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Insights into Editorial: The litchi link?: on Bihar encephalitis deaths

Insights into Editorial: The litchi link?: on Bihar encephalitis deaths




The outbreak of acute encephalitis syndrome (AES) in Bihar has led to close to 350 cases and around 100 deaths.

While the causes of AES are still researched, the association with hypoglycaemia and litchi fruit has drawn attention.

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.

If dextrose infusion is not started within four hours after the onset of symptoms, the brain cells may not recover but will die.

As a result, children suffer from various aspects of brain damage, such as speech getting affected, mental retardation, muscle stiffness/weakness, etc., even if they survive.


Causes for Acute Encephalitis Syndrome:

The most common causes of acute encephalitis syndrome are traced to a bacteria or a virus and it takes at least a few days before presenting serious symptoms and deaths, the toxin in litchi causes serious problems overnight.

While well-nourished children who eat the fruit remain unaffected even if they go to bed on an empty stomach, the under-nourished ones are at grave risk.

Blood glucose falls sharply causing severe brain malfunction (encephalopathy), leading to seizures and coma, and death in many cases.

This is because under-nourished children lack sufficient glucose reserve in the form of glycogen and the production of glucose from non-carbohydrate source is blocked midway leading to low blood sugar level.

This causes serious brain function derangement and seizures.

While 5% dextrose infusion serves the purpose in cases of general low blood sugar, children suffering from acute hypoglycaemic encephalopathy can be saved only by infusing 10% dextrose within four hours of illness onset.


Is litchi fruit responsible for causing hypoglycaemic encephalopathy?

In 2012-2013, a two-member team headed by virologist Dr. T. Jacob John 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.

What precisely causes the brain inflammation is not clear. Heat and humidity could be factors, and also genetic predisposition because not all the children in a family fall ill despite the same conditions.


Hypoglycaemic Encephalopathy can be treated:

Full and complete recovery can be achieved if children with hypoglycaemic encephalopathy are infused with 10% dextrose within four hours after the onset of symptoms.

Infusing 10% dextrose not only restores blood sugar to a safe level but also stops the production of amino acid that is toxic to brain cells by shutting down the body’s attempt to convert fatty acid into glucose.

Together with dextrose infusion, infusing 3% saline solution helps in reducing oedema of brain cells.

The concentration of ions in the fluid outside the brain cells becomes more than what is inside the cell and this causes the fluid from the cells to come out thus reducing oedema and damage to brain cells.

Using 5% dextrose, as is the norm in general low blood sugar level cases, may help children with hypoglycaemic encephalopathy recover from hypoglycaemia, but the accumulation of amino acid is not turned off. And so, even if children survive, they will suffer from brain damage.



Recovery is rapid and complete if 10% dextrose is infused within the golden hours. Infusing a higher concentration of dextrose is necessary to completely stop the attempt by the body to produce glucose from non-carbohydrate source.

If encephalopathy was indeed the cause of death, this simple medical intervention could have saved many lives. Dextrose infusion could have been done even as children were being transported to hospitals in ambulances. The failures were at the stages of both prevention and care.

To prevent illness and reduce mortality in the region, the main recommendations are minimising lychee consumption, ensuring receipt of an evening meal and implementing rapid glucose correction for suspected illness.

To get a sense of what these numbers mean, the WHO’s prescription could be touchstone. It advises governments to maintain a ratio of one doctor for every thousand persons or 100 for a lakh.