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Transcript of 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.
Bengis et al. (2004);
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.
Bengis et al. (2004);
Gibbs (2005)
Increased human-animal contact More chance of a ‘host-jump’ to humans. This would
then allow transmission between animals and humans.
Bengis et al. (2004);
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.
Bengis et al. (2004);
Broglia & Kapel (2011)
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
Bengis et al. (2004);
Broglia & Kapel (2011)
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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