Category: COVID

Which Entryway a Coronavirus Uses Affects its Infection Severity

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Until now, the reason why some coronaviruses such as SARS-CoV-2 affect humans more severely than other seasonal ones has eluded scientists. Now, results published in Nature have provided a piece of the puzzle by identifying a gateway used by the seasonal coronavirus HKU1 to enter human cells. HKU1 binds to a different receptor than SARS-CoV-2, which may partly explain the difference in severity between these two coronaviruses.

Receptors provide a useful means of figuring out coronavirus transmissibility and pathology as part of surveillance work on viral evolution. Seven coronaviruses are known for their ability to infect humans. Four of these are generally mild: HKU1, 229E, NL63 and OC43, while the other three are more pathogenic: SARS-CoV-1, Mers-CoV and SARS-CoV-2.

The HKU1 virus was first identified in an elderly patient with severe pneumonia in Hong Kong in 2005. Like SARS-CoV-2, HKU1 mainly infects upper respiratory tract cells. However, it rarely affects the bronchi and alveoli in the lungs. The HKU1 virus causes colds and other mild respiratory symptoms. Complications may also occur, including severe respiratory tract infections, particularly in young children, the elderly and immunocompromised individuals. It is estimated that 70% of children are infected before the age of 6. In total, 75 to 95% of the global population has been exposed to HKU1, which is comparable to other seasonal human coronaviruses.

At the cellular level, coronavirus spike proteins are cleaved after binding to their receptors. This cleavage phenomenon is vital for viral fusion, entry and multiplication. Some coronaviruses (SARS-CoV-2 and NL63) use the ACE2 receptor as a gateway for entering cells. Until now, HKU1 and OC43 were the only coronaviruses with unknown receptors.

Through collaboration between scientists at eight Institut Pasteur units, it was possible to identify the TMPRSS2 enzyme as the receptor to which HKU1 binds to enter cells. Once binding has occurred, TMPRSS2 triggers fusion of HKU1 with the cell, leading to viral infection. Through a combination of techniques performed in vitro and in cell culture, the scientists demonstrated that the TMPRSS2 receptor has high affinity with the HKU1 spike, which is not the case for SARS-CoV-2.

“Once a receptor has been identified for a virus, it is possible to characterise target cells more accurately, while also gaining insights on viral entry and multiplication mechanisms and infection pathophysiology,” comments, Olivier Schwartz, co-last author of the study and Head of the Institut Pasteur’s Virus and Immunity unit.

“Our findings also shed light on the various evolution strategies employed by coronaviruses, which use TMPRSS2 either to bind to target cells or trigger fusion and viral entry,” adds Julian Buchrieser, co-last author of the study and scientist in the Institut Pasteur’s Virus and Immunity unit.

These human-pathogenic viruses’ use of different receptors probably affects their degree of severity. Receptor levels vary among respiratory tract cells, thus influencing the sensitivity of cells to infection and viral spread. Once the route of viral entry into cells is known, it should also be possible to fight infection more effectively by developing targeted therapies and assess the risk of virulence posed by any future emerging coronaviruses.

In parallel with this work, Institut Pasteur teams led by Pierre Lafaye and Felix Rey have developed and characterised nano-antibodies (very small antibodies) that inhibit HKU1 infection by binding to the TMPRSS2 receptor. These reagents have been patented for potential therapeutic activities.

Source: Institut Pasteur

Study Finds Urological Effects of SARS-CoV-2 Infection in Men

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A study published in the Journal of Internal Medicine indicates that SARS-CoV-2 infection may worsen lower urinary tract symptoms (LUTS) in men. The study researchers found that a enlarged prostate as a result of COVID was involved.

The study included 17 986 men receiving medication for LUTS within the public healthcare system of Hong Kong in 2021–2022, half of whom had SARS-CoV-2 infection. The group with SARS-CoV-2 had significantly higher rates of retention of urine (4.55% versus 0.86%); blood in the urine (1.36% versus 0.41%); clinical urinary tract infection (4.31% versus 1.49%); bacteria in the urine (9.02% versus 1.97%); and addition of 5-alpha reductase inhibitors, which are drugs prescribed for enlarged prostate. (0.50% versus 0.02%). These urological manifestations occurred regardless of COVID severity.

The findings might relate to the presence of certain proteins targeted by SARS-CoV-2 that are known to be expressed in the prostate.

“We are excited to be the first to report the effects of COVID on complications of benign prostatic hyperplasia – or enlarged prostate – and also demonstrate the alarming extent of its urological effects,” said corresponding author Alex Qinyang Liu, MD, of Prince of Wales Hospital, in Hong Kong.

Source: Wiley

Not Just ‘Long COVID’: Researchers Find ‘Long Colds’

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A new study from Queen Mary University of London, published in The Lancet’s EClinicalMedicine, has found that people may experience long-term symptoms, termed ‘long colds’, after non-COVID acute respiratory infections.

The ‘long cold’s’ most common symptoms included coughing, stomach pain, and diarrhoea more than four weeks after the initial infection. While the severity of an illness appears to be a key driver of risk of long-term symptoms, just why some people suffer extended symptoms while others do not is a focus of further research.

The findings suggest that there may be long-lasting health impacts following non-COVID acute respiratory infections such as colds, influenza, or pneumonia, that are currently going unrecognised. However, the researchers do not yet have evidence suggesting that the symptoms have the same severity or duration as long COVID.

The research compared the prevalence and severity of long-term symptoms after an episode of COVID versus an episode of another acute respiratory infection that tested negative for COVID. Those recovering from COVID were more likely to experience light-headedness or dizziness and problems with taste and smell compared to those who had a non-COVID respiratory infection.

While long COVID is now a recognised condition, there have been few studies comparing long-term symptoms following SARS-CoV-2 coronavirus infection versus other respiratory infections.

The study is the latest output from COVIDENCE UK, Queen Mary University of London’s national study of COVID, launched back in 2020 and still in follow-up, with over 19 000 participants enrolled. This study analysed data from 10 171 UK adults, with responses collected via questionnaires and statistical analysis carried out to identify symptom clusters.

Giulia Vivaldi, researcher on COVIDENCE UK from Queen Mary University of London and the lead author of the study, said: “Our findings shine a light not only on the impact of long COVID on people’s lives, but also other respiratory infections. A lack of awareness – or even the lack of a common term – prevents both reporting and diagnosis of these conditions.

“As research into long COVID continues, we need to take the opportunity to investigate and consider the lasting effects of other acute respiratory infections.

“These ‘long’ infections are so difficult to diagnose and treat primarily because of a lack of diagnostic tests and there being so many possible symptoms. There have been more than 200 investigated for long COVID alone.”

Source: Queen Mary University of London

Does COVID Infection or Vaccination Worsen Migraines?

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Headaches are a frequent complaint of those with a COVID infection, or have received a COVID vaccination, and it is thought that it may subsequently increase the frequency of migraines. To put this to the test, an observational study published in the European Journal of Neurology investigated the effects on migraine frequency of having had either been infected with COVID or having received a COVID vaccination.

Among 550 adults who had received migraine-related care at a Spanish headache clinic, 44.9% (247) reported COVID at least once and 83.3% (458) had been vaccinated; 61 patients (24.7%) reported migraine worsening since COVID and 52 (11.4%) since vaccination.

In participants who perceived that their migraines worsened, those who had been infected were 2.5-times more likely to be concerned about migraine worsening and patients who had been vaccinated were 17.3-times more likely to have this concern.

When investigators examined patients’ e-diary information, they observed no significant difference in headache frequency one month before and after infection or vaccination, even when comparing patients with and without self-reported migraine worsening.

“In the case of COVID-19, we reported previously that indeed headache is a frequent and disabling symptom of the infection; yet, it may not necessarily be linked to an increase in migraine frequency,” the authors wrote. “In light of our results, we believe that clinicians should deliver to patients a more reassuring message that COVID-19 and COVID-19 vaccines may marginally affect migraine course and that probably the impact of the infection and vaccines is less than the individual rhythmicity to have attacks. This information may help minimise their worry.”

Source: Wiley

New SARS-CoV-2 Variant BA.2.86 not as Resistant to Antibodies as First Feared

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Researchers studying the new SARS-CoV-2 variant BA.2.86 have found that the new variant was not significantly more resistant to antibodies than several other circulating variants. Their study, published in The Lancet Infectious Diseases, also showed that antibody levels to BA.2.86 were significantly higher after a wave of XBB infections compared to before, suggesting that the vaccines based on XBB should provide some cross-protection to BA.2.86.

The recently emerged BA.2.86 is very different from any other currently circulating variants. It includes many mutations in the spike gene, reminiscent of the emergence of Omicron.  The virus uses the viral spike to infect cells and is the main target for our antibodies.  When the spike mutates, it comes with the risk that our antibodies are less effective against this new ‘variant’, and therefore that our protection from infection is reduced and that vaccines may need to be updated.

“We engineered a spike gene that matches that of the BA.2.86 variant and tested the blood of Stockholm blood donors (specifically those donations made very recently) to see how effective their antibodies are against this new variant. We found that although BA.2.86 was quite resistant to neutralising antibodies, it wasn’t significantly more resistant than a number of other variants that are also circulating”, says Daniel Sheward, lead author of the study and Postdoctoral researcher in Benjamin Murrell’s team at Karolinska Institutet.

An important question is whether upcoming updated vaccines that are based on the XBB variant will boost protection against BA.2.86.  To determine whether antibodies triggered by infection with XBB may be effective against this new variant, Ben Murrell’s team also compared samples taken before and after XBB spread in Sweden.

“We also found that antibody levels to BA.2.86 were significantly higher after a wave of XBB infections compared to before, suggesting that the vaccines based on XBB should provide some cross-protection to BA.2.86. However, BA.2.86 was resistant to all available monoclonal antibody therapeutics that we tested,” says Daniel Sheward.

Public health agencies need to know what the current level of immunity to this new variant is, and whether the vaccines are sufficient must be updated.  Monoclonal antibodies also represent an important option for some patient groups, such as the immunocompromised – for the clinicians, it’s important to know which if any, monoclonal antibody therapeutics will be effective against the variants that are circulating.  

“I think the main message is that there is currently no reason to be alarmed over this new variant and that it’s probably a good idea to get a booster vaccine when they are offered.  However, another ‘omicron-like’ event is also a reminder that we shouldn’t get complacent”, says Benjamin Murrell, Principal researcher at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet.

Source: Karolinska Institutet

Study Explains a Link between COVID and Increased Cardiovascular Risk

Source: Wikimedia CC0

A study published in the journal Nature Cardiovascular Research shows that SARS-CoV-2 can directly infect the arteries of the heart and cause the fatty plaque inside arteries to become highly inflamed, increasing the risk of heart attack and stroke. The findings may help explain why certain people who get COVID have a greater chance of developing cardiovascular disease, or if they already have it, develop more heart-related complications.

In the National Institutes of Health (NIH)-funded study, researchers focused on older people with atherosclerotic plaque, who died from COVID. However, because the researchers found the virus infects and replicates in the arteries no matter the levels of plaque, the findings could have broader implications for anybody who gets COVID.

“Since the early days of the pandemic, we have known that people who had COVID have an increased risk for cardiovascular disease or stroke up to one year after infection,” said Michelle Olive, PhD, acting associate director of the Basic and Early Translational Research Program at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH. “We believe we have uncovered one of the reasons why.”

Though previous studies have shown that SARS-CoV-2 can directly infect tissues such as the brain and lungs, less was known about its effect on the coronary arteries. Researchers knew that after the virus reaches the cells, the body’s immune system sends in macrophages to help clear the virus. In the arteries, macrophages also help remove cholesterol, and when they become overloaded with cholesterol, they morph into a specialised type of cell called foam cells.

The researchers thought that if SARS-CoV-2 could directly infect arterial cells, the macrophages that normally are turned loose might increase inflammation in the existing plaque, explained Chiara Giannarelli, MD, PhD, associate professor in the departments of medicine and pathology at New York University’s Grossman School of Medicine and senior author on the study. To test their theory, Giannarelli and her team took tissue from the coronary arteries and plaque of people who had died from COVID and confirmed the virus was in those tissues. Then they took arterial and plaque cells – including macrophages and foam cells – from healthy patients and infected them with SARS-CoV-2 in a lab dish. They found that the virus had also infected those cells and tissues.

Additionally, the researchers found that when they compared the infection rates of SARS-CoV-2, they showed that the virus infects macrophages at a higher rate than other arterial cells. Cholesterol-laden foam cells were the most susceptible to infection and unable to readily clear the virus. This suggested that foam cells might act as a reservoir of SARS-CoV-2 in the atherosclerotic plaque. Having more build-up of plaque, and thus a greater number of foam cells, could increase the severity or persistence of COVID.

The researchers then looked at the predicted inflammation in the plaque after infecting it with the virus. They observed the release of inflammatory cytokines, also known to promote the formation of even more plaque. The cytokines were released by infected macrophages and foam cells. The researchers said this may help explain why people who have underlying plaque buildup and then get COVID may have cardiovascular complications long after getting the infection.  

“This study is incredibly important as it adds to the larger body of work to better understand COVID,” said Olive. “This is just one more study that demonstrates how the virus both infects and causes inflammation in many cells and tissues throughout the body. Ultimately, this is information that will inform future research on both acute and Long COVID.”

Though the findings conclusively show that SARS-CoV-2 can infect and replicate in the macrophages of plaques and arterial cells, they are only relevant to the original strains of SARS-CoV-2 that circulated in New York City between May 2020 and May 2021. The study was conducted in a small cohort of older individuals, all of whom had atherosclerosis and other medical conditions; therefore, the results cannot be generalised to younger, healthy individuals.

Source: National Institutes of Health

‘Long COVID’ Risks are Inflated by Flawed Research, Reviewers Find

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‘Long COVID’ is a mysterious constellation of symptoms associated with having recovered from COVID infection – but how many cases represent a true condition, and how many fall under a poorly-defined umbrella of currently known ones? Overly broad definitions, a lack of appropriate, or any, comparison groups, among other things, in studies looking at the epidemiology of the condition have distorted the risks, say the authors of a review published in BMJ Evidence-based Medicine.

This is further compounded by inclusion of poorly conducted studies into systematic reviews and pooled data analyses that end up overstating the risk yet again, they add. 

Likely consequences include increased public anxiety and healthcare spend; misdiagnoses; and diversion of funds from those who really do have other long term conditions secondary to COVID infection, suggest the researchers.

Many after-effects of COVID infection include post-ICU syndrome, which is a constellation of health issues that are present when the patient is in intensive care and which persist after discharge home, and shortness of breath following pneumonia. The trouble is that these are common to many upper respiratory viruses, the researchers point out.

None of the working definitions of ‘long COVID’ used by influential health bodies, such as the US Centers for Disease Control and Prevention, the World Health Organization, the UK National Institute for Health and Care Excellence (NICE), Scottish Intercollegiate Guidelines Network (SIGN), and the Royal College of General Practitioners requires a causal link between SARS-CoV2 and a range of symptoms. 

Not only should comparator (control) groups be included in ‘long COVID’ studies, when they often aren’t, but they should also be properly matched to cases, ideally by age, sex, geography, socioeconomic status and, if possible, underlying health and health behaviours, which they rarely are, say the researchers.

During the early stages of the pandemic, when SARS-CoV-2 testing wasn’t widely available, studies were more likely to include a non-representative sample of SARS-CoV-2-positive patients by including fewer patients with mild or no symptoms.

This is known as sampling bias, which occurs when certain members of a population have a higher probability of being included in a study sample than others, potentially limiting the generalisability of a study’s findings, explain the researchers.

“Our analysis indicates that, in addition to including appropriately matched controls, there is a need for better case definitions and more stringent [‘long COVID’] criteria, which should include continuous symptoms after confirmed SARS-CoV-2 infection and take into consideration baseline characteristics, including physical and mental health, which may contribute to an individual’s post COVID experience, “ they write, adding that the umbrella term ‘long COVID’ should be jettisoned in favour of different terms for specific after effects.

While the results of high quality population studies on ‘long COVID’ in adults and children have been reassuring, they point out,  the body of research “is replete with studies with critical biases” they add, setting out common pitfalls.

“Ultimately, biomedicine must seek to aid all people who are suffering. In order to do so, the best scientific methods and analysis must be applied. Inappropriate definitions and flawed methods do not serve those whom medicine seeks to help,” they insist.

“Improving standards of evidence generation is the ideal method to take long COVID seriously, improve outcomes, and avoid the risks of misdiagnosis and inappropriate treatment,” they include.

Source: EurekAlert!

From Molecule to the Shelf

Bada Pharasi, CEO of The Innovative Pharmaceutical Association of South Africa (IPASA)

Lessons from the COVID-19 pandemic have underlined the importance of continued investment into pharmaceutical innovation and R&D to not only bring life-saving medications to those in need, but to improve public health outcomes, writes Bada Pharasi, CEO of The Innovative Pharmaceutical Association of South Africa (IPASA).

From treatments for cancer, cardiovascular diseases and more recently, the COVID-19 vaccine, the pharmaceutical industry has made significant progress in the development of over 470 medications in the last 10 years alone.1

While the innovative pharmaceutical process typically takes between 10 and 15 years from discovery to regulatory approval2 – owing to factors including immense R&D costs, regulatory compliance, and the protection of patents3 – the fast-tracked development and approval of COVID-19 vaccines laid bare the need for pharmaceutical companies to be prepared to mitigate the risk of future outbreaks – and this means continued investment in innovation and R&D.

The pandemic underlined the need for countries to be prepared for outbreaks on the horizon. To ensure we can meet the next challenge, pharmaceutical innovations must match the pace at which diseases mutate. This kind of innovation is non-negotiable and requires continued investment as a safeguard against losing lives and endangering South Africa’s fragile healthcare system.

As we are in the midst of a cholera epidemic, as well as the recent measles outbreak,4 it’s important to continue driving innovation to treat diseases, with medicines developed by innovative pharmaceutical companies benefiting millions across the country every day.

This is evidenced by mortality rates for HIV/AIDS and TB in the country falling by 59.2% and 55.7% between 2007 and 2017, with at least 60 new medicines currently in the R&D pipeline to treat TB.5

While patents in pharmaceutical innovation protect the originators’ intellectual property, it is important that innovative medications be developed to ensure a continuous pipeline of access to generics once the patent has lost its exclusivity. This will drive consumer accessibility and affordability of life-saving treatments and medications that may otherwise be unattainable for many.

As we continue racing against the proverbial clock in protecting against current and future diseases, pharmaceutical companies should continue to invest in innovation and R&D to outsmart existing dreaded diseases, and provide agility and preparedness should the next unknown pandemic threaten. Our health, and lives, depend on it.

References:
1. #AlwaysInnovating: The pharmaceutical innovation journey [Internet]. IFPMA. 2023 [cited 2023 Jun 28]. Available from: https://www.ifpma.org/initiatives/alwaysinnovating/
2. Derep M. What’s the average time to bring a drug to market in 2022? [Internet]. N-SIDE; 2022 [cited 2023 Jun 28]. Available from: https://lifesciences.n-side.com/blog/what-is-the-average-time-to-bring-a-drug-to-market-in-2022
3. Ancliff S. 10 challenges facing the pharmaceutical industry in 2024 [Internet]. [cited 2023 Jun 29]. Available from: https://blog.i-nexus.com/10-challenges-facing-the-pharmaceutical-industry
4. Yoganathan V. Prepare for more pandemics in the future, experts warn [Internet]. Juta MedicalBrief. Medical Brief; 2023 [cited 2023 Jun 30]. Available from: https://www.medicalbrief.co.za/prepare-for-more-pandemic-in-the-future-experts-warn/
5. South Africa – the innovative hub for pharmaceutical development [Internet]. B2B Central. New Media; 2021 [cited 2023 Jun 29]. Available from: https://www.b2bcentral.co.za/why-south-africa-is-an-innovation-hub-for-pharmaceuticals/

Long COVID’s ‘Blue Legs’ Syndrome in Need of Greater Awareness

An unusual case of a Long Covid patient’s legs turning blue after 10 minutes of standing highlights the need for greater awareness of this symptom among people with the condition, according to new research published in the Lancet.

The paper, authored by Dr Manoj Sivan at the University of Leeds, focuses on the case of one 33-year man who developed with acrocyanosis – venous pooling of blood in the legs.

A minute after standing, the patient’s legs began to redden and became increasingly blue over time, with veins becoming more prominent. After 10 minutes the colour was much more pronounced, with the patient describing a heavy, itchy sensation in his legs. His original colour returned two minutes after he returned to a non-standing position.

The patient said he had started to experience the discolouration since his COVID-19 infection. He was diagnosed with postural orthostatic tachycardia syndrome (POTS), a condition that causes an abnormal increase in heart rate on standing.

Dr Sivan, Associate Clinical Professor and Honorary Consultant in Rehabilitation Medicine in the University of Leeds’ School of Medicine, said: “This was a striking case of acrocyanosis in a patient who had not experienced it before his COVID-19 infection.

“Patients experiencing this may not be aware that it can be a symptom of Long Covid and dysautonomia and may feel concerned about what they are seeing. Similarly, clinicians may not be aware of the link between acrocyanosis and Long Covid.

“We need to ensure that there is more awareness of dysautonomia in Long Covid so that clinicians have the tools they need to manage patients appropriately.”

Long Covid affects multiple systems in the body and has an array of symptoms, affecting patients’ ability to perform daily activities. The condition also affects the autonomic nervous system, which is responsible for regulating blood pressure and heart rate.

Acrocyanosis has previously been observed in children with dysfunction of the autonomic nervous system (dysautonomia), a common symptom of post-viral syndromes.

Previous research by Dr Sivan’s team has shown that both dysautonomia and POTS frequently develop in people with Long Covid.

Dysautonomia is also seen in a number of other long-term conditions such as Fibromyalgia and Myalgic Encephalomyelitis, also known as Chronic Fatigue Syndrome or ME.

Dr Sivan said: “We need more awareness about dysautonomia in long term conditions; more effective assessment and management approaches, and further research into the syndrome. This will enable both patients and clinicians to better manage these conditions.”

The research is the latest work by the team in the field of autonomic medicine. Other developments include a home test for people with symptoms of autonomic dysfunction in conditions such as long COVID, chronic fatigue syndrome, fibromyalgia, and diabetes 1 and 2, where people experience dizziness or blackouts.

Source: University of Leeds

Wristbands a Breeding Ground for Bacteria, Including E. Coli

Photo by Jonathan Borba on Unsplash

The COVID pandemic took disinfecting to new heights. Now, a new study has uncovered a niche for bacteria to colonise: despite being worn daily, routine cleaning of wristbands is generally overlooked or simply ignored. Researchers from Florida Atlantic University tested wristbands of various materials to determine their risk for harbouring potentially harmful pathogenic bacteria, and found that plastic and rubber bands had a particularly high load, especially if worn at the gym.

For the study, researchers tested plastic, rubber, cloth, leather and metal (gold and silver) wristbands to see if there is a correlation between wristband material and the prevalence of bacteria. They investigated the hygienic state of these various types of wristbands worn by active individuals and identified the best protocols to properly disinfect them.

Using standard microbiological assays, researchers looked at bacterial counts, type of bacteria and their distribution on the wristband surfaces. They also conducted a bacteria susceptibility assay study screening the effectiveness of three different disinfectant solutions: Lysol™ Disinfectant Spray; 70% ethanol, commonly used in hospitals and alcohol wipes; and a more natural solution, apple cider vinegar.

Results of the study, published in the journal Advances in Infectious Diseases, suggest you stick with the ‘gold standard’ or at least silver the next time you purchase a wristband. Nearly all wristbands (95%) were contaminated. However, rubber and plastic wristbands had higher bacterial counts, while metal ones, especially gold and silver, had little to no bacteria.

“Plastic and rubber wristbands may provide a more appropriate environment for bacterial growth as porous and static surfaces tend to attract and be colonissd by bacteria,” said Nwadiuto Esiobu, PhD, senior author and a professor of biological sciences in the Charles E. Schmidt College of Science.

The most important predictor of wristband bacteria load was the texture of wristband material and activity (hygiene) of the subject at sampling time. There were no significant differences between males and females in the occurrence or distribution of the bacteria groups.

Intestinal organisms of the genera Escherichia, specifically E. coli. Staphylococcus spp was prevalent on 85% of the wristbands; researchers found Pseudomonas spp on 30% of the wristbands; and they found E. coli bacteria on 60% of the wristbands, which most commonly begins infection through faecal-oral transmission.

The gym-goer showed the highest staphylococcal counts, which emphasises the necessity of sanitising wristbands after engaging in rigorous activity at the gym or at home.

“The quantity and taxonomy of bacteria we found on the wristbands show that there is a need for regular sanitation of these surfaces,” said Esiobu. “Even at relatively low numbers these pathogens are of public health significance. Importantly, the ability of many of these bacteria to significantly affect the health of immunocompromised hosts indicates a special need for health care workers and others in hospital environments to regularly sanitize these surfaces.”

Findings from the study showed that Lysol™ Disinfectant Spray and 70% ethanol were highly effective regardless of the wristband material with 99.99% kill rate within 30 seconds. Apple cider vinegar was not as potent and required a full two-minute exposure to reduce bacterial counts. While these common household disinfectants all proved at least somewhat effective on all materials (rubber, plastic, cloth and metal), antibacterial efficacy was significantly increased at two minutes compared to thirty seconds.

Different disinfectants, depending on their active ingredients, kill bacteria in different ways, such as by disrupting cell membrane integrity, altering or removing proteins or interfering with metabolic activities.

“Other potential forms of bacterial transmission and facilitation of infection, such as earbuds or cell phones, should be similarly studied,” said Esiobu.

Source: Florida Atlantic University