Category: Diseases, Syndromes and Conditions

Categories : Diseases, Syndromes and ConditionsTags :

What Time at Night a Malaria Mosquito Bites Impacts Infection

On By ModernMedia
Photo by Ekamelev on Unsplash

Researchers have discovered that what time of the night a malaria-bearing mosquito bites may have significant effect on the subsequent infection’s severity.

When mice are infected in the middle of the night with the parasites causing cerebral malaria, the symptoms of the disease are less severe than for those inflected during the day, and the spread of the parasites within the hosts is more limited, research teams from McGill University, the Douglas Research Centre and the Research Institute of the McGill University Health Centre have discovered.

Malaria is a mosquito-borne infectious disease that affects hundreds of millions of people worldwide. It kills more than half a million people each year, most of them children. Cerebral malaria is the deadliest form of the disease.

The researchers’ findings, published in the journals iScience and ImmunoHorizons, have the potential to lead to new treatment practices based on aligning medication with our circadian rhythms.

How circadian rhythms of host and parasite interact

Circadian rhythms are defined as physiological and behavioral oscillations with cycles of approximately 24 hours, matching the Earth’s rotation, that persist in the absence of environmental timing cues. These rhythms are regulated by a master clock in the brain, as well as by clocks located in most other organs and cell types throughout the organism.

“We explored how the circadian rhythms of both the host and the malaria parasite interact to affect the severity of the disease and the host’s ability to fight off the parasite,” said Priscilla Carvalho Cabral, a recent McGill PhD graduate who carried out the experiments described in two recent studies on the subject.

Nicolas Cermakian, Director of the Laboratory of Molecular Chronobiology, and the corresponding author of the two studies, noted, “The difference in a host’s response to infection depending on the time of day suggests that their circadian rhythms could be influencing the progression of the disease. How such immune clocks impact malaria has not been looked at before.”

An important advance in knowledge

In parasites and their animal hosts, as well as in most living organisms, many bodily functions are under circadian control. It is known, for instance, that the replication of malaria parasites inside the red blood cells of a host follows a daily rhythm. Previous work from the same team has already shown that another serious parasitic disease, leishmaniasis, is affected by host clocks: the time of infection influences the replication of the parasite as well as the immune response to it. In the new studies, the same was found to be true for cerebral malaria.

“Our results represent an important advance in knowledge since many of the mechanisms driving the rhythms in susceptibility to diseases, especially parasitic diseases, remain largely unknown,” says Martin Olivier, Director of the Laboratory for the Study of Host-Parasite Interaction, a professor in McGill’s Department of Microbiology and Immunology and co-author of the two studies.

Source: McGill University

Categories : Diseases, Syndromes and ConditionsTags :

Kidney Damage in Lupus Comes from an Unexpected Source

On By ModernMedia
When the NKp46 receptor of the ILCs is blocked (right), the lupus nephritis recedes. Blue: cell nuclei.
Credit: Charité | Frauke Schreiber

A Berlin-led research team has uncovered critical regulators of severe kidney damage in patients with the autoimmune disorder lupus. A small, specialised population of immune cells – called innate lymphoid cells (ILCs) – trigger an avalanche of effects that cause harmful kidney inflammation, also known as lupus nephritis.

The research, published this week in Nature, upends conventional wisdom that autoantibodies are primarily responsible for lupus nephritis.

“While autoantibodies are required for tissue damage, they are by themselves not sufficient. Our work reveals that ILCs are required to amplify the organ damage,” says Dr Masatoshi Kanda, a senior paper author who was a Humboldt Fellow at Max Delbrück Center and is now at the Department of Rheumatology and Clinical Immunology, Sapporo Medical University in Japan.

Lupus, or systemic lupus erythematosus, is most often diagnosed between the ages of 15 and 45. Symptoms can range from mild to severe. But what causes kidney damage in some patients – some to the point of requiring dialysis – has been unclear.

“The role of ILCs in lupus or lupus nephritis was entirely unknown,” says Professor Antigoni Triantafyllopoulou, a senior paper author at the German Rheumatology Research Center (DRFZ), an institute of the Leibniz Association, and at the Department of Rheumatology and Clinical Immunology at Charité – Universitätsmedizin Berlin. “We have now identified most of the circuit controlled by ILCs by looking at the whole kidney at single-cell resolution.”

Unusual immune cells

ILCs are a small group of immune cells that – unlike most other immune cells that circulate throughout the body – live in a specific tissue or organ.

“They are in the tissue all the time, from the time of embryonic development, which makes them very different from other immune cells,” says Professor Andreas Diefenbach, a senior paper author and director of the Institute of Microbiology, Infectious Diseases and Immunology at Charité – Universitätsmedizin Berlin.

Diefenbach’s lab was among those that discovered ILCs in the mid-2000s. Most of his research is focused on ILCs in the gut and how they modify tissue function. In this study, Triantafyllopoulou and Kanda teamed up with his group and Dr Mir-Farzin Mashreghi at the DRFZ to find out whether ILCs were present in the kidney and what role they might play in lupus nephritis.

The whole single-cell picture

To unravel this mystery, the team turned to single-cell RNA sequencing, which identifies genes that are active, or “switched on,” in individual cells and helps researchers understand the cell’s identity and function.

Kanda, a rheumatologist who was studying bioinformatics in Professor Norbert Hübner’s lab at the Max Delbrück Center at the time, developed a specialized protocol for single-cell RNA sequencing of mouse and human kidneys. “Masatoshi’s protocol was very good at pulling out and preserving multiple types of kidney cells, which gave us a much more complete overview of how lupus affects the whole kidney,” explains Triantafyllopoulou. The team sequenced nearly 100 000 individual kidney and immune cells of various types and functions.

The key receptor

Through experiments in mice, the team learned that a subgroup of ILCs with a receptor called NKp46 must be present and activated to cause lupus nephritis. When NKp46 is activated, this subgroup of cells ramped up production of a protein called GM-CSF, which stimulates invading macrophages to multiply. In the kidney, a flood of incoming macrophages caused severe tissue damage and fibrosis.

“These ILCs are really amplifiers in this system,” Diefenbach says. “They are small in population, but they seem to fertilise the whole process.”

When the team blocked NKp46 with antibodies or the receptor was genetically removed, kidney tissue damage was minimal. They also blocked GM-CSF with similar anti-inflammatory effects.

“Critically, autoantibody levels did not change when NKp46 was inhibited, but kidney tissue damage was reduced, which shows autoantibodies are not directly responsible for kidney inflammation,” Triantafyllopoulou explains.

The team also compared the results to sequencing data from tissue taken from human patients with lupus and found ILCs present, though more work is required to fully understand how to target ILCs in human kidneys. Nevertheless, the insights gained through these detailed studies point to new antibody therapies for patients with severe forms of lupus. The hope is to prevent the need for kidney dialysis in these patients.

Source: Max Delbrück Center for Molecular Medicine in the Helmholtz Association

Categories : Diseases, Syndromes and Conditions Neurodegenerative DiseasesTags :

Shingles Increases Risk of Cognitive Decline in Later Life

On By ModernMedia

The risk was higher for men who were carriers of a gene linked to dementia

Photo by Mari Lezhava on Unsplash

A new study led by investigators from Brigham and Women’s Hospital found that an episode of shingles is associated with about a 20 percent higher long-term risk of subjective cognitive decline. The study’s findings provide additional support for getting the shingles vaccine to decrease risk of developing shingles, according to the researchers. Their results are published in Alzheimer’s Research & Therapy.

“Our findings show long-term implications of shingles and highlight the importance of public health efforts to prevent and promote uptake of the shingles vaccine,” said corresponding author Sharon Curhan, MD, of the Channing Division for Network Medicine at Brigham and Women’s Hospital. “Given the growing number of Americans at risk for this painful and often disabling disease and the availability of a very effective vaccine, shingles vaccination could provide a valuable opportunity to reduce the burden of shingles and possibly reduce the burden of subsequent cognitive decline.”

Shingles, medically known as “herpes zoster,” is a viral infection that often causes a painful rash. Shingles is caused by the varicella zoster virus (VZV), the same virus that causes chickenpox. After a person has chickenpox, the virus stays in their body for the rest of their life. Most of the time, our immune system keeps the virus at bay. Years and even decades later, the virus may reactivate as shingles.

Almost all individuals in the US age 50 years and older have been infected with VZV and are therefore at risk for shingles. There’s a growing body of evidence that herpes viruses, including VZV, can influence cognitive decline. Subjective cognitive decline is an individual’s self-perceived experience of worsening or more frequent confusion or memory loss. It is a form of cognitive impairment and is one of the earliest noticeable symptoms of Alzheimer’s disease and related dementias.

Previous studies of shingles and dementia have been conflicting. Some research indicates that shingles increases the risk of dementia, while others indicate there’s no association or a negative association. In recent studies, the shingles vaccine was associated with a reduced risk of dementia.

To learn more about the link between shingles and cognitive decline, Curhan and her team used data from three large, well-characterized studies of men and women over long periods: The Nurses’ Health Study, the Nurses’ Health Study 2, and the Health Professionals Follow-Up Study. The study included 149,327 participants who completed health status surveys every two years, including questions about shingles episodes and cognitive decline. They compared those who had shingles with those who didn’t.

Curhan designed the study with first author Tian-Shin Yeh, formerly of the Harvard TH Chan School of Public Health. The researchers found that a history of shingles was significantly and independently associated with a higher risk – approximately 20% higher – of subjective cognitive decline in both women and men. That risk was higher among men who were carriers of the gene APOE4, which is linked to cognitive impairment and dementia. That same association wasn’t present in the women.

Researchers don’t know the mechanisms that link the virus to cognitive health, but there are several possible ways it may contribute to cognitive decline. There is growing evidence linking VZV to vascular disease, called VZV vasculopathy, in which the virus causes damage to blood vessels in the brain or body. Curhan’s group previously found that shingles was associated with higher long-term risk of stroke or heart disease.

Other mechanisms that may explain how the virus may lead to cognitive decline include causing inflammation in the brain, directly damaging the nerve and brain cells, and the activation of other herpesviruses.

The limitations of this research include that it was an observational study, information was based on self-report, and included a mostly white, highly educated population. In future studies, the researchers hope to learn more about preventing shingles and its complications.

“We’re evaluating to see if we can identify risk factors that could be modified to help reduce people’s risk of developing shingles,” Curhan said. “We also want to study whether the shingles vaccine can help reduce the risk of adverse health outcomes from shingles, such as cardiovascular disease and cognitive decline.” 

Source: Brigham and Women’s Hospital

Categories : Diseases, Syndromes and ConditionsTags :

WHO Declares International Public Health Emergency over Mpox Outbreak

On By ModernMedia
Mpox (monkeypox) virus. Source: NIH

WHO Director-General Dr Tedros Adhanom Ghebreyesus has determined that the upsurge of mpox in the Democratic Republic of the Congo (DRC) and a growing number of countries in Africa constitutes a public health emergency of international concern (PHEIC) under the International Health Regulations (2005) (IHR).

Dr Tedros’s declaration came on the advice of an IHR Emergency Committee of independent experts who met earlier in the day to review data presented by experts from WHO and affected countries. The Committee informed the Director-General that it considers the upsurge of mpox to be a PHEIC, with potential to spread further across countries in Africa and possibly outside the continent.

The Director-General will share the report of the Committee’s meeting and, based on the advice of the Committee, issue temporary recommendations to countries.

In declaring the PHEIC, Dr Tedros said, “The emergence of a new clade of mpox, its rapid spread in eastern DRC, and the reporting of cases in several neighbouring countries are very worrying. On top of outbreaks of other mpox clades in DRC and other countries in Africa, it’s clear that a coordinated international response is needed to stop these outbreaks and save lives.”

WHO Regional Director for Africa Dr Matshidiso Moeti said, “Significant efforts are already underway in close collaboration with communities and governments, with our country teams working on the frontlines to help reinforce measures to curb mpox. With the growing spread of the virus, we’re scaling up further through coordinated international action to support countries bring the outbreaks to an end.”

Committee Chair Professor Dimie Ogoina said, “The current upsurge of mpox in parts of Africa, along with the spread of a new sexually transmissible strain of the monkeypox virus, is an emergency, not only for Africa, but for the entire globe. Mpox, originating in Africa, was neglected there, and later caused a global outbreak in 2022. It is time to act decisively to prevent history from repeating itself.”

This PHEIC determination is the second in two years relating to mpox. Caused by an Orthopoxvirus, mpox was first detected in humans in 1970, in the DRC. The disease is considered endemic to countries in central and west Africa.

In July 2022, the multi-country outbreak of mpox was declared a PHEIC as it spread rapidly via sexual contact across a range of countries where the virus had not been seen before. That PHEIC was declared over in May 2023 after there had been a sustained decline in global cases.

Mpox has been reported in the DRC for more than a decade, and the number of cases reported each year has increased steadily over that period. Last year, reported cases increased significantly, and already the number of cases reported so far this year has exceeded last year’s total, with more than 15 600 cases and 537 deaths.

The emergence last year and rapid spread of a new virus strain in DRC, clade 1b, which appears to be spreading mainly through sexual networks, and its detection in countries neighbouring the DRC is especially concerning, and one of the main reasons for the declaration of the PHEIC.

In the past month, over 100 laboratory-confirmed cases of clade 1b have been reported in four countries neighbouring the DRC that have not reported mpox before: Burundi, Kenya, Rwanda and Uganda. Experts believe the true number of cases to be higher as a large proportion of clinically compatible cases have not been tested.

Several outbreaks of different clades of mpox have occurred in different countries, with different modes of transmission and different levels of risk.

The two vaccines currently in use for mpox are recommended by WHO’s Strategic Advisory Group of Experts on Immunization, and are also approved by WHO-listed national regulatory authorities, as well as by individual countries including Nigeria and the DRC.

Last week, the Director-General triggered the process for Emergency Use Listing for mpox vaccines, which will accelerate vaccine access for lower-income countries which have not yet issued their own national regulatory approval. Emergency Use Listing also enables partners including Gavi and UNICEF to procure vaccines for distribution.

WHO is working with countries and vaccine manufacturers on potential vaccine donations, and coordinating with partners through the interim Medical Countermeasures Network to facilitate equitable access to vaccines, therapeutics, diagnostics and other tools.

WHO anticipates an immediate funding requirement of an initial US$ 15 million to support surveillance, preparedness and response activities. A needs assessment is being undertaken across the three levels of the Organization.

To allow for an immediate scale up, WHO has released US$ 1.45 million from the WHO Contingency Fund for Emergencies and may need to release more in the coming days. The Organization appeals to donors to fund the full extent of needs of the mpox response.

Source: WHO

Categories : Diseases, Syndromes and Conditions HospitalsTags :

Klebsiella Thrives in Nutrient-deprived Hospital Environments

On By ModernMedia
Photo by Hush Naidoo Jade Photography on Unsplash

Scientists at ADA Forsyth Institute (AFI) have identified a critical factor that may contribute to the spread of hospital-acquired infections (HAIs), shedding light on why these infections are so difficult to combat. Their study reveals that the dangerous multidrug resistant (MDR) pathogen, Klebsiella, thrives under nutrient-deprived polymicrobial community conditions found in hospital environments.

According to the World Health Organization, HAIs pose significant risks to patients, often resulting in prolonged hospital stays, severe health complications, and a 10% mortality rate. One of the well-known challenging aspects of treating HAIs is the pathogens’ MDR. In a recent study published in Microbiome, AFI scientists discovered that Klebsiella colonising a healthy person not only have natural MDR capability, but also dominate the bacterial community when starved of nutrients.

“Our research demonstrated that Klebsiella can outcompete other microorganisms in its community when deprived of nutrients,” said Batbileg Bor, PhD, associate professor at AFI and principal investigator of the study. “We analysed samples of saliva and nasal fluids to observe Klebsiella‘s response to starvation conditions. Remarkably, in such conditions, Klebsiella rapidly proliferates, dominating the entire microbial community as all other bacteria die off.”

Starvation environments

Klebsiella is one of the top three pathogens responsible for HAIs, including pneumonia and irritable bowel disease. As colonising opportunistic pathogens, they naturally inhabit the oral and nasal cavities of healthy individuals but can become pathogenic under certain conditions. “Hospital environments provide ideal conditions for Klebsiella to spread,” explained Dr Bor. “Nasal or saliva droplets on hospital surfaces, sink drains, and the mouths and throats of patients on ventilators, are all starvation environments.”

Dr Bor further elaborated, “When a patient is placed on a ventilator, they stop receiving food by mouth, causing the bacteria in their mouth to be deprived of nutrients and Klebsiella possibly outcompete other oral bacteria. The oral and nasal cavities may serve as reservoirs for multiple opportunistic pathogens this way.”

Additionally, Klebsiella can derive nutrients from dead bacteria, allowing it to survive for extended periods under starvation conditions. The researchers found that whenever Klebsiella was present in the oral or nasal samples, they persisted for over 120 days after being deprived of nutrition.

Other notable findings from the study include the observation that Klebsiella from the oral cavity, which harbours a diverse microbial community, was less prevalent and abundant than those from the nasal cavity, a less diverse environment. These findings suggest that microbial diversity and specific commensal (non-pathogenic) saliva bacteria may play a crucial role in limiting the overgrowth of Klebsiella species. 

The groundbreaking research conducted by AFI scientists offers new insights into the transmission and spread of hospital-acquired infections, paving the way for more effective prevention and treatment strategies.

Source: Forsyth Institute

Categories : Diseases, Syndromes and Conditions Environmental EffectsTags :

Does Air Pollution Affect Lupus Risk?

On By ModernMedia
Photo by Kouji Tsuru on Pexels

New research published in Arthritis & Rheumatology indicates that chronic exposure to air pollutants may increase the risk of developing lupus, an autoimmune disease that affects multiple organs.

For the study, investigators analysed data on 459 815 participants from the UK Biobank. A total of 399 lupus cases were identified during a median follow-up of 11.77 years. Air pollutant exposure was linked with a greater likelihood of developing lupus. Individuals with a high genetic risk and high air pollution exposure had the highest risk of developing lupus compared with those with low genetic risk and low air pollution exposure.

“Our study provides crucial insights into the air pollution contributing to autoimmune diseases. The findings can inform the development of stricter air quality regulations to mitigate exposure to harmful pollutants, thereby reducing the risk of lupus,” said co–corresponding author Yaohua Tian, PhD, of the Huazhong University of Science and Technology, in China.

Source: Wiley

Categories : Diseases, Syndromes and ConditionsTags :

After an Infection, Brain Inflammation Triggers Muscle Weakness

On By ModernMedia
Photo by Andrea Piacquadio

Infections and neurodegenerative diseases cause inflammation in the brain. But for unknown reasons, patients with brain inflammation often develop muscle problems that seem to be independent of the central nervous system. Now, researchers at Washington University School of Medicine in St. Louis have revealed how brain inflammation releases a specific protein that travels from the brain to the muscles and causes a loss of muscle function.

The study, published in Science Immunology, also identified ways to block this process, which could have implications for treating or preventing the muscle wasting sometimes associated with inflammatory diseases, including bacterial infections, Alzheimer’s disease and long COVID.

“We are interested in understanding the very deep muscle fatigue that is associated with some common illnesses,” said senior author Aaron Johnson, PhD, an associate professor of developmental biology. “Our study suggests that when we get sick, messenger proteins from the brain travel through the bloodstream and reduce energy levels in skeletal muscle. This is more than a lack of motivation to move because we don’t feel well. These processes reduce energy levels in skeletal muscle, decreasing the capacity to move and function normally.”

Fruit fly and mouse models

To investigate the effects of brain inflammation on muscle function, the researchers modelled three different types of diseases – an E. coli bacterial infection, a SARS-CoV-2 viral infection and Alzheimer’s. When the brain is exposed to inflammatory proteins characteristic of these diseases, damaging chemicals called reactive oxygen species build up. The reactive oxygen species cause brain cells to produce an immune-related molecule called interleukin-6 (IL-6), which travels throughout the body via the bloodstream. The researchers found that IL-6 in mice – and the corresponding protein in fruit flies – reduced energy production in muscles’ mitochondria, the energy factories of cells.

“Flies and mice that had COVID-associated proteins in the brain showed reduced motor function – the flies didn’t climb as well as they should have, and the mice didn’t run as well or as much as control mice,” Johnson said. “We saw similar effects on muscle function when the brain was exposed to bacterial-associated proteins and the Alzheimer’s protein amyloid beta. We also see evidence that this effect can become chronic. Even if an infection is cleared quickly, the reduced muscle performance remains many days longer in our experiments.”

Johnson, along with collaborators at the University of Florida and first author Shuo Yang, PhD (who did this work as a postdoctoral researcher in Johnson’s lab) make the case that the same processes are likely relevant in people. The bacterial brain infection meningitis is known to increase IL-6 levels and can be associated with muscle issues in some patients, for instance. Among COVID-19 patients, inflammatory SARS-CoV-2 proteins have been found in the brain during autopsy, and many long COVID patients report extreme fatigue and muscle weakness even long after the initial infection has cleared. Patients with Alzheimer’s disease also show increased levels of IL-6 in the blood as well as muscle weakness.

Potential treatment targets

The study pinpoints potential targets for preventing or treating muscle weakness related to brain inflammation. The researchers found that IL-6 activates what is called the JAK-STAT pathway in muscle, and this is what causes the reduced energy production of mitochondria. Several therapeutics already approved by the Food and Drug Administration for other diseases can block this pathway. JAK inhibitors as well as several monoclonal antibodies against IL-6 are approved to treat various types of arthritis and manage other inflammatory conditions.

“We’re not sure why the brain produces a protein signal that is so damaging to muscle function across so many different disease categories,” Johnson said. “If we want to speculate about possible reasons this process has stayed with us over the course of human evolution, despite the damage it does, it could be a way for the brain to reallocate resources to itself as it fights off disease. We need more research to better understand this process and its consequences throughout the body.

“In the meantime, we hope our study encourages more clinical research into this pathway and whether existing treatments that block various parts of it can help the many patients who experience this type of debilitating muscle fatigue,” he said.

Source: Washington University School of Medicine

Categories : Diseases, Syndromes and ConditionsTags :

Debunking Myths About Mpox

On By ModernMedia
Mpox (monkeypox) virus. Source: NIH

Myths are widely held beliefs about various issues, including illness and disease. They come about through frequent storytelling and retelling. Dr Themba Hadebe, Clinical Executive at Bonitas Medical Fund, helps debunks myths about monkeypox (mpox).

Myth 1: Mpox (formerly monkeypox) is a new disease created in a lab

Fact: The mpox virus was discovered in Denmark (1958) in a colony of monkeys at a laboratory kept for research.  The first reported human case was in 1970 in the DRC. Mpox is a zoonotic disease, meaning it can be spread between animals and people. It is found regularly in parts of Central and West Africa and can spread from person to person or occasionally from animals to people.  

Myth 2: Mpox comes from monkeys

Fact: Despite its name, monkeypox does not come from monkeys. The disease earned the name when the ‘pox like’ outbreaks happened in the research monkeys. While monkeys can get mpox, they are not the reservoir (where a disease typically grows and multiplies). The reservoir appears to be rodents.

Myth 3:  Only a handful of people have contracted mpox

Fact: Globally, more than 97 000 cases and 186 deaths were reported across 117 countries in the first four months of 2024. South Africa is among the countries currently experiencing an outbreak.  On the 5 July, it was reported that the number of mpox cases in the country has risen to 20. This after four more cases have been confirmed in Gauteng and KwaZulu-Natal in the last few days.

15 patients have, however been given a clean bill of health.

Myth 4:  It is easy to diagnose mpox

Fact: It is easy to mistake mpox for something else. While the rash can be mistaken for chickenpox, shingles or herpes, there are differences between these rashes. Symptoms of mpox include fever, sore throat, headache, muscle aches, back pain, low energy and swollen lymph nodes. Fever, muscle aches and a sore throat appear first. The rash begins on the face and spreads over the body, extending to the palms of the hands and soles of the feet and develops over 2-4 weeks in stages. The ‘pox’ dip in the centre before crusting over.

Laboratory confirmation is required. A sample of one of the sores is diagnosed by a PCR test for the virus (MPXV).

Myth 5: Mpox is easily treated

Fact: ‘Currently,’ says the National Institute for Communicable Diseases (NICD), ‘there is no registered treatment for mpox in South Africa. However, the World Health Organization (WHO) recommends the use of TPOXX for treatment of severe cases, in immunocompromised people’. However, the Department of Health (DoH) has only obtained this treatment, with approval on a compassionate use basis, for the five known patients with severe disease.

There is no mpox vaccine currently available in South Africa.

Myth 6: You can get mpox from being in a crowd or from a public toilet seat

Fact: Mpox is not like Covid-19 which is highly contagious. It spreads through direct contact via blood, bodily fluid, skin or mucous lesions or respiratory droplets.

It can also spread though bites and scratches. Studies have shown that the virus can stay on surfaces but it is not spreading in that way or in a public setting. The risk of airborne transmission appears low.

Myth 7: Mpox is deadly

Fact: While mpox lesions can look similar to smallpox lesions, mpox infections are much milder and are rarely fatal. That said, symptoms can be severe in some patients, needing hospitalisation and, in rare cases, result in death. It is, however, painful and very unpleasant. So, it is important to avoid infection.

Myth 8: Mpox is sexually transmitted

Fact: You can become infected though close, direct contact with the lesions, rash, scabs or certain bodily fluids of someone who has mpox. Even though this could imply transmission though sexual activity, it is not limited to that.  You can also be exposed if you are in close physical proximity to infected people, such as spouses or young children who sleep in the same bed.

Myth 9: I can’t protect myself from getting Mpox

Fact:  You can take precautions: Avoid handling clothes, sheets, blankets or other materials that have been in contact with an infected animal or person. Wash your hands well with soap and water after any contact with an infected person or animal and clean and disinfect surfaces. Practice safe sex and use personal protective equipment (PPE) when caring for someone infected with the virus.

Myth 10:  You can’t stop other people being infected by you

Fact: You may not protect them by 100% but you can isolate. Also, alert people who have had recent contact with you.  Wash your hands regularly with soap and water or use hand sanitiser, especially before or after touching sore and disinfected shared spaces.  Cover lesions when around other people, keep skin dry and uncovered (unless in a room with someone else).

Mpox is a notifiable medical condition but is treatable, if you are concerned, call the DoH toll free number of 0800 029 999 but remember, your GP is your first port of call for all your healthcare needs.

Categories : Diseases, Syndromes and Conditions Mental HealthTags :

Dengue Linked to Heightened Short- and Long-term Risk of Depression in Taiwan

On By ModernMedia

New study also uncovers short-term links with sleep disorders

Photo by Ekamelev on Unsplash

Analysis of the medical records of nearly 50 000 people who experienced dengue fever in Taiwan suggests that this disease is associated with elevated short- and long-term risk of depression. Hsin-I Shih and colleagues of National Cheng Kung University and National Health Research Institutes, Taiwan present these findings in the open-access journal PLOS Neglected Tropical Diseases.

People may develop dengue fever after being bitten by a mosquito carrying the dengue virus. Dengue fever can be mild, but it can also progress to life-threatening severity, and some people may have long-term health effects. Prior research has uncovered links between active dengue fever and psychiatric disorders, such as depression and anxiety. However, few studies have examined the long-term risk of such disorders after a dengue infection.

To address this knowledge gap, Shih and colleagues analysed the medical records of 45 334 dengue patients in Taiwan and, for comparison, 226 670 patients who did not experience dengue. Covering the years 2002 to 2015, the researchers examined whether dengue patients were more likely to develop anxiety, depressive disorders, and sleep disorders at various time points after infection. To help account for other factors that could influence mental health, the dengue patients were grouped with demographically similar non-dengue patients for statistical analysis.

The researchers found that the dengue patients had a greater likelihood of developing a depressive order across all timeframes, including less than three months, three to 12 months, and more than 12 months after their infection. Sleep disorders were only elevated within three to 12 months post-infection, and there was no observable elevated risk of anxiety.

Taking a closer look at patients whose dengue was severe enough for them to be hospitalized, the researchers found an elevated risk of anxiety disorders within the first three months of infection, as well as elevated risk of sleep disorders in the first 12 months. This subgroup also had elevated risk of depression across timeframes.

These findings suggest a potential link between dengue fever and subsequent depressive disorder. However, further research is needed to determine whether dengue contributes directly to development of depression, or if the association is due to some indirect mechanism.

The authors add: “This study highlights a significant association between dengue fever and an elevated risk of depression in both the short and long term, underscoring the need for further research into the mental health impacts of dengue infection.”

Provided by PLOS

Categories : Diseases, Syndromes and Conditions Pain ManagementTags :

In Knee Osteoarthritis, Inactivity may be more Complex than Believed

On By ModernMedia
Photo by Towfiqu barbhuiya

Knee osteoarthritis (OA) is a common cause of pain and joint stiffness. And while physical activity is known to ease symptoms, only one in 10 people regularly exercise. Understanding what contributes to patients’ inactivity is the focus of a world first study from the University of South Australia. Here, researchers have found that people with knee OA unconsciously believe that activity may be dangerous to their condition, despite medical advice telling them otherwise.

The study, published in PAIN, found that of those surveyed, 69% of people with knee pain had stronger implicit (unconscious) beliefs that exercise was dangerous than the average person without pain. It’s an interesting finding that not only highlights the conflicted nature of pain and exercise, but also that what people say and what people think, deep down, may be entirely different things.

Lead researcher, and UniSA PhD candidate based at SAHMRI, Brian Pulling, says the research provides valuable insights for clinicians treating people with knee OA.

“Research shows that physical activity is good for people with knee OA, but most people with this condition do not move enough to support joint or general health,” Pulling says.

“To understand why people with OA might not be active, research studies typically use questionnaires to assess fear of moving. But unfortunately, questionnaires are limited – what we feel deep down (and how our system naturally reacts to something that is threatening) may be different to what we report. And we still know that many people are avoiding exercise, so we wanted to know why.”

To assess this, the researchers developed a tool that can detect and evaluate people’s implicit beliefs about exercise; that is, whether they unconsciously think activity is dangerous for their condition.

“We found that that even among those who said they were not fearful about exercise, they held unconscious beliefs that movement was dangerous,” Pulling says.

“Our research shows that people have complicated beliefs about exercise, and that they sometimes say one thing if asked directly yet hold a completely different implicit belief.

“People are not aware that what they say doesn’t match what they choose on the new task; they are not misrepresenting their beliefs.

“This research suggests that to fully understand how someone feels about an activity, we must go beyond just asking directly, because their implicit beliefs can sometimes be a better predictor of actual behaviour than what people report. That’s where our tool is useful.”

The online implicit association test presents a series of words and images to which a participant must quickly associate with being either safe or dangerous. The tool intentionally promotes instant responses to avoid deliberation and other influencing factors (such as responding how they think they should respond).

Associate Professor Tasha Stanton says that the new tool has the potential to identify a group of people who may have challenges increasing their activity levels and undertaking exercise.

“What people say and what people do are often two different things, Assoc Prof Stanton says.

“Having access to more accurate and insightful information will help health professionals better support their patients to engage with activity and exercise. It may also open opportunities for pain science education, exposure-based therapy, or cognitive functional therapy…things that would not usually be considered for someone who said that they were not scared to exercise.”

Researchers are now looking to see if implicit beliefs are directly associated with behaviour and are asking for people to complete the Implicit Association Test (takes seven minutes). At the end of the test participants are given their results in comparison to the rest of the population.

To take the test, please click here: https://unisasurveys.qualtrics.com/jfe/form/SV_0OZKUqzBNtiKGF0

Source: University of South Australia