will a zoonotic disease ever destroy the human race

Will a zoonotic disease ever destroy the human race? A

critical review

Shona Redman

Word Count: 1496

INTRODUCTION

Zoonotic diseases, which spread from animal hosts to humans (Homo sapiens) (Center for

Disease Control and Prevention (CDC) 2013), account for most human diseases (Cleaveland

et al. 2001). Previous zoonotic pandemics include Spanish influenza (Influenzavirus A),

responsible for 50 million deaths in two years (Johnson & Mueller 2002), and more recently

severe acute respiratory syndrome, SARS, (Coronavirus) has killed 774 people (CDC 2012).

Numerous Hollywood films have depicted a zoonotic disease wiping out humanity. In this

essay the feasibility of this notion will be discussed by analysing whether any naturally

occurring bacterium, virus or parasite could achieve such devastation.

EMERGENCE OF ZOONOTIC DISEASES

To create a pandemic a disease must emerge or re-emerge (Cleaveland et al. 2001; Bengis et

al. 2004), with zoonotic disease emergence increasing due to socio-economic, environmental

and ecological factors (Table 1).

Table 1. Factors affecting the emergence of zoonotic diseases

Factor causing emergence How it aids emergence References

Increasing human population Creates areas of high human density in which the

disease can spread rapidly. Migration to urban areas in

search of jobs, education etc. moves pathogen to new

areas.

Bengis et al. (2004);

Gibbs (2005);

Jones et al. (2008);

Broglia & Kapel (2011)

Increased frequency and speed of

travel

Trains and aeroplanes allow humans to travel long

distances relatively quickly to spread a disease to non-

endemic areas before symptoms appear.


Gibbs (2005);

Christou (2011)

Changing agricultural practices Increased intensity allows easy transmission of disease

through a livestock population; may cause viral

amplification.

Livestock are being kept in ways that allow transfer of

pathogens between wild and domestic hosts.


Gibbs (2005)

Increased human-animal contact More chance of a ‘host-jump’ to humans. This would

then allow transmission between animals and humans.


Blancou et al. (2005)

Increased movement of animals

and animal products by humans

Allows geographical spread of pathogen and exposes

new human populations to the disease.



Environmental changes that alter

host and vector distributions e.g.

deforestation

Disease can spread in a new area.

New susceptible human populations exposed to

infected hosts and vectors



Emergence of new strains and

breakdown of host’s defences

Can infect more people and have deadlier effects. Blancou et al. (2005);

Jones et al. (2008);

Colwell et al. (2011)

Of the pathogens being considered, viruses are most likely to emerge and achieve

global spread (Cleveland et al. 2001; Gibbs 2005; Johnson et al. 2015). Bacteria are also

responsible for a high proportion of emerging infectious diseases (Jones et al. 2008) and

amongst parasites, protozoans are most likely to emerge (Chomel 2008). Once emerged it is

down to the biology of the disease to establish the disease within the human population.

PROPERTIES AFFECTING THE PANDEMIC POTENTIAL OF ZOONOTIC DISEASES

For a zoonosis to induce a pandemic its properties must facilitate rapid transmission and

spread amongst humans (Figure 1).

Figure 1. Diagram showing the ideal properties of a zoonotic disease capable of wiping out humanity

Bacterium

Multiple

hosts

Widespread or

travels long

distances Asymptomatic

reservoirs One a

domesticated

species

Host

Properties

Transmission

Time frame

Pathogenicity

Evading control

Droplet spread

Human-to-human

Disease agent

Virus

Long infectious

period

Latency < Incubation

Antibiotic resistance Viral mutation

50-100%

mortality but not

straightaway

Suppress

immune system

Secondary method

Animal hosts

Zoonoses commonly have primary hosts with close contact and evolutionary similarity to

domesticated species so the pathogen can mutate and use these domestic species as an

intermediate to infecting humans (Cleaveland et al. 2001; Wiethoelter et al. 2015).

Additionally, the host would ideally have global distribution or travel long distances, as is the

case with migratory birds (Olsen et al. 2006).

Multi-host pathogens are more likely to emerge, have a broad geographic spread and

cause human-to-human transmission (Cleaveland et al. 2001; Johnson et al. 2015). These

additional hosts may be asymptomatic reservoirs which are particularly problematic for

disease control (Mandl et al. 2015). Therefore, to destroy humanity a disease should exhibit

host plasticity with some asymptomatic hosts so that the pathogen may spread unnoticed.

Transmission method

Different disease agents generally rely on certain transmission routes to infect humans

(Figure 2). Due to their little human-to-human transmission and exploitation of easily

controlled transmission routes (i.e. oral and vector) (Centre for Food Security and Public

Health, CFSPH 2006; World Health Organisation, WHO 2016b), parasites are unlikely to

destroy humanity so will not be considered further. Additionally, vector-mediated

transmission alone is not feasible for a global pandemic, although it can facilitate spread of a

pathogen across the vector’s range and between multiple host species (Johnson et al. 2015).

Comparatively, bacteria and viruses exploit multiple, harder to control, transmission routes

(Figure 2) and have an increased ability to transmit between humans, making them a greater

pandemic threat (Christou 2011).

Figure 2. Diagram showing the typical transmission routes of zoonotic diseases to humans.

(Key: red star for bacteria; yellow for parasites; green for viruses). References: CFSPH (2006) and CDC (2016).

Time frame of disease

The incubation, latency and infectious periods of a disease determine how long an individual

is asymptomatic and then infectious for (Lessler et al. 2009). Incubation periods vary hugely

but are typically under two weeks for most bacteria and viruses (Table 2). A short incubation

period means disease transmission starts earlier but a longer period means the host has more

time to spread the disease undetected but also to be cured before symptoms appear (Osmond

1998).

Direct Indirect

Biological vector

Via bite to skin

Fomite

Via contact with an inanimate

object that is carrying the

pathogen e.g. food, water

Airborne

Via inhalation of droplet nuclei

suspended in air

Droplet Spread

Via inhalation of droplets spread a

few feet by sneezing, talking etc.

Direct contact

Via skin-to-skin contact, biting etc.

with an infected individual or contact

with infected soil, vegetation or

faeces.

Table 2. Characteristics of example bacterial and viral zoonoses (Adapted from Trevino 2012a, b)

Disease Animal hosts Person-to-

person?

Vector? Transmission route(s) Human (H) &

animal (A) incubation periods

Mortality rate Some typical clinical signs in humans Additional references

Leptospirosis

(Leptospira species)

Farm animals; dogs;

rodents; seals

No No Ingestion of contaminated

water; inhalation; direct contact with urine

H: 7-12 days

A: 4-12 days

4-18% Fever; headache; jaundice; acute renal

failure; pulmonary haemorrhage

Edwards et al. (1990);

Dupont et al. (1997); Bharti et al. (2003)

Lyme Disease

(Borrelia burgdorferi)

Horses; dogs; rodents;

deer; birds

No Yes Ticks H: 7-14 days

A: 2-5 months

Low “Bulls-eye” rash; fever; headache; stiff

neck; chronic recurring arthritis

Barbour (1998)

Scott et al. (2001)

Bovine Tuberculosis

(Mycobacterium

bovis)

Badgers; farm animals;

dogs; cats

No No Ingestion of unpasteurised

milk; inhalation

H&A: Variable Unknown May be asymptomatic; signs depend on

infection route but may include bone &

joint lesions, meningitis and pneumonia

Nugent (2011)

Plague

(Yersinia pestis)

Primary host: Rodents

Secondary hosts: Dogs; cats

Yes Yes Direct contact with

infected animals and fleas; inhalation

H: 1-7 days

A: 1-6 days

30-60% during Black Death;

8% during modern outbreaks

Flu-like signs; “buboes”- enlarged tender

lymph nodes; rapid pneumonia; respiratory failure; shock; death

Butler (2013);

WHO (2016a)

Influenza H5N1 strain

(Influenzavirus)

Chickens; waterfowl; pigs Not

confirmed yet

No Inhalation; direct contact

with nasal secretions

H: 1-4 days

A: 1-7 days

33-51% in 3 outbreaks Fever; chills; headache; weakness;

sneezing; sore throat; cough; pneumonia; death

Gubareva et al. (1998);

Horimoto & Kawaoka (2001); Bengis et al. (2004);

Kallio-Kokko et al. (2005)

Rabies (Lyssavirus)

Usually dogs, foxes and bats

Possible but not

confirmed

No Direct contact between infected saliva and skin

abrasions or mucous

membrane; airborne; organ

transplants

H: 2 days to >6 months but typically

20-60 days

A: 10 days to 6

months

Near 100% Headache; fever; abnormal behaviour; paralysis; difficulty swallowing; delirium;

hydrophobia; convulsions; death

Plotkin (2000); Kallio-Kokko et al. (2005);

Sudarshan et al. (2007)

West Nile virus

(Flavivirus)

Primary host: birds

Dead-end host: horses

Rarely Yes Culex mosquito bites;

direct contact with infected

animals, blood or tissues; organ transplants and

blood transfusions

H: 3-14 days

A: Unknown

2-7% 80% do not show any symptoms but

symptoms of severe diseases include:

fever, neck stiffness, disorientation, convulsions, muscle weakness, coma and

paralysis

Hubálek & Halouzka (1999);

Asnis et al. (2000);

Bengis et al. (2004); Gibbs (2005);

WHO (2011)

Severe Acute Respiratory Syndrome

(SARS)

(Coronavirus)

Bats; civets Yes No Droplet spread H: 2-16 days A: Unknown

10% during 2002-2003 epidemic

Fever; myalgia; cough; pneumonia; lesions; acute respiratory distress

syndrome

Lee et al. (2003); Peiris et al. (2003a, b);

Lau et al. (2005);

Cameron et al. (2008)

Nipah virus (Henipavirus)

Reservoir host: bats Primary host: pigs

Yes No Droplet spread; direct contact with mucous

membranes and skin

abrasions

H: Several days-2 months but usually

<2 weeks

A: 7-14 days

32% during 1999 epidemic Fever; headache; dizziness; vomiting; decreased consciousness; hypertension

Goh et al. (2000); Bengis et al. (2004);

Lau et al. (2005);

CFSPH (2016)

If the latency period is shorter than the incubation period, the disease can spread

through a population, before symptoms, and associated control, begin (Fraser et al. 2004;

Kallio-Kokko et al. 2005). Furthermore, to infect all humans, a disease should have a long

infectious period, but this again gives the host time to be treated and cured. The ideal

solution to avoid detection may be for a disease to be completely asymptomatic. However,

symptoms often aid transmission (Wolfe et al. 2007; CDC 2012), and an asymptomatic

disease would unlikely be pathogenic enough to destroy the human population.

Mortality rates

Logically, to kill all humans, a zoonosis should have a 100% mortality rate however, this has

only been seen in rabies (Kallio-Kokko et al. 2005) because some individuals have natural

resistance to a disease (Pancino et al. 2010). Furthermore, high virulence hinders human-to-

human transmission because infected individuals are quarantined or incapacitated so unable

to travel (Ewald 1996). Consequently, it may be more beneficial for a disease to have a

mortality rate around 50% but with effective transmission between humans to ensure the

population declines (Omran 1971). However, the disease would likely be controlled before

causing complete extinction and most current bacterial and viral zoonoses have mortality

rates much lower than 50% (Table 2), indicating that they are probably incapable of the feat

being considered here.

A disease could also cause indirect mortality by dampening down the immune system

(Zolopa et al. 2009). This is seen in Human Immunodeficiency Virus (HIV), where the

immune system is compromised, and in SARS and influenza A, where an excessive innate

immune response compromises the adaptive immune system (Kash et al. 2006; Cameron et

al. 2008). However, humans possess a range of control methods to limit mortality.

PREVENTION OF ZOONOTIC PANDEMICS

Human intervention and natural limitations in a disease itself can prevent a zoonotic

pandemic.

Control methods

Surveillance of zoonoses is critical in identifying a pandemic threat or start of an outbreak

(Blancou et al. 2005; Christou 2011). Surveillance relies on information collected by official

health systems and international cooperation (Blancou et al. 2005) so that early detection and

effective control of pathogens similar to previous ones can occur.

Current control methods attempt to eradicate the pathogen through prophylaxis

(Blancou et al. 2005). Sanitary prophylaxis involves slaughtering infected animals whilst

medical prophylaxis focuses on vaccinating animal hosts and humans (Blancou et al. 2005).

To be effective a vaccine only needs to be administered to enough individuals that population

immunity is achieved (Alexander & Brown 2000). New molecular cloning techniques help to

develop new vaccines (Corbel 1997), for example, marked vaccines which distinguish

between infected and vaccinated individuals so that sanitary prophylaxis is accurate (Blancou

et al. 2005).

Additional control methods include banning the international trade of infected animals

(Gibbs 2005) and wiping out biological vectors or preventing their contact with humans

(WHO 2016b). Human-to-human transmission can be controlled through good hygiene (Seto

et al. 2003) and treatment of early stage disease with antibiotics and anti-viral drugs (Bengis

et al. 2004; WHO 2016a), which reduce symptoms in 70-90% of patients (Alexander &

Brown 2000; Zolopa et al. 2009).

Natural prevention mechanisms

An important natural factor limiting a zoonosis is the geographical limitation of animal hosts

and vectors which contains the disease in certain regions unless humans spread it globally

themselves (Gubler 1998; Colwell et al. 2011). However, even if this was achieved, small,

isolated populations would avoid infection. Additionally, natural selection often selects for

less virulent disease strains so that infected individuals transmit the disease before death; this

means that over time a pathogen becomes less dangerous (Ewald 1996). However, pathogens

can overcome these preventative measures through mutations or by exploiting pre-existing

limitations in control methods.

EVASION OF CONTROL

Limitations of control methods allow pathogens to evade detection and control. International

support is required for surveillance in developing countries, meaning that many diseases are

neglected in areas most at risk from the next zoonotic pandemic (Jones et al. 2008; Christou

2011). Additionally, some countries do not publish information that will affect trade or

tourism; this is often the most important information for international disease surveillance

(Blancou et al. 2005).

Sanitary prophylaxis effectiveness is limited by wild animal and reservoir hosts, and

global disease spread (Mandl et al. 2015). Whereas, medical prophylaxis is often used in

developing countries to reduce prevalence because limited finances prevent eradication

(Blancou et al. 2005). Furthermore, vaccines are often not developed for wildlife hosts

because of a lack of profit for pharmaceutical companies (Blancou et al. 2005).

Worryingly, control measures can initiate the evolution of new disease strains to

which control is ineffective and humans lack immunity to. This occurs due to new selection

pressures imposed by vaccines, anti-viral drugs and antibiotics, or due to antigenic drift and

shift within viruses (Gern & Falco 2000; Kallio-Kokko et al. 2005). Influenza is particularly

renowned for its mutation ability (Box 1). Additionally, multi-stage pathology can make later

stages of bacterial infection harder to treat (Gern & Falco 2000), but health authorities focus

less on bacterial zoonoses due to the availability of antibiotics (Blancou et al. 2005).

Box 1. A case study of the potential pandemic threat of Influenza H5N1

CONCLUSION

Overall, it is highly unlikely that a zoonosis could ever destroy the human race, especially

one caused by a parasite due to the limitations associated with their transmission. However,

even if a bacterium or virus evolved with all the ideal characteristics, the disease would still

need to achieve global spread and a near 100% mortality rate. This is unlikely because some

individuals will have natural resistance, and natural selection facilitates evolution of less

virulent strains to ensure survival of the disease agent in the population.

Influenza H5N1 (Avian flu)

Influenza H5N1 is a negative-strand RNA orthomyxovirus that is of pandemic concern because of several reasons:

RNA viruses are especially likely to emerge (Cleveland et al. 2001; Wiethoelter et al. 2015).

Mutations occur frequently through antigenic drift and shift. This creates new strains to which humans have

not been previously exposed to and makes developing vaccines difficult (Carrat & Flahault 2007).

Pigs (Sus scrofa domesticus) can be infected by both avian and human influenza strains so facilitate genetic

re-assortment to create new emerging diseases (Castrucci et al. 1993; Bengis et al. 2004).

Pathogenicity and ability to adapt to new hosts i.e. domestic birds and humans, can be increased by

mutations (Castrucci et al. 1993; Kallio-Kokko et al. 2005).

It is highly contagious and can be spread around the world by migratory birds (Olsen et al. 2006).

It has previously resulted in epidemics and pandemics with up to 50% mortality (Horimoto & Kawaoka

2001; Bengis et al. 2004).

Short latency period means management must be implemented rapidly (Kallio-Kokko et al. 2005).

Potential to cause tissue damage by an excessive innate immune response which can compromise the

adaptive immune system (Kash et al. 2006).

However, there are limitations to H5N1’s pandemic potential:

No evidence of human-to-human transmission (Gibbs 2005).

Control can be achieved by slaughtering poultry in infected areas (Alexander & Brown 2000; Gibbs 2005).

Effective antiviral drugs e.g. amantadine and zanamivir (Hayden et al. 1997; Gubareva et al. 1998;

Alexander & Brown 2000)

To overcome these limitations, the H5N1 strain would need to mutate to allow human-to-human transmission and to

become resistant to anti-viral drugs. However, it is still unlikely H5N1 could wipe out the human population

because some people have previously been exposed to the virus and so have some immunity. To overcome this a

mutation would need to create a new strain (no longer H5N1) or increase pathogenicity.

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will a zoonotic disease ever destroy the human race

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