Tuberculosis and leprosy

2. Etgiology and pathogenesis
 Mycobacterium tuberculosis
 Infection with atypical mycobacteria can clinically closely resemble
M.tuberculosis infection of the skin
 Manifestation of M.tuberculosis infection of skin depends on several
fectors
 Immunity
○ Specific immunity – depending on whether the exposure to bacteria is primary or
secondary
○ General immunity – depending on nutritional status, immunosuppression etc.
 Route of entry (hemetogenous or contiguous spread or exogenous
inoculation
 Bacterial load

3. Clinical features
 Cutaneous tuberculosis include
 Lupus vulgaris
 Scrofuloderma
 Tuberculosis verrucosa cutis
 Tuberculides

5. Lupus vulgaris
 Definition:
Chronic dermal infection with Mycobacterium tuberculosis
or Mycobacterium bovis.
 Pathogenesis:
Lupus vulgaris is usually the result of endogenous
reactivation; the mycobacteria reach the dermis by direct
spread from lymph nodes, or by hematogenous or
lymphatic spread.
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6. Clinical features:
 Large red-brown atrophic patches or plaques with telangiectases.
 Sites of predilection include face (especially nose and ears),
breasts, and thighs.
 Crusts, ulceration, and destruction of adjacent tissue (cartilage of
ear or nose) lead to mutilation.
 Classic lesion is the lupus nodule,2–3mm slightly elevated papule
at periphery.
 On diascopy, characteristic “apple jelly” color surrounded by pale
border.
 When one presses on a lupus nodule with a sound, one can break
through with little pain: sound phenomenon.
 The histologic equivalent of a lupus nodule is a tubercle.
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7. Morphology
 Single lesions
 Well-demarcated, annular or arcuate plaques which slowly
extend centrifugally
 Periphery shows erythematous to brownish
 Deep-seated nodules which may stand as apple jelly
nodules on diascopy.
 Over period of time, the center becomes atrophic (paper
thin), depigmented and scarred
 New nodules may appear within area or scarring

8. Localization Complications
 Buttocks
 Upper extremities
 Face
 Ulceration
 Hypertrophic lesions
 Squamous cell
carcinoma - rarely

10.  Scrofuloderma is a cutaneous tuberculosis due
to direct extension of infection from an
underlying tuberculous focus present in lymph
nodes
 Cervical
 Axillary
 Inguinal
 A bone or a joint

11. Tuberculosis Cutis Colliquativa
 Synonyms: Scrofuloderma.
 Definition: Subcutaneous tuberculosis with development of cold
abscesses and spread to skin.
 Epidemiology: Patients are usually young children or elderly
people.
 Pathogenesis:
 Scrofuloderma: Spread of subcutaneous tuberculosis into
subcutaneous fat and then skin from infected lymph node,
bone, or other tissue.
 Tuberculous gumma: Hematogenous spread of mycobacteria
with multiple liquefying cold abscesses that break though to the
skin.
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12. Morphology
 Initially the lesion manifests as a bluish red, painless
swelling, which breaks open after several weeks to form
sinuses
 Mouth of the sinus is irregular and has a blue undermined
edge.
 The sinuses discharge watery or caseous material
 Ulcers (when present) are linear or serpiginous with
undermined, bluish edge, and a floor with granulation tissue
 Base formed of underlying tuberculous focus – lymph nodes,
bone or joint

13. Clinical features
 Usually the lymph nodes of the neck and submandibular region
are involved.
 They are infected from the primary pulmonary tuberculosis or
directly infected from the tonsils (in the past when milk infected
with Mycobacterium bovis was ingested).
 Initially indolent blue-red nodules (cold abscesses) that enlarge
and break down.
 The ulcers are bizarre, undermined, and tend to form fistulas.
 Healing occurs after years, with typical strands of scarring.
 Hematogenous lesions involve the trunk and extremities, often
with simultaneous lesions in bones (fingers, sternum, ribs).
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14. Localization
 Lymph nodes
 Cervical
 Axillary
 Inguinal
 Legs –from tuberculous osteomyelitis
 Skin over sternoclavicular joint

16. Tuberculosis Cutis Verrucosa
 Definition: Exogenous reinfection in individual with
intact specific immune response; very uncommon.
 Pathogenesis: Two sources of infection:
 Infected human material: Injuries during autopsies or
other medical services,known as prosector’s wart.
 Infected cows: Now very rare, but used to be common
in slaughterhouse workers and butchers.
 Clinical features: Solitary verrucous papule or nodule,
no lupus nodules, central clearing.
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17. Morphology
 Single verrucous nodule with a serpiginous edge and
erythematous areola.
 The base is indurated
 Fissures of the warty plaque discharge pus and the center
may show some scarring
 Lymphadenopathy is rare
 Sites – trauma-prone sites – hands and feet

18. Tuberculids
 Definition: In the past tuberculid was defined as a
reaction to Mycobacterium tuberculosis without direct
infection; it included many diseases with
granulomatous histology but no connection to
tuberculosis, such as rosacea.
 As tuberculosis became more rare, it became clear that
the connections were tenuous.
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19. Investigations
 To confirm diagnosis of tuberculosis
 Biopsy – caseating granuloma is pathognomonic of
tuberculosis
 Isolation of M.tuberculosis
 Mantoux test
 To rule out concomitant tuberculosis in other organs
 Chest X-ray – to rule out pulmonary tuberculosis
 X-ray of bonesjoints – to rule out underlying bone or joint
tuberculosis in scrofuloderma
 Fine needle aspiration cytology – of enlarged lymph nodes

20. Points for diagnosis
 The diagnosis of cutaneous tuberculosis is
based on
 Chronicity of lesions
 Characteristic morphology
 Characteristic histology of a caseating granuloma

21. Treatment
 Standard antituberculosis therapy with four drugs for 8
weeks followed by two drugs for 16 weeks is
recommended.
 Isoniazid
 Rifampicin
 Ethambutol
 Pyrazinamide

23. Etiology
 Mycobacterium leprae
 Route of infection is not established
 Type of disease which develops, depends on the
immunological response and not on the virulence of
the organism
 M.leprae cannot be cultured in vitro, but can be grown
in animal models.
 Leprosy is a global disease

24. Classification
 Depending on clinicopathological, immunological and
bacteriological features leprosy is classified into polar
leprosy and borderline leprosy
 Tuberculoid leprosy
 Borderline tuberculoid
 Mid borderline
 Borderline lepromatous
 Lepromatous leprosy

25.  Only two polar forms, tuberculoid leprosy (seen in
patients with very good immunity) and lepromatous
leprosy (seen in patients with poor immunity) are stable.
 The other forms are instable.
 The disease may worsen from borderline tuberculoid -
mid borderline - borderline lepromatous.
 With treatment the disease may move in the opposite
direction.
 There are three other types of leprosy which are seen
 Indeterminate leprosy
 Histoid leprosy
 Neuritic leprosy

26. Clinical features - Prototype skin
lesions
 Can be single or multiple
 Are usually hypopigmented, may be erythematous
 Are usually macules or plaques, papules or nodules may
be seen
 May be well-defined or poorly defined
 Show epidermal or dermal atrophy, so lesions appear shiny
 Show loss of hair and sweating
 Show an-hypo-esthesia

27. Nerve involvement
 Thickened peripheral nerves is typical
 A thickened nerve is accompanied by signs of nerve
damage in form of lossreduction of sensation in skin
lesions or distal part of extremities – glove and stocking
anesthesia
 Weakness of muscles supplied by the affected nerve
 Nodularity and tenderness may be present.

28. Indetermined leprosy
 Seen on face of children in endemic areas
 Always a macule
 Atrophic
 Hypoesthetic or normoesthetic
 Hypopigmented or slightly erythematous
 With or without nerve thickening

29. Indeterminate leprosy:
 The initial cutaneous manifestations of leprosy are
subtle and not specific.
 Initially erythematous patch, which in darker-skinned
individuals appears pale; most cases resolve, some
advance into more severe disease.
 Differential diagnostic considerations include vitiligo,
nevus anemicus, nevus depigmentosus,
postinflammatory hypopigmentation, pityriasis alba,
tinea versicolor
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30. Tuberculoid leprosy
 Localized form of infection
 One (or two) asymmetrically located lesions
 Macules or plaques
 Well-defined
 Hypopigmented
 Anesthetic
 Often with an active border
 Hair loss
 Thickening or regional nerve

31. Tuberculoid leprosy:
 Skin findings: One or multiple erythematous or scaly, well-
circumscribed macules or patches; usually hypo- or
anesthetic.
 Differential diagnostic considerations include lupus
vulgaris, chronic cutaneous lupus erythematosus (discoid),
tinea corporis.
 All patients have nerve involvement.
 Inflammation of Schwann cells leads to thickening of
peripheral nerves.
 Course generally benign.
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32. Lepromatous leprosy
 Systemic disease, characterized by extensive
cutaneous, neural and systemic involvement
 Facial lesions
 Diffuse infiltration of the face, ear lobules alae
nasi
 Loss of lateral third of the eyebrows
 Facial deformities – now rare

33. Lepromatous leprosy:
 Papular and nodular lesions symmetrically distributed.
Often start on nose and ears, later involve hands, arms,
buttocks. Facial lesions can be markedly swollen (leonine
facies) with loss of eyebrows (Lucio sign).
 Nasal secretions rich in organisms.
 Complications include orchitis, facial mutilation,
neurotrophic ulcers, flexion contractures of hands, foot
drop.
 Differential diagnostic considerations include myxedema,
neurofibromatosis, post-kala-azar dermal leishmaniasis
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34. Cutaneous lesions
 Numerous, symmetrically located
 Different types
 Macules – small, hypopigmentederythematous, minimal
hypoesthesia
 Papulonodules – most frequent type, dull red papules and
nodules or diffusely infiltrated skin
 Other manifestations of leprosy include peripheral
anesthesia, trophic ulcers and motor dysfunction

35. Nerve involvement
 Bilaterally symmetrical peripheral nerve thickening
 Nerves may become tender
 Systemic involvement
 Lymphadenopathy
 Hepatoplenomegaly
 Ocular involvement
 Testicular atrophy

36. Borderline leprosy:
 More lesions, more widespread and less sharply
defined than in tuberculoid form.
 Usually symmetrical on trunk but may be asymmetric
 on face.
 Less likely to have scale.
 Nerve involvement less prominent
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37. BT leprosy
 Lesions are large, hypopigmented macules or plaques
 Differ from TT
 Less sharply demarcated, having satellite lesions
 More in number
 Less asymmetrical
 Less hypoesthetic
 Few nerves may be asymmetrically thickened

38. BL leprosy
 Differs from LL
 Lesions are bilateral
 Less symmetrical
 Lesions may be hypoesthetic
 Lesions are small, but larger than LL
 Peripheral nerve involvement is bilateral with tendency to
asymmetry

39. BB leprosy
 Numerous lesions
 Asymmetrically
 Erythematous raised annular plaques with central
clearing
 Hypoesthetis
 Multiple asymmetrically thickened nerves

40. Complications
 Facial deformities
 Disabilities of hands and visible hand deformity
 Disabilities of eyes
 Motor deficits
 Trophic ulcers
 Testicular dysfunction
 Renal involvement

41. Diagnostic approach:
 Skin biopsy; histological examination; Ziehl–Neelsen works well in
lepromatous leprosy. For paucibacillary forms, PCR is available, but has
not been as effective as hoped.
 Nasal smear or scraping from tissue fluid from ear in lepromatous
leprosy reveals numerous organisms on Ziehl–Neelsen stain.
 Neurological examination (anesthetic patches, enlarged nerves).
 Lepromin test (Mitsuda test): Injection of an extract from lepromatous
tissue; positive response is development of nodule after 3–4weeks in
tuberculoid leprosy.
 False-positive serological tests for syphilis in lepromatous leprosy.
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42. Therapy:
 Current WHO recommendations:
– Tuberculoid leprosy: Dapsone 100mg daily and
rifampicin 600mg monthly for 6–9months.
– Single lesion (tuberculoid or indeterminate): Dapsone
600mg, ofloxacin 400mg, and minocycline 100mg as
single dose.
– Lepromatous leprosy: Dapsone 100mg daily;
clofazimine 150mg, and rifampicin 600mg monthly for 12–
18months.
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