Poliomyelitis

Poliomyelitis

poliomyelitis, called polio for short (from the Greek πολιός, poliós: 'grey'; and µυελός, myelós: 'of or relating to the spinal cord') or infantile paralysis, is an infectious disease that mainly affects the nervous system. The disease is caused by the poliovirus. It is called infantile because the people who contract the disease are mainly children. It is transmitted from person to person through respiratory secretions or by the fecal-oral route. Most polio infections are asymptomatic. In only 1% of cases, the virus enters the central nervous system (CNS) via the bloodstream. Within the CNS, poliovirus preferentially infects and destroys motor neurons, causing muscle weakness and acute flaccid paralysis.

Polio is more likely to occur in children ages 4 to 15 in temperate climates, with warm summers and slightly cold winters. It is a highly infectious disease, but it is combated with vaccination. the illness afects the central nervous system. In its acute form it causes inflammation in the motor neurons of the spinal cord and brain and leads to paralysis, muscle atrophy and very often deformity. In the worst case it can cause permanent paralysis or death by paralyzing the diaphragm.

October 24 is World Polio Day.

History

Egyptian funerary stole from the period of Amenhotep II1400 a. C.), showing a palace official with poliomyelitis.

Polio was first described by the German Jakob Heine in 1840. During acute polio epidemics in the early 19th century , several categories of polio were defined to classify the extent and severity of the disease. Two basic patterns of polio infection were described: a minor one, which did not affect the central nervous system (CNS), called abortive polio, and major illness, with or without paralysis.

Polio began to be controlled in 1949 when bacteriologist John Franklin Enders managed to grow the virus in tissues in the laboratory. Based on this technique, the epidemiologist Jonas Edward Salk developed a vaccine for the three known types of polio. After the relevant clinical tests that demonstrated that it was safe, inoculation began in 1954. The Salk vaccine, as it is known, is injectable.

In 1964, another vaccine, developed by Albert Sabin, was licensed. It was called trivalent because it attacked the three types of viruses mentioned. Unlike the Salk vaccine, it was administered orally, so Sabin very quickly replaced Salk.

In a very short time there were massive vaccination campaigns and as a consequence of all this, on June 21, 2002, the World Health Organization (WHO) declared the European region free of the polio virus. This region is made up of fifty-one countries and eight hundred and fifty million inhabitants. The last case in this region occurred in Turkey in November 1998. America was the first region in the world to be certified free of wild polio in 1994, having the last case in Peru in 1991.

In 1988, the WHO launched a global eradication program. "When we started the eradication campaign in 1988, polio paralyzed more than a thousand children every day," reported Dr Gro Harlem Brundtland, then WHO director-general, adding: "In 2001, there were far fewer than thousand cases throughout the year. Polio is only active in less than ten countries anymore.

In May 2014, the WHO issued an alert note regarding the spread of polio in endemic and non-endemic areas, specifically Pakistan and Afghanistan in Central Asia, Syria and Iraq in the Middle East, and Cameroon and Equatorial Guinea in central Africa.

On October 24, 2019, the WHO confirmed the worldwide eradication of type 3 polio.

Epidemiology

The World Health Organization declares an area free of a disease when three years go by without any cases.

In 1994, the WHO considered the region of America (36 countries) free of polio, in the year 2000 it did so with the region of the Pacific (37 countries, including China). In June 2002, Europe was declared a polio-free zone, which represents for its 870 million inhabitants “the greatest achievement of the new millennium in terms of health public”^{[citation required]}.

The WHO began its campaign to eradicate polio in 1988. At that time it was still endemic throughout the world, and in fact that year there were 350,000 infected. During 2005, only about 1,880 people worldwide contracted the disease. At the beginning of 2006, and after having been eradicated from Egypt and Niger, the WHO declared that there were only three countries left in the world where the disease was still endemic. These were Nigeria, Pakistan and Afghanistan. The WHO, Unicef, the Centers for Disease Control and Prevention of the United States (CDC) and Rotary International announced that they would redouble their efforts in those countries, with which they estimated that in two more years there would be no new cases of the disease. disease. Then it would take three more years for polio to be officially declared eradicated.

If successful, it would be the third infectious disease to be eliminated from the face of the Earth. The first was smallpox, and the second was rinderpest. However, in 2014, this objective was still not close, since the transmission of the virus and the presence of the disease had been verified in various countries, such as: Pakistan, Afghanistan, Iraq, Syria, Nigeria, Equatorial Guinea, Cameroon and Ethiopia. A total of 68 cases were reported in the first 4 months of 2014, including some in non-endemic countries (in 2013 there were 417 registered cases).

On October 24, 2019, the WHO confirmed the worldwide eradication of type 3 polio.

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  A girl receiving oral poliomyelitis vaccine

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  Administration of oral vaccine in Valencia, 1963

Etiology

Polio is an infection caused by a member of the Enterovirus genus known as poliovirus (PV). This group of RNA viruses prefers the gastrointestinal tract and infects and causes disease only in humans. Its structure is very simple, composed of a single sense (+) RNA genome enclosed in a protein shell called a capsid. In addition to protecting the genetic material of the virus, poliovirus capsid proteins allow exclusive infection of certain types of cells in the host. 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 sequence. All three serotypes are extremely virulent. and produce the same symptoms of the disease. PV1 is the most common form, and the one most closely related to paralysis caused by polio.

People exposed to the virus, either by infection or by immunization with the polio vaccine, develop protective immunity. Immune individuals have IgA antibodies to polio present in the tonsils and gastrointestinal tract and are capable of blocking virus replication, whereas IgG and IgM antibodies to PV can prevent spread of the virus to motor neurons of the nervous system. central. Infection or vaccination with one poliovirus serotype does not provide immunity against the other serotypes, and full immunity requires exposure to each serotype.

Transmission

Polio is highly contagious and spreads easily from person to person. In endemic areas, wild poliovirus is capable of infecting virtually the entire human population. Polio is a seasonal disease in temperate climates, with the peak of transmission occurring in summer and autumn. These seasonal differences are much less pronounced in the tropics. The time between the first exposure and the appearance of the first symptoms, known as the incubation period, is normally between 6 to 20 days, with a maximum separation of 3 to 35 days. The virus particles are excreted in the feces during several weeks after the initial infection. The disease is transmitted mainly through the fecal-oral route, through ingestion of contaminated food or water. It is sometimes transmitted via the oral-oral route, a mode especially visible in areas with good sanitation and hygiene. The virus is most infectious between days 7-10 prior to the onset of symptoms, but transmission is possible as long as the virus remains in saliva or feces.

Factors that increase the risk of polio infection or affect the severity of the disease include immune deficiency, malnutrition, tonsillectomy, physical activity immediately after the onset of paralysis, injury to muscle skeletal disease due to injection of vaccines or therapeutic agents, and pregnancy. Although the virus can cross the placenta during pregnancy, the fetus does not appear to be affected by maternal infection or maternal vaccination against polio. In addition, maternal antibodies cross the placenta, providing passive immunity that protects the infant from polio infection during the first months of life.

Pathogenesis

During active infection, Poliovirus enters the body through the mouth, infecting the first cells it comes into contact with in the pharynx and intestinal mucosa. It gains entry into cells by binding to an immunoglobulin-like receptor, known as the poliovirus receptor or CD155, on the cell's surface. The virus then hijacks the host cell's own machinery, and begins to play. Poliovirus multiplies in gastrointestinal cells for about a week, from where it spreads to the tonsils—specifically the dendritic follicular cells residing in the tonsillar germinal centers—intestinal lymphoid tissue, including Peyer's patch M cells, and the cervical and deep mesenteric nodes, where it multiplies abundantly. The virus is subsequently absorbed into the bloodstream.

The presence of the virus in the bloodstream—known as primary viremia—allows it to be widely distributed throughout the body. Poliovirus can survive and multiply within the bloodstream and lymphatics for long periods, sometimes up to 17 weeks. In a small percentage of cases, it can spread and reproduce in other sites, such as brown fat, reticuloendothelial, and muscle tissues.. This sustained replication is one of the main causes of an increase in viraemia, and leads to the appearance of catarrhal symptoms. Rarely, the infection manages to progress in such a way that the virus invades the central nervous system, causing a localized inflammatory response. In most of these cases, what is caused is a self-limited inflammation of the meninges, the layers of tissue that surround the brain, which is known as non-paralytic aseptic meningitis. CNS penetration offers no benefit to the virus, and is likely no more than an accidental deviation from normal gastrointestinal infection. The mechanisms by which polio spreads to the CNS are poorly understood, but appear to be all an opportunistic event, largely independent of the age or sex of the person.

Post-polio syndrome (PPS) is a condition that strikes survivors of polio. Approximately 20-40% of people who recover from polio may develop PPS. The onset of PPS can occur anytime from 10 to 40 years after the onset of infection and can slowly progress over ten years, producing symptoms such as extreme fatigue, muscle pain, and muscle atrophy in new muscle fibers as well as those previously affected.

Classification

The term poliomyelitis refers to the disease caused by any of the three serotypes of poliovirus. Two patterns of polio infection are commonly described: a mild disease that is not associated with the central nervous system (CNS), sometimes called abortive poliomyelitis, and a form that is associated with severe CNS disease, which can be or non-paralytic. In most people with a normal immune system, a poliovirus infection turns out to be asymptomatic. Occasionally the infection produces minor symptoms, which may include upper respiratory tract infection (sore throat and fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain, constipation, or, rarely, diarrhea), catarrh, and similar illnesses.

The virus enters the central nervous system in about 3% of infections. Most patients with nonparalytic CNS touch develop aseptic meningitis, with symptoms of headache, neck, back, abdominal and extremity pain, fever, vomiting, lethargy, and irritability. Approximately 1 in 200 to 1 in Within 1,000 cases, the disease progresses to the paralytic form, in which the muscles become weak, hypotonic and with poorly controlled movements, and finally completely paralyzed, a condition known as acute flaccid paralysis. Depending on the site of the paralysis, paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal. Encephalitis, an infection of the brain tissue itself, can occur rarely and is usually limited to children. It is characterized by confusion, mental status changes, headaches, fever, seizures, and less frequently spastic paralysis.

Clinical picture

In more than 95% of cases, the infection is asymptomatic, so that the disease has an inapparent course in them but is capable of stimulating an antibody-forming immune response. Other much less common forms include a severe respiratory variety, bulbar paralytic poliomyelitis, polioencephalitis, and monophasic forms. Much more frequently catarrhal, pre-paralytic and paralytic forms are recorded.

Abortive Polio

Followed by an incubation period of 7-14 days, there is approximately three days of illness characterized by fever, sore throat, fatigue, and often diarrhea and vomiting. For more than three quarters of these patients, the consequence is improvement, which is where the word abortive comes from: the end of the course of the infection. Central nervous system (CNS) cells are not affected.

Pre-paralytic poliomyelitis

Approximately 5% of symptomatic patients may have central nervous system involvement, in which the previous symptoms, the prodrome, install the current disease. After this febrile phase and seizures of approximately one week, these patients develop aseptic meningitis that appears as a biphasic complex. The first characterized by a recurring fever of about 39 °C (degrees Celsius) and headache and stiff neck. The cerebrospinal fluid may have a slight increase in cell number and a slight increase in protein concentration. The second phase usually presents with meningeal irritation and involvement of the autonomic nervous system.

Paralytic Polio

Spinal cord, illustration of the motor fibers of the previous asta, which is most affected in paralytic poliomyelitis.

Usually starts with a fever, which occurs 5 to 7 days before other symptoms. Then appear extreme fatigue, muscle pain and muscle atrophy that causes flaccid, proximal and asymmetric paralysis and can even affect breathing and swallowing. It is a very rare course, occurring in 0.01% of symptomatic patients. After several years, due to paralysis and the evolution of spinal static, disorders such as scoliosis and permanent deformities appear.

Diagnosis

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

A laboratory diagnosis is usually made based on the recovery of poliovirus from a stool sample or a pharyngeal swab. Antibodies against poliovirus can be of diagnostic utility, and are generally detected in the blood of infected patients early in the course of infection. Analysis of cerebrospinal fluid (CSF), which is obtained by lumbar puncture, usually reveals an increased number of white blood cells (mainly lymphocytes) and a slightly elevated level of protein. Detection of the virus in the CSF is diagnostic of paralytic poliomyelitis, but it rarely occurs.

In case poliovirus is isolated from a patient experiencing acute flaccid paralysis, tests are done through oligonucleotide (genetic) mapping or, more recently, PCR amplification, to determine if it is a virus. "wild type" (ie, the virus found in nature) or "vaccine type" (derived from a strain of poliovirus used to produce the polio vaccine). It is important to determine the source of the virus, because for each reported case of paralytic poliomyelitis caused by wild poliovirus, it is estimated that there would be another 200-3000 asymptomatic and contagious carriers of the virus.

Prevention

Two types of polio vaccine are used worldwide. The first was developed by Jonas Salk, first tested in 1952, and released by Salk on April 12, 1955. The second vaccine was an oral vaccine developed by Albert Sabin using attenuated poliovirus. Clinical trials of the Sabin vaccine began in 1957 and it was licensed in 1962.

Current situation

Eradication

In April 2013, at the World Vaccine Summit in Abu Dhabi, the World Health Organization launched the program Comprehensive Strategic Plan for Polio Eradication and Endgame 2013‒2019 , which sought to eradicate polio in the world by 2019. According to data from this institution, in 1988, 350,000 cases were reported in at least 125 countries where the disease was endemic, while in 2016 only 37 newly infected. The poliovirus type 2 was declared eradicated in 1999 and the poliovirus type 3, in 2012; since then only type 1 has persisted, the transmission of which occurs naturally only in Afghanistan and Pakistan.

2014 international emergency declaration

On May 14, 2014, according to WHO monitoring, cases continue to be reported in endemic countries (Pakistan and Afghanistan) and new cases are reported in non-endemic areas (Equatorial Guinea, Cameroon, Iraq, Syria, Ethiopia). This situation indicates the dangerous progression of polio that motivates the declaration of international emergency.

The work of Frida Kahlo and polio

In 1913, when she was only 6 years old, the Mexican painter Frida Kahlo contracted this disease, which forced her to remain in bed for 9 months and left her right leg thinner than her left for life. As a consequence of this, there are various works of hers where the painter reflects the loneliness she felt during her illness. Some of his most famous works linked to poliomyelitis and the loneliness of his childhood are: Four inhabitants of Mexico City (1938), Girl with a death mask or She Plays Alone (1938) and Day of the Dead.