Category: Infection

Doxycycline is an antibiotic in the tetracycline family used to treat acute bacterial sinus infections in people allergic to penicillin. It is also commonly used to treat acne, skin infections like cellulitis, and some sexually transmitted infections (STIs). Doxycycline is sometimes prescribed as an alternative to amoxicillin, another antibiotic used for sinus infections, in people allergic to penicillin-type antibiotics. This article will discuss doxycycline’s role as an antibiotic in treating sinus infections, how it works, and what to expect when taking doxycycline for a sinus infection. Getty Images / WLADIMIR BULGAR/SCIENCE PHOTO LIBRARY How Does Doxycycline Work for a Sinus Infection? Doxycycline blocks bacteria from producing proteins needed to replicate, thereby preventing bacteria from multiplying further. Doxycycline does not kill bacteria; it is considered bacteriostatic, meaning that it suppresses the growth of bacteria. Doxycycline and other antibiotics only work for bacterial sinus infections, though. They will not treat viral infections. How to Take Doxycycline for a Sinus Infection Doxycycline for sinusitis is usually prescribed as 100 milligrams (mg) twice daily for five to seven days. Alternatively, it can be taken at 200 milligrams once a day. Some formulations of doxycycline are best taken on an empty stomach, while others can be taken with or without food. Ask your pharmacist about the specific formulation you are receiving at the pharmacy. If taking doxycycline irritates your stomach, you can try taking it with food or milk to prevent this. Be sure to swallow the capsule or tablet with a large amount of water to ensure that it does not remain in the esophagus, where it could cause irritation. How Long Will Doxycycline Take to Work? Symptoms of acute sinusitis should begin to improve three to five days after starting doxycycline. To clear the infection, take doxycycline for the entire prescribed duration, usually five to seven days. It’s important to continue to take your medication even if you begin to feel better. Stopping your antibiotic regimen early can contribute to antibiotic resistance, and your infection could return. What Side Effects Should I Expect? Like other antibiotics, doxycycline can sometimes cause side effects. However, it is generally considered well tolerated among most people. Side effects of doxycycline may include: Photosensitivity: Doxycycline can make your skin more sensitive to the sun. Avoid prolonged sun exposure, and wear sunscreen and protective clothing to cover your skin in the sun while taking this antibiotic. Diarrhea: Diarrhea is a common side effect of antibiotics that usually clears once antibiotics are finished. Call your healthcare provider if the diarrhea is severe, does not stop, or is bloody. Other gastrointestinal-related issues, like stomach upset and nausea/vomiting Serious side effects of doxycycline may include: Severe allergic skin reaction: Doxycycline can sometimes cause skin reactions that can progress to severe and life-threatening. If you notice a sudden allergic skin reaction, stop taking doxycycline and seek care from a healthcare provider immediately. C. diff diarrhea: C. difficile diarrhea can occur up to two months after taking antibiotics. See a healthcare provider for evaluation if you experience large amounts of watery diarrhea or bloody diarrhea. Intracranial hypertension (pseudotumor cerebri): Doxycycline has been associated with an increase in intracranial pressure. Symptoms include headache, blurred vision, double vision, or vision loss. If visual disturbance occurs while taking doxycycline, seek a prompt eye evaluation. Precautions Doxycycline should not be taken during pregnancy, as it can harm a fetus. Because doxycycline can cause permanent tooth discoloration in developing teeth, it should not be used in children 8 years and younger unless the benefits outweigh the risk (e.g., treatment of anthrax, Rocky Mountain spotted fever). Alternative Treatments for a Sinus Infection The usual first-line antibiotic chosen for treating a bacterial sinus infection in people who are not allergic to penicillin is Amoxil (amoxicillin) or Augmentin (amoxicillin-clavulanate). The other antibiotic option besides doxycycline for people allergic to penicillin is a respiratory fluoroquinolone such as levofloxacin or Avelox (moxifloxacin). Over-the-counter (OTC) products can help with symptomatic relief. These can include: Summary Doxycycline is a tetracycline antibiotic prescribed for acute bacterial sinusitis. It is usually the treatment of choice for people who cannot take penicillin. It’s typically prescribed for five to seven days and is tolerated with minimal side effects by most people. You should start to feel better within three to five days of starting doxycycline; if you don’t feel better or your symptoms worsen, this could mean a virus or a resistant bacteria cause your sinus infection. You should return to a healthcare provider for reevaluation. Frequently Asked Questions Doxycycline is similarly effective to amoxicillin for treating a sinus infection. Amoxicillin is usually chosen in people who do not have an allergy to penicillin, while doxycycline is used in people with a history of penicillin allergy. If you have no improvement in symptoms after taking doxycycline for three to five days, contact your healthcare provider. Potential causes for non-response include sinusitis caused by a virus or resistant bacteria. You might need a different treatment. Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy. By Carrie Yuan, PharmD Carrie Yuan PharmD is a clinical pharmacist with expertise in chronic disease medication management for conditions encountered in primary care. Share Feedback Was this page helpful? Thanks for your feedback! What is your feedback? Other Helpful Report an Error

This article summarizes an opinion piece in the Proceedings of the National Academy of Science. It explores the history and language of the “standard model” of infectious disease, SIR – Susceptible, Infectious, Recovered. Infectious – the Germ Theory In 1890 Robert Koch published his criteria for the causal relationship between microbes and disease, setting the stage for the germ theory of disease. The influence of this theory cannot be overestimated – it has explained our global life expectancy remaining stubbornly stuck at two to three decades. It allows us to act upon that information with “the advent of hygiene, vaccines, aseptic surgery, and antibiotics….” His first postulate states that a given pathogen is found in all patients with the corresponding disease and not in healthy individuals. But as herpes zoster and COVID clearly demonstrate, that is not true – many patients are host to the microorganism, but far fewer have clinical manifestations, “the corresponding disease.” Tuberculosis is another example of an “infection enigma.” Mycobacterium tuberculosis, the infectious agent of the continuing global problem of tuberculosis, is estimated to reside in 25% of the global population. Yet 90% of those individuals have a latent form, where the mycobacterium is present, it is not contagious, and the patient has no clinical manifestations. René Dubos, more than 70 years ago, recognized these “silent” infections must be due to “a recent causal “weakening” of the sick host, after infection, but before the development of disease.” Those weakenings, or as he described, “changing circumstances,” were attributable to external environmental stressors, “ecological” in the sense that the stress originated in the environment, which could also, in turn, be modified by the host. Vaccines, social distancing, and masks are all environmental modifications. Susceptibility Moving toward genetics Sickle cell anemia or sickle cell disease (SCD) is an inherited disorder, an abnormality in the hemoglobin molecule that reduces oxygen transport ability and causes clumping and clotting. The resultant clumps and clots obstruct blood flow in the smaller vessels and provoke extremely painful sickle cell crises damaging organs like the kidneys. In 1949 a South African geneticist, Anthony C. Allison, was faced with a puzzle. When the hemoglobin abnormality of SCD is found in both genes contributed by the parents, the disease is fatal. But he discovered that upwards to 20% of the Kenyans he assessed had the far less lethal trait, one, not two, abnormal genes. He reported in 1954 that the underlying reason for such a high percentage was that “sickle cell trait provides large African populations with 10-­fold greater protection against the risk of cerebral malaria…[a] population level has never been surpassed by candidate gene or genome-­wide approaches.” Several other notable examples of susceptibility to infections and our underlying genetics exist. Bacterial appendicitis is infectious but not contagious. There are familial clusters of appendicitis. Studies of tuberculosis in twins from the 30s and 40s show a more significant “sharing” of TB with genetically identical (monozygotic) twins at 90% than dizygotic twins, born with differing genetics, at 20% The 1980 HIV epidemic demonstrated how an acquired immunodeficiency could result in specific rare infections, like pneumocystis pneumonia (PCP), caused by the fungus Pneumocystis jirovecii. Similarly, the immunosuppression from drugs used to suppress rejection in transplantation resulted in infections labeled “opportunistic.” All of these instances, from recognizable, overt immunologic compromise, strongly suggest a role for genetics in increasing or decreasing the susceptibility of a host to an infectious organism. Immunity is a spectrum Not all genetic errors affect every individual with the error – a genetic finding termed incomplete penetrance (complete penetrance affects all individuals with the error). The presence of a BRCA (BReast CAncer) gene mutation reduces tumor suppression elevating the risk of breast and ovarian cancer in those with the mutation. Women with a BRCA1 mutation have a penetrance, a clinical manifestation, of 55 to 72%; those with BRCA2 have a penetrance of 45 to 69%. Some inborn errors occur in cytokines; the small protein foot soldiers invoked in immunity’s inflammatory response. Job’s Syndrome, a rare syndrome involving an error in the interleukin cytokine, results in recurrent skin staph infections. [1] Our immunologic responses are not always correct, and we may develop antibodies to ourselves, termed autoantibodies. The presence of autoantibodies may mimic inborn errors in cytokines by reducing the numbers and effectiveness of the normal cytokines, creating an “autoimmune phenocopy” of a disease. Antibodies to one of the interferons (IFN-­α), another of the cytokines involved in our immune defense against viruses, is present in about 1% of adults under age 65 but increase to 4 to 7% in older populations. In a study of 3,595 hospitalized patients with “severe” COVID, autoantibodies to IFN-­α were found in 13.6% and were present in 18% of the patients who died. In a new study reported in Nature, the same research group identified a variant of the HLA gene that confers a more robust immunity to COVID. In their study, 13,000 individuals in a donor registry, whose genes had been characterized were found to be positive for COVID. But 10% of those individuals were symptom-free. Roughly 20% of these symptom-free individuals had a specific mutation of their HLA-B gene that made them “especially potent at clearing SARS-CoV-2.” And when that mutation, which has an incidence of roughly 10% in those with European ancestry, is homozygous (coming from both mother and father), it increases the likelihood of remaining asymptomatic in the presence of a positive COVID test 8-fold. A new paradigm “It is, admittedly, difficult to measure the weights of causal factors, and comparing the respective contributions of the germ and host theories is intellectually challenging.” It is the nature of scientific knowledge to build upon the work already done. The development of the germ theory as the explanation of infection has served us well, but it was developed before we had knowledge of immunity, let alone an immune system. For all its explanatory power, the germ theory could not incorporate what Donald Rumsfeld characterized as the “unknown unknowns.” Our understanding

Sepsis (Adobe Stock, unknown) A recent cost-consequence analysis in Critical Care Explorations has revealed that utilizing the IntelliSep Index (ISI) for early sepsis diagnosis in the emergency department (ED) is both more effective and less expensive in preventing mortality compared to procalcitonin. Christopher S. Hollenbeak, PhD, Department Head of Health Policy and Administration and Professor of Surgery and Public Health Sciences at Penn State University, answered questions from Infection Control Today® (ICT®) about the study. “Sepsis causes 270,000 deaths and costs $38 billion annually in the United States, “according to the authors of the study. “Most cases of sepsis present in the emergency department (ED), where rapid diagnosis remains challenging. The IntelliSep Index (ISI) is a novel diagnostic test that analyzes characteristics of WBC [white blood cell] structure and provides a reliable early signal for sepsis. This study performs a cost-consequence analysis of the ISI relative to procalcitonin for early sepsis diagnosis in the ED.” ICT: A summary of the key findings and why they are important. Christopher S. Hollenbeak, PhD, Department Head of Health Policy and Administration and Professor of Surgery and Public Health Sciences at Penn State University, (Photo courtesy of Cytovale) Christopher S. Hollenbeak, PhD: Our team performed a cost-consequence analysis to evaluate the health economics of using a new IntelliSep test to inform sepsis care in the ED. In this analysis, IntelliSep was compared to procalcitonin (PCT), a biomarker related to bacterial infection evaluated as a sepsis indicator and performed similarly to the standard of care. The study supported the hypothesis that using Intellisep as part of the sepsis diagnostic strategy may provide effective reductions in the clinical and financial burden of treating sepsis compared to a procalcitonin diagnostic strategy. The IntelliSep test could serve as an invaluable element of sepsis care by quickly and efficiently focusing care on those with the highest risk of sepsis while expediting the care of those with lower risk. ICT: What is the practical application of the key findings for infection preventionists from this study? CSH: The search for solutions and improvements in sepsis care has become increasingly complicated as the incidence of sepsis continues to rise due to increased awareness, changes in the population’s risk profile, such as increasing age and comorbidities, and the impact of the COVID-19 pandemic on pre-existing workforce shortages. Solutions that will safely reduce the cost of care without sacrificing outcomes will require addressing the many factors driving the soaring economic burden of the disease in this new, post-pandemic era of medicine. This study suggests that risk stratification informed by the IntelliSep test could improve survival for patients with sepsis as compared to that reported with PTC and do so with an expected cost of more than $800 less than that for PCT. This finding is important given that outcomes in sepsis have been proven dependent upon prompt recognition and action. ICT: What results surprised you, if any? CSH: One of the more surprising aspects of the study is that an IntelliSep-informed treatment process saves, on average, over $800 per patient tested while also providing a small mortality benefit. This indicates that the IntelliSep test may enable centers to decrease the economic burden of sepsis and achieve better clinical outcomes. And while the study design relies on many assumptions, it is a home run. ICT: What, if any, future research will there be related to this one CSH: Great question. This study approximates the health-economic outcomes of using the IntelliSep test to inform clinical care of potentially septic patients. The IntelliSep test recently received FDA Clearance. Applying the test in the care environment will offer another opportunity to capture clinical and financial outcome information and add additional information to this work. ICT: Is there anything else that you would like to add? CSH: In our evaluation, the IntelliSep test showed that using the test to inform sepsis care is clinically and economically superior to a strategy informed by PCT. This performance is encouraging, given that the test can be performed in under 10 minutes and utilizes whole blood from a standard EDTA draw. Given its performance and fit within hospital workflows, the trial represents a promising new development in managing sepsis patients.

The BDN Opinion section operates independently and does not set newsroom policies or contribute to reporting or editing articles elsewhere in the newspaper or on bangordailynews.com. Lisa Jarvis is a Bloomberg Opinion columnist covering biotech, health care and the pharmaceutical industry. Even as COVID has faded into the background for most of the public, our curiosity about the virus’s idiosyncrasies hasn’t waned. Why does one member of a household suffer a hacking cough but another not even a sniffle? Why does long COVID afflict some and not others? A cluster of new studies suggests some of the answers lie in our genes. What scientists are learning could help them develop better vaccines in the future — either for new variants of COVID-19 or entirely new forms of SARS. Mild cases or asymptomatic infections have been relatively unstudied. Scientists’ focus on the sickest patients wasn’t just because of the urgency to save lives, but because it’s simply easier to study people in a controlled setting like a hospital. Collecting DNA, sequencing it and then tracking healthy people out in the community is an impossibly tall order. A team of researchers, led by the University of California, San Francisco’s Jill Hollenbach, found a clever way of getting around that problem by tapping into a group of people who had already given up their DNA: bone marrow donors. The team invited donors to participate in an ongoing project at UCSF called the COVID-19 Citizen Science Study. Hollenbach’s team recruited nearly 30,000 volunteers to download an app and, when they eventually tested positive for the virus, complete a questionnaire about their symptoms. Although they’ve been collecting data from that cohort for years now, this study was limited to the time before people were vaccinated so the results could be cleanly interpreted, Hollenbach said. They were looking for differences in a group of genes called HLA (short for human leukocyte antigen) that carry the recipes for proteins that help our immune cells distinguish between our own biological detritus and unwelcome invaders. The proteins show little pieces of viruses to our T-cells, which take this as an invitation to attack. Because T-cells have a long memory, they swoop in again fast the next time a similar virus invades. The researchers found that people who carried one copy of a version of a gene called HLA-B*15:01 were more than twice as likely to remain asymptomatic after being infected with COVID. And people who inherited two copies of the gene (one from each parent) were eight times more likely to never suffer symptoms. Hollenbach’s team found that this particular flavor of HLA is very good at recognizing garden variety coronaviruses, and the T-cells exposed to those were later very good at detecting important bits of SARS-CoV-2. In other words, people with this variant who also had, say, a common cold “have this kind of superpower” of managing their COVID infection to the point where they don’t have symptoms, she explains. “I think their findings are very exciting,” said Jean-Laurent Casanova, a Rockefeller University scientist who studies the relationship between our genes and susceptibility to infectious diseases. “It suggests that T-cells are involved in the early phase of SARS-CoV-2 infection, and that a strong T-cell response can blunt infection and prevent clinical manifestations.” @media ( min-width: 300px ){.newspack_global_ad.block_64c05594055dc{min-height: 100px;}} Another study, yet to be peer reviewed, offers genetic ties to the other end of the spectrum: when people suffer lingering symptoms. Researchers compared about 6,500 people with a long COVID diagnosis to nearly a million people without. People were 1.6 times more likely to develop long COVID if they had a variant in a gene called FOXP4. That same gene is also known to be a culprit in lung cancer and severe COVID. While these studies help explain the wide range of responses to the virus, many questions remain unanswered. For example, why were some people not just asymptomatically infected, but never infected? Casanova is interested in, say, that “health care worker without a mask in 2020 that has repeatedly tested negative, negative, negative. They’re seemingly resistant to infection and we think there’s a genetic basis for that.” His lab is currently analyzing some 2,000 genomes among that group to try to fish out the gene responsible. Scientists would also like to understand if there are genes involved in other, rarer situations, like the people whose infections cause brain swelling, or others that get a form of heart inflammation called myocarditis after getting the mRNA vaccines. @media ( min-width: 300px ){.newspack_global_ad.block_64c0559418de4{min-height: 100px;}} Like all science, understanding the genetic link to susceptibility is just pulling on the first thread. So much other work needs to be done to unravel the rest. Hollenbach’s findings about asymptomatic COVID, for example, should prompt more exploration into alternate approaches to vaccination. The existing vaccines all try to prevent infection altogether, but there could be merit in focusing on vaccines designed to take advantage of that memory T-cell response that seems to work so well for people with the right genetics. “Maybe you get infected, but manage it so quickly and effectively that you don’t experience illness,” she said. It is important to keep unraveling these mysteries. They teach us about better ways to address this virus, which we know is here to stay, and also contribute to the broader understanding of how genes shape the immune response. More articles from the BDN

Naegleria fowleri, the amoeba responsible for the child’s death, enters the body via the nose and travels to the brain where it begins destroying tissue. (Image credit: Shutterstock) A 2-year-old boy in Nevada has died after being infected with a “brain-eating” amoeba after visiting a natural hot spring in the state. In a statement published July 20, the Nevada Division of Public and Behavioral Health (DPBH) announced that the boy — named Woodrow Bundy, according to a Facebook post from his family — was likely exposed to the microbe at Ash Springs in Lincoln County. According to the DPBH, the Centers for Disease Control and Prevention (CDC) confirmed that the child’s condition was caused by Naegleria fowleri, a single-cell organism known to cause such brain infections. Typically found in soil and warm fresh water, such as lakes, rivers, hot springs and sometimes freshwater spouting from splash pads, the amoeba can cause a rare but deadly infection of the brain, known as primary amebic meningoencephalitis (PAM). “If you wind up getting infected with it, chances are you’re going to die,” Brian Labus, an epidemiologist and associate professor at the University of Nevada, told FOX5. “Very few people have actually survived this type of infection.” Related: ‘Brain-eating’ amoeba ruled out in ‘cluster of illnesses’ in Oklahoma. What could the cause be? CDC figures show that, of the 154 people known to have been infected by N. fowleri between 1962 and 2021, only four have survived. People typically become infected when water carrying the amoeba enters their nose, likely during swimming or diving, and travels up to the brain via nerves in the nasal cavity. From there, N. fowleri begins to destroy brain tissue, resulting in its nickname as a “brain-eating amoeba.” “It progresses rather rapidly because it’s actively destroying brain tissue, so it’s very difficult for your body to deal with something like that and fight it off,” Labus told FOX5. Symptoms of PAM usually begin around five days after exposure to the amoeba, the CDC states, and they can include headaches, fever, nausea or vomiting. At later stages of the disease, victims may experience a stiff neck and confusion and show a lack of attention to people and surroundings, and they may also develop seizures or hallucinations. They may even fall into a coma. Usually, a patient will die around five days after symptoms emerge. According to the CDC, young boys like Bundy are at the highest risk of being infected with N. fowleri, compared to other demographics. The reason why is unclear, but the agency suggests this could be because boys more often take part in water activities, such as diving and playing in the sediment at the bottom of lakes and rivers. (The DPBH didn’t note whether Bundy was swimming at the time of his exposure or potentially encountered the amoeba some other way.) N. fowleri can’t be spread from one person to another — it enters the body only through exposure to contaminated water. The DPBH noted that there is “no means to eliminate the ameba from fresh bodies of water,” so people should “always assume there is a risk,” of exposure, even if that risk is extremely low. “The only sure way to prevent an infection is to avoid water-related activities in warm fresh water, especially during summer months,” the CDC notes. People who choose to swim, however, can reduce their risk of infection by stopping water going up their nose. This could involve avoiding diving, using nose clips or not putting your head under water, the CDC suggests.

This article summarizes an opinion piece in the Proceedings of the National Academy of Science. It explores the history and language of the “standard model” of infectious disease, SIR – Susceptible, Infectious, Recovered. Infectious – the Germ Theory In 1890 Robert Koch published his criteria for the causal relationship between microbes and disease, setting the stage for the germ theory of disease. The influence of this theory cannot be overestimated – it has explained our global life expectancy remaining stubbornly stuck at two to three decades. It allows us to act upon that information with “the advent of hygiene, vaccines, aseptic surgery, and antibiotics….” His first postulate states that a given pathogen is found in all patients with the corresponding disease and not in healthy individuals. But as herpes zoster and COVID clearly demonstrate, that is not true – many patients are host to the microorganism, but far fewer have clinical manifestations, “the corresponding disease.” Tuberculosis is another example of an “infection enigma.” Mycobacterium tuberculosis, the infectious agent of the continuing global problem of tuberculosis, is estimated to reside in 25% of the global population. Yet 90% of those individuals have a latent form, where the mycobacterium is present, it is not contagious, and the patient has no clinical manifestations. René Dubos, more than 70 years ago, recognized these “silent” infections must be due to “a recent causal “weakening” of the sick host, after infection, but before the development of disease.” Those weakenings, or as he described, “changing circumstances,” were attributable to external environmental stressors, “ecological” in the sense that the stress originated in the environment, which could also, in turn, be modified by the host. Vaccines, social distancing, and masks are all environmental modifications. Susceptibility Moving toward genetics Sickle cell anemia or sickle cell disease (SCD) is an inherited disorder, an abnormality in the hemoglobin molecule that reduces oxygen transport ability and causes clumping and clotting. The resultant clumps and clots obstruct blood flow in the smaller vessels and provoke extremely painful sickle cell crises damaging organs like the kidneys. In 1949 a South African geneticist, Anthony C. Allison, was faced with a puzzle. When the hemoglobin abnormality of SCD is found in both genes contributed by the parents, the disease is fatal. But he discovered that upwards to 20% of the Kenyans he assessed had the far less lethal trait, one, not two, abnormal genes. He reported in 1954 that the underlying reason for such a high percentage was that “sickle cell trait provides large African populations with 10-­fold greater protection against the risk of cerebral malaria…[a] population level has never been surpassed by candidate gene or genome-­wide approaches.” Several other notable examples of susceptibility to infections and our underlying genetics exist. Bacterial appendicitis is infectious but not contagious. There are familial clusters of appendicitis. Studies of tuberculosis in twins from the 30s and 40s show a more significant “sharing” of TB with genetically identical (monozygotic) twins at 90% than dizygotic twins, born with differing genetics, at 20% The 1980 HIV epidemic demonstrated how an acquired immunodeficiency could result in specific rare infections, like pneumocystis pneumonia (PCP), caused by the fungus Pneumocystis jirovecii. Similarly, the immunosuppression from drugs used to suppress rejection in transplantation resulted in infections labeled “opportunistic.” All of these instances, from recognizable, overt immunologic compromise, strongly suggest a role for genetics in increasing or decreasing the susceptibility of a host to an infectious organism. Immunity is a spectrum Not all genetic errors affect every individual with the error – a genetic finding termed incomplete penetrance (complete penetrance affects all individuals with the error). The presence of a BRCA (BReast CAncer) gene mutation reduces tumor suppression elevating the risk of breast and ovarian cancer in those with the mutation. Women with a BRCA1 mutation have a penetrance, a clinical manifestation, of 55 to 72%; those with BRCA2 have a penetrance of 45 to 69%. Some inborn errors occur in cytokines; the small protein foot soldiers invoked in immunity’s inflammatory response. Job’s Syndrome, a rare syndrome involving an error in the interleukin cytokine, results in recurrent skin staph infections. [1] Our immunologic responses are not always correct, and we may develop antibodies to ourselves, termed autoantibodies. The presence of autoantibodies may mimic inborn errors in cytokines by reducing the numbers and effectiveness of the normal cytokines, creating an “autoimmune phenocopy” of a disease. Antibodies to one of the interferons (IFN-­α), another of the cytokines involved in our immune defense against viruses, is present in about 1% of adults under age 65 but increase to 4 to 7% in older populations. In a study of 3,595 hospitalized patients with “severe” COVID, autoantibodies to IFN-­α were found in 13.6% and were present in 18% of the patients who died. In a new study reported in Nature, the same research group identified a variant of the HLA gene that confers a more robust immunity to COVID. In their study, 13,000 individuals in a donor registry, whose genes had been characterized were found to be positive for COVID. But 10% of those individuals were symptom-free. Roughly 20% of these symptom-free individuals had a specific mutation of their HLA-B gene that made them “especially potent at clearing SARS-CoV-2.” And when that mutation, which has an incidence of roughly 10% in those with European ancestry, is homozygous (coming from both mother and father), it increases the likelihood of remaining asymptomatic in the presence of a positive COVID test 8-fold. A new paradigm “It is, admittedly, difficult to measure the weights of causal factors, and comparing the respective contributions of the germ and host theories is intellectually challenging.” It is the nature of scientific knowledge to build upon the work already done. The development of the germ theory as the explanation of infection has served us well, but it was developed before we had knowledge of immunity, let alone an immune system. For all its explanatory power, the germ theory could not incorporate what Donald Rumsfeld characterized as the “unknown unknowns.” Our understanding

Certain types of infection have previously been linked to cognitive impairment, including SARS-CoV-2, especially among patients experiencing long COVID-19; however, it is unclear whether these cognitive deficits can improve over time. To analyze whether these symptoms improve more than a year post infection, a study published in eClinicalMedicine performed 2 rounds of cognitive testing to conduct longitudinal tracking of cognitive performance and deficits up to 2 years after being infected with the virus. Image credit: bizoo_n – stock.adobe.com Past studies have analyzed small, hospitalized cohorts during the first year of the pandemic (prior to vaccination) with somewhat short follow-up (approximately 6-12 months since infection). Further, few studies have used a longitudinal approach to assess the individuals’ cognitive trajectories and whether recovery can influence cognitive performance, according to the authors of the current study. The United Kingdom COVID Symptom Study Biobank (CSSB) held 2 rounds of testing. Round 1 was conducted between July 12, 2021, and August 27, 2021, and round 2 between April 28, 2022, and June 21, 2022), to assess the effects of COVID-19 exposures on cognitive accuracy and reaction times. The virus’s presences, correlations, magnitude, and persistence of effects are relatively unexplored within community-based cases, according to the investigators. There was a total of 3335 individuals who completed round 1, of whom 1768 had also completed round 2. Study participants were divided into 5 groups depending on their infection status and the associated symptom durations at the time of study invitation. Case group 1 included individuals with positive SARS-CoV-2 test but no associated symptoms (asymptomatic COVID); case group 2 included individuals with positive SARS-CoV-2 test with between 1 and 13 days of associated symptoms; case group 3 included individuals with positive SARS-CoV-2 test and at least 28 days of associated symptoms (long COVID); control group 1 included individuals with negative SARS-CoV-2 test with at least 28 days of symptoms at the time of test (long non-COVID); and control group 2 (“healthy controls”) included individuals with negative SARS-CoV-2 test associated with 1-3 consecutive days of symptoms at the time of test with a low symptom burden (healthy non-COVID). In both rounds 1 and 2 of assessment, participants completed 12 different cognitive tasks that assessed different cognitive domains, including working memory, attention, reasoning, and motor control, with a longitudinal analysis assessing change in performance between the 2 rounds. Effects of COVID-19 impairment on cognitive accuracy and reaction times were evaluated, as well as how ongoing symptoms after COVID-19 infection influenced self-perceived recovery. The study results indicate that individuals with community-based SARS-CoV-2 infection present cognitive deficits in performance accuracy compared to their non-infected counterparts when among groups with a ≥12-week symptom duration following infection. Additionally, they presented no evidence that SARS-CoV-2 infection had impacted their reaction time when completing the cognitive tasks. These individuals had self-reported as not being fully recovered. For those who had discernable deficits at initial testing, longitudinal follow-up indicated that the deficits persisted for nearly 2 years since infection. Alternatively, the individuals who reported feeling recovered presented no impairment, including those who experienced long-term illness or symptoms. The findings are similar to a previous study that had reported higher cognitive performance for the 42 participants who self-reported being recovered compared to 117 who experienced ongoing symptoms. The recovery rate was highly correlated with the duration of symptoms, which showed a recovery rate of only 17% for those with ≥12-week symptom duration at 38 weeks since infection. Limitations of the current study include potential selection and participation biases, findings were limited by the CSSB cohort composition, and data that would further contribute to the study were lacking (i.e., prior neurovascular and neurodegenerative comorbidities, cognitive assessment data prior to infection). Further, the study relied on participants voluntarily logging their symptoms and COVID-19 test results for the researchers to derive their infection status and duration of symptoms. Reference Cheetham N J, Penfold R, Giunchiglia V, et al. The effects of COVID-19 on cognitive performance in a community-based cohort: a COVID symptom study biobank prospective cohort study.eClinicalMedicine. Volume 0, Issue 0, 102086 https://doi.org/10.1016/j.eclinm.2023.102086

Urinary tract infections are not only painful, unpleasant, and potentially hazardous but also present a considerable challenge for physicians. They’re difficult to diagnose quickly, and conventional diagnostic typically methods take several days. These are several days in which the doctor usually prescribes a treatment, without being sure whether or not it will actually be effective. Electron micrograph of phages. Image credits: Matthew Dunne / ScopeM / ETH Zurich. A team of researchers at ETH Zurich wanted to have a better diagnostic tool. In partnership with Balgrist University Hospital, they have developed a rapid test that uses bacteriophages — viruses that infect bacteria — to identify the pathogens that cause the infection. The team genetically modified the phages to make them more efficient to target bacteria. Each type of phage targets only one particular type or strain of bacteria. The researchers led by Martin Loessner are now taking advantage of this characteristic with their new rapid test. Better testing for bladder infections Initially, the researchers focused on identifying phages capable of effectively targeting the three primary bacteria responsible for urinary tract infections: Escherichia coli, Klebsiella, and Enterococci. These natural phages then underwent modifications to prompt any bacteria they infect to generate a readily detectable light signal. This method enabled the researchers to reliably detect the pathogenic bacteria from a urine sample in less than four hours – instead of the several days of conventional methods. It’s still early days, but once further refined, the approach could enable the researchers to prescribe antibiotics right after diagnosis. But it doesn’t end there. This method also allows doctors to predict which patients are likely to respond well to tailored phage therapy. This is because the strength of the light signal produced during the assay shows how efficient the phages are in attacking bacteria. The stronger the glow, the better the bacterium will respond to the therapy — so clinicians can prescribe the most effective treatment from the get go. Phage therapies go way back but were largely left behind in Western countries with the discovery of penicillin. However, as antibiotic resistance increases, they are increasingly becoming a subject of interest. They also have the important advantage of going after one single bacterium, instead of trying to cover a wide spectrum, as many antibiotics do. However, previous approaches had one problem. “Phages aren’t interested in completely killing their host, the pathogenic bacterium,” Samuel Kilcher, a study author, said in a statement. To address this, the team genetically modified the phages. These can now produce new phages in the infected host and their own antibiotics. “There are also many academic and commercial clinical trials underway worldwide that are systematically investigating the potential of natural and genetically optimized phages,” Matthew Dunne, study author, said in a statement. However, there’s a long way before this happens, as extensive clinical studies still need to be carried out. While this was only a proof of concept for now, the team will now test its efficacy in a clinical trial with a group of selected patients. The findings were published in this study and in this one, both in the journal Nature Communications.

Two cases of Vibrio, a potentially serious and sometimes fatal illness, were reported in Dare County from July 20 to 25, the local health department announced today. The new cases bring the statewide total to 47 so far this year, according to North Carolina health department data. This number is significantly higher than the 31 cases reported for all of 2017. In 2019, the state logged 41 cases. Vibrio bacteria is found naturally in warm sea water and brackish water. People can contract Vibrio by getting the contaminated water in open wounds, cuts, sores, punctures or burns. For example, people who cut themselves while peeling crabs or stepping on sharp objects on the shore and then coming into contact with the bacteria can be at risk. People can also become ill with Vibrio after eating raw or undercooked shellfish, especially oysters. Signs of infection include fever and chills, nausea or vomiting, or a skin infection that appears red and warm to the touch. People should seek medical attention immediately if they are experiencing symptoms after eating shellfish or being exposed to seawater. Those at higher risk for infection and complications include those with compromised immune systems, especially those with chronic liver disease: https://www.cdc.gov/vibrio/faq.html. Ocean temperatures along the North Carolina coast are running five to seven degrees above average for July. (Map: NOAA) Most cases of Vibrio in the U.S. occur from May through October, when water temperatures are warm. But climate change is heating up the oceans, lengthening the seasons when the bacteria can thrive — and extending the Vibrio’s range farther north. This summer abnormally hot marine waters have spread from the Gulf of Mexico, the Caribbean and north to the mid-Atlantic. For example, at Oregon Inlet on the Outer Banks the water temperature today is 87.3 degrees, according to federal weather data. The average water temperature for July at that monitoring station is 80.3 degrees. Farther south in Beaufort, the water is 86.9 degrees, more than seven degrees higher than the monthly average. At 85.5 degrees, Wilmington and Wrightsville are running five to seven degrees hotter than average. The USDA reported last month that climate change is expected to increase the human and financial costs of Vibrio infections. According to scientific projections, U.S. cases of illness from Vibrio infections could increase 50% by 2090 compared with 1995 because of higher sea surface temperatures associated with moderate increases in greenhouse gas concentrations, the USDA report said. Annual total cost of these illnesses more than doubles from nearly $2.6 billion in 1995 to $6.1 billion in 2090 (in 2022 dollars), based on this scenario. About 95% of total costs are attributable to deaths caused by Vibrio infections, according to the USDA.

TUESDAY, July 25, 2023 (HealthDay News) — Results from more than 26,000 respiratory tests in late 2022 found simultaneous infections with COVID-19, influenza or respiratory syncytial virus (RSV) in more than 1% of positive tests. Co-infections were especially widespread in children and teens. In people under age 21, researchers saw a 6% co-infection rate of SARS-CoV-2 and influenza A.