Endotoxins are fragments of bacterial cell walls that are released when bacteria die. Because cockroaches consume a wide range of materials, they host a diverse gut microbiome. Previous studies have shown that these insects shed large quantities of endotoxins through their droppings. Although humans and household pets can also produce endotoxins, the researchers found that a major portion of those detected in household dust originated from cockroach feces.

"Endotoxins are important to human health, as inhalation of these components has been shown to provoke allergic responses," said Coby Schal, the Blanton J. Whitmire Distinguished Professor of Entomology at NC State and co-corresponding author of the study. "Past surveys in U.S. homes found endotoxin levels much higher in homes with self-reported evidence of cockroaches; that association is stronger in low-income homes than in single-family homes."

How the Study Was Conducted

The research took place in multi-unit apartment complexes in Raleigh, North Carolina. Scientists measured the scale of cockroach infestations alongside concentrations of allergens and endotoxins in each home. To establish baseline readings, both settled and airborne dust samples were collected before any treatment began.

The findings revealed that infested homes contained high amounts of endotoxins, with female cockroaches producing roughly twice as much as males.

"Female cockroaches eat more than males, so more endotoxins are shed from their fecal matter," explained Madhavi Kakumanu, an NC State research scholar in Schal's lab and co-corresponding author of the paper. She noted that kitchens typically contained more endotoxins than bedrooms, since they provide abundant food sources for cockroaches.

Testing Pest Control's Effectiveness

The infested apartments were split into two categories: untreated homes and those that received professional extermination to remove cockroaches. Researchers also included a control group of residences with no infestation. Dust and insect samples were collected again at three and six months.

Homes that remained untreated consistently showed high levels of both allergens and endotoxins throughout the study. In contrast, most units that underwent extermination were cleared of cockroaches and showed substantial reductions in both allergens and endotoxins.

"When you eliminate cockroaches, you eliminate their allergens. Small decreases in cockroaches don't lower allergen levels because the remaining live cockroaches deposit more allergens," Schal said. "Endotoxins significantly decreased in homes where cockroaches were eliminated. This paper shows that the cockroach is the most important depositor of endotoxin in infested homes."

Kakumanu added, "We also saw that allergens and endotoxins can be airborne."

Next Steps: Exploring Health Effects

Schal noted that future research will look at how cockroach allergens and endotoxins interact in animal models of asthma, such as mice.

"There exists the implication that asthma can be worse due to interactions between allergens and endotoxins," he said. "We want to see if that is the case in mice."

The research was published in The Journal of Allergy and Clinical Immunology: Global. Co-authors include NC State's Richard G. Santangelo, Zachary C. DeVries from the University of Kentucky, and Jeffrey Siegel from the University of Toronto.

Funding was provided by the U.S. Department of Housing and Urban Development Healthy Homes program (NCHHU0053-19, NCHHU0081-24); the Alfred P. Sloan Foundation (2013-5-35 MBE); a Pilot Project from the Center for Human Health and the Environment under P30ES025128 from the National Institute of Environmental Health Sciences; the National Institute of Allergy and Infectious Diseases of the National Institutes of Health (award number 1R21AI187857-01); the Research Capacity Fund (HATCH) (project NC02639) from the U.S. Department of Agriculture National Institute of Food and Agriculture; and the Blanton J. Whitmire Endowment at North Carolina State University.

For the first time, researchers from the Wellcome Sanger Institute, the University of Oslo, the University of Helsinki, Aalto University in Finland, and their collaborators have been able to estimate how efficiently one person can pass gut bacteria to others. This kind of calculation, which measures transmission rates, has previously been possible mainly for viruses.

Tracking Dangerous Strains Across Populations

The study, published today (November 4) in Nature Communications, examined three key E. coli strains circulating in the UK and Norway. Two of these strains are resistant to several common classes of antibiotics. They are also the most frequent causes of urinary tract and bloodstream infections in both countries. The researchers suggest that better monitoring of these strains could guide public health responses and help prevent outbreaks of infections that are difficult to treat.

In the long term, gaining insight into the genetic factors that help E. coli spread could lead to more targeted therapies and reduce reliance on broad-spectrum antibiotics. The approach developed in this study could also be adapted to investigate other bacterial pathogens and improve strategies for managing invasive infections.

E. coli is one of the leading causes of infections around the world.¹ While most strains are harmless and normally inhabit the gut, the bacteria can enter the body through direct contact such as kissing or indirect means like shared surfaces, food, or living spaces. When E. coli moves into areas such as the urinary tract, it can cause serious illness, including sepsis, especially in people with weakened immune systems.

Antibiotic resistance has made these infections even more concerning. In the UK, more than 40 percent of E. coli bloodstream infections are now resistant to a key antibiotic,² reflecting a global trend of rising resistance levels.

Applying Viral-Style Transmission Metrics to Bacteria

Scientists often describe how infectious a pathogen is using the basic reproduction number, known as R0. This number estimates how many new cases a single infected person might cause. It is typically applied to viruses and helps predict whether an outbreak will expand or decline. Until now, researchers have been unable to assign an R0 value to bacteria that normally colonize the gut, since they often live in the body without triggering illness.

To overcome this, the team combined data from the UK Baby Biome Study with genomic information from E. coli bloodstream infection surveillance programs in the UK and Norway, previously compiled by the Wellcome Sanger Institute.

Using a software platform called ELFI³ (Engine for Likelihood-Free Inference), the researchers built a new model capable of estimating R0 for the three major E. coli strains studied.

Their results showed that one particular strain, known as ST131-A, can spread between people as rapidly as some viruses that have caused global outbreaks, including the swine flu (H1N1). This is particularly striking because E. coli is not spread through airborne droplets like flu viruses are.

The two other strains studied, ST131-C1 and ST131-C2, are resistant to multiple antibiotic classes but spread much more slowly among healthy individuals. However, in hospitals and other healthcare environments, where patients are more vulnerable and contact is frequent, these resistant strains could move through populations much faster.

Understanding R0 for Bacteria

Assigning an R0 value to bacteria opens the door to a clearer understanding of how bacterial infections spread. It also helps identify which strains pose the greatest threat and could inform public health strategies to better protect people with compromised immune systems.

Fanni Ojala, M.Sc., co-first author at Aalto University in Finland, explained: "By having a large amount of systematically collected data, it was possible to build a simulation model to predict R0 for E. coli. To our knowledge, this was not just a first for E. coli, but a first for any bacteria that live in our gut microbiome. Now that we have this model, it could be possible to apply it to other bacterial strains in the future, allowing us to understand, track, and hopefully prevent the spread of antibiotic-resistant infections."

Dr. Trevor Lawley, Group Leader at the Wellcome Sanger Institute and co-lead of the UK Baby Biome Study, who was not involved in this research, noted: "E. coli is one of the first bacteria that can be found in a baby's gut, and in order to understand how our bacteria shape our health, we need to know where we start -- which is why the UK Baby Biome study is so important. It is great to see that our UK Baby Biome study data are being used by others to uncover new insights and methods that will hopefully benefit us all."

A New Lens on Bacterial Genetics

Professor Jukka Corander, senior author at the Wellcome Sanger Institute and the University of Oslo, added: "Having the R0 for E. coli allows us to see the spread of bacteria through the population in much clearer detail, and compare this to other infections. Now that we can see how rapidly some of these bacterial strains spread, it is necessary to understand their genetic drivers. Understanding the genetics of specific strains could lead to new ways to diagnose and treat these in healthcare settings, which is especially important for bacteria that are already resistant to multiple types of antibiotics."

The success of this study relied on extensive genomic data from the UK and Norway, all sequenced at the Wellcome Sanger Institute. This large-scale data made it possible to identify transmission patterns in detail. The datasets originated from earlier studies published in The Lancet Microbe,^4,5 which laid the foundation for the modeling breakthrough achieved in this new research.

Notes

1. Antimicrobial Resistance Collaborators. (2022) 'Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis.' The Lancet. DOI: 1016/S0140-6736(21)02724-0
2. UK Health Security Agency. New data shows 148 severe antibiotic-resistant infections a day in 2021. Available at: https://www.gov.uk/government/news/new-data-shows-148-severe-antibiotic-resistant-infections-a-day-in-2021#:~:text=Over%20two-fifths%20of%20E,as%20cefiderocol%20to%20identify%20resistance^[1]
3. ELFI can be found: https://www.elfi.ai/^[2]
4. R. A. Gladstone, et al. (2021) ' Emergence and dissemination of antimicrobial resistance in Escherichia coli causing bloodstream infections in Norway in 2002-17: a nationwide, longitudinal, microbial population genomic study' Lancet Microbe. DOI: 10.1016/S2666-5247(21)00031-8.
5. A. K. Pontinen, et al. (2024) 'Modulation of multidrug-resistant clone success in Escherichia coli populations: a longitudinal, multi-country, genomic and antibiotic usage cohort study' Lancet Microbe. DOI: 10.1016/S2666-5247(23)00292-6.

Glaucoma occurs when retinal ganglion cells (RGCs) and their axons become damaged. These delicate nerve cells, located at the back of the eye, carry visual information to the brain. Once they deteriorate, vision loss begins. Current therapies mainly reduce pressure inside the eye, but none effectively protect RGCs from harm. This gap in treatment highlights the urgent need for neuroprotective strategies that can preserve these critical nerve cells.

Searching for Biomarkers and Protective Treatments

Pawan Singh, a researcher at Mizzou's School of Medicine, is dedicated to finding both biomarkers that reveal glaucoma early and therapies that safeguard the optic nerve. His team recently discovered that glaucoma patients have lower levels of two naturally occurring molecules, agmatine and thiamine, in the clear fluid at the front of the eye compared with individuals without the disease. These small molecules, known as metabolites, may serve as early indicators that can be detected through testing.

"In several cases, people do not find out they have glaucoma until they are older and their eye pressure is elevated," Singh explained. "Our long-term goal is to see if doctors could one day do a simple blood test to check for these biomarkers. If they can, hopefully they will be able to catch the disease much earlier, before vision loss occurs, so patients can receive treatment sooner."

Promising Clues for Future Treatments

Beyond diagnosis, the discovery offers hope for new therapies. Singh's pre-clinical research suggests that agmatine and thiamine may help protect RGCs and maintain visual function, offering neuroprotective potential. These molecules could eventually be developed into treatments, possibly in the form of eye drops or supplements, that slow or prevent vision loss from glaucoma.

"Mizzou's impressive research infrastructure and our collaborative team help make this research possible," Singh said. "While more work needs to be done, the eye doctors I have spoken to here at Mizzou are very excited about this research, so I am proud and hopeful for the future."

The findings were published in Investigative Ophthalmology and Visual Science under the title "Metabolomic profiling of aqueous humor from glaucoma patients identifies metabolites with anti-inflammatory and neuroprotective potential in mice."