Credits: Canva
Health officials are sounding the alarm across the Gulf Coast and beyond as cases of Vibrio vulnificus—a rare but lethal “flesh-eating” bacteria—are climbing to levels that have experts deeply concerned. This year alone, infections have killed multiple people in Florida, Louisiana, and North Carolina, with reports trickling in from other coastal states. For a bacterium that kills roughly one in five people it infects, this uptick is not a statistic anyone takes lightly.
Historically, Vibrio vulnificus was an uncommon public health threat, with Louisiana, for example, averaging around seven cases a year over the last decade. In 2023, that number has more than doubled to 17 confirmed infections, four of which proved fatal. Florida, a state with a much larger coastline and higher exposure risk, has already reported 16 cases and at least five deaths. North Carolina has also logged multiple cases and one confirmed death.
While these numbers may seem small compared to seasonal flu or other infections, the stakes are higher: this bacteria can destroy tissue, trigger sepsis, and kill within days. Even with hospitalization, survival is not guaranteed.
Vibrio vulnificus is perhaps most infamous for its causing of necrotizing fasciitis—a swift, virulent infection that kills skin, fat, and muscle tissue. The "flesh-eating" moniker is no hyperbole. Once within the body, the bacteria reproduce rapidly, secreting toxins that kill surrounding tissue and break down the body's defense mechanisms. Two major routes of infection exist:
Through open sores: If you have an open cut, scrape, or even a new tattoo and come in contact with seawater or brackish water that contains the bacteria, you may be in danger.
Through infected seafood: Consuming raw or improperly cooked shellfish—particularly oysters—can deposit the bacteria right into your gut.
Once infection sets in, symptoms can appear within hours. These include redness, swelling, pain, fever, blistering lesions, and in severe cases, septic shock. Without swift medical treatment, death can occur in just a couple of days.
There’s no single explanation for the spike in cases, but scientists and public health agencies are looking closely at several factors.
Warmer waters: Vibrio vulnificus thrives in warm, brackish waters. Between May and October, Gulf Coast water temperatures are ideal breeding grounds. Climate change is pushing average ocean temperatures higher, expanding the bacteria’s habitat farther north than ever before. In recent years, infections have been documented in states like Connecticut and New York—places previously considered low risk.
Storm activity: Hurricanes and tropical storms stir up coastal waters, spreading the bacteria into new areas and concentrating it in floodwaters. Florida’s “extremely active” hurricane seasons in recent years may have amplified exposure.
Environmental shifts: Researchers are investigating unusually high levels of plankton and chlorophyll in parts of Florida’s panhandle waters, which may correlate with surges in Vibrio populations.
For survivors, the road back to health can be long and grueling. In severe wound infections, surgeons often have to remove infected tissue, sometimes leading to amputations. One Florida patient described doctors marking the spread of infection up his leg with a pen to track its progress—three weeks of hospitalization and aggressive antibiotics eventually saved his limb. Others are not so fortunate.
According to the Centers for Disease Control and Prevention (CDC), about 80,000 cases of vibriosis occur in the US each year, most linked to milder Vibrio species causing gastrointestinal illness. But Vibrio vulnificus is different: it’s less common but far deadlier. Roughly 20% of infections result in death.
While anyone can contract Vibrio vulnificus, certain groups face a much higher risk of severe illness or death. These include:
For these groups, even minor exposure can quickly escalate into a life-threatening infection.
Public health agencies are urging people—especially in Gulf Coast states—to take precautions:
Seek medical attention immediately if you notice signs of infection after exposure. Early treatment with antibiotics can dramatically improve survival odds.
As global patterns change and ocean waters heat up, scientists caution that infections from Vibrio vulnificus will become increasingly prevalent in regions that aren't used to them. Local reports over the last decade indicate the bacteria spreading up the northeastern seaboard, with sporadic cases reaching as far north as New England.
This growth highlights the fact that Vibrio vulnificus is no longer simply a "Gulf Coast issue" – it's a viable threat to any warm coastal area. And with more individuals looking for beach holidays and seafood meals in warm-weather months, awareness joins prevention as paramount.
The increase in fatal Vibrio vulnificus infections is a reminder of the way evolving environmental conditions, human activity, and microbial behavior combine in perilous ways. While the infection remains rare compared to other illnesses, its high fatality rate makes it a serious public health concern.
For now, health experts aren’t calling for people to avoid the ocean entirely but they are urging caution. Cover wounds, skip the raw oysters if you’re in a high-risk group, and don’t ignore early symptoms. Infections can escalate quickly, but with swift recognition and medical treatment, many lives can be saved. The challenge is making sure people know the risk before they wade in.c
Credits: AP
Nobel Peace Prize 2025: It was 1am at night, when Mary Brunkow's phone began to ring, assuming it to be a spam call, she put it on "do not disturb" and went back to sleep. Her husband too ignored the rings, only to be woken up along with their dog a few minutes later, when the Associated Press photographer showed up at their door. This is when Brunkow realized that she had won a Nobel Prize.
Brunkow along with two other scientists Fred Ramsdell and Shimon Sakaguchi had won the Nobel Prize "for their discoveries concerning peripheral immune tolerance".
It refers to the mechanisms by which the immune system prevents self-reactive immune cells, especially the T-cells from attacking healthy tissues once they are already in the body's circulation.
The three are award for their work that revealed the existence and function of these special class of T-cell, called the regulatory T-cells, which act as brakes on immune responses, preventing autoreactivity. They also discovered the gene FOXP3, whose proper function is essential to the development and operation of regulatory T-cells. Their discovery revealed that mutation in FOXP3 genes is what leads to serious autoimmune disorders.
Long before FOXP3, Sakaguchi, who is a professor at Osaka University in Japan, resurrected and rigorously defined the concept of regulatory T cells, also called Tregs. In 1995, he published work that showed that a subset of T-cells marked by CD25 along with CD4 could suppress autoimmune responses in mice. Those cells would be later called as the regulatory T-cell. It was his discovery which became the "brake" the immune system needed.
Before Sakaguchi's work, the existence of regulatory T-cells was speculative, even controversial. The idea was dismissed because the evidence was murky. His work also opened the possibility that one day we may enhance regulatory T-cell functions in autoimmune diseases or inhibit it in cancer settings.
While Sakaguchi defined the Treg population, Brunkow and Ramsdell filled the gap by discovering FOXP3, the gene whose expression is necessary for Treg development.
They studied that in mice, a peculiar strain known as "scurfy" mice, spontaneously developed lethal autoimmunity, which was manifested by scaly, flaky skin, enlarged lymph nodes and spleens, and early death. They showed that the scurfy phenotype is caused by a mutation on the X chromosome in a previously unknown gene which they named FOXP3.
Their discovery also showed that in humans, a rare autoimmune syndrome called IPEX, which is characterized by immune dysregulation, polyedendocrinopathy, entropathy, X-linked inheritance is caused by mutations in the human equivalent, FOXP3. They thus, directly connected the mouse mutation and human disease that proved that FOXP3 is central to immune self-tolerance.
Without functional FOXP3, regulatory T-cells fail to form or function, and immune system launches damaging attacks on normal tissues.
Their discovery is important as it can be used to treat autoimmune diseases like Type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, and many more.
The scope for cancer immunotherapy and tolerance during organ transplantation also broadens with the discovery. As with the FOXP3, it becomes possible to design therapies that block Treg suppression locally, enabling the immune system to better recognize and attack tumors. In terms of organ transplantation, with Tregs, it may become feasible to engineer Tregs that home to transplanted organs and locally suppress rejection.
The Nobel press release and news sources note that more than 200 clinical trials are already underway based on regulatory T cell / peripheral tolerance ideas.
Credits: Canva
A recent report from Santé publique France highlights a significant rise in suspected COVID-related visits to emergency departments across the country during the week of September 15–21, 2025 (week 37). Compared with the previous week (September 8–14, week 36), hospital visits linked to COVID increased by 43% among children under 15, with 156 additional visits, and by 29% among adults, with 224 more visits.
Cases among adults had already started climbing the week before. This surge comes as a new SARS-CoV-2 variant, nicknamed “Frankenstein,” becomes increasingly common in France. Here is everything you need to know about this variant, its symptoms, and how to protect yourself.
According to the World Health Organization (WHO), this rise is associated with the emergence of a new variant called XFG. It is nicknamed “Frankenstein” because it is a recombinant, meaning it contains genetic material from two different COVID-19 subtypes, LF.7 and LP.8.1.2. The WHO has classified XFG as a variant under monitoring since June 25, 2025, and it is spreading in several countries worldwide. Current evidence suggests that the public health risk remains low, and approved COVID vaccines are expected to continue preventing severe disease and symptomatic infection. Countries in Southeast Asia have also reported increases in both new cases and hospitalisations in areas where XFG has been widely detected.
Although XFG appears to spread more easily than other variants, experts say it does not seem to cause more severe illness. “The vast majority of infections are mild and resolve within a few days with rest,” said Dr. Gérald Kierzek. Infectious disease specialist Anne-Claude Crémieux added that, so far, there are no signs the variant is more dangerous than previous strains.
Symptoms of the Frankenstein Variant
The symptoms of XFG are similar to those seen with previous COVID-19 variants and are generally mild, resembling a common cold. These may include:
The nickname “Frankenstein” reflects the variant’s hybrid nature, as it combines genetic material from multiple COVID-19 subtypes.
There is no treatment specific to XFG, so care follows the same principles used for other COVID variants.
Research on the Frankenstein variant is ongoing. Since the disease can affect individuals differently, taking personal precautions and consulting a doctor when symptoms appear remain essential.
Credits: Canva
The oral cholera vaccine Shanchol, made in Hyderabad and first developed by Shantha Biotechnics, has received World Health Organization (WHO) prequalification after its production was recently revived under new management. The clearance allows global procurement agencies such as UNICEF, Gavi, and PAHO to source the vaccine for countries where cholera continues to have a serious public health threat, according to GCBC Vaccines. With the approval in place, here’s a closer look at the vaccine, how it works, and why it matters.
Dr. K.I. Varaprasad Reddy, founder of Shantha Biotechnics, said, “Shanchol was designed to be an affordable and accessible answer for countries that struggle with repeated cholera outbreaks. The WHO’s prequalification continues that mission.”
Shanchol is an oral, inactivated, bivalent cholera vaccine that protects against Vibrio cholerae, the bacteria responsible for the disease. The name itself is a brand term rather than an abbreviation.
Type of vaccine: Shanchol is a killed whole-cell vaccine, which means it contains dead cholera bacteria. These are used to train the immune system without causing infection. Being bivalent, it offers protection against the two major cholera strains, O1 and O139.
Originally created by Shantha Biotechnics, the vaccine later came under Sanofi’s ownership, which eventually halted its production. Manufacturing has now resumed under GCBC Vaccines, part of the Gland Family Office. With WHO prequalification restored, Shanchol will once again be distributed globally to support vaccination programs.
Oral cholera vaccines (OCVs) such as Shanchol and Dukoral are tools in preventing the spread of cholera, a severe diarrheal disease caused by Vibrio cholerae. Taken orally, they help trigger an immune response in the intestine that limits bacterial infection. These vaccines are especially valuable in areas with poor sanitation and limited access to clean water.
Vishy Chebrol, Executive Director of GCBC Vaccines, said the company’s priority is to ensure that vaccines reach the countries that need them most, affordably and consistently. “We are also working to bring more affordable and innovative vaccines to global markets, continuing Shantha’s legacy of improving access to life-saving immunization,” he added.
With WHO’s renewed approval, Shanchol, a bivalent, killed whole-cell oral cholera vaccine effective against Vibrio cholerae O1 and O139, will continue to be supplied worldwide to meet growing demand and support national immunization programmes.
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