93 immunized kids affected by polio in Bihar

Patna, Nov. 5 -- There is some 'very disturbing' news for health planners in Bihar. Of the 98 cases of poliomyelitis detected in Bihar till October 30 this year, 93 children had been administered seven doses of oral polio vaccine (OPV). One child had been given three doses and the vaccination status of the other four kids is unknown. Not surprising therefore, those in the know of things are now passing the buck.

The data, collected under the National Polio Surveillance Programme (NPSP) of the World Health Organisation (WHO), has baffled experts, many of whom have started questioning the usefulness of the OPV. "The latest statistics of polio cases in Bihar is perplexing. Either the affected children suffer from serious immunity deficiency or the OPV has failed to produce required immunity in them," said Dr Gopal Krishna, State immunisation officer. Dr Hemant Shukla, in-charge of the NPSP and WHO representative in Bihar, evaded queries on the data saying: "I am not the authorised person to comment on the issue." Principal Health Secretary CK Mishra could not be contacted despite repeated efforts by HT.

The WHO provides technical support to the polio elimination programme while the United Nations International Children's Emergency Fund (UNICEF) takes care of the social mobilisation aspect of the exercise. The State government executes the work as per the directives issued by the Union Ministry of Health and Family Welfare. "The agencies involved in the programme are groping in the dark," said a senior doctor on condition of anonymity. " Their hit and trial tactics to eradicate the debilitating disease has failed to deliver the goods, " he added. In 2007, when they concentrated on eliminating P1 polio virus, the P3 virus went wild and affected 459 kids. In 2009, when they focused their attention on the P3, the P1 afflicted 34 children.

The alarming rate of growth registered in polio cases also raises serious questions on the quality of teams deployed or whether, all teams shown as deployed are actually there or not. Data now suggests that when anti-polio activity was said to have been intensified in north Bihar, the number of cases abnormally increased in central parts of the State. And when they came to central Bihar, the number of those afflicted rose significantly in north Bihar. In the current year, Saharsa district has reported maximum number of cases (22), followed by Khagaria (15) and Patna (13), the doctor said.
 The agencies have also tried all types of vaccines: monovalent, trivalent etc. to contain the disease. Dr SP Srivastava, former head of department (HoD) of pediatrics, Patna Medical College and Hospital (PMCH), believes that one of the major factors for recurrence of the cases is that the vaccine has failed to act on the changing genetic mutation of the virus.

Dr Sujit Kumar Sinha, president of the Indian Academy of Paediatrics (IAP), Patna chapter, believes that immunity status of the child should be examined before the administration of the OPV. Some other doctors blame poor sanitation and population density for the high incidence of polio. The issue is being taken up at the two-day meeting of the Indian Expert Advisory Group on polio, beginning in New Delhi on Thursday.

There was something of an epidemic of poliomyelitis, or polio for short, in the early 1950s, but it is an old disease; both my parents had mild cases around World War I. In its most severe form it could paralyze or deform the spine, legs or lungs. Nobody knew how the virus was transmitted; public swimming pools came under suspicion for a time, and September was known to be the worst month of the "polio season." And so there was polio insurance, which covered families for the cost of such treatment as was available. But little could be done, then or now, besides physical therapy on paralyzed limbs or the purchase of a respirator machine-known as an "iron lung" -- for paralyzed breathing muscles. Polio's most famous victim was Franklin D. Roosevelt, a paraplegic. He encouraged the work of the March of Dimes, which funded research in the disease, and it was his image that appeared on the new dime issued in 1946. Finally, in 1955, Dr Jonas Salk introduced an effective vaccine, followed by another from Dr. Albert Sabin a few years later, and a nationwide vaccination program transformed polio into a bad memory.

The Polio Crusade

THE POLIO CRUSADE IN AMERICAN EXPERIENCE A GOOD VIDEO THE STORY OF THE POLIO CRUSADE pays tribute to a time when Americans banded together to conquer a terrible disease. The medical breakthrough saved countless lives and had a pervasive impact on American philanthropy that ... Continue reading..http://www.pbs.org/wgbh/americanexperience/polio/

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