Acute encephalitis syndrome (AES) in Bihar’s Muzaffarpur has so far claimed over 110 children. At present, more than 400 children with AES have been admitted to various hospitals. Most of the deaths have been attributed to low blood sugar level (hypoglycaemia).
What is acute encephalitis syndrome (AES)?
Acute encephalitis syndrome or AES is a basket term used for referring to hospitals, children with clinical neurological manifestation that includes mental confusion, disorientation, convulsion, delirium, or coma. Meningitis caused by virus or bacteria, encephalitis (mostly Japanese encephalitis) caused by virus, encephalopathy, cerebral malaria, and scrub typhus caused by bacteria are collectively called acute encephalitis syndrome. While virus or bacteria cause all the other conditions, encephalopathy is biochemical in origin and hence very different from the rest.
There are different types of encephalopathy. In the present case, the encephalopathy is associated with hypoglycaemia and hence called hypoglycaemic encephalopathy.
Is encephalitis different from hypoglycaemic encephalopathy?
Yes, the two conditions are very different and show very different symptoms and clinical manifestations.
Fever on the very first day is one of the symptoms of encephalitis before the brain dysfunction begins. While fever is seen in children in the case of hypoglycaemic encephalopathy, fever is always after the onset of brain dysfunction (actually due to brain dysfunction). And not all children exhibit fever. Some children have no fever, while others may have mild or very high fever.
The blood sugar level is usually normal in children with encephalitis but is low in the children with hypoglycaemic encephalopathy.
In the case of encephalitis, one-two days of fever (due to virus infection) is followed by the onset of symptoms caused by the brain getting affected. However, in hypoglycaemic encephalopathy, children go to bed without any illness but manifest with symptoms such vomiting, convulsion and semi-consciousness early next day morning (4 a.m.-7 a.m.). At that time, the blood sugar level will be low and hence the name hypoglycemic encephalopathy.
The most important difference between the two is the presence of white blood cells in the cerebrospinal fluid. In encephalitis, there are more white blood cells per unit volume of cerebrospinal fluid, which is a reflection of inflammation in the brain. In contrast, no increase in white blood cells is seen in hypoglycaemic encephalopathy as there is no inflammation in the brain.
Is encephalitis or hypoglycaemia encephalopathy that killed over 110 children in Muzaffarpur?
In a majority of cases, children died due to hypoglycaemic encephalopathy. According to a June 18 Press Information Bureau (PIB) press release, hypoglycaemia (low blood sugar level) was reported in “high percentage” of children who died in Muzaffarpur. Unlike hypoglycaemic encephalopathy, encephalitis does not cause low blood sugar level so death in a high percentage of children couldn’t have been due to encephalitis.
Is litchi fruit responsible for causing hypoglycaemic encephalopathy?
In 2012-2013, a two-member team headed by virologist Dr. T. Jacob John suspected, and next year confirmed, a toxin found in litchi fruit that was responsible for causing the hypoglycaemic encephalopathy. In 2017, a large Indo-U.S. team confirmed the role of the toxin. The toxin is called methylene cyclopropyl glycine (MCPG).
Early morning, there is normal tendency for blood sugar to dip, after several hours of no food intake. Undernourished children who had gone to sleep without a meal at night develop hypoglycaemia. The brain needs normal levels of glucose in the blood. The liver is unable to supply the need. So the alternate pathway of glucose synthesis, called fatty acid oxidation, is turned on. That pathway is blocked by MCPG.
Litchi does not cause any harm in well-nourished children, but only in undernourished children who had eaten litchi fruit the previous day and had gone to bed on empty stomach.