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Leprosy pp 75-110 | Cite as

Clinical Features

  • Enrico Nunzi
  • Cesare Massone
  • Salvatore Noto
Chapter

Abstract

The wide range of cutaneous clinical features of leprosy arises from the interaction between Mycobacterium leprae and the cell-mediated immunity of patients; clinical aspects can be seen in a spectrum (Ridley–Jopling) which ranges from the tuberculoid (TT) hyperergic pole to the lepromatous (LL) anergic pole. TT is characterized by single or a few lesions (macules, plaques, and papules) grouped together, asymmetric arrangement, well-defined edges, and anesthetic dry surface. LL is characterized by large number of lesions (macules, plaques, and nodules), smooth surface, preserved sensitivity, presence of acid-fast bacilli (AFB), and symmetric distribution pattern. Between these two extreme forms there is an interpolar or borderline group where it is possible to distinguish BT, BB, and BL. BT leprosy has anesthetic, asymmetric lesions (which include macules, plaques, and papules). In the middle part of the spectrum (BB form) there is high immunological instability with propensity for type 1 leprosy reaction. The BB form is clinically characterized by lesions with symmetric distribution, polymorphic aspect, and AFB presence in lesions. The BL form has symmetric arrangement of lesions (macules, plaques, and nodules), but they are fewer than in the anergic LL form and they contain AFB.

Keywords

Lepromatous Leprosy Tuberculoid Leprosy Leprosy Reaction Annular Lesion Skin Smear 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. 1.
    Sehgal VN, Srivastava G (1987) Indeterminate leprosy. A passing phase in the evolution of leprosy. Lepr Rev 58:291–294PubMedGoogle Scholar
  2. 2.
    Nunzi E, Fiallo P (1995) Leprosy: a dicotomous disease. Eur J Dermatol 5:649–652Google Scholar
  3. 3.
    Noto S, Clapasson A, Nunzi E (2007) Classification of leprosy: the mystery of “reactional tuberculoid”. G Ital Dermatol Venereol 142:294–295Google Scholar
  4. 4.
    WHO Expert Committee on Leprosy (1988) WHO Technical report series n. 874. Seventh report p7Google Scholar
  5. 5.
    Uplekar MW, Antia NH (1986) Clinical and histopathological observations on pure neuritic leprosy. Indian J Lepr 58:513–521PubMedGoogle Scholar
  6. 6.
    Jopling WH (1956) Borderline (Dimorphous) leprosy maintaining a polyneuritic form for eight years: a case report. Trans R Soc Trop Med Hyg 50:478–480PubMedCrossRefGoogle Scholar
  7. 7.
    Yoder LJ, Jacobson RR, Job CK (1985) A single skin lesion—an unusual presentation of lepromatous leprosy. Int J Lepr 53:554–558Google Scholar
  8. 8.
    Mascaro JM, Ferrando J, Gratacos R (1981) Leopromatous leprosy clinically localized to one-half of the face. Report of a case. Int J Lepr 49:315–316Google Scholar
  9. 9.
    Maroja MF, Lima LL, Pereira PMR, De Oliveira RML, Massone C (2010) Zoster-like segmental presentation of Lepromatous leprosy. Lepr Rev (in press)Google Scholar
  10. 10.
    Taylor PM (1982) The Clinical Diagnosis of dapsone resistant leprosy. Lepr India 54:117–122PubMedGoogle Scholar
  11. 11.
    Price EW, Fitzhebert M (1966) Histoid (hight-resistance) lepromatous leprosy. Int J Lepr 34:367–374Google Scholar
  12. 12.
    Kroll JJ, Shapiro L (1973) The histoid variety of lepromatous leprosy. Int J Dermatol 13:74–78CrossRefGoogle Scholar

Copyright information

© Springer-Verlag Italia 2012

Authors and Affiliations

  1. 1.Department of DermatologyUniversidad Tecnica Particular de LojaLojaEcuador
  2. 2.Department of DermatologyMedical University of GrazGrazAustria
  3. 3.Consultant for: Centre for Research in Leprosy and Tropical Dermatology (CIRLEP)University of GenoaGenoaItaly

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