8/01/2011

There I established a laboratory to study viruses, and to train other scientists to become virologists.



The purpose of this weblog is to teach you about viruses and viral disease. This topic is not one that everyone understands, yet nearly everyone would like to. I was most disturbed when the Secretary of Health and Human Services, Tommy G. Thompson, referred to the anthrax bacillus as a virus. That incident crystallized in my mind the need to better educate the public about viruses.
I am your host at Virology blog - Vincent Racaniello Ph.D., Professor of Microbiology at Columbia University Medical Center. Why am I qualified to teach you virology? I have been studying viruses for over 30 years, starting in 1975, when I entered the Ph.D. program in Biomedical Sciences at Mt. Sinai School of Medicine of the City University of New York. My thesis research, in the laboratory of Dr. Peter Palese, was focussed on influenza viruses. In 1979 I joined the laboratory of Dr. David Baltimore at Massachusetts Institute of Technology, where I did postdoctoral work on poliovirus. In 1982 I joined the faculty  in the Department of Microbiology at Columbia University College of Physicians & Surgeons in New York City. There I established a laboratory to study viruses, and to train other scientists to become virologists. Over the years we have studied a variety of viruses including poliovirus, echovirus, enterovirus 70, rhinovirus, and hepatitis C virus. As principal investigator of my laboratory, I oversee the research  that is carried out by Ph.D. students and postdoctoral fellows. I also teach virology to graduate students, as well as medical, dental, and nursing students.
Since I think about viruses every day, and I have always been interested in teaching others about viruses, this blog seemed to be an ideal forum to convey some of my knowledge on this topic.
Read more http://www.virology.ws/about/

From Polio Australian Incorporate   e-Bulletin , Congratulations for share this excellent link.


Poliomyelitis after a twelve year incubation period 
Virology Blog — 30 June 2011 

Polio this week As of Wednesday 27 July 2011
Wild poliovirus (WPV) cases 



México Post Polio a la vanguardia en el Síndrome de Post Polio

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

video

movie

movie2

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