Journal of Postgraduate Medicine
 Open access journal indexed with Index Medicus & ISI's SCI  
Users online: 2479  
Home | Subscribe | Feedback | Login 
About Latest Articles Back-Issues Articlesmenu-bullet Search Instructions Online Submission Subscribe Etcetera Contact
 
  NAVIGATE Here 
  Search
 
 :: Next article
 :: Previous article 
 :: Table of Contents
  
 RESOURCE Links
 ::  Similar in PUBMED
 ::  Search Pubmed for
 ::  Search in Google Scholar for
 ::Related articles
 ::  [PDF Not available] *
 ::  Citation Manager
 ::  Access Statistics
 ::  Reader Comments
 ::  Email Alert *
 ::  Add to My List *
* Registration required (free) 


  IN THIS Article
 ::  Introduction
 ::  Case report
 ::  Discussion
 ::  Acknowledgement
 ::  References

 Article Access Statistics
    Viewed4473    
    Printed68    
    Emailed3    
    PDF Downloaded0    
    Comments [Add]    

Recommend this journal


   
Year : 1984  |  Volume : 30  |  Issue : 1  |  Page : 57-9

Is there a recrudescence of poliomyelitis? (a case report).







How to cite this article:
Dalvi S G, Bhatt A D, Parab M H. Is there a recrudescence of poliomyelitis? (a case report). J Postgrad Med 1984;30:57


How to cite this URL:
Dalvi S G, Bhatt A D, Parab M H. Is there a recrudescence of poliomyelitis? (a case report). J Postgrad Med [serial online] 1984 [cited 2020 Nov 27];30:57. Available from: https://www.jpgmonline.com/text.asp?1984/30/1/57/5495




  ::   Introduction Top

Poliomyelitis is a disease of infantile age. However, the disease has shown a rising incidence in adults in the western countries. We commonly come across this disease in children but it is rarely encountered in adults in our country. Because of its infrequency in adults it becomes important to discuss its clinical, immunological, and epidemiological significance. Hence, we report here a case of poliomyelitis affecting a young man of 25 years.

  ::   Case report Top

K.A., a 28 year old male, developed fever with chills and shooting pain in the right lower limb for which he was given an intramuscular injection in the right thigh. Two days later he noticed weakness of the right lower limb followed by weakness of the left lower limb. He developed transient constipation and difficulty in passing urine, which disappeared in a day after his admission on 25th April 1981. There was no history of taking any vaccinations in the recent past or childhood.
His physical examination revealed bilateral flaccid paraplegia with grade 0 power. He had areflexia in the lower limbs and plantars were absent. There were no fasciculations and there was no sensory impairment. At this stage he was thought to have either spinal cord lesion in a stage of shock or anterior horn cell or anterior root lesion. In view of the febrile episode at the onset an infectious aetiology was considered.
Investigations showed a normal haemoglobin and blood count. His urine, stool, BUN, blood sugar and serum electrolyte values were normal. Dorso-lumbar spine X-rays were normal. Cerebrospinal fluid done on 28-4-1981 revealed 24 mg% proteins, 92 mg% sugar, 720 mg% chlorides and 28 lymphocytes on smear. The colloidal gold curve was normal. CSF and blood VDRL were negative.
The clinical picture remained unchanged for a month. An electromyographic examination done showed an anterior horn cell lesion. Repeat spinal fluid examination on 4-6-1981 showed 49 mg% proteins with 1 lymphocyte. Viral studies failed to reveal any antibody in the C.S.F. but blood showed positive antibodies to poliovirus type I in a titre of 1:32, type II in a titre of 1:128 and type III in a titre of 1:128. Since the clinical picture and EMG suggested an anterior horn cell lesion following an infectious process, a possibility of. poliomyelites was considered, which was confirmed by the repeat viral studies after 6 weeks, which showed a 16 fold rise in the titre of antibodies to poliovirus type I, the new value being 1:512. The other two poliovirus antibodies did not show any rise and remained at 1:128.
His course in the ward with passive and active physiotherapy and assisted mobilization showed steady improvement in the muscle tone and power and the patient could walk with minimal support. He was discharged 14 weeks after the onset of the illness.

  ::   Discussion Top

This patient showed anterior horn cell disease with a rising antibody titre against poliovirus type I suggesting infection by poliovirus type I.[5] Acute poliomyelitis in our country is believed to be confined to infantile age. Hence this occurrence of disease in an adult brings out certain important points.
The history of poliomyelitis began with its description as a children's or infant's disease, the disease occurring rarely after the age of 25 years. The propencity of infants to develop this disease is attributed to falling maternal antibody titres and rising opportunities for virus contact in unhygienic areas. The relative immunity of adults in our country is due to appearance and persistence of neutralising antibodies to virus, following a single or repeated subclinical infection.[4]
The behaviour of the disease in our country till now confirms to the cases observed in the highly developed countries during the last century. However, during the last two decades the trend has changed in the developed countries. During and after the second world war, the incidence rose steadily in adults.[2] In the city of New York, Sabin noticed a rising incidence of poliomyelitis in the age group of 5-9 years between 1916 and 1944.[10] By 1944, Copenhagan had 53% of poliomyelitis cases occurring in adolescents of 15 years and above.[3] Olin observed a similar trend in Sweden between 1905 and 1950.[7]
The features of this adult poliomyelitis are different from the infantile disease in the following way[5]:
1. Biphasic course i.e. minor illness followed by major episode is unusual in adults.
2. Adults have a gradual onset of vague symptoms and a long prodromal period lasting upto a week.
3. More often, the disease is severe in adults. There is a greater frequency of pain, quadriparesis and respiratory muscle paralysis. Bulbospinal disease is common after 30 years and hence mortality is higher.
4. Females are more commonly and severely affected after the age of 15 years. Males run a milder course.
The mild course with good recovery in our patient does confirm the last two observations. However, the onset of the disease at this late age may be due to following factors. The patient was never immunised in childhood or was never exposed to minor infection. However "most normal subjects above a certain age have at least one type of neutralising antibody despite lack of history of clinical manifestations of poliomyelitis."[3] In 1952, Banker noticed that 90% of our population above 4 years of age have positive antibodies.[1] Studies in Eskimos have shown persistence of antibodies upto 30-40 years.[8] If our patient also had such persistent antibody titres, then the present episode signifies a new infection with poliomyelitis type I virus. This possibility raises certain new epidemiological problems.
1. Are we heading towards the western trend with improvement in child health and immunisation? The implications of above observations in western countries suggest that with development towards higher standards and better awareness of hygienic conditions in more and more countries, they too may experience epidemics of poliomyelitis of increasing severity affecting, on an average, older and older age group.[9] If this trend follows in our country, we will face an economic crisis with increasing number of man hours lost from work and rising number of physically handicapped.
2. Is there a recrudscence of poliomyelitis? Our viral studies in a female patient with similar clinical and electromyographic findings did not show a rising titre against poliomyelitis. Hence the answer to this problem at this stage is not possible and requires further detailed epidemiological work.
3. In 1969, Melnick et al[6] observed the titres to be declining in 20-30% of immunised children over a period of 5 years. Hence, booster doses are required to maintain a protective level of antibodies. This has been already recommended by American Academy of pediatrics.[6],[11] In view of these observations should there be a booster dose/immunisation programme against poliomyelitis for adults?

  ::   Acknowledgement Top

We are thankful to Dr. C. K. Deshpande, Dean, K.E.M. Hospital and Seth G.S. Medical College, for permission to publish the paper.

  ::   References Top

1.Banker, D. D.: Preliminary observations on antibody patterns against certain viruses among inhabitants of Bombay City. Ind. J. Med. Sci., 6: 733-745, 1952.  Back to cited text no. 1    
2.Brain, L. and Walton, J. N.: "Brains Disease of The Nervous System," 7th Edition, E.L.B.S. and Oxford University Press. London, 1969, p. 453.  Back to cited text no. 2    
3.Debre, R. and Cellars, I.: "Clinical virology. The Evaluation and Management of Human Viral Infections". W. B. Saunders Company, Philadelphia, London and Toronto, 1970.  Back to cited text no. 3    
4.Gear, J. H. S.: Distribution of antibodies to poliomyelitis virus in general population. In, "Papers and Discussions" presented at the Third International Poliomyelitis Conference, J. B. Lippincott and Co., Philadelphia, 1955, p. 138-139.  Back to cited text no. 4    
5.Horsefall, F. C. and Tamm, I.: "Virus and Rickettsial Infections of Man." 4th Edition, J. B. Lippincott and Co., Philadelphia, 1965.  Back to cited text no. 5    
6.Melnick, J. L., Burckhardt, M., Taber, C. H. and Erckman, P. L.: Developing gap in immunity to poliomyelitis in an urban area. J. Amer. Med. Assoc., 209: 1181-1185, 1969.  Back to cited text no. 6    
7.Olin, G.: The epidemiological pattern of poliomyelites in Sweden from 1905 to 1950. In, "Papers and Discussions". presented at the Second International Poliomyelites Conference, J. B. Lippincott Company, Philadelphia, 1952, pp. 357-375, cited by Debre' and Cellars.[3].   Back to cited text no. 7    
8.Paul, J. R., Riorden, J. T. and Melnick, J. L.: Antibodies to 3 different antigenic types of poliomyelitis virus in sera from North Alaskan Eskimos. Amer. J. Hyg. 54: 275-285, 1951. Quoted in "Papers and Discussions" presented at the Third International Poliomyelitis Conference, J. B. Lippincott Company, Philadelphia, 1955, p. 146.  Back to cited text no. 8    
9.Payne, A. M. M.: Poliomyelitis as a world problem. In, "Papers and Discussions" presented at the Third International Poliomyelitis Conference, J. B. Lippincott Company, Philadelphia, 1955, p. 393-400.  Back to cited text no. 9    
10.Sabin, A. B.: Epidemiological pattern of poliomyelitis in different parts of the world. In, "Papers and Discussions." Presented at the First International Poliomyelitis Conference, J. B. Lippincott Company, Philadelphia, 1949, pp. 3-33, Cited by Debre and Cellars.[3]  Back to cited text no. 10    
11.Weinstein, L.: Poliomyelitis-a persistent problem. New Engl. J. Med., 288: 370-372. 1973.  Back to cited text no. 11    

Top
Print this article  Email this article
Previous article Next article
Online since 12th February '04
2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
Published by Wolters Kluwer - Medknow