lecture of 51 slide

1. Acute Flaccid Paralysis
( GBS and Poliomyelitis )
By
Dr . Magdy Shafik Ramadan
Senior Pediatric and Neonatology consultant
M.S, Diploma, Ph.D of Pediatrics

2. Introduction
Acute flaccid paralysis (AFP) is defined as
onset of paralysis ( <4 weeks ) in a child (age < 15
years) for which no obvious cause has been found;
or, a paralysis in a person of any age in whom polio
is suspected.
• The Paralysis is associated with loss of muscle tone
andloss of eflexes.
• Reporting of all AFP cases less than 15 years of age is
mandatory in India.
• All AFP cases should be investigated within 48 hours.

3. Anatomical localization and Etiolgical
agents in Acute Flaccid Paralysis
EtiologyAnatomical site
PoliovirusAnterior Horn Cell
HSV, CMV, rabiesDorsal root ganglia
Acute transverse myelitisSpinal Cord
GBS,,
Vit b12 deficiency, diphtheria, rabies,
Heavy metals,
Hypokalemia
Peripheral nerves
Myasthenia crisis, organophosphorus
poisoning, botulism
Neuromuscular junctionNeuromuscular
junction
Polymyositis, SLE, Lyme diseas,
toxoplasmosis
Muscle

4. Clinical assessment
EtiologyOnset of Paralysis
GBS, traumatic neuritis,
transverse
myelitis, myasthenia crisis,
viral myositis
Within hours to few
days
Polio, Japanese B Encephalitis,
Tick bite
paralysis
Within 2-3 weeks
Lyme disease, Post diphtheritic
polyneuropathy
Weeks to months
RabiesMonths to years

5. DiseaseProgression of
paralysis
Traumatic neuropathyMaximum Deficit at
onset
Poliomyelitis, Japanese
B encephalitis
Hours to few days
GBS, Varicella zoster,
Tick bite paralysis
Up to 2-4 weeks
Lyme disease and
polymyositis
Few weeks to months

6. DiseaseTopography
Poliomyelitis, Japanese B
encephalitis,
Traumatic neuropathy
Asymetric involvement
GBS, Transverse myelitis,
rabies, botulism
Symmetric involvement

7. DiseaseClinical Feature
Neuropathy secondary to
neurotropic viruses (Rabies,
varicella zoster)
GBS
Transverse myelitis
Lyme disease
Traumatic neuropathy
Sensory features
DiseaGBG V ses of AHC, peripheral
nerves and in spinal shock
phase of cord diseases
DTR-Areflexia
Transverse myelitisBladder Bowel involvement
Polio and non polio enteroviruses,
other neurotropic
viruses and occasionaly with
transverse myelitis, viral
myositis
Fever at onset of paralysis

8. Investigations
• Serum Potassium
• MRI Spine with contrast
• NCS, NST and EMG
• CSF Examination
• Serum Creatinine phosphokinase
• Urine for porphobilinogen
• Lyme’s serology

9. Guillain-Barre Syndrome

10. Introduction
.. It is an acute inflammatory demyelinating
Polyradiculo neuropathy
• It is an acute diffuse post-infective disease
causing
generalized paralysis and areflexia.
The average age of incidence is 4-8 years, and rare below
2 years

11. Clinical Features
A progressive ascending, symmetrical paralysis
coming on
over hours, days to a few weeks is the hallmark
of GBS.
Pain and refusal to walk are the presenting
symptoms.
Cranial nerve involvement in 50% cases.
Autonomic manifestations seen in one third
patients

12. Motor weakness:
– Begins in lower limbs and progressively
involves trunk, upper limbs, diaphragm,
respiratory, pharyngeal and laryngeal muscles.
– May also involve lower cranial nerves
– Proximal muscles involved more in limbs.
– Progression of paralysis for 4-10 days.
– Areflexia

13. Consciousness is normal.
Cranial Nerves:
– 7th nerve bilateral involvement is frequently
seen
Sensory symptoms
– No objective sensory loss.
– There may be distal impairment of vibration
and position sense.

14. Lab Features
CSF :
Normal pressure
• Xanthochromic appearance
• Raised CSF protein 1-10 g/l (100-
1000mg/dl)
ALBUMINOCYTOLOGICAL DISSOSCIATION:
•Cell count normal, no pleocytosis
– Proteins : elevated, twice the normal limit

15. Nerve conduction velocity studies.
Electromyography:
Nerve Biopsy
Serum Creatinine kinase may be normal to
elevated

16. Treatment
Supportive care : Ventilation, physiotherpary
IVIG :
Indications:
• Acute GBS of less than 2 weeks
• • Inability to walk unaided
• • Bulbar weakness.
Dose : 0.4mg/kg/day for 5 days

17. Plasmapharesis
Dose : 200-250 ml/kg/bodyweight of plasma
is removed on alternate days in 4-6 sittings
for 8- 12 days.
Complications:
• CVS complication
• Dysautonomia
• Hepatitis and AIDS

18. Poliomyelitis

19. Introduction
Greek poliós= "grey", myelós= marrow, and the
suffix - itis= inflammation
First described by British physician Micheal
Underwood in 1799 referring to it as
"debility of the lower extremities.
Epidemiology:
Poliovirus: belongs to “Picorna” viruses
which are small RNAcontaining viruses. Non
Enveloped.

20. Human is the only reservoir. It multiplies in the
intestine and spreads via faeco-oral route.
The maximum excretion of virus occurs just before
the onset of paralysis and during the first 2
weeks after the onset of paralysis.
However, virus is intermittently excreated for upto
2 months after infection.
Three antigenically distinct serotypes. Type1, 2
and 3

21. Polio virus can remain active for several days at
room temperature and can be stored
indefinitely at -20 degree C.
Most frequent cause of epidemic polio is
Type 1 followed by type 3.
The primary site of replication is small
intestine and regional lymph nodes.
Poliovirus accesses the CNS via peripheral
nerves and primarily infects motor neuron
cells in the spinal cord (the anterior horn cells)
and the medulla oblongata.

22. Infants born to mothers with few antibodies
are protected for a few weeks.

23. Clinical manifestations

24. ACTIVE IMMUNIZATION
Oral (Sabin) Polio Vaccine:
1961 by Albert Sabin, Live attenuated
vaccine.
• Provide both humoral and Mucosal (Gut)
immunity.
Mucosal intestinal immunity prevent
infection with wild polio virus.

25. Intestinal immunity is the main reason why mass
campaigns with OPV can rapidly stop person
to person transmission of wild polio virus.
Immunity probably lifelong.
Shed in stool for up to 6 weeks following
vaccination.

26. Risks associated with use of OPV
Vaccine Associated Paralytic Poliomyelitis:
Those cases of AFP, which have residual
weakness 60 days after onset of paralysis and
from whose stool samples, vaccine related
poliovirus is isolated.
In some recipient of OPV, there is genetic
change ( <1%), in the VP1 gene of vaccine
virus.

27. This minor change turns the vaccine virus
virulent.
Causes paralysis in recipient (recipient VAPP) or
among unimmunized close contacts (contact
VAPP)
1 case of VAPP occurs after 2.3 million first
doses, and after 12 million subsequent doses.

28. Vaccine derived Poliovirus:
There is a greater genetic change (1-15%) in
the VP1 gene of the vaccine virus.
It has potential for human infection and
paralysis.
Types of VDPV :
1) cVDPV (Circulating vaccine derived polio
virus ) : A cVDPV is associated with sustained
person to person transmission and is
circulating in the community under conditions
of low population immunity, with evidence of
causing 2 or more paralytic cases.

29. 2) iVDPV (Immununo deficiency –related
vaccine –derived polio virus) reported in
immunodeficient patients who have
prolonged infections after exposure to OPV.
• 3) aVDPV (ambiguous vaccine derived polio
virus) currently have unclassified source (i.e.,
a single isolate from a healthy or non-
immunodeficient person; environmental
isolates without an associated AFP case).

30. Inactivated (Salk) vaccine:
Developed in 1955 by Dr Jonas Salk.
• Consists of inactivated polio strains of all
three types.
• Excellent humoral immunity.
• Gives Mucosal protection but not mucosal
immunity.
• No risk of VAPP or VDPV.
• 0.5 ml IM or SC or a fractional dose of 0.1ml
Intradermal.

31. National Immunization Schedule:
– bOPV at birth,6-10-14 weeks followed by
booster at 15- 18month.
– IPV at 14 week (0.5ml)
– In some states Fractional doses of IPV at 6 and
14 weeks instead of IM dose.
The IAP Schedule : ‘Sequential IPV-OPV schedule’
– bOPV at birth
– IPV at 6-10-14 weeks
– bOPV at 6 and 9 month
– IPV at 15-18 month
– bOPV at 5 year

32. Pulse Polio Immunization (PPI)
Program
Following the Global Polio Eradication Initiative
of WHO in 1988, GOI conducted the first
round of PPI consisting of 2 immunization
days 6 wks apart on 9th dec 1995 and 20th jan
. 1996

33. Strategy adopted:
The basic strategy for eradicating polio
consisted of:
a) Immunizing every child below 1 year with at
least 3 doses of OPV.
b) National Immunization Days during which
every child below 5 years gets 2 additional
doses of OPV on 2 days separated by 4 to 6
weeks.
c)Surveillance of AFP to identify all reservoirs of
wild poliovirus transmission.

34. • d) Extensive house-to-house immunization
mopping –up campaigns in the final stages
where wild poliovirus transmission per sists.
Key Points :
Targeted all children upto 3 yrs later on WHO
increased the age upto 5 yrs.
PPI occurs in two rounds about 4-6 wks apart
during low transmission season of polio , i.e.
Between nov to feb.

35. These doses are extra dose which supplements
and do not replace the doses received during
immunization services.
• There is no minimum interval between PPI
and scheduled OPV doses.
On 26 May 2012, the World Health Assembly
declared the completion of poliovirus
eradication to be a “programmatic emergency
for global public health” and called for the
development of comprehensive polio endgame
strategy.

36. • In response to this directive, the GPEI
developed Polio Eradication & Endgame
Strategic Plan (PEESP) 2013-2018.
• This strategy shall prevent circulating VDPV
by augmenting the immunity induced by
earlier doses of trivalent OPV.
• By 2019 there shall be complete cessation
of OPV

37. AFP-SURVEILLANCE
Nationwide AFP (acute flaccid paralysis)
surveillance is the gold standard for
detecting cases of poliomyelitis.
• Surveillance identifies new cases and
detects importation of wild poliovirus.

38. The four steps of surveillance are:
1. Finding and reporting children with
AFP.
2. Transporting stool samples for
analysis.
3. Isolating and identifying poliovirus
in the laboratory.
4. Mapping the virus to determine the
origin of the virus strain.

39. Finding and reporting children with acute
flaccid paralysis (AFP) surveillance
1-The first links in the surveillance chain are staff in all
health facilities- from district health centres to large
hospitals.
• 2- They must promptly report every case of AFP in
any child under 15 years of age.
3-The number of AFP cases reported each year is
used as an indicators of a country’s ability to detect
polio-even in countries where disease no longer
occurs.

40. A country’s surveillance system needs to be
sensitive enough to detect at least one case of
AFP for every 100,000 children under 15- even
in absence of polio.

41. Transporting stool samples for
analysis
1-Two stool specimens should be collected at an
interval of 24 to 48 hours apart and within 14 days of
onset of paralysis.
2-However, when AFP cases are seen late (i.e. greater
than 2 weeks after paralysis onset), stool specimen
may be collected up to 60 days after onset of
paralysis.
• 3-The specimen should be placed in a clean
container such as wide mouth plastic or glass bottle
with screw on cap.

42. 4-It need not be autoclaved, but should be
cleaned.
5-At least ‘one thumb sized’ 8 gm of stool is
required.
• 6-Stool sample should be adequate and in
good condition accompanied by all details as
required by laboratories.

43. Isolating Poliovirus
If poliovirus is isolated the next step is to
distinguish between wild and vaccine related.
If wild polio virus is isolated then identify which
of the two surviving types of wild virus is
involved.

44. Mapping The Virus
1- Once wild poliovirus has been identified further tests
are carried out to determine where the strain may have
originated.
2-By determining the genetic makeup of virus, wild virus
can be compared to others and classified into genetic
families which cluster in defined geographic areas.
3-When polio has been pinpointed to a precise geographical
area, it is possible to identify the source of importation of
poliovirus- both long range and cross border

45. Environmental Surveillance
• Environmental surveillance involves testing
sewage or other environmental samples for
the presence of poliovirus.
• Environmental surveillance often confirms
wild poliovirus infections in the absence of
cases of paralysis.
• Systematic environmental sampling provides
important supplementary surveillance data.

47. •‫عام‬ ‫منذ‬ ‫األطفال‬ ‫شلل‬ ‫من‬ ‫خالية‬ ‫مصر‬ ‫أصبحت‬2004.‫وقد‬
‫عن‬ ‫أبلغ‬‫أسيوط‬ ‫مدينة‬ ‫من‬ ‫حالة‬ ‫آخر‬‫أيار‬ ‫في‬/‫مايو‬2004.
‫عن‬ ‫وأبلغ‬‫بيئة‬ ‫عينة‬ ‫آخر‬‫بها‬‫أصلي‬ ‫بري‬ ‫فيروس‬‫في‬‫كانون‬
‫الثاني‬/‫يناير‬2005.‫نهاية‬ ‫وفي‬‫عام‬2008،‫اكتشاف‬ ‫تم‬
‫البيئية‬ ‫البرية‬ ‫الفيروسات‬ ‫من‬ ‫فيروسين‬‫ج‬ ‫من‬ ‫وافدة‬‫نوب‬
‫التوالي‬ ‫على‬ ‫والهند‬ ‫السودان‬.‫؟؟‬
•‫في‬ ‫اكتشفت‬ ‫فقد‬ ،‫السودان‬ ‫شمال‬ ‫من‬ ‫وافدة‬ ‫حالة‬ ‫أحدث‬ ‫أما‬
‫األول‬ ‫كانون‬/‫عام‬ ‫ديسمبر‬2010‫الصرف‬ ‫مياه‬ ‫عينة‬ ‫من‬
‫أسوان‬ ‫مدينة‬ ‫من‬ ‫أخذها‬ ‫تم‬ ‫الصحي‬.

48. ‫الحاد‬ ‫الرخو‬ ‫األطفال‬ ‫شلل‬ ‫ترصد‬
•‫تسعي‬ ‫مطلع‬ ‫منذ‬ ‫الترصد‬ ‫تقارير‬ ‫إعداد‬ ‫في‬ ‫مصر‬ ‫بدأت‬‫نيات‬
‫العشرين‬ ‫القرن‬.‫عام‬ ‫وفي‬1996‫إلى‬ ‫مصر‬ ‫تحولت‬ ،
‫الح‬ ‫تم‬ ،‫الحين‬ ‫ذلك‬ ‫ومنذ‬ ،‫الفيروسية‬ ‫الحاالت‬ ‫تصنيف‬‫على‬ ‫فاظ‬
‫معاي‬ ‫حدود‬ ‫في‬ ‫الحاد‬ ‫الرخو‬ ‫األطفال‬ ‫شلل‬ ‫ترصد‬ ‫مؤشرات‬‫ير‬
‫للمنظمة‬ ‫النموذجية‬ ‫اإلشهاد‬.

50. Jonas Salk Albert Sabin
George Guillain
Jean Barre
Thanks.