It's unclear why colon cancer cases have doubled in people under 55 over the past two decades, a staggering rise that has alarmed doctors and cancer researchers.

But part of the story could be colibactin, a toxin made by certain strains of E. coli and other bacteria. In a study out this week, researchers have identified a strong link between this DNA-damaging toxin and colon cancer among younger patients.

The team, based at the University of California, San Diego, analyzed tissue samples from close to 1,000 colorectal cancer patients across four continents. They found the majority had cancers bearing mutations that signaled a past encounter with colibactin.

"You can think of it as the weapon system of a bacteria to fight other bacteria and to defend themselves," says Ludmil Alexandrov, the lead author of the study, which was published in Nature this week.

Strikingly, those under the age of 40 with early-onset colon cancer were three to five times more likely to have these mutations than those in their 70s and older.

The thinking goes that in some people, this bacterial weaponry — technically called a "genotoxin" — can get directed at their gut cells, seeding mutations that put them at increased risk of developing colorectal cancer.

According to their data, this exposure isn't ongoing when the cancer is diagnosed. Instead, it appears to have happened during childhood.

"Our estimate is that it happens within the first 10 years of life," Alexandrov says. "So if you get that mutation at age 5, that puts you 20 to 30 years ahead of schedule for getting colorectal cancer."

While the study shows a strong association, the data can't prove colibactin caused these patients to develop cancer at a younger age. And researchers in the field don't expect E. coli, or any single microbe for that matter, to be the skeleton key for the surge in colorectal cancer.

"That would be too simple," says Christian Jobin, a microbiome researcher at the University of Florida.

More likely, he says, colibactin — studied closely in E. coli but produced by other bacteria, too — is one "hit" among many to our microbiome, which together may place some people on a faster trajectory for developing cancer.

What triggers a DNA-damaging toxin

The study is a new clue into the rise in colorectal cancer in the young. Scientists believe some confluence of environmental factors, including diet, a sedentary lifestyle, medication and so on, is driving this steep rise.

These could be having downstream effects on the microbes in our gut like E. coli.

"It's been really perplexing," says Dr. Neelendu Dey, a gastroenterologist whose lab focuses on the gut microbiome at the Fred Hutchinson Cancer Center. "The microbes that may contribute to cancer risk are tricky to understand."

The family of microbes to which E. coli belongs is actually the most prevalent type of bacteria in your gut during the very early stages of life.

About 20% to 30% of people have strains of E. coli that can synthesize this toxin, but that doesn't mean it's necessarily having "deleterious effects," says Jobin, whose lab has pioneered related research.

In other words, it's not some new infectious agent that simply needs to be eliminated.

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Antibiotics use and nutrition, could be at play

Because they sequenced the genome of cancer from patients all over the globe, Alexandrov says the researchers could tell these mutations related to colibactin are actually quite rare in more "rural, non-industrialized" regions of Africa and Asia, whereas they turn up more frequently in the U.S. and Western Europe.

That evidence, coupled with the findings that it's a result of early childhood exposure, gives them a handful of hypotheses about what could be at play.

He says some of their top suspects are the mode of birth (cesarean section vs. vaginal delivery), breastfeeding, the use of antibiotics and nutrition, for example whether children were fed ultra processed foods.

"All of these factors are known to substantially affect the microbiome and there is some evidence they may impact this [colibactin producing] bacteria, but we really need to investigate each one carefully."

Dey views all of these as plausible, particularly antibiotics, given that other research teams have linked early-life antibiotic use to increased risk of colorectal cancer later on.

More broadly, he says he hopes researchers can eventually find microbes that serve as "biomarkers" for identifying people at risk of developing pre-cancers. And, perhaps down the line, drugs can be designed to target toxins like colibactin to counter their harmful effects.

Poliovirus has been detected in a sample of Perth's wastewater, health officials have revealed.

Authorities said the detection in mid-April was evidence of a vaccine-derived poliovirus Type 2 strain, similar to what has been identified in Africa, Europe and Papua New Guinea in recent years.

Western Australia's chief health officer, Dr Clare Huppatz, said it was the first time this particular strain had been detected in Australia, but presented a very low risk to the population.

The potential for this strain to circulate in a highly vaccinated population is very low, and the poliovirus vaccination coverage in WA children is 92 per cent."

Dr Huppatz noted the presence of the virus in wastewater in Europe during 2024 and 2025 did not lead to anyone developing the disease.

“This finding is most likely from someone who has travelled overseas and is shedding this virus strain," she said.

"This sort of detection has occurred in Europe on several occasions across four different countries where this same strain has been detected in the wastewater.

"On each of those occasions it hasn't led to outbreaks, in fact it hasn't led to any single cases of disease."

But Dr Huppatz said the case served as a reminder for people to be fully vaccinated against the disease while it still circulated overseas.

"It is a timely reminder that polio virus is still circulating around the world and of course with international travel it is something we could be exposed to even in Perth," she said.

University of New South Wales medical epidemiologist Dr Abrar Chughtai said there had been similar detections in Australia recently.

“Australia previously detected vaccine-derived poliovirus in Melbourne wastewater in 2024, linked to an unvaccinated traveller," he said.

"Similar detections have occurred globally in many countries ... mainly in under-immunised populations, with no subsequent outbreaks."

[..]

History of polio in Australia

According to the Australian Institute of Health and Welfare (AIHW), Australia was declared polio-free in 2000.

"Although there has been no known local transmission of the poliovirus in Australia since 1972, there remains a risk of the importation of polio from overseas," its website reads.

Since 1987, the only case of polio detected in Australia was in 2007 when an overseas-born student acquired the disease during a visit to a country with known ongoing polio transmission, according to the AIHW.

The previous two epidemics of polio in Australia were in 1956, and from 1960 to 1962.

Cases of polio sharply declined after 1956, when the vaccine was introduced.

An alarming new report, jointly written by Hepatitis Queensland and the Cancer Council Queensland, found Queenslanders are dying from liver cancer at more than triple the rate than in the 1980s.

It contains statistics showing Queensland liver cancer deaths have risen from 1.6 deaths per 100,000 population in the 1980s to 5.1 per 100,000 in 2018–2022, the latest data available.

"The steady increase in liver cancer incidence observed in Queensland mirrors trends seen nationally and internationally, where liver cancer has become one of the fastest-growing causes of cancer mortality," the report says.

It will be released publicly today and contains estimates that about 48,000 Queenslanders are living with chronic hepatitis B or C. [~1% of the population]

Modelling suggests 20–30 per cent of cases have not yet been diagnosed and "true prevalence may be underestimated", the report says.

Hepatitis Queensland CEO Anna Hawkes says Queenslanders most in need of care are often not receiving it.

"We have the tools to test, treat, and care for people with hepatitis B and C," she says.

[...]

Liver cancer survival among Queenslanders remains poor compared with most other cancers, although "five-year relative survival has improved from 8.6 per cent in the 1980s to 24.1 per cent in 2018–2022".

Dr Hawkes warns hepatitis C symptoms can be silent or flu-like, such as having fatigue and a fever.

"If you have had cosmetic surgery or dental work done overseas, a backyard tattoo or used drugs recreationally, even decades ago, don't ignore ongoing flu-like symptoms," she says.

"Ask your doctor to be tested for hepatitis."

Cancer Council Queensland chief operating officer Mena Waller says Queensland has a clear opportunity to reduce preventable liver cancer and improve outcomes across the population, particularly among at-risk groups, such as First Nations people.

Between 2018–2022, more than 1,600 Queenslanders died of liver cancer.

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Note: the main article details the experiences of one person with hepatitis that provides some personal insight into the burden of the disease.

WHO just released their Global Hepatitis Report 2026. A couple of the key points.

Global burden in 2024: There were an estimated 240 million people living with chronic HBV infection globally, equivalent to 2.9% of the global population in 2024. In the same year, an estimated 47 million people were living with HCV infection, equivalent to 0.6% of the global population.

Hepatitis remains a major cause of preventable death: In 2024, an estimated 1.3 million people died from viral hepatitis B and C–related cirrhosis and liver cancer. Chronic HBV infection caused about 1.1 million deaths, an increase of 17% since 2015. Hepatitis C infection caused about 240 000 deaths, a 12% reduction since 2015.

Treatment coverage remains critically low: Less than 5% of the 240 million people living with chronic HBV infection were receiving treatment in 2024, despite around 50% being eligible under WHO 2024 HBV treatment guidelines. Since 2015, only 20% of people eligible for HCV treatment had received it. In 2024, 11 million people who had been diagnosed with HCV infection were not yet on treatment.

Too many children are still getting infected with chronic HBV: In 2024, global chronic HBV prevalence among children under 5 years was 0.6%, down from 0.8% in 2015 but well above the 2030 target of 0.1%. The highest burden among children is in the WHO African Region, where prevalence exceeds 1% in most countries and in the range of 2–5% in several countries. Eighty‑five countries have now achieved the target of 0.1% prevalence of HBV infection in children aged under 5 years.