By Dr Poonam Khetrapal Singh, WHO Regional Director for South-East Asia

On the sixth anniversary of the last case of wild poliovirus in the South-East Asia Region, World Health Organization commends countries in the Region for their continued efforts to protect children against this crippling virus and maintain the Region’s polio-free status, despite challenging conditions.
Poliovirus  Image/CDC
Poliovirus Image/CDC
Amid a global shortage of injectable inactivated polio vaccine (IPV), countries in the WHO South-East Asia Region are opting to use fractional doses of IPV, an evidence-based intervention that not only ensures continued protection of children against all types of polioviruses, but also helps save vaccine – a move bound to positively impact global vaccine supply in the coming years.
India became the first country globally to introduce fractional doses of IPV in childhood immunization programme in eight of its 36 states / union territories in early 2016. The initiative is now being scaled up nationwide. Sri Lanka followed suit in July 2016. Bangladesh has decided to introduce fractional IPV doses this year. Other countries in the Region are also considering a shift to the use of fractional IPV doses in their immunization schedule.
Studies have confirmed that two fractional doses (one fractional dose is one-fifth of a full dose) of IPV, given twice to infants – first at the age of six weeks and then at 14 weeks – provide the same protection against all polioviruses as does one full dose of IPV.
By using fractional IPV, countries are saving vaccine and vaccine cost, without compromising on the protection that the vaccine provides to children against polio.
Since polio-free certification on 27 March 2014, all countries in WHO South-East Asia Region have been working towards timely implementation of the global polio end game strategy to achieve a polio-free world.
South-East Asia was the first WHO Region to complete the polio vaccine switch from the traditionally used trivalent oral polio vaccine (tOPV) to the bivalent vaccine (bOPV) to prevent any paralysis caused by type 2 poliovirus strain in tOPV.
As a part of the global polio endgame strategy, countries in the Region have introduced IPV to supplement the oral polio vaccine (OPV), and ensure protection against all types of polioviruses, while the programme globally strives towards stopping poliovirus transmission and cessation of OPV use.
The date – 13 January – the last time that wild poliovirus crippled a child in WHO South-East Asia Region in the year 2011, should be a reminder to all countries of the continued need to reach every child with polio vaccines and to strengthen disease surveillance so that poliovirus does not return to cripple children in our Region.

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    Erradicación de La poliomielitis

    Polio Tricisilla Adaptada

    March Of Dimes Polio History

    Dr. Bruno




    A 41-year-old man developed an acute illness at the age of 9 months during which, following a viral illness with headache, he developed severe weakness and wasting of the limbs of the left side. After several months he began to recover, such that he was able to walk at the age of 2 years and later was able to run, although he was never very good at sports. He had stable function until the age of 18 when he began to notice greater than usual difficulty lifting heavy objects. By the age of 25 he was noticing progressive difficulty walking due to weakness of both legs, and he noticed that the right calf had become larger. The symptoms became more noticeable over the course of the next 10 years and ultimately both upper as well as both lower limbs had become noticeably weaker.

    On examination there was wasting of the muscles of upper and lower limbs on the left, and massively hypertrophied gastrocnemius, soleus and tensor fascia late on the right. The calf circumference on the right exceeded that on the left by 10 cm (figure1). The right shoulder girdle, triceps, thenar eminence and small muscles of the hand were wasted and there was winging of both scapulae. The right quadriceps was also wasted. The wasted muscles were also weak but the hypertrophied right ankle plantar flexors had normal power. The tendon reflexes were absent in the lower limbs and present in the upper limbs, although the right triceps was reduced. The remainder of the examination was normal.

    Figure 1

    The patient's legs, showing massive enlargement of the right calf and wasting on the left


    What is that nature of the acute illness in infancy?
    What is the nature of the subsequent deterioration?
    What investigations should be performed?
    What is the differential diagnosis of the cause of the progressive calf hypertrophy?



    An acute paralytic illness which follows symptoms of a viral infection with or without signs of meningitis is typical of poliomyelitis. Usually caused by one of the three polio viruses, it may also occur following vaccination and following infections with other enteroviruses.1 Other disorders which would cause a similar syndrome but with upper motor neurone signs would include acute vascular lesions, meningoencephalitis and acute disseminated encephalomyelitis.


    A progressive functional deterioration many years after paralytic poliomyelitis is well known, although its pathogenesis is not fully understood.2 It is a diagnosis of exclusion; a careful search for alternative causes, for example, orthopaedic deformities such as osteoarthritis or worsening scoliosis, superimposed neurological disorders such as entrapment neuropathies or coincidental muscle disease or neuropathy, and general medical causes such as respiratory complications and endocrinopathies.3


    Investigations revealed normal blood count and erythrocyte sedimentation rate and normal biochemistry apart from a raised creatine kinase at 330 IU/l (normal range 60–120 IU/l), which is commonly seen in cases of ongoing denervation. Electromyography showed evidence of denervation in the right APB and FDI with polyphasic motor units and complex repetitive discharges, no spontaneous activity in the left calf and large polyphasic units in the right calf consistent with chronic partial denervation. Motor and sensory conduction velocities were normal. A lumbar myelogram was normal. Magnetic resonance imaging (MRI) scan of the calves is shown in figure2.

    Figure 2

    Axial T1 weighted MRI scan (TR 588 ms, TE 15 ms) of the calves, showing gross muscle atrophy and replacement by adipose tissue on the left, and hypertrophy of the muscles on the right, with only minor adipose tissue deposition


    The differential diagnosis of the progressive calf hypertrophy is given in the box.

    Causes of calf muscle hypertrophy

    Chronic partial denervation

    • radiculopathy

    • peripheral neuropathy

    • hereditary motor and sensory neuropathy

    • spinal muscular atrophy

    • following paralytic poliomyelitis

      Neuromyotonia and myokymia

    • Isaac's syndrome

    • generalised myokymia

    • neurotonia

    • continuous muscle fibre activity due to: chronic inflammatory demyelinating polyradiculopathy, Guillain Barre syndrome, myasthenia gravis, thymoma, thyrotoxicosis, thyroiditis

      Muscular dystrophies



    • tumours

    • amyloidosis

    • cysticercosis

      Link here