Nipah virus: Clinical manifestation and diagnosis


Nipah virus, a paramyxovirus (a group of viruses related to respiratory disease) associated with Hendra virus, first emerged in Malaysia in 1998. The virus can cause asymptomatic infections and fatal encephalitis. Malaysia has had no more cases since 1999, but outbreaks continue to occur in Bangladesh and India. 

In the Malaysia-Singapore outbreak, transmission occurred primarily through contact with pigs; whereas in Bangladesh and India, it is associated with ingestion of contaminated date palm sap and human-to-human transmission. Bats are the primary reservoirs. Currently, there are no therapeutic ways of treating the infection; supportive care is the only treatment.

Discovery of the virus

Virologists isolated a virus from the cerebrospinal fluid of an encephalitis patient. The electron microscope revealed characters similar to Paramyxoviridae. Eventually, they proposed the name Nipah virus because of its origin.

The first outbreak was in Malaysia from a pig farm industry. The subsequent outbreaks were observed in India and Bangladesh. The two different strains of the virus– NiV-MY and NiV-BD– expressed various symptoms.

NiV-BD vs. NiV-MY: Difference in symptoms of infection

The genome of the virus approximates to 18000 nucleotides with two strains- NiV-BD and NiV-MY. The genome size increases with virus pathogenesis. The interhost transmission is not clear yet.

Although the strains are not distinguishable, they may be different in certain aspects. Studies indicated that NiV-BD is more pathogenic than NiV-MY. The antibody therapy treatment is narrow for NiV-BD. Studies also suggest that NiV-BD infection resulted in more oral shedding and a higher replication rate in the respiratory tract. This difference may explain the contrasting situation in India and Bangladesh– more respiratory complications, shorter incubation period, and high fatality rate.

Human to human transmission of Nipah virus

The Malaysian outbreak reported person-to-person transmission, especially in families of affected index cases. The health care workers, primarily focused on encephalitic individuals, were at significant risk. Although a few nurses tested positive for Nipah in the serum analysis, they were declared as negative results.

They had no anti-neutralizing antibodies and expressed no symptoms of the infection. Apart from serum analysis, an MRI scan revealed affected brain regions similar to acute and asymptomatic Nipah virus infection.

In contrast, Bangladesh and India had many reported cases of human to human transmission. Authorities in India recommend not to eat raw date palm sap and not to enter abandoned wells to avoid contracting the virus.

Other routes of transmission include close contact with affected animals like pigs, dogs, horses, and bats. The secretions from these animals are the primary source of first contact infection.

Clinical manifestation of Nipah virus

When the Nipah virus enters the human body, the immune response includes the release of cytokines and interleukins. In the later stages, the virus makes its way into the epithelial cells of the lungs. It eventually enters the bloodstream. By studying the overall pathway of the virus, it is evident that the infection can lead to multiple organ failure. It also includes renal failure and bleeding from the gastrointestinal tract.

The incubation period ranges from four days to two months, with an average of fewer than two weeks. Common symptoms that gradually develop into encephalitis include fever, headache, nausea, and general discomfort with a high rise in temperature. The viral inclusions in different parts were diagnosed by electron microscopy. Patients also expressed reduced levels of brainstem dysfunction– pupillary reflexes, vasomotor changes, and seizures. Cerebellar signs are also common.

A unique feature of the infection is relapse and late-onset of encephalitic symptoms. The most extended delay recorded in the late-onset of symptoms is 11yr.

Diagnosis of the virus in human

  • It causes systemic vasculitis, thrombosis, and necrosis in the central nervous system.
  • Its presence was witnessed in endothelial cells, causing cell damage.
  • Nipah was also present in smooth muscle cells of blood vessels leading to syncytial giant cell formation.

The viral antigens are also present in neurons leading to severe neurological complications and brain ailments. The virus gains entry into the CNS via olfactory nerves. It includes psychiatric defects– depression and personality changes. While others exhibit cognitive deficits– attention, verbal, mental confusion, and visual memory, these deficits are due to the disruptions in the blood-brain barrier. The condition can worsen, leading to a coma if left untreated.

The presence of Nipah in these regions is crucial to the diagnosis and pathogenesis of the virus.

The respiratory manifestation of the infection

Though Nipah virus infection primarily affects the CNS, it also affects multiple organs to various degrees, especially the respiratory system. In the initial stages, the diagnosis is confirmed by its presence in epithelial cells and alveoli of the respiratory system. This condition leads to acute respiratory distress syndrome. The first identified cases of respiratory distress in the Nipah virus were in Malaysia, although it was not evident. It may also be ventilator-associated and asymptomatic pneumonia. Coughing along with a sore throat is evident in the initial stages. 

In contrast, a few patients in Singapore expressed only respiratory symptoms and no encephalitis. Bangladesh and India rated high on the respiratory distress due to Nipah virus, with a large part involved in acute respiratory distress syndrome. This difference is due to the affected Nipah virus strain.

There is no vaccine for the virus. The treatment includes supportive care. Creating a vaccine is challenging because of its rapid mutations.

Related: Zika virus: reason behind microcephalic fetuses

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