Have you ever wondered why most disinfectants indicate they kill 99.9% or 99.99% of germs, but never promise to wipe out all of them? Perhaps the thought has crossed your mind mid-way through cleaning your kitchen or bathroom.

Surely, in a world where science is able to do all sorts of amazing things, someone would have invented a disinfectant that is 100% effective?

The answer to this conundrum requires understanding a bit of microbiology and a bit of mathematics.

What is a disinfectant?

A disinfectant is a substance used to kill or inactivate bacteria, viruses and other microbes on inanimate objects.

There are literally millions of microbes on surfaces and objects in our domestic environment. While most microbes are not harmful (and some are even good for us) a small proportion can make us sick.

Although disinfection can include physical interventions such as heat treatment or the use of UV light, typically when we think of disinfectants we are referring to the use of chemicals to kill microbes on surfaces or objects.

Chemical disinfectants often contain active ingredients such as alcohols, chlorine compounds and hydrogen peroxide which can target vital components of different microbes to kill them.

The maths of microbial elimination

In the past few years we’ve all become familiar with the concept of exponential growth in the context of the spread of COVID cases.

This is where numbers grow at an ever-accelerating rate, which can lead to an explosion in the size of something very quickly. For example, if a colony of 100 bacteria doubles every hour, in 24 hours’ time the population of bacteria would be more than 1.5 billion.

Conversely, the killing or inactivating of microbes follows a logarithmic decay pattern, which is essentially the opposite of exponential growth. Here, while the number of microbes decreases over time, the rate of death becomes slower as the number of microbes becomes smaller.

For example, if a particular disinfectant kills 90% of bacteria every minute, after one minute, only 10% of the original bacteria will remain. After the next minute, 10% of that remaining 10% (or 1% of the original amount) will remain, and so on.

Because of this logarithmic decay pattern, it’s not possible to ever claim you can kill 100% of any microbial population. You can only ever scientifically say that you are able to reduce the microbial load by a proportion of the initial population. This is why most disinfectants sold for domestic use indicate they kill 99.9% of germs.

Other products such as hand sanitisers and disinfectant wipes, which also often purport to kill 99.9% of germs, follow the same principle.

Real-world implications

As with a lot of science, things get a bit more complicated in the real world than they are in the laboratory. There are a number of other factors to consider when assessing how well a disinfectant is likely to remove microbes from a surface.

One of these factors is the size of the initial microbial population that you’re trying to get rid of. That is, the more contaminated a surface is, the harder the disinfectant needs to work to eliminate the microbes.

If for example you were to start off with only 100 microbes on a surface or object, and you removed 99.9% of these using a disinfectant, you could have a lot of confidence that you have effectively removed all the microbes from that surface or object (called sterilisation).

In contrast, if you have a large initial microbial population of hundreds of millions or billions of microbes contaminating a surface, even reducing the microbial load by 99.9% may still mean there are potentially millions of microbes remaining on the surface.

Time is is a key factor that determines how effectively microbes are killed. So exposing a highly contaminated surface to disinfectant for a longer period is one way to ensure you kill more of the microbial population.

This is why if you look closely at the labels of many common household disinfectants, they will often suggest that to disinfect you should apply the product then wait a specified time before wiping clean. So always consult the label on the product you’re using.

Other factors such as temperature, humidity and the type of surface also influence how well a disinfectant works outside the lab.

Similarly, microbes in the real world may be either more or less sensitive to disinfection than those used for testing in the lab.

Disinfectants are one part infection control

The sensible use of disinfectants plays an important role in our daily lives in reducing our exposure to pathogens (microbes that cause illness). They can therefore reduce our chances of getting sick.

The fact disinfectants can’t be shown to be 100% effective from a scientific perspective in no way detracts from their importance in infection control. But their use should always be complemented by other infection control practices, such as hand washing, to reduce the risk of infection.

Hassan Vally, Associate Professor, Epidemiology, Deakin University

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

A recent study has suggested Shingrix, a relatively new vaccine given to protect older adults against shingles, may delay the onset of dementia.

This might seem like a bizarre link, but actually, research has previously shown an older version of the shingles vaccine, Zostavax, reduced the risk of dementia.

In this new study, published last week in the journal Nature Medicine, researchers from the United Kingdom found Shingrix delayed dementia onset by 17% compared with Zostavax.

So how did the researchers work this out, and how could a shingles vaccine affect dementia risk?

From Zostavax to Shingrix

Shingles is a viral infection caused by the varicella-zoster virus. It causes painful rashes, and affects older people in particular.

Previously, Zostavax was used to vaccinate against shingles. It was administered as a single shot and provided good protection for about five years.

Shingrix has been developed based on a newer vaccine technology, and is thought to offer stronger and longer-lasting protection. Given in two doses, it’s now the preferred option for shingles vaccination in Australia and elsewhere.

In November 2023, Shingrix replaced Zostavax on the National Immunisation Program, making it available for free to those at highest risk of complications from shingles. This includes all adults aged 65 and over, First Nations people aged 50 and older, and younger adults with certain medical conditions that affect their immune systems.

What the study found

Shingrix was approved by the US Food and Drugs Administration in October 2017. The researchers in the new study used the transition from Zostavax to Shingrix in the United States as an opportunity for research.

They selected 103,837 people who received Zostavax (between October 2014 and September 2017) and compared them with 103,837 people who received Shingrix (between November 2017 and October 2020).

By analysing data from electronic health records, they found people who received Shingrix had a 17% increase in “diagnosis-free time” during the follow-up period (up to six years after vaccination) compared with those who received Zostavax. This was equivalent to an average of 164 extra days without a dementia diagnosis.

The researchers also compared the shingles vaccines to other vaccines: influenza, and a combined vaccine for tetanus, diphtheria and pertussis. Shingrix and Zostavax performed around 14–27% better in lowering the risk of a dementia diagnosis, with Shingrix associated with a greater improvement.

The benefits of Shingrix in terms of dementia risk were significant for both sexes, but more pronounced for women. This is not entirely surprising, because we know women have a higher risk of developing dementia due to interplay of biological factors. These include being more sensitive to certain genetic mutations associated with dementia and hormonal differences.

Why the link?

The idea that vaccination against viral infection can lower the risk of dementia has been around for more than two decades. Associations have been observed between vaccines, such as those for diphtheria, tetanus, polio and influenza, and subsequent dementia risk.

Research has shown Zostavax vaccination can reduce the risk of developing dementia by 20% compared with people who are unvaccinated.

But it may not be that the vaccines themselves protect against dementia. Rather, it may be the resulting lack of viral infection creating this effect. Research indicates bacterial infections in the gut, as well as viral infections, are associated with a higher risk of dementia.

Notably, untreated infections with herpes simplex (herpes) virus – closely related to the varicella-zoster virus that causes shingles – can significantly increase the risk of developing dementia. Research has also shown shingles increases the risk of a later dementia diagnosis.

The mechanism is not entirely clear. But there are two potential pathways which may help us understand why infections could increase the risk of dementia.

First, certain molecules are produced when a baby is developing in the womb to help with the body’s development. These molecules have the potential to cause inflammation and accelerate ageing, so the production of these molecules is silenced around birth. However, viral infections such as shingles can reactivate the production of these molecules in adult life which could hypothetically lead to dementia.

Second, in Alzheimer’s disease, a specific protein called Amyloid-β go rogue and kill brain cells. Certain proteins produced by viruses such as COVID and bad gut bacteria have the potential to support Amyloid-β in its toxic form. In laboratory conditions, these proteins have been shown to accelerate the onset of dementia.

What does this all mean?

With an ageing population, the burden of dementia is only likely to become greater in the years to come. There’s a lot more we have to learn about the causes of the disease and what we can potentially do to prevent and treat it.

This new study has some limitations. For example, time without a diagnosis doesn’t necessarily mean time without disease. Some people may have underlying disease with delayed diagnosis.

This research indicates Shingrix could have a silent benefit, but it’s too early to suggest we can use antiviral vaccines to prevent dementia.

Overall, we need more research exploring in greater detail how infections are linked with dementia. This will help us understand the root causes of dementia and design potential therapies.

Ibrahim Javed, Enterprise and NHMRC Emerging Leadership Fellow, UniSA Clinical & Health Sciences, University of South Australia

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