Thursday, May 14, 2026

Fw: Ref.: (LML) Update about Hantavirus breakout


 

Leprosy Mailing List –  May 14,  2026

 

Ref.:  (LML)  Update about Hantavirus breakout 

From: Francesca Cando Gajete, Manila, the Philippines

____________________________________________________________________________

Note editor: This is not about leprosy, but otherwise an interesting story. I assume that many of you have followed this saga, but may be some are not in the position to receive such news. Normally, we would not publish such information, but in this case we made an exception.

 

 

Dear Pieter,

 

Sharing this latest update from Dr Edsel Maurice Salvana, Infectious Diseases Consultant Researcher WHO DOH

 

HANTAVIRUS Latest update: There are now eleven cases, nine of which have been confirmed. The three new cases are one American, one French woman and one Spaniard. There have been no additional deaths from the initial three. Most passengers and crew have disembarked and are being quarantined. Contact tracing is ongoing for passengers who disembarked earlier and who may have exposed others. 

 

As long as protocols are followed and everyone cooperates, the risk of further transmission remains LOW. Stay safe.

 

Outbreak in the High Seas

 

The recent report of an outbreak of hantavirus on a cruise ship gave feelings of double déjà vu to those of us in the infectious diseases field. The first déjà vu moment is that of the COVID-19 outbreak on the cruise ship the Diamond Princess, which was the first such SARS-CoV-2 outbreak of its nature and resulted in the ship being bounced around, and finally allowed to dock and discharge its beleaguered passengers after two weeks of quarantine. The second déjà vu moment is the hantavirus infection that claimed the lives of classical pianist Betsy Arakawa and, by extension, her husband Gene Hackman in their New Mexico home just over a year ago. Betsy had apparently contracted hantavirus pulmonary syndrome from rodent nests found around their house and subsequently died at home, while Gene Hackman who had advanced Alzheimer’s was unable to call for help and died of heart failure.

 

The current outbreak on the cruise ship MV Hondius has already killed three people as I write this article, and at least five others have fallen ill. Six of the eight cases have tested positive for the Andes hantavirus on genomic sequencing. The rest of the sick patients are presumed to have hantavirus infection until they can be properly tested since they are showing symptoms consistent with the disease. The ship is currently docked off the coast of Praia in Cape Verde, and some of the sick passengers have been evacuated. The rest of the passengers and crew are likely going to be quarantined either onboard or transferred to a facility for this purpose. The MV Hondius originated from Argentina, where hantavirus is endemic, particularly the Andes virus which is the only hantavirus that has been documented to be capable of human-to-human transmission. According to reports, the cruise ship also stopped in Uruguay and Chile where there have been periodic outbreaks of hantavirus. Authorities in these countries are racing to find the potential source and contain any local infections as well.

 

What is hantavirus? Hantavirus is a family of viruses that can cause two distinct deadly syndromes: hantavirus pulmonary syndrome (HPS) and hemorrhagic fever with renal syndrome (HFRS). Hantavirus disease usually starts off with a flu-like illness characterized by fever, malaise, muscle pain and headaches and can easily be mistaken for more common illnesses. Patients who progress to HPS end up with shortness of breath that can progress to severe respiratory failure and death. If they survive, recovery can be prolonged for up to six months. Patients who progress to HFRS have symptoms that are very similar to leptospirosis, with decreased urine output, bleeding in the urine and the stool, and potentially bleeding in the lungs as well. Low platelets can be found in both syndromes, and so hantavirus infection can be mistaken for dengue fever.

 

Hantavirus is a zoonosis, which is an infectious disease transmitted from animals. The natural host of hantaviruses are rodents, and humans are infected when they inhale aerosolized dried rodent feces, urine or saliva. Rodents do not manifest signs of symptoms of disease, and so these serve as persistent reservoirs of infection. Hantaviruses are found all over the world.

 

Hantaan virus was the very first hantavirus to be described and gave the virus family its name. It was discovered during the Korean War when it caused an outbreak of HFRS among soldiers stationed along the Hantan River. Hantaviruses in the Americas (New World hantavirus) such as Sin Nombre and Andes can cause HPS which have a 30 to 60% mortality. Old World hantaviruses include Hantaan, Seoul, Puumala and Dubrava-Belgrade viruses and these cause the relatively milder HFRS with a mortality rate of 1-15%. Puumanla and Dubrava-Berlgrade viruses cause less severe disease than Hantaan and Seoul.

 

There are no effective antivirals for any of the hantaviruses. Supportive care for HPS is the mainstay of treatment, including the use of ventilators and high-flow oxygen to support recovery of lung function. For HFRS, hydration and management of electrolytes is crucial. In case of renal failure, dialysis may be necessary either as a temporary measure if the kidneys recover, or as an ongoing measure until renal transplant can be performed. There is no widely available vaccine for hantavirus. Some inactivated vaccines have been developed in China and Korea and seem effective for preventing HFRS although the duration of protection is unclear. Other vaccines are in development including DNA, protein and virus-like particles formats and preliminary results are promising.

 

Prevention of infection starts with good pest control to minimize exposure to aerosolized mouse droppings. Wearing protective equipment such as masks when cleaning out rodent nests, especially those with dried mouse droppings, can decrease the risk of exposure and infection. It is still unclear how human to human transmission occurs with the Andes virus. Previous reports suggest close contact, but at least one transmission event occurred with only transient contact between the infected case and the subsequent victim. 

The transmission pattern on the MV Hondius remains unclear. The victims could have all been exposed to rat droppings at the same time and manifested disease at different times. The incubation period of the Andes virus can take up to six weeks, and so there is a possibility of a single exposure. However, the previous documentation of human-to-human transmission for this specific hantavirus also makes it possible that some of the infected patients were subsequently exposed onboard to the sick passengers. Active investigation is ongoing and contact tracing for those passengers that were able to leave before the vessel was quarantined is being done.

 

One of the most important questions I get asked a lot is whether there is a chance this could turn into another pandemic. The World Health Organization (WHO) has already stated that this is unlikely. While the current outbreak seems to involve human-to-human transmission, this usually occurs only with prolonged and close contact. The period in which a patient is contagious is very short and only happens when he or she has a fever. The fever typically lasts only one day, although the other symptoms can persist. Finally, the long incubation period means that proper contact tracing and quarantine can interrupt transmission. Hantavirus can be controlled and contained. The most important thing is that we remain vigilant and listen to properly vetted advice from trustworthy sources like WHO and the Department of Health.

 

A guide especially for our seafarers and travelers.

 

Francesca

 

Dr Francesca Cando Gajete, MHA,FPLS

Member, WHO DOH ADHOC NTAG NTDS 

Member, International Leprosy Association 

Former National Leprosy Control Program Manager 

email address: francesca_gajete@yahoo.com

____________________________________________________________________________

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

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

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


--
You received this message because you are subscribed to the Google Groups "Leprosy Mailing List" group.
To unsubscribe from this group and stop receiving emails from it, send an email to leprosymailinglist+unsubscribe@googlegroups.com.
To view this discussion visit https://groups.google.com/d/msgid/leprosymailinglist/d5e5589d-9f98-4c4e-b95a-a21e7c509bd2n%40googlegroups.com.

Sunday, May 10, 2026

Fw: Ref.: (LML) Did capsule P have a dramatic impact?


 

Leprosy Mailing List –  May 10,  2026

 

Ref.:  (LML) Did capsule P have a dramatic impact?

From:  Joel Almeida, Mumbai, India

____________________________________________________________________________

 

 

Dear Pieter,

ref: (LML) Did capsule P have a dramatic impact (LML May 5, 2026)?

re capsule X, para 3

Correct:


15% decrease in incidence rate of PB with 2 to 5 lesions, between the initial 2 years and years 3 and 4.



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


--
You received this message because you are subscribed to the Google Groups "Leprosy Mailing List" group.
To unsubscribe from this group and stop receiving emails from it, send an email to leprosymailinglist+unsubscribe@googlegroups.com.
To view this discussion visit https://groups.google.com/d/msgid/leprosymailinglist/ac4f807b-559d-4161-85b9-182c9aa6b3e3n%40googlegroups.com.

Fw: Ref.: (LML) Macrophages and eyes/hands/feet


 

 

Leprosy Mailing List –  May 10,  2026

 

Ref.:  (LML) Macrophages and eyes/hands/feet

From:  Joel Almeida, Mumbai, India

____________________________________________________________________________

 

Dear Pieter and colleagues

Macrophages form an important first line of defence. They can limit or even eliminate the bacillus, including via autophagy and vit D-induced cathelicidin. Most of the genomic polymorphisms known to modify  the risk of HD, and LL HD, are related to macrophage function (hLife 2024;2:6–17). The well-known importance of nutrition, schooling, income etc is likely to be partly via upholding macrophage function. Infection with the bacilli has been demonstrated in as many as 50% of all individuals in endemic areas [BMJ. 1973; 3:557-559],  but new cases of disease are relatively rare in endemic populations, often <1 in 10,000/year. Apparently, most infected persons self-limit or eliminate the bacilli without signs of disease, or sequelae, or onward transmission. They are harmless.

Macrophage function unfortunately can be subverted, by producing bacillary debris (eg., DNA) in the cytosol (J Inf Dis 2016, 214:311-320). Once the bacilli within macrophages are damaged by any means, the resulting molecular cascade of harm (cGAS-STING-IRF3-IFNB-OASL) suppresses autophagy and cathelicidin (J Inf Dis 2016, 214:311-320). The disarmed macrophage is vulnerable to regrowth or reinfection when anti-microbial cover is prematurely withdrawn. The bacillary debris is not cleared immediately, given suppression of autophagy. Therefore the duration of anti-microbial cover is no less important than bactericidal potency. As long as concentrated viable bacilli remain available in the household, or market place, or workplace, or neighbourhood, the disarmed macrophage following the withdrawal of anti-microbial protection forms a hospitable niche for bacilli to replicate.

Bacilli replicate by elongation [Nature Comms (2020) 11:452], boosting the surface area and surface virulence factors per bacillus (Mce1A for invasiveness/cell entry [PLoS Negl Trop Dis 13(3): e0006704] and PGL1 for damage to axonal mitochondria via macrophage iNOS- excess NO [Cell (2017)170, 973–985]). Replicating bacilli have high phenotypic virulence. The predicted outcome of prematurely withdrawn antimicrobials is boosted transmission, more frequent multi-case households, more "silent" nerve damage via PGL1-iNOS-NO. Worse, visible deformity via "silent" nerve damage is predicted to more frequently form the first detectable sign of disease in a subclinically infected contact who was given chemoprophylaxis.

 

Is it wise to sabotage macrophage defences in asymptomatic contacts? 

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


--
You received this message because you are subscribed to the Google Groups "Leprosy Mailing List" group.
To unsubscribe from this group and stop receiving emails from it, send an email to leprosymailinglist+unsubscribe@googlegroups.com.
To view this discussion visit https://groups.google.com/d/msgid/leprosymailinglist/96f866fe-6d05-40cc-8bb2-446114d9bdean%40googlegroups.com.

Friday, May 8, 2026

Fw: Ref.: (LML) Need for rethinking on chemoprophylaxis strategies for leprosy control


 

 

 

Leprosy Mailing List –  May 8,  2026

 

Ref.:  (LML) Need for rethinking on chemoprophylaxis strategies for leprosy control

From: Ben Naafs, Munnekeburen, the Netherlands

____________________________________________________________________________

 

Dear Pieter and colleagues,

 

We like to refer to the following article in the attached file:

Need for rethinking on chemoprophylaxis strategies for leprosy control

By Bhushan Kumar, Sukhdeep Singh, Tarun Narang , Nusrat Shafiq, , Sunil Dogra

Department of Dermatology, Shalby Hospital, Punjab, Departments of

Dermatology, Venereology and Leprology and Clinical Pharmacology,

Institute of Medical Education and Research, Chandigarh, India

 

 

I read with pleasure the above article voicing worries I also have. The solution; treat the index case and examen the contacts and treat the ones needed treatment and vaccinate with BCG or similar vaccine is a good one.

 

You will prevent leprosy in the contacts who can develop a protective immunity. But they need a booster if this booster is not supplied by the environmental bacteria.

The problem stays with the ones who can not develop protective immunity and will, when infected, develop polar Lepromatous Leprosy.

 

The patients with a high BI should be treated longer then the WHO advises and followed up with serology in order to detect early a relapse or reinfection. Polar Lepromatous Leprosy patients in an endemic society should be treated for life. Remember Almeida’s contributions!

With 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

 


--
You received this message because you are subscribed to the Google Groups "Leprosy Mailing List" group.
To unsubscribe from this group and stop receiving emails from it, send an email to leprosymailinglist+unsubscribe@googlegroups.com.
To view this discussion visit https://groups.google.com/d/msgid/leprosymailinglist/f36f6dca-404b-4586-8ca2-5cf4707aad35n%40googlegroups.com.

Tuesday, May 5, 2026

Fw: (LML) Did capsule P have a dramatic impact?


 

Leprosy Mailing List –  May 5,  2026

 

Ref.:  (LML) Did capsule P have a dramatic impact?

From: Joel Almeida, Mumbai, India

____________________________________________________________________________

 

Dear Pieter and colleagues,

A randomised controlled trial revealed a relatively large drop in incident single lesion cases of HD. This was after using a certain capsule (P) once among contacts of index cases. The incidence rate fell from 14/10k person-years during years 1 and 2 of follow-up, to only 4.3/10k p-yrs during years 3 and 4. This was a 69% reduction in incidence rate between the initial and later years. During that time the incidence rate of PB HD with 2 to 5 lesions also declined, but by 60%. The incidence rate of MB HD also declined, but by 40%. These too were relatively large and rapid declines. 

Could capsule P be the definitive solution to HD? First consider the comparator arm.

The comparator arm used a different capsule (X) once, and failed to show such a dramatic drop in incidence rate between the initial and later years. Instead, there was a numerical increase in incidence rate, of 12% in single lesion HD, 70% increase in PB with 2 to 5 lesions, and 60% increase in MB HD, between the initial 2 years and years 3 and 4.

Interestingly, the risk of incident HD was numerically higher in contacts of PB index cases vs contacts of MB index cases, but only in the capsule P arm. In the capsule X arm, the usual pattern of risk was observed: numerically higher risk in contacts of MB index cases vs contacts of PB index cases.

Before considering capsule P for the family members of your patients, know that the trial did not report the incidence rate of visible deformity at diagnosis. Therefore neither P nor X could be considered safe on the basis of the trial outcomes.

What were the capsules?
P was placebo. X was rifampicin. (Moet et al 2004 Lepr Rev, Moet et al 2008 Br Med J, Feenstra et al 2012 Lepr Rev).

Why did the P arm alone show a numerically higher risk of HD in contacts of PB index cases vs MB index cases? Most likely because of undiagnosed inapparent LL cases among the contacts of PB index cases, occurring disproportionately in the P arm. 

Why was placebo so dramatically effective in years 3 and 4? Nine incident MB cases were diagnosed in the P arm by year 2, and were removed from the infectious pool by starting them on full MDT. By contrast, only four incident MB cases in the X arm were similarly removed by year 2.  The 9 incident MB cases diagnosed in the P arm by year 2 are likely to have included one or more previously inapparent LL cases that were initially (and understandably) classed as healthy contacts of PB index cases.

Placebo is unlikely to have had a dramatic effect between the initial two years and the latter two years. The excess cases in the placebo arm during years 1 and 2 are likely to have been due to undiagnosed LL cases occurring disproportionately in the placebo arm, shedding astronomical numbers of viable bacilli (10^7 per day or even per nose blow, Davey and Rees 1974 Lepr Rev). Based on the whole set of observations, diagnosis of inapparent LL followed by prompt full MDT treatment appears highly effective. The overwhelming importance of undiagnosed LL cases together with the reported numerical excess risk of HD in the PB index clusters of the placebo arm, somewhat undermine the reliability of conclusions from this trial.

Inapparent LL cases seem overwhelmingly important in maintaining transmission.

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


--
You received this message because you are subscribed to the Google Groups "Leprosy Mailing List" group.
To unsubscribe from this group and stop receiving emails from it, send an email to leprosymailinglist+unsubscribe@googlegroups.com.
To view this discussion visit https://groups.google.com/d/msgid/leprosymailinglist/c46b9f6d-305f-49b2-901f-ae51b5054459n%40googlegroups.com.

Friday, April 24, 2026

Fw: Ref.: (LML) Animals and human participants

 

Leprosy Mailing List –  April 24,  2026

 

Ref.:  (LML) Animals and human participants

From:  Joel Almeida, Mumbai, India

____________________________________________________________________________

 

Dear Pieter and colleagues,

Armadillos offer a useful model of H. Disease. Many aspects including nerve damage, immunobiology, deformity, immunomodulation, anti-microbial potency etc can be studied there. 

Human participants in endemic countries are not always rich, influential or highly schooled. They do not have easy ways of telling whether and when experiments with potential serious harm or even fatality are being done on them. Even the experimenters might not be omniscient about the underlying biology.

Would it be a bad idea to first examine the underlying biology of an intervention in vitro or tissue culture or animal models, before experimenting on people?

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


--
You received this message because you are subscribed to the Google Groups "Leprosy Mailing List" group.
To unsubscribe from this group and stop receiving emails from it, send an email to leprosymailinglist+unsubscribe@googlegroups.com.
To view this discussion visit https://groups.google.com/d/msgid/leprosymailinglist/3bf43b67-8594-4982-9550-5187a10f3053n%40googlegroups.com.

Fw: Ref.: (LML) Animals and human participants


 

Leprosy Mailing List –  April 24,  2026

 

Ref.:  (LML) Animals and human participants

From:  Joel Almeida, Mumbai, India

____________________________________________________________________________

 

Dear Pieter and colleagues,

Armadillos offer a useful model of H. Disease. Many aspects including nerve damage, immunobiology, deformity, immunomodulation, anti-microbial potency etc can be studied there. 

Human participants in endemic countries are not always rich, influential or highly schooled. They do not have easy ways of telling whether and when experiments with potential serious harm or even fatality are being done on them. Even the experimenters might not be omniscient about the underlying biology.

Would it be a bad idea to first examine the underlying biology of an intervention in vitro or tissue culture or animal models, before experimenting on people?

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


--
You received this message because you are subscribed to the Google Groups "Leprosy Mailing List" group.
To unsubscribe from this group and stop receiving emails from it, send an email to leprosymailinglist+unsubscribe@googlegroups.com.
To view this discussion visit https://groups.google.com/d/msgid/leprosymailinglist/3bf43b67-8594-4982-9550-5187a10f3053n%40googlegroups.com.