poliomyelitis(redirected from bulbar poliomyelitis)
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infantile paralysis,acute viral infection, mainly of children but also affecting older persons. Historically, there were three immunologic types of poliomyelitis virus, but two of three types of the wild virus have been eradicated; exposure to one type produced immunity only to that type, so infection with another type was still possible. Spread of the infection is primarily through contact with an infected person. Most people who contract polio either exhibit no symptoms or experience only minor illness; however, such individuals can harbor the virus and spread it to others. Less than 1% of the people who get infected develop paralysis.
The virus enters the body by way of the mouth, invades the bloodstream, and may be carried to the central nervous system, where it causes lesions of the gray matter of the spinal cord and brain. The illness begins with fever, headache, stiff neck and back, and muscle pain and tenderness. If there is involvement of the central nervous system, paralysis ensues. Of those patients who develop paralytic poliomyelitis, about 25% sustain severe permanent disability, another 25% have mild disabilities, and 50% recover with no residual paralysis. The disease is usually fatal if the nerve cells in the brain are attacked (bulbar poliomyelitis), causing paralysis of essential muscles, such as those controlling swallowing, heartbeat, and respiration. There is no specific drug for treatment. For reasons not clearly understood, some people who have had severe polio experience postpolio syndrome, a condition in which new weakness and pain occurs years later in previously affected muscles.
The incidence of poliomyelitis declined radically in the United States when a mass immunization program with the SalkSalk, Jonas Edward,
1914–95, American physician and microbiologist, b. New York City, B.S. College of the City of New York, 1934, M.D. New York Univ. College of Medicine, 1939. He did research on the influenza virus at the Univ.
..... Click the link for more information. vaccine, a preparation made from killed organisms and injected, was begun in 1955. A live-virus vaccine had earlier been developed (1948) by Hilary KoprowskiKoprowski, Hilary,
1916–2013, Polish-American microbiologist and immunologist, b. Warsaw, M.D. Univ. of Warsaw, 1939. He fled Poland after the Nazi invasion (1939), making his way to Brazil where he worked in the Rockefeller Foundation's yellow-fever service.
..... Click the link for more information. , but it was never approved for use in the United States. By 1961 the SabinSabin, Albert Bruce
, 1906–93, American physician and microbiologist, b. Bialystock, Russia, grad. New York Univ. (B.S., 1928; M.D., 1931). He emigrated to the United States in 1921 and was naturalized in 1930.
..... Click the link for more information. vaccine, a preparation made from weakened living organisms and taken orally, was released for use. Since then the disease has been virtually eliminated in the Americas, Europe, and Australasia, but vaccination programs continue because of polio's existence in other parts of the world (mainly areas of South Asia and West Africa) and the ease of travel.
In 1988 the World Health Organization began a global vaccination campaign to eradicate the disease—which continued to paralyze hundreds of thousands of children each year—by 2000. Although the date of eradication was later pushed back to 2005 (and even later a set deadline was abandoned), there were by 2003 less than a thousand new cases of polio worldwide. In 2003–4, however, the campaign was slowed when Muslim states in N Nigeria refused to use vaccines they believed would sterilize women, leading to an increase in cases there and in neighboring countries and to outbreaks of the disease in 17 countries including Yemen and Indonesia. Since then there have been other outbreaks, from various sources, in some African nations, in Central Asia, in Syria (as a result of its civil war), and in Papua New Guinea. The last known case of type 2 poliomyelitis occurred in 1999, and that of type 3 in 2012. In 2016 the formulation of the vaccine was altered to remove the eradicated type 2 poliovirus. According to WHO, endemic transmission of wild polio continues to occur only Afghanistan and Pakistan. Outbreaks of polio due to inadequate community vaccination levels that do not prevent the natural transmission and occasional mutation of the weakened strain used in the vaccine continue to occur in some areas free of wild polio.
An acute infectious viral disease which in its serious form affects the central nervous system and, by destruction of motor neurons in the spinal cord, produces flaccid paralysis. However, about 99% of infections are either inapparent or very mild. See Animal virus, Central nervous system
The virus probably enters the body through the mouth; primary multiplication occurs in the throat and intestine. Transitory viremia occurs; the blood seems to be the most likely route to the central nervous system. The severity of the infection may range from a completely inapparent through minor influenzalike illness, or an aseptic meningitis syndrome (nonparalytic poliomyelitis) with stiff and painful back and neck, to the severe forms of paralytic and bulbar poliomyelitis. In all clinical types, virus is regularly present in the enteric tract. In paralytic poliomyelitis the usual course begins as a minor illness but progresses, sometimes with an intervening recession of symptoms (hence biphasic), to flaccid paralysis of varying degree and persistence. When the motor neurons affected are those of the diaphragm or of the intercostal muscles, respiratory paralysis occurs. Bulbar poliomyelitis results from viral attack on the medulla (bulb of the brain) or higher brain centers, with respiratory, vasomotor, facial, palatal, or pharyngeal disturbances.
Poliomyelitis occurs throughout the world. In temperate zones it appears chiefly in summer and fall, although winter outbreaks have been known. It occurs in all age groups, but less frequently in adults because of their acquired immunity. The virus is spread by human contact; the nature of the contact is not clear, but it appears to be associated with familial contact and with interfamily contact among young children. The virus may be present in flies.
Inactivated poliovirus vaccine (Salk; IPV), prepared from virus grown in monkey kidney cultures, was developed and first used in the United States, but oral poliovirus vaccine (Sabin; OPV) is now generally used throughout the world. The oral vaccine is a living, attenuated virus.
(also called infantile paralysis), an acute infectious disease caused by lesions of the gray matter of the spinal cord and characterized chiefly by disease of the nervous system.
The scientific study of poliomyelitis was begun by the German orthopedist J. Heine (1840), the Russian neuropathologist A. Ia. Kozhevnikov (1883), and the Swedish pediatrician K. Medin (1890), researchers who demonstrated the independent and infectious character of the disease. The incidence of poliomyelitis in the mid-20th century was of epidemic proportions in many European and North American countries. The use of vaccines resulted in a rapid decline in incidence and led to complete eradication of the disease in many areas: in the USSR, for example, it no longer existed after 1959. The American scientists J. Salk and A. Sabin and such Soviet scientists as M. P. Chuma-kov and A. A. Smorodintsev were instrumental in developing the vaccines.
Poliomyelitis is caused by an enterovirus existing in three independent types, I, II, and III. The source of infection is a person with the disease or an asymptomatic carrier. The causative agent is eliminated through the mouth for several days and then with the feces for several weeks, sometimes for months. The infection may be transmitted by inhaling the droplet-borne virus, but infection by swallowing, resulting from infected hands or food, is more common. Flies may also carry the virus.
Poliomyelitis occurs most often in summer and fall and generally attacks children from six months to five years of age. Type I virus is responsible for most cases. After entering the body, it multiplies in the Waldeyer’s ring, intestine, and regional lymph nodes. It penetrates the blood and sometimes the central nervous system, inflicting injury especially to the motor cells of the anterior horns of the spinal cord and the nuclei of the cranial nerves. In most cases, the clinical course is asymptomatic and the infection can be detected only by laboratory tests. In other cases, symptoms appear after an incubation period of three to 35 days (generally from nine to 11 days).
A distinction is made between nonparalytic poliomyelitis, which includes the abortive and meningeal types, and paralytic poliomyelitis. The abortive type is characterized by such general nonspecific symptoms as catarrhal manifestations, gastrointestinal disturbances, general weakness, and fever. From the epidemiological standpoint it is the most dangerous type. The meningeal type is manifested by serious meningitis. In the most common paralytic type, spinal poliomyelitis, the general symptoms of infection are followed by paralysis of muscle groups innervated by motor cells of the spinal cord. The muscles most often affected are the quadriceps and adductors of the legs, the flexors and extensors of the feet, and the deltoid, triceps, and supinators of the forearms. Paralysis of the diaphragm is particularly dangerous because it causes severe respiratory disturbances.
The bulbar type of poliomyelitis is caused by lesions of different sections of the medulla oblongata, and the pontine type by lesions of the nucleus of the facial nerve. The nonparalytic types of the disease usually end in complete recovery. With the paralytic types, the functions of the affected muscles are partially restored in some cases and the defect may persist for a long time, sometimes for life. The most severe cases, especially those involving the respiratory centers of the medulla oblongata, may be fatal. The diagnosis of the disease is based on clinical, epidemiological, and laboratory findings.
Poliomyelitis is treated by bed rest, pain-relieving drugs, tranquilizers, and application of heat. Patients with the paralytic types are treated by means of drugs and physical and orthopedic therapy when the progression of the paralysis ceases, at a point between the fourth and sixth weeks of the disease’s course; they later receive periodic treatment at a sanatorium or health resort. Treatment of respiratory disorders includes resuscitation procedures.
The principal method of preventing poliomyelitis is immunization with live vaccine. Children are given several scheduled vaccinations at intervals of a month or more from the age of two months. The vaccine is administered orally in the form of drops or candy. Persons who contract poliomyelitis are hospitalized and the site of the infection is disinfected. In the USSR, the Institute of Poliomyelitis and Viral Encephalitides of the Academy of Medical Sciences of the USSR (founded 1955) is in charge of efforts to control poliomyelitis.
REFERENCESChumakov, M. P., I. M. Prisman, and T. S. Zatsepin. Poliomielit—detskii spinnomozgovoi paralich. Moscow, 1953.
Epidemicheskii poliomielit. Moscow, 1957.
Poliomielit. Moscow, 1957. (Translated from English.)
Drozdov, S. G. Poliomielit i egoprofilaktika v razlichnykh stranakh mira. Moscow, 1967.
S. G. DROZDOV