NIGERIA: Vitamin A handouts boost polio vaccine acceptance

NIGERIA: Vitamin A handouts boost polio vaccine acceptance
14 Jun 2010 12:40:07 GMT
Source: IRIN
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MAIDUGURI, 14 June 2010 (IRIN) - Campaigns to distribute Vitamin A supplements to reduce high rates of child mortality and morbidity in northern Nigeria have had the unexpected side-effect of encouraging heavily stigmatized polio immunizations in the region.

Helen Keller International (HKI) started administering Vitamin A to children under five in northern Nigerian states in 2001 to protect them against river blindness, which is endemic in some states, including Borno. [http://www.irinnews.org/Report.aspx?ReportId=89167]

Vitamin A can reduce under-five deaths by 30 percent, according to the UN World Health Organization (WHO), and reduce malaria infection rates in children by one-third. [http://www.irinnews.org/Report.aspx?ReportId=85015]
As a result, the treatment tends to be welcomed by parents. Realizing this, health officials and international NGOs started to use Vitamin A to entice parents into accepting the polio vaccine. In 2007, Nigeria's National Council on Health integrated polio vaccines with the government's bi-annual Immunization Plus Days, when inoculations against measles, yellow fever, worms and Vitamin A were also administered.
"The inclusion of Vitamin A as a component of the integrated immunization campaign has helped in polio vaccine acceptance and is helping in the polio eradication drive," Susan Ojomo, UNICEF child survival and development manager in charge of 10 northern states, told IRIN.
Nigeria hopes to eradicate poliomyelitis by 2015 but resistance to the vaccine among some religious groups and traditional leaders in northern states had hampered the fight and led the infection to spread to the country's once polio-free neighbours. [http://www.irinnews.org/Report.aspx?ReportId=87407; http://www.irinnews.org/Report.aspx?ReportId=74624]
"Now almost every household brings its under-fives for polio immunization once it is accompanied by a Vitamin A supplement," local government immunization officer Mamman Isa told IRIN from the town of Biu, 200km south of Maiduguri.
Political commitment
These efforts have made a difference, said Oliver Rosenbauer, spokesman for the WHO Polio Eradication Initiative, but deeper engagement from state authorities and individual religious leaders has also increased acceptance. "We have always had strong political commitment at the national level, but this was inconsistent at the district and local level until last year," he told IRIN.
In 2009, state governors signed up to the "Abuja Commitment to Eradicate Polio." They engaged civil society leaders to ensure vaccinators were carefully selected and well-trained; polio campaigns were well-organized and had the right amount of vaccines. "This has had a real trickle-down effect," he said. [http://www.reliefweb.int/rw/rwb.nsf/db900sid/KHII-7RX9QN?OpenDocument]
At the same time, the Sultan of Sokoto state in the north formed the Traditional Northern Leaders' Forum to try to engage religious and traditional leaders in the fight.
"Resistance was never the only reason there is polio in Nigeria. Before, vaccinators didn't have maps; they didn't have the right number of vaccines; they weren't kept cold enough; and communities weren't engaged in immunizations – to get those fixed, you need this kind of local level leadership," said Rosenbauer.
The number of polio cases has plummeted by 99 percent – from 289 to three – in June 2010 versus June 2009, says WHO.
Polio campaigners must also ensure they achieve 100 percent coverage, warns Rosenbauer. Some 85 out of 700 local government areas in the north are still considered "high or very high-risk", he says; and in some areas 20 percent of children are still being missed. "The [targeting] trend is better, but needs to be built on. If we take our foot off the accelerator - this is an endemic-prone disease and it will come roaring back in no time."

The Polio Crusade

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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