Poliomyelitis

introduction, historical background, history of polio vaccine, definition, epidemiology, mode of transmission, pathogenesis and its phase, clinical presentation - preparalytic and paralytic stages. acute stage, convalescent stage, recovery stage, residual stage or post polio syndrome. investigations, medical treatment, surgical management , rehabilitation

1. MRS. M.PRADEEPA MPT (NEURO) VICE PRINICIPAL PPG COLLEGE OF PHYSIOTHERAPY COIMBATORE, TAMILNADU, INDIA POLIOMYELITIS

2. Introduction Polio also known as poliomyelitis is a highly contagious disease caused by a virus that attacks the nervous system A major cause of paralysis and death 30 yrs ago, now rare with the introduction of effective vaccines and improved sanitation.

3. Prehistory The effects of polio have been known since prehistory Egyptian paintings and carvings depict healthy people with withered limbs, and children walking with canes at a young age.

4. History of Polio The first clinical description was provided by the English physician Michael Underwood in 1789, where he refers to polio as "a debility of the lower extremities" The work of physicians  Jakob Heine in 1840 and Karl Oskar Medin in 1890 led to it being known as  Heine– Medin disease. The disease was later called  infantile paralysis , based on its propensity to affect children.

5. First US Polio Epidemic The first major documented polio outbreak in the United States occurred in Rutland County, Vermont (1894). Eighteen deaths and 132 cases of permanent paralysis were reported. Charles Caverly , MD, was one of the first physicians to recognize that polio could occur with or without paralysis.

6. Contagious Nature of Polio Discovered The contagious nature of polio would be established in 1905. After a series of polio epidemics in Sweden, Ivar Wickman (1872-1914) published two important findings about polio. First, he suggested that polio was a contagious disease that could be spread from person to person. Second, he recognized that polio could be present in people who did not appear to have a severe form of the disease. These cases are known as abortive cases.

7. Poliovirus Identified In Vienna, Karl Landsteiner, MD (1868-1943), and Erwin Popper, MD (1879-1955), announced that the infectious agent in polio was a virus. Popper and Landsteiner deduced the viral nature of polio by carefully filtering preparations of spinal cord fluid from a person who had died of polio. The filters were known to trap bacteria. When Popper and Landsteiner injected the filtered preparations into monkeys, the monkeys developed polio. The researchers then concluded that an infectious particle smaller than bacteria caused the disease. Poliovirus itself would not be visible to researchers until the 1950s, when the electron microscope was available.

8. Flexner Investigates Polio Immunity - 1910 At the Rockefeller Institute for Medical Research in New York, Simon Flexner, MD (1863-1946), showed that “germicidal substances” were present in the blood of monkeys that had survived polio. Other researchers reported similar results with humans. These substances were neutralizing antibodies to polio. Researchers took this finding to indicate that a vaccine might be used to induce antibody production to fight the virus.

9. The Iron Lung - 1929 Philip Drinker, PhD (1894-1972), and Charles McKhann , MD (1898-1988), at Boston Children’s Hospital and Harvard published a paper describing successful use of an artificial respirator for patients suffering from paralytic polio. The machine, first known as the Drinker respirator and later as the iron lung, would provide temporary and in some cases, permanent breathing support for people suffering paralysis of the diaphragm and intracostal muscles, which are essential for respiration.

10. More Than One Type of Poliovirus Proposed – 1931 & 1949 Australian researchers Frank M. Burnet (1899-1985) and Jean Macnamara (1899-1968) infected monkeys with polio from a fatal human case of the disease. The monkeys had recovered from a previous case of polio and yet were paralyzed by the new infection. Their work showed that there was more than one type of poliovirus, and that previous infection with one type did not confer immunity to another type. The implication was clear: a polio vaccine would need to provide protection from all types of polio. It would be 20 years before David Bodian and Isabel Morgan (1949) would demonstrate that there are three types of polioviruses.

11. Polio vaccine The first polio vaccine, known as inactivated poliovirus vaccine (IPV) or  Salk vaccine , was developed in the early 1950s by American physician  Jonas Salk . This vaccine contains killed virus and is given by injection. In the 1960s a second type of polio vaccine, known as oral poliovirus vaccine (OPV) or  Sabin vaccine , named for its inventor American physician and microbiologist  Albert Sabin , was developed. OPV contains live attenuated (weakened) virus and is given orally.   Vaccines, whether killed or live, may contain strains of all three poliovirus serotypes—PV1, PV2, and PV3—or of just one or two (serotypes are closely related though distinguishable forms). 

12. Polio in India The Indian Council of Medical Research (ICMR) had established a Polio Research Unit (now Enterovirus Research Centre, EVRC) Mumbai in 1949. Data on epidemiology of urban poliomyelitis analysis were collected by pioneers. The second polio research unit in India was the Enterovirus Laboratory, established in 1964, in the Christian Medical College (CMC), Vellore, Tamil Nadu. Polio immunization using imported OPV was introduced in Mumbai by the city corporation in 1964 and in Vellore by CMC in 1965. Until early 1990s India was hyperendemic for polio, with an average of 500 to 1000 children getting paralysed daily.  India, vaccination against polio started on 1978 with Expanded Programme on Immunization (EPI). By 1999, it covered around 60% of infants, giving three doses of OPV to each. (PULSE POLIO PROGRAM) The last reported cases of wild polio in India were in West Bengal and Gujarat on 13 January 2011 India received polio-free certification along with the entire South-East Asia Region of WHO on 27th March 2014 by WHO

13. Etymology The term derives from the Ancient Greek  poliós meaning "grey“ and myelós referring to the grey matter of the spinal cord, and the suffix  - itis , which denotes inflammation of the spinal cord's grey matter, although a severe infection can extend into the brainstem and even higher structures, resulting in  polio encephal itis , resulting in inability to breathe, requiring mechanical assistance such as an iron lung

14. Definition An acute viral infection in which the anterior horn cells of the spinal cord and motor nuclei of the brain stem are selectively involved.

15. Etiology The poliovirus is a picornavirus (RNA virus). Three immunological distinct strains have been isolated Type-1-Brunhilde, Type-2-Lanchi, Type-3-Leon. Immunity to one does not result in immunity to the other two.

16. Mode of Transmission Spread by faecal/oral route. Inhalation or entry through conjunctiva of droplets of respiratory secretions may also be possible modes of entry in close contacts of patients in early stage of disease.  Once ingested the virus multiplies in the nasopharynx and gastrointestinal tract. Penetration of GI tract results in viraemia but CNS involvement occurs in only a very small proportion. Most infected patients are asymptomatic. Virus excretion continues in the faeces for as long as three months after the initial infection – carrier state

17. MODE OF TRANSMISSION

18. Pathogenesis

19. Pathophysiology of polio infection in nervous system Only 5% of infected patients have selective nervous system involvement after viremia . The poliovirus enters the nervous system by either crossing the blood-brain barrier or by axonal transportation from a peripheral nerve. It can cause nervous system infection by involving the precentral gyrus, thalamus, hypothalamus, motor nuclei of the brainstem and surrounding reticular formation, vestibular and cerebellar nuclei, and neurons of the anterior and intermediate columns of the spinal cord. The nerve cells undergo central chromatolysis along with an inflammatory reaction while multiplication of the virus precedes onset of paralysis. As the chromatolysis process goes on further, muscle paralysis or even atrophy appears when fewer than 10% of neurons survive in the corresponding cord segments. Gliosis develops when the inflammatory infiltrate has subsided, but most surviving neurons show full recovery.

20. Pathogenesis

21. Pathogenesis

22. Clinical presentation Prodromal stage or pre paralytic stage Paralytic stage – can further divided into Acute stage Convalescent stage Stage of recovery Residual stage or post polio syndrome

23. Preparalyitc stage Few hours to a few days and 1 to 3 days is the usual duration. Fever, malaise, sweating, Headache, Sore throat, Slight Cough and Diarrhea or constipation. It may improve or progress to severe symptoms like Backache Joint pains. Pyrexia of variable duration and severity. Mild neck stiffness. Irritability.

24. Acute stage 3 to 6 weeks from the onset of Poliomyelitis. Muscle tenderness is the most important sign  seen in this stage esp in calf muscles

25. Convalescent stage Duration 3 months. Spinal Type: Asymmetric paralysis. Paralysis develops; widespread or localised; ascending or descending, maximal 24 hours after onset of this stage. The lower limb muscles are more often involved. Muscles fasciculate. Muscle pain worsens May involve respiratory muscles. Flexion contractures of hip, knee and equinus deformity of the ankle are common.

26. Bulbar Type: Involvement muscles innervated by crainal nerve - Pharyngeal, laryngeal, lingual and facial weakness The early signs of respiratory involvement includes breathing difficulty, feeling of suffocation, slight cyanosis, use of sternomastoids , alae nasae and other accessory muscles of respiration. Spinobulbar : This type has a combination of both spinal and bulbar type. Postencephalic : Mental disturbance, coma, paralysis of facial muscles, symptoms similar to meningitis like headache, vomiting, neck stiffness may occur

27. Recovery stage This stage extends for almost 2 years. Thus muscle in the polio patient can be strengthened to their maximum capacity upto 2 years.

28. Residual stage or Post Polio Syndrome Post - polio syndrome  (PPS) is a condition that affects  polio  survivors years  after  recovery from an initial acute attack of the  poliomyelitis  virus. Halstead introduced the term "post-polio syndrome" in 1986, and he published revised criteria for diagnosing PPS in 1991, in which new muscle weakness was introduced  Other terms -  "late effects of polio" ( LEoP ) and " postpolio muscular atrophy." 

29. Criteria for the diagnosis of PPS were published by March of Dimes  Prior paralytic poliomyelitis with evidence of motor neuron loss, as confirmed by history of the acute paralytic illness, signs of residual weakness and atrophy of muscles on neurologic examination, and signs of denervation electromyography (EMG) A period of partial or complete functional recovery after acute paralytic poliomyelitis, followed by an interval (usually 15 y or more) of stable neurologic function Gradual or sudden onset of progressive and persistent new muscle weakness or abnormal muscle fatigability (decreased endurance), with or without generalized fatigue, muscle atrophy, or muscle or joint pain; sudden onset may follow a period of inactivity, or trauma or surgery; less commonly, symptoms attributed to PPS include new problems with breathing or swallowing. Symptoms persist for at least a year Exclusion of other neurologic, medical, and orthopedic problems as causes of symptoms

30. Pathophysiology of PPS Pathology in post polio syndrome is not well understood but several hypothesis had been formulated. Disintegration of overused motor units: Decompensation of a chronic denervation and reinnervation process to the extent that the remaining healthy motor neurons can no longer maintain new sprouts; thus, denervation exceeds reinnervation .   Reactivation of polio virus: Motor neuronal loss due to reactivation of a persistent latent virus. Immune system dysfunction: Foci of perivascular and interstitial inflammatory cells have been found on 50% of biopsies of patients with PPS. Activated T cells and immunoglobulin M and immunoglobulin G antibodies specific for gangliosides also have been found. The loss of strength due to the usual stresses of aging and weight gain can produce PPS .  Infection of the polio survivor's motor neurons by an enterovirus that is different from the one responsible for the patient's polio

31. Signs and Symptoms of PPS Progressive muscle and joint weakness and pain General fatigue and exhaustion with minimal activity Muscle atrophy Breathing or swallowing problems Sleep-related breathing disorders, such as sleep apnea Decreased tolerance of cold temperatures Flat-back syndrome

32. Investigations CSF Examination: Mildly elevated protein content in CSF from 40 to 50 mg/100 ml Throat washing: Throat washing is taken and assessed for the virus. The washings are incubated at a favourable atmosphere in a culture media. Stool samples are also examined for polio virus Blood tests: Blood is tested for antibodies for polio virus. Fingerprinting the polio virus Once the polio virus is isolated it is tested by a special test called oligonucleotide mapping (fingerprinting) or genomic sequencing. This is essentially looking at the genetic sequence of the virus to detect if the origin of the virus is “wild type” or “vaccine like”. Wild type virus naturally occurs in the environment and may occur as 3 subtypes – P1, P2 and P3. Vaccine like virus is derived after a spontaneous mutation of the genes of the virus in the polio vaccine.

33. Investigations Plain radiograph and CT With acute infection, no radiographic features are typically evident. Chronically, findings are characterized by atrophy of involved areas, including of bone and muscle, which may be similar to other neuromuscular disorders. MRI Neuroimaging may reveal ALS-like abnormalities in the affected areas of the ventral motor tracts in the spine and/or motor cortex, which are characteristically hyperintense . Extensive fatty muscle atrophy may be seen in affected areas of the musculoskeletal system, which may be unilateral or bilateral. 

34. Treatment No treatment, Supportive measures Prevention - Vaccination: Salk and Sabin vaccination Acute stage: Rest-The child should not be over handled. Isolation Booster dose Nutrition-Diet rich in" Protein". Sister Kenny's Bath: This is a form of moist heat. This helps to resolve inflammation to some extent. Massage should not be given as it may cause more damage due to which the patient may not be able to walk later on

35. Convalescent stage Treatment Muscle Charting. Positioning. Changing the position-Turning the patient every 2 to 4 hours and night prevents bed sores and keeps the skin dry Residual stage treatment Patient is given combination of stretching, strengthening and calliperization . Tailor-made calipers and splints can prevent the deformity from aggravating. Eg ., knee calipers , below knee brace, AFO, KAFO etc.,

36. Orthopaedic operations in patients with residual poliomyelitis The subcutaneous method of division: Hip and knee contractures of over 30 degree – (factor responsible for the deformity in young child is a tight tensor fascia lata and ilio-tibial band. In the older child or adult, other ligamentous and tendinous structures play an important part and must be divided as well) Tendon transfer to re-establish muscle power Muscle transplantation to replace a paralysed muscle Stabilization of relaxed or flail joint Arthrodesis Limb lengthening Joint replacement surgery Ilizarov techniques

37. Rehabilitation Physical therapy Occupational therapy Speech therapy Vocational therapy

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