Are rising lower respiratory infection hospital admissions linked to dirty air?

The Covid crisis highlighted gaps in our understanding of the role that air pollution plays in infections.

A flurry of studies carried out during and after the crisis allowed a UK government advisory group to conclude that long-term exposure to air pollution may contribute to worse coronavirus symptoms. The group offered examples that included a study of more than 3 million people in Denmark that showed air pollution added to the risk of death or hospital admission with severe Covid, especially in the least well off.


Now a study led by the Barcelona Institute for Global Health has examined whether long-term exposure to air pollution is a factor in hospital admissions for lower respiratory infections (LRIs). LRIs include chest infections, pneumonia and bronchitis and place a large and increasing burden on health services. Alone, they accounted for a 15% increase in the rate of hospital admissions in the UK between 1999 and 2019.

Prof Cathryn Tonne, who led the study, said: “We have so much evidence of the negative health effects of air pollution on a wide range of health outcomes. We were surprised to see how limited the evidence still was for air pollution and LRIs in adults.”

Nearly 4 million adults in Catalonia were studied over a five-year period. During this time, 94,000 people were admitted to hospital with LRIs – almost 60,000 of these had flu or pneumonia. Their health records were then compared with air pollution in their neighbourhoods. People over 65, and especially men with blood pressure problems, were most vulnerable to needing hospital admission with an LRI that was worsened by air pollution. This included particle pollution and exposure to nitrogen dioxide, a pollutant from diesel exhaust and burning fossil gas. Men living in the most polluted 25% of neighbourhoods had a 50% increased chance of being admitted to hospital with these infections compared with those in cleaner areas, but even here the risk was not zero.

Tonne said: “Importantly, we also observed positive associations between air pollution and hospital admission for LRI even at relatively low pollution concentrations. Continuing to reduce air pollution will have broad health benefits. This includes reducing the risk of hospital admission for common respiratory infections, particularly among vulnerable people.”

In 2022, Prof Sir Stephen Holgate chaired an inquiry by the UK Academy of Medical Sciences into the health burden from respiratory infections that the UK experiences each winter. Commenting on the study from Catalonia, Holgate said: “It is known that air pollution episodes trigger hospital admissions for serious lung infections. This study of nearly 4 million people clearly shows that long-term exposure to outdoor particulate pollution and nitrogen dioxide also drives infection-related hospital admissions.

here is a lot at stake

The world’s most powerful man is using his office to punish journalistic organisations that won’t follow his orders or who report critically on his policies. Donald Trump’s actions against the press include bans, lawsuits and hand-picking his own pool of reporters.

But the global threat against the press is bigger than just Trump.

Economic and authoritarian forces around the globe are challenging journalists’ ability to report. An independent press, one that those in power can’t simply overrule, is crucial to democracy. Figures such as Trump and Hungary’s Viktor Orbán want to crush it through exclusion and influence.

The Guardian is a global news organisation that will stand up to attacks on the free press. We have no interest serving those with immense power or immense wealth.

We are owned by an independent trust devoted only to protecting and defending our journalism. That means we don’t have a billionaire owner dictating what our reporters can cover or what opinions our columnists can have, or shareholders demanding a quick return.

The global situation is shifting hour by hour, making this an extremely challenging moment. It will take brave, well-funded, committed, quality journalism to call out what is happening.

Website: International Conference on Infectious Diseases

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Hormonal Contraceptives and Allergies: Is There a Link?

TOPLINE:

Among women, the use of systemic hormonal contraceptives is independently associated with an increased likelihood of having allergic rhinitis, a study showed.

METHODOLOGY:

Researchers analyzed data from 46,205 women in the United States (average age, 30.9 years) to examine associations between the use of systemic hormonal contraceptives and the risk for rhinitis, which encompasses nasal symptoms like sneezing, congestion, itching, or rhinorrhea.
Overall, 4606 participants had a diagnosis of rhinitis, of whom 92.4% had allergic rhinitis and 7.6% had nonallergic rhinitis.
Contraceptives were classified as progestin-only or estrogen-containing.

TAKEAWAY:

Participants using systemic hormonal contraceptives had 32% higher odds of having allergic rhinitis (adjusted odds ratio [aOR], 1.32; 95% CI, 1.20-1.44) than those not using systemic hormonal contraceptives, the researchers reported.
Progestin-only contraceptives (aOR, 1.29; 95% CI, 1.12-1.48) and estrogen-containing contraceptives (aOR, 1.35; 95% CI, 1.21-1.51) were associated with an increased risk for allergic rhinitis.
No significant associations were observed for nonallergic rhinitis.

IN PRACTICE:

“Clinicians may have a higher vigilance for rhinitis symptoms in adult women taking systemic hormonal contraceptives,” the study authors wrote.

SOURCE:

Richard G. Chiu, with the University of Illinois Chicago, was the corresponding author of the study, which was published online on March 21 in Laryngoscope Investigative Otolaryngology.

LIMITATIONS:

The duration of exposure to hormonal contraceptives was not always clear from medication records. The study had a cross-sectional design and did not establish a causal relationship between hormonal contraceptive use and rhinitis.

Website: International Conference on Infectious Diseases

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England, Wales and Northern Ireland Imported Zika Cases Reach New Highs

(Vax-Before-Travel News)

Recent data from the UK Health Security Agency (UKHSA) show that the number of imported Zika cases in England, Wales, and Northern Ireland (EWNI) increased last year.

On March 27, 2025, the UKHSA disclosed that the number of Zika virus disease cases reached 16 in England, Wales, and Northern Ireland during 2024, compared to 8 cases in 2023.

Most Zika-infected travellers returned to EWNI from South-Eastern Asia, where countries reported locally acquired infections.

For example, since 2016, the Zika virus has been reported in India's 16 different states/union territories.

Dr. Philip Veal, Consultant in Public Health at the UKHSA, stated in a media release, "It is essential to take precautions against mosquito-borne infections such as dengue while travelling abroad. Simple steps, such as using insect repellent, covering exposed skin, and sleeping under insecticide-treated bed nets, can reduce the risk of mosquito-borne infections."

Although Zika virus cases are rarely reported and don't often cause serious illness, the infection poses a significant risk to pregnant women, as it can be passed to the fetus.

An Original Investigation published by JAMA Public Health in January 2025 found that children born with congenital Zika syndrome (CZS) had a 13.10-fold higher hazard of death compared with those without CZS.

This health risk is well-known in the Region of the Americas, where Zika infections have substantially increased.

Over 42,127 ZIka cases were confirmed in the Americas in 2024, with the highest proportion of Zika cases reported in Argentina, Brazil, Bolivia, Colombia, and Costa Rica.

The U.S. CDC says Zika-spreading mosquitoes are found throughout Puerto Rico, where the Department of Health reported 16 cases in 2024.

In 2023, over 37,659 Zika cases were reported by various countries in the Americas.

As of March 31, 2025, no drug or vaccine prevents Zika virus infection. However, Zika vaccine candidates are conducting clinical trials in 2025.

Website: International Conference on Infectious Diseases

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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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