You might have heard of something called “cryptosporidiosis” recently, closely followed by warnings to stay away from your local swimming pool if you’ve had diarrhoea.

More than 700 cases of this gastrointestinal disease were reported in Queensland in January, which is 13 times more than in January last year. Just under 500 cases have been recorded in New South Wales this year to-date, while other states have similarly reported an increase in the number of cryptosporidiosis infections in recent months.

Cryptosporidiosis has been listed as a national notifiable disease in Australia since 2001.
But what exactly is it, and should we be worried?

What causes cryptosporidiosis, and who is affected?

Cryptosporidiosis is the disease caused by the parasite Cryptosporidium, of which there are two types that can make us sick. Cryptosporidum hominis only affects humans and is the major cause of recent outbreaks in Australia, while Cryptosporidium parvum can also affect animals.

The infection is spread by spores called oocysts in the stools of humans and animals. When ingested, these oocysts migrate and mature in the small bowel. They damage the small bowel lining and can lead to diarrhoea, nausea, vomiting, fever and abdominal discomfort.

Most people develop symptoms anywhere from one to 12 days after becoming infected. Usually these symptoms resolve within two weeks, but the illness may last longer and can be severe in those with a weakened immune system.

Children and the elderly tend to be the most commonly affected. Cryptosporidiosis is more prevalent in young children, particularly those under five, but the disease can affect people of any age.

So how do we catch it?

Most major outbreaks of cryptosporidiosis have been due to people drinking contaminated water. The largest recorded outbreak occurred in Milwaukee in 1993 where 403,000 people were believed to have been infected.

Cryptosporidium oocysts are very small in size and in Milwaukee they passed through the filtration system of one of the water treatment plants undetected, infecting the city’s water supply. As few as ten oocysts can cause infection, making it possible for contaminated drinking water to affect a very large number of people.

Four days after infection a person with cryptosporidiosis can shed up to ten billion oocysts into their stool a day, with the shedding persisting for about two weeks. This is why one infected person in a swimming pool can infect the entire pool in a single visit.

Cryptosporidium oocysts excreted in the faeces of infected humans and animals can also reach natural bodies of water such as beaches, rivers and lakes directly through sewer pipes or indirectly such as in manure transported with surface runoff after heavy rain.

One study which modelled Cryptosporidium concentrations in rivers around the world estimated there are anywhere from 100 to one million oocysts in a litre of river water.

In Australia, cryptosporidiosis outbreaks tend to occur during the late spring and early summer periods when there’s an increase in recreational water activities such as swimming in natural water holes, water catchments and public pools. We don’t know exactly why cases have seen such a surge this summer compared to other years, but we know Cryptosporidium is very infectious.

Oocysts have been found in foods such as fresh vegetables and seafood but these are not common sources of infection in Australia.

What about chlorine?

Contrary to popular belief, chlorine doesn’t kill off all infectious microbes in a swimming pool. Cryptosporidium oocysts are hardy, thick-walled and resistant to chlorine and acid. They are not destroyed by chlorine at the normal concentrations found in swimming pools.

We also know oocysts can be significantly protected from the effects of chlorine in swimming pools by faecal material, so the presence of even small amounts of faecal matter contaminated with Cryptosporidium in a swimming pool would necessitate closure and a thorough decontamination.

Young children and in particular children in nappies are known to increase the potential for disease transmission in recreational water. Proper nappy changing, frequent bathroom breaks and showering before swimming to remove faecal residue are helpful ways to reduce the risk.

Some sensible precautions

Other measures you can take to reduce yours and others’ risk of cryptosporidiosis include:

• avoid swimming in natural waters such as rivers and creeks during and for at least three days after heavy rain
• avoid swimming in beaches for at least one day after heavy rain
• avoid drinking untreated water such as water from rivers or springs. If you need to drink untreated water, boiling it first will kill the Cryptosporidium
• avoid swallowing water when swimming if you can
• if you’ve had diarrhoea, avoid swimming for at least two weeks after it has resolved
• avoid sharing towels or linen for at least two weeks after diarrhoea has resolved
• avoid sharing, touching or preparing food that other people may eat for at least 48 hours after diarrhoea has resolved
• wash your hands with soap and water after going to the bathroom or before preparing food (Cryptosporidium is not killed by alcohol gels and sanitisers).

Not all cases of diarrhoea are due to cryptosporidiosis. There are many other causes of infectious gastroenteritis and because the vast majority of the time recovery is uneventful you don’t need to see a doctor unless very unwell. If you do suspect you may have cryptosporidiosis you can ask your doctor to refer you for a stool test.

Vincent Ho, Associate Professor and clinical academic gastroenterologist, Western Sydney University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Alzheimer’s disease, a progressive neurodegenerative disorder that affects millions worldwide, has a long preclinical stage. It potentially begins decades before clinical symptoms become apparent.

But as our new research suggests, blood biomarkers in combination with self-reported memory concerns could offer an early clue to how Alzheimer’s disease develops across the life course.

This means midlife could be a critical window for promoting brain health.

For our study, we used data from the world-leading Dunedin Study at the University of Otago, which has been following a cohort of people for more than 50 years.

We found a certain protein known as pTau181 was associated with self-reported concerns about memory and thinking skills.

Notably, study participants were only 45 years old at the time of assessment. People typically aren’t diagnosed with dementia until their 70s or older.

In recent years, we’ve seen advances in pharmaceutical treatments for Alzheimer’s disease. However, these are not cures. At best, they slow disease progression but they don’t preserve or restore cognitive function lost during more advanced stages.

It is likely these treatments work best when taken early, which makes it more important to identify the earliest signs of Alzheimer’s disease.

Preventing dementia

Different types of dementia can look similar during the early stages of disease, but the treatment and course of progression differ significantly for each type of dementia.

In the past, Alzheimer’s disease could only be definitively diagnosed postmortem, or more recently with invasive testing such as a lumbar puncture. But researchers are now working on identifying blood biomarkers that could offer a minimally invasive way to identify people at higher risk of developing Alzheimer’s disease.

Detecting Alzheimer’s disease in its earliest stages could provide an opportunity for prevention and offer the greatest benefits for brain health and ageing.

This may involve lifestyle changes, such as supporting people to be physically active and continuing to engage in social activities, and addressing modifiable risk factors such as hypertension or hearing loss.

Preventive approaches work more effectively the earlier they are implemented. Studying middle-aged populations is therefore important for identifying early risk profiles for Alzheimer’s, long before the disease would be diagnosed.

When forgetfulness becomes a sign of disease

As people get older, they often notice their memory isn’t as good as it used to be.

Forgetfulness is common and usually benign as people age. But in some people, these memory issues may indicate something else is going on.

Recent research shows subtle subjective changes in cognition often occur long before diagnosis and might be the first moment the disease is felt.

Screening for biological markers, in combination with subjective reports of memory function, could help distinguish the earliest signs of Alzheimer’s disease pathology from normal ageing.

Proteins such as pTau181 are much higher in people with Alzheimer’s disease, but we don’t know yet when this protein begins to accumulate.

Our findings add to the growing evidence that the earliest signs of dementia may show up long before diagnosis. They also show that self-reported cognitive concerns may be an early warning sign for Alzheimer’s, even in midlife.

Interestingly, we didn’t find that the pTau181 biomarker was associated with MRI brain scan measures or cognitive test performance at age 45.

There are at least two possible explanations for this.

Perhaps pTau181 increases during the earliest stages of Alzheimer’s disease, when people first start to notice their memory worsening but no changes are shown yet in MRI scans. Or it could be that elevated pTau181 is not related to Alzheimer’s disease risk in midlife, and the protein is only useful for detecting Alzheimer’s in older adults.

We don’t know enough yet, but will be following the same group of people as they get older to continue this research.

Ashleigh Barrett-Young, Research Fellow in Brain Health, University of Otago

This article is republished from The Conversation under a Creative Commons license. Read the original article.