Wildlife & Biodiversity

Understanding zoonotic diseases: ‘Global human interaction has eased transmission’

Globalisation and population explosion have led to increase in human-to-human transmission of viruses, says Sanath Krishna Muliya, project scientist at Wildlife Institute of India

By Ishan Kukreti
Published: Thursday 07 May 2020

The origins of the novel coronavirus SARS-CoV-2, largely unknown nearly five months after the first COVID-19 case was discovered, have baffled the scientific community. The novel coronavirus recognises, with high probability, a zoonotic origin. This has shone the spotlight on the nature of zoonotic diseases.

Down to Earth spoke to Sanath Krishna Muliya, project scientist, Wildlife Institute of India, to understand the burden of zoonotic diseases and how vulnerable humans are to zoonoses. Edited excerpts:

Ishan Kukreti: What is the zoonoses disease burden globally? What is its distribution in the developed and developing countries?

Sanath Krishna Muliya: Infectious diseases are currently the second-most leading cause of death and the leading cause of disability-adjusted life years in humans worldwide.

More than 30 new pathogens capable of causing such diseases have been identified worldwide in the last four decades; some of them have managed to jump between species. The diseases caused by these viruses include influenza, human immunodeficiency virus (HIV), Kyasanur forest disease, Rabies, Nipah, Hendra, Ebola, Zika and COVID-19.  

A virus would not judge if it spread in a developed, developing or under-developed country — it just has to propagate.  West Nile Virus, Zika, Ebola or COVID-19 — all have spread even in the most advanced countries.

IK: Nipah Viral Encephalitis is a classic example of emergence of bat-borne virus due to economic boom, habitat destruction and climate change.

SKM: Nipah Virus (NiV) infection started as an accidental zoonotic infection in Malaysia from their natural reservoirs — the pteropid bats or fruit bats.

Named after the Nipah river village in Malaysia, wherein the first known human outbreak took place, the encephalitic disease has been so far reported from Malaysia, Singapore, the Philippines, Bangladesh and India with up to 75 per cent mortality rate.

Even after 22 years since its first occurrence, NiV outbreaks are still being reported from the continent causing considerable morbidity and deaths.

A retrospective study to identify the cause showed that a series of events, including deforestation for pulpwood and industrial plantation, slash-and-burn procedure for palm oil industry, etc in Indonesia resulted in the formation of a severe haze throughout much of Southeast Asia in the months directly preceding the Nipah outbreak in Malaysia.

This, in conjunction with severe 1997-1998 El Niño Southern Oscillation (ENSO) event, led to mass migration of pteropid bats to Malaysia, which was also concurrently experiencing upsurge of large-scale piggeries due to rapid economic progression.

All these factors led to the spillover of a novel paramyxovirus from its reservoir host bat to the domestic pig, and ultimately to human population. This highlights the importance of anthropogenic changes that led to the emergence of a novel bat-borne infection in humans.

Subsequent outbreaks in Bangladesh and India also highlighted how social and cultural attributes of humans can lead to emergence of diseases.

Contrary to bat-pig-human transmission in Malaysia, bat-human spread through consumption of contaminated food (raw date palm liquor, half-eaten fruits, etc) and human-human transmissions through nosocomial infections (infection or toxin that exists in a certain location) and through care-giving were prominent modes of transmission in Bangladesh and India.


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IK: Could you explain in detail the factors which make it possible for viruses to jump from animals to humans and also, from humans to humans?

SKM: For any infectious disease, be it emerging or established, there are three major requirements that are often referred to as epidemiological triad: A causative agent, a host and an environment. The spread sets off when the host and agent are brought together.

In case of most spillover events, the causative viruses or their precursor strains already existed in the system through the ‘sylvatic cycle/enzootic cycle’, which is a natural transmission cycle of a viral pathogen within its natural animal host (bats for Rabies and Nipah; macaques and rodents for Kyasanur Forest Disease, etc).

Now most of these natural hosts are either immune to such viruses due to co-evolution and acquired immunity or through physiological adaptations over the years.

In addition to the triad, contact between natural host and the novel recipient host is a precondition for virus transfer and disease emergence. Viruses are versatile in nature. Some of them have the ability to affect a vast range of hosts, while some have evolved themselves to allow efficient infection and transmission within the new host.

When such viruses get exposed to a naïve population such as that of humans, they are not immune to the virus, thereby creating potential for emergence of novel infectious diseases.    

All the above traits, in addition to a network of human attributes like sociological, ecological and environmental changes, have greatly altered the probability of such potentially pathogenic viruses to come into contact with us.

While these human activities have not only caused unwanted changes in historic host-pathogen interactions, they have also orchestrated the unprecedented convergence of various pathogens on spatial and temporal scale, leading to widespread disease outbreaks and subsequent tragic loss of human life at an epidemic scale.

 The best examples: 

  • Kyasanur Forest Disease: Habitat destruction for agricultural activities and increased human movement for logging and cattle grazing in Karnataka’s Kyasanur Forest area brought the virus in contact with humans. Before the outbreak, the virus was naturally circulating through a wildlife-tick vector cycle.
  • SARS-CoV: It started as accidental spillover among people due to wildlife trade in China. The novel virus most likely originated from horseshoe bats via recombination events among existing SARS coronaviruses in species such as civets in live animal markets. This shows how such events create a potential hotspot for disease emergence by creating unnatural environment for viruses, which can then evolve and jump species barriers rapidly.
  • Nipah: Explained in earlier response. 

IK: Has there been an increase in the human-to-human transmission of viruses? If yes, why?

SKM: There been an increase in human-to-human transmission of viruses. There are numerous reasons for this, the most important being globalisation and population explosion.

For any given virus, the density of the vulnerable host population is a crucial component — both to sustain itself in the system as well as in transmission/propagation.

The unprecedented population growth, ensuing population explosion and overcrowding have all made us one of the most vulnerable mammalian species. Our trade, travel and global human interaction patterns have further eased the transmission pathways for such viruses.

Consider Ebola. The disease is not new to Africa; its first outbreak dates back to 1976.

The initial outbreaks were restricted to one-two countries during individual episodes and they gradually faded out. The 2013-2014 outbreak in West Africa, however, was the largest ever recorded and differed dramatically from the previous outbreaks in its duration, number of people affected and geographic extent.

More than 5,000 confirmed human cases were recorded, with a mortality rate of 50 per cent. The correlation between this and population attributes were as follows:

  • Population growth has been dramatic in the region, with population densities (people/kilometre square) increasing by 223 per cent, 178 per cent, and 275 per cent in Guinea (1960–2012), Sierra Leone and Liberia respectively (1961–2013).
  • Rural-to-urban migration and growth in the affected countries significantly increased here; the proportion of the population that is now urbanised increased significantly in Guinea (248 per cent, 1960–2013), Sierra Leone and Liberia (130 per cent and 163 per cent respectively in 1960–2013). All major Ebola outbreaks were in such urbanised setups with high human densities.
  • The location of the index case (the first case in the outbreak) was Guéckédou, Guinea, a small village bordering Sierra Leone and Liberia. Travel restrictions between these countries were minimal. Infected individuals from Guéckédou moved rapidly from the originally infected village into other major urban centres in all three countries, eventually leading to a major outbreak in the region. International air travel further propagated the disease as far as Americas through tourists, migrants of healthcare workers. 

IK: Does the difference in human and animal immunity systems make us more vulnerable to zoonoses?

SKM: It is quite complicated. Yes, there are differences among human and animal immune systems.

However, the reasons that we are more vulnerable are different. Some of the viruses are just novel to us and our immune system is not equipped to respond to it.

For example, in the acute respiratory infections with SARS-CoV and influenza A, our system over-responds by massive innate immune activation, causing local tissue damage and compromising the generation of protective adaptive immune responses.

On the other hand, it is crucial to understand the dynamics between virus and their natural reservoirs.

Bats, for example, have acquired innate immunity to numerous viruses (which are now identified as zoonotic) due to genetic, physiological and behavioural adaptations. They have developed the ability to harbour them with no clinical signs of diseases.

Looking the sheer number of such viruses being identified in bats and their ability to not get affected, it becomes clear that bats and such viruses have co-evolved over millions of years. It is highly unlikely that their ability to ‘asymptomatically carry viruses’ is a recently acquired trait.

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