What Is the Incubation Period of Japanese Encephalitis?

Japanese encephalitis is a prevalent infectious disease in the Asia-Pacific region, characterized by its lack of specific treatment. It has an annual incidence rate of 67,900 cases, with a mortality rate of 25-30%.

Additionally, 50% of survivors experience severe neurological sequelae. Thus, understanding Japanese encephalitis is crucial for safeguarding public health.

1. Japanese Encephalitis Characteristics

Japanese encephalitis is an acute blood-borne infectious ailment affecting both adults and children. It stems from the Japanese encephalitis virus, a member of the Flavivirus genus within the Togaviridae family. This virus is heat-resistant, inactivated at 56 degrees Celsius for 30 minutes or 2 minutes at 100 degrees Celsius, and can endure in a frozen state for several years.

The primary sources of Japanese encephalitis are wild birds and livestock, including pigs, buffaloes, cows, and horses.

Transmission occurs through Culex mosquitoes, which serve as disease vectors. These mosquitoes become infected with the virus after feeding on infected animals and subsequently transmit it to humans through mosquito bites. Culex mosquitoes thrive during the summer, contributing to the prevalence of Japanese encephalitis, especially from May to July.

2. Incubation Period of Japanese Encephalitis

The incubation period for Japanese encephalitis typically spans 5 to 14 days, with an average duration of one week. During this period, patients typically remain asymptomatic.
Key phases include:

• Onset Phase:

This phase coincides with the virus's traversal of the blood-brain barrier, leading to cerebral edema and the emergence of meningeal syndrome symptoms.

The disease begins abruptly with a high fever of 39 - 40°C or higher, accompanied by symptoms such as headaches, abdominal pain, nausea, and vomiting.

In the initial 1 - 2 days, patients may experience neck stiffness, increased muscle tone, eye movement disturbances, confusion or loss of consciousness, and heightened tendon and bone reflexes.
Some young children may exhibit symptoms resembling bacterial infections or food poisoning, including loose stools, abdominal pain, and vomiting.

• Full-blown Phase:

Spanning from days 3 - 4 to days 6 - 7 of the disease, this phase witnesses the virus penetrating brain parenchyma, resulting in the destruction of nerve cells.

Prominent symptoms during this stage include signs of brain damage and focal neurological impairment.

On days 3 - 4 of the disease, symptoms from the onset phase do not diminish but intensify. Patients progress from excited delirium to altered consciousness, eventually descending into a deep coma.

Autonomic nervous system dysfunctions become more pronounced, marked by profuse sweating, variable skin coloration, breathing difficulties, increased bronchial secretions, rapid and weak pulses, and elevated blood pressure.

Patients may experience delirium, hallucinations, agitation, increased muscle tone, leading to convulsive postures and spasms, or facial and limb muscle tremors. Some may enter a fixed, postured state.

Local symptoms encompass limb and cranial nerve paralysis, particularly involving the ophthalmic and facial nerves (VII).

Most fatalities occur within the initial 7 days, with survivors having a more favorable prognosis.

Laboratory Testing:

White blood cell counts typically increase by 15,000-20,000/mm3, primarily due to a 75-85% increase in neutrophils, along with elevated erythrocyte sedimentation rates.
Cerebrospinal fluid aspiration and testing reveal.