Treatment of Psoriasis by phototherapy

1. Gockerman's regimen

Tar + UV light

2. Ingram's regimen

Anthrlin + UV exposure

Eczema= dermatitis

Group of inflammatory skin diseases with similar clinical and

Histopathological presentation 💥💥

Clinical features of acute eczema

Itching

Papules

Vesicles

Oozing

Crusting

Erythema

Edema

Chronic eczema clinical features

Chronically itchy

Lichenified

Histopathology

Acute eczema

Fluid droplet accumulation in between the epidermal cells: spongiosis

Chronic eczema

Hyperkeratosis

Acanthosis

Chronic infiltrate in dermis

Classification of eczema

Two categories

Exogenous
Endogenous

Exogenous eczema

Divided into two groups

1. Irritation causing chemicals: irritant contact dermatitis ICD

Depends on the irritancy of substance like pH, concentration, temperature

Everybody is susceptible if sufficient conc used for sufficient duration

No prior exposure needed

No priming

No sensitization

No memory T cell

2. Prior exposure to chemical, sensitization: Allergic contact dermatitis

ACD

Individual susceptibility eg. Family history of Atopy

Delayed type HS

Thus requires prior exposure

Requires priming

Sensitization required

Memory T cells involved

ICD is more common than ACD

Cumulative ICD

Repeated exposure to sub acute damage

eg. Housewives eczema aka chronic hand eczema

Other examples of ICD

Nappy rash coz of urine and feces in diaper

Chemical burn

Thermal burn

Acute insect bite reaction

Most common cause of ICD are 1. Water 2. Detergents

Diagnosis

Patch test is not useful, infact harmful

Diagnosis of ACD

Patch test is confirmatory

Patch test

Apply the chemicals / allergens under occlusion

Site

Most preferred is back

Arm and buttocks can be used

Reading at 48 hours and rereading at 96 hours is recommended

Precautions

Do not test on inflamed skin coz penetration will be more and difficult to
take readings as already inflamed

Pt eczema should be reasonably controlled or else multiple false positive

reaction ka Angry Beck phenomena

Pt should not be on steroids/ immunosuppressants : false negative result

Positive site shows

Edema

Vesicles

Pustules indicating irritant reaction

Most common allergens

Nickel is the most common

Most common air borne allergen varies from country to country

India: Parthenium hysterophorus aka Congress grass (look for picture )

Most common allergen in females

Vegetables

Berloque dermatitis

Exogenous eczema because of photo allergic reactions to cosmetics

Classically eu de cologne

It contains Bergemot oil derived from a citrus plant, this produced the
Photosensitivity

Produces erythema and vesicles in acute stage

Chronic: pigmentation at the site of application

It felt as a black necklace

Berloque is is a trinklet/ charm/ necklace

Thus berloque dermatitis represents a linear, streaky pigmentation at the

site of cosmetic use

Aroma chemically means a closed ring structure, thus all can cause
photosensitive reactions

Melanosis is dark pigmentation due to long term use of cosmetics

Management of exogenous eczema

1. Identify, if possible, do a patch test

2. Removal/ protection

3. Topical corticosteroids + antihistamines

If severe: systemic corticosteroids or immunosuppressive drugs

Endogenous eczema

Atopic dermatitis

Atopy
A= out
Topy= place

Excessive and abnormal immune response

If involves skin: produces atopic dermatitis

If nares: allergic rhinitis

Bronchi: bronchial asthma

These 3 are called the triad of Atopy

Etiopathogenesis

Mostly same for all three

1. Strong family history

2. More in urban and industrialized societies than in poor countries: this is

ka Hygeine Hypothesis

If Child is born and within first 2-3 months exposed to several Ag, less
allergies develop

3. Increased IgE

4. Increased eosinophils

5. Increased RAST positivity to common household allergens, usually

many

Radio allergen sorbent test

Specific IgE seen

6. Decreased CMI: increased bacterial, fungal and viral infection

7. Abnormal vascular response

If skin stroked, normally wheal and flare response seen

In chronic urticaria : dermatographism, excessive response

In atopic dermatitis : white dermatographism due to vasoconstriction

White lines on stroking the skin

A pt has pigmented patch, it is stroked: wheal and flare reaction seen in

the patch

This is called as Darier's sign seen in urticaria pigmentosa

Thus urticaria pigmentosa is a cutaneous Mastocytosis

Central to Pathogenesis of Atopic dermatitis is increased TEWL

Trans epidermal water loss

Coz of this

Skin becomes dry and skin cracks

Through these cracks, entry of allergens and irritants

Irritants produce irritation and response is itching which leads to

scratching

As the scratching continues, more and more inflammatory mediators

accumulate resulting in a viscous cycle of itch- scratch- itch cycle

Leads to acute eczema in acute settings

In chronic conditions: Lichenification

Meanwhile allergens leads to sensitization and lead to further aggravation

of the vicious cycle

Clinical features
Usually seen after more than equal to 3 months of age

Xerotic skin

Acute and chronic eczematous lesion

Sites

In infantile phase, upto 2 years

Face> trunk> extensors of extremities

Childhood phase 2-12 years

More lesion on the flexure aspect

Adult phase

Flexures but localized

Flexures typically affected are ante cubital fossa, most typical

Popliteal fossa

Neck

Submammary folds

Spare axilla and groin

Stigmata of Atopy

Dry dandruff

Lateral madarosis aka Hertoghe's sign: lateral half of eyelids are lost and
underlying skin shows sclerosis

Accessory and deep lines under the eyes aka Dennie's lines or Dennie
Morgan folds

Keratoconus

Anterior sub capsular cataract

Peri orbital darkness aka allergic Shiner

Or peri orbital pallor aka Headlight sign

Horizontal groove on the dorsum of nose called Allergic salute

Ill defined, finely scaly, hypo pigmented macules: Pityriasis Alba

Recurrent lip eczema / dermatitis

Recurrent ear lobe dermatitis

Recurrent nipple dermatitis

Hyperkeratotic follicular papules over extensor: Keratosis pilaris

Antenna sign: central plug of keratin jetting out like an antenna

Hyper linear palms indicates hyper responsive immune system

Pt. CMI is decreased and viral infections common

HSV infection is severe in Atopy

Umblicated necrotic vesicles which are extensive ka Eczema Herpeticum

aka Kaposi's Varicelliform eruption

Rarely also seen in other conditions like

Seborrheic dermatitis

Reiter's dermatitis

Darier's disease

Compare eczema Herpeticum with

Eczema vaccinatum

Severe widespread vesiculopustular necrotic lesions after vaccinia

virus( used for small pox vaccination) inoculation in atopics

It is specific for vaccinia virus and not vaccination

Management

Diagnosed by clinical signs based on criteria and no lab test is diagnostic

Biopsy will only tells whether acute or chronic atopic eczema

Hanifen and Rajka criteria

1. Itchy rash which is chronic or chronically relapsing( no itch, no Atopy)

2. Typical morphology and distribution for age

3. Family or personal history of Atopy

Minor criterias

All the points discussed above like stigmata, IgE etc.

Thus atopic dermatitis is an Itch that rashes

Or
Itch is the disease

Treatment
1. Reduce the transdermal water loss TEWL

Emollients like oils, paraffin etc

2. Avoidance of irritants like soaps, woolen and fiber clothes, hot water

3. Antihistamines

4. Topical CS

5. Topical tacrolimus/ Pimecrolimus: Calcineurin inhibitors

If very severe

Immunosuppressants

Oral CS

In adults, phototherapy

Thus pt ??

Seborrheic dermatitis

Endogenous dermatitis of Seborrheic areas

Thus two concepts

Typical sites

Typical morphology

Typical sites

Scalp

Central face

Nasolabial fold

T zone of face

Central chest

Upper back

Typical morphology

1. Erythema topped with greasy, dirty looking, yellowish, adherent scales

2. Increased prevalence in Parkinson's disease, Mental retardation,

stroke, Down's syndrome

Increased incidence in HIV

3. Seborrhea is not necessary (+/-)

4. Males> females

5. Increased no. of Malessezia species(pityrosporum ovale, commensal

skin fungus) but a controversy persists whether it is the cause or a result
of the disease

More likely to be the cause

Blepharitis is also an associated feature

Treatment
Mild steroids( avoid halogenated potent steroids)

Topical antifungals containing ZPTO Zn Pyrithion, Ketoconazole, selenium

sulfide

Systemic antifungals

Cradle cap is a type of Seborrheic dermatitis in infants

Nummular dermatitis aka discoid eczema

Coin or disc shaped

Endogenous dermatitis with coin shaped or discoid lesions

Xerotic eczema/ Asteotic eczema/ Eczema Craquealae

Old age

Extensor aspect of limbs

Winter season

Dry and cracked lesions: Crazy paving pattern

Lichen simplex chronicus

Circumscribed neuro dermatitis

Idiopathic disorder

History of chronic localized itching

Classically at sites like

Wrist

Ankle

Knee

Elbow

Neck

Genitals

Nerve endings usually become bulbous in any chronic itching condition

Pompholyx
Earlier ka dyshydriotic eczema

Recurrent, deep seated, itchy, sago grain like( tapioca) vesicles on hands/
feet/ finger/ toes

Pompholyx means bubbles

Some pts are atopic

Some can have nickel HS

Poison ivy dermatitis

Toxicodendron is the poison family

It is not a contact dermatitis

It is a ACD

Airborne allergic dermatitis

Exposed parts

Drug induced P. Rosea

Gold, Arsenic, bismuth, lithium, metronidazole , barbiturates, captopril,

methopromazide

Lichen nitidus

Idiopathic

Asso with Lichen planus are controversial

Clinical features

Minute, pin head size, shiny, hypo pigmented or skin colored papules
arranged in groups over wrist, hand, extensor extremities and genitals

Biopsy reveals Claw clutching a ball appearance

Epidermis shows basal cell degeneration

Epitheloid cells

Lymphocytes, elongated rete ridges

May be self limited

Treatment with topical steroids if needed

Lichen striatum
Small ,1-3 mm papules

Could be shiny, erythematous or finely scaled

Arranged in 1-3 cm linear bands of papules usually over extremities

Seem to follow the lines of Blaschko( lines of migration of cells in embryo)

Follow patterns, on the front of the trunk, linear and S shaped on flanks
and overall pattern like a fountain spray.

Importance is that cutaneous mosaic disorders or Nevi follow these lines

of developmental migration

Evidence suggests that it could be a viral infection

Etiology not known

Self limiting

May be longer duration(6-12 months)

Pastia lines are linear petechiae in folds of skin seen in scarlet fever

Figurate erythemas

1. Erythema multiforme

Etiology

HSV>>>>>>mycoplasma and other infections >>>> drugs

Morphology

Target lesion/ bulls eye lesion/ iris lesion

Violaceous then white the red

classical sites are

Acral: extremities, palm, soles, genitals

Facial : lips

Earlier erythema multiforme, SJS and TEN were considered a spectrum.

Now EM is separated from the two.

SJS/ TEN are most severe drug reactions

Characterized by

Cutaneous purpuric macules(incomplete target lesions while EM have

complete)

Peeling of epidermis That is

Epidermal detachment

Or

Epidermal peeling sign

Or

Pseudo nikolsky sign

In SJS, less than 10% of BSA affected

In TEN, more than 30%

In between it's called transitional TEN or SJS/TEN overlap

SJS/TEN are almost always drug induced

Antilepileptics: phenytoin, carbamazepine and there may be an overlap

amongst these thus valproate may be used

Antibiotics: sulfonamides

Treatment

Remove offender

Supportive treatment

Erythema migrans/ erythema chronicum migrans

Slowly enlarging annular erythema

Asso with Lyme's disease: Borrelia Burgdoferri

It may be seen in primary disease around the site of tick bite and later in
secondary disease as multiple similar small lesion all over the body

Erythema marginatum
Associated with Rheumatic fever

Transient, evanescent, asymptomatic, reticular erythema

Chicken wire appearance

Becomes more apparent on heat application or exercise

Erythema gyratum repens

Associated with malignancies

Most common and characteristic with Ca lung

First reported with Ca breast

Morphology

Cut section of tree trunk: wood grain pattern

Concentric ring of erythema and scaling

Chronic itching

Treatment of underlying cause

Erythema annulare Centrifugum

Reactive phenomena Associated with drugs> infections >malignancies

Malignancies are uncommon if not rare

Morphology

Annular erythema with a trailing scale

Thus Inner edge has scales

Biopsy

Extravasation of RBC and Coat sleeve appearance of perivascular

lymphocyte

treat the underlying cause

Necrolytic migratory erythema

Presents with

Peri orificial necrosis and erosion

Paraneoplastic condition associated with Glucagonoma

Granuloma annulare

Associated with DM( not seen in all)

Morphology

Skin colored, asymptomatic, papules which coalesce together in annular

configuration with central clearing

on stretching the skin, individual papules

Can be appreciated

Site

Knuckle areas of joints of hand and feet, dorsal aspect

If the lesions are traumatized, some patients have resolution

Ka Reverse Koebners phenomena

In few cases, In Vitiligo pts, undergoing surgical treatment, there is

repigmentation of non operated sites: Remote Reverse Koebners
phenomena

Urticaria and Angioedema

Urticaria involves superficial dermis

Angioedema involves deep dermis or subcutis

Urticaria divided into acute and chronic, time line being 6 weeks

Types and causes

Acute urticaria due to drugs, food, infections

Urticaria can be mediated by contact: contact urticaria

Can also be caused by non immune mechanism

Eg.

Radio contrast medium

Urticaria pigmentosa

Mastocytosis

Darier's sign

Pt can have a heat or cold urticaria

Solar urticaria: only on sun exposure

Cholinergic urticaria: increased Ach discharge or stress like exercise,

sweat, heat, sunlight

Will be associated with sweating

Vibratory urticaria

Delayed pressure urticaria: on removal or on continued pressure( tight

belt)

Most common cause

Chronic Idiopathic urticaria

Urticaria is associated with wheals

Treatment

H1 antihistamines

Initially non sedatives are preferred

Increase the dose

Add another anti histamine

Add H2 blocker

If nothing works

Steroids or immunosuppressants

Hereditary angioedema

Recurrent

Family history

H/o abdominal pain and angioedema

NO ITCHING

Lip, eye, tongue, glottic swelling( medical emergency)

Type 1 Hereditary Angio Neurotic edema HANE

Quincke's disease

Due to C1 esterase inhibitor deficiency

Type 2

C1 esterase inhibitor is normal in amount but function abnormal

Type 3

C1 esterase inhibitor with normal amount and function

Seen in females

??? Asso with hormones

First investigation

C4 levels is the screening test

Treatment

Type 1: replacement therapy with C1 EI concentrate or if required, FFP for

acute episodes

Type 2 has same treatment

Type 3: danazol

Sexually transmitted diseases

Not all infections cause disease or symptoms

Hence the preferred term is STI

Venereal disease is an old legal term for classical STD's

Many organisms produce similar signs and symptoms or Syndromes

Eg.

Genital ulcers

Urethral discharge

Inguinal nodes

Approach to treatment : Syndromic treatment

Treat all the common cause of the syndrome without etiological

confirmation

Genital ulcer disease syndrome

Can be caused by

Chancre: treponema pallidum,

Chancroid: H. Ducrei , painful

Herpes HSV 2>1, painful

Donovanosis= Granuloma inguinale caused by Calymmatobacterium /

Klebsiella granulare

Lympho granuloma venereum LGV: C. Trachomatis L1,L2,L3

Try to differentiate between these causes on the basis of

incubation period

Lesional features

Lymph node enlargement

Chancre of primary syphilis

IP is 9-90 days and average of 3 weeks

Thus pt presents around 1 month of contact

Lesional features

Chancre is single, painless, punched out ulcer with sharp borders and
clear granulation tissue on the ulcer floor

Non tender

Does not bleed

Firm/ cartilaginous/ button like/ indurated/ nickel in flannel feel

Lymph node

Bilateral

Symmetrical

Multiple

Firm

Freely mobile

Discrete

Painless

Non tender

Non fluctuant thus No abscess formation

Non matted

Thus all put together: Shotty LN

Chancroid
Opposite of chancre

IP is short, 3-10 days

Lesion

Multiple

Painful

Undermined borders: ulcer much deeper than visible on surface

Dirty necrotic tissue on the floor

Tender to touch

Bleeds on manipulation

Absolutely soft thus aka soft sore/ soft chancre

lymph node

Usually unilateral

Painful and tender

Fluctuant and abscess forming

Adherent to the overlying skin

All above combined is called a Bubo

It ruptures through a single sinus

It infects surrounding skin forming a giant chancroid

Thus it is a ruptured inguinal Bubo

LGV

IP = 3-30 days

Lesion

Transient or absent

Thus it is a GUD without a GU

If at all seen, herpetiform vesicle

Lymph node

Unilateral

Painful and tender (genital ulcer is painless)

Abscess forming

More matting

Multilocular abscess

Multiple discharging sinuses

No infection of surrounding skin

Lymph nodes above and below the inguinal ligament are affected

sign of groove seen on lateral view

Granuloma inguinale/ donovanosis

IP = 8-80 days

Lesion

Starts as a painless papule

ulcerates

Becomes a Granulomatous mass which has a beefy red surface, is

friable( bleeds easily)

Gradually lesion develops overhanging everted edges

Now resembles squamous cell Ca morphology

Lymph nodes

Not enlarged

Uncommonly a granuloma may be formed in the sub cutaneous tissue in

the inguinal area ka Pseudo Bubo

Herpes Genitalis

HSV 2>> HSV 1

IP= 6-21 days(1-3 weeks)

Clinical features

When HSV enters, seroconversion happens

First episode/ Primary is either asymptomatic or severely symptomatic

In HSV 2 infections, 50% are symptomatic

Recurrences are usually less severe than primary If it happened at all

Clinical features are

Grouped vesicular eruptions which in primary are more numerous, deeper,

punched out, more pain and tenderness, more systemic features

Lymph node may be bilateral, tender, firm

Duration of 3-4 weeks

Recurrences are less in number

Superficial

Serpiginous erosion

Less pain

Less systemic features

No lymph node or unilateral if at all

Duration of 1 week

Syndromic management of genital ulcer disease GUD

If H/o recurrences and grouped vesicles

Treat with acyclovir

If absent

Treat for Chancre + chancroid

Chancre treatment is injection benzathine penicillin 2.4 million IU IM

divided on two buttocks

Chancroid: Azithromycin 1 gm stat

Urethral discharge syndrome

In males

Etiology

N. Gonorrhea

C. Trachomatis (D-K)

Generally speaking, gonorrhea is more symptomatic than chlamydia but

not always and reverse can be true

30-50% pt may have co infection

This dual antibiotic treatment for all pt

Gram stain of the discharge showing Intracellular gram negative

diplococcus is almost 90% sensitive and specific in male urethra but
unreliable in throat, cervix and rectum

NACO recommendation

Cefixime tab 400 mg for gonorrhea stat

Azithromycin 1 gm stat

Vaginal discharge syndrome

Always do a speculum examination

Decide whether a VDS or a cervical DS

If VDS

Candida

Trichomonas

Bacterial vaginosis

Treat by

Tab fluconazole + tab Secnidazole 2 gm stat

If no speculum exam done or pt or her partner is high risk, treated for

both VDS and CDS

If cervical

N. Gonorrhea

C. Trachomatis

Urethritis in females is caused by coli forms

Inguinal Bubo syndrome

Etiology

Chancroid + LGV

Tab azithromycin for chancroid

Tab doxycycline 100 mg bd for 21 days

Scrotal swellings
Epididymitis

Etiology

Gonorrhea and chlamydia

(Treated by single dose azithromycin and cefixime according to doctors

manual)

But

This has to be followed

Cefixime 400 mg bd for 7 days

Doxycycline 100 mg nd for 14 days

Lower abdominal pain

PID

Etiology

N. Gonorrhea

C. Trachomatis

Anaerobes

Cefixime+ azithromycin + Secnidazole

Cefotetan can be given as cefixime won't be sufficient

Genital warts
HPV 6>>>11

16,18,31,33,51 etc

Condyloma Acuminata

Rough irregular filiform surface

Or

Irregular raspberry like masses

Diagnosis is clinical

Treated by Podophyllin

In pregnancy, cryotherapy done

World over

Herpes is the most common STD according to WHO

NACO says Chancre is the most common

Thus choose gonorrhea more than syphilis

In USA , HPV is the commonest STI

Secondary syphilis

Follicular syphilae: itchy rash

Primary syphilis

Extragenital chancre, most common on lip

Absent in Syphilis d'emblee

Direct intravascular inoculation , produces secondary without primary

syphilis

Coronal sulcus is the most common site in males

Mucous patch

Many merge

Irregular margins

Snail track ulcer

Condyloma lata

Flat topped, greyish, macerated, oozy papules over muco cutaneous

junctions

Eg.

Anogenital skin

Differentiate with C. Acuminata

Moth eaten Alopecia, non scarring

Hypo pigmented/ depigmented lesion on neck ka Circle of Venus

S2 (secondary syphilis) lesion along the hairline is called Corona Veneris

Posterior hair line ends below C4

Maximum possibility of isolating treponema pallidum is in secondary

syphilis

Infectivity of the lesion

Mucous patch> C. Lata> Chancre> other secondary lesion

After 8-12 weeks

Secondary heals

Pt has no sign symptoms but VDRL continues to be positive

This is latent syphilis

Upto two years, early latency

25% of these relapse usually within one year! as they relapse! the lesions
are mainly of secondary type but rarely can develop at site of healed
chancre: Chancre Redux

Late latency is beyond 2 years

70% remain latent

30% developing Into tertiary either : gumma, CNS, cvs involvement

Tertiary syphilis

Treponema difficult to isolate

Benign tertiary syphilis is called gumma or gummatous symphilis

Most commonly located on shin area

Clinically punched out ulcer

Floor covered with sticky, wash leather slough: gummy mass

Heal with tissue paper scars

As one heals, other one pops up in the periphery

Gumma can also affect brain

Congenital syphilis

Treponema pallidum is shown to cross the placenta throughout the

pregnancy but no disease is caused in the first trimester

Syphilis is not a cause of first trimester abortion, >16 weeks

Kassowitz law

Serially improving outcomes of pregnancies

Infectivity is continuously going down

Congenital syphilis divided into

Early: <2 years

Late: >2 years

Stigmata

Early CS
History of LBW

Hematological picture: hemolytic anemia

Leukopenia

Thrombocytopenia

Lympho reticular

Generalized lymphadenopathy

Hepatosplenomegaly

Jaundice

Muco cutaneous features

Running nose with blood discharge: Snuffles

This is because of septal perforation and later forms the stigmata of

depressed nasal bridge

Pt can have S2 type rash usually by 3-4 weeks of age

Rarely at birth or within first week: vesico bullous lesion in hands and feet
ka Syphilitic pemphigus

C. Lata or mucous patch could be present

Musculoskeletal features

Osteochondritis usually within first six month of life

Severe pain

Refuses to move limb: Pseudo paralysis of Parot

X ray of knee joint shows irregular radioluscency at upper medial tibia

Cat bite sign aka Wimberger sign

Late congenital syphilis

Most common presentation is interstitial keratitis

Called as Salmon patch in the vascular phase

Gumma like lesion or gumma

If present in palate or bones is called Parot's nodes

CVS is generally spared

Osteochondritis is not seen

Only osteitis and peri osteitis may be seen

Certain tell tale signs

Stigmata

Cranio tabes

Frontal bossing

Olympian brow

Interstitial keratitis

Hutchinson's teeth

Nerve deafness

Above three constitute hutchinson's triad

Mulberry molars

Depressed nasal bridge

Peri oral furrowing: Rhagades

High arched palate

Short little finger: Dubois sign

Increased carrying angle of elbow

Higemonakis sign: swelling near medial end of clavicle

Sabre shin: bent tibia

Salt pepper fundus

Clutton's joint: both knees involved, seen in congenital, don't confuse

with Charcot's joints seen in tertiary

Investigation

For ulcerated vesico bullous lesion

Chancre or C. Lata

Dark field microscopy

All cases of suspected sexually transmitted genital ulcer should be

first investigated with dark field microscopy to rule in or rule out of
syphilis

Not very useful in mucosal lesions as difficult to differentiate with the

commensal treponema

Serological test for syphilis STS

Two types

Non treponemal: non specific

VDRL

RPR

Treponemal: specific

TP immobilization test TPI

TPHA

FTA ABS

New tests

TPPA particle agglutination

EIA enzyme immuno assay

Traditional method

Screen with RPR or VDRL

Confirm with TPHA / FTA ABS

Reverse sequence testing

As incidence is going down

Screen with TPPA/ EIA

if negative, pt considered normal

If positive, non treponemal test

If positive

Syphilis

Or treated syphilis if negative: do another confirmatory test

Like TPHA / FTA

VDRL / RPR

RPR > VDRL for non treponemal test

VDRL is used for CSF

IP for VDRL is 4-6 weeks of incubation

Average IP of chancre is 3 weeks

Thus VDRL would be negative in initial two weeks

Thus dark ground microscopy has to be done

False positive VDRL

Old age

Infectious mononucleosis

Lepromatous leprosy

SLE

Pregnancy( probably not increased any more than normal but traditional
false positive)

HIV is not a cause here

False negative VDRL

Incubation period of initial two weeks

Very high levels of Ab and blocking Ab, no flocculation seen, pro zone
phenomena: do in serial dilutions: then would be positive

Titers follow/ parallel the disease activity and these can be done to follow
up the pt unlike treponemal test which are positive for life

Specific / Treponemal tests

Traditionally TPHA was considered most specific

FTA ABS : most sensitive and first serological test that is positive

Currently

In sensitivity

TPPA/EIA > FTA> TPHA

Specificity

TPPA/EIA > TPHA> FTA

IgM FTA ABS

First test to be positive

May be important for congenital syphilis but no commercially formulation

available

Rx

Primary

Secondary

Early latency

Early relapsing syphilis

All above are early syphilis

Injection benzathine penicillin 2.4 million IU single dose

Late latent

Gumma

Treated by

Inj benzathine penicillin 2.4 million IU weekly for 3 weeks

Thus total dose of 7.2

Neurosyphilis

Ocular syphilis

Aqueous crystalline penicillin G IV infusion

For CVS syphilis

Same as late syphilis but under the cover of steroids to prevent

cardiovascular collapse

Congenital syphilis

Treated by equivalent doses of penicillins

Either

Benzathine or crystalline

Some ppl prefer procaine penicillin

Important aspect is to treat whom

1. Cases of confirmed congenital syphilis

2. Presumed congenital syphilis

All of them have to have a VDRL positive mother

If mother had no treatment:

If treated within 4 weeks of delivery

Treated with a non penicillin regime

If VDRL of infant is four fold higher than mother

IgM FTA ABS positive

TPHA of infant is of no use in an infant as it is positive because of mother

Pregnant patient with syphilis

Penicillin only

If penicillin allergy

Desensitize and give a full dose of penicillin

But now NACO says

Erythromycin + treat the baby at birth with penicillin as transfer not

prevented by erythromycin

Obliterative end arteritis and plasmacytic infiltrates are seen in all stages
of syphilis

Other STD related points

Chancroid
Intradermal test called ITO test, outdated

No serological test for chancroid

Gram stain shows a school of fish, tram track, rail road, red snapper
appearance

Other investigations

Gram stain has about 50% sensitivity

Biopsy was the traditional gold standard

Now WHO says gold standard is culture

Treated by azithromycin

HSV
Gold standard is viral culture

Serology not very helpful

Tzanck smear: multi nucleated giant cells

LGV
Intradermal test: Frei's test, outdated

Investigation

Most important is LCR> PCR

These are nucleic acid amplification test NAAT

If can't be done

Go to serology

MIF> CFT

In females and receptive MSM

Inguinal Bubo syndrome is seldom seen

Coz in female, deep part of introitus and cervix drains into peri rectal and
iliac nodes rather than inguinal nodes

Esthiomine : giant elephantiasis of vulva , can occur in LGV

Pain

Tenesmus

Pus discharge from anus

Lymph discharge

Constipation

Pencil stool

Perforation

Peritonitis

Carcinoma

This is Abdomino rectal syndrome

Donovanosis
Diagnosis by touch smear

Tissue smear

Crush smear

Impression smear

Also done in cutaneous leishmaniasis

Intracellular bipolar staining bodies known as Donovan bodies

Closed safety pin appearance

Treatment of syphilis with HIV

Treat according to stage, no change in management

Leprosy

Annual new case detection rate

10.78/ lac population

Prevalence

0.68/10000 in 2011-12

0.73 in 12-13

Proportion of multi bacillary is 49.92%

Female: 37%

Children:10%

Visible deformity or grade 2 deformity is 3.45 %

Most common type in India : not possible to comment

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