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PubMedDate not supplied

Evaluation of cell mediated immunity in the histopathologic spectrum of leprosy using lymphocyte transformation test.

Lymphocyte transformation in response to PHA, M. leprae and BCG with the use of measurements of 3H-thymidine uptake, was studied in 10 normal controls, and 71 leprosy patients of different types histologically classified according to the Ridley-Jopling scale. Lepromin and PPD tests were done in each one of them. It was found that there was a generalized depression of immune responsiveness to PHA in all forms of leprosy. The immune responsiveness of lymphocytes to M. leprae continuously and gradually increases from the lepromatous (LL) towards the tuberculoid (TT) end of the spectrum. The loss of immune response of lymphocytes from lepromatous patients to M. leprae is specific as evidenced by their capacity to respond selectively to BCG when PPD-positive, irrespective of their place in the leprosy spectrum.

Antigens, Bacterial↗

PubMed1994

A longitudinal study of immunologic reactivity in leprosy patients treated with immunotherapy.

More than 150 leprosy patients treated with multidrug therapy (MDT) plus immunotherapy (IMT) with a mixture of heat-killed Mycobacterium leprae plus live BCG were studied in relation to humoral and cell-mediated immune responses. Many previously had received prolonged sulfone monotherapy. Patients received 2 to 10 doses of IMT in a period of 1 to 3 years, depending upon their clinical form of leprosy. The patients were followed up for 5 to 10 years with repeated determinations of antibody levels to phenolic glycolipid-I; lymphoproliferative (LTT) responses to soluble extract of M. leprae, to whole bacilli and to BCG, skin-test responses and bacterial indexes (BIs). After MDT plus IMT there was a statistically significant decrease of antibody levels in the multibacillary (MB) group. The BI decreased proportionally to the ELISA results. LTT increased to M. leprae antigens, especially to soluble extract, in a high percentage of these patients (34% of LL patients positive). Lepromin positivity in MB patients increased from 5% initially positive to 75% at the cut-off during this follow up. These results show substantial early and persistent cell-mediated reactivity to M. leprae in many MB patients treated with MDT-IMT, confirming and expanding previously published data.

Antibodies, Bacterial↗

PubMed1995

Neuritic leprosy: further progression and significance.

Sixteen neuritic cases have been seen developing cutaneous lesions. These cutaneous lesions by and large appear within 4 months after the diagnosis of neuritic leprosy. Leprosy pathology in cutaneous lesions has been found ranging between indeterminate and borderline lepromatous group. Development of cutaneous lesions does not seem to be influenced by age, sex or number of nerves or lepromin status. Neither lesions seem to appear in any particular part of the body. Therapy, duration and type i.e. monodrug or multidrug, also does not seem to influence the development of cutaneous lesions in either way. It appears that neuritic cases with either very early (indeterminate) or with advanced multibacillary neural pathology may develop skin lesions. Skin lesion possibly appear following reversal reaction in skin. Cases with newly developed skin lesions well respond to standard therapy. Development of cutaneous lesions by neuritic cases possibly indicates towards the natural history of the disease, conforming to the hypothesis that leprosy is basically neural in inception and that all other forms emerge from it.

Adult↗

PubMed1995

Enhancement in the histological diagnosis of indeterminate leprosy by demonstration of mycobacterial antigens.

In a clinico-pathological study of Indeterminate leprosy, fifty-six cases were chosen based on specified clinical criteria. Their clinical features were noted, the smears for acid fast bacilli (AFB) were prepared from lesions, lepromin inoculation and biopsies were performed from the lesional edges. They were subsequently treated with a modified extended WHO regimen for paucibacillary leprosy. On routine hematoxylin eosin (HE) and Fite-Faraco staining of paraffin embedded sections, histopathological confirmation of Indeterminate leprosy was observed in only 17/56 (31%) of the clinically diagnosed cases whereas the remaining were labelled as non-specific pathology. Histometric analysis of all HE stained sections did not show any characteristic finding which could be considered as characteristic and discriminatory for Indeterminate leprosy. Immunoperoxidase staining for demonstration of mycobacterial antigen by direct staining procedure using conjugated rabbit anti-BCG and indirect three step procedure using primary rabbit anti-BCG and avidin biotin complex, was next performed on the sections exhibiting non-specific pathology. With the direct immunoperoxidase method, antigen was demonstrable in (11/35) 31% of the cases. The more sensitive indirect method could demonstrate the presence of antigen in (21/35) 60% of the cases. This study thus shows that demonstration of mycobacterial antigen by simple and inexpensive immunoperoxidase techniques enhances the histopathologic diagnosis of Indeterminate leprosy.

Adolescent↗

PubMed1997

Regional lymphadenitis following antileprosy vaccine BCG with killed Mycobacterium leprae.

Phase-II and extended Phase-II studies were conducted in three different sets of the population in Thiruthani Taluk, Chengalpattu District, South India, involving BCG and killed Mycobacterium leprae (KML) combination vaccines to ascertain the acceptability of the vaccines. In the Phase-II study, 997 healthy volunteers were vaccinated on individual randomization with one of the vaccines arms: BCG 0.1 mg + 6 x 10(8) KML, BCG 0.1 mg + 5 x 10(7) KML, BCG 0.1 mg + 5 x 10(6) KML, BCG, 0.1 mg or normal saline. Blood samples were taken and the serum was tested for antibody levels against phenolic glycolipid-I (PGL-I) and the 35-kDa protein of M. leprae. In this study, we observed regional suppurative adenitis in 6% (6 out of 100), 3% (3 out of 100), and 3% (3 out of 100) of the vaccinees in the BCG 0.1 mg + 6 x 10(8) KML, BCG 0.1 mg + 5 x 10(7) KML, and BCG 0.1 mg + 5 x 10(6) KML vaccine arms, respectively, in the 13-70 year age group. Earlier BCG scar status, skin-test reactions to lepromin-A, Rees' MLSA, and serum antibody levels against PGL-I and the 35-kDa protein did not help to identify the group at risk of developing suppurative adenitis. Suppurative adenitis appears to have a different relationship between the age of the subject and the dose of the vaccine. In order to overcome the problem of regional suppurative adenitis and to know the mechanism involved, an extended Phase-II study was conducted in similar groups of the population by reducing the BCG and KML doses, i.e., with BCG 0.05 mg + 6 x 10(8) KML, BCG 0.05 mg + 5 x 10(7) KML, and BCG 0.01 mg + 5 x 10(7) KML. Biopsy specimens were collected from lymph nodes of the suppurative adenitis cases and were subjected for culture and histopathological examination. The observations showed that regional suppurative adenitis could be reduced to 1% in the BCG 0.05 + 6 x 10(8) KML group, 0.5% in the BCG 0.05 + 5 x 10(7) KML group, and 0.5% in the BCG 0.01 + 5 x 10(7) KML group. This phenomenon of suppurative adenitis appears to be related to the total dose of mycobacterial antigens. Suppurative adenitis was seen by weeks 18 and 20 post-vaccination in the latter two lower doses; whereas it was seen by week 8 in the higher dose of the combination vaccines. No case of suppurative adenitis was observed in the BCG 0.1 mg group. Culture and histopathology ruled out the possibilities of progressive BCG infection and superadded infection. Considering the above results, BCG 0.05 mg + 6 x 10(8) KML was acceptable for a large-scale vaccine trial in South India.

Adolescent↗

PubMed1981

The monocyte-macrophage system in granulomatous inflammation.

Granulomas may be immunologically induced or non-immunologically induced. In immunologically induced granulomas cells of the monocyte-macrophage series take on the appearance of epitheloid cells. Ultrastructurally epithelioid cells may have a secretory appearance with much rough endoplasmic reticulum or take on highly degenerate vesicular appearance. Other epithelioid cells look like activated macrophages. Secretory epithelioid cells may be found associated with acute local inflammation as in borderline tuberculoid leprosy in reaction, the lepromin reaction, following injection of BCG vaccine and in experimental zirconium granulomas. In these situations there may also be strong histological and biochemical evidence of increased fibroblast activity and collagen synthesis. It is suggested that these cells are actively secreting a fibroblast-activating factor. Epithelioid cells may lose their Fc receptors, undifferentiated macrophages in lepromatous leprosy can lose their C3 receptors. It is suggested that in a number of situations granuloma formation may be associated with complement activation through the alternative pathway as in the case of mycobacterial granulomas. Toxic granulomas produced by metals may be caused by C3 being split by plasmin after conversion from plasminogen by activation of the Hageman factor.

Animals↗

PubMed1985

Biological, chemical, immunological and staining properties of bacteria isolated from tissues of leprosy patients.

Two kinds of microorganisms are found in tissue of leprosy patients: Mycobacterium leprae (ML) and leprosy derived corynebacteria (LDC). ML from untreated patients has an alcohol-acid-fastness, which is lost upon treatment with antibiotics and immune response (tuberculoid leprosy). Vulnerable ML thus produced can be reversibly de-stained by organic solvent: in tissue sections from tuberculoid and treated patients, more bacteria are, thus, revealed by the Wade-Fite than by the Ziehl-Neelsen procedure. Organisms of genera Corynebacterium, Mycobacterium and Nocardia (CMN group), have DNA with %GC contents of 50-70, 69-72, and 68-70 respectively. GC values of DNA from ML and LDC are close to 56%. DNA from different LDC strains display high homology among them and low homology with reference corynebacteria. CMN cell wall consists of interconnected peptidoglycan and polysaccharide-mycolate complex. Peptidoglycan of LDC (and known CMN) has the polysaccharide backbone linked to a tetrapeptide of L-Ala, D-Glu, m-DAP (meso-diaminopimelate), D-Ala. In ML, L-Ala is replaced by glycine. Mycobacterial wall polysaccharides (that of ML is unknown) are branched arabinogalactans with end arabinoses linked to C70 to C90 mycolates. LDC peripheral polysaccharides are arabinogalactomannans with arabinose and mannose lateral strands. Mycolic acids of LDC are of corynomycolic type (C32, C34 and C36 with 1-4 double bonds) and those of ML are of mycobacterial type. Components of CMN wall and cytoplasm are immunologically active as antigens (polysaccharides, proteins), haptens (lipids) and adjuvants (peptidoglycans). Strong intrageneric and weak intergenera crossreactions are observed among CMN bacteria: LDC preparations, however, crossreact strongly with ML and mycobacteria, and weakly with reference corynebacteria. LDC in leprosy tissues can, thus, be revealed as well by fluorescent anti-LDC antisera as by anti-ML antisera. The main crossreacting component is antigen M1 of LDC, which corresponds to antigens Ag 7 of ML and Ag60 of BCG, the active components of lepromin and tuberculin (known reagents for cutaneous tests). Antigen M1 has a polysaccharide moiety crossreacting with the wall polysaccharide of LDC.(ABSTRACT TRUNCATED AT 400 WORDS)

Corynebacterium↗

PubMed1988

Metabolism of the TMA group of antigens during the growth cycle of mycobacteria.

The TMA (thermostable macromolecular antigens) group includes A60 of Mycobacterium tuberculosis and A7 of M. leprae, active components of tuberculin and lepromin. We have previously described the purification and composition of A60, and its ability to elicit immune reactions of humoral and cellular type. In the present work, the intracellular and extracellular distribution and composition of A60 have been traced, as a function of the replication cycle, in static surface cultures of M. bovis. In exponentially-growing mycobacteria, most A60 was present in the cytoplasm and had a high protein/polysaccharide ratio: this ratio, as well as the level of cytoplasmic A60, decreased after cessation of cell proliferation. The A60 fraction located within the cell wall increased during the stationary phase, but its protein/polysaccharide ratio underwent minor changes. A release of cellular polypeptides and polysaccharides into the extracellular fluid occurred during the declining and lysing phases: a fraction of it was represented by A60. This explains the practice of old tuberculin preparation by autoclaving filtrates of autolysed mycobacterial cultures. The pattern of an A60-like antigen in shaken homogeneous cultures of M. smegmatis was similar (most antigen present in cytoplasm during growth, increase of the wall fraction in stationary phase, and extracellular release during the declining phase).

Antigens, Bacterial↗

PubMedDate not supplied

Genetically restricted suppressor T-cell clones derived from lepromatous leprosy lesions.

Leprosy is a spectral disease in which immune responses to Mycobacterium leprae correlate with the clinical, bacteriological and histopathological manifestations of disease, so study of its pathology provides insights into immunoregulatory mechanisms in man. At the tuberculoid pole, patients have few lesions in the skin which contain rare organisms and are able to mount strong cell-mediated immune responses to M. leprae antigens. In contrast, at the lepromatous pole, patients have disseminated skin lesions containing large numbers of acid-fast bacilli and are selectively unresponsive to antigens of M. leprae. M. leprae-induced suppressor cells derived from peripheral blood have been reported to be active in vitro, yet their in vivo significance has remained unclear. Because the focal point of the immune response to M. leprae is the skin lesion consisting of lymphocytes and macrophages, we have recently developed methods for isolating lymphocytes from skin biopsies of leprosy patients. We report here that two T8 clones derived from lepromatous leprosy skin biopsies, in the presence of lepromin, suppress concanavalin A (Con-A) responses both of peripheral blood mononuclear cells and of T4 clones in an HLA-D (HLA, histocompatibility locus antigen)-restricted manner. Moreover, these T8 clones suppressed responses of HLA-D-matched, but not HLA-D-mismatched antigen-responsive T4 clones to M. leprae antigens, indicating that T-cell suppression is major histocompatibility complex (MHC)-restricted at some level in man.

Antigens, Bacterial↗

PubMed2003

Segregation of HLA/TNF region is linked to leprosy clinical spectrum in families displaying mixed leprosy subtypes.

Each year an estimated 600000 new leprosy cases are diagnosed worldwide. The spectrum of the disease varies widely from limited tuberculoid forms to extensive lepromatous forms. A measure of the risk to develop lepromatous forms of leprosy is provided by the extent of skin reactivity to lepromin (Mitsuda reaction). To address a postulated oligogenic control of leprosy pathogenesis, we investigated in the present study linkage of leprosy susceptibility, leprosy clinical subtypes, and extent of the Mitsuda reaction to six chromosomal regions carrying known or suspected leprosy susceptibility loci. The only significant result obtained was linkage of leprosy clinical subtype to the HLA/TNF region on human chromosome 6p21 (P(corrected)=0.00126). In addition, we established that within the same family different HLA/TNF haplotypes segregate into patients with different leprosy subtypes directly demonstrating the importance of this genome region for the control of clinical leprosy presentation.

Chromosomes, Human, Pair 6↗

PubMed2001

Sequential erythema nodosum leprosum and reversal reaction with similar lesional cytokine mRNA patterns in a borderline leprosy patient.

We compare the clinical and histological data with the immunological status of a borderline leprosy patient who experienced an erythema nodosum leprosum (ENL) reaction followed by a reversal reaction (RR) after 12 weeks of anti-inflammatory treatment (pentoxifylline, PTX, 1200 mg daily). Skin biopsies, serum and blood samples were collected sequentially during the reactional episodes. At the outset of RR, the patient's lymphocytes secreted interferon (IFN) -gamma and there was a positive lymphoproliferative test in response to Mycobacterium leprae, which had been absent during ENL. The lepromin reaction reversed from negative (0 mm) at diagnosis, to positive (3 mm) 3 months after the development of RR. Tumour necrosis factor (TNF) -alpha levels in the serum decreased after 1 week of treatment and increased slightly thereafter. The immunohistochemical data for ENL showed a diffuse dermal and hypodermal infiltrate composed of mononuclear cells and neutrophils, while RR was characterized by an epithelioid granulomatous infiltrate with a marked presence of gammadelta T cells. Reverse transcription-polymerase chain reaction showed a mixed cytokine profile characterized by the expression of TNF-alpha, IFN-gamma, interleukin (IL) -6, IL-10 and IL-12 mRNA in the skin, which persisted throughout the development of ENL and RR lesions. IL-4 mRNA, first detected after 7 days of PTX treatment, was still present during RR. The results suggest the emergence of an initial Th0-like cytokine profile in ENL, typical of a state of immunoactivation, before conditions optimal for the appearance of an antigen-specific cell-mediated immune response and gammadelta T-cell migration are created.

Adult↗

PubMed2000

Co-stimulatory signals increase the reactivity of gammadelta T cells towards mycobacterial antigens.

Although it has been shown that gammadelta T lymphocytes are able to react with different cell-associated or soluble antigens, the immune repertoire of these cells appears to be skewed to the recognition of mycobacterial antigens. We have studied the number and reactivity of gammadelta T cells towards several mycobacterial antigens in patients with tuberculosis and leprosy, as well as their healthy contacts and control individuals. We found an increased number of Vdelta2+ cells in healthy contacts (PPD+ and lepromin+) and tuberculoid leprosy patients. The gammadelta T cells from lepromatous leprosy showed a decreased response to all antigens tested, but some of these patients exhibited a significant response to the 30-kD glycoprotein of Mycobacterium tuberculosis. Interestingly, the reactivity of gammadelta T cells against mycobacterial antigens was significantly increased by costimulatory signals generated through CD7, LFA-1, CD50 and CD69 in all groups. However, signalling through CD69 did not enhance the responsiveness of gammadelta lymphocytes from lepromatous patients. On the other hand, the in vitro blockade of IL-10 with a specific antibody enhanced the cell proliferation of gammadelta lymphocytes from lepromatous leprosy patients, whereas exogenous IL-10 had an opposite effect in most individuals studied. These results suggest the potential role of different cell membrane receptors in the regulation of gammadelta T cell proliferation induced by mycobacteria, as well as the possible involvement of IL-10 in this phenomenon.

Antibodies, Monoclonal↗

PubMed1992

A major T cell antigen of Mycobacterium leprae is a 10-kD heat-shock cognate protein.

Several mycobacterial antigens, identified by monoclonal antibodies and patient sera, have been found to be homologous to stress or heat-shock proteins (hsp) defined in Escherichia coli and yeast. A major antigen recognized by most Mycobacterium leprae-reactive human T cell lines and cell wall-reactive T cell clones is a 10-kD protein that has now been cloned and sequenced. The predicted amino acid sequence of this protein is 44% homologous to the hsp 10 (GroES) of E. coli. The purified native and recombinant 10-kD protein was found to be a stronger stimulator of peripheral blood T cell proliferation than other native and recombinant M. leprae proteins tested. The degree of reactivity paralleled the response to intact M. leprae throughout the spectrum of leprosy. Limiting-dilution analysis of peripheral blood lymphocytes from a patient contact and a tuberculoid patient indicated that approximately one third of M. leprae-reactive T cell precursors responded to the 10-kD antigen. T cell lines derived from lepromin skin tests were strongly responsive to the 10-kD protein. T cell clones reactive to both the purified native and recombinant 10-kD antigens recognized M. leprae-specific epitopes as well as epitopes crossreactive with the cognate antigen of M. tuberculosis. Further, the purified hsp 10 elicited strong delayed-type hypersensitivity reactions in guinea pigs sensitized to M. leprae. The strong T cell responses against the M. leprae 10-kD protein suggest a role for this heat-shock cognate protein in the protective/resistant responses to infection.

Amino Acid Sequence↗

PubMedDate not supplied

Properties of microorganisms isolated from human leprosy lesions.

Diphtheroids, which in addition to Mycobacterium leprae are present in human leprosy lesions, were identified as true corynebacteria by DNA and cell wall analysis. Peptidoglycan (adjuvant) of these leprosy-derived corynebacteria (LDC) consists of N-acetylglycosaminyl-N-acetyl(glycolyl)-muramic acid and L-Ala-D-Glu(NH2)-(L)-meso-A2pm-(L)-D-Ala (A2pm = diaminopimelic acid). (The amino group of the tetrapeptide is attached to the carboxyl group of the muramate). Peripheral polysaccharide (antigen) is arabinogalactomannan with lateral chains of mannofuranose and arabinofuranose. To the latter are linked mycolic acids containing groups of isomers with 24-36 carbon atoms and containing between zero and four double bonds. DNAs of LDC isolates have a guanine + cytosine content of 56% and demonstrate a high degree of homology. LDC ribosomes cross-react with antisera against mycobacteria and with sera from patients with leprosy. Thermostable antigen M of LDC cross-reacts with the main antigens of tuberculin and lepromin. LDC thus represents a homogeneous and unique group of corynebacteria immunologically related to M. leprae. Leprosy might be the result of a pathogenic cooperation between both organisms, as suggested by the enhancement of M. leprae growth rate promoted in mice by living LDC.

Cell Wall↗

PubMedDate not supplied

Leprosy: cause, transmission, and a new theory of pathogenesis.

Leprosy is generally accepted as being caused by Mycobacterium leprae, an acid-fast organism often present in great numbers in certain forms of leprosy. However, it has not been possible to confirm with scientifically acceptable evidence that this entity is the cause of leprosy; laboratory cultivation, an essential factor in the proof, has not been accomplished with the acid-fast bodies seen in leprotic tissue. The mechanisms of transmission of the disease also remain conjectural; prolonged, close contact and transmission by nasal droplet have both been proposed, and, while the latter fits the pattern of disease, both remain unproved. It is proposed that the causative agent of leprosy is not a difficult-to-transmit agent but, rather, an organism that has evolved a highly efficient state of parasitism in stable types of populations and that everyone in the population harbors the leprosy parasite at some time. The majority of the population incubate subclinical infections at various levels; clinical leprosy arises from within the pool of subclinical infection in the endemic population rather than by transmission from an index case. A theory of complete infection of endemic populations is consistent with the rate of development and distribution of positive lepromin reactions among healthy persons in endemic regions and provides an explanation for the difficulty in controlling leprosy in endemic populations by isolation of patients or by therapy for clinical cases.

Humans↗

PubMed1989

Interactions between simian immunodeficiency virus and Mycobacterium leprae in experimentally inoculated rhesus monkeys.

Thirty-four rhesus monkeys were inoculated with Mycobacterium leprae inoculum isolated from sooty mangabey monkeys with leprosy. Later it was learned that one of the M. leprae-donor mangabeys was asymptomatically infected with simian immunodeficiency virus (SIV). Thus, five of the rhesus monkey were coinoculated with M. leprae and SIV. Three of the five became SIV-positive and developed signs of leprosy and an AIDS-like illness. Two animals remained healthy. The coinoculated leprosy-positive rhesus monkeys developed leprosy despite serologic response patterns to M. leprae antigens that usually indicate leprosy resistance. Three (60%) of the five SIV-positive rhesus monkeys developed leprosy compared with 21% of the animals who received SIV-free M. leprae inocula. Diminished lepromin skin test responses and decreasing T-helper cell percentages were observed in SIV-coinoculated rhesus monkeys with leprosy. These observations suggest that SIV increases the susceptibility of rhesus monkeys to leprosy, possibly related to loss of T-helper cell function.

Animals↗

PubMed1993

Combined multidrug and Mycobacterium w vaccine therapy in patients with multibacillary leprosy.

Immunotherapy with Mycobacterium w vaccine was attempted in patients with borderline-borderline, borderline lepromatous (BL), or lepromatous leprosy (LL) to determine whether immunization can hasten recovery and reduce treatment time by invigorating cell-mediated immunity. Mycobacterium w, a nonpathogenic, rapidly growing, atypical mycobacterium, shares a number of common B and T cell determinants with Mycobacterium leprae and Mycobacterium tuberculosis. Patients receiving the vaccine had rapid clinical improvement and accelerated bacteriologic clearance. After treatment with vaccine for 2 years, 13 of 31 BL and LL patients were bacteriologically negative as were 5 of 25 controls. Vaccinated patients had one of two distinct histologic features, either an upgrading in the disease spectrum or complete clearance of granuloma. Some 80% of lepromin conversions were in BL and LL patients who received vaccine versus none and 14.3% of BL and LL controls, respectively. Thirteen of 17 vaccinated LL patients were released from treatment after 2 years in contrast to 2 of 15 controls.

Bacterial Vaccines↗

PubMed1999

Macular lesions in leprosy: a clinical, bacteriological and histopathological study.

Among 150 untreated patients of leprosy, 19 had only macular lesions; three were of the indeterminate type, and eight each were of the tuberculoid and the borderline types, according to the Indian Association of Leprologists (IAL, 1981) classification. The clinical, bacteriological, and histopathological parameters of these 19 patients were studied both before and after six months of WHO Multi Drug Therapy (MDT/1982). A single macule was present in seven (36.84%) patients. In twelve (63.16%), two or more were seen. In eighteen (94.74%), one or more peripheral nerves were enlarged. The size of the macules varied from 5 to 15 cm, and there were no changes seen even after treatment. In most (94.74%) of the patients, the macules were hypopigmented. The surfaces were rough and dry in seven (36.84%) but smooth in the other twelve (63.16%). The margins were well defined in the seven (36.84%) patients with single macules but ill defined in the other twelve (63.16%). After six months of antileprosy treatment, the single macules showed some resolution. Slit skin smear examination was negative in all cases before and after treatment. Clinico-histopathological correlations were seen in only six (31.58%) patients; the clinical diagnoses were indeterminate and tuberculoid leprosy in three (15.79%) patients each. In the indeterminate group, the clinico-histopathological correlation was 100%; it was 37.50% in the tuberculoid group. There were no correlations between the clinical and histopathological parameters in thirteen (68.42%) cases. After six months of treatment, the histopathology became nonspecific in all patients. The lepromin test was positive in six (31.58%) patients; four were of the tuberculoid group and one each from the indeterminate and borderline leprosy groups. Hence, although macular lesions can be seen throughout the leprosy spectrum, it is difficult to correlate their clinical, bacteriological and histopathological parameters.

Adolescent↗