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Sunday, 4 June 2017

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Will Neuropathy Diagnosis Go Over The Fiscal Cliff


 Today's post comes from the Neuropathy Association E-news letter for November 2012 (see link below) and highlights a potentially very difficult time for neuropathy patients in the United States. Hopefully solutions can be found, now that plunging off the fiscal cliff has been temporarily averted but these sort of spending cuts are just the sort that will remain on the statute books irrespective of macro decision making in Washington. Not that EMGs are the be all and end all of neuropathy testing (a patient's account of symptoms is more often than not enough to confirm diagnosis) but EMGs and the like are useful tools in establishing the extent of neuropathic damage and certainly in measuring its progress. If you are living in the USA it may well be worth reading and supporting this  campaign by the Neuropathy Association.

 

A MESSAGE FROM THE PRESIDENT AND CEO
Tina Tockarshewsky November 2012

Dear Friend,

A clear and present danger for our community is now upon us, and your support is essential.

It was recently announced in the 2013 Medicare Physician Fee Schedule from the Centers for Medicare & Medicaid Services (CMS) that reimbursement payments to physicians for needle electromyography (EMG) tests and nerve conduction studies (NCSs) will be severely reduced by 30%-70% beginning on January 1, 2013. EMG and NCSs are the primary diagnostic tools for peripheral neuropathy as well as other neuromuscular diseases like ALS, MS, and Parkinson’s. Implementing these cuts will deny millions access to proper diagnosis and care.

We are hearing from many physicians that they will no longer be able to afford to practice neuromuscular medicine...and many currently in practice will simply stop seeing Medicare patients!

This Neurological Fiscal Cliff Will Hurt Neuropathy Patients!
 
This is a crisis unlike any we have ever known before…and is a potential game changer for ALL patients and medical professionals working with the neuropathy community. Early diagnoses will be reduced and misdiagnoses will increase. Patient access and care will suffer, exacerbating the challenges already facing neuropathy patients.

A 2010 poll by The Neuropathy Association showed that many patients already face significant delays in diagnosis, during which irreparable nerve damage continues:

Neuropathy Diagnosis 2012
 
Two Ways You Can Help
First: In the coming days, we will announce a process for contacting members of Congress and posting comments on these proposed changes on the Centers for Medicare & Medicaid Services website. Please watch your emails for this announcement and respond immediately. Please also know that we are working with our medical professional society partners to respond to this crisis.
And keep in mind that other insurers follow Medicare’s actions. So, even if you are not on Medicare, this change has the potential to impact everyone in the neuropathy community.

Second: Support our year-end fundraising efforts, and KEEP US IN THE FIGHT. In these difficult times for the economy and the Association, your generous contributions are our lifeline – and help protect your interests as well as those of untold numbers of future patients.
Thank you for taking action.

Neurologists to See Cuts in 2013 Medicare Payments
The Center for Medicare and Medicaid Services (CMS) recently released new code values that could result in decreased payments to neurologists. Specifically, physicians who provide nerve conduction and needle EMG services will face dramatic cuts of more than 50 percent for some services starting January 1, 2013. This is a drastic cut that will be especially hard on neurology practices large and small, many of which rely on these services to meet their bottom line. Patients also will pay the price with less access to these services. Private health insurers often follow Medicare payment rules as well, which will exacerbate the situation.
- American Academy of Neurology


Editor’s Note: Please refer to the President and CEO's message above for more information about this breaking issue that negatively impacts access to critical evaluation and care for people with neuropathy, and how The Neuropathy Association is working with the American Academy of Neurology, the American Association of Neuromuscular & Electrodiagnostic Medicine, and the American Academy of Physical Medicine & Rehabilitation to address this issue.

http://www.neuropathy.org/site/PageServer?pagename=Resources_PubArchivesM_E

BED BUGS CAN TRANSMIT PARASITE THAT CAUSES CHAGAS DISEASE



The bed bug may be just as dangerous as its sinister cousin, the triatomine, or "kissing" bug. A new study from Penn Medicine researchers in the Center for Clinical Epidemiology and Biostatistics demonstrated that bed bugs, like the triatomines, can transmit Trypanosoma cruzi, the parasite that causes Chagas disease, one of the most prevalent and deadly diseases in the Americas.
The role of the bloodsucking triatomine bugs as vectors of Chagas disease -- which affects 6 to 8 million worldwide, mostly in Latin America, and kills about 50,000 a year -- has long been recognized. The insects infect people not through their bite but feces, which they deposit on their sleeping host, often around the face, after feeding. Bed bugs, on the other hand, are usually considered disease-free nuisances whose victims are left with only itchy welts from bites and sleepless nights.
In a study published online this week in the American Journal of Tropical Medicine and Hygiene, senior author Michael Z. Levy, PhD, assistant professor in the department of Biostatistics and Epidemiology at the University of Pennsylvania's Perelman School of Medicine, and researchers at the Universidad Peruana Cayetano Heredia in Peru conducted a series of laboratory experiments that demonstrated bi-directional transmission of T. cruzi between mice and bed bugs.
In the first experiment run at the Zoonotic Disease Research Center in Arequipa, Peru, the researchers exposed 10 mice infected with the parasite to 20 uninfected bed bugs every three days for a month. Of about 2,000 bed bugs used in the experiment, the majority acquired T. cruzi after feeding on the mice. In a separate experiment to test transmission from bug to mouse, they found that 9 out of 12 (75 percent) uninfected mice acquired the parasite after each one lived for 30 days with 20 infected bed bugs.
In a third experiment, investigators succeeded in infecting mice by placing feces of infected bed bugs on the animal's skin that had either been inflamed by bed bug bites, or scraped with a needle. Four out of 10 mice (40 percent) acquired the parasite by this manner; 1 out of 5 (20 percent) were infected when the skin was broken by the insect's bites only. A final experiment performed at the Penn bed bug lab in Philadelphia demonstrated that bed bugs, like triatomines, defecate when they feed.
"We've shown that the bed bug can acquire and transmit the parasite. Our next step is to determine whether they are, or will become, an important player in the epidemiology of Chagas disease," Levy said. "There are some reasons to worry -- bed bugs have more frequent contact with people than kissing bugs, and there are more of them in infested houses, giving them ample opportunity to transmit the parasite. But perhaps there is something important we don't yet understand about them that mitigates the threat."
T. cruzi is also especially at home in the guts of bed bugs. "I've never seen so many parasites in an insect," said Renzo Salazar, a biologist at the Universidad Peruana Cayetano Heredia and co-author on the study. "I expected a scenario with very low infection, but we found many parasites -- they really replicate well in the gut of the bed bugs."
Wicked Cousins
Bed bugs and kissing bugs are distant cousins but share many striking similarities. Both insects hide in household cracks and crevices waiting for nightfall and the opportunity to feed on sleeping hosts. They are from the same order of insects (Hemiptera) and both only feed on blood. (One main difference is their size: kissing bugs are five times as big as a bed bug). With so much in common, it seemed logical to the authors that the kissing bug's most infamous trait, the transmission of T. cruzi, is also shared by the bed bug.
Other investigators have shared this suspicion. In 1912, just three years after Carlos Chagas described the transmission of the disease by kissing bugs, French parasitologist Émile Brumpt recounted that he had infected almost 100 bed bugs exposed to an infectious mouse, and then used them to infect two healthy mice. Decades later an Argentine group replicated his work. These experiments, largely ignored during the recent bed bug resurgence, missed one key point.
"Mice can hunt and eat bed bugs," said Ricardo Castillo-Neyra, DVM, PhD, coauthor and postdoctoral fellow at the Universidad Peruana Cayetano Heredia and Penn. "The older studies were almost certainly only documenting oral transmission of the parasite. Our work shows for the first time that bed bugs can transmit the parasite when their feces are in contact with broken skin, the route by which humans are usually infected."
Emerging Problem
More people in the U.S. are infected with T. cruzi now than ever before. The Centers for Disease Control and Prevention estimates that the number of Chagas disease cases in the U.S. today could be as high as 300,000.
"There have always been triatomine bugs and cases of Chagas disease in the U.S., but the kissing bugs we have here don't come into homes frequently like the more dangerous species in South and Central America do," Levy said. "I am much more concerned about the role of bed bugs. They are already here -- in our homes, in our beds and in high numbers. What we found has thrown a wrench in the way I think about transmission, and where Chagas disease could emerge next."
Equally worrying is the invasion of bed bugs into areas where Chagas disease is prevalent, especially in countries where traditional insect vectors of the parasite have been nearly eliminated, Levy said. In these areas, bed bugs will be repeatedly exposed to T. cruzi, and could re-spark transmission where it had been extinguished.
"Bed bugs are harder to kill than triatomines due to their resistance to common insecticides." Levy said. "No one is prepared for large scale bed bug control. If the parasite starts to spread through bed bugs, decades of progress on Chagas disease control in the Americas could be erased, and we would have no means at our disposal to repeat what had been accomplished."
Often referred to as a silent killer, Chagas disease is hard to diagnose in its early stages because the symptoms are mild or absent. The parasites are hidden mainly in the heart and digestive muscle and over time can cause cardiac disorders and sometimes digestive or neurological problems. In later years, the infection can lead to sudden death or heart failure caused by progressive destruction of the heart muscle. Although there are some drugs to treat Chagas disease, they become less effective the longer a person is infected.
The long asymptomatic period of Chagas disease complicates surveillance for new outbreaks of transmission. In Arequipa, Peru, thousands became infected with the parasite before a case appeared in the hospital. The same could happen in cities in the United States if the parasite were to emerge in the bed bug populations, the authors say.
"Carlos Chagas discovered T. cruzi in triatomine insects before he saw a single case of the disease," Levy said. "We need to learn from his intuition -- check the bugs for the parasite."




Foot Problems With Neuropathy


Today's post from wecare.ca/blog (see link below) talks almost exclusively to diabetes patients with neuropathic foot problems and doesn't mention HIV as also being a possible cause of neuropathy (Not surprising; there are more than a hundred causes!) but that doesn't take away from the fact that the symptoms and possible problems for your feet are exactly the same and once neuropathy is established, have the same cause. If you're trawling the Net for information about neuropathy you will more often than not be directed by your search engine to diabetes sites purely because diabetes is the best known and most common cause of neuropathy. It's important to realise that you're in the right place, even if your own cause is very different. Most of the symptoms of peripheral neuropathy are the same for all and many of the treatments are the same too. Today's post gives everyone with neuropathy some useful information as to why their feet are playing up and why ulcers etc may be appearing. Having absorbed this, it may be wise to look further to neuropathy sites associated with your own cause or causes but all information gathered will be useful to you in learning to live with the problem.



The Pins and Needles of Peripheral Neuropathy

November 12th, 2012 | Posted by
SueKelly in Care Connections

Most people know what it is like to experience the numbing effect of ‘pins and needles’. But if you are diabetic or suffer from circulatory problems – this ailment can be a serious and ongoing concern.

Peripheral neuropathy is damage to the nerves in the limbs and particularly the feet where the body’s nerves are the longest. The risk of developing neuropathy increases the longer a person has been afflicted with diabetes or congestive heart failure or other circulatory problems. The nerve damage prevents people from knowing when their feet are too hot, too cold or sore or painful. Therefore a person loses the warning signs that their feet could be in jeopardy. This is called “loss of protective sensation”.

Loss of protective sensation (LOPS) contributes significantly to ulcer development. In healthy individuals, irritants like bunions, blisters or calluses may cause an unconscious change of gait. In people living with diabetes who experience LOPS as a result of peripheral neuropathy, no discomfort is felt, so pressure on specific sites is continued, directly affecting the development of ulcers. Early detection of LOPS and implementation of preventative strategies will reduce the rates of limb-threatening complications.

Many foot ulcers begin in innocent ways. As a visiting nurse I was always curious how a problem started and would ask my clients what was the first sign that brought them to the doctor? Often the response was one of embarrassment and foolishness as they described the simple way it began – a blister, a piece of torn skin or a small amount of bleeding. The harmless scratch burgeoned from a trivial occurrence to a condition that threatened the maintenance of limbs and in some cases, life.

The following signs may be an indication that you have peripheral neuropathy or decreased circulation. If you have any one of these symptoms, make an appointment to see your health care professional.


Signs of Peripheral Neuropathy

Signs of Poor Circulation

Pain, tingling, burning and numbness that starts in the feet and slowly progresses up the calves; tends to be worse at night

Inability to detect excessive heat such as in a bath or a heating pad

Any small sore, cut or ingrown toenails

Weakness in small muscles of the feet that cause the toes to claw, or in more serious cases foot drop will develop

A change in gait

Swelling or redness on any part of the foot

The existence of a bunion, callus, corn or wart

Absence of foot pulses

A pale colour of the feet when the feet are raised

Feet that feel cold

Pain at rest

Pain at night relieved by hanging the feet over the side of the bed

A blue colour to the toes

A reddish colour of the feet

Swelling of the feet


Given the alarming statistics of foot problems in patients living with diabetes, it is prudent to assess all diabetics for their level of risk related to foot problems. Special attention needs to be paid to the elderly and over-weight clients. In older clients limited mobility and poor eyesight may prevent them from properly examining their feet – a task that should be done daily. In obese patients, excessive weight will be an impediment to easy foot inspection.

People with diabetic foot ulcers face incredible challenges in their family, social and work lives, which sometimes affect their sense of self-worth. From the ease with which the ulcers seem to develop, to the future unpredictability imposed by the condition, people describe the dramatic impact that having a foot ulcer has on their activities of daily living. There is a great deal of stress and fear that comes with the uncertainty of not knowing when and if the ulcer will heal and in some cases whether or not amputation will become an eventuality.

To learn more about taking care of your feet, read the blog
7 Steps to Healthier Feet for Diabetics and do all you can to ensure a healthier and independent future.

http://www.wecare.ca/blog/?p=562

Saturday, 3 June 2017

NEW ANTIBIOTIC ATTACK S DRUG RESISTANT MICROBES



The multitude of microbes scientists have found populating the human body have good, bad and mostly mysterious implications for our health. But when something goes wrong, we defend ourselves with the undiscriminating brute force of traditional antibiotics, which wipe out everything at once, regardless of the consequences.

Researchers at Rockefeller University and their collaborators are working on a smarter antibiotic. And in research to be published October 5 in Nature Biotechnology, the team describes a 'programmable' antibiotic technique that selectively targets the bad bugs, particularly those harboring antibiotic resistance genes, while leaving other, more innocent microbes alone.
"In experiments, we succeeded in instructing a bacterial enzyme, known as Cas9, to target a particular DNA sequence and cut it up," says lead researcher Luciano Marraffini, head of the Laboratory of Bacteriology. "This selective approach leaves the healthy microbial community intact, and our experiments suggest that by doing so you can keep resistance in check and so prevent certain types of secondary infections, eliminating two serious hazards associated with treatment by classical antibiotics."
The new approach could, for instance, reduce the risk of C. diff, a severe infection of the colon, caused by the Clostridium difficile bacterium, that is associated with prolonged courses of harsh antibiotics and is a growing public health concern.
The Cas9 enzyme is part of a defense system that bacteria use to protect themselves against viruses. The team coopted this bacterial version of an immune system, known as a CRISPR (clustered regularly interspaced short palindromic repeats) system and turned it against some of the microbes. CRISPR systems contain unique genetic sequences called spacers that correspond to sequences in viruses. CRISPR-associated enzymes, including Cas9, use these spacer sequences as guides to identify and destroy viral invaders.
The researchers were able to direct Cas9 at targets of their choosing by engineering spacer sequences to match bacterial genes then inserting these sequences into a cell along with the Cas9 gene. The cell's own machinery then turns on the system. Depending on the location of the target in a bacterial cell, Cas9 may kill the cell or it may eradicate the target gene. In some cases, a treatment may prevent a cell from acquiring resistance, they found.
"We previously showed that if Cas9 is programmed with a target from a bacterial genome, it will kill the bacteria. Building on that work, we selected guide sequences that enabled us to selectively kill a particular strain of microbe from within a mixed population," says first author David Bikard, a former Rockefeller postdoc who is now at the Pasteur Institute in Paris.
In initial experiments, Bikard and colleagues targeted a strain of the common skin and respiratory bacteria Staphylococcus aureus that is resistant to the antibiotic kanamycin. Treatment by Cas9 programmed to target a part of the resistance gene killed most of the resistant Staph, but left behind the kanamycin-susceptible Staph.
Targeted bacterial genocide is only one option. Bacteria share genes, including those conferring drug resistance, in the form of rings of DNA known as plasmids. In a second series of experiments, researchers turned Cas9 on tetracycline resistance-harboring plasmids in a strain of the potentially deadly multidrug resistant bacteriaStaphylococcus aureus (MRSA). Not only did the resistant cells become sensitive to tetracycline after Cas9 destroyed the plasmids, but the arrival of Cas9 in other Staphcells acted as an immunization, preventing them from taking on resistance-carrying plasmids.
And, in a final set of experiments, conducted in collaboration with Vincent Fischetti's Laboratory of Bacterial Pathogenesis and Immunology, adjunct faculty member Chad Euler confirmed their test tube results on living skin, by using Cas9 to selectively kill kanamycin-resistant Staph infecting the shaved backs of mice.
In spite of the promising results, the delivery system needs improvement. The researchers used bacteria-infecting viruses to inject the programmed Cas9 enzymes into the bacterial cells, but these viruses only attack specific types of cells. Scientists need to devise a less discriminating method of delivery, before the technology can be used to develop a new class of antibiotics, Marraffini says.
In addition to its potential as a much-needed new weapon against drug-resistant microbes, the new system could also be used to advance research on the complex populations of microbes in the body, about which very little is known. "There are enormous microbial communities in the human body," Marraffini says. "Programmable Cas9 enzymes may make it possible to analyze these populations by eliminating their members, one by one, and studying the effects."