Poliomyelitis: A Comprehensive Overview of the Disease

Poliomylitis
 
Dr. Abbas
 
Etiology
 
 
Epidemiology
Paralysis is the most devastating effect of polio
virus infection
Although 90-95 % infection-subclinical
Eradicated in most of countries
except Nigeria, Afghanistan and
Pakistan
Universal vaccination
strategy and improved
sanitation: key factor in
eradication
 
Transmission
 
Pathogenesis
Pathogenesis(contd..)
Vaccine strain of polio do not
replicate in CNS.
 
Reversion occur in small
intestine and reaches to CNS
via. Peripheral nerves
 
                                      Infection
Traverse neural pathways and multiple site within CNS
Perineural inflammation and destruction
Petachial hemorrhages and  inflammatory edema
Primarily infect motor neuron in anterior horn cells and medulla
oblongata(cranial nerve nuclei)
Involvement of reticular formation that controlled vitals may have
catastrophic out come
Pathogenesis(contd..)
 
Involvement of dorsal horn
and  dorsal root ganglias of
spinal cord results in
hyperesthesia and
myalgias:typical of acute
polimyelitis
Other neuron  affected are the
nuclie in the vermis of
cerebellum, substantia
nigra,thatmus,hypothalmus
 
Clinical features
I.P- 8-12 days ,ranges from 5- 35 days
Infection with wild polio virus may follow several courses
 
 
Abortive  poliomyelitis
Non specific flu like illness.
phgysical examination
: non specific pharyngitis,
abdominal or muscular tenderness and weakness
Recovery : complete without sequelae
 
 
Non- Paralytic poliomyelitis
Sign of abortive poliomyelitis but more intense
Headache, nausea, vomiting , sore throat, neck & spinal rigidity,
fleeting paralysis of bladder and constipation.
Changes in Reflexes may precede before onset of paralysis
.
Superficial reflexes, cremastric, abdominal  and reflexes of
,spinal, gluteal muscle.
Spinal and gluteal reflexes disappear before other reflexes
.
Changes in DTR occur after 8-24 hrs after superficial reflexes
diminished.
DTR are absent with paralysis
Sensory defect don’t occur in poliomyelitis
Recovery : complete
 
Paralytic poliomyelitis
Spinal
Bulbar
Encephalitis
Paralysis
Appears  3-8days after the initial symptoms
Clinical features of paralytic polio
caused by wild or vaccine strain
are comparable
Spinal paralytic polio
 ist phase
Symptoms similar to abortive polio
Patient appear to feel better for 2-5 days
Biphasic disease
Severe headache and fever and exacerbation of previous symptoms.
Severe muscle pain sensory and motor phenomenon.
Physical examination: distribution of paralysis characteristically
spotty
After 1-2 days asymmetric  flaccid paralysis occur
Involvement of 1 leg is most common , followed by involvement of
1 leg and 1 arm
Proximal areas of the extremities tend to be involved to a greater
extent.
 
Polio Paralysis
Some  times biphasic phase
absent.
50-60% cases  h/o IM
injection before
paralysis(provocation
paralysis)
Paralysis start .
Little recovery from paralysis
noticed during ist  few days
but not beyond 6 months.
Return  of strength and
reflexes is slow and & may
continue to improve as long as
18 months after the acute ds.
Atrophy of limb ,growth
failure and deformity  finally
evident
 
 
Bulbar Polio
Dysfunction of cranial nerve and medullary
centers without involving spinal cord
Respiratory difficulty, paralysis of extraoccular, facial and
masticatory muscles.
1-nasal twang to the voice or cry.
2-inability swallow smoothly ,
3-absence of effective coughing
4-nasal regurgitation of saliva
5-deviation of palate, uvula, tongue
6-involvement of vitals centre in the medulla
7-paralysis of 1 or both vocal cords
8- Rope sign
: acute angulations b/w chin and larynx
caused by weakness of hyoid muscle
 
 
Polioencephalitis
Rare form of disease
Higher centre of brain
severely involved
Seizure, coma ,spastic paralysis,
irritability, disorientation,
drowsinesss,cranial nerve paralysis,
deaths
 
 
Diagnosis
Paralysis in any unimmunized or partially immunized
children
VAPP  should be considered in any child with paralysis
developed 7-14 days after receiving OPV.
Combination of fever ,headache, neck
and back pain,assymmetric flaccid
paralysis without sensory loss.
WHO recommends lab diagnosis of polio must be done by
isolation and identification of polio virus in the stool ,with
specific identification of wild –type and vaccine strains.
In suspected of poliomyelitis two stool sample
collected 24-48 hrs apart
80-90% isolation of virus  in acute phase.
< 20% isolation b/w 3-4 weeks
Ideally 8-10gm stool sample
Proper cold chain
 
 
Differential diagnosis
All causes of acute
flaccid paralysis
 
 
AFP
Paralysis of acute onset i.e less than 4weeks and
affected limbs are floppy or flaccid or limp.
Tone diminished, DTR  diminished.
Sensation not affected
Case definition
: any child aged less than 15yrs
who has acute onset flaccid paralysis for which
no obvious cause(severe trauma, electrolyte
imbalance) is found or paralytic illness in a
person of any age in which polio is suspected
AFP
causes
Disorder of muscle: e.g.
polymyositis, viral myositis
 
Treatment
 
             only     
supportive
 
Prevention
 
WHO recommends 4 strategy for global
eradication of polio-
1-routine vaccination
2-NIDs
3-AFP surveillance
3- Mop-up immunization
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Poliomyelitis, commonly known as polio, is caused by a non-enveloped, positive, single-stranded RNA virus belonging to the Picornaviridae family. Paralysis is the most severe consequence of polio infection, with transmission occurring through the fecal-oral route. The virus primarily infects the GI tract before spreading to the central nervous system, leading to devastating effects. Vaccination and sanitation play a crucial role in eradicating the disease, which has been successful in most countries but remains endemic in Nigeria, Afghanistan, and Pakistan.


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  1. Poliomylitis Dr. Abbas

  2. Etiology Non- enveloped,positiv e ,single sranded R.N.A virus Picornaviridae, genus - enterovirus 3- serotypes- 1,2,3 Sensitive heat and light

  3. Epidemiology Paralysis is the most devastating effect of polio virus infection Although 90-95 % infection-subclinical Universal vaccination strategy and improved sanitation: key factor in eradication Eradicated in most of countries except Nigeria, Afghanistan and Pakistan

  4. Transmission virus excreted in feces 2weeks before the onset of paralysis to several weeks after the onset of symptoms Human are only reservoir Spread by feco- oral route

  5. Pathogenesis Infection via GI tract Primary site of infection M cells of mucosa Wild type polio viruses reaches CNS along peripheral nerves Regional lymph node Virus seeds multiple sites :RE systems, brown fat,skeletal muscle Primary viremia after 2-3 days

  6. Pathogenesis(contd..) Vaccine strain of polio do not replicate in CNS. Occasional revertants(by nucleoside subtitution) of these vaccine strain developed a neurovirulent phenotype and cause Vaccine acquired paralytic poliomylitis Reversion occur in small intestine and reaches to CNS via. Peripheral nerves

  7. Pathogenesis(contd..) Infection Traverse neural pathways and multiple site within CNS Perineural inflammation and destruction Petachial hemorrhages and inflammatory edema Primarily infect motor neuron in anterior horn cells and medulla oblongata(cranial nerve nuclei) Involvement of reticular formation that controlled vitals may have catastrophic out come

  8. Involvement of dorsal horn and dorsal root ganglias of spinal cord results in hyperesthesia and myalgias:typical of acute polimyelitis Other neuron affected are the nuclie in the vermis of cerebellum, substantia nigra,thatmus,hypothalmus

  9. Clinical features I.P- 8-12 days ,ranges from 5- 35 days Infection with wild polio virus may follow several courses Inapparant Abortive Non-paralytic Paralytic 90-95% 5% 1% 0.1%

  10. Abortive poliomyelitis Non specific flu like illness. phgysical examination: non specific pharyngitis, abdominal or muscular tenderness and weakness Recovery : complete without sequelae

  11. Non- Paralytic poliomyelitis Sign of abortive poliomyelitis but more intense Headache, nausea, vomiting , sore throat, neck & spinal rigidity, fleeting paralysis of bladder and constipation. Changes in Reflexes may precede before onset of paralysis. Superficial reflexes, cremastric, abdominal and reflexes of ,spinal, gluteal muscle. Spinal and gluteal reflexes disappear before other reflexes. Changes in DTR occur after 8-24 hrs after superficial reflexes diminished. DTR are absent with paralysis Sensory defect don t occur in poliomyelitis Recovery : complete

  12. Paralytic poliomyelitis Spinal Bulbar Encephalitis Paralysis Appears 3-8days after the initial symptoms Clinical features of paralytic polio caused by wild or vaccine strain are comparable

  13. Spinal paralytic polio Biphasic disease ist phase Symptoms similar to abortive polio Patient appear to feel better for 2-5 days Severe headache and fever and exacerbation of previous symptoms. Severe muscle pain sensory and motor phenomenon. Physical examination: distribution of paralysis characteristically spotty After 1-2 days asymmetric flaccid paralysis occur Involvement of 1 leg is most common , followed by involvement of 1 leg and 1 arm Proximal areas of the extremities tend to be involved to a greater extent.

  14. Polio Paralysis Some times biphasic phase absent. 50-60% cases h/o IM injection before paralysis(provocation paralysis) Paralysis start . Little recovery from paralysis noticed during ist few days but not beyond 6 months. Return of strength and reflexes is slow and & may continue to improve as long as 18 months after the acute ds. Atrophy of limb ,growth failure and deformity finally evident

  15. Bulbar Polio Dysfunction of cranial nerve and medullary centers without involving spinal cord Respiratory difficulty, paralysis of extraoccular, facial and masticatory muscles. 1-nasal twang to the voice or cry. 2-inability swallow smoothly , 3-absence of effective coughing 4-nasal regurgitation of saliva 5-deviation of palate, uvula, tongue 6-involvement of vitals centre in the medulla 7-paralysis of 1 or both vocal cords 8- Rope sign: acute angulations b/w chin and larynx caused by weakness of hyoid muscle

  16. Polioencephalitis Rare form of disease Higher centre of brain severely involved Seizure, coma ,spastic paralysis, irritability, disorientation, drowsinesss,cranial nerve paralysis, deaths

  17. Diagnosis Paralysis in any unimmunized or partially immunized children VAPP should be considered in any child with paralysis developed 7-14 days after receiving OPV. Combination of fever ,headache, neck and back pain,assymmetric flaccid paralysis without sensory loss. WHO recommends lab diagnosis of polio must be done by isolation and identification of polio virus in the stool ,with specific identification of wild type and vaccine strains.

  18. In suspected of poliomyelitis two stool sample collected 24-48 hrs apart 80-90% isolation of virus in acute phase. < 20% isolation b/w 3-4 weeks Ideally 8-10gm stool sample Proper cold chain

  19. Differential diagnosis All causes of acute flaccid paralysis

  20. AFP Paralysis of acute onset i.e less than 4weeks and affected limbs are floppy or flaccid or limp. Tone diminished, DTR diminished. Sensation not affected Case definition: any child aged less than 15yrs who has acute onset flaccid paralysis for which no obvious cause(severe trauma, electrolyte imbalance) is found or paralytic illness in a person of any age in which polio is suspected

  21. AFP causes Anterior horn cells disorder Disoreder of neuromuscu lar junction Metabolic disorder Acute traumatic neuritis e.g. GB Neuropathi es poliomyelitis,n onpolioenterov irus,west nile virus syndrome e.g. e.G myasthenia gravis hypokalemia Disorder of muscle: e.g. polymyositis, viral myositis

  22. Treatment only supportive

  23. Prevention WHO recommends 4 strategy for global eradication of polio- 1-routine vaccination 2-NIDs 3-AFP surveillance 3- Mop-up immunization

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