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Vaccination

Vaccination is the administration of antigenic material (a vaccine) to stimulate adaptive immunity to a disease. Vaccines can prevent or ameliorate the effects of infection by many pathogens. There is strong evidence for the efficacy of many vaccines, such as the influenza vaccine,[1] the HPV vaccine[2] and the chicken pox vaccine[3] among others. Vaccination is generally considered to be the most effective method of preventing infectious diseases. The material administered can either be live but weakened forms of pathogens (bacteria or viruses), killed or inactivated forms of these pathogens, or purified material such as proteins.


Smallpox was likely the first disease people tried to prevent by purposely inoculating themselves with other types of infections.[4] In 1718, Lady Mary Wortley Montagu reported that the Turks had a habit of deliberately inoculating themselves with fluid taken from mild cases of smallpox, and that she had inoculated her own children.[5] Before 1796 when British physician Edward Jenner tested the possibility of using the cowpox vaccine as an immunization for smallpox in humans for the first time, at least six people had done the same several years earlier: a person whose identity is unknown, England, (about 1771); a Mrs. Sevel, Germany (about 1772); a Mr. Jensen, Germany (about 1770); Benjamin Jesty, England, in 1774; a Mrs. Rendall, England (about 1782); and Peter Plett, Germany, in 1791.[6]

The word vaccination was first used by Edward Jenner in 1796. Louis Pasteur furthered the concept through his pioneering work in microbiology. Vaccination (Latin: vacca—cow) is so named because the first vaccine was derived from a virus affecting cows—the relatively benign cowpox virus—which provides a degree of immunity to smallpox, a contagious and deadly disease. In common speech, 'vaccination' and 'immunization' generally have the same colloquial meaning. This distinguishes it from inoculation which uses unweakened live pathogens, although in common usage either is used to refer to an immunization. The word "vaccination" was originally used specifically to describe the injection of smallpox vaccine.[4][6]

Vaccination efforts have been met with some controversy since their inception, on scientific, ethical, political, medical safety, religious, and other grounds. In rare cases, vaccinations can injure people and, in the United States, they may receive compensation for those injuries under the National Vaccine Injury Compensation Program. Early success and compulsion brought widespread acceptance, and mass vaccination campaigns were undertaken which are credited with greatly reducing the incidence of many diseases in numerous geographic regions.

Mechanism of function

In the generic sense, the process of artificial induction of immunity, in an effort to protect against infectious disease, works by 'priming' the immune system with an 'immunogen'. Stimulating immune response, via use of an infectious agent, is known as immunization. Vaccinations involve the administration of one or more immunogens, which can be administered in several forms.

Some vaccines are administered after the patient already has contracted a disease. Vaccinia given after exposure to smallpox, within the first three days, is reported to attenuate the disease considerably, and vaccination up to a week after exposure likely offers some protection from disease or may modify the severity of disease.[7] The first rabies immunization was given by Louis Pasteur to a child after he was bitten by a rabid dog. Subsequently it was found that proper post-exposure prophylaxis (PEP) of potential rabies cases within 14 days infection provides complete protection against the disease.[8] Other examples include experimental AIDS, cancer and Alzheimer's disease vaccines. The essential empiricism behind such immunizations is that the vaccine triggers an immune response more rapidly than the natural infection itself.

Most vaccines are given by hypodermic injection as they are not absorbed reliably through the intestines. Live attenuated polio, some typhoid and some cholera vaccines are given orally in order to produce immunity based in the bowel.

Adjuvants and preservatives

Vaccines typically contain one or more adjuvants, used to boost the immune response. Tetanus toxoid, for instance, is usually adsorbed onto alum. This presents the antigen in such a way as to produce a greater action than the simple aqueous tetanus toxoid. People who get an excessive reaction to adsorbed tetanus toxoid may be given the simple vaccine when time for a booster occurs.

In the preparation for the 1990 Gulf campaign, Pertussis vaccine (not acellular) was used as an adjuvant for Anthrax vaccine. This produces a more rapid immune response than giving only the Anthrax, which is of some benefit if exposure might be imminent.

They may also contain preservatives, which are used to prevent contamination with bacteria or fungi. Until recent years, the preservative thiomersal was used in many vaccines that did not contain live virus. As of 2005, the only childhood vaccine in the U.S. that contains thiomersal in greater than trace amounts is the influenza vaccine,[1] which is currently recommended only for children with certain risk factors.[9] Single-dose Influenza vaccines supplied in the UK do not list Thiomersal (its UK name) in the ingredients. Preservatives may be used at various stages of production of vaccines, and the most sophisticated methods of measurement might detect traces of them in the finished product, as they may in the environment and population as a whole.[2]

Vaccination versus inoculation

Many times these words are used interchangeably, as if they were synonyms. In fact they are different things. As doctor Byron Plant explains: "Vaccination is the more commonly used term which actually consists of a "safe" injection of a sample taken from a cow suffering from cowpox... Inoculation, a practice probably as old as the disease itself, is the injection of the variola virus taken from a pustule or scab of a smallpox sufferer into the superficial layers of the skin, commonly on the upper arm of the subject. Often inoculation was done "arm to arm" or less effectively "scab to arm"...[10]

Vaccination began in the 18th century with the work of Edward Jenner.[11][12][13]

Types

All vaccinations work by presenting a foreign antigen to the immune system in order to evoke an immune response, but there are several ways to do this. The four main types that are currently in clinical use are as follows:

  1. An inactivated vaccine consists of virus particles which are grown in culture and then killed using a method such as heat or formaldehyde. The virus particles are destroyed and cannot replicate, but the virus capsid proteins are intact enough to be recognized and remembered by the immune system and evoke a response. When manufactured correctly, the vaccine is not infectious, but improper inactivation can result in intact and infectious particles. Since the properly produced vaccine does not reproduce, booster shots are required periodically to reinforce the immune response.
  2. In an attenuated vaccine, live virus particles with very low virulence are administered. They will reproduce, but very slowly. Since they do reproduce and continue to present antigen beyond the initial vaccination, boosters are required less often. These vaccines are produced by passaging virus in cell cultures, in animals, or at suboptimal temperatures, allowing selection of less virulent strains, or by mutagenesis or targeted deletions in genes required for virulence. There is a small risk of reversion to virulence, this risk is smaller in vaccines with deletions. Attenuated vaccines also cannot be used by immunocompromised individuals.
  3. Virus-like particle vaccines consist of viral protein(s) derived from the structural proteins of a virus. These proteins can self-assemble into particles that resemble the virus from which they were derived but lack viral nucleic acid, meaning that they are not infectious. Because of their highly repetitive, multivalent structure, virus-like particles are typically more immunogenic than subunit vaccines (described below). The human papillomavirus and Hepatitis B virus vaccines are two virus-like particle-based vaccines currently in clinical use.
  4. A subunit vaccine presents an antigen to the immune system without introducing viral particles, whole or otherwise. One method of production involves isolation of a specific protein from a virus or bacterium (such as a bacterial toxin) and administering this by itself. A weakness of this technique is that isolated proteins may have a different three-dimensional structure than the protein in its normal context, and will induce antibodies that may not recognize the infectious organism. In addition, subunit vaccines often elicit weaker antibody responses than the other classes of vaccines.

A number of other vaccine strategies are under experimental investigation. These include DNA vaccination and recombinant viral vectors.

Early forms of inoculation may have been developed in ancient China.[4] Scholar Ole Lund comments: "The earliest documented examples of vaccination are from India and China in the 17th century, where vaccination with powdered scabs from people infected with smallpox was used to protect against the disease. Smallpox used to be a common disease throughout the world and 20% to 30% of infected persons died from the disease. Smallpox was responsible for 8% to 20% of all deaths in several European countries in the 18th century. The tradition of inoculation may have originated in India in 1000 BCE."[14] The mention of inoculation in the Sact'eya Grantham, an Ayurvedic text, was noted by the French scholar Henri Marie Husson in the journal Dictionaire des sciences me`dicales.[15] Almroth Wright, the professor of pathology at Netley, further helped shape the future of vaccination by conducting limited experiments on the professional staff at Netly, including himself. The outcome of these experiments resulted in further development of vaccination in Europe.[16] The Anatolian Ottoman Turks knew about methods of inoculation.This kind of inoculation and other forms of variolation were introduced into England by Lady Montagu, a famous English letter-writer and wife of the English ambassador at Istanbul between 1716 and 1718, who'd almost died from smallpox as a young adult and was physically scarred from it. She came across the Turkish methods of inoculation, consenting to have her son inoculated by the Embassy surgeon Charles Maitland in the Turkish way. Lady Montagu wrote to her sister and friends in England describing the process in details. On her return to England she continued to propagate the Turkish tradition of inoculation and had many of her relatives inoculated. The breakthrough came when a scientific description of the inoculation operation was submitted to the Royal Society in 1724 by Dr Emmanual Timoni, who had been the Montagu’s family physician in Istanbul. Inoculation was adopted both in England and in France nearly half a century before Jenner's famous smallpox vaccine of 1796.[17]

Since then vaccination campaigns have spread throughout the globe, sometimes prescribed by law or regulations (See Vaccination Acts). Vaccines are now used to fight a wide variety of disease threats besides smallpox. Louis Pasteur further developed the technique during the 19th century, extending its use to protecting against bacterial anthrax and viral rabies. The method Pasteur used entailed treating the infectious agents for those diseases so they lost the ability to cause serious disease. Pasteur adopted the name vaccine as a generic term in honor of Jenner's discovery, which Pasteur's work built upon.

A doctor performing a typhoid vaccination in Texas, 1943.

Prior to vaccination with cowpox, the only known protection against smallpox was inoculation or variolation (Variola - the Smallpox viruses) where a small amount of live smallpox virus was administered to the patient; this carried the serious risk that the patient would be killed or seriously ill. The death rate from variolation was reported to be around a tenth of that from natural infection with Variola, and the immunity provided was considered quite reliable. Factors contributing to the efficacy of variolation probably include the choices of Variola Minor strains used, the relatively low number of cells infected in the first phase of multiplication following initial exposure, and the exposure route used, via the skin or nasal lining rather than inhalation of droplets into the lungs.

Consistency would suggest the activity should have predated Jenner's description of an effective vaccination system, and there is some history relating to opposition to the older and more hazardous procedure of variolation[citation needed].

In modern times, the first vaccine-preventable disease targeted for eradication was smallpox. The World Health Organization (WHO) coordinated the global effort to eradicate this disease. The last naturally occurring case of smallpox occurred in Somalia in 1977.

Maurice Hilleman was the most prolific of inventors of vaccines. He developed successful vaccines for measles, mumps, hepatitis A, hepatitis B, chickenpox, meningitis, pneumonia and Haemophilus influenzae bacteria.[18]

In 1988, the governing body of WHO targeted polio for eradication by the year 2000. Although the target was missed, eradication is very close. The next eradication target would most likely be measles, which has declined since the introduction of measles vaccination in 1963.

In 2000, the Global Alliance for Vaccines and Immunization was established to strengthen routine vaccinations and introduce new and under-used vaccines in countries with a per capita GDP of under US$1000. GAVI is now entering its second phase of funding, which extends through 2014.

Society and culture

Poster for vaccination against smallpox. Main article: Vaccination policy Further information: Vaccine controversy and Vaccine injury

In an attempt to eliminate the risk of outbreaks of some diseases, at various times several governments and other institutions have instituted policies requiring vaccination for all people. For example, an 1853 law required universal vaccination against smallpox in England and Wales, with fines levied on people who did not comply. Common contemporary U.S. vaccination policies require that children receive common vaccinations before entering public school.

Beginning with early vaccination in the nineteenth century, these policies were resisted by a variety of groups, collectively called anti-vaccinationists, who object on scientific, ethical, political, medical safety, religious, and other grounds. Common objections are that vaccinations do not work, that compulsory vaccination represents excessive government intervention in personal matters, or that the proposed vaccinations are not sufficiently safe.[19] Many modern vaccination policies allow exemptions for people who have compromised immune systems, allergies to the components used in vaccinations or strongly held objections.[20]

Allegations of vaccine injuries in recent decades have appeared in litigation in the U.S. Some families have won substantial awards from sympathetic juries, even though most public health officials believed that the claims of injuries were unfounded.[21] In response, several vaccine makers stopped production, threatening public health, and laws were passed to shield makers from liabilities stemming from vaccine injury claims.[21]

In countries with limited financial resources, limited coverage is a major problem causing unnecessary morbidity and mortality. Mean coverage may often appear fairly adequate. However, when analyzed in detail, effective coverage may nevertherless be rather poor.[22] More affluent countries are able to subsidize vaccinations for at-risk groups, resulting in more comprehensive and effective cover. In Australia, for example, the Government subsidizes vaccinations for seniors and indigenous Australians.[23]

Public Health Law Research,[24] an independent organization, reported in 2009 that there is insufficient evidence to assess the effectiveness of requiring vaccinations as a condition for specified jobs as a means of reducing incidence of specific diseases among particularly vulnerable populations;[25] that there is sufficient evidence supporting the effectiveness of requiring vaccinations as a condition for attending child care facilities and schools.;[26] and that there is strong evidence supporting the effectiveness of standing orders, which allow healthcare workers without prescription authority to administer vaccine as a public health intervention aimed at increasing vaccination rates.[27]

An HIV vaccine that protects vaccinated individuals from HIV infection is the goal of many HIV research programmes. Currently, there is no effective vaccine against HIV, the virus that causes AIDS. Vaccine development is one of several strategies to reduce the worldwide harm from AIDS, with other approaches based upon antiviral treatments such as highly active antiretroviral therapy (HAART) and social approaches such as safe sex prevention and awareness campaigns.

There is evidence that a vaccine may be possible. Work with monoclonal antibodies (MAb) has proven that the human body can defend itself against HIV, and certain individuals remain asymptomatic for decades after HIV infection. Potential candidates for antibodies and early stage results from clinical trials have been announced. However these are early results, and have not been developed to the point of human testing, or have not been replicated.

Malaria is a mosquito-borne infectious disease of humans caused by eukaryotic protists of the genus Plasmodium. It is widespread in tropical and subtropical regions, including much of Sub-Saharan Africa, Asia and the Americas. Malaria is very prevalent in these regions because they have significant amounts of rain fall and consistent hot temperatures. These warm, consistent temperatures and moisture provide mosquitos with the environment they need to breed continuously.[1] The cause of the disease is a protozoan, discovered in 1880, by Charles Louis Alphonse Laveran while he was working in the military hospital in Constantine, Algeria and observed the parasites in a blood smear taken from a patient who had just died of malaria.[2] The disease results from the multiplication of malaria parasites within red blood cells, causing symptoms that typically include fever and headache, in severe cases progressing to coma, and death.

Four species of Plasmodium can infect and be transmitted by humans. Severe disease is largely caused by Plasmodium falciparum. Malaria caused by Plasmodium vivax, Plasmodium ovale and Plasmodium malariae is generally a milder disease that is rarely fatal. A fifth species, Plasmodium knowlesi, is a zoonosis that causes malaria in macaques but can also infect humans.[3][4]

Malaria transmission can be reduced by preventing mosquito bites by distribution of inexpensive mosquito nets and insect repellents, or by mosquito-control measures such as spraying insecticides inside houses and draining standing water where mosquitoes lay their eggs. Although many are under development, the challenge of producing a widely available vaccine that provides a high level of protection for a sustained period is still to be met.[5] Two drugs are also available to prevent malaria in travellers to malaria-endemic countries (prophylaxis).

A variety of antimalarial medications are available. In the last 5 years, treatment of P. falciparum infections in endemic countries has been transformed by the use of combinations of drugs containing an artemisinin derivative. Severe malaria is treated with intravenous or intramuscular quinine or, increasingly, the artemisinin derivative artesunate [6] which is superior to quinine in both children and adults.[7] Resistance has developed to several antimalarial drugs, most notably chloroquine.[8]

Each year, there are more than 225 million cases of malaria,[9] killing around 781,000 people each year according to the World Health Organisation's 2010 World Malaria Report,[10] 2.23% of deaths worldwide. The majority of deaths are of young children in sub-Saharan Africa.[11] Ninety percent of malaria-related deaths occur in sub-Saharan Africa. Malaria is commonly associated with poverty, and can indeed be a cause of poverty[12] and a major hindrance to economic development.

Hepatitis (plural hepatitides) is a medical condition defined by the inflammation of the liver and characterized by the presence of inflammatory cells in the tissue of the organ. The name is from the Greek hepar (παρ), the root being hepat- (πατ-), meaning liver, and suffix -itis, meaning "inflammation" (c. 1727).[1] The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis.

Hepatitis may occur with limited or no symptoms, but often leads to jaundice, anorexia (poor appetite) and malaise. Hepatitis is acute when it lasts less than six months and chronic when it persists longer. A group of viruses known as the hepatitis viruses cause most cases of hepatitis worldwide, but it can also be due to toxins (notably alcohol, certain medications, some industrial organic solvents and plants), other infections and autoimmune diseases.

Hepatitis B is an infectious illness caused by hepatitis B virus (HBV) which infects the liver of hominoidea, including humans, and causes an inflammation called hepatitis. Originally known as "serum hepatitis",[1] the disease has caused epidemics in parts of Asia and Africa, and it is endemic in China.[2] About a quarter of the world's population, more than 2 billion people, have been infected with the hepatitis B virus.[3] This includes 350 million chronic carriers of the virus.[4] Transmission of hepatitis B virus results from exposure to infectious blood or body fluids such as semen and vaginal fluids, while viral DNA has been detected in the saliva, tears, and urine of chronic carriers with high titer DNA in serum. Perinatal infection is a major route of infection in endemic (mainly developing) countries.[5] Other risk factors for developing HBV infection include working in a health care setting, transfusions, and dialysis, acupuncture, tattooing, extended overseas travel and residence in an institution. [6] [3][7] However, Hepatitis B viruses cannot be spread by casual contact, such as holding hands, sharing eating utensils or drinking glasses, breast-feeding, kissing, hugging, coughing, or sneezing.[8]

The acute illness causes liver inflammation, vomiting, jaundice and rarely, death. Chronic hepatitis B may eventually cause liver cirrhosis and liver cancer—a fatal disease with very poor response to current chemotherapy.[9] The infection is preventable by vaccination.[10]

Hepatitis B virus is an hepadnavirushepa from hepatotrophic and dna because it is a DNA virus[11]—and it has a circular genome composed of partially double-stranded DNA. The viruses replicate through an RNA intermediate form by reverse transcription, and in this respect they are similar to retroviruses.[12] Although replication takes place in the liver, the virus spreads to the blood where virus-specific proteins and their corresponding antibodies are found in infected people. Blood tests for these proteins and antibodies are used to diagnose the infection.

The inaugural International Hepatitis C Awareness day, coordinated by various European and Middle Eastern Patient Groups, took place October 1 2004[4], however many patient groups continued to mark 'hepatitis day' on disparate dates[5].

In 2007 the World Hepatitis Alliance was formed to unite worldwide hepatitis B and hepatitis C patient groups and bring more public and political[4] attention to the issue of viral hepatitis.[6]

With input of its members (organisations from around the world working in the field of hepatitis), the newly titled World Hepatitis Day was switched to May 19, and launched with the campaign slogan 'Am I Number 12?' in 2008. ‘Am I Number 12?’ referred to the worldwide statistic that 1 in 12 people are living with viral hepatitis B or hepatitis C[6], and the slogan was translated into 40 different languages for use by patient organisations worldwide, and also displayed in banner form on several public landmarks.[7]

'Am I number 12' was maintained as the theme for the 2009 World Hepatitis Day, with many alliance members also creating a hepatitis themed '12 asks of government'[8].

In 2010 the third annual World Hepatitis Day was held, with a new theme of 'This is hepatitis' given prominence. This is hepatitis gave a renewed focus to the human stories behind viral hepatitis.[9]. 'This is Hepatitis' will be retained as the theme for 2011.[10]

Following the adoption of a viral hepatitis resolution during the 63rd World Health Assembly in May 2010, World Hepatitis Day was given global endorsement as the primary focus for national and international awareness-raising efforts and the date was changed to July 28 (in honour of Nobel Laureate Prof. Blumberg, discoverer of the hepatitis B virus, who celebrates his birthday on that date).[11] The resolution resolves that:

"1. 28 July shall be designated as World Hepatitis Day in order to provide an opportunity for education and greater understanding of viral hepatitis as a global public health problem, and to stimulate the strengthening of preventive and control measures of this disease in Member States;"[12]

The Theme

World Hepatitis Day dates, names, and themes 2004–present

Date

Name

Theme

1 October 2004

International Hepatitis C Awareness Day[13]

"You have company"

1 October 2005

World Hepatitis C Awareness Day[14]

"Hepatitis C - A Priority Today"

1 October 2006

World Hepatitis Awareness Day[15]

"Get tested"

1 October 2007

World Hepatitis Awareness Day[16]

"Get tested"

19 May 2008

World Hepatitis Day[17]

"Am I number 12?"

19 May 2009

World Hepatitis Day[18]

"Am I number 12?"

19 May 2010

World Hepatitis Day[18]

"This is hepatitis"

28 July 2011

World Hepatitis Day[19]

"This is hepatitis"

Prevalence

Of the 350 million to 400 million individuals worldwide infected with the hepatitis B virus (HBV), one-third reside in China, with 130 million carriers and 30 million chronically infected.[2][3] Since the Expanded Program on Immunization (EPI) beginning 1992, the prevalence of HBV has declined, especially among children 3 to 12 years old.[4][5] During a 5-year period, 10.0% of patients with chronic hepatitis developed cirrhosis, and 20.3% of the cases with compensated cirrhosis progressed to decompensated cirrhosis. 6.5% of the people with cirrhosis and chronic hepatitis progressed to hepatocellular carcinoma (HCC). 5-year survival for compensated cirrhosis is 55%, that for decompensated cirrhosis is 14%, and that for HCC is less than 5%.[6] Every year, 300,000 people die from HBV-related diseases in China, including 180,000 patients with HCC.[7] However, the incidence of hepatitis B is still increasing, from 21.9 in 100,000 people in 1990 to 53.3 in 100,000 in 2003.[8] That increase has occurred despite a vaccination program for newborn babies since the 1990s, which showed good effectiveness for reducing chronic HBV infection in children.[9]

Transmission

The reason for this increased HBV infection is unknown, because hepatitis B has no clear transmission routes in many people in China, although both neonatal infection and horizontal transmission during early childhood are still the most common routes. During and before the Cultural revolution many of the cases came from unsafe needles that carried the virus. This was due to the fact that medicine in that time was rather poor in quality and was reduced to one room hospitals.

Public awareness

Public awareness of the disease, which is spread through the exchange of bodily fluids, is not as high as it is for HIV and AIDS. In some rural areas, doctors have reused syringes and unknowingly spread the disease, particularly among children.

Vaccination

By 2006, China has successfully immunised 11.1 million children living in the country's poorest provinces against hepatitis B according to the Chinese health ministry, and the Global Alliance for Vaccines and Immunization (GAVI). However, China still has a long way to go before immunisation levels reach a percentage able to limit the spread of hepatitis B. China's health minister, Gao Qiang told a Beijing press conference that the project, while effective, has covered only one third of all children born in China since the project began in 2002. This does not mean the rest of China's children went unvaccinated. However, even within the project's target area, over one million newborns went unvaccinated each year because of access issues; health-care costs, lack of birth attendants, and the remoteness of their birthplaces, such as herder's huts, mountain villages, and remote farms.

Until 2005, when a law banning the practice was passed, parents were charged fees for the administration of the vaccine. Even though the GAVI alliance (whose partners include UNICEF and the WHO), and Chinese government were providing the vaccine and one-use needles free of charge, health-care workers charged fees that parents were unwilling or unable to pay. China is in urgent need of a comprehensive hepatitis B vaccination program. Surveillance is still poor infection rates are estimates based on a 1992 epidemiological survey. Those estimates put the disease burden at 120 million people chronically infected with hepatitis B, one third of the burden (360 million) estimated by the WHO.

China's national target is to reach greater than 85% vaccination. The joint project with the GAVI alliance has shown that this is feasible with three quarters of the 1301 project counties reporting that 85% or more children received three doses of HepB vaccine. In hospitals designated project hospitals, the percentage of newborns vaccinated within 24 hours of birth in project hospitals is now over 90%. However, the overall newborn vaccination rate in the region covered by the GAVI alliance/government joint project was 70%, lower than the 75% they hoped to achieve.

Achieving long-term success will require "assuring no new financial barriers arise", said Julian Lob-Levyt, Executive Secretary of the GAVI Alliance. "This is one of the greatest challenges and the solution lies not just within China but with a global community mobilized to ensure access to vaccine financing for all developing nations."

Home to a large population of ethnic minorities of low socioeconomic status, the Qinghai province is a remote, often neglected, rural region of China with a high prevalence of chronic hepatitis B. Since many children 5 years of age and older in Qinghai were not vaccinated against the hepatitis B virus at birth, a private-public partnership was formed between the Ping and Amy Chao Foundation, the ZeShan Foundation, the Asian Liver Center at Stanford University, the China Center for Disease Control and Prevention, the Chinese Foundation for Hepatitis Prevention and Control, and the Qinghai government. Using the existing provincial China CDC structure, this private-public partnership in Qinghai resulted in a unique two-part school-based immunization program to educate and provide free Hep B vaccination for all children in kindergarten and grade school within the region.[10]

Between 2006 and 2008, this program demonstrated the feasibility and successful implementation of:

  1. A province-wide catch-up vaccination program that reached 600,000 children in 2,200 schools, and
  2. A hepatitis B education program incorporated into the school curriculum.

Impact: The success of this large scale province-wide demonstration program led the Chinese government to announce the adoption of a new policy beginning in 2009 to provide free catch-up hepatitis B vaccination for all children in China under the age of 15 who have not been vaccinated.

Treatment

Because a high load of HBV in patients is the main cause of hepatitis progression, the ultimate goal in treatment is to eradicate the virus before irreversible liver damage occurs.[11]

Unfortunately, there are no agents available with high enough efficacy and safety to fully eradicate HBV. Neither interferon alpha, including standard and pegylated forms, nor nucleotide analogues (including lamivudine, adefovir dipivoxil, and most recently, entecavir) could eradicate HBV covalently-closed-circular DNA in liver cells, which is the replication model for HBV recurrence. However, no agents are available to break through the host's immune tolerance to HBV, which is another important reason for persistent infection with HBV,[12] although some patients respond well temporarily to administration of interferon and nucleotide analogues alone or in combination regimens.[13] Some traditional Chinese herbs, such as kushenin (Sophora flavescens) and some complex prescriptions, have some efficacy as antivirals and in the protection of liver function, although the specific mechanism and components need to be identified. The current treatment in China is the combination of antiviral agents (lamivudine, adefovir dipivoxil), immune modulators (interferon alpha, peginterferon alpha, thymosin), and hepatic protectors (such as glycyrrhizin, essentiale, glucurolactone). The Chinese spend around Ɲ900 billion (US$110 billion) on these regimens every year.[14] Apart from cost, patients and carriers of HBV infection are often confronted with tough conditions and social pressures, although such discrimination is illegal in China.

Chinese drug regulation authorities have approved Swiss pharmaceutical firm Novartis AG's drug Sebivo, a brand name for telbivudine, as a treatment for chronic hepatitis B in February 2007. The decision comes shortly after Sebivo was recommended for approval in the European Union. The medicine was developed jointly by Novartis and U.S. biotech firm Idenix Pharmaceuticals Inc and has been shown in trials to produce significantly greater viral suppression compared to the commonly used treatment lamivudine. Sebivo won its first major approval in Switzerland in September 2006

Measles, also known as rubeola or morbilli, is an infection of the respiratory system caused by a virus, specifically a paramyxovirus of the genus Morbillivirus. Morbilliviruses, like other paramyxoviruses, are enveloped, single-stranded, negative-sense RNA viruses. Symptoms include fever, cough, runny nose, red eyes and a generalized, maculopapular, erythematous rash.

Measles (also sometimes known as English Measles) is spread through respiration (contact with fluids from an infected person's nose and mouth, either directly or through aerosol transmission), and is highly contagious—90% of people without immunity sharing living space with an infected person will catch it. The infection has an average incubation period of 14 days (range six to 19 days) and infectivity lasts from two to four days prior, until two to five days following the onset of the rash (i.e. four to 9 days infectivity in total).[1]

An alternative name for measles in English-speaking countries is rubeola, which is sometimes confused with rubella (German measles); the diseases are unrelated.[2][3] Signs and symptoms


A person infected with measles. This patient presented on the third pre-eruptive day with “Koplik spots” indicative of the beginning onset of measles.

The classical symptoms of measles include four-day fevers and the three Cs—cough, coryza (runny nose) and conjunctivitis (red eyes). The fever may reach up to 40 °C (104 °F). Koplik's spots seen inside the mouth are pathognomonic (diagnostic) for measles, but are not often seen, even in real cases of measles, because they are transient and may disappear within a day of arising.

The characteristic measles rash is classically described as a generalized, maculopapular, erythematous rash that begins several days after the fever starts. It starts on the head before spreading to cover most of the body, often causing itching. The rash is said to "stain", changing color from red to dark brown, before disappearing.[citation needed] The measles rash appears two to four days after initial symptoms, and lasts for up to eight days.[4]

Complications

Complications with measles are relatively common, ranging from relatively mild and less serious diarrhea, to pneumonia, Otitis media and acute encephalitis (and rarely subacute sclerosing panencephalitis); corneal ulceration leading to corneal scarring. Complications are usually more severe in adults who catch the virus.

Between 1987 and 2000, the case fatality rate across the United States was three measles-attributable deaths per 1000 cases, or 0.3% (177 deaths / 67,032 cases).[5] In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%.[5] In immunocompromised patients (e.g. people with AIDS) the fatality rate is approximately 30%.[6]

Patients with the measles should be placed on respiratory precautions.[further explanation needed][7] It is believed that patients should always be isolated from populations until recovery is confirmed, such as several days after disappearance of rash and symptoms of complications.

Humans are the only known natural host of measles, although the virus can infect some other primate species.

Diagnosis

Clinical diagnosis of measles requires a history of fever of at least three days, with at least one of the three C's (cough, coryza, conjunctivitis). Observation of Koplik's spots is also diagnostic of measles.

Alternatively, laboratory diagnosis of measles can be done with confirmation of positive measles IgM antibodies or isolation of measles virus RNA from respiratory specimens. In patients where phlebotomy not possible, saliva can be collected for salivary measles-specific IgA testing. Positive contact with other patients known to have measles adds strong epidemiological evidence to the diagnosis. The contact with any infected person in any way, including semen through sex, saliva, or mucus, can cause infection.

Prevention

Rates of measles vaccination worldwide Measles cases reported in the United States before and after introduction of the vaccine

Measles cases reported in England and Wales before and after the introduction of the vaccine, coverage was not widespread enough for herd immunity to interrupt episodic outbreaks until after the MMR vaccine was introduced in 1988.

In developed countries, most children are immunized against measles by the age of 18 months, generally as part of a three-part MMR vaccine (measles, mumps, and rubella). The vaccination is generally not given earlier than this because children younger than 18 months usually retain antimeasles immunoglobulins (antibodies) transmitted from the mother during pregnancy. A second dose is usually given to children between the ages of four and five, to increase rates of immunity. Vaccination rates have been high enough to make measles relatively uncommon. Even a single case in a college dormitory or similar setting is often met with a local vaccination program, in case any of the people exposed are not already immune.

In developing countries where measles is highly endemic, WHO doctors recommend two doses of vaccine be given at six and nine months of age. The vaccine should be given whether the child is HIV-infected or not.[8] The vaccine is less effective in HIV-infected infants, but the risk of adverse reactions is low. Measles vaccination programs are often used to deliver other child health interventions, as well, such as bed nets to protect against malaria, antiparasite medicine and vitamin A supplements, and so contribute to the reduction of child deaths from other causes.[9]

Unvaccinated populations are at risk for the disease. Traditionally low vaccination rates in northern Nigeria dropped further in the early 2000s when radical preachers promoted a rumor that polio vaccines were a Western plot to sterilize Muslims and infect them with HIV. The number of cases of measles rose significantly, and hundreds of children died.[10]

Claims of a connection between the MMR vaccine and autism were raised in a 1998 paper in The Lancet, a respected British medical journal.[11] Later investigation by Sunday Times journalist Brian Deer discovered the lead author of the article, Andrew Wakefield, had multiple undeclared conflicts of interest,[12] and had broken other ethical codes. The Lancet paper was later retracted, and Wakefield was found guilty by the General Medical Council of serious professional misconduct in May 2010, and was struck off the Medical Register, meaning he could no longer practise as a doctor in the UK.[13] The research was declared fraudulent in 2011 by the BMJ.[14] Scientific evidence provides no support for the hypothesis that MMR plays a role in causing autism.[15]

In January 2010, a study of Polish children found vaccination with the measles, mumps, and rubella vaccine was not a risk factor for development of autistic disorder; in fact, the vaccinated patients had a slightly reduced risk of autistic disorder, although the mechanism of action is unknown, and the result may have been coincidental.[16] The autism-related MMR study in Britain caused use of the vaccine to plunge, and measles cases came back: 2007 saw 971 cases in England and Wales, the biggest rise in occurrence in measles cases since records began in 1995.[17] A 2005 measles outbreak in Indiana was attributed to children whose parents refused vaccination.[18]

Treatment

There is no specific treatment for measles. Most patients with uncomplicated measles will recover with rest and supportive treatment. It is, however, important to seek medical advice if the patient becomes more unwell, as they may be developing complications.

Some patients will develop pneumonia as a sequel to the measles. Other complications include ear infections, bronchitis, and encephalitis. Acute measles encephalitis has a mortality rate of 15%. While there is no specific treatment for measles encephalitis, antibiotics are required for bacterial pneumonia, sinusitis, and bronchitis that can follow measles.

All other treatment addresses symptoms, with ibuprofen, or acetaminophen (paracetamol) to reduce fever and pain and, if required, a fast-acting bronchodilator for cough. As for aspirin, some research has suggested a correlation between children who take aspirin and the development of Reye's syndrome.[19] Some research has shown aspirin may not be the only medication associated with Reye's, and even antiemetics have been implicated,[20] with the point being the link between aspirin use in children and Reye's syndrome development is weak at best, if not actually nonexistent.[19][21] Nevertheless, most health authorities still caution against the use of aspirin for any fevers in children under 16[22][23][24][25]

The use of vitamin A in treatment has been investigated. A systematic review of trials into its use found no significant reduction in overall mortality, but it did reduce mortality in children aged under two years.[26][27][28]

Prognosis

While the vast majority of patients survive measles, complications occur fairly frequently, and may include bronchitis, and panencephalitis which is potentially fatal. Also, even if the patient is not concerned about death or sequela from the measles, the person may spread the disease to an immunocompromised patient, for whom the risk of death is much higher, due to complications such as giant cell pneumonia. Acute measles encephalitis is another serious risk of measles virus infection. It typically occurs two days to one week after the breakout of the measles exanthem, and begins with very high fever, severe headache, convulsions, and altered mentation. Patient may become comatose, and death or brain injury may occur.[29]

Poliomyelitis, often called polio or infantile paralysis, is an acute viral infectious disease spread from person to person, primarily via the fecal-oral route.[1] The term derives from the Greek poliós (πολιός), meaning "grey", myelós (µυελός), referring to the "spinal cord", and the suffix -itis, which denotes inflammation.[2]

Although around 90% of polio infections cause no symptoms at all, affected individuals can exhibit a range of symptoms if the virus enters the blood stream.[3] In about 1% of cases the virus enters the central nervous system, preferentially infecting and destroying motor neurons, leading to muscle weakness and acute flaccid paralysis. Different types of paralysis may occur, depending on the nerves involved. Spinal polio is the most common form, characterized by asymmetric paralysis that most often involves the legs. Bulbar polio leads to weakness of muscles innervated by cranial nerves. Bulbospinal polio is a combination of bulbar and spinal paralysis.[4]

Poliomyelitis was first recognized as a distinct condition by Jakob Heine in 1840.[5] Its causative agent, poliovirus, was identified in 1908 by Karl Landsteiner.[5] Although major polio epidemics were unknown before the late 19th century, polio was one of the most dreaded childhood diseases of the 20th century. Polio epidemics have crippled thousands of people, mostly young children; the disease has caused paralysis and death for much of human history. Polio had existed for thousands of years quietly as an endemic pathogen until the 1880s, when major epidemics began to occur in Europe; soon after, widespread epidemics appeared in the United States.[6]

By 1910, much of the world experienced a dramatic increase in polio cases and frequent epidemics became regular events, primarily in cities during the summer months. These epidemics—which left thousands of children and adults paralyzed—provided the impetus for a "Great Race" towards the development of a vaccine. Developed in the 1950s, polio vaccines are credited with reducing the global number of polio cases per year from many hundreds of thousands to around a thousand.[7] Enhanced vaccination efforts led by the World Health Organization, UNICEF, and Rotary International could result in global eradication of the disease.[8][9]

Classification

Outcomes of poliovirus infection

Outcome

Proportion of cases[4]

Asymptomatic

90–95%

Minor illness

4–8%

Non-paralytic aseptic
meningitis

1–2%

Paralytic poliomyelitis

0.1–0.5%

— Spinal polio

79% of paralytic cases

— Bulbospinal polio

19% of paralytic cases

— Bulbar polio

2% of paralytic cases

The term poliomyelitis is used to identify the disease caused by any of the three serotypes of poliovirus. Two basic patterns of polio infection are described: a minor illness which does not involve the central nervous system (CNS), sometimes called abortive poliomyelitis, and a major illness involving the CNS, which may be paralytic or non-paralytic.[10] In most people with a normal immune system, a poliovirus infection is asymptomatic. Rarely the infection produces minor symptoms; these may include upper respiratory tract infection (sore throat and fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and influenza-like illness.[4]

The virus enters the central nervous system in about 3% of infections. Most patients with CNS involvement develop non-paralytic aseptic meningitis, with symptoms of headache, neck, back, abdominal and extremity pain, fever, vomiting, lethargy and irritability.[2][11] Approximately 1 in 1000 to 1 in 200 cases progress to paralytic disease, in which the muscles become weak, floppy and poorly controlled, and finally completely paralyzed; this condition is known as acute flaccid paralysis.[12] Depending on the site of paralysis, paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal. Encephalitis, an infection of the brain tissue itself, can occur in rare cases and is usually restricted to infants. It is characterized by confusion, changes in mental status, headaches, fever, and less commonly seizures and spastic paralysis.[13]

Cause: Poliovirus-----A TEM micrograph of poliovirus

Poliomyelitis is caused by infection with a member of the genus Enterovirus known as poliovirus (PV). This group of RNA viruses colonize the gastrointestinal tract[1] — specifically the oropharynx and the intestine. The incubation time (to the first signs and symptoms) ranges from 3 to 35 days with a more common span of 6 to 20 days.[4] PV infects and causes disease in humans alone.[3] Its structure is very simple, composed of a single (+) sense RNA genome enclosed in a protein shell called a capsid.[3] In addition to protecting the virus’s genetic material, the capsid proteins enable poliovirus to infect certain types of cells. Three serotypes of poliovirus have been identified—poliovirus type 1 (PV1), type 2 (PV2), and type 3 (PV3)—each with a slightly different capsid protein.[14] All three are extremely virulent and produce the same disease symptoms.[3] PV1 is the most commonly encountered form, and the one most closely associated with paralysis.[15]

Individuals who are exposed to the virus, either through infection or by immunization with polio vaccine, develop immunity. In immune individuals, IgA antibodies against poliovirus are present in the tonsils and gastrointestinal tract and are able to block virus replication; IgG and IgM antibodies against PV can prevent the spread of the virus to motor neurons of the central nervous system.[16] Infection or vaccination with one serotype of poliovirus does not provide immunity against the other serotypes, and full immunity requires exposure to each serotype.[16]

A rare condition with a similar presentation, non-poliovirus poliomyelitis, may result from infections with non-poliovirus enteroviruses.[17]

Transmission

Poliomyelitis is highly contagious via the oral-oral (oropharyngeal source) and fecal-oral (intestinal source) routes.[16] In endemic areas, wild polioviruses can infect virtually the entire human population.[18] It is seasonal in temperate climates, with peak transmission occurring in summer and autumn.[16] These seasonal differences are far less pronounced in tropical areas.[18] The time between first exposure and first symptoms, known as the incubation period, is usually 6 to 20 days, with a maximum range of 3 to 35 days.[19] Virus particles are excreted in the feces for several weeks following initial infection.[19] The disease is transmitted primarily via the fecal-oral route, by ingesting contaminated food or water. It is occasionally transmitted via the oral-oral route,[15] a mode especially visible in areas with good sanitation and hygiene.[16] Polio is most infectious between 7–10 days before and 7–10 days after the appearance of symptoms, but transmission is possible as long as the virus remains in the saliva or feces.[15]

Factors that increase the risk of polio infection or affect the severity of the disease include immune deficiency,[20] malnutrition,[21] tonsillectomy,[22] physical activity immediately following the onset of paralysis,[23] skeletal muscle injury due to injection of vaccines or therapeutic agents,[24] and pregnancy.[25] Although the virus can cross the placenta during pregnancy, the fetus does not appear to be affected by either maternal infection or polio vaccination.[26] Maternal antibodies also cross the placenta, providing passive immunity that protects the infant from polio infection during the first few months of life.[27]

As a precaution against infection, public swimming pools were often closed in affected areas during poliomyelitis epidemics.

Pathophysiology-----A blockage of the lumbar anterior spinal cord artery due to polio (PV3)

Poliovirus enters the body through the mouth, infecting the first cells it comes in contact with—the pharynx (throat) and intestinal mucosa. It gains entry by binding to an immunoglobulin-like receptor, known as the poliovirus receptor or CD155, on the cell membrane.[28] The virus then hijacks the host cell's own machinery, and begins to replicate. Poliovirus divides within gastrointestinal cells for about a week, from where it spreads to the tonsils (specifically the follicular dendritic cells residing within the tonsilar germinal centers), the intestinal lymphoid tissue including the M cells of Peyer's patches, and the deep cervical and mesenteric lymph nodes, where it multiplies abundantly. The virus is subsequently absorbed into the bloodstream.[29]

Known as viremia, the presence of virus in the bloodstream enables it to be widely distributed throughout the body. Poliovirus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks.[30] In a small percentage of cases, it can spread and replicate in other sites such as brown fat, the reticuloendothelial tissues, and muscle.[31] This sustained replication causes a major viremia, and leads to the development of minor influenza-like symptoms. Rarely, this may progress and the virus may invade the central nervous system, provoking a local inflammatory response. In most cases this causes a self-limiting inflammation of the meninges, the layers of tissue surrounding the brain, which is known as non-paralytic aseptic meningitis.[2] Penetration of the CNS provides no known benefit to the virus, and is quite possibly an incidental deviation of a normal gastrointestinal infection.[32] The mechanisms by which poliovirus spreads to the CNS are poorly understood, but it appears to be primarily a chance event—largely independent of the age, gender, or socioeconomic position of the individual.[32]

Paralytic polio------Denervation of skeletal muscle tissue secondary to poliovirus infection can lead to paralysis.

In around 1% of infections, poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex. This leads to the development of paralytic poliomyelitis, the various forms of which (spinal, bulbar, and bulbospinal) vary only with the amount of neuronal damage and inflammation that occurs, and the region of the CNS that is affected.

The destruction of neuronal cells produces lesions within the spinal ganglia; these may also occur in the reticular formation, vestibular nuclei, cerebellar vermis, and deep cerebellar nuclei.[32] Inflammation associated with nerve cell destruction often alters the color and appearance of the gray matter in the spinal column, causing it to appear reddish and swollen.[2] Other destructive changes associated with paralytic disease occur in the forebrain region, specifically the hypothalamus and thalamus.[32] The molecular mechanisms by which poliovirus causes paralytic disease are poorly understood.

Early symptoms of paralytic polio include high fever, headache, stiffness in the back and neck, asymmetrical weakness of various muscles, sensitivity to touch, difficulty swallowing, muscle pain, loss of superficial and deep reflexes, paresthesia (pins and needles), irritability, constipation, or difficulty urinating. Paralysis generally develops one to ten days after early symptoms begin, progresses for two to three days, and is usually complete by the time the fever breaks.[33]

The likelihood of developing paralytic polio increases with age, as does the extent of paralysis. In children, non-paralytic meningitis is the most likely consequence of CNS involvement, and paralysis occurs in only 1 in 1000 cases. In adults, paralysis occurs in 1 in 75 cases.[34] In children under five years of age, paralysis of one leg is most common; in adults, extensive paralysis of the chest and abdomen also affecting all four limbs—quadriplegia—is more likely.[35] Paralysis rates also vary depending on the serotype of the infecting poliovirus; the highest rates of paralysis (1 in 200) are associated with poliovirus type 1, the lowest rates (1 in 2,000) are associated with type 2.[36]

Spinal polio------The location of motor neurons in the anterior horn cells of the spinal column.

Spinal polio is the most common form of paralytic poliomyelitis; it results from viral invasion of the motor neurons of the anterior horn cells, or the ventral (front) gray matter section in the spinal column, which are responsible for movement of the muscles, including those of the trunk, limbs and the intercostal muscles.[12] Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia. When spinal neurons die, Wallerian degeneration takes place, leading to weakness of those muscles formerly innervated by the now dead neurons.[37] With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed.[12] Progression to maximum paralysis is rapid (two to four days), and is usually associated with fever and muscle pain.[37] Deep tendon reflexes are also affected, and are usually absent or diminished; sensation (the ability to feel) in the paralyzed limbs, however, is not affected.[37]

The extent of spinal paralysis depends on the region of the cord affected, which may be cervical, thoracic, or lumbar.[38] The virus may affect muscles on both sides of the body, but more often the paralysis is asymmetrical.[29] Any limb or combination of limbs may be affected—one leg, one arm, or both legs and both arms. Paralysis is often more severe proximally (where the limb joins the body) than distally (the fingertips and toes).[29]

Bulbar polio------The location and anatomy of the bulbar region (in orange)

Making up about 2% of cases of paralytic polio, bulbar polio occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem.[4] The bulbar region is a white matter pathway that connects the cerebral cortex to the brain stem. The destruction of these nerves weakens the muscles supplied by the cranial nerves, producing symptoms of encephalitis, and causes difficulty breathing, speaking and swallowing.[11] Critical nerves affected are the glossopharyngeal nerve, which partially controls swallowing and functions in the throat, tongue movement and taste; the vagus nerve, which sends signals to the heart, intestines, and lungs; and the accessory nerve, which controls upper neck movement. Due to the effect on swallowing, secretions of mucus may build up in the airway causing suffocation.[33] Other signs and symptoms include facial weakness, caused by destruction of the trigeminal nerve and facial nerve, which innervate the cheeks, tear ducts, gums, and muscles of the face, among other structures; double vision; difficulty in chewing; and abnormal respiratory rate, depth, and rhythm, which may lead to respiratory arrest. Pulmonary edema and shock are also possible, and may be fatal.[38]

Bulbospinal polio

Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms; this subtype is called respiratory polio or bulbospinal polio.[4] Here, the virus affects the upper part of the cervical spinal cord (C3 through C5), and paralysis of the diaphragm occurs. The critical nerves affected are the phrenic nerve, which drives the diaphragm to inflate the lungs, and those that drive the muscles needed for swallowing. By destroying these nerves this form of polio affects breathing, making it difficult or impossible for the patient to breathe without the support of a ventilator. It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions.[39]

Diagnosis

Paralytic poliomyelitis may be clinically suspected in individuals experiencing acute onset of flaccid paralysis in one or more limbs with decreased or absent tendon reflexes in the affected limbs that cannot be attributed to another apparent cause, and without sensory or cognitive loss.[40]

A laboratory diagnosis is usually made based on recovery of poliovirus from a stool sample or a swab of the pharynx. Antibodies to poliovirus can be diagnostic, and are generally detected in the blood of infected patients early in the course of infection.[4] Analysis of the patient's cerebrospinal fluid (CSF), which is collected by a lumbar puncture ("spinal tap"), reveals an increased number of white blood cells (primarily lymphocytes) and a mildly elevated protein level. Detection of virus in the CSF is diagnostic of paralytic polio, but rarely occurs.[4]

If poliovirus is isolated from a patient experiencing acute flaccid paralysis, it is further tested through oligonucleotide mapping (genetic fingerprinting), or more recently by PCR amplification, to determine whether it is "wild type" (that is, the virus encountered in nature) or "vaccine type" (derived from a strain of poliovirus used to produce polio vaccine).[41] It is important to determine the source of the virus because for each reported case of paralytic polio caused by wild poliovirus, it is estimated that another 200 to 3,000 contagious asymptomatic carriers exist.[42]

Prevention:Passive immunization

In 1950, William Hammon at the University of Pittsburgh purified the gamma globulin component of the blood plasma of polio survivors.[43] Hammon proposed that the gamma globulin, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. The results of a large clinical trial were promising; the gamma globulin was shown to be about 80% effective in preventing the development of paralytic poliomyelitis.[44] It was also shown to reduce the severity of the disease in patients that developed polio.[43] The gamma globulin approach was later deemed impractical for widespread use, however, due in large part to the limited supply of blood plasma, and the medical community turned its focus to the development of a polio vaccine.[45]

Vaccine: Polio vaccine-----A child receives oral polio vaccine.

Two types of vaccine are used throughout the world to combat polio. Both types induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus, thereby protecting both individual vaccine recipients and the wider community (so-called herd immunity).[46]

The first candidate polio vaccine, based on one serotype of a live but attenuated (weakened) virus, was developed by the virologist Hilary Koprowski. Koprowski's prototype vaccine was given to an eight-year-old boy on February 27, 1950.[47] Koprowski continued to work on the vaccine throughout the 1950s, leading to large-scale trials in the then Belgian Congo and the vaccination of seven million children in Poland against serotypes PV1 and PV3 between 1958 and 1960.[48]

The second inactivated virus vaccine was developed in 1952 by Jonas Salk at the University of Pittsburgh, and announced to the world on April 12, 1955.[49] The Salk vaccine, or inactivated poliovirus vaccine (IPV), is based on poliovirus grown in a type of monkey kidney tissue culture (Vero cell line), which is chemically inactivated with formalin.[16] After two doses of IPV (given by injection), 90% or more of individuals develop protective antibody to all three serotypes of poliovirus, and at least 99% are immune to poliovirus following three doses.[4]

Subsequently, Albert Sabin developed another live, oral polio vaccine (OPV). It was produced by the repeated passage of the virus through non-human cells at sub-physiological temperatures.[50] The attenuated poliovirus in the Sabin vaccine replicates very efficiently in the gut, the primary site of wild poliovirus infection and replication, but the vaccine strain is unable to replicate efficiently within nervous system tissue.[51] A single dose of Sabin's oral polio vaccine produces immunity to all three poliovirus serotypes in approximately 50% of recipients. Three doses of live-attenuated OPV produce protective antibody to all three poliovirus types in more than 95% of recipients.[4] Human trials of Sabin's vaccine began in 1957,[52] and in 1958 it was selected, in competition with the live vaccines of Koprowski and other researchers, by the US National Institutes of Health.[48] It was licensed in 1962[52] and rapidly became the only polio vaccine used worldwide.[48]

Because OPV is inexpensive, easy to administer, and produces excellent immunity in the intestine (which helps prevent infection with wild virus in areas where it is endemic), it has been the vaccine of choice for controlling poliomyelitis in many countries.[53] On very rare occasions (about 1 case per 750,000 vaccine recipients) the attenuated virus in OPV reverts into a form that can paralyze.[19] Most industrialized countries have switched to IPV, which cannot revert, either as the sole vaccine against poliomyelitis or in combination with oral polio vaccine.[54]

Treatment-----A modern negative pressure ventilator (iron lung)

There is no cure for polio. The focus of modern treatment has been on providing relief of symptoms, speeding recovery and preventing complications. Supportive measures include antibiotics to prevent infections in weakened muscles, analgesics for pain, moderate exercise and a nutritious diet.[55] Treatment of polio often requires long-term rehabilitation, including physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery.[38]

Portable ventilators may be required to support breathing. Historically, a noninvasive negative-pressure ventilator, more commonly called an iron lung, was used to artificially maintain respiration during an acute polio infection until a person could breathe independently (generally about one to two weeks). Today many polio survivors with permanent respiratory paralysis use modern jacket-type negative-pressure ventilators that are worn over the chest and abdomen.[56]

Other historical treatments for polio include hydrotherapy, electrotherapy, massage and passive motion exercises, and surgical treatments such as tendon lengthening and nerve grafting.[12] Devices such as rigid braces and body casts—which tended to cause muscle atrophy due to the limited movement of the user—were also touted as effective treatments.[57]

Prognosis

Patients with abortive polio infections recover completely. In those that develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery.[58] In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within four to six weeks after onset.[58] Half the patients with spinal polio recover fully; one quarter recover with mild disability and the remaining quarter are left with severe disability.[59] The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of viremia, and inversely proportional to the degree of immunity.[32] Spinal polio is rarely fatal.[33]

A child with a deformity of her right leg due to polio

Without respiratory support, consequences of poliomyelitis with respiratory involvement include suffocation or pneumonia from aspiration of secretions.[56] Overall, 5–10% of patients with paralytic polio die due to the paralysis of muscles used for breathing. The mortality rate varies by age: 2–5% of children and up to 15–30% of adults die.[4] Bulbar polio often causes death if respiratory support is not provided;[39] with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient.[4][60] When positive pressure ventilators are available, the mortality can be reduced to 15%.[61]

Recovery

Many cases of poliomyelitis result in only temporary paralysis.[12] Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months.[58] The neurophysiological processes involved in recovery following acute paralytic poliomyelitis are quite effective; muscles are able to retain normal strength even if half the original motor neurons have been lost.[62] Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.[58]

One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[63] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[64] restoring the fibers' capacity to contract and improving strength.[65] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units:[34] a single motor neuron that once controlled 200 muscle cells might control 800 to 1000 cells. Other mechanisms that occur during the rehabilitation phase, and contribute to muscle strength restoration, include myofiber hypertrophy—enlargement of muscle fibers through exercise and activity—and transformation of type II muscle fibers to type I muscle fibers.[64][66]

In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis. These include the use of weaker muscles at a higher than usual intensity relative to the muscle's maximal capacity, enhancing athletic development of previously little-used muscles, and using ligaments for stability, which enables greater mobility.[66]

Complications

Residual complications of paralytic polio often occur following the initial recovery process.[11] Muscle paresis and paralysis can sometimes result in skeletal deformities, tightening of the joints and movement disability. Once the muscles in the limb become flaccid, they may interfere with the function of other muscles. A typical manifestation of this problem is equinus foot (similar to club foot). This deformity develops when the muscles that pull the toes downward are working, but those that pull it upward are not, and the foot naturally tends to drop toward the ground. If the problem is left untreated, the Achilles tendons at the back of the foot retract and the foot cannot take on a normal position. Polio victims that develop equinus foot cannot walk properly because they cannot put their heel on the ground. A similar situation can develop if the arms become paralyzed.[67] In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps and leans to one side, in turn leading to deformities of the spine (such as scoliosis).[67] Osteoporosis and increased likelihood of bone fractures may occur. Extended use of braces or wheelchairs may cause compression neuropathy, as well as a loss of proper function of the veins in the legs, due to pooling of blood in paralyzed lower limbs.[39][68] Complications from prolonged immobility involving the lungs, kidneys and heart include pulmonary edema, aspiration pneumonia, urinary tract infections, kidney stones, paralytic ileus, myocarditis and cor pulmonale.[39][68]

Post-polio syndrome-------Post-polio syndrome

Around a quarter of individuals who survive paralytic polio in childhood develop additional symptoms decades after recovering from the acute infection, notably muscle weakness, extreme fatigue, or paralysis. This condition is known as post-polio syndrome (PPS) or post-polio sequelae.[69] The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic disease.[70][71] Factors that increase the risk of PPS include the length of time since acute poliovirus infection, the presence of permanent residual impairment after recovery from the acute illness, and both overuse and disuse of neurons.[69] Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.[4]

Eradication-----Disability-adjusted life year for poliomyelitis per 100,000 inhabitants.

no data----≤ 0.35---0.35-0.7--0.7-1.05---1.05-1.4---1.4-1.75---1.75-2.1---2.1-2.45---2.45-2.8

2.8-3.15---3.15-3.5----3.5-3.85-----≥ 3.85


WHO 2002----
Poliomyelitis eradication

While now rare in the Western world, polio is still endemic to South Asia and Nigeria. Following the widespread use of poliovirus vaccine in the mid-1950s, the incidence of poliomyelitis declined dramatically in many industrialized countries. A global effort to eradicate polio began in 1988, led by the World Health Organization, UNICEF, and The Rotary Foundation.[72] These efforts have reduced the number of annual diagnosed cases by 99%; from an estimated 350,000 cases in 1988 to a low of 483 cases in 2001, after which it has remained at a level of about 1,000 cases per year (1,606 in 2009).[73][74][75] Polio is one of only two diseases currently the subject of a global eradication program, the other being Guinea worm disease. If the global Polio Eradication initiative is successful before that for Guinea worm or any other disease, it would be only the third time humankind has ever completely eradicated a disease, after smallpox in 1979[76] and rinderpest in 2010.[77] A number of eradication milestones have already been reached, and several regions of the world have been certified polio-free. The Americas were declared polio-free in 1994.[78] In 2000 polio was officially eliminated in 36 Western Pacific countries, including China and Australia.[79][80] Europe was declared polio-free in 2002.[81] As of 2006, polio remains endemic in only four countries: Nigeria, India (specifically Uttar Pradesh and Bihar), Pakistan, and Afghanistan,[73][82] although it continues to cause epidemics in other nearby countries due to hidden or reestablished transmission.[83]