29 oct. 2017

New vaccine for fibromyalgia treatment that actually work.





By Donna Gregory Burch
If someone could give you a vaccine that would cure your fibromyalgia, would you do it? That may sound like a dream, but it’s closer to reality than you might think. Los Angeles-based biomedical firm EpicGenetics and Massachusetts General Hospital researchers are seeking approval from the U.S. Food and Drug Administration (FDA) to conduct a clinical trial next year to test the Bacille Calmette-Guerin (BCG) vaccine as a potential treatment for fibromyalgia.
BCG is a generic tuberculosis vaccine that is almost a 100 years old and has been safely administered millions of times,” explained Dr. Denise Faustman, head of the Faustman Lab at Massachusetts General Hospital. “For over 10 years, our research group at Massachusetts General Hospital have been actively investigating the role that the BCG vaccine could play in treating various forms of autoimmunity. Our current focus is type 1 diabetes, but globally BCG is being tested in a number of autoimmune diseases. Over the next two years we will begin clinical testing of BCG in fibromyalgia.”
According to the World Health Organization, more than 100 million children are given the BCG vaccine each year. It’s mainly used in developing countries where tuberculosis is still active. The BCG vaccine is not available in the United States because of the low risk of infection. In the U.S., BCG is used in a small number of patients to treat bladder cancer.
So, the obvious question is why would a vaccine for an infectious lung condition be used for fibromyalgia? The answer lies within the immune system.
Vaccines are typically given to healthy people to prevent infection. In this case, however, the BCG vaccine would be administered to fibromyalgia patients in an effort to quell their symptoms.
When EpicGenetics was tasked with creating a diagnostic test for fibromyalgia several years ago, researchers ran all sorts of lab tests on fibromyalgia patients to figure out how they differed from healthy control subjects and what might be causing their symptoms. Researchers discovered several white blood cell abnormalities in fibromyalgia patients, leading them to conclude symptoms are associated with a suppressed immune system.
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“We believe [the term] fibromyalgia is a misnomer,” said Dr. Bruce Gillis, EpicGenetics’ CEO. “These people aren’t suffering with anything that’s affecting the muscles, per say. What they are suffering with is their immune system cannot produce normal quantities of protective proteins. …There are cells in the immune system called peripheral blood mononuclear cells. They are not producing normal quantities of the protective proteins called chemokines and cytokines.”
The finding led to the development of the FM/a blood test for fibromyalgia. (Yes, despite what your doctors may have told you, there IS a blood test for fibromyalgia! It’s just not widely accepted in the medical community.) The test analyzes the levels of four chemokines and cytokines found at reduced levels in fibromyalgia patients. These four chemokines and cytokines just happen to be the same ones that are boosted by the BCG vaccine.
“Given what’s been published in the medical literature, we believe this vaccine will reverse the immune system abnormalities [of fibromyalgia],” Gillis said.
Gillis and Faustman are seeking FDA approval to administer the first BCG vaccines to fibromyalgia patients early next year.
“This is the first time ever that a direct treatment of fibromyalgia will be done,” Gillis said. “As you know, the medications [currently on the market] for fibromyalgia only treat symptoms. They have no immune system benefits. [The pharmaceutical companies] concede they’re only treating symptoms but you need to treat the disease, and that’s why we’re moving ahead with the vaccine application [to the FDA].”
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If Gillis’ theory holds true, then “the chemokines and cytokines that are deficient in patients with fibromyalgia will no longer be deficient [once the BCG vaccine is administered],” Gillis said. “Production levels will normalize, and you have to assume then that their symptoms will disappear. … We think we are on the cusp of something major.”
Because the vaccine has such a long history, it’s not expected to cause any major side effects in patients.
The BCG vaccine is anticipated to cost $20-$25 per dose – a nominal amount when compared to the ongoing expense of taking pharmaceuticals every day.
“We think a fibromyalgia patient would need one or two doses maximum so you can understand why I’m not getting much support from drug companies,” Gillis said.
In addition to the vaccine trial, EpicGenetics is partnering with the University of California, Los Angeles (UCLA) and the University of Illinois College of Medicine Chicago to sequence the genomes of up to 250,000 fibromyalgia patients.
“We’re looking for any type of genetic patterns or anomalies or mutations,” Gillis said.
Patients who test positive for fibromyalgia using the FM/a test will be able to participate in the genomic study.
The FM/a test currently costs $936 but is covered by some insurance companies and Medicare. EpicGenetics’ support team helps patients determine if their insurance company will cover the test. A no-interest payment plan is available for people who are uninsured or whose insurance won’t cover the test.
If you’d like to learn more about the FM/a test, visit FMTest.com. Click here to read more about EpicGenetics’ fibromyalgia genome project and the BCG vaccine study. If you’re interested in having the FM/a test, please fill out the application form on the home page at FMTest.com. If you have additional questions or experience any issues with submitting the form, you can email the company at ask@epicgtx.com or call (310) 277-4600.
About Author:
Donna Gregory Burch was diagnosed with fibromyalgia in 2014 after several years of unexplained pain, fatigue and other symptoms. She was later diagnosed with chronic Lyme disease. Donna covers news, treatments, research and practical tips for living better with fibromyalgia and Lyme on her blog, FedUpwithFatigue.com. You can also find her onFacebook and Twitter. Donna is an award-winning journalist whose work has appeared online and in newspapers and magazines throughout Virginia, Delaware and Pennsylvania. She lives in Delaware with her husband and their many fur babies.
Source: prohealth.com

Post Polio Litaff, Association A.C _APPLAC Mexico

9 oct. 2017

Trump policy set to hinder war on polio in Pakistan: report


THE EXPRESS TRIBUNE > PAKISTAN

Experts looking into the crippling impact of polio in Pakistan and Afghanistan have stated that the biggest obstacle is not lack of money, but the mistrust of the western governments who bankroll the vaccines, The Guardian reported.

And now US President Donald Trump is about to deepen that mistrust. If the US continues to threat Pakistan, the anti-US sentiment will increase dramatically, which have led to attacks on polio workers and prompted tribal leaders to ban vaccination campaigns.
It would not be the first time the US has got in the way of the war on polio. The fight against polio suffered its biggest blow in 2011 when the CIA concocted a fake hepatitis vaccination campaign as part of its efforts to find Osama bin Laden. The Taliban issued fatwas and murdered dozens of health workers. In 2014, Pakistan recorded more than 300 polio cases.
In his recently announced South Asia strategy, Trump signaled a tougher line on Pakistan, “We have been paying Pakistan billions and billions of dollars at the same time they are housing the very terrorists that we are fighting. But that will have to change, and that will change immediately,” he said.
“It is hard to predict how local communities will respond to health workers if bombings pick up,” said Monica Martinez-Bravo, a researcher at CEMFI and co-author of a new paper on mistrust of vaccines in Pakistan. But she documented a clear correlation between support for militant groups at times a result of air campaigns, will decline in immunisation rates.
Bombings complicate access for immunisers, and insurgents have used polio to demand a halt to airstrikes in return for allowing vaccinations. This year, in Kunduz in northern Afghanistan, the Taliban banned inoculations for 15 months, relenting only when a 14-month-old girl contracted polio.
Since the Global Polio Eradication Initiative was launched in 1988, an estimated 16 million people have been saved from paralysis, and 1.5 million children from death. The virus loiters in the environment. Last week, standing above a river in Rawalpindi overflowing with sewage after the monsoon rains, Sarwat Boobak, area coordinator for WHO, said her team had detected wild polio, a sign that people were still shedding the virus, even in the capital Islamabad.
A long-time polio worker, Boobak fled her home town of Karachi in 2012 after the CIA vaccination scheme was revealed. “Our work suffered so much after that,” she said.
The backlash predominantly hit female health workers who make up the backbone of vaccination teams. Since then, at least 41 polio workers have been killed in Pakistan, as have several polio workers in Afghanistan. An overwhelming majority of Pakistanis welcome vaccination workers, a few refusals can keep the disease alive.
“Polio vaccines are produced in western countries, and are made out of pig fat or contain alcohol, the two things that are forbidden in Islam,” said Akbar Wazir, a tribal elder from North Waziristan. Equally false are beliefs that vaccines transmit HIV or cause sterilisation.
Such misconceptions grew stronger after the CIA ruse, said Martinez-Bravo. “Once people found credible evidence for one claim, it lent credibility to the others,” she said. This year, 250,000 Pakistani polio workers will target 38 million children who require a course of 10-15 vaccinations. A campaign of that magnitude requires goodwill from communities.


“Certain elements don’t want the Pakistani government to succeed, including in polio campaigns,” said Rana Muhammad Safdar, emergency coordinator for polio eradication in Pakistan. He would not rule out that military operations could endanger vaccination campaigns. “By now we have been able to prevent 500,000 paralysis cases in Pakistan alone,” he said. “We all must be extra careful.”
Post Polio Litaff, Association A.C _APPLAC Mexico

5 oct. 2017

Study Provides New Insight Into Patients’ Healing Journeys

Researchers developed model of how people transcend suffering to find healing.

Article ID: 681075
Released: 13-Sep-2017 5:05 PM EDT
  • Credit: Sara Warber
    This model of the "healing journey" describes how people who are ill re-establish a sense of integrity and wholeness. Researchers' thematic analysis of patient interviews found that healing is a complex, long-term process facilitated by persistence and trusting relationships.
The study is one of few to examine healing from the patient perspective. “The findings are helpful because they show, from the lived experience of people who are suffering, how the winding path of healing happens,” said co-author Kurt C. Stange, MD, PhD, a Distinguished University Professor at Case Western Reserve University and a Scholar of the Institute for Integrative Health, which helped fund the study.
The authors performed thematic analyses of in-depth interviews with 23 patients who had a variety of medical, psychological, and social issues. All had experienced healing, defined as “recovering a sense of integrity and wholeness after experiencing illness and suffering.” Interviews were conducted by the first author, John Glenn Scott, MD, PhD, for an earlier study of healing relationships between doctors and patients.
Using a combination of qualitative methods to analyze the transcripts, the authors identified emerging themes and developed a model illustrating the healing journey. The process it depicts begins with a wounding event, causing suffering, defined as “the experience of distress when the intactness or integrity of the person is threatened.” Its degree and quality are related to the individual’s characteristics, relationships, and stage of life. Through persistence, the suffering person forms safe, trusting relationships with helpers, who in turn, enable the person to gain resources, such as positivity. The cycle of acquiring relationships and resources repeats indefinitely, fostering beneficial attributes, such as self-acceptance. These contribute to a restored sense of wholeness and integrity, which constitutes healing.
Healing Journey Model
Transcript analyses revealed that healing was an erratic, long-term process, experienced uniquely by each person with their individual circumstances. The authors wrote: “People in the sample experienced healing journeys that spanned a spectrum from overcoming unspeakable trauma and then becoming healers themselves, to everyday heroes functioning well despite ongoing serious health challenges.”
The study found that people on healing journeys created connections with a wide range of helpers, including not only family, friends, and health professionals, but also non-human sources of support, such as pets, spirituality, and personal interests. Crucial to forming connections were a feeling of safety and a sense of trust that connections would be conducive to healing. These relationships proved instrumental in helping participants develop skills and resources through observation and practice, including the ability to reframe suffering in a positive light, the choice to adopt an optimistic attitude, and the capacity to take responsibility for one’s recovery from illness.
The authors note that the healing journey was recursive in nature, not step-wise.  Mustering persistence and battling despair, people continually formed connections and gained new resources. As a result, they gradually found relief from suffering and began to exhibit emergent characteristics: a sense of hope, self-acceptance, and a desire to help others—the immediate precursors to healing.
Importantly, the authors go on to say that restoring a sense of integrity and wholeness doesn’t require the absence of illness. None of the study participants was cured, yet as the authors point out, “they were all able to transcend their suffering and in some sense to flourish.”
The authors are hopeful the study will influence a shift in the way patients and health care practitioners think about and approach healing. “By filling a gap in understanding the healing process, the study’s findings may offer hope to those who are suffering and guide how they respond to their state of illness,” said Dr. Stange. “Likewise, greater understanding of patients’ journeys may positively inform the way health professionals, caregivers, and communities support those who are ill.”
Other authors include two Institute for Integrative Health Scholars, Paul Dieppe, MD, FRCP, FFPH (University of Exeter Medical School) and David Jones, MD (The Institute for Functional Medicine), as well as Sara L. Warber, MD (University of Michigan Medical School), and John Glenn Scott, MD, PhD (Northeastern Vermont Regional Hospital, Dartmouth Geisel School of Medicine).
In addition to funding from the Institute for Integrative Health, Dr. Jones received some support from the Institute for Functional Medicine, and Dr. Stange received some support from a Clinical Research Professorship from the American Cancer Society.
# # #
About The Institute for Integrative Health
A non-profit organization based in Baltimore, the Institute for Integrative Health was founded by Brian Berman, MD, in 2007 to catalyze new ideas in health, understand the complex network of factors that influence health, and promote the well-being of individuals and communities. Learn more at www.tiih.org.
Media contact: Robin Yasinow, The Institute for Integrative Health, 410-299-5437, ryasinow@tiih.org

Post Polio Litaff, Association A.C _APPLAC Mexico

2 oct. 2017

Estructura Neuronal



La neurona posee determinadas particularidades que hacen de ella una unidad funcional muy especial. Una característica fundamental le es exclusiva: la escasa posibilidad de renovación de las células degeneradas. De modo que el cerebro humano que inicialmente posee aproximadamente 1011neuronas, suele perder alrededor de 50.000 a 100.000 sin que se produzca reparación de esta pérdida. Las neuronas son estructural y funcionalmente unidades celulares, tienen la característica de recibir estímulos nerviosos provenientes de otras neuronas, ya sean excitatorios o inhibitorios, y conducir el impulso nervioso.

Las neuronas poseen proteínas específicas como lo son: la GP-350 soluble unida a la membrana, es específica del cerebro y está localizada en las células piramidales y estrelladas; la sinaptina contenida en las vesículas sinápticas y en las membranas plasmáticas de la sinapsis; la D1, D2 y D3 son proteínas específicas del cerebro, localizadas en las membranas sinápticas y que difieren en su peso molecular y la P-400, proteína que está unida a las membranas y que se halla solamente en la capa molecular del cerebelo, donde existe en las dendritas de las células de Purkinje.
Las neuronas son células que poseen dos grandes y notables propiedades como son: la irritabilidad, que le confiere a la célula la capacidad de respuesta a agentes físicos y químicos con la iniciación de un impulso y la conductibilidad, la cual le proporciona la capacidad de transmitir los impulsos de un sitio a otro. El grado en que estén desarrolladas estas dos propiedades protoplasmáticas en las neuronas, junto con la gran diversidad de formas y tamaños de los cuerpos celulares y la longitud de sus prolongaciones distinguen a este tipo de células de otras. El término neurona se refiere a la célula nerviosa completa, incluyendo su núcleo, citoplasma que lo rodea, denominado pericarión, y una o más extensiones protoplasmáticas, las cuales suelen ser axones y/o dendritas.
Por lo general los somas de las neuronas están agrupados en una especie de masa. En el SNC se les denomina núcleos a los grandes cuerpos celulares no encapsulados; en el SNP, generalmente estos grupos están encapsulados y se les conoce como ganglios.
La neurona es la célula fundamental y básica del sistema nervioso. Es una célula alargada, especializada en conducir impulsos nerviosos. En las neuronas se pueden distinguir tres partes fundamentales, que son: el citón o soma o cuerpo celular, corresponde a la parte más voluminosa de la neurona. Aquí se puede observar una estructura esférica llamada núcleo. Éste contiene la información que dirige la actividad de la neurona. Además, el soma se encuentra el citoplasma. En él se ubican otras estructuras que son importantes para el funcionamiento de la neurona, las dendritas, que son prolongaciones cortas que se originan del soma neural. Su función es recibir impulsos de otras neuronas y enviarlas hasta el soma de la neurona. El axón, es una prolongación única y larga. En algunas ocasiones, puede medir hasta un metro de longitud. Su función es sacar el impulso desde el soma neuronal y conducirlo hasta otro lugar del sistema.

El cuerpo de la célula nerviosa, como el de las otras células, que consiste esencialmente en una masa de citoplasma en el cual está incluido el núcleo; está limitado por su lado externo por una membrana plasmática. Es a menudo el volumen del citoplasma dentro del cuerpo de la célula es mucho menor que el volumen del citoplasma en las neuritas.
  • Núcleo: por lo común se encuentra en el centro del cuerpo celular. Es grande, redondeado pálido y contiene finos gránulos de cromatina muy dispersos. Por lo general las neuronas poseen un único núcleo que está relacionado con la síntesis de ácido ribononucleico RNA. El gran tamaño probablemente se deba a la alta tasa de síntesis proteica, necesario para mantener el nivel de proteínas en el gran volumen citoplasmático presente en las largas neuritas y el cuerpo celular.
  • Sustancia de Nissl: consiste en gránulos que se distribuyen en todo el citoplasma del cuerpo celular excepto en la región del axón. Las micrografías muestran que la sustancia de Nissl está compuesta por retículo endoplasmático rugoso dispuestos en forma de cisternas anchas apiladas unas sobre otras. Dado que los ribosomas contienen RNA, la sustancia de Nissl es basófila y puede verse muy bien con tinción azul de touluidina u otras anilinas básicas y microscopio óptico. Es responsable de la síntesis de proteínas, las cuales fluyen a lo largo de las dendritas y el axón y reemplazan a las proteínas que se destruyen durante la actividad celular. La fatiga o lesión neuronal ocasiona que la sustancia de Nissl se movilice y concentre en la periferia del citoplasma. Esto se conoce con el nombre de cromatólisis.
  • Aparato de Golgi: cuando se ve con microscopio óptico, después de una tinción de plata y osmio, aparece como una red de hebras ondulantes irregulares alrededor del núcleo. En micrografías electrónicas aparece como racimos de cisternas aplanadas y vesículas pequeñas formadas por retículos endoplasmáticos lisos. Las proteínas producidas por la sustancia de Nissl son transferidas al aparato de Golgi donde se almacenan transitoriamente y se le pueden agregar hidratos de carbono. Las macromoléculas pueden ser empaquetadas para su transporte hasta las terminaciones nerviosas. También se le cree activo en la producción de lisosomas y en la síntesis de las membranas celulares.
  • Mitocondrias: Dispersas en todo el cuerpo celular, las dendritas y el axón. Tienen forma de esfera o de bastón. En las micrografías electrónicas las paredes muestran doble membrana. La membrana interna exhibe pliegues o crestas que se proyectan hacia adentro de la mitocondria. Poseen muchas enzimas que toman parte en el ciclo de la respiración, por lo tanto son importantes para producir energía.
  • Neurofibrillas: Con microscopio óptico se observan numerosas fibrillas que corren paralelas entre si a través del cuerpo celular hacia las neuritas (tinción de plata). Con microscopio electrónico se ven como haces de microfilamentos de aproximadamente 7 mm de diámetro. Contienen actina y miosina y es probable que ayuden al transporte celular.
  • Microtúbulos: Se ven con microscopio electrónico y son similares a aquellos observados en otro tipo de células. Tienen unos 20 a 30 nm de diámetro y se hallan entremezclados con los microfilamentos. Se extienden por todo el cuerpo celular y sus prolongaciones. Se cree que la función de los microtúbulos es el transporte de sustancias desde el cuerpo celular hacia los extremos dístales de las prolongaciones celulares.
  • Lisosomas: Son vesículas limitadas por una membrana de alrededor de 8 nm de diámetro. Sirven a la célula actuando como limpiadores intracelulares y contienen enzimas hidrolíticas.
  • Centríolos: Son pequeñas estructuras pares que se hallan en las células inmaduras en proceso de división. También se hallan centríolos en las células maduras, en las cuáles se cree que intervienen en el mantenimiento de los microtúbulos.
  • Lipofusina: Se presenta como gránulos pardo amarillentos dentro del citoplasma. Se estima que se forman como resultado de la actividad lisosomal y representan un subproducto metabólico. Se acumula con la edad.
  • Melanina: Los gránulos de melanina se encuentran en el citoplasma de las células en ciertas partes del encéfalo, como por ejemplo la sustancia negra del encéfalo. Su presencia está relacionada con la capacidad para sintetizar catecolaminas por parte de aquellas neuronas cuyo neurotransmisor es la dopamina.
La superficie celular o membrana, que limita la neurona, reviste una especial importancia por su papel en la inclinación y la transmisión de los impulsos nerviosos. Elplasmalemao membrana plasmática es una doble capa de moléculas de fosfolípidos que tiene cadenas de hidrocarburos hidrofóbicos orientados directamente hacia el aspecto medial de la membrana. Dentro de esta estructura se encuentran moléculas de proteínas, de las cuales algunas pasan a través de todo el espesor de este estrato y proporcionan canales hidrofílicos a través de los cuales los iones inorgánicos entran o salen de la célula. Los iones comunes (sodio, potasio, calcio y cloro) poseen un canal molecular específico. Los canales tienen una entrada que regula la carga eléctrica o voltaje, lo cual significa que se abre y cierra en respuesta a cambios de potencial eléctrico a través de la membrana.
El núcleo de este tipo de células es voluminoso hasta de 20 mm de diámetro, de forma esférica y situado en el centro del cuerpo nuclear, incluyendo una heterocromatina que se halla en cantidad pequeña y marginada en la superficie interna de la cubierta nuclear.
El cuerpo celular o pericarión suele ser grande en comparación con otras células y varía de 4 a 135 mm de diámetro, su forma es variable en extremo, y depende del número y orientación de sus prolongaciones.
El aparato de Golgi es un organelo citoplasmático provisto de acúmulos de cisternas aplanadas, estrechamente, yuxtapuestas, las cuales se encuentran apiladas y rodeadas por muchas vesículas pequeñas, es un sistema continuo agranular o de superficie lisa. La superficie es el área donde se adhieren los carbohidratos de algunas proteínas, que posteriormente se convierten en glucoproteínas, estas se transportan en forma de vesículas en dirección distal o a lo largo de las prolongaciones citoplasmáticas para renovar las vesículas sinápticas en los bulbos terminales de las terminaciones axónicas y también contribuyen a la renovación de la membrana neuronal (Roselli, 1997).
Los lisosomas son grandes vesículas que contienen enzimas que catalizan la descomposición de moléculas grandes no necesarias, generalmente son numerosas.
Las mitocondrias son organelos citoplasmáticos dispersos en el pericarión, dendritas y axones; son esféricos en forma de bastoncillo, o filamentosas, tienen una longitud de 0.2 a 1.0 mm y un diámetro de 0.2 mm. Las mitocondrias de las neuronas muestran su característica de membrana doble periférica con crestas o pliegues internos. En estas se depositan las enzimas que tienen que ver con diversos aspectos del metabolismo celular, incluyendo la respiración y la fosforilación; son el sitio donde se produce energía en las reacciones de la fisiología celular (Jones, et al., 1985).
El axón de una neurona principalmente está rodeado por una vaina de mielina, que empieza cerca del origen del axón y finaliza en las cercanías de sus ramas terminales en el sistema nervioso, la mielina es depositada por los oligodendrocitos y esta formada esencialmente por capas estrechamente superpuestas a sus membranas plasmáticas. La cubierta de mielina, por tanto, tiene una composición lipoproteíca y unas interrupciones llamadas nódulos de Ranvier, las cuales indican los sitios donde se unen las porciones formadas por diferentes oligodendrocitos contiguos. Los canales de sodio y sus poros que regulan el voltaje se presentan únicamente en los nodos de un axón mielinizado, de manera que ocurren solo en esos sitios movimientos iónicos en la conducción de ese impulso.

La envoltura de mielina aísla el axón entre los nodos y así hay una conducción casi instantánea del potencial de acción de un nodo al inmediato. Esta conducción saltatoria permite una señalización mucho más rápida en el axón mielinizado que en el amielínico. El grosor de la capa de mielina y la distancia entre los nodos tiende a ser directamente proporcional al diámetro y a la longitud del axón; la conducción del impulso nervioso es más rápida cuando el diámetro de la fibra nerviosa es mayor (Meyer, 1985).

También los axones de las neuronas se agrupan a menudo. En el SNC se les llaman tractos a los haces o masas de axones que llevan información u ordenes motoras de una clase completa. Los tractos forman la materia blanca del SNC. En el SNP, se llamannervios a los haces discretos de axones que traen información hacia el SNC desde las estructuras periféricas y conducen órdenes motoras hacia las glándulas y los músculos (Meyer, 1985).
Las dendritas salen del cuerpo de la neurona y se ramifican en su cercanía; sus ramas pueden ser profusas e intrincadas. El citoplasma de las dendritas llamado dendroplasma, se parece al del pericarión, con retículo endoplásmico granular (sustancia cromatofílica o de Nilss). Se presenta en los troncos proximales de las dendritas y en los sitios donde se ramifican; en algunas neuronas; las ramas pequeñas tienen un gran número de diminutas salientes, llamadas espinas dendríticas, que participan en la sinapsis. La superficie del cuerpo celular puede ser incluida como área receptora de la neurona; en las neuronas motoras de la médula espinal, por ejemplo, gran número de terminaciones axónicas hace sinapsis con el cuerpo celular y también con las dendritas (Palo, 1997).
Las neuronas, al igual que las otras células de la glía poseen prolongaciones celulares filamentosas de naturaleza proteica que les confieren resistencia mecánica. Dentro de estos se distinguen tres tipos de organelos alargados: microtúbulos, microfilamentos y filamentos intermedios; representados químicamente por los neurotúbulos, estructuras localizadas en el interior de los axones, compuestas de tubulina asociada a proteínas denominadas dineínas y diseñadas para proporcionar rigidez y fortaleza mecánica a las prolongaciones filamentosas de neuronas y células gliales, también toman parte en las funciones dinámicas, tales como transporte axoplásmico y fluidez de las membranas celulares; neurofilamentos que representan a los filamentos intermediarios que son organulos citoplasmáticos fibrosos del sistema nervioso, su estructura proteica no es clara, pero se sabe que no están compuestos de tubulina ni actinia, están involucrados en el mecanismo de transporte axónico y suelen conferir una resistencia adicional a las prolongaciones largas y microfilamentos, compuestos de actina capaces de interaccionar con la miosina de una forma que sugiere que forman parte de un mecanismo contráctil y, por lo tanto, están involucrados en el movimiento.
Jairo Alfonso Tovar Franco, Ph.D.
2.1.6. Fase VI: Muerte neuronal.
No se sabe cómo viene determinada la especificidad en la supervivencia de las conexiones sinápticas. Posiblemente, una formación excesiva inicial de conexiones viene seguida por una degeneración de todas, excepto las correctas. Está es la denominada hipótesis de la muerte celular. Durante el desarrollo del SNC se generan un gran número de neuronas que han de ser selectivamente eliminadas.

Las neuronas necesitan determinados factores de crecimiento para sobrevivir, puesto que los niveles de estos factores son muy bajos, las neuronas compiten por ellos, de tal manera, que si no pueden conseguirlos, mueren. Este fenómeno se denomina muerte celular natural . Se han descrito tres clases diferentes de factores de crecimiento por los que compiten las neuronas: el factor de crecimiento nervioso (NGF), el factor neurotrófico derivado del cerebro (BDNF) y la neurotrofina-3 (NT-3). Los tres pertenecen a la familia de factores de crecimiento nervioso.
La cascada de señales intracelulares implicada en la protección de la muerte apoptótica generada por deprivación de señales de supervivencia.
La muerte celular programada (PCP; también denominada apoptosis) ocurre de manera natural durante el desarrollo
del sistema nervioso y esta regulada por la actividad de un conjunto de genes.
La muerte por apoptosis se caracteriza por la
existencia de condensación de la cromatina, fragmentación del DNA, desorganización del citoesqueleto, etc.

Existen evidencias de que la muerte apoptotica ocurre en diversos estados neuropatológicos como ALS, enfermedades de Parkinson y Alzheimer y como consecuencia de procesos de isquemia en el cerebro. El concepto de que la muerte neuronal que se observa en dichas circunstancias puede ser, en una importante proporción, de naturaleza apoptótica, ha llevado a intentar investigar los mecanismos subyacente en la apoptosis neuronal con el fin de poder diseñar estrategias terapéuticas que logren paliar los efectos de dichas patologías. Para ello, y entre otras estrategias, se han utilizado varios modelos de apoptosis en cultivos neuronales.
Uno de estos modelos son las neuronas granulares de cerebelo. Se pueden obtener cultivos muy homogéneos de estas células, que solamente logran sobrevivir in vitro
Una de las hipótesis de trabajo propuestas, indica que la despolarización inducida por la alta concentración de KCl provocaría la liberación de peptidos, que actuando a través de sus receptores podrían aumentar la concentración intracelular de AMP cíclico. 
Este aumento en la concentración de nucleótido cíclico seria un elemento clave en la cascada celular de supervivencia generada por una elevada concentración de KCl.En este sentido, se ha descrito que el PACAP parece tener un afecto anti-apoptotico en este modelo, que estaría mediado por la activación de la adenilato ciclasa y posterior activación de la vía de las quinasas MEK-ERK.

Post Polio Litaff, Association A.C _APPLAC Mexico

Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger, UNITED STATES, 2017


Compliant version of the schedule

Print PDF document of this schedule

These recommendations must be read with the footnotes that follow. For those who fall behind or start late, provide catch-up vaccination at the earliest opportunity as indicated by the green bars in tables below. To determine minimum intervals between doses, see the catch-up schedule. School entry and adolescent vaccine age groups are 4-6 yrs, 11-12 yrs, and 16 yrs.

Birth to 15 Months

VaccineBirth1 mo2 mos4 mos6 mos9 mos12 mos15 mos
Hepatitis B1 (HepB)1stdose←2nddose→ ←3rd dose→
Rotavirus2 (RV)
RV1 (2-dose series); RV5 (3-dose series)
  1stdose2nddoseSee footnote 2   
Diphtheria, tetanus, & acellular pertussis3 (DTaP: <7 a="" yrs="">  1stdose2nddose3rd dose ←4thdose→
Haemophilus influenzae type b4 (Hib)  1stdose2nddoseSee footnote 4 ←3rd or 4th dose,
See footnote 4
Pneumococcal conjugate5 (PCV13)  1stdose2nddose3rd dose ←4th dose→
Inactivated poliovirus6 (IPV:<18 a="" yrs="">  1stdose2nddose←3rd dose→
Influenza7 (IIV)    Annual vaccination (IIV) 1 or 2 doses
Measles, mumps, rubella8 (MMR)    See footnote 8←1st dose→
Varicella9 (VAR)      ←1st dose→
Hepatitis A10 (HepA)      ←2 dose series, See footnote 10
Meningococcal11 (Hib-MenCY ≥ 6 weeks; MenACWY-D ≥9 mos; MenACWY-CRM ≥ 2 mos)   See footnote 11
Tetanus, diphtheria, & acellular pertussis12 (Tdap: ≥7 yrs)        
Human papillomavirus13 (HPV)        
Meningococcal B11        
Pneumococcal polysaccharide5 (PPSV23)        

Legend

 Range of recommended ages for all children Range of recommended ages for catch-up immunization Range of recommended ages for certain high-risk groups Range of recommended ages for non-high-risk groups that may receive vaccine, subject to individual clinical decision making No recommendation

18 Months to 18 Years

Vaccines18 mos19-23 mos2-3 yrs4-6 yrs7-10 yrs11-12 yrs13-15 yrs16 yrs17-18 yrs
Hepatitis B1 (HepB)←3rddose→
Rotavirus2 (RV)
RV1 (2-dose series); RV5 (3-dose series)
         
Diphtheria, tetanus, & acellular pertussis3 (DTaP: <7 a="" yrs="">←4thdose→ 5thdose     
Haemophilus influenzae type b4 (Hib)  
Pneumococcal conjugate5 (PCV13)  
Inactivated poliovirus6 (IPV:<18 a="" yrs="">←3rddose→ 4thdose   
Influenza7 (IIV)Annual vaccination (IIV) 1 or 2 dosesAnnual vaccination (IIV) 1 dose only
Measles, mumps, rubella8 (MMR) 2nddose 
Varicella9 (VAR) 2nddose 
Hepatitis A10 (HepA)←2 dose series, See footnote 10 
 
Meningococcal11 (Hib-MenCY ≥ 6 weeks; MenACWY-D ≥9 mos; MenACWY-CRM ≥ 2 mos) See footnote 11 1st dose 2nddose 
Tetanus, diphtheria, & acellular pertussis12 (Tdap: ≥7 yrs)     Tdap 
Human papillomavirus13 (HPV)      See footnote 13 
 
Meningococcal B11       See footnote 11
    
Pneumococcal polysaccharide5(PPSV23)  See footnote 5
Note: The above recommendations must be read along with the footnotes of this schedule.

Footnotes

Recommended Immunization Schedule for Persons Age 0 Through 18 Years

United States, 2017
For further guidance on the use of the vaccines mentioned below, see the ACIP Recommendations.
For vaccine recommendations for persons 19 years of age and older, see the adult immunization schedule.
See additional notes for Recommended Immunization Schedule for Persons Age 0 Through 18 Years and Catch–up Immunization Schedule.
  1.  Hepatitis B (HepB) vaccine. (Minimum age: birth)
    Routine vaccination:
    At birth
    • Administer monovalent HepB vaccine to all newborns within 24 hours of birth.
    • For infants born to hepatitis B surface antigen (HBsAg)–positive mothers, administer HepB vaccine and 0.5 mL of hepatitis B immune globulin (HBIG) within 12 hours of birth. These infants should be tested for HBsAg and antibody to HBsAg (anti–HBs) at age 9 through 12 months (preferably at the next well–child visit) or 1 to 2 months after completion of the HepB series if the series was delayed.
    • If mother’s HBsAg status is unknown, within 12 hours of birth, administer HepB vaccine regardless of birth weight. For infants weighing less than 2,000 grams, administer HBIG in addition to HepB vaccine within 12 hours of birth. Determine mother’s HBsAg status as soon as possible and, if mother is HBsAg–positive, also administer HBIG to infants weighing 2,000 grams or more as soon as possible, but no later than age 7 days.
    Doses following the birth dose
    • The second dose should be administered at age 1 or 2 months. Monovalent HepB vaccine should be used for doses administered before age 6 weeks.
    • Infants who did not receive a birth dose should receive 3 doses of a HepB–containing vaccine on a schedule of 0, 1 to 2 months, and 6 months, starting as soon as feasible. See Catch–up Schedule.
    • Administer the second dose 1 to 2 months after the first dose (minimum interval of 4 weeks); administer the third dose at least 8 weeks after the second dose AND at least 16 weeks after the first dose. The final (third or fourth) dose in the HepB vaccine series should be administered no earlier than age 24 weeks.
    • Administration of a total of 4 doses of HepB vaccine is permitted when a combination vaccine containing HepB is administered after the birth dose.
    Catch–up vaccination:
    • Unvaccinated persons should complete a 3–dose series.
    • A 2–dose series (doses separated by at least 4 months) of adult formulation Recombivax HB is licensed for use in children aged 11 through 15 years.
    • For other catch–up guidance, see Catch–up Schedule.
  2.  Rotavirus (RV) vaccines. (Minimum age: 6 weeks for both RV1 [Rotarix] and RV5 [RotaTeq])
    Routine vaccination:
    • Administer a series of RV vaccine to all infants as follows:
      1. If Rotarix is used, administer a 2–dose series at ages 2 and 4 months.
      2. If RotaTeq is used, administer a 3–dose series at ages 2, 4, and 6 months.
      3. If any dose in the series was RotaTeq or vaccine product is unknown for any dose in the series, a total of 3 doses of RV vaccine should be administered.
    Catch–up vaccination:
    • The maximum age for the first dose in the series is 14 weeks, 6 days; vaccination should not be initiated for infants aged 15 weeks, 0 days, or older.
    • The maximum age for the final dose in the series is 8 months, 0 days.
    • For other catch–up guidance, see Catch–up Schedule.
  3.  Diphtheria and tetanus toxoids and acellular pertussis (DTaP) vaccine. (Minimum age: 6 weeks. Exception: DTaP–IPV [Kinrix, Quadracel]: 4 years)
    Routine vaccination:
    • Administer a 5–dose series of DTaP vaccine at ages 2, 4, 6, 15 through 18 months, and 4 through 6 years. The fourth dose may be administered as early as age 12 months, provided at least 6 months have elapsed since the third dose.
    • Inadvertent administration of fourth DTaP dose early: If the fourth dose of DTaP was administered at least 4 months after the third dose of DTaP and the child was 12 months of age or older, it does not need to be repeated.
    Catch–up vaccination:
    • The fifth dose of DTaP vaccine is not necessary if the fourth dose was administered at age 4 years or older.
    • For other catch–up guidance, see Catch–up Schedule.
  4.  Haemophilus influenzae type b (Hib) conjugate vaccine. (Minimum age: 6 weeks for PRP–T [ActHIB, DTaP–IPV/Hib (Pentacel), Hiberix, and Hib–MenCY (MenHibrix)], PRP–OMP [PedvaxHIB])
    Routine vaccination:
    • Administer a 2– or 3–dose Hib vaccine primary series and a booster dose (dose 3 or 4, depending on vaccine used in primary series) at age 12 through 15 months to complete a full Hib vaccine series.
    • The primary series with ActHIB, MenHibrix, Hiberix, or Pentacel consists of 3 doses and should be administered at ages 2, 4, and 6 months. The primary series with PedvaxHIB consists of 2 doses and should be administered at ages 2 and 4 months; a dose at age 6 months is not indicated.
    • One booster dose (dose 3 or 4, depending on vaccine used in primary series) of any Hib vaccine should be administered at age 12 through 15 months.
    • For recommendations on the use of MenHibrix in patients at increased risk for meningococcal disease, refer to the meningococcal vaccine footnotes and also to MMWR February 28, 2014/63(RR01):1–13[32 pages].
    Catch–up vaccination:
    • If dose 1 was administered at ages 12 through 14 months, administer a second (final) dose at least 8 weeks after dose 1, regardless of Hib vaccine used in the primary series.
    • If both doses were PRP–OMP (PedvaxHIB or COMVAX) and were administered before the first birthday, the third (and final) dose should be administered at age 12 through 59 months and at least 8 weeks after the second dose.
    • If the first dose was administered at age 7 through 11 months, administer the second dose at least 4 weeks later and a third (and final) dose at age 12 through 15 months or 8 weeks after second dose, whichever is later.
    • If first dose is administered before the first birthday and second dose administered at younger than 15 months, a third (and final) dose should be administered 8 weeks later.
    • For unvaccinated children aged 15–59 months, administer only 1 dose.
    • For other catch–up guidance, see Catch–up Schedule. For catch–up guidance related to MenHibrix, see the meningococcal vaccine footnotes and also MMWR February 28, 2014/63(RR01):1–13[32 pages].
    Vaccination of persons with high–risk conditions:
    • Children aged 12 through 59 months who are at increased risk for Hib disease, including chemotherapy recipients and those with anatomic or functional asplenia (including sickle cell disease), human immunodeficiency virus (HIV) infection, immunoglobulin deficiency, or early component complement deficiency, who have received either no doses or only 1 dose of Hib vaccine before 12 months of age, should receive 2 additional doses of Hib vaccine, 8 weeks apart; children who received 2 or more doses of Hib vaccine before age 12 months should receive 1 additional dose.
    • For patients younger than age 5 years undergoing chemotherapy or radiation treatment who received a Hib vaccine dose(s) within 14 days of starting therapy or during therapy, repeat the dose(s) at least 3 months following therapy completion.
    • Recipients of hematopoietic stem cell transplant (HSCT) should be revaccinated with a 3–dose regimen of Hib vaccine starting 6 to 12 months after successful transplant, regardless of vaccination history; doses should be administered at least 4 weeks apart.
    • A single dose of any Hib–containing vaccine should be administered to unimmunized* children and adolescents age 15 months and older undergoing an elective splenectomy; if possible, vaccine should be administered at least 14 days before procedure.
    • Hib vaccine is not routinely recommended for patients 5 years or older. However, 1 dose of Hib vaccine should be administered to unimmunized* persons aged 5 years or older who have anatomic or functional asplenia (including sickle cell disease) and unimmunized* persons age 5 through 18 years with HIV infection.
    Patients who have not received a primary series and booster dose or at least 1 dose of Hib vaccine after 14 months of age are considered unimmunized.
  5.  Pneumococcal vaccines. (Minimum age: 6 weeks for PCV13, 2 years for PPSV23)
    Routine vaccination with PCV13:
    • Administer a 4–dose series of PCV13 at ages 2, 4, and 6 months and at age 12 through 15 months.
    Catch–up vaccination with PCV13:
    • Administer 1 dose of PCV13 to all healthy children aged 24 through 59 months who are not completely vaccinated for their age.
    • For other catch–up guidance, see Catch–up Schedule.
    Vaccination of persons with high–risk conditions with PCV13 and PPSV23:
    • All recommended PCV13 doses should be administered prior to PPSV23 vaccination if possible.
    • For children aged 2 through 5 years with any of the following conditions: chronic heart disease (particularly cyanotic congenital heart disease and cardiac failure); chronic lung disease (including asthma if treated with high–dose oral corticosteroid therapy); diabetes mellitus; cerebrospinal fluid leak; cochlear implant; sickle cell disease and other hemoglobinopathies; anatomic or functional asplenia; HIV infection; chronic renal failure; nephrotic syndrome; diseases associated with treatment with immunosuppressive drugs or radiation therapy, including malignant neoplasms, leukemias, lymphomas, and Hodgkin disease; solid organ transplantation; or congenital immunodeficiency:
      1. Administer 1 dose of PCV13 if any incomplete schedule of 3 doses of PCV13 was received previously.
      2. Administer 2 doses of PCV13 at least 8 weeks apart if unvaccinated or any incomplete schedule of fewer than 3 doses of PCV13 was received previously.
      3. The minimum interval between doses of PCV13 is 8 weeks.
      4. For children with no history of PPSV23 vaccination, administer PPSV23 at least 8 weeks after the most recent dose of PCV13.
    • For children aged 6 through 18 years who have cerebrospinal fluid leak; cochlear implant; sickle cell disease and other hemoglobinopathies; anatomic or functional asplenia; congenital or acquired immunodeficiencies; HIV infection; chronic renal failure; nephrotic syndrome; diseases associated with treatment with immunosuppressive drugs or radiation therapy, including malignant neoplasms, leukemias, lymphomas, and Hodgkin disease; generalized malignancy; solid organ transplantation; or multiple myeloma:
      1. If neither PCV13 nor PPSV23 has been received previously, administer 1 dose of PCV13 now and 1 dose of PPSV23 at least 8 weeks later.
      2. If PCV13 has been received previously but PPSV23 has not, administer 1 dose of PPSV23 at least 8 weeks after the most recent dose of PCV13.
      3. If PPSV23 has been received but PCV13 has not, administer 1 dose of PCV13 at least 8 weeks after the most recent dose of PPSV23.
    • For children aged 6 through 18 years with chronic heart disease (particularly cyanotic congenital heart disease and cardiac failure), chronic lung disease (including asthma if treated with high–dose oral corticosteroid therapy), diabetes mellitus, alcoholism, or chronic liver disease, who have not received PPSV23, administer 1 dose of PPSV23. If PCV13 has been received previously, then PPSV23 should be administered at least 8 weeks after any prior PCV13 dose.
    • A single revaccination with PPSV23 should be administered 5 years after the first dose to children with sickle cell disease or other hemoglobinopathies; anatomic or functional asplenia; congenital or acquired immunodeficiencies; HIV infection; chronic renal failure; nephrotic syndrome; diseases associated with treatment with immunosuppressive drugs or radiation therapy, including malignant neoplasms, leukemias, lymphomas, and Hodgkin disease; generalized malignancy; solid organ transplantation; or multiple myeloma.
  6.  Inactivated poliovirus vaccine (IPV). (Minimum age: 6 weeks)
    Routine vaccination:
    • Administer a 4–dose series of IPV at ages 2, 4, 6 through 18 months, and 4 through 6 years. The final dose in the series should be administered on or after the fourth birthday and at least 6 months after the previous dose.
    Catch–up vaccination:
    • In the first 6 months of life, minimum age and minimum intervals are only recommended if the person is at risk for imminent exposure to circulating poliovirus (i.e., travel to a polio–endemic region or during an outbreak).
    • If 4 or more doses are administered before age 4 years, an additional dose should be administered at age 4 through 6 years and at least 6 months after the previous dose.
    • A fourth dose is not necessary if the third dose was administered at age 4 years or older and at least 6 months after the previous dose.
    • If both OPV and IPV were administered as part of a series, a total of 4 doses should be administered, regardless of the child’s current age. If only OPV was administered, and all doses were given prior to age 4 years, 1 dose of IPV should be given at 4 years or older, at least 4 weeks after the last OPV dose.
    • IPV is not routinely recommended for U.S. residents aged 18 years or older.
    • For other catch–up guidance, see Catch–up Schedule.
  7.  Influenza vaccines. (Minimum age: 6 months for inactivated influenza vaccine [IIV], 18 years for recombinant influenza vaccine [RIV])
    Routine vaccination:
    • Administer influenza vaccine annually to all children beginning at age 6 months. For the 2016–17 season, use of live attenuated influenza vaccine (LAIV) is not recommended.
    For children aged 6 months through 8 years:
    • For the 2016–17 season, administer 2 doses (separated by at least 4 weeks) to children who are receiving influenza vaccine for the first time or who have not previously received ≥2 doses of trivalent or quadrivalent influenza vaccine before July 1, 2016. For additional guidance, follow dosing guidelines in the 2016–17 ACIP influenza vaccine recommendations (seeMMWR August 26, 2016;65(5):1–54[56 pages].
    • For the 2017–18 season, follow dosing guidelines in the 2017–18 ACIP influenza vaccine recommendations.
    For persons aged 9 years and older:
    • Administer 1 dose.
  8.  Measles, mumps, and rubella (MMR) vaccine. (Minimum age: 12 months for routine vaccination)
    Routine vaccination:
    • Administer a 2–dose series of MMR vaccine at ages 12 through 15 months and 4 through 6 years. The second dose may be administered before age 4 years, provided at least 4 weeks have elapsed since the first dose.
    • Administer 1 dose of MMR vaccine to infants aged 6 through 11 months before departure from the United States for international travel. These children should be revaccinated with 2 doses of MMR vaccine, the first at age 12 through 15 months (12 months if the child remains in an area where disease risk is high), and the second dose at least 4 weeks later.
    • Administer 2 doses of MMR vaccine to children aged 12 months and older before departure from the United States for international travel. The first dose should be administered on or after age 12 months and the second dose at least 4 weeks later.
    Catch–up vaccination:
    • Ensure that all school–aged children and adolescents have had 2 doses of MMR vaccine; the minimum interval between the 2 doses is 4 weeks.
  9.  Varicella (VAR) vaccine. (Minimum age: 12 months)
    Routine vaccination:
    • Administer a 2–dose series of VAR vaccine at ages 12 through 15 months and 4 through 6 years. The second dose may be administered before age 4 years, provided at least 3 months have elapsed since the first dose. If the second dose was administered at least 4 weeks after the first dose, it can be accepted as valid.
    Catch–up vaccination:
    • Ensure that all persons aged 7 through 18 years without evidence of immunity (see MMWR 2007;56[No. RR–4][48 pages]), have 2 doses of varicella vaccine. For children aged 7 through 12 years, the recommended minimum interval between doses is 3 months (if the second dose was administered at least 4 weeks after the first dose, it can be accepted as valid); for persons aged 13 years and older, the minimum interval between doses is 4 weeks.
  10.  Hepatitis A (HepA) vaccine. (Minimum age: 12 months)
    Routine vaccination:
    • Initiate the 2–dose HepA vaccine series at ages 12 through 23 months; separate the 2 doses by 6 to 18 months.
    • Children who have received 1 dose of HepA vaccine before age 24 months should receive a second dose 6 to 18 months after the first dose.
    • For any person aged 2 years and older who has not already received the HepA vaccine series, 2 doses of HepA vaccine separated by 6 to 18 months may be administered if immunity against hepatitis A virus infection is desired.
    Catch–up vaccination:
    • The minimum interval between the 2 doses is 6 months.
    Special populations:
    • Administer 2 doses of HepA vaccine at least 6 months apart to previously unvaccinated persons who live in areas where vaccination programs target older children, or who are at increased risk for infection. This includes persons traveling to or working in countries that have high or intermediate endemicity of infection; men having sex with men; users of injection and non–injection illicit drugs; persons who work with HAV–infected primates or with HAV in a research laboratory; persons with clotting–factor disorders; persons with chronic liver disease; and persons who anticipate close, personal contact (e.g., household or regular babysitting) with an international adoptee during the first 60 days after arrival in the United States from a country with high or intermediate endemicity. The first dose should be administered as soon as the adoption is planned, ideally, 2 or more weeks before the arrival of the adoptee.
  11.  Meningococcal vaccines. (Minimum age: 6 weeks for Hib–MenCY [MenHibrix], 2 months for MenACWY–CRM [Menveo], 9 months for MenACWY–D [Menactra], 10 years for serogroup B meningococcal [MenB] vaccines: MenB–4C [Bexsero] and MenB–FHbp [Trumenba])
    Routine vaccination:
    • Administer a single dose of Menactra or Menveo vaccine at age 11 through 12 years, with a booster dose at age 16 years.
    • For children aged 2 months through 18 years with high–risk conditions, see “Meningococcal conjugate ACWY vaccination of persons with high–risk conditions and other persons at increased risk” and “Meningococcal B vaccination of persons with high–risk conditions and other persons at increased risk of disease” see below.
    Catch–up vaccination:
    • Administer Menactra or Menveo vaccine at age 13 through 18 years if not previously vaccinated.
    • If the first dose is administered at age 13 through 15 years, a booster dose should be administered at age 16 through 18 years, with a minimum interval of at least 8 weeks between doses.
    • If the first dose is administered at age 16 years or older, a booster dose is not needed.
    • For other catch–up guidance, see Catch–up Schedule.
    Clinical discretion:
    • Young adults aged 16 through 23 years (preferred age range is 16 through 18 years) who are not at increased risk for meningococcal disease may be vaccinated with a 2–dose series of either Bexsero (0, ≥1 month) or Trumenba (0, 6 months) vaccine to provide short–term protection against most strains of serogroup B meningococcal disease. The two MenB vaccines are not interchangeable; the same vaccine product must be used for all doses.
    • If the second dose of Trumenba is given at an interval of <6 4="" 6="" a="" after="" and="" at="" be="" between="" dose="" doses="" first="" given="" interval="" is="" least="" li="" minimum="" months="" second="" should="" the="" third="" weeks.="">
    Meningococcal conjugate ACWY vaccination of persons with high–risk conditions and other persons at increased risk:
    Children with anatomic or functional asplenia (including sickle cell disease), children with HIV infection, or children with persistent complement component deficiency (includes persons with inherited or chronic deficiencies in C3, C5–9, properdin, factor D, factor H, or taking eculizumab [Soliris]):
    • Menveo
      • Children who initiate vaccination at 8 weeks. Administer doses at ages 2, 4, 6, and 12 months.
      • Unvaccinated children who initiate vaccination at 7 through 23 months. Administer 2 primary doses, with the second dose at least 12 weeks after the first dose AND after the first birthday.
      • Children 24 months and older who have not received a complete series. Administer 2 primary doses at least 8 weeks apart.
    • MenHibrix
      • Children who initiate vaccination at 6 weeks. Administer doses at ages 2, 4, 6, and 12 through 15 months.
      • If the first dose of MenHibrix is given at or after age 12 months, a total of 2 doses should be given at least 8 weeks apart to ensure protection against serogroups C and Y meningococcal disease.
    • Menactra
      • Children with anatomic or functional asplenia or HIV infection
        • Children 24 months and older who have not received a complete series. Administer 2 primary doses at least 8 weeks apart. If Menactra is administered to a child with asplenia (including sickle cell disease) or HIV infection, do not administer Menactra until age 2 years and at least 4 weeks after the completion of all PCV13 doses.
      • Children with persistent complement component deficiency
        • Children 9 through 23 months. Administer 2 primary doses at least 12 weeks apart.
        • Children 24 months and older who have not received a complete series. Administer 2 primary doses at least 8 weeks apart.
      • All high–risk children
        • If Menactra is to be administered to a child at high risk for meningococcal disease, it is recommended that Menactra be given either before or at the same time as DTaP.
    Meningococcal B vaccination of persons with high–risk conditions and other persons at increased risk of disease:
    Children with anatomic or functional asplenia (including sickle cell disease) or children with persistent complement component deficiency (includes persons with inherited or chronic deficiencies in C3, C5–9, properdin, factor D, factor H, or taking eculizumab [Soliris]):
    • Bexsero or Trumenba
      • Persons 10 years or older who have not received a complete series. Administer a 2–dose series of Bexsero, with doses at least 1 month apart, or a 3–dose series of Trumenba, with the second dose at least 1–2 months after the first and the third dose at least 6 months after the first. The two MenB vaccines are not interchangeable; the same vaccine product must be used for all doses.
    For children who travel to or reside in countries in which meningococcal disease is hyperendemic or epidemic, including countries in the African meningitis belt or the Hajj:
    • Administer an age–appropriate formulation and series of Menactra or Menveo for protection against serogroups A and W meningococcal disease. Prior receipt of MenHibrix is not sufficient for children traveling to the meningitis belt or the Hajj because it does not contain serogroups A or W.
    For children at risk during an outbreak attributable to a vaccine serogroup:
    • For serogroup A, C, W, or Y: Administer or complete an age– and formulation–appropriate series of MenHibrix, Menactra, or Menveo.
    • For serogroup B: Administer a 2–dose series of Bexsero, with doses at least 1 month apart, or a 3–dose series of Trumenba, with the second dose at least 1–2 months after the first and the third dose at least 6 months after the first. The two MenB vaccines are not interchangeable; the same vaccine product must be used for all doses.
    For MenACWY booster doses among persons with high–risk conditions, refer to MMWR 2013;62(RR02):1–22[32 pages]MMWR June 20, 2014;63(24):527–530[16 pages], and MMWR November 4, 2016; 65(43):1189–1194[6 pages].
    For other catch–up recommendations for these persons and complete information on use of meningococcal vaccines, including guidance related to vaccination of persons at increased risk of infection, see meningococcal MMWR publications.
  12.  Tetanus and diphtheria toxoids and acellular pertussis (Tdap) vaccine. (Minimum age: 10 years for both Boostrix and Adacel)
    Routine vaccination:
    • Administer 1 dose of Tdap vaccine to all adolescents aged 11 through 12 years.
    • Tdap may be administered regardless of the interval since the last tetanus and diphtheria toxoid–containing vaccine.
    • Administer 1 dose of Tdap vaccine to pregnant adolescents during each pregnancy (preferably during the early part of gestational weeks 27 through 36), regardless of time since prior Td or Tdap vaccination.
    Catch–up vaccination:
    • Persons aged 7 years and older who are not fully immunized with DTaP vaccine should receive Tdap vaccine as 1 dose (preferably the first) in the catch–up series; if additional doses are needed, use Td vaccine. For children 7 through 10 years who receive a dose of Tdap as part of the catch–up series, an adolescent Tdap vaccine dose at age 11 through 12 years may be administered.
    • Persons aged 11 through 18 years who have not received Tdap vaccine should receive a dose, followed by tetanus and diphtheria toxoids (Td) booster doses every 10 years thereafter.
    • Inadvertent doses of DTaP vaccine:
      • If administered inadvertently to a child aged 7 through 10 years, the dose may count as part of the catch–up series. This dose may count as the adolescent Tdap dose, or the child may receive a Tdap booster dose at age 11 through 12 years.
      • If administered inadvertently to an adolescent aged 11 through 18 years, the dose should be counted as the adolescent Tdap booster.
    • For other catch–up guidance, see Catch–up Schedule.

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Polio Film

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video

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Polio Video

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Enlaces

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www.postpoliolitaff.org/
Postpoliolitaff.- Asociación Post Polio Litaff A.C Primera Organización oficial sobre Síndrome de Post Poliomielitis En México.


Polio y Efectos Secundarios SPP
http://polioyspp.blogspot.com/
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