Ilmu Kesehatan Kulit dan Kelamin

Referat
Fakultas Kedokteran
Januari 2019
Universitas Pattimura

Cutaneous Tuberculosis

Karel Josafat Romario Souhoka

2017-84-035

Pembimbing:
dr. Rita Sugiono Tanamal, Sp.KK

Dibawakan Dalam Rangka Tugas Kepaniteraan Klinik

Bagian Ilmu Kesehatan Kulit dan Kelamin
Fakultas Kedokteran
Universitas Pattimura
1 Ambon
2019
 Introduction
 WHO report in 2017 it is estimated that the incidence of
TB cases reaches 10 million  1.3 million people die

 In 2011, Indonesia was placed sequentially after India,

China and South Africa with 0.38 -0.54 million TB cases

 TB: infectious disease caused by Mycobacterium

tuberculosis, which generally attacks the lungs and can
cause changes in the skin

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 Incidence of this disease has declined in the past decade 
increasing availability of antituberculosis and BCG vaccines

 Clinical presentation: chronic lesions, painless, non-

pathognomonic, can be small papules and erythema to large
tuberculomas

 Definitive diagnosis is made based on culture

 Standard therapy for tuberculosis is 2RHZE / 4RH for 6

months

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 Objectives
Explain Explain what is cutaneous TB

about Explain the epidemiology of cutaneous TB

cutaneous
TB Describe the etiology of cutaneous TB

Explain the pathogenesis of cutaneous TB

Describe the clinical manifestations and differential diagnosis of

cutaneous TB
Tracing the diagnosis of cutaneous TB

Explain the management of cutaneous TB

Explain the prognosis of cutaneous TB

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 Definition & Epidemiology
 Cutaneous tuberculosis is tuberculosis of the skin caused by
M. tuberculosis, M. bovis, and in certain circumstances by BCG

 WHO in 2017 it is estimated that the incidence of TB cases

reaches 10 million  1.3 million people die

 1% of all TB cases are cutaneous TB  in India there could be

1,847,000 new cases (1999)  annual incidence of cutaneous
TB is 18000 cases

 Skrofuloderma and lupus vulgaris are the most common forms

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 Etiology
 M. tuberculosis has germ shaped rods measuring 3 x 0.5
µm, not sporous and not symmetrical, immotile

 Obligate aerobic, slow growth, up to 37 ° C

 Antigens are on the cell wall (fat component)  slow

type hypersensitivity

 The phosphatida fraction causes tubercle reactions with

caseous necrosis in tissues

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 Bacteriological examination:
 Microscopy
 Preparation was colored Ziehl-
Neelsen. Acid-resistant bacteria: red
acid-resistant basil, solid, fragmented,
or granular stems with separate
arrangements, such as stick brooms, Picture of Basil acid resistant in Ziehl-Neelsen
or bunches (ZN) staining

Result Means

Ther is no BTA in 100 field of view Negative

1-9 BTA/100 field of view Count BTA

10-99/100 field of view +

1-10/50 field of view ++

>10/20 field of view +++

 Culture : On Lowenstein Jensen

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 Pathogenesis
 Infections are usually through inhalation of infectious droplets,
sometimes can also be through ingestion or direct contact

 Damage the integrity of the skin or mucous membrane 

Path of entry

 Cutaneous TB can occur through direct contact or

perkontinuitatum from lesions of the underlying skin tissue
such as lymph nodes, bones, digestive and pulmonary

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 The infection  slow-type hyperactivity ( 2-10 weeks) 
tuberculin examination (+)
 Only 5% of infected individuals become sick. 10% cases
become latent (post-primary TB)
 Risk factor:
 Number of bacteria
 Frequency of coughing or sneezing
 Host's immune status
 Frequency and duration of exposure
 Poorly ventilated and moist conditions
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 The form of spread of cutaneous TB
can be through:
• Direct spread of organs under the skin
infected with tuberculosis (scrofuloderma)
• Inoculation of the skin around the orifice of
the internal organs affected by tuberculosis
(orifice tuberculosis)
• Hematogenously (miliary tuberculosis)
• Lymphogen (lupus vulgaris)
• Directly enter the skin in the event of barrier
damage (cutaneous verrucous tuberculosis)

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 Classification

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Clinical manifestation and differential
diagnosis
 Primary Inoculation Tuberculous (PIT)
 Tuberculous chancre,Tuberculous primary complex

 Inoculation of M. tuberculosis to the skin in individuals without

natural / acquired immunity

 Early lesions contain multibacillary organisms  paucibacillary

 Children >>

 DD: Syphilis, tularemia, bartonellosis, sporotrichosis, other

Mycobacterioses

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  Initial lesions occurring within 2-4 weeks can be brownish
papules, indolent nodules or ulcers (chancre), resonant walls,
hemorrhagic granule base until crusting

 Predilection: face, hands, lower limbs (traumatic location)

 Wound healing can cover active lesions below it, causing cold
abscess formation  sinus formation

 Regional lymphadenopathy (after 4-8 weeks)

 Fever (+/-), painless paronychia (+/-)

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 Picture. Primary inoculation tuberculosis. Note tuberculous
charce on the thigh and regional lymphadenopathy. A positive
tuberculin reaction is noted on the arm

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 Tuberculosis Veruccosa Cutis (TVC)
 Warty tuberculosis

 The paucibacillary form is caused by exogenous reinfection

(inoculation) in individuals with high immunity who have
previously been sensitized

 Especially occurs in adults, children

 DD: Warts or keratosis, hyperkeratotic lupus vulgaris,

blastomycosis, chromomycosis, tertiary syphilis

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  Inoculation: minor injuries

 Predilection: Places of trauma (lower limbs and legs, hands)

 Skin lesions can be papules or pustules with purplish

inflammatory halo which becomes hyperkeratotic (often
mistaken for warts) and then develops into verucous plaques
with irregular edges

 Can be crescent shaped due to spreading serpiginous

 Lymphadenopathy is rare

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 Picture. Tuberculosis verrucosa cutis on the
back of the hand

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 Lupus Vulgaris (LV)
 The form of chronic, progressive, post-primary, paucibacillary
cutaneous tuberculosis, in individuals with moderate immunity and
high tuberculin sensitivity

 Woman >>

 The way of infection: exogenous and endogenous through

hematogenous, lymphatic, or transmission from other body parts

 DD: Sarcoidosis, limphocytoma, discoid LE, tertiary syphilis, leprosy

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  The initial lesions in the form of macules / papules become
anular, gelatinous, small, red-brownish plaques

 Diaskopi: apple-jelly nodule

 Lesion has a discoidal elevation with an atrophic area

 There are 5 forms of LV:

 Plaque form, ulcerative and mutilating form, vegetating form, tumor-
like form, papular and nodular form

 Predilection: face and extremities

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 Pictures. A) Slightly raised, brownish plaque of lupus vulgaris.
B) Large plaque of lupus vulgaris of 10 years,during involving
the cheek, jaw, and ear.

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 Scrofuloderma
 Tuberculosis colliquativa cutis

 Subcutaneous tuberculosis, secondary to percontinuitatum

from the underlying tissue that is infected with TB (KGB, joints,
bones

 Children & adults >>

 DD: Lymphadenitis bacterial non-tuberculosis, M. scrofulaceum

infection, hidradenitis supurativa

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  Initially formed or blue-reddish nodule formation (non-
inflammatory) in the glands / joints that are infected 
periadenitis attachment to surrounding tissue  cold abscess
formation irregular, livid, resonant wall, closed granulation
tissue pus seropurulen  yellowish crusting or matrix, even
skin bridge

 Predilection: parotid, submandibular, supraclavicular

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 Picture. Scrofuloderma in the clavicular region. Note abscess
formation, ulceration, and extrusion of purulent and caseous
material.

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 Metastatic Tuberculous Abcscess
 Tuberculous gumma

 Hematogenous forms of primary focus (usually pulmonary)

single/multiple lesions

 Generally in malnourished children, immunosuppressed

conditions, or basic lymphoma disease

 DD: Gumma syphilis, leishmaniasis, deep dermatophytosis

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  Skin abnormalities in the form of subcutaneous nodules, firm
borders or abscesses

 Sometimes ulcers can be found

 Predilection: extremities >> body

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 Picture. Tuberculous guma on the right foot. There are well-
defined subcutaneous nodules.

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 Orificial Tuberculosis
 Tuberculosis ulcerosa cutis et mucosae
 TB infection in the mucosa or around the orifice due to
autoinoculation of mycobacteria from the progression of
tuberculosis of internal organs such as lung, intestinal, sometimes
genitourinary
 Multibacillary form
 Man >> Woman
 DD: Syphilis lesions (painless), aphthous ulcer, squamous cell
carcinoma

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  Yellowish or reddish nodules can become ulcers with a typical
punched-out appearance, circular, uneven edges, mucosa
around the edema

 The base of the ulcer appears as multiple yellowish tubercles

and easily bleeds

 Pain (+), dysphagia (+)

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 Picture. Orificial tuberculosis in advanced cavitary pulmonary
tuberculosis

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 Acute Millary Tuberculosis
 Tuberculosis cutis miliaris disseminata

 Associated with miliary TB, hematogenous spread,

mycobacteria spread from the focus of infection in the lung /
meningen to the skin.Tuberculin reaction (-)

 Occurs in children/immunocompromised status (HIV/measles)

 Skin lesions in the form of well-defined erythema, papules,

vesicles, pustules or hemorrhagic lesions

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 Picture. Miliary tuberculosis or diseminated TB. Appearance
of miliary sized vesicles

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 Diagnosis
 Absolute citeria  CULTURE

 Relative criteria:
 Evidence or history of active tuberculosis in other sites

 Clinical history and physical appearance

 The presence of acid-fast bacilli

 Tuberculous granulomas seen on histology

 Positive Mantoux test.

 Response to anti-tuberculosis therapy

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 Treatment
 The purpose of giving antituberculosis:
 Extracellular basil which is free to divide
 Basil is dormant in cells and caseous tissue
 Basil in macrophages and inflammatory lesions is slow to divide
Recommended Dose
Antituberculous drug Daily 3x/week

Dose Maximum Dose Maximum

(mg/kgBB) (mg/kgBB) (mg)

Isoniazid (H) 5 300 mg/hari 10 900

Rifampisin (R) 10 450-600 mg/hari 10 600

Pirazinamid (Z) 30 15 mg/kgBB/hari 35 -

Etambutol (E) 15 1.5-2 g/hari 30 -

Streptomisin (S)* 15 500-700 mg/hari 15 1000

Treatment recommendations are 2HRZE / 4HR which rarely causes resistance compared to alternative 2HRZE / 4H3R3
therapies.

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 Therapy of cutaneous tuberculosis (same as pulmonary
tuberculosis) is divided into 2 phases:
 Phase I: eradication of the bacillus which is rapidly dividing and
is an intensive phase with a combination of several drugs for 2
months

 Phase II: instantly kills the dormant bacillus and is a further

phase consisting of isoniazid and rifampicin for 4 months

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 Prognosis
 All types of cutaneous tuberculosis begin to respond to
treatment at the sixth week

 Response failure: related to diagnosis, compliance with

medication, and the presence of drug resistance

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 THANK YOU

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