Enterovirus
Dongyou Liu in Handbook of Foodborne Diseases, 2018
Poliomyelitis (also known as infantile paralysis, acute anterior poliomyelitis, or polio) is an acute infection with poliovirus, which may manifest as subclinical illness (90%–95% of cases); abortive poliomyelitis (a nonspecific minor illness in young children, with slight fever, malaise, headache, sore throat, and vomiting; 4%–8% of cases); nonparalytic poliomyelitis (aseptic meningitis without paralysis, with deep muscle pain, hyperesthesias, paresthesias, urinary retention, and muscle spasms; 1% of cases); or paralytic poliomyelitis (flaccid weakness of various muscle groups, due to viral invasion into the central nervous system, along with dysphagia, nasal regurgitation, nasal voice, pharyngeal paralysis, and skeletal muscle paralysis; <1% of cases). Although polio has been eradicated with extensive vaccination in most parts of the world, cases still occur in regions with incomplete immunization (e.g., Pakistan, Afghanistan, and Nigeria) [24].
Health promotion and person-to-person disease outbreaks
Glenn Laverack in Health Promotion in Disease Outbreaks and Health Emergencies, 2017
Polio (poliomyelitis) is a highly infectious disease caused by a virus. It invades the nervous system and can cause irreversible paralysis in a matter of hours. Polio mainly affects children under 5 years old and is spread through person-to-person contact and through the contamination of water and food. When a child is infected with poliovirus, the virus enters the body through the mouth and multiplies in the intestine. It is then shed into the environment through the faeces where it can spread rapidly through a community, especially in overcrowded conditions of poor hygiene and sanitation. However, if a sufficient number of people, including children, are immunised against polio, the virus is unable to find susceptible people to infect and eventually is eradicated. Most people infected with the poliovirus have no signs of illness and are unaware that they have been infected. In others, initial symptoms include fever, fatigue, headache, vomiting, stiffness in the neck and pain in the limbs. The symptomless people can then spread the infection to others before the first case of polio emerges. For this reason, a single confirmed case of polio paralysis is considered to be evidence of an outbreak, particularly in countries where very few cases normally occur.
Taming the Enemy
Norman Begg in The Remarkable Story of Vaccines, 2023
These attenuated vaccines (often referred to as live attenuated vaccines or replicating vaccines) have a number of advantages over inactivated vaccines. Because they are alive, they grow and multiply in your body. This means your immune system gets a continuous stimulus over several days or even weeks. Live attenuated vaccines provide stronger, and longer-lasting immunity than killed ones. Yellow fever is a live attenuated vaccine; a single dose will protect you for life. There are some downsides, however. The ability of live vaccines to multiply means that they can produce symptoms of the disease, albeit a much milder version. Measles vaccine is a good example. It’s quite common for a child to develop a rash and mild fever about a week after the vaccine; a “mini measles”. Very rarely, a live vaccine can produce a full-blown version of the disease. Paralysis following live polio vaccination (the version that is given by mouth) occurs at a rate of about one per 2 million doses. This is still much better than the actual disease, where up to one in ten people who are infected will get paralysis, however, it is one of the reasons why most polio vaccines given nowadays are the killed version, which cannot cause paralysis. Another drawback of live vaccines is that they cannot be given to people with severely weakened immune systems, as they may not be able to control the replication of the organism. Examples of live attenuated vaccines include measles, mumps, rubella, yellow fever, BCG (for tuberculosis) and oral polio vaccine.
Growing up with a disability following paralytic poliomyelitis: experiences from persons with late effects of polio
Published in Disability and Rehabilitation, 2021
Catharina Sjödahl Hammarlund, Jan Lexell, Christina Brogårdh
The analysis uncovered a number of subcategories, which were then put into three categories. (1) “Memories of falling ill, being immobilized and needing physical treatment” consisting of four subcategories: (a) Disabilities following acute paralytic poliomyelitis, (b) Being sent away for treatment, (c) Surgical treatment and physiotherapy, and (d) Orthoses to facilitate mobility. (2) “Managing social encounters and living up to the expectations of others” comprised four subcategories: (a) Alienation due to activity limitations, (b) Feeling looked upon as different, (c) Meeting peers and making friends, and (d) Managing a situation without complaining. (3) “Various psychological strategies for adapting” contained three subcategories: (a) Trying to blend in, (b) Choosing to focus on positive aspects of life, and (c) Building a self-image and trust in the ability to manage (Figure 1).
Quality of life for post-polio syndrome: a patient derived, Rasch standard scale
Published in Disability and Rehabilitation, 2018
Carolyn A. Young, Anne-Marie C. Quincey, Samantha M. Wong, Alan Tennant
Poliomyelitis (polio) is an acute, communicable disease caused by poliovirus. The illness has varying degrees of severity, including rapid onset of acute flaccid paralysis. Prior to the development of vaccination programmes in the 1950s, polio was widespread. For example, in America in 1952, there were more than 21,000 paralytic cases.[1] Despite concerted efforts by the WHO and others, such as Rotary International, to ensure widespread vaccination and the eradication of polio, outbreaks of polio continue. From 1976–1995, there were 48 outbreaks of paralytic poliomyelitis, with a cumulative total of ∼17,000 cases reported worldwide.[2] Europe had been declared free of poliovirus from 2002 until an outbreak in 2010 in Tajikistan.[3] A 60% increase in confirmed cases of polio in Pakistan between 2009 and 2010 is a reminder of the persistence of the disease.[4]
Adolf Kussmaul (1822–1902), and the naming of “poliomyelitis”
Published in Journal of the History of the Neurosciences, 2022
Nadeem Toodayan, Eric Matteson
Although some features of the illness might certainly be accounted for by an attack of paralytic polio, the symptom complex of progressive but self-limiting paraparesis with peripheral sensory and autonomic symptoms in the absence of a distinct central sensory level (which could indicate transverse myelitis) may be better explained by an acute inflammatory demyelinating polyradiculoneuropathy, or Guillain-Barre syndrome.1It was not until 1875 that Wilhelm Erb (1840–1921) and Carl Westphal (1833–1890) first indicated the clinical importance of deep tendon reflexes (Louis and Louis 2002), and this is why Kussmaul did not comment on such findings in his own case. We would expect the reflexes to be diminished in this instance. Kussmaul himself had originally described such a syndrome in the same year Octave Landry (1826–1865) coined the term “acute ascending paralysis” (Landry 1859), but he could not identify an anatomical or toxic cause for the disease (vide infra). Indeed, the term “Kussmaul-Landry paralysis” was in use before the name Guillain-Barre syndrome was popularized (Fischer 1931, 87), and was apparently the first of a number of eponymous clinical entities to be later linked to Kussmaul’s name (see Table 1).
Related Knowledge Centers
- Antibody
- Paresthesia
- Poliovirus
- Flaccid Paralysis
- Infection
- Headache
- Post-Polio Syndrome
- Fecal–Oral Route
- Feces
- Physician