Category: Infection

Animals and humans coexist with a vast array of microorganisms known as the microbiome, forming a relationship that can range from mutually beneficial to pathogenic. To safeguard against harmful pathogens and maintain the presence of beneficial microorganisms, animals have evolved various defenses.One is small antimicrobial peptides (AMPs), small peptides that combat invading microbes. AMPs are crucial immune effectors in plants and animals, fighting against potential infections while also influencing the composition of the host’s microbiome. While previous studies have shown that AMPs evolve rapidly, little was known about the driving forces behind this evolution. For example, different animals have different “repertoires” of AMP genes, while lacking others found elsewhere. Understanding the evolutionary “logic” behind this is important not just as an ecological study, but also for the development of strategies to prevent infections by targeting specific microbial threats. Now, a study led by three scientists at EPFL (École Polytechnique Fédérale de Lausanne) in Switzerland has uncovered the selective pressures driving the evolution of AMPs and how they control bacteria in the host’s microbiome. The work was carried out by Bruno Lemaitre’s group at EPFL’s School of Life Sciences, led by Mark Hanson (now at the University of Exeter) and Lena Grollmus. It is published in Science. The researchers focused on diptericin (Dpt), a small antimicrobial peptide that mainly defends flies against Gram-negative bacteria, disrupting their bacterial membrane. Looking at the fruit fly, Drosophila, the team examined how diptericins function and evolve in response to their microbial environment. The team discovered that different types of diptericins, known as DptA and DptB, play specific roles in the fruit fly’s defense against different bacteria. By screening Drosophila mutants lacking specific AMP gene families, the researchers found that DptA is effective against Providencia rettgeri, a natural pathogen of Drosophila. Meanwhile, DptB helped the host resist infection by multiple species of Acetobacter, some of which reside in the fruit fly’s gut and help its physiology and development. In contrast, DptA played no significant role against Acetobacter and DptB played no significant role against Providencia. Evolutionary history Analyzing the evolutionary history of the diptericin genes, the scientists found two instances of convergent evolution that lead to DptB-like genes in fruit flies that feed on fruit, an environment associated with high levels of Acetobacter. This suggests that DptB evolved to control Acetobacter in the ancestral fruit-feeding Drosophila. The study also found that fruit flies with different ecological niches, such as mushroom-feeding or being plant-parasites, had either lost the DptB gene or both DptA and DptB genes, corresponding to an absence of Acetobacter or both Providencia and Acetobacter, respectively. Variations in DptA and DptB sequences were found to predict the host’s resistance to infection by these bacteria throughout the Drosophila genus. This highlights the evolutionary adaptation of the fly’s immune repertoire to combat specific microbes prevalent in its surroundings. To validate their findings, the researchers infected various Drosophila species with different variants of DptA and DptB genes. The researchers said the results were striking: the resistance of the host to infection by P. rettgeri and Acetobacter was readily predicted just by the presence and polymorphism of the DptA or DptB genes, even across fly species separated by almost 50 million years of evolution. The work sheds light on the dynamics that shape the host’s immune system and how the host’s defenses adapt to combat specific pathogens while fostering beneficial microorganisms. The findings propose a new model of AMP-microbiome evolution, incorporating gene duplication, sequence convergence, and gene loss, all guided by the host’s ecology and microbiome. This model explains why different species possess specific repertoires of AMPs, offering insights into how host immune systems rapidly adapt to the suite of microbes associated with a new ecological niche. “The way our bodies fight infections is very complex,” Hanson said. “But this sort of research helps us to view our immune system in a new light. It helps us ask: ‘why is our immune system made the way it is?’ That can help us learn how to fight infections, including ones that resist antibiotics.” Looking to expand your network? Build relationships with world-leading academic teams at 250+ institutes. ADVERTISEMENT

IF YOU’RE a contact lens wearer, you might thinking taking a dip in the pool with your lenses in is harmless. But opticians have warned that even a quick swim can cause some serious damage to your peepers – the last thing you want when you’re on holiday. 1 Even a quick dip with your contact lenses could allow bacteria to enter your eyes According to Nimmi Mistry, professional services optician at Vision Direct, water tends to be rife with bacteria, whether it’s tap, sea or swimming pool water. This matters because contact lenses are “exceptionally porous and absorbent”, she told Huffington Post. Exposing your lenses to water when you swim means bacteria is more likely to spread across their surface. As a result, even a quick dip in the pool or sea could put you at greater risk of developing a sight-threatening eye infection. While chlorine is added to swimming pool water to kill germs, it can’t eradicate all of them according to Nimmi. It might also irritate you peepers too, she added. “As soft lenses are exceptionally porous, the bacteria and the chlorine in pool water can still easily reach and harm your eyes,” the optician explained. Your risk of a nasty infection is even higher when swimming in the sea, rivers or lakes, or indulging in water sports, because natural bodies of water are rife with bacteria. Acanthamoeba is one of the most dangerous organisms found in these sources and can result in a rare but serious eye infection, Acanthamoeba keratitis. Most read in Health “If left untreated, this infection may lead to inflammation of the cornea, resulting in vision loss and sight-threatening complications down the line,” Nimmi stressed. The signs of acanthamoeba keratitis you need to know Acanthamoeba causes Acanthamoeba keratitis when it infects the transparent outer covering of the eye called the cornea. Acanthamoeba amebas are very common in nature and can be found in bodies of water (for example, lakes and oceans), soil, and air, medics at the CDC state. The symptoms can be similar to those of other eye infections and can last for several weeks or several months. The main signs to look for include: Eye pain Eye redness Blurred vision Sensitivity to light Sensation of something in the eye Excessive tearing If you have any of the above then you should see an eye doctor. Experts at the CDC said that eventually Acanthamoeba keratitis will cause pain and vision loss if left untreated. It’s understandable that you don’t want to plunge into the water while not being able to see at all. In this case, the optician suggested you opt for daily disposable contact lenses instead of reusable ones and wear tight-fitting waterproof swimming goggles. It’s best to throw out the reusable lenses afterwards, she added. If you don’t want to tear through reusable lenses on your holiday, Nimmi suggested buying some prescription goggles – it means you’ll also be foregoing wearing lenses while swimming altogether, lessening your chances of infection. If you want to stick to your reusable lenses, Dr Vicki Chan suggested you remove them while you’re swimming and popping them back in afterwards.

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Home Health Eye Flu Cases Rise in Delhi: How Long Does it Last And How to Treat it? The monsoon’s humid and damp conditions provide an ideal breeding ground for the viruses or bacteria responsible for these infections to spread rapidly, he said. Eye Flu Cases Rise in Delhi: How Long Does it Last And How to Treat it? The national capital is inundated with Yamuna River water. There has been a sudden outbreak of eye flu in Delhi owing to these cases of conjunctivitis and other eye infections are on the rise in Delhi, with many doctors cautioning that it is “highly contagious” and proper hygiene behaviour needs to be maintained to check its spread. Doctors at both government and private hospitals said they have been receiving cases largely from the younger population in the city. It is a “self-limiting infection” and each individual immunity will have a role to play in the course of the disease. The monsoon’s humid and damp conditions provide an ideal breeding ground for the viruses or bacteria responsible for these infections to spread rapidly, he said. To stop the spread of the infection, touching of eyes should be the least, contact of the same with others should be avoided, and isolation of school children for 3-5 days in case of infection after which if the treatment is started they can be non-infective. You may like to read How Long Eye Flu Will Last? Typically, eye flu lasts about a few days to around two weeks. Pink eye is also of two types. One has due to viruses like herpes or adenovirus. This usually lasts from 10-14 days and in severe cases, it may go on for about a month long. The other one a bacterial pink eye, which may last for around 10 days. According to Healthline, a virus that causes viral pink eye can spread from your nose to your eyes, or you can catch it when someone sneezes or coughs and the droplets come in contact with your eyes. Bacteria cause bacterial pink eye. Usually, the bacteria spreads to your eyes from your respiratory system or skin. You can also catch the bacterial pink eye if you: HOW TO TREAT EYE FLU? Eyr flu is spreading like wildfire in Delhi and is regarded as highly contagious as well. Symptoms are watery discharge in the eyes, redness, congestion, photophobia, hemorrhages in the superficial layer of the eye. The management is through antibiotic eye drops, eye ointments, topical decongestants, lubricants and some oral anti-allergic. According to experts, eye flu can be treated with cold compression of the eye through ice packs. Cases of conjunctivitis and skin allergy are mostly being reported from relief camps housing people affected by the flooding in parts of Delhi, city Health Minister Saurabh Bharadwaj said on July 17. RECOMMENDED STORIES Published Date: July 25, 2023 2:21 PM IST –> <!– Comments – Join the Discussion –> Don’t Miss Out on the Latest Updates.Subscribe to Our Newsletter Today! Subscribe Now

The deadly H5N1 bird flu virus has crossed the species barrier to infect large numbers of domestic cats for the first time, according to the World Health Organization (WHO). On Monday the Geneva based health watchdog, which has been monitoring the spread of H5N1 around the world in recent months, said it had confirmed that 29 cats in Poland had tested positive for the virus. “This is the first report of high numbers of cats infected with avian influenza A(H5N1) spread over a wide geographical area within any country”, said the WHO. Fourteen cats are reported to have been euthanised, and a further 11 died. “Some cats developed severe symptoms including difficulty in breathing, bloody diarrhoea, and neurological signs, with rapid deterioration and death in some cases. “In total, 20 cats had neurological signs, 19 had respiratory signs, and 17 had both neurological and respiratory signs”. 1807 International report On June 27, the IHR National Focal Point of Poland notified WHO of unusual deaths in cats across the country. Last week the European Centre for Disease Prevention and Control (ECDC) issued a report saying there were “several uncertainties … regarding the source of infection” and the WHO said on Monday that the source of the infection in cats remained “unknown”. It added: “There are several possibilities for the source of infection, among which the cats could have had direct or indirect contact with infected birds or their environments, ate infected birds, or ate food contaminated with the virus”. Local media have linked the outbreak to contaminated meat. Out of the 24 cats which positive for H5N1, 13 were said to have been found to have been fed raw poultry meat. It was reported a woman living in Chełmek, southern Poland, fed her cat raw chicken purchased from a large supermarket chain before its death. Within days of eating the meat, the cat became drowsy and was taken to the vet by her owner, who suspected a cold. The day after the visit the cat “began to lose her balance, fell off the chair, her hind legs were paralysed, she stopped walking and eating completely,” the vet told the Polish newspaper Gazeta Wyborcza. Antibiotics and steroids did not help and the cat died just seven days after eating the raw meat. ‘Virus is evolving’ The World Organisation for Animal Health said that the wide geographical distribution of cases suggests that the primary mode of spread in these cases is not cat-to-cat transmission but instead linked to a common source. However, experts have also highlighted that the virus extracted from the cats in Poland exhibits two mutations that facilitate better transmission in mammals. Media reports from Poland cite the director of the National Veterinary Institute in Puławy stating that, “they have detected two mutations that indicate that the A(H5N1) virus is evolving to multiply more easily in mammals”. Although ECDC assessments show the current risk to the general public is low, it is considered moderate in persons exposed to infected cats, particularly if they belong to a vulnerable population group. In total, the deaths of around 70 domestic cats since June 23 are being investigated, according to local media . It follows reports of five dogs and one cat testing positive for H5N1 at a poultry farm in Brescia, Italy, on July 7. The farm is experiencing an outbreak of avian flu, the ECDC said in its latest report on communicable disease threats in Europe. Chile also last week reported the deaths of 13,000 sea lions as a result of bird flu, up from previous estimates of 9,000. How worried should we be about avian flu? Over the past two years, a new strain of H5N1 avian influenza, which transmits easily among birds, has caused devastation in wild and domestic flocks across the globe. There have been concerns that the increased spread offers more opportunities for the virus to jump to people, especially as more and more mammals have been infected. In April, the virus was found to “efficiently” spread between ferrets in a laboratory, the first study confirming that the virus can spread from mammal to mammal. Last week the UK Health Security Agency (UKHSA) issued the following chart showing the increasing spread of the H5N1 virus in mammals around the world. It noted that although there have been human cases – including three in the UK – there have been no confirmed cases of human to human transmission (or indeed of mammal to mammal transmission) here or anywhere else in the world. Protect yourself and your family by learning more about Global Health Security

A sinus infection, or sinusitis, is when you have an inflamed or stuffy nose or fluid buildup in your sinuses. The fluid build-up provides an environment where germs associated with viruses or bacteria can grow. There are several causes of sinus infections, with the most common cause being the common cold. You may have a sinus infection from other causes, including a benign growth in the sinuses called nasal polyps or allergies. In this article, you’ll learn more about the common causes of sinus infections so you can narrow down the potential cause of your sinus infection as well as treatments, risk factors and prevention. damircudic / Getty Images The Main Causes of Sinus Infections The three main causes of sinus infections are: Infection, typically caused by viruses or bacteria Nasal polyps (benign growths that contain mucus) Allergies such as seasonal allergies or allergies to environmental triggers A Common Cause of Acute Sinusitis The common cold is the most common cause for acute sinusitis or sudden sinus infection. It usually is caused by a viral infection, although bacteria and fungi can also lead to acute sinus infections. How Long Does Acute Sinusitis Last? Acute sinus infections can last anywhere from three to eight weeks. The risk for sudden sinus infection caused by bacteria or fungi is greater in people with compromised immune systems. Common Causes of Chronic Sinusitis Common causes of chronic sinusitis include: Allergies to pollen, dust, mold, or fungi spores Nasal polyps Tumors Fractures Chronic sinusitis in adults is most often caused by nasal swelling and inflammation associated with allergies. These allergies trigger the release of histamines to the affected area, which cause nasal passageway inflammation. Structural differences, including polyps, fractures, or a narrowing within the nasal cavity, can also promote chronic infection. This is because when the nasal passage is blocked in any way, fluid buildup can occur and prevent proper drainage. What Makes a Sinus Infection Chronic Any sinus infection lasting longer than eight weeks is considered chronic sinusitis. People who live with asthma, cystic fibrosis, and immune system challenges have a greater chance of developing chronic sinusitis. Sinus Infection Symptoms The most common symptoms of sinus infection include: Runny nose or stuffy nose Facial pain or pressure Headache Mucus dripping down the throat (postnasal drip) Greenish nasal discharge Enlarged lymph nodes Sore throat Cough Bad breath despite brushing teeth These symptoms can last around 10 days, but you should be seeing improvements as the days pass. Sinus Infection Treatment A sinus infection may or may not require antibiotic treatment. Most sinus infections will resolve without antibiotic treatment. Your healthcare provider can help determine whether antibiotics are necessary. Usually, taking unnecessary antibiotics won’t help your condition, and overuse of antibiotics can result in unwanted side effects, including antibiotic resistance (when germs develop the ability to fight off the drugs used to kill them). In some cases, your healthcare provider will suggest a method called watchful waiting or delayed antibiotic prescribing, as follows: Watchful waiting is when your healthcare provider monitors symptoms for two or three days before deciding whether to prescribe antibiotics. Two or three days is enough time to see if your immune system will fight the infection independently. Delayed prescribing is when your healthcare provider writes the antibiotic prescription but asks you to wait two to three days before filling it to see if it’s necessary or if your symptoms are improving. Methods of at-home treatment include: Nasal decongestant sprays: These sprays can taken up to four days. They help reduce swelling and promote free-flowing drainage from the nasal cavity. Antihistamines: These medications can help reduce inflammation caused by allergy-induced infection. Combination medications: These include both decongestant medication and antihistamines. These should only be taken for a sinus infection after consultation with a healthcare provider or allergist. Topical prescription nasal corticosteroid sprays: These drugs help reduce inflammation and swelling but can also be effective in reducing the size of nasal polyps if they are obstructing airflow. Home Remedies to Help Sinus Infections There are ways of feeling better when you have a sinus infection. A common home remedy for sinus infection is using a nasal saline rinse. Saline rinses are a sanitary way to help clear the nasal passageway. Other at-home remedies for sinus infection relief include: Using a warm compress over the nose and forehead area to help relieve pressure and promote drainage Breathing in clean steam from hot water Using a humidifier to keep at-home air moist and prevent nasal passage dryness Drinking plenty of water to help loosen mucus Sleeping with your head elevated What Are the Risk Factors for Sinus Infections? Risk factors play a role in who will experience sinus infections, and how often. Common risk factors for sinus infections include: A previous, recent cold Seasonal allergies Exposure to smoke, including secondhand smoke Structural differences including being born with a narrow nasal passageway or developing a nasal polyp Compromised immune system Taking medications or drugs that weaken the immune system’s defenses Is Sinus Surgery Necessary to Reduce Risk? People who are born with narrow nasal passageways may be advised to seek surgical remedy if they have chronic sinus infections. This is an effective way of reducing this common risk factor for sinus infection. Can Sinusitis Be Prevented? There are several ways you can help protect yourself from having a sinus infection. These include general methods of preventing infection or spreading illness that can help keep yourself and others healthy. Prevention efforts include: Wash your hands thoroughly and frequently. Stay up-to-date on vaccines including the flu vaccine but also the pneumococcal vaccine. Avoid smoking or exposure to secondhand smoke. Avoid close contact with someone with a sinus infection or upper respiratory infection. Consider getting a humidifier to help keep the household air moist (be sure to stay on top of cleaning your humidifier). When to Contact a Healthcare Provider If you’re experiencing repeat infections or if you have multiple sinus infections in a single year, it’s time to consider

Early in the COVID-19 pandemic, doctors started to notice something striking. For what was originally described as a respiratory virus, SARS-CoV-2 seemed to have a strong effect on the brain, causing everything from loss of taste and smell and brain fog to, in serious cases, stroke. NYU Langone Health, a New York city research hospital, started collating those anecdotes in hopes of better understanding how the virus affects the brain and nervous system. Years later, the project has morphed from focusing solely on acute symptoms to also tracking the long-term neurologic issues that some people with Long COVID experience, says program director Dr. Sharon Meropol. The list of neurocognitive issues that Meropol’s team and other researchers must track is extensive: cognitive decline, changes in brain size and structure, depression and suicidal thinking, tremors, seizures, memory loss, and new or worsened dementia have all been linked to previous SARS-CoV-2 infections. In some cases, these longer-term problems occur even in patients with relatively mild COVID-19. The “Holy Grail” question now, Meropol says, is what’s going on in the brains of COVID-19 patients—and how to reverse the damage. Gray matters If you were to look at the brain of someone infected by certain viruses, like rabies, you would see “virus teeming everywhere. It’s black and white” that the brain is infected, says Dr. Avindra Nath, clinical director of the National Institute of Neurological Disorders and Stroke (NINDS). More from TIME With SARS-CoV-2, there’s more gray area. Early in the pandemic, Nath and his colleagues scanned and physically analyzed the brains of 13 people who died from COVID-19. They didn’t find the SARS-CoV-2 virus in those brains—but they did find significant damage to their blood vessels, which were coated with antibodies. It looked to Nath like the body’s immune system had gone haywire in response to the virus, causing it to attack its own blood vessels and setting off a cascade of effects that led to significant inflammation in the brain, potentially culminating in fatal damage to the part that controls breathing. In people who survive COVID-19, brain inflammation may also explain years-long symptoms like brain fog and memory loss—though “we don’t know for sure,” Nath says. Dr. Lara Jehi, who researches COVID-19 and the brain at the Cleveland Clinic, also points to inflammation as a possible trigger for COVID-19’s neurologic symptoms. She’s found evidence of abnormal inflammation in people with chronic post-COVID headaches. And in a 2021 study, Jehi and her colleagues compared the brains of people with Long COVID and Alzheimer’s disease. “We found many areas of overlap between the two, and these areas of overlap centered on…inflammation in the brain and microscopic injuries to the blood vessels,” she says. Going into that study, Jehi says, her team wanted to determine whether the SARS-CoV-2 virus was entering the brain and causing damage directly, or triggering an immune response that led to brain changes. Their findings pointed to the latter—but researchers still haven’t ruled out the possibility that the virus has direct effects on the brain. Virus in the brain Since Nath’s brain-scanning project early in the pandemic, other researchers have found the virus in the brains of people who died from COVID-19. For a 2022 paper in Nature, researchers analyzed brain tissue of 11 people who had COVID-19 when they died. In all but one of those individuals, the researchers found the virus’ genetic material in central-nervous-system tissue—which, they wrote, “prov[ed] definitively that SARS-CoV-2 is capable of infecting and replicating within the human brain.” To Nath, however, that’s still an open question, and one worthy of more research. His team has continued to study the brains of COVID-19 patients and has yet to find concrete evidence of the SARS-CoV-2 virus in those organs. In one instance, he says, they found viral proteins—but not the full virus—in biopsied tissue from someone who had COVID-19 at the time they were undergoing brain surgery for epilepsy. Researchers behind an April 2023 study not yet been peer-reviewed also found SARS-CoV-2 spike proteins—which are found on the virus’ surface and allow it to enter human cells—in the brains of people who died from COVID-19. But the research is “inconsistent,” Nath says. “Some have found it, some have not, and some people who have found it, have found very small amounts. There’s still a gap in knowledge there.” Dr. Wes Ely, who researches brain disease at Vanderbilt University Medical Center, says he’s convinced SARS-CoV-2 can attack the “support cells” of the brain, or those ensure neurons are able to keep the brain and body functioning normally. Damaging these support cells, Ely says, can kick off a domino effect that leads to tissue death in the brain. But, Ely says, “almost certainly there are multiple processes going on”—it could be that the virus both directly affects the brain and causes changes to the immune system that lead to neurocognitive issues. “We’re not looking for a magic bullet that will solve all these problems” at once, he says. While there may not be a single solution, that doesn’t mean there’s no solution. Ely has found that “cognitive rehab,” a process of rebuilding the brain’s function through targeted mental exercises, can help people who develop similar cognitive decline after stays in the intensive-care unit. That approach could be risky for people with Long COVID, many of whom experience worsened symptoms after mental or physical exertion, Ely says—but changing the immune system’s function in hopes of reducing inflammation in the brains of people with Long COVID is another promising route. NINDS is currently enrolling patients for a study on immunotherapy as a potential treatment for neurologic Long COVID. That approach is particularly exciting, Nath says, because it entails a therapy that is already used to treat a range of autoimmune and neurologic conditions—so if it proves effective, it could be rolled out to Long COVID patients relatively quickly. Some preliminary research also suggests blood-thinning drugs may help breakup tiny “microclots” in the blood that are linked to systemic inflammation, potentially relieving

In a recent study posted to the medRxiv* preprint server, researchers compared the association between neuroimaging markers of dementia: brain volume, hippocampal volume, white matter lesions or hyperintensity volume, and antibodies to common infection across three population-based cohort studies in the United Kingdom (UK). Study: Common infections and neuroimaging markers of dementia in three UK cohort studies. Image Credit: NewAfrica/Shutterstock.com *Important notice: medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information. Background All three markers tested in this study were associated with brain structure and pathology changes clinically relevant to subclinical dementia triggered by neurodegenerative diseases, like Alzheimer’s disease (AD) and cerebral small vessel disease. First, the researchers examined whether seropositivity and exposure to all examined pathogens were associated with neuroimaging outcomes; further, they tested these associations using the apolipoprotein E (APOE) genotype as an interaction term. Furthermore, they assessed associations of antibody titers against each pathogen, indicating recent reactivation with these neuroimaging outcomes. Neurotropic pathogens – such as herpes simplex virus (HSV) – can directly infect the central nervous system (CNS) cells, possibly triggering amyloid-ß pathology, neuroinflammation, and neuronal loss, all of which have been implicated in dementia etiology. However, in the absence of large-scale serology data, it remains challenging to define previous infections. Thus, examining relationships between multiple common infections and subclinical markers of dementia prospectively – across well-characterized population-based studies – could facilitate a more comprehensive understanding of their role in dementia risk. In addition, assessing whether pathogen exposure may interact with established risk or protective factors of dementia could provide insights into possible at-risk groups. About the study In the present study, researchers applied a validated fluorescence bead-based multiplex serology panel to the UK Biobank (UKB), the MRC National Survey of Health and Development (NSHD), and Southall and Brent Revisited (SABRE) to measure serum immunoglobulin G (IgG) against antigens from a wide range of pathogens with outcomes among several settings in parallel. An adaptation of the same panel assayed 18 pathogens in 1,813 and 1,423 NSHD and SABRE participants, respectively. In UKB, they assayed 21 pathogens among 9,429 participants at baseline and an additional 260 at follow-up. They quantified antibody responses or seroreactivity indicating prior infection for each pathogen using median fluorescence intensity units and between one and six antigens per pathogen. To measure total exposure to multiple pathogens, they derived two pathogen burden index (PBI) scores, total PBI and neurotropic PBI indicating the sum of serostatuses to 17 pathogens and 11 neurotropic pathogens, including herpes simplex viruses (HSV), Toxoplasma gondii, and John Cunningham (JC) virus, respectively. The latter held more clinical relevance to neurological outcomes. Next, the team derived tertiles in the serology and neuroimaging samples to group antibody responses of seropositive samples in seroreactivity analyses. Seroreactivity values formed a variety of non-normal distributions. For NSHD and UKB, the team used neuroimaging measures assessed via brain magnetic resonance imaging five to 11 years and one to 13 after blood sampling for serology assaying, respectively. However, for SABRE, they used neuroimaging measures collected at the same time as blood sampling for serology assaying. For all three cohorts, they quantified brain volume and hippocampal volume using in-house using Geodesic Information Flows. Likewise, they used an automatic algorithm, Bayesian Model Selection (BaMoS), for deriving white matter hyperintensities. Further, the researchers used directly genotyped data for APOE genotypes using rs7412 and rs429358 single nucleotide polymorphisms (SNPs). Subsequently, they developed APOE e4 and APOE e2 non-carrier/carrier, where the latter were heterozygoushomozygous for the alleles e4 and e2, respectively. Related Stories Then, they used random-effects models with a maximum likelihood estimator for meta-analysis of findings across studies. Multiplying regression coefficients deduced in white matter lesion volumes analyses by 100 transformed them to sympercents. They used the Benjamini-Hochberg procedure with an alpha of 0.05 to correct findings from meta-analyses of serostatus outcome, seroreactivity, and APOE interaction analyses and fetch the false discovery rate (FDR). An I2 statistics >50% or Q-p value<0.05 indicated significant heterogeneity in all included studies. The team applied three linear regression models in the primary analyses to evaluate associations between serology variables and neuroimaging outcomes. While Model one included total intracranial volume and other technical covariates, Model two adjusted for Model one and age, gender, and ethnicity covariates. Model three adjusted for model one and two covariates and social, behavioral, and lifestyle confounders. These measures reflected trackable, long-term characteristic differences. In statistical modeling of seroreactivity analyses, they modeled tertiles as an ordinal variable and investigated pathogens with a seroprevalence >5% in all studies. The team used the same models accounting for ten genetic principal components during APOE interaction analyses to assess whether pathogen burden relationships with outcomes varied by APOE genotype, including APOE e4 and APOE e2 carrier statuses as interaction terms. Notably, they conducted APOE e4 and APOE e2 analyses separately. The team also conducted several secondary and sensitivity analyses. Results The present study had 2,632 participants with available serology measures and data on at least one neuroimaging outcome, of which 438, 1,259, and 935 belonged to the NSHD, SABRE, and UKB cohorts, respectively. Likewise, the study encompassed 17 pathogens with relevant serology data. For the APOE genotype interactions study, the authors had genetic data of 1,810 participants after quality control, of which data of 413, 593, and 804 participants came from the NSH, SABRE, and UKB cohorts, respectively. Of 593 SABRE participants, 314 and 279 were of European and South Asian ethnicities, respectively. The authors found minimal or no evidence of any associations in most instances. Accordingly, the findings for HSV concerning neuroimaging outcomes were null though it is the most studied pathogen with an alleged link with AD. Likewise, the findings for many other pathogens with serological markers on the study panel with alleged links to AD and other causes of dementia were null. These findings, at least for HSV, agreed with several previous studies. Moreover, the authors found no convincing evidence of associations of pathogen burden scores

In a recent study published in the Frontiers in Immunology Journal, a group of researchers examined the immune response and potential cross-protection in hospitalized patients with breakthrough infections caused by the Delta and Omicron variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). ​​​​​​​Study: Immune responses in COVID-19 patients during breakthrough infection with SARS-CoV-2 variants Delta, Omicron-BA.1 and Omicron-BA.5. Image Credit: Naeblys/Shutterstock.com Background The coronavirus disease 19 (COVID-19) pandemic has resulted in millions of infections and deaths worldwide. Vaccines have been crucial in reducing the spread of the virus. Messenger ribonucleic acid (mRNA) vaccines like Comirnaty and Spikevax have been widely administered in Germany, effectively protecting against SARS-CoV-2. However, new variants of concern, such as Omicron, have emerged, posing challenges to vaccine effectiveness. Omicron is particularly evasive to antibodies generated by vaccines. Despite breakthrough infections among vaccinated people, most remain protected from severe illness. However, the immune response to specific Omicron sub-variants, viz. BA.1 and BA.5, are not well understood. About the study The study population involved 52 hospitalized patients with confirmed SARS-CoV-2 breakthrough infections and a control group of 28 individuals without SARS-CoV-2 infection. Among the patients, 25 were infected with the Delta variant, 15 with the Omicron-BA.1 variant, and 12 with the Omicron-BA.5 variant. Most Delta-infected individuals were double vaccinated, while most Omicron-BA.1 patients were double or triple vaccinated, and all Omicron-BA.5 patients had received a booster dose. The control group had varying levels of vaccination. Patient samples, including blood samples and nasopharyngeal swabs, were collected for analysis. To characterize the SARS-CoV-2 strains and immune responses, viral ribonucleic acid (RNA) was isolated and sequenced, and phylogenetic analysis was performed. The study also measured immunoglobulin G (IgG) antibodies against the SARS-CoV-2 spike protein and IgM/IgG antibodies against the nucleocapsid protein using enzyme-linked immunosorbent assay (ELISA). Neutralization assays were conducted to assess the ability of patient sera to neutralize different SARS-CoV-2 variants. Additionally, an Interferon-gamma (IFN-γ) enzyme-linked immunosorbent spot (ELISpot) assay was performed to evaluate the cell-mediated response to the virus. Statistical analyses were conducted to assess significant differences between groups using tests such as Kruskal-Wallis, Mann-Whitney U, Wilcoxon signed-rank, and Fisher’s exact tests. Correlation coefficients were calculated using Spearman’s rank analysis. Study results The study conducted sequencing and phylogenetic analysis of the SARS-CoV-2 variants causing infections. Researchers reported that most breakthrough infections occurred in individuals who had received at least one vaccine dose, with varying vaccination levels in the control group. Related Stories Whole genome sequencing of clinical isolates revealed that patients were infected with the Delta variant or the Omicron sub-lineages viz. BA.1 and BA.5. Further, when serum samples were tested for SARS-CoV-2-specific antibodies using ELISA, most samples were positive for subunit 1 (S1)-specific IgG antibodies, indicating a humoral immune response. Antibody levels against the nucleocapsid protein (NCP) were much lower than S1. There were no significant variations in antibody levels between different breakthrough infection groups based on the vaccine status. Neutralization assays were performed to evaluate the ability of patient sera to neutralize different SARS-CoV-2 variants. Sera from breakthrough-infected patients showed reduced neutralization capacity against Omicron sub-lineages BA.5 and BA.1 compared to Alpha, Delta, and wild-type variants. However, patients with Delta breakthrough infections who received two vaccine doses had a significantly enhanced neutralizing antibody response against the Delta variant compared to uninfected controls. Cellular immunity was assessed using an IFN-γ ELISpot assay. Double-vaccinated Delta-infected patients showed the highest response to NCP stimulation, followed by boosted patients infected with the BA.5 variant. Delta-infected patients responded significantly more to wildtype S protein than BA.1-infected patients. All groups showed a lower response to mutated SARS-CoV-2 variants. Correlations were observed between neutralizing antibody titers, S1-specific IgG antibody levels, and the cellular immune response. The highest correlation between neutralizing antibody titers against Alpha and wild-type variants was found. However, the correlation was lower for Delta and Omicron variants. A correlation was also found between S1-specific IgG antibody concentrations and the cellular immune responses against wildtype, but not against SARS-CoV-2 variants. Discussion The study highlights several important findings. Firstly, the neutralizing antibody titers against the Omicron sub-variants were significantly reduced compared to other variants, indicating a substantial immune escape of these sub-variants. This aligns with previous research showing their ability to evade antibodies from vaccinated or infected individuals with other Omicron sub-lineages. The study demonstrated a strain-specific enhancement of neutralizing immunity in patients with Delta and Omicron-BA.1 breakthrough infections. Delta infections significantly enhanced neutralizing antibody titers against Delta, surpassing the levels observed against the wildtype strain. Similarly, Omicron-BA.1 breakthrough infections enhanced neutralizing antibody titers against BA.1 and Delta, suggesting cross-reactive immunity between these variants. However, BA.5 breakthrough infections did not result in an immune boost, indicating that BA.5 has a weaker effect on humoral immunity and may increase the risk of reinfections. The study also assessed cellular immunity using an IFN-γ ELISpot assay. The response to distinctly mutated regions of all SARS-CoV-2 variants was weak, possibly due to the early stage of infection at the time of sample collection. However, all patient groups exhibited a strong IFN-γ response when stimulated with the spike protein of the Wuhan wildtype, indicating a robust cellular immune response regardless of vaccination status or variant causing breakthrough infection. Conclusions The study provides valuable insights into the immune response to breakthrough infections with Delta and Omicron variants. The reduced neutralizing antibody titers against Omicron sub-variants highlight the challenge posed by these highly evasive variants. The findings of strain-specific immune boosting and the lack of immune enhancement in BA.5 infections contribute to our understanding of vaccine effectiveness and the potential for reinfections with emerging variants. Journal reference:

Surgical site infection (SSI) in plastic, reconstructive and aesthetic surgery (ERCP) is quite uncommon compared to other surgical specialities but remains one of the main complications. The aim of our study was to provide feedback on the systematic investigation of SSI in ERCP. This is a monocentric retrospective study, including all paediatric and adult patients who have undergone ERCP surgery between 01/01/2014 and 31/12/2021. During this period, the department systematically investigated all SSI cases. Eight thousand eight hundred and seventy-eight surgical procedures were performed. The SSI rate was 0.34%. Thirty SSIs (19W,11M), with a mean age of 56 years (none paediatric), were investigated. Twenty-seven patients suffered from comorbidities. The surgical indications included 17 cases of skin cancer, 7 cases of weight loss, 4 cases of breast reconstruction, 1 lipoma, 1 pectus excavatum. Eleven surgeries consisted in lymphnode procedures (8 sentinel lymphnodes, 3 curage). The average operating time was 116minutes. Nineteen patients received antibiotic prophylaxis. The average time to onset of SSI after surgery was 10 days. The most prevalent bacteria were commensals of the skin flora and the digestive tract. Apart from surgical management, 100% of patients were treated with antibiotics. High age, multiple comorbidities, long, combined procedures, placement of equipment, lymph node surgery, post-operative punctures on implanted equipment, are all risks factors for SSI. The implementation of a systematic monitoring of SSI within our department has provided us with the opportunity to analyse our data in real time and allow us to adjust our practices if necessary. This process can be used in other plastic reconstructive and aesthetic surgery departments. The collection and analysis of SSIs is both easily done and the procedure is well standardized. The assistance of the operational hygiene team is a key asset for the success of this project. The development of this type of procedure on a national level could be an asset to improve the management of SSI by taking advantage of the experience of a larger number of centres.Copyright © 2023 Elsevier Masson SAS. All rights reserved.