Have you ever wondered which infectious agents could cause a real-life “zombie outbreak”?

Simon Odekunle

Since their conception in the 1600s by Haitian slaves (Mariani, 2016), zombies have grown to be a staple of 21st century pop culture. Originally depicted as slow, mindless, cumbersome creatures, believed to be the soulless bodies of slaves who had committed suicide (Mariani, 2016), the depiction of zombies has since somewhat changed, with many modern media formats now portraying them as rabid and voracious killing machines craving human flesh. It is perhaps due to the diversity in the types of threats that zombies can pose that has inspired their use in many media forms – for example, they are often used to induce tension and emphasise the direness of the protagonist’s situation in popular blockbuster movies such as World War Z, I Am Legend, and in TV shows such as The Walking Dead and Game of Thrones.

Nowadays, most formats use “scientific” means to explain how “zombiism” arises. Gone are the mystic and spiritual origins. These have long been substituted by viruses or genetic defects which induce zombie-like traits, such as an insatiable thirst for human flesh and hyper-violent behaviour. Wondering whether these descriptions were based mainly in science or pseudoscience, I decided to investigate some real life diseases, to see if there were any which could cause a potential “zombie outbreak”. The criteria needed to make it onto my list were as follows:

  • The infectious agent responsible for causing the disease must be blood-borne
  • The disease must induce behavioural changes in the host similar to those exhibited by zombies
  • The disease must be capable of causing some form of outbreak

And so, without further ado, let’s get into it.

Rabies

Angry white dog biting a stick

Dog bites are the most common source of human rabies cases worldwide (Image Source)

The viral inflammatory disease, rabies, is an obvious first candidate. Rabies gets its name from the Latin word rabere which means “to rage/rave” (Mahadevan et al., 2016), and it is arguably the disease that induces behaviour most like that of the ‘modern zombie’ – in particular, the behaviour of zombies depicted in movies such as I Am Legend and World War Z. Some of the ‘modern zombie’-like symptoms induced by rabies include hydrophobia, aerophobia, heliophobia and, of course, heightened aggression (Mahadevan et al., 2016).

Rabies viral encephalitis is an inflammation of the brain caused by the neurotropic rabies virus (a member of the Rhabdoviridae family). Rabies virus is transmitted primarily through bites from domesticated animals and rodents, and also through mucous membrane exposure (e.g. open wounds) (Mahadevan et al., 2016). Once within the host, the virus enters an incubation period (IP) during which it remains near the inoculation site, replicating at low levels in nearby skeletal muscle (Mahadevan et al., 2016). After the IP, the virus proceeds to the neuromuscular junctions and/or muscle spindles, where it has access to the nervous system through the unmyelinated nerve endings (Mahadevan et al., 2016). Upon reaching the central nervous system (CNS), rapid replication occurs within the dorsal root ganglion of the host, and from there the virus spreads to other organs around the body (Mahadevan et al., 2016). All of this leads to the aforementioned ‘modern zombie’-like symptoms, as well as to confusion (alternating with periods of lucidity); autonomic dysfunction (leading to jerky movements); pupil dilation; and excessive sweating (Mahadevan et al., 2016). If that doesn’t describe a zombie, I don’t know what does.

Creutzfeldt-Jakob Disease

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CJD is a degenerative neurological disease caused by prions (Image Source)

Another prime candidate is Creutzfeldt-Jakob Disease (CJD) – the human equivalent of bovine spongiform encephalopathy (BSE) (also known as mad cow disease). CJD is not caused by a pathogenic organism but rather by misfolded prion proteins in the brain. Prion diseases, such as CJD, are associated with the conversion of α-helix rich prion proteins (PrPC) into insoluble β-sheet-rich scrapie-like aggregates (PrPSc). These aggregates have virus-like properties in that they are self-propagating and can cause fatal diseases (Chen and Dong, 2016). CJD is the most common human prion disease, and CJD cases are split into three different catalogues: sporadic, genetic, and acquired (Chen and Dong, 2016). The sporadic and genetic forms of CJD arise randomly from within the host, while acquired CJD arises usually from the consumption of PrPSc-contaminated foods, such as beef from a cow with BSE (Chen and Dong, 2016). Once inside the host, the PrPSc enters the CNS and begins propagating until disease occurs – after which the patient soon dies (Chen and Dong, 2016). The IP length of CJD, like rabies, can vary dramatically – ranging from a couple of months to over 30 years, depending on numerous factors.

Early-stage CJD patients can display zombie-like symptoms such as confusion, memory loss, lack of coordinated muscle movement, and aggressive behaviour.

Sleeping Sickness

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Sleeping sickness is a parasitic disease which, if left untreated, is virtually always fatal (Image Source)

Patients of the last candidate have been documented behaving more like ‘classic zombies’. Officially known as human African trypanosomiasis (HAT), sleeping sickness (SS) is caused by parasitic protozoa called trypanosomes (mostly Trypanosoma brucei gambiense), and is transmitted by the blood-sucking tsetse fly indigenous to sub-Saharan Africa (Kennedy, 2013). SS is a wasting disease and has been responsible for major pandemics in the past. Perhaps the most notable of these was between 1896 and 1906, when it is estimated that SS caused the deaths of hundreds of thousands of people (Kennedy, 2013). Early-stage HAT is often misdiagnosed as malaria due to their clinical similarities, although HAT quickly produces more severe symptoms such as jaundice and several cardiac issues (Kennedy, 2013). Late-stage HAT is when the neurological symptoms begin to appear and patients begin to truly act like zombies. Late-stage HAT patients typically suffer from mental and motor disturbances such as tremors, gait irregularities and abnormal reflexes (Kennedy, 2013). A reversal of the patient’s diurnal and nocturnal patterns can also occur, leading to nocturnal insomnia and daytime somnolence (Kennedy, 2013). Other behavioural symptoms include increased irritability and hallucinations – typical zombie behaviour.

Conclusion

So, there you have it. Those are the three main zombie-related harbingers of the end of civilisation as we know it. Or perhaps not quite. Fortunately, while all three diseases have the potential to cause a “zombie outbreak”, none are likely to cause an outbreak of major concern. The indeterminate IP lengths and low transmission rates of rabies and CJD, make large-scale pandemics highly unlikely (despite new cases of both diseases emerging regularly in Europe and North America). Furthermore, while HAT still affects thousands of people annually (Kennedy, 2013), recent advances in the prevention of insect-borne diseases, as well as significant health-care system improvements in regions where HAT is endemic, have greatly reduced the likelihood of HAT pandemics occurring. Thus, unless the infectious agents which cause these diseases mutate in a drastic manner, like the Ebola virus – wherein transmission rates might increase rapidly, and death might occur at a lower rate or at a later stage in pathogenesis – pandemics are unlikely to happen. Alternatively, perhaps a mutation will grant these infectious agents the ability to reanimate dead bodies – like the ‘zombie-ant’ fungus, Ophiocordyceps unilateralis – thereby creating true human zombies. Either way, I don’t want to be around to find out.

References:

  1. Chen, C. and Dong, X.P. (2016) Epidemiological characteristics of human prion diseases. Infectious Diseases of Poverty. 5, 47.
  2. Kennedy, P.G.E. (2013) Clinical features, diagnosis, and treatment of human African trypanosomiasis (sleeping sickness). The Lancet Neurology. 12(2), 186–94.
  3. Mahadevan, A., Suja, M.S., Mani, R.S. and Shankar, S.K. (2016) Perspectives in diagnosis and treatment of rabies viral encephalitis: insights from pathogenesis. The American Society for Experimental NeuroTherapeutics. 13(3), 477–92.
  4. Mariani, M. (2016) The Tragic, Forgotten History of Zombies [online]
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