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Published17 hours agoSharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesBy Patience Atuhaire BBC News, KampalaAn Ebola patient has died at a hospital in Uganda’s capital, the health ministry has confirmed.He was the 19th victim in the current outbreak of the deadly virus but the first to die in Kampala.There have been 54 confirmed cases in Uganda but no others have been recorded in the city.Twenty people have recovered including five medics from the first hospital where a case was treated. They were discharged on Tuesday.The person who died in Kampala was already known to the authorities as having potentially come into contact with the virus. Why is Uganda’s Ebola outbreak so serious?He was from outside the city but Health Minister Dr Jane Ruth Aceng said the man ran away from his village, disguised his identity and visited a traditional healer in a different region.He died at Kiruddu National Referral Hospital last Friday, but the death has only just been confirmed.Dr Aceng said that teams which treated him were alert to the dangers and had protected themselves, because the patient arrived at the hospital when he was seriously ill. Forty-two people who he may have come into contact with have been identified and are being followed up. Ebola spreads between humans by direct contact with bodily fluids and contaminated environments. Funerals can be a particular risk if mourners have direct contact with the body.Dr Aceng added that there are currently no other confirmed Ebola cases in Kampala, although the city and surrounding districts are considered high risk.The outbreak began in September in Mubende district, 80km (50 miles) west of the capital.A 24-year-old-man was the first known Ebola death, and six members of his family also died. Four health workers have also been among the victims, including a doctor from Tanzania.Medics had previously expressed concern about the lack of adequate personal protective equipment (PPE) such as gloves and masks. They had also called for Mubende to be put under quarantine.However, President Yoweri Museveni ruled out restrictions, saying: “Ebola is not spread like corona[virus]” as it is not an airborne disease.No effective Ebola vaccine is available yet, because the Sudan strain circulating in central Uganda is different to the Zaire strain that has afflicted West Africa and the Democratic Republic of Congo and which can be immunised against.Experts say it is unrealistic to think Ebola will ever be eradicated, but with swift action and effective contact tracing it is now easier to prevent a crisis.More on this storyWhy is Uganda’s Ebola outbreak so serious?30 SeptemberDoctors in Ebola zone strike over safety fears26 September

An Australian nation-wide population-based follow-up study published in the Journal of Dental Research (JDR) has provided evidence that exposure to fluoridated water by young children was not negatively associated with child emotional, behavioral development and executive functioning in their adolescent years.
The study by Professor Loc Do of the University of Queensland Faculty of Health and Behavioural Sciences, School of Dentistry and colleagues examined the effect of early childhood exposures to water fluoridation on measures of school-age executive functioning and emotional and behavioral development in a population-based sample. This longitudinal follow-up study used information from Australia’s National Child Oral Health Study of 2012-14. Children aged 5-10 years at the baseline were contacted again after 7-8 years, before they had turned 18 years of age.
Percent lifetime exposed to fluoridated water (%LEFW) from birth to the age of five years was estimated from residential history and postcode-level fluoride levels in public tap water. Measures of children’s emotional and behavioral development were assessed by the Strength and Difficulties Questionnaire (SDQ), and executive functioning was measured by the Behavior Inventory of Executive Functioning (BRIEF). Multivariable regression models were generated to compare the associations between the exposure and the primary outcomes, controlled for covariates. An equivalence test was also conducted to compare the primary outcomes of those who had 100%LEFW against those with 0%LEFW.
Sensitivity analysis was also conducted. A total of 2,682 children completed SDQ and BRIEF, with mean scores of 7.0 (95%CI: 6.6, 7.4) and 45.3 (44.7, 45.8), respectively. Those with lower %LEFW tended to have poorer scores on the SDQ and BRIEF. Multivariable regression models reported no association between exposure to fluoridated water and the SDQ and BRIEF scores. Low household income, identifying as Indigenous, and having a neurodevelopmental diagnosis were associated with poorer SDQ/BRIEF scores.
The study concluded that exposure to fluoridated water during the first five years of life was not associated with altered measures of child emotional and behavioral development and executive functioning. Children who had been exposed to fluoridated water for their whole early childhood had their measures of emotional, behavioral development and executive functioning at least equivalent to that of children who had no exposure to fluoridated water.
“Water fluoridation is unquestionably effective in preventing dental caries, and this study is an important addition to the body of literature documenting the safety of water fluoridation,” said IADR President Brian O’Connell, Dean of the Faculty of Health Sciences, Trinity College Dublin, Ireland. “The IADR recently reaffirmed its support for water fluoridation as this public health measure has a high benefit/cost ratio and benefits deprived communities the most, thus reducing health inequalities.”
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Cerebral aneurysms appear in 5% to 8% of the general population. The blood vessel rupture and resultant blood leakage within the brain can lead to severe stroke or fatal consequences. Over one quarter of patients who experience a hemorrhagic stroke die before reaching a health care facility.
Predicting the rupture of aneurysms is crucial for medical prevention and treatment. In Physics of Fluids, by AIP Publishing, researchers from the Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, and the Indian Institute of Technology Madras, developed a patient-specific mathematical model to examine what aneurysm parameters influence rupture risk prior to surgery.
Aneurysms occur when the weakest point of a blood vessel thins, expands, and, after a certain limit, bursts. In the case of cerebral aneurysms such as internal carotid artery bifurcation aneurysm, blood leaks into the intracranial cavity
“Since clinicians encounter these aneurysms at various growth stages, it motivated us to analyze internal carotid artery aneurysms in a systematic manner,” said B. Jayanand Sudhir, of the Sree Chitra Tirunal Institute for Medical Sciences and Technology. “The current study is a sincere and systematic attempt to address the dynamics of blood flow at various stages to understand the initiation, progression, and rupture risk.”
The team examined the aspect ratio and size ratio of aneurysms, which describe the shape and size characteristics of the bulge in a holistic manner. As these parameters increase and the aneurysm expands, the stress applied against the aneurysm walls and the time blood spends within the aneurysm increase. This leads the probability of rupture to rise.
Patient-specific computed tomography scans are fed into the model, which reconstructs the geometry and blood flow of the aneurysm. It then uses mathematical equations to describe the fluid flow, generating information about the blood vessel walls and blood flow patterns.
“This was feasible due to the access we had to the national supercomputing cluster for performing the computational fluid dynamics-based simulations,” said S.V. Patnaik of the Indian Institute of Technology Madras.
“The novelty of this work lies in close collaboration and amalgamation of expertise from clinical and engineering backgrounds,” said Sudhir. “The aneurysm models were of different shapes, which helped us build and understand the complexity of flow structures in multilobed cerebral aneurysms.”
Multilobed aneurysms, which include more than one balloonlike pocket of expanding blood, contained more complex blood flow structures than their single-lobed counterparts.
The authors hope to transform the rupture risk predictions into a user-friendly software to help clinicians and neurosurgeons prioritize and manage high-risk patients. They plan to use the model to assess the effectiveness of different treatment options for aneurysms.
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In a long-term prospective study of more than 600 older participants, Johns Hopkins Medicine researchers say they have evidence that higher levels of cell-free DNA circulating in the blood may signal increased risk of chronic inflammation associated with early signs of frailty and dementia.
The findings, published Oct. 11 in the Journal of Alzheimer’s Disease, could advance the search for relatively simple blood tests that detect risk of Alzheimer’s disease and other forms of cognitive decline.
Circulating cell-free genomic DNA, (ccf-gDNA) is a long identified product of natural cell death in the body. As cells die via apoptosis (programed cell death), the cells shrink, degrade their plasma membrane, and ultimately rupture and release their contents into the body, including DNA fragments. These fragments end up as free-range DNA in the bloodstream.
“These ccf-gDNA fragments may trigger long-term chronic inflammatory reactions that have previously been linked to the premature destruction and aging of tissues and organs, including the brain,” says Peter Abadir, M.D., associate professor of geriatric medicine and gerontology at the Johns Hopkins University School of Medicine. “The body sees these ccf-gDNA fragments as something that needs to be removed, therefore the body’s immune system is running at a higher rate than it should. Such immune system overdrive may be a factor in identifying the onset of dementia.”
For the new study, the researchers tested the blood of 631 people with the average age of 79 who showed no cognitive impairment when the study began. Participants received yearly physical and cognitive testing, at the time of each blood draw. Researchers found that during the eight-year study period, higher levels of ccf-gDNA in the blood were associated with increased cognitive decline and worsening frailty.
Alzheimer’s disease affects an estimated 6.5 million people in the United States, according to the Alzheimer’s Association, and there are no known cures or effective therapies. However, the potential of a blood test to identify those most at risk or in early stages could lead to supportive services and other interventions to plan for, compensate for or slow down worsening symptoms.
“Our world population is aging quickly. We have so many advances that have helped extend our life span, so the goal now is to live healthier as we age,” says Lolita Nidadavolu, M.D., Ph.D., assistant professor of geriatric medicine and gerontology at the Johns Hopkins University School of Medicine. “Dementia and frailty are increasing in frequency. Many people know someone affected by these conditions. With a single blood draw, we may have the potential to identify people who can benefit from early interventions.”
Moving forward, researchers say they hope to learn more about the cellular origins of ccf-gDNA fragments. If researchers can identify that a large amount of these fragments are coming from a specific type of cell, it is hoped that they can advance the search for drugs that target the aging and dementia process.
Other scientists who contributed to this research are Danielle Feger, Yuqiong Wu, Alden Gross, Jeremy Walston and Esther Oh of Johns Hopkins, and David Bennett and Francine Grodstein of Rush University.
This research was funded by the BrightFocus Foundation, the Johns Hopkins University Claude D. Pepper Older Americans Independence Center (which is funded by the National Institute on Aging of the National Institutes of Health), the Nathan W. and Margaret T. Shock Aging Research Foundation and the Nathan Shock Scholar in Aging Research Award. This study was also supported by the National Institute on Aging’s translational aging research training program and the institute’s epidemiology and biostatistics of aging program.
The authors have no conflict of interest to report.
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Adults with a genetic form of childhood-onset blindness experienced striking recoveries of night vision within days of receiving an experimental gene therapy, according to researchers at the Scheie Eye Institute in the Perelman School of Medicine at the University of Pennsylvania.
The patients had Leber Congenital Amaurosis (LCA), a congenital blindness caused by mutations in the gene GUCY2D. The researchers, whose findings are reported in the journal iScience, delivered AAV gene therapy, which carries the DNA of the healthy version of the gene, into the retina of one eye for each of the patients in accordance with the clinical trial protocol. Within days of being treated, each patient showed large increases, in the treated eye, of visual functions mediated by rod-type photoreceptor cells. Rod cells are extremely sensitive to light and account for most of the human capacity for low-light vision.
“These exciting results demonstrate that the basic molecular machinery of phototransduction remains largely intact in some cases of LCA, and thus can be amenable to gene therapy even after decades of blindness,” said study lead author Samuel G. Jacobson, MD, PhD, a professor of Ophthalmology at Penn.
LCA is one of the most common congenital blindness conditions, affecting roughly one in 40,000 newborns. The degree of vision loss can vary from one LCA patient to another but all such patients have severe visual disability from the earliest months of life. There are more than two dozen genes whose dysfunction can cause LCA.
Up to 20 percent of LCA cases are caused by mutations in GUCY2D, a gene that encodes a key protein needed in retinal photoreceptor cells for the “phototransduction cascade” — the process that converts light to neuronal signals. Prior imaging studies have shown that patients with this form of LCA tend to have relatively preserved photoreceptor cells, especially in rod-rich areas, hinting that rod-based phototransduction could work again if functional GUCY2D were present. Early results with low doses of the gene therapy, reported last year, were consistent with this idea.
The researchers used higher doses of the gene therapy in two patients, a 19- year-old man and a 32-year-old woman, who had particularly severe rod-based visual deficits. In daylight, the patients had some, albeit greatly impaired, visual function, but at night they were effectively blind, with light sensitivity on the order of 10,000 to 100,000 times less than normal.
The researchers administered the therapy to just one eye in each patient, so the treated eye could be compared to the untreated eye to gauge treatment effects. The retinal surgery was performed by Allen C. Ho, MD, a professor of Ophthalmology at Thomas Jefferson University and Wills Eye Hospital. Tests revealed that, in both patients, the treated eyes became thousands of times more light-sensitive in low-light conditions, substantially correcting the original visual deficits. The researchers used, in all, nine complementary methods to measure the patients’ light sensitivity and functional vision. These included a test of room navigation skills in low-light conditions and a test of involuntary pupil responses to light. The tests consistently showed major improvements in rod-based, low-light vision, and the patients also noted functional improvements in their everyday lives, such as “can [now] make out objects and people in the dark.”
“Just as striking was the rapidity of the improvement following therapy. Within eight days, both patients were already showing measurable efficacy,” said study co-author Artur V. Cideciyan, PhD, a research professor of Ophthalmology at Penn.
To the researchers, the results confirm that GUCY2D gene therapy to restores rod-based photoreceptor functions — and suggest that GUCY2D-LCA patients with more severe rod-based dysfunction are likely to benefit most dramatically from the therapy. The practical message is that there should be an emphasis on rod vision measurements at screening of LCA candidates and in monitoring them throughout a treatment trial.
The findings, the researchers said, also underscore the remarkable fact that in some patients with severe congenital vision loss, the retinal cell networks that mediate vision remain largely alive and intact, and need only the resupply of a missing protein to start working again, more or less immediately.
The ongoing clinical trial is registered at clinicaltrials.gov as trial NCT03920007.
Support for the research was provided by Atsena Therapeutics, Inc., the developer of the GUCY2D gene therapy; the National Institutes of Health (R01 EY11522); and by a CURE Formula grant from the Pennsylvania Department of Health.

Electronic gaming can precipitate life-threatening cardiac arrhythmias in susceptible children whose predisposition may have been previously unrecognized, according to a new report in Heart Rhythm, the official journal of the Heart Rhythm Society, the Cardiac Electrophysiology Society, and the Pediatric & Congenital Electrophysiology Society, published by Elsevier. The investigators documented an uncommon, but distinct pattern among children who lose consciousness while playing electronic (video) games.
“Video games may represent a serious risk to some children with arrhythmic conditions; they might be lethal in patients with predisposing, but often previously unrecognized arrhythmic conditions,” explained lead investigator Claire M. Lawley, MBBS, PhD, The Heart Centre for Children, Sydney Children’s Hospitals Network, Sydney, Australia. “Children who suddenly lose consciousness while electronic gaming should be assessed by a heart specialist as this could be the first sign of a serious heart problem.”
The investigators performed a systematic review of literature and initiated a multisite international outreach effort to identify cases of children with sudden loss of consciousness while playing video games. Across the 22 cases they found, multiplayer war gaming was the most frequent trigger. Some children died following a cardiac arrest. Subsequent diagnoses of several heart rhythm conditions put the children at continuing risk. Catecholaminergic polymorphic ventricular tachycardia (CPVT) and congenital long QT syndrome (LQTS) types 1 and 2 were the most common underlying causes.
There was a high incidence of potentially relevant genetic variants (63%) among the patients, which has significant implications for their families. In some cases, the investigation of a child who lost consciousness during video gaming led to many family members being diagnosed with an important familial heart rhythm problem. “Families and healthcare teams should think about safety precautions around electronic gaming in children who have a condition where dangerous fast heart rhythms are a risk,” noted Dr. Lawley.
The investigators attributed adrenergic stimulation related to the emotionally charged electronic gaming environment as the pathophysiological basis for this phenomenon. Electronic gaming is not always the “safe alternative” to competitive sports it is often considered. At the time of the cardiac incidents, many of the patients were in excited states, having just won or lost games, or were engaging in conflict with companions.
“We already know that some children have heart conditions that can put them at risk when playing competitive sports, but we were shocked to discover that some patients were having life-threatening blackouts during video gaming,” added co-investigator Christian Turner, MBBS, The Heart Centre for Children, Sydney Children’s Hospitals Network, Sydney, Australia. “Video gaming was something I previously thought would be an alternative ‘safe activity.’ This is a really important discovery. We need to ensure everyone knows how important it is to get checked out when someone has had a blacking out episode in these circumstances.”
The study notes that while this phenomenon is not a common occurrence, it is becoming more prevalent. “Having looked after children with heart rhythm problems for more than 25 years, I was staggered to see how widespread this emerging presentation is, and to find that a number of children had even died from it. All of the collaborators are keen to publicize this phenomenon so our colleagues across the globe can recognize it and protect these children and their families,” noted co-investigator of the study, Jonathan Skinner, MBChB, MD, also from Sydney.
As an accompanying editorial Daniel Sohinki, MD, MSc, Department of Cardiology, Augusta University, Augusta, GA, USA, and coauthors pointed out that, “exertion should be understood to encompass activities outside of traditional competitive athletics. Appropriate counseling regarding the risks of intense video gameplay should be targeted in children with a pro-arrhythmic cardiac diagnosis, and in any child with a history of exertional syncope of undetermined etiology. Further, any future screening programs aimed at identifying athletes at risk for malignant arrhythmias should encompass athletes being considered for participation in eSports.”
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Women with polycystic ovary syndrome (PCOS) in Alabama may be more likely to have excessive hair growth and insulin resistance, whereas women with PCOS in California may be more likely to have higher testosterone levels, according to new research published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
PCOS affects 7-10% of women of childbearing age and is the most common cause of infertility. In the United States, an estimated 5 to 6 million women have PCOS, but the disorder is still underdiagnosed. Women are diagnosed with PCOS if they have two of the following criteria: androgen excess (excess male sex hormones such as testosterone), ovulatory dysfunction and polycystic ovaries.
“Our study found geographical differences in PCOS in black and white women, suggesting there are both genetic and environmental influences on how this disease manifests,” said Margareta D. Pisarska, M.D., of Cedars-Sinai in Los Angeles, Calif. “Ongoing research is needed to identify modifiable risk factors for PCOS that may be race and ethnicity-specific to bring precision medicine to the management of this disease.”
The researchers compared data from 1,610 black and white women with PCOS in Alabama and California. They found regional differences in the way these women met criteria for the diagnosis of PCOS and in symptoms associated with PCOS, with some variations among black and white women.
Overall, there were many similarities among the races. Women with PCOS in Alabama were more likely to have excessive hair growth and insulin resistance, whereas women with PCOS in California were more likely to have higher levels of testosterone.
When comparing black women with PCOS in Alabama and California, the average body mass index (BMI) did not differ between the locations, whereas in white women with PCOS, the average BMI was higher in Alabama than California.
“Since we have now identified that there are geo-epidemiologic differences, we intend to do follow up studies comparing black and white women with PCOS, controlling for geo-epidemiologic differences,” Pisarska said. “Furthermore, we are trying to look at factors that are contributing to these differences in order to tailor treatments based on specific needs for improvements in care for all women with PCOS.”
Other authors of this study include Katherine VanHise, Jessica L. Chan, Sahar Wertheimer, Roy G. Handelsman, Ekaterina Clark, Rae Buttle and Erica T. Wang of Cedars-Sinai Medical Center; and Ricardo Azziz of the University of Alabama at Birmingham in Birmingham, Ala. and the University of Albany, SUNY, in Albany, N.Y.
The study received funding from the National Institutes of Health and Helping Hand of Los Angeles, Inc.
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When a highly contagious strain of avian influenza began racing across the United States this spring, the Raptor Center at the University of Minnesota, prepared for an influx of ailing birds.“But we never could have anticipated the flood of patients that arrived,” said Dr. Victoria Hall, executive director of the center, which provides medical care for birds of prey.From late March to early June of this year, Dr. Hall and her colleagues saw more than 180 flu-afflicted birds, including scores of great horned owls, red-tailed hawks and bald eagles. Many were severely ill, suffering from seizures or unable to see or stand. Caring for these animals — just one of which survived — was emotional, draining work that required long hours in personal protective equipment, including Tyvek suits and respirators.So it came as an immense relief when cases tailed off this summer, falling to just one in July and zero in August.But in September, the sick raptors returned. Last month, the center had 11 confirmed cases of the avian flu, Dr. Hall said: “It’s definitely coming back through.”This year’s avian influenza outbreak is the worst the United States has experienced since 2015, the last time the country was hit hard by bird flu. So far, the virus has affected 47 million farmed birds, nearly the same number as in the 2014-15 season.But by all other measures, this year’s outbreak is “radically different than what we’ve seen before,” said Bryan Richards, the emerging disease coordinator at the National Wildlife Health Center, which is part of the U.S. Geological Survey.This year’s is more wide-ranging, spreading to almost every state, and is having a much greater effect on wild birds, infecting more than 100 species in North America, according to Mr. Richards. (The virus currently poses little risk to humans, experts say.)And, unlike in 2015, the virus did not fizzle out over the summer. Instead, it continued to circulate in wild birds, many of which spend their summers in the Arctic.Now, as wild birds fly south for the winter, they are bringing the virus with them. Cases are climbing again in a number of northern states and popping up for the first time in some southern ones, such as Mississippi, Arkansas and New Mexico.More on BirdsAn Epic Flight: In search of an endless summer, bar-tailed godwits fly 7,000 miles each year — from Alaska to New Zealand. And they do it without stopping to eat, drink or rest.An Uneven Crisis: The risk of extinction, a study suggests, is not randomly or equally spread across the avian family. Instead, the most distinctive birds are likely to vanish first.Hammering Away: A study shows that woodpeckers do not absorb shocks during pecking and they likely aren’t being concussed either.A Beloved Bird Call: The corncrake’s loud cry was once a common sound of summer in Ireland, but these days it can seldom be heard. Efforts are underway to bring it back. Poultry farms are familiar with the risks of avian influenza, but for many zoos, rehabilitation centers and facilities that house wild birds, it is a formidable new threat. They are bracing themselves for a resurgence — and wondering whether the virus is here to stay.“We’ll just have to be on alert,” said Dr. Trevor Zachariah, the director of veterinary programs at Florida’s Brevard Zoo, where infected wild vultures keep finding their way onto the property. “We may have to live with this.”Spring surgeA scarlet macaw living in a temporary, behind-the-scenes habitat at the Brevard Zoo in Melbourne, Fla.Brevard ZooAvian influenza wings its way around the world in the bodies of migrating birds, especially in water birds such as ducks, geese and gulls. Some of these birds, which can carry the virus without showing symptoms, share summer habitats in the Arctic, where they may swap pathogens, picking up new flu strains.“It’s like bringing the kids to day care from different suburbs,” said Dr. Keith Poulsen, director of the Wisconsin Veterinary Diagnostic Laboratory. “As they commingle, that’s where the virus moves around on a global scale.”As infected birds migrate, they shed the virus in their feces, mucus and saliva, seeding infections in flocks of farmed fowl, in which some flu strains can be fatal.The current outbreak began in late 2021, when a highly pathogenic strain of flu known as Eurasian H5N1 was detected in birds in Eastern Canada. The virus made its way down the Atlantic coast to Florida and then exploded this spring, when migrating birds carried the pathogen north and west.Along the way, it not only infiltrated hundreds of commercial flocks but also began felling wild birds, taking out entire families of owls and triggering die-offs of geese and gulls.“We’ve never seen anything like this before,” said Ashton Kluttz, the executive director of the Bird Rescue Center in Sonoma County, Calif., which created extra makeshift hospitals to handle the patient load.(The virus also found its way into mammals, from foxes to seals.)Rehabilitation centers, sanctuaries and zoos have scrambled to put new precautions in place, moving vulnerable birds inside and suspending public programs. After Tri-State Bird Rescue & Research, in Delaware, identified its first case in February — triggering a three-week quarantine — it adopted new disinfection protocols and stopped accepting waterfowl from other rehabilitation centers.“We have — fortunately, knock wood — not had an outbreak at our center,” said Lisa Smith, the rescue’s executive director. But, she added, “We know the virus is still out there.”Fall flightsFlamingos at the San Diego Zoo were moved to a covered habitat.Ken Bohn/San Diego ZooCases ebbed in many places this summer, but the virus never completely disappeared. Now, it’s on the move.Blue-winged teal, a species related to ducks, are among the first species to fly south in the fall. In mid-September, three hunter-harvested teal tested positive for the virus in Mississippi, marking the first detections in that state. The finding affirms that, “Yes, the virus persisted in northern latitudes through the summer,” Mr. Richards said. “And it’s coming back on the wings of wild waterfowl.”Wisconsin began to see a spike in wild bird infections around Labor Day, Dr. Poulsen said, and recently documented its first poultry outbreaks since May. “We were really hoping that we were out of the woods,” he said.The virus appears to be making a comeback in other northern regions, including Minnesota, North Dakota and Alberta, Canada. So far, experts have said, the surge has been smaller than it was in the spring. “But there’s lots more geese and ducks to come down out of the Arctic,” said Margo Pybus, a provincial wildlife disease specialist at Alberta’s Fish and Wildlife Division.Farther south, wildlife facilities are preparing for a flood of fall migrants. Southern California was spared in the spring, but Dr. Hendrik Nollens, the vice president of wildlife health at the San Diego Zoo Wildlife Alliance, does not expect to be so lucky this fall.The San Diego Zoo and its sister facility, the San Diego Zoo Safari Park, covered their outdoor aviaries and removed food and water sources that might attract avian interlopers, even going so far as to drain a pond popular with wild ducks. They also moved 900 birds into more protected habitats — “a herculean effort” that involved relocating hundreds of flamingos, Dr. Nollens said.To pull off the feat, employees guided many of the flamingos into enclosed trailers, which delivered the animals to covered or indoor habitats. Staff members modified these new spaces to suit the leggy wading birds, adding feeding pools, trimming low-hanging tree branches and raising the sprinklers designed to keep their feathers in fine fettle.When the flamingos will return home is unclear. “When do we stop doing these things is actually a tough challenge,” Dr. Nollens said. “We don’t know what’s going to happen from here.”The long haulA great horned owl being examined at the Bird Rescue Center in Sonoma County, Calif.Joshua Asel/Bird Rescue CenterThe signs from Europe, where the outbreaks began earlier than they did in North America, were not encouraging. There, the virus has persisted through multiple migration cycles, fueling “the largest avian flu epidemic” ever observed on the continent, according the European Center for Disease Prevention and Control.Although the scope and scale of future outbreaks is hard to predict, scientists said that they expected the virus to persist through the winter, then to travel north again in the spring. “I don’t see any reason to suggest this is going to go away anytime soon,” Mr. Richards said.And if the virus does stick around? “It is going to have huge implications for anybody with either permanently captive or transitory captive wildlife in their care,” Dr. Hall said.The Raptor Center plans to continue testing all incoming patients for the virus indefinitely and is considering building a more permanent triage and quarantine area, she added. In California, the Bird Rescue Center recently decided to add an avian influenza unit to its new facility, which is not slated to open until at least late 2023.The Oregon Zoo, which moved many of its birds indoors in August, does not want to keep the animals cooped up for long. “It’s just not good welfare,” said Dr. Carlos Sanchez, the zoo’s head veterinarian. “They need the space to move. They need the sun.” So employees are working to reopen aviaries with new precautions in place, such as foot baths where visitors can disinfect their shoes.In the long run, managing the risks may require facilities to be watchful and nimble, tightening and loosening precautions as outbreaks flare and fade.At the Pittsburgh Zoo & PPG Aquarium, for instance, employees will return to wearing full P.P.E., as they did this spring, if the virus is reported in the surrounding county, said Dr. Justin Rosenberg, an associate veterinarian at the zoo.After the spring surge, combined with more than two years of coronavirus-related precautions, there is definite “preparedness fatigue,” Dr. Rosenberg acknowledged.But the zoo is eager to protect its avian charges, which include flamingos, ostriches and a 3-year-old duck with “one of the best names that I have encountered,” Dr. Rosenberg said. “We are doing whatever we can to keep Ritz Quacker safe.”A great horned owl that was treated for bird flu at the University of Minnesota Raptor Center this spring, and a rare survivor, was released into the wild.The Raptor Center

Published2 days agoSharecloseShare pageCopy linkAbout sharingImage source, ABC/Talissa SigantoBy Matt PreceyBBC EastA former boss of NHS hospitals in England accused of corruption in Australia has had his case thrown out of court.Prosecutors in Brisbane have dropped charges against Malcolm Stamp, who had been accused of nepotism and other offences. The Queensland Office of the Director of Public Prosecutions confirmed the matter had been discontinued.Mr Stamp, who lives in Norfolk, has been contacted for comment.The case centred on Mr Stamp’s time as chief executive of the Metro North Health and Hospital Service in Brisbane between 2013 and 2014.The Queensland Crime and Corruption Commission (CCC) had charged him with dishonestly seeking to procure a job for his daughter at the hospital and trying to cover it up.At the time the CCC alleged Mr Stamp had “corruptly arranged for a co-offender to hire his daughter and for the Metro North Hospital and Health Service to pay her wage to a company linked to a co-offender”.Mr Stamp appeared before Brisbane Magistrates Court in July after reportedly facing extradition proceedings.No ‘reasonable prospects’Under Australian law, a magistrate has to consider whether there is enough evidence for the case to proceed to trial.The prosecution made the announcement when the hearing resumed last week following an adjournment.The 69-year-old held a number of high level NHS posts before moving to Australia.He was chief executive of a string of NHS trusts including Addenbrooke’s Hospital in Cambridge, the Norfolk & Norwich Hospital, Mid Essex Hospitals and University Hospitals of Coventry and Warwickshire.A spokesman for the Office of the Director of Public Prosecutions said: “We can confirm that the matter was discontinued on 7th October 2022.”Following a consideration of the available evidence, including that given at committal hearing, a determination was made that there were not reasonable prospects of conviction”. Find BBC News: East of England on Facebook, Instagram and Twitter. If you have a story suggestion email eastofenglandnews@bbc.co.ukMore on this storyFormer NHS boss appears in court in Australia28 JulyEx-NHS boss charged with corruption in Australia11 June 2020Ex-hospital boss ‘faces extradition’ over warrant17 February 2020MPs attack private hospital deal3 May 2006MPs condemn ‘capitalist’ NHS deal3 May 2006

BROKEN ARROW, Okla. — It was Lachlan Rutledge’s sixth birthday, but as he mustered a laborious breath and blew out one candle, it was his mother who made a wish: for a pediatric hospital bed in northeast Oklahoma.The kindergartner has a connective tissue disorder, severe allergies and asthma. Those conditions repeatedly landed him in the pediatric intensive care unit at Ascension St. John Medical Center in Tulsa, with collapsed veins and oxygen levels so low, he was unresponsive to his mother’s voice.But in April the hospital closed its children’s floor to make room for more adult beds. So on a September morning, after coming down with Covid for the fourth time and with what looked like bilateral pneumonia, Lachlan was struggling to breathe in an overcrowded emergency room at the Children’s Hospital at Saint Francis — the only remaining inpatient pediatric option in Tulsa.“We’re always preparing for battle. It’s just a question of where we’re going to fight,” said his mother, Aurora Rutledge, looking frightened as she twisted the blonde ringlets that poked out from under Lachlan’s Spider-Man headphones. Hospitals around the country, from regional medical centers to smaller local facilities are closing down pediatric units. The reason is stark economics: Institutions make more money from adult patients.In April, Henrico Doctors’ Hospital in Richmond, Va., ended its pediatric inpatient services. In July, Tufts Children’s Hospital in Boston followed suit. Shriners Children’s New England said it will close its inpatient unit by the end of the year. Pediatric units in Colorado Springs, Raleigh, N.C., and Doylestown, Pa., have closed as well.“They’re asking: Should we take care of kids we don’t make any money off of, or use the bed for an adult who needs a bunch of expensive tests?” said Dr. Daniel Rauch, chief of pediatric hospital medicine for Tufts Medicine, who headed its general pediatric unit until it closed over the summer. “If you’re a hospital, that’s a no-brainer.”Lachlan’s backpack is full of EpiPens and medications — and clear labeling — to manage his allergies when he’s at school.Melissa Lukenbaugh for The New York TimesMany hospitals have converted children’s beds to adult I.C.U. beds during the pandemic and are reluctant to change them back. Now, staff shortages, inflation — drug costs have increased 37 percent per patient compared to prepandemic levels — low Medicaid reimbursement and dwindling federal subsidies granted during the pandemic have left some health centers operating on negative margins and eager to prioritize the most profitable patients. Young patients like Lachlan, who has private insurance, occupy beds to recover from infections or asthma attacks but don’t undergo lucrative, billable procedures — like joint or heart surgeries — that are more common among aging patients.Physician reimbursement through Medicaid, the insurance program for low-income people, is often only about 70 percent of the amount reimbursed through Medicare, the insurance program for elderly people of all incomes. More than a third of children in the United States are enrolled in Medicaid.There have been no aggressive legislative efforts to keep hospitals from closing or shrinking their pediatric units. Democratic senators introduced a bill last year to grant funding to specialized children’s hospitals to improve their infrastructure, but it has not moved past the assigned committee.Health policy experts say an important solution would be to encourage hospitals to care for children by increasing Medicaid reimbursement rates. But even higher Medicaid and private rates wouldn’t come close to what hospitals can charge for remunerative adult procedures, and with many state budgets already strained, experts say the regulatory move is unrealistic.Hospitals that no longer admit children rely on transferring them to pediatric units at other hospitals. But when even the largest pediatric floors in the country are at capacity, the pileup of critically ill children in E.R.s can cause patients’ conditions to worsen.An E.R. crushLachlan during a recent visit to the overcrowded emergency room at The Children’s Hospital at Saint Francis — the only remaining inpatient pediatric option in Tulsa.Emily Baumgaertner/The New York Times“Picu kids don’t belong here,” an overwhelmed E.R. doctor in a small Boston area hospital wrote two weeks ago to his hospital’s chief medical officer in an expletive-ridden text message reviewed by The Times. (P.I.C.U. is the acronym for pediatric I.C.U. The text message was shared on the condition that the hospital not be identified.)Every I.C.U. for children in Boston was full at the time, and the nearest open beds were in New Haven, Conn., and Vermont. The doctor who sent the text message considered intubating the child in the E.R. while he waited for a closer bed to become available.As children return to school, waves of illnesses are overrunning many of the units that remain.“Forget the two-week January crush. We couldn’t find beds in May or August or September,” said Dr. Melissa Mauro-Small, the chief of pediatrics at Signature Healthcare Brockton Hospital, near Boston. “There is no more respiratory season. It’s respiratory season year-round.”A hospital in Plymouth, Mass., that had not transferred a patient to Dr. Mauro-Small’s hospital in a decade did so six times in 10 days recently, she said. The E.R. staff at Lowell General Hospital outside Boston had to ask eight hospitals across New England whether they had room for an intubated 2-year-old, according to patient charts reviewed by The Times. It transferred another patient to the closest I.C.U. bed available — in Maine.“At some point, this was going to become a crisis,” Dr. Mauro-Small said. “And here we are.”St. John Medical Center in Tulsa had been a community treasure for almost a century when Ascension acquired it in 2013. The closure of the pediatric unit triggered opposition from both families and referring pediatricians.Dr. Michael Stratton, a pediatrician in Muskogee, Okla., said Ascension St. John had been “the number one place to send a child,” and its pediatric unit closure had been “such a huge disservice to all of eastern Oklahoma.”Lachlan’s morning routine involves time with the inhaler after breakfast while preparing for school.Melissa Lukenbaugh for The New York TimesA spokeswoman for Ascension St. John, where Lachlan had been admitted to the I.C.U. three times before the closure, declined to be interviewed but said in an email that the closure was driven by a demand for more adult beds. She also pointed to past statements that said the Children’s Hospital at Saint Francis was “more than capable of picking up the slack.”A spokeswoman for the Children’s Hospital at Saint Francis said that it had occasionally reached full capacity and that the staff transferred about 23 patients to other facilities, including in Arkansas, so far this year.The E.R. “was busy even prior to the closure of the St. John’s pediatric unit,” she said. Still, she said the hospital had not become overburdened. “Volume is fairly consistent with what we usually see on a seasonal basis,” she said.Some Oklahoman families with chronically ill children say they routinely drive to Memphis, St. Louis and Rochester, Minn., for care. The distances cause financial strain and, in the worst cases, cause them to forgo care, said Katy Kozhimannil, director of the University of Minnesota Rural Health Research Center.For those in rural communities, pediatric closures have made travel to what Dr. Rauch calls “bread-and-butter pediatrics” untenable. Sixteen-year-old Johnny in Childress, Texas, had to be home-schooled so he could travel eight hours to Dallas for dialysis treatment three times a week, according to his doctor.Jamaal Bets His Medicine, a 2-year-old with an autoimmune disease in Fort Kipp, Mont., routinely takes an 11-hour trip to Billings, Mont., to receive infusions, his mother, Patricia, said.‘Children are not small adults’Lachlan and his mother, Aurora Rutledge, outside the Saint Francis Emergency Center.Melissa Lukenbaugh for The New York TimesThe decline of local access to children’s inpatient care began over a decade ago and accelerated during the pandemic. Between 2008 and 2018 — the most recent national data available — pediatric inpatient units in the United States decreased almost 20 percent, and nearly a quarter of children found themselves farther from their nearest pediatric unit.The steepest decline in pediatric inpatient beds was in rural regions, where large health systems acquired community hospitals and consolidated pediatrics to one campus. Centering pediatric care in specialized centers can erode a local hospital’s ability to care for a critically ill child, doctors say.“Children are not small adults,” said Dr. Meredith Volle, a pediatrician at Southern Illinois University School of Medicine in Springfield, Ill., who routinely sees patients who travel from two to three hours away. The number of pediatric beds in Illinois has declined, and 48 of its counties now have no pediatrician at all.“When nurses and respiratory therapists become less comfortable with children’s cases, when the units don’t have child-sized equipment,” Dr. Volle said, “at a certain point, you really shouldn’t treat kids anymore because you don’t treat them often enough to be good at it.”Critically ill children are four times as likely to die in hospitals and twice as likely to die in trauma centers that scored low on a “pediatric readiness” test, according to research. Only one-third of children in a national research survey had access to an emergency department deemed highly “pediatric-ready,” and of those, nine out of 10 lived closer to a less-prepared one.A parent who is unaware of the wide variability, said Dr. Katherine Remick, the executive director of the National Pediatric Readiness Quality Initiative, “could make a split-second decision that changes their child’s fate.”Lachlan’s life“We’re always preparing for battle. It’s just a question of where we’re going to fight,” said Ms. Rutledge.Melissa Lukenbaugh for The New York TimesThe Rutledge family lives in Broken Arrow, a sunny Tulsa suburb with a frozen custard shop and a dentistry called Super Smiles. Their front porch is home to potted succulents, an abandoned scooter and a 140-pound Great Dane named Thor.But their lives are far from ordinary. The last time Lachlan needed to see an allergy specialist, his mother packed the car with his nebulizer and medications for a 14-hour drive to Denver, leaving her husband, their two other sons and her mother, who was undergoing chemotherapy, for two weeks. Later, when doctors told her that Lachlan’s disorder appeared to be causing stomach ulcers — but that the sole pediatric gastroenterologist at Saint Francis wasn’t available for months — she began planning a journey to Dallas.On the September morning that Lachlan was in St. Francis struggling to breathe, the E.R. was so busy that Ms. Rutledge hooked him up to a pulse oximeter herself, quieting the monitor’s settings so it wouldn’t frighten him every time his heart rate spiked.Lachlan tugged at his collar bone, his chest looking retracted. Five hours later, he still hadn’t been admitted. Ms. Rutledge’s hands trembled and tears streamed down her face.“I know you guys are exhausted at this hospital, and I get it,” she shouted, leaning over Lachlan’s bed to level her eyes with the attending physician on the other side. “But you will not send this child home so he can watch his own vitals drop.”Lachlan was discharged from the E.R. after 10 hours with a course of steroids to fight the inflammation in his lungs. He sleeps in his parents’ bedroom so they can check his oxygen levels and administer nebulizer treatments every few hours throughout the night.