Warfarin-Associated Nonuremic Calciphylaxis
Deadly fungal infection that doctors have been fearing now reported in U.S.
A strain of Candida auris cultured in a petri dish at the Centers for Disease Control and Prevention. (Shawn Lockhart/CDC)
Nearly three dozen people in the United States have been diagnosed with a deadly and highly drug-resistant fungal infection since federal health officials first warned U.S. clinicians last June to be on the lookout for the emerging pathogen that has been spreading around the world.
The fungus, a strain of a kind of yeast known as Candida auris, has been reported in a dozen countries on five continents starting in 2009, when it was found in an ear infection in a patient in Japan. Since then, the fungus has been reported in Colombia, India, Israel, Kenya, Kuwait, Pakistan, South Korea, Venezuela and the United Kingdom.
Unlike garden variety yeast infections, this one causes serious bloodstream infections, spreads easily from person to person in health-care settings, and survives for months on skin and for weeks on bed rails, chairs and other hospital equipment. Some strains are resistant to all three major classes of antifungal drugs. Based on information from a limited number of patients, up to 60 percent of people with these infection have died. Many of them also had other serious underlying illnesses.
Those at greatest risk are individuals who have been in intensive care for a long time or who are on ventilators or have central line catheters inserted into a large vein.
In the United States, the largest number of infections has been reported in New York, with at least 28 cases, according to the Centers for Disease Control and Prevention. Infections have also been reported in Illinois, Maryland, Massachusetts and New Jersey. Last June, the CDC sent an urgent alert to clinicians to start looking for the infections, which are difficult to identify with standard laboratory methods.
“As soon as we put out that alert, we started to get information about cases and now we know more about how it spreads and how it’s acting,” Tom Chiller, the CDC’s top fungal expert, said in an interview Thursday. The CDC now tracks the number of infections
, updating the case count every few weeks.
In addition to the 35 infected patients, an additional 18 were carrying the organism but weren’t sickened by it.
The microbe is among a group of newly emerging drug-resistant threats, health officials said.
“These pathogens are increasing, they’re new, they’re scary and they’re very difficult to combat,” said Anne Schuchat, CDC’s acting director, during a briefing in Washington this week about the growing danger from antimicrobial resistance.
Of the first seven cases that were reported to the CDC last fall, four patients had bloodstream infections and died during the weeks to months after the pathogen was identified. Officials said they couldn’t be sure whether the deaths were caused by the infection because all the individuals had other serious medical conditions. Five patients had the fungus initially isolated from blood, one from urine, and one from the ear.
The infection is still relatively rare. “It’s really hitting the sickest of the sick,” Chiller said.
So far, the fungus doesn’t seem to be evolving into new strains within the United States. Because the country doesn’t yet have any “homegrown” strains of the deadly fungus, “it gives us a better opportunity to contain it and stop it from spreading,” Chiller said.
In other countries, infections have been resistant to all three major types of antifungal drugs, but so far the U.S. cases have been treatable with existing drugs.
Because invasive bloodstream infections with Candida are common in hospitalized patients in the United States, health officials are concerned that this deadly strain could “get into that mix,” Chiller said. Unlike Candida infections in the mouth, throat or vagina (which are typically called yeast infections), invasive yeast infections can affect the blood, heart, brain, eyes, bones and other parts of the body and are more dangerous.
Among infectious disease clinicians and laboratory personnel, infections involving fungi don’t typically ring the same kind of alarm bells as antibiotic-resistant bacteria — until now.
“This is a paradigm shift, because Candida is not generally thought of as highly resistant or passed person to person,” Chiller said.
Since the CDC issued its alert in June, the agency has provided funds and additional expertise to help regional laboratories and hospitals identify the organism.
Hospital Floors May Pose a Larger Health Risk Than Previously Thought
Hospital room floors may be an overlooked source of infection, according to a study published in the March issue of the American Journal of Infection Control, Because items in the patient’s room may touch the floor, pathogens on hospital floors can rapidly move to the hands and high-touch surfaces throughout a hospital room.
“Understanding gaps in infection prevention is critically important for institutions seeking to improve the quality of care offered to patients,” said 2017 APIC president Linda Greene, RN, MPS, CIC, FAPIC. “Even though most facilities believe they are taking the proper precautions, this study points out the importance of ensuring cleanliness of the hospital environment and the need for education of both staff and patients on this issue.”
In the study by Abhishek Deshpande, MD, PhD, and colleagues, researchers cultured 318 floor sites from 159 patient rooms (two sites per room) in five Cleveland-area hospitals. The hospital rooms included both C. difficile infection (CDI) isolation rooms and non-CDI rooms. Researchers also cultured hands (gloved and bare) as well as other high-touch surfaces such as clothing, call buttons, medical devices, linens, and medical supplies.
The researchers found that floors in patient rooms were often contaminated with Methicillin-resistant Staphylococcus aureus (MRSA), VRE, and C. difficile, with C. difficile being the most frequently recovered pathogen found in both CDI isolation rooms and non-CDI rooms.
Of 100 occupied rooms surveyed, 41 percent had one or more high-touch objects in contact with the floor. These included personal items, medical devices, and supplies. MRSA, VRE, and C. difficile were recovered from 6 (18 percent), 2 (6 percent), and 1 (3 percent), respectively of bare or gloved hands that handled the items.
“Efforts to improve disinfection in the hospital environment usually focus on surfaces that are frequently touched by the hands of healthcare workers or patients,” said Deshpande, et al. “Although healthcare facility floors are often heavily contaminated, limited attention has been paid to disinfection of floors because they are not frequently touched. The results of our study suggest that floors in hospital rooms could be an underappreciated source for dissemination of pathogens and are an important area for additional research.”
Reference: “Are hospital ﬂoors an underappreciated reservoir for transmission of health care-associated pathogens?” Abhishek Deshpande; Jennifer L. Cadnum; Dennis Fertelli; Brett Sitzlar; Priyaleela Thota; Thriveen Sankar C.; Annette Jencso; Heba Alhmidi; Sreelatha Koganti; and Curtis J. Donskey appears in the American Journal of Infection Control, Volume 45, Issue 3 (March 2017).
Autoimmune Diseases Linked to Dementia
A new study provides additional evidence linking autoimmune diseases to dementia, including Alzheimer’s disease (AD).
Researchers showed that compared with a control group admitted to the hospital for another reason, people hospitalized with an autoimmune disease were more likely to be later admitted with dementia.
“Fundamentally, this is an epidemiology study using the power of big numbers of patients to look at a hypothesis, namely that Alzheimer’s disease may have an autoimmune component, and our bottom line in epidemiological and population terms is that yes, the study supports that hypothesis,” study author Michael J. Goldacre, emeritus professor of public health, University of Oxford, United Kingdom, told Medscape Medical News.
It’s important for clinicians to recognize that their patients with multiple sclerosis, type 1 diabetes, rheumatoid arthritis, or other autoimmune disorders may have an increased risk for dementia, said Dr Goldacre.
The study was published online March 1 in the Journal of Epidemiology & Community Health.
Common Chronic Diseases
Researchers used the Hospital Episode Statistics database, which includes clinical, demographic, and administrative information on hospital admissions (including day cases) in England. They constructed retrospective cohorts of patients admitted to the hospital with a range of autoimmune diseases and followed them to see which patients were later admitted with a record of dementia.
The 25 diseases on the list for evaluation included those that are common and chronic and for which there’s an accepted autoimmune component. The list did not include type 1 diabetes because, as Dr Goldacre explained, he and his colleagues had already published a paper that linked diabetes with subsequent dementia.
The researchers also constructed a control cohort of patients hospitalized with various other medical and surgical conditions and injuries.
From April 1, 1998, to March 31, 2012, over 1.8 million people were admitted to the hospital with an autoimmune disease. The number in the different autoimmune groups ranged from 1019 for Goodpasture’s syndrome (where antibodies attack the lungs and kidneys), to 316,043 for rheumatoid arthritis (RA). About 7 million people were included in the control cohort.
The autoimmune disease cohort that eventually had the most dementia cases (48,146) was myxoedema (hypothyroidism). This condition “is quite common in elderly people, particularly women,” commented Dr Goldacre.
Overall, patients admitted to the hospital with an autoimmune disease were 20% more likely to have a subsequent admission for dementia than those without an admission for an autoimmune disease (adjusted rate ratio [RR], 1.20; 95% confidence interval [CI], 1.19 – 1.21).
Of the 25 diseases studied, 18 showed significant positive associations with dementia at P < .05 (with 14 significant at P < .001), including multiple sclerosis (RR, 1.97; 95% CI, 1.88 – 2.07), psoriasis (RR, 1.29; 95% CI, 1.25 – 1.34), and systemic lupus erythematosus (RR, 1.46; 95% CI, 1.32 – 1.61).
The authors noted that by chance alone, only one or two would be significant at P = .05.
However, although significant, effect sizes were small.
“As risks go, it’s a relatively small elevation,” said Dr Goldacre. “Risks start to seem important at the individual patient level when they are about two-fold or over, when the risk is something like doubled.”
Researchers found no notable differences in the RRs for dementia after excluding cases of dementia recorded within a year of the autoimmune disease admission. This suggests that the dementia diagnosis was not the result of being admitted soon after an autoimmune disease admission.
Investigators subdivided patients admitted with a record of dementia into those having AD and those having vascular dementia.
Of the 81,502 people with an autoimmune disease and dementia, 20,032 had a record of AD and 22,536 a record of vascular dementia. The risk for vascular dementia after an admission with an autoimmune disease was higher (RR, 1.28; 95% CI, 1.26 – 1.31) than the risk for AD (RR, 1.06; 95% CI, 1.04 – 1.08).
“We think that’s probably because these autoimmune diseases are themselves conditions that predispose to atherosclerotic vascular disease,” said Dr Goldacre.
Some autoimmune diseases were associated with an elevated risk for future vascular dementia but not AD. This was the case for RA, where the RR for vascular dementia was 1.16 (95% CI, 1.12 – 1.20) but for AD, it was 0.89 (95% CI, 0.86 – 0.93).
“We might have been tempted to just dismiss the seemingly protective effect — the inverse relationship between RA and AD — were it not for the fact that others have reported on that before, so it’s not an entirely sort of eccentric finding,” said Dr. Goldacre.
The finding helps support the hypothesis that nonsteroidal anti-inflammatory drugs (NSAIDs) protect against AD. “People with rheumatoid arthritis generally take NSAIDs to manage their condition, so if rheumatoid arthritis is at least partially a proxy for NSAID use, the real association may be between NSAID use and a reduced risk of AD,” write the authors.
Since dementia subgroups were not well coded on hospital records, the authors cautioned that the separate analyses of AD and vascular dementia should be viewed with caution.
In analyzing the data separately for men and women, the researchers found that the adjusted RRs for dementia were broadly similar when they looked at individual diseases, but for all of them together, the RR was higher in men than women.
Dr Goldacre pointed out that autoimmune diseases are generally more common in women than men. “It’s often the case that the sex with the lower disease frequency has outcomes that are worse than the sex with the higher disease frequency.”
For example, he said, although women don’t develop myocardial infarction as often as men, they tend to have a slightly higher death rate from it, he said. “I am highly speculative, but that pattern might fit here.”
The researchers also analyzed the data according to time interval between the autoimmune disease and dementia admissions. Most associations remained significant for 5 or more years, although they were generally stronger with shorter time intervals.
Medscape Medical News invited James A. Hendrix, PhD, director, Global Science Initiatives, Alzheimer’s Association, to comment on the study.
“We certainly are seeing more and more research on the link between AD and the immune system and neuroinflammation,” said Dr Hendrix. “This kind of paper helps show that there is something going on and we need to do more research to really understand it.”
An “emerging” field of research for the Alzheimer’s Association is developing anti-inflammatory agents targeted to the brain, he said.
“A possible strategy would be to develop a drug that has excellent brain penetration and has brain-specific targets, so it targets the microglia or other cells in the brain that are associated with the immune system and neuroinflammation.”
Another strategy might be to “repurpose” anti-inflammatory drugs and see whether they can affect neuroinflammation with limited side effects.
“We will leave no stone unturned with this,” said Dr Hendrix.
Indeed, last summer, the Alzheimer’s Association announced a $7 million investment in clinical trials targeting brain inflammation (see Medscape Medical News’ coverage of the Part the Cloud Challenge on Neuroinflammation).
Dr Hendrix said the association between RA and vascular dementia uncovered by the study was news to him. “That says that we really don’t have a good understanding of the role of the immune system and inflammation when it comes to vascular dementia. For me, that was the one of the things that stood out in the paper generally.”
He outlined a number of “caveats” to the research. For one thing, the authors looked only at hospital records. “These were people who went into hospital complaining of an autoimmune disease or disorder, so it was probably pretty severe to force them to go to a hospital for care,” said Dr Hendrix.
Also, only about half of those who developed dementia were classified as having AD or vascular dementia. “It’s really challenging under the best of circumstances to do a differential diagnosis of dementia,” said Dr Hendrix.
The Unit of Health-Care Epidemiology was funded by the English National Institute for Health Research to build the linked data set. The authors have disclosed no relevant financial relationships.
J Epidemiol Community Health. Published online March 1, 2017. Abstract
Eczema Relief: Probiotic Lotion Shows Early Promise
Scanning electron microscopic image of Staphylococcus aureus bacteria (orange).
Credit: CDC/Jeff Hageman, MHS
Over the years, people suffering from eczema have slathered their skin with lotions containing everything from avocado oil to zinc oxide. So, what about a lotion that features bacteria as the active ingredient? That might seem like the last thing a person with a skin problem would want to do, but it’s actually a very real possibility, based on new findings that build upon the growing realization that many microbes living in and on the human body—our microbiome—are essential for good health. The idea behind such a bacterial lotion is that good bugs can displace bad bugs.
Eczema is a noncontagious inflammatory skin condition characterized by a dry, itchy rash. It most commonly affects the cheeks, arms, and legs. Previous studies have suggested that the balance of microbes present on people with eczema is different than on those with healthy skin . One major difference is a proliferation of a bad type of bacteria, called Staphylococcus aureus.
Recently, an NIH-funded research team found that healthy human skin harbors beneficial strains of Staphylococcus bacteria with the power to keep Staph aureus in check. To see if there might be a way to restore this natural balance artificially, the researchers created a lotion containing the protective bacteria and tested it on the arms of volunteers who had eczema . Just 24 hours after one dose of the lotion was applied, the researchers found the volunteers’ skin had greatly reduced levels of Staph aureus. While further study is needed to learn whether the treatment can improve skin health, the findings suggest that similar lotions might offer a new approach for treating eczema and other skin conditions. Think of it as a probiotic for the skin!
In their study published in Science Translational Medicine, Richard Gallo, of the University of California, San Diego and his colleagues, set out to connect the dots between eczema, Staph aureus, and changes to the skin microbiome. Step one involved swabbing the forearms of 30 people with healthy skin and almost 50 people with outbreaks of the most common form of eczema, atopic dermatitis. From each swab, the researchers isolated hundreds of bacterial colonies and tested their ability to inhibit the growth of Staph aureus in lab dishes.
Gallo’s team found that bacterial strains collected from the skin of healthy people showed antimicrobial activity that inhibited the growth of Staph aureus. The researchers traced that inhibition to previously unknown antimicrobial peptides produced by certain strains of Staphylococcus hominis and Staphylococcus epidermidis, which are benign bacteria that are quite abundant on the skin. The researchers then discovered that the antimicrobial strains not only kill Staph aureus quite effectively, they do so without causing harm to other beneficial bacteria commonly found on healthy skin. In contrast to the healthy people, people with eczema had much lower levels of the two strains of protective bacteria.
Based on encouraging results in a mouse model, Gallo and his colleague initiated a Phase I clinical trial involving five volunteers with atopic dermatitis that tested positive for Staph aureus. To beef up the amount of protective Staph bacteria on the volunteers’ skin, the researchers took a small sample of each patients’ skin micriobiome, grew up more of the good Staph strains in the lab, and used them to create a personalized probiotic lotion. The volunteers then each received a single dose of probiotic lotion on one arm and regular lotion on the other. Twenty-four hours later, it was clear—the probiotic lotion reduced levels of the bad bug, Staph aureus, on the participants’ skin.
The researchers report that a larger human clinical trial is now underway, designed to test whether continued use of probiotic lotion can provide lasting protection against Staph aureus and improve eczema symptoms. Hopefully, the promise of these new findings can provide some encouragement to the more than 31 million Americans, many of them children, who now suffer from eczema
The immune-system-targeting drug is delivered through the skin through a process called epicutaneous immunotherapy.
Inside each patch is a sprayed-on sample of peanut protein. Once you put it on, the protein makes its way into your immune system through your skin.
Since it’s delivered this way, the allergen never makes it to the blood stream, which would cause the allergic reaction you’re trying to avoid.
Based on the data from DBV’s phase two trial, those who used the patch for three years at the 250 microgram dose (the highest dose) had the best responses to the treatment.
The patch treatment is a departure from the way allergies are typically treated.
Typically, the only way to lessen an allergic reaction is through ‘desensitisation’, a process in which you gradually introduce small amounts of the allergen into your body. In the case of peanut allergies, that means eating the peanut outright.
The problem with this method is that it can be risky, since it can cause an allergic reaction that spreads throughout the body through the blood stream.
Other, more common methods, for treating allergies have been focused around treating the symptoms of the allergic reaction; i.e. using antihistamines like Benadryl or shots of epinephrine in extreme cases.
Beyond peanut allergies, DBV is developing patches to treat other food allergies such as milk and eggs – among the most common food allergies – and other non-food allergies that are connected to asthma.
The company’s also exploring treatments for Crohn’s disease, celiac disease, and type 1 diabetes that use the same immunotherapy technology.
This article was originally published by Business Insider.
Carri’s Corner – The Quality Payment Program/MIPS/APMs – How do you begin?
Taking care of and making patients healthier is the main concern of clinicians. As a special gift, Medicare has devoted itself to help you focus on quality care! The MACRA final rule has introduced, as you all know by now, the Quality Payment Program (QPP) where clinicians either choose the MIPS (Merit-Based Incentive Payment System) or the APMs (Advanced Alternative Payment Models) track. It was published this past October and the new programs begin in 2017, with payment adjustments beginning in 2019. Most providers will be part of the MIPS program which combines elements of three programs whose performance period ended in 2016: PQRS, VM, and the Medicare EHR incentive program. I am sure many of you have already begun the work, however for some who really do not understand what the new programs are about, I thought I would do my best to explain what I know.
MIPS is comprised of four performance categories which include Quality (formerly PQRS), Cost (formerly Value-Based Modifier),Improvement Activities (this is new) and Advancing Care Information (formerly Meaningful Use). Performance will be measured for clinicians under these categories and a final score will be issued. For the first year, clinicians will be able to pick their pace and participate as minimally or as fully as they are able to. Data will then be received by CMS, who will then issue feedback to clinicians to let them know how they performed under the MIPS program. Higher scores will be associated with higher reimbursement in 2019.
Let’s look at how you can begin participating in MIPS. First, you must determine if you are eligible. Next you need to decide if you will be submitting as an individual or a group and lastly you must decide your method of submission and verify its capabilities.
As you prepare to partake, I would like to offer a few suggestions. Begin with considering your practice’s readiness and evaluate your ability to begin reporting data for the 2017 transition year. Then, review the Pick Your Pace options as to whether you would like to participate as a test, partial or full-year. Start selecting your measures and/or improvement activities. CMS has given clinicians increased flexibility to choose the improvement activities and measures, within the performance categories, that are most meaningful to their practice. You may choose one or more performance categories, the more you choose the more your reimbursement will be. Go to https://qpp.cms.gov/ and click on explore measures. There you will find a list of specialties, unfortunately Podiatry is not yet listed, but you can find quality measures that apply to your specialty. Verify the information you need to report and review the specifications for any measures you will be reporting. As you care for and treat your patients during 2017, you will be tracking your data. Finally, you will take that captured data and submit it to CMS by March 31, 2018.
Hopefully every physician in our group, who is eligible, is prepared. The better prepared and the more you participate in MIPS, the more you will get paid.
For any technical support, or any other questions on these programs go to QPP.cms.gov
Next month in Carri’s Corner- Part 2 explanation of MIPS including more specific information on elements of reporting, length of participation, performance categories and scoring.
Please contact me for guidance with EHR programs that can help with MIPS and reporting.
I would also like to remind everyone that we are available for any billing help that you need. We can take on your whole account or customize our service to what you need. How is you AR doing? Please do not hesitate to contact us for help. We are Sammy experts and also work on other systems.