Friday, October 29, 2010

Lupus vulgaris


*A chronic and progressive form of cuteneous TB that occurs in tuberculin sensitive patients. In most series it is the most common form of cut. TB.
*Lesion appears in normal skin as a result of direct extension of underlying tuberculous foci, of lymphatic or hematogenous spread, after primary inoculation, BCG vaccination or in scars of old scrofuloderma.
*Lesion mostly invove the head and neck.
*Reappearance of new nodules within a previously atrophic or scarred lesion is characteristic.
*Cartilage within the affected area is progressively destroyed(lupus vorax)
*Bone is usually spared.
*Clinical variants include;
*a)plaque form
*b)ulerating
*c)vegetative
*d)nodular
*Lesions often persist for years before diagnosis
*And can be disfiguring
*Patients with lupus vulgaris and PTB have a 4-10 fold higher mortality than PTB alone.
*In long standing lupus vulgaris,squamous cell carcinoma can occur and be confused with the disease itself.http://www.answers.com/topic/lupus-vulgaris

TB cutis orificialis


*Results from autoinoculation of mycobacteria into the periorificial skin and mucous membranes in patient with advanced TB. Underlying disease can be pulmonary,intestinal or genitourinary Tb. Infectious mycobacteria shed from these foci are inoculated into surrounding mucous membranes and skin.
*Tuberclin sensitivity is strong and patients are typically older men.
*The tip and lateral margin of the tongue are affected most frequently. 
*Lesions start as red papules that evolve into painful,soft punched out shallow ulcers.
*Usually patients that develop orificial TB have severe internal organ disease and appearance of this lesion portends a poor prognosis.http://en.wikipedia.org/wiki/Tuberculosis_cutis_orificialis

scrofuloderma


*Result from break of skin overlying a tuberculous focus,usually at a lymph node but also at the skin over infected bones or joints.
*Historically a high prevalence was found in children infected with m.bovis .
*The oral or tonsillar primary lesion progresses to cervical adenitis, formation of cold abscesses and secondary breakdown of the overlying skin.
*Tubercle bacilli can be isolated from purulent discharge.
*Tuberculin sensitivity is usually marked. 
*Spontaneous healing can occur but often takes years. Lupus vulgaris may develop in the vicinity of healing scrofuloderma.
*Metastatic tuberculous abscesses is a variant of scrofuloderma that occurs following hematogenous  spread of mycobacteria to skin in tuberculin sensitive individuals.
*Typically occurs in malnourished children or severely immunosupressed patients.

Miliary TB of skin


*A rare manifestation of fulminant miliary TB resulting from hematogenous  spread of mycobacteria to multiple organ, including skin.
*The initial site of infection is usually pulmonary or meningeal.occur predominantly in children.
*Tuberculin sensitivity is absent  and bacillary load high.
*Currently numerous instances are reported in the immunocompromised.
*Disseminated lesions occur on all parts of the body especially the trunk.
*Lesions erupt as small, red macule or papules.purpura, vesicle and central necrosis are common.
*Affected patient are gravely ill and prognosis poor.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1673824/

TB verrucosa cutis


*This an indolent warty plaque that occurs as a direct inoculation of TB into the skin of individuals previously infected with m.tuberculosis or m.bovis. Re-infection TB can result from accidental exposure to tuberculous tissues in high risk groups such as physicians, pathologists and laboratory workers(anatomist`s wart, verruca necrogenica) 
*Farmers ,butchers and veterinarians contract this form of re-infection TB from tuberculous cattle.
*Lesions most commonly occur on the hands and in children the lower extremities.
*Infection starts as an asymptomatic plaque of mistaken for verruca vulgaris. 
*The lesion may show central involution with atrophic scar or form massive excrescences with fissures.the later may discharge pus.
*Regional nodes are not affected unless secondary infection occurs.http://emedicine.medscape.com/article/1105317-overview
 

Primary inoculation TB


*Results from introduction of mycobactria to an individual who was not previously infected with TB or was immunized with the m.bovis.
*After entry they multiply in tissue macrophages and spread to regional lymph node. An inflammatory papule develops in 2-4 wks at the inoculation sites that breaks down into a firm, non healing shallow, nontender. Undermined ulcer with a granulomatous base. Painless lymphadenopathy is evident 3-8 wks.
*Numerous bacilli are present at the inoculation site and regional lymph node. This ulceroglandular complex is the skin analog of the Ghon complex.
*As with all Tb infection the clinical course depends upon the host immune response . Tuberculin sensitivity usually is coincident with the development of lymphadenopaty. Epitheloid granulomas are evident in the skin and lymph node. 
*The primary lesion heals with scaring after 1-3 month. With a less effective host immune response, bacterial load remains high and healing is delayed for up to 12 month. regional nodes may suppurate,erode and perforate the surface of the overlying skin(scrofuloderma).latent foci of infection can remain at the site and progress to lupus vulgaris or TB verrucosa cutis.
     

CUTENEOUS TB


*VARIANTS
*Primary inoculation TB
*TB verrucosa cutis
*Miliary TB of  skin
*Scrofuloderma
*TB cutis orificialis
*Lupus vulgaris