ATOPIC DERMATITIS PART 2 is an itchy, chronic, or chronically relapsing, inflammatory skin condition that occurs most commonly during early infancy and childhood..pptx

Outline
 Introduction
- Morphology - Description- Approach
 Bacterial infections of the skin ( common )
- Impetigo, Echtyma
- Folliculitis, Furuncle, Carbuncle
- Cellulitis, Erysipelas
 Fungal infections
- Superficial & Deep
- P. Versicolor
- Onychomycosis

CTD…
 Dermatitis/ Eczema
- Atopic Dermatitis( AD)
- Seborrheic Dermatitis(SD)
- Contact Dermatitis (CD)
- Lichen Simplex Chronicus (LSC)
 Infestations
- Scabies
- Onchocerciasis
 Leishmaniasis

CTD….
 HSV,HZV,MC & Warts
 Cut. TB & Leprosy
 Papulosquamous disorders
- Psoriasis
- Pityriasis Rosea
- Lichen Planus

CTD….
 Disorders of skin appendages
- Acne
- Rosacea
- Periorificial Dermatitis ( POD )
 Disorders of pigmentations
- Vitiligo
- Melasma
- Postinflammatory hypo/hyperpigmentation(PIH)

CTD….
 Drug eruptions and related disorders
- Drug Reaction
- Urticaria
 Cutaneous manifestations of HIV/AIDS
 Sexually transmitted infections (STIs)

CTD….
 Practical session
 Exam

Introduction to
Dermatology
 “He who studies skin disease & fails to study the lesion first will never learn
dermatology.” Siemens(1891–1969)
to read words, one must recognize letters;
to read the skin, one must recognize basic skin lesions.
For Health Officer Students
Solomon H ( MD,Dermatovenereologist)

 OVERVIEW OF THE SKIN
 Dermatology is the field of medicine that deals with the
macroscopic study of skin, adjacent mucosa (oral and genital)
and cutaneous adnexa
 Skin is the largest organ in the body ~5 kg & covers 2 m2
 is a dynamic, complex, integrated arrangement of cells,
tissues, and matrix elements that mediates a diverse array of
functions
 There are two types of skin :
 Glaberous skin - Non hair bearing area
 Non glaberous skin - Hair bearing area

 Has three major regions:
Epidermis:
 The outermost part of the skin
 major permeability barrier, innate immune function, adhesion,
and ultraviolet protection
Dermis:
 major structural element, three types of components—cellular,
fibrous matrix, and diffuse and filamentous matrix
 also site of vascular, lymphatic, and nerve networks
Hypodermis (subcutis):
 mechanical integrity, contains the larger source vessels and
nerves

 The epidermis may be divided into the ff
zones:

 Skin Appendages
 Pilosebaceous unit
 Hair follicle
 Sebaceous gland
 Arrector pilli muscle
 Apocrine glands
 Eccrine sweat glands
 Nails

 Functions of the skin
 Physical barrier
 Mechanical protection
 UV protection
 Thermoregulation
 Immunological function
 Sensory and autonomic function
 Vitamin D synthesis
 Excretion
 Sociosexual function

Primary lesions ...vs... Secondary lesions
 basic/uncomplicated lesions
Macule
patch
Papule
plaque
Nodule
Vesicle
bulla
Pustule,... etc.
 develop as the 10
lesion evolve
 are created by scratching or
infection
Crust
Scale
fissure
Erosion
Ulceration
Excoriation
Atrophy
Lichenification, ...etc.

Macule
 non-palpable, flat lesion, area
of variegated colour in the
skin/mucosa.
 Hyper pigmented
 Hypo pigmented
 Size:- <0.5cm
 pytriasis versicolor
 Pytriasis rosea

Patches  large macule
 flat area of the skin/mucosa
with varied colour
 Size:- > 0.5cm
Eg:
 Vitiligo
 Melasma

Papules
 elevated solid lesion
(i.e most of its part is above the
plane)
 Size:- 0.5cm in diameter
 E.gs with d/t shape & color:
 Flat-toped…. LP
 Dome shaped…. MC
 Red papule---- Rosacea
 Purple---LP

Plaques  broad papule
 plateau-like, elevated,
superficial, solid lesion
 Size:- >0.5cm
 Often formed by the
confluence of papules
 Eg. – psoriasis

Nodules  big papule
 Circumscribed/round,
ellipsoid, elevated, solid,
palpable lesion
 Size:- >0.5cm
 Eg.
 A.vulgaris
 Melanoma
 Lipoma
 Tumour :- is large nodule
( >2cm)

Vesicles
 fluid cavity, elevated lesions
 Size:- </=0.5cm
 Eg. Herpes Zoster

Blisters/ Bullae large vesicle
 fluid cavity , elevated lesions
 Size:- >0.5cm
 Develop from vesicles through
coalescence or enlargement,
 Eg.
 Impetigo
 Pemphigus Vulgaris
 Bullous Pemphigoid

Pustules
 circumscribed raised cavity in
the epidermis containing pus
 collection of leukocytes,
cellular debris +/-
bacteria
 Size:- may vary
 heal w/o scarring

Abscess large pustules
 localized collection of
purulent material deep in the
dermis/ subcutis
 is a pink warm, tender,
erythematous, fluctuant
nodule
 Associated with systemic
symptoms

Crusts
 hard deposits of dried serum,
pus, or blood, usually mixed
with epithelial and sometimes
bacterial debris
 appearance depends on the
nature of the secretion
 Yellowish brown -serous
 Yellowish green -
purulent
 Reddish black -
hemorrhage

Scales
 Accumulation of stratum
corneum due to increased
proliferation and/or delayed
desquamation
 Size :- ranges from fine dust-
like particles to extensive
parchment-like sheet

Fissures/cracks
 linear loss of continuity of
the skin surface or mucosae
 Result from excessive tension
or decreased elasticity of the
involved tissues

Erosions
 moist, circumscribed,
depressed lesion that results
from loss of all or a portion
of the viable epidermis
 May result from
trauma/scratching,
maceration, rupture of
vesicle / bullae, or
epidermal necrosis
 Unless secondarily infected,
heal without scarring

Ulcer
 “breach in the skin” in
which there has been
destruction of the epidermis
& at least the upper dermis
 heal with scarring

Excoriation
 are surface excavations
(small superficial defect)of
epidermis that result from :
 Local trauma
 scratching
 itchy skin conditions

Lichenification
 reactive thickening of the
epidermis
 induced by repeated
rubbing of the skin

Atrophy
 Decrease in the size of a
cell, tissue, organ, or part
of a body
– thinning of the epidermis,
leading to wrinkling and a
shiny appearance( paper thin )

Striae
 Are linear depression of the
skin
 Result from changes of the
reticular dermis that occur
with rapid stretching of the
skin
 1st
appear as pink to red in
colour & raised, later
become paler & flat

Scars
 abnormal
proliferation of fibrous
tissues that replaces
previously normal
collagen
 Usually follows
ulceration, surgery or
infection breaching
the reticular dermis

Approach to Patient
History Taking
1. Identification( name, age, sex, address,
occupation, etc)
2. Chief compliant with duration
3. HPI
 Elaboration of c/c
 Onset of lesion( site & progress)
 Periodicity
 recurring/remitting condition?
 Prior Dx & biopsy result
 Aggravating/relieving factors
 +ve/-ve pertinent Hx
( specific & nonspecific
symptoms)
 Medication Hx ( previous Rx &
response)
4. Past/known medical Illnesses
*medical,
*surgical,
*psychiatric,
*oncologic,
*gynecologic/obstetric,
*autoimmune diseases
5. Personal ,Family & social Hx
6. Review of systems
* HEENT, LGS, RS, CVS, Abd, GUT,
MSS, IS, NS

Physical Exam( inspection & palpation)
 GA (initial clinical impression)
 V/S ( BP, PR, RR, Temp)
 from Head –to- Toe
In practice many prefer,
brief Hx initially Perform
P/E then more detailed Hx .
Current Recommendations,
brief P/E initially obtain Hx
then return to more focused
P/E
 Complete cutaneous exam
includes:
* Entire Skin surface
* Mucous membrane
* Hair
* Nail

Four cardinal features in complete P/E
1. Morphology of skin lesions( i.e. the
types)
2. Shape/configuration of lesions
3. Arrangement of lesion
4. Distribution of lesions

1. Morphology of skin lesions
types(either 1ry or 2ry) for each lesions
 Palpation of the lesions:
 Simple palpation
 Blunt pressure
 Squeezing/pinching
 Stretching
 Rubbing
 Scratching
 Three major xics:
1. Colour
2. Consistency
3. Anatomy of the skin primarily
affected
 Check also:
 Deviation in temperature
 Mobility
 Presence of tenderness
 Margination

2.Shape/configuration of individual lesions
 Annular/ring-like ---
T.corporis
 Discoid/nummular---NE,
Psoriasis
 Polycyclic---- Urticaria
 Umblicated------MC
 Linear ---- LP
 Serpinigous ----Larva migrans
 Targetoid---- EM

3. Arrangement of lesions
 Grouped/
Herpetiform---HSV
infections
 Scattered/discrete
 Guttate-----Guttate
psoriasis

4. Distribution of lesions
 Dermatomal/ Zosteriform---
HZ
 Lymphangitic---Sporotrichosis
 Symmetry--- psoriasis
 Flexor----AD,
 Extensor---psoriasis
 Acral --- melanoma
 Truncal--- p.roesa
 Universal---Vitiligo
 Localised --- LCL
 Generalized ---LP

Appropriate Investigations
Common Laboratory tests as needed
 Hematologic tests
 Chemistries
 Serologic tests
 Stool tests
 Urinary tests
 Histology of skin biopsy
 Bacteriology & mycology, etc
Skin tests as needed
 Imaging modalities as needed

BACTERIAL INFECTIONS
OF THE SKIN
FOR HEALTH OFFICER STUDENTS
SOLOMON H ( MD,
DERMATOVENEREOLOGIST )

Introduction
 Bacterial skin infections occur when there is a
cut ,break in the skin due to trauma .
 Impetigo, folliculitis and cellulitis are the
most frequently seen bacterial skin infections.
 Infections with pyogenic (pus forming)
bacteria
 usually Staphylococcus aureus and/or
Streptococci (usually Group A β haemolytic
Streptococci - GABS)

Staphylococcus
- Commonly carried in nose(35%),
perineum (20%),
axillae and toe webs (5-10%)
- Staphylococcus causes impetigo, folliculitis, and
carbuncles plus deeper infections.
 Streptococcusus
- Rarely found on normal skin, often in throat
(10%),occasionally in nose
- Causes cellulitis, lymphangitis, regional
lymphadenitis

 Superficial Cutaneous infections
Impetigo
 infections in the epidermis
 Untreated pyodermas can extend to
the
dermis, resulting in ecthyma
 Two types

1) Non-Bullous Impetigo
 70% of impetigo
 industrialized countries -- S. aureus and less often
by group A streptococcus in developing countries
– group A streptococcus remains a common cause
 Occurs in children of all ages and adults
 pruritus

 Cutaneous Lesions
 initially a transient vesicle or pustule  honey-
coloured crusted plaque
 Surrounding erythema
 May regional LAP
 May progress to - Ecthyma

2) Bullous Impetigo
 more common in newborns and infants
 rapid progression of vesicles to flaccid bullae
 bullae arises on normal skin
 fluid clear yellow- dark yellow – turbid – may
crust

 Diagnosis
o Gram stain
o Culture
o Histology
 Treatment
 good hygiene removal of crusts.
 Antibiotics
- topical if mild – mupirocin , fusidic acid,
- Systemic if severe, multiple lesions,
- cloxacillin, erythromycin, amoxi+ clavulanic
acid, cephalexin

 Ecthyma
 usually a consequence of neglected impetigo
 characterized by thickly crusted erosions or
ulcerations
 Caused by Group A Strept and/or Staph
 Commonest in children or debilitated adults

 most commonly on the lower extremities
 ulcer has a “punched out” appearance
 Covered with dirty greyish-yellow crust
 heals slowly
 Treat as impetigo

 Folliculitis
 a pyoderma that begins within the hair follicle
 a small, fragile, dome-shaped pustule occurs at
the infundibulum (ostium or opening) of a hair
follicle
 Children – scalp
 Adults - beard area, axillae, extremities, and
buttocks
 Can complicate to Furuncles if untreated

 Furuncles – boil
 deep-seated inflammatory nodule that develops
around a hair follicle
 areas with friction, occlusion, and perspiration
 usually from a preceding, more superficial
folliculitis
 solitary or multiple
 hard, tender, red folliculocentric nodule
 undergoes abscess formation  Ruptures

 Carbuncle
 more extensive, deeper, communicating lesion
 develops when multiple, closely set furuncles coalesce
 more serious inflammation
 red and indurated, and multiple pustules soon appear
on the surface, draining externally around multiple
hair follicles  scar
 fever and malaise

 beware of bacteremia from such lesions esp when
appears on the face
 Treatment
 a systemic antibiotic as impetigo for mild cases
 severe infections or infections in a dangerous areas
- maximal antibiotic dosage by the parenteral
route
 drain if abscess

 Erysipelas
 caused by group A β- hemolytic streptococcus
 acute infection of skin- level of part of dermis
 superficial cellulitis with marked dermal
lymphatic vessel involvement
 face or a lower extremity
 superficial erythema, edema with a sharply
defined margin to normal tissue

 Cellulitis
 infection extends deeper into the dermis and
subcutaneous tissue
 S. aureus and GAS – common causes
 looks erysipelas but lack of distinct margins,
deeper edema, surface bulla/necrosis
 can go deep if untreated – fasciitis
 regional LAP
 portal of entry evident in half of cases

Treatment
 Supportive
- rest, immobilization, elevation &
analgesia.
 Dressings
-cool sterile saline dressings for
removal of purulent exudates and
necrotic tissue


Drug treatment
 pt with mild cases of cellulitis can be treated out
patient with drugs covering streptococcus and
staphylococcus.
Cephalexin ,Flucloxacillin / Dicloxacillin 500mg po
QID.
Clarithromycin 500 mg po BID for penicillin allergic
pts.
Azithromycin
Clindamycin
CHOICE OF ANTIBIOTIC FOR PARENTRAL THERAPHY;
depends on the suspected or proven etiology.
B.penicillin,flucloxacillin,ceftriaxone,vancomycin,clind
amycin….

SUPERFICIAL FUNGAL
INFECTION & P.
VERSICOLOR
FOR HEALTH OFFICER
STUDENTS
SOLOMON. H ( MD,
DERMATOVENEREOLOGIST )

Superficial fungal infection
 The commonest type of fungal infection in the body
 Are caused by fungi capable of superficially invading
the skin
 are Dermatophytes, Candida species & Malassezia
species
 Can be subdivided into those that induce
 no/minimal inflammatory response (tinea
versicolor)

 TINEA CAPITIS
Synonyms
Ringworm of the scalp
 dermatophyte infection of hair and scalp, typically
caused by Trichophyton and Microsporum species
EPIDEMIOLOGY.
 Common between 3 and 14 years of age.
 decrease in incidence after puberty ------The
fungistatic effect of fatty acids in sebum.

CLINICAL FINDINGS
 In general, dermatophyte infection of the scalp
results in hair loss, scaling and varying degrees of an
inflammatory response.
 Non- inflammatory Vs Inflammatory
• Seborrheic type • Kerion
• Gray patch • Favus
• Black dot • Agminate folliculitis

Noninflammatory Type
1) “ Seborrheic ” type
 Scale is the predominant feature
 Seen most commonly with M. audouinii or M. ferrugineum.
2) “Gray patch” tinea capitis
 Partial alopecia(nonscarring), often well demarcated
erythematous circular in shape, showing numerous broken-off
hairs
 Fine scaling with fairly sharp margin.
 Hair shaft becomes brittle, breaking off at or slightly above
scalp.
 Small patches coalesce, forming larger patches.
 Patches often occur on the occiput

 “Gray patch” type. A large, round
hyperkeratotic plaque of alopecia due
to breaking off of hair shafts close to
the surface, giving the appearance of a
mowed wheat field on the scalp of a
child.
Seborrheic ” type. With mild scalp
scaling
mild scalp
scaling

3) “Black Dot” tinea Capitis
 Least inflammatory form
 Commonly caused by --T. tonsurans and T. violaceum.
 Hairs broken off at the level of the scalp leave behind
grouped black dots within patches of polygonal shaped
alopecia with finger-like margins.
 The alopecia may occur in discrete patches or involve the
entire scalp.

Inflammatory Type
1) “ Kerion ” tinea capitis
 The most severe pattern of reaction
 is a painful or pruritic , boggy inflammatory mass studded
with broken loose hairs and follicular orifices oozing with pus.
 Maybe followed by scarring alopecia
 Lymphadenopathy is frequent.

2) “ Agminate folliculitis ” tinea capitis
 Less severe inflammation than kerion with
sharply defined, dull red plaques studded with
follicular pustules.
3) “ Favus ” tinea capitis
 Latin, “honeycomb”
 characterized by thick yellow crusts - scutula
composed of skin debris and hyphae that
 Trichophyton schoenleinii is the most common

Diagnostic procedure
 KOH
 CULTURE
 HISTOPATHLOGY

TREATMENT
 oral antifungal treatment--- since dermatophytes
penetrating the follicle are usually out of reach for
topically applied agents.
GRISEOFULVIN
 taken with a fatty meal to facilitate absorption
 Dosage ---20–25 mg/kg/day for 45days
 Common side effects include photosensitivity,
headache, and gastrointestinal(GI) upset.
TERBINAFINE
 Doses of 3–6 mg/kg/day for 4–8 weeks
 Side effects; GI upset , increase liver enzymes level

ITRACONAZOLE
 At doses of 5 mg/kg/day for 2–4 weeks
FLUCONAZOLE
 6 mg/kg/day for 30 days is effective in curing tinea
capitis
 is the only oral antifungal agent approved for children
younger than two years.
ADJUVANT THERAPY
 ketoconazole (2%), and Selenium sulfide (1%
and2.5%), are shampoo preparations that help
eradicate dermatophytes from the scalp of children.

TINEA FACIEI
 is infection of the glabrous skin of the face with a dermatophyte
fungus
 all dermatophytes must be considered potentially capable of
producing this condition.
Clinical features
 itching, burning and exacerbation after sun exposure are
common.
 atypical features are more common
 Erythema is usual, scaling(in less than 2/3 of pts)
 annular or circinate lesions
 induration with a raised margin (in about half)
Management
 In localized cases, topical (azoles)therapy
 Widespread – oralTerbinafine, Fluconazole or Itraconazole is
generally preferred.

TINEA CORPORIS
• Ringworm of the body
 refers to any dermatophytosis of glabrous skin except palms, soles, and the groin. most
commonly by T. Rubrum
 Characteristic lesions are annular (circular), usually sharply marginated with a raised
edge & centrally cleared plaque
TREATMENT
 Localized- Topical terbinafine or azole twice daily for 2-4 weeks
 Widespread- Oral terbinafine or fluconazole or itraconazole

TINEA PEDIS AND TINEA MANUUM
 Tinea pedis --- dermatophytosis of the feet,
 Tinea manuum ---involves the palmar and interdigital areas of
the hands, have fine dry scaling accentuation of the flexural
creases
 Infection of the dorsal aspects of feet and hands is
considered to be tinea corporis.
 EPIDEMIOLOGY.
 T. pedis and T. manuum are the most common
dermatophytoses.
 Incidence of T. pedis is higher among those using communal
baths, showers or pools.
 ETIOLOGY---are caused predominantly by T. rubrum (most
common),T. interdigitale, and E. floccosum.

Management
 Mild and moderate interdigital disease
• Topical imidazole twice daily for 4 weeks
• Topical terbinafine twice daily for 7 days
 Severe form - Oral terbinafine or fluconazole or
itraconazole
 Most cases clear with 2–4 weeks of treatment

TINEA CRURIS
 is a dermatophytosis of the groin, genitalia, pubic
area, and perianal skin.
 The three most common causative agents are E.
floccosum, T. rubrum and T.mentagrophytes
 is the second-most common type of
dermatophytosis worldwide
 exacerbated by occlusion and humid climates.
 presents classically as a well-marginated annular
plaque with a scaly raised border which extends
from the inguinal fold on to the inner thigh, often
bilaterally.
 Treatment

 Tinea cruris. Annular eythematous
plaques with a raised scaling border
expanding from the inguinal on the inner
thighs and pubic region.

Tinea incognito
 are ringworm infections modified by corticosteroids
(systemic or topical)
 the raised margin is diminished, Scaling is lost and the
inflmmation is reduced.
 Whatever site is affected, it is often best to treat steroid‐
modified ringworm with oral therapy,
Tinea corporis: tinea
incognito.
Erythematous patches on
the buttocks, some with
sharp margination, others
with clearing, and
excoriations.

DERMATOPHYTID (ID) REACTION
 is a non infective cutaneous eruption representing
‐
an allergic response to a distant focus of
dermatophyte infection.
Criteria
(1) dermatophytosis on another part of body,
(2) absence of fungal elements from the id eruption,
(3) resolution of the id eruption with clearing of the
primary dermatophyte infection

 P.versicolor
 ‘ Pityriasis’ – scaling
 ‘ Versicolor’- varied colors
 It is a superficial fungal infection.
 It is mild, asymptomatic and non-contagious.

Epidemiology
 P.versicolor occurs worldwide, but the highest
incidence is found in tropical climates.
 Most commonly affects adolescents and young adults.
 Both sexes are affected.
 No racial predilection.

Pathogenesis
Gene
tics Hum
id
envir
onm
ent
Hyp
erhi
drosi
s
Imm
uno
supp
ressi
on
Use
of
topic
al
skin
oils
Maln
utriti
on
OCP

Clinical findings
 P. Versicolor is typically asymptomatic.
 Most common sites are upper back, upper arm,
chest, neck, & abdomen.
 The typical presentation is scaly oval to round
macules scattered over seborrheic areas.

Diagnosis
 Clinical
 KOH
 Culture
Management
 Topical agents
 A variety of topical medications are effective.
 The usual time to recovery is 2–4 weeks.

Ketoconazole shampoo 2% is applied
on to affected areas and left for 5-10
minutes prior to rinsing; for 3
consecutive days or twice weekly for 2–
3 weeks.
Ketoconazole 2% cream twice daily
for 1-2wks
Terbinafine 1% cream applied twice
daily for one week.

Cont…
 Systemic treatment
• Indicated for patients with extensive disease, frequent
recurrences, or for whom topical agents have failed.
 Fluconazole
• 300 mg once weekly for two weeks
• 400 mg stat
 Itraconazole
 200-400mg /day from 3 – 7 days
 400 mg stat
 Ketoconazole
 200 mg daily for 7-10 days
• 400mg stat

&
DEEP FUNGAL INFECTION
FOR H/O STUDENTS
SOLOMON. H
(DERMATOVENEREOLOGI
ST)

Onychomycosis
 Onychomycosis :- is an Invasion of the nail plate by
dermatophyte fungi, nondermatophyte fungi or
yeasts.
 Synonyms
• Ringworm of the nails
• Tinea unguium
 Tinea unguium - refers strictly to dermatophyte
infection of the nail plate.

Risk factors
 Tinea pedis
 Hot and humid environment
 Increasing age
 Diabetes
 Poor venous and lymphatic drainage
 tight-fitting shoe
 HIV
 Smoking
 Nail trauma

Etiology
 Onychomycosis is caused by:-
- Dermatophytes:- 90%
- Non dermatophytic molds :- 3%-5%
- Yeasts :- 5%-17%

Dermatophytes
 Trichophyton rubrum ~71%
 Trichophyton mentagrophytes ~20%
 T. tonsurans
 T. violaceum
 T. soudanense
 Epidermophyton floccosum

Non Dermatophytic
Molds
• Scopulariopsis brevicaulis - common
• Fusarium spp.
• Aspergillus spp.
• Acremonium
• Scytalidium hyalinum
• Scytalidium dimidiatum
 The nondermatophyte molds most commonly occur
in antecedently diseased or aged nails.

Yeasts
 Candida albicans - >70%
 C. parapsilosis
 C. tropicalis
 C. krusei
 Occurs in conjunction with chronic
mucocutaneous candidiasis.

7 distinct patterns
1. Distal/lateral subungual onychomycosis (DLSO)
2. Superficial onychomycosis (SO)
3. Proximal subungual onychomycosis (PSO)
4. Endonyx onychomycosis (EO)
5. Mixed pattern onychomycosis (MPO)
6. Totally dystrophic onychomycosis(TDO)
7. Secondary onychomycosis

1.
1-Distal and Lateral subungual onychomycosis
(DLSO)
 It is the most common type
 Most often caused by
 T. rubrum
 T. mentagrophytes.
 A small percentage of cases are caused by
 E. floccosum, T. tonsurans, T. violaceum.

Cont’d
 It is characterized by
yellow-brown
discoloration of the nail
plate, onycholysis, and
subungual
hyperkeratosis.

2- Superficial white
onychomycosis(SWO)
 Common causes are:
- T. mentagrophytes
- T. rubrum

There will be direct invasion
of the dorsal nail plate
resulting in powdery
white to dull yellow
sharply Bordered patches
any-where on the surface of the nail.

3-Proximal Subungual
onychomycosis (PSO)
 Caused by - T. rubrum,Fusarium,C. albicans & Aspergillus
 Particularly affects immunocompromised pts (RVI)
 resulting a white to beige opacity on the proximal
nail plate.

4- Endonyx onychomycosis
 Mostly caused by dermatophytes
- T. soudanense
- T. violaceum
 Invasion occurs from the top surface
of the nail plate and result in scarred
with pits

5-Mixed pattern onychomycosis (MPO)

 Different patterns of nail plate infection are often
seen,
 The commonest are
 PSO and SO or
 DLSO and SO
 DLSO and PSO
 These almost always require oral therapy.

6-Totally dystrophic onychomycosis(TDO)
 The organism directly invades the nail plate, and the
proximal and lateral nail folds become increasingly thick,
until the nail becomes totally dystrophic.
 Mainly by Candida albicans & Trichophyton rubrum

7-Secondary onychomycosis
 Fungal nail plate invasion may occur secondary to
other nail pathologies.
eg, psoriasis, Lichen planus, Contact dermatitis ,
and traumatic nail dystrophy.
 Diagnosis based on clinical suspicion is particularly
difficult and laboratory investigations are necessary
to confirm the presence of fungi.

Diagnosis
1- Direct microscopic (KOH solution)
2- Fungal culture
3- Nail biopsy

Management of Onychomycosis
1. Topical therapy (Ciclopirox or Amorolfine)
2. Systemic antifungal therapy, either alone or in
combination with a topical agent.
 Fluconazole
 Itraconazole
 Terbinafine
3. Surgical intervention

 Introduction
 Deep Fungal infection : Subcutaneous mycoses
 The most common subcutaneous mycoses :-
 Mycetoma
 Chromoblastomycosis
 Sporotrichosis

1) Mycetoma
 Greek word from “Fungal Tumor”.
 Synonyms: Madura foot
 Localized, Specific, Chronic,
Granulomatous ,Progressive inflammatory &
disfiguring disease that involve the subcutaneous
tissue.
 Triad of mycetoma :-
1) painless subcutaneous mass,
2) Sinuses and
3) The discharge of grains are pathognomonic

 Sites of mycetoma
 Common Site
 Foot – 70%
 Hands – 12%
 Knee
 Arm
 Leg
 Head & neck
 Thigh
 Perineum

2) CHROMOBLASTOMYCOSIS
 is chronic fungal infection of skin and subcutaneous
tissue caused by fungi that implanted to skin from
environment.
 Mainly found in soil enriched by organic waste,
decaying woods and vegetation.
 Primary lesion is erythematous papule
or warty growth that enlarge assuming
various size & shape

 Disease can present clinically in 05 variant
(Nodular, Tumor, Plaque, Verrucous & Cicatricial )

3) Sporotrichosis
 Synonym: Rose Gardner’s Disease
 Is a subacute or chronic; subcutaneous or systemic
fungal infection caused by the dimorphic fungus
Sporothrix schenckii and closely related species.
 Cutaneous forms
 Lymphocutaneous sporotrichosis
 Fixed cutaneous sporotrichosis
 Disseminated cutaneous form
 Atypical varieties( mycetoma-like or cellulitic
forms)

Lymphatic
Fixed cutaneous
Disseminated
cutaneous

 DIAGNOSIS
 Diagnosis depends on clinical , pathological &
imaging finding.
 Requires laboratory evaluation:
 Grain color, texture & microscopy
 Histopathology
 Serology
 FNA
 Culture (gold standard)
 Imaging

 MANAGEMENT
Treatment options are:
*antifungal chemotherapy
itraconazole
terbinafine
Amphotericin B
*physical methods
cryotherapy
thermotherapy
* surgical
* combination therapy

Dr. Solomon .H (MD, Dermatovenereologist )

Introduction
 Dermatitis : is a general term for skin
inflammation.
 -Dermatitis and eczema
- considered synonyms
- dermatitis – includes all type of cutaneous
inflammation
- all eczema are dermatitis but all dermatitis
may not be eczema

 The 04 most common types of
dermatitis;
1) Atopic Dermatitis ( AD )
2) Seborrhic Dermatitis ( SD )
3) Contact Dermatitis ( CD )
4) Lichen Simplex Chronicus ( LSC )

 ATOPIC DERMATITIS (AD)
 AD is an itchy, chronic, or chronically relapsing,
inflammatory skin condition that occurs most commonly
during early infancy and childhood.
 A common disease occurring worldwide at any age
( usually onset is before 5 yrs.)
 Has 3 phases ( varying in morphology , distribution….)
 Infantile
 Childhood
 Adulthood

Pathogenesis –Multifactorial
Genetic factors
Immune
dysfunction
Environmental
factors

Clinical features
 Depend on:
 Age
 Stage of the disease
 History
 Self or family Hx of atopy
 Pruritis
o Cardinal feature in AD
o Night > day
o Leads to excoriation, pruritic papules , lichenification &
eczematous skin lesion
 Chronic or relapsing nature of the disease

 P/E
 Acute stage
o Edematous, erythmatous Papules, vesicles ,
& serous exudates
 Sub-acute stage
o Erythematous , excoriated, scaling papules
& plaques
 Chronic stage
o Thickened plaques of skin, lichenification,
pruritic nodules

Con..
 Infantile AD ( 3mons-2yrs )
 Distribution
o Face ,scalp ,& extensor surface of the
extremities
o Diaper area is generally spared
 Morphology
o Acute stage predominates
o Secondary infection & LAP are common
 Has chronic on & off type course

Con..
 Childhood AD
 From 2- 12 yrs
 Distribution
o Flexural sites of the extremities ,
o Sides of the neck and
o Hand can be commonly involved
 Morphology
o Chronic stage

Con..
 Adult AD ( >12yrs )
 Distribution
o More generalized
o Flexural sites of the extremities , nipple , lip
 Morphology
o Chronic lesions

Associated features
 Xerosis
 Keratosis pillaris
 Ichthyosis vulgaris
 Dennie–Morgan lines
 Palmoplantar hyperlinearity
 Pitryiasis alba
 Cheilitis
 Lichenification
 Prurigo nodularis
 Nipple eczema

DIAGNOSIS
 Is made clinically and is based on historical feature
,morphology and distribution of skin lesions and
associated clinical signs
 Haniﬁn and Rajka’s diagnostic criteria appear to
be valid for both adults and children

 Hanifin-Rajka criteria (1980)

Management
 Heath Education
 Skin hydration
 Pharmacologic therapy
 Rx of complications
 Identification & flare factors

 SEBORRHEIC DERMATITIS (SD)

common, chronic papulosquamous disorder
affecting infants and adults
 characteristically found distinctive morphology with
pink to erythematous,, superficial patches and plaques
sharply marginated lesions covered with a yellow, branny
and sometimes greasy scale.
 distinctive distribution in areas with a rich supply of sebaceous
glands
 namely the scalp, face and upper trunk In some cases the flexures

 ETIOLOGY AND
PATHOGENESIS
Seborriec
dermatitis
patient
susceptibility.
sebaceous
activity
yeast
Malessezia,
immunologic
abnormality

 Clinical Patterns in SD
INFANTILE SD
 Scalp (cradle cap),
 Trunk (flexures and napkin area),
ADULT SD
 Scalp,
 Face,
 eyelids (blepharitis),
 Trunk

 Infantile SD
 Infants commonly develop a greasy adherent scale on the vertex
of the scalp during the first wk of life - Cradle cap
 Seborrheic dermatitis occurs in infants between the ages of 3 weeks
and 12 months
 10% infants< one month of age
 Peak prevalence at the age of 3 months- 70%
 7% of children aged one to two years

Widespread pattern of seborrheic dermatitis with
psoriasiform lesions on the trunk and groin.

 ADULT SD
It is usually characterized by
 well demarcated erythematous plaques with greasy-
looking, yellowish scales distributed on areas rich in
sebaceous glands such as the
 scalp
 the external ear
 the center of the face
 periocular
 the upper part of the trunk
 intertriginous areas including
(inguinal, inframammary, and axillary)

Management
Infantile SD
 Initial treatment should be conservative
 Application of an emollient to the scalp to loosen the scales, followed
by removal of scales with a soft brush or fine-tooth comb
 white petrolatum
 vegetable oil
 mineral oil
 baby oil
 In more extensive or persistent cases
 low-potency topical corticosteroids applied once per day for one
week
 ketoconazole 2% cream or shampoo twice per week for two weeks.

Mangement…
Adult SD
 The main goals of therapy
 To clear the visible signs of the disease
 To ameliorate the associated symptoms, especially pruritus
 Treatments to control dandruff and seborrheic
dermatitis includes;
 Keratolytic- SA, Sulfur
 Antimicrobial- Imidazoles

Management
Dandruff
 Dandruff responds to more frequent
shampooing
with medicated shampoos

Management…
SD
 Can be treated with shampoos
 Selenium sulfide (1%–2.5%)
 Imidazoles (1%–2% ketoconazole shampoo, creams,
lotions, or foams)
Ciclopirox (cream, gel, and shampoo)
Salicylic acid (shampoos, creams)

 CONTACT DERMATITIS
(CD)
 A dermatitis a non contagious inflammatory
condition caused by substances coming in contact
with the skin is called contact dermatitis
 Two types
* Allergic contact dermatitis (ACD)
* Irritant contact dermatitis (ICD)

 ALLERGIC CONTACT DERMATITIS
(acd)
 ACD is a delayed type of hypersensitivity
reaction elicited due to contact of the skin to a
specific allergen
 Previous history of sensitization of the skin is
required
 20% of CD

Etiology
 50% of the cases are caused by 25 known
allergens
 Metals
 Preservatives
 Topical antibiotics
 Fragrance compounds
 Others

Nickel
 Most common
Allergy tested
 Component of jewelry,
belt buckles, buttons

Neomycin sulfate
 Topical antibiotic
 Found in preparations
like bacitracin, hemorrhoid
creams, otic and
ophthalmic medications

Formaldehyde
 Colorless gas
in cosmetics,
textile, paint,
cigarette
smoke,
and plastic
bottles

Cobalt
 Metal found in association with nickel and
chromium for hardness and strength
 Found in jewelry,
buttons, cosmetics,
hair dyes,
joint replacement,
ceramics, enamel,
cement paint

Clinical features
 THOROUGH HISTORY
 Early lesions appear
as pruritic papules
and vesicles with
erythematous base

 With chronicity comes lichenification

 Diagnosis
 KOH to R/O fungal infection
 Patch Test remains the gold standard diagnostic modality
 Approaches for treatment
 Identify and avoid cause
 Symptomatic treatment
 Corticosteroids
 Topical immunomodulators
 Phototherapy
 Immunosuppressive agents

 Irritant contactDermatitis
(ICD)
 Non-specific response of the skin by
inflammation due to direct cytotoxic effects of
chemicals
 80% of CD
 Manifested by erythema, mild edema and
scaling
 It is a diagnosis by exclusion

Etiology
1. Acids
2. Alkalis
3. Metal salts
4. Solvents
5. Alcohols
6. Detergents and cleansers
7. Plastics
8. Food
9. Water
10. Bodily fluids
11. Fabric fibers
12. Plants

ICD types
 Acute
- acute often single exposure.
 Delayed acute
- delayed 12-24hr or longer.
 Chronic
- Slowly developing over months to years.

Diagnosis
 Thorough history and physical examination
 Lab:
 KOH
 Direct microscopy
 Patch test
 Skin biopsy

Treatment
 Emergency management
 Patient education
 Steroids and immunomodulators
 Photochemotherapy

 LICHEN SIMPLEX CHRONICUS (LSC)
 LSC is a chronic dermatitis caused by repeated
skin scratching and/or rubbing.
 Scratching or rubbing causes further itching and
then further scratching and/or rubbing, creating a
vicious circle (itch–scratch cycle).

Etiology
 LSC is not a primary process
 Conditions that can lead to a scratch-itch cycle that can
cause lichen simplex chronicus include:
 Insect bites
 Scars (eg, traumatic, postherpetic/zoster )
 Eczema (atopic dermatitis)
 Psoriasis,
 Scabies
 Acne Keloidalis Nuchae ( AKN)
 Dry skin (xerosis)
 Poor circulation in legs (venous insufficiency)
 Anxiety and stress

Epidemiology
o Frequency
 Exact frequency in the general population is unknown. In
one study, 12% of aging patients with pruritic skin had
lichen simplex chronicus
o Race
 No differences are reported
o Sex
 Lichen simplex chronicus is observed more commonly in
females than in males with a 2-to-1 ratio.
o Age
 Lichen simplex chronicus occurs mostly in mid-to-late
adulthood, with highest prevalence in persons aged 30-50
years.

Clinical features
 LSC is characterized by
pruritic, dry, scaling,
hyperpigmented,
lichenified plaques (single
or multiple) in irregular,
oval, or angular shapes.
 It involves easily reached
sites
 Lower legs
 Arms
 Neck
 Upper trunk and
 Genital region

 Diagnosis
 Clinical
 KOH
 Histology
 Treatment
 Treatment of the cause of the itch
 Education and behavioral changes
 Corticosteroids (most often topical but sometimes
injected intralesionally)
 Antihistamines
 emollients, and
 Topical or oral antibiotics if infection is present

INFESTATIONS
Solomon H ( MD, Dermatovenereologist )

Scabies
Synonyms
• Itch mite infestation
 Scabies is a human skin infestation caused by
the penetration of the obligate human parasitic
mite Sarcoptes scabiei var. hominis into the
epidermis.

Transmission
 Scabies can be transmitted
directly by close personal contact, sexual or otherwise
 indirectly via fomite transmission.
 Spread of the infestation between family members &
close contacts is common

Clinical Findings
 IP ranges from days to months.
 2-6 wks initial exposure - pruritus & cutaneous
lesions, the host's immune system becomes
sensitized to the mite or its byproducts – type IV
hypersensitivity reaction
 itching is severe & usually worst at night ,
exacerbated by a hot bath or shower.

CTD…
 Cutaneous lesions are symmetrical.
 Lesions appear mainly
 interdigital webs ,sides of the fingers
 volar aspects of the wrists & lateral palms
 elbows
 Axillae
 Waist & buttocks
 Feet
 scrotum & penis in men
 labia, nipple & areolae in women

An imaginary circle
intersecting the main
sites of involvement—
 axillae,
elbow flexures
Wrists
 hands
crotch
has long been called
the circle of Hebra.

1° scabies lesions
 First manifestation of the infestation
 small erythematous papules – 1-3mm , rarely contain
mites, hypersensitivity rxn
 Vesicles – discrete lesions filled w clear fluid ,if old –
cloudy
 burrows - tunnel that a female mite excavates
(pathognomonic sign )

In infants/young children
 Generalized, including
scalp & face
 Conc. on palms, soles,
body folds.
 Atypical lesions:
vesicles,bullae,
pustules, nodules
 vesicle or pustule
containing the mite
may be noted at the

In elderly
 All skin surfaces are susceptible, including
the scalp and face
 Altered inflammatory response may delay
dx
 In bedridden pts - concentrated on the back.
 Crustation is common

Diagnosis
 Clinical diagnosis
 The epidemiologic history (e.g. pruritus in household
members or close personal contacts),
 the distribution and types of lesions, and
 pruritus
 definitive diagnosis - microscopic identification of the
scabies mites, eggs, or fecal pellets (scybala).

Treatment
 Rx includes administration of scabicidal agent
 Antipruritic agent such as sedating
antihistamine
 An appropriate antimicrobial agent if
secondarily infected
 Provision of detailed verbal and written
instructions is critical for compliance and
complete eradication of scabies.
 Proper preventive & control measures

TREATMENT FOR SCABIES
Drug Dose Comments
Permethrin 5% cream
Apply for 8 hours, repeat in
7 days
Most common treatment
presently; pregnancy
category B, tolerance seems
to be developing
Benzyl benzoate 10% lotion
(BBL)
Apply for8- 24 hours for 03
consecutive days, repeat
after 01 week
available in our set up , use
above 02years; C/Is –
pregnancy or lactation
Crotamiton 10% cream
/lotion
Apply for 8 hours on days
1,
2, 3, and 8
Has antipruritic qualities;
effectiveness is marginal
Precipitated sulfur 2%–10% Apply for 8 hours on days
1, 2, 3
Considered safe in neonates
and during pregnancy;
limited efficacy data;
inexpensive
Ivermectin 200 µg/kg Taken orally on day 1 and 8 Highly effective with good

ONCHOCERCIASIS
 Onchocerciasis is a filarial disease
caused by the filarial nematode,
Onchocerca volvulus
predominantly affecting cutaneous
and ocular tissues
Also known as:
 River blindness
 Erysipela de la costa -in central
America
 Swoda- Arabic for “black”
 Craw-craw- west Africa

EPIDEMIOLOGY
 one of the
debilitating neglected
tropical diseases
(NTDs)
 > 99 % in 27
countries in sub-
Saharan Africa

EPIDEMIOLOGY
 races and sex- no reported differences
 Socioeconomic - occupation as related to
exposure to black fly bites, i.e, farmers,
fishermen - contributing factor
 Age- ↑ age results in cumulative exposure
in endemic areas
 Onchocerciasis -2nd
, leading infectious cause
of blindness worldwide

In Ethiopia
 In Mainly the western
parts i.e from the
Takazi valley in the
northwest, to the
Omo valley in the
southwest are
affected
 The main endemic
focal areas are;
 Kefa-Sheka and
Bench Maji zone
in south west
 Pawi –Metema in
North West

VECTOR
 Onchocerciasis is transmitted by the
bite of infected black flies of the
genus Simulium and family Simulidae
 Breed in fast flowing streams
and rivers
 Highly oxygenated water
required for maturation of the
larvae
 They tends to stay within 2 km of
its breeding site.
 S. kaffaense- in Ethiopia

THE PARASITE
Helmin
ths
Nematodes(ro
und worms)
Intestinal
Tissue
Filaria
e
Onchocerc
a volvulus
Trematodes(F
lukes)
Cestodes
(Tape worms)

CLINICAL FEATURES
 Cutaneous
 ophthalmologic
 chronic, systemic, and localized manifestations
(Weight loss and growth arrest ),appear ~ 1–3 years
after the bite of the black fly.
 Vary by geographic location

ONCHOCERCAL DERMATITIS
 Clinical manifestations are highly variable due to:
• Chronicity, age, geographic area, immune
responsiveness
 On history patient might have:
 Generalized itching
 rash
 Skin color changes
 Itchy eyes, redness or photophobia
 Weight loss
 Generalized myalgia

 Six different patterns of skin changes have been
described in onchocerciasis:
1. Acute papular onchodermatitis
2.Chronic papular onchodermatitis
3. Lichenified onchodermatitis
4. Atrophy
5. Depigmentation
6. Onchocercal nodules( onchocercomata)

1. Acute papular onchodermatitis
 In children and in the
earliest cases in endemic
areas,
 most often- face,
extremities, and trunk,
on exposed site
 small pruritic papules,
vesicles and pustules,
 sometimes with
associated erythema and
edema.

2.Chronic papular onchodermatitis
 Comprises larger lichenoid
papules
 Are often symmetrically
distributed over buttocks,
waist, and shoulders
 Post inflammatory
hyperpigmentation is
common
 may be accompanied by
acute lesions elsewhere

3. Lichenified Onchodermatitis (LOD)
 most commonly in young patients
 is found mainly in East Africa Sudan , Ethiopia and
Yemen
 is less common in West Africa or South America
 In LOD, pruritus is severe and often asymmetrical.

3. Lichenified onchodermatitis
(LOD)
 Hyper pigmented,
lichenified plaques
 lymph nodes in the
affected region are
often enlarged.
 When a single limb is
involved, the condition
may be referred to as
“sowda”.

4. ATROPHY (ATR)
 mimics the normal effects of
aging,
 dry and shiny, with fine
wrinkles resembling tissue
paper
 most frequently on the
buttocks
, shoulders or lower limbs
 may be associated with
decreased sweating or hair
growth
 long-standing
onchocerciasis
 may develop after any of the
patterns or arise de novo
 An extreme form - known as

HANGING GROIN
 is atrophy affecting the skin
of the groin and anterior
thigh.
 Inguinal lymph nodes
enlarge in a sling of atrophic
skin on the medial thigh,
 then as the nodes shrink and
become fibrotic, they leave
redundant folds of loose
skin.

5. DEPIGMENTATION (DPM)
 on the anterior tibialis
in large patches,
 can be found on the
abdomen or lateral groin
 “leopard skin”.
 Complete Pigment loss
within the patch, except
for perifollicular islands
of retained normal
pigmentation.

6. ONCHOCERCAL
NODULES(ONCHOCERCOMATA)
 Firm, painless, freely
mobile subcutaneous
nodule,
 often located over a bony
prominence
 comprised of 2–3 adult
worms
 Onchocerciasis -2nd
, leading
infectious cause of blindness
worldwide

 OCULAR
MANIFESTATIONS
 may result in blindness rates
in endemic communities of
5–10%
 1st
ocular sign - presence of
microfilariae in the eye (slit-
lamp examination)
 Other manifestations include
 Punctate keratits
 Sclerosing keratitis
 Uveatis
 Optic atrophy
 Onchocoreoretinitis

 DIAGNOSIS
 history of compatible
epidemiologic exposure and
clinical manifestations
 SKIN SNIPS
 SLIT-LAMP
EXAMINATION
 MAZZOTTI TEST
 PATCH TEST
 SEROLOGY
 PATHOLOGY
 Ultrasonography

SKIN SNIPS
 with a corneoscleral
punch
 or with a small needle
and disposable razor
blade .
 bloodless specimen
from the level of the
dermal papillae.
 from site with highest
numbers of microfilariae.

MAZZOTTI TEST
 Patient is given 50 mg oral dose of
diethylcarbamazine (DEC)
microfilarial death  ↑ pruritus
about 20 to 90 minutes later an
acute papular rash with edema,
fever, cough and mus.skeletal
symptom
 Symptoms peak in 24 hours &
subside - 48 to 72 hours.
 severe systemic reactions can
develop, including pulmonary
edema, visual loss, collapse, and
death
 not as routine test
 C/I- in those heavily
infected and with
optic nerve disease

 TREATMENT
IVERMECTIN
 drug of choice
 is effective efficient at killing microfilariae
but does not kill the adult worm.
 MOA
- agonist of the parasite neurotransmitter,
induces an influx of C l through channels
- probably impairs the release of microfilariae
from the female adult worm already after the
first dose.

IVERMECTIN…
 Dosage: Single oral dose of 150micrograms/kg
 should be continuously given once or twice a year
until patients are:
• asymptomatic,
• for the duration of the lives of adult worms or
• for people residing in endemic area.
• For those no more living in endemic area, single dose
and a repeat dose in relapse.
 Mass treatment - 6 to 12 monthly intervals
for 10 to 16 years.

IVERMECTIN…
 ADRs: Myalgia, dizziness, fever, headache,
lymphadenopathy, skin rash or itching,
postural hypotension
 C/Is: Pregnancy, hypersensitivity to
ivermectin.
 P/C: Breast-feeding
 Blood should be obtained to evaluate for
evidence of L. loa microfilariae prior to
administration of ivermectin

 Macro Filaricidal Therapy
 Doxycylline
 is used to kill the Wolbachia bacteria that
live in adult worms
 be effective in sterilizing the female worms
and reducing their numbers over a period of
four to six weeks
 200 mg/day for 6 weeks
 Ivermectin alone Rx- reappearance of
dermal microfilariae 4 months after therapy
 combined with doxycycline, absence of

microfilariae that lasts for 18 months

Treatment…
 Diethyl carbamazepine(DEC)
 Alternative, but rarely used
 may cause severe exacerbation of skin and eye
disease, even blindness
 induces the Mazzotti
In heavily infested patients, prednisone 40 mg
daily, starting the day before DEC and continuing
for a few days until the reaction has settled

 Nodulectomy
 Particularly in lightly infected
individuals,

Complications
 major complication is visual impairment and
blindness
 Inguinal and femoral hernias
 dermatologic aspects - psychosocial and
socioeconomic effects as well

Preventive measures
 no vaccine to prevent onchocerciasis
 vector control, chemotherapy, and personal
protection measures from biting during the
day
 Mass drug administration with ivermectin
administration at 6 to 12 monthly intervals for
10 to 16 years Significant impact on the
burden of skin and ocular disease
 Spraying black fly breeding sites with
larvicides

VIRAL INFECTIONS OF
SKIN AND MUCOSA
Solomon. H ( MD,
Dermatovenereologist )

 Introduction
 Viruses are obligatory intracellular parasites
 Human herpes viruses replicate within the nucleus
 Cxed by their ability to produce latent but life long
infection
 Vast majority of infected persons remain asymptomatic..
 Common infection:-
 HSV
 VZV ( HZ & CHICKEN POX)
 MC and
 HPV ( Warts )

 HERPES SIMPLEX VIRUS (HSV)
INFECTION
 HSV virus interaction with human host has 3
components
1, 1˚infection (1st
HSV infection , without preexisting
Ab to HSV1 or HSV 2)
2, latency in sensory ganglion
3, reactivation resulting in recurrent infection with
asymptomatic viral shedding or clinical manifestation

 Epidemiology
 1/3 of world population has experienced a
symptomatic HSV infection
 Caused by 2 types of HSV viruses
 HSV 1 =mucocutaneous presentation
Mostly associated with orofacial disease
 HSV 2 -> associated with genital & perigenital
infection
 Age of Onset Most commonly young adults;
range, infancy to old age.

 Transmission
 Most transmission usually occurs;
 skin-skin,
 skin-mucosa,
 mucosa-skin contact.
 Increased HSV-1 transmission associated with;
 crowded living conditions and
 lower socioeconomic status

 Clinical features
 Classical herpes lesions are divided into 03 stages;
1) Developmental – prodrome,erythema,papule
2) Disease – vesicle, ulcerate or crust
3) Resolution – dry flaking,& residual swelling

 DIAGNOSIS
 Clinical
 Direct Microscopy = Tzanck Smear
 Viral cultures
 PCR
 Serological assays
 Direct fluorescent antibody assay(DFA)
 Histology

 MANAGEMENT
 Topical Antiviral Therapy:-
 Approved for herpes labialis; minimal efficacy.
 Acyclovir 5% ointment Apply QID daily for 7 days
 Penciclovir 1% cream Apply QID daily for 7 days
 Systemic Therapy
 Acyclovir
 Valacyclovir
 Famciclovir
 Prevention:- Skin-to-skin contact should be avoided

 HERPES ZOSTER VIRUS INFECTIONS
 An acute dermatomal infection associated with reactivation
of VZV
 Characterized by Unilateral pain
 A vesicular or bullous eruption limited to a dermatome(s)
innervated by a corresponding sensory ganglion
 Typically a disease of adulthood
 20% - healthy adults
 50% - immunocompromised persons.

Cont..
 IP:14/15 days(10-23 days).
 A typical patient is infectious :
 1-2 days (rarely,3-4 days) before the exanthem appears.
 For 4 or 5 days thereafter (untill the last crop of vesicles has
crusted).
 Immunocompromised patients are infectious for a longer
period of time.

Risk factors for HZ
 Older age
 Cellular immune dysfunction
 Bone marrow & solid organ transplantation
 Hematological malignancies and solid tumors
HIV
 Chemotherapy , Corticosteroid
 Gender : Females
 Race : whites
 Trauma or surgery in affected dermatome

 Clinical Manifestations
 Herpes Zoster-
1.Prodromal
2.Rash
1.Prodrome
 Pain & paraesthesia in the involved dermatome for
several days before the rash
 Vary from superficial itching, tingling, burning to
deep, severe, or lancinating pain.

Cont
2. Rash :
Skin Lesions
 The most distinctive feature : localization & distribution of
the rash
 Unilateral, dermatomal
 Evolve more slowly
Usually. Consist of grouped vesicles

.
days
s

 Distribution
 Unilateral, dermatomal .
 Two or more contiguous dermatomes may be
involved.
 Site of Predilection ;
 Thoracic (>50%),
 Ophthalmic (10–20%),
 Lumbosacral and cervical (10–20%).

 Management
 Constitutional symptoms Bed rest,
nonsteroidal anti-inflammatory drugs,
(Ibuprophen) , acteaminophene
& TCA ( Amitriptyline)
 Calamine lotion
 Systemic antibiotics for bacterial cellulitis.
 Topical antiviral treatment for herpes zoster is
not effective
 Acyclovir 800 mg PO four times daily for 7–10
days(≤72 h )
 Ophthalmologic evaluation is needed

 Complication of HZ
Cutaneous viseral
 Bacterial super-infection - pneumonitis
 Scaring -hepatitis
 Zoster gangliosum - esophagitis
 Cutaneous dissemination - gastritis
neurologic -pericarditis
 PHN
 TM
 Meningioencephalitis
 Autonomic
 CN palsy
 Deafness
 Ocular complications(uveitis, keratitis,
conjunctivitis,scleritis… necrosis of the eye lid)

Varicella (chickenpox)
 French . - ‘chiche-pois’ for chickpea (the vesicle size).
 Old English . - ‘gican’- to itch.
 An acute & highly contagious viral exanthem that
occurs as a result of primary infection by VZV.
 Worldwide distribution.
 Prevaccination era :
90% <10 yrs .
 < 5% of individuals , >15 yrs of age.
 98% of the adult cases affected are seropositive.

 Transmission
• Respiratory Tract / Direct contact
• Highly contagious : 80-90% 0f susceptible household
contacts develop disease
 IP:14/15 days(10-23 days)
 A typical patient is infectious :
 1-2 days (rarely,3-4 days) before the exanthem appears.
 For 4 or 5 days thereafter (until the last crop of vesicles
has crusted)
 Immunocompromised patients are infectious for a
longer period of time

CLINICAL FINDINGS
 VARICELLA – two phases.
1.Prodromal
2.Rash
1.PRODROME- 2-3 days.
Fever, headache, malaise, backache, anorexia
Dry cough & sore throat
Fever
Absent / Rise to 40.5 c°.
Usually persists as long as new lesions continue to
appear
Pruritus
The most distressing symptom
Usually present throughout the vesicular stage

2.Rash- :
 Begins on the Face & Scalp ---Trunk---Extremities.
 Appear in successive crops, Scattered.
 Macule Papules Vesicles Pustules Crusts
 Typical vesicle: superficial & thin-walled, surrounded by an irregular area of
erythema (“Dewdrop on a rose petal ”)
 Vesicles may develop in MM (mouth, nose…) ---Rupture rapidly ---Shallow
ulcers

Cont.
 Rash of varicella
Begins on face & scalp
Erythematous macules &
papules
Vesicles & pustules
Dew drop in a rose petal

Treatment
 Strict isolation
 Adequate hydration
 Adequate rest
 Cool compresses, or calamine lotion locally
 antihistamines
 Antipyretics – not salicylates (avoid aspirin)
Why????
 Antibiotics for secondary bacterial infection
 Antiviral treatments
Acylovir 20mg/kg for 5 days ( 2-12 yrs)
8-15 yrs -acyclovir 400-800mg 5x a day 5 days

 MOLLUSCUM CONTAGIOSUM
 Molluscum contagiosum (MC) is a self-limited epidermal viral
infection caused by Molluscum contagiosum virus ( pox virus)
.
 Risk groups
 Children
 Sexually active adults
 Immunocompromised: HIV/AIDS, organ transplant
recipients
 Transmission: Skin-to-skin contact
 characterized by smooth, dome-shaped discrete papules that
occasionally develop surrounding areas of scale and erythema
(molluscum dermatitis)

 Clinical manifestations
 Skin-colored papules; often umbilicated
 Few to many of lesions
 HIV/AIDS: large nodules; confluent
 Course:
 Usually asymptomatic
 Healthy persons: MC resolves spontaneously
 HIV/AIDS: if not successfully treated with
antiretroviral therapy (ART), MC can become huge
and confluent.

 Management
 Treatment of lesions:
o 5% imiquimod cream applied at bedtime 3–5 times per
week for up to 1–3 months
o 5% KOH applied at bedtime once per day
o curettage and
o cryotherapy freezing lesions for 10–15 seconds
 Prevention:
o Avoid skin-to-skin contact with individual having MC
o HIV-infected individuals with MC in the beard area
should be advised to minimize shaving facial hair

 HUMAN PAPILLOMAVIRUS
INFECTIONS
 Human papillomaviruses (HPV) are
ubiquitous in
humans, causing
▪ Subclinical infection
▪ Wide variety of benign clinical lesions on skin
and mucous membranes
 They also have a role in the oncogenesis of
cutaneous and mucosal premalignancies :
 Squamous cell carcinoma in situ (SCCIS)
 Invasive SCC

Introduction
 Warts (verrucaea) :-
are benign proliferations of the skin and mucosa that
are caused by infection with papillomaviruses(PVs).
 Based on anatomic location, histopathology &
biology, HPV infections are categorized as;
1. cutaneous(non-genital) and
2. genital-mucosal types

Epidemiology
 INCIDENCE:- > 10% in children
16% in general population
increases 50- 100X in immunodeficient
• AGE:- children & young adults
Peak 12 – 16 years of age
 SEX:- girls > boys
 GEOGRAPHICAL: - in low socio-economic societies
 RACE:- no racial predilection
 MORTALITY:- benign & self-limiting condition but small percentage of
malignant transformation occurs

Transmission
 direct skin-to-skin contact
 fomite spread
 swimming pool or shower-room floors
 habitual nail biting
 Shaving
 Occupational (handlers of meat, fish & poultry)
 Iatrogenic
N.B. No convincing evidence for blood-borne
dissemination

 Cutaneous HPV infections occur commonly in the
general population:
 Common warts: (Verruca Vulgaris )Represent
approximately 70% of all cutaneous warts
 Plantar warts: (Verruca Plantaris) Common in older
children and young adults
 Flat warts: (Verruca Plana) Occur in children and adults,
 Mucosal warts:
Condyloma acuminatum (genital wart)
Most prevalent sexually transmitted infection.

Verruca plana A 12-year-old male kidney transplant recipient. Multiple brown
keratotic papules are seen on the forehead and scalp.

 Genital warts (condyloma accuminata)
 Papillomatous cauliflower-like lesions
 Seen in external genitalia of both sexes , perianal
region and in anal canal
 May affect the urethral meatus, urethra, vagina
or cervix.
 form huge lesions causing discomfort and
irritation.
 in children raises the suspicion of sexual abuse

Complications
 Ulceration
 bleeding
 Secondary infection
 mechanical obstruction
 Malignant transformation
 Anxiety, depression, other psychiatric components
 Feeling of guiltiness

Rx Options of Cutaneous wart
1.destructive
Salicylic acid
Cryotherapy
Thermocautery/curettage
and cautery
TCA/BCA
KOH
2.antiproliferative
Podophyllin
Bleomycin
Retinoids
3.immunomodulatory
modalities
Topical
sensitization
Cimetidine
Intralesional
immunotherapy
Imiqumoid
4.virucidals
Formaldehyde
Glutaraldehyde

PILOSEBACEOUS DISORDERS
Dr. Solomon H (MD, Dermatovenereologist )

SKIN APPENDAGES
 Include :-
 Pilosebaceous units
 hair apparatus, sebaceous gland,
arrector pili muscle, & in some areas
apocrine glands
 Nails
 Sweat glands
 eccrine , apocrine, apoeccrine
 Common pilosebaceous
disorders:
 Acne
 Rosacea
 POD

 ACNE VULGARIS
Synonym: ■Acne
 is a self-limited chronic inflammatory disorder of the
pilosebaceous unit that is seen primarily in adolescents
 It is characterized by -seborrhoea, the formation of open
and closed comedones, erythematous papules and
pustules
 In more severe cases nodules, deep pustules and
pseudocysts

EPIDIMOLOGY
Age: Seen primarily in adolescents
- All age groups may be affected
-can also be seen in neonatal and infentile age
 often heralds the onset of puberty
Sex

In adolescents →boys > girls(16-18)
 post adolescent → women> men

 ETIOLOGY AND PATHOGENESIS
 Four key elements
1. Follicular hyperkeratinization
2. Increased sebum production
3. Propionibacterium acne within
the follicle
4. Inflammation
 Other factors
 Hormonal Influences
 Androgen
 Estrogen
 Corticotropin-releasing
hormone
 Dietary Factors
 Genetics
 Stress

CLINICAL FINDINGS
 Most report gradual onset of lesions around puberty
can be seen in the neonatal or infantile age
 Usually asymptomatic
Local symptoms may include pain or itching (rare)
 Systemic symptoms are most often absent
 The primary site → face
 to lesser degree → the back, chest, and shoulders

Clinical features
NONINFLAMMATORY INFLAMMATORY
 Closed comedones
(whiteheads)
 open comedones
(blackheads)
 Papules
 pustules
 nodules
 ‘cysts’

Noninflammatory
lesions
(comedones)
 predominant lesions
In very young patients
Closed comedones
(whiteheads)
 Appear as 1-mm
pale or yellow,
slightly elevated,
small papules

Open comedones
(blackheads)
 Appears as a flat
or slightly raised
lesion with a
central dark-
colored follicular
impaction of
keratin and lipid

CLASSIFICATION
 Mild acne
 Comedones are the predominant lesions
 Less number of papules and nodule
 Moderate acne
 More papules and pustules on the face
 Comedones
 Lesions could also be present on the trunk
 Severe Acne
 Widespread papulopustular lesions
 Nodules, cysts
 Nodular acne with systemic symptoms

HISTORY AND PHYSICAL EXAMINATION OF THE ACNE PATIENT
History Physical examination
Sex
Age
Motivation
Lifestyle/hobbies
Occupation
Current and previous treatments
Use of cosmetics, sunscreens,
cleansers, moisturizers
Menstrual history
Medications
• Corticosteroids
• Oral contraceptives
• Anabolic steroids
• Other (e.g. lithium, EGFR inhibitors)
Concomitant illnesses
Skin type (e.g. oily versus dry)
Skin color/phototype
Distribution of acne
• Face (e.g. “T-zone”, cheeks, jawline)
• Neck, chest, back, upper arms
Overall degree of involvement (mild,
moderate or severe)
Lesion morphology
• Comedones
• Inflammatory papules
• Pustules
• Cysts
• Sinus tracts
Scarring
• Pitted
• Hypertrophic
• Atrophic
Postinflammatory pigmentary changes
Diagnosis

General recommendation
 Patients with Mild acne
Topical therapy
 Patients with Moderate acne
Topical & Oral Therapies
 Patients with Severe acne
Oral isotretinoin

 Management
 includes:
General measures
Topical therapy
Systemic therapy

Topical Options
 Topical Benzoyl Peroxide
 Topical antibiotics
 Topical Retinoids
 Topical Salicylic acid
 Topical Azelaic acid
 Topical Sulfur
 Combination therapy

Systemic Therapy
 Systemic Antibiotics,
 Hormonal Therapy,
 Oral Retinoids

ROSACEA
 The word “ Rosacea ” originates from the feminine
Latin word “ Rosaceus ” meaning Rose coloured.
 Rosacea is a common, chronic skin disorder that
presents with a variety of clinical manifestations
primarily localized on the central face.
 The usual age of onset is between 30–50 years.
 Women commonly affected than men.

 Pathogenesis
 Genetics
 Ultraviolet radiation
 Microbes
 Vascular hyperreactivity
 Epidermal barrier dysfunction

TF
Spicy
foods
Alcohol
Sun
exposure
Emotion
al stress
Temperatu
re extremes
Heavy
exercise
Infectio
n
Medica
tions

Classification
1) Erythematotelangiectatic Rosacea
2) Papulopustular Rosacea
3) Phymatous Rosacea
4) Ocular Rosacea

1) Erythematotelangiectatic
Rosacea
 Persistent centrofacial erythema and
flushing along with telangiectases, central
face edema, burning and stinging,
roughness or scaling, or any combination
of these signs and symptoms
 Mild, moderate, and severe sub-types are
recognized

2) Papulopustular Rosacea
 Persistent central facial erythema with
transient papules, pustules, or both in a
central facial distribution.
 Burning and stinging less common, and
flushing less severe than ETR.
 Mild, moderate, or severe

3) Phymatous Rosacea
 Thickened skin, nodularities, and
irregular surface contours in convex areas
 Mild, moderate or severe subtypes

4) Ocular Rosacea
 May manifest as blepharitis, conjunctivitis, iritis, scleritis, and
keratitis
 Photophobia, pain, burning, itching & foreign body sensation
may be part of the ocular symptom complex.
 Mild, moderate, or severe

 General measures
 Specific measures
 Topical therapy
 Oral therapy
MANAGEMENT

PERIORIFICIAL DERMATITIS
 Periorificial dermatitis is an inflammatory skin
disorder of young women and children.
 It is characterized by small, discrete papules and
pustules in a periorificial distribution,
predominantly around the mouth.
 Women between the ages of 16 and 45 constitute
the vast majority of patients affected by POD.

 Pathogenesis
 The pathways that lead to the development of POD are not well
understood.
 Topical corticosteroid use is frequently reported in association
with POD.
 Fluorinated toothpaste, skin moisturizers and cosmetic products
 Deficiencies in skin barrier function and features of atopy have
been detected at increased frequency in patients with POD.

Management
 Avoid triggering factors like corticosteroids…..
 For milder cases, initial application of topical
metronidazole alone may suffice.
 Oral tetracycline, doxycycline, or minocycline for a
course of 8 to 10 weeks
 Oral erythromycin for children under 8 and TTC
allergic patients.

LEISHMANIASIS &
LEPROSY
FOR HEALTH OFFICER STUDENTS
SOLOMON H ( MD, DERMATOVENEREOLOGIST )

CUTANEOUS & MUCOCUTANEOUS LEISHMANIASIS
 Leishmaniasis: An Infectious disease caused
by intracellular protozoan parasites of the
genus Leishmania.
 Infect the skin, mucosa, and the viscera.
 Transmission is via the bite of female
sandflies from the genera Phlebotomus &
Lutzomyia.

 Old World (OW)
 Mediterranean basin,
Southern Europe,
Central Africa, and
parts of Southern
and Central Asia
 L. major or L. tropica,
L. infantum or L.
aethiopica
 New World (NW)
 Central and South
America
 L. mexicana and L.
braziliensis

 Mucocutane
ous
leishmaniasis is
endemic in Central
America and the
northern regions of
South America
 Visceral
leishmaniasis has
a worldwide
distribution, but
most frequently in
Africa and Asia

 Leishmania are dimorphic parasites
 Promastigote - 10–20 µm
 Spindle-shaped
 Motile with single anterior flagellum
 In the gut of the sandfly or in culture
 Amastigote - 2–6 µm
 Oval & nonmotile
 In the host reticuloendothelial system

 The several species of Leishmania causing human
infections are classified under 4 complexes:
1) Tropica (L. tropica, L. major, L.minor, L. aethiopica)
2) Mexicana (L. mexicana,L. amazonensis, L. pifanoi, and L.
venezuelensis)
3) Braziliensis or viannia (L.brasiliensis, L.guyanensis, L.
panamensis, and L.peruviana)
4) Donovani (L. donovani, L. infantum, L. chagasi,L. sinesis)

Vector
 Sandyfly
 Phlebotomus - OW
 Lutzomyia - NW
 Found in cracks, rodent burrows,
termite hills , forests
Transmission:
Bite from infected sandflies
Congenital
Parenteral (bld transfusion, needle sharing)

CLINICAL MANIFESTATION
 Depending on the degree of the cell mediated host
immune response & the type ,virulence of Leishmania sp.
z clinical classification are:
I. Cutaneous leishmaniasis
II. Mucocutaneous leishmaniasis
III. Visceral leishmaniasis

 CUTANEOUS
LEISHMANIASIS
 Clinical spectrum – subclinical, localize and disseminated
 Factors that determine the clinical spectrum:
 Parasite virulence factors: leishmania species
 The genetic susceptibility: vector & host
 Host Factor: immune response
 Cutaneous leishmaniasis can be further subdivided
in to;
1. Localized CL
2. Diffuse CL
3. Leishmaniasis Recidivans
4. Post Kala-azar Dermal Leishmaniasis

1. Localized CL
Due to L. major
 Ip – 1wk to 3 mo.
 A red nodules appear
 After 2 wks crust form
 Marked and persistent
crusting

Due to L. tropica
 Longer IP & course
 Small brownish nodule
 Shallow ulceration
at the center
 After 8-12 mths regress
leaving scar

Due to L. aethopica
 Central face
 Satellite papules
 Heal over 2-5 yrs
 Nasal involvement &
edema of face

2. Diffuse CL
 When an individual failed to mount
immune response (CMI) to
the leishmania parasites.
 L.aethopica – OW
 L.mexicana – NW
 Disseminated non ulcerated
nodules heavily loaded
with parasite
 Chronic, relapse after therapy
 Mimics lepromatous leprosy

3. Leishmaniasis Recidivans
 Caused mostly by
L. tropica
L.brasiliensis
 Papules appear close to or
on scar of old lesion
 Apple-jelly nodules
 Host reaction-exaggerated
hypersensitivity

4. Post Kala- azar Dermal Leishmaniasis
 A sequel to VL that has cured
following adequate treatment.
 Rash develops after a year or
so after a course of therapy for VL
 Mostly seen in RVI pts
 Lesion appear as macular, papular,
and nodules over the face, trunk,
and extremities.

Mucocutaneous leishmaniasis
 Chronic progressive spread of
CL to the nasal, pharyngeal,
buccal mucosa
 Due to L.aethopica &L.braziliensis

DIAGNOSIS
 A high index of suspicion - clinical
 Confirmation is by identification of the organism.
 Slit skin smear
 FN aspirates- marrow, spleen, LNs
 Culture
 NNN (Novy-Mac Neal-Nicolle’s) media
 Gold standard
 Positive in 1-3 wks
 Histopathology
 Serology
 PCR

Management
 Observation/ Local wound care
 Topical therapy
 Infiltration 1-2ml SSG( IL-SSG)
 Topical paromomycin
 Cryotherapy
 Heating 40-42c
 Systemic Therapy
 Pentavalent antimonials compounds
 Sodium stibogluconate - 20 mg/kg for 28 days.
 Meglumine antimoniate -20 mg/kg for 20 days
 Pentamidine
 Miltefosine
 Amphotericin B

LEPROSY
 Definition : is a chronic granulomatous infectious
disease caused by Mycobacteriuem leprea
 The term leprosy is derived from the Greek word
lepros , which means scaly. In Ethiopia…
 Rarely cause mortality , but is disabling ,deforming ,&
stigmatizing disease.
 Age
 Occur at all ages ranging from early infancy to very old
age
 Sex-slightly higher in males

Con..
 Principally affects the cooler areas of the body
including:
 Skin
 Peripheral nerves
 Testis
 Anterior chamber of the eye
 Upper respiratory tract
 It is Gram-positive, acid fast bacillus,
Noncultivable & Non toxin producing bacteria

Mode of transmission
 Not fully understood
 Respiratory droplets
 Skin contact (Direct Vs indirect , intact Vs broken
skin )
 Ingestion (Breast milk of
lepromatous leprosy mother)

Risk factors for disease devt .
 The majority of individuals exposed to the
organism don’t develop the disease.
 Risk factors include:
 Close contact(household , intimate, frequent &
prolonged )
 The type of leprosy in the index patient
 Genetic factors
 Host immunity ( old
age ,immunocompromised )

The WHO classification
Paucibacillary (PB) Leprosy
 One to five leprosy skin lesions.
 Only one nerve trunk enlarged
 AFB is negative
Multibacillary (MB) Leprosy
 Six or more skin lesions.
 If there is involvement (enlargement) of more
than one nerve
 AFB is positive

Ridley-Jopling classification
 Types ( TT , BT, BB ,BL ,LLs LLp )

Polar Tubercloid leprosy
( TT )
 Strong immunity as manifested by spontaneous
cure or absence of downgrading.
 Lesions: sharply marginated plaque with annular
configuration , firmly indurated, elevated,
erythematous, scaly, dry, hairless, and often
hypopigmented.

Borderline tubercloid ( BT )
 Has adequate immunity to limit the diseases & bacillary
growth but not to self cure
 Lesions – plaques or papules, annular configuration is
common but minimal elevation ,scaling,induration,
erythema & satellite lesions

Borderline leprosy ( BB )
 The immunologic midpoint or mid-zone of the
granulomatous spectrum
 Lesions – Annular lesions with sharply
marginated interior and exterior margins,
 large plaques with islands of clinically normal skin
within the plaque, giving a “Swiss cheese”
appearance

Borderline lepromatous leprosy (BL)
 Immunity is low to control bacillary proliferation but
adequate to cause tissue damage (nerve damage).
 Lesions – Dimorphic -poorly marginated outer border
(lepromatous like) but a sharply marginated inner one
(tuberculoid like),

Lepromatous leprosy ( LL )
 Diminished CMI toward M. leprae permits unrestricted
bacillary replication and widely disseminated, multiorgan
disease
 Lesions: Poorly defined nodules are the most common lesions,
usually up to 2 cm in diameter, and are symmetrically
distributed
 A conjunction of skin folding and nodule formation produces
the “leonine faces”
 Hair loss is most common in the eyebrows/eyelashes
( madarosis )
 Nose involvement
 Edema –stuffiness, epistaxis & increased secretion
 cartilage & bone involvement- the pathognomic “saddle-
nose’’ deformity

Lateral P. N Radial N ulnar N
posterior tibial N

Lagophthalms & corneal
opacification

 Clinical presentation
 The cardinal signs of leprosy are:
1) Definite loss of sensation in hypo-pigmented or
reddish skin lesion.
2) Thickened or enlarged peripheral nerve with
or without tenderness
3) The presence of acid-fast bacilli in a slit skin
smear.
 Presence of one or more of the three cardinal
is a confirmatory to a leprosy case

 Clinical findings
 History
 Risk for those born or resident in endemic area
 Duration of symptoms, history of previous Rx
 Peripheral neuropathy, nasal stuffiness, ocular
symptoms
- 90% Hx of numbness first→ sometimes years before
the skin lesions appear
 /Temp. → light touch → pain → deep pressure/
 Especially apparent in hands & feet
 complaint of burn or an ulcer

 Examination ‫׃‬
Cutaneous lesions
- character, number & distribution
- Hypopigmented macule, plaque
- may or may not be hypoesthetic
• Neuropathies
- assess for hypoesthesia /light touch, pinprick/
anhidrosis
-ulnar, median, radial cutaneous N, peroneal N,
post.tibial N
- enlargement , tenderness

 Diagnosis.
 Criteria for Diagnosis.
 Cardinal signs of leprosy
 Presence of AFB in slit skin smear ( SSS )
 Histopathology - confirmation

Slit Skin Smear ( SSS )
What? Staining a skin sample with ZNS
Why? Confirm diagnosis ( BI/MI )
Classify
Follow
Where? Border of Suspected lesions, tip of earlobe,
above eyebrow, chin, extensor surface of the forearm,
buttocks and trunk “2 sites”
How ? An incision 5 mm long and 3 mm deep-blade is
turned at right angles to cut

 TREATMENT
 PB – Multidrug therapy( MDT) regimen
Child <10yrs
 Rifampicin 300mg monthly
 Dapsone 25mg daily
10 – 14yrs
>15yrs

 MB – MDT regimen
Child <10yrs
 Clofazimine 100mg monthly
 Clofazimine 50mg 2x/week
10 – 14yrs
 Clofazimine 150mg monthly
 Clofazimine 50mg every other day

ATOPIC DERMATITIS PART 2 is an itchy, chronic, or chronically relapsing, inflammatory skin condition that occurs most commonly during early infancy and childhood..pptx

ATOPIC DERMATITIS PART 2 is an itchy, chronic, or chronically relapsing, inflammatory skin condition that occurs most commonly during early infancy and childhood..pptx

More Related Content

Similar to ATOPIC DERMATITIS PART 2 is an itchy, chronic, or chronically relapsing, inflammatory skin condition that occurs most commonly during early infancy and childhood..pptx

More from masresha22

Recently uploaded

ATOPIC DERMATITIS PART 2 is an itchy, chronic, or chronically relapsing, inflammatory skin condition that occurs most commonly during early infancy and childhood..pptx

Editor's Notes