At What Age Should the First Polio Vaccine Be Given Chapter 27 Chapter Review Quizlet
Neurohospitalist. 2014 Oct; iv(4): 223–229.
Poliomyelitis
Historical Facts, Epidemiology, and Current Challenges in Eradication
Human Mohan Mehndiratta
oneSection of Neurology, Janakpuri Superspeciality Hospital, Janakpuri, New Delhi, India
Prachi Mehndiratta
2Section of Neurology, subspecialty sectionalisation Vascular neurology-StrokeDepartment of Neurology, subspecialty segmentation Vascular neurology-Stroke, University of Virginia, Charlottesville, VA, The states
Renuka Pande
3Section of Microbiology, Janakpuri Superspeciality Infirmary, New Delhi, Republic of india
Monitoring Editor: Jennifer Lyons
Abstract
Poliomyelitis is a highly infectious disease caused by a virus belonging to the Picornaviridae family. It finds a mention even in aboriginal Egyptian paintings and carvings. The clinical features are varied ranging from mild cases of respiratory disease, gastroenteritis, and malaise to severe forms of paralysis. These have been categorized into inapparent infection without symptoms, mild illness (abortive poliomyelitis), hygienic meningitis (nonparalytic poliomyelitis), and paralytic poliomyelitis. This disease has been associated with crippling deformities affecting thousands of lives throughout the earth. Only due to the perseverance and determination of great scientists in 1900s, the genomic structure of the virus and its pathogenesis could be elucidated. Contribution of Salk and Sabin in the form of vaccines—oral polio vaccine (OPV) and the inactivated polio vaccine—heralded a scientific revolution. In 1994, the World Health Organization (WHO) Region of The Americas was certified polio costless followed by the WHO Western Pacific Region in 2000 and the WHO European Region in June 2002 of the iii types of wild poliovirus (types 1, two, and iii). In 2013, only three countries remained polio endemic—Nigeria, Pakistan, and Afghanistan. Global eradication of polio is imperative else the threat of an outbreak will hover forever. Today, all the governments of the world in collaboration with WHO stand up unified in their fight against poliomyelitis and the task when achieved will pave the way for eliminating other infections in future.
Keywords: poliomyelitis, infectious disease medicine, epidemiology
Introduction
Eradication of polio is a success story for medicine and public health and teaches us much virtually how to combat infectious diseases. Poliovirus has been used as a model virus because a large torso of research data exists on the concrete, chemical, and biological properties of the virus, vaccination is available, and it is like shooting fish in a barrel to culture every bit compared to other viruses. The word poliomyelitis originates from the Greek word "polio" meaning "grayness" and "myelon" meaning "marrow." It is an infectious disease caused by the poliovirus, a fellow member of the genus Enterovirus, belonging to the Picornaviridae family.i Poliomyelitis is an sectional homo disease transmitted from a patient or a symptom-free carrier through the fecal-oral route. Manifestations are varied ranging from asymptomatic (most common) to the nigh severe forms of debilitating paralysis. Historians have laid proof of the existence of poliomyelitis in aboriginal times. Egyptian paintings from the period 1403 to 1365 BC draw children with deformed limbs, walking with sticks. In 1789, an English md Michael Underwood gave the first clinical description where he referred to polio every bit "debility of the lower extremities." Polio was known as Heine-Medin disease due to the contributions of physicians Jakob Heine and Karl Oskar Medin in 1840.2,3
In the United States, localized paralytic polio epidemics began to appear around 1900. In June 1916, a directive was issued by the US public health regime in Brooklyn, New York, regarding the existence of an epidemic of polio. More than than 27 000 patients were reported, and fatality was more than 6000 in the state. At that place were more 2000 deaths in New York City solitary.4Authorities realized that they were dealing with an uncontrollable problem when a polio epidemic began to announced each summer. The crescendo came in 1940 to 1950 when "polio" came to be associated as the "wrath of God." Quarantine of exposed children led to widespread panic and anxiety among the parents.iv,five
An urgent medical revolution came in the form of polio vaccines introduced in 1950 by Salk and Sabin. The number of cases of polio decreased from nearly 58 000 to only 5600 in a year's time. Further decline in number of cases was seen afterward the second wave of mass immunization. By 1961, only 161 cases were recorded. The last case of paralytic polio through endemic transmission was recorded in 1979 in the midwest United States. In 1988, Globe Health System (WHO) passed a resolution to gratis the earth from wild-type polio past 2000 in the class of Global Polio Eradication Initiative. In 1994, the WHO Region of The Americas was certified polio costless followed by the WHO Western Pacific Region in 2000. World Health Organization European Region was declared polio free of the 3 types of wild poliovirus (types ane, 2, and 3) in June 2002. A globe map depicting polio-endemic countries, regions of recent outbreak of poliovirus, and countries at high gamble of poliovirus outbreak is depicted as Figure 1.
World map showing polio-endemic countries' outbreak of wild poliovirus in polio-complimentary regions and countries at higher propensity of wild poliovirus outbreak in the year 2013.
Pathogenesis
Poliovirus has a diameter of 25 to thirty nm. Its outer coat or capsid is composed of 60 protomers each made of 4 virion proteins VP1, VP2, VP3, and VP4 bundled in icosahedral symmetry. All the four virions are fabricated of 8 strands of protein bundled in β sheet array forming a β barrel. Due to the intermingling of various proteins, loops are created, which serve as antigenic sites for combination with respective antibodies. Three serotypes of poliovirus have been recognized as types ane, 2, and 3. The prototype strains are Brunhilde and Mahoney strains for type 1, Lansing and MEFI for type 2, and Leon and Saukett for blazon 3. Each of the viruses has been crystallized and studied in detail.1,6
The poliovirus enters the oropharynx and multiplies locally in the tonsils, lymph nodes of the neck, and then after in Peyer patches and small intestine. The incubation period ranges from two to 35 days. There is also a hypothesis to propose that sometimes, virus enters the claret stream and then secondarily invades the tonsils.vi After 3 to 5 days, the virus is shed in stool and also can be recovered from the throat swabs of exposed patients. This period may be entirely asymptomatic or mild viremic symptoms may be seen. Self-limiting episodes of gastroenteritis, respiratory tract infection, and influenza-like illness can occur. The viremia may subside due to the appearance of antibodies or spread to the central nervous system (CNS) via bloodstream. Published literature as well points to spread via the afferent nerve pathway in the brain equally virus has special affinity for cellular receptor CD155 that helps in cell attachment and entry.seven The virus primarily causes destruction attributable to its cytopathic nature. In that location is extensive damage to the anterior horn cells of the spinal cord. This causes limb paralysis. The virus may spread to the posterior horn cells, motor neuron of the thalamus, and hypothalamus. In bulbar form of poliomyelitis, there is involvement of brain stalk, which may be fatal. Histological appearance of the afflicted brain cells shows vacuolation and infiltration. There is accumulation of plasma cells, polymorphonuclear neutrophils, and microglia. Infected cells get phagocytosed past macrophages causing degeneration of axons. Widespread muscular atrophy occurs leading to flaccid paralysis. Death usually occurs due to respiratory paralysis in farthermost cases. Postpolio syndrome (PPS) tin occur 25 to 30 years after the initial paralytic attack.8 In PPS, progressive musculus cloudburst is seen probably due to ongoing motor neuron deterioration. Another hypothesis suggests abnormal presence of cytokines possibly due to the persisting poliovirus in the encephalon and spinal cord.half dozen
Modes of Manual
The spread of the disease is through the fecal-oral route. The dissemination of the virus in the feces is the reason of information technology being a highly communicable disease. Maximum excretion of the virus is seen in ii to 3 days prior and 1 week after appearance of symptoms.
The spread is rapid in areas with poor sanitation, especially among the nonimmune population. The propagation of the virus is mainly seen in summer months in temperate regions. Tropical regions have no such distinction.
Poliomyelitis has been present endemically through infection among susceptible infants. Mainly due to the presence of antibodies to all the 3 serotypes of the virus (types ane, 2, and 3) in women of childbearing historic period and also due to the protective effect of maternal antibody, infants can be infected and protected simultaneously without whatever residual effects. The disease changed its form from owned to causing diverse outbreaks of paralysis only in the belatedly 19th century. Improper sanitation facilities and lack of personal hygiene were establish to be the nearly important contributory factors, which led to infants getting exposed to the virus at an age beyond the protection of maternal antibodies.4,9
Clinical Presentation
Clinical features have been classified co-ordinate to the severity of symptoms. The majority of exposed patients (around 95%) are asymptomatic. During this catamenia, in that location is shedding of the virus in stool and it tin can be isolated from pharynx swabs too. The ratio of asymptomatic to paralytic cases ranges from 50:1 to 1000:1.ten Bootless poliomyelitis, which is a mild viremic grade, accounts for around iv% to 8% of infections. At that place may be gastroenteritis, influenza-like illness, and mild respiratory tract infections, which ordinarily subside within one week. Around 1% of the clinical cases present equally aseptic meningitis.9 There can be severe muscle spasm of the neck, dorsum, and lower limbs, which follows a brief prodrome like the one in abortive poliomyelitis. Complete recovery usually takes place within x days. The almost astringent class, paralytic poliomyelitis, which is seen in less than 1% of patients, presents as excruciating episodes of pain in back and lower limbs. In children, the affliction may nowadays in biphasic form—a catamenia of prodrome followed by a brief symptom-free catamenia of seven to 10 days and then appearance of asymmetrical paralysis of limbs. Flaccid paralysis is the hallmark with loss of deep tendon reflexes somewhen.ix
Recovery may be complete in some patients simply if loss of motor functions persists across 12 months, lifelong disability ensues. The 3 forms of paralytic poliomyelitis are spinal poliomyelitis, which is most common, bulbar poliomyelitis (two%), and a combination of above ii, bulbospinal poliomyelitis (around 19%)iv Bulbar poliomyelitis has the maximum fatality every bit the brain stem neurons are involved. In PPS, there is progressive muscular weakness, joint deterioration, and increasing skeletal deformities. Fatigue, post-obit even minimal physical activity may lead to astringent handicap of the twenty-four hours-to-mean solar day functioning.
Laboratory Diagnosis
The current method of diagnosis is polymerase concatenation reaction (PCR) for detection of poliovirus, which can exist isolated from samples of stool, pharynx swabs, blood, and cerebrospinal fluid (CSF). Stool samples of the infected person are the master sample source. The virus is excreted intermittently for a long menses of ane to 2 months later on infection. In all, 80% of exposed people excrete the virus in the first ii weeks, which declines to around 25% in the third week. Therefore, 2 samples of stool must be collected ideally at an interval of 24 hours within 2 weeks' fourth dimension for maximizing the chances of isolation of virus.11 Presence of the virus in the oropharynx is ordinarily early in the infection. The virus tin rarely be isolated from CSF in cases of aseptic meningitis. During get-go phase of viremia (3-5 days after infection), virus tin exist isolated from claret, but it is non of diagnostic importance.
Cell Civilization
Initially the virus was cultivated in Rhesus and Cyanomolgus monkey cell lines, but these methods are not preferred at present. At present, human cell lines like human amnion prison cell line and human embryo cell line are generally preferred methods. In India, polio laboratories work on RD cell line ,which is derived from human rhabdomyosarcoma and L20B cell line, which are very specific for poliovirus.11 Virus growth is determined by its cytopathic consequence on the jail cell lines. This usually occurs inside seven days of inoculation. If the cytopathic changes are seen only in RD cell line, inoculation is done in L20B prison cell line to ostend poliovirus. The isolate is then subjected to neutralization tests using specific antisera for serotyping. Tests are likewise done to confirm whether the isolate is a wild strain or a vaccine-derived one. These tests are called intratypic differentiation tests.11 These are either based on the principle of enzyme-linked immunosorbent analysis or based on the hybridization techniques.
Serology
A iv-fold rise in antibody titer is essential for confirmation of the infection. Neutralizing antibodies appear very early in the affliction process and persist for life.
Molecular Methods
Samples like CSF and serum give a poor yield of virus in culture. In add-on, cell culture is technically laborious and time consuming. These challenges have been addressed by the addition of PCR in the armamentarium of diagnostic tests. Information technology has revolutionized the isolation of poliovirus. Polio-specific PCR primers have been designed, which assist in the isolation of the virus.12
Genetic sequencing of the virus is essential to decide its origin and mode of transmission in cases of outbreak. When the world today stands on the brink of polio eradication, firsthand identification of the genome of the outbreak isolate is imperative. Whether information technology is a recirculating strain or an imported one, the noesis will assist in curbing transmission.
Management
In the earlier times, when the epidemics of polio were frequent, there was absolute lack of noesis regarding the management aspects of this crippling disease. Astute cases required firsthand relief from hurting, and rehabilitation was a challenge for chronic cases with deformities. Various strategies to manage these cases were in vogue at that time. A lot of experimentation was also involved. One of the earliest descriptions regarding direction strategies of polio is the heroic work of Sister Elizabeth Kenny (an Australian nurse). She used hot packs to relieve musculus spasms in early stages of the disease13 and discouraged the practice of prolonged immobilization of affected limbs. A large number of patients were benefited.
The first mod rehabilitation eye dedicated to patients with polio was prepare in 1926 by President Franklin Theodore Roosevelt in the U.s..xiv
Later, new inventions were introduced to offer relief to the sick patients. One such musical instrument was the Iron Lung Car.15 Information technology was used in patients with respiratory paralysis to prolong their lives by assisted respiration. The drawbacks were the mammoth size, technical adjustments, and cost gene.
Modern medicine has contributed tremendously to the direction of polio. In the recovery stage, remedial exercises are prescribed to assist the paralyzed muscles. Appropriate orthotic devices have been designed to prevent deformities due to musculus imbalance16,17 Diverse sessions of intense physiotherapy are necessary for rehabilitation and recovery. Surgical management includes tendon transplant, contracture relieving surgeries, and joint replacement surgeries.eighteen Illizarov technique, an orthopedic technique used to stabilize and rehabilitate the limb has also been now increasingly used for correction of deformities.xix
Prevention
Salk and Sabin conducted numerous trials on their own blood relations, pets, and school children, which ultimately led to their moment of victory. It is a piffling known fact that more than 100 000 monkeys were killed for the benefit of humanity during development of the polio vaccine.20 The history of vaccines would be incomplete without mentioning the contribution of Dr David Bodian.21 He described the pathogenesis of the disease and the 3 antigenic types of poliovirus forth with his squad.22
Herd Immunity
Herd amnesty supplements to polio vaccination. Amongst those individuals who receive oral polio vaccine (OPV), only 95% develop immunity. Information technology is necessary to understand that the population in whom the vaccine fails are nonetheless protected past the immunity of those around them.
Numerous hurdles and setbacks were encountered earlier routine vaccination became reality for polio. In 1 incident, around 200 people became sick and eleven died after vaccination. This led to anticipation and anxiety regarding the safety of immunization. Subsequently investigation constitute out that an inferior quality batch of inactivated polio vaccine produced by a particular drug company was backside this mishap.23 This laid to rest the feet and apprehension regarding polio vaccination.
Sabin continued to work on a live weakened strain that provided gut immunity but did not invade the CNS. He got the vaccine OPV licensed in 1962. Details about the constitution, mode of delivery, efficacy, and safety contour about the vaccines are described in Table one.23,24
Table 1.
Comparison of Oral Polio Vaccine (OPV) and Inactivated Polio Vaccine (IPV).
| Property of Vaccine | Oral Polio Vaccine | Inactivated Polio Vaccine |
|---|---|---|
| Grooming | Alive attenuated poliovirus serotypes (Sabin types 1, 2, and 3), in a 10:i:three ratio, respectively. | Strain of each of the 3 serotypes that have been inactivated (killed) with formalin, adsorbed onto adjuvants. The final vaccine mixture contains 40, viii, and 32 d-antigen units of serotypes 1, 2, and 3, respectively. |
| Valency | Trivalent OPV (tOPV) and monovalent, confronting blazon one (mOPV1) and against type 3 (mOPV3) bivalent (blazon i and blazon 3) OPVs (bOPVs) | Only 1-type trivalent |
| Storage | +2°C to +viii°C. Should be protected from calorie-free. Any vaccine showing particulate thing, turbidity, or change in color should exist discarded | +2°C to +8°C. Should exist protected from light. Any vaccine showing particulate matter, turbidity, or modify in color should be discarded |
| Pathogenesis | Produce a local allowed response in the intestines. Mucosal immunity decreases the replication and shedding of the virus | Antibodies are produced against the polio virus which provide humoral amnesty, thus decreasing the replication of the virus. |
| Assistants | Through mouth every bit drops | Intramuscularly into the upper arm or anterolateral thigh, can be administered alone or in combination with other vaccines |
| Recommended dosage | No longer in use in polio-complimentary countries like The states and Britain. Used routinely but in polio campaigns in loftier adventure and endemic areas | A total of 5 doses of vaccine at the appropriate intervals |
| Vaccine efficacy | Amnesty from oral poliovirus vaccine is probably lifelong. OPV produces excellent gut immunity | The duration of immunity with IPV is not known with certainty. Highly effective in producing immunity to poliovirus and protection from paralytic poliomyelitis. No gut amnesty |
| Adverse effects | Vaccine-associated paralytic poliomyelitis (VAPP) outbreaks due to circulating vaccine-derived poliovirus (cVDPV) | Adverse events following administration of IPV are very mild and transient |
Current Status in India
The National Polio Surveillance Project launched in 1988 in collaboration with WHO had the sole objective of making India polio free.11 The initiative in India came in the form of "Pulse Polio" in 1995 to 1996, an immunization entrada launched by the Regime of India. Nether this extensive drive, two drops of OPV was given to all children younger than 5 years of age. Due to the dedicated active surveillance of acute flaccid paralysis cases, the results were impressive. As compared to 24 000 cases in 1988, the number of cases reported in 2003 were but 134. At the end of 2003, Nigeria, Bharat, Pakistan, Niger, Transitional islamic state of afghanistan, and Egypt25 were the only countries in the earth that remained polio endemic. For Republic of india to obtain global polio eradication certificate, it was crucial that all laboratory sources of wild polioviruses are destroyed. For this, a National Task Force on Laboratory Containment of Wild Polio Virus was constituted.26 This job forcefulness was led by The Director Full general of Indian Council of Medical Inquiry. It was following the guidelines of the Global Action Programme, which emphasized the conception of a national inventory of all the wild polioviruses and potentially poliovirus-infected materials. In India, the final reported instance was in the state of West Bengal on January 13, 2011. On February 25, 2012, WHO directed that Bharat be struck off from the listing of polio-endemic countries. In 2013, simply 3 countries remain polio endemic—Nigeria, Islamic republic of pakistan, and Afghanista.27,28 India has recently completed the 2-year milestone of becoming polio free and is expected to receive a global polio eradication document in 2014.29
Current Challenges in the Earth
The last divers case of natural polio in the United Kingdom was in the yr 1984. Betwixt 1985 and 2002, 40 cases of paralytic polio were reported.24 Of these, 30 were vaccine-associated paralytic polio. In 6 patients, the infection was contracted overseas, and in 5 patients, the source of infection was unknown. The wild virus was non detected. In 2000, an outbreak occurred in Hispaniola.seven The causative isolate was a recombinant of the vaccine strain and an unknown virus. Vaccine-associated paralytic poliomyelitis will go along to be a serious result as long as OPV is beingness used. Scientific data prove beyond doubt that polio eradication will too require the eventual disuse of OPV, otherwise in that location will be resurgence in a polio-free world due to vaccine-associated paralytic polio and polio outbreaks due to circulating vaccine-derived polioviruses. Polio-costless countries will be nether a constant threat of importing a vaccine-derived poliovirus from places where OPV is used. But the greatest challenge is to terminate the transmission of the wild strain circulation. In 2012, WHO alleged completion of polio eradication a Programmatic Emergency. The Stop Manual of Polio (Terminate) plan was launched to strengthen surveillance and promote maximum vaccination campaigns.30 Many factors pose challenges to complete eradication. Geographically difficult terrains make vaccine commitment difficult. At that place are serious sanitation problems. In some areas, cooperation from the local assistants is lacking. Some religious factions have been candidature against the vaccine drive.31 The crunch is non independent within the political boundaries of countries merely spill over in the form of wild strains existence exported to polio-free areas. One such recent outbreak occurred in Xinjiang province of China in 2011.32 This region had been certified polio gratuitous for the past 10 years. Investigation traced the origin to a wild polio strain from Pakistan. Outbreak management on a colossal scale was launched to comprise this outbreak. Oral polio vaccine of 43.seven one thousand thousand doses was delivered in v rounds of vaccination. This report reiterates the already known fact that until the fourth dimension polio is exterminated from all the countries, polio-gratis countries will exist under threat. The efforts of thousands of people working religiously for decades should not go waste.
Footnotes
Annunciation of Conflicting Interests: The authors declared the following potential conflicts of involvement with respect to the enquiry, authorship, and/or publication of this article: Dr Prachi Mehndiratta did 3 months voluntary service in polio eradication program during her medical graduation.
Funding: The authors received no fiscal support for the research, authorship, and/or publication of this article.
References
1. Bodian D, Horstmann DM. Polioviruses. In: Horsfall FL, Tamm I, eds. Viral and Rickettsial infections of Human being. 4th ed. Philadelphia, PA: JB Lippincott Co;1965: 430–473 [Google Scholar]
two. Daniel TM, Robbins FC, eds. A history of poliomyelitis. Polio. Rochester, New York: University of Rochester Press; 1997:5–22 [Google Scholar]
v. Trevelyan B, Smallman-Raynor M, Cliff A. The spatial dynamics of poliomyelitis in the United States: from epidemic emergence to vaccine-induced retreat, 1910–1971. Ann Assoc Am Geogr. 2005;95(2):269–293 [PMC free article] [PubMed] [Google Scholar]
6. Schaulies JS, Schaulies SS, Meulen VT. Infections of the central nervous system. In: Topley and Wilson's Microbiology and Microbial Infections, Virology. Vol. 2. tenth ed. Wiley-Blackwell; 2005:1401–1498 [Google Scholar]
7. He Y, Mueller South, Chipman PR, et al. . Complexes of poliovirus serotypes with their common cellular receptor, CD155. J Virol. 2003;77(eight):4827–4835 [PMC free commodity] [PubMed] [Google Scholar]
8. Gonzalez H, Khademi M, Borg K, Olssonet T. Intravenous immunoglobulin treatment of the mail service-polio syndrome: sustained furnishings on quality of life variables and cytokine expression afterward one year follow upwards. J Neuroinflammation. 2012;9:167. [PMC gratis article] [PubMed] [Google Scholar]
9. McQuillen D, McQuillen M. Poliomyelitis. In: Jones Royden H, ed. Netter's Neurology. Philadelphia, PA; Elsevier Saunders; 2005:597–601 [Google Scholar]
12. Chezzi C. Rapid diagnosis of poliovirus infection past PCR distension. J Clin Microbiol. 1996;34(vii):1722–1725 [PMC free commodity] [PubMed] [Google Scholar]
13. Oppewal SR. Sis Elizabeth Kenny, an Australian nurse, and treatment of poliomyelitis victims. Image J Nurs Sch. 1997;29(1):83–88 [PubMed] [Google Scholar]
15. Wilson D. Braces, wheelchairs, and iron lungs: the paralyzed body and the machinery of rehabilitation in the polio epidemics. J Med Humanit. 2005;26(ii-3):173–190 [PubMed] [Google Scholar]
16. Jubelt B. Post-polio syndrome. Curr Treat Options Neurol. 2004;6(two):87–93 [PubMed] [Google Scholar]
17. Brehm A, Beelen A, Doorenbosch CA, Harlaar J, Nollet F. Effect of carbon composite knee–ankle–foot orthoses on walking efficiency and gait in former polio patients. J Rehabil Med. 2007;39(eight):651–657 [PubMed] [Google Scholar]
19. Kocaoglu Yard, Eralp L, Atalar Air conditioning, Bilen Iron. Correction of complex human foot deformities using the Ilizarov external fixator. J Foot Ankle Surg. 2002;41(1):30–39 [PubMed] [Google Scholar]
20. National Museum of American History. Polio: 2 vaccines. http://amhistory.si.edu/polio/virusvaccine/vacraces2.html. Accessed November 24, 2013 [Google Scholar]
21. Nathanson N. David Bodian's contribution to the evolution of poliovirus vaccine. Am J Epidemiol. 2005;161(3):207–212 [PubMed] [Google Scholar]
22. Bodian D. Pathogenesis of poliomyelitis. Am J Public Wellness Nations Wellness. 1952;42(11):1388–1402 [PMC gratis article] [PubMed] [Google Scholar]
26. National Task Force for Containment of Wild Polio Virus. http://www.npspindia.org/. Accessed Dec 4, 2013
30. CDC. The global polio eradication initiative end transmission of polio (STOP) program—1999-2013. MMWR Morb Mortal Wkly Rep. 2013;62(24):501–503 [PMC free article] [PubMed] [Google Scholar]
31. Bhaumik S. Polio eradication: current status and challenges. J Fam Med Primary Care. 2012;1(2):84–85 [PMC free article] [PubMed] [Google Scholar]
32. Luo HM, Zhang Y, Wang XQ. Identification and command of a poliomyelitis outbreak in Xinjiang, China. N Engl J Med. 2013;369(21):1981–1990 [PubMed] [Google Scholar]
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