Fatigue to Infection: 5 early symptoms of blood cancer, know which tests should be done

Cancer is a disease that causes the death of about 10 million people every year. It is the second leading cause of death. There are many types of cancer, one of them is blood cancer, which is also known as hematologic cancer. As soon as the name of blood cancer comes to mind, the first thing that comes to mind is death! But if you become aware of this disease, then it can be prevented with the help of treatment. Now, when we spoke to Dr Vigyan Mishra, Lab Head at Newberg Diagnostics, Noida, he explained the ways to recognise the symptoms of this disease and which tests should be done to detect blood cancer.

These symptoms start appearing when blood cancer occurs:

• Tiredness: It is one of the earliest symptoms that accompany blood cancer. However, the intensity of the fatigue is usually severe and not responsive to rest.
• Increased Infections: Blood cancer tends to attack the immune system, and patients are susceptible to being prone to infections. Patients come to be exposed to colds, flu, or any other infection multiple times.
• Easy Bruising: The early signs can be easy bruising, nosebleeds or bleeding gums. The reason is again the lack of platelets.
• Enlarged Lymph Nodes: Swollen lymph nodes in the neck, armpits or groin are considered an early sign of lymphoma- one of the types of blood cancer.
• Fever and Night Sweats: Unexplained fever and night sweats can sometimes be some of the earliest presentations of blood cancer. Most patients will say that they come and go, without a self-evident cause, for example, an infection.

Take the following tests to diagnose blood cancer:

• CBC Test (Complete Blood Count Test): The first step that a doctor takes when he suspects a diagnosis of blood cancer is to suggest a CBC test. It measures the extent of red blood cells, white blood cells, and even the presence of platelets in the blood.
• Bone Marrow Biopsy: This test shows if any disease is affecting the blood cells or the marrow. It also tells how much the disease has spread. During bone marrow biopsy, an examiner inserts a needle into the hip bone for examination. For leukaemia, lymphoma and myeloma patients, this test forms an important part.
• Flow Cytometry: This process measures the physical or chemical characteristics of cells in a sample of blood or bone marrow. This will enable the search to be made for cancerous cells, which can then be taken into consideration in diagnosis.
• Imaging Tests: Here, areas of the body where lymph nodes are enlarged are scanned. To do so, X-rays, ultrasounds, CT scans, or PET scans are carried out on these patients to see if the patient has any tumours or other signs of cancerous nature related to blood cancer.
• Cytogenetic Testing: This test analyses a sample of blood, tissue, or bone marrow of an individual to check for genetic abnormalities.

Website: International Conference on Infectious Diseases

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Mitigating Chronic Disease Depends on Infection Prevention

Infection as One of Many Root Causes of Chronic Disease

Humans are afflicted by an alphabet soup of health conditions. One fact that holds true across the spectrum is that disease is complicated. Science has shown us time and again that there is no single root cause of disease—there are roots. There’s a root for genetics, one for the microbiome, another for age. There are roots for diet and environmental factors, like pollution or toxins (e.g., pesticides). And there is a root for infection.

While infection has historically been viewed through a “get infected, get better, move on” lens, we know that this isn’t entirely accurate. Getting better isn’t a given, and infection can spur long-term health disruptions and conditions, sometimes years after an infection occurred.

Epstein-Barr virus (EBV), for instance, is tied to multiple sclerosis and cancer; other viruses, including human papillomavirus (HPV) and hepatitis B and C, also cause cancer. Heart disease, depression and diabetes are some of many outcomes associated with Long COVID—a long-term implication of SARS-CoV-2 infection characterized by a laundry list of conditions in both children and adults. Conditions like inflammatory bowel disease, psoriasis and even obesity may also have infectious underpinnings. And while viruses are key culprits, other types of microbes, like bacteria, are triggers of infection-fueled health issues (e.g., chronic Lyme disease), as well. Some mechanisms underlying infectious-chronic disease connections are known (for example, how EBV disrupts DNA to spur cancer development), while many, such as those modulating Long COVID, are active areas of investigation.

There is no “1 size fits all” when it comes to the development and progression of disease; there may be similarities and trends within a population, but everyone is a little bit different. It is, thus, prudent to explore all factors with roles to play—and infectious disease increasingly appears to be one of them. Maintaining focus on the infection factor is particularly important in an era defined by the spread of pathogens with known chronic health implications (SARS-CoV-2), as well as unknown or emerging pathogens whose impacts are less clear.

Preventing Infections Helps Prevent Some Chronic Diseases

If infection is a possible steppingstone toward chronic disease, it stands to reason that efforts toward understanding and preventing the former can, and do, apply to the latter. Take HPV—the cause of genital warts and one of the most prolific sexually transmitted viruses in the world—as an example.

Through extensive research, scientists found that HPV is integral in the development of certain cancers (e.g., cervical cancer). They went on to discover the viral proteins that cause host cells to continuously reproduce and become cancerous, as well as the surface proteins that modulate viral cellular binding and internalization.

Additional investigation showed that those surface proteins self-assemble into virus-like particles (VLPs)—essentially, viruses without any genetic material inside. What did scientists do with that information? They made a stellar vaccine. HPV vaccines, comprised of VLPs from different HPV types, train the immune system to recognize viral particles and destroy them. They are more than 90% effective at preventing cancer—a particularly devastating chronic disease—triggered by the virus.

This is just 1 case, and the path from molecular insights to useful tools, like vaccines, differs in the context of other infections. The point is that harnessing and advancing knowledge of the infectious process leads to tactics that simultaneously minimize the risk of both acute and chronic health problems. It is also absolutely worth exploring how modifications in, for instance, diet or environmental pollution support long-term health. The idea is that investigating chronic disease requires a “yes, and” approach, with the understanding that insights into infection are not extraneous, but necessary.

More Than Vaccines

Such insights lead to advancements that go beyond vaccines, too. This is not to say vaccines aren’t crucial—they are. But it’s worth noting that the more scientists study infectious disease, the more they can develop novel, external methods to manage them as well.

For instance, studies on the molecular make-up of SARS-CoV-2 informed the development of a device that detects the virus in the air within 5 minutes and with 77-83% accuracy; a biosensor with a similar detection time was recently developed for avian influenza A (H5N1). Such devices offer real-time methods for monitoring the presence of viruses to inform disease control measures. Knowing how environmental variables, like carbon dioxide (CO2) levels, which rise in places like crowded rooms, impact viral survival can further influence how buildings are designed and ventilated to lower the risk of infection. Researchers are also inventing tools like a portable device that sterilizes virus-containing aerosols generated by patients during clinical respiratory care, with potential use in non-clinical environments, as well as innovative surface coatings that kill microbes in minutes and for extended periods of time.

Collectively, these examples demonstrate multi-faceted approaches for mitigating problematic microbes. By, again, looking ahead, those methods have the potential to not only influence short-term health, but also long-term health. Think about it in the context of Long COVID: coupling improved air filtration with technologies that detect and kill SARS-CoV-2 could help lower the chances of (repeat) infection and, in turn, its associated chronic outcomes.

Healthy Science, Healthy People

Of course, how one thinks about and approaches studying chronic diseases is meaningless if one can’t study them at all. Funding and staffing cuts at and by U.S. federal research agencies undermine efforts to investigate all roots of disease, which negatively affects the development of countermeasures, like new medications. As such, while it is critical to examine chronic disease without disregarding known risk factors (i.e., infection), it is even more crucial, in this moment, to protect the health and integrity of the scientific enterprise to ensure those examinations can happen at all. Our long-term health depends on it.

Contact your representatives to share the impact recent executive orders and funding caps have on your work and scientific research in their district and state.

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Do bacteria age or are they immortal?

The term “aging” generally conjures up images of graying hair, slowing pace, and the eventual appearance of wrinkles. Yet, beyond these physical markers, aging is a fundamentally cellular and molecular process, even for organisms like bacteria, which also experience age-related changes.

From humble single-celled organisms to complex mammalian systems, all living organisms experience the impact of passing time, according to a recent report from the American Society for Microbiology.

As they age, cells accumulate damage that impairs function, leading to numerous age-related disorders in humans. But what about bacteria? Can these single-celled entities feel the passage of time?

Bacteria age and binary fission factor

Bacteria, being single-celled organisms, propagate differently from humans. Rather than sexual reproduction, they undergo a process known as binary fission.

In this process, they duplicate their DNA and divide into two, resulting in rapid replication. Interestingly, the fastest-growing bacterium can split in less than 10 minutes.

Historically, it was believed that bacteria, thanks to binary fission’s symmetrical nature, did not age. After all, this process results in a parent and offspring identical in age, leading to a concept dubbed “functional immortality.”

Aging, it was assumed, required an asymmetric division where the parent is older than the offspring.

Aging of bacteria

Contrary to the longstanding belief, evidence emerged in 2005, suggesting that, like us, bacteria do age. The researchers found that Escherichia coli (E. coli) exhibit differences between “old” and “new” (parent and offspring) cells.

These distinctions became evident as scientists watched the cells divide under a microscope, noting that older cells’ growth rate and offspring production decline over time.

Moreover, the senior cells died more frequently than their younger counterparts. Clearly, despite similar appearances, cells underwent divisions that left them functionally asymmetric and susceptible to aging.

Asymmetry to the rescue

So, how does this asymmetry help? It turns out, this type of division is crucial for the population’s overall fitness.

An asymmetric division maintains variance, the variety upon which natural selection acts. More variation typically means a better chance of survival under changing conditions.

One of the key players in this aging process is protein aggregation. This process occurs in bacteria and eukaryotic cells and is associated with age-related diseases in humans, such as Alzheimer’s and Parkinson’s, where harmful protein clumps can lead to cell death.

In bacteria, scientists found a smart way of dealing with this problem. As a feature of asymmetric division, older cells accumulate these proteins segregating age-related damage and keeping their offspring looking “younger” at the molecular level.

Cellular states of stress

Another culprit contributing to aging, both in humans and bacteria, is stress. E. coli cells activate a stress state inside the cell to survive mutations accumulated over their lifetimes.

Some of these mutations, while not lethal, can negatively impact the cell’s fitness by causing a critical protein to lose its function.

In a study analyzing the effects of over 60 different nonlethal loss-of-function mutations in E. coli, researchers found that these mutants increased their metabolic activity to compensate for lost protein function.

Still, this adaptation comes at a cost. These cells grow slower and enter a state similar to purgatory faster than non-mutants, especially in nutrient-poor environments.

The findings suggest an “aging cost” associated with maintaining resistance to stress on a population level. Could understanding bacterial aging lead us to new antibiotic targets? Might this ancient mechanism of aging shed light on certain human diseases perpetuated through cellular stress states?

Complexities of aging

Time and age certainly doesn’t stand still for anyone, humans and bacteria included. But perhaps bacteria’s susceptibility to aging is a blessing in disguise.

These hardy organisms make excellent subjects for studying the nuances of aging, given their rapid growth and the ability to observe numerous generations in a single experiment. After all, understanding the complexity of aging is inherent to unlocking the mysteries of life itself.

The discovery that bacteria are not eternal beings, as once thought, but vulnerable to aging like all living organisms, signifies the interconnectedness of life at every level.

The concept of time, aging, and the decline in function straddle across the biological spectrum, making it possible to draw parallels between the simplest life forms and the most complex ones.

Website: International Conference on Infectious Diseases

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Toxoplasma gondii – the good guy?

Can a pathogen ‘change its spots’? Apparently, with a bit of genetic engineering, it can. Shahar Bracha and colleagues have engineered Toxoplasma gondii to deliver beneficial proteins to the brain of mice, leading to its potential future use as a carrier of therapeutic proteins for people suffering from neurological diseases

Toxoplasma gondii is a parasitic protozoan that can infect pretty much all warm blooded animals. It is estimated that a third to half of the human population are infected with Toxoplasma – and many remain asymptomatic. However, it can lead to toxoplasmosis – which manifests as behavioural or neuropsychiatric changes in the animal (for example, Toxoplasma, a common parasite that makes you angry). It can also be passed on to fetuses, impacting their development or causing miscarriages. Whilst the parasites can infect most animals, it can only reproduce sexually inside feline hosts and the oocytes are shed in cat feces- this is why pregnant women are advised not to change cat litter trays.

Unsurprisingly, a lot of work has gone into studying this parasite and how it works (an example was highlighted in Hilary Hurd’s blog last week Immune-induced change in gut microbiota plays a role in pathology caused by Toxoplasma gondii infection), with the ultimate aim of being able better prevent, control or treat infections. We therefore know quite a bit about how the parasite is able to breach the blood – brain barrier in order to cause disease.

What we (the general public) probably were not expecting is that researchers would go beyond that and look for ways exploit, for our own benefit, the finely-tuned, highly evolved mechanisms the parasite would normally employ to spread through the Central Nervous system and cause disease. However, this is exactly what Shahar Barcha and her team have done.

Building on work already done using this parasite to deliver proteins to host cells, the team of researchers leveraged two of the three secretory organelles the parasite uses, rhoptry and dense granules secretory organelles, to deliver large therapeutic proteins intracellularly to the host or patient.

Parasites were engineered to express selected beneficial neuroproteins fused to carrier proteins (toxofilin for rhoptry targeting and GRA16 for dense granule targeting) for testing in vitro. Further to this, the team also tested the potential for multiple protein development by creating a T. gondii line that simultaneously expressed rhoptry and dense granules.

Initial tests of these engineered parasites occurred in human tissue cell lines, neurons and brain organoids. The next steps were to inject these engineered parasites into mice. For this, a new line of T.gondii with lower virulence was developed, and inoculated intraperitoneally into the mice. Inoculated mice showed high levels of cysts and confirmed that MECP2, a protein that is needed for normal functioning of nerve cells, was indeed delivered to the brain.

Overall, the studies by Shahar Barcha and team show that T.gondii could be a versatile carrier for therapeutics that are needed to be delivered intracellularly. Certainly, using the parasite helps bypass many of the difficulties researchers and clinicians currently encounter in getting therapeutic proteins and molecules to the areas of the body that they are needed. There does need to be considerably more research and testing conducted before it can be used on humans, and for specific diseases.

My own personal feeling is its use as therapeutics should be monitored and regulated closely, solely because it is a pathogenic parasite (even if engineered to be less virulent). However, also from a personal perspective, these studies do bring much needed hope to many people who suffer from neurological diseases where there isn’t a cure, and currently no chance of reversing the disease.

Website: International Conference on Infectious Diseases

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Outbreak Investigation of Salmonella: Mini Pastries (January 2025)

Product

Recalled Sweet Cream-brand mini pastries with best by dates from 2025/06/17 through 2025/11/15 (June 17 - November 15, 2025).

The food service customers who received the recalled product have been contacted directly by the distributing firms, and the recalled product should no longer be available for sale.
Symptoms of Salmonella Infection:

Illness usually occurs within 12 to 72 hours after eating food that is contaminated with Salmonella, and the symptoms usually lasts four to seven days. Symptoms include diarrhea, fever, and abdominal cramps. Children younger than five, the elderly, and people with weakened immune systems are more likely to have severe infections.

Stores Affected

Recalled mini pastries were distributed in FL, NJ, NY, and PA to food service locations such as hotel cafes, bakeries, institutions, and restaurants. The mini pastries were also served at catered events. The firm directly notified customers who received the recalled product, and the recalled product should no longer be available for sale.

Recommendation

The recalled product should no longer be available for sale; however, food service customers who received the recalled product should follow FDA’s safe handling and cleaning recommendations and use extra care in cleaning and sanitizing any surfaces and containers that may have come in contact with recalled products to reduce the risk of cross-contamination.
Contact your healthcare provider if you think you may have developed symptoms of a Salmonella infection.

Current Update

The FDA and CDC, in collaboration with state and local partners, investigated an outbreak of Salmonella infections linked to recalled Sweet Cream-brand mini pastry products with best by dates from 2025/06/17 through 2025/11/15 (June 17 - November 15, 2025).

As of March 14, 2025, a total of 18 people infected with the outbreak strain of Salmonella have been reported from 7 states. Of the 12 people for whom information is available, one person has been hospitalized. No deaths have been reported. Of the 7 people interviewed, 5 (71%) reported eating pastries.

Under the Laboratory Flexible Funding Model (LFFM) program, the Communicable Disease Service within the New Jersey Department of Health (NJDOH), collaborated with the City of Paterson Division of Health and the Public Health and Environmental Laboratories to collect and analyze Sweet Cream-brand mini pastry samples from a warehouse that received the recalled product. Three samples tested positive for Salmonella and are a Whole Genome Sequencing (WGS) match to the outbreak strain.

To further protect public health and prevent violative product from entering the U.S., FDA has added Mini Patisserie Ready to Eat (RTE) pastries from the Italian manufacturer, Sweet Cream S.R.L.S., to the Red List of Import Alert #99-19, “Detention Without Physical Examination of Food Products Due to the Presence of Salmonella.” This import alert informs FDA field staff that they may detain shipments of these pastries from Sweet Cream S.R.L.S. without physical examination.

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What Have Been Some Recent Advancements In Neonatal Care? Know From A Doctor

Neonatal care encompasses not only the treatment of acute medical conditions, but also preventive measures aimed at reducing the risk of infections, encouraging breastfeeding, and ensuring proper nutrition for infants under the guidance of a neonatologist. Read on to know more.

Neonatal care: Neonatal care is a specialised care offered to sick or premature babies in a hospital's neonatal unit. It has seemingly undergone significant changes in recent years, leading to remarkable improvements in the survival rates of full-term and premature infants. In this article, we discuss the treatment options and technologies that have been transforming the landscape of neonatal care, ultimately saving the lives of millions of babies with serious health complications after birth. According to Dr Anish Pillai, lead consultant-neonatology and paediatrics, Motherhood Hospitals, Kharghar, Navi Mumbai, the integration of advanced medical technologies has become a relieving factor for both parents and care providers. Neonatologists are now better-equipped to ensure that infants with various ailments at birth recover effectively and achieve developmental milestones according to their age.

Understanding The Advancements In Neonatal Care

Advanced Antenatal Care

Dr Pillai states that improvement in antenatal care during pregnancy, along with regular high-quality scans can detect most congenital defects prior to delivery. This prepares the family and medical team to anticipate and treat complications in a more comprehensive manner. Timely identification and management of risk factors during pregnancy can also reduce the burden of prematurity.

Advanced Respiratory Support

Many premature babies are born with respiratory issues and require immediate ventilation management. Innovations like high-frequency oscillatory ventilation and advanced non-invasive techniques have significantly improved respiratory support strategies; enhancing outcomes for neonates with breathing difficulty.

Nutrition Innovations

Adequate nutrition is vital for the healthy growth and development of premature infants. Innovations such as breast milk banks and human milk-based fortifiers cater specifically to their nutritional needs, ensuring that every infant receives the best possible start in life. Even babies who are too sick to tolerate mother's milk can be given parenteral nutrition using umbilical lines and infusion pumps. Growth monitoring tools in mobile apps have made tracking of baby's growth and development easy.

Telemedicine

Telemedicine has transformed neonatal care by allowing healthcare professionals to monitor the health of premature infants remotely. Parents can seek expert help conveniently, reducing the need for long-distance travel and enabling timely interventions.

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Scientists discover new part of the immune system

A new part of the immune system has been discovered and it is a goldmine of potential antibiotics, scientists have said.

They've shown a part of the body known to recycle proteins has a secret mode that can spew out an arsenal of bacteria-killing chemicals.

The researchers in Israel say it transforms our understanding of how we are protected against infection.

And gives a new place to look for antibiotics to tackle the growing problem of superbugs that resist our current drugs.

The discovery centres on the proteasome – a tiny structure that is found in every cell of the body.

Its main role is to chop up old proteins into smaller chunks so they can be recycled to make new ones.

But a series of experiments, detailed in the journal Nature, shows the proteasome detects when a cell has been infected by bacteria.

It then changes structure and role. It starts transforming old proteins into weapons that can rip open the outer layer of bacteria to kill them.

Prof Yifat Merbl, from the Weizmann Institute of Science, told me: "This is really exciting, because we never knew that this was happening.

"We discovered a novel mechanism of immunity that is allowing us to have a defence against bacterial infection.

"It's happening throughout our body in all the cells, and generates a whole new class of potential natural antibiotics."

The research team went through a process they called "dumpster diving" to find these natural antibiotics.

They were tested on bacteria growing in the laboratory and on mice with pneumonia and sepsis. The researchers said they were getting results comparable to some established antibiotics.

And when the researchers took cells in the laboratory and disabled the proteasome they were far easier to infect with bacteria like Salmonella.

Prof Daniel Davis, the head of life sciences and an immunologist at Imperial College London, said the findings were "extremely provocative and very interesting" as they changed our understanding of how our body fights infection.

"What's really exciting about this, is it's a totally undiscovered process by which anti-germ molecules are made inside our cells, it feels profoundly important and surprising."

But he cautioned that turning this into a new source of antibiotics is an idea that "still needs to be tested" and that will take time.

More than a million people a year are estimated to die from infections that are resistant to drugs like antibiotics.

But despite the need, there has been a lack of research into developing new antibiotics to keep up with demand.

Against that bleak background, having somewhere new to look is a source of optimism for some scientists.

Dr Lindsey Edwards, a senior lecturer in microbiology at King's College London, told the BBC: "It's a potential goldmine for new antibiotics, that's quite exciting.

"In previous years it's been digging up soil [to find new antibiotics], it is wild that it's something we have within us, but comes down to having the technology to be able to detect these things."

She also says there could be fewer issues with developing them into drugs because they are already products of the human body so the "safety side of it might be a lot easier".

Website: International Conference on Infectious Diseases

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Multidrug-Resistant Fungal Pathogens No Match for New Antibiotic Mandimycin

Scientists have unveiled mandimycin—a newly discovered antibiotic with unparalleled properties that may revolutionize multidrug-resistant (MDR) fungal infection treatment—according to a study in Nature. Unlike conventional antibiotics, mandimycin boasts a unique mode of action: targeting fungal cell membrane phospholipids, disrupting ion balance, and sidestepping resistance mechanisms. Its potent, broad-spectrum fungicidal effects mark a significant leap in combating hard-to-treat fungal infections, offering hope in the battle against resilient superbugs.


s from an ambitious analysis by researchers from China Pharmaceutical University and Shandong University of over 316,000 bacterial genomes, pinpointing biosynthetic gene clusters (BGCs) encoding mycosamine-rich polyene macrolides. Mandimycin’s structure is a marvel of nature: a 38-membered macrolactone ring adorned with three unique sugars, including a rare dideoxysaccharide. This intricate composition gives mandimycin extraordinary solubility—9,700 times higher than the gold-standard antifungal amphotericin B—overcoming longstanding challenges of poor bioavailability in antifungal agents.

In laboratory tests, mandimycin exhibited potent, broad-spectrum efficacy against deadly MDR fungal pathogens, including Candida, Cryptococcus, and Aspergillus species, identified as critical threats by the World Health Organization. Remarkably, its minimum inhibitory concentrations (MICs) ranged from just 0.125 to 2 μg/mL, demonstrating robust fungicidal activity. Unlike existing polyene antifungals that target ergosterol in fungal cell membranes, mandimycin operates through a novel mechanism. It binds specifically to essential phospholipids, such as phosphatidylinositol, disrupting membrane integrity and inducing cell collapse. This unique mode of action circumvents cross-resistance to existing antifungals, a frequent hurdle in combating MDR strains.

A safer, more effective antifungal

The antibiotic’s resistance profile is equally impressive. Despite rigorous attempts, researchers could not generate resistant fungal mutants—a rarity in antifungal research. Structural studies revealed that mandimycin’s antifungal potency relies heavily on its dideoxysaccharide moiety, underscoring its importance in phospholipid binding. Compared to amphotericin B, mandimycin demonstrated dramatically lower nephrotoxicity and no hemolytic effects, even at high concentrations. Testing in human renal and other cell lines revealed 7–22 times weaker toxicity for mandimycin, and in vivo mouse studies showed minimal kidney injury markers at doses as high as 30 mg/kg.
Mandimycin also exhibited exceptional antifungal efficacy against MDR Candida albicans, achieving a 100% survival rate in mice at 10 mg/kg and significantly reducing fungal burdens in major organs. The drug proved potent across various delivery methods, including subcutaneous, intravenous, and oral administration. With favorable pharmacokinetics and no observable side effects, mandimycin outperformed amphotericin B in both safety and effectiveness, marking a critical step forward in combating MDR fungal infections.

Mandimycin represents a new frontier in antifungal therapy, blending potent efficacy with innovative action. With its potential to address rising fungal infections in immunocompromised patients and overcome antifungal resistance, mandimycin could transform global healthcare landscapes. This discovery not only highlights the unexplored potential of microbial biodiversity but also offers hope against the escalating threat of antifungal resistance.

Website: International Conference on Infectious Diseases

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Clinical Overview of Rabies

Overview

Rabies is a fatal but preventable viral disease, which can spread to people and pets through bites and scratches from an infected animal. Rabies can cause severe disease and death if urgent medical care is not sought after a rabies exposure. The virus is fatal if rabies-related medical care, called postexposure prophylaxis or PEP, is not started before symptoms begin to show.

Rabies is rare in people in the United States, with only 1 to 3 cases reported each year. However, each year about 60,000 Americans receive PEP following an exposure.

Who is at risk

There have been no confirmed instances of human-to-human transmission of rabies virus aside from those attributable to organ and tissue transplantation. Rabies virus is transmitted through direct contact with infectious tissue or fluids. Rabies virus is not transmitted through contaminated objects or materials such as clothes or bedding.

Healthcare workers providing care to patients with suspected or confirmed rabies should protect themselves by using standard precautions. Healthcare workers caring for patients with rabies do not pose a risk to their families or community.

Exposure risks

People and pets can be exposed to rabies through bites and scratches from animals infected with rabies. In the U.S., rabies is mostly found in wild animals like bats, raccoons, skunks, and foxes. But in many other countries, dogs are still carriers of rabies.

It's crucial to inquire about recent contact with wild animals, especially if the patient has been scratched or bitten. Also, ask about recent travel to areas where rabies in dogs is prevalent.

How it spreads

Rabies is spread when an infected animal, usually wild, bites or scratches other animals or people. The virus is usually carried in saliva or mucus and spreads through broken skin.

Signs and symptoms

After a rabies exposure, the rabies virus must travel to the brain before it can cause symptoms. This time between exposure and the appearance of symptoms is the incubation period, and it may last for weeks to months.

The first symptoms of rabies may be like the flu, including weakness or discomfort, fever, or headache. There also may be discomfort, prickling, or an itching sensation at the site of the bite. These symptoms may last for several days. Usually, severe disease appears within two weeks of the first symptoms, when the rabies virus causes brain dysfunction. Common signs include anxiety, confusion, agitation, and hallucinations.

Once clinical signs of rabies appear, the disease is nearly always fatal, and treatment is typically supportive.

Rabies postexposure prophylaxis (PEP)

For people who have never had a rabies vaccine, rabies PEP consists of wound washing, a dose of human rabies immune globulin (HRIG), and a rabies vaccine given at the time of the first medical visit. Then, it includes a dose of vaccine given again on days 3, 7, and 14 after the first dose.

Pregnancy is not a contraindication for rabies PEP and exposure to rabies or a rabies diagnosis in the mother does not require pregnancy termination. More information on PEP can be found here.

Website: International Conference on Infectious Diseases

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Influenza

Overview

Flu, also called influenza, is an infection of the nose, throat and lungs, which are part of the respiratory system. The flu is caused by a virus. Influenza viruses are different from the "stomach flu" viruses that cause diarrhea and vomiting.

Most people with the flu get better on their own. But sometimes, influenza and its complications can be deadly. To help protect against seasonal flu, you can get an annual flu shot. Although the vaccine isn't 100% effective, it lowers the chances of having severe complications from the flu. This is especially true for people who are at high risk of flu complications.

Aside from the vaccine, you can take other steps to help prevent infection with the flu. You can clean and disinfect surfaces, wash hands, and keep the air around you moving.

Symptoms

The viruses that cause flu spread at high levels during certain times of the year in the Northern and Southern hemispheres. These are called flu seasons. In North America, flu season usually runs between October and May.

Symptoms of the flu such as a sore throat and a runny or stuffy nose are common. You may also get these symptoms with other illness such as a cold. But colds tend to start slowly, and the flu tends to come on quickly, within two or three days after you come in contact with the virus. And while a cold can be miserable, you usually feel much worse with the flu.

Other common flu symptoms include:

• Fever.
• Cough.
• Headache.
• Muscle aches.
• Feeling very tired.
• Sweating and chills.

In children, these symptoms may show up more generally as being fussy or irritable. Children also are more likely than adults to have ear pain, feel sick to the stomach, vomit or have diarrhea with the flu.

Risk factors

There are a range of factors that may raise your risk of catching a flu virus or having complications from a flu infection.

Older and younger age

Seasonal influenza tends to have worse outcomes in young children, especially those age 2 years and younger. Adults older than age 65 also tend to have worse outcomes.

Living conditions

People who live in facilities with many other residents, such as nursing homes, are more likely to get the flu.

Weakened immune system

An immune system that doesn't quickly clear out flu virus may raise the risk of getting the flu or getting flu complications. People may have a weakened immune system response from birth, due to illness, or due to disease treatment or medicine.

Chronic illnesses

Chronic conditions may increase the risk of influenza complications. Examples include asthma and other lung diseases, diabetes, heart disease, nervous system diseases, previous history of stroke, metabolic disorders, problems with the airway, and kidney, liver or blood disease.

Race or ethnicity

In the United States, people who are Native American or Alaska Native, Black, or Latino may have a higher risk of needing care in the hospital for influenza.

Aspirin therapy

Young people on long-term aspirin therapy are at risk of developing Reye's syndrome if infected with the influenza virus.

Pregnancy

Pregnant people are more likely to develop influenza complications, particularly in the second and third trimesters.

Obesity

People with a body mass index (BMI) of 40 or higher have an increased risk of flu complications.

Controlling the spread of infection

The influenza vaccine isn't 100% effective. So it's important to take steps to lower the spread of infection, including:

• Wash your hands. Wash your hands well and often with soap and water for at least 20 seconds. If soap and water aren't available, use an alcohol-based hand sanitizer with at least 60% alcohol. Make sure friends and family that you're around regularly, especially kids, know the importance of hand-washing.
• Avoid touching your face. Keeping your hands away from your eyes, nose and mouth helps keep germs away from those places.
• Cover your coughs and sneezes. Cough or sneeze into a tissue or your elbow. Then wash your hands.
• Clean surfaces. Regularly clean often-touched surfaces to prevent spread of infection from touching a surface with the virus on it and then your face.
• Avoid crowds. The flu spreads easily wherever people gather — in child care centers, schools, office buildings and auditoriums and on public transportation. By avoiding crowds during peak flu season, you lower your chances of infection.

Website: International Conference on Infectious Diseases

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First vaccine against epizootic haemorrhagic disease recommended for approval

EMA has recommended the approval of Hepizovac, the first vaccine against epizootic haemorrhagic disease (EHD) authorised in the EU for use in cattle. This new vaccine provides protection against the recently emerged serotype 8 of the epizootic haemorrhagic disease virus (EHDV), which has been responsible for recent outbreaks in Europe.

What is EHD?

EHD is an infectious disease that primarily affects domestic and wild ruminants, like deer. The virus is transmitted through the bite of midges that have fed on infected animals. Infection with EHDV can lead to severe clinical signs in cattle, including fever, nose and mouth sores, drooling, eye inflammation, and respiratory distress. In some cases, it can result in death. Despite the severity of the disease in affected animals, the EHDV is not a risk to human health, as it is not known to cause disease in humans under any conditions.

The vaccine

Hepizovac contains an inactivated form of the EHDV serotype 8 along with adjuvants to help stimulate the immune response. The vaccine is available as a ready-to-use suspension for injection.

The efficacy of the vaccine was assessed in a study that compared the protection against EHDV in vaccinated and unvaccinated calves. After two doses, given 21 days apart, vaccinated animals showed a significant reduction in the amount of virus present in the blood.

Hepizovac was approved under exceptional circumstances considering recent outbreaks of EHD in cattle herds, for which no vaccines were previously available. The approval was granted due to the urgent need for a solution to control the spread of this disease, which has had a significant impact on animal health and agricultural economies. Although certain safety, quality, and efficacy data were not fully available, the Committee for Medicinal Products for Veterinary Use (CVMP) determined that the benefit of the immediate availability of the vaccine outweighed these risks.

Based on the risk assessment conducted as part of the evaluation of all veterinary products, the vaccine is not expected to pose a risk to human or animal health or the environment, if used according to the product information.

The CVMP opinion will now be sent to the European Commission for the adoption of the decision on the EU-wide marketing authorisation of Hepizovac.

Website: International Conference on Infectious Diseases

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Inside Antarctica’s plague-infested penguin colonies

Antonio Alcamí shuddered when he saw that a new plague — which had already caused the death of hundreds of millions of birds around the world — was leaping to the Americas and sweeping relentlessly from north to south, on its way to Antarctica, killing tens of thousands of marine mammals in its path.

Few people were as uniquely prepared as he was — a virologist specializing in lethal viruses, already hardened by the treacherous polar terrain — so he proposed setting up a laboratory at the Spanish Army’s Gabriel de Castilla Antarctic Base.

On February 24, 2024, Alcamí and his colleague Ángela Vázquez confirmed for the first time the presence of the highly pathogenic avian influenza virus in Antarctica. He immediately had a bold idea: he would set up a floating laboratory aboard a sailboat, allowing him to navigate through penguin colonies and find out what was happening. Two journalists from EL PAÍS joined him for a day, documenting his odyssey as he followed the trail of the plague.

The expedition, backed by the Spanish National Research Council (CSIC), set sail on January 14 from southern Argentina aboard a chartered Australian sailboat, the Australis. Just 23 meters long, the vessel was packed with eight scientists and three crew members. Their makeshift diagnostic laboratory occupied a tiny storage room — wedged between sacks of potatoes and onions. The researchers slept in claustrophobic bunk cabins. It was an unprecedented and revolutionary approach to conducting cutting-edge science in Antarctica.

Alcamí, 64, is well aware of the threat of lethal pathogens. He works with the World Health Organization as an advisor on smallpox, a virus that killed 300 million people in the 20th century until, thanks to vaccination, it became the first disease eradicated from the planet. Alcamí and his colleagues take extreme precautions when disembarking at the penguin colonies, braving harsh, almost unbearable conditions. They suit up in full waterproof gear — blizzard goggles, gloves, and masks — shielding themselves against temperatures that often plunge to -15°C and hurricane-force winds. On February 22, at a penguin colony on Livingston Island, the acrid stench of guano saturates the air, while the deafening squawks of thousands of tightly packed birds reverberate in their heads.

The floating laboratory has been cruising the coast of the Antarctic Peninsula — the portion of the continent closest to South America — for six weeks. The virus now appears to be everywhere. The team has detected it in 24 of the 27 sites visited, in nine bird species (cormorants, kelp gulls, Antarctic pigeons, southern fulmars, skuas, giant petrels, and three types of penguins) and four mammal species (fur seals and leopard, crabeater, and Weddell seals). Of the nearly 750 animals tested, one in four tested positive.

After detecting the first case in Antarctica a year ago in skuas — seabirds similar to seagulls — Alcamí feared a catastrophic outbreak in penguin colonies, where hundreds of thousands of the species can crowd together. “The reality is that this hasn’t happened. We’ve found some infected animals and little mortality, which suggests that penguins are more resistant to this disease than we thought. This is very good news,” says Alcamí, a virologist from the Severo Ochoa Center for Molecular Biology, a joint institute of the CSIC and the Autonomous University of Madrid.

Other Antarctic species are more vulnerable. “Although we haven’t seen a devastating effect on penguins, we are beginning to see a significant impact on many birds and, especially, marine mammals. My concern is that in the medium term this will become one of the most significant infections of the last century in Antarctica,” warns Alcamí. “Just because we don’t see marine mammal carcasses doesn’t mean they aren’t dying, because they are possibly dying at sea, where we don’t see them.”

“The avian flu we’re seeing has acquired the ability to infect the brain. And that’s what makes it unique. That’s what makes it so deadly,” explains Alcamí. Infected animals succumb amid tremors and convulsions.

While veterinarians dissect penguin carcasses on land, looking for symptoms in the brain and lungs, the virologist returns to the sailboat. His final report from the expedition warns that the virus has been identified in half of the carcasses analyzed, often with extremely high viral loads, suggesting that avian flu is causing “significant mortality” in various species, such as skuas.

“Sometimes we’ve found 40 or 60 carcasses of these birds. They’re very susceptible. The virus is having a tremendous effect on their population,” says Alcamí. “We must remember that penguins aren’t the only representatives of Antarctica. This continent is home to many unique species, and they all must be preserved.”

Their colleagues Begoña Aguado, Ángela Vázquez, and Rafael González proudly showcase the sailboat’s unusual high-tech laboratory, where they work from sunrise to sunset in cramped, spartan conditions. The deafening hum of the electric generator is a constant backdrop, and the temperature rarely rises above freezing.

Some scientists have expressed skepticism about the high number of positive cases, citing concerns over potential sample contamination. But Alcamí’s team stands firm, insisting they have rigorously verified their findings. The first season of the expedition, conducted a year ago, made the cover of the prestigious journal Nature Microbiology.

The new mission has been made possible thanks to a €300,000 ($325,000) donation from the Spanish Union of Insurers and Reinsurers, along with logistical support from the Juan Carlos I Antarctic Base — a cutting-edge CSIC research facility funded by the Ministry of Science on the remote Livingston Island.

Website: International Conference on Infectious Diseases

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