Download File

SKIN
INFECTIONS
BACTERIA
 VIRUSES
 FUNGI

NORMAL SKIN FLORA
The resident flora of skin is a mixture of harmless
staphylococcus epidermidis, corynebacterium
spp.,propionibacterium spp.,brevibacteium spp.,
malassezia spp.
 In a minority, carry it in their nostrils, perineum or
armpits.

BACTERIAL INFECTIONS
PYODERMAS :
Infections of skin and appendages commonly by
S.aureus,Strep.pyogenes or both.
 S.Aureus
NonfollicularBullous impetigo, impedigo contagiosa*, ecthyma*
Follicularsuperficial folliculitis, deep folliculitis, furuncle, carbuncle
 Strep.pyogenes
Localizedimpetigo contagiosa*,ecthyma*
Spreadingerysipelas, cellulitis

*-Caused by one and/or both the organigms
IMPETIGO
Types:
impetigo contagiosa
Bullous impetigo
Causes
 Staphylococci, streptococci, or
by both together
 Bullous type is usually caused
by Staphylococcus aureus
 The crusted ulcerated type is
caused by β- haemolytic strains
of streptococci.
 Highly contagious
IMPETIGO CONTAGIOSA









Epidemiology:
 Prevalence: Frequent, often occuring in epidemics.
Age :preschool and young school children
Gender:adults,male>females
Clinical features:
Thin walled bulla on an erythematous base , ruputres rapidly to
form an exudative plaque covered with honey –colored crusts.The
lesion spreads peripherally without central healing and many
lesions may coalesce to form polycyclic plaque.Removal of the crust
reveals an erosion.
Usually multiple lesions, particularly around the face.
Regional lympadenopathy is frequent,
Constitutional symptoms may occur
Complications: Acute glomerulonephritis
PRESENTATIONS
BULLOUS IMPETIGO


Epidemiology: Sporadic
Age: new borns and infants

Clinical features:
Bullae, containing turbid fluid, without an erythematous
halo,rupture after few days to form thin, varnish like
crusts.Lesion may heal in the center to form annular
plaques.
Mucous membranes may be involved.
Site: face and other parts

Complications:





lymphadenopathy
staphylococcal scalded skin syndrome
DIFFERENTIAL DIAGNOSIS
Herpes simplex
 Eczema
 Scalp lice
 Bullous/contagiosum

INVESTIGATION


Diagnosis is usually made on clinical grounds
Gram stains or swabs are sent to the laboratory
for culture, but treatment must not be held up
until the results are available.
TREATMENT

General measures:

local hygiene,gentle removal of the crust after softening
with topical agent and compressing thems and application
of a topical antibiotic such as neomycin, fusidic acid
mupirocin or bacitracin is effective.
Systemic antibiotics (such as flucloxacillin,amoxyclavulanic acid, erythromycin or cefalexin) are needed
for severe cases
 If a nephritogenic strain of streptococcus is suspected
(penicillin V).

FURUNCULOSIS (BOILS)

A furuncle is an acute pustular infection of a hair
follicle, usually with Staphylococcus aureus
PRESENTATION AND COURSE
A tender red nodule which enlarges
 Later may discharge pus
 Its central ‘core’ before healing leave a scar
 Site-face, axillae, buttocks and perineal region
 Most patients have one or two boils
 The sudden appearance of many furuncles
suggests a virulent staphylococcus including
strains of community- acquired MRSA.

CHRONIC FURUNCULOSIS

Susceptibility of follicles or colonization of nares
or groins by pathogenic bacteria.
PREDISPOSING FACTORS
Nasal or perineal carriage
 Diabetes,hiv
 Underlying skin disease-scabies, atopic dermatitis

COMPLICATIONS

Septicemia
DIFFERENTIAL DIAGNOSIS


Based on clinical diagnosis
Hidradenitis suppurativa should be considered if
only the groin and axillae are involved.
INVESTIGATIONS IN CHRONIC
FURUNCULOSIS
General examination: look for underlying skin
disease (e.g. scabies, pediculosis, eczema).
 Test the urine for sugar.
 Full blood count.
 Culture swabs from lesions and carrier sites
(nostrils, perineum) of the patient and immediate
family. Test both to identify the organism and to
evaluate sensitivity to various antibiotics.
 Immunological evaluation only if the patient has
recurrent or unusual internal infections too.

TREATMENT
Acute episodes moist hot fomentation,topical antibiotics
 simple incision and drainage.
 An appropriate systemic antibiotic is needed
when

Many furuncles are erupting
 When fever is present or
 When the patient is immunosuppressed

Daily bath using an antiseptic soap.
 Improve hygiene and nutritional state
 Chronic: antibiotics topical and systemic

STAPHYLOCOCCUS SCALDED SKIN
SYNDROME(SSSS)
Erythema and tenderness are followed by the
loosening of large areas of overlying epidermis
 In children, the condition is usually caused by a
hematological spread of exotoxin produced by
staphylococcal infection elsewhere (e.g. impetigo
or conjunctivitis or otitis)which cause split in
upper layers of epidermis.
 No mucosal involvement
 Good prognosis


In adults with widespread
exfoliation, consider toxic
epidermal necrolysis
Staphylococcal scalded skin
syndrome in a child.
The overlying epidermis is loosening
in the red areas
INVESTIGATION AND TREATMENT
Gm stain and culture
 Supportive and nursing care
 Systemic antibiotics iv then later
oral drugs(antistaph.)

CARBUNCLE







A group of adjacent hair follicles becomes deeply
infected with Staphylococcus aureus
Swollen painful suppurating area of discharging
pus from several points. Commonest site back and
neck and thigh
The pain and systemic upset are greater than
those of a boil.
Diabetes and Sys.steroid therapy must be
excluded and Pus culture should be done
Treatment needs both topical and systemic
antibiotics(flucloxacillin or other penicillinase
resistant antiiotics).
Incision and drainage have been shown to speed
up healing, although it is not always easy when
there are multiple deep pus-filled pockets.
Consider the possibility of a fungal kerion in
unresponsive carbuncles.
TOXIC SHOCK SYNDROME








Life threatening disease
A staphylococcal toxin is also responsible for this condition
Mostly in females during or imediately after menstuation and is
associated with use of highly absorbent intravaginal tampons.
High fever , systemic upset (myalgia, headache, sore throat and
vomiting),generalised erythematous blancing rash and
hypotension
Multisystem involvement withen hrs
Erythema – and sometimes circulatory collapse
A week or two later- characteristic desquamation, most marked
on the fingers and hands.
Immediate resuscitation ,systemic antibiotics (fluclox or
vancomycin) and irrigation of the underlying infected site are
needed.
STREPTOCOCCAL INFECTIONS
Erysipelas
 Cellulitis
 Necrotizing fasciitis

ERYSIPELAS
It is superficial spreading puoderma while cellulitis
is deeper and often the 2 coesist.
 The causative streptococci usually gain their entry
through a split in the skin (e.g. between the toes or
under an ear lobe).


The first warning of an attack

Malaise
 Shivering
 Fever
After a few hours the affected area of skin becomes

 red,
and the eruption spreads with a well-defined advancing edge.
Blisters may develop on the red plaques.
 Untreated, the condition can even be fatal.
 It responds rapidly to systemic penicillin.

Erysipelas
CELLULITIS








This inflammation of the skin occurs at a deeper level than
erysipelas.
The subcutaneous tissues are involved and the area is more
raised and swollen.
The erythema is less marginated than in erysipelas.
Cellulitis often follows an injury,most common site is lower limbs
Favours areas of hypostatic oedema.
Streptococci, staphylococci or other organisms may be the cause.
Treatment is elevation, rest,NSAIDS – sometimes in hospital
Systemic antibiotics-Penicillin(erythromycin),if recurrent
chemoprophylacis with long acting penicillin (benzathine
penicillin)
Cellulitis
Leprosy




Leprosy (Hansen's disease) is a chronic granulomatous disease
affecting skin and nerve.
Causative organism:
Mycobacterium leprae(AFB)
Infection:
 nasal droplets followed by haematogenous spread to skin and
nerve.
The clinical features depend on the immunological status of the host
and not on the virulence of the organism :
good cell mediated response -localized infection
poor immunological response -generalized inf.of skin along with
visceral involvement seen.
PATHOGENESIS




At the tuberculoid pole,
well-expressed CMI and delayed hypersensitivity control bacillary
multiplication; organised epithelioid granulomas are seen in tissue
biopsies.
Th1-type response to M. leprae, producing interleukin-2 (IL-2) and
interferon-γ (IFN-γ), and positive lepromin (a soluble M. leprae
preparation) skin tests. This strong cell-mediated response clears antigen,
but with local tissue destruction.
In the lepromatous form,
there is abundant bacillary multiplication in Schwann cells and the
perineurium.


have a specific cell-mediated T-cell and macrophage anergy to M. leprae
and poor lymphocyte responses to M. leprae antigens in vitro. They are
negative on lepromin skin testing. They produce Th2-type cytokines. Nerve
damage occurs across the spectrum in skin lesions and peripheral nerves.
Between these two poles is a continuum, varying from patients with
moderate CMI (borderline tuberculoid) to patients with little cellular
response (borderline lepromatous).
Classification
Lepromatous
Borderline lepromatous(BL)
Borderline
Borderline tuberculoid(BT)
Tuberculoid
CARDINAL FEATURES OF LEPROSY
Skin lesions, typically anaesthetic at tuberculoid end of spectrum
Thickened peripheral nerves
Acid-fast bacilli on skin smears or biopsy
PRESENTATION

Lepromatous leprosy
Skin


macules numerous, hypopigmented and erythematous or plaques,
papules, or diffuse infiltration of the skin occur.
In advanced cases: nodular lesion especially on ears face and
eyebrows are lost
 Leonie facies-thickened brow and lobes of the ear
Late features



Nerve enlargement and damage
Anaesthesia. In skin lesions the small dermal sensory and
autonomic nerve fibres are damaged, causing local sensory loss
(touch,heat,pain,numbness)and loss of sweating
(anhydrosis)within that area. First in the distal aspects of the
forearms and lower legs later ‘glove and stocking’distribution and
eventually over the trunk and face.
Weakness and wasting of muscles of hands feet and face




Testes atropy, impotence, gynaecomastia
Mucosa of nose mouth pharynx and larynx:rhinitis
hoarsenes, perforationof nasal septum and palate larygeal
obstruction.
Bones of hands feet and face: cystic lesions of phalanges
permitting fracture loss of upper incisor teeth and nasal
spine leaking to nasal collapse
Eye involvement. Blindness due to leprosy is a devastating
complication for a patient with anaesthetic hands and feet.
Eyelid closure is impaired when the facial (7th) nerve is
affected. Damage to the trigeminal (5th) nerve causes
anaesthesia of the cornea and conjunctiva. The cornea is
then susceptible to trauma and ulceration.
Tuberculoid leprosy: Depigmentation
with a palpable erythematous rim at
the upper edge.
The ‘leonine’ facies of lepromatous
leprosy
PRESENTATION

Tuberculoid leprosy

one or few solitary lesions in skin and peripheral nerves
Skin lesions

Macular or raised as plapues or as rings with flat center

The lesion is hypopigmented in dark skins coppery in pale skins

Well defined margin surface is dry and scaly

Lesion are of any size and occur any where

Loss of sensation is early and marked
Peripheral neuropathy.
o
Thickened nerves, sensory loss and dysfucn of muscles(asthenia)supplied
by that peripheral nerve

'sites of predilection'. ulnar (above elbow)nerve-claw hand

median (wrist or above elbow), radial (humerus) -wrist drop,

radial cutaneous (wrist),common peroneal (knee), posterior tibial

facial nerve as it crosses the zygomatic arch, and great auricular in the
posterior triangle of the neck.






Borderline or dimorphous(BLand BT)leprosy
Lesion are intermediate in character betn lepromatous and
tubrculoid or as a mixture of them
Borderline leprosy is unstable
Borderline lepromatous leprosy (BL) is characterised by
widespread small macules. They may experience both type 1 and
type 2 reactions. Peripheral nerve involvement is widespread.
Borderline tuberculoid (BT) The skin lesions are similar to those
in tuberculoid leprosy but are more numerous. Damage to
peripheral nerves may be widespread and severe. These patients
are prone to type 1 reactions with consequent nerve damage.
Pure neural leprosy This occurs principally in India and accounts
for 10% of patients. There is asymmetrical involvement of
peripheral nerve trunks and no visible skin lesions. On nerve
biopsy all types of leprosy have been found.
CLINICAL CHARACTERISTICS OF THE POLAR FORMS OF LEPROSY
Clinical and tissuespecific features
Lepromatous
Tuberculoid
Skin and nerves
Number and distribution
Widely disseminated
One or a few sites, asymmetrical
Poor
Never
Good
Common
Slight hypopigmentation
Slight erythema
Smooth, shiny
None
Impaired late
Marked hypopigmentation
Coppery or red
Dry, scaly
Common
Impaired early
Late
Early and marked
Skin lesions
Definition
Clarity of margin
Elevation of margin
Colour
Dark skin
Light skin
Surface
Central healing
Sweat and hair growth
Loss of sensation
Nerve enlargement
and damage
Late
Early and marked
Bacilli (bacterial
index)
Many (5 or 6+)
Absent (0)
Natural outcome
Progression
Healing
Other tissues
Upper respiratory mucosa,
eye, testes, bones, muscle
None
Reactions
Immune complexes
Cell-mediated
SPECTRUM OF LEPROSY
TUBERCULOID VS.
LEPROMATOUS LEPROSY
TUBERCULOID VS.LEPROMATOUS LEPROSY
LEPROSY REACTIONS


Leprosy reactions are events superimposed on the cardinal
features .Type 1 (reversal) reactions These occur in 30% of
borderline patients (BT, BB, BL) and are delayed
hypersensitivity reactions caused by increased recognition
of M. leprae antigens in skin and nerve sites.
Type 2 (erythema nodosum leprosum-ENL) reactions These
are partly due to immune complex deposition and occur in
BL and LL patients who produce antibodies and have a
high antigen load.
REACTIONS IN LEPROSY
Lepra reaction type 1
(reversal)
Lepra rection type 2
(erythema nodosum
leprosum)
Mechanism
Cell-mediated
hypersensitivity
Immune complexes
Clinical features
Painful tender nerves,
loss of function
Swollen skin lesions'
New skin lesions
Rarely fever
Tender papules and
nodules; may ulcerate
Painful tender nerves,
loss of function
Iritis, orchitis, myositis,
lymphadenitis
Fever, oedema
Management
Mild:aspirin 600mg 6hly
Severe:prednisoline 4080mg reducing over 39mths
Mild:aspirin 600mg 6hly
Severe: thalidomide2 or
prednisolone 40-80 mg,
reducing over 1-6
months; local if eye
involved3

Indicated for any new impairment of nerve or eye function.
1% hydrocortisone drops or ointment and 1% atropine drops.




Differential diagnosis
Skin The anaesthesia of tuberculoid and borderline
tuberculoid lesions differentiates them from fungal
pityriasis versicolor, vitiligo, post-inflammatory
depigmentation, psoriasis and eczema.
The presence of acid-fast bacilli in smears differentiates
lepromatous nodules from onchocerciasis, Kaposi's sarcoma
and post-kala-azar dermal leishmaniasis.
Nerves Leprosy is the most common cause of peripheral
nerve thickening. Uncommon conditions such as CharcotMarie-Tooth disease and amyloid are differentiated from
leprosy by the absence of skin lesions and acid-fast bacilli.
Comparison should always be made with nerves on the
other side. The causes of other polyneuropathies such as
HIV infection, diabetes, alcoholism, vasculitides and heavy
metal poisoning should all be considered where
appropriate.






Investigations
The diagnosis is clinical, made by finding a cardinal sign of
leprosy and supported by finding acid-fast bacilli in slit skin
smears or typical histology in a skin or sensory nerve
biopsy.
Skin lesions should be tested for anaesthesia.
The peripheral nerves should be palpated for thickening
and tendernessand motor and sensory test to be done.CNS
is unaffected.
Slit skin smears : The bacterial load is assessed by scraping
dermal material on to a glass slide. The smears are then
stained and acid-fast bacilli are scored on a logarithmic
scale: the bacterial index (BI). Smears are useful for
confirming the diagnosis and monitoring response to
treatment.
Lepromin test.
 This is of no use in the diagnosis of leprosy but, once the
diagnosis has been made, it will help to decide which
type of disease is present (positive in tuberculoid type).
Management
 PRINCIPLES OF LEPROSY TREATMENT
 Stop the infection with chemotherapy
 Treat reactions
 Educate the patient about leprosy
 Prevent disability
 Support the patient socially and psychologically
 All leprosy patients should be given an
appropriate multidrug combination. Patients can
be classified into paucibacillary (skin smearnegative tuberculoid and BT) and multibacillary
(skin smear-positive BT, all BB, BL and
LL).Multibacillary patients with an initial BI>4
need longer treatment and should be treated to
smear negativity(24mths)

MODIFIED WHO-RECOMMENDED MULTIDRUG THERAPY
REGIMENS IN LEPROSY
Type of
leprosy*
M onthly supervised drug
treatment
Daily selfadministered
drug
treatment
Duration of
treatment
Paucibacillar
y
Rifampicin 600 mg
Dapsone 100
mg
6mth
Multibacillary
Rifampicin 600 mg
Clofazimine 300 mg
Clofazimine 50
mg Dapsone
100 mg
12mth
Paucibacillar
y single-lesion
Ofloxacin 400 mg
Rifampicin 600 mg
Minocycline 100 mg




Single dose
WHO classification for field use when slit skin smears are not available
paucibacillary single-lesion leprosy (one skin lesion)
paucibacillary (2-5 skin lesions)
multibacillary (more than 5 skin lesions).
In this field classification WHO recommends treatment of multibacillary patients for 12
months only.






Patient education: Reassurance that after 3 days of
chemotherapy they are not infectious and can lead a
normal social life.
Prevention of disability
Physiotherapy can prevent contractures, muscle atrophy
and over-stretching of paralysed muscles. Anaesthetic feet
need protective footwear.
Social, psychological and economic rehabilitation .
Prognosis The majority of patients, especially those who
have no nerve damage at the time of diagnosis, do well on
MDT, with resolution of skin lesions. Borderline patients
are at risk of developing type 1 reactions which may result
in devastating nerve damage.
Prevention and control case detection and providing MDT.
BCG vaccination has been shown to give good but variable
protection against leprosy.
CUTANEOUS TUBERCULOSIS
CUTANEOUS TUBERCULOSIS
 Cutaneous
tuberculosis- is highly variable
in its clinical presentation, depending on
the immunologic status of the patient and
the route of inoculation of mycobacteria
into the skin.
 In most cases, the organism reaches the
skin via lymphatic or hematogenous
spread.
 Exogenous inoculation cutaneous
tuberculosis does occur.
CLASSIFICATION OF CUTANEOUS
TUBERCULOSIS

Exogenous Infection



Endogenous Spread






Primary inoculation tuberculosis (PIT): via
percutaneous inoculation, occurs at the inoculated site
in a nonimmune host( tuberculous chancre ).
Tuberculosis verrucosa cutis (TVC): via percutaneous
inoculation, occurs at the inoculated site in an
individual with prior tuberculosis infection.
Lupus vulgaris (LV)
Scrofuloderma (SD)
Metastatic tuberculosis abscess (MTA)/ tuberculous
gumma
Acute miliary tuberculosis (AMT)
Orificial tuberculosis (OT)
Tuberculosis due to BCG
Immunization(tuberculides)
EPIDEMIOLOGY

Age of Onset- AMT more common in infants and adults
with advanced immunodeficiency. PIT more common in
infants. SD more common in adolescents, elderly. LV
affects all ages.

Sex- LV more common in females. TVC more common in
males.

Race- Tuberculosis in blacks, in general, less favorable
prognosis than in whites.


Occupation- TVC: previously in physicians, medical
students, and pathologists as verruca necrogenica,
anatomist’s wart, postmortem wart; in butchers and
farmers from Mycobacterium bovis.
Etiology- The obligate human pathogenic mycobacteria:
M. tuberculosis, M. bovis, and occasionally, bacillus
Calmette-Guérin (BCG)
EPIDEMIOLOGY

Predisposing factors for tuberculosis includ


The type of clinical lesion depends on the route of
cutaneous inoculation and the immunologic
status of the host.


poverty, crowding, HIV infection.
Cutaneous inoculation results in a tuberculous chancre
in the nonimmune host but TVC in the immune host.
Modes of endogenous spread to skin include the
following:



direct extension from underlying tuberculous infection,
i.e., lymphadenitis or tuberculosis of bones and joints,
results in SD;
lymphatic spread to skin, results in LV;
hematogenous dissemination, results in AMT, LV, or
MTA.
PHYSICAL EXAMINATION
Primary Inoculation Tuberculosis
 Initially, papule occurs at the inoculation site 2 to 4 weeks
after the wound.

Lesion enlarges to a painless ulcer, with shallow granular
base and multiple tiny abscesses or, alternatively, may be
covered by thick crust.

Deeper inoculation results in subcutaneous abscess.

Most common on exposed skin at sites of minor injuries.

Oral lesions occur after ingestion of bovine bacilli in
nonpasteurized Milk.
PRIMARY INOCULATION TUBERCULOSIS
PHYSICAL EXAMINATION
Tuberculosis Verrucosa Cutis
 Initial papule with violaceous halo.
Evolves to hyperkeratotic, warty, firm
plaque . Clefts and fissures occur from
which pus and keratinous material can be
expressed. Border often irregular. Lesions
are usually single, but multiple lesions
occur. Most commonly on dorsolateral
hands and fingers. In children, lower
extremities, knees. No lymphadenopathy.
TUBERCULOSIS VERRUCOSA CUTIS
PHYSICAL EXAMINATION
Lupus Vulgaris
 Initial flat papule is ill-defined and soft and
evolves into well-defined, irregular plaque.
Reddish-brown: diascopy reveals an “apple
jelly”color.
 Hypertrophic forms result in soft tumorous
nodules.
 Ulcerative forms present as punched-out, often
serpiginous ulcers surrounded by soft, brownish
infiltrate.
 Usually solitary, but several sites may occur.
 Most lesions on the head and neck, most often on
nose and ears or scalp. Lesions on trunk and
extremities rare.
LUPUS VULGARIS
PHYSICAL EXAMINATION
Scrofuloderma






Firm subcutaneous nodule that initially is freely movable;
the lesion then becomes doughy and evolves into an
irregular, deep-seated nodule or plaque that liquefies and
perforates.
Ulcers and irregular sinuses, usually of linear or
serpiginous shape, discharge pus.
Edges are undermined, inverted, and dissecting
subcutaneous pockets and bridging scars.
Most often occurs in the parotidal, submandibular, and
supraclavicular regions; lateral neck;
SD most often results from contiguous spread from affected
lymph nodes or tuberculous bones (phalanges, sternum,
ribs) or joints.
SCROFULODERMA
PHYSICAL EXAMINATION
Metastatic Tuberculosis Abscess
 Also called tuberculous gumma.
 Subcutaneous abscess, nontender, “cold,”
fluctuant. Coalescing with overlying skin,
breaking down and forming fistulas and ulcers.
 Single or multiple lesions, often at sites of
previous trauma.
PHYSICAL EXAMINATION
Acute Miliary Tuberculosis
 Also called Exanthem.
 Disseminated lesions are minute macules and
papules or purpuric lesions. Sometimes vesicular
and crusted.
 Removal of crust reveals umbilication.
 Disseminated on all parts of the body,
particularly the trunk.
PHYSICAL EXAMINATION
Orificial Tuberculosis
 Small yellowish nodule on mucosa breaks down
to form painful circular or irregular ulcer with
undermined borders and pseudomembranous
material. Surrounding mucosa swollen,
edematous, and inflamed.
 Since OT results from autoinoculation of
mycobacteria from progressive tuberculosis of
internal organs, it is usually found on the oral,
pharyngeal (pulmonary tuberculosis), vulvar
(genitourinary tuberculosis), and anal (intestinal
tuberculosis) mucous membranes.
 Lesions may be single or multiple, and in the
mouth most often occur on the tongue, soft and
hard palate, or lips. OT may occur in a tooth
socket after tooth extraction
ORIFICIAL TUBERCULOSIS
DIFFERENTIAL DIAGNOSIS

Primary Inoculation Tuberculosis
Chancriform syndrome:
Primary syphilis with chancre,
 Cat-scratch disease,

DIFFERENTIAL DIAGNOSIS

Tuberculosis Verrucosa Cutis





Verruca vulgaris,
Pyoderma,
Blastomycosis,
Hypertrophic lichen planus,
SCC.
DIFFERENTIAL DIAGNOSIS
 Lupus








Vulgaris
Sarcoidosis,
Lymphoma,
Chronic cutaneous lupus erythematosus,
Tertiary syphilis,
Leprosy,
Blastomycosis,
Lupoid leishmaniasis,
Pyodermas.
DIFFERENTIAL DIAGNOSIS

Scrofuloderma





Invasive fungal infections,
Actinomycosis,
Tertiary syphilis,
Acne conglobata,
Hidradenitis suppurativa.
DIFFERENTIAL DIAGNOSIS
 Metastatic
Tuberculosis Abscess
Invasive fungal infections,
 Hidradenitis,
 Tertiary Syphilis.

 Orificial
Tuberculosis
Aphthous ulcers,
 Histoplasmosis,
 Syphilis,
 SCC.

LABORATORY EXAMINATIONS
Dermatopathology
 PIT: initially nonspecific inflammation; after 3 to
6 weeks, epithelioid cells, Langhans giant cells,
lymphocytes, caseation necrosis.
 AMT: nonspecific inflammation and vasculitis.
 All other forms of CTb show more or less typical
tuberculous histopathology;
 TVC is characterized by massive
pseudoepitheliomatous hyperplasia of epidermis
and abscesses.
 Mycobacteria are found in PIT, SD, AMT, MTA,
OT, but only with difficulty or not at all in LV
and TVC.
LABORATORY EXAMINATIONS


Culture Yields mycobacteria also from lesions of
LV and TVC.
PCR Can be used to identify M. tuberculosis
DNA in tissue specimens.
LABORATORY EXAMINATIONS
Skin Testing
 PIT: Patient converts from intradermal skin test
negative to positive during the first weeks of the
infection.
 AMT: usually negative.
 SD, MTA, and OT: may be negative or positive
depending on state of immunity.
 LV and TVC: positive.
DIAGNOSIS


Clinical Examinations.
Histological findinging confirmed by isolation of
M. tuberculosis on culture or by PCR.
COURSE AND PROGNOSIS
 The
course of CT is quite variable,
depending on the type of cutaneous
infection, amount of inoculum, extent of
extracutaneous infection, age of the
patient, immune status, and therapy.
 PIT: without treatment, usually resolves
within 12 months, with some residual
scarring. Rarely, LV develops at site of
PIT.
 Tuberculosis due to BCG immunization:
depends on general state of immunity.
 It may assume appearance and course of
PIT, LV, or SD; in the immune
compromised it may lead to MTA or AMT.
MANAGEMENT
Only PIT and TVC limited to the skin.
 All other patterns of CT are associated with
systemic infection that has disseminated
secondarily to the skin.
 As such, therapy should be aimed at achieving a
cure, avoiding relapse, and preventing emergence
of drug-resistant mutants.

TREATMENT

Standard antituberculosis therapy with 4 drugs for 8wks
followed by 2 drugs for 16 wks is recommended . All drugs
should be taken on an empty stomach once daily
Treatment of cutaneous tuberculosis
Intensive phase
Maintenance
phase
duration
drugs
Daily dose
8wks
Isoniazide
5mg/kg
Rifampicin
10mg/kg
Ethambutol
15mg/kg
Pyrazinamide
30mg/kg
Isoniazide
5mg/kg
Rifampicin
10mg/kg
16 wks