Our macrocosm is flooded with enormous numbers of wild flora and fauna along with the kaleidoscope of niches that support an enormous range of vertebrate and invertebrate species. Infectious pathogens, originating in wild animals is turning out to be increasingly imperative throughout the globe in recent decades due to substantial impacts on human wellbeing, agricultural production, wildlife-based economies and wildlife conservation. The emergence of these pathogens as noteworthy health issues is associated with a range of causal factors, most of them linked to the sharp and exponential rise of global human activity.
Discussing their patterns of transmission, two types are evident. In one pattern, human-to-human transmission occurs, which maintains the infection for some period of time or permanently e.g, Immunodeficiency virus/HIV, Influenza A, Ebola virus and severe acute respiratory syndrome. In the second pattern, direct or vector-mediated animal-to-human transmission is seen like in case of Rabies, Nipah virus, West Nile virus, Hantavirus, Lyme Borreliosis, Plague, Tularemia, Leptospirosis and Ehrlichiosis thereby posing a serious health implication globally.
As we know Nipah virus is under limelight, it is one of the recently emerging viruses that have caused serious illness in hundreds of humans and animals. Nipah virus, Similar to Hendra virus are highly pathogenic paramyxoviruses for which bats have been implicated as the natural host. These bats are within the genus Pteropus in the family Pteropodidae, or Old world fruit bats and are commonly referred to as flying foxes that caused serious disease outbreaks in humans and livestock in Australia, Malaysia, Singapore and Bangladesh. Several features distinguish henipaviruses from other paramyxoviruses like the extra length of Henipa virus genome, wide host range by naturally infecting flying foxes, horses, pigs, cats, dogs, humans, and experimental investigations have extended this host range to include guinea pigs and hamsters.
Nipah virus was first isolated in 1999 from pigs and adult human males in peninsular Malaysia and then in Singapore with the symptoms of fever and encephalitis, and some with respiratory illness. Most of the humans affected in the Malaysian outbreak had a history of direct contact with live pigs, and most were adult male. A slightly different NiV emerged in Bangladesh and India in 2001 and continues to cause regular outbreaks of fatal encephalitis in humans, with evidence of direct bat-to-human and human-to-human transmission and mortality of between 70%and 100%. NiV has been classified as BSL-4 selected agent and possess several characteristics which make them highly adaptable for their use as bioterror agents.
Discussing about the clinical presentation of disease; it is a complex systemic illness affecting multiple organ systems. In terrestrial species, Nipah virus displays a predominantly respiratory or neurological tropism, depending on the host. In swine, respiratory signs dominate especially in young animals showing signs of pyrexia, nasal discharge, rapid and laboured respiration and a notable, harsh and non-productive cough, giving rise to the name ‘barking-pig-disease. In addition, a multifocal neurological illness has also been observed in growing pigs, together with sudden death in mature animals. When the Nipah virus hunt human patients, a wide gamut of clinical manifestations are seen which ranges from mild symptoms of pyrexia, headache and drowsiness, to a severe, fatal acute encephalitic syndrome.
Distinctive clinical signs such as areflexia, hypotonia, abnormal pupillary response, tachycardia, hypertension, abnormal doll’s-eye reflex, and segmental myoclonus are recorded by the clinicians that suggest involvement of the brain-stem and upper cervical cord. Moreover, absent or reduced tendon reflexes with hypotonia, segmental myoclonus that is characterized by focal, rhythmic jerking of muscles, prominently involving the diaphragm are witnessed. Not only this, other muscle groups in the arms, legs, neck and face may be affected as well. The seizures observed in Nipah virus infection are mainly in the form of generalized tonic clonic. If chest x-rays performed, abnormal findings have been reported but without primary lung disease. But in some cases atypical pneumonia with abnormal chest x-rays recorded. Infection with NiV can also take a more chronic course (in excess of 4 years), with serious neurological disease followed by a non-encephalitic or asymptomatic infection.
The recurrence of neurological manifestations has also been noted in patients who had previously recovered from acute encephalitis (relapsed encephalitis). With respect to the diagnostics of Nipah virus there are cornucopias of diagnostic tools and tests get done like in other neurological insults, unsurprisingly, Cerebrospinal fluid (CSF) assessment reveals anomalous findings of elevated protein levels /or elevated white cell counts in many patients with Nipah virus infection. Glucose levels generally reported within normal limits. Thrombocytopenia, leukopenia and elevated levels of Alanine and aspartate aminotransferases are recorded but with normal blood urea, creatinine and electrolyte levels. IgM and IgG antibody detection via (ELISA) tests in serum and CSF are critical to the diagnosis of NiV infection. The ELISA tests for the antibodies have high specificity and are therefore useful as a screening test.
Serum neutralization tests are also available that could be useful as a confirmatory test for NiV infection. Apart from serologic diagnosis of NiV infection, MRI imaging of brain has proved to be a useful diagnostic aid particularly in acute encephalitis. Typically, in acute NiV encephalitis, on MRI the brain shows multiple, disseminated, small discrete hyperintense lesions mainly in the subcortical and deep white matter, and occasionally in the cortex. Ribavirin, a very broad-spectrum virustatic agent, which showed varying degrees of efficacy against viruses such as respiratory syncytial virus, influenza and measles, was tried on an empirical basis in NiV-infected patients.
There are ways to reduce the risk of developing NiV infections. For example, individuals should avoid date palm sap and any bats or potentially infected domestic animals such as infected pigs. The WHO suggests that health care professionals wear gloves and other protective clothing during any pig slaughtering and culling procedures. Avoid contagion, the communication of disease from one person to another by close contact. Medical caregivers should employ quarantine methods and use barrier methods such as gloves, masks, and disposable gowns, as they are at high risk of person-to-person transmission of NiV. The lessons that could be learned from serious outbreaks such as NiV are many. Politicians should learn not to meddle but leave it to trained professionals like scientists and doctors to establish and publicize the cause of outbreaks. Among the scientists and doctors themselves, greater cooperation and freer dissemination of accurate information, both locally and internationally, would be helpful. Scientists must share their expertise and knowledge to help stop the outbreak.
Keeping an open mind for new possibilities is also important; without this we could never have discovered this new virus. From the scientific point of view, improved, reliable diagnostic aids have to be developed quickly, especially those that do not require viral culture. Animal models of NiV infection have to be found to further understand its pathogenesis, particularly with regard to the mechanisms, including immune mechanisms, involved in relapsed and late-onset NiV encephalitis. Suitable models could also be useful to assess therapies using Ribavirin and other newer drugs or modalities. In the long run we have to be concerned about the ecological impact of human activities, including our existing animal husbandry practices, which are now thought to be a likely contributory factor for the emergence of new viruses
Dr. Abrar-Ul-Haq Wani can be reached at dr.abrar79@gmail.com
