INTERNATIONAL JOURNAL OF LEPROSY^ Volume 48, Number 2Printed in the U.S.A.

Striated Muscle in Four Categories of Leprosy.I. Histology and Histochemistryi

Shirin M. Daver, Darab K. Dastur,C. R. Revankar, and J. S. Shah'

Muscle changes in leprosy have been re-ported infrequently despite the fact thatmore than 20% of leprosy patients sufferfrom motor deficits and paralysis of mus-cles ("'). In fact, according to the AmericanLeprosy Missions, leprosy "causes morehand paralysis than all other diseases puttogether."

Hoggan ( 2") has been credited with theearliest report of muscular atrophy in lep-rosy. From their own considerable clinicaland some pathological experience of nerveand muscle tissue in leprosy, Hansen andLooft (''), as far hack as 1895, agreed withthe suggestion of Hoggan that "the mus-cular affection in leprosy" was essentiallyan atrophy and secondary to the neuritis.The various stages of degeneration of themyoneural endings and denervation atro-phy were described by Dastur ( 1). M. lep-rae have been reported in the muscle, main-ly between striated muscle fibers, byIshihara ( 2 '), Convit, et al. ( 1 ), and Pearson,et al. ( 27) and in intramuscular nerve twigsby Dastur (I). Harman ('") rightly stressedthe frequent bacillation of smooth musclefibers in the skin, the lips, and the nipple inlepromatous leprosy.

Most detailed reports dealing with path-ological changes in nerves omit any men-tion of skeletal muscle changes. Convit, etal. (") described degenerative changes inthe muscle as "leprous myositis." In astudy of muscles, intramuscular nerves,and nerve endings in leprosy, Dastur ( 4 .")

' Received for publication on 22 May 1979; acceptedfor publication in revised form on 28 February 1980.

2 S. M. Daver, M.Sc., Senior Research Assistant;D. K. Dastur, M.D., D.Sc., F.A.M.S., F.R.C.Path.,Professor of Neuropathology; Neuropathology Unit,Post-Graduate Research Laboratories, J. J. Group ofHospitals, Bombay-400 008, India; C. R. Revankar,M.B.B.S., D.V.D., Medical Officer; J. S. Shah, M.B.,M.S., Hon. Plastic Surgeon; Acworth Leprosy Hos-pital, Bombay-400 031, India.

stressed the relative infrequency of changesconsistent with a leprous myositis (in lessthan 10% of specimens), which was at timessecondary to intramuscular leprous neuri-tis. This has been reviewed recently ( 23). Tothe best of our knowledge, the histochem-istry of muscle in leprosy has not been stud-ied at all.

In the present study, histological changes,as seen in frozen and paraffin embeddedsections of striated muscle, are reported.Ultrastructural examination of the muscleof the same cases has also been carried outand will be reported in the second paper ofthis series ( 7 ).

MATERIALS AND METHODSClinical material. The clinical material

comprised 4 groups of leprosy patients. Ex-cept for group IV, all the patients were re-porting as fresh, untreated cases to the out-patient department of Acworth LeprosyHospital, where they were examined, se-lected, and biopsied.

The 7 patients of group I manifested veryearly non-lepromatous leprosy, generally ofthe early macular tuberculoid variety. Theywere bacteriologically negative as deter-mined from smears of skin clips of the cu-taneous lesion and the ear lobule. Each pa-tient had only I or 2 small skin lesions,which were flat, hypopigmented, and hyp-esthetic to anesthetic. A full thickness bi-opsy of the periphery of the skin lesion,which included a part of the surroundingnormal skin, was carried out in each case.The essential finding in variously stainedparaffin sections of these biopsies was thepresence of few or many inflammatory ex-udates consisting of small mononuclearcells with only a stray larger mononuclearcell. Epithelioid cells or giant cells were notseen. Lepra cells or bacilli were not en-countered in any specimen. None of thepatients had any signs or symptoms refer-able to the peripheral nerves except for

140

48, 2^Dover, et al.: Histo/ogy of Muscle in Leprosy^141

slight tenderness of the ulnar nerve in 2 pa-tients. None of them showed any weaknessof the ulnar or median nerve supplied mus-cles of the hand or forearm nor wasting orweakness of the muscles of the lower limb.

The 2 patients of group II had untreatedtuberculoid leprosy of long duration andwere also bacteriologically negative on ex-amination of skin smears or of the fullthickness skin biopsies. There were multi-ple skin lesions which were small or large,generally pale, and occasionally well de-fined with raised edges. Paraffin sections ofthe biopsy specimen of I of these lesionsshowed a florid mononuclear cell reaction,with more large mononuclear cells than inbiopsies of group 1. One of the 2 specimensshowed prominent epithelioid cells and afew giant cells organized to form "tuber-cles' . and also clear infiltration of the deepdermal nerves. Of the peripheral nerves,the ulnar was most thickened, but othernerves of both the upper and lower limbswere also found thickened on palpation.The ulnar supplied hand muscles werefound weak in both cases with wasting inI case (the one with the more severe reac-tion in the skin lesion described above).

Group III comprised 5 patients with es-tablished untreated lepromatous leprosy.They were bacteriologically positive witha large number of acid-fast bacilli in boththe skin clip and nasal smears. Biopsy spec-imens of the skin from the edges of the in-cision on the hand showed a few exudateswith lepra cells in addition to small mono-nucleus. There were no discrete lesions,but there was generalized infiltration of theskin, including thickening of the ear lob-ules. The ulnar, greater auricular, and othernerves were found thickened and tender.Two of the patients showed weakness andwasting of hand muscles with contracturesof the medial fingers: one showed weaknesshut no wasting: and 2 others were unre-markable in respect to the power of thesemuscles.

The 7 patients of group IV were of thelepromatous type and had taken the pre-scribed course of treatment with dapsone(DDS), 100 mg daily for 6 days a week, con-tinuously for 11/2 to 6 years. The dapsone/creatinine ratio in urine was measured in allpatients of this group and was found to bewithin normal limits for patients taking this

dose of dapsone (35 and over) in 6 of them.In I patient (J/45), this ratio was markedlylow (10.5), indicating that he alone waseither not taking treatment adequately ornot absorbing his dapsone. All patientswere bacteriologically positive on skin clipand nasal smear examination with predom-inantly granular forms of AFB at the timeof biopsy. At this time, 6 of the patientsshowed no overt cutaneous lesions. Onepatient (J/45) presented with ill-definedcongestive lesions with a nodular surfaceover the ears, along the forearm, and on thehand, which probably represented either aform of reactive leprosy or an allergic re-action since these did not contain bacilli,and the patient was afebrile and asympto-matic. At operation, there were clear adhe-sions between the skin and the first dorsalinterosseous muscle in these patients. Ofthe peripheral nerves, the ulnar was foundthickened in all, and in I case, the radialand lateral popliteal nerves were also thick-ened. There was weakness of adduction/ab-duction of the thumb and fingers in 3 of the7 patients (including J/45), the power of thehand muscles being normal in the others.Patient J/45 also showed wasting of thesemuscles.

Surgical procedure. The first dorsal in-terosseous muscle was biopsied in all thecases except 4 cases of group I where theflexor carpi ulnaris was biopsied. The for-mer muscle was biopsied because the nerveselected for simultaneous study was the in-dex branch of the radial cutaneous nervefrom the dorsum of the hand, and the latterwas biopsied along with I or 2 funiculi ofthe ulnar nerves in and above the elbowgroove by the plastic surgeon (J.S.S.), as-sisted by the neuropathologist (D.K.D.).The other important reason for the selec-tion of these particular pairs of nerve andmuscle biopsies was the well-known factthat these 2 nerves, the radial ( 6 ) and theulnar Oh are damaged early and selectivelyin leprosy of all types.

Laboratory methods. For routine histol-ogy the specimens were fixed in formalin,blocked in paraffin, and the sections stainedwith hematoxylin and eosin. For quantita-tion, the smallest fiber diameter in formalinfixed and frozen cross sections was mea-sured by stage and eyepiece micrometry,and fiber size spectra were plotted.

3D

142^ International Journal of Leprosy^ 1980

41%.40.rift& Jitti% $1.5..7704

FIG. Ia. (NP/K/6): Weak muscle from a patientwith lepromatous leprosy, showing muscle fascicles

with small or large well-defined or ill-defined groups

of atrophic fibers contrasting with the better preservedfibers. (II. & x250)

A portion of the biopsy specimen wassnap-frozen in isopentane cooled in dry ice,and I() ,um sections cut in a cryostat at–20°C. The histochemical reactions stud-ied for determining fiber types were succin-ic dehydrogenase ( 17 ), adenosine triphos-phatase ( 25), and phosphorylase ( 2"). Thethiolacetic acid esterase method of Wach-stein, et al. ("") was followed for the dem-onstration of acetylcholinesterase at themotor end-plates.

RESULTSHistology. Striated muscles from the pa-

tients in group I revealed a normal histol-ogy of well-organized fascicles with com-pactly arranged fibers. Fiber diametermeasurements showed that there were nofibers smaller than than 34 ,um in size, theaverage diameter being 52 ,um in frozensections and 40 tan in paraffin sections.

Of the 2 specimens in group II, atrophywas evidenced as a generalized reductionin the size of all the fibers in I case and asgroups of small fibers in the other patient,who was clinically more severely affectedand who showed the florid tuberculoid re-action in the skin. The average fiber diam-eter was lower than that in group I (25.5pin in paraffin sections).

In group III, 2 patients who had no wast-ing or weakness of their hand musclesshowed an essentially normal histologicalpicture. The others, who presented withwasting, weakness, or clawing of fingers,showed atrophy (Figs. Ia and lb), at timesthe entire muscle being made up of verysmall fibers and fascicles (Figs. 2a and 2b).Muscle fibers from the atrophic areasshowed angularity and nuclear prominence.

K - 6

1111111111pH. Fibre Diameter (um)

FIG. lb . Histogram of fiber diameters of the samemuscle shows a large proportion (56%) of small-sized

fibers below 2(1 pm in site and a very small proportion

(I5%) above 40 pm.

In addition to the atrophy, 2 cases alsoshowed some myopathic features. In someareas, there was moderate to marked vari-ation of fiber size and rounding, some fibersshowing central nucleation. Occasionalmuscle fibers undergoinc, necrosis, evi-denced by collections of large mononuclearcells, were also seen (Fig. 3a) in the patientwith moderate weakness of the hand mus-cles and early contractures (see clinicalmaterial).

The biopsies in group IV showed mainlylarge fascicles with compactly arranged fi-bers. These fibers showed little or no vari-ation in size except in I case (with mildweakness of the hand muscles) where I or2 groups of atrophic fibers were seen. Theaverage frozen fiber diameter in these caseswas 51 p.m (comparable to that in group I)except in I specimen (1\11 3/J/45, see clinicalmaterial), where all the fascicles were madeup of highly atrophic fibers (average fiberdiameter-20 ,um). Slightly more than theusual variation in fiber size was found inspecimens from 3 of the 7 cases of thisgroup, all 3 of whom had clinically unaf-fected muscles.

Fite-Faracco stained sections showedacid-fast bacilli (AFB) in 3 of the 5 untreat-ed lepromatous patients (group III). Thesebacilli were not within the muscle fibers hutin an exudate between fibers in I case (Fig.3b) and in endothelial cells of blood vesselsin the other 2 cases (Fig. 3c). AFB weredetected in the muscle in only I of the 7treated lepromatous cases (group IV) andagain in a vessel wall.

nn

48, 2^Duvet-, et al.: Histology of Muscle in Leprosy^143

FIG. 2a. (NP1K13 I): Weak muscle from a lepro-

!maims patient: an entire fascicle made up of angulatedatrophic fibers with apparent nuclear increase between

2 other fascicles with polygonal normal-sized fibers.

(H. & E., x250)

Enzyme histochemistry. Histochemicalpreparations for succinic dehydrogenase(SDH), phosphorylase, and myosin adeno-sine triphosphatase (ATPase) revealedType I and Type II fibers to he well distrib-uted in a checkerboard pattern in all biop-sies of group I, especially as seen by theATPase reaction (Fig. 4a). An actual countshowed the average ratio of Type I to TypeII fibers to be 1:1.6 for the flexor carpi uI-naris (FCU) and I:1 for the first dorsal in-terosseous muscles. The histograms for thediameters of the 2 fiber types confirmed theimpression that there was no appreciabledifference between the fiber types with re-spect to size.

Similar preparations of the specimens ingroup II showed a preponderance of TypeI fibers (Type I:Type II = 1:0.4). In someareas the Type II fibers were grouped to-gether, giving type grouping.

In group III, the muscle biopsies againshowed type preponderance and typegrouping. The graph of fiber types clearlyshows the Type II fibers to include smalland large sized fibers whereas the Type Ifibers were of uniform size. In addition, theclinically weak muscles showing atrophy inparaffin sections contained small fibers ofboth types. Sometimes, there were groupsof atrophic fibers all belonging to Type II,thereby manifesting type atrophy (Fig. 4b).

All the specimens of group IV showed afairly constant picture of Type I prepon-derance, and most of them showed typegrouping without atrophy (Fig. 5a). Thus,type grouping was encountered in clinically

K-31

20^

HI& E(Ple:1;4

(Paraffin)ewn

' 10

tot

0 1^I 2^ 0

Fibre Diameter (um)

FIG. 2h. Histogram of fiber diameters, showing awide range of size. The very small fibers (under 20

pcm) represent the atrophic fascicle and the larger fi-bers the lateral fascicles in Fig. 2a.

weak muscles as well as in those whichwere clinically unaffected. In the I muscleshowing severe atrophy (NP/J/45), theatrophic fibers were of both types, hut thelarger fibers were mainly of Type II (Fig.5b).

Preparations of cholinesterase reaction atmotor end-plates revealed a rich spray ofinnervation in the muscles of group IV pa-tients (Fig. 6a). In contrast, in the speci-mens showing fiber atrophy in groups IIand III, the end-plates were scanty andtended to he abnormally expanded withoutlying droplets of activity (Fig. 6h).

DISCUSSIONHistology. The most conspicuous change

in the present material was a decrease inthe size of the muscle fibers. The atrophiedfibers occurred in well-defined or ill-definedgroups, and many were angulated, con-forming to the classical description of de-nervation ('), and were probably secondaryto leprous neuritis. The only report on the

r

wit. •Fin. 3a. (NP/K/39): Slightly weak muscle from an

untreated lepromatous patient, showing a longitudinal

section of muscle fibers, I of them undergoing necrosis

and replaced by a collection of large mononuclear cells(phagocytes). (H. & E., x625)

144 International Journal of Leprosy 1980

FIG. 3h. (NP/J/993): Perivascular exudate between

muscle fibers, showing a number of acid-fast bacilli.Note the large cluster on the neurovascular bundle

arching onto the fiber on the right (arrow). (Fite-Far-

acco, x1400)

l'IG. 4a. (NP/I/976): Muscle showing no clinical

wasting or weakness: normal checkerboard pattern of

dark Type II fibers and lightly stained Type I fibers.

The 2 types of fibers are seen in equal proportions.

(ATPase x100)

tgl• ?Oft44 4. 177..sh OM* rei•Ci

correlation between clinical and histologi-cal features of skeletal muscle in leprosy isthat of Dastur ( 1 ) on 60 patients, the major-ity of whom were non-lepromatous. Thelargest number of muscle specimens show-ing normal or only slightly affected histol-ogy was encountered among patients withclinically unaffected muscles (12 of 15).Correspondingly, the largest number ofspecimens showing pronounced pathologi-cal changes was derived from patients withclinically severely affected muscles (20 outof 28). Groups of atrophic fibers along withfloccular and vacuolar change in the sar-coplasm were seen by Slotwiner, et al. ( 25 )in muscles from patients with leprosy whowere negative for acid fast bacilli.

For many years atrophy of muscle fiberswas considered to be an effect of denerva-tion only. The occurrence of sarcoplasmic

411i^4riir -44 ^ii. ....* \^411

FIG. 3c. (NP/K/31): A single rod-shaped bacillus

(arrow) in an endothelial cell of a blood vessel. (Fite-

Faracco, x1400)

changes in otherwise well-defined neuro-genic disease with no evidence of any otherprocess was subsequently noted by Engel(9 in spinal muscular atrophy. Drachman,et al. (") have provided striking evidence ofthe myopathic histopathology of muscle inlong standing neurogenic atrophy. Drach-man, et al. CI found many features of"myopathy, — including inflammatory, de-generative, and regenerative changes with-in a month after experimental denervationof extraocular muscles.

In our observations reported here, onlyneurogenic changes were seen in the estab-lished tuberculoid group, the duration of

4h. (NP/K/6): Better preserved fascicle madeup of larger Type I fibers; a group of atrophic Type II

fibers in the center (arrow) and parts of 2 fascicles

with atrophic 'Type I fibers (in lower left corner), rep-

resenting type atrophy in a clinically weak muscle

from an untreated lepromatous patient. (ATPasex 100)

48, 2^Darer, et al.: Histology of Muscle in Leprosy^145

5a. (NP/J/201): Clinically unaffected muscle:parts of 3-4 fascicles showing mainly pale Type I fi-bers. Note the central fascicle with a group of darkType II fihers, suggesting type grouping without atro-phy. I ATPase x1001

symptoms being approximately the same inthe untreated tuberculoid and lepromatousgroups. Myopathic changes, i.e., fiber sizevariation, some rounding and occasionalcentral nucleation, inflammation, and ne-crosis were encountered, in addition toconsiderable atrophy, in the lepromatouscases. Considering the light microscopicfindings only, 2 of the 5 muscles from un-treated lepromatous cases and 2 of the 7from treated lepromatous patients showedacid-fast bacilli, generally in the inflamma-tory exudate between muscle fibers or fas-cicles. It may he recalled that 3 of the 6lepromatous patients of Dastur ( 1 ) showedintramuscular bacilli, in 2 cases in interfas-

^4IP^.^pit^as, t

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e.^1 ^4^1

■IC^1

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►i 4

, .^t im .1^•

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FIG. 6a. (NP/J/245): Clinically normal muscle froma treated lepromatous patient, showing a normal com-plement of motor end-plates. Note that there is gen-erally I end-plate on I muscle fiber. (Cholinesterasex100)

cicular nerves and in I instance betweenmuscle fibers. Likewise, of the 2 other in-stances when bacilli were seen in relationto intrafusal muscle fibers (within the"spindle"), by Patel, et al. ( 2") in a patientand by Edwards (") in a mouse, they wereclearly on the muscle fiber (') (and not with-in it) and in the capsule cells of the spindle("), respectively.

Histochemistry. There has been some ar-gument whether a given denervative pro-cess acts selectively on I or another typeof muscle fiber. In long standing denerva-tion of muscle, the atrophic fibers are ofboth types histochemically, thus helping to

Ftc. 5h. (NP/J/45): Clinically weak and wastedmuscle, showing severe atrophy of fibers, both paleType I and dark Type II fibers being atrophied exceptat lower left quadrant where there is a cluster of smallType II fibers representing type atrophy. Type II fi-bers constitute the majority of the better preservedfibers. (Phosphorylase x100)

FIG. 6h. (NP/K/6): Weak muscle from a patientwith lepromatous leprosy, showing motor end-platesof varying size and shape including some which appearexpanded (split arrows) and sonic shrunken (arrows).the latter on atrophied fibers. (Cholinesterase x320)

146^ International Journal of Leprosy^ 1980

distinguish this condition from those withselective atrophy of I fiber type. "Typeatrophy" of any fiber type is generally ac-cepted to indicate a denervation processparticularly affecting anterior horn cells( " '). To the best of our knowledge, the pres-ent investigation reports for the first timehistochemical findings on the striated mus-cle in leprosy.

In the present observations, there was nopreferential atrophy of either type in thespecimens of the tuberculoid group where-as some "type atrophy," especially ofType II fibers, was observed in the lepro-matous group. Type II fiber atrophy hasbeen recorded in such diverse situations asmental retardation ( 2 ) and collagen vasculardisease (''). Perhaps this occurrence ofType 11 fiber atrophy should signify that themuscle is inactive. "Type grouping,"another activity characteristic of denerva-tion, probably represents a process of rein-nervation of previously denervated fibers.It is usually a feature of long standing andrelatively slowly progressive neuropathies.Type grouping was seen in our material inthe lepromatous groups.

Histologically normal looking muscle re-vealed a rich supply of motor end-plates,demonstrated by their cholinesterase activ-ity. In the atrophic muscles, the end-plateswere scanty, and at times they could not hediscerned at all in the severely affectedcases. Lubinska ( 22) found an abrupt fall incholinesterase activity after denervation offast and slow muscles of the rat at birth.The slow muscles were more affected thanthe fast. Miledi and Slater ( 2 ') found thatcholinesterase was clearly visible in bothnormal and denervated muscle even severalmonths after nerve degeneration.

The elongated or multiple end-platesseen in myasthenia gravis might he causedby a change in the muscle fiber surfacemembrane consequent to the interruptionof neuromuscular transmission (' 2 ). Duchen(") has suggested that interruption of neu-romuscular transmission may he responsi-ble for axon sprouting. He observedmarked sprouting following intramuscularinjection of botulinum toxin. When the ax-onal sprouts make contact with the surfaceof a muscle fiber, they appear to induce inthe sarcolemma, by invagination, the for-mation of a groove constituting a miniature

synapse. The synapse formation is readilydetected in acetylcholinesterase prepara-tions because of the rich acetylcholinester-ase activity of the invaginated sarcolemma.The development of new end-plates seemsto result in the formation of a structure ex-ceeding in size and complexity the originalend-plates ("2). The few end-plates whichappear larger, with multiple droplets, in theleprosy muscle could therefore be due toreinnervation by axonal sprouting. At-tempts at regeneration were reported as arare occurrence in vitally stained whole-mount preparations in leprosy patients ( 4 ).

In these 4 groups, there was some cor-relation between clinically detected mus-cular weakness, on the one hand, and great-er atrophy (in all groups) and degeneration(in groups III and IV) by all parameters oflight microscopy, on the other. These find-ings are confirmed by subsequent electron-microscopic examinations ( 7 ).

SUMMARYThis histological and histochemical study

of muscle in leprosy was carried out in viewof the paucity of such studies despite thefact that leprosy is the single largest causeof motor deficit and paralysis. There were21 patients who fell into 4 groups: thosewith very early non-lepromatous leprosy(group I, 7), untreated tuberculoid leprosyof long duration (group II, 2), untreated lep-romatous leprosy (group III, 5), and treatedlepromatous leprosy (group IV, 7). A nor-mal histological and histochemical pictureon paraffin and frozen sections stained forATPase and succinic dehydrogenase (SDH)reactions was seen in group 1. While groupsII and III revealed muscle fiber atrophy andtype preponderance, group III also showeddegeneration of some fiber, inflammatoryor necrotic reaction, and, histochemically,type atrophy or grouping. The treated lep-romatous group showed similar hut milderand less frequent changes. Fite-Faraccostained paraffin sections showed acid-fast-bacilli in and around blood vessels betweenmuscle fiber in 2 specimens each of groupsIII and IV. In frozen sections stained forcholinesterase reaction, motor end-plateswere well preserved in groups I and IV hutappeared to he scanty in biopsies of groupII and shrunken or expanded in group III.On the whole, lepromatous leprosy showed

48, 2^Darer, et al.: Histology of Muscle in Leprosy^147

the maximum changes in and around mus-cle fibers, and there was fair clinico-path-ologic correlation in all the groups.

RESUMENEste estuclio histolOgico e histoquimico Lie los intis-

culos en la lepra se realize en vista de IL) escaso de

este tipo de estudios, no ohstante que la lepra es la

was importante causa Unica de disfunción motora yparalisis. Se estudiaron 21 pacientes organizados en

4 grupos: pacientes con lepra muy temprana no lepro-

matosa (grupo I, 7), pacientes con lepra tuberculoidede muy larga evoltici6n y sin tratamiento (grupo II, 2),

pacientes con lepra Icpromatosti sin tratar (grupo III,

5), y pacientes con lepra lepromatosa tratada (grupoIV, 7). En el grupo I sc observO on cuadro histolOgico

e histoquimico normal en los cortes en parafina y en

los cortes en congelación tefiidos para visualizar la

actividad de ATPasti y de SDI!. Los grupos II y III

mostraron evidencias de atrOfia de la fibra muscular

y preponderancia de tipo, el grupo III tambien mostro

degeneraci6n de algunits fibres, reaccion inflamatoria

o necrOtica e, histoquimicamentc, atr6fia de tip() 0

agrupanfiento. El grupo de los lepromatosos tratadosmostro camhios similares pero moderados y menus

frecuentes. En dos especimenes del grupo III y en dosdel grupo IV, los curies en parafina tefiidos por Fite-

Faracco mostraron la presencia de bacilos acido me-

sistentes en y alrrededor de los vasos sanguincos,entre las fihras musculares. En los cortes en conge-

laci6n tefiidos para colinesterasa, las placas terminatesmotoras estuvieron hien preservadas en los grupos I

y IV pero aparecieron escasas en los especimenes de

los grupos II y III, con atrófia grupal.

RESUMEOn a décide de procéder a Line etude histologique

et histochimique du muscle dans la lepre, car de telles

etudes soot mares, et ce, inalgre le fait que la lèpre soilla principale cause de deficit moteur et de paralysie.

On a considéré 21 malades, qui pouvaient etre classés

en quatre groupes. Le groupe I, compost:. de 7 ma-lades, reprenait ceux avec tine lepre non lépromateuse

tres precoce. Le deuxieme groupe était constitue pardes !naiades atteints de lepre tuberculoide depuis long-

temps, et non Mikes. Ce groupe se composait de 2

personnes. Le troiseme groupe reprenait les maladessouffrant de lepre lepromateuse et non traites, soil 5personnes. Quant au quatrieme groupe, it s'agissait de

lepre lépromateuse traitée, 7 malades en tout. Dans legroupe I, on a observe des aspects histologiques et

histochimiques normaux, dans des coupes congelees

et enrollees de paraffine, colorées pour mettre en evi-

dence les reactions it l'ATPase et a la SDH. Alors queles groupes II et III révélaient Line atrophic des fibres

musculaires, caractéristique du type de lepre, legroupe III montrait également tine degeneration de

quelques fibres, de meme qu'une reaction inllamma-toire ou nécrotique et, du point de vue histochimique,

Lie I'atrophie caractéristique du groupe. Le groupe le-

promateux traits montrait des modifications ana-

logues, mais plus discretes et moins fréquentes. Lescoupes colorées par la méthode de Fite-Faracco a laparaffine, revélaient des bacilles-acido-resistants dansles vaisseaux, de nléme qu'autour des vaisseaux,

entre les fibres musculaires, et ceci dans deux échan-tillons appartemint effectivement aux groupes III etIV. Dans des coupes congelées, colorees pour [mitre

en evidence la reaction a la cholinesterase, les plaquestermimiles dans les muscles moteurs étitient hien prés-

ervées dans les malades des groupes I et IV, mais

apparaissaient plus mares dans les biopsies provenantdes groupes II et III montrant par ailleurs de l'atrophiccaractéristique de ces groupes.

Acknowledgements. The greater part of this work

was carried out on a research grant from the American

Leprosy Missions, Inc., Bloomfield, New Jersey,

U.S.A., and the terminal part on a grant from theBombay Hospital Trust, Bombay Hospital, Bombay,

to both of which grateful acknowledgement is record-ed. Special thanks are due to the Sir Hormusjee Mody

and Lady Manekhai Mody Trust, Bombay, for general

support of research activities at the NeuropathologyUnit as also to the Nerve-Muscle Research Cell (Dr.

Daya Manghani, In-charge) of the Bombay Hospital,for facilities provided.

Thanks are due to Dr. K. K. Koticha, Superinten-dent, Acworth Leprosy Hospital, for facilities provid-

ed; to Miss N. Patkar, Mr. N. Solanki, and Mr. V.

Darekar of the Neuropathology Unit for the routinehistopathological procedures and the photographicprints.

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