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Cutaneous tuberculosis can take many forms. These are classified below.
Innoculation:
| • | painless brown-red papule develops into a nodule which may ulcerate |
| • | ddx of chancriform conditions – deep fungal (sporotrichosis, blastomycosis, histoplasmosis, coccidioidomycosis), nocardiosis, syphilis, leishmaniasis, yaws, tularemia, atypical mycobacterium |
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| • | wart-like lesions on back of hands (AKA Prosector’s wart) |
| • | previously sensitized individual with reasonably strong immunity against M. tuberculosis |
| • | ddx: wart, blastomycosis, chromomycosis (i.e. send fungal culture), bromoderma, or M. marinum (differentiated only by culture) |
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Endogenous Continuous Spread:
| • | = tuberculous involvement of the skin by direct extension |
| • | presents clinically as a cutaneous sinus, most often draining underlying tuberculous lymphadenitis or osteomyelitis |
| • | ddx: atypical mycobacteria infection, actinomycosis, coccidioidomycosis, mycetoma |
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Hematogenous Spread to Skin:
| • | originates from TB elsewhere in the body by hematogenous, lymphatic or contiguous spread |
| • | brown plaque; 90% on head or neck (face most frequent) |
| • | nodules which ulcerate or resolve with scar |
| • | histology = classic tubercles (+/- caseation) |
| • | ddx: sarcoid, chronic DLE, tertiary syphilis, leprosy, deep fungal |
| • | softness of lesion, brownish-red color, (with apple jelly diascopy), and slow evolution are characteristics of LV helpful in diagnosis |
| • | occurs in patients with strong immunity therefore a negative tuberculin test provides strong evidence against the diagnosis of LV (tissue culture = gold standard) |
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| • | appears in the setting of fulminant TB of the lung or meninges |
| • | generally, patients have other unmistakable signs of severe miliary tuberculosis |
| • | because this represents uncontrolled hematogenous infection, the tuberculin test is negative |
| • | skin biopsy – diffuse suppurative inflammation with predominantly PML’s; acid-fast bacilli abundant |
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Tuberculids:
| • | finding of TB DNA by PCR suggests that the tuberculids also represent hematogenous dissemination of TB which is quickly controlled by the host, usually resulting in the absence of detectable organisms |
| • | occur in persons with strong immunity to tuberculosis (always PPD +) |
| • | tend to be bilaterally symmetrical eruptions because they result from hematogenous dissemination |
| • | successive crops, symmetrically, on extensor extremities (elbows, knees, dorsal hands, buttocks) |
| • | varioliform scarring follows the lesions |
| • | ddx: PLEVA, papulopustular secondary syphilis, LyP, perforating GA, perforating collagenosis |
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| • | minute, keratotic, discrete papules scattered over the trunk |
| • | the lesions are arranged in nummular or discoid groups |
| • | as a rule, they appear in patients with TB of the bone or lymph nodes |
| • | ddx: lichen nitidus, lichen planus, secondary syphilis, sarcoid |
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| • | with or without ulceration, posterior lower calf, 80% women |
| • | ddx: (idiopathic) nodular vasculitis, erythema nodosum (short duration, rapid development, does not ulcerate, and affects chiefly the anterior rather than the posterior calves), syphilitic gumma (usually unilateral and single) |
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Subtype and PPD status: (quiz yourself - these all make sense so you don't need to rote memorize)
tuberculoid chancer PPD negative? (by definition they are naive to TB, but will now turn PPD +, timing?)
tuberculosis cutis verruciformis PPD +
scrofuloderma strong PPD+
lupus vulgaris strong PPD+
acute miliary TB PPD negative/ weak
papulonecrotic tuberculid strong PPD+
erythema induratum strong PPD+
lichen scrofulosorum strong PPD+
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