M.G.R. MEDICAL UNI CHENNAI MAY - 2019 OGICAL TOSIS” the LEPROSY) GY IVERSITY

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Page 1: CLINICO EPIDEMIOLOGICAL, MYCOLOGICAL STUDY OF ...repository-tnmgrmu.ac.in/10948/1/202000119karunya.pdffounder of mycology. He also described ectothrix and endothrix infection of hair

“CLINICO EPIDEMIOLOGICAL, MYCOLOGICAL

STUDY OF CHRONIC DERMATOPHYTOSIS”

Dissertation submitted in partial fulfilment

M.D. (DERMATOLOGY, VENEREOLOGY & LEPROSY)

DEPARTMENT OF DERMATOLOGY

MADRAS MEDICAL COLLEGE

THE TAMILNADU DR. M.G.R. MEDICAL UNIVERSITY

CLINICO EPIDEMIOLOGICAL, MYCOLOGICAL

STUDY OF CHRONIC DERMATOPHYTOSIS”

Dissertation submitted in partial fulfilment of the

Requirements for the degree of

(DERMATOLOGY, VENEREOLOGY & LEPROSY)

BRANCH XX

DEPARTMENT OF DERMATOLOGY

MADRAS MEDICAL COLLEGE

CHENNAI - 600 003

THE TAMILNADU DR. M.G.R. MEDICAL UNIVERSITY

CHENNAI

MAY - 2019

CLINICO EPIDEMIOLOGICAL, MYCOLOGICAL

STUDY OF CHRONIC DERMATOPHYTOSIS”

of the

(DERMATOLOGY, VENEREOLOGY & LEPROSY)

DEPARTMENT OF DERMATOLOGY

THE TAMILNADU DR. M.G.R. MEDICAL UNIVERSITY

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CERTIFICATE

This is to certify that the dissertation titled

“CLINICO EPIDEMIOLOGICAL, MYCOLOGICAL STUDY OF

CHRONIC DERMATOPHYTOSIS” is a bonafide work done by

DR.KARUNYA.S, Post graduate student of the Department of

Dermatology, Venereology and Leprosy, Madras Medical College,

Chennai - 3, during the academic year 2016 - 2019. This work has not

previously formed the basis for the award of any degree.

Prof. Dr. A. RAMESH, Prof Dr.U.R. DHANALAKSHMI,

M.D., D.D.,DNB, (DVL) MD.,D.D., DNB Professor,

Professor, Professor and Head, Department of Dermatology, Department of Dermatology, Madras Medical College, Madras Medical College, Chennai- 600 003 Rajiv Gandhi Govt.General Hospital, Chennai- 600 003.

Prof.Dr.R.JAYANTHI, MD., FRCP(Glasg).

Dean, Madras Medical College & Rajiv Gandhi Govt General Hospital,

Chennai - 600 003.

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DECLARATION

The dissertation entitled “CLINICO EPIDEMIOLOGICAL,

MYCOLOGICAL STUDY OF CHRONIC DERMATOPHYTOSIS”

is a bonafide work done by Dr. KARUNYA S, Department of Dermatology,

Venereology and Leprosy, Madras Medical College, Chennai - 3,

during the academic year 2016 - 2019 under the guidance of

Prof. DR. A. RAMESH M.D., D.D., DNB (DVL) Professor, Department of

Dermatology, Madras Medical College, Chennai -3.

This dissertation is submitted to The Tamil Nadu Dr. M.G.R. Medical

University, Chennai towards partial fulfillment of the rules and regulations for

the award of M.D Degree in Dermatology, Venereology and Leprosy

(BRANCH – XX)

Prof. Dr. A. RAMESH, M.D.,D.D.,DNB (DVL),

Professor, Department of Dermatology,

Madras Medical College,

Chennai - 600 003.

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DECLARATION

I, Dr.KARUNYA. S, solemnly declare that this dissertation titled

“CLINICO EPIDEMIOLOGICAL, MYCOLOGICAL STUDY OF

CHRONIC DERMATOPHYTOSIS” is a bonafide work done by me at

Madras Medical College during 2016 - 2019 under the guidance and

supervision of Prof.U. R.DHANALAKSHMI, M.D., D.D., D.N.B., Professor

and Head of the Department, Department of Dermatology, Madras Medical

College, Chennai-600003.

This dissertation is submitted to The Tamil Nadu Dr. M.G.R. Medical

University, Chennai towards partial fulfillment of the rules and regulations for

the award of M.D Degree in Dermatology, Venereology and Leprosy

(BRANCH – XX).

(DR. KARUNYA S)

PLACE :

DATE :

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SPECIAL ACKNOWLEDGEMENT

My sincere thanks to Prof.Dr.R.JAYANTHI MD., FRCP(Glasg)

Dean, Madras Medical College, Chennai-3 for allowing me to do this

dissertation and utilize the Institutional facilities.

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ACKNOWLEDGEMENT

I am grateful to Prof. Dr. U.R. DHANALAKSHMI, M.D., D.D.,

D.N.B., Professor and Head of the Department, Department of Dermatology,

Madras Medical College, for her advice, guidance, motivation and

encouragement for my study.

I would like to express my sincere and heartfelt gratitude to

Prof. Dr. S. KALAIVANI, M.D., D.V., Director and Professor, Institute of

Venereology, for her kindness and support throughout the study.

I sincerely thank My Guide Prof. Dr. A. RAMESH, M.D., D.D.,DNB,

Professor, Department of Dermatology, for his valuable support. He has been a

source of constant motivation and encouragement throughout the study. I am

extremely grateful to him for guiding me throughout the study.

I sincerely thank Prof. Dr. S. NIRMALA MD., Professor, Department

of Dermatology for her constant help and support.

I thank Prof. Dr. R. PRIYAVATHANI ANNIE MALATHY, M.D.,

D.D., D.N.B., M.N.A.M.S., Professor, Department of Dermatology for her

advice and encouragement.

I thank Prof. Dr.V.SAMPATH, M.D., Professor Department of

Dermatology for his invaluable guidance, advice and encouragement.

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I wish to thank Prof. Dr.S.KUMARAVEL M.D., D.D., and

Prof.Dr.J.MANJULA M.D., DNB., former Associate Professor, Dermatology

for theirs support and motivation

I humbly thank my Co-Guide, Dr.R.MADHU, M.D.,(DERM).,D.C.H.

Assistant professor, Department of Dermatology for her valuable guidance

throughout my work. I would like to express my sincere and heartfelt gratitude

for the time which she devoted for my research project.

I extend my gratitude to DR.V.N.S.AHAMEDSHARIFF, M.D.D.V.L.,

Dr.B.VIJAYALAKHSMI, M.D.D.V.L., Dr.R.MANIPRIYA, M.D.D.V.L.,

D.C.H. and Dr.K.DEEPA, M.D.D.V.L., Dr.C.L.CHITRA, M.D.DVL,

Dr.S.VENKATESAN MD, DNB., Dr.TAMILSELVI MDDVL, Assistant

professors, Department of Dermatology for their kind support and

encouragement.

I express my thanks Dr.SAMUEL JEYARAJ DANIEL M.D.,

Dr.K.UMA MAHESHWARI M.D.D.V.L., my former assistant professors,

Department of Dermatology, for their support and help

I also thank my STD Associate Professor Dr.C.VIJAYBASKAR,

M.D.D.V.L my Assistant Professors Dr.P.PRABAHAR, M.D.D.V.L.,

Dr.H.DHANASELVI, M.D.D.V.L., Dr.K.GAYATHRI, M.D.D.V.L.,

Dr.T.VASANTHY M.D.D.V.L., Dr.E.BALASUBRAMANIAN,

M.D.D.V.L, Dr.R.SNEKAVALLI M.D.D.V.L., Dr.VANATHY MD.DVL

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and Dr. C.DURGAVATHI MDDVL, DD Institute of Venereology for their

able guidance

I express my thanks to Dr.C.VIDHYA, M.D.DVL., Dr. R.HEMA

MALINI, M.D.D.V.L., former assistant professors, Institute of Venereology

for their able guidance

I am thankful to My Colleagues for their support throughout the study.

I am also grateful to All Paramedical Staffs for rendering timely help to

complete my study. Last but not the least I am profoundly grateful to All

Patients for their cooperation and participation in this study. They have been

the principal source of knowledge which I have gained during the course of my

clinical research.

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CERTIFICATE - II

This is to certify that this dissertation work titled “CLINICO

EPIDEMIOLOGICAL, MYCOLOGICAL STUDY OF CHRONIC

DERMATOPHYTOSIS” of the candidate Dr.KARUNYA. S, with

registration Number 201630006 for the award of M.D. in the branch of

DERMOTOLOGY, VENEREOLOGY AND LEPROSY.

I personally verified the urkund.com website for the purpose of

plagiarism Check. I found that the uploaded thesis file contains from

introduction to conclusion pages and result shows 3 percentage of plagiarism

in the dissertation.

Guide and Supervisor Sign with Seal

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CONTENTS

SL.NO. TITLE PAGE NO

1. INTRODUCTION 1

2. REVIEW OF LITERATURE 3

3. AIMS AND OBJECTIVES 51

4. MATERIAL AND METHODS 52

5. OBSERVATION AND RESULTS 54

6. CLINICAL IMAGES

7. DISCUSSION 77

8. CONCLUSION 89

9. REFERENCES

10. ANNEXURES

10.1 ABBREVIATIONS

10.2 PROFOMA

10.3 INFORMATION SHEET

10.4 CONSENT FORM

10.5 ETHICAL COMMITTEE AND APPROVAL CERTIFICATE

10.6 MASTER CHART

10.7 KEY FOR MASTER CHART

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INTRODUCTION

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1

INTRODUCTION

Fungi are the most common cause of skin infections in developing

countries. Fungal infections are divided into superficial, subcutaneous and

deep. Superficial mycoses are fungal infections that invade fully keratinized

tissues like stratum corneum of epidermis, nail and hair.1Superficial fungal

infections account for 20-25% of world population with dermatophytosis being

most common.2 They include more common infections like Dermatophytosis,

Pityriasis versicolor, Candidiasis and the rare infections like Tinea nigra and

piedra.1

Dermatophytois (ring worm or tinea) ,an infection of skin and its

derivatives caused by closely related group of fungi known as dermatophytes

belonging to three genera namely Trichophyton, Microsporum and

Epidermophyton, characterized by scaly plaques with papules in the periphery

with central clearing.1

According to Kaaman et al, “Chronic dermatophytosis refers to

persistent or recurrent episodes of dermatophytosis lasting for more than one

year despite adequate treatment with topical and systemic antifungal agents”.3

Hay in the past considered chronicity, “when the infection persisted

continuously for 3 years inspite of treatment with griseofulvin for 3 months”.4

In the recent times, duration of infection being redefined, Chronic

dermatophytosis refers to “patients who had the infection for more than

6 months to 1 year period with or without recurrence inspite of being treated”.5

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2

Dermatophytosis has evolved as one of the major public health

problems over the last 4 to 5 years in India , a tropical country with hot and

humid climate, causing severe discomfort and disability to the patients,

especially when the infection tends to be chronic and recurrent, wherein

there is a remarkable adverse impact on the quality and life of patients.6

This study is intended to find out the various predisposing factors,

clinical presentations, etiological agents of chronic dermatophytosis and to

study the clinicomycological correlation in patients with chronic

dermatophytosis

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REVIEW OF LITERATURE

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3

REVIEW OF LITERATURE

HISTORY:

Robert Remark in 1837, observed an unusual structure from scalp

infection, favus using microscope. Later Johann l Schonlein described it as

fungi. Then the unusual organism was cultured and found to be infectious again

by Remark in 1845, which he named as Acherion. In 1835, Agostino Bassi,

called as “Father Of Mycology”, established that fungus Beauveria bassania

was the causative agent of the disease muscardine in silk worms, that can be

transmitted from one to another which is widespread geographically .In 1842,

the clinical and microscopic features and contagious nature of causative agent

of favus was described by David Gruby, a Parisch physician, who was the real

founder of mycology. He also described ectothrix and endothrix infection of

hair and named the causative organism as Microsporum audounii and

Trichophyton tonsurans.7

Raymond Sabouraud, “Father of Medical Mycology” in 1910 published

‘Les Teignes’ in which he classified dermatophytes into 4 genera as Acherion,

Epidermophyton, Microsporum and Trichophyton. Then Chester Emmons

eliminated the genus Acherion in 1934 from Sabouraud’s classification and

based on mycological principles, the dermatophytes were again reclassified

into rest of three genera.7

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4

Dermatophytosis is a type of superficial mycoses caused by a group of

closely related filamentous fungi called dermatophytes.8 The word

‘dermatophyte’ means ‘skin plant’ which is a misnomer as these are fungi and

are not phylogenitically related to plants. Dermatophytosis is also called as

‘tinea’ or ‘ringworm’, ‘Tinea’ literally menas ‘worm’ / ‘insect larva’ (cloth

moth) that was thought by Romans to have caused this infection. It is used to

describe serpentine and annular lesions of skin.9

DEFINITION:

Naive infection of dermaophytosis means a given subject is not

previously exposed to a particular infection of a given disease or treatment for

that disease.10

Chronic dermatophytosis refers to “patients who had the infection for a

period of more than 6 months to 1 year duration with or without recurrence

inspite of being adequately treated ”.5

Dermatophytosis is considered to be recurrent when there is re-

occurrence of the disease (lesions) within few weeks (< 6 weeks) after

completion of the treatment.10

Chronic and recurrent dermatophytosis causes significant distress

socially, emotionally and financially to the patients. Relapse denotes the

occurrence of dermatophytosis (lesions), after a longer period of infection-free

interval (6–8 weeks) in a patient who has been cured clinically10. Familial

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5

clustering and connubial cases are reported in patients with chronic

dermatophytosis with even infants presenting with extensive tinea corporis.11

EPIDEMEOLOGY:

Superficial mycoses affects 20-25% of world population of which

dermatophytosis is predominant.2 Lifetime risk of acquiring dermatophytosis is

10–15%.12 There is an increase in the prevalence of dermatophytosis over the

past 4–5 years across the country. It is difficult to decide between the terms

“epidemic” and “hyperendemic” to describe this current alarming situation of

increased incidence and prevalence of superficial dermatophytosis in india.13

Dermatophytosis is more common in the tropical and subtropical countries, due

to the hot and humid climate. India is a tropical country, with hot summer in

the western region , hot and humid weather in the southern states and the

relatively humid weather with high rainfall in the northeastern states,which

predisposes dermatophytosis. Various studies across the country shows the rise

in prevalence of dermatophytosis from 58.5 %during 1995–96 to 91.2 % in

2016 12

Transmission of infection to humans occurs either through direct contact

with an infected person, animal and soil or from infected desquamated

keratinocytes or from hair, that is shed with fungal spores on the floor of

houses, swimming pools, locker rooms, hotel rugs, clothes, towels, bed linens,

pillow covers, furniture, theater seats, farm fences, combs, hair brushes, caps,

and infected toys too in case of children with tinea capitis. Spores are viable for

12-20 months in a suitable environment.12

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6

Geographic Location:

Dermatophytes are found worldwide (Trichophyton rubrum ,

T.mentagrophytes var. interdigitale, Microsporum canis, and Epidermophyton

floccosum). Specific geographic predilection are noted in case of T.

Schoenleinii (Eurasia, Africa), T. soudanense (Africa), T.violaceum (Asia,

Africa, and Europe, ) and T.concentricum (Pacific Islands, Far East, and

India).13The Prevalence of dermatophytosis is influenced by multiple factors

such as migration, environment, host immunity, industrialization, global travel,

socioeconomic conditions, cultural practices and clinical type.12

Most of the studies across India have shown T. rubrum as the most

common organism followed by T. mentagrophytes as the codominant species.12

Simultaneous rise in the prevalence of T. mentagrophytes has been documented

in the various studies done in different cities all over the country including

Amritsar, Patiala, and Lucknow in north India, Kolkata in the east, Ahmedabad

in the west and Tirupati and Chennai in south India. Few studies also reported

T. mentagrophytes to be the most common organism followed by T. rubrum as

quoted in the table below

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Table 1: Changing scenario of dermatophytes in south India14-20

City Period Study T.

Rubrum

T.

Menta

T.

Viol

T.

Tons

E.

Floc Others

Hubli14 2007–08 Noronha et al 38.3 48.3 5 t.verr-

8.3

Tirupati15 2011 Surekha et al 64 20 4 t.ver 12

Chennai16 2011-14 Ramaraj et al 48.9 44.75 3.49 0.7 m.gyp-

1.4 Chennai17

2014

Kumaran et al 22.4 67.34 m.can-

6.1 Kakinada18

2015 Parameshwari

et al 50 35.7 8.35 m.gyp-

4.3

Shimoga19 2016 Manjunath 38.57 22.85 4.28 1.4 m.aud-

21.4

Pudhucherry20 2017 Jegadesh et al 12 64 20

t.schon

-2.08

Table 2: Changing scenario in North India

City Period Study T.

Rubrum

T.

Menta

T.

Viol

T.

Tons

E.

Floc Others

Ranchi26 2012-2015 Singh et al 63.2 26.4 - 2.94 5.8 -

Uttarkhand24 2013 Kainthola

et al 28.15 42.85 - - 42.85 t.verr-

28.57

Amristar23 2013-2015

Kansra et al

24.29 46.43 3.57 - -

t.ver-

12.14 t.sch-

11.43 Kashmir21 2014 Munir et al 52.94 29.42 - - - -

Tanda22 2016 Kaur et al 32 48.2 3.6 10.7 - Ndm-

39

Lucknow25 2016 Khan et al 5.6 37 27.8 -

m.aud-5.6

ndm-14.8

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Table 3: Changing scenario in central, West and East India

City Period Study T.

Rubrum

T.

Ment

a

T.

Viol

T.

To

ns

E.

Flo

c

Others

Cuttack37 2009-2011 Prasad et al 48.2 26.3 8.7 1.7 m.aud-

2.6,t.sch-11.4

Jaipur27

2011-2014 Agarwal et al

34.2

37.9

11.3

8.3

m.aud-6.2

Manipur34 2010-2012 Singh et al 47.54 22.95 1.63

3.27 19.69

Kolkotta36 2011-2014 Gosh et al 22.2 21.6 2.11 t.verr-3.8

Loni32 2013 Bose et al 33.3 21.3 2 m.gyp-

1.3 Meghalaya35 2013 Lyngdoh 30.3 28.9

26.3

2.6 t.verr-7.9

Ahmedhabad28

2014 chandasama 52.1 26.05 1.68

0.84

m.gyp-

3.3

Bhopal33 2014 Gupta et al 41.3 28.3 15.2

6.5 t.verr-

8.7

Mumbai30 2015 Amodkumar et al

42.85 37.14 20 m.gyp-9.7

Pune31 2016 Sharma 40 36 8 10.66

Ndm-2.5

Valsad29 2016 Patel IHC 3 18 21.23

3 m.can-21.2

Sex Ratio and Age Group:

In the past studies have shown that dermatophytosis is more common in

males than females in the ratio of 3:1.This is attributed to the increased

physical activity and increased time spent outdoor in hot humid climatic

conditions. But in recent times, studies have shown that there is a change in

the sex ratio from 2.6:1 to 1.05:1. This may be due to more women working

outdoors and also due to wearing of tight clothing and synthetic garments

which predispose to dermatophytosis.5,38 Females are commonly affected in

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9

third to fourth decades.12 Hesitancy and embarrassment leads to substantial

under-reporting, particularly in women.5

Urban Vs Rural and Socioeconomic Status:

In the past, dermatophytosis was found to be more common in the rural

community or in people belonging to low socioeconomic status.38,39,40 However

in the recent year, dermatophytosis has been increasingly prevalent among

middle and higher socio economic group living in urban areas.15,26,41,42

Occupation:

Dermatophytosis are more common in manual laborer working

outdoors, but in the present days, it seems to be more common among students,

professionals and business men.22,24,43

Intra familial Infection:

There is increased incidence of infection among the family members

producing chronic and recurrent Dermatophytosis.14,22,44 Connubial cases and

infants with extensive tinea corporis have been reported.12

ETIOLOGY:

Dermatophytes are hyaline septate moulds belong to Kingdom:- Fungi,

Phylum:- Ascomycota, Order:-Oonyganeles, Family:- Arthrodermatacea. The

family Arthrodermatacea has approximately 40 species divided among the

three genera, Trichophyton, Microsporum and Epidermophyton,. Trichophyton

rubrum and T.mentagrophytes found to be the most common species.7

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CLASSIFICATION OF DERMATOPHYTES:

I. Based on the habitat and host , dermatophytes are classified as

Anthropophilic, Zoophilic, Geophilic organisms.(table4)

Anthropophilic: These fungi adapt human as host and elicit a chronic

interactable infection with minimal inflammation. They are transmitted among

humans by direct contact or through fomites.45

Zoophilic: These fungi are transmitted from animals ( such as cats,

dogs, rabbits, guinea pig, birds, horses and cattle) to humans. Exposed areas

such as face, beard, scalp and arms are the common sites of involvement. They

are transmitted by direct contact through animals or indirect through fomites.

Acute and intense inflammatory response occurs in humans to this fungi.45

Geophilic: These fungi cause sporadic infection of human by direct contact

with soil. Spores of these organisms are long lived and have the potential to

produce epidemic. They also produce intense inflammatory type of infection.45

Table 4: Ecological classification of dermatophytes45

HABITAT DERMATOPHYTE

HOST

Anthropophilic

-Restricted to human host -Transmitted from one person to another -Produces mild but chronic lesions

T.rubrum

T. tonsurans

T. interdigitale

T. schoenleinii

T. soudanense

T. violaceum

T. concentricum

T. audouinii

T.ferrugineum

Epidermophyton

floccosum

Human

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II. Based on the species of individual genera45

(Table 5)

Table 5: Classification of Dermatopytes based on Genera45

Epidermophyton Microsporum Trichophyton

E. Floccosum M.audoinii

M.persicolor

M.praecox

M.canis

M.fulvum

M.gallinae

M.nanum

M.racemosum

M.gypseum

M.cookei

M.ferrugineum

M.vanbreuseghemii

T.rubrum

T.mentagrophytes

T.interdigitale

T.tonsurans

T.equinum

T.erinacei

T.verrucosum

T.violaceum

T.schoenleinii

T.simii

T.concentricun

III. Based on the Macroscopic and microscopic colony morphology

Macroscopic colony morphology and microscopic features in lactopenol

cotton blue mount (LPCB) are used for identification of individual species

Zoophilic

-Found in animals -Sporadically affect humans -Produces highly inflammatory lesions

T.mentagrophytes

T.interdigitale

M. nanum

M. galinae

T.simii

T.verrucosum

T.ennacei

Microsporum canis

M. persicolor

Rodents rodents Poultry Cattle Rodents Cats, dogs, horses Hedgehogs Pigs Primates Rodents

Geophilic

- Grow in soil -Sporadically infect humans -Produce marked inflammatory lesion

T. eboreum

T.terrestre

M.cookie

M.persicolor

T.vanbreuseghemii

M. gypseum

Soil

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(table-6). Macroscopic characteristics include color, appearance, surface,

texture, reverse pigmentation and diffusion of pigment into media. Microscopy

includes the presence or absence of micro and macro conidia and its

appearance differs for each species that helps in identification.46

Table 6: Microscopic features of Dermatophytes in LPCB mount7,45

:

S.no Genes Macroconidia Microconidia

1 Trichophyton(invades -skin, hair & nails)

Smooth walled fusiform, pencil/clavate / cylindrical large numbers than microcondia

Abundant than macroconidia rarely scarce/ absent clavate/teardrop/ pyriform shaped/ spherical along the hyphae-singly / clusters.

2 Epidermophyton

-skin & nail

Smooth walled broadly clavate, singly or in banana like clusters.

Absent

3 Microsporum

-skin & hair

Rough walls, egg shaped/ fusiform large in number than microconidia

Usually seen, pyriform/ clavate Singly along the hyphae.

IV. Based on integument affected it is classified as follows.45

(Table 7)

Table 7: Integument affected by Dermatophytes45

S.No Genera Skin Hair Nail

1 Trichophyton X X X

2 Microsporum X X -

3 Epidermophyton X - X

M.persicolor and T.concentricum does not invade hair.46

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PREDISPOSING FACTORS OF CHRONIC DERMATOPHYTOSIS:

AGENT FACTORS:

� T. rubrum is the most common organism causing chronic dermatophytosis

of the glabrous skin .3,5,47,48 The ubiquitous presence, easy transmission and

the ability of this fungus to cause non inflammatory chronic skin lesions

are some of the important factors responsible for the high incidence of

chronic infection. It is a resilient fungus and survives in the environment

outside the body as spores until it gets a warm, moist area of skin, where it

readily colonizes.5T.rubrum has the ability to evade host defence by

producing larger cell wall mannan than other dermatophytes. Mannan

moiety present in the cell wall in larger amounts result in intense inhibition

of lymphocyte proliferation. It reduces the keratinocyte proliferation and

causes slow turnover of cells, thus explaining the chronicity of infection

Mannan acts as a potent immunosuppressor by suppressing lymphocyte

proliferation, inhibiting complement activation and polymorphonuclear

leucocytes3,5,49

� Individuals with T.rubrum present a negative delayed hypersensitivity

reaction to trichophytin. They are more likely to have either no reactivity or

only immediate reactivity (74%), while patients with T. mentagrophytes are

more likely to have delayed reactivity with or without immediate reactivity

(85%).50

� T.rubrum escapes immune system by inhibiting the most important

pathways in antigen processing and presentation. Patients with T.rubrum

infection have lower level of free radicals and nitric oxide release (20–30%)

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than patients with chronic dermatophytosis infected from other species,

which leads to defective killing mechanism. The toll-like receptor 4 is down

regulated by T. rubrum further decreases the inflammatory response by

decreasing production of pro-inflammatory cytokine and recruitment of

neutrophils. The cellular milieu of these patients has decreased level of

inflammatory cytokines such as interleukin-1β (IL-1β), tumor necrosis

factor-α, IL-6, IL-8, and increased the production of anti-inflammatory

cytokines such as IL-10. Immune evasion makes the organism to survive in

the stratum corneum for long duration and produces spores in large

numbers.5

� T.rubrum and T. mentagrophytes have the ability to survive as spores for

long time upto 7 months and 9 to 15 months respectively.53

T. mentagrophytes and M. gypseum were found to survive on towel for

more than 25 weeks and in swimming pool water for 1 week . Higher

occurrence of T. mentagrophytes are found in the house dust of infected

persons.52Spores then complete the lifecycle, desquamate from skin and

make the organism plentiful in human habitatats which also makes it as a

common cause of chronic dermatophytosis.5

� Glycoprotein present in the cell wall of T. mentagrophytes has cross

reactivity with human blood group isoantigen A causing chronicity and

wide spread infection53

� T. rubrum and T. mentagrophytes exhibit dimorphism and could be induced

to form germination tubes at pH 712

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� Other organisms causing chronic infection are T.schonleinii, T.violaceum,

T.verrucosum, T.simii, E.floccosum, M.canis and M.gypseum.5

HOST FACTORS:

The clinical manifestations of dermatophytosis may also depend on host

factors such as site of invasion, physiological variation of host skin barrier, age

of patient, obesity, immunosuppressive state, and acquired conditions such as

excessive sun exposure.13 Anatomical characteristics of affected area which

include the presence of skin folds, sebaceous glands,variable thickness of the

corny layer, and vellus hair follicle involvement also affects the typical

centripetal progression and favours inflammation and crusting.45

� Atopic individuals have an immunological predisposition to chronic

infection. Defective cell mediated immunity and shift to Th2 pathway with

high levels of IgE4 and IgG in people with atopy make them more

predisposed to chronic dermatophytosis.5 They have 3 fold increased risk of

chronic infection. IgE levels elevated in atopic individuals forms complexes

with dermatophyte antigen there by antagonizing it and so it is not available

for activation of CMI producing chronic widespread dermatophytosis.3

Conversely atopic dermatitis can be exacerbated in chronic dermatophytic

infection due to trichophyton sensitivity. This is called as Atopic-chronic

dermatophytosis syndrome.5

� In normal individuals, macrophages and neutrophils migrate in response to

dermatophytic invasion and kill the pathogen by phagocytosis ,which was

found to be defective in chronic dermatophytosis.520-30% of patients with

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chronic infection produce low levels of free radicals and nitric oxide

indicating a defective killing mechanism.5,54The cellular milieu of patients

with chronic infection has decreased inflammatory cytokines such as IL-1β,

TNF α, ,IL-6,IL-8 and increases the production of anti-inflammatory

cytokines such as IL-10.5

� In autosomal recessive mutation of genes encoding CARD9 protein, due to

the lack of or low level of functioning CARD9 protein, patients are not able

to control the invasiveness of dermatophytes such as T.rubrum

and T.verrucosum.54 CARD9 is an adaptor protein downstream to several

immune receptors such as dectin-1, dectin-2, and mincle, which recognize

fungal structures and are involved in the regulation of multiple downstream

pathways of anti-fungal response, found to be associated with severe

fungal infections of varied clinical presentations ranging from candidal

meningitis to recurrent dermatophytic infection of skin and nails.

Dermatophytosis with invasion of bone, central nervous system and lymph

nodes have been reported.5,49,54

� Dectin 2, a c type lectin pattern recognition receptor on dendritic cells , on

binding to hyphal elements induces Th17 type of inflammatory response.

Mutation in adapter molecule dectin-1 and dectin-2 results in failure of th17

activation ,which is associated with susceptibility to chronic mucocutaneous

candidiasis and chronic dermatophytosis.5,45

� Patients with HLA A26 and HLA AW33 have been shown to have an

increased frequency of chronic tinea pedis.3

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� Chronic dermatophytosis is one of the common cutaneous association in

patients with diabetes mellitus.49,55 But prevalence of diabetes mellitus in

dermatophytosis has been observed to be the same as in general

population.56 There is no correlation between dermatophytosis and duration

of diabetes mellitus, blood sugar level and complications. Onychomycosis

has been found to be common in diabetes mellitus. The dry moccasin type

of tinea pedis is often misdiagnosed as dry skin in diabetic patients3,56

� Chronic dermatophytosis is common in patients with icthyosis vulgaris,

especially in x-linked form, because of slow turnover of epidermis and

delayed desquamation of stratum corneum. The thick retention of keratin

acts as a good nidus for multiplication of fungi which lays bed for chronic

infection.57

� In HIV infection, due to immunosuppression which leads to chronic, non

inflammatory extensive disease. Onychomycosis is common in patients

with CD4 count 370 cells/cubic mm. In patients with low cd4 count ,the

common presentation is proximal subungual onychomycosis.58

� Bronchial asthma associated with chronic dermatophytosis is attributed to

allergic bronchial hyper reactivity to trichophytin antigen. The amino acid

sequences of trichophytin are identical to various enzymes which are

responsible for both fungal pathogenesis and allergic disease. Allergens

also causes rhinosinusitis and symptomatic late onset intrinsic type of

asthma.59

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� Chronic dermatophytosis has also seen to be associated with psoriasis,

chronic mucocutaneous candidiasis, cushing syndrome, cancer

chemotherapy, radiotherapy, internal malignancies, pulmonary tuberculosis,

collagen vascular diseases, rheumatoid arthritis, peripheral vascular

diseases, hypertrichosis, acne, cutaneous tags and contact dermatitis with

kum kum.55,60

� Clothing types and habits, poor personal hygiene, sharing of towels with

others, soap used for bathing, Close contact with animals or soil harboring

and swimming habit are some of the modifiable risk factors for

development of chronic infection. Close association among people,

unhygienic habits, tight underwear without aeration, synthetic dresses,

exhausting physical work like exercises, long working hours under the sun,

all of which lead to profuse sweating and result in increased dampness and

warmth of the body altogether facilitating skin surface perfect nidus of

infection.61

� Most common predisposing factor in adults is excessive perspiration

contributed by occlusive clothing which provides an environment for the

dermatophytes to thrive. Individuals participating in contact sports, such as

football, wrestling, or rugby, are at increased risk of acquiring a tinea

infection. Autoinoculation by dermatophytes elsewhere in the body,

especially the foot or groin, is also causative.12

� Patients who take bath once a day(in case of excess sweating)or once in

two days or more than that are more prone to chronic infection because they

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fail to exfoliate skin scales, producing more fungal load leading to chronic

infection.12,60Sharing of bath towels, toiletries, beddings, soaps, combs, foot

wear and other household articles are responsible for transmission of

disease among the family members, resulting in persistence of infection

for long duration.61Areas such as public showers, health club bathing

facilities, swimming pools, changing rooms and toilets will contain layers

of skin shed from an infected person. The shed skin contains fungal spores

and individuals with fissured or hyperhydrotic skin conditions are at risk

for infection.12,61

� Individuals with low paying jobs and residing in slums with distinct lack of

basic amenities like electricity, proper sanitation, access to piped water,

poor garbage disposal has been associated with presence of zoophilic type

of dermatophytes owing to presence of rodents rats. This is a common

phenomenon in slums characterized by heaps of garbage around living

houses. Rodents scavenging into houses in search of food maybe reservoirs

of fungal pathogens.12,61

DRUG RESISTANCE:

Emergence of antifungal resistance due to irrational use of antifungals

against cutaneous mycosis.62-65 It can be clinical, microbiological or a

combination of two. Microbioiologic resistance is the non susceptibility of a

fungus to an antifungal agent to the in vitro susceptibility, in which the

minimum inhibitory concentrations(MICs) of the drugs exceed the susceptible

breakpoint for that fungus.62 Primary resistance is seen naturally among fungi

without prior exposure to the drug. Secondary resistance is due to previously

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susceptible strains after exposure to the anti fungal agent, which is due to

altered gene expression. Both primary and secondary resistance to antifungal

agents is on the rise in recent years.66,67Clinical resistance means persistence or

progression of an infection even after adequate treatment with antimicrobial

therapy. This may be due to incorrect diagnosis, suboptimal dosage,

immunosuppression and or duration of therapy.62,63

In vivo resistance is because of antifungal misuse as patients fail to

finish the full course of treatment. Inadequate dosage leads to failure in

clearing the organism completely, encouraging the growth of resistant strains.

Another mechanism of resistance is biofilm formation by dermatophytes,

which confers resistance to both antimicrobial agents and host immunity.68,69

Over the counter (OTC) medications and rampant use of topical steroid

and antifungal combination(TSAF) creams by patient themselves or

unrestricted prescriptions by quacks and general practitioners. Misdiagnosing

other skin conditions as fungal infection and treating those with suboptimal

and irrational dose of medications leads to development of resistance. Cost of

antifungal drugs may also be responsible for non adherence or poor compliance

of patients. Drug interactions may lead to decreased bioavailability of the

antifungal drug leading to treatment failure.5,63,68

PATHOGENISIS:

The pathogenesis of dermatophytosis comprises the complex interaction

between host, agent and the environment. The host factors which attribute to

infection includes diabetes mellitus(DM),long term steroidtherapy, atopy,

lymphomas, asthma, cushing syndrome and immune compromised status.

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Some areas of the body are more prone to get dermatophyte infection namely

the intertriginous areas where excessive sweating ,maceration and alkaline pH

which favours the growth of the dermatophytes.70 Natural infection is acquired

by deposition of viable arthrospores or hyphae on the surface of individual.

After inoculation into the skin, under favourable conditions the infection

progresses through the following stages namely adherence, penertration,

invasion.45

After competing with normal flora, dermaophytes secrete proteases

that degrade spinghosines produced by keratinocytes and fatty acids produced

by sebaceous glands. Adhesion of fungus to epithelial cells is mediated by

adhesin in case of T.rubrum and microfibrills in case of T.mentagrophytes.71,72

Dermatophytes are provided with an arsenal of proteases aimed at the digestion

of the keratin network into assimilable oligopeptides or amino acids.71The

arthroconidia then germinates and the hyphae formed prolong radially in

multiple directions.72.Once the hyphae is formed , the spores starts germinating

and penetrate the stratum corneum of skin at a rate faster than desquamation.

Penetration is accompanied by dermatophytes secreting multiple serine-

subtilisins and metallo -endoproteases (fungalysins) formerly called keratinases

that are found almost exclusively in the dermatophytes. These dermatophytic

keratinolytic proteases cannot act before disulfide bridges are reduced within

the compact protein network constituting keratinized tissues. This was recently

shown to depend from a sulfite efflux pump encoded by the Ssu1 gene. Sulfite

excretion by this transporter allows sulfitolysis of proteins, rendering them

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accessible for proteases, and functions in the same time as a possible

detoxification pathway, a future target for new anti-fungal treatments. The

protease production in T.rubrum is highly host specific showing reduced

physiological activity when growing on their preferred host.

Fungal mannans in the dermatophyte cell wall have immuno-inhibitory effects

.In case of T.rubrum, cell wall mannans seem to be involved in an

immunosuppression, inhibiting lymphoproliferative response of mononuclear

leukocytes in response to fungal antigens. Although specific suppressor T cells

are eventually activated during persistent infections, target cells are mainly

monocytes rather than lymphocytes. Trichophyton rubrum mannans may also

decrease the keratinocyte proliferation rate, directly or via lymphocyte function

alteration, contributing significantly to the chronicity of T. rubrum infection.71

After penetration, all dermatophytes have the ability to invade skin , but

invasion of hair and nail varies with species. Fungal metabolic products

diffuse through the malphigian layer to cause erythema, vesicle or even pustule

formation along with pruritus. The degree of inflammation, varies according to

the dermatophyte species, the host species and the pathophysiological status of

the host. In general, the zoophilic species cause more inflammatory infections,

which may heal spontaneously and result in relative resistance to re-infection.

The anthropophilic species causes chronic, ill defined infections, which leads

to decreased resistance for re-infection. Primary infection produces negative

trichophytin test and minimal inflammation (mild erythema and scaling) due to

increased keratinocyte turnover.71

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HOST RESPONSE

INNATE IMMUNITY:

Dectin 1 and dectin 2 activate toll like receptor TLR 2 and TLR 4 by

recognising the beta glucan in the cell wall of dermatophytes. Activation of

TLR induces the production of IL-6TNFα,IL-17,IL-10, and stimulates adaptive

immunity.70

ADATIVE IMMUNITY

HUMORAL IMMUNITY: Hypersensitivity response to trichophytin antigen

is because of its association with increased levels of IgE and IgE4 antibodies

and Th2 cytokine production leads to chronic infection. Th2 cells produces IL-

4 which leads to antibody isotype switching.70

CELL MEDIATED IMMUNITY:

Cell mediated immunity is protective in dermatophytes. Macrophage cells

secrete IFN α and IFN β causing delayed hypersensitivity reaction(DTH). A

positive DTH skin test correlates with acute inflammatory response and

clearance of infection. Increased immediate hypersensitivity response is

associated with chronicity of infection. However immunity to infection

depends on the dermatophyte species, host and patho physiological status of the

host.75

Serum inhibitory factors such as ferritin, beta globulin,α2 macroglobulin,

unsaturated transferrin, and other metal chelators that bind to iron are essential

for growth of dermatophytes that controls the infection in host.76,77 Adults have

natural resisitance to tinea capitis due to the presence of long chain saturated

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fatty acids which are fungistatic and fungicidal .78 Commensal yeast causes

lipolysis and increases the level of fatty acids and thereby inhibiting fungi.79

CLINICAL FEATURES:

The clinical manifestation of dermatophytes depends on the size of inoculum,

causative agent, site of body involved and immunity of the host.13 They are as

follows

Dermatophytoses of Keratinized epidermis

� Tinea corporis � Tinea cruris � Tinea faciei � Tinea manuum � Tinea pedis � Tinea incognito

Dermatophytoses of Hair � Tinea capitis � Tinea barbae � Dermatophytic

folliculitis Majocchi’s granuloma

Dermatophytoses of nails (onychomycosis): Onychomycosis is a term used for all fungal infections of the nail and includes those due to dermatophytes as well as nondermatophytes

Tinea corporis is most commonly caused by T. rubrum; however, the

inflammatory type is caused by T. verrucosum, T. mentagrophytes, M. canis,

and M. gypseum. The most common causative agents for Tinea cruris, Tinea

pedis, and Tinea manuum are E. floccosum, T. rubrum, and T.

mentagrophytes.12 The typical incubation period is 1 to 3 weeks.45

TINEA CORPORIS:

Synonyms: Tinea circinata/ Tinea glabrosa / Ringworm of the body.

Tinea corporis is ringworm of glabrous skin. Fungi affects non hairy

skin of body like trunk and limbs excluding scalp, nails, groin, beard, face,

hands and feet. T.rubrum, T.mentagrophytes, M.canis and rarely M.audounii

are the common organisms causing tinea corporis.13 In case of family members

of children with Tinea capitis and wrestlers, T.tonsurans is commonly isolated.

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T.corporis in wrestlers called as Tinea gladiatorum. They present singly or

multiple erythematous, circinate lesions, in plaques, papules, vesicles or

pustules, with centrifugal growth, in such a way periphery is more active, with

a tendency to central healing.80 When granulomatous infections occur, and

with pustules around the follicles, it is called Majocchi granuloma.

Inflammation is minimal with Tinea corporis when compared to Tinea capitis

or Tinea barbae. Pustules, vesicles or frank bulla are seen in case of

inflammatory lesions.13,80

Variants of Tinea corporis include Tinea profunda, Tinea imbricata,

Bullous Tinea Corporis, Perifollicular granulomatous papules (majocchi’s

granuloma). T.profunda is characterized by kerion like lesion with a red boggy

pustular surface.80(table-8)

Table-8: Variants of Tinea Corporis12

Type Organism Clinical feature

Tinea profunda T. verrucosum An intense inflammatory reaction against zoophilic fungi can result in large pustular lesions or a kerion with a red, boggy, pustular surface. The follicular pustules represent the deep invasion of organism into hair follicle

Majocchi’s granuloma (dermatophytic granuloma)

T. rubrum Women with tinea pedis or onychomycosis who shave their legs, get perifollicular papulopustules or granulamatous nodules. This dermatophytic folliculitis is a foreign body granulomatous reaction in the dermisafter response to the fungal elements because of follicular rupture

Tinea imbricate

T. concentricum Plaque with erythematous concentric annular rings

Bullous tinea corporis

T. rubrum Intense inflammatory response causes vesicles at the margins

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TINEA IMBRICATA:

One type of chronic recurrent dermatophytosis is Tinea imbricata (TI),

caused by anthropophilic dermatophytes T.concentricum which has many local

synonyms such as Kaskado in Papua, Kihis in Central Kalimantan, Chimbere

in Bolivia, and Le pita in Tokelau island. It is endemic in certain parts of the

world, for instance in Polynesia (“Tokelau” ), and in Brazil (Mato grosso and

Cmazônia), where it is called “chimberê”.6 TI is endemic in several remote and

isolated tropical areas in South Pacific, South-East Asia, Central and South

America, and Mexico.1 It is a genetically mediated and race dependent

dermatophytosis. Inherited as autosomal recessive which affects both sexes and

all ages. Infection starts as a scaling ring, centrifugal spread follows, but within

the area of central clearing a second wave of scaling soon arises and it is

repeated further to produce concentric rings. Whole body can be affected and

its natural course is prolonged. Intense puritis leads to lichenification.

Hypopigmentation may also be seen.6

MAJOCCHI’SGRANULOMA:

It is commonly seen in women with Tinea pedis or onychomycosis.

Fungus affects dermal and subcutaneous tissue and it is present in two forms,

namely perifollicular papule or nodule in immunocompetant individuals and

deep nodular plaque or abscess form in immuo-compromised patients

Pathogenesis is due to fungal elements in the dermis after follicular rupture

eliciting a foreign body granulomatous reaction. Hair follicle acts as a

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reservoirand so lesionsinvolving hair follicles are usually resistant to treatment

and leads to chronic infection or recurrence .56

TINEA CRURIS:

Synonym: Ringworm of groin, Jock itch, Gym itch, Dhoti itch, Eczema

marginatum13,81

It is the dermatophytosis of groin, surrounding pubic area, perineum and

perianal areas. Tinea cruris is common in men who wear tight fitting garments.

It is the second most common dermatophytosis in the World after Tinea pedis.

It is more common in men than women and in the adults more than

children.12T.rubrum, T.mentagrophytes and E.floccosum are the most common

organisms isolated. It is common in hot and humid climate characterized by

itchy, erythematous plaques, with sharp margin extending from groin to thighs.

T.rubrum mostly causes chronic nodular infection and it extends from groin to

buttock, abdomen and lower back. The lesions produced by T.mentagrophytes

are vesicular and inflammatory.13

TINEA FACIEI:

Glabrous facial skin infection of dermatophytes is called Tinea faciei.

T.mentagrophytes, T.rubrum and T.tonsurans are the most common organisms

isolated13. It excludes moustache and beard areas of adult males, clinically

characterized by well circumscribed plaques with elevated margins and central

clearing. Cheek, nose, periorbital area, chin and forehead are the most common

sites involved. Simple papules, flat patches of erythema, few vesicles or

pustules can occur due to steroid application. Due to photosensitivity and

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frequent absence of scaling it can be confused with discoid lupus

erythematosus or polymorphic light eruption.80 Examination of scalp is

important to rule out glabrous type of Tinea capitis.7

TINEA BARBAE:

Synonym: Ringworm of beard, Barber’s itch.

Trichomycosis affecting the beard areas of face and neck with hair

shaft invasion. T.veruccosum and T.mentagrophytes are the common species

causing Tinea barbae. M.canis, T.violaceum, T.schonleinii, T.rubrum and

T.tonsurans are other species isolated occasionally.13 (table-9)

TABLE-9 : CLINICAL TYPES OF TINEA BARBAE12,80

Clinical types

Organism

Clinical feature

Deep inflammatory Zoophilic organisms like T.mentagrophytes

var.

mentagrophytes

and T.verrucosum

The clinical presentation is severe with intense inflammation and multiple follicular pustules resembling kerion . Hairs are loose or broken, and depilation is easy and painless. Constitutional symptoms such as malaise, fever, and lymphadenopathy may be present; scarring alopecia may develop

Superficial Anthropophilic T. violaceum

Lesions similar to bacterial folliculitis with mild erythema along with perifollicular papules and pustules, leading to exudation and crusting

Circinate T.rubrum Dry scaly erythematous lesions with active border and central clearing resembling tinea corporis. Hairs are usually spared

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TINEA MANUUM:

Dermatophytosis of palmar aspect of hand is called Tinea manuum.

Infection of dorsal surface of hand is referred as Tinea corporis, T.rubrum,

E.floccosum and T.mentagrophytes and rarely T.violaceum and T.erinacei are

mostly islolated. Most common clinical presentation is diffuse hyperkeratosis

of palm and fingers with characteristic accentuation of flexural creases.13

TINEA CAPITIS:

Synonyms: Ringworm of scalp, Tinea tonsurans, Herpes tosurans.

Dermatophyte infection of scalp hair shaft is Tinea capitis. Children in

the age group between 3 to 14 years of age are most commonly affected. Adult

and adolescents are protected, because of the fungistatic nature of sebum, but it

can occur in any age group. Infection can be ectothrix and endothrix, in which

arthroconidia are seen outside and within the hair shaft respectively. Organisms

causing ectothrix are M.audouinii, M.canis, M.equinum, M.ferrugineum.

Endothrix is caused by T.tonsurans, , T.violaceum, T.yaoundei,T.soundanense,

T.gourvilii.13 E.floccossum and T.concentricum wil not cause scalp hair

infection . Clinical presentation may be inflammatory, non-inflammatory or

mixed type. Kerion, favus, abscess and pustular types are inflammatory types

while grey patch, block dot, sebrorrheic dermatitis like, alopecia areata like and

glabrous type are the non-inflammatory manifestations.80

TINEA UNGIUUM AND ONYCHOMYCOSIS:

Fungal infection of nail is called as onychomycosis. Dermatophytic

infection of nail is called as Tinea unguium. T.rubrum, T.mentagrophytes and

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E.floccosum are the most common organisms isolated. Onychomycosis

clinically presents as Distal lateral subungual onychomycosis, White

superficial onychomycosis, Proximal subungual onychomycosis, Endonyx and

Total dystrophic onychomycosis.13

Most common clinical presentation is distal lateral subungual

onychomycosis. T.rubrum is the common etiologicalagent isolated. Clinically

presents with subungal hyperkeratosis with discolouration of distal and lateral

aspect of nail. In proximal subungal type of onychomycosis, infection starts at

the cuticle and gradually spreads upto the tip of nail and it is the most common

in patients with AIDS.80T. interdigitale is the most common organism causing

Superficial white onychomycosis and it produces white patches or pits on the

nail surface. Black superficial onychomycosis is caused by melanized non

dermatophytic fungus – Neocytalidium dimidiatum. Endonyx is due to infection

ofT.soudanese and T.violaceum. Crumbling and disappearanceof nail plate

expose hypertrophic nail bed and is seen in total dystrophic

onychomycosis.13,80

TINEA PEDIS:

Dermatophytic infection of soles and interdigital web spaces of the feet

is called tinea pedis. It is more common in adult males wearing shoes due to

occlusion and maceration of the toe clefts. T.rubrum, T.mentagrophytes and

E.floccosum are common organisms isolated in patients with Tinea pedis.13

Various clinicalmorphologies include chronic scaly hyperkeratotic (Moccasin),

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inflammatory (vesicular),ulcerative types andchronic interdigital. Complex

interaction between dermatophytes commonly T.rubrum, bacteria and rarely

Candida causes interdigitale infection.

It includes 2 forms, 1)Dermatophytosis simplex presents with scaling

and fissuring,2)Dermatophytosis complex characterized by highly macerated

malodorous leucokeratotic lesions. Mocassin type is charachterised by chronic

mild dry hyperkeratotic lesions commonly caused by T.rubrum or severe

variant with cracked inflamed skin and erythema. Vesiculobullous type shows

small vesicles especially on the arch and sides of the foot and

T.mentagrophytesis the most common causative agent. Ulcerative type presents

with maceration, denudation, oozing affecting the soles.80

TWO FEET ONE HAND SYNDROME:

The feet are involved before the hands become infected. Patients relate

that tinea manuum developed in the hand after scratching the soles of the feet

or after picking the toe nails.82

TINEA INCOGNITO:

Tinea incognito is the term generally used for steroid modified cases of

dermatophytosis.13,83 In tinea incognito, the classical well-defined lesions

become modified. They become ill defined with reduced itching and

inflammation with spread of lesion. In many dermatoses like melasma,

psoriasis, pemphigus, etc., which are steroid responsive, there can be

superimposed tinea especially at occlusive sites. Therefore, before initiation of

steroid, any occult foci of fungal infection like, tinea corporis, tinea pedis and

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onychomycosis must be ruled out.12 Recent reports suggest that cases of

incognito lesion develop after tacrolimus and pimecrolimus as well. It is being

proposed that these manifestations are due to resilient organisms rather than

resistant organisms. Lesions can be asymptomatic without inflammation and

scaling,very pruritic, deep painful folliculitis like lesion or deep follicular

papules or pustules that are violaceous. Atrophy of epidermis is seen. Typical

annular pattern is lost. T.rubrum and T.mentagrophytes is are isolated.83

Table 10: Difference between classical Tinea and Tinea Incognito12

Classic Tinea Tinea Incognito

Itching present Minimal itching until steroid is applied; if steroid withdrawn, irritation/itching

Oval or circular plaque with sharply defined borders and central clearing, erythema Peripheral vesiculation may be present

Polymorphic with scattered papules, pustules, and hyperpigmentation with diffuse blanching Erythema with telangiectasis

Margins are raised Margins are less raised

Scaly lesions Less scaly

Less irritable Irritable

Less chance of recurrence and dissemination

More chance of recurrence and dissemination

Clinical clues to diagnose tinea incognito are ill-defined skin lesion with

diffuse scaling of long duration , lesions occurring at sites like face, trunk,

genitalia, unresponsiveness to topical corticosteroids (including combination

therapy)or initial subsidence of symptoms followed by exacerbation in

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cessation of therapy ,unresponsiveness to topical calcineurin inhibitor,

Presence of occult tinea like interdigital space, Patient on immunosuppressive

treatment for conditions like autoimmune dermatological and medical

condition.12

TINEA INDECISIVA (PSEUDO IMBRICATA):

Tinea pseudoimbricata is so named because of its clinical resemblance to

the infection typically caused by Trichophyton concentricum. Similar clinical

presentation have been described in patients treated with topical corticosteroids

and in those with some form of immunosuppression. Due to prolonged

alternating use of antifungals and topical steroids, dermatophyte lesions are

characterized by widespread annular concentric erythematous rings similar to

tinea imbricata produced as a result of cyclical immune suppression by topical

corticosteroid followed by reinfection due to early discontinuation of topical

antifungals . Defense against infection depends on both innate (e.g. b-

defensins) and acquired T cell-mediated immune mechanisms that result in

erythema and scaling. In T. concentricum infections, acquired immunity is

weakly expressed in genetically predisposed individuals, or modulation of

immunity by dermatophytes. A ring effect similar to that described here can be

explained by the fact that although host reaction occurs in response to actively

metabolizing fungal cells, these are only partially inhibited as a result of

concomitant topical steroid treatment or immunosuppression. When local

immune responses decline below a key threshold, the fungal genes are switched

on again and instigate another zone of host induced inflammatory response.

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This may be repeated several times, resulting in concentric rings of scaling and

inflammation that reflect the alternating activation and deactivation of defense

mechanisms.84

DERMATOPHYTID:

Id reaction may occur after starting treatment with antifungal therapy ,

as a result of cell mediated immune response. It is a nonfungal, generally

pruritic, papular, or vesicular eruption that typically begins on the face, then

spreads to the trunk and extremities. The eruption is usually follicular,

lichenoid, or papulosquamous, rarely morbilliform or scarlatiniform. The most

common site of involvement are on the hands and sides of the fingers with

associated tinea of the feet. These lesions are mostly vesicular, extremely

pruritic, and tender. Secondary bacterial infection may occur. Diagnosis is

mainly by the demonstration of fungal hyphae at a site distant from the

dermatophytid, absence of etiological agent in the id reaction lesion and

resolution of the lesions as the infection subsides.45

CHRONIC AND RECURRENT INFECTION:

Most common clinical presentation in case of chronic dermatophytosis

is tinea corporis. The commonest site in chronic infection is around the waist

followed by groin and back. Non inflammatory lesions with hyperpigmentation

and secondary lichenification can occur in chronic dermatophytosis lesion

caused by Trichophyton rubrum.85 The most common site of infection in

chronic dermatophytosis associated with psoriasis,86diabetes,87 hereditary

palmoplantar keratoderma,HIV88 is Tinea pedis. Tinea cruris is most common

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in males with chronic dermatophytosis. Tinea faciei resembles discoid lupus

erythematosus when it occurs bilaterally on face.85 Chronic infection caused by

T.mentagrophytes are relatively smaller in size and inflammatory .

Erythematous lesions with pustules, vesicles and granulomatous features may

be seen.89

ATYPICAL TINEA:

Atypical manifestation of cutaneous dermatophytosis mimics other

dermatoses. They are common in immune compromised patients resulting in

chronic disease. Atypical presentations resembles psoriasis , eczema ,

erythema multiforme , lupus erythematosus , dermatitis herpetiformis , rosacea

, impetigo , polymorphus light eruption , pyoderma , bullous lesion ,

eczematous, pseudomemranous , purpuric or nodular lesions,circumscribed

scleroderma, crusty circular plaques, white paint‑like dots, molluscum .Most

common atypical presentation observed are eczema like tinea.83 Even Patients

with previous cutaneous dermatitis not taking systemic/topical steroids also had

modified morphology. Now due to rampant use of topical steroid antifungal

combo preparations, tinea has now qualified for the category of great imitator

similar to syphilis, sarcoidosis and mycosis fungoides. The organisms most

commonly implicated in atypical tinea are T.rubrum,T,mentagrophytes,

M.canis, M.gypseum, M.audouinii, T.tonsurans, T.verrucosum, T.violaceum,

E.floccosum.83

Another variant of dermatophytosis frequently seen all over India in the

recent years is recurrent infection or tinea recidiveans. Steroids abuse in the

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form of combination formulation may be one of the most important

predisposing factors in these resilient forms of dermatophytosis. It is being

proposed that these manifestations are due to resilient organism than resistant.83

Trichophyton rubrum syndrome 10is defined as,

(a) skin lesions at the following four sites:

(1) feet, often involving soles; (2) hands, often involving palms; (3) nails; and

(4) at least one lesion in another location other than (1) (2) or (3), except for the

groin.

(b) positive microscopic analyses of potassium hydroxide preparations of skin

scrapings, in all four locations.

(c) identification of Trichophyton rubrum by cell culture at three of the four

locations at least. For diagnosis of Trichophyton rurum syndrome, the criteria

(a) and (b) and (c) have to be fulfilled.10

DEEP DERMATOPHYTOSIS:

Deep dermatophytosis is a rare clinical entity characterized by

infection of dermis, subcutis and internal visceral organs. It presents as nodular

lesions with an indolent course in association with superficial fungal infection

and the absence of hair follicle involvement. It is distinct entityfrom majocchi’s

granuloma.83

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TINEA RECIDIVEANS:

Resistance is characterized by non-responsiveness for treatment whereas

the tinea recidiveans or recurrent forms are characterized by response to

treatment initially and relapse within a week of stopping treatment or while on

treatment. It is characterized by lesions appearing at the periphery of the

healing patches .83

LABORATORY INVESTIGATION:

Scraping should be collected from the active margin of the lesion. It is

then transported to the laboratory in a pre-sterilized black chart paper, so the

specimen is kept dry and hence prevents the bacterial contamination. Various

tests used for confirmation of the diagnosis of dermatophytosis are:

a) Direct microscopic examination with 10-20% potassium hydroxide

b) Culture

c) Hair perforatin test

d) Urease test

e) Vitamin test

f) Growth on rice grain

g) Growth on 1% peptone agar

h) Wood’s lamp examination

i) Histopathology

j) Dermoscopy

k) Polymerase chain reaction and Nuclei acid sequence based amplification

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l) Matrix Associated Laser Desorption Ionization Time Of Flight Mass

Spectrometry

m) Reflectance confocal microscopy

Collection of specimen:

Samples used are skin scales, nail clippings and hairs. The lesion to be

scraped is cleaned with 70% ethyl alcohol and sterile gauge. Using cotton balls

for cleaning may confuse with fungal elements during microscopic

examination.80Blunt scalpel sterilized by heating is used to collect the scales

from the advancing edge of the lesion. Scraping should be done starting from

the center to the edge of the lesion across the margin. In case of vesicles or

bulla, roof top examination is done. In case of nails, nail clipping and

subungual keratin is used as sample. In case of hair root examination, it is done

by plucking the basal root portion of hair is and the scales in the scalp are

alsoscraped.7

a. Direct microscopic examination using 10% potassium hydroxide

(KOH)

Examination of scraping done with 10-20% potassium hydroxide is a

quick and imperative bed side tool for diagnosis. One drop of 10% KOH is

added to the specimen on the glass slide and a cover slip is placed over it and

pressed down firmly to attain the monolayer of cells. KOH is used to digest the

protein and disrupt the keratin aiding the better visualization of fungal

elements.90 Other agents that have been used are 10% sodium sulphide

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solution, 35% dimethyl suphoxide, dimethyl acetamide, dimethyl

formamide.13Then after a waiting for 10-15 minutes, slide is viewed under low

power (10x) and high power (40x) to look for the fungal elements.

Congo red, Methylene blue and Cotton blue are some of the special

stains used to increase the difference between the skin and fungus. Acridine

orange or Calcafluor white stains or Blankophor P Fussing in sodium sulphide

solution are used in case of fluorescence microscopy.13The most sensitive

method as Fluorescent staining diaminostilbene) with optical brighteners these

substances bind to main cell wall component of fungi, chitin. Presence of

refractile, long branching, hyaline septate hyphae with or without arthrospores

is found to be positive. Air bubbles and cotton fibers are common artifacts.91,92

b. Culture

Sabouraud’s dextose agar (SDA) medium is the most commonly used

media for isolation of dermatophytes .Composition of medium includes

peptone 1%, dextrose 4%, agar 2%, ph 5.6, chloramphenicol 0.05 g/l,

cycloheximide 0.5 g/dl. Emmons modification is 2% dextrose instead of 4%,

neopeptone instead of peptone, ph 6.8-7. Cycloheximide and chloramphenicol

inhibits the growth of non dermatophytic mould and bacteria respectively. In

case of non dermatophytic infection of palms, soles and nail, cycloheximide

free media is used. Cultures are incubated for atleast 4 weeks at the temperature

of 28 degree celsius before it is considered as negative or no growth .45 Growth

occurs in 7-14 days.13,93

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Dermatophytic test medium (DTM) is used as an alternative culture

method with ph indicator phenol red incorporated in the medium. The medium

turns red because of the proteolytic activity of dermatophytes thereby

increasing the ph to 8 or above .If there is growth of saprophytes, media

remains amber. The medium turns yellow if there is non-dermatophyte mould.

If there is no change in color for up to two weeks, medium is discarded .False

positive reaction is observed due to growth of Histoplasma capsulatum, and

Blastomyces dermtitis.45

Dermatophyte identification medium (DTM) is also used for presumptive

identification of dermatophytes. After an inoculation of 24-48 hours, if there is

dermatophyte growth, then the color changes from greenish blue to purple.

False positive results are low when compared to DTM .7 Media used for

conidiation are Potatodextose agar, Cornmeal agar, and sterile unfortified

polished rice.Macroscopic appearance of colony is examined for color of

surface, presence or absence of reverse pigmentation, texture and growth

rate.The colony is subjected to tease mount and stained with lactophenol cotton

blue and examined under microscope.46 Microconidia and macroconidia are

examined and their structural characteristics are used in species identification.If

the species identification in the above method is not confirmatory, slide culture

is prepared and examined for characteristic morphology enriched medium like

potato dextrose agar is used for sporulation.92 Urease test , growth on rice

grains,in vitro hair perforation test are some of the other physiological tests

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done. ,if Microsporum species is suspected and nutritional requirement if a

Trichophyton is suspected.46

Table 11: Genus Trichophyton7,13,46

Agent Colony Surface Reverse Microscopy

i. T.rubrum13

(5 forms) 1. Downy – most common

White downy / cottony and dome shaped

Dark brown initially and turns red after 3-4 weeks

Microconida- small tear drop shaped, along the side of hyphae.bird on fence appearance

2. Melanoid Similar to downy Brown melanoid t to red pigment on reverse

Tear drop shaped microconidia along the sides of hyphae.

3. Dysgonic – slow growing

Tiny, deep red colonies

- -

4. Granular form

Powdery/ granular brown topic radial folding

Reddish brown reverse

Tear shaped microconidea -smooth thin walled cylindrical pencil shaped macroconidia

5. Yellow form

Smooth,leathery, surface yellow to downy

Yellow on reverse

-

ii. T.interdigitale13 Fast growing White powdery surface with creamy center

Tan or reddish brown with pale edge

Spherical microconidia in clusters -macroconidia present

iii.

T.mentagrophytes13

Rapidly growing

Intensely granular surface is fully white or cream centre, edge- thinner, spiky/ stellate

Yellow, tan or red brown

Spherical microconidia in grape like clusters, spiral hyphae and thin walled cylindrical macroconida may be present.

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iv. T.tonsurans13 Slow growing Velvety/ powdery surface grey, cream yellow in color ,surface circlular or radial folds are present

Chocolate brown/mahogany or yellow.

Variable micro conidiae – balloon shaped /clavate microconidia and stacked matches like macroconidia – large numbers chlamydoconidia seen microconidia are present.

v. T.schonleinii13 Glabrous/velvety heaped and the periphery is folded with fringe of hyphae at the edge of medium

White to cream Pale Dichotomously branching hyphae with flattened tips

vi. T.verrucosum13 Slow growing White or grey waxy - 26 deg c – short hyphae along with terminal chlamydoconidia clavate or elongate microconidia along the sides of hyphae - rat tailed macroconidia

vii. T.violaceum13 Slow growing

Waxy or leathery in texture Deep purple to red in color

- Micro and macro conidia are usually absent. Chlamydoconia and distorted hyphae may be present.

viii.

T.soundanense13

Slow growing Glabrous/leathery/ brittle in texture with characteristic stellate/eye lash fringe around the edge. Color apricot to yellow

- stiff and brush like hyphae, regularly septate with zigzag appearance of arthroconidia

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Table 12: Genus Microsporum and Epidermophyton:7,13

Agent Colony Surface Reverse Microscopy

M.audouinii Glabrous to velvety like a mouse fur

White to tan colour,silky growth , thicker, downy white surface

Salmon pink to tan colour

Terminal and intercalary chlamydoconidia seen. racquet hyphae present

M.canis Rapid growth Coarse colones. fluffy to wooly / hairy texture. Surface White to pale yellow

Deep yellow to orange

Macroconidia –large spindle shaped, thick walled .it has an asymmetrical knob ,it has up to 16 cells

M.gypseum Rapidly growing

Floccose or powdery growth in texture. Cinnamon colured . Surface buff / fawn

Range from colorless to deep mahogany brown

macroconidia seenas clusters in large numbers. cylindrical to fusiform shaped,echinulations present, thin walled 4 to 6 septa seen- racquet and pectinate hyphae may be present

Epidermophyton

floccosum13 Grows rapidly form velvety or sude like colonies with central or radial folds

Khakhi or olive green

Light to dark brown

Large clavate macroconidia maximum of upto six cells seen, apex rounded. Microconidia – absent Chlamydoconidia – large numbers in older cultures.

DERMATOPHYTE IDENTIFICATION: This is done on the basis of

colony characteristics,physiologic tests and microscopic morphology.

Dermatophytes can be distinguished based on the appearance of macroconidia.

Few physiological tthere to confirm the identification of some species. In

additionto this special amino acid tests and requirements of vitamin can

differentiate trichohyton species from others. The property of the organism to

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hydrolyse urea is used to differentiate T.mentagrophytes (urease positive) and

T. rubrum (urease negative).94

c. Hair perforation test

The colonies to be tested is inoculated on the sterile hair suspended in

distilled water supplemented along with yeast extract and incubated at 28

degree celsius for 2 weeks. The hair is then examined for wedge shaped

penetrations that are perpendicular to the hair axis.7 The test is positive in case

of T. mentagrophytes and M.canis .Penetrations are not seen with T.rubrum and

M.equinum.94

d. Urease test

The colonies to be tested is inoculcated in to the sterilized urea agar

base and is mixed with sterile molten agar ,then it is incubated at 28 degree

celsius for 7 days. Hydrolysis of urea is observed by T.mentagrophytes and

turns the color from yellow to magenta red, while T.rubrum does not.94

e. Vitamin test

Vitamin test help us to differentiate Trichophyton species based on their

requirement of vitamins for growth . T.tonsurans,T.concentrum and

T.violaceum require thiamine. T.verucosum requires thiamine and inositol,

while nicotinic acid is required for T.equinum, T.meigninii uses histidine.

Agar free inoculum from soa medium is inoculated into Trichophyton agar 1-7

namely Agar – 1: casein based – vitamin free and it is used as control,Agar 2: –

inositol,Agar 3 :- thaimine +inositol, Agar 4: – thiamine ,Agar 5 – nicotinic

acid,Agar 6 – ammonium nitrate - vitamin free control,Agar 7 – histidine and

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incubated for 2-3 weeks at 26 degree celsius. Based on the requirements of the

vitamins as said above, the organisms are identified. Sorbitol utilization

differentiatesT.rubrum (positive) andT.mentagrophytes (negative).7

f. Growth on rice grain

The test organism is inoculated onto the surface of ordinary white rice

coated with distilled water (autoclaved) and incubated at 26 degree celsius. The

growth of the organism is assesed after 2-3 weeks. Microsporum audouinii

grows poorly while other species of Microsporum shows growth. The

significance of this test is to differentiate M.audouinii from other species of

microsporum.7

g. Growth on 1% Peptone Agar

Pink color colonies are produced by Microsporum persicolor while

T.mentagrophytes remains white.7

h. Wood’s Lamp examination

Wood’s lamp examination is done in school children to screen for tinea

capitis. Microsporum species and T.schoenleinii shows green fluorescence.

Black dot type of tinea capitis does not fluoresce.94

i. Histopathology

Histopathological examination is helpful in the diagnosis of Majocchi’s

granuloma .KOH examination of scales on the surface of Majocchi’s

granuloma is often negative. Hyphae are visualized in stratum corneum with

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hematoxylin and eosin staining. Periodic–acid shiff and Gomori methanamine

silver are some of the special stains used to highlight the hyphae.94 In early

stages fungus in epidermisshows a toxic reaction similar to that of acute,

subacute or chronic dermatitis. In chronic tinea corporis, hyperkeratosis and

parakeratosis are seen in dry scaly plaques . ‘sandwich sign’ indicates the

presence of hyphae in the stratum corneum between two zones of cornified

cells. In case of immunodeficiency, granulomas are surrounded by an

eosinophilic matrix of splendore hoeppli material .95

j. Dermoscopy

Comma hairs, curve hairs, fractured hairshaft, corkscrew hairs, morse

code hairs, transluscent hair are seen in the case of Tinea capitis.94,96

Charachteristic scaly plaques of tinea corporis in dermoscopy show scaly

plaques , translucent hairs , follicular pustules , broken hairs , corkscrew hair ,

black dots , dystrophic hair and Morse code hair and rarely Empty follicles.97

k. Polymerase Chain Reaction (Pcr) And Nucleic Acid Sequence Based

Amplification:

Rapid and early diagnosis of infection and also helpful in identifying

drug resistance against antiungals.96

UNIPLEX PCR: They areIn house PCR assays helps to differentiate

dermatophytes from skin scales. The sensitivity and specificity of the test was

80.1% and 80.6 on par with the cultures.96

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47

MULTIPLEX PCR: It helps in the identification of 21 dermatophytic

pathogens along with subsequent DNA detection by agarose gel

electrophoresis. Nested-PCR, Real-Time PCR, Multiplex PCR, Restriction

Fragment Length Polymorphism (RFLP), Amplified Fragment Length

Polymorphism (AFLP), Random Amplified Polymorphic DNA (RAPD), DNA

microarray and other nucleic acid based techniques provide faster, easier, and

confident species-level diagnostic approach which may lead to an effective

treatment at early stage of dermatophytosis.96

l. NEWER METHODS – MALDI TOF:Matrix Associated Laser Desorption

Ionization Time Of Fight Mass Spectrometry is done based on the

biochemical characteristic and proteolytic degradation products of fungal

infection. The peptide patterns are identified by comparison of known peptide

spectra from skin disorders stored already in the database. This method is

very rapid and helps in the simultaneous identification of up to 64

dermatophyte strains. Results are obtained in 24 hrs.96

k. Reflectance confocal microscopy

It is a noninvasive.It helps in vivo imaging of epidermis and also upto

superficial dermis at cellular level resolution to identify the fungal and

parasitic infection of skin. Fungal hyphal elements with branching are detected

over an erythematous annular scaly patch.96

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48

TREATMENT

The mainstay of management lies in counseling the patients regarding the

general measures and making them to strictly adhere to it. It is important to

stress that compliance to treatment is very important.

General measures: 12,98

� Bathing twice in cold water in hot and humid climate and to wipe dry and

then wear clothes.

� Avoidance of tight clothing and synthetic garments. Patients should be

encouraged to use cotton garments.

� Patients with Tinea cruris patients are instructed to wear box-type inner

garments,remove the waistband and change the under garments everyday.

They are advised to remove the hair on genitalia regularly

� Patients with Tinea pedis should be better advised to use open foot wear

and cotton socks.

� To minimize exposure to fomites by avoidance of sharing of soaps, towels,

clothes, towels, bed linen, and combs should be practiced and are washed

regularly. Washing clothes at 60°c has found to eliminate dermatophytes.99

Infected clothes and socks to be washed separately. Sunlight is the best

disinfectant. So washed clothes should be turned inside out while drying in

sunlight.

� People staying in hostel are instructed to iron the clothes or use well-dried

inner garments.

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49

� Mechanical removal of any material containing keratin, such as shed skin

and hairs, facilitates disinfection. Vacuuming is considered as the best

method in the western world . Wet mopping may be ideal in our country.

After mechanical removal, washable surfaces should be cleaned thoroughly

with detergent and hot water.

� All bed linens and towels should be scrubbed, and washed with hot water

and detergent. Cleaning and disinfection of the surroundings shoud be

repeated at least once in a week until all affected persons have eliminated

the fungal infection.

� Patients with Tinea pedis should be better advised to use open foot wear

and cotton socks.

� Patients should be explained about the adverse effects of steroids and

instructed to strictly avoid using OTC preparations and other self

medications

� Obese patients are encouraged to lose weight.

TOPICAL THERAPY:

Topical therapy is indicated when patients have few localized lesions,

during the first trimester of pregnancy, systemic antifungals are

contraindicated. Topical antifungals (AFA) are usally used in combination

with systemic antifungal therapy. Topical antifungal have the advantage of

availability of increased concentration of the drug at the lesional site. Azoles

namely triazoles and imidazoles, allylamines,tolnaftate, ciclopiroxolamine

benzylamines, and whitfield ointment. “ RULE OF TWO ”98 is to be followed

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50

with the exception of luliconazole which is to be applied once a day ,with the

topical antifungal creams are being applied 2 cm beyond the margin of the

lesion for a minimum of atleast 2 weeks beyond the complete clinical

resolution.98

SYSTEMIC THERAPY:

Multiple site involvement, localized tinea not respnding to topical AFAs,

extensive/chronic/recurrent infections, Tinea capitis, Tinea pedis and Tinea

manuum are indications for systemic AFAs. Systemic antifungals used in

management of dermatophytosis are fluconazole, ketoconazole, itraconazole,

terbinafine and griseofulvin. Systemic ketoconazole is no longer approved by

FDA for superficial fungal infection due to the adverse effect of

hepatotoxicity.

Table 13: Systemic antifungals

Reference Griseofulvin Fluconazole Itraconazole Terbinafine

Rook’s dermatology 9th edn, 201613

1g/day -4 weeks - 100 mg/day x 2 to 4 weeks

250 mg/ day for 2-3 weeks

Fitzpatrick’s dermatology -8th edn, 201245

500 mg/ day x 2-4 weeks

150-300 mg/ w-eek x 4-6 weeks

100 mg/ day x 1 week

250 mg/ day x 2-4 weeks

Bolognia dermatology 3rd edn, 20121

500-1000mg/day (microsize) or 375-500mg/day (ultramicronise) x 2-4 weeks

150-200 mg/ week x 2-4 weeks

200 mg/ day x 1 week

250 mg/day x 1 week

IADVL book of dermatology 4th edn,2015100

500 mg/day x 4-8 weeks

150- 300 mg/ week x4-6 weeks

200-400 mg / day x 1 week

250 mg/day x 2 weeks

Senthamilselvi G-handbook of dermatomycol ogy 1st edn101

500 mg / day x 6 weeks

3mg/kg biweekly x 6 weeks

100 mg/day x 2 weeks or 200 mg/ day x 1 week

5mg/kg x2 weeks

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AIMS AND OBJECTIVES

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51

AIMS AND OBJECTIVES

1) To study the epidemiological aspects of chronic dermatophytosis.

2) To study the various clinical presentations in patients with chronic

dermatophytosis.

3) To study the various associations in patients with chronic dermatophytosis.

4) To isolate the various etiological agents in patients with chronic

dermatophytosis

5) To study the clinico mycological correlation of chronic dermatophytosis

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MATERIAL AND METHODS

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52

MATERIALS AND METHODS

STUDY CENTRE :

The study was conducted in Mycology section, Department of Dermatology,

Madras Medical college / Rajiv Gandhi Government General Hospital,

Chennai- 3

INCLUSION CRITERIA:

1) Patients attending or referred to Mycology Outpatient department who

had the disease for more than 6 months duration in spite of having

completed treatmentwith or without recurrence.

2) KOH positivity in scrapings for fungus

EXCLUSION CRITERIA:

1. KOH negativity of scraping for dermatophytosis

2. Tinea capitis,Onychomycosis,Tinea pedis

STUDY PROCEDURE:

One hundred patients with history of chronic dermatophytosis was selected for

the study. Detailed case history of each patient was taken with reference to

name, sex,age, Inpatient/Outpatient number,address, occupation, marital

status, chief complaints, duration of symptoms, previous treatment

history(topical and systemic) and other associated comorbidities such as

diabetes, tuberculosis, immunosuppressive states (HIV, , anemia , malnutrition,

transplant patients, internal malignancy,) and hobbies, personal hygiene,

clothing habits, history of other members affected in the family sharing of

fomites like towels, bed linen, history of pet animals in homewas noted. Past

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53

history of similar infections waa also noted. General and systemic

examinations were done. Clinical features like site of involvement, shape nad

number of lesions, size of lesions was noted. Palms, soles ,nail and mucosa

was examined. Blood hemogram, random blood sugar,serum electrolytes ,tests

of renal and liver function ,ELISA for HIV was done if indicated . Scraping

was done from the active margin in the periphery and was viewed for the

presence of long thin branched hyalinized septate hyphae in KOH .All the

specimens which are KOH positive was subjected to SDA culture. The area to

be scraped was cleaned with 70% alcohol ,scales are scraped and was

inoculated into Sabouraud's Dextrose Agar medium and kept at 28 degree

celsius in an incubator. Macroscopic appearance of the colony was observed

weekly for 2 to 3 weeks. Microscopic appearance of the colony in lacto phenol

cotton blue was noted

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OBSERVATION AND RESULTS

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SEX DISTIBUTION

Out of the 100 patients, 30 patients were males and 70 were females

sex ratio of males to females

Table 14: Sex Distribution in patients with chronic dermatophytosis

Sex No

Male

Female

Chart-1: Sex Distribution in patients with chronic dermatophytosis

AGE WISE DISTRIBUTION

In our study,

age of 38 years. The most commonly affected age group was 21

25 (25%) patients closely followed by

23 (23%) patients and

affected males was

54

RESULTS

SEX DISTIBUTION:

100 patients, 30 patients were males and 70 were females

to females of 1:2.3.Mean age group was 35 years

Sex Distribution in patients with chronic dermatophytosis

No of Patients ( N=100) Percentage (%)

30

70

1: Sex Distribution in patients with chronic dermatophytosis

AGE WISE DISTRIBUTION:

age of the patients ranged from 5 to 75 years with a mean

years. The most commonly affected age group was 21

closely followed by the age group between

patients and 21 (21%)patients in 41-50 years. Maximum

in the age group of 21-30 years with 12

30%

70%

SEX DISTRIBUTION

MALE FEMALE

100 patients, 30 patients were males and 70 were females with the

of 1:2.3.Mean age group was 35 years (Table 14).

Sex Distribution in patients with chronic dermatophytosis

Percentage (%)

30

70

1: Sex Distribution in patients with chronic dermatophytosis.

patients ranged from 5 to 75 years with a mean

years. The most commonly affected age group was 21-30 years with

the age group between 31-40 years with

ximum number of

with 12 (40%)patients

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while the highest number of affected females was

years with19 (27.1%) patients

Table 15: Sex Wise Age Distribution

AGE

MALE (N=30)

<=20YRS

21-30YRS

31-40YRS

41-50YRS

>50YRS

0.0%

5.0%

10.0%

15.0%

20.0%

25.0%

30.0%

35.0%

40.0%

<=20yrs

16.7% 17.1%

SEXWISE AGE DISTRIBUTION (%)

55

while the highest number of affected females was in the age group of 31

(27.1%) patients. (Table 15)

Sex Wise Age Distribution

SEX

MALE (N=30) FEMALE (N=70)

5(16.7%) 12(17.1%)

12(40%) 13(18.6%)

4(13.3%) 19(27.1%)

4(13.3%) 17(24.3%)

5(16.7%) 9(12.9%)

Chart-2: Sex Wise Age Distribution

21-30yrs 31-40yrs 41-50yrs >50yrs

Age

40.0%

13.3% 13.3%

16.7%17.1%18.6%

27.1%

24.3%

12.9%

SEXWISE AGE DISTRIBUTION (%)

in the age group of 31-40

TOTAL (100%)

17(17%)

25(25%)

23(23%)

21(21%)

14(14%)

Male

Female

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SOCIOECONOMIC STATUS

Out of the 100 patients

status followed by

status and 3 (3%) patients from higher socioeconomic status.

Table 16: Socioeconomic status.

Socioeconomic status

Lower SES(<20,000/annum)

Middle SES (>40,000/annum)

Higher SES

0

10

20

30

40

50

60

SOCIO ECONOMIC STATUS (%)

56

SOCIOECONOMIC STATUS:

100 patients, 51 (51%) patients belonged to lower socioeconomic

46 (46%) patients belonging to middle socioeconomic

(3%) patients from higher socioeconomic status. (Tabl

Socioeconomic status.

ocioeconomic status(SES) No of patients (n=100)

Lower SES(<20,000/annum) 51

Middle SES (>40,000/annum) 46

3

Chart-3:Socioeconomic status.

HigherSES

Middle SES (>40,000/annum)

Lower SES(<20,000/annum)

3

46

51

SOCIO ECONOMIC STATUS (%)

HigherSES

Middle SES (>40,000/annum)

Lower SES(<20,000/annum)

, 51 (51%) patients belonged to lower socioeconomic

to middle socioeconomic

(Table 16)

Percentage (%)

51

46

3

Lower SES(<20,000/annum)

SOCIO ECONOMIC STATUS (%)

HigherSES

Middle SES (>40,000/annum)

Lower SES(<20,000/annum)

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RURAL/URBAN DISTRIBUTION

Among the 100 patients, 45

followed by 36 (36%) patients

from semiurban area

Table 17: Residence locality

Residence locality

Urban

Rural

Semi urban

RESIDENCE LOCALITY

57

RURAL/URBAN DISTRIBUTION

100 patients, 45 (45%) patients were from urban area,

(36%) patients from rural area while 19 (19%)

from semiurban area. (Table 17)

Residence locality

No of patients P

45

36

19

36%

19%

45%

RESIDENCE LOCALITY

RURAL SEMI URBAN URBAN

Chart-4: Residence locality

were from urban area,

(19%) patients were

Percentage (%)

45.0

36.0

19.0

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OCCUPATIONAL STATUS:

Thirty (30%) patients o

patients were outdoor labourers, 23

office employees and 1 (1%)

Table 18: Occupational Status

Occupation

House Wife

Outdoor Labourers

Student

Office Employees

Hospital Worker

HOUSE WIFE

STUDENT

OFFICE EMPLOYEES

OUTDOOR LABOURERS

HOSPITAL WORKER

58

OCCUPATIONAL STATUS:

Thirty (30%) patients out of the 100 patients were house wives

patients were outdoor labourers, 23 (23%)patients were students,21

and 1 (1%) patient was a hospital worker. (Table 18)

Occupational Status

No of patients (n=100) Percentage

30

25

23

21

1

Chart-5: Occupational Status

30%

23%

21%

25%

1%

OCCUPATION (%)

OFFICE EMPLOYEES

OUTDOOR LABOURERS

HOSPITAL WORKER

were house wives, 25 (25%)

patients were students,21 (21%)were

. (Table 18)

Percentage (%)

30

25

23

21

1

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DURATION OF INECTION

Sixty (60%) patients o

6months – 1year , followed by

(6%)patients and more than 3 years in 3

Table 19: Duration

Duration

0.5-1 YR

1-2 YRS

2-3 YRS

>3 YRS

Chart

Out of the 100 patients

had persistent infection while

(Table 20),with less than

episodes in 20 (35.7%)

60

DURATION OF INFECTION (%)

59

DURATION OF INECTION:

(60%) patients out of the 100 patients, had infection ranging from

1year , followed by 1-2 years in 32 (32%)patients, 2

patients and more than 3 years in 3 (3%)patients. (Table 1

Duration of Infecction

No of patients (n=100) Percentage

60

32

6

2

Chart-6: Duration of Infecction

100 patients, 44 (44%) patients with chronic dermatophytosis

had persistent infection while 56 (56%) patients had intermittentmanifestation

with less than 3 episodes in 36 (64.3%) patients

(35.7%) patients out of the 56 patients (Table 2

60

32

62

DURATION OF INFECTION (%)

0.5-1 YR 1-2 YRS 2-3 YRS >3 YRS

had infection ranging from

patients, 2-3 years in 6

19)

Percentage (%)

60

32

6

2

chronic dermatophytosis

intermittentmanifestation

patients and more than 3

(Table 21).

DURATION OF INFECTION (%)

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Table 20: Course of infection in patients with chronic dermatophytosis

Persistent/Episodic

Episodic

Persistent

Chart-7: Course o

Table 21: No of episodes in patients with chronic dermatophytosis

Episodes

<=3

>3

Chart-8: No of episodes in patients with chronic dermatophytosis

60

Course of infection in patients with chronic dermatophytosis

No of patients (n=100) Percentage (%)

56 44

of Infection in Patients with Chronic Dermatophytosis

No of episodes in patients with chronic dermatophytosis

No of patients (n=100) Percentage

36 20

8: No of episodes in patients with chronic dermatophytosis

44%56%

PERSISTENT/ EPISODIC (%)

PERSISTENT

EPISODIC

64%

36%

EPISODES (%)

<=3

>3

Course of infection in patients with chronic dermatophytosis

ercentage (%)

56 44

Chronic Dermatophytosis

No of episodes in patients with chronic dermatophytosis

Percentage

64.3 35.7

8: No of episodes in patients with chronic dermatophytosis

<=3

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TREATMENT HISTORY:

In the present study

(OTC) drugs of which 23 (out of 30

58.6%) were females.

patients. These were

approached family physicians. Forty nine

applied topical steroid antifungal(TSAF)

males,18(60%) patients had abused TSAF creams while 31(44.3%) females out

of 70 had applied these creams.

22 (73.3%) of males,

Table 22: Treatment history

Treatment history

OTC Drugs Prescription Drugs Topical Steroid Use Poor compliance

0%

Topical sterioids use

OTC drugs

Prescription drugs

Poor compliance

SEX WISE DISTRIBUTION OF

61

TREATMENT HISTORY:

present study, 64 patients gave history of use of Over the counter

of which 23 (out of 30-76.6%) were males and 41(out of 70

58.6%) were females. patients Use of prescribed drugs was observed in 87

. These were the patients who had used OTC drugs and subsequently

approached family physicians. Forty nine patients gave history

opical steroid antifungal(TSAF) combination creams

males,18(60%) patients had abused TSAF creams while 31(44.3%) females out

of 70 had applied these creams. History of poor compliance was observed in

, and 53 (75.5%) of females (Table 22)

Treatment history

Sex

Male Female

23(35.9%) 41(64.125(28.7%) 62(71.3

18(36.7%) 31(63.322(29.3) 53(70.6%)

Chart 9: Treatment history

18

23

25

22

31

41

62

53

0% 20% 40% 60% 80%

SEX WISE DISTRIBUTION OF

TREATMENT HISTORY

patients gave history of use of Over the counter

76.6%) were males and 41(out of 70-

was observed in 87

d used OTC drugs and subsequently

history of having

combination creams. Among the 30

males,18(60%) patients had abused TSAF creams while 31(44.3%) females out

History of poor compliance was observed in

Total Female

41(64.1%) 64 62(71.3%) 87 31(63.3%) 49

70.6%) 75

80% 100%

SEX WISE DISTRIBUTION OF

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ASSOCIATION:

Out of the 100 patients, 35

which 11 (31.4%)

hypertension, 10 (28.6%)

5 (14.3%) patients

3(8.6%) patients had ischemic heart disease

neurological disorder

Table 22: Comorbidities

Comorbidities

Diabetes Mellitus Hypertension Diabetes & Hypertension Atopy Cancer Cardiac disease Neurological disease

DM & HT

ATOPY

CANCER

CARDIAC DISEASE

NEUROLOGICAL DISEASE

62

100 patients, 35 of them had association with co morbidities, of

which 11 (31.4%) patients had diabetes mellitus,2 (5.7%)

(28.6%) patients had both diabetes mellitus and hypertension,

had history of atopy, 3 (8.6%) patients had cancer

had ischemic heart disease and 1 (2.9%) patient had

neurological disorder. (Table 23).

Comorbidities

Comorbidities No of patients (n=100)

11 2

ypertension 10 5 3 3

Neurological disease 1

Chart 10: Comorbidities

DM

HT

DM & HT

ATOPY

CANCER

CARDIAC DISEASE

NEUROLOGICAL DISEASE

2

5

3

3

1

COMORBIDITIES

with co morbidities, of

(5.7%) patients had

patients had both diabetes mellitus and hypertension,

ad history of atopy, 3 (8.6%) patients had cancer and

(2.9%) patient had

Percentage

31.4 5.7

28.6 14.3 8.6 8.6 2.9

11

10

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63

PERSONAL HISTORY:

Out of the 100 patients, 85 (85%) patients took bath daily, 14 (14%)

patients took bath once in 2 days and 1 (1%) patient used to take bath once in a

week. Among the 100 patients, 52 (52%)patients did not wipe after bathing of

which 14 (26.9%) were males and 38 (73.1%) were females. Sharing of fomites

such as towels, clothes and bed linen was observed in 78 (78%) patients.

Twenty three out of 100 patients gave the history of washing clothes once in 3

days.Eight patients had pet animals in their home. Out of the 70 females ,51

patients gave the history of working in kitchen of which 23patients worked in

kitchen for less than 2 hours and 28 worked in kitchen for more than 2 hours

especially during the hot afternoons.(Table 24)

Table 24: Personal Habits

Personal habits Sex Total

Male Female

Bathing habits

Daily 24(28.2%) 61(71.8%) 85

Once in 2 days 6(42.8%) 8(57.2%) 14

Once in a week 0(0%) 1(100%) 1

Dressing without wiping 14(26.9%) 38(73.1%) 52

Sharing fomites 23(29.4%) 55(70.6%) 78

Wearing unwashed clothes 8(34.8%) 15(65.2%) 23

Pet animals 3(37.5%) 5(62.5%) 8

Hours in kitchen <=2hrs 0(0%) 23(100%) 23

>2hrs 0(0%) 28(100%) 28

No kitchen work 30(61.2%) 19(38.8%) 49

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DRESSING HABITS

Out of the30 males 17 (56.7%) patients wore jeans

patients used v shaped inner garments,15

wearing waist / wrist band and 11 (36.7%) patients gave

foot wear. (Table 25)

0

10

20

30

40

50

60

70

80

90

64

Chart 11: Personal Habits

DRESSING HABITS – MALE:

30 males 17 (56.7%) patients wore jeans regularly,9

shaped inner garments,15 (50%) patients gave h

wearing waist / wrist band and 11 (36.7%) patients gave history of using closed

)

PERSONAL HABBITS

regularly,9 (30%)

patients gave history of

history of using closed

Male

Female

Total

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Table 25: Male dressing habits

Dresses

Jeans

Waist band/ wrist band

Shoes/ closed foot wear

Inner garments V shaped

DRESSING HABITS

Out of the 70 females in the study, 44 (62.9%) patients wore synthetic

garments, 17 (24.3%) patients use

jeans, 31 (44.3%) pati

used closed foot wear. (Table 2

0.0%

10.0%

20.0%

30.0%

40.0%

50.0%

60.0%

JEANS

56.7%

DRESSING HABITS

65

Male dressing habits

Dresses Male (n=30)

17(56.7%)

Waist band/ wrist band 15(50%)

Shoes/ closed foot wear 11(36.7%)

shaped 9(30%)

Chart-12:Male dressing habits

DRESSING HABITS – FEMALE:

70 females in the study, 44 (62.9%) patients wore synthetic

garments, 17 (24.3%) patients used leggings regularly, 3 (4.3%) patients wore

jeans, 31 (44.3%) patients used wrist band/ anklets and 10 (14.3%) patients

used closed foot wear. (Table 26)

JEANS INNER

GARMENTS

WAIST BAND/

WRIST BAND

SHOES/ CLOSED

FOOT WEAR

56.7%

30.0%

50.0%

DRESSING HABITS - MALE

Male (n=30)

17(56.7%)

15(50%)

11(36.7%)

9(30%)

70 females in the study, 44 (62.9%) patients wore synthetic

leggings regularly, 3 (4.3%) patients wore

10 (14.3%) patients

SHOES/ CLOSED

FOOT WEAR

36.7%

MALE

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Table 26: Female dressing habits

DRESSES

Synthetic garments

Waist band/ wrist band

Leggings

Shoes/ closed foot wear

Jeans

FAMILY HISTORY:

Out of the 100 pati

members being affected with

16 were males. Among

membersand 19 (36.5%)

family. Among the 16 males,13

patients had more than 3

0.0%

10.0%

20.0%

30.0%

40.0%

50.0%

60.0%

70.0%

JEANS

66

Female dressing habits

DRESSES FEMALE (N=70)

44(62.9%)

wrist band 31(44.3%)

17(24.3%)

Shoes/ closed foot wear 10(14.3%)

3(4.3%)

Chart-13: Female dressing habits

FAMILY HISTORY:

100 patients, 68 (68%) patients gave history of other family

affected with dermatophytosis of which 52 were females while

Among the 52 females , 33 (63.5.7%) patients had less than 3

(36.5%) patients had more than 3 members affected in the

16 males,13 (81.2%) patients had less than

patients had more than 3 members affected in the family. (Table 2

JEANS LEGGINGS SYNTHETIC

GARMENTS

WAIST

BAND/

WRIST BAND

SHOES/

CLOSED

FOOT WEAR

DRESSING HABITS - FEMALE

FEMALE (N=70)

44(62.9%)

31(44.3%)

17(24.3%)

10(14.3%)

3(4.3%)

history of other family

of which 52 were females while

patients had less than 3

patients had more than 3 members affected in the

patients had less than 3 and3 (18.8%)

(Table 27)

SHOES/

CLOSED

FOOT WEAR

FEMALE

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Table 27: Infection among family members

Family members affected

<3 members >=3 members

Chart

BODY SURFACE AREA(BSA) :

Out of the 100 patients in the study ,

than 40% of BSA, 15(15% )with <

30% and 9(9%) with 11

TABLE 28: Body surface area

BSA

<10%

11-20%

21-30%

>40%

0.0%

<3 Members

>=3 Members

67

Infection among family members

amily members affected Sex

Male (n=16) Female (n=52)

13(81.2%) 33(63.5%) 3(18.8%) 19(36.5%)

Chart-14:Infection among family members

BODY SURFACE AREA(BSA) :

Out of the 100 patients in the study , 62(62%) of patients had in more

15(15% )with <10% BSA involvement,14(14%) with 21

30% and 9(9%) with 11-20%(table 28)

: Body surface area

Number of patients

15

9

14

62

0.0% 20.0% 40.0% 60.0% 80.0% 100.0%

81.3%

18.8%

63.5%

36.5%

FAMILY HISTORY

Total

46(67.6%) 22(32.4%)

:Infection among family members

of patients had in more

10% BSA involvement,14(14%) with 21-

%

15

9

14

62

Female

Male

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CLINICAL TYPE OF DERMATOPHYTOSIS:

Out of the 100 patients

had single clinical type

clinical presentations.

ISOLATED CLINICAL TYPES:

Among the 9 patients with single clinic

most common presentation seen in 6

females and 1 male, followed by 2

included 2 females and 1 patient with tinea faciei who was a male.

Table 29:

Isolated clinical types

Tinea Corporis TineaGlutealis Tinea Faciei

68

CLINICAL TYPE OF DERMATOPHYTOSIS:

100 patients, 9 (9%) patients with chronic dermatop

had single clinical type, while 91 (91%) patients had combination

s.

Chart-15:Clinical presentation

ISOLATED CLINICAL TYPES:

9 patients with single clinical type, tinea corporis

most common presentation seen in 6 (66.6%) patients which included

and 1 male, followed by 2 (22.2%) patients with tinea glutealis which

2 females and 1 patient with tinea faciei who was a male.

clinical types Sex

Male Female

1 5 0 2 1 0

9

91

with chronic dermatophytosis

patients had combination of various

al type, tinea corporis was the

which included 5

h tinea glutealis which

2 females and 1 patient with tinea faciei who was a male. (Table 29)

Total

(n=9)

6(66.6%) 2(2.22)

1(11.1%)

SINGLE

COMBINED

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69

COMBINATION CLINICAL TYPES:

Among the 91 patients, combination of tinea corporis and tinea cruris

was most common presentation seen in 35(23.07%) patients and was more

common in 21(17.1%) females, followed by tinea corporis, tinea cruris and

tinea axillaris seen in 15 patients which is also more common in females.

(Table 29) (Fig 1-19, 25-33, 39, 43, 47)

Table 30: Combination Clinical Types

Combination Clinical Types Sex Total

N=91(100%) Male Female

T.Corporis+T.Cruris 14(40%) 21(60%) 35(38.4%)

T.Corporis+T.Axillaris+T.Cruris. 1(5%) 19(95%) 20 (21.9%)

T.Corporis+T.Axillaris+T.Cruris+T.Facei 2(22.2%) 7(77.7%) 9(9.89%)

T.Corporis+T.Cruris+T.Facei 3(60%) 2(40%) 5(5.49%)

T.Corporis+T.Axillaris 0(0%) 4(100%) 4(4.39%)

T.Corporis+T.Axillaris+T.Cruris+T.Manuum 2(50%) 2(50%) 4(4.39%)

T.Corporis+T.Axillaris+T.Facei 1(50%) 1(50%) 2(2.19%)

T.Corporis+T.Axillaris+T.cruris+ T.Capitis 0(0%) 2(100%) 2(2.19%)

T.Corporis+T.Cruris 1(50%) 1(50%) 2(2.19%)

T.Corporis+T.Cruris+T.Facei 1(50%) 1(50%) 2(2.19%)

T.Corporis+T.Axillaris+T.Cruris+T.Glutealis+T.Facei+T.Manuum

0(0%) 1(100%) 1(1.09%)

T.Corporis+T.Axillaris+T.Cruris+T.Facei+T.Manuum+T.Ped

1(100%) 0(0%) 1(1.09%)

T.Corporis+T.Axillaris+T.Cruris+T.Facei+T.Ped

0(0%) 1(100%) 1(1.09%)

T.Corporis+T.Axillaris+T.Cruris+T.Ped 1(100%) 0(0%) 1(1.09%)

T.Corporis+T.Axillaris+T cruris+T.Manuum 0(0%) 1(100%) 1(1.09%)

T.Corporis+T.Cruris+T.Facei+T.Manuum 1(100%) 0(0%) 1(1.09%)

T.Corporis+T.Cruris+T.Pedis 0(0%) 1(100%) 1(1.09%)

T.Corporis+T.Facei+T.Capitis 1(100%) 0(0%) 1(1.09%)

T.Corporis+T.Manuum 0(0%) 1(100%) 1(1.09%)

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70

Clinical presentation of steroid modified Tinea:

Among the 49 patients who had abused TSAF combination

creams,46(100%) preented with erythema,12(26.1 )patients had pustules, 9

(19.5%) had ring within ring appearance(tinea pseudoimbricata),vesicles and

erythrodermic presentation in 1(3.12%) each patient (Fig 14-18)

Overall distribution of clinical types:

Due to combination of clinical types, total number of clinical pattern

observed was 258,of which tinea corporis was the most common seen in 97

(37.5%) patients, followed by tinea cruris in 74 (28.7%) patients, tinea axillaris

in 46 (17.9%) patients , tinea faciei in 24 (9.3%) patients ,tinea manuum in 11

(4.3%) patients ,tinea pedis in 4 (1.6 %) patients and glabrous type of tinea

capitis in 2 (0.7%) patients. (Table 31)

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Table 31: Overall distribution of clinical types of chronic dermatophytosis

Clinical types

T.Corporis

T.Cruris

T.Axillaris

T.Facei

T.Manuum

T.pedis

T. capitis

Total

Chart-16: Overall distribution of clinical types of chronic dermatophytosis

74

71

Overall distribution of clinical types of chronic dermatophytosis

linical types No of patients Percentage

97

74

46

24

11

4

2

258

: Overall distribution of clinical types of chronic dermatophytosis

97

46

74

2411 24

CLINICAL TYPES

Overall distribution of clinical types of chronic dermatophytosis

Percentage (%)

37.5

28.7

17.9

9.3

4.3

1.6

0.7

100

: Overall distribution of clinical types of chronic dermatophytosis

T.CORPORIS

T.AXILLARIS

T.CRURIS

T.FACEI

T.MANUUM

T.CAPITIS

T. PEDIS

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72

KOH MOUNT AND CULTURE:

There was 100 percent positivity of KOH mount as it was the inclusion

criteria. Out of the100 patients,83 (83%) patients were found to be culture

positive for dermatophyte in SDA and17(17%) were found to be negative.

(Table 32)

Table 32: Culture results

KOH & CULTURE KOH +VE

CULTURE +VE

KOH +VE

CULTURE –VE

N=100 83 17

Chart-17:Culture results

83%

17%

CULTURE

POSITIVE NEGATIVE

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73

ISOLATION OF DERMATOPHYTE SPECIES:

Among the 83 isolates, Trichophyton mentagrophytes complex (Fig 20-

23) was the most common species isolated in 53(63.9%)patients, followed by

Trichophyton rubrum (Fig 34-37) in 26 (31.3%)patients, Trichophyton

tonsurans (Fig 44-45) in 2 (2.4%) patients. Trichophyton verrucosum (Fig 50-

51) and Microsporum gypseum (Fig 44-45) isolated in 1 patient(1.2%) each.

(Table 33)

Table 33: Isolation of species

Species No of patients Percentage (%)

Trichophyton.mentagrophytes complex 53 63.9%

Trichophyton.rubrum 26 31.3%

Trichophyton.tonsurans 2 2.4%

Trichophyton.verrucosum 1 1.2%

Microsporum.gypseum 1 1.2%

TOTAL 83 100

Chart 18: Isolation of species

Trichophyton.m

entagrophytes

complex

Trichophyton.r

ubrum

Trichophyton.t

onsurans

Trichophyton.v

errucosum

Microsporum.g

ypseum

Percentage 63.9 31.3 2.4 1.2 1.2

0

10

20

30

40

50

60

70

Isolation of species

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GENDER WISE DIST

In the present study

out of the 30 males and 60(85%) patients out of 70 females

isolates in females,43 (71.7%) were

followedby T.rubrum

T.tonsurans (Fig 39)

(Fig 43) each. Among the 23 culture positive isolates in males ,12 isolates were

T.rubrum followed by 10 isolates with

T.tonsurans (Table 3

Table 34:

Species

Trichophyton.mentagrophytes complex

Trichophyton.rubrum

Trichophyton.tonsurans

Trichophyton.verrucosum

Microsporum.gypseum

Trichophyton.mentagrophytes complex

Trichophyton.rubrum

Trichophyton.tonsurans

Trichophyton.verrucosum

Microsporum.gypseum

SEXWISE DISTRIBUTION OF SPECIES

Figure

74

NDER WISE DISTRIBUTION OF CULTURE ISOLATES

In the present study, culture positivity was seen in 23( 76.6%) patients

out of the 30 males and 60(85%) patients out of 70 females

isolates in females,43 (71.7%) were T.mentagrophytes complex

.rubrum (Fig 25-33) seen in 14 female patients and 1 patient with

(Fig 39), T.verrucosum (Fig 47) and Microsporum gypseum

each. Among the 23 culture positive isolates in males ,12 isolates were

followed by 10 isolates with T.mentagrophytes and 1 patient with

(Table 34)

Sex

Male (n=23) Female (n=60)

Trichophyton.mentagrophytes complex 10(43.5%) 43(71.7%)

12(52.2%) 14(23.3%)

Trichophyton.tonsurans 1(4.3%) 1(1.7%)

Trichophyton.verrucosum 0(0%) 1(1.7%)

Microsporum.gypseum 0(0%) 1(1.7%)

0.0% 10.0% 20.0% 30.0% 40.0% 50.0% 60.0%

Trichophyton.mentagrophytes complex

Trichophyton.rubrum

Trichophyton.tonsurans

Trichophyton.verrucosum

Microsporum.gypseum

43.5%

52.2%

4.3%

23.3%

1.7%

1.7%

1.7%

SEXWISE DISTRIBUTION OF SPECIES

Female Male

Figure 19. Gender wise distribution of species

ISOLATES:

culture positivity was seen in 23( 76.6%) patients

out of the 30 males and 60(85%) patients out of 70 females. Among the 60

complex (Fig 1-19)

and 1 patient with

Microsporum gypseum

each. Among the 23 culture positive isolates in males ,12 isolates were

and 1 patient with

Total

N=83 (n=60)

43(71.7%) 53(63.9%)

14(23.3%) 26(31.3%)

2(2.4%)

1(1.2%)

1(1.2%)

60.0% 70.0% 80.0%

52.2%

71.7%

SEXWISE DISTRIBUTION OF SPECIES

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CLINICOMYCOLOGICAL CORRELATION

Among the

from patients with inflammatory

(28.3%) were found to cause

infected with of

noninflammatory lesions while

4(15.4%) patients.

noninflammatory clinical presentation

Microsporumgypseum

inflammatory lesions. (Table 3

Table 35: Morphology of lesion

Tr icho p hy to n .m enta g ro p hy te

Tr icho p hy to n . rub rum

Tricho p hy to n . to nsura ns

Tr icho p hy to n . verruco sum

Micro sp o rum .g yp seum

NON INFLAMMATORY

Species Isolated

Trichophyton.mentagrop

hytes complex

Trichophyton.rubrum

Trichophyton.tonsurans

Trichophyton.verrucosum

Microsporum.gypseum

75

CLINICOMYCOLOGICAL CORRELATION:

the 53 isolates of T.mentagrophytes,38(71.7%)

inflammatory type of chronic dermatophytosis,

were found to cause non inflammatory lesions.Out of 26 patients

of Trichophyton rubrum,22(84.6%)

noninflammatory lesions while inflammatory lesions were observed in

Two patients infected with Trichophyton tonsurans

inflammatory clinical presentation. Both patient

Microsporumgypseum and Trichophyton verrucosum

s. (Table 35)

: Morphology of lesion

Chart 20. Morphology of lesion

Tr icho p hy to n .m enta g ro p hy te…

Tricho p hy to n . rub rum

Tricho p hy to n . to nsura ns

Tr icho p hy to n . verruco sum

Micro sp o rum .g yp seum

15

22

2

38

1

1

NMORPHOLOGY OF LESION

NON INFLAMMATORY INFLAMMATORY

Non Inflammatory

Lesions (N=39) %

Inflammatory

Lesions

Trichophyton.mentagrop15 28.3

22 84.6 Trichophyton.tonsurans 2 100

Trichophyton.verrucosum 0 0 gypseum 0 0

38(71.7%) were isolated

type of chronic dermatophytosis, while 15

Out of 26 patients

patients had

inflammatory lesions were observed in only

Trichophyton tonsuranshad

atientsinfected with

presented with

4

INFLAMMATORY

Inflammatory

Lesions (N=46) (%)

38 71.7

4 15.3 0 0

1 100 1 100

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Among 46 patients with inflammatory lesions,

in all 46 patients, pustule

appearance was seen in 9

patient and diffuse erythroderma

Among the presentation with

observed in this study are eczematous, psoriasiform, lichenoid, hyperpigmented

and diffuse scaly types

Table 36: Types of inflammatory in patients of chronic dermatophytosis

Inflammatory lesions

Erythema

Pustules

Ring in ring

Vesicular lesion

Erythrodermic

Chart 21. Types of inflammatory in patients of chronic dermatophytosis

TYPES OF INFLAMMATORY

76

patients with inflammatory lesions, erythema was observed

patients, pustules were seen in 12 (26.1%) patients

appearance was seen in 9 (19.5%) patients, vesicular lesion seen in 1

fuse erythroderma was seen in 1 (2.17%) patient

Among the presentation with noninflammatory lesions

observed in this study are eczematous, psoriasiform, lichenoid, hyperpigmented

and diffuse scaly types

Types of inflammatory in patients of chronic dermatophytosis

Inflammatory lesions Number of patients Percentage

46

12

9

1

1

. Types of inflammatory in patients of chronic dermatophytosis

46

129

11

TYPES OF INFLAMMATORY

LESIONS

NO OF PATIENTS

erythema was observed

in 12 (26.1%) patients, ring within ring

patients, vesicular lesion seen in 1 (2.17%)

was seen in 1 (2.17%) patient. (Table 36)

noninflammatory lesions various pattern

observed in this study are eczematous, psoriasiform, lichenoid, hyperpigmented

Types of inflammatory in patients of chronic dermatophytosis

Percentage (%)

100

26.1

19.5

3.12

3.12

. Types of inflammatory in patients of chronic dermatophytosis

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KOH wet mount

Figure A. KOH wet mount scrapping shows characteristic hyaline

long branching septate hyphae

Figure B. KOH showing arthrospores

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TRICHOPHYTON

MENTAGROPHYTES

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Various Clinical Presentation

Figure 1: Anular lesion of tinea corporis with

erythematous papules at periphery

Figure 2 Tinea corporis – annular with

erythematous scaly rim

Figure 3 Tinea axillaris with large scales and

erythema

Figure 4 Tinea corporis with steroid induced

Depigmentation

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Figure 5. Tinea corporis with hyper

pigmentation and break through

lesions

Figure 6. Scaly tinea corporis with

tinea glutealis

Figure 7. Lichenified psoarisaform plaque of

tinea corporis in lumbosacral region

Figure 8. Tinea faciei

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Figure 9. Tinea corporis and tinea axillaris

with double ring

Figure 10. Tinea axillaris with multiple

annular lesions

Figure 11. Pustular lesions of Tinea axillaris Figure 12. Tinea glutealis

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Figure 13,14 & 15 – Extensive dermatophytosis

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Figure 16. Tinea corporis – Erythematous

plaques

Figure 17. Tinea pseudoimbricata

Figure 18. Lichenified hyper pigmented

plaques

Figure 19. Vesiculopustular type of tinea

corporis

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Macroscopic Morphology of Culture

Figure 20 A&B. White cottony colonies with raised central tuft and reddish brown reverse

Figure 21 A&B white cottony colonies with raised central tuft and yellowish reverse

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Microscopic Morphology of Slide Culture

in LPCB Mount

Figure 22 Spherical Microconidia arranged in Clusters

Figure 23 Spiral hyphae along with spherical microconidia in clusters

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Figure 24 A & B. Macroscopic Morphology of Culture with Reverse

Figure 24 A

Figure 24 B

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TRICHOPHYTON

RUBRUM

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Clinical Presentation

Figure 25 Hyperpigmented form of tinea

corporis with diffuse scaling

Figure 26 Tinea Corporis

Figure 27 Tinea corporis Figure 28. Tinea glutealis

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Figure 29 A & B. Extensive Dermatophytosis

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Figure 30 Tinea cruris in a obese female Figure 31. Inflammatory type of Tinea

axillaris

Figure 32. Tinea Faciei Figure 33. Scaly lichenoid plaque of tinea

corporis in waist

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Macroscopic Morphology of Culture

Figure 34 A&B White granular colonies with central folding and yellow brown reverse

Figure 35 A&B White granular colonies with central foldings and deep red brown reverse

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Microscopic Morphology of slide culture

in LPCB mount

Figure 36 Tear drop shaped microconidia arranged along the sides of hyphae “Bird on the fence

appearance “

Figure 37 Smooth thin walled multi septate cylindrical macroconidia along with tear drop

shaped microconidia

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Figure 38 A & B. Macroscopic morphology

of culture and reverse

Figure 38 A

Figure 38 B

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TRICHOPHYTON

TONSURANS

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Clinical Presentation

Figure 39 A&B Scaly lichenified plaques of tinea corporis

Macroscopic Morphology of Culture and Reverse

Figure 40 A&B White powdery colonies with central fold and brown reverse

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Microscopic Morphology of Colonies in Slide

Culture in LPCB Mount

Figure 41 Intercalary chlamydoconidia

Figure 42 Balloon microconidia

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MICROSPORUM GYPSEUM

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Clinical Presentation

Figure 43 A

Figure 43 B

43 A & B. Inflammatory plaques of tinea corporis

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Macroscopic Morphology of Culture and Reverse

Figure 44 A&B Young creamy colonies with buffy

surface and yellow reverse

Figure 45A&B Old flat spreading deep cream coloured

colonies and reddish brown reverse

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Microscopic morphology of slide culture

in LPCB mount

Figure 46 Macroconidia in large numbers

Figure 47 4-6 Celled macroconidia with symmetrical rough walles echinulations and terminal

end slightly rounded

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TRICHOPHYTON

VERRUCOSUM

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Clinical Presentation

Figure 48 A&B Inflammatory type of tinea corporis

Figure 49 Tinea Glutealis

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Macroscopic Morphology of Culture and Reverse

Figure 50 A&B small button large disc shaped white coloured

colonies with raised centre and flat peripheries

&

Yellow brown reverse

Microscopic Morphology of Slide Culture

in LPCB Mount

Figure 51 A Chains of chlamydoconidia

Figure 51 B Short septae with broad ends

divided to form antler horn hyphae

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DISCUSSION

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DISCUSSION

In the present study, most common age group involved was between

21-30 years(25%) followed by 23% in the age group of 31 – 40 years which

differs from the studies done on chronic dermatophytosis by Karthika et al48 (

31.6%) in 2016andZachariya et al102 ( 32%) in 2017who observed patients in

the age group of 31-40 yearsto be the most commonly affected. Study on socio

demographic status of dermatophytosis by Mahalakshmi et al103 also observed

that patients in the age group of 21-40 years were most commonly affected

which is similar to our observation of 48 % patients seen in this age

group.103This is also similar to the observation of other studies of

dermatophytosis like Ramraj et al(21-40 years).16This was in contrast to the

study by Senthamil Selvi et al101done in 2000,3 in which most common age

group affected was between 41-50 years. The youngest patient in this study

was an 8 year old boy, while the oldest was a 74 years old female. The mean

age of patients in this study was 35 years which is close to the findings by

Senthamil Selvi et al ( 39.3 years in 1998)55, and Hay et al (41 and ,44 years in

198285 and 1979104) in their studies on patients with chronic dermatophytosis.

. In this study, males were most commonly affected in the age group of 21-30

years(40%) which is similar to the observation made by Senthamil Selvi et al101

in 2000 and Mahalakshmi et al (56%).103 However females were found to be

most affected in the age group of 31-40 years which is in concordance with

study conducted by Karthika et al.48. In the current scenario of increased

prevalence of chronic dermatophytosis in India, patients in the third and fourth

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decade seems to be more vulnerable to develop chronic dermatophytosis

because of their life style and increased physical activity which leads to

excessive sweating . Socialization is also high in this age group compared to

other age groups which eventually results in transmission of infection.

In the study group, females were predominantly affected (70%) than

males 30%with Male to female ratio was 1:2.3 which is close to the findings of

Karthika et al48 (males 40% and females 30% in the ratio of 1:1.5). and

Zachariya et al102 ( 66%females and 34% males in the ratio of 1:3).This is in

contrast to observations made by Senthamil Selvi et al3 (74.6% males and

33.9% females),Hay et al in 1979(68.8% males and 31.3% females),Hay et al

in 1990(60% males and 40%) in which males outnumber females.3,88,104

However females were most commonly affected in the age group of 31-50

years in this study which is in concordance with observations of Senthamil

selvi et el in 2000.3The female predominance in the recent studies in contrast to

the studies done in the past during (1980-2000) can be attributed to increase in

health awareness, accessibility to health care and female working population

With regard to the occupation of the patients in this study, housewives

were the most common (30%), followed by outdoor labourers(25%),

students(23%) and office employees (21%), which is slightly different with the

findings by Zachariya et al 102manual labourers(56%), housewives(20%)).102

However the percentage of patients infected in both the studies were almost

similar. This is also similar to the observations made by others studies of

dermatophytosis like Gupta et al33, Ghosh et al36 and Singh et al105. Outdoor

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manual labourers are affected in 25% of patients in our study which us in

concordant to the observation made by Mahalakshmi et al.103This is explained

by the nature of work done by house wives and manual labourers, as the latter

tend to work more in outdoors in hot and humid climate leading to excessive

sweating resulting in an ideal milieu for dermatophytes to germinate. Increased

occurrence in students and office employees are attributed to the habit of

wearing tight synthetic garments and long working hours.

In the present study of 100 patients, 51% of patients belonged to lower

socioeconomic status while 46% were from middle class which is close to the

observations of Mahalakshmi et al103(50%). Renganathan et al,39 Rathode et

al41 and Parameshwari et al18 are some of the other studies of dermatophytosis

which showed similar results.However, it was lesser when compared with the

results observed by Zachariya et al who reported 86% in lower socio economic

status and Janardhan et al who observed that majority of his patients belonged

to the lower socioeconomic status. This could be explained by the fact that the

former study population comprised of 66% females who were mostly working

in paddy fields and 52% of manual labourers. In the latter study by Janardhan

et al, 64% of the study group was from the rural background. In contrast, our

institution is a tertiary care centre located in a city, catering to mixed

population. Increased occurrence in the middle SES in this study may be due to

the current scenario of increased prevalence of chronic, recurrent and

recalcitrant dermatophytosis which occurs irrespective of SES, probably due to

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the strong interplay between the host , environment, agent and the

pharmacological factors.

Among the patients in the study group , most of them (45%)were from

urban locality, which is similar to the observations made by Mitruka et al

(56%),107 Gosh RR et al36(57%) and Kucheria et al(71%).107 Our centre being

a tertiary care unit located in a metropolis caters to people belonging to urban,

semi-urban and rural population in and around the city. Patients from rural area

comprised of 36% in consistence withthat of Kucheria et al(29%)108 , but

lesser than the finding by Munir et al (61%)21Thiscould be substantiated by the

fact that farmers and manual labourers formed the majority of the study group.

House wives were the most common group of patients comprising 30%

followed by manual labourers (25%), students (23%) and office employees

(21%) in this study. Zacharia M et al,102 however had reported that manual

labourers formed the majority of his patients comprising of 52% followed by

house wives (20%), students (18%) and patients with indoor work (10%). This

difference could be attributed to the fact that his study was done in a centre

located in the coastal district of Kerala visited by a lot of manual labourers,

while the present study was conducted in a tertiary centre in a Metropolis.

Increasing occurrence of chronic dermatophytosis among the students and

office employees signifies the change in the scenario of chronicity which was

earlier thought to be associated with low socioeconomic status and

immunosuppression among the other factors.

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The mean duration of infection was 1.35 years with majority of patients

(60%) having the infection continuously or intermittently between 6 months to

1 year. This is much lesser compared to the observations by Karthika et al (7.35

years)48 and Khosarvi et al (8.7 years).109The difference in mean duration of

infection may reflect the improvement in behavior of patients seeking treatment

earlier compared to the yester years.

In this study, 49% of patients gave history of use of topical steroid

creams which is almost close to the 56% observed by Zacharia M et al.ref Most

of the topical steroid antifungal combination creams available in India contain

a potent steroid molecule, 1 or 2 antibacterials and 1 antifungal drug. Patients

tend to use these creams intermittently over prolonged duration as there is a

subjective improvement in symptoms followed by cessation after which there is

a flare and then the patient resumes the application of the cream. This causes

profound local immunosuppression due to the steroids and barrier dysfunction

due to the loss of normal skin microflora caused by the antibacterial

components resulting in the skin becoming susceptible to develop chronic and

persistent dermatophytosis.11

Diabetes mellitus (DM) was the most common association with 54.2%

of patients ,in which patient had only diabetes in 31.4% followed by

combination of diabetes and hypertension (28.6%) . This is in concordance

with results from earlier studies by Prasad et al and Karthika et al who reported

a prevalence of 17.3% and 26.7% respectively.48,110 Though in all the above

studies including the present , diabetes mellitus seems to be the most common

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association, 52% of patients associated with diabetes in this study reflects the

increasing incidence of DM in India. This is in contrast to the results from the

studies by Senthamil selvi et al3 in 2000 with 7% , Khosravi et al109(8%) and

Zacharia et al (8%).102In our study , atopic diathesis was associated with 14.3%

of patients which is in similar to the observations of 13.3% by Prasad et al110

and 20 % with Karthika et al.48Carcinoma was seen in 8.6 % of patients in our

study which explains the persistence of infection in immunosuppressed

patients.

In the present study , synthetic garments were used by 44% of patients

which is similar to the observation made by Poluri et al with 40.32%111 and

Mahalakshmi et al with 50%.103 Modern trend seen in both men and women

preferring to wear jeans, leggings and tight synthetic garments irrespective of

the socioeconomic strata, which definitely does not suit the hot and humid

climate that is prevalent in India, makes them more vulnerable to develop

chronic dermatophytosis, due to the persistent sweating resulting in a contusive

milieu for the dermatophytes to thrive well. It was found that 85% used to take

bath once daily,14% tookbath once in 2 days and 1% took bath once in a week.

This was consistent with the findings of Narasimmalu et al112 (78% took bath

once a day,14% took bath once in two days).This is also similar to the

observations of Mahalakshmi et al in which poor personal hygiene was noted in

73.7% of patients with chronic dermatophytosis .103In our study, 52% did not

have the habit of wiping properly after bathing which was also the observation

made by Das K et al.113Sharing of fomites was observed in 78% of patients of

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which 23 were males (76.7%) and 55 were females(78.6%)which is very close

to the results observed by Zacharia et al102 (80)% . History of close contact

with pet animals, cattle and goats was found in 8 % of patients which was less

than the 20% observed by Zachariya et al.105

In this study,68% of patients had history of family members being

affected with dermatophytosis, of which 48% had less than 3 and 22 % had

more than 3 members affected . This finding was exactly similar to the results

of Mahalakshmi et al103 (68%), who also reported that 58% of patients with

duration less than 6 months had family members affected which was less than

that observed in the patients with chronic infection. Transmission among

family members was explained by sharing of fomites in seen in 78% of the

patients in the study group, overcrowding and low socioeconomic status. Our

finding is in contrast to that of Zachariya et al102 who reported that 20% of

patients had family members being affected. This could be attributed to the fact

that prolonged working hours under the Sun observed in his study population

which was mainly agriculture workers and manual labourers, was the major

contributing factor for the chronicity rather than the persistence of infection

due to sharing of fomites among the family members. Frequency of family

members being infected in the studies by Mahajan S et al (30.9%) and

Kucheria M et al (33%) was less than that in the present study.108,116

Body surface area involvement of more than 40% was seen in62% of the

patients . This is in concordance to the observation of Prasad et al110 who

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reported that patients with chronic dermatophytosis were found to have more

than 40% BSA affected.

In the present study, 9% of patients had single clinical type of lesion,

while 91% had multiple types. Multiple site involvement with more than one

type of clinical presentation was seen in 78% of patients by Karthika et al

which is less than that in our study.48Among the isolated clinical types

observed in this study, tinea corporis was the most common presentation seen

in 66.6% of patients followed by 22.2% of patients with tinea glutealis.In

contrast, tinea cruris was the most common single clinical type seen in 28 % of

patients in the study by Zachariya et al102. This is quite understandable as 52%

of his study population were manual labourers who were more prone for

developing tinea cruris. Among the 91% of patients with combination of

clinical types, combination of tinea corporis and tinea cruris was the most

common type seen in 35.8 % of patients followed by tinea corporis , cruris and

axillaris seen in 21.9 % of them. Both types were more common in females

than males (60% and 95% respectively). Though Zachariya et al102also reported

the combination of tinea corporis and tinea cruris to be the most common type,

he reported a higher rate of 56%, as manual labourers who are more

predisposed to excessive sweating formed a major proportion of his study

group. In our present study, overall 258 clinical types were observed ,Tinea

coporis was the most common type seen in 37.5% of patients followed by

tinea cruris in 74 patients(28.7%), Tinea axillaris in 46 patients(17.9%) , Tinea

faciei in 24 patients(9.3%) ,. Karthika et al48 also observed tinea corporis to be

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the commonest type of presentation seen in 36.2% of patients which is very

similar to our observation. Our results are also close to the observation made by

Surendran et al115study ( tinea corporis – 44.3%, tinea cruris -38.2%) of

dermatophytosis. But the most common clinical type observed by Senthamil

selvi et al in 199855 and 20003 was tinea cruris followed by tinea corporis. In

this stufy, commonest site affected was back in men and waist in women which

is in accordance with the previous studies by Senthamil Selvi et al in 20003 and

Karthika et al.3,48 This pattern of distribution may be attributed to highly humid

environment as well as the dressing pattern of the patients in which occlusive

dressing along with excessive sweating and moisture result in persistence or

recurrent infection with dermatophytes.

Among the 49% patients with steroid modified tinea, various clinical

presentations seen were eczematous, psoriasiform, pustular, vesicular, atrophic,

pseudoimbricata and erythrodermic forms which is in similar to the

observations of Dutta B et al who also had various clinical presentations like

psoriasiform, eczematous, malar rash, follicultis, maculopapaular rash, rosacea

like, striae, depigmentation with scaling etc. Patients with steroid modified

tinea require longer duration of treatment.

In our study, among the scrapings from 100 patients with KOH

positivity subjected to culture in modified SDA, 83% showed isolates positive

for dermatophytes which was higher than 52%, that was observed by Karthika

et al107,41.3% by Prasad et al110,68% by Zachariya et al102,66.6% by Senthamil

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selvi et al in 199855 and 71% observed by Bindhu et al116 , but was lower than

87.3% reported by Ghosh et al.36

In this study, Trichophyton mentagrophytescomplex was the most

common dermatophyte(63.9%) and Trichophyton rubrum(31.3) being the

second common isolate.this is in contrast to the studies on chronic

dermatophytosis such as Sentamil selvi et al,3 Karthika et al,48 Prasad et al110

and Zachariya et al102 whichis shown in the table-

Table 37 Studies on Chronic Dermatophytosis

Study T.rubrum T.mentagrophytes

Senthamil selvi et al 1998 64.5% 25%

Karthika et al at 2016 46% 34.6%

Prasad et al at 2016 17.3% -

Zachariya et al 41.2% 11.8%

Current literature in India is not available to know the prevalence of

T.mentagrophytes complex among the patients with chronic

dermatophytosis.However this study on chronic dermatophytosis is in con

cordance with the observations of other studies like Kumaran et al17(67.34%

and 22.4%), Jagadesh et al 18(64% and 12%),Noronha et al19(48.3% and

38.3%), Kaur et al25(48.2% and 32%),Kansara et al 23(46.43 % and

24.29%),Kainthola et al24(42.85% and 28.15%) of T.mentagrophytes and

T.rubrum respectively .This reflects the change in the trend of the causative

organism of dermatophytes in India which is considered as one of the most

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important factorsthat has led to the increased prevalence of chronic and

recurrent dermatophytosis.

In this study inflammatory lesions were seen in 71.7% of the patients

from whom T.mentagrophytes complex was isolated and 15.3% of the

patients with T.rubrum as isolate. It is a known observation that inflammatory

lesions are produced by zoophilic organism but in the current scenario of

increased prevalence of T,mentagrophytes complex ,speciation is very pertinent

to decide on the anthropophilc or zoophilic species of the organism .However

speciation of T.mentagrophytes complex has evolved into a complex issue as

most of the patients with inflammatory lesions do not give history of contact

with animals.T.rubrum has always been known to be the major causative agent

of chronic dermatophytosis charecterised by non inflammatory lesions.

Inflammatory lesions seen due to T.rubrum warrants further studies. It is not

known whether inflammatory lesions in the absence of contact with animals

due to T.mentagrophytes or T.rubrum could be due to the local

immunosuppression produced by the rampant abuse of TSAF combination

creams, virulence of the organism, increased fungal load or theinterplay

between the host immunity and the organism. Noniflammatory lesions were

seen in 86.6% of patients with T.rubrum isolate and 15.3% of patients with

T.mentagrophytes complex isolate. The clinical presentation of lesions

produced by the former is mostly large geographic,diffuse, scaly , lichenified

or hyperpigmented which is similar to the observations by Senthamil selvi et

al3 in 2000 and Karthika et al48.

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LIMITATION :

Speciation of T.mentagrophytes complex could not be done due to the

non availability of research laboratory facilities

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CONCLUSION

� Most common age group affected was 21-30 years followed by 31-40 years

� Females were predominantly affected than males

� Proportion of patients belonging to both lower and middle socioeconomic

status was almost equal

� Most of the patients were from urban and semiurban areas

� Housewives were most commonly affected followed by manual labourers

� Most of the patients had infection for more than 6 months to 1 year

� Episodic manifestations are common, with more than 3 episodes being

common than continuous clinical manifestations

� Most of the patients had used over the counter drugs, while almost half of

the patients had used topical steroid anti fungal combination creams

� Diabetes mellitus was the most common association in this study

� Use of topical steroid anti fungal combination creams, poor compliance,

sharing of fomites, wearing leggings/jeans, synthetic dresses and unwashed

dresses kept in wardrobe, spending time more than 2 hours in kitchen

during noon were some of factors that played a role in predisposition to

chronic dermatophytosis

� Infection of multiple family members were noted in most of the patients

� Most of the patient with chronic dermatophytosis had more than 40% BSA

� Occurrence of multiple clinical types in an individual patient was more

common than single type.

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� Overall, Tinea corporis was the most common clinical presentation

followed by tinea cruris

� Multiple combination of tinea corporis and tinea cruris was the most

common clinical presentation seen among the various combination clinical

types

� In patient who had abused TSAF combination creams, various clinical

presentations observed were erythema, atrophy, ring within ring

appearance(tinea pseudoimbricata), pustules, vesicles and erythrodermic

forms.

� Culture was positive in 83 patients

� Trichophyton mentagrophytes complex was the most common organism

isolated followed by Trichophyton rubrum, Trichophyton tonsurans,

Trichophyton verrucosum and Microsporum gypseum.

� Majority of the patients infected by T.mentagrophytes complex presented

with inflammatory lesions

� Most of the patients from whom T.rubrum was isolated had non

inflammatory lesions

In the past predisposing factor for chronic dermatophytosis considered

were obesity, diabetes mellitus, immunosuppresion, atopy, etc. but in the

current scenario of tinea epidemic, in India rampant abuse of topical steroid

creams, sharing of fomites, wearing synthetic tight clothing and poor

compliance seems to play a major role in predisposition to chronicity of

dermatophytosis.

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The exact reason for the shift of the organismfrom T.rubrum which has

been the most common organism implicated in chronic dermatophytosis

worldwide to T.mentagrophytes remains an enigma which necessitates further

studies on the environmental factors ,mycological, antifungal susceptibility ,

molecular and genomic aspects of dermatophytosis.

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BIBLIOGRAPHY

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REFERENCES

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2. Panda S, Verma S. The menace of dermatophytosis in India: The evidence that we need. Indian J Dermatol Venereol Leprol 2017;83:281-4

3. Senthamil Selvi G, Kamalam A, Ajitha doss K, Thambiah A S. The dermatophytes in relation to the sites in non chronic and chronic dermatophytes. Current Advances in medical mycology, 1996, PP 151 –156.

4. Hay RJ and Brostoff.Immune response in patients with trichophyton rubrum infections.Clin.Exp Dermatology 1977:2:373-80

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25. Kaur I, Thakur K, Sood A, Mahajan VK, Gupta PK, Chauhan S, et al. Clinico-mycological profile of clinically diagnosed cases of dermatophytosis in North India: a prospective cross-sectional study. Int J Health Sci Res. 2016;6(8):54-60

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48. 48.Karthika Sivaprakasam, Balaji Govindan,A Clinico-Mycological Study of Chronic Dermatophytosis of More Than Years Duration

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Volume : 5 | Issue : 6 | June 2016 • ISSN No 2277 - 8179 | IF : 3.508 | IC Value : 69.48

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73. Sandy Vermout. Pathogenesis of dermatophytosis. Mycopathologia 2008;166:267-75.

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75. García-Romero MT, Arenas R. New insights into genes, immunity, and the occurrence of dermatophytosis. J Invest Dermatol2015;135:655-7

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77. King RD, Khan HA, Foye JC, Greenberg JH, Jones HE. Transferrin, iron and dermatophytes. Serum dermatophyte inhibitory component definitely identified as unsaturated transferrin. J Lab Clin Med 1975;86:204-12.

78. Rothman S, Smiljanic A, Shapiro AL. The spontaneous cure of tinea capitis in puberty. J.InvestDermatol 1947;8:81-97.

79. Lorincz AL, Priestley JO, Jacobs PH. Evidence of a humoral mechanism which prevents growth of dermatophytes. J Invest Dermatol1958;31:15-7.

80. Sumitsethi, Surabhi Sinha. Superficial Fungal Infections: Dermatophytes.In:Sarkar R, Desai S R, editors. Fungal diseases. World clindermatol. 2016;3(1):14-40(22)

81. Payam Behzadi1, Elham Behzadi, Reza Ranjbar1. Molecular Biology Research Center, Baqiyatallah University of Medical Sciences,Dermatophyte fungi: Infections, Diagnosis and Treatment Tehran, IRAN

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84. Topical steroid-induced tinea pseudoimbricata: a striking form of tinea incognito: Roderick J. Hay, MD, DM, FRCP Department of Dermatology King’s College London UK

85. Hay RJ, Shernan G. Chronic dermatophyte infections II. Br.J.Dermatol 1982 Feb; 106 (2): 191-8.

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86. Svejgaard E, Epidemiology and Clinical features of Dermatomycosis and Dermatophytosis Acta Deen Venereol. Suppl (Stockh), 1986 ; 121 : 19 – 26.

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90. Amodkumar Yadav, AD Urhekar, Vijay Mane et al. Optimization and Isolation of Dermatophytes from Clinical Samples and In Vitro Antifungal Susceptibility Testing By Disc Diffusion Method. Research and Reviews: Journal of Microbiology and Biotechnology Volume 2 Issue 3 July – September, 2013

91. De HoogGS ,Guarro J , Gene J , Figueras MJ , eds. Atlas of Clinical Fungi. Baarn : Central bureauvoor Schimmelcultures / Universitat Rovirai Virgili, 2000.

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93. Vignesh D, SathyaPriyaSankar,SelvaSudha,aclinical studyof a superficial dermatophytic infection in kanchipuram , National Journal of Medical Research & Yoga Science; Jan2015:Vol.-1,Issue-2,P.22-24,ISSN 2395-2911

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96. Alok Kumar Sahoo and Rahul Mahajan PMID: 27057486 PMCID: PMC4804599 Management of tinea corporis, tinea cruris, and tinea pedis: A comprehensive review Indian Dermatol Online J. 2016 Mar-Apr; 7(2): 77–86.doi: 10.4103/2229-5178.178099

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102. Meriya Zacharia 1 , Balachandran Parapattu Kunjukunju Clinical profile of patients with chronic dermatophytosis- a descriptive study from a tertiary care centre in Kerala J. Evid. Based Med. Healthc., pISSN- 2349-2562, eISSN- 2349-2570/ Vol. 4/Issue 47/June 12, 2017

103. Mahalakshmi R.*, Apoorva R., Jefferson Joshua Dermatophytosis: clinical profile and association between sociodemographic factors and duration of infection . Int J Res Dermatol. 2017 Jun;3(2):282-285

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ANNEXURES

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10.1 ABBREVIATIONS

SDA - Sabouraud Dextrose Agar

KOH - Potassium Hydroxide

GMS - Gomori Methamine Silver

PAS - Periodic Acid Schiff

SES - Socio Economic Status

MIC - Minimum Inhibitory Concentration

OTC - Over The Counter

HIV - Human Immunodeficiency Virus

MALDITOF - Matrix Associated Laser Desorption Ionization Time Of

Fight Mass Spectrometry

TSAF - Topical Steroid Antifungals

TI - Tinea Imbricata

DTM - Dermatophyte Test Medium

PCR - Polymerase Chain Reaction

RFLP - Restriction Fragment Length Polymorphism ,

AFLP - Amplified Fragment Length Polymorphism ,

RAPD - Random Amplified Polymorphic Dna

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10.2 PROFOMA

Case No:

Name: Age: Sex: OP No:

Address: Occupation: Phone number:

Rural /urban: Community: Income:

CHIEF COMPLAINTS:

Duration: Total -

Present illness - Frequency:

TREATMENT HISTORY:

Historyof selfmedication/OTC drugs/prescription from doctors

Topical-episode: duration:

Systemic-episode: duration:

PAST HISTORY:

Comorbidities-

HT/ DM/ TB/ BA/ EPILEPSY/ HIV

Renal/ hepatic/ cardiac diseases / malignancy/ transplant patients

Chronic intake of steroids - Connective Tissue Disorders/ Atopy

PERSONAL HISTORY:

Hobbies - gym / walkingDiet

MARITALHISTORY : Married / unmarried

FAMILY HISTORY :

Total No. of members :

Number affected :

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H/O SHARING : Towels / Pillows / Bedsheets / Dresses

BATHING HABITS : Daily / once in ___ dayswiping:yes/no

H/O habit of wearing dresses after bath without wiping

CLOTHING HABITS : MALES – jeans / inner garments

FEMALES – leggings /synthetic garments:

H/O no of hours spent in kitchen:

H/O wearing waist band / wrist band

H/O wearing shoes / close type of foot wear

GENERAL EXAMINATION: General condition- Build-

Anemia/ Jaundice/ Pedal edema/ Generalized lymphadenopathy

Systemic Examination :

CVS

RS

ABDOMEN

CNS

Others

DERMATOLOGICAL EXAMINATION:

Site of involvement: Tineacorporis/ T.axillaris/ T.cruris/ T.glutealis/

T.faciei/ T.manuum/Glaborous type of T.capitis

Size of lesions:

Number of lesions:

Shape:

Surface:

Periphery of lesions:

Ring within ring appearance:

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Erythema:

Pustules:

Pigmentation:

Diffuse scaling:

Vesicular:

Granulomatous/Verrucous

Others:

Palms and soles:

Nails:

Scalp, hair, mucosa:

INVESTIGATIONS

1. Blood haemogram

2. Blood sugar

3. RFT

4. LFT

5. Serum electrolytes

6. Potassium hydroxide mount

7. Culture

TREATMENT GIVEN: topical and Systemic antifungals

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10.3 INFORMATION TO PARTICIPANTS

Investigators : Dr.S. Karunya

Dr.A.Ramesh

Dr.R.Madhu

Name of Participant:

Title: CLINICO EPIDEMIOLOGICAL AND MYCOLOGICAL STUDY OF

CHRONIC DERMATOPHYTOSIS

You are invited to take part in this study. The information in this document is meant to help you decide whether or not to take part. Please feel free to ask if you have any queries or concerns

We are conducting a study on“CLINICO EPIDEMIOLOGICAL AND

MYCOLOGICAL STUDY OF CHRONIC DERMATOPHYTOSIS” among patients attending Rajiv Gandhi Government General Hospital, Chennai

• And for that your participation may be valuable to us.

• The purpose of this study is to determine the epidemiology, clinical profile, associated co morbid condition and various predisposing conditions of chronic dermatophytosis.

• In this study history of patient will be taken, examination will be done and clinical photographs will be taken without disclosing the identity of patients, sample from patient(scales)will be subjected to KOH mount and examined under light microscope for fungal hyphal elements, if found positive fungal culture will be done. Routine blood test will be taken and specific treatment will be given based on diagnosis.

• The privacy of the patients in the research will be maintained throughout the study. In the event of any publication or presentation resulting from the research, no personally identifiable information will be shared.

• Taking part in this study is voluntary. You are free to decide whether to participate in this study or to withdraw at any time; your decision will not result in any loss of benefits to which you are otherwise entitled.

• The results of the special study may be intimated to you at the end of the study period or during the study if anything is found abnormal which may aid in the management or treatment.

Signature of Investigator Signature of the Participant

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10.4 PATIENT CONSENT FORM

Title of the study:

CLINICO EPIDEMIOLOGICAL AND MYCOLOGICAL STUDY OF

CHRONIC DERMATOPHYTOSIS

Name of the Participant:

Name of the Principal investigator : Dr.S. Karunya.

Name of the Institution : Rajiv Gandhi Government General

Hospital, Chennai

Documentation of the informed consent

1. I ___________________________ have read the information in this form (or it has been read for me). I was free to ask any questions and they have been answered. I am over 18 years of age and exercising my free power of choice, hereby give my consent to be included as a participant in the study.

2. I have read and understood this consent form and the information provided to me.

3. I have had the consent document explained to me.

4. I have been explained about the nature of the study.

5. I have been explained about my rights and responsibilities by the Investigator.

6. I am aware of the fact that I can opt out of the study at any time without having to give any reason and this will not affect my future treatment in this hospital

7. I hereby give permission to the investigators to release the information obtained from me as result of participation in this study to the sponsors, regulatory authorities, govt. agencies and IEC.I understand that they are publicly published

8. I have understood that my identity will be kept confidential if my data are publicly presented.

9. I have had my questions answered to my satisfaction.

10. I have decided to be in the research study

11. I am aware that if I have any question during this study, I should contact at one of the addresses listed above. By signing this consent form I attest that the information given in this document has been clearly explained to me and apparently understood by me. I will be given a copy of this consent document.

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Name and signature/thumb impression of the participant (or legal representative if participant incompetent)

_______________ _________________ _________________

Name Signature Date

Name and signature of impartial witness (required for illiterate patients):

________________ __________________ _________________

Name Signature Date

Address and contact number of the impartial witness:

Name and Signature of the investigator or his representative obtaining consent:

________________ __________________ ________________

Name Signature Date

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10

.6 M

AS

TE

R C

HA

RT

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10.7 KEY FOR MASTER CHART

L - Low Socioeconomic Class

M - Middle Socioeconomic Class

H - High Socioeconomic Class

Ru - Trichophyton Rubrum

ME - Trichophyton Mentagrophytes

V - Trichophyton Verrucosum

T - Trichophyton Tonsurans

Gyp - Microsporum Gypseum

Wnl - Within Normal Limits

R - Rural

U - Urban

+ - Yes

- - No