Leprosy Mailing List Blog

Friday, August 7, 2026

Fw: Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works

Leprosy Mailing List – August 7, 2026

Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works

From: Claudio Guedes Salgado, Marituba, Brazil

____________________________________________________________________________

Dear Pieter,

I have followed with great interest the recent exchange initiated by Joel Almeida, followed by the thoughtful comments from Benedict Quao and Ben Naafs about the “(LML) Long-lasting adverse impact of chemoprophylaxis & what actually works”.

Rather than focusing exclusively on the proposed biological mechanism, I believe the discussion has now reached a broader and perhaps more important scientific question: what level of evidence is required before a preventive intervention is considered sufficiently safe for widespread implementation?

Joel Almeida proposes a biological hypothesis that seeks to explain the epidemiological observations reported in a recent publication. Benedict Quao rightly reminds us that ecological associations should not be interpreted as proof of causality and that mechanistic hypotheses must remain clearly distinguished from experimental evidence. Ben Naafs, in turn, accepts several of Benedict's methodological criticisms while simultaneously reminding us that the available evidence is also insufficient to conclude that SDR-PEP is free from important long-term adverse consequences.

To me, this is the central point.

Regardless of whether Joel's proposed mechanism ultimately proves correct, the current discussion highlights an important limitation of the existing evidence base. Most SDR studies were designed to evaluate reductions in case detection, operational feasibility, implementation, or acceptability. They were not specifically designed to investigate delayed clinical outcomes such as multibacillary disease, nerve function impairment, immunological reactions, or grade 2 disability.

This distinction is important.

Operational feasibility is not equivalent to long-term clinical safety.

Likewise, high acceptance of a single tablet should not be interpreted as evidence supporting the intervention itself. In communities where Hansen's disease remains a feared condition, acceptance of a simple preventive intervention is naturally expected. Acceptance tells us that implementation is possible; it does not tell us whether the intervention is the optimal strategy or whether all clinically relevant risks have been adequately evaluated.

Another aspect deserves attention. The pivotal COLEP trial demonstrated a protective effect primarily during the first two years of follow-up. Thereafter, this advantage was no longer statistically demonstrable. Subsequent multicountry studies have contributed valuable information regarding implementation and feasibility, but relatively few, if any, have been specifically designed to determine whether SDR provides sustained protection or whether it influences clinically relevant long-term outcomes.

Another issue that deserves far greater attention is the quality of contact examination itself.

The effectiveness and safety of any chemoprophylaxis programme depend fundamentally on correctly identifying who truly does not have Hansen's disease before SDR is administered. This requires experienced clinical evaluation. Unfortunately, global expertise in clinical leprosy has declined considerably since the WHO declaration of leprosy elimination as a public health problem in 2000. In many endemic countries, relatively few health professionals have extensive experience in recognizing early, subtle, oligosymptomatic or predominantly neural forms of the disease.

Our own experience strongly supports this concern. Following the structured training of 55 physicians as leprologists in the Brazilian state of Mato Grosso, case detection increased substantially, particularly in the municipalities where these specialists are now practicing (de Medeiros Junior NF, Salgado CG, Andrade VLG, Maluf GA. Hanseníase no Brasil: Mato Grosso em foco. Cuiabá: Tribunal de Contas do Estado de Mato Grosso; 2024). This observation suggests that one limiting factor in Hansen's disease control is not simply transmission itself, but the capacity to recognize disease early and accurately.

This naturally raises an important question for current SDR programmes: who is examining contacts before they receive chemoprophylaxis, and what level of expertise is required to confidently exclude early Hansen's disease?

An equally important question concerns diagnostic support. In the settings where SDR trials are being conducted, or where SDR has already been incorporated into control programmes, are complementary diagnostic tools routinely available? Are serological assays such as anti-PGL-I IgM, molecular methods such as RLEP qPCR, or high-resolution peripheral nerve ultrasonography being systematically used to improve the detection of oligosymptomatic or subclinical disease before chemoprophylaxis is offered?

If the answer is no, then an unavoidable concern remains: individuals with early or unrecognized Hansen's disease may be incorrectly classified as healthy contacts and consequently receive a single dose of rifampicin instead of prompt multidrug therapy followed by appropriate neurological monitoring.

Several additional questions therefore remain unanswered.

Could administration of SDR to contacts with unrecognized subclinical disease delay diagnosis rather than prevent disease?

Could this contribute to later multibacillary presentations or increased disability?

Has nerve function impairment been systematically monitored after SDR administration with the same rigor routinely recommended during multidrug therapy?

Have studies been adequately powered and specifically designed to detect delayed neurological or immunological outcomes?

Has the possibility of altered transmission dynamics, rather than simply altered case detection, been sufficiently explored?

Has the potential selection of rifampicin-resistant organisms, whether in Mycobacterium leprae or other bacteria exposed within the community, been adequately investigated under conditions of large-scale administration?

Finally, could widespread confidence in chemoprophylaxis inadvertently reduce the emphasis placed on what remains the cornerstone of Hansen's disease control: careful clinical examination, experienced assessment of contacts, early diagnosis, and longitudinal follow-up?

None of these questions demonstrates that SDR-PEP is harmful.

Equally, however, none has yet been answered sufficiently to conclude that SDR-PEP is unequivocally safe under routine programmatic conditions.

In science, absence of evidence of harm should never be confused with evidence of absence of harm.

The present discussion should therefore not be viewed as being for or against SDR. Rather, it should encourage the Hansen's disease community to generate the level of evidence that such a globally promoted intervention deserves. Future studies should move beyond operational feasibility and short-term case detection to include rigorous clinical assessment by experienced leprologists, systematic evaluation of nerve function, disability, multibacillary disease, reactions, molecular diagnosis, antimicrobial resistance, and prolonged follow-up.

Perhaps the first question should not be "Should SDR be given to this contact?" Rather, it should be "How certain are we that this individual truly does not already have Hansen's disease?" Until we can answer that question with confidence, caution remains both scientifically justified and clinically prudent.

Kind regards,

Claudio Salgado

====================================================

Claudio Guedes Salgado, MD, PhD

Full Professor
Institute of Biological Sciences
Federal University of Pará
Coordinator of the Biological Sciences II Area at CAPES, Brazil
Former President of Brazil Hansen's Disease Society (SBH), 2018-2023
International Relations Advisor for the SBH
Elected Councillor for the Americas 2025–2028 International Leprosy Association (ILA)
Dermato-Immunology Lab
Av. João Paulo II, 113
Bairro: Dom Aristides
Marituba - Pará - Brasil
CEP: 67200-000
Phone: +55-91-3201-7033
Cell phone: +55-91-991465641

E-mails: csalgado@ufpa.br and claudioguedessalgado@gmail.com

Lattes CV (Brazil format): http://lattes.cnpq.br/2310734509396125

ORCID ID: https://orcid.org/0000-0003-3961-7764

LinkedIn: https://www.linkedin.com/in/claudio-guedes-salgado/
Instagram: https://www.instagram.com/claudiosalgado/

Facebook: https://www.facebook.com/claudioguedessalgado

Map to the Lab: https://goo.gl/maps/7omyd54wy7z

____________________________________________________________

LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << edit...@gmail.com

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Fw: Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works

Leprosy Mailing List – August 7, 2026

Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works

From: Joel Almeida, Mumbai, India

____________________________________________________________________________

Dear Pieter and colleagues,

Respectful thanks to the correspondent (Dr. Benedict Quao) for his interest in the original letter (LML 9 and 11 July 2026).

Low‑income individuals are disproportionately represented among new HD (leprosy) cases and their families. Many have minimal schooling, and rely on manual labour to escape destitution and hunger. Safeguarding their eyes, hands and feet is therefore paramount. This is why so many esteemed colleagues are working to match the rapid declines in MB HD (multibacillary leprosy) documented in Weifang (China), Malta, Jordan, Chile, Vietnam, Thailand, Karonga, Ecuador and elsewhere—using steadily improving diagnosis and full free antimicrobial treatment together with regular check-ups, without chemoprophylaxis. It is also why, in endemic areas, nasal swabs from ALL asymptomatic individuals are needed, to identify cryptic LL high‑shedders and rapidly end transmission.

The correspondent doubts that asymptomatic individuals exist who shed large quantities of viable M. leprae. Yet Davey and Rees (1974, Lepr Rev 45(2):121–34) provided clear evidence:
“Highly bacilliferous discharges were encountered in early lepromatous leprosy, indicating nasal involvement far more severe than external appearances suggested… millions of bacilli are discharged daily in nasal secretions from lepromatous patients with active and, importantly, early disease. When these millions of bacilli are being discharged from the nose the patients may well be unaware that they have leprosy and clinically they have insignificant skin lesions…”
They estimated "an average output/day from the nose of an active lepromatous patient of 31 ,000,000 live organisms and an average of 19,000,000 live Myco. leprae from a single early morning specimen of nasal discharge" Without bacillary replication in the nose, it is very difficult to explain how nearly 20 million bacilli appear in one specimen of nasal discharge. These facts illustrate why nasal swabs from all asymptomatic persons in a cluster, analysed by semi‑quantitative mLAMP (DNA or RNA as desired), are critical for prompt full treatment and rapid reduction of transmission. Semi-quantitative means those who shed astronomical numbers of bacilli in nasal discharges are distinguished from transient nasal carriers of trivial numbers of bacilli.

Regarding São Luís (Maranhão), where no chemoprophylaxis was used: the original letter noted that it is “producing among the world’s most rapid declines of new MB HD: e.g. from 279 new MB in 2023 to only 200 in 2025.” It further stated that introducing nasal swabs for semi‑quantitative mLAMP could accelerate this decline and end transmission within weeks. That was the intended message. Extending the point: failure to introduce nasal swabs for ALL asymptomatics risks missing cryptic LL high shedders. That can keep open the floodgates of infection, putting at risk São Luís’ remarkable achievements.

When serious harm is demonstrated from an intervention, the burden of proof shifts to proponents of the intervention to demonstrate safety.

What does the RCT evidence show? All RCTs failed to report on incident G2D (visible deformity at diagnosis) as an outcome. However, three RCTs reported incident MB HD as an outcome. MB carries a far higher risk of nerve damage than PB (Croft et al 2000 Lancet) and is therefore a useful proxy for risk of G2D. Contrary to the correspondent’s assertion, an excess of incident MB cases in arm 2 (household‑contact PEP clusters) versus arm 1 (non‑PEP control clusters) is evident in raw RCT data. Two of the only three RCTs that included incident MB HD as an outcome—PEOPLE and MALTALEP—show this excess o incident MB. Incident MB is an outcome, not a subgroup; the denominator is the same as for all other outcomes. The third RCT (COLEP), at full protocol duration (4 years), showed no statistically valid protection against incident MB HD, and incident MB cases even increased numerically between years 1/2 and 3/4, contrasting with a concurrent 40% DECREASE in incidence in the PLACEBO arm. This contrast between rapid decline in the placebo group and concurrent INCREASE in the chemoprophylaxis arm is important, as is excess incident MB HD in household PEP arm 2 clusters vs non-PEP arm 1 clusters of the other two RCTs. Contacts who received short‑term chemoprophylaxis and then developed visible deformity before diagnosis will derive no comfort from concealment of RCT signals of harm. They are not in a position to gamble with their eyes, hands and feet.

Further evidence of harm comes from India, indicating that short‑term chemoprophylaxis is an important factor in causing visible deformity before diagnosis (Ind J Lepr 2026, 97:175-188). The article is available at: https://doi.org/10.5281/zenodo.21344996

The correspondent apparently also overlooked the most relevant part of the OASL article by de Toledo Pinto et al. (2016) who reported:
“MdTHP‑1 cells [macrophages] were lipofected with M. leprae DNA… IFNB and OASL mRNA levels were significantly increased after 72 hours of infection, compared with the unlipofected culture.”
Lipofection means that foreign DNA within liposomes (fat droplets) was delivered into the cytosol of macrophages. This was M. leprae DNA: neither killed bacilli nor live bacilli.
Given established biology:
1. One or a few antimicrobial doses damage intracellular bacilli, producing bacillary debris in macrophage cytosol.
2. Cytosolic bacillary DNA activates cGAS → cGAMP → STING → IRF3 → IFN‑β.
3. IFN‑β upregulates OASL, which suppresses autophagy and cathelicidin.
Autophagy is the primary mechanism by which macrophages clear debris and bacilli. Vitamin‑D‑induced cathelicidin is a critical antimicrobial peptide.

Cytosolic DNA sensing via cGAS is foundational immunology, grounded in the work of Zhijian “James” Chen (Lasker Award 2024, Japan Prize 2026 etc.). The default expectation is that this highly conserved and universal sequence occurs. Proponents of PEP must demonstrate how and why it is uniquely absent in the case of bacillary debris produced by one or a few antimicrobial doses. That burden of proof is nowhere near being discharged.

When bacilli replicate by elongation, their surface area increases, and their numbers increase. Given the role of the surface virulence factor PGL‑1 in non‑inflammatory nerve damage (Madigan et al., Cell 2017 http://dx.doi.org/10.1016/j.cell.2017.07.030 ), and the surface virulence factor Mce1A in cell entry (Fadlitha et al 2019 https://doi.org/10.1371/journal.pntd.0006704 ) proponents of PEP must demonstrate that actively replicating bacilli are phenotypically safer for humans than dormant bacilli: less invasive and less damaging to nerves. That burden is nowhere near being discharged.

The PEPHans vs non‑PEP comparison in the original letter(s) (9 and 11 July) aligns with convergent patterns across multiple datasets and biological levels. %G2D (visible deformity at diagnosis) normally indicates delayed diagnosis. Yet the displayed data show that intensified active case finding (increased proportion detected by contact tracing) was accompanied by an increase—not a decrease—in %G2D. This reversal of the usual pattern occurred only in PEPHans areas. Biological acceleration of nerve damage is expected to result in a significantly higher percentage of new cases presenting with G2D as the first detectable sign of HD in PEP areas. PEPHans began in 2016, continued till 2019, and the harms remained evident as recently as 2024.

The new case detection rate of MB HD in the PEPHans municipalities was similar to the non-PEP areas of Maranhão (around 4 to 5 per 10k population/year) until the dramatic drop attributable to COVID disruptions. The physical distancing of COVID together with disruption in case finding activities is likely to be responsible for the dramatic drop in both areas. However, physical distancing of COVID had no lasting epidemiological benefit in PEPHans municipalities. High virulent bacilli circulating and incubating in PEPHans municipalities not only nullified any epidemiological benefit but also demonstrably increased the risk of G2D among new cases. Only in non-PEP Maranhão municipalities was the drop in new cases maintained and even accelerated later (aided no doubt by boosted household income thanks to Bolsa Familia cash payments). Newly detected LL cases in São Luís (Maranhão) declined from 52 (2023) to 27 (2025). This favourable outcome in PEP-free places such as São Luís needs to be reinforced by introducing nasal swabs for ALL asymptomatics in case clusters. Then transmission can be ended rapidly, and sustained by periodic mop-up surveillance.

Conclusion:

Human eyes, hands and feet are at stake. The burden of proof is on proponents of short-term chemoprophylaxis to demonstrate that highly conserved and universal macrophage biology is somehow absent in the case of damage to intracellular bacilli by one or a few doses of anti-microbials. That burden is not remotely close to being discharged. The universal macrophage biology is illustrated by a range of epidemiological observations. Short-term chemoprophylaxis not only boosts the risk of new MB HD as shown in the raw data of RCTs, but also is predicted by the biology, and illustrated by convergent epidemiological observations, to be an avoidable risk factor for visible deformity before diagnosis. Brazil and the USA, both scientific powerhouses in macrophage biology and HD research, set good examples to the world by avoiding chemoprophylaxis. Leading groups in countries such as India are also applying science to the protection of their people's eyes, hands and feet.

Short-term chemoprophylaxis was introduced and promoted on the demonstrably false premise that good diagnosis and full free anti-microbial treatment are incapable of reducing transmission. Many places, as listed near the start, showed relatively rapid decline of new MB HD using good diagnosis and full free anti-microbial treatment, without the demonstrable harms of short-term chemoprophylaxis. With semi-quantitative mLAMP on nasal swabs from ALL asymptomatics, all cryptic high-shedders can be made non-infectious within days or weeks. Instead of concentrated viable bacilli being transmitted back and forth indefinitely between persons with genomes predisposing to LL type of HD, elimination of concentrated viable bacilli from a cluster can be achieved in days or weeks.

Is such rapid success undesirable? Is human safety optional?

Safety message for a low‑income person in an endemic area:

Under no circumstances should you accept short‑term chemoprophylaxis for yourself or your loved ones. It can disarm your defender cells, allowing bacilli to replicate and damage your nerves, with risk of visible deformity before diagnosis. Instead, request full examination for signs of HD and a nasal swab to test for high bacillary loads. If either is positive, demand full free treatment with regular check‑ups to protect your nerves. This is also how HD transmission can be ended rapidly.

With all sincerity,

Joel Almeida

____________________________________________________________________________

LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << edit...@gmail.com

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Wednesday, August 5, 2026

Fw: Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works

Leprosy Mailing List – August 8, 2026

Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works

From: Ben Naafs, Munnekeburen, the Netherlands

____________________________________________________________________________

Dear Pieter,

I read with interest the points made by Benedict Quao (LML, August 4, 2026) and in his reaction on Joël Almeda’s contributions about PEP. LML is an open forum for raising doubts and having reasoned discussions between the different actors active in the field of leprosy. PEP is one the items that is discussed most frequently in the past years. I hope that more persons will share their views on this subject. For me it was a trigger again. I will follow his points.

1. Interpretation of the PEP data.

I fully agree that there could well be a serious selection basis.

A longer pre-intervention period should indeed be included.

However, I think that a short time intervention like PEP will not kill all bacilli in a MB patient. All MB patients will stay MB patients. PEP may even induce a more active disease with reactivity and more nerve damage (which is the worry of Joël). The follow up in PEP studies is not specifically looking for this, one looks mainly for new diseases developing and according to me often for too short period of time. That the contact tracing is more intensive in PEP then in non-PEP areas should not occur in a good PEP trial.

A good PEP trial should indeed require analyses of the baseline situation and in mine opinion have a long enough follow-up.

2. Interpretation of STING/OASL

I go with the interpretation that the autophagy is regulated by the infective burden and less by the dead bacilli.

3. Persistence of bacterial debris.

It is very likely that dead bacteria (debris) after killing stay in the macrophages and disappear slowly. It is certainly shown in biopsies over time that it disappears very slowly particularly Lipoarabinomannan (LAM). Thus, this is demonstrated.

4. Emergence of “high-virulence” bacilli.

In a macrophage most bacilli are already death. Short “treatment” (PEP) will kill a few more. The remaining living bacteria continue dividing. Whether they do it faster I do not know. It may look as if the MI in the beginning goes up quicker, but I also doubt high-virulence. That means for me that they infect more easily, and I agree that has never been shown.

5. Linking these mechanisms to increased MB disease and disability.

I agree that the mentioned theories of mechanisms do not hold. But the observation that there are more active disease and more nerve damage could be true. But you must look for it. Killing bacteria expose other antigenic determinants leading to immunoreactivity and even reactions and thus more nerve damage. It was seen in the seventies when one tried Rifa monotherapy and it was one of the reasons that in the 80^th leprologists warned against it, (Among others Thuur Cap (Jozef Arthur Cap) and Jan Warndorff. As far as I have seen the PEP programs did not look specifically for it.

6. Expected effect of chemoprophylaxis

I wonder whether you may call PEP chemoprophylaxis. It is in fact a too short “treatment” particularly for MB patients. Each time after a trial one was basically dissatisfied and started a new, stronger or longer treatment and at a moment added BCG. You say the limited efficacy may not be interpreted as harm. You have not looked for harm such as nerve damage or reactions. But it diminishes trust in the health worker when it has only a limited effect. (And to me that is harm}

And an extra remark: from HIV we know that only 20% of infected people can develop leprosy. That is why for the borderline patients BCG is so helpful. This fact is not taken in account as far as I read the PEP articles.

7. Asymptomatic “high shedders” as main reservoir of transmission.

There may be high shedders, but I cannot define them. But probably most MB are shedders. When you treat them properly the reservoir for transmission most likely goes down, ergo the number of new patients.

A. An open door. But be aware that some MB patients, particularly the ones that are undertreated, (something that is due to the too short MB treatment in the WHO advice), may be asymptomatic as active MB patients. I feel these could be the ones Joël means. But wait for his answer.

B. If you do a good survey, you will find in high endemic area’s a great number of patients who seem “asymptomatic” to a less experienced leprologist. Thus, we can’t say that is not demonstrated. Concerning the nasal carriers: The nose is like a vacuum cleaner and most people in a high endemic area may have temporarily live and dead bacilli in the nose. Look at the PGL-1 serology in these areas. It is unlikely that they do not contribute to the M. leprae pool. Concerning mLAMP, this is still being studied. But when used properly it may be an important extra tool to study and thereafter become useful against the M. leprae pool.

C. Indeed, DNA does not indicate live bacilli only the presence of bacilli dead or alive. RNA detection is needed.

Dear Benedict, my thanks for your extensive analyses and I hope my views will stimulate additional discussions on this important area.

High Regards,

Ben

____________________________________________________________________________

LML - S Deepak, B Naafs, S Noto and P Schreuder

LML blog link: http://leprosymailinglist.blogspot.it/

Contact: Dr Pieter Schreuder << edit...@gmail.com

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Tuesday, August 4, 2026

Fw: Ref.: (LML) Infolep monthly overview of new publications on leprosy. July, 2026

Leprosy Mailing List – August 4, 2026

Ref.: (LML) Infolep monthly overview of new publications on leprosy. July, 2026

From: Elizabeth Talatu Williams, Amsterdam, the Netherlands

____________________________________________________________________________

Dear colleagues,

We are pleased to share the July 2026 edition of the Infolep newsletter, featuring recent publications, case reports, and global updates from the leprosy field.

Infolep announces the publication of the Prevention of Leprosy: Single-Dose Rifampicin Post-Exposure Prophylaxis (SDR-PEP) Toolkit, developed by the GPZL SDR-PEP Sub-group. This toolkit brings together materials, tools, and key documents developed based on experience gained from projects and programmes implemented across diverse leprosy-endemic settings and contexts. Access the toolkit here.

This month's featured articles explore the psychosocial impact of disability and stigma among persons affected by leprosy and lymphatic filariasis, healthcare access and community knowledge in Malawi, and active case detection among incarcerated populations in Brazil. We also feature several case reports highlighting diverse clinical presentations of leprosy and the continued importance of early diagnosis.

It also includes new research on innovative approaches to leprosy control, including teleinterconsultation for disability surveillance, the development and validation of a chatbot for managing leprosy lesions, advances in biomarker discovery, and studies on disease transmission, maternal and childhood leprosy, and programme implementation across endemic settings.

Just two months to go until the 17th Annual NTD NGO Network (NNN) Conference, taking place in Kigali, Rwanda, from 29 September to 1 October 2026. Registrations are still open, don't miss the opportunity to join global partners working to eliminate neglected tropical diseases.

Stay tuned to Infolep for more updates, resources, news, and tools that support your work in leprosy.

Warm regards,
Elizabeth Talatu Williams

www.leprosy-information.org
info@infolep.org

Featured Research Spotlight

The psychosocial impact of disability and stigma among persons affected by leprosy and lymphatic filariasis in India
van Wijk R, Agarwal A, Nayak P, et al. PLOS mental health. 2026; 3 (7): 1 – 16

Beyond elimination: Assessing healthcare access, knowledge, attitudes, and practices regarding leprosy among communities in Lilongwe and Balaka districts of Malawi
Singano N, Lubanga A, Kacheyo J, et al. PLoS neglected tropical diseases. 2026; 20 (7): 1 - 15.

Hidden burden of leprosy in incarcerated populations in northeast Brazil: active case detection and serological assessment
de Lucena TS, Galani LC, Barbosa LD, et al. European Journal of Clinical Microbiology & Infectious Diseases. Springer Science and Business Media LLC. 2026.

Other New Publications

Feel free to contact us to receive full-text versions if these cannot be found through the Infolep portal.

Immune Dysregulation and Community Health Factors in Maternal and Childhood Leprosy: A Partial Least Squares-Structural Equation Modelling Study
Prakoeswa FRS, Endaryanto A, Prakoeswa CRS. Infection & Chemotherapy. XMLink. 2026; 58 (2): 224.

Temporal and spatial patterns of Leprosy in Uganda, 2020-2024: A nationwide surveillance analysis
Abbo G, Migisha R, Mfitundinda E, et al. PLoS neglected tropical diseases. 2026; 20 (7): 1 - 14.

Teleinterconsultation as a strategy to support surveillance of physical disability in leprosy in the state of Maranhão, Brazil
Neves ACFB, Matos SOV, Pereira VF, et al. Ciência & Saúde Coletiva. FapUNIFESP (SciELO). 2026; 31 (5): 1 - 8.

Development and validation of a chatbot for managing leprosy lesions
Martins RMG, Alves DDA, Alves SAA, et al. Ciência & Saúde Coletiva. FapUNIFESP (SciELO). 2026; 31 (5): 1 - 11.

Mass Spectrometry-Based Metabolomics in Formalin-Fixed Paraffin-Embedded Skin Biopsies Identifies Potential Candidate Biomarkers for Leprosy Progression Across the Ridley–Jopling Clinical Spectrum
Pereira NV, Dornelas BDC, Costa WVTD, et al. Microorganisms. MDPI AG. 2026; 14 (7): 1 - 21.

A retrospective review of leprosy diagnosed histopathologically from skin biopsy specimens in central South Africa
van Wyk R, le Grange D, Budding L. Southern African journal of infectious diseases. 2026; 41 (1): 1 - 9.

Transmission Interruption of Leprosy in the Philippines: An Update on the Current Program Priorities and Interventions
Fatunmbi BS, Taruc AY, Sanikullah KH, et al. Tropical Medicine and Infectious Disease. MDPI AG. 2026; 11 (7) : 1 - 13.

Medical students’ self-perception about Leprosy at a university in the amazon region
Pinho Rodrigues VI, Coelho Yano K, Costa Quaresma T, et al. Revista Brasileira de Neurologia. Revista Brasileira de Neurologia. 2026; 62 (2): 1 - 6.

The Correlation Between Knowledge and Family Support for Self-Care of Leprosy Patients
Saleh NC, Armaijn L, Sakurawati A. Asian Journal of Engineering, Social and Health. Ridwan Institute. 2026; 5 (7): 727 - 734.

Renal Involvement in Leprosy in the Multidrug Therapy Era: Current Evidence and Clinical Monitoring
de Oliveira K, Corrêa LMDA, Brandão LKV, et al. Current Tropical Medicine Reports. Springer Science and Business Media LLC. 2026; 13 (1): 1 - 13.

Case Reports

A Six Year Old Boy with Lepromatous Leprosy: A Case Report Revealing an Unsolved Mystery
Sobhan S, Farook M. Mymensingh medical journal: MMJ. 2026; 35 (3): 959-964.

Oral Diagnosis of Lepromatous Leprosy in a Hyperendemic Region of Brazil
Rosa A, Alves M, Dorta R. Head and neck pathology. 2026.

Evidence of autochthonous transmission of leprosy, causing an outbreak in a family
Mansoori N, Farzaneh T, Sofizadeh A. Leprosy Review. Lepra. 2026; 97 (2): 1 - 5.

Paucibacillary leprosy presenting as fibular neuropathy: A case of autochthonous zoonotic exposure in endemic Florida
Ruffing K. PLoS neglected tropical diseases. 2026; 20 (6): 1 - 5.

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Friday, August 7, 2026

Fw: Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works

Fw: Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works

Wednesday, August 5, 2026

Fw: Ref.: (LML) Long-lasting adverse impact of chemoprophylaxis & what actually works

Tuesday, August 4, 2026

Fw: Ref.: (LML) Infolep monthly overview of new publications on leprosy. July, 2026

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