258^ International .lourilal 01 . Leprosy^ 1983

components of lepra cells. Int. J. Lepr. 28 (1960)22-37.

8. KtiANoir: AR, V. R. Pathology. olleprosy. In: /Ap-t:H.9• in 'Amu and Practice. 2nd ed. Cochrane. R.G. and Davey, T. E., eds. Bristol: John Wright &Sons Limited. 1964. pp. 125-151.

9. Nit s. K. I he significance or the vacuole mVirchow lepra cells and the distribution of lepracells in certain organs. Tok■o .1. Med. Affair, 2066(1918) 1-7. English translation in Int. J. Lepr. 4(1936) 491-507.

10. SAKURAI, 1. and SKINSNES, 0. K. Lipids in leprosy.2. Histochemistry of lipids in human leprosy. Int.J. Lepr. 38 (1970) 389-41)3.

11. Surat. K. Ilistopathologieal studies on humanleprosy. IV. Itistochemical analysis of abnormalfats in lepromatous leprosy especially on it de-position in lymph nodes. Lepro 27(1958)216-227.

12. l'AstAmoio, 7., NisintiRA, M., IIAR \ ‘, N. andDv T. Electron microscopy of ultra-thin sec-

tions of lepra cells and .11. hprae. Int. .1.1.epr. 26(1958) 1-8.

Co-incident (Simultaneous) Dapsone Sensitivity andDapsone-resistant Leprosy

To THE EDIT OR:

It was interesting to read the letter of Dr.McDougall and Dr. Felton Ross [1.11_, 50(1982) 214-215] concerning co-incident (si-multaneous) dapsone sensitivity and dap-sone-resistant leprosy. They ask whetherleprosy workers in other parts of the worldhave observed findings similar to theirs.

This occurrence was first proved by work-ers from the British Medical ResearchCouncil's unit in Sungei Buloh, Malaysia,in the initial series of papers which provedthe existence of sullbne-resistant leprosy.

Our Indian patient No. 5075 was No. 1in the first seven cases we studied for resis-tance ( 2 ) and also No. 1 in the more detailedreport printed in 1966 ('). Although the sen-sitivity tests that were first performed foundhim to have a strain of dapsone-sensitiveorganisms. his Morphological Index did notdiminish as much as might have been ex-pected after six months on injectible DDS(600 mg weekly).

This case was reported in much greaterdetail in 1968 as "A Case of 'Partial' Resis-tance" (') which describes how his Mor-phological Index fluctuated wildly while onsulfone treatment. In March 1963 the biop-sies (we always took two from different sites)showed definite active lepromas and he wastreated with 300 mg of dapsone twice week-ly. About eight months later further biopsiesseemed quiescent although Dr. Ridley not-

ed "one more than the other." In April 1964however the biopsies again showed defi-nitely active leprosy. In the next eightmonths he had a severe bout of emhemanodosum leprosum which we believe is as-sociated with successful anti-mvcobacterialtherapy. yet by February 1965 the biopsiesstill showed definite evidence of activity. Atthat time he was put on clolazimine therapyand from then on got steadily better by allcriteria—clinical, bacteriological, andpathological.

we were treat i ng a pat i ent whose i n i t i a l

lesions showed dapsone sensitivity but whoimproved and then got worse while undertreatment—the skin plaques got smaller buta diffuse skin infiltration appeared.

In those early days we were not yet ableto recognize the clinical appearance of sul-fone-resistant leprosy, but in retrospect it isobvious that this patient had some lesionscontaining resistant organisms and otherswith sensitive organisms. We said in oursummary that it was likely that more casesof this type will be found. Apparently thisis now the case.

We must therefore accept that resistantleprosy may be due to two things:

1) The development of a resistant clonein a patient most of whose bacilli are sul-fone-sensitive. It is a moot point whetherthis clone develops because of inadequatetherapy or whether it was always there and

51, 2^ Correspondence^ 259

only revealed when the sensitive populationdisappeared.

2) Any lepromatous patient under satis-factory sulfone treatment is liable to catcha resistant form of leprosy, particularly ifsuch immunologically susceptible individ-uals are living in a place where other caseswith resistant organisms are likely to befound.

Some time ago I was asked to write anarticle for the "house paper" of a famousleprosari urn and I wrote to the effect thatleprosaria should be closed down—it wasnot published. It seems to me to be the heightof stupidity to send lepromatous patientsfor admission to a hospital where, almostby definition, they are likely to meet sul-lone-resistant mycobacteria. If this contin-ues (to repeat our warning of 15 years ago).

it is likely that more cases of this type willbe found.

—John FL S. Pettit. M.D.. F.R.C.P.Won/ .303China In.syrance Building174 Milan Twinkle Abdul RahmanKuala Lumpur„Ilala•.sla

REFERENCESI. PLARsoN, J. NI. IL.^ iii, I „I. II. S. and Rrrs. R. J.

W. Studies in sullone resistance in leprosy. 3. Acase of "partial - resistance. Int. J. Lei - . 36 (1968)171-178.

2. 1 3 1:1 - 1 it, .1. H. S. and RiTs, R. J. W. Sulphone re-sistance in leprosy. An experimental and clinicalstudy. Lancet 2 (1964) 673-674.

3. I, J. Ii. S.. RI rs, R. J. W. and Rummri. D. S.Studies in sullone resistance in leprosy. I. Detection()leases. Int. J. Leff. 34 (1966) 375-390.

Serum Levels of C3-activator (Antifactor B) in Leprosy

To rHe Eorroit:There have been previous reports that

during the eruption of crops of erythemanodosum leprosum (EN L) raised C2 and C3levels in the sera of patients have been ob-served ( 1' 7 ). These two components are in-volved in the classical immune complexpathway of complement activation.

(73-activator (Antifactor 13) is involved inthe alternative pathway activation of com-plement ( 1 ), and recently .1/ycobacteriumleprac bacilli have been shown to activatethe alternative pathway of complement ( 3 ).It was considered pertinent to determinehow the value of C3-activator varies in theleprosy sera, particularly during ENL wheninitially immune complexes and .11. lepracbacilli could activate both paths of comple-ment separately.

Sera were collected from 9 ENL, 3 non-ENL and I borderline patients from Japanand Addis Ababa, Ethiopia. The concen-trations of C3-activator, the third compo-nent of complement (C3c) and immuno-globulins (1gG, IgA and IgM) in the patients'sera were determined by the radial im-

munodiffusion method of Mancini. et al.('). using the standard immunoglobulin seraand the Partigen " immunodiflusion platesmanufactured by I3ehringwerke AG (1\ lar-burg-Lahn) of West Germany.

Measured 5 pl volumes of the standardsof Ig(i, IgA, IgM, C3c, and C3-activatorwere introduced into the first three wells andthe same volume of test sera introduced intothe remaining nine wells of each plate. The13 mg/m1 protein standard plasma used for(73-activator determination was used neat,diluted 1:2 and diluted 1:4 for the threestandard wells. All the plates were allowedto stand at room temperature for 48-72 hrbefore the diameters of precipitin ringswhich developed around the wells weremeasured, using a Behringwerke precisionmeasuring viewer. Graphs were plotted ofring diameters against the logarithm of thestandard concentration, and the concentra-tions in the samples were determined fromthe plots. The results are given in The Table.

Moderate increases in the serum levels ofC3-activator were observed only in ENLcases. The lowest values were observed in