1. Mycobacterial Infections Dr Qassim S. Al- Chalabi

2. Mycobacterial infections They include many pathogens of man, the most important of which are:  M. tuberculosis.  M. leprae.  Atypical mycobacteria.

3. Cutaneous TB The resident Cutaneous TB is caused by M. tuberculosis, an acid and alcohol-fast bacillus. Recently, there is increase in incidence of cutaneous TB due to HIV epidermis, a rise in resistant strains of M. tuberculosis & a decline in TB control efforts

4. Classification of cutaneous TB I)Inoculation TB from an exogenous source Tuberculous chancre. TB verrucosa cutis. II)Secondary TB from an endogenous source: Contiguous spread: scrofuloderma. Autoinoculation: orificial TB. III)Hematogenous TB Lupus vulgaris. Acute miliary TB. Tuberculous gumma. IV)Tuberculids Papulo-necrotic tuberculids. Lichen scrofulosorum. Erythema induratum (Bazin) IMP

5. Primary inoculation complex “Tuberculous chancre” Results from exogenous direct inoculation of M. tuberculosis into skin or mucosa of an individual not previously infected with TB, mainly children. Usually on face or extremities as asymptomatic brownish-red papule or nodule that erodes to form an indurated, non-tender ulcer with sharply demarcated undermined edges. There is prominent regional lymphadenopathy. Tuberculin test is –ve.

6. Tuberculosis verrucosa cutis “TVC” – Warty TB Results from exogenous direct inoculation of M. tuberculosis into the skin of an individual with high degree of immunity. Usually on hands, knees & ankles as asymptomatic papule that slowly evolves into a warty hyperkeratotic irregular plaque that enlarges by peripheral extension.

7. Scrofuloderma From direct extension to the skin from underlying tuberculous focus, usually a LN but sometimes a bone, joint or epididymis. A bluish-red nodule that breaks down to form an ulcer with bluish undermined edges & floor covered with soft granulation tissue. Progression & scarring produce irregular adherent masses. Healing occurs with characteristic puckered scarring.

8. Tuberculosis cutis orificialis In the mucosa or the skin adjoining orifices in a patient with advanced internal TB with weak tuberculin reaction. Painful shallow ulcers with undermined bluish edges with no tendency to heal spontaneously. It occurs around the mouth, anus or genitalia.

9. Lupus vulgaris “LV” The most common type of cutaneous TB. It starts in childhood & progresses very slowly. Tuberculin test is ++ve. It appears commonly on face, neck (90% of cases) or buttocks & limbs, as sharply demarcated, serpiginous reddish-brown soft plaque composed of deep seated nodules.

10. Lupus vulgaris (Cont’d) Slow peripheral extension leading to thin, contractile & unhealthy scar (i.e. new lesions appear in areas of atrophy). Scarring & destruction of underlying structures as nose or ear cartilage usually occurs with various mutilations as microstomia & ectropion, … etc. SCC & less commonly BCC may develop at the margin.

11. Lupus vulgaris (Cont’d) Diascopy test Pressing of LV lesions with a glass slide, to diminish vascularity, yellowish-brown spots appear “apple jelly” nodules.

12. Tuberculosis Cutis Orificialis ScrofulodermaLupus VulgarisTuberculosis Verrucosa Cutis Tuberculous Chancre Autoinoculation from underlying advanced visceral tuberculosis Contiguous spread onto skin from underlying tuberculous infection Hematogenous, lymphatic, or contiguous spread from distant site of tuberculous infection Exogenous reinfectionPrimary (exogenous) inoculation Sensitized host with diminishing immunity Sensitized host with low immunity · Sensitized host with moderate to high immunity Sensitized host with strong immunity Non-sensitized host · Multi-bacillaryMulti- or pauci- bacillary Pauci-bacillaryPaucibacillaryPauci- or Multibacillary, Punched-out ulcers with undermined edges· On mucocutaneous junctions of mouth, genitalia Subcutaneous nodules with purulent or caseous drainage· May develop sinuses and ulcers with granulating bases· Occurs over cervical LN Brownish-red plaque· “Apple- jelly” color on diascopy. Head/neck involvement in 90% of cases Slowly growing verrucous plaques with irregular borders Typically on hand Painless red-brown papule that ulcerates Tuberculous primary complex: regional lymphadenopathy, 3-8 weeks post infection

13. Treatment of TB cutis Isoniazid (INH), usually up to 300 mg daily in adults, orally for 6 ms. Rifampicin, 50 kg  600 mg daily orally for 6 ms. Pyrazinamide, for the 1 st 2 ms. Ethambutol, for the 1 st 2 ms (15 mg/kg) daily. All drugs are taken on an empty stomach once daily.

14. Drug regimens Initial phase, for 2-3 months using at least 3 drugs (e.g. INH, rifampicin and ethambutol). Continuation phase, for several months usually with 2 drugs only (e.g. INH & rifampicin).

15. Tuberculids Tuberculids are a group of skin eruptions associated with an underlying or silent focus of TB. The bacilli are absent from the lesions. The lesions are bilateral & symmetrical occurring in crops with a tendency to spontaneous healing.

16. Papulonecrotic tuberculids Recurring symmetric crops of non-itchy, dusky-red papules on extensor surface of extremities, face, ears & buttocks which undergo central necrosis & heal with pigmented pitted scars. Lichen scrofulosum Grouped, closely set, minute lichenoid, slightly scaly, reddish-brown, often peri-follicular papules. They commonly occur on the trunk & heal without scarring. Erythema induratum “of Basin’s” deep purplish ulcerating nodules occur on the backs of the lower legs, usually in women with a poor ‘chilblain’ type of circulation.

18. Leprosy (Hansen’s disease)

19. Leprosy (Hansen’s dis.) It is a chronic infectious dis., affecting primarily the peripheral nerves & secondarily the skin, mucous membranes & internal organs. More prevalent in tropical & subtropical areas of Africa, south east Asia & Latin America. The estimated no. of leprosy cases in the world  after the introduction of multidrug therapy “MDT” from 12 million in 1980’s to 2.7 million in 1994.

21. Etiology Leprosy (Cont’d) Mycobacterium leprae which is an obligate intracellular parasite. It could be stained by Ziehl-Neelsen method where it is an acid-fast bacillus “AFB”.. It doesn’t grow in usual media, however can be inoculated in mice foot pads & in aramdillo. M. leprae multiplies slowly, so leprosy develops slowly in ms & yrs as compared with hrs & days in case of bacterial dis.

22. Mode of infection Leprosy (Cont’d) Through prolonged close contact of susceptible individual with an open case of leprosy (i.e. untreated pts with multibacillary leprosy with +ve nasal scrapings). Infection may occur through droplet air-borne inf., contact with ulcerated lesions, blood borne. It can be transmitted via the placenta. Genetic predisposition plays an important role. Incubation period= The incubation time for tuberculoid leprosy is up to 5 years and for lepromatous disease may be 20 years or longer.

23. Classification

24. Lepromatous Leprosy.Tuberculoid Leprosy.Clinical features Many organ except GIT,CNS and lungSkin & nerveStructure involvement Innumerable, widespread, symmetrical1-2 (mainly face) asymmetrical No. of lesions Macules, papules & nodules, thickness of face (leonine facies), loss of eyebrow, alopecia Sharply marginated hypopigmented macule, slightly raised purplish rim, hairless Shape of lesion Most peripheral nerves thickened Thickened in vicinity of lesion (great auricle, ulner radial nerve) Involvement of nerve Glove & stocking anesthesia, trophic ulcer of periphery & muscle paralysis Hypoaesthesia & loss of sweating in lesion Manifestation of nerve involvement Nasal crusting, epistaxes, saddle nose, keratitis, infertility NoneOther manifestation YesNoInfectious

26. Leprosy (Cont’d) Slit smears. Nasal scrapings. Skin biopsy Nerve biopsy Lepromin test: is a non-specific test of delayed hypersensitivity reaction, which is of value in classifying a case of leprosy. It is an important prognostic test and is not a diagnostic one. The test is strongly positive in TT type, weakly positive in BT and is negative in BB, BL and LL types. Diagnosis of leprosy

27. Multi-drug therapy (Cont’d) PaucibacillaryMultibacillary Daily (taken at home) Dapsone 100 mg Once a month (taken under supervision) Rifampicin 600 mg 6 months Daily (taken at home) Dapsone 100 mg + clofazimine 50 mg Once a month (taken under supervision) Rifampicin 600 mg + clofazimine 300 mg At least 2 years, preferably until –ve skin smears are obtained. Regimen Duration of ttt

28. Reaction in leprosy Two types of reactions may occur: Type I reaction Type II reaction Type of leprosy Precipitating factor Cause Clinical features Systemic disturbances Associated features Mostly borderline Drug Change in cell- mediated immunity Signs of acute inflammation of existing lesions Unusual Nerve swelling with pain & tenderness Mostly LL & BL Drug & pregnancy Immune complex syndrome Erythema nodosum leprosum (ENL) Fever, malaise, etc. are common Oedema of hands & feet, iritis, mild nerve damage

29. Treatment of leprosy (Cont’d) II)Treatment of reactions Precipitated factors, e.g. immunization, pregnancy & intercurrent inf. should be avoided. Chemotherapy is continued at the usual dosage. Mild reaction: aspirin 600 mg/4-6 hrs or chloroquine 150 mg/8 hrs.

30. Treatment of leprosy (Cont’d) Type I Prednisolone starting at 50-80 mg daily & gradually reducing the dose especially in severe cases. Type II Thalidomide 400 mg at night, never to women in child-bearing period due to its teratogenic effects.

31. Treatment of leprosy (Cont’d) Type II (Cont’d) Clofazimine, increasing the dose to 300 mg daily & reduced gradually to normal within 2 ms to avoid toxicity. Prednisone 30 mg tab. initially, if thalidomide is contraindicated. III)Educate the patient

32. That’s all for today