'Superbug from India resistant to all available antibiotics'

January 16, 2017

Washington, Jan 16: A woman in the US died after being infected by a superbug during her visit to India, say doctors who found that the "nightmare" bacteria was resistant to all available antibiotics.

bacteriaThe infection was caused by carbapenem-resistant Enterobacteriaceae (CRE), a multidrug-resistant organism associated with high mortality.

While CRE are not new to the US, what was new in this case is that the infection was resistant or non-susceptible to all available antimicrobial drugs, researchers said.

The 70-year-old patient in the US was admitted to an acute care hospital last year after an extended trip to India.

She was given a primary diagnosis of systemic inflammatory response syndrome, likely resulting from an infected right hip seroma. The infection was serious; none of the 14 antibiotics physicians used to treat the woman worked.

After the CRE - identified as Klebsiella pneumoniae - was confirmed by lab testing, an isolate from a wound specimen was sent to the CDC for further susceptibility testing and to determine the mechanism of resistance.

That testing confirmed the presence of New Delhi metallo-beta-lactamase (NDM-1), an enzyme that directly breaks down carbapenems, a powerful class of antibiotics that are often used to treat multidrug-resistant infections.

The US Centres for Disease Control and Prevention's antimicrobial testing showed the isolate was resistant to 26 different antibiotics, including all aminoglycosides and polymixins - another class of last-resort antibiotics.

It was also intermittently resistant to tigecycline, an antibiotic developed specifically to overcome drug-resistant organisms. Essentially, there were no treatment options.

Meanwhile, the patient's condition was deteriorating quickly. She died of septic shock in early September last year, less than two months after admission. The woman had been in India for two years and had been hospitalised at least four times there for a right femur fracture and a subsequent hip fracture.

"We feel comfortable saying that she most likely obtained the bug in India," said Lei Chen, senior epidemiologist with the Washoe County Health District in the US.

CRE have been labelled as a "nightmare" bacteria not only because they are already resistant to most antibiotics, but also because they spread easily in hospital settings.

The enzymes that enable resistance are carried on mobile pieces of DNA known as plasmids that can spread to other types of bacteria. NDM-1 enzyme is particularly mobile, researchers said.

"It's what we call a promiscuous plasmid, that seems to move easily between species," said Alex Kallen, a CDC medical epidemiologist.

When CRE bacteria enter the bloodstream, they can be deadly. CRE bacteria kill up to half of patients who get bloodstream infections from them.

NDM-1 was originally identified in 2009 in a Swedish patient who had been hospitalised in India.

The research was published in CDC's Morbidity and Mortality Weekly Report (MMWR).

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Agencies
June 17,2020

Leading physicians are celebrating a small dose of good news that arrived Tuesday about dexamethasone, a cheap and widely used steroid shown to be able to save lives among COVID-19 patients, but also cautioning against releasing study results by press release during a global health emergency, like in the case of the latest dexamethasone study by University of Oxford.

"It will be great news if dexamethasone, a cheap steroid, really does cut deaths by one-third in ventilated patients with COVID19, but after all the retractions and walk backs, it is unacceptable to tout study results by press release without releasing the paper", Atul Gawande, surgeon and CEO of Haven Healthcare, tweeted.

"Bottom line is, good news," Dr. Fauci, America's foremost infectious diseases expert told a US newswire on Tuesday, soon after the dexamethasone results were announced in the UK.

Fauci, who has long championed the therapeutics-first view said that dexamethasone is a "significant improvement" in the available therapeutic options currently available.

On Medical Twitter and Facebook, doctors broadly agree that dexamethasone use aligns well with the way COVID19 attacks the body's immune system. Fauci said the results in the Oxford study make "perfect sense" in that context.

"We should see the number of people who actually survive go up, if the study holds up," virologist and epidemiologist Dr. Joseph Fair told a television network.

Global coronavirus cases crossed 8 million on Tuesday. In the US, Texas and Florida are facing a new wave of cases after lifting lockdown orders earlier than medical experts recommended. Amidst the relentless graph upwards, the dexamethasone study results injected hope for better survival rates among those most seriously ill.

World Health Organization chief scientist Soumya Swaminathan welcomed the results from the randomised control trial.

Dr Eugene Gu, Founder and CEO of CoolQuit tweeted that he is "genuinely impressed" with the UK dexamethasone trial. This may be a "game changer", he wrote.

"There's no conflict of interest as dexamethasone is a generic steroid. The mechanism of action makes sense because steroids can reduce cytokine storms and overactive immune systems that makes COVID-19 so deadly. The number needed to treat is 8 ventilated patients which is great."

The Oxford study found that dexamethasone reduced deaths by 35 percent in patients who needed treatment with breathing machines and by 20 percent in those only needing supplemental oxygen. Dexamethasone was one of 5 drugs studied in a large clinical trial in the United Kingdom named RECOVERY, short for Randomised Evaluation of COVID-19 Therapy.

Peter Horby, chief investigator of the University of Oxford clinical trial, said dexamethasone is the first drug to be shown to improve survival in COVID-19. Details of the study have not been released. The trial organisers said they made their announcement via a news release because of "the public health importance of these results." According to Horby's public comments, there was a lot of initial resistance to studying steroids.

During the study, 2,104 patients were randomly selected to be given 6 milligrams of dexamethasone once a day (either by mouth or by intravenous injection) for 10 days. That group was compared with 4,321 patients who received the usual care alone.

Researchers estimated that dexamethasone would prevent one death for every eight patients treated while on ventilators and one for every 25 patients on extra oxygen alone.

UK experts have called the study results a breakthrough in the fight against the virus. The researchers have promised they would publish the results soon.

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Agencies
January 26,2020

High-protein diets may help people lose weight and build muscle, but there is a downside to it --a greater heart attack risk. Researchers now report that high-protein diets boost artery-clogging plaque.

The research in mice showed that high-protein diets spur unstable plaque -- the kind most prone to rupturing and causing blocked arteries.

More plaque buildup in the arteries, particularly if it's unstable, increases the risk of heart attack.

"There are clear weight-loss benefits to high-protein diets, which has boosted their popularity in recent years," said senior author Babak Razani, associate professor at Washington University School of Medicine in St. Louis, Missouri.

"But animal studies and some large epidemiological studies in people have linked high dietary protein to cardiovascular problems. We decided to take a look at whether there is truly a causal link between high dietary protein and poorer cardiovascular health," Razani added.

The researchers studied mice who were fed a high-fat diet to deliberately induce atherosclerosis, or plaque buildup in the arteries.

Some of the mice received a high-fat diet that was also high in protein. And others were fed a high-fat, low-protein diet for comparison.

The mice on the high-fat, high-protein diet developed worse atherosclerosis -- about 30 per cent more plaque in the arteries -- than mice on the high-fat, normal-protein diet, despite the fact that the mice eating more protein did not gain weight, unlike the mice on the high-fat, normal-protein diet.

"A couple of a scoop of protein powder in a milkshake or smoothie adds something like 40 grams of protein -- almost equivalent to the daily recommended intake," Razani said.

"To see if protein has an effect on cardiovascular health, we tripled the amount of protein that the mice receive in the high-fat, high-protein diet -- keeping the fat constant. Protein went from 15 per cent to 46 per cent of calories for these mice".

Plaque contains a mix of fat, cholesterol, calcium deposits and dead cells. Past work by Razani's team and other groups has shown that immune cells called macrophages work to clean up plaque in the arteries.

But the environment inside plaque can overwhelm these cells, and when such cells die, they make the problem worse, contributing to plaque buildup and increasing plaque complexity.

"In mice on the high-protein diet, their plaques were a macrophage graveyard," Razani informed.

To understand how high dietary protein might increase plaque complexity, Razani and his colleagues also studied the path protein takes after it has been digested -- broken down into its original building blocks, called amino acids.

"This study is not the first to show a telltale increase in plaque with high-protein diets, but it offers a deeper understanding of the impact of high protein with the detailed analysis of the plaques," said Razani.

"This work not only defines the critical processes underlying the cardiovascular risks of dietary protein but also lays the groundwork for targeting these pathways in treating heart disease," he added.

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Agencies
July 30,2020

New York, Jul 30: Can the coronavirus spread through the air? Yes, it's possible.

The World Health Organisation recently acknowledged the possibility that Covid-19 might be spread in the air under certain conditions.

Recent Covid-19 outbreaks in crowded indoor settings — restaurants, nightclubs and choir practices — suggest the virus can hang around in the air long enough to potentially infect others if social distancing measures are not strictly enforced.

Experts say the lack of ventilation in these situations is thought to have contributed to spread, and might have allowed the virus to linger in the air longer than normal.

In a report published in May, researchers found that talking produced respiratory droplets that could remain in the air in a closed environment for about eight to 14 minutes.

The WHO says those most at risk from airborne spread are doctors and nurses who perform specialized procedures such as inserting a breathing tube or putting patients on a ventilator.

Medical authorities recommend the use of protective masks and other equipment when doing such procedures.

Scientists maintain it's far less risky to be outside than indoors because virus droplets disperse in the fresh air, reducing the chances of Covid-19 transmission.

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