May 2, 2017

On the brink of eradication: Why polio research matters



IMAGE: THIS IMAGE SHOWS A TRANSMISSION ELECTRON MICROGRAPH OF POLIOVIRUSES. view more 
CREDIT: DR GRAHAM BEARDS AT EN.WIKIPEDIA
Poliovirus research offers insights into other viruses that impact global health

In the decades since Dr. Jonas Salk developed the first polio vaccine, cases of polio have exponentially declined. Though once widespread epidemic, the highly infectious childhood disease is now close to global eradication. 

The question remains: why would researchers spend time and resources studying a virus already on the brink of total eradication? 
In a new Research Matters article, PLOS Pathogens author and microbiologist at the University of Texas Southwestern Medical Center, Julie K. Pfeiffer discusses why she studies poliovirus, and shares how her research has affected the study of other viruses. 
For Dr. Pfeiffer, there are several benefits to studying poliovirus. Poliovirus "grows like a weed", able to produce immense stocks that are easy and safe to work with since its genome can be targeted, mutations can be made within days, and a vaccine already exists for it. 
Most importantly, because poliovirus has already been exhaustively studied, it can serve as a useful model system, a virus that can be studied to understand the workings of other similar viruses.
Early in her career, Dr. Pfeiffer showed that RNA viruses such as poliovirus, benefited from a "sloppy replication strategy". As RNA viruses replicated, they produced genetic mutations, some of which benefited them. This discovery was later used show that other RNA viruses including chikungunya, also relied on sloppy replication strategies. 
In addition, Dr. Pfeiffer's research has shown that poliovirus "sticks to bacteria", aiding its infection and transmission. Her work, along that of other research groups, has shown that many gut viruses rely on intestinal bacteria to infect humans. Dr. Pfeiffer's findings were applied to human norovirus, a virus that can lead to severe infections with explosive vomiting and diarrhea, opening the door to prevention strategies. 
By studying an eradicated virus like poliovirus, scientists like Dr. Pfeiffer can learn more about other viruses that pose a threat to public health such as Ebola, Zika, and influenza. This type of basic research could potentially lead to new treatments and vaccines for these viruses. 
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In your coverage please use this URL to provide access to the freely available article in PLOS Pathogenshttp://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006330
Citation: Pfeiffer JK (2017) The importance of model systems: Why we study a virus on the brink of global eradication. PLoS Pathog 13(4): e1006330. doi:10.1371/journal.ppat.1006330
Funding: Dr. Pfeiffer's work is supported by NIH R01 AI74668, NIH R21 AI114927, a Burroughs Wellcome Fund Investigators in the Pathogenesis of Infectious Diseases Award, and a Faculty Scholar grant from the Howard Hughes Medical Institute. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The author has declared that no competing interests exist.
Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

May 1, 2017

Postpolio Syndrome Symptoms


Postpolio Syndrome

Synonyms and related keywords: PPS
  • Central 
    • Pathogenesis can include chronic pain, type A personality, depression, dysfunctional reticular-activated system, sleep disorders, and respiratory dysfunction. 
    • PPS produces somnolence and difficulty in concentrating and remembering.
  • Peripheral 
    • Pathogenesis may be metabolic exhaustion of the enlarged motor units, neuromuscular junction transmission defects, scarring within the motor neurons, or loss of motor units due to aging. 
    • PPS produces decreased muscular endurance and increased muscular fatigability.
  • Weakness 
    • A number of functional etiologies for weakness have been hypothesized, including disuse, overuse, and chronic weakness, as well as weight gain. 
    • Asymmetric and scattered weakness may be present. 
    • Some authors have found evidence that previously unaffected muscles later become weak; in these cases, they discovered that the patient was unaware or had not been told that the particular muscle had been affected during the acute episode.
  • Muscle pain 
    • Deep aching pain may be a component of a myofascial pain syndrome or fibromyalgia. 
    • This feature is extremely prevalent in PPS.
  • Gait disturbance: Difficulty with gait is caused by progressive weakness, pain, osteoarthritis, or joint instability; it is common in patients who previously used assistive devices but later discarded them.
  • Respiratory problems 
    • Respiratory disorders are most prevalent in patients with residual respiratory muscle weakness. 
    • These changes cause chronic microatelectasis, diminished pulmonary compliance, increased chest wall tightness, chronic alveolar hypoventilation, decreased cough and expiratory flow, and decreased clearing of secretions. 
    • The new respiratory difficulties are not only related to new respiratory muscle weakness but also to scoliosis, pulmonary emphysema, cardiovascular insufficiency, or poor posture. 
    • A central component also may occur because acute bulbar polio often affects the medullary structures, including the reticular formation and sleep regulatory system.
  • Swallowing problems 
    • These difficulties can occur in patients with bulbar and nonbulbar postpolio. 
    • Subclinical asymmetrical weakness in the pharyngeal constrictor muscles is almost always present in all postpolio muscular atrophy (PPMA) patients, including those who do not complain of new swallowing difficulties.
  • Autonomic dysfunction: The cause is unclear; the peripheral component could include muscular atrophy and, therefore, diminished heat production.
  • Sleep apnea
  • This disorder is not uncommon in patients left with residual bulbar dysfunction or severe respiratory compromise.
  • Sleep apnea appears to be due to a combination of the following:
    • Central apnea, due to a residual dysfunction of the surviving bulbar reticular neurons 
    • Obstructive apnea, due to pharyngeal weakness and increased musculoskeletal deformities from scoliosis or emphysema 
    • PPMA, resulting in diminished muscle strength of the respiratory, intercostal, and abdominal muscle groups
  • Flat back syndrome
  • Another possible symptom in some patients with PPS is the flat back syndrome, which consists of the inability to stand erect because of forward flexion of the trunk and pain in the low back and legs.
  • The flat back syndrome typically occurs in patients with diminished lumbar lordosis as a result of instrumentation of the spine for scoliosis, vertebral fracture, or degenerative joint disease.
  • The trunk extensor musculature plays an essential role in maintaining upright posture, and it may be that PPS-related weakness in this musculature represents a major contributing factor to the flat back syndrome in these patients.


Author: Flor M Muñiz, MD, Staff Physician, Department of Physical Medicine and Rehabilitation, Thomas Jefferson UniversityCoauthor(s): Gerald Herbison, MD, Clinical Professor, Department of Physical Medicine and Rehabilitation, Thomas Jefferson University
Flor M Muñiz, MD, is a member of the following medical societies: American Medical Association
Editor(s): Martin K Childers, DO, Associate Professor, Department of Physical Medicine and Rehabilitation, University of Missouri School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; Kat Kolaski, MD, Adjunct Clinical Assistant Professor, Department of Pediatrics, University of North Carolina; Director, Pediatric and Adolescent Rehabilitation, Charlotte Institute of Rehabilitation; Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center; and Denise I Campagnolo, MD, MS, Clinical Director of Spinal Cord Injury Program, Associate Professor, Department of Physical Medicine and Rehabilitation, New Jersey Medical School


Post Polio Litaff, Association A.C _APPLAC Mexico

Mayo Clinic Epidural Stimulation Trial Enables Movement and Stepping





On April 3, the Mayo Clinic published the results of a new trial that further validates the effectiveness of epidural stimulation for functional improvement in spinal cord injury subjects. In this trial, a 26-year-old, three years out from a motor-complete SCI at T6, regained volitional motor function below his level of injury while using an implanted epidural stimulation device. The study sought to replicate the results of a previous epidural stimulation trial conducted at the University of Louisville, in collaboration with the research team of V. Reggie Edgerton at UCLA.
The Mayo Clinic trial began with the subject, Jered Chinnock, undergoing 22 weeks of three times per week locomotor and task-specific strength training. Following the initial period of motor training, surgeons implanted an epidural stimulation device made by Medtronics and FDA approved for pain (with off-label approval for functional rehabilitation purposes) and connected it to an electrode array positioned on the dorsal epidural surface of the lumbosacral spine. After three weeks of post-surgical recovery, the team began epidural stimulation — with Chinnock attempting volitional leg movements while researchers tuned the settings of the stimulation device.
In the first two weeks of epidural stimulation, with the device turned on, Chinnock was able to:
•  Control his muscles while lying on his side, resulting in leg movements
•  Make step-like motions while lying on his side and standing with partial support
•  Stand independently using his arms on support bars for balance
Previous trials had produced standing and some volitional movement of lower limbs while reclining, but only after 17 weeks of stimulation and motor rehabilitation. The Mayo Clinic trial marks the first time a subject has been able to voluntarily make step-like movements while standing with partial support, and is the quickest turnaround for functional improvement with epidural stimulation.
“We’re really excited, because our results went beyond our expectations,” says neurosurgeon Kendall Lee, M.D., Ph.D., principal investigator and director of Mayo Clinic’s Neural Engineering Laboratory. “These are initial findings, but the patient is continuing to make progress.”
The preliminary results in this trial show functional return only while the epidural stimulation device is turned on. Previous studies have shown that after prolonged therapy, some volitional control of previously paralyzed muscles remains even when the stimulator is turned off.
It remains to be seen if Chinnock will regain even more function with continued therapy and adjustment of the stimulation settings, but even the initial findings are enough to show that functional return with epidural stimulation continues to move forward, one step at a time.
For more about Chinnock’s journey, see the below video.



Post Polio Litaff, Association A.C _APPLAC Mexico

Apr 29, 2017

Let the EVIDENCE speak: Did Vaccines Save Us?


There is a perception out there that vaccines saved us from the deadly diseases of the 19th and 20th centuries. But did they?
Please review the evidence below.
You will see that in developed nations, mortality from these diseases declined dramatically before vaccines came in, with the trend heading downward (smallpox and polio excepted, they have different stories). This was largely even before antibiotics were widely used.
Vaccine protagonists argue we can see the worth of vaccines better by looking at graphs showing disease incidence (morbidity), rather than by looking at mortality. However death rates give us the most accurate picture of what is going on—incidence data only includes reported cases, and many cases of disease are never reported, but deaths usually are.
Also, although incidence data show declining disease rates after introduction of some vaccines, this is not significant if those diseases had become mild in the vast majority of cases anyway, due to improvements in the health of populations.
If the slope of a mortality graph is pointing downwards for a long time with no vaccine, it’s reasonable to expect it would continue to go down if not interfered with, and that serious side effects of the disease would be declining too.
England and Wales measles mortality 1839 to 1978.

US measles mortality 1900 to 1988.






(Record of mortality in England and Wales for 95 years as provided by the

Office of National Statistics, published 1997; Report to The Honourable Sir George Cornewall Lewis, Bart, MP, Her Majesty’s Principal Secretary of State for the Home Department, June 30, 1860, pp. a4, 205; Essay on Vaccination by Charles T. Pearce, MD, Member of the Royal College of Surgeons of England; Parliamentary Papers, the 62nd Annual Return of the Registrar General 1899 (1891–1898))
Whooping cough (pertussis) mortality Australia 1870 to 1970
Diphtheria mortality, in England and Wales. Diphtheria vaccination began in 1920, and became widespread in the 1940s.



Diphtheria mortality UK vs USA. An early form of the diphtheria vaccine in limited use from 1920, widespread vaccination early 1940s (UK), late 1940s (USA).







Mumps mortality in England and Wales, 1901 to 1999 (mumps vaccination started 1988, in MMR)



England and Wales mortality for measles, scarlet fever, whooping cough (pertussis), diphtheria and smallpox, 1838 to 1978. Note – there was no vaccine for scarlet fever.

United States mortality rates from various infectious diseases from 1900 to 1965. Notice the diphtheria and typhoid graphs almost match each other, despite the fact there was no widespread use of a typhoid vaccine. There was no vaccine for scarlet fever.
(Vital Statistics of the United States 1937, 1938, 1943, 1944, 1949, 1960, 1967, 1976, 1987, 1992; Historical Statistics of the United States— Colonial Times to 1970 Part 1; Health, United States, 2004, US Department of Health and Human Services; Vital Records & Health Data Development Section, Michigan Department of Community Health; US Census Bureau, Statistical Abstract of the United States: 2003; Reported Cases and Deaths from Vaccine Preventable Diseases, United States, 1950–2008)
Massachusetts tuberculosis, diphtheria, typhoid, measles, and smallpox mortality rates from 1861 to 1970 (although US national records did not begin until 1900, records in some cities began earlier, and give us a chance to see what was going on before 1900). There was no widespread use of a vaccine for typhoid.


(Historical Statistics of the United States—Colonial Times to 1970 Part 1, Bureau of the Census, p. 63)
FRANCE measles mortality rate. Note – measles vaccination rate was less than 20% in 1983 and less than 40% in 1989.
US influenza and pneumonia mortality rates 1900 to 2002, vaccination was introduced early 1970s
Note – Influenza and pneumonia are bundled together, because influenza leads to pneumonia, and the exact cause of death cannot be determined (when your country or state health authorities declare X thousand people died from influenza, know that pneumonia deaths are included in that figure).
Above graph magnified, 1960 to 2002, includes vaccine coverage in blue
This is what US investigative journalist Sharyl Attkisson wrote in 2014:
“An important and definitive “mainstream” government study done nearly a decade ago got little attention because the science came down on the wrong side. It found that after decades and billions of dollars spent promoting flu shots for the elderly, the mass vaccination program did not result in saving lives. In fact, the death rate among the elderly increased substantially.”
Read it here: Govt. Researchers: Flu Shots Not Effective in Elderly, After All
And flu pandemics?
In 2011 Professor Collignon, professor of microbiology at the Australian National University and director of infectious diseases at Canberra Hospital, had this to say, regarding Australia’s 2009 swine flu episode:
“What was a bit surprising when we looked at some of the data from Canada and Hong Kong in the last year is that people who have been vaccinated in 2008 with the seasonal or ordinary vaccine seemed to have twice the risk of getting swine flu compared to the people who hadn’t received that vaccine.
“Some interesting data has become available which suggests that if you get immunised with the seasonal vaccine, you get less broad protection than if you get a natural infection.
“It is particularly relevant for children because it is a condition they call original antigenic sin, which basically means if you get infected with a natural virus, that gives you not only protection against that virus but similar viruses or even in fact quite different flu viruses in the next year.
“We may be perversely setting ourselves up that if something really new and nasty comes along, that people who have been vaccinated may in fact be more susceptible compared to getting this natural infection.
Tetanus mortality England and Wales 1901 to 1999. Vaccine widespread in late 1940s.
Note – The numbers of farm labourers fell by half after the second world war, and the increase in mechanisation reduced the chances of the types of  injuries likely to result in tetanus.
Tetanus mortality England and Wales 1901 to 1999. Vaccine widespread in late 1940s.
From the CDC (US gov):
“Tetanus is not contagious from person to person. It is the only vaccine-preventable disease that is infectious but not contagious.”
and
A marked decrease in mortality from tetanus occurred from the early 1900s to the late 1940s. In the late 1940s, tetanus toxoid was introduced into routine childhood immunization”
http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/tetanus.pdf
Meningitis in Australia


The Hib vaccine was introduced to reduce bacterial meningitis – bacterial meningitis can be caused by a wide variety of bacteria but the Hib bacterium was the predominant one found in bacterial meningitis cases at the time. The Hib vaccine has indeed reduced the incidence of Hib infections, but has it reduced meningitis deaths? Or have other bacteria simply taken over?

Meningitis all ages in Australia, 1907 to 2007Meningitis Australia under fives. Note – the Hib vaccine greatly reduced most Hib infections in just 2 years, so the meningitis occurring after 1995 has been caused by other bacteria (there are unlimited species and strains of bacteria that can cause this type of infection).
Meningitis Australia under fives, 1960 to 2006
Australian graphs are from Fooling Ourselves: on the fundamental value of vaccinesby Greg Beattie
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