10/20/2014

Sindh’s latest polio victim received vaccine only once

By Saher Baloch

Published Sep 25, 2014 06:11am
BILAL in the lap of his uncle in their home on Wednesday.—White Star
BILAL in the lap of his uncle in their home on Wednesday.—White Star

KARACHI: Two-year-old Hazrat Bilal looks at people around him with tired eyes. His uncle, Abdul Razzaq, tries to get his attention by calling his name but Bilal looks up for a few seconds before looking away. 
Presently residing in Liaquatabad’s Khamosh Colony, Bilal is one of the five children to have contracted polio recently. 
This is the 14th case in Karachi and 15th across Sindh making its way among the 171 polio cases in Pakistan at present. 
On Wednesday afternoon, the family sat in one of the empty rooms inside their home to discuss what went wrong with Bilal. As his father, Khayal Mohammad, was busy at the roadside restaurant owned by the family, his uncle Abdul Razzaq spoke on his behalf. “He was really ill a month back,” he says as he tries to swaddle Bilal’s lower body with a wrapping sheet. “Our family doctor at the nearest Imam Zainul Abideen Hospital thought that he had got a meningitis fever as his neck arms and upper body had no movement in them. We shifted him to the National Institute of Child Health immediately soon after the doctor asked us to.”
The child had diarrhoea and fever for almost a week before being taken to the hospital, the family says. On being taken to the NICH, the doctors there asked them to wait for a ventilator to be available that alarmed the parents. “He almost made it to the ventilator but was declared ‘out of danger’ after five hours. He was admitted in the hospital for 13 days after that,” says Razzaq. 
During this time, Bilal couldn’t sit properly. His arms were also paralysed for a while until he started making some improvement but he is in a much better condition now. 
His mother Zakiya (last name not given), a 25-year-old woman, however, says that he still cries at night. “He wakes up in the middle of the night and cries till morning, and then there are times that he doesn’t wake up at all,” she says. Sitting in her lap, the child’s left foot is motionless until someone from the family touches it to make a point, making him wince in pain. Bilal is the youngest among Zakiya’s four children. She says, “I gave birth to him at home, back in my village in Tor Ghar tehsil of Khyber Pakhtunkhwa. There are no hospitals over there so he didn’t get immunised. It was only when I brought him to Karachi as a one-year-old that he got polio drops from a polio team that had come to our doorstep.” The mother said that was the only time the child had received the polio vaccine until he got seriously sick a month back. 
The home, where12 more children apart from Bilal live, houses five families, says Razzaq. “We are very scared for them now. Their immunisation was done at a private hospital after we saw what happened to Bilal. We have never refused immunisation by the polio teams. What happened to Bilal was maybe because of the sheer laziness on our part, I think. We thought nothing would happen to him,” he adds. 
The patriarch of the family, Gohar Ali Khan, moved to Karachi in the 1950s from Tor Ghar tehsil. He owns a number of restaurants in Liaquatabad, managed and supervised by his five sons. Sitting in the same room as his family, he quietly eats his lunch at the time of the interview, remarking later, “There were no immunisations during our times, and yet I survived for so long.” On hearing that, his son says that he has had a bypass surgery and is a sugar patient on medicines at the moment. 
The family has been waiting for Bilal’s reports which were sent to the National Institute of Health in Islamabad for further verification, making him, what senior paediatrician Dr Ghaffar Billo calls, a “suspected polio case”. 
Dr Billo says a polio case can be further verified after sending it to the Centre for Disease Control (CDC) in Atlanta, Georgia for gene identification, if the parents want to be completely sure. “But since we don’t have the basic practice of taking children for vaccinations, going for an advanced option like this becomes a luxury availed by only a few people,” he adds. 
Immunisation coverage
About the current crop of cases specifically in Sindh, Dr Billo says the routine immunisation programme till the 1980s “was the best period for Pakistan as it covered 95 per cent of the children. The World Health Organisation started a national immunisation programme worldwide in 1988 but in Pakistan it kicked off in 1994. That period in between, where there was no activity with regard to polio, left the space for the virus to take its hold.” 
Also, since then, he explains, “The population coverage for polio remained between 65 and 75 per cent; whereas it should be 95 per cent otherwise it won’t have the desired impact. So in a way, 35 per cent of our population has always remained uncovered with regard to polio immunisation, be it Fata, KP, Quetta or Qilla Abdullah in Balochistan.” 
In Bilal’s case, he says, “One dose a year won’t make a difference, as it takes at least seven to 10 doses, with proper monthly gaps, to ensure immunity.” 
Executive District Officer for Health Dr Zafar Aijaz says there are around “325 centres for polio immunisation across Karachi. And we, on our part, have been requesting the families to come to these centres to get their children immunised.” 
He insists that it’s not only a job of government hospitals “but community at large to ensure there is awareness about polio”. 
Like Dr Billo, Dr Aijaz also says that routine immunisation “is the main concern of our department. If routine immunisation is properly sustained and followed it will help us fight other diseases too.” 
However, Dr Billo says that unless and until, “There's proper reportage of cases and a genuine utilization of funds we’ll be faced with same problems over and over again.” 
Published in Dawn, September 25th, 2014

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Erradicación de La poliomielitis

Polio Tricisilla Adaptada

March Of Dimes Polio History

Dr. Bruno

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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

Questions

1
What is that nature of the acute illness in infancy?
2
What is the nature of the subsequent deterioration?
3
What investigations should be performed?
4
What is the differential diagnosis of the cause of the progressive calf hypertrophy?

Answers

QUESTION 1

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.

QUESTION 2

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

QUESTION 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

QUESTION 4

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

    Myositis

    Infiltration

  • tumours

  • amyloidosis

  • cysticercosis

    Link here