Pseudo Chancre redux

A gamma or a lesion of tertiary syphilis at the site of healed chancre

Leprosy

0.73/10000 is the currents prevalence

Etiology

M. Leprae

Generation time: 13-14 days

Source: only viable source is open, that is untreated case of multi bacillary
leprosy

Naturally occurring in Armadillo, but transfer to humans is yet to be

proved

Route of exit from the patients: respiratory route

Route of entry: respiratory or droplet, much more common than per

cutaneous if any in tuberculoid type of leprosy

Other routes are questionable: GI tract infection, insect bites

Vertical transmission is least likely

Fate of the bacilli

M. Leprae

Enters the body

More than 90% of ppl are able to kill all the M. Leprae completely

In 10%, bacilli not killed properly and an infection results

Early indeterminate phase

75% pts completely recover in 3-4 months

In remaining 25%, if cell mediated immunity good, tuberculoid

If immunity compromised, lepromatous

In immunity +/- , borderline

Lepromin test
Marker of CMI status

In indeterminate pt, Lepromin negative, CMI decreased, lepromatous

Lepromin positive, no disease or tuberculoid

Clinical features
Spectral concept

Is determined by the host CMI

Tuberculoid type, CMI high, nerve damage happens coz of the immune
response

While in lepromatous, the nerve injury happens late as CMI low

Although the disease is preserved to a small area in tuberculoid while

widespread in lepromatous

Classifications
Ridley and Jopling classification
Based on 4 parameters

1. Clinical

2. Bacteriological ( split skin smears)

3. Histopathological

4. Immunological ( Lepromin testing)

If all 4 are available

Then leprosy pt can be divided into 5 groups

TT

BT

BB

BL

LL

with CMI decreasing as we descend

Ridley jopling is not purely clinical, instead is used for research purposes
and has not got any therapeutic significance

Thus

Indian classification / IAL classification

Clinical or clinico- bacteriological

Tuberculoid

Lepromatous

Borderline (is not = BB)

Have dimorphic features, both lepromatous and tuberculoid

Indeterminate type

Pure neuritic leprosy

This also has no therapeutic significance

WHO classification/ operational/ working classification

Completely clinical

No slit smears required

No investigations needed

Treatment can be started on clinical grounds alone

NLEP modifications of WHO classification

Paucibacillary and multi bacillary

No of lesions
PB: less than equal to 5

MB: more than equal to 6

No. Of nerves

1 is Pb

2 pr more is MB

AFB

Zero is PB

MB is, even if one bacilli

Even if one criteria fulfills MB, consider it MB so that under treatment

does not happen

Indeterminate leprosy

Early form

Mostly seen in children, more than adults

Lesions are macules, thus never raised

If a palpable lesion, it can not be indeterminate

Non scaly( dierentiate from P. Alba)

Lesions are never ANESTHETIC

Sensory loss is mild or absent

Atrophy +/-

Nerve involvement is +/-

3/4th of the pt heal in 3-4 month of time spontaneously

No. of lesions is usually is 1-3

Biopsy shows perineural lymphocytic infiltrate

AFB smears : may be positive or negative

Most common site is face

Q. Saucer right way up: always answer TT

Q. Pesudopodia( jagged border) : borderline > BT > BB

Q. Satellites: borderline > BT > BB

Q. Punched out lesion: BB > borderline

Q. Inverted saucer: borderline > BL > BB

Q. Bizzare: borderline > BB > BT

Q. Most common nerve involvement: posterior tibial> ulnar nerve

Q. Most common cranial nerve: facial > trigeminal

Q. Modalities lost: sensory loss is always first> motor > autonomic

Q. Sensation loss: temperature is the first sensation to go > pain > touch>
pressure and vibration

Q. Warmth and cold dierentiation > warmth(44 degree C) > cold (27
degree C) > hot( perceived as pain) > pain > touch

Pressure and vibration are preserved till late

Lepromatous leprosy besides the macular forms also develops of the

forehead, zygoma, ear lobes, nose

Plus nodules

In the infiltrated area

Plus

Depressed nasal bridge

Plus

Madarosis

Plus

Loss of teeth giving rise to Leonine facies

Nasal symptoms are earliest: epistaxis, nasal crusting

Oil smeared appearance

Male genital tract is involved producing testicular atrophy, gynecomastia,

loss of testicular sensations

Females genital tract is typically spared

Histoid leprosy
Characterized by papules and nodules on non infiltrated normal skin

6+ but no globi( cigar shaped arrangement on slit skin smear)

Biopsy reveals spindle shaped cells in whorls

In past Histoid/ Wade leprosy indicated dapsone mono therapy resistance

and relapse

Most new cases are de novo Histoid

Lucio Leprosy/ Latapi/ Lepra Bonita

Aka beautiful leprosy

Diuse infiltrative form

No skin lesion

In early disease, skin is shiny, less wrinkles

Later on nerve, hair involvement develops

Described in Mexico

Biopsy shows endothelial invasion

Q. On deformities in leprosy

0: no deformity

1: glove and stocking anesthesia

2: any visible deformity

Eye

0: no deformity

2: any eye deformity

Most common deformity: plantar ulcer could be the answe

Go with claw hand > plantar ulcer

Reactions in leprosy

Acute clinical presentations

Two types

Type 1 reaction: CMI mediated, type 4 HS

Seen in immunologically unstable

BT, BB, BL

Not in stable TT and LL

Usually seen in within first 6 months of treatment

Increased CMI produces accelerated killing of the bacilli producing the

acute episode

So the skin lesions become erythematous, Edematous, tender

Nerves: acute neuritis or nerve abscess and nerve function impairment

No new skin develop coz CMI is upgrading

Predominantly a Th1 reaction with IL-1 and interferon as mediators

Aka as upgrading or reversal reaction coz CMI is going up

Rarely and questionably downgrading reactions can occur, new lesions

will develop

Systemic features are less

Treatment

Do not stop MDT

If mild symptoms, NSAID

Moderate/ severe/ neuritic : oral steroids

Nerve abscess

Should be drained

Type 2 reaction: immune complex mediated, type 3 HS

Multisystem disease

Seen in 50% LL, 25% BL

Seen after the 6 months of treatment

Systemic features are present: fever, joint pain, malaise

Skin: tender, red, painful nodules: erythema nodosum leprosum ENL

No change in the existing skin lesion of leprosy

Eye: iridocyclitis

Kidney: GN

Neuritis

Hepatitis

Treatment

Mild: NSAID

Moderate/ severe

1: oral steroids

2: oral steroids + clofazimine

3: thalidomide( recurrent and non responding cases)

Lucio phenomena
Is a type of Type 2 reaction

Aka type 3 Lepra reaction

Because of gross endothelial damage: infarcts in skin, no nodules seen

It is an episode in Lucio leprosy patient

Q. Nerve abscess most commonly seen in BT and ulnar nerve

Q. Usually biopsy taken from radial cutaneous as easily accessible

Q. Mouse foot pad inoculation is most sensitive for drug ecacy and not
morphological index

Q. Lepromin test is not diagnostic

Treatment regime

MB leprosy

Rifampicin 600 mg once a month

Clofazimine:300 mg once a month and 50 mg daily

Dapsone: 100 mg daily

Duration 12 months, preferably within 18 months

PB

Rifampicin 600 mg once a month

Dapsone 100 mg daily

Duration 6 months, preferably 9 months

No follow up , fixed duration treatment

Sign of activity of disease

Appearance of new lesion

Increase in size or erythema of lesions

New nerve involvement

Signs of reversal reaction

Mycobacterial infections

Two morphology

Plaque

Ulcer

Plaque morphology
Erythematous plaques

Annular

Central atrophy and scarring

Peripheral activity and spread

With advancing and receding edges

Usually asymptomatic

Ulcer morphology
Well defined

Asymptomatic

Bluish margins

Undermined edges

Cheesy/ Caseous center

Atypical mycobacterial infection

1. Swimming pool granuloma/ fish tank granuloma

Mycobacterium Marinum( Balnei)

Plaque form

Usually on the exposed skin

By inoculation and exposure to swimming pools, aquariums or sea water

Immunosuppression +/-

No LN enlarged

ATT has poor results

Minocycline is most eective

2. Buruli ulcer
M. Ulcerans

Mainly in certain districts of Africa

Children, immuno suppressed and malnourished more aected

Also asso with exposure to aquatic environment

Ulcer form

Ulcer becomes wider and wider, deeper and deeper till it leads to
exposure of underlying structure like fascia, muscles and even bones

Even then, LN is not enlarged

Eect of ATT is poor

Early surgical excision and grafting for larger lesions is the preferred
treatment

Typical tubercular infections

Primary: in non sensitized hosts, no prior exposure to the bacteria

Secondary: in sensitized hosts, reinfection or reactivation and spread

Tuberculids: HS reaction

Primary cutaneous TB
5% of cutaneous TB
Only route of entry: inoculation

Mostly in children

Site of entry: ulcer forms

Within few weeks: draining LN enlargement

This combo is analogous to Ghon's complex in the lung

Aka tubercular chancre

Tuberculin test negative

There could be a seroconversion later and it could be positive

Secondary cutaneous TB

1. Lupus vulgaris
Previously sensitized

Route of entry: hematogenous, lymphatic, or inoculation: although

predominantly endogenous

Classical plaque form

Diascopy test: shows apple jelly colored nodules

Probing: soft on probing( unlike sarcoidosis, which has a grainy feel)

Easily gives way on pressure with match stick: match stick sign and

Not the Match box sign: delusion of Parasitosis , parts of normal skin kept
in container like match box and presented to the physician as evidence of
insects in the skin

Lupus vulgaris is the most common( also in India)

Face is most common site in he developed western countries

In India, buttocks and extremeties> face

2. Tubercular wart/ tuberculosis verrucosa Cutis/ Anatomist wart/

prosecutors wart
Don't confuse with Butchers wart which is seen in HIV

CMI is high

Route of entry is inoculation

Plaque form with verrucous, rough , irregular, fissured warty surface in

areas of activity

Feet > hands

Q. Farmer with a single warty lesion on foot: TBVC

3. Scrofuloderma

Route of transmission

Contiguous spread

Mostly from LN to skin

Can also come from lacrimal glands, bones, ligaments, seminal vesicles

Classic ulcer

However it is fixed to the underlying source like matted LN

Most common cutaneous TB in children

4. Tubercular Gumma
Route of transmission is hematogenous

Pt has an internal focus of TB and there is temporary Immunosuppression

Now it spreads hematogenously

Reaches skin

Multiple ulcers

But NOT fixed to the underlying tissue

5. Orificial TB / TB cutis orificialis

Internal advanced end stage TB

Like TB of lungs

Because of the end stage, there is severe Immunosuppression

The sputum is full of AFB, it starts to infect the self tissue like mouth,
gums, lips, tongue

Auto inoculation

Ulcers

Severe Immunosuppression thus tuberculin negative: this is called

terminal Anergy

Tuberculids

Id eruptions: hypersensitivity rashes

If due to TB, it is called tuberculid

If by bacteria, bacterid

Dermatophyte: dermatophytid

Conditions needed

1. Focus of non cutaneous TB

2. Rash on the skin that parallels the disease activity of underlying focus

3. Skin lesions should be AFB negative

Examples

1. Papulonecrotic tuberculid PNT

Starts as a painless papule, undergoes central wedge shaped necrosis

heals with a depressed scar

Predominantly seen on LL> UL > face

2. Erythema induratum
Bazin's disease

Ulcers on calf in women

3. Lichen scrofulosorum
Children and adolescents

Most common underlining focus is TB LN

Clinical features

Minute, pinhead sized, shiny/ and or hyperkeratotic papules grouped in

indescrete patches on trunk > extremities

Biopsy shows epithelial cell granulomas

Surrounding hair follicles and sweat glands

Treatment

Same as TB

Diascopy: to look under pressure

Glass Slides used

Bacterial infections

Ecthyma: ulcer with a crust

Common Ecthyma: Ecthyma Pyogenicum by staph and strep

Ecthyma gangrenosum: pseudomonas

Ecthyma contagiosum: para pox viral infection

Zoonosi with sheep and goat

Veldt sore= desert sore

Type of Ecthyma caused by diphtheroids and streptococci

Seen mainly on exposed skin

Ecthyma heals with scarring

Impetigo heals without scarring

Impetigo has two forms

Bullous( always staph)

Non bullous

Non bullous/ common impetigo/ impetigo contagiosa

Vesicles and Honey colored crust

Around the perinasal> face

Etiology is controversial

First Streptococcal pyogenes then Staphylococcal

Heals without scarring

Erysipeloid

Caused by erysiplothrix

Purplish, painful, tender erythematous lesion

Seen in butchers

Erysipelas
Always streptococcal

Previously dierentiated from cellulitis

in modern and current world, both are synonymous

Erythrasma

Chladymia minutissimum
Reddish, thin, tiny scale, macule/ plaques with a wrinkled appearance in
the intertriginous areas

Web space> groin! axilla

Woods lamp: cord red fluorescence

Treatment by erythromycin

Woods lamp
Light source covered with nickel oxide and barium silicate filter

It blocks the visible light

Only black light comes out which is UV

Wavelength peaks between 360-365 nm

Uses

Tinea capitis of ectothrix variety caused by microsporum species

Pteriding : green fluorescence

As the spores are on the outside

Erythrasma
Coproporphyin produces coral red fluorescense

Pseudomonas: pyocyanin and pyoverdin , blue green

P. Versicolor: golden or yellow

Porphyria : red fluorescence of urine and serum

Serum in all

Urine in all except erythropoietin proto porphyria

In EPP, there is no P in the pee

Vitiligo

Ash leaf macules of tuberous sclerosis

Nevus depigmentosus (achromicus)

Decreased melaonosis

Optical window

Become more apparent on woods lamp examination

In nevus anemicus and worono ring( psoriasis)

No melanin problem, only vasoconstriction

No optical window thus on woods lamp examination

These become either non accentuated or attenuated, merge with the

surrounding

Epidermal pigmentation like freckle becomes accentuated

Dermal pigmentation on the other hand become attenuated

Corynebacterium skin infections

1. Erythrasma
2. Veldt sore
3. Pitted keratolysis: holes in soles

4. Trichomycosis: axillaris, pubis

Should be called trichobacteriosis

Yellowish/ pinkish concretions/ granules along the hair shaft

Fungal infections

Three areas

Surface mycosis
Superficial cutaneous mycosis
Deep cutaneous mycosis

Surface mycosis
Three diseases
Pityriasis versicolor
Tenia Nigra
Piedra

Superficial
Dermatophytes
Candida

Deep
Sporotrichosis
Chromoblastomycosis

Pityriasis versicolor
Aka tinea versicolor

Etiology

Malessezia furfur

Furfur is a combination of 6 species

It's a normal commensal in the upper part of the hair follicles in sebum
rich areas

When environment becomes moist and wet

Multiply

Move up

Aect the surface of stratum corneum

Thus recurrent in rainy season.

Initial lesions are peri follicular

Soon large irregular patches

Can have both hypo and hyper pigmented lesions

Scaly patches of many colors

Male > female

Site

Trunk> neck, face

Scales are easily dislodged with nail: nail sign/ Besigner sign

With scotch tape: en mass removal: Coup de Ongle sign

KOH

Spore + hyphae

Spaghetti and meat balls

Grapes and bananas

Ziti and meatballs

Wood lamp

Yellow fluorescense

Treatment

Griseofulvin not to be used

Topical and systemic anti fungals can be used

Oral terbinafine is not eective

Tinea Nigra
Non scaly, brown/ black, irregular, macules on palms and on soles

Etiology

Hoartae wernickii

Exophiala or Phaeranellomyces

Treatment

Scraping

Topical antifungals

Piedra

Nodules along the hair shaft

Dark or light colored

Dark: Black Piedra caused by Piedraria hoartae

Light: white Piedra caused by trichsporum beigelii ( combo of species) or

T. Cutaneum

Nodules

Fruity bodies of fungus

Non fluorescent

Dicult to dislodge

Best to shave

Formalin based shampoo can be tried

Or topical antifungals

Recently terbinafine has shown to be eective

Superficial cutaneous mycosis

Dermatophytoses

3 genera

Microsporum does not aect nail

Epidermophyton does not aect hair

Trichophyton aects all three

Source

1. Anthrophilic

2. Zoophilic

3. Geophilic

Anthrophilic is least inflammatory

Geophylic is moderately inflammatory

Zoophilic are severely inflammatory

Keratinophylic fungi

Live in stratum corneum

Tinea capitis

Caused by all dermatophytes except

epidermophyton floccosum

Trichophyton concentricum

Trichophyton memtagrophytes variety interdigitale

Pt group

Disease of school going child

Types

1. Grey patch TC

Ectothrix

Microsporum species

Scaly itchy scalp

Alopecia and grey luster less hair

Woods lamp

Green fluorescence

2. Black dot TC

Endothrix infection

Hair breaks at scalp surface

No scaling of the scalp

Trichophyton species

3. Kerion

Tender, cystic, boggy swelling with pus discharge through multiple hair
openings

Heals with scarring Alopecia

Zoophilic and geophilic organisms like

Microsporum memtagrophytes variety memtagrophyte

Or microsporum canines

4. Favus

Endemic in J and K

Trichophyton schoenleni

Yellow colored cup shaped crusts pierced in the center with the hair

These crusts are also ka Scutula

Koh : air bubbles within hair shaft

Griseofulvin is the Doc

For kerion: add a short course of steroids

For favus: screen and treat other close contacts coz it is endemic

Most common etiology of TC

Worldwide: microsporum

India: trichophyton violaceum

USA: trichophyton tonsurens

Most common dermatophyte causing human infection: T. Rubrum

Most common dermatophytoses is T. Pedis

Tenia is aka ring worm

Annular, central clearing, peripheral itchy scaly Excoriations

Tinea incognito

Modified by topical steroids or systemic steroids

Itching and redness is less but spread is more

T. Rubrum

Red color in culture medium

Lesions can be white, red black

T. Pedis

3 types

Moccasin : dry / scaly, caused by rubrum

Bullous type: multilocular, caused by T. Memtagrophyte

Interdigital: athletes foot, caused by rubrum

T. Mannum

Unilateral, erythema, scaling, itch

Most scales apparent within creases

Onychomycosis / T. Ungum

Proximal onychomycosis , least common, marker of HIV

Distal onychomycosis , most common

White onychomycosis : superficial onychomycosis

Distal onychomycosis

Discoloration

Crumbling

Tunnels

Sub ungual hyperkeratosis

White onychomycosis

Caused by T. Memtagrophyte

Rest all caused by rubrum

Rx

Terbinafine

6 weeks for finger nails

12 weeks for toe nails

Griseofulvin used to be given

6 months for FN

12 months for TN

Candidiasis

Predisposing conditions
Normal commensal

Becomes pathogenic due to

Local factors

Denture

Obesity

Systemic factors

DM

HIV

Uremia

Broad spectrum ABX therapy

Malignancy

Morphology

Erythematous plaques and not a white plaque

Satellite pustules surrounded it

Intertriginous areas

KOH shows pseudo hyphae

Deep cutaneous mycosis

Sporotrichosis

Etiology: Sporothrix schankeii

Inoculation of wooden implant

Rose gardener disease

Nodules and ulcer

In 15% , only at site of inoculation: fixed cutaneous sporotrichosis

In the rest

Along the lymphatics, linear lymphatic spread

Known as Sporotrichoid pattern

Biopsy

Foreign body granuloma

Eosinophilic material

Cigar shaped fungal bodies

Treatment

Ostracon azalea is the new treatment

Earlier saturated solution of KI

Chromoblastomycosis

Verrucous cauliflower like masses

Caused by pigmented fungi

Eg. Phialophora verrucosa

Treated by surgery plus antifungals

T. Cruris

Jock itch or Dhobi itch or eczema marginatum