Clinics in Dermatology (2015) 33, 3845

Histopathology of the lepromatous skin biopsy

Cesare Massone, MD a,, Workalemahu Alemu Belachew, MD b , Antonio Schettini, MD c
a

Department of Dermatology, Medical University of Graz, Graz, Austria

Mekelle University, College of Health Science, Mekelle, Ethiopia
c
Fundation Alfredo Da Matta, Manaus, Amazonas, Brazil
b

Abstract The histopathology of lepromatous skin varies according to the cell-mediated immunity of the
host against Mycobacterium leprae. In tuberculoid and borderline tuberculoid leprosy, epithelioid
noncaseating granulomas predominate, and acid-fast bacilli (AFB) are absent or only rarely present. In
borderline lepromatous and lepromatous leprosy, the infiltrate is composed of macrophages with a
vacuolar cytoplasm, lymphocytes, and plasma cells. AFB are numerous. Edema inside and outside the
epithelioid granulomas, together with the appearance of large giant cells, are the main features of type 1
reactions. A conspicuous neutrophilic infiltrate in the subcutis with or without vasculitis is found in
erythema nodosum leprosum. The main histopathologic features of leprosy and its particular forms are
discussed in this review.
2015 Elsevier Inc. All rights reserved.

The main feature of the vast majority of leprosy biopsy

specimens is a granulomatous infiltrate that has different
features according to the form of leprosy, the time and site of
the biopsy, the presence of a leprosy reaction, and therapy.
The clinical spectrum of leprosy correlates in most of cases
(but not in all) directly with histopathologic results, reflecting
the different grade of cell-mediated immune response (CMI) of
the host against Mycobacterium leprae.14
Although leprosy is a routine diagnosis and well-known
issue in endemic areas, recognition may become difficult in
nonendemic areas, where leprosy may be misdiagnosed as
many different inflammatory dermatoses. In fact, due to
increased immigration from endemic areas, leprosy cases
might be more commonly observed in nonendemic areas,
such as Europe.5
To formulate a correct diagnosis and classification of
leprosy, three cardinal points are needed. First, histopathologic diagnosis of leprosy is impossible without exact

Corresponding author. Tel.: +43 316 385 13235; fax: +43 316 385
14957.
E-mail address: cesare.massone@gmail.com (C. Massone).
http://dx.doi.org/10.1016/j.clindermatol.2014.10.003
0738-081X/ 2015 Elsevier Inc. All rights reserved.

clinical data, such as anamnesis (origin or travels to endemic

countries; contact with leprosy patients; household leprosy
cases); number, distribution, and type of the lesions;
presence or absence of anesthesia; therapies; and other
pertinent signs and symptoms (e.g., of type 1 or type 2
reaction). The final diagnosis and classification of a leprosy
patient in a referral center should always be formulated on a
detailed clinical-pathologic correlation. Second, the skin
biopsy has to be correctly performed: It must be deep (at least
4 mm punch biopsy including part of the subcutaneous fat)
and without artifacts (squeeze).6 Lastly, a representative part
of the lesion must be biopsied. This means that in
indeterminate leprosy (IL) the center of a small hypopigmented lesion (or better, the center of the anesthetic area) or
the border of an annular macule has to be biopsied. In
tuberculoid (TT), borderline tuberculoid (BT), and borderline borderline leprosy (BB) the infiltrated margins are
diagnostic; in borderline lepromatous (BL) and lepromatous
leprosy (LL), the center of a macule, plaque, or nodule. If a
type 1 reaction (T1R) is suspected, the most edematous and
infiltrated area of the lesion has to be biopsied, whereas in
cases of erythema nodosum leprosum (ENL) the biopsy must
be deep to include the subcutaneous fat.6,7

Histopathology of the lepromatous skin biopsy

Hematoxylin and eosin (H&E) and Fite-Faraco (FF)
stains must be performed on each biopsy specimen by an
experienced laboratory technician. Serial sections are
sometimes needed. Immunohistochemistry of the lymphocytic
infiltrate is never necessary for the diagnosis. Polymerase
chain reaction (PCR) for M. leprae is useful only in a limited
number of cases.
FF is the method of choice for staining AFB; control
sections should be used; and whenever there is doubt, there
should be no hesitation in staining further sections.14
There are several recipes for modified stain for AFB.14,6
AFB are assessed on histopathologic sections exactly in
the same way as in the smear, according to the following
logarithmic indices (bacterial index of granuloma [BIG]):
0: Absence of bacilli
1 +: 1-10 bacilli in 100 high-power fields (HPFs)
2 +: 1-10 bacilli in 10 HPFs
3 +: 1-10 bacilli for HPFs
4 +: 10-100 for HPFs
5 +: 100-1000 for HPFs
6 +: Many clumps, globi (N 1000 bacilli)
Unfortunately, the Ridley-Jopling clinical classification does
not always correlate with the histologic features, and in some
cases, there is a discrepancy between clinical and histopathologic classification. Different authors found an overall agreement between clinical type and histologic type, 58% and 70%,
respectively, with the major disparity observed in borderline
cases.14

39

Tuberculoid leprosy
The granulomatous infiltrate is more often multifocal,
with a typical periadnexal (with involvement of the arrector
pili muscle and sweat glands) and perineural distribution,
both in the superficial and deep portions of the dermis. Skin
adnexa may be also infiltrated and destroyed by the
granulomas (Figure 4). Extension of the infiltrate to the
subcutis is possible.
The granulomas are noncaseating and formed by mature
epitheliod cells, encapsulated by many lymphocytes
(Figures 1 and 2). Numerous large Langhans cells are
pathognomonic. Multinucleated giant cells may be present,
whereas plasma cells are absent. Fibrin in the center of the
granuloma is not observed. The epidermis is often atrophic
and eroded by the granulomas present in the superficial
dermis. There is no clear subepidermal zone.
Nerves are enlarged and swollen. The perinerium is intact
and may be surrounded by lymphocytes. In other cases,
nerves are infiltrated by the granulomas, and they may be
destroyed beyond recognition. Rarely, a patch of fibrinoid
necrosis may be observed. A careful search may reveal few
remnants of nerve tissue in the granuloma. Some authors
report that S100 stain is superior to H&E in identifying nerve
fragmentation in TT, but S100 staining is usually not needed.
AFB are usually absent (AFB: 0 to 1 +) and PCR is negative
in most cases.14
The main differential diagnoses are sarcoidosis, tuberculosis, leishmaniasis, and secondary syphilis. The presence of
plasma cells should suggest consideration of leishmaniasis.
The presence of prominent epidermal hyperplasia favors deep
mycoses, tuberculosis, and leishmaniasis.9,10

Histopathologic patterns of leprosy

The inflammatory cells present in leprosy lesions are
epithelioid cells, macrophages, lymphocytes, plasma cells,
and in specific cases also neutrophils and mast cells.8
According to CMI response to M. leprae, different types of
granulomatous reaction can be observed. Epithelioid cells
are usually seen in TT and BT, whereas foamy macrophages
characterize the infiltrate of BL and LL. The infiltrate can
often touch the epidermis in TT, but only rarely in BT, and
typically spares the epidermis in BB, BL, and LL. Rarely the
infiltrate may be found in the superficial dermis only; more
usually it involves all the dermis and sometimes also the
subcutis. Some cases may be characterized by a prominent
lymphocytic infiltrate, resulting in a diagnostic pitfall. In
each biopsy the nerves have to be carefully checked. The
presence of AFB inside the nerve is diagnostic of leprosy.
Although the polar forms TT and LL are quite easily
diagnosed and classified, borderline cases may sometimes
present overlapping features. For this reason, combinations
of symbols, such as TT-BT, BT-BB, BB-BL and BL-LL, are
used for those cases that show intermediate features among
two groups.14

Fig. 1 Tuberculoid (TT). Multifocal granulomatous infiltrate

in the superficial and deep dermis, periadnexal and perineural.
The granulomas are focally in contact with the epidermis.

40

Fig. 2 Tuberculoid (TT) granulomas are characterized by

noncaseating mature epithelioid cells and are surrounded by
many lymphocytes.

Borderline tuberculoid leprosy

BT presents a similar infiltrate to TT. The main
differences reside in the lesser maturation of epithelioid
cells and in particular the presence of the lymphocytes within
and not only around the granulomas; moreover, granulomas
are less organized and tubercle formation is less prominent
(Figure 3). Undifferentiated, medium-sized giant cells are
typical of BT. The epidermis may or may not be eroded by
granulomas. Nerves typically are moderately swollen and
have perineural and intraneural granulomas. The perineurium is infiltrated by lymphocytes. AFB are 0 to 2 +. PCR is
positive in almost half of cases.14 The main differential
diagnoses are sarcoidosis, tuberculosis, leishmaniasis, and
secondary syphilis.9,10

Borderline borderline leprosy

BB is also characterized by granulomas with immature
epithelioid cells but without the formation of well-defined

Fig. 3 In borderline tuberculoid (BT) granulomas the epithelioid

cells are less mature than in BT and lymphocytes are not only
around but also infiltrate the granulomas.

C. Massone et al.

Fig. 4 Borderline lepromatous (BL). Macrophage granulomas

that infiltrate the superficial and deep dermis, also with periadnexal
and perineural distribution, but that are always separated by the
epidermis by a typical narrow zone (Unna band).

epithelioid granulomas. Giant cells are not present, and

lymphocytes are diffusely distributed. Macrophages represent a fairly significant proportion of cells. There is often
edema. The epidermis is atrophic. The subepidermal zone is
not involved. Nerves are not swollen but are infiltrated by
epithelioid cells and lymphocytes and partly destroyed. A
lamination of the perineurium (reactive proliferation of
perineural cells) may be observed. AFB are 3 to 4 +. PCR is
positive in only almost all cases.14

Borderline lepromatous leprosy

The infiltrate in BL is characterized by the presence of
macrophages (so-called macrophage granuloma) admixed
with lymphocytes. In some cases, lymphocytes predominate
over macrophages (Figures 4-7). A solitary clump of

Fig. 5 Borderline lepromatous (BL). The macrophages have

small vacuoles in the cytoplasm, and there are several lymphocytes
invading the granuloma. Plasma cells are present.

Histopathology of the lepromatous skin biopsy

41

Fig. 6 Borderline lepromatous (BL). In some cases lymphocytes

predominate over macrophages. In these cases the diagnosis might
be a challenge.

epithelioid cells among the macrophages may be found. The

infiltrate can be diffuse, patchy nodular, perivascular, or
periadnexal but always separated from the epidermis by a
typically narrow zone (Unna band) of collagen. Macrophages
have a more or less prominent foamy cytoplasm, especially in
regressing lesions, but no large vacuoles are usually found.
Plasma cells are present. Nerves have an onion-skin
perineurium with lymphocytes forming a cuff around a nerve
bundle. AFB (4 to 5 +) are present inside macrophages,
Schwann cells, endothelial cells, and arrector pili muscles.14

Lepromatous leprosy

Fig. 8 Lepromatous leprosy (LL). Patchy nodular infiltrate of

macrophages in the all dermis without granuloma formation.
A clear grenz zone in the superficial dermis between the infiltrate
and the epidermis is typically present.

LL is characterized by collections and sheets of

macrophages diffusely distributed in the dermis (but also a
patchy nodular arrangement can be found). Lymphocytes
and plasma cells are diffusely scattered or in a clump. There
are no epithelioid cells. The epidermis is atrophic, and a clear
grenz zone (Unna band) in the superficial dermis between the
infiltrate and the epidermis is typically present (Figure 8).
Skin adnexa are surrounded by macrophages and are

atrophic. The infiltrate can extend to the deep dermis and

subcutaneous fat.
Macrophages present as a gray cytoplasm with foamy
changes (lepra cells, Virchow cells; Figure 9) in variable
amount from mild foamy appearance in early lesions to large
vacuoles in older or regressing lesions (occurring also in
multinucleated giant cells; Figure 10).

Fig. 7 Borderline lepromatous (BL) (same case as Figure 6).

A predominately lymphocytic infiltrate is observed also around the
eccrine glands and nerves.

Fig. 9 Lepromatous leprosy (LL). Macrophages present a gray

cytoplasm with mild foamy changes (lepra cells, Virchow cells in
early lesions). Plasma cells are present.

42

C. Massone et al.

Fig. 10 Lepromatous leprosy (LL). In older or regressing lesions,

large vacuoles appear.

Fig. 12 Acid-fast bacilli (AFB) are granular or fragmented in

patients while receiving or shortly after multidrug therapy (MDT).

Nerves have a perineural collection of macrophages and may

have an onion-skin perineurium but without significant
infiltration, or they may be fairly normal. Nerves may be
somewhat hyaline or fibrosed but not swollen.
Numerous AFB (5-6 +) are present within macrophages,
sweat and sebaceous glands, hair follicles, arrector pili
muscles, Schwann cells, perineural cells, and vascular
endothelium. AFB may be arranged in parallel array, or
forming clusters, or densely packed in large masses known as
globi (Figure 11). AFB have a solid appearance in
untreated patients, whereas they are granular or fragmented
in patients during or shortly after multidrug therapy (MDT;
Figure 12).PCR is obviously positive in both LL and BL and
is not necessary for the diagnosis.14
The histopathologic differential diagnoses of both LL
and BL mainly include other diseases that produce
foamy macrophages, such as xanthomas and xanthogranulomas, postkala-azar dermal leishmaniasis, paraffinoma,
and rarely infections caused by other nontuberculous
(atypical) mycobacteria.9,10

Indeterminate leprosy
Indeterminate leprosy (IL) is characterized by a superficial or more often superficial and deep perivascular and
periadnexal lymphohistiocitic infiltrate. In some cases, the
infiltrate is more prominent around the adnexa (sweat and
sebaceous glands, hair follicles) than around the vessels.
Mast cells are increased, whereas granulomas are absent. The
epidermis may present with focal vacuolar degeneration of
basal keratinocytes and exocytosis of lymphocytes. A
perineural infiltrate can be seen in one third of cases, and
lymphocytes cuffing the nerve fibrils are a good hint for
the diagnosis. Nerves, however, are not enlarged.
AFB are difficult to find, and FF serial sections are needed
to find single or small groups of AFB in a nerve. The
subepidermal zone just beneath the basal layer and the
arrector pili muscles are sites where AFB might be also
found. PCR is positive only in a small proportion of cases,
being in these cases of some help for the diagnosis.14,11
Diagnosis of IL without detailed clinical information is not
possible, because the histopathologic differential diagnosis
includes the large group of dermatides with a perivascular and
periadnexal lymphohistiocytic infiltrate.9,10

Leprosy reactions
Type 1 reaction

Fig. 11 Lepromatous leprosy (LL). Numerous solid acid-fast bacilli

(AFB) are present solitarily or in globules.

T1R occur mainly in BT and BB and sometimes also in

BL patients. On the background of a BT, BB, or BL,
histopathologic result, the histologic features that characterize T1R are the presence of edema in the superficial dermis
and edema in the granuloma with disorganization of the
granuloma, the appearance of foreign body giant cells
(sometimes with vacuoles due to intracellular edema), large
Langhans giant cells with epidermal erosion with spongiosis
(Figures 13 and 14), and fibroplasia in the dermis. In severe

Histopathology of the lepromatous skin biopsy

Fig. 13 Borderline tuberculoid (BT) with type 1 reaction (T1R).

Edema in the papillary dermis but also inside the granuloma with
disorganization of the granuloma and presence of large Langhans
giant cells.

43

Fig. 15 Erythema nodosum leprosum (ENL). A neutrophilic

infiltrate is present together with foamy macrophages.

The term erythema nodosum leprosum is a misnomer that

communicates misinformation to clinicians and histopathologists alike. The definition of ENL is inappropriate, mainly as
regards its clinical similarity with true EN: The term type 2
leprosy reaction would be more appropriate.
ENL can occur in both LL and (less commonly) BL. Two
different variants have been described histopathologically. One
has been reported by Ridley as pink node type or classic ENL

(or a mild form of ENL; Figure 15). Typically, the infiltrate is

centered on small granulomas in the subcutis with clusters of
neutrophils around old foamy macrophages. Eosinophils, plasma
cells, and mast cells are present. Even if in histopathologic
textbooks ENL has been classified as a mostly lobular panniculitis
with vasculitis, it should be stressed that vasculitis is not a
conspicuous feature of classic ENL. In fact, classic features of
small or medium vessel vasculitis, necrotizing changes, and
thrombus formation have been reported in classic ENL lesions in
almost 25% of cases. ENL is a dynamic process and of course the
time of the biopsy influences the histopathologic features. In fact,
vasculitic changes are more often seen in really early lesions.
Opposed to this concept, in necrotizing ENL (or severe ENL;
Figure 16) the vasculitic changes with neutrophilic infiltrate,
hemorrhages, and thrombi can be severe and may produce
degeneration of the collagen with necrosis of both dermis and
epidermis (clinically ulcerated lesions). In these cases ENL may
resolve with dermal fibrosis.
Solid AFB will be found in lesions coming from untreated
patients, whereas granular or fragmented AFB are usually
seen in patients undergoing therapy. In cases occurring long
after MDT, FF can be negative.14,12

Fig. 14 Borderline tuberculoid (BT) with type 1 reaction (T1R).

Edema in the granuloma with disorganization of the granuloma and
presence of many lymphocytes and of large Langhans giant cells.

Fig. 16 Necrotizing erythema nodosum leprosum (ENL) or

severe ENL. In this case a leukocytoclastic vasculitis with
neutrophils and hemorrhages coexists with Virchow cells.

reactions, breakdown of the granuloma and even necrosis or

ulceration can occur, and few collections of neutrophils may
be found. As T1R subside, there is a reduction in the edema
and formation of well-organized tubercles. The five key
features are dermal edema, intragranuloma edema, giant cell
size, giant cell numbers, and HLA-DR expression.12,13
If T1Rs occur in BL, epithelioid granulomas with giant
cells and edema are observed together with Virchow cells
and macrophage granuloma.14,12,13

Erythema nodosum leprosum

44
The main histologic differential diagnoses include LucioAlvarado phenomenon (see below), true EN, erythema
induratum Bazin, Sweet syndrome, pyoderma gangrenosum,
and deep mycotic infections.9,10

Particular forms of leprosy

Histoid leprosy
The term histoid leprosy (HL) was coined by Wade in
1963 to describe firm, reddish, or skin-colored, dome-shaped
or oval papules and nodules, regular in contour with
translucent shiny and stretched overlying skin, that on
histologic examination have a circumscribed macrophage
granuloma with the predominance of spindle-shaped cells or
polygonal cells and unusually large numbers of AFB. Some
cases may resemble a fibrohystiocytic tumor. A small
collection of foamy macrophages may be present.
HL is a clinical and pathologic variant of multibacillary
leprosy usually occurring in patients receiving long-term
diaminodiphenylsulfone therapy, with initial improvement
followed by relapse.14,14

Lucio-Latapi leprosy
Lucio-Latapi leprosy is a distinct form of lepromatous
leprosy reported mainly in Mexico but also in areas of Central
America and South America. It is characterized by a diffuse
nonnodular infiltration of the skin. Histopathologically, it is
similar to LL, with diffuse infiltration of Virchow cells.15

Lucio-Alvarado phenomenon
Patients with Lucio-Latapi leprosy may develop fever,
arthralgias, myalgias, and very painful red or purpuric
macules, of irregular shapes, angulated or stellar, on the
lower legs, thighs, hip, trunk, and upper limbs. Histopathologically, there is epidermal necrosis, ulceration, features of
diffuse lepromatous leprosy in the dermis with numerous AFB,
and a panvasculitis of both superficial and deep vessels. In
particular, a lobular panniculitis is found, with the mediumsized arteries infiltrated by macrophages with the consequent
narrowing of their lumens, occlusion, and ischemic changes.16

Regressive lesions
During or after MDT can be confirmed to have had
successful treatment by histopathologic conformation; however, clearance of the infiltrate and of AFB may take several
years, depending on granuloma fraction and the BIG.
Perineural granulomas in TT may persist 18 months after the
cessation of effective therapy.14

C. Massone et al.
The epithelioid granulomas gradually disappear in TT and
BT. They may assume the picture of nonspecific perivascular
chronic inflammation, mainly constituted by lymphocytes.
BL and LL regressive lesions have a fatty degeneration
with the appearance of more and larger vacuoles (even giant
vacuoles, especially in LL) and with a diffuse lymphocytic
infiltrate. AFB are granular or fragmented, and their number
may also shrink. Skin adnexa are atrophic and disappear
without fibrosis. Nerve bundles are replaced by fibrosis.
Foamy cells disappear slowly, leaving a perivascular
lymphocytic infiltrate with few foamy cells. After successful
MDT, lesions can histologically clear in 2 to 5 years or more,
but in some patients, a few foamy cells may persist for their
lifetime for unexplained reasons.14

Relapse
Relapse may take place at the site of a preexisting lesion, in
a fully resolved site, or in a previously not involved site. In
relapsing TT and BT, epithelioid granulomatous Langerhan
giant cells reappear with the same distribution as in active
lesions. Differentiating relapse from T1R is extremely difficult.
In BL and LL relapse, in addition, small and large foci of
newly arrived lymphocytes and spindle-shaped macrophages
with pink granular cytoplasm are identified along with a few
small clumps of foamy macrophages. The main feature is the
reappearance of solid-staining AFB in biopsy specimens. The
coexistence of granular or fragmented AFB is also possible.
It is not possible to distinguish histologically between a
relapse and a reinfection.14,17

Diagnostic clues
Histologic features that should always induce consideration
of leprosy and exclusion through biopsy in a patient coming
from endemic areas are as follows:
Epithelioid granulomas with multifocal distribution
Erosion of the epidermis by epithelioid granulomas
and without epidermal hyperplasia
Perineural and periadnexal granulomatous infiltrate
Swollen and enlarged nerves
Necrosis of a nerve
Perineural lymphocytic infiltrate with elongated shape
at the dermal-epidermal junction
A lyphmo histioxyxtic infiltrate that is more prominent
around the adnexa than around the vessels
Macrophage granuloma with foamy cells with a
grenz zone
Foamy cells with large vacuoles
Onion-skin infiltrate around nerves
Neutrophils in a macrophage granuloma with
foamy cells

Histopathology of the lepromatous skin biopsy

A plasma cell with 6 Ls: lues, lupus vulgaris, Lyme/
borelliosis, leprosy, leishmaniasis, lymphoma9
The pale infiltrate: lues, lupus vulgaris, leprosy, leishmaniasis9

References
1. Ridley DS. Pathogenesis of Leprosy and Related Diseases. London:
Wright. 1988250.
2. Ridley DS. Histological classification and the immunological spectrum
of leprosy. Bull World Health Organ. 1974;51:451.
3. Job CK. Pathology of leprosy. In: Hastings RC, ed. Leprosy. 2nd ed.
Edinburgh: Churchill Livingstone; 1994. p. 193-224.
4. Massone C. Histopathology of the skin. In: Nunzi E, Massone C, eds.
Leprosy, A Practical Guide. Berlin: Springer; 2012. p. 115-136.
5. Massone C, Nunzi E, Cerroni L. Histopathologic diagnosis of leprosy in
a nonendemic area. Am J Dermatopathol. 2010;32:417-419.
6. Singh A, Weng X, Nath I. Skin biopsy in leprosy. In: Khopkar U, ed.
Skin BiopsyPerspectives. Rijeka, Croatia: InTech; 2011. p. 73-86.
7. Ridley DS. Skin Biopsy in Leprosy. Basel, Switzerland: Ciba-Geigy.
1977:63.

45
8. Mahaisavariya P, Jiamton S, Manonukul J, Khemngern S. Mast cells
in leprosy and leprosy reaction. Int J Dermatol. 2000;39:274-277.
9. Weedon D. Skin Pathology. 3rd ed. London: Elsevier. 2010.
10. Ackerman AB. Histologic Diagnosis of Inflammatory Skin Diseases.
2nd ed. Baltimore: Williams & Wilkins. 1997:522.
11. Liu TC, Yen LZ, Ye GY, Dung GJ. Histology of indeterminate leprosy.
Int J Lepr Other Mycobact Dis. 1982;50:172-176.
12. Ridley DS. Reactions in leprosy. Lepr Rev. 1969;40:77-81.
13. Lockwood DN, Lucas SB, Desikan KV, Ebenezer G, Suneetha S,
Nicholls P. The histological diagnosis of leprosy type 1 reactions:
Identification of key variables and an analysis of the process of
histological diagnosis. J Clin Pathol. 2008;61:595-600.
14. Pradeep NS, Nanda Kumar G. A clinical and histopathological study of
histoid leprosy. Int J Dermatol. 2013;52:580-586.
15. Magaa M. LucioLatapi leprosy. In: Nunzi E, Massone C, eds.
Leprosy, A Practical Guide. Berlin: Springer; 2012. p. 111-114.
16. Magaa M. Lucios phenomenon. In: Nunzi E, Massone C, eds.
Leprosy, A Practical Guide. Berlin: Springer; 2012. p. 241-244.
17. Shetty VP, Wakade AV, Ghate SD, Pai VV. Clinical, bacteriological
and histopathological study of 62 referral relapse cases between Jan
2004 and Dec 2009 at the Foundation for Medical Research, Mumbai.
Lepr Rev. 2011;82:235-243.