Dev Aditya Tomar

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Xenotransplantation: Pigs and Humans

Dev Aditya Tomar — Tue, 03 Mar 2026 09:47:05 +0000

Ethically and legally sourced organs are always in demand. The high demand and low supply result in an unfortunately high mortality rate, not due to transplantation, but due to waiting for one. In India, the gap between demand and available organs is staggering—roughly 150,000–200,000 patients are waiting for kidney transplants, yet only a few thousand transplants occur.

Here comes the idea of xenotransplantation: where one transplants organs, tissues, or cells from one species into another. In recent years, this idea has shifted from science fiction [Frankenstein] to clinical reality. In 2025–2026 alone, xenotransplants have moved from an idea to the first structured clinical trials, thus offering a potential solution to one of medicine’s most persistent problems.

This article unveils what xenotransplantation actually is, how pig organs are genetically edited, the real-world anecdotes, the challenges that remain, and what the future might look like.

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DEFINING XENOTRANSPLANTATION

Types of Transplants or Grafts

Transplantation is the process of transferring cell, tissue or organ from one being to another. Now, they might be:

Autograft: Tissue or organ is transplanted from one part of a person’s body to another part of the same person.
Isograft: Tissue is transferred between genetically identical individuals (e.g., identical twins).
Allograft: A tissue or organ is transferred from one person to another (same species, not genetically identical).
Xenograft: Transplantation of organs or tissues between different species

For practical reasons, the primary animal used is the pig, though some research uses primates or other species. In modern medicine, xenotransplants are being developed for kidneys (for end-stage renal disease), hearts (for severe heart failure), livers (for acute or chronic liver failure), Islet cells (for type 1 diabetes), and skin and corneal tissues (for burns and eye‑disease patients).

BUT WHY PIGS?

Just like how Mendel selected Pisum sativum [Sweet pea] for his genetic experiments, pigs seem to have been selected for cultivating xenotransplants. Here are the reasons:

Similar size and anatomy

Pig hearts and kidneys are roughly the same.
Their physiology is also close enough that early‑stage transplants can restore basic function of the organ

Rapid and scalable breeding

Thanks to their high reproductive capacity, a large number of pigs can be procured in a shorter amount of time.
This means, in theory, that thousands of “organ-ready” pigs could be bred on demand, unlike the limited supply of human donor organs.

Advanced genetic‑editing tools

CRISPR and other gene‑editing technologies have made it possible to make tailor-made organs fitting an individual.
In landmark cases, pig kidneys and hearts used in humans carried up to 69 different genetic edits.

Because of this combination—anatomy, scalability, and genetic programmability—pigs have become the workhorse species for modern xenotransplantation.

GENETICALLY ENGINEERED PIGS

In short, we can say there are 3 major goals for genetic engineering:

Prevention of Transplant Rejection

Human immune systems has the ability to detect “self” from “non-self” antigens. Pig antigens like α‑Gal (Galactose‑α‑1,3‑galactose) and other glycan antigens are flagged as “foreign”. This led to hyperacute graft rejections within minutes in early xenotransplant attempts.

The scientists now use CRISPR to overcome this problem. Recent successful pig‑kidney cases involved multiple antigen‑knockout edits plus human‑gene insertions to fine-tune compatibility.

But preventing rejection isn’t just about removing pig markers. The compatibility can also be increased by the addition of human genes.

CD46, CD55, CD59: Regulate the complement system
Thrombomodulin, EPCR (endothelial protein C receptor): Reduce abnormal clotting within the graft [major cause of early failure]
CD47: Prevents phagocytosis of pig cells
HO‑1 (heme‑oxygenase‑1): Has anti-inflammatory and protective effects on blood vessels inside the organ

In one landmark pig‑kidney transplant (2024–2025), the donor pig carried 69 different genetic edits—a mix of knockouts, knock-ins, and knockdowns. This genetically engineered organ functioned in a human recipient for over 270 days (nearly nine months).

Tackling Thrombosis

Thrombotic Microangiopathy

One of the biggest issues in early xenotransplantation was thrombotic microangiopathy. It is the development of multiple clots in small blood vessels of the organ, leading to ischaemia and death of the tissue.

The solution has been twofold:

Engineering pig organs with human clot-regulating genes (thrombomodulin, EPCR, CD47, etc.).
Providing immunosuppressive and anticoagulant drug regimens around the time of transplant.

Chances of Zoonotic Infections

Pigs are a host to several different viruses, including porcine endogenous retroviruses (PERVs). These viruses are integrated in the pig’s DNA and can, in theory, infect human cells, raising concerns about long-term safety.

Recent advances include:

Gene‑editing PERVs out of the pig genome using CRISPR.
Protocols to check for any viral activation or transmission.

So far, no PERV transmission has been definitively documented in human xenotransplant cases, but the risk remains a key focus of regulatory scrutiny.

REAL-WORLD XENOTRANSPLANT CASES

Now let’s look at the most recent cases of xenotransplants…

Pig Kidney

The first truly durable pig-kidney transplant in a human was a compassionate use case in 2024–2025. A patient with end-stage kidney disease and no hope of a human donor received a kidney from a 69‑gene-edited pig.

Key outcomes:

Normal filtration function, reducing the need for dialysis.
The patient reported improved energy, better appetite, and fewer complications tied to chronic dialysis.
The graft survived for over 270 days, far longer than any previous pig‑kidney xenotransplant.

In 2026, the first FDA‑sanctioned clinical trial for pig‑to‑human kidney xenotransplantation began in the United States at major centers including NYU Langone, Massachusetts General Hospital, and Johns Hopkins.

These trials are small, closely monitored, and follow strict protocols for patient selection, immunosuppression, and follow‑up.

Organizations like the National Kidney Foundation have also highlighted that clinical trials for pig‑to‑human kidney transplantation are now officially underway.

Pig Heart

In the early 2020s, the first pig‑to‑human heart transplants under compassionate‑use protocols made headlines. Some recipients survived for weeks to months, far longer than was expected.

The associated risks were immense, but each case provided critical data:

Response of human immune cells
Better drug combinations to balance rejection prevention and side effects.
Better protocols for selecting recipients

In 2025–2026, the International Society for Heart and Lung Transplantation (ISHLT) published a consensus statement that lays out strict guidelines for clinical cardiac xenotransplantation. These include:

Which human antirejection drugs are acceptable?
How to monitor for rejection and infection?
How to manage informed consent and long-term follow-up?

This document is essentially a “blueprint” for bringing pig‑heart transplants out of the emergency room and into structured clinical practice.

Pig Liver

In 2025, a world‑first pig‑to‑human liver xenotransplant in a living patient was reported in China. The recipient, a patient with severe liver failure, received a 6‑gene‑edited miniature‑pig liver.

This liver functioned for several weeks, providing metabolic support and buying time for the patient’s condition to stabilize. While the graft did not last years, it demonstrated that pig livers can replace a human’s liver, even for a short duration.

Reports from the European Association for the Study of the Liver (EASL) and other liver‑disease societies now frame pig‑liver xenotransplants as a potential bridge for acute‑liver‑failure patients who would otherwise die within days.

Other Pig Transplants

Researchers are also exploring pig‑derived islet‑cell transplants for type 1 diabetes.

Scientists are also looking at:

Pig‑skin grafts for burn patients (providing temporary coverage until human‑skin grafts can be prepared).
Pig‑corneal transplants for patients with corneal scarring or infection.

RESPONSE OF HUMAN IMMUNE SYSTEM

Xenotransplantation is a constant battle against the immune system. The body’s reaction to a pig organ typically follows a sequence:

Types of Graft Rejection

Hyperacute and Acute Rejection

In early attempts, the immune system would destroy pig organs within minutes to hours via hyperacute rejection. This happened because:

Human antibodies bound to pig‑specific antigens.
The complement system activation, causing massive blood‑clotting and organ destruction.

Modern gene editing and immunosuppression have reduced the incidence dramatically, but low‑level immune activity often still occurs over days to months.

Chronic Immune Reactions

Even with genetic modifications, the human immune system continues to interact with the pig graft in the long run.

A 2026 immunology paper analyzing the first long‑lasting pig‑kidney xenograft showed that:

Certain immune‑cell subsets remained active even months after transplant.
Gene‑expression patterns in the graft revealed subtle changes reflective of ongoing immune stress.

Thrombosis and Coagulation

Thrombotic microangiopathy remains one of the toughest issues. Pig‑human blood‑clotting systems are not perfectly aligned, so:

Microclots form in small vessels inside the graft.
Over time, these clots block blood flow and cause organ failure.

Solutions now include:

Genetic insertion of human-like clot-regulating genes (thrombomodulin, EPCR, CD47).
Careful use of anticoagulant drugs around the transplant window.

These interventions have significantly reduced early clotting-related failures in recent xenotransplants.

Infection and Viral Risks

The final concern is infection, especially from pig-specific viruses. Regulators and clinicians are carefully monitoring:

Porcine endogenous retroviruses (PERVs): As mentioned earlier, CRISPR is being used to delete or inactivate PERVs from donor pigs.
Other pathogens: Pigs are raised in strict biosecure facilities, and organs are screened for bacteria, parasites, and common viruses.

Post‑transplant, patients undergo regular testing for any sign of viral or microbial transmission.

To date, there is no confirmed case of PERV transmission from pig‑to‑human xenografts, but the risk is treated as a top‑priority issue.

Porcine endogenous retroviruses

SIGNIFICANCE IN HUMAN PATIENTS

The primary driver of xenotransplantation is the uneven demand and supply chain. Xenotransplantation offers a possible way to close this gap by:

Providing on‑demand organs not dependent on sudden accidents or deaths.
Reducing waiting times and mortality for patients on dialysis, in heart‑failure clinics, or on liver‑support systems.
Offering time for more options: a pig organ can keep someone alive and stable until a human organ becomes available.

For patients, the benefits are profound, including and not limited to improved quality of life, greater predictability, and potential longevity.

CHALLENGES AND ETHICAL QUESTIONS

Despite the promise, xenotransplantation is still high‑risk, experimental surgery with major open questions.

Long‑Term Survival and Function

Even the best‑case pig‑kidney xenografts have so far lasted months, not decades. Long‑term outcomes—like 10‑ or 20‑year survival—are still unknown.

Immunosuppression and Side Effects

Xenotransplant recipients need strong immunosuppressive drugs to suppress their immune systems enough to accept the pig organ. These drugs:

Increase susceptibility to infections.
Raise the risk of cancer.
Can cause kidney damage, diabetes, and other metabolic problems.

Ethical Considerations

Xenotransplantation raises serious ethical issues:

Is it acceptable to breed and modify pigs solely for human organ harvesting?
Patients in end‑stage disease may feel pressured to accept experimental procedures with uncertain outcomes.
Will xenotransplants become another tool for the wealthy, while the poor remain on dialysis or in heart‑failure clinics?

Cost and Scalability

Right now, xenotransplantation is extremely expensive: gene editing, pathogen‑controlled breeding, surgery, and long‑term monitoring all carry high costs.

Scaling this technology to hundreds of thousands of patients worldwide will require dramatic cost reductions and technological simplification.

REFERENCES

Tao P and Zhou K (2025) Recent progress in pig-to-human kidney xenotransplantation. Front. Immunol. 16:1735113. doi: 10.3389/fimmu.2025.1735113

Shirini, Kasra et al. “Xenotransplantation Literature Update: January-June 2025.” Xenotransplantation vol. 32,4 (2025): e70072. doi:10.1111/xen.70072

Clinical Trials for Pig-to-Human Kidney Transplantation Are Here. National Kidney Foundation. August 05, 2025.

Guilherme T. Ribas et al, Immune profiling in a living human recipient of a gene-edited pig kidney, Nature Medicine (2026). DOI: 10.1038/s41591-025-04053-3

U.S. FDA page summarizing regulatory concerns, infection risks, and oversight of animal‑to‑human transplants. Link.

International Society for Heart and Lung Transplantation document on rules for patient selection, immunosuppression, and monitoring in pig‑heart xenotransplants. 20 February 2026.

National Kidney Foundation‑style page explaining what xenotransplantation is, how it works, and where trials stand. Link.

Telemedicine: The Guide to Digital Healthcare in 2026

Dev Aditya Tomar — Sun, 01 Mar 2026 13:08:27 +0000

Telemedicine is no longer a futuristic concept, but rather a reality of how people receive healthcare nowadays. In simple terms, telemedicine is the practice of delivering medical services remotely, using technology such as video calls, apps, messaging, and remote‑monitoring devices. That is, one can get expert opinion with only a click now!

The COVID-19 pandemic has significantly accelerated its evolution from a niche “backup option” into a mainstream model of care. It is now being used for routine check-ups, chronic‑disease management, mental‑health counselling, emergency triage, and even remote‑surgical support.

In India, eSanjeevani portal and private‑sector apps are already being promoted and put into use.

Table of Contents

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WHAT IS TELEMEDICINE?

PATIENT'S BENEFITS

DOCTORS AND TELEMEDICINE

REGULATIONS, PRIVACY AND ETHICS

TELEMEDICINE IMPLEMENTATION GUIDE BY WHO

CASE STUDY: eSANJEEVANI

Lessons & Future Plans

CHALLENGES AND LIMITATIONS

THE FUTURE OF TELEMEDICINE

REFERENCES

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WHAT IS TELEMEDICINE?

Many people use “telemedicine” and “telehealth” interchangeably, but :

Telemedicine refers to clinical services delivered at a distance [like consultations, prescriptions, and follow-ups]
Telehealth is a broader umbrella comprising of telemedicine, remote monitoring, health‑education courses, and public‑health campaigns delivered through digital channels.

Within telemedicine, there are three main modes:

Live‑interactive video visits
Store‑and‑forward: Patients or local clinics send photos, scans, and lab reports to a specialist who reviews them later and issues a report or recommendation
Remote patient monitoring (RPM): Patients use devices (blood‑pressure cuffs, glucose meters, smartwatches, ECG patches) that transmit data to clinicians, who then track trends and intervene when needed.

In India, telemedicine has been formally guided by the Telemedicine Practice Guidelines (2020), updated in 2026. It requires the doctors to be registered, patient identity to be verified, proper documentation, informed consent, and treatment with the same professional standards as in-person visits.

PATIENT'S BENEFITS

For patients, telemedicine is primarily about access, convenience, and continuity.

Telemedicine removes geography as a barrier to expertise.
No long queues, no crowded waiting rooms. Also, greater compliance would be observed in cases of multiple regular follow-ups.
For Chronic‑disease management, like diabetes, hypertension, heart failure, chronic kidney disease, and autoimmune conditions. It can schedule regular check-ins, track lab results, and watch trends from home devices, helping the patient prevent avoidable hospitalizations.
Tele‑counselling and tele‑psychiatry let people seek help from the privacy of their homes, reducing stigma and shame
Post‑treatment and rehabilitation. After surgery, or hospital discharge, patients can receive physiotherapy guidance and nutrition coaching easily.

DOCTORS AND TELEMEDICINE

With a skewed doctor-to-population ratio here in India, telemedicine can provide a structure, thus decreasing OPD crowd, waiting time, and delivery of urgent care.

The following are some possible scenarios:

Pre‑visit triage: A patient can fill out an online, listing his symptoms, medications, and allergies. This information is then forwarded to the physician before the call starts.
During the visit: The platform can access the patient’s medical history, lab results.
Post‑visit automation: After the call, the system can auto‑generate notes, send prescription orders as suggested, schedule follow-up reminders, and flag patients with notifiable diseases.

REGULATIONS, PRIVACY AND ETHICS

Because telemedicine deals with highly sensitive health data, it sits at the intersection of law, ethics, and technology.

In India, the 2026‑updated Telemedicine Practice Guidelines stress that the same professional standards apply whether care is given in‑person or remotely.
Patients must be clearly informed about how their data are stored, who can access it, and how long records are kept. Teleconsultation records must be as complete and secure as physical‑chart notes.
End-to-end encryption is a must, for maintaining patient’s privacy. Another possibility could be integrating the private telemedicine data into national digital‑health platforms such as India’s Ayushman Bharat Digital Mission (ABDM).

Telemedicine Practice Guidelines, India

Strict scrutiny over AI-generated results should be kept. Confirming the result with a physician could be one step towards it.

TELEMEDICINE IMPLEMENTATION GUIDE BY WHO

CASE STUDY: eSANJEEVANI

Launched in 2018 by the Ministry of Health & Family Welfare, Government of India, eSanjeevani is a cloud-based national telemedicine platform developed by C-DAC, Mohali. It was integrated with Ayushman Bharat Health & Wellness Centres (HWCs).

Objectives

Its main objectives were to:

Address shortage of doctors and specialists at primary level
Reduce burden on district and tertiary hospitals
Create electronic health records and ensure continuity of care

During COVID-19 lockdown (when OPDs were closed), it was expanded into eSanjeevaniOPD, a free patient-to-doctor teleconsultation service for all citizens.

Parts of eSanjeevani

Patient to Doctor Telemedicine

Assisted Telemedicine

It has two components :

eSanjeevaniHWC (Hub-and-Spoke Model)
- Health worker to doctor teleconsultation
- Used at rural HWCs
- EMR created → patient connected to doctor → ePrescription issued → medicines dispensed locally
eSanjeevaniOPD
- Direct patient-to-doctor consultation via web/mobile app
- Patient registers → receives token → waits in virtual queue → doctor consults → prescription issued

Issues Faced

Scaling issues
No SOPs initially [Standard Operating Procedures]
Digital illiteracy among health workers
Low public trust in telemedicine
Demand spikes

Their Solutions

Shifted to hyperscale cloud system
Developed and revised SOPs with MoHFW
Extensive training & trial sessions
Awareness campaigns & user guides
Continuous monitoring & forecasting

Lessons & Future Plans

Higher internet penetration increased usage, but demand was strong even in low-connectivity and remote areas.
Strong local technical support ensured 99.5% uptime.
Integrated with Ayushman Bharat Digital Mission for health records linkage.
Expanding to eSanjeevani 2.0 with AI features, multilingual interface, and capacity for 1 million consultations/day.

CHALLENGES AND LIMITATIONS

Despite having positive effects on the current healthcare infrastructure, it comes along with some challenges.

Digital divide: People may lack stable internet, smartphones, or the digital literacy to use apps.
Physical‑exam limitations: Conditions like acute abdominal pain, complex injuries, and certain surgical cases would still require in-person exams, palpation, or imaging that cannot be fully replicated remotely.
Privacy and commercialization risks: Breaches, misuse of data, or aggressive marketing practices can erode patient trust too.

THE FUTURE OF TELEMEDICINE

Instead of “in‑person vs. telemedicine,” the future is hybrid care—mixing face‑to‑face visits, video consults, phone calls, and remote monitoring based on each patient’s needs and condition.
As smartwatches, continuous glucose monitors, ECG patches, and implantable devices become more accurate and affordable, telemedicine dashboards will receive richer, real-time data streams, thus enabling earlier intervention.
Telemedicine will be a key tool for delivering specialist care in low‑resource and remote regions, including tribal belts and underserved districts of India, where building enough hospitals and training enough specialists in‑person is physically and financially challenging.

REFERENCES

Consolidated telemedicine implementation guide. 9 November 2022 Publication. ISBN: 978 92 4 005918 4

eSanjeevani, National Telemedicine Service. Link.

Is HbA1c not useful in Indian Population?

Dev Aditya Tomar — Sun, 22 Feb 2026 07:33:50 +0000

HbA1c or Glycated Haemoglobin is a term known to almost all Indians, thanks to the high prevalence of diabetes not only in their direct family but also in their community. Be it a healthcare worker or a member of the general public, I can surely say that you must know a diabetes patient personally, may it be your friend, family or a loved one.

HbA1c is widely used as a diagnostic and monitoring method for diabetes in general. Even with the availability of other tests like OGTT, FBS, PPBS, it still remains the preferred mode of classifying people into diabetics and non-diabetics. This is perhaps due to the following advantages:

No fasting required
Depicts the trend of the previous 2-3 months
Adopted in guidelines [WHO, ADA]

However, depending on HbA1c as the sole criteria for diagnosis and monitoring of diabetes can lead to the misinterpretation, specially in Indian populations. This effect is seen due to the enormous burden of haematological abnormalities [IDA], genetic factors [G6PD deficiency], social and metabolic influences.

The Article “The limitations and fallacies of relying on glycosylated haemoglobin for diagnosing and monitoring diabetes in Indian population” highlights the discordance between HbA1c and blood glucose levels, with a special focus on people with altered erythrocytic dynamics.

My article tries to describe all of it in a much simpler way, so that you can digest the information easily and also get to know about medical topics, without obsessing over the minute details.

Special thanks to Shambik Sir [my Physics teacher] for telling me about this article published in The Lancet Regional Health – Southeast Asia, 2026.

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STRUCTURE OF THE STUDY

Search Terms

HbA1c
glycated haemoglobin
diabetes
diagnosis
oral glucose tolerance test (OGTT)
iron deficiency anaemia
hemoglobinopathies
G6PD deficiency
Polycythaemia
erythrocyte lifespan
South Asians
India

Filters

To select

observational studies
randomized controlled trials
meta-analyses
national survey reports
clinical guidelines

Grouping

HbA1c as a :

Diagnostic tool [Compared to OGTT, FBS]
Monitoring marker [Compared to SMBG, CGM, Fructosamine, Glycated albumin]

Selection Criteria

If they provided data on

Discordance between HbA1c and glucose-based indices
Diagnostic or monitoring performance in the presence of hematologic disorders
Alternative biomarkers such as fructosamine, glycated albumin, or 1,5-anhydroglucitol.

Special Emphasis

On studies focused on the effect of haematological conditions on HbA1c.

HbA1c AND BLOOD GLUCOSE

Blood Test for HbA1c

HbA1c is hailed as the gold standard test for assessment of glycaemic control. It is used for the diagnosis of prediabetes and diabetes. This choice can be attributed to:

Convenience [no fasting]
Stability before analysis
Relatively low variation among individuals

The American Diabetes Association guidelines give the following cut-offs for classification of diabetes :

< 5.7% : Normal
5.7 to < 6.5% : Prediabetes
> 6.5% : Diabetes

On the other hand, here’s what WHO says about it :

HbA1c can be used as a diagnostic test for diabetes if stringent quality assurance tests are in place and assays are standardized to criteria aligned to the international reference values, and there are no conditions present which preclude its accurate measurement.
An HbA1c of 6.5% is recommended as the cut point for diagnosing diabetes.
A value of less than 6.5% does not exclude diabetes diagnosed using glucose tests.
Quality of evidence assessed by GRADE: moderate
Strength of recommendation based on GRADE criteria: conditional

In short, it has pointed out the specific requirements, only under which the credibility of the test is assured.

American Diabetes Association Guidelines

In the Indian scenario, these are quite often overlooked, thus simplifying and increasing the “efficiency” of the diagnostic and monitoring process. It leads to either misdiagnosing or overdiagnosis of diabetes, hindering the treatment plan, prolonging the latent period, and increasing the risk of complications like diabetic neuropathy, retinopathy, etc.

When the HbA1c and mean glucose concentrations were compared using various methods like Continuous Glucose Monitoring Systems [CGMS], Fasting Plasma Glucose, Self-Monitoring of Blood Glucose, a discordance was observed between them. The causes of the variations are individually discussed in the upcoming topic.

So, to remove such variations, the researchers proposed 2 related indices.

Glycation Gap [GGap] : Predicted HbA1c from plasma fructosamine – Measured HbA1c
Haemoglobin Glycation Index [HGI] : Measured HbA1c – Predicted HbA1c from fasting plasma glucose level

CAUSES OF DIVERGENCE IN INDIA

Four major causes are underlined in the paper. They are :

Haematological Abnormalities
Standardisation of Assays
National Glyco-haemoglobin Standardisation Programme
Seasonal variation

Haematological Abnormalities

Here, a table was provided with different causes and their underlying mechanisms. In short, it talks about three cases in general:

FALSE LOW HbA1c

Due to the following causes, RBC lifespan decreases, thus decreasing the time it gets for glycation of Haemoglobin.

Haemolytic anaemia
G6PD deficiency (subclinical haemolysis)
Acute blood loss (increased young RBCs)
Pregnancy (increased RBC turnover, haemodilution)
Chronic liver disease (hypersplenism, bleeding)
Chronic renal failure (Decreased RBC survival)
Recent blood transfusion (dilution effect)
High-dose vitamin C (assay interference / Decreased glycation)

FALSE HIGH HbA1c

It is opposite to false low HbA1c. Here, the lifespan increases, thus increasing glycation time.

Iron deficiency anaemia (IDA) (Increased glycation, prolonged RBC life)
Polycythaemia (prolonged RBC lifespan)

UNRELIABLE OR VARIABLE HbA1c

It is due to a mix of the mechanisms or because it interferes with the assay.

Hemoglobinopathies (variant & method dependent)
Chronic renal failure (carbamylated Hb interference)
Alcohol abuse
Liver disease
High BMI (obesity)
Race/ethnicity differences (e.g., South Asians, African origin)
Elderly (RBC morphology changes)
Recent transfusion
Hypertriglyceridemia, hyperbilirubinemia
Lead poisoning
Drugs: opioids, salicylates, ribavirin, vitamin E
Asplenia
Assay variation
Seasonal variation (noted in Indian population)

In India, we see high rates of IDA (affecting an estimated 25%–68% depending on age, sex, and study region), hemoglobinopathies ((0.37%-5.9%), with regional and ethnic variation), and G6PD deficiency (7.7–8.5% with high prevalence in tribal group).

G6PD deficiency alone resulted in a median delay of 4.1 years in diabetes diagnosis and a 37% increase in microvascular complications.

Standardisation of Assays

Many laboratories use methods other than High-performance liquid chromatography (HPLC) for the assessment of HbA1c. Even ion-exchange HPLC, which is widely employed in Indian labs, may yield uninterpretable results in individuals with silent haemoglobin variants.

National Glyco-haemoglobin Standardisation Programme

A survey of 310 Indian laboratories found that 75% used HbA1c for diabetes mellitus diagnosis, but only 70% of these assays were National Glyco-haemoglobin Standardization Programme (NGSP)- certified. It shows the possibility of gaps in quality assurance between different labs throughout India.

Thus, the labs need to adopt standardised NGSP-certified HbA1c methods for better diagnosis.

Seasonal Variations

HbA1c levels are highest during the monsoon (June–September) and lowest during autumn (October–November). In patients with well-controlled diabetes, HbA1c tends to rise during winter and the monsoon. However, in patients with HbA1c ≥ 6.5%, levels tend to decrease during the monsoon and autumn.

OTHER APPROACHES

To assess glycemia, we can adopt alternative and complementary approaches as listed below.

Self-Monitoring of Blood Glucose [SMBG]
Fructosamine
Continuous Glucose Monitoring
Flash Glucose Monitoring
Glycated Albumin
1,5-Anhydroglucitol
Haemoglobin Glycation Index

Self Monitoring of Blood Glucose

CLINICAL & POLICY IMPLICATIONS

For Diagnosis

Standardised OGTT as Gold Standard

For Monitoring

HbA1c (measured using a standardized and NGSP-certified assay) should be interpreted
With serial fasting and postprandial blood glucose values.
CGMS if affordable and available.

REFERENCE

The limitations and fallacies of relying on glycosylated hemoglobin for diagnosing and monitoring diabetes in Indian populations. Samajdar, Shambo Samrat et al. The Lancet Regional Health - Southeast Asia, Volume 45, 100724

Use of Glycated Haemoglobin (HbA1c) in the Diagnosis of Diabetes Mellitus. Abbreviated Report of a WHO Consultation. WHO/NMH/CHP/CPM/11.1

Nipah Virus : Is it an Emergency?

Dev Aditya Tomar — Sun, 01 Feb 2026 07:27:22 +0000

Nipah virus (NiV) is a highly virulent zoonotic pathogen that represents a major public health concern because of its high fatality rate and ability to spread between humans. The virus was first recognized during an outbreak in Malaysia in 1998–1999 and is classified under the Henipavirus genus of the Paramyxoviridae family. Fruit bats of the Pteropus genus serve as the natural reservoir, and human infection can occur through direct contact with bats, via intermediate animal hosts such as pigs, or through close contact with infected persons.

Clinically, Nipah virus infection demonstrates a broad spectrum of manifestations, ranging from asymptomatic cases to severe respiratory disease and lethal encephalitis. Reported case fatality rates vary from 40% to 75%, depending on the outbreak and the level of healthcare support available. Repeated outbreaks in South and Southeast Asia, particularly in India and Bangladesh, underscore the virus’s significant epidemic potential.

We'll discus the topic under the epidemiological triad [Agent, Host, Environment], Transmission, its Symptoms, Treatment and Prevention.

Table of Contents

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AGENT FACTOR

Structure

Genome Organization

Mechanism of Viral Entry

Role of Epherin Receptor

HOST FACTORS

Natural Reservoir

Intermediate Animal Hosts

Human Host

Human to Human Transmission

ENVIRONMENTAL FACTORS

Habitat Loss and Deforestation

Urbanisation and Agricultural Expansion

Climate and Seasons

Food Contamination Practices

Livestock and Animal Housing

PATHOGENESIS

Viral Entry into Host

Primary Replication

Viremia and Dissemination

Endothelial Infection and Vasculitis

Neuroinvasion

Respiratory System Involvement

Immunopathology

Unique Feature

MODES OF TRANSMISSION

Neurological Involvement

Differential Diagnosis

MANAGEMENT

Symptomatic Treatment

Drugs under Study

PREVENTATIVE MEASURES

Prevention of Bat-to-Human Transmission

Prevention of Animal-to-Human Transmission

Prevention of Human-to-Human Transmission

Infection Control in Healthcare Settings

Public Health Measures

Vaccination

SITUATION IN INDIA

REFERENCES

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AGENT FACTOR

Nipah virus (NiV) belongs to the Paramyxoviridae family and is classified under the Henipavirus genus. Owing to its high virulence, significant mortality rate, and the lack of an effective antiviral therapy or licensed vaccine, NiV is designated as a Biosafety Level-4 (BSL-4) pathogen.

Structure

Although NiV shares similarities with other paramyxoviruses, it exhibits certain distinct structural features.

Presence of reticular cytoplasmic inclusions located near the endoplasmic reticulum
Comparatively larger virion size.

Such ultrastructural differences help distinguish NiV from classical paramyxoviruses, despite overall structural resemblance.

Nipah Virus under Microscope

Genome Organization

Nipah virus is a negative-sense, single-stranded, non-segmented, enveloped RNA virus exhibiting helical symmetry. The viral genome is approximately 18.2 kilobases in length and consists of six genes arranged in a 3′–5′ orientation.

These genes encode essential viral proteins : Nucleocapsid protein, Phosphoprotein, Matrix protein, Fusion glycoprotein, Attachment glycoprotein, and the Large polymerase protein.

The nucleocapsid protein, phosphoprotein, and large polymerase protein together form the viral ribonucleoprotein complex, which is essential for viral replication and transcription.
The matrix protein plays a crucial role in viral assembly and budding, linking the ribonucleoprotein core to the viral envelope.

Mechanism of Viral Entry

Viral entry into host cells is mediated by two surface glycoproteins: the attachment glycoprotein and the fusion glycoprotein.
The attachment glycoprotein binds to specific host cell receptors, initiating viral entry.
This interaction triggers activation of the fusion glycoprotein, which undergoes cleavage into two subunits, F1 and F2.
The F1 subunit is primarily responsible for mediating the fusion of the viral envelope with the host cell membrane, allowing entry of the viral genome into the cell.

Role of Epherin Receptor

Research has shown that binding of the host cell receptor ephrin-B2 to the Nipah virus attachment glycoprotein induces allosteric conformational changes. These changes activate the fusion glycoprotein and facilitate receptor-dependent viral entry into host cells, particularly in endothelial and neuronal tissues.

HOST FACTORS

Host factors play a crucial role in determining susceptibility, disease severity, and transmission dynamics of Nipah virus (NiV) infection.

Fruit Bats

Natural Reservoir

Fruit bats of the Pteropus genus serve as the natural reservoir of Nipah virus. Infected bats remain largely asymptomatic while shedding the virus in saliva, urine, feces, and partially eaten fruits. Their ability to fly long distances and their close proximity to human habitats facilitate viral spillover events.

Intermediate Animal Hosts

Certain domestic animals can act as intermediate hosts, amplifying viral transmission. Pigs played a major role during the initial outbreak in Malaysia, where close contact between infected pigs and humans led to widespread transmission. Other animals, such as horses and goats, have also been found to be susceptible, although their role in large-scale outbreaks remains limited.

Human Host

Humans are accidental hosts of Nipah virus infection. Factors such as close contact with infected animals, consumption of contaminated food products, and exposure to infected individuals increase the risk of infection. Healthcare workers and family caregivers are particularly vulnerable due to prolonged and close exposure to infected patients.

Nipah virus exhibits a strong affinity for ephrin-B2 and ephrin-B3 receptors present on host cells. These receptors are highly expressed on endothelial cells, neurons, and respiratory epithelium, explaining the virus’s predilection for the nervous system and lungs. Binding of the viral attachment glycoprotein to these receptors facilitates viral entry and cell-to-cell spread.

The innate immune response is the first line of defense against Nipah virus infection. However, NiV has developed mechanisms to evade host immunity, particularly by inhibiting interferon signaling pathways. Impaired early immune responses contribute to high viral replication and severe disease.

Disease severity is influenced by host-related factors such as age, nutritional status, comorbidities, and immune competence. Delayed healthcare access and inadequate supportive care further exacerbate disease outcomes. Host genetic factors may also play a role, although these are not yet fully understood.

Human to Human Transmission

Host behaviours significantly affect transmission. Practices such as inadequate infection control, lack of personal protective equipment, and close physical contact with infected individuals increase the risk of secondary transmission. Cultural practices involving caregiving and burial rituals may also contribute to virus spread during outbreaks.

ENVIRONMENTAL FACTORS

Environmental factors play a critical role in the emergence, transmission, and recurrence of Nipah virus outbreaks. These factors influence bat ecology, human–animal interactions, and opportunities for viral spillover.

Habitat Loss and Deforestation

Deforestation and large-scale land-use changes disrupt the natural habitats of fruit bats (Pteropus species), forcing them to migrate closer to human settlements. Loss of forest cover reduces natural food sources for bats, increasing their reliance on cultivated fruits and agricultural areas, thereby enhancing the risk of viral transmission to humans and domestic animals.

Urbanisation and Agricultural Expansion

Rapid urbanization and expansion of agricultural activities bring humans, livestock, and wildlife into closer contact.

Deforestation and Habitat Loss

Orchards and farms established near bat roosting sites facilitate contamination of fruits, animal feed, and water sources with bat saliva, urine, or feces, creating conditions favorable for Nipah virus spillover.

Climate and Seasons

Seasonal variations significantly influence Nipah virus transmission. In South Asia, outbreaks commonly occur during winter months, coinciding with increased consumption of raw date palm sap. Climatic factors such as temperature changes, rainfall patterns, and drought affect bat feeding behavior, viral shedding, and human exposure risks.

Date Pal Sap Collection

Food Contamination Practices

Traditional food-harvesting and storage practices contribute to environmental exposure. Collection of raw date palm sap in open containers allows contamination by bats, serving as a major route of Nipah virus transmission in Bangladesh and parts of India.

Similarly, consumption of partially eaten fruits discarded by bats increases infection risk.

Livestock and Animal Housing

Poor livestock housing conditions, particularly pig farming near fruit trees or bat habitats, increase the risk of animal infection and viral amplification. Environmental contamination of animal feed and water sources can facilitate rapid spread among livestock, which may then transmit the virus to humans.

PATHOGENESIS

Viral Entry into Host

Infection begins when Nipah virus enters the human body through the respiratory tract, oral mucosa, or gastrointestinal tract. The viral attachment glycoprotein binds to host cell receptors, primarily ephrin-B2 and ephrin-B3, which are abundantly expressed on endothelial cells, neurons, and respiratory epithelial cells.

This receptor binding triggers activation of the viral fusion glycoprotein, allowing fusion of the viral envelope with the host cell membrane and entry of the viral genome into the cell.

Primary Replication

Following entry, the virus undergoes primary replication at the site of entry, particularly in respiratory epithelial cells. The viral ribonucleoprotein complex initiates transcription and replication of viral RNA in the host cell cytoplasm, leading to production of new virions.

Viremia and Dissemination

Pathogenesis of Nipah Virus Infection

After initial replication, Nipah virus spreads through the bloodstream, resulting in viremia. The virus disseminates to multiple organs, including the lungs, central nervous system, spleen, kidneys, and heart. Endothelial cells serve as major targets, facilitating widespread vascular involvement.

Endothelial Infection and Vasculitis

A hallmark of Nipah virus pathogenesis is infection of vascular endothelial cells, leading to endothelial dysfunction and systemic vasculitis. Viral replication in endothelial cells causes inflammation, thrombosis, increased vascular permeability, and microinfarctions. These vascular changes contribute significantly to tissue ischemia and organ damage.

Neuroinvasion

Nipah virus demonstrates marked neurotropism. The virus gains access to the central nervous system either through hematogenous spread across the blood–brain barrier or via infected endothelial cells. Once in the brain, viral replication leads to neuronal damage, inflammation, and necrosis, resulting in acute encephalitis, seizures, altered consciousness, and coma.

Respiratory System Involvement

Infection of respiratory epithelium and pulmonary endothelium leads to acute respiratory distress characterized by cough, dyspnea, and hypoxia. Extensive alveolar damage and pulmonary edema may occur, contributing to high mortality and increased risk of human-to-human transmission via respiratory secretions.

Immunopathology

Nipah virus has evolved mechanisms to suppress the host innate immune response, particularly by inhibiting interferon signaling pathways. This immune evasion allows uncontrolled viral replication and delays effective antiviral responses, contributing to disease severity.

Excessive immune activation in later stages may lead to cytokine release and inflammatory tissue damage. The combined effects of direct viral cytotoxicity and immune-mediated injury exacerbate organ dysfunction.

Unique Feature

A unique feature of Nipah virus infection is the occurrence of relapsing or late-onset encephalitis weeks to months after apparent recovery. This is believed to result from persistent viral infection or reactivation within the central nervous system.

MODES OF TRANSMISSION

Bat-To-Human, Animal-To-Human, Human-To-Human Transmission

Bat-To-Human

Fruit bats (Pteropus species), the natural reservoir of Nipah virus, transmit the virus to humans through contamination of food or water with their saliva, urine, or feces. Consumption of raw or partially processed date palm sap contaminated by bats is a well-documented route of transmission. Eating fruits partially eaten or contaminated by bats also increases the risk of infection.

Animal-To-Human

Domestic animals, particularly pigs, can act as intermediate hosts and amplify the virus. Humans may become infected through close contact with infected animals, their respiratory secretions, blood, or tissues. This mode of transmission was prominent during the initial outbreaks in Malaysia among pig farmers and slaughterhouse workers.

Human-To-Human

Person-to-person transmission has been documented in several outbreaks, especially in healthcare and household settings. Transmission occurs through close contact with infected individuals, exposure to respiratory droplets, body fluids, or contaminated surfaces.

Transmission

Caregivers and healthcare workers are at increased risk in the absence of adequate infection control measures.

Nosocomial

Hospital-based transmission occurs when appropriate infection prevention and control practices are not followed. Aerosol-generating procedures, improper use of personal protective equipment, and inadequate isolation facilities contribute to nosocomial spread.

CLINICAL FEATURES

The incubation period typically ranges from 5 to 14 days, but in some cases may extend up to 45 days.

Some individuals may remain asymptomatic or develop only mild illness. However, even mild cases may progress rapidly to severe disease.

Prodromal Symptoms

Initial symptoms are non-specific and may resemble common viral illnesses, including : Fever, Headache, Myalgia, Fatigue, Sore throat, Nausea and vomiting.

Respiratory Symptoms

Respiratory involvement is common and may be mild or severe. Features include:

Cough, Shortness of breath,
Chest discomfort
Acute respiratory distress syndrome (ARDS) in severe cases

Respiratory symptoms increase the risk of human-to-human transmission.

Neurological Involvement

Neurological involvement is a hallmark of Nipah virus infection and often indicates severe disease. Features include:

Altered sensorium
Drowsiness or confusion
Seizures
Focal neurological deficits
Acute encephalitis leading to coma

Other Symptoms

Systemic involvement may result from widespread vasculitis and endothelial damage, leading to:

Hypotension
Tachycardia
Multiorgan dysfunction

A distinctive feature of Nipah virus infection is relapsing or late-onset encephalitis, occurring weeks to months after apparent recovery. Symptoms include behavioral changes, seizures, and neurological deterioration.

Complications

Severe encephalitis
Respiratory failure
Multiorgan failure
Death [Case Fatality Rate is 40-75%]

DIAGNOSIS

Early and accurate diagnosis of Nipah virus infection is essential for patient management and outbreak control. Due to the high infectivity of the virus, diagnostic testing is performed in specialized high-containment laboratories.

Specimen

Blood (serum, plasma)
Cerebrospinal fluid (CSF)
Throat and nasal swabs
Urine
Respiratory secretions

RNA Detection

Reverse Transcriptase–Polymerase Chain Reaction (RT-PCR) is the gold standard for early diagnosis. It detects Nipah virus RNA in clinical specimens and is highly sensitive and specific. RT-PCR is most useful during the acute phase of infection.

Serology

Serological assays are used to detect antibodies against Nipah virus:

IgM antibodies - recent or acute infection
IgG antibodies - past exposure or recovery

Enzyme-linked immunosorbent assay (ELISA) is commonly used for antibody detection.

Nipah Virus (VERO NR596 Cells) Malaysia Strain

Virus Isolation

Virus isolation can be performed in cell culture but is restricted to Biosafety Level-4 (BSL-4) laboratories due to the high risk involved. This method is primarily used for research and confirmatory purposes rather than routine diagnosis.

Imaging

Although not confirmatory, imaging studies support diagnosis:

MRI brain may show multiple small hyperintense lesions suggestive of encephalitis
Chest X-ray / CT scan may reveal pulmonary infiltrates or ARDS

Immunohistochemistry

Immunohistochemical staining of tissue samples can detect viral antigens in affected organs, particularly in fatal cases. This method helps in post-mortem diagnosis and pathological studies.

Differential Diagnosis

Japanese encephalitis,
Herpes simplex encephalitis,
Dengue,
Leptospirosis, and
COVID-19.

MANAGEMENT

Currently, there is no specific antiviral therapy or licensed vaccine available for Nipah virus infection. Management is largely supportive, with emphasis on early diagnosis, intensive care, and strict infection control measures.

Symptomatic Treatment

Management of fever and pain
Adequate hydration and electrolyte balance
Nutritional support
Patients with severe disease require admission to intensive care units.
Respiratory Support :
- Respiratory complications are common and may progress rapidly. Management includes:
- Oxygen therapy
- Non-invasive or invasive mechanical ventilation in cases of respiratory failure
- Management of acute respiratory distress syndrome (ARDS)
Neurological Management :
- Patients with encephalitis require careful neurological monitoring. Management includes:
- Control of seizures using antiepileptic drugs
- Measures to reduce raised intracranial pressure
- Maintenance of airway protection in unconscious patients

Drugs under Study

Drug Name	Effect in Humans	Effect in Animals	In-Vitro Test
Ribavirin	In Malaysia outbreak during 1998/1999, a 36% reduction in mortality. In 2018 outbreak in Kerala, out of 23 cases showed 2 survivors. (drug given orally)	No effect in animals	-
Remdesivir (GS-5734; Veklury®)	Not tested in humans	Shows 100% survival rate in AGM model against NiV-B	-
Favipiravir (T-705; Avigan®)	Not tested in humans	Full protection against NiV- M	-
Griffithsin (GRFT)	Not tested in humans	In syrian hamster model against NiV-B shows 15% and 35% survival rate.	-
4’ azidocytidine (R1479)	Not tested in humans	Not tested in animals	Shows activity against NiV, but its prodrug is inactive; therefore withdrawn from clinical trials
4′-chloromethyl-2′-deoxy-2′-fluorocytidine (ALS-8112)	Phase I and II of clinical trials against respiratory syncytial virus infection	Not tested in animals	Strong effect against NiV in vitro at low micromolar range.
Lipopeptide fusion inhibitors	50% survival rate in Syrian golden hamster’s model. In AGMs model shows 33% survival rate.	-	-

PREVENTATIVE MEASURES

Prevention of Bat-to-Human Transmission

Avoid consumption of raw or unprocessed date palm sap.
Use physical barriers (such as bamboo skirts or covers) to prevent bats from accessing sap collection pots.
Wash and peel fruits thoroughly before consumption.
Avoid eating fruits that appear partially eaten or contaminated by bats.

Prevention of Animal-to-Human Transmission

Maintain proper animal housing away from fruit trees and bat habitats.
Implement biosecurity measures in livestock farms, especially pig farms.
Use protective gloves and clothing when handling sick animals.
Promptly isolate and report illness in domestic animals.

Prevention of Human-to-Human Transmission

Early identification and isolation of suspected and confirmed cases.
Use of personal protective equipment (PPE) by healthcare workers and caregivers.
Avoid direct contact with body fluids of infected individuals.
Safe burial practices with minimal handling of the deceased.

Infection Control in Healthcare Settings

Adherence to standard, contact, and droplet precautions.
Use of N95 masks during aerosol-generating procedures.
Proper disinfection of hospital equipment and patient environments.
Training healthcare workers in infection prevention and control practices.

Public Health Measures

Strengthening surveillance systems for early outbreak detection.
Rapid contact tracing and monitoring of exposed individuals.
Quarantine of high-risk contacts when necessary.
Timely risk communication and public awareness campaigns.

Vaccination

Vaccine Name	Country	Phase of Trial
ChAdOx1	United States (Oxford)	Phase 2
PHV02	United States	Phase 1
mRNA-1215	United States	Phase 1
HeV-sG-V	USA	Phase 1
CD40.NiV	Vaccine Research Institute of the ANRS MIE/Inserm	-

SITUATION IN INDIA

Scroll.in

In West Bengal (North 24 Parganas district), two laboratory-confirmed cases of Nipah virus infection were reported in late December 2025 and confirmed in January 2026. Both patients are young healthcare workers (nurses) from the same private hospital.

One patient has shown clinical improvement while the other remained critically ill as of the latest reports.

Over ~190 contacts (including health workers and community contacts) were identified and tested; none have tested positive or shown symptoms.

The World Health Organization said that the risk posed by the Nipah virus was “moderate at the sub-national level, and low at the national, the regional and global levels”. The World Health Organization said it assessed the risk from Nipah to be “moderate” at the sub-national level as no specific drugs or vaccines against it are available, and because early diagnosis is difficult.

REFERENCES

Pandey H, Pandey P, Jakhmola V, et al. A Comprehensive Review of Nipah Virus: From Epidemics to Approaches of Management. J Pure Appl Microbiol. 2024;18(3):1502-1514. doi: 10.22207/JPAM.18.3.33

Rana S, Negi P, Devi M, Butola M, Ansori ANM, Jakhmola V. Systematic Review On New Face of Monkeypox Virus. J Pure Appl Microbiol. 2022;16(suppl 1):3119-3129.

Thomas B, Chandran P, Lilabi MP, et al. Nipah virus infection in Kozhikode, Kerala, South India, in 2018: epidemiology of an outbreak of an emerging disease. Indian J Community Med. 2019;44(4):383-387.

Looi LM, Chua KB. Lessons from the Nipah virus outbreak in Malaysia. Malays J Pathol. 2007;29(2):63-67.

Clayton BA. Nipah virus: transmission of a zoonotic paramyxovirus. Curr Opin Virol. 2017;22:97-104.

Johnson K, Vu M, Freiberg AN. Recent advances in combating Nipah virus. Fac Rev. 2021;10.

Oxford scientists launch first human vaccine trials for deadly Nipah virus. 2024. Retrieved from Link.

Monath TP, Nichols R, Feldmann F, et al. Immunological correlates of protection afforded by PHV02 live, attenuated recombinant vesicular stomatitis virus vector vaccine against Nipah virus disease. Front Immunol. 2023;14:1216225

National Institutes of Health. NIH launches clinical trial of mRNA Nipah virus vaccine.2022. Retrieved from Link.

Rodrigue V, Gravagna K, Yao J, Nafade V, Basta NE. Current progress towards prevention of Nipah and Hendra disease in humans: A scoping review of vaccine and monoclonal antibody candidates being evaluated in clinical trials. Trop Med Int Health. 202429(5):354-364.

A promising vaccine against Nipah virus infection. 2024. Retrieved from Link.

Nipah virus fact sheet. WHO. Retrieved from WHO.

Nipah virus: WHO says low risk of disease spreading beyond India, no travel curbs needed. Scroll.in. Retrieved from Scroll.in.

Artificial Sweeteners and Cognitive Decline: How Low-Calorie Sweeteners Impact Brain Health

Dev Aditya Tomar — Wed, 22 Oct 2025 06:45:32 +0000

Artificial sweeteners have become a popular alternative to sugar, promising the same sweetness without the added calories. From diet sodas to sugar-free desserts, these low- and no-calorie sweeteners are widely used by individuals aiming to manage weight, control blood sugar, or reduce sugar intake. While their short-term metabolic benefits are well-documented, emerging research is raising concerns about their long-term effects on brain health. Recent studies suggest that regular consumption of artificial sweeteners may be linked to cognitive decline, memory impairment, and neuroinflammation. In this article, we explore the mechanisms behind these effects, review the latest scientific evidence, and discuss what this means for individuals concerned about mental and metabolic health.

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ARTIFICIAL SWEETENERS

EXTRA-ORAL MECHANISMS:

EFFECTS OF ARTIFICIAL SWEETENERS

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ARTIFICIAL SWEETENERS

Artificial sweeteners are synthetic sugar substitutes that provide a sweet taste without the added calories of regular sugar. They are widely used in foods and beverages such as diet sodas, sugar-free desserts, and chewing gums to help reduce calorie intake and manage blood sugar levels. Common examples include aspartame, saccharin, sucralose, and stevia (a plant-derived natural sweetener often grouped with artificial ones).

These sweeteners are much sweeter than sugar, meaning only small amounts are needed to achieve the desired

sweetness. They are particularly beneficial for people with diabetes or those aiming to control weight. However, their long-term safety and health effects have been subjects of scientific debate, prompting ongoing research and regulatory monitoring.

But Why?

Artificial sweeteners were created as substitutes for sugar to address the increasing demand for low-calorie and diabetes-friendly alternatives. During the early 20th century, growing concern about health issues such as obesity, diabetes, and tooth decay encouraged the search for safer sweetening options that could provide sweetness without harmful effects. These substitutes were intended to help lower calorie consumption, support weight control, and maintain stable blood sugar levels. They also proved especially useful during periods of sugar scarcity—like World War I and II—when alternative sweeteners were needed for food manufacturing.

Are they sweet?

Mechanism of Action

Non-nutritive sweeteners (NNSs) are not physiologically inert and can influence feeding and metabolism through various peripheral and central mechanisms. These mechanisms include actions on oral and extra-oral sweet taste receptors, effects on metabolic hormone secretion, cognitive processes like reward learning, memory, and taste perception, and gut microbiota.

ORAL MECHANISMS:

Sweet taste perception begins in the oral cavity when sweet tastants bind to T1R2/T1R3 G-protein coupled receptors. NNSs bind with high affinity to these receptors, even at low concentrations, to elicit sweet taste.
Prolonged NNS stimulation might increase sensory adaptation and reduce sweet taste sensitivity, potentially affecting the acceptability of both caloric and non-caloric sweeteners.
In vitro studies suggest NNSs cause greater down-regulation of taste receptor subunits compared to caloric sweeteners, indicating that adaptation magnitude may depend on binding affinity or receptor interactions.
Unlike caloric sweeteners, NNSs do not consistently produce cross-adaptation and can sometimes enhance the intensity of sweet stimuli, especially caloric ones.
Early exposure to NNSs, such as acesulfame potassium (AceK) in maternal milk, has been shown to increase preference thresholds for saccharin and sucrose in adult mice, accompanied by changes in taste signal transduction proteins.
Neuroimaging studies in heavy NNS users have revealed altered taste processing, including an inverse association between NNS use and brain responses (BOLD) in the amygdala and insula to sucrose.

EXTRA-ORAL MECHANISMS:

Functional sweet taste receptors are present in various extra-oral tissues, including the brain, pancreas, and gut, where they are involved in metabolic processes like glucose sensing, satiety hormone secretion, and glycemic control.
In vitro, both caloric and non-caloric sweeteners can stimulate the secretion of incretin hormones (GLP-1 and GIP) from enteroendocrine cells via a T1R3-dependent mechanism.
Both natural and non-nutritive sweeteners increase the expression and membrane trafficking of glucose transporters SGLT-1 and GLUT2 through their actions on intestinal sweet taste receptors.
Studies in mice have demonstrated that NNS administration increases SGLT-1- and GLUT2-dependent glucose absorption. However, some studies have not observed acute effects of NNS consumption on hormone secretion or glycemic excursion in naive rats.

EFFECTS OF ARTIFICIAL SWEETENERS

Alternative sweeteners and potential action mechanisms.

The potential mechanisms by which artificial sweeteners (AS) influence the development of type 2 diabetes (T2D) and cardiovascular complications are complex and multifactorial. By interacting with the sweet taste receptor family (T1R), artificial sweeteners can enhance insulin sensitivity, promote glucose uptake, and increase the expression of LDL receptors. Additionally, they may help reduce the formation of advanced glycation end products (AGEs), reactive oxygen species (ROS), and inflammatory mediators such as TNF-α, IL-6, and intracellular NF-κB.

However, overstimulation of the associated G protein pathways due to excessive intake of artificial sweeteners may have adverse effects.

This includes promoting weight gain, insulin resistance, increased intestinal permeability, and chronic inflammation, all of which contribute to the development of metabolic disorders and related comorbidities.

COGNITIVE DECLINE

An 8-Year Prospective Study was done to find out the "Association Between Consumption of Low- and No-Calorie Artificial Sweeteners and Cognitive Decline". It was published on 3rd September, 2025 and here's what it says :

Stats

12,772 participants
Mean age 51.9 ± 9.0 years
54.8% women
43.2% Black/mixed race
Mean consumption of LNCSs was 92.1 ± 90.1 mg/d.

Summary

Recent research has suggested a possible link between the consumption of certain low- and no-calorie sweeteners (LNCSs) — including aspartame, saccharin, acesulfame-K, erythritol, sorbitol, and xylitol — and accelerated cognitive decline. Higher intake of these sweeteners has been associated with a faster reduction in global cognitive performance, particularly affecting memory and verbal fluency. Participants consuming the highest amounts of combined LNCSs demonstrated a more rapid decline in verbal fluency and overall cognition in non-diabetic individuals, and a greater decline in memory and cognitive function among those with diabetes.

The most recent evidence, published in Neurology — the medical journal of the American Academy of Neurology, was supported by the Brazilian Ministry of Health, the Ministry of Science, Technology, and Innovation, and the National Council for Scientific and Technological Development.

It found that regular consumption of these sweeteners, including tagatose, was linked to declines in memory and overall cognitive ability equivalent to approximately 1.6 years of additional brain aging. These findings suggest that frequent intake of artificial and low-calorie sweeteners may have potential long-term implications for brain health.

Researchers found a link in people under 60 but not older than 60. Do note that, while the study found links, it does not prove that sweeteners cause cognitive decline.

"Correlation does not equal to Causation"

Similar Studies

While numerous animal studies have demonstrated a link between excessive sugar intake and impaired cognitive function, the precise effects of sugars on human cognition remained uncertain.

On 25th Dec, 2023, a systematic review and meta-analysis aimed to assess existing evidence, and the overall quality of research exploring the impact of free and added sugars on cognitive performance in healthy individuals.

Most cohort studies and eight of nine cross-sectional studies reported a significant positive association between higher added sugar consumption and an increased risk of cognitive decline. Conversely, four studies noted a lower risk of cognitive impairment among individuals consuming natural fructose-rich foods, such as fruits.

The majority of randomized controlled trials focused on the short-term effects of glucose on cognitive facilitation, emphasizing that optimal brain function depends on well-regulated blood glucose levels tailored to individual physiology. Overall, the findings underscore the potential harmful effects of excessive, long-term, or prenatal exposure to added sugars on cognitive health.

However, further research is still necessary to clarify the distinct roles of free and added sugars in influencing human cognition.

Mechanism

Effects of Artificial Sweeteners on Brain Health.

Dr. Arbind Kumar Choudhary, Associate Professor, Department of Physiology, All India Institute of Medical Science, Raebareli, Uttar Pradesh, India in his research suggests that artificial sweeteners such as aspartame, sucralose, and saccharin may contribute to oxidative stress and neuroinflammation, disrupt the integrity of the blood-brain barrier, and alter cerebral blood flow, potentially accelerating cognitive decline.

These sweeteners may also affect the gut microbiome, impairing the gut-brain axis and exacerbating neurocognitive issues. Individuals with metabolic conditions such as type 2 diabetes and obesity may be particularly vulnerable, facing an increased risk of cognitive impairment and neurodegenerative diseases.

While artificial sweeteners can provide short-term metabolic benefits, their potential long-term effects on brain health remain a concern. Given their widespread use in India amid rising rates of metabolic and neurodegenerative disorders, there is an urgent need for targeted research to evaluate their safety and long-term neurological impact.

REFERENCES

Aspartame and Other Sweeteners in Food. US FDA.

Burke MV, Small DM. Physiological mechanisms by which non-nutritive sweeteners may impact body weight and metabolism. Physiol Behav. 2015 Dec 1;152(Pt B):381-8. doi: 10.1016/j.physbeh.2015.05.036. Epub 2015 Jun 3. PMID: 26048305; PMCID: PMC4661139.

Concetta Schiano, Vincenzo Grimaldi, Michele Scognamiglio, Dario Costa, Andrea Soricelli, Giovanni Francesco Nicoletti, Claudio Napoli, Soft drinks and sweeteners intake: Possible contribution to the development of metabolic syndrome and cardiovascular diseases. Beneficial or detrimental action of alternative sweeteners?, Food Research International, Volume 142,
2021, 110220, ISSN 0963-9969, https://doi.org/10.1016/j.foodres.2021.110220.

Gillespie KM, White MJ, Kemps E, Moore H, Dymond A, Bartlett SE. The Impact of Free and Added Sugars on Cognitive Function: A Systematic Review and Meta-Analysis. Nutrients. 2023 Dec 25;16(1):75. doi: 10.3390/nu16010075. PMID: 38201905; PMCID: PMC10780393.

CHOUDHARY, Arbind Kumar. Artificial Sweeteners on Brain Health: Neurovascular Changes and Cognitive Decline in Indian Population. Medical Research Archives, [S.l.], v. 13, n. 4, apr. 2025. ISSN 2375-1924. Available at: <https://esmed.org/MRA/mra/article/view/6388>. Date accessed: 22 oct. 2025. doi: https://doi.org/10.18103/mra.v13i4.6388.

Natalia Gomes Gonçalves, Euridice Martinez-Steele, Paulo A. Lotufo , Isabela Bensenor , Alessandra C. Goulart, Sandhi Maria Barreto , Luana Giatti , Carolina Perim de Faria, Maria del Carmen Bisi Molina, Paulo Caramelli , Dirce Maria Marchioni, and Claudia Kimie Suemoto.

Association Between Consumption of Low- and No-Calorie Artificial Sweeteners and Cognitive Decline. Neurology Journals. Volume 105 | Number 7. October 07, 2025

ORS : Oral Rehydration Salt Solution

Dev Aditya Tomar — Sat, 18 Oct 2025 09:04:06 +0000

On 15th October, 2025, the Food Safety and Standards Authority of India (FSSAI), has issued a directive requiring all food and beverage companies to cease using the term “ORS” (Oral Rehydration Solution) on their products. The order extends to all instances where the term appears on its own, with any prefix or suffix, or as part of a trademark or brand name.

On this note, I would like to expand more on the topic of Oral Rehydration Solution, its constituents and uses as directed by WHO while touching on the clarification issued by FSSAI.

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BASIC TERMINOLOGIES

Dehydration

Rehydration

Oral Rehydration Therapy (ORT)

ORAL REHYDRATION SALT SOLUTION

Constituents

Difference between the Old and the New

Role of the Constituents

Previous Stance on ORS

Clarification dated 15th Oct, 2025

Dr. Sivaranjani Santosh

References

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BASIC TERMINOLOGIES

Dehydration

Loss of water and dissolved salts from the body, occurring, for instance, as a result of diarrhoea.

Rehydration

The correction of dehydration.

Oral Rehydration Therapy (ORT)

The administration of fluid by mouth to prevent or correct the dehydration that is a consequence of diarrhoea.

ORAL REHYDRATION SALT SOLUTION

Oral Rehydration Salts (ORS) is the internationally recognized non-proprietary name for a scientifically formulated glucose-electrolyte solution developed in 1969. It was approved, recommended, and distributed by the World Health Organization (WHO) and UNICEF as a life-saving medical formulation for the prevention and treatment of dehydration caused by diarrhea and other conditions leading to fluid loss. It remains a cornerstone of primary healthcare and is classified as an essential medicine by the WHO for its proven safety, affordability, and effectiveness.

Constituents

Given below is the list of ingredients present in the New ORS solution as advised by WHO.

Dissolution of an ORS sachet in drinking water yields the following concentrations :

Difference between the Old and the New

The 'Old' ORS formulation is known as the Standard WHO ORS whereas the 'New' one is called the Reduced Osmolarity ORS. Previously, the ORS had a total osmolarity of 311 mOsm/l, but a consultative technical meeting held in New York (USA) in July 2001 reviewed various studies evaluating this approach. During the meeting, experts provided technical recommendations to WHO and UNICEF regarding the efficacy and safety of reduced osmolarity ORS for treating children with acute non-cholera diarrhea, as well as adults and children suffering from cholera.

These studies showed that the efficacy of ORS solution for treatment of children with acute non-cholera diarrhoea is improved by reducing its osmolarity. In a combined analysis of this study and studies with other reduced osmolarity ORS solutions stool output was also reduced by about 20% and the incidence of vomiting by about 30%.

However, it remains uncertain whether this finding can be confidently applied to patients with severe cholera-induced diarrhea, in whom electrolyte losses are extensive. In such cases, the risk of developing hyponatremia may be heightened, potentially leading to adverse clinical outcomes and diminishing the benefits of using reduced osmolarity ORS.

Role of the Constituents

Glucose : Facilitates the absorption of sodium (and hence water) on a 1:1 molar basis in the
small intestine
Sodium and Potassium : To replace the body losses of these essential ions during
diarrhoea (and vomiting)
Citrate : Corrects the acidosis that occurs as a result of diarrhoea and dehydration.

Uses

DEHYDRATION :

While the mortality rate among children under five suffering from acute diarrhea has declined remarkably—from about 4.5 million deaths annually in 1979 to 1.6 million in 2002—acute diarrhea still remains a significant cause of illness and death among children in developing countries.

The introduction of Oral Rehydration Salts (ORS) and Oral Rehydration Therapy (ORT) by UNICEF and WHO in the late 1970s represented a major milestone in global child health. During the 1990s, these therapies were estimated to have saved more than one million young lives each year by effectively preventing deaths from dehydration caused by diarrhea.

Nevertheless, recent trends indicate a concerning decline in both awareness and the correct use of home-based treatments for diarrhea, including ORT, in several countries—threatening to undermine decades of progress in reducing child mortality.

Hence, the healthcare workers are advised to : [Detailed]

Treat dehydration with ORS solution (or with an IV electrolyte solution in cases of severe dehydration) &

Provide children with 20 mg per day of zinc supplementation for 10–14 days (10 mg per day for infants under six months old)

For cause-specific mortality: The World Health Report2003, WHO, Geneva. For malnutrition: Pelletier, D. L., E. A. Frongillo, and J. P. Habicht, ‘Epidemiologic evidence for a potentiating effect of malnutrition on child mortality’,American Journal of Public Health, vol. 83, no. 8, August 1993, pp. 1130-1133.

OTHERS :

In a study about ORS as alternative to IV fluids in adult burn patients with >15% TBSA burn injuries, it was observed that :

there were no major significant differences between the study group and control group.
Even where there was a significant difference, apart from blood pressure in the first hour of the first day, the study group never crossed safe limits for other parameters.
WHO-ORS with 5gm salt tablets, given according to Sørenson’s formula, is a safe and efficient alternative for IV resuscitation.
It could even be a substitute, particularly in low resource settings and fire disasters.

FSSAI

FSSAI, or the Food Safety and Standards Authority of India, is an independent statutory body responsible for establishing and enforcing food standards in India, ensuring that all food products are safe, hygienic, and fit for human consumption.

Previous Stance on ORS

Earlier directives from the Centre, issued on July 14, 2022, and February 2, 2024, permitted the use of the term “ORS” on product labels as part of a trademark with a prefix or suffix. This was allowed only provided the label included the disclaimer: “The product is NOT an ORS formula as recommended by WHO.”

Clarification dated 15th Oct, 2025

FSSAI has reiterated that, following a fresh review, the use of the term “ORS” in any form—whether as part of a trademark or otherwise—on products like fruit-based, non-carbonated, or ready-to-drink beverages violates the Food Safety and Standards Act.

The authority emphasized that such labeling can mislead consumers by being false, deceptive, ambiguous, or inaccurate.

Additionally, FSSAI warned that products in breach of this rule may incur penalties under Sections 52 and 53 of the Food Safety and Standards Act, 2006.

Dr. Sivaranjani Santosh

Dr Sivaranjani Santosh, paediatrician, says the following...

“It's a huge relief. That means now I know that no child will die, no adult will die because of worsening of diarrhoea, because of these drinks. ORS is supposed to save lives. It's a wonder drug of the 20th century. It's supposed to save lives. It's supposed to rehydrate us. It is like Amrut for us. And here, people have labelled their high sugar drinks as ORS with a suffix or prefix. And for the past 14 years, they have been cheating the public, deceptive labelling, unethical marketing, pharmacies, hospitals, schools, everywhere,”

In 2022, Dr. Santosh filed a PIL in the Telangana High Court against companies labeling sweetened fruit juices as ORS without meeting WHO standards, citing high sugar content and inconsistent electrolytes.

The case drew the attention of then Health Secretary Rajesh Bhushan, prompting judicial and regulatory review. FSSAI initially restricted the use of ‘ORS’ on labels and ads on April 8, 2022, but temporarily relaxed the rule on July 14, 2022, allowing companies with registered trademarks to continue using the term until a final ruling by the Controller General of Patents, Designs and Trademarks.

Dr. Santosh’s eight-year campaign shed light on companies marketing sugar-heavy drinks as ORS, falsely suggesting health benefits. Her advocacy emphasized the risks these products pose, especially to children and people with diabetes. And finally, FSSAI has now given is new directive in favour of her campaign.

References

Kim Y, Hahn S, Garner P. Reduced osmolarity oral rehydration solution for treating dehydration caused by acute diarrhoea in children. Cochrane Database Syst Rev. 2001;2002(2):CD002847. doi: 10.1002/14651858.CD002847. Update in: Cochrane Database Syst Rev. 2002;(1):CD002847. doi: 10.1002/14651858.CD002847. PMID: 11406049; PMCID: PMC6532752.

Moghazy AM, Adly OA, Elbadawy MA, Hashem RE. Evaluation of who oral rehydration solution (ORS) and salt tablets in resuscitating adult patients with burns covering more than 15% of total body surface area (TBSA). Ann Burns Fire Disasters. 2016 Mar 31;29(1):43-47. PMID: 27857652; PMCID: PMC5108229.

Clarification regarding Order dated 14.10.2025 on withdrawal of permissions for use of the term “ORS” along with brand names. Dated 15th October 2025. FSSAI. Retrieved from https://fssai.gov.in/advisories.php.

Oral rehydration salts. Production of the new ORS. 1 January 2006 | Guideline. WHO. Link.

Clinical Management of Acute Diarrhea. WHO/UNICEF Joint Statement.

Antimicrobial Resistance : A Report by WHO

Dev Aditya Tomar — Fri, 17 Oct 2025 08:17:20 +0000

The WHO’s Global Antimicrobial Resistance Surveillance System (GLASS) report highlights a sharp increase in antibiotic resistance, particularly in low- and middle-income nations such as India, where healthcare systems are often fragile.

Drawing on data from more than 23 million bacterial infections reported in over 100 countries, the report reveals that between 2018 and 2023, over 40% of antibiotics have become ineffective against common infections of the bloodstream, urinary tract, digestive system, and reproductive organs.

In 2021 alone, bacterial infections caused an estimated 7.7 million deaths globally, with drug resistance contributing to 4.71 million of those and directly causing 1.14 million fatalities.

This article delves deeper into the topic of antimicrobial resistance and its current effects worldwide and in India.

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INTRODUCTION

Antimicrobial resistance (AMR) is emerging as one of the most serious challenges to global health, weakening the power of critical medicines and increasing the danger posed by infections that were once easily treatable, as well as by routine medical procedures.

Through its Global Antimicrobial Resistance and Use Surveillance System (GLASS), the World Health Organization (WHO) helps nations establish robust surveillance systems and produce comparable data that can drive informed public health policies.

On 13 October 2025, WHO published Global antibiotic resistance surveillance report 2025, which offers a comprehensive global picture of antibiotic resistance patterns, drawing on evidence from more than 23 million confirmed cases of bloodstream, urinary, gastrointestinal, and urogenital infections (including gonorrhoea). The findings are based on data submitted by 104 countries in 2023 and 110 countries over the 2016–2023 period.

If you'd like to understand what AMR [Antimicrobial Resistance] is, then please look at this article. The following is a synopsis of the detailed analysis provided by WHO.

AT A GLANCE

Since the launch of GLASS in 2016, antimicrobial resistance (AMR) data have been submitted by 110 countries, including three territories and regions. Participation has expanded significantly—from just 25 countries in 2016 to 104 in 2023, reflecting a growth of more than 300%.

The steady increase in reporting underscores the growing global recognition of the importance of sharing surveillance data as a collective public health responsibility. Despite these improvements, considerable gaps in data availability and reporting continue to hinder a complete global picture.

In 2023, antibiotic resistance was detected in roughly one out of every six laboratory-confirmed bacterial infections worldwide. The highest resistance levels were found in urinary tract infections (1:3 cases) and bloodstream infections (1:6).

Lower resistance rates were observed in gastrointestinal infections (1:15) and urogenital gonorrhoeal infections (1:125).

Trends of AMR: median annual change in percentage, 2018–2023.

Geographically, the South-East Asia and Eastern Mediterranean regions reported the greatest burden, with nearly one in three infections showing resistance, followed by the African Region, where one in five infections were resistant—both surpassing the global median.

Conversely, resistance was less prevalent in the European Region (one in ten) and lowest in the Western Pacific Region (one in eleven), highlighting marked regional differences.

Median national percentage of AMR in bloodstream infections by AMR surveillance coverage, 2023.

Between 2018 and 2023, antimicrobial resistance (AMR) has risen in 40% of the pathogen–antibiotic combinations tracked for global trends, with annual relative increases ranging from 5% to 15%, depending on the specific combination.

Resistance is notably growing against “Watch” antibiotics in the AWaRe (Access, Watch, Reserve) classification—particularly carbapenems and fluoroquinolones—among major Gram-negative pathogens such as Acinetobacter spp., E. coli, K. pneumoniae, and Salmonella spp.

This trend is concerning because these drugs are critical for treating severe infections. The rise in AMR is narrowing empirical treatment options and prompting a shift from oral to intravenous therapies, with increased dependence on second-line and last-resort antibiotics.

Here are some representations of the Percentage antibiotic resistance to ceftriaxone in N. gonorrhoeae urogenital infections, 2023

Percentage AMR

Global trends in percentage AMR by infection type: median annual change (2018–2023) and 2023 percentage resistance estimates :

INDIAN STATS

The numbers below were a part of Global antibiotic resistance surveillance report 2025 :

Blood Stream Infections

DRUGS

NO. OF INFECTIONS WITH AST, 2023

NO. OF INFECTIONS WITH AST, 2018-2023

% RESISTANCE

Acinetobacter - Imipenem

9946

30,983

71.2

E. coli - Cefotaxime

6564

25,744

78.5

E. coli - Imipenem

8962

30,295

32.3

E. coli - IIIrd Gen Cephalosporins

6564

17,527

79.4

K. pneumoniae - Cefotaxime

6132

24,864

79.6

K. pneumoniae - Imipenem

9065

32,301

61.2

Salmonella - Ciprofloxacin

S. aureus - Methicillin

8373

37,592

50.9

S. pneumoniae - Penicillin G

Gastrointestinal Infections

DRUGS

NO. OF INFECTIONS WITH AST, 2023

NO. OF INFECTIONS WITH AST, 2018-2023

% RESISTANCE

Salmonella - Ciprofloxacin

340

1084

28.9

Shigella - Ciprofloxacin

186

82.1

Urinary Tract Infections

DRUGS

NO. OF INFECTIONS WITH AST, 2023

NO. OF INFECTIONS WITH AST, 2018-2023

% RESISTANCE

E. coli - Cefotaxime

51,874

174,593

73.5

E. coli - Imipenem

64,488

206,402

19.2

K. pneumoniae - Cefotaxime

13,440

44,535

69.9

K. pneumoniae - Imipenem

18,739

59,460

40.3

Urogenital Infections

DRUGS

NO. OF INFECTIONS WITH AST, 2023

NO. OF INFECTIONS WITH AST, 2018-2023

% RESISTANCE

N. gonorrhoea - Ceftriaxone

AMRSN, 2013

Antimicrobial resistance (AMR) represents a significant public health challenge in India, a country with a high prevalence of infectious diseases and extensive, often unregulated, antibiotic use. Accurate assessment of the AMR burden is essential to understand its consequences, while knowledge of local resistance trends is critical for developing both empirical and pathogen-specific treatment strategies suited to varied epidemiological contexts.

In view of this, to generate relevant evidence on the extent of drug resistance and a nationally representative reliable data on AMR which was not existent from India, ICMR initiated Antimicrobial Resistance Surveillance and Research Network (AMRSN) in 2013.

Goals :

Establish network of hospitals to monitor trends in the antimicrobial susceptibility profile of clinically important bacteria and fungi limited to human health.
Include comprehensive molecular studies for identifying the clonality of drug-resistant pathogens and their transmission dynamics to enable better understanding of AMR in the Indian context and develop suitable interventions.
Disseminate information on AMR in pathogenic organisms to stakeholders to promote interventions that reduce AMR.
Create data management system for data collection and analysis.

Focus :

Enterobacteriaceae causing sepsis,
Gram negative non-fermenters,
Enteric fever pathogens,
Diarrheagenic bacterial organisms,
Gram positives: staphylococci and enterococci and
Fungal pathogens (excluded in WHO priority pathogens)-yeasts (Candida and Cryptococcus spp.) and mycelial fungi (Aspergillus spp. and Zygomycetes spp.)

Collaboration with Institutes :

Diarrheagenic bacterial organisms, CMC, Vellore
Enteric fever pathogens: AIIMS, New Delhi
Enterobacteriaceae causing sepsis: PGIMER, Chandigarh
Gram negative non fermenters: CMC, Vellore
Gram positives including MRSA: JIPMER, Pondicherry
Fungal infections: PGIMER, Chandigarh

REFERENCES

India's Antimicrobial Resistance Surveillance & Research Initiative, ICMR. Link.

Global antibiotic resistance surveillance report 2025. 13 October 2025 | Global report. WHO. ISBN: 978924011633. Link.

Global antibiotic resistance surveillance report 2025: summary13 October 2025 | Executive summary. WHO Reference Number: B09585. Link.

Understanding Nobel Prize : Year 2025

Dev Aditya Tomar — Tue, 14 Oct 2025 16:10:31 +0000

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