Bihar Deaths: Misreporting Aggravates Failed State

A study of hypoglycaemic encephalopathy, which is actually the disease that killed children in Bihar, will lead one to the root cause of malnutrition, a condition for which the state is responsible


As of 28 June, 167 children have died in Bihar of a certain disease that has assumed the scale of an epidemic. “Encephalitis” and “litchi” have turned buzzwords in Google searches as well as mainstream media. However, medical professionals have identified the root cause of the deaths as malnutrition while the deaths are falsely being attributed to litchis. The press and public are being misled to believe that the disease is encephalitis (a variation of which is Japanese encephalitis), as most of the media space on this issue has been dominated by politicians and administrators instead of medical professionals.

Misreporting from Bihar

Reports from Bihar have used the term AES (acute encephalitis syndrome) despite the knowledge that not all AES cases are due to hypoglycaemic encephalopathy (the real disease in this case). AES is a broad umbrella under which come Japanese encephalitis, meningitis, cerebral malaria and hypoglycaemic encephalopathy.

Identifying and understanding the root cause of the epidemic in Bihar will enable the healthcare machinery to tackle and prevent such deaths in future.

Hypoglycaemic encephalopathy ≠ Encephalitis

Are encephalopathy and encephalitis the same? Well, often in medical jargon, they are used interchangeably. However, encephalopathy, simply put, refers to a disease of the brain. It is preceded by the term that explains the cause behind it. In this case, hypoglycaemia or low blood sugar. In contrast, encephalitis is an inflammation of the brain caused by viruses such as herpes simplex, western Nile virus or often bacteria. The blood sugar level in encephalitis victims can be normal in contrast to that in hypoglycaemic encephalopathy.

Encephalitis victims often experience very high fever, seizures and an altered mental state. In contrast, the victims of hypoglycaemic encephalopathy do not experience any fever before brain dysfunction occurs. Children go to bed without exhibiting any symptom, but during the early morning hours (4-7 AM), they experience high fever, vomiting and loss of consciousness.

In encephalitis, the white blood cell count is high, indicating inflammation of the brain. However, the children suffering from hypoglycaemic encephalopathy do not have increased white blood cell count, they have normal white blood cell levels.

Hence, characterising the disease under “AES”, which the public often interprets as encephalitis, is rather inaccurate, as the real disease is being hidden under a generic term.

Litchi of Bihar not to blame

Following news reports filed by lay reporters, one may be tempted to think that litchi is behind the deaths in Muzaffarpur, Bihar. This is due to a misinterpretation of a paper published by Dr Jacob John who had identified a neurotoxin in litchi as methylene cyclopropyl glycine (MCPG),the agent responsible for the deaths.

However, Dr John never said MCPG was the cause of the death but rather the trigger when children are malnourished and go to bed on an empty stomach or when they have not eaten for long periods. He recently confirmed that it was perfectly safe to eat litchis but

“Special care has to be taken to ensure that severely malnourished children who eat litchi have a meal before going to bed.”

Figure 1 glycolysis and glycogenolysis
Figure 1

So, how does MCPG or the litchi toxin affect undernourished kids?

As shown in Figure 1, the liver stores excess glucose in our blood from the food we eat as glycogen reserves through a process called glycogenesis. When our blood glucose gets depleted, let’s say due to long periods of absence of food, the liver starts breaking down these glycogen reserves into glucose through a process called glycogenolysis. Now, our blood once again has glucose required for our energy and bodily functions. What happens when we run out of glycogen?

As shown in Figure 2, our liver starts utilising amino acids and free fatty acids (non-carbohydrate sources) to convert them into glucose for energy. This process is called gluconeogenesis.

Figure 2

Thus, our body once again has glucose available for energy and bodily functions. However, when litchi is consumed on an empty stomach or by malnourished children, the MCPG toxin inhibits the process of gluconeogenesis releasing amino acids that are toxic for the brain. Thus, malnourishment and the trigger of litchi consumption becomes a deadly combination. The amino acids released due to the incomplete gluconeogenesis causes brain oedema and the children start suffering from convulsions, high fever and eventual death if not attended in time.

A few health officials have attributed the deaths to high heat and humidity. However, these are false claims, as most of these symptoms manifest during 4-7 AM when the temperature is lower than that during the day.

Prevention and cure

As banal as it sounds, the prevention of this disease simply lies in consuming food and not eating litchis in an empty stomach or in a malnourished state. Even the treatment is rather simple if children are administered an intravenous dose of 10% dextrose within four hours of showing the symptoms, their lives will be saved. While doctors have received a lot of flak for no fault of theirs, the fact remains they have saved many children who were admitted to the hospitals in time.

What is clearly evident is that these deaths are entirely preventable and have been caused due to sheer ignorance, lack of education and poor state machinery in Bihar.


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