How rotavirus causes severe gastrointestinal disease

Rotavirus is a major cause of diarrhea and vomiting, especially in children, that results in approximately 128,000 deaths annually. The virus triggers the disease by infecting enterocyte cells in the small intestine, but only a fraction of the susceptible cells has the virus. In the mid-90s, scientists proposed that the small portion of infected cells promotes severe disease by sending out signals that disrupt the normal function of neighboring uninfected cells, but the nature of the signal has remained a mystery.

In the current study published in the journal Science, a team led by researchers at Baylor College of Medicine discovered that rotavirus-infected cells release signaling molecules, identified as adenosine diphosphate (ADP), which binds its cellular receptor P2Y1 on neighboring cells. Activating P2Y1 by ADP results in signals called intercellular calcium waves in these uninfected cells. Disrupting ADP binding to its receptor reduced the severity of diarrhea in a mouse model of the disease, suggesting that targeting the P2Y1 may be an effective strategy to control viral diarrhea in human populations.

“In our previous studies using fluorescent calcium sensors and time-lapse imaging, we discovered that rotavirus-infected cells display aberrant calcium signals that we can visualize as bright pulses of intercellular calcium waves that radiate from the infected cells,” said corresponding author Dr. Joseph Hyser, assistant professor of virology and microbiology and member of the Alkek Center for Metagenomic and Microbiome Research at Baylor. “Calcium signaling was known to be associated with various aspects of rotavirus infection and our work revealed the dynamic nature of the alterations induced by rotavirus.”

In the current study, the researchers conducted the experiments using a lower dose of the virus and noticed that it was not just the virus-infected cells that showed dynamic calcium signaling, but also the adjacent uninfected cells surrounding the infected cells produced pulses of calcium waves that were coordinated with those of the infected cells. This observation suggested that the infected cells could be triggering intercellular calcium waves in the uninfected cells.

The researchers connected their observation to a concept proposed in the mid-90s suggesting that rotavirus-infected cells send signals to neighboring uninfected cells that disrupt their function, promoting diarrhea and vomiting.

“Our videos of live fluorescent microscopy showing intercellular calcium wave signaling in both rotavirus-infected and uninfected cells provided an unprecedented means to investigate the nature of the proposed signal, which had not been identified,” said first author Dr. Alexandra L. Chang-Graham, an M.D./Ph.D. student in the Medical Scientist Training Program who completed her Ph.D. thesis working in the Hyser lab.

Finding the signal

Chang-Graham, Hyser and their colleagues worked with three different laboratory models to identify the signal that triggers intercellular calcium waves on uninfected cells. They used a monkey kidney cell line commonly used to study rotavirus. They also worked with human intestinal enteroids, a cultivation system that recapitulates many of the characteristics of the human infection and a neonatal mouse model of rotavirus infection and diarrhea. Their studies showed that suspected triggers of calcium waves, such as prostaglandin E2 and nitric oxide, did not elicit a calcium response. Then they tested ATP and ADP, known mediators of calcium signaling that had not been previously associated with rotavirus infection. They found that rotavirus-infected cells triggered intercellular calcium waves by releasing ADP that binds to its receptor, P2Y1, on uninfected neighboring cells. Knocking out the P2Y1 gene, which prevents ADP from signaling, reduced intercellular calcium waves.

“Across the three model systems we consistently found evidence that rotavirus-infected cells signal uninfected cells with ADP and that this contributes to the severity of the disease,” Chang-Graham said. “We consider it paradigm shifting that the actual signal, ADP, was not even on the radar before.”

ADP signaling is involved in triggering severe rotavirus symptoms

Further studies revealed previously unknown roles of ADP on rotavirus infection and replication, shining a spotlight on ADP as an important trigger of the multiple factors involved in severe diarrhea and vomiting caused by rotavirus. For instance, the researchers found evidence that ADP signaling increases rotavirus infection, the expression of inflammatory cytokine IL1-alpha and the secretion of serotonin, an inducer of diarrhea. ADP signaling also increases the expression of enzymes that produce prostaglandin and nitric oxide, potentially causing the increases in those compounds observed in rotavirus infection. Preventing ADP signaling and intercellular calcium waves reduced the production of the compounds mentioned above.

“Finally, we determined that inhibiting the P2Y1 receptor reduced the severity of rotavirus-induced diarrhea in a mouse model,” Chang-Graham said. “Using intercellular calcium waves, rotavirus amplifies its ability to cause disease beyond the cells it directly infects. This is the first virus identified to activate ADP-mediated intercellular calcium waves. This may be a strategy that other viruses also use to cause disease in their hosts.”

“Our findings add a new and very potent signaling pathway into the causative mechanisms of rotavirus diarrhea,” Hyser said. “In terms of treatment, this is exciting because currently some drugs targeting P2Y1 are undergoing preclinical testing as anticlotting drugs. It’s possible that such drugs could be repurposed, if proven to be safe for children, to be used to treat diarrhea caused by rotavirus infection.”

Other contributors to this work include Jacob L. Perry, Kristen A. Engevik, Francesca J. Scribano, J. Thomas Gebert, Heather A. Danhof, Joel C. Nelson, Joseph S. Kellen, Alicia C. Strtak, Narayan P. Sastri, Mary K. Estes and Robert A. Britton at Baylor College of Medicine. Melinda A. Engevik and James Versalovic are affiliated with Baylor and Texas Children’s Hospital.

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Predicting preterm births

Predicting preterm birth can be difficult, especially for women who have not given birth. It has long been known that the best predictor of preterm birth is someone who has had a prior preterm birth; however, this information is helpful only in second and subsequent pregnancies. For women in their first pregnancy, it is a challenge for obstetricians and midwives to advise them on their risks. To address this issue, researchers at Baylor College of Medicine and Texas Children’s Hospital studied how family history can predict preterm birth. Their findings were published in the American Journal of Obstetrics & Gynecology.

“This is a retrospective study of prospective data,” said Dr. Kjersti Aagaard, professor of obstetrics and gynecology at Baylor and Texas Children’s Hospital. “We developed a biobank and data repository called PeriBank where we consistently asked our pregnant patients a set of questions about their familial history. We were able to take that detailed data and determine if that specific woman’s family history did or did not predict her delivering preterm.”

Once familial information was gathered, the research team was able to answer questions to quantify estimates of risk for preterm birth based on the pregnant patient’s family history of preterm birth in herself, her sister(s), her mother, grandmothers and aunts and great-aunts. Their findings showed scenarios for women who have previously given birth (multiparous), as well as women who have never given birth (nulliparous). If a nulliparous woman herself was born preterm, her relative risk for delivering preterm was 1.75-fold higher. If her sister delivered preterm, her relative risk was 2.25-fold higher. If her grandmother or aunt delivered preterm, there was no significant increase of risk. If a multiparous mother with no prior preterm births was born preterm herself, her risk was 1.84-fold higher. However, if her sister, grandmother or aunt delivered preterm, there was no significant increase.

“We’ve managed over the years to collect data from a very large population of pregnant women that reflect Houston. There was considerable diversity by race, ethnicity, culture and socioeconomic status. This was a key strength of our study. With this breadth and depth of data reflective of the diversity of Houston, we were able to ask some good questions, which gave us really important information about ‘heritability’ of risk,” Aagaard said.

The research team showed that preterm births cannot be fully attributed to genetics, Aagaard said. Family members may share DNA or genetic code, but the same generation of family members are more likely to share social determinants or have experienced systemic racism and bias. This was best demonstrated by their finding that a history of preterm birth in the pregnant woman or her sister was significantly associated with preterm birth, while a grandmother or aunt was not. These same-generation predictors are generally thought to reflect more about common environmental or social exposures (or a combination of limited genetics plus common exposures) than genetic linkages.

“We know that for the majority of women who deliver a baby preterm, we cannot say that the cause of that preterm birth was in whole or in part genetics. Rather, this study provides subtle but important clues that it is more likely the shared familial background and its exposures that render risk,” Aagaard said. “We hope others will similarly be mindful of those subtle characteristics when looking at heritability and risk. We remain committed to finding the underlying true causal and driving factors. In the meantime, we provide for the first time some reliable risk estimates for first time moms based on their and their family history of preterm birth.”

Other contributors to this work include Amanda Koire and Derrick Chu.

This work was funded by the March of Dimes Preterm Birth Research Initiative (KA) and the NIH (1R01NR014792; KA).

Story Source:

Materials provided by Baylor College of Medicine. Note: Content may be edited for style and length.

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Meta-Lists

While you may have plenty of experience of making lists, such as for your to-dos and goals, have you ever thought of making a meta-list? A meta-list is a list of lists.

Which lists do you think it would be worthwhile to create?

Here’s an example of a meta-list:

  • Places to visit
  • Goals to achieve
  • Skills to develop
  • Experiences to share with a relationship partner
  • Programming languages to learn
  • Technologies to study
  • Potential purchases to research
  • Exercises or types of workouts to try
  • Exercise equipment to acquire for a home gym
  • Fears to face and overcome
  • Kitchen items to replace or upgrade
  • Home maintenance tasks to do
  • Home upgrades to do
  • New business ideas
  • New product or service ideas
  • New marketing campaign ideas
  • Email list providers to investigate
  • Web hosting platforms to evaluate
  • Sexual experiences to have
  • Coaching programs and personal development courses to invest in
  • Books to read
  • Movies to watch
  • Games to play
  • Apps to try
  • Websites to check out
  • Articles to read
  • Videos to watch
  • Dietary improvements to make
  • Favorite healthy recipes
  • Favorite wines
  • Favorite Star Trek episodes
  • Fitness milestones to achieve
  • Yoga positions
  • Best running shoes
  • Investment opportunities to research
  • Holiday gifts to buy for friends and family
  • Activities that make you happy
  • Most effective productivity practices
  • Personal values
  • Favorite memories
  • Restaurants to try
  • National parks to visit

So a meta-list is like a shopping list of shopping lists, not just for buying items at a store but for experiences to have across many areas of life.

I’ve maintained a lot of lists over the years, including many like the ones above, and I’ll tell you that they’re easy to create, but they also require tremendous patience. It’s one thing to work on a singular list of goals, but when you have many such lists, it can easily feel overwhelming at first.

When you see how easy it is to brainstorm items and how long it takes to actually do them, you may be tempted to abandon the practice, but I urge you to stick with it. There is a payoff, but it takes time.

Those lists can help you stay alert for when some item on some list becomes more accessible than usual, encouraging you to snag an opportunity while it’s hot. You can also periodically skim your lists to grab new ideas to explore. Such lists are great for whenever your life starts becoming a bit stale or predictable – they can give you so many ideas for mixing things up.

When it comes to meta-lists, think in terms of decades, not just months or years. You may have an item on one of your lists that you don’t get to for 20 years, but it’s still satisfying to check it off.

There were many items I added to a list during my 20s, and I didn’t finally get to it until my 40s. Some examples include traveling to various European countries, going skydiving, doing an extended water fast, going to Disney World and Epcot Center, and reading several Mark Twain books including Tom Sawyer, Huckleberry Finn, and A Connecticut Yankee in King Arthur’s Court.

Note that you don’t have to fill in all of these lists at once. Just create your one meta-list of the lists you may want to create. Then create a stub for each list, such as in the Notes or Reminders app on your phone. Whenever an idea for any of these lists pops into your mind, such as a movie a friend recommends, you can easily add it to the appropriate list. You can even do this verbally by telling a smart device to do it for you. Rachelle and I use our Apple Watches to add items to the grocery list whenever an item runs low. Then we’ll automatically have access to that list on our watches and phones whenever we’re out.

You can also use crowdsourcing to populate some of your lists. Ask people for book and movie recommendations, for instance. You may be surprised at how efficient this is. A single Facebook post can fill up your movie queue with some outstanding gems.

Lists are relatively easy to maintain since they just sit there till you need them. I especially find it helpful to have a “books to read” list since then I’m never left wondering what to read next. Most items on my list were suggested by friends.

While it may take time to fill out a bunch of lists, it only takes a few minutes to create a meta-list. Why not take a short break to do it right now? You could even copy the one I brainstormed above and edit it to suit your needs.

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Health24.com | Poor nutrition in poorer countries: Children in these nations grow up much shorter than elsewhere

  • There are few global studies on the height and BMI of children 
  • Research was conducted to fill this information gap 
  • There is a height difference of 20cm between the tallest and shortest adolescent populations>

Limited data exist on the health and nutrition of school-aged children and adolescents on a global level. A global analysis, led by Imperial College London, was recently published in The Lancet. The study examined the height and weight of groups aged between five and 19 years. 

The world’s tallest kids

Researchers assessed growth trends among 65 million participants between 1985 to 2019 – based on data pooled from 2 181 population-based studies.

An average difference of 20cm was found between adolescents from the world’s tallest and shortest populations. The tallest were from the Netherlands, Montenegro, Estonia, and Bosnia and Herzegovina (boys); and the Netherlands, Montenegro, Denmark, and Iceland (girls). And the world’s shortest kids lived in Timor-Leste, Laos, the Solomon Islands, and Papua New Guinea (boys); and Guatemala, Bangladesh, Nepal, and Timor-Leste (girls).

South African kids not among the healthiest

In the case of South Africa, the findings indicated that local girls tended to gain too much weight for their height.

The study also showed that around the age of five years, South African children were at optimal height, but once they reached 19 years they were shorter than recommended by the World Health Organization for that age group.

In their paper, researchers said: “The unhealthiest changes – gaining too little height, too much weight for their height compared with children in other countries, or both – occurred in many countries in sub-Saharan Africa.” 

Good nutrition is vital

This kind of study is of great importance as it shows that good nutrition is vital in young children to ensure good outcomes. Researchers warned that good nutrition in the early life of a child is vital as it can impact the rest of their life, and, if neglected, can lead to stunted growth and obesity.

Image credit: Unsplash

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Health24.com | Study highlights heart-health issues for adults who were preemies

  • Before the 1970s, the survival rate of extremely preterm babies was below 10%
  • A new study studied changes during adult years in individuals who were born very preterm
  • It was found that the extremely premature group tended to develop more heart issues as adults

Erin Wegener was a tiny baby facing enormous challenges.

Born at 29 weeks’ gestation, she weighed only 1 pound, 14 ounces (0.5kg). Her first three months were lived in the neonatal intensive care unit. Family photos show her covered in gauze, sustained by too many tubes to count. Her entire hand just about fit inside her father’s wedding ring.

Her parents were warned she could face a lifetime of mental and physical challenges. But today, she’s working as a music therapist in the same hospital system in Grand Rapids, Michigan, where she was born.

The doctors’ most dire warnings didn’t come true, and her premature birth has never been much of a factor in her adult life. “I feel very thankful that I have not had a lot of health issues growing up,” she said.

Cardiovascular health score

Wegener was born in 1985, just a few years before breakthroughs in treatment allowed many more extremely low birth weight babies to survive. As that wave of children enters adulthood, a new study is revealing details about possible risks to their heart health.

Research published in the American Heart Association journal Hypertension compared cardiovascular health among two groups of Australians born in 1991 and 1992, as they turned 25 years old. The 165 participants in the first group were born extremely preterm (earlier than 28 weeks’ gestation) or with an extremely low birth weight (below 2.2 pounds). The 127 participants in the second group were born at term and at normal weights.

Researchers looked at several factors related to heart health and calculated a cardiovascular health score for each person. Overall, the extremely premature/low birth weight group had a less favourable rating than the term-born group, specifically for blood pressure, exercise capacity, fasting blood glucose (a marker of diabetes) and visceral abdominal fat (“belly fat”, which has been linked to heart disease, cancer and more).

It was known that people born early are prone to such problems, said the study’s lead author Dr Jeanie Cheong, a professor at the Royal Women’s Hospital in Melbourne, Australia. But the new research sought to tie the risks together for an overall view, she said. “We looked at all these factors cumulatively, rather than individually, thus providing a holistic view to health.”

Her work is part of the ongoing Victorian Infant Collaborative Study, which has been monitoring a group of Australians since their birth in 1991 or 1992. That’s the era when some treatments became widespread – such as corticosteroids for at-risk pregnant women to accelerate lung growth of babies in utero or using wetting-like agents called surfactants to treat immature lungs in premature babies.

Gender differences

Those treatments led to what Cheong called an exponential rise in survival over a short period for preemies. Before the 1970s, the survival rate of extremely preterm babies was below 10%, she said. By the early 1990s, that rate had soared to nearly 70%. It’s now at 87%, according to a separate study published recently in BMJ Open that Cheong led.

But the new study confirms other investigations about preemies’ long-term cardiovascular risk and adds details, said Dr Anne Monique Nuyt, a professor of paediatrics at the University of Montreal and head of neonatology at CHU Sainte-Justine hospital in Montreal. She was not involved in the new research.

“It’s one of the very first reports showing changes during adult years in individuals who were born very preterm.” Because they evaluated the participants at age 18, researchers discovered, for example, that the preterm group gained more weight between 18 and 25 than the normal birth weight group.

Nuyt, co-leader of a separate long-term study of premature infants, said the new work also confirmed earlier findings of gender differences in preemies’ future heart risks. Males scored worse for blood pressure, exercise tolerance and belly fat.

Cheong said the findings shouldn’t worry individuals born early. But “it is even more important for them to have close health surveillance and adopt healthy lifestyle choices, something that we all should do regardless,” she said.

Miracle of survival

The new study also showed the rate of smoking among former preemies is as high as in the general population, which Nuyt called worrisome. After all, many required oxygen right up until their parents took them home.

“We know smoking is very bad for the lungs. And it’s very bad for the heart, and it’s very bad for blood pressure. So if there’s one group that should not at all smoke, it’s these extremely low birth weight or extremely preterm individuals,” said Nuyt, who co-wrote a review paper published recently in Hypertension that called for greater awareness of the links between premature birth and heart problems.

“All physicians, all health care providers should be asking their patients, ‘Do you know your birth weight? Do you know whether you were born very tiny or very premature?'” she said.

Wegener, now 35, isn’t aware of any heart issues. And as the mother of three – with another baby due in April – she’s grateful for what she considers the miracle of her survival and long-term health. “I feel very fortunate.”

American Heart Association Newscovers heart and brain health. Not all views expressed in this story reflect the official position of the American Heart Association. Copyright is owned or held by the American Heart Association, Inc., and all rights are reserved. 

Image credit: iStock

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Health24.com | SEE | Smoking worsens Covid-19 infection in the airways, new study reveals

  • Several studies have found that smoking cigarettes increases the risk of severe Covid-19 and death 
  • However, until now, scientists haven’t fully understood how this happens
  • In a new study, UCLA researchers show how cigarette smoke blocks the first line of defence against infections

Since the early days of the pandemic, questions have been raised about the link between smoking and Covid-19, the disease caused by SARS-CoV-2.

In June this year, the World Health Organization stated that, based on existing literature assessing the association between smoking and Covid-19, there was “insufficient information to confirm any link between tobacco or nicotine in the prevention or treatment of Covid-19”.

However, more recent studies have shown that while smokers are not at risk of contracting infection, their risk of severe disease and death, once infected, is higher than that of non-smokers, although the ways that cigarette smoke exposure affects airway cell infection by SARS-CoV-2 have not been very clear.

A new study by scientists at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at the University of California has helped understand how this happens by investigating SARS-CoV-2 infection on a cellular and molecular level – using a model of airway tissue created from human cells.  

Their report was published in Cell Stem Cell.

The study

To perform their study, the scientists employed a platform known as an air-liquid interface culture. Essentially, this is grown from human airway stem cells and closely replicates how the airways behave and function in humans.

The airways carry air breathed in through the nose and mouth to the lungs, also functioning as the body’s first line of defence against airborne pathogens, such as viruses, the authors noted.

“Our model replicates the upper part of the airways, which is the first place the virus hits,” said Brigitte Gomperts, a professor of pulmonary medicine and member of the UCLA Jonsson Comprehensive Cancer Center.

“This is the part that produces mucus to trap viruses, bacteria and toxins and contains cells with finger-like projections that beat that mucus up and out of the body.”

This type of model, Gomperts explained, has previously been used to study lung diseases for over a decade and has been shown to mimic the changes in the airway that can be seen in someone that smokes.

‘Smoking cigarettes is like creating holes in these walls’

The air-liquid cultures used in the study were grown from airway stem cells that were taken from the lungs of five young, healthy, non-smoking tissue donors.

To replicate the effects of smoking, the researchers exposed these airway interface cultures to cigarette smoke for three minutes per day over four days.

They then infected the cultures exposed to cigarette smoke (along with identical cultures that had not been exposed) with live SARS-CoV-2 viruses.

The two groups were compared. In the models exposed to smoke, the researchers saw between two and three times more infected cells.

stem cell stem
Image source: UCLA Broad Stem Cell Research Center/Cell Stem Cell

A more in-depth analysis led to the conclusion that smoking resulted in more severe infection, at least in part, by blocking the activity of interferons (which play a critical role in the body’s early immune response to fight the virus).

“If you think of the airways like the high walls that protect a castle, smoking cigarettes is like creating holes in these walls,” Gomperts said.

“Smoking reduces the natural defences, and that allows the virus to set in.”

READ | Covid-19 deaths: Surprise findings on smoking and other insights from study of 17m patients

READ | Covid-19 is more severe in smokers, an analysis of 19 studies show

READ | Why the cigarette ban during lockdown? Five medical experts weigh in

Image: Basil MK/Pexels

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News24.com | SEE | Smoking worsens Covid-19 infection in the airways, new study reveals

  • Several studies have found that smoking cigarettes increases the risk of severe Covid-19 and death 
  • However, until now, scientists haven’t fully understood how this happens
  • In a new study, UCLA researchers show how cigarette smoke blocks the first line of defence against infections

Since the early days of the pandemic, questions have been raised about the link between smoking and Covid-19, the disease caused by SARS-CoV-2.

In June this year, the World Health Organization stated that, based on existing literature assessing the association between smoking and Covid-19, there was “insufficient information to confirm any link between tobacco or nicotine in the prevention or treatment of Covid-19”.

However, more recent studies have shown that while smokers are not at risk of contracting infection, their risk of severe disease and death, once infected, is higher than that of non-smokers, although the ways that cigarette smoke exposure affects airway cell infection by SARS-CoV-2 have not been very clear.

A new study by scientists at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at the University of California has helped understand how this happens by investigating SARS-CoV-2 infection on a cellular and molecular level – using a model of airway tissue created from human cells.  

Their report was published in Cell Stem Cell.

The study

To perform their study, the scientists employed a platform known as an air-liquid interface culture. Essentially, this is grown from human airway stem cells and closely replicates how the airways behave and function in humans.

The airways carry air breathed in through the nose and mouth to the lungs, also functioning as the body’s first line of defence against airborne pathogens, such as viruses, the authors noted.

“Our model replicates the upper part of the airways, which is the first place the virus hits,” said Brigitte Gomperts, a professor of pulmonary medicine and member of the UCLA Jonsson Comprehensive Cancer Center.

“This is the part that produces mucus to trap viruses, bacteria and toxins and contains cells with finger-like projections that beat that mucus up and out of the body.”

This type of model, Gomperts explained, has previously been used to study lung diseases for over a decade and has been shown to mimic the changes in the airway that can be seen in someone that smokes.

‘Smoking cigarettes is like creating holes in these walls’

The air-liquid cultures used in the study were grown from airway stem cells that were taken from the lungs of five young, healthy, non-smoking tissue donors.

To replicate the effects of smoking, the researchers exposed these airway interface cultures to cigarette smoke for three minutes per day over four days.

They then infected the cultures exposed to cigarette smoke (along with identical cultures that had not been exposed) with live SARS-CoV-2 viruses.

The two groups were compared. In the models exposed to smoke, the researchers saw between two and three times more infected cells.

stem cell stem
Image source: UCLA Broad Stem Cell Research Center/Cell Stem Cell

A more in-depth analysis led to the conclusion that smoking resulted in more severe infection, at least in part, by blocking the activity of interferons (which play a critical role in the body’s early immune response to fight the virus).

“If you think of the airways like the high walls that protect a castle, smoking cigarettes is like creating holes in these walls,” Gomperts said.

“Smoking reduces the natural defences, and that allows the virus to set in.”

READ | Covid-19 deaths: Surprise findings on smoking and other insights from study of 17m patients

READ | Covid-19 is more severe in smokers, an analysis of 19 studies show

READ | Why the cigarette ban during lockdown? Five medical experts weigh in

Image: Basil MK/Pexels

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Health24.com | Covid-19 collateral damage: When hand sanitisers become a double-edged sword

  • The rise in the use of alcohol-based hand sanitisers has increased the incidence of hand eczema
  • Hand eczema presents as a red itchy, sometimes burning or even tender, rash
  • Adequate skincare should, therefore, be prioritised, especially among healthcare workers

When Covid-19 started spreading across the globe, the World Health Organisation (WHO) and the Centers for Disease Control and Prevention recommended that the best way to prevent Covid-19 infection is through physical distancing, wearing cloth masks, as well as frequent and proper handwashing and surface decontamination. 

The call for regular handwashing led to an exponential rise in the use of alcohol-based hand sanitisers, which has increased the incidence of hand eczema in healthcare workers as well as the general population.

Two kinds of hand eczema

Hand eczema characteristically presents as a red itchy, sometimes burning or even tender, rash. The rash may be dry with cracked and scaly skin, or wet with blisters, oozing and crusting. Certain individuals, such as those with underlying atopic (a general disposition to develop) eczema, are at greater risk of developing alcohol rub hand eczema due to the inherent impaired barrier function of the skin characterising this condition. 

In a study from Hubei province in China, 434 healthcare workers were interviewed, with 321 (74%) reporting that they sanitise their hands more than 10 times per day. Of those healthcare workers, 246 (76.6%) reported symptoms of hand eczema, with the most common being irritant contact hand eczema and less commonly allergic contact hand eczema. 

Another study from Milan reported that from 9 March to 4 May 2020 there were 24 new cases of hand eczema in the general population related to the use of alcohol-based sanitisers.

Some of the issues with alcohol-based hand sanitisers include the use of non-standard formulae (meaning that methanol is used instead of ethanol); types of alcohol such as isopropyl alcohol vs. ethanol; as well as varying amounts of alcohol (<60%). The various recipes making the rounds on social media in the early days of lockdown illustrate this point. 

“Irritant” contact hand eczema may develop in anyone whose hands are exposed to irritants such as water, soap, or alcohol hand sanitisers. “Allergic” contact hand eczema, on the contrary,  will only develop in those who have been primed to develop skin irritation to certain substances such as nickel, latex or colophony (found in adhesives, cosmetics and printing ink).

Debilitating and painful disease

An intact skin usually deters from the development of the latter form of hand eczema. Irritants assist in disrupting the skin barrier, improving the likelihood of developing allergic contact hand eczema. 

Alcohol rub hand eczema can become a debilitating and painful disease, resulting in work absenteeism which can severely impair the delivery of essential services. The increased frequency of handwashing and use of alcohol hand sanitiser associated with Covid-19 prevention dramatically increases the likelihood of developing allergic contact hand eczema, which may greatly impact quality of life as well as cause occupational difficulties in the long run. 

Apart from the discomfort of dry, itchy skin, the breaks in the skin can serve as a point of entry for Covid-19 because of viral receptors in the blood vessels of the skin. Painful, dry skin could also inadvertently decrease hand hygiene compliance which further increases the risk of disease transmission in these individuals. Prevention is therefore essential. 

It has become clear that the Covid-19 pandemic will persist for the foreseeable future. Equally clear has been the gargantuan impact of this viral infection. Therefore, the importance of following protective guidelines, such as outlined by health and government organisations, is undeniable and should be closely adhered to.  

The WHO has recommended a 60% alcohol-containing hand sanitiser with 1.45% glycerol as a moisturising agent to protect healthcare workers, and now the frequently sanitising public, from the complications of excessive alcohol hand rub usage. The minimum amount of glycerol required to decrease the risk of hand eczema is not known, although studies have shown that even lower levels than the recommended 1.45% glycerol were effective to protect the skin from excessive drying.

Moisturisers few and far between

Further recommendations include the use of an emollient-containing hand cream immediately after sanitising. Although this is a useful measure to prevent alcohol rub dermatitis, one study showed that only approximately one in five healthcare workers did so after using alcohol hand rub. This figure is highly unlikely to be higher among the general public. 

Sanitising stations are located everywhere in hospitals and public areas and have been an important means of combating the spread of Covid-19. However, moisturisers are few and far between, hence the increased incidence of alcohol rub hand eczema during the pandemic.

Adequate skin care could increase hand hygiene compliance and should therefore be prioritised, especially among healthcare workers. Furthermore, preventative measures are critical to allay the next, albeit completely different wave, that of allergic contact hand eczema – another unintended health consequence of Covid-19. 

*Dr Suretha Kannenberg is a Consultant Dermatologist in the Division of Dermatology at Stellenbosch University. Sergio Alves and Allison Arendse are 5th-year medical students in the same division. This is a revised version of their article recently published in the South African Medical Journal.

Image credit: Unsplash

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