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PubMed2000

A clinical prediction rule for nerve-function impairment in leprosy patients.

BACKGROUND: Nerve-function impairment (NFI) commonly occurs during or after chemotherapy in leprosy and is the key pathological process leading to disability and handicap. We describe the development of a simple clinical prediction rule for estimating the risk of NFI occurrence. METHODS: New leprosy cases who presented to a centre in Bangladesh were recruited and followed up for 2 years in a field setting. We used multivariable regression analysis by Cox's proportional hazards model to identify predictive variables for NFI. Discriminative ability was measured by a concordance statistic. Internal validity was assessed with bootstrap resampling techniques. FINDINGS: 2510 patients were followed up for 2 years, 166 developed NFI. A simple model was developed with leprosy group (either paucibacillary leprosy [PB] or multibacillary leprosy [MB]) and the presence of any nerve-function loss at registration as predictive variables. Patients with PB leprosy and no nerve-function loss had a 1.3% (95% CI 0.8-1.8%) risk of developing NFI within 2 years of registration; patients with PB leprosy and nerve-function loss, or patients with MB leprosy and no nerve-function loss had a 16.0% (12-20%) risk; and patients with MB leprosy with nerve-function loss had a 65% (56-73%) risk. INTERPRETATION: Our prediction rule can be used to plan surveillance of new leprosy patients. Patients at low risk of NFI may need no follow-up beyond their course of chemotherapy (6 months); patients with intermediate risk need a minimum of 1 year of surveillance; and patients with high risk should have at least 2 years of surveillance for new NFI. Current recommendations for surveillance of patients with leprosy (for the duration of chemotherapy only) exclude an important group of patients who are at risk of developing NFI after completion of treatment.

Adolescent↗
PubMed1984

Defective production of monocyte-activating cytokines in lepromatous leprosy.

We have examined the capacity of monocytes from patients with leprosy to undergo activation and the capacity of mononuclear cells from these patients to incorporate [3H]thymidine and produce monocyte-activating cytokines. Monocytes from patients with either lepromatous or tuberculoid leprosy were activated by concanavalin A (Con A)-induced mononuclear cell supernatants generated from the leukocytes of a normal person. Monocytes activated by these supernatants strongly inhibited L. pneumophila multiplication, and the degree of inhibition was comparable in both groups of patients. Mononuclear cells from patients with either form of leprosy responded comparably to Con A with vigorous [3H]thymidine incorporation. Mononuclear cells from patients with tuberculoid leprosy also vigorously incorporated [3H]thymidine in response to M. leprae antigens. In contrast, mononuclear cells from patients with lepromatous leprosy did not exhibit significant [3H]thymidine incorporation in response to M. leprae antigens. The capacity of mononuclear cells to generate monocyte-activating cytokines generally paralleled their capacity to incorporate [3H]thymidine in response to Con A and M. leprae. Mononuclear cells from patients with either form of leprosy responded to Con A with the production of cytokines (supernatants) able to activate normal monocytes, expressed by inhibition of L. pneumophila multiplication. However Con A-induced supernatants from patients with lepromatous leprosy were less potent than Con A-induced supernatants from patients with tuberculoid leprosy. Mononuclear cells from patients with tuberculoid leprosy responded to M. leprae antigens with the production of potent monocyte-activating supernatants. In contrast, mononuclear cells from patients with lepromatous leprosy did not produce monocyte-activating cytokines in response to M. leprae antigens. These studies support the hypothesis that the immunological defect in lepromatous leprosy results from a failure to activate mononuclear phagocytes rather than from an intrinsic inability of these cells to be activated. We suggest that the failure to activate mononuclear phagocytes stems from defective production of monocyte-activating cytokines in response to M. leprae antigens.

Adult↗
PubMed2003

Expression of CC and CXC chemokines and chemokine receptors in human leprosy skin lesions.

We have investigated the expression of chemokines and their receptors in leprosy skin lesions using immunohistochemistry. Skin biopsies from 25 leprosy patients across the leprosy spectrum, 11 patients undergoing type I reversal reactions and four normal donors were immunostained by ABC peroxidase method using antibodies against CC and CXC chemokines and their receptors. Using an in situ hybridization technique we have also studied the expression of monocyte chemoattractant protein 1 (MCP-1), RANTES and interleukin (IL)-8 chemokines mRNA in leprosy skin lesions. Chemokines and receptor expression was detected in all leprosy skin biopsies. Expression of CC chemokines MCP-1 (P < 0.01) and RANTES (P < 0.01) were elevated significantly in borderline tuberculoid leprosy in reversal reaction compared to non-reactional borderline tuberculoid leprosy, but there was no difference in the expression of IL-8 chemokine. Surprisingly, there was no significant difference in the expression of CC (CCR2 and CCR5) and CXC (CXCR2) chemokine receptors across the leprosy spectrum. Similarly, there was no significant difference in the expression of mRNA for MCP-1, regulated upon activation normal T cell expressed and secreted (RANTES) and IL-8 chemokines. Here, the presence of a neutrophil chemoattractant IL-8 in leprosy lesions, which do not contain neutrophils, suggests strongly a role of IL-8 as a monocyte and lymphocyte recruiter in leprosy lesions. These results suggest that the chemokines and their receptors, which are known to chemoattract T lymphocytes and macrophages, are involved in assembling the cellular infiltrate found in lesions across the leprosy spectrum.

CD4-Positive T-Lymphocytes↗
PubMed1973

Cytochemical reactions of human leprosy bacilli and mycobacteria: ultrastructural implications.

Leprosy bacilli harvested from freshly biopsied tissue from cases of lepromatous, borderline and histoid leprosy were, in conjunction with Mycobacterium lepraemurium and representative mycobacteria, examined cytochemically with and without their pyridine-extractable acid-fastness. Unlike the mycobacteria, unextracted leprosy bacilli failed to give a positive response to the periodic acid Schiff test or to take up Sudan black B, toluidine blue O, alkaline methylene blue or safranin O. Once their acid-fastness was removed with pyridine, leprosy bacilli were stained by all of the foregoing dyes except Sudan black B, under this condition they remained gram positive. While permanent loss of acid-fastness from leprosy bacilli always resulted in a loss of acid hematein-fixing material (Smith-Dietrich-Baker tests), the reverse was not true. Mild aqueous saponification, bromination, or sequential treatment with lipase and phospholipase D resulted in a loss of acid hematein-positivity but not acid-fastness. After pyridine extraction, bromination, or aqueous saponification, true mycobacteria lost neither their acid hematein-positivity nor their acid-fastness. The acid hematein-positive material and the acid-fastness of both leprosy bacilli and mycobacteria were lost after treatment with alkaline ethanol. These cytochemical findings are discussed in the light of what is known of the ultrastructure of leprosy bacilli and mycobacteria, and of the occurrence of a dl-3, 4-dihydroxyphenylalanine oxidase in leprosy bacilli but not in mycobacteria. An effort is made to explain the rather unique cytochemical properties of leprosy bacilli. Since pyridine-extractable acid-fastness (and acid hematein-positivity) serve to distinguish human leprosy bacilli from M. lepraemurium, one or the other, or both, are suggested as bases for differentiating these two organisms in animal experiments designed to show the in vivo propagation of human leprosy bacilli.

Acids↗
PubMed2002

Leprosy: a problem solved by 2000?

It is now the year 2001, and in many endemic regions leprosy remains a public health problem by any definition. It is clear that defining leprosy purely by prevalence side-steps some of the real issues. There is still much to do to solve the problem of leprosy. Control programmes require better tests for early diagnosis if leprosy is to be reduced much further. Treatment of the infection and of reactions is still far from ideal, whilst an effective vaccine would be valuable in high-risk regions. Research into the true incidence in each endemic area is essential, and control programs of the future will need a more detailed understanding of the transmission of M. leprae to permit new logical interventions. Leprosy remains a devastating disease. Much of the damage that it inflicts is irreversible, and leads to disability and stigmatization. This is perhaps the greatest problem posed. It is easy to dwell on the successes of the elimination campaign, so diverting attention from those populations of 'cured' patients who still suffer from the consequences of infection. Leprosy should be regarded as a problem unsolved so long as patients continue to present with disabilities. WHO has carried out a highly successful campaign in reducing the prevalence of leprosy, and this needs to be acknowledged, but what is happening to the incidence in core endemic areas? Maintaining this success, however, may be an even greater struggle if funding is withdrawn and vertical programmes are absorbed into national health structures. We must take heed of the historian George Santayana, 'those who cannot remember the past are condemned to repeat it'. We should take the example of tuberculosis as a warning of the dangers of ignoring a disease before it has been fully controlled, and strive to continue the leprosy elimination programmes until there are no new cases presenting with disability. The World Health Organisation has shown that leprosy is an eminently treatable disease, and has prepared the ground. The leprosy elimination campaigns truly are 'at a height... ready to decline'. Can it be that this is the chance to take leprosy 'at the flood'? If so, perhaps an extension of the elimination programs beyond the year 2001 would indeed 'lead to fortune'.

Global Health↗
PubMed2003

Screening for leprosy in immigrants--a decision analysis model.

Almost all leprosy cases reported in industrialized countries occur amongst immigrants or refugees from developing countries where leprosy continues to be an important health issue. Screening for leprosy is an important question for governments in countries with immigration and refugee programmes. A decision analysis framework is used to evaluate leprosy screening. The analysis uses a set of criteria and parameters regarding leprosy screening, and available data to estimate the number of cases which would be detected by a leprosy screening programme of immigrants from countries with different leprosy prevalences, compared with a policy of waiting for immigrants who develop symptomatic clinical diseases to present for health care. In a cohort of 100,000 immigrants from high leprosy prevalence regions (3.6/10,000), screening would detect 32 of the 42 cases which would arise in the destination country over the 14 years after migration; from medium prevalence areas (0.7/10,000) 6.3 of the total 8.1 cases would be detected, and from low prevalence regions (0.2/10,000) 1.8 of 2.3 cases. Using Australian data, the migrant mix would produce 74 leprosy cases from 10 years intake; screening would detect 54, and 19 would be diagnosed subsequently after migration. Screening would only produce significant case-yield amongst immigrants from regions or social groups with high leprosy prevalence. Since the number of immigrants to Australia from countries of higher endemnicity is not large routine leprosy screening would have a small impact on case incidence.

Australia↗
PubMed2004

Risk factors for the development of clinical leprosy among contacts, and their relevance for targeted interventions.

Existing knowledge on risk factors for the development of clinical leprosy among contacts of known leprosy patients is reviewed with the aim to identify factors associated with leprosy among contacts that have potential for developing effective targeted interventions in leprosy control. Different definitions of 'contact' have been used and most studies on this subject were among so-called household members. Yet several studies indicate that contacts found in other places than the household are also at risk of developing leprosy. The type of leprosy and the bacterial index are the main patient-related factors involved in transmission, but also contacts of PB patients have a higher risk of contracting leprosy as compared to the general population. The most important contact-related factors are the closeness and intensity of the contact and inherited susceptibility, while the role of age and sex of the contacts is not clear. The role of socio-economic factors is also vague. The significance of immunological and molecular markers in relation to risk of transmitting or developing leprosy is not yet fully understood, but there is an indication that contacts who are sero-positive for anti-PGL-I antibodies are at increased risk of developing clinical leprosy. The presence of a BCG scar is likely to be related to a lower risk. Analogies with tuberculosis suggest that the 'stone-in-the-pond' approach to control may be applicable to leprosy too. Sputum smear negative tuberculosis patients are known to spread the bacteria to others. This analogy strengthens the suggestion that the contacts of paucibacillary leprosy cases should also be included in contact tracing and examination. It is concluded that targeted interventions should be aimed at close contacts of both MB and PB patients inside and outside the household, particularly when genetically related.

Adolescent↗
PubMed1998

[Evaluation of the elimination of leprosy in Burkina Faso].

During May and June 1997, we conducted a rapid survey on leprosy prevalence in 30 villages. It was to assess reaching of the leprosy elimination threshold (one case per 10,000 inhabitants) in Burkina Faso. We drew lots for the villages in ten provinces among which five had the highest prevalence rates of leprosy in 1996 and five had the lowest prevalence rates. We added a leprosy elimination monitoring to the survey. This monitoring consisted of visits to the health centers covering the 30 villages. We interviewed and clinically examined 33 cases of leprosy in treatment in those health centers. We found fifty-one patients of leprosy in visited villages. The prevalence rate of leprosy (6.74 per 10,000 inhabitants) was twice higher than the prevalence rate registered in the same villages. We detected 28 new cases of leprosy during the survey. Proportion of hidden cases of leprosy were 54.9%. We estimated geographical coverage of MDT at 75% in the 10 provinces. Eight of the 27 visited health centers (29.6%) did not get sufficient supply. The cure rate has fallen from 93 to 73 per cent between 1992 and 1997. Our results show that leprosy elimination threshold is not reached in Burkina Faso. Leprosy control activities that were declining during the last five years need to be reinforced.

Adolescent↗
PubMed2006

HLA and leprosy in the pre and postgenomic eras.

Leprosy has intrigued immunologists for many decades. Despite minimal genetic variation between Mycobacterium leprae isolates worldwide, two completely different forms of the disease can develop in the susceptible human host: localized, tuberculoid, or paucibacillary leprosy, which can heal spontaneously, and disseminating, lepromatous, or multibacillary leprosy, which is progressive if untreated. The questions which host factors regulate these very different outcomes of infection, by what mechanisms, and whether these can be used to combat disease remain unanswered. Leprosy has been one of the very first human diseases in which human leukocyte antigen (HLA) genes were demonstrated to codetermine disease outcome. Jon van Rood was among the earliest researchers to recognize the potential of this ancient disease as a human model to dissect the role of HLA in disease. Decades later, it is now clear that HLA molecules display highly allele-specific peptide binding capacity. This restricts antigen presentation to M. leprae-reactive T cells and controls the magnitude of the ensuing immune response. Furthermore, specific peptide/HLA class II complexes can also determine the quality of the immune response by selectively activating regulatory (suppressor) T cells. All these factors are believed to contribute to leprosy disease susceptibility. Despite the global reduction in leprosy disease prevalence, new case detection rates remain invariably high, demonstrating that treatment alone does not block transmission of leprosy. Better tools for early detection of preclinical M. leprae infection, likely the major source of unidentified transmission, therefore is a priority. Newly developed HLA-based bioinformatic tools now provide novel opportunities to help combat this disease. Here, we describe recent work using HLA-DR peptide binding algorithms in combination with recently elucidated genome sequences of several different mycobacteria. Using this postgenomic HLA-based approach, we were able to identify 12 candidate genes that were unique to M. leprae and were predicted to contain T cell epitopes restricted via several major HLA-DR alleles. Five of these antigens (ML0576, ML1989, ML1990, ML2283, ML2567) were indeed able to induce significant T cell responses in paucibacillary leprosy patients and M. leprae-exposed healthy controls but not in most multibacillary leprosy patients, tuberculosis patients, or endemic controls. 71% of M. leprae-exposed healthy controls that did not have antibodies to the M. leprae-specific phenolic glycolipid-I responded to one or more M. leprae antigen(s), highlighting the potential added value of these unique M. leprae proteins in diagnosing early infection. Thus current state-of-the-art HLA immunogenetics can provide new tools for specific diagnosis of M. leprae infection, which can impact our understanding of leprosy transmission and can lead to improved intervention.

Amino Acid Motifs↗
PubMedDate not supplied

Serum adenosine deaminase levels in reactional and non-reactional leprosy.

BACKGROUND AND AIMS: Altered serum adenosine deaminase (ADA) levels have been recorded in various diseases involving lymphocytes and/or lymphoreticular system including leprosy. The study was planned to evaluate alterations in serum ADA levels, if any, in reactional and non-reactional leprosy. METHODS: Eighty patients of leprosy, comprising 60 patients of non-reactional leprosy and 20 patients of reactional leprosy were studied along with 20 normal healthy controls. Five milliliters of venous blood was collected and ADA levels were estimated by the method of Giusti (1974). RESULTS: There were 54 males and 26 females. The age of the patients ranged from 5 years to 62 years. The duration of leprosy ranged from 15 days to 3 years. The mean serum ADA level in normal controls was 10.31 +/- 0.58 u/L. The serum ADA levels were raised in leprosy patients, significantly so in multibacillary patients. The serum ADA levels were higher in patients of leprosy with reaction. CONCLUSIONS: The study showed significantly high serum ADA levels in multibacillary leprosy and this was further increased in patients of leprosy with reaction. This may be because of increased lymphoreticular activity during the reactional phases.

Adenosine↗
PubMed2003

R-R interval variation and the sympathetic skin response in the assessment of the autonomic nervous system in leprosy patients.

OBJECTIVES: The aim of this study was to evaluate possible autonomic nervous system (ANS) dysfunction in leprosy patients with the sympathetic skin response (SSR) and the heart rate (R-R) interval variation (RRIV) measurements which are easy and reliable methods for evaluation of autonomic functions. MATERIAL AND METHODS: We studied 37 lepromatous leprosy patients (mean age: 38 +/- 17 years, range 23-62 years, 20 females and 17 males) and 35 age-matched healthy subjects (mean age: 34.19 +/- 12.74 years, range 24-48 years, 20 females and 15 males). Non-invasive bedside tests (orthostatic test, Valsalva ratio), R-R interval variation (RRIV) during at rest and deep breathing, the SSR latency and amplitude from both palms, and nerve conduction parameters were studied in all the subjects. RESULTS: The mean values of RRIV in leprosy patients during at rest [mean RRIV in patients, 17.42 +/- 8.64% vs controls, 22.71 +/- 3.77% (P < 0.05)] and during deep breathing [mean RRIV in patients, 21.64 +/- 9.08% vs controls, 30.70 +/- 5.99% (P < 0.005)] was significantly lower compared with the controls. The mean latency of SSR in leprosy patients [mean SSR latency in patients, 1.72 +/- 1.13 ms vs controls, 1.30 +/- 0.41 ms (P < 0.05)] was significantly prolonged compared with the controls. The mean amplitude of SSR in leprosy patients [mean SSR amplitude in patients, 0.54 +/- 0.57 microV vs controls, 1.02 +/- 0.56 microV (P > 0.05)] was smaller compared with the controls, but this difference was not significant. The mean Valsalva ratio in leprosy patients [mean in patients, 1.11 +/- 0.13 vs controls, 1.16 +/- 0.07 (P > 0.05)] was smaller compared with the controls, but not statistically significant. The mean difference of systolic and diastolic blood pressure between supine rest and during standing in leprosy patients were higher compared with the controls [mean systolic pressure in patients, 7 +/- 6 mmHg vs controls, 6 +/- 8 mmHg (P > 0.05) and mean diastolic pressure in patients, 3 +/- 3 mmHg vs controls, 3 +/- 2 mmHg (P > 0.05)], but they did not reach statistical significance. Furthermore, lower RRIV and the prolonged SSR latencies in leprosy patients were closely correlated to some parameters of sensorimotor nerve conduction and each other [median nerve distal latency and RRIV, r = -0.67 (P < 0.05), ulnar nerve distal latency and RRIV, r = -0.59 (P < 0.05), RRIV and SSR latency, r = -0.33 (P < 0.02)]. These data indicate that leprosy patients have the functional abnormalities of ANS. CONCLUSION: We conclude that combined use of these two tests, both of which can be easily and rapidly performed in the electromyogram (EMG) laboratory using standard equipment, allows separate testing of parasympathetic and sympathetic function, and are very sensitive methods in assessing of ANS function in peripheral neuropathy in leprosy patients.

Adult↗
PubMed2004

Increased incidence of cytoplasmic ANCA (cANCA) and other autoantibodies in leprosy patients from western India.

The prevalence of various autoantibodies was studied in 75 leprosy patients comprising eight patients with lepromatous leprosy (LL), 36 patients with borderline lepromatous leprosy (BL) and 31 patients with borderline tuberculoid leprosy (BT), along with 100 normal controls. Certain autoantibodies such as anti-nuclear antibodies (ANA), anti-single stranded DNA (anti-ssDNA) and anti-neutrophil cytoplasmic antibodies (ANCA) were raised among leprosy patients. When ANCA specificities to anti-myeloperoxidase (anti-MPO), anti-proteinase3 (anti-PR3) and anti-lactoferrin (anti-LF) were studied, it was found that the patterns of immunofluorescence such as perinuclear (p-ANCA), cytoplasmic (c-ANCA) and atypical (X-ANCA) and specificity by ELISA to anti-MPO, anti-PR3 and anti-LF varied in the LL, BL and BT groups. However, a higher amount of c-ANCA was observed in 62.5% of leprosy cases, while the incidences of p-ANCA and X-ANCA were lower. The LL group showed a higher incidence of autoantibodies as compared with the BL and BT groups, along with a male preponderance for autoantibody development. Some unusual antibody profiles such as 'X'-ANCA were also observed. The study suggests that autoantibody formation could be quite prevalent and also variable in the spectrum of leprosy cases, and there seems to be a serological overlap among leprosy and autoimmune disease, which could have pathogenetic importance in the leprosy patients developing complications.

Adult↗
PubMed1989

Hormone profile in leprosy.

Hormone profile were carried out in 35 male cases of leprosy. They were divided into tuberculoid leprosy, borderline leprosy, lepromatous leprosy and lepra reaction. Serum testosterone, follicle-stimulating hormone, Luteinizing hormone, and Oestradiol level were measured in these cases of leprosy. It was observed that serum testosterone were significantly low in lepromatous leprosy (P less than 0.001) and lepra reaction (P less than 0.01). The serum levels of follicle-stimulating hormone and luteinizing hormone were significantly high in lepromatous leprosy (P less than 0.02) and lepra reaction (P less than 0.05). Serum Oestradiol was raised in approx. 60% cases in borderline leprosy, lepromatous leprosy and lepra reaction.

Adult↗
PubMed1989

Lymphoproliferation and in vitro antibody synthesis in leprosy patients.

An in vitro system to assess B-cell function in leprosy patients is described. In vitro lymphoproliferation and antibody synthesis by peripheral blood mononuclear cells (PBMC) in response to pokeweed mitogen (PWM) and Formalin-treated Staphylococcus aureus Cowan I (FSA) from 31 leprosy patients and 13 healthy controls were studied. DNA synthesis was induced by both PWM and FSA in PBMC from all of the leprosy patients and control subjects. Lepromatous leprosy (LL) patients' cells showed higher responses to both PWM and FSA. However, these increases were not statistically significant. The levels of secreted IgM, IgG, or IgA were examined in the 7-day culture supernatants of PBMC cultured with or without PWM or FSA using an enzyme-linked immunosorbent assay. Wide individual variations were observed in in vitro antibody synthesis. IgM secretion in PBMC from normal subjects and various groups of leprosy patients in response to PWM and FSA was comparable. In vitro IgG secretion in response to PWM was the highest in cells from LL patients; it was significantly decreased in cells from tuberculoid leprosy (TT) patients (p less than 0.01). The levels in cells from borderline leprosy (BB) patients were intermediate in response to the same mitogen. Cells from leprosy patients as a group showed a higher spontaneous secretion of IgA in comparison with cells from normal subjects. Overall, the in vitro Ig secretion by PBMC in different patient groups appears to reproduce the spectrum of antibody levels observed in patients in vivo. Thus, the present in vitro culture system may help to delineate the mechanisms of B-cell dysregulation in leprosy.

Antibodies, Bacterial↗
PubMed1994

Epidemiologic characteristics of leprosy reactions.

An 8-year prospective study of a cohort of 176 newly diagnosed leprosy patients was conducted to examine the possible influence of age, sex, multidrug therapy (MDT), and duration of illness on the risk of either type 1 or type 2 reactions. Patients were enrolled over a 5-year period (1984-1989) and followed for a minimum of 3 years. All reactions studied were severe enough to warrant hospital admission. Overall, 45% of this cohort developed a reaction; 32% of patients considered at risk developed type 1 reactions, and 37% of patients considered at risk developed type 2 reactions. Despite the predominance of men among the leprosy patients, type 1 reactions occurred with significantly greater frequency in women, and did not appear to be influenced by age of onset of leprosy. Individuals experiencing one type 1 reaction were not likely to experience a recurrence, suggesting that the immunologic mechanisms of this reaction may be limited or regulated by genetic or immunologic factors. Type 2 reactions, on the other hand, occurred with equal frequency in both males and females, but were highly associated with onset of leprosy in the second decade of life. Individuals who experienced type 2 reactions often had one or more recurrence of the reaction. No increased risk was seen for either reaction with longer duration of leprosy or longer duration of treatment. The mechanisms by which these differences relate to the pathogenesis of leprosy reactions remains unclear, but future studies of clinical and immunological parameters of leprosy reactions may benefit from stratification of data by gender and age of onset of leprosy in addition to the routine grouping of results by leprosy classification.

Adolescent↗
PubMed2005

Leprosy: too complex a disease for a simple elimination paradigm.

Can leprosy be eliminated? This paper considers the question against the background of the WHO programme to eliminate leprosy. In 1991 the World Health Assembly set a target of eliminating leprosy as a public health problem by 2000. Elimination was defined as reaching a prevalence of < 1 case per 10 000 people. The elimination programme has been successful in delivering highly effective antibiotic therapy worldwide. However, despite this advance, new-case detection rates remain stable in countries with the highest rates of endemic leprosy, such as Brazil and India. This suggests that infection has not been adequately controlled by antibiotics alone. Leprosy is perhaps more appropriately classed as a chronic stable disease than as an acute infectious disease responsive to elimination strategies. In many countries activities to control and treat leprosy are being integrated into the general health-care system. This reduces the stigma associated with leprosy. However, leprosy causes long-term immunological complications, disability and deformity. The health-care activities of treating and preventing disabilities need to be provided in an integrated setting. Detecting new cases and monitoring disability caused by leprosy will be a challenge. One solution is to implement long-term surveillance in selected countries with the highest rates of endemic disease so that an accurate estimate of the burden of leprosy can be determined. It is also critical that broad-based research into this challenging disease continues until the problems are truly solved.

Communicable Disease Control↗
PubMed1994

Ocular manifestations of leprosy in a noninstitutionalized community in the United States.

OBJECTIVE: Our goal was to delineate the epidemiologic and clinical patterns of ocular leprosy in an outpatient setting in the United States. DESIGN: Examinations were performed in 61 consecutive outpatients seen in a Midwestern leprosy clinic. PATIENTS: Forty-three male and 18 female patients were examined. The patients' origins included Southeast Asia (24 patients [39%]), Latin America (23 patients [38%]), India (nine patients [15%]), Europe or North America (two patients [3%]), Africa (two patients [3%]), and the Middle East (one patient [2%]). RESULTS: Thirty-nine percent of patients were classified as having polar lepromatous leprosy; 18%, borderline lepromatous leprosy; 3%, borderline borderline leprosy; 36%, borderline tuberculoid leprosy; 2%, polar tuberculoid leprosy; and 2%, indeterminate leprosy. Ninety-six percent of patients had a best-corrected visual acuity of 20/40 or better. Ocular findings included madarosis (28 patients [46%]), subconjunctival fibrosis (18 patients [30%]), punctate epithelial keratopathy (17 patients [28%]), posterior subcapsular cataract (10 patients [16%]), corneal hypesthesia (10 patients [16%]), lagophthalmos (seven patients [11%]), corneal pannus (six patients [10%]), entropion (five patients [8%]), prominent or beaded corneal nerves (four patients [7%]), iridocyclitis (four patients [7%]), focal avascular keratitis (three patients [5%]), scleritis (three patients [5%]), interstitial keratitis (two patients [3%]), iris pearls (two patients [3%]), and ocular clofazimine crystals (two patients [3%]). Madarosis, corneal hypesthesia, and posterior subcapsular cataracts were significantly associated with disease duration (P < .05). CONCLUSION: We report herein a relatively low frequency of visual impairment attributable to leprosy in our series compared with that seen among institutionalized leprous patients. However, since 48% of subjects had one or more sight-threatening complications as a result of their disease, a program of regular ophthalmic follow-up is strongly advocated for all patients with leprosy.

Adolescent↗
PubMed1995

Complex segregation analysis of leprosy in southern Vietnam.

To investigate the nature of the genetic component controlling susceptibility to leprosy and its subtypes, 402 nuclear families were ascertained through a leprosy patient followed at the Dermatology Hospital in Ho Chi Minh City, Vietnam; 285 families were of Vietnamese origin and 117 were of Chinese origin with a higher proportion of lepromatous forms among Chinese patients. Segregation analyses were conducted using the model developed by Abel and Bonney [(1990) Genet Epidemiol 7:391-407], which accounted for variable age of onset and time-dependent covariates. Three phenotypes were considered: leprosy per se (all forms of leprosy together), nonlepromatous leprosy, and lepromatous leprosy. For each of this phenotype, analyses were performed on the whole sample and separately on the Vietnamese and the Chinese families. The results showed that a single Mendelian gene could not account for the familial distributions of leprosy per se and its two subtypes in the whole sample. However, these results were different according to the ethnic origin of the families. In the Vietnamese subsample, there was evidence for a codominant major gene with residual familial dependences for the leprosy per se phenotype, and borderline rejection of the Mendelian transmission hypothesis for the nonlepromatous phenotype. In Chinese families, strong rejection of Mendelian transmission was obtained in the analysis of leprosy per se, and no evidence for a familial component in the distribution of the nonlepromatous phenotype was observed. For the lepromatous phenotype, the discrimination between models was poor, and no definitive conclusion could be reached. Referring to immunological data, we suggest that these results could be explained by a heterogeneity in the definition of the lepromatous phenotype. It is likely that progress in the understanding of the genetic components involved in the expression of leprosy will come from a better definition of the phenotype under study, and immunological studies are ongoing in this population to investigate this hypothesis.

Adolescent↗