1. MYCOBACTERIAl INFECTIONS

2. Cutaneous Tuberculosis achronic grnulomatous disease caused by Mycobacteril TB.there are four major categories of cutaneousTB: 1-Inculation from an exogenous source(prmary inculation TB and tuberculosis verrcosa cutis). 2-Endogenous cutaneous spread contagiously or by autoiculation(scrofulderma,Tuberculosis cutis oroficials). 3-Hematogenous spread to the skin(Lupus vulgaris,&miliary TB).

3. 4-Tuberculides(erythema induratum<bazin disease>,papulonecrotic tuberculide,and lichen scrofulsorum). Tuberculine Testing: * It is designed to detect cell-mediated immune response to M.tuberculosis. *It remains the most useful method of identifying infected persons. *The test becomes positive between 2nd and 10th weeks following infection and remains positive for many years. *The intradermal or Montoux test ,the injection of 5TU and the test read h. after intradermal injection. *Induration and erythema measuring 5mm or more considered positive in HIV patient, those with risk factors,recent close contact,healed TB, those with chest x-ray findings of healed TB.

4. 5mm or larger in chidren is considered positive after exposure to patient with active TB. *If it measures more than 10 mm is considered positive in inject drug users,low incom patient in high prevalence countries . *Induration more than 15mm positive in all others . * Reactivity to tuberculine testing is impaired in(lymphoproliferative diseases,sarcoidosis,corticosteroids,and immunosuppressive medications,sever protein deficiency, chr. renal failure).

5. BCG vaccination:
Is aliving attenuated bovine tubercle bacillus used to enhance immunity to tuberculosis.
Is given only to tuberculine negative persons.
It is effective in reducing childhood TB if given to neonates .once the patient has been vaccinated the tuberculine test becomes positive.
Dermatologic (specific)complications of BCG(persistant regional lymphadenitis,scrofulderma,lupus vulgaris,excessive ulceration may occur if BCG is inculated too deeply).
Non specific complications include(urticaria,erythema nodosum,erythema multiform,and granuloma annulare).
Occasionally BCG will cause progressive local dissemination or even fatal disease in immunocompetent host.

6. Inculation cutaneous TB from exogenous source: -primary inculation TB(TB chancre) *It develops at sites of inculation of tubercle Bacilli into tuberculosis free individual. *Regional lymphadenopathy usually occur completing the complex. *It occurs chievly in children and affects the face or extermities,in previously traumatized skin including sites of tattoos and nose piercing or mucosa. *The earliest lesion appearing 2-4 weeks after inculation is apainless ,brown-red papule

8. Which develop into indurated nodule or plague that may ulcerate
Which develop into indurated nodule or plague that may ulcerate.This is TB chancre. *prominent regional lymphadenopathy appears 3-8 weeks after infection,cold supperative and draining sinuses may appear over involved lymph nodes. *spontaneous healing usually occurs within one year. DDx: chancriform conditions(syphilis,leshmaniasis,yaws,atypical mycobacterial disease). - Tuberculosis verrcusa cutis(prosector wart): *Happen from exogenous inculation of bacilli into the skin of previously sensitized person with strong immunity against M.TB.

9. The tuberculine test is strongly positive
*The tuberculine test is strongly positive. *Clinically the lesion begins asmall papule,which becomes hyperkeratotic,resembling wart.the lesion enlarge by peripheral expansion with or without central clearing. *lesions are almost always solitary, and regional adenopathy usually present only if secondary bacterial infection occurs. *Frequent locations are on the dorsa of the hands in adults,and the ankles and buttocks in children. *the lesions seldom ulcerate & may heal spontaneously. DDx: -atypical mycobacteria-Majocchi granuloma- - Verruccous epidermal nevus- hypertrophic lichen planus. - Verruca vulgaris.

12. Cutaneous TB from endogenous source
Scrofulderma:is atuberculous involvement of the skin by direct extention,usually from underlying tuberculous lymphadenitis.It occurs over cervical lymph nodes but also over bone or around joints.
Clinically the lesions begin as subcutaneous masses,which enlarge to form nodules.Suppuration occur centrally,they may be erythematous or skin colored and skin temperture not increased over the mass,lesions may drain forming sinuses.
Sccrofulderma heals with characteristic cord like scars,allowing the diagnosis to be made years later.

15. DDx:Atypical mycobacteria-Sporotrichosis-Actinomycosis
DDx:Atypical mycobacteria-Sporotrichosis-Actinomycosis. -Tuberculosis cutis orificialis: *It is aform of cutaneous TB that occurs at mucocutaneous borders of the nose,mouth,anus,urinary meatus and vagina. *Itis from active underlying visceral TB(larynx,lung,intestine,genitourinary TB.). Tuberculine test(+),& lesions usually ulcerat.

16. CLINICAL FINDINGS. A small yellowish or reddish
nodule appears on the mucosa and breaks down
to form a soft ulcer with a typical punched-out appearance,
undermined edges, and circular or irregular border Lesions may be single or multiple and are extremely painful, resulting
in dysphagia.

19. Cutaneous TB from hematogenous spread.
Lupus Vulgaris: It may appear at sites of inoculation, at scofulderma scars, or most commonly at distant sites from the initial infectious focus. Most patients with high immunity to TB & +ve tuberculine test.
Clinically consist of single plague composed of grouped red-brown papules which when blanched by diascopic pressure have pale,brownish-yellow apple jelly color.
90% of lupus vulgaris lesion occur on the head and neck.
DDx; -Colloid milia-Acne vulgaris-Rosacea-Sarcoidosis.

22. Miliary TB: Appear in the setting of fulminant TB of the lungs and meninges.
Tuberculides: Are agroup of skin eruptions associated with an underlying or silent focus of TB,it includes:-papulonecrotic tuberculide- lichen scrofolsorum-Erythema induratum.

23. Diagnosis of cutaneous TB
1-Biopsy with acid- fast staining should be done when history and physical examination suggest cutaneous TB.
2-PCR testing is increasingly used to identify mycobact.DNA in tissue specimens.
3-Culture remains the gold standard.

24. Treatment
HIV testing is recommended for all patients because may require longer courses.
For all form multidrug therapy is recommended.
The initial phase of treatment is intensive for rapid destruction of mycobacteria.During this(8-weeks)period,INH,rifampin,pyrazinamide,and ethambutol.
The continuation phase cnsist of two-drug combination either(INH & rifampin)or in non HIV pts INH&rifapentin.The usual minimal durationis 18 weeks.

25. Hansens Disease(leprosy) achronic granulomatous disease,caused by mycobacteriam leprae,principally acquired during childhood,young adulthood.Skin, peripheral nervous system,upper resp.tract,eyes,and testes are the major sites of involvment. Etiology: Myco.lrprae is aweekly acid fast organisms,has not been cultured in vitro. *Infect skin and cutaneous nerves. *Grows best in cooler areas(skin,nerves,upper res.tract,anterior chamber of eye&testes). *Sparing warmer areas of skin(axilla,groin,scalp&midline of back.)

26. Host:Humans are the main reservoirs
Host:Humans are the main reservoirs.Wild armadillos also Transmission: Possible transmission include nasal droplets,contact with infected soil,insect vectors. *Inculation via skin( bites,scratches,small wounds,tattoos). *Inhalatio into nasal passages or lungs.

27. Predisposing Factors: 1-Residence in endemic area
Predisposing Factors: 1-Residence in endemic area. 2-Having ablood relative with leprosy. 3-poverty(malnutrition). 4-Contact with affected armadillos. SEX: Males >Females. Incubation period: 2-40 yrs(most common 5-7 yrs) Clinical features: the clinical spectrrum depends on the host cell mediated immunity to M. leprae. * Patients who develop clinical disease classified into in two groups( patients with few organisms in tissues paucibacillary,and patients with large number of organisms are termed multibacillry).

28. Types of leprosy Tuberculoid leprosy Borderline leprosy
Lepromatous leprosy
High resistance
Intermediate resistance
Low resistance
Organisms hard to find
Many organisms
Non-infectious
Some organisms
Infectious
Localized lesion
Scattered lesion
Generalized lesion

29. Usually the onset is insidious
*Usually the onset is insidious. * prodromal symptoms are generaly so slight that the disease is not recognized until the appearance of cutaneous eruption. *The first manifestation in 90% of patients is numbness. *The earliest sensory changes are loss of discrimination of cold and heat, and loss light touch,most often in the feet and hands. * Often the first lesions is solitary,ill defined,hypopigmented macule that merges into the surrounding skin on the cheeks, upper arms,thighs,buttocks.

30. Difference between tuberculoid and lepromatous leprosy
Tuberculoid(paucibacillary)
Lepromatous leprosy(multibacillary)
Involvment
Skin&nerves only Asymmetrical
Many tissues Symmetrical
One or two only
Commonly on face
Innumerable widspread

31. Continuation of differences
Lesions
Sharply marginated hypopigmented macules slightly raised purplish rim ,hairless
Widspread macules,papules,nodules plagues thickened on face(leonine facies)
Involvment of nerves
Thickened in vicinity of lesions
Most peripheral nerves thickened
Hyposthesia of lesion,absent sweating of lesion
Lesion not hyposthetic but glove and stock anesthesia

32. Diagnosis: Culture
M. leprae has not been cultured in vitro; however, it does grow when inoculated into the mouse foot pad. Routine bacterial cultures to rule out secondary infection.
PCR
M. leprae DNA detected by this technique makes the diagnosis of early paucibacillary leprosy and identifies M. leprae after therapy Diagnosis
Made if one or more of the cardinal findings are detected: patient from endemic area, skin lesions characteristic of leprosy with diminished or loss of sensation, enlarged peripheral nerves, finding of M. leprae in skin or, less commonly, other sites.

33. Differential Diagnosis
A number of skin diseases may be confused with leprosy. Hypopigmented
and hyperpigmented lesions may mimic pityriasis alba,
pityriasis versicolor, mycosis fungoides or sarcoidosis. The circinate
erythematous plaques may be misdiagnosed as tinea corporis,
sarcoidosis, lichen planus, psoriasis or mycosis fungoides. The differential
diagnosis of the infiltrated plaques or nodules includes leishmaniasis,
syphilis, sarcoidosis, lymphoma and cutaneous tuberculosisI2,1".
The neurologic findings may be confused with other types of peripheral
neuropathy (e.g. due to diabetes mellitus, nutritional disorders,
vasculitis, poliomyelitis or syringomyelia), while the deforming acral
features may suggest Dupuytren's contractu res, scleroderma, tabes
dorsalis, or other diseases associated with neuropathic changes 11,12,1".
The differential diagnosis of a type 1 reaction includes acute lupus
erythematosus, cellulitis and drug reactions, while in patients with
type 2 reactions, the possibility of other vasculitides and panniculitides
needs to be considered. The latter includes erythema nodosum which

37. If organisms are found on skin smears the patients are said to be multibacillary(LL). *If the results are negative skin smears(and the patients had five or fewer lesions)they are called paucibacillary(TL). Treatment: * In paucibacillary(Tuberculoid Lep.): -Rifampin 600mg/day+Dapson 100mg/day for 12 months. *In multibacillary(lepromatous Lep.): -Dapson 100mg/day+50mg/day of clofazimine+600mg/day of rifampin for 2 years.

38. At the end of treatment ,visible skin lesions may still be present
At the end of treatment ,visible skin lesions may still be present . * special care is needed with 2 types of lepra reactions that can occur during treatment. Type 1 reactions:are caused by cell mediated immune inflammation within exisisting skin lesions. They generally occur with borderline leprosy. Type 2 reactions:are mediated by immune complexes and occur in lepromatous patients. -Type 1 reaction present with inflammation of exisistng lesions,no systemic symptoms,lesions swell erythematous tender. -Treatment of type 1 reac. :-Steroid(prednisolone),clofazmine,cyclosporine

39. Type 1 reaction

40. Type 2 reaction

41. Type 2 reac. Occure in half of patients with borderline lepromatous or lepromatous lep. * It is called erythema nodosum leprosum.(Type 2). *present with multisystemic involvment and accompanied by systemic symptoms (fever, myalgia,arthralgia,anorexia). *Skin lesions are erythematous subcutaneous &dermal nodulesmwiddely distributed,donot occur at sites of exisiting lesions,which can ulcerate, and favor extensor arms & medial thighs. -Treatment of type 2 reac.:- Thalidomide drug of choice.

43. Prevention
BCG vaccination.
Chemoprphylaxis sometimes used.