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Poliomyelitis
Poliomyelitis
Poliomyelitis
Polio= gray matter Myelitis= inflammation of the spinal cord One in 200 infections leads to irreversible paralysis. Among those paralyzed, 5% to 10% die due to respiratory failure. Polio cases have decreased by over 99% since 1988, from an estimated 350 000 cases then, to 1352 reported cases in 2010. In 2012, only three countries (Afghanistan, Nigeria and Pakistan) remain polio-endemic, down from more than 125 in 1988.
Endemic
1988
Importation
2012
It is a viral infection There are three types of poliovirus (P1, P2, P3) It is contagious: usually spread by fecal- oral route. The polio viruses are extremely hardy and can retain infectivity for several days at room temperature. Rapidly inactivated by heat, formaldehyde, chlorine, UV. Only harmful to humans.
Epidemiology
Epidemiology
Most affects children under the age of 5 years in developing tropical countries. Incubation period ranges from 4 to 35 days
Epidemiology
The
most devastating result of polio is paralysis, although 90-95% of infections are in apparent but induce clinical immunity. Non paralytic illness occur in about 5% of all infection with paralytic polio occurring in 1/1000 infections among infants to about 1/100 infections in adolescents. In developed prior to vaccination paralytic polio occurred in adolescents. Conversely in developing countries with poor sanitation infection in life results in infantile paralysis
Poor
sanitation and overcrowding have permitted the continuous transmission in certain poor countries in Africa and Asia
Pathogenesis
Mode of transmission
sanitation, droplet is common mode of transmission during the acute phase of the disease when the virus is in the throat.
5- Indirect contact with articles contaminated with pharyngeal discharge of infected person. Inlet The mouth and nose
Pathogenesis
Entry
in mouth In contact host wild and vaccine strains of polio gain entry via GIT , multiplies in mucosa of small intestine. The virus seeds multiple sites including reticuloedothelial system, brown fat deposits and skeletal muscles Wild polio virus probably accesses the CNS via peripheral nerves. Vaccines strain do not replicate in CNS a feature that accounts for the safety of vaccine strains
The polio virus primarily affects motor neurons in spinal cord and medulla oblongata.
Other
neurons affected are the nuclei in roof of vermis of cerebellum, the substantia nigra, occasionally red nuclei, variable involvement of thalamus, hypothalamic, and pallidal nuclei and motor cortex.
Risk factors
Immune
deficiency Pregnancy Poor sanitation and hygiene Poverty Unimmunized status, especially if <5 years Tonsillectomy: a risk factor for bulbar paralysis. Intramuscular injections or trauma Genetics: No genetic susceptibility has been identified.
Clinical manifestations
Inapparent infection
Paralytic polio
Abortive polio
NonParalytic polio
Response to Infection
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Clinical manifestations
Follow
one of several course In apparent infection (90-95%) Abortive poliomyelitis Nonparalytic poliomyelitis Paralytic poliomyelitis
Inapparent infection
90-95% No
disease No sequelae
Abortive poliomyelitis
5% of patient occurs 1-2 week after infection. Many include fever, pharyngitis, headache, anorexia, nausea, and vomiting. Illness is short Menigoencephalitis in 1% Physical exam is normal Recovery is complete and no neurologic signs.
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Non paralytic
1% Signs
of abortive poliomyelitis are more intense headache, nausea vomiting, stiffness of posterior muscles of neck, trunk, and limbs. Nuchal rigidity and spinal rigidity are the basis of diagnosis. Gentle forward flexion of occiput and neck elicits nuchal rigidity Fleeting paralysis of bladder and constipation are frequent
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Non paralytic
Head
drop present AF tense. Reflexes are normal. Changes in reflex indicate impending paralysis
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Paralytic Poliomyelitis
Paralytic
disease occurs 0.1% of those who become infected with the polio virus. 1)Spinal paralytic poliomyelitis. 2)Bulbar poliomyelitis 3)Polioencephalitis
Paralytic Poliomyelitis
Weakness is clinically detectable only when more than 50% of the nerve cells supplying the muscle have been destroyed.
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phase corresponds to abortive poliomyelitis 2nd phase is spinal paralytic poliomyelitis. Feels better for 2 to 5 days Severe headache, fever, severe muscle pain, sensory and motor phenomena may develop. Distribution of paralysis is characteristically spotty Within 1-2 days AFP occur with involvement of one leg more common followed by involvement of one arm Initially hyperactive DTR followed by diminished or absence of reflexes. Sensation intact
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Bulbar Poliomyelitis
Dysfunction
of cranial nerves and medullary centers, may occur without apparent involvement of spinal cord Clinical findings along with respiratory difficulty include 1)Nasal twang 2)Inability to swallow 3)Absence of effective coughing 4)Nasal regurgitation of saliva and fluids 5)Deviation of palate, uvula & tongue 6)Irregularities of HR, resp. BP, temperature. 7)Paralysis of 1 or both vocal cords.
Bulbar Poliomyelitis
Ascending
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Polioencephalitis
Rare
Seizures,
coma, and spastic paralysis with increased reflexes may be observed. The manifestations are common to any other cause of encephalitis and can be attributed to poliovirus only with specific viral diagnosis or of accompanied by flaccid paralysis
Clinical Evolution
Diagnosis
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Diagnosis
Polio
should be considered in unimmunized or partially immunized child with paralytic disease. VAPP should be considered in any child who has received OPV within 7-14 days. Confirmation by isolation and identification of virus in stools. In suspected AFP cases 2 stool samples should be collected at 24-48 hours apart and sent to WHO certified laboratory for analysis.
Diagnosis
Cerebrospinal Fluid: Leukocytosis, Increased protein, Normal glucose. Serology Obtain stool, blood and throat samples for viral serology, demonstrating a four fold rise in IgG is helpful but not always easy. Positive IgM is diagnostic.
Diagnosis
Electrodiagnostic
Motor
nerve studies: show normal to mildly slowed conduction velocities and low to normal amplitudes. may be helpful to evaluate involvement of anterior horn of the spinal cord or other findings.
MRI
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Condition
Clinical finding
Onset of paralysis
Pleocyt osis
yes
Yes
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Progression of paralysis
GBS
Preceding infection, bilateral facial weakness Preceding Mycoplasma pneumoniae Schistosomas, other parasitic or viral infection
Hours to 10 days
yes
+ -
no
yes
Yes early
yes
yes
The 32nd President of the United States, Roosevelt has been by far the most famous polio survivor in the public mind. However, his age (39 years) and many features of his illness are more consistent with a diagnosis of Guillain-Barr syndrome
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Progression of paralysis
yes
multifactori al
no
no
no
no
Conditi on
Clinical finding
Onset of paralysis
Progression of paralysis
Viral myositis Hypokal meic periodic paralysis Critical illness polyneu ropathy Flaccid limbs and respiratory weakness
pseudo paralysis Proximal limb, respiratory muscle Acute following systemic inflammat ory response syndrome/
no yes + _
no no
Hours to days + _
yes
+ _
no
Treatment
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Treatment
No
specific antiviral treatment All intramuscular injections and surgical procedure are contraindicated. Close monitoring of respiratory and cardiovascular functioning is essential during the acute stage of poliomyelitis along with fever control and pain relievers for muscle spasms. Treatment is symptomatic.
Treatment-Abortive
Analgesics Bed
& sedatives
Treatment-non paralytic
Above
mentioned methods Hot packs & hot tub baths Firm bed Foot board or splint Gentle physical therapy
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Paralytic poliomyelitis
Rest Neutral position of limbs. Active and passive movement of limbs when pain disappears. In pure bulbar poliomyelitis maintain airway. Fluid and electrolyte equilibrium should be maintained by giving IV because in 1st first few days tube or oral feeding may incite vomiting. BP should be monitored because HT is not uncommon Mechanical respirators are often needed
Treatment of polio often requires long-term rehabilitation, including physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery.
Complications
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Complications
Acute
Prognosis
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Prognosis
The
outcome of abortive poliomyelitis, aseptic meningitis syndromes is uniformly good with death being exceedingly rare and with no long term sequelae. In severe bulbar poliomyelitis the mortality is as high as 60%. The recovery phase last for 6 months beyond which persistent paralysis is permanent
In 1960 Summer Olympics in Rome Rudolph became the 1st American woman to win 3 gold medals
Wilma Rudolph ,born prematurely at 4.5 lbs. she contracted infantile paralysis at age 4. She recovered, but wore a brace on her left leg and foot until she was 9. She was required to wear an orthopaedic shoe for support of her foot for another 2years. until she was 12 years old she had also survived bouts of scarlet fever, whooping cough, chickenpox, & measles.
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Risk factors: increasing length of time since acute poliovirus infection, more severe initial polio, presence of permanent residual impairment after recovery from acute illness initial polio at older age, female gender.
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PPS
diagnostic criteria Prior paralytic poliomyelitis History of acute paralytic illness, residual weakness and muscle atrophy on examination, and signs of denervation on electromyography (EMG) Partial or complete functional recovery followed by15 yrs or more of stable neurologic function. New muscle weakness or abnormal muscle fatigability (decreased endurance) with or without generalized fatigue, atrophy, muscle and joint pain. Symptoms should persist for at least one year.
Jonas Salk
Global Eradication
Albert Sabin
only affects humans, there are no known animal reservoirs An effective, inexpensive vaccine is available: Oral Polio Vaccine (OPV) Immunity is life long There are no chronic carriers Half life of excreted virus in the sewage is 48hrs ( spread occurs only during this period)
Global eradication
Global Eradication
WHO
polio Routine immunization National immunization days Acute flaccid surveillance Mop-up immunization
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