[Solomon T, Kneen R, Dung NM, Khal1h Vc, Thuy TTN, Ha DQ et al. Poliomyelitis-like illness due to Japanese encephalitis virus. Lancet 1998; 351: 1094-1097].
The study was conducted in 22 consecutive Vietnamese children who presented with acute flaccid paralysis. These children had rapid onset of weakness in one or more limbs, hyptonia, reduced or absent tendon reflexes and no upper motor neuron sign. After clinical assessment at inclusion in the study, all children were subjected to routine assessment of blood and cerebrospinal fluid (CSF) biochemical parameters. Virological cultures and antiviral antibody measurements were performed in serum, CSF and feces. For viological study, 88 age-matched children with diphtheria were also recruited. A year later children were reassessed clinically and electrophysiological (electromyography and nerve conduction) studies were done.
On observation, out of 22 selected children, 12 had virological evidence of Japaneseencephalitis virus (JEV) infection, eight had no evidence of JEV infection, and in two the results were non-diagnostic. Among control patients' only one had virological evidence of JEV infection. In only one patient among non-diagnositc result wild poliovirus type-l was isolated: In JEV infected children onset of weakness was more rapid, asymmetrical and was less likely to involve upper limbs. In these children the acute flaccid paralysis was more profound, and was followed by a short febrile prodromal illness. Seven of the eight
JEV negative patients fitted in to the Asbury's criteria(1) of Guillian-Barre syndrome compared with one of the 12 JEV
infected patients. Subsequent development of features suggestive of encephalitis (coma, convulsions, extrapyramidal. manifestations and up going plantar reflex) and meningeal inflammation (nuchal rigidity, stiff spine and CSF pleocytosis) were observed more frequently (four patients) in JEV infected children; only one of JEV negative patient had these manifestations. Bulbar paralysis, involvement of other cranial
nerves and evidence of autonomic involvement (transient hypertension) was more frequent in JEV-negative
patients. However, equal number of patients in both the groups had evidence of
respiratory paralysis. Mortality was observed only in JEV-negative patients as two patients died due to respiratory paralysis. At the time of discharge higher number patients among JEV infected group could not walk. Thirteen (eight JEV positive) of the 18 survivors returned for follow-up. Patients with JEV infection had greater disability and were more likely to have asymmetric muscle wasting (all eight patients) while JEV-negative
children (two of five) had symmetrical wasting. Nerve conduction studies and
electromyography were suggestive of anterior horn cell involvement in JEV-positive group. However, two out of 5 JEV-negative children had electrophysiological evidence of previous demyelinating polyneuropathy.
Acute flaccid paralysis is the term used in public health programs to identify suspected patients with paralytic disease consistent with acute poliomyelitis. It is
characterized by rapid onset of weakness of limbs, often with weakness of respiratory muscles and difficulty in swallowing, progressing to maximum severity within 1- 10 days. In some developing countries the incidence of acute flaccid paralysis remains high despite decrease in the proportion of virologically confirmed poliomyelitis(2). Paralytic disease due to enteroviruses other than poliovirus occurs sporadically and is usually less severe than poliomyelitis. Most cases are due to enterovirus 70 to 71(3) or to coxsackie virus A7. Gullian-Barre syndrome is also associated with entero-virus infections. Polio like illness has been observed in some young adult cases of acute hemorrhagic conjuctivitis caused by enterovirus 70, during epidemics. Mumps virus may occasionally be associated with transverse myelitis and Gullian-Barre syndrome and present with acute flaccid paralysis. In certain circumstances oral polio-vaccine (OPV) can cause acute flaccid paralysis. The risk of developing polio-myelitis after OPV is estimated at 1 case per 2.5 million doses administered. The risk of developing paralytic disease after OPV is about 2000 times higher among immuno-deficient children. Intramuscular injections during the first month after vaccination are associated with high risk of vaccine-associated paralysis(4). Whether there is an in- creased risk of Gullian-Barre syndrome following OPV is controversial(5).
Clinically poliomyelitis is quite difficult to distinguish from other causes
of acute flaccid paralysis. Oostvogel et al.(6) observed fever to be a good parameter to distinguish poliomyelitis from other infectious diseases or Gullian-Barre syndrome.
Other Causes of Acute Flaccid Paralysis in Children
1. Transverse myelitis
2. Gullian-Barre syndrome
" Axonal" variety
3. Post-injection sciatic
3. Diphtheric polyneuropathy
5. Human rabies and post-rabies vaccine
In this article Solomon et al. from Vietnam discovered a totally new viral cause for acute flaccid paralysis in children. The clinical features were similar to that of poliomyelitis, and they thought it to be an
important factor for continuing high incidence of acute flaccid paralysis in this region. In endemic areas like India where Japanese encephalitis as well as poliomyelitis still have a very high incidence, it will be difficult to differentiate between these two diseases on clinical grounds alone. However, presence of urinary retention, pyramidal
tract signs and encephalitis are rare complications of poliomyelitis, and will suggest possibility of JEV infection producing acute flaccid paralysis. Another important implication of this study is that JEV
infection in children can produce damage to the anterior horn cells of spinal cord, as is seen in patients of poliomyelitis. Whether long-term complications of poliomyelitis (like post-polio syndrome) are also associated with JEV
infection, would be interesting to know, as a large number of patients with progressive and non-progressive asymmetrical muscle wasting are frequently encountered in neurology practice of a JEV endemic area.
In his comment on this paper Arya(7) suggested that the CNS involvement in these patients should have been documented by magnetic resonance imaging (MRI) of brain and spinal cord. Wakamato et al.(8) earlier had observed MRI abnormalities in the dorsal region of the pons to the upper part of the thoracic spinal cord in a 7 month old infant with poliomyelitis like illness. There were hypointense T-l weighted lesions with bilateral anterior horn involvement MRI may prove valuable in detecting target neurons in brain or spinal cord that were likely to be affected in Japanese encephalitis virus.
Thus, acute flaccid paralysis is a syndrome with several possible causes and will continue to occur world-wide even after complete eradication of poliovirus. Japanese encephalitis virus, which is known to produce severe meningo-encephalomyelitis, should also be considered in the differential diagnosis of patients with polio-like illness in endemic areas.
Ravindra Kumar Garg,
Department of Neurology,
Institute of Medical Sciences,
Banaras Hindu University,
Varanasi,221 005, India.
Asbury AK. Diagnostic considerations in Gullian-Barre syndrome. Ann Neurol
1981; 9(Suppl): 1-5.
Tangermann RB, Bilous J,Maher C, Aylword, Schnur A, Sato Y, et al. Poliomyelitis eradication in the western Pacific
Infect Dis 1997; 175 (Suppl) S97-
Melnick JL. Enterovirus type 71 infection: A varied clinical pattern sometimes mimicking paralytic poliomyelitis. Rev Infect Dis 1994; 6 (Suppl-2): S387-S390.
Strebel PM, lon-Nedelcu N, Baughman AL, Sutter RW, Cochi SL. Intramuscular . injections within 30 days of immunization with oral poliovirus vaccine: A risk factor for vaccine-associated paralytic poliomyelitis. N Engl
Med 1995; 332: 500-505.
Salisbury DM. Association between oral poliovaccine and Gullian-Barre syndrome? Lancet 1998; 351: 79-80.
Oostvogal PM, Conyn-van Spaendon .CK, Hirasing RA, van Loon AM. Surveillance of acute flaccid paralysis in the Nether- lands, 1992"1994. Bull WHO 1998; 76: 55- 62.
Arya Sc. Japanese encephalitis virus and poliomyelitis like illness. Lancet 1998; 351: 1964.
Wakamato H, Marimato T, Nagao H, Matsuda H. MRI in polimyelitis-like syndrome. Pediatr Radial 1992; 22: 533- 534..
[Shatrugna V, Raman L, Uma K, Sujatha T. Interaction between
vitamin A and iron. Effects of supplements in pregnancy. Internat
1997; 67: 145-148].
The present study was carried out to assess the vitamin A status and effect of
vita- min A and iron supplementation on vita- min A levels during pregnancy in
rural women. Two hundred and eighty two pregnant women at different weeks of
gestation attending rural health center were recruited for investigations.
Baseline vitamin A status was assessed in fasting blood samples of these women.
Of these, 145 vitamin A supplementation in form of vita- min A fortification of
sugar has a positive impact on iron metabolism and nutrition without change in
intake of iron(4). There are studies which suggest that vitamin A deficiency
results in anemia and supplementation of vitamin A improves hemoglobin levels in
Further from the present report and previous. studies(1,2,4,5) it is apparent
that understanding interactions between different vitamins and minerals during
pregnancy have practical implications for formulating large scale
supplementation programmes in the community.
Kalawati Saran Chidren's Hospital
and Lady Hardinge Medical College,
New Delhi 110 001,
1. Panth M, Shatrugna V, Yasodhara P, Sivakumar B.
Effect of vitamin A supplementation on hemoglobin and vitamin A
levels during pregnancy. Brit J Nutr 1990; 64: 351-358.
2. Venkatachalam PS, Belavaday B, Gopalan C. Studies of vitamin A nutritional
status of mothers and infants in poor communi- ties of India. J Pediatr 1962;
3. Guha DK, Walia BNS, Tondon BN, Deo MG, Ghai OP. Small bowel changes in iron
deficiency anemia in childhood. Arch Dis Child 1968; 43: 239-244.
4. Mejia LA, Arroyave G. The effect of vitamin A fortification of sugar on iron
metabolism in preschool children in Guate-mala. Amer J Clin Nutr 1977; 30: 1175-
5. Mohanram M, Kulkarni KA, Reddy V. Hematological studies in vitamin A
deficient children. Internat J Vit Nutr 1977; 47: 389-393.