Parasites are organisms that live on or in another host organism and redirect its resources for themselves. They are nearly as old as life itself, having existed since before the days of the last universal common ancestor of all life (Forterre & Prangishvili, 2009). Parasites’ effects on their host range from miniscule to lethal, and they are a huge driving force in shaping host populations (Minchella & Scott, 1991). Their impact on the biosphere is enormous: 50% of known species are parasites, parasitism is the most common consumer strategy on the planet, and parasitism has independently evolved dozens of times in different clades (R. Poulin & Morand, 2000).
All known animal species carry parasites. Commonly, ‘disease’ or ‘microparasite’ refer to microscopic organisms like fungi, bacteria, protozoa, viruses, etc., and “parasite” or “macroparasite” to animal parasites. (‘Disease’ can also refer to non-parasitic conditions, such as cancer or diabetes, but will be used here to mean parasitic conditions.) Macroparasites are further divided into “ectoparasites”, which live on a host’s exterior (e.g. ticks) and “endoparasites”, which live inside a host, usually in the intestinal tract (e.g. tapeworms). An organism that necessarily kills its host is called a parasitoid. All of these organisms use the parasitic consumer strategy (O’Donoghue, 2010).
This piece looks at the scale of the parasite load on wild animals, and the effects of parasites on wild-animal suffering. There is an appendix on ways in which researchers measure parasite and disease load and the challenges associated with these measurements.
- 1 Introduction
- 2 The extent of parasitism in nature
- 3 Negative impacts from disease / parasites
- 4 Reducing harms from parasitism
- 5 Conclusion
- 6 Appendix: Measuring parasite / disease load in wild animals
- 7 Bibliography
The extent of parasitism in nature
What is the parasite load on the typical wild animal?
Many large animals are infected with at least one parasite at any given time. This table describes some findings on parasitism in populations or on individual vertebrates. It was based on available data with some eye towards a diverse range of species. It is not comprehensive.
63% have nematodes or nematode eggs in feces
|Kestrel||84.3% have protozoan blood parasites||(Dawson & Bortolotti, 2000)|
|Red grouse||Individuals have 2000-9000 nematodes of a single species in the caeca alone (a small part of the bird intestine)||(Newborn & Foster, 2002)|
|Female blue tits||89.1% have protozoan blood parasites||(Tomás, Merino, Moreno, Morales, & Martínez-de La Puente, 2007)|
|Soay sheep (wild, during a population crash)||100% have gastrointestinal worms|
100% have biting ked flies, sometimes over 1000/sheep
|Elk in Yellowstone National Park||48.7%-57% have gastrointestinal parasites||(Barber-Meyer, White, & Mech, 2007)|
|Snowshoe hare||15+ individual nematode parasites (lung and intestine) per animal||(Sovell & Holmes, 1996)|
|European eel||84% have at least one helminth, crustacean, or metazoan parasite||(Ternengo, Levron, Desideri, & Marchand, 2005)|
|Lungless salamanders||71.5% have ectoparasitic mites on the skin||(Maksimowich & Mathis, 2000)|
|Humans||16% have intestinal nematodes (mostly in China and Sub-Saharan Africa)||(de Silva et al., 2003)|
How common are other infectious diseases in the wild?
Wild animals have their own epidemics, which are called epizootics, as well as circulating diseases (like colds or flus in humans). Overviews of epizootic prevalence in animals are rare in the literature, but epizootics are common in nature.
Some well-studied epizootics include tasmanian devil facial tumor disease (“Tasmanian devil facial tumour disease (DFTD) — Transmissible Cancer Group,” 2015), chronic wasting disease in deer and elk (U.S. Geological Survey: National Wildlife Health Center, 2002), Newcastle disease in waterbirds (Glaser et al., 1999), and white-nose syndrome in bats (“USGS National Wildlife Health Center – White-Nose Syndrome (WNS),” n.d.).
Some epizootics are traced to spillover events. This is when a parasite normally hosted in one species ‘spills over’ into a novel host where it’s unusually successful, and sometimes causes a huge outbreak. Much of the existing research on spillover in wild animals is on topics of human health or veterinary interest, e.g., on diseases that spill over from animals to humans or livestock. For instance, these include transfer of bovine tuberculosis from white-tailed deer to cattle (Sorensen, van Beest, & Brook, 2014), as well as influenza, ebola, or anthrax. Researchers also commonly study animal disease as it affects conservation of endangered populations. Spillover events that have been studied include canine distemper virus spreading from domestic dogs into African wild dogs and black-footed ferrets (Daszak, Cunningham, & Hyatt, 2000) or avian malaria altering the distribution of bird populations in Hawaii (Scott, 1988). Whether or not the species are endangered, the fact that most pathogens have multiple hosts (Woolhouse, Taylor, & Haydon, 2001) suggests that spillover between wild populations is frequent, if often unobserved.
What factors affect parasite load and disease?
Researchers look at two metrics to study the magnitude of parasitic burden on a species or an individual: richness or diversity, which is the total number of infecting parasitic species, and abundance, which is the quantity of individual parasites. Both of these are correlated, though not directly – more diverse ecosystems frequently, although not always, have more abundance and biomass (Cardinale et al., 2007) (Stachowicz, Bruno, & Duffy, 2007).
Richness and abundance across species and populations
When looking at whole species or populations of a species, researchers usually examine richness.
Parasitic richness among different species depends on a variety of factors. In mammals, phylogeny is a major factor (Nunn, Altizer, Jones, & Sechrest, 2003). Bordes and Morand (1998( writes that “[endo]parasite species richness seems to be an attribute of host species such as any other host life history trait,” meaning that geographically separated populations of the same species tend to have similar endoparasite abundance. (Bordes & Morand, 2011) Aside from that, crucial factors are population size (Morand & Poulin, 1998), density, and range. Animals that are densely crowded or have wide geographic ranges will host more diverse endoparasites than species that are less densely crowded or have smaller ranges (Stanko, Miklisová, Goüy de Bellocq, & Morand, 2002), generally because this results in more opportunities for parasites to spread between members.
Non-autochthonous1Not originating in the place where found; non-native or introduced populations have fewer parasites than autochthonous2Originating in the place where found; native or local. populations. (Torchin, Lafferty, Dobson, McKenzie, & Kuris, 2003)
Larger species both ingest more endoparasites and have more surface area for ectoparasites. Animals that eat a larger volume of food, e.g. primates that eat nutrient-poor leaves versus nutrient-rich fruit, have more exposure to parasites (Nunn et al., 2003).
From insects to human beings, social animals have more parasites and infectious diseases than solitary animals, because potential hosts are more densely concentrated. Competition between individuals can also increase risk of parasitism (Kappeler, Cremer, & Nunn, 2015). For example, sparring dear transmit papovavirus through open wounds, which leads to skin tumors (Sorensen et al., 2014). Some parasites even increase their hosts’ tendency to group together, thus improving their chances of successfully spreading (Yong, 2013).
Richness and abundance in individual animals
Parasite load varies drastically between individuals. Old and juvenile animals are more likely to have (and die from) parasites. Older animals have also generally accumulated more non-lethal parasites over their lives, which may still exact a fitness cost (Lester, 1984). Other contributing factors include an individual’s sex and reproductive status, degree of hunger or starvation, and stress from other causes (Scott, 1988).
Some individuals have unusually high levels of parasites. They may become ‘superspreaders’, individuals that have disproportionately large effects on the flow of disease in the population. The effect is well-known in both human and animal outbreaks. The reason this happens in some individuals but not others is somewhat unclear, but may have to do with unusual illness characteristics that lead to higher rates of spread – for instance, humans with Staphylococcus aureus colonizing the respiratory system are more likely to transmit it to others than those where it colonizes the skin, its usual location (Stein, 2011).
Negative impacts from disease / parasites
Why might we not expect parasites to be particularly harmful?
There are several unintuitive reasons we wouldn’t necessarily expect parasites to cause much harm or suffering to their hosts.
One of these is the complicated nature of parasitism. Parasitism is a form of symbiosis, an umbrella category that also includes mutualism (both organisms benefit from an association) and commensalism (where one organism benefits and another is unaffected.) These categories are not clearly delineated in nature. Parasite status can vary from species to species (both host and symbiote), and even from individual to individual (opportunistic pathogens are ordinarily commensal species that become parasitic when their environment changes, such as the host weakening) (Brown, Cornforth, & Mideo, 2012).
Either way, pathogenicity of an organism isn’t an innate characteristic, it’s highly based on the organism’s particular interactions with the host. Sometimes, most of the harm of a pathogen comes from the immune response it triggers, rather than direct bodily harm. Other pathogens do redirect host resources, but do not provoke a significant immune response or cause tissue damage and only harm their hosts slightly (Casadevall & Pirofski, 1999). Some of these do not even impact host fitness (Kelly, Hatcher, & Dunn, 2003). Researchers sometimes separate host resistance to parasites (the ability to avoid infection) from tolerance (the ability to limit harm from infection) (Råberg, Graham, & Read, 2009).
Some animals have behavioral strategies to deal with parasites, like preening in birds or social grooming in mammals. Animals from butterflies to sparrows to elephants seek out anti-parasitic compounds, either to prevent parasites (e.g. sparrows preferentially lining their nests with insecticidal cigarette butts) or in response to an active infection (e.g. sick chimpanzees seeking out noxious plant leaves to eat, and stopping when they recover) (Shurkin, 2014). Some entire species, like cleaner wrasses or oxpecker birds, survive by removing parasites from other animals (Goldman, n.d.). These could suggest that external parasites no longer bother host animals with relationships to these species. Such behaviors certainly mitigate the negative effects of parasites.
Organisms traditionally considered ‘parasites’ even sometimes provide benefits to their hosts. Untreated parasitic worm infections in humans have been linked to less exacerbation from multiple sclerosis and lower rates of allergies and asthma. The causal mechanism might be either general immune system suppression leading to fewer inappropriate immune responses (for instance, allergies, where the immune system reacts to innocuous stimuli), or perhaps that historically, contact with parasites was an important part of priming appropriate immunoregulation (Rook, 2009). In such a case, conclusively determining if a parasite is overall “harmful” to an animal is difficult.
Experimental manipulation is perhaps the soundest way of determining if a symbiote overall harms its host, and by what means. Other studies establish correlation. (See the appendix for details on the kinds of studies that are used.) Of course, for some parasites that kill or cause enormous physical damage to their hosts, negative effects are more obvious.
Are wild animals harmed by parasites?
Studies in various host-parasite systems generally find a variety of negative and sometimes neutral effects from parasite infection. Unfortunately, many animals have not been studied in depth, and there are many criteria we might use as indicators of experienced suffering, so we should be cautious about drawing sweeping conclusions.
Effects on overall wellbeing
Some consequences from parasites are direct and well-established. Parasites increase their host’s susceptibility to predation. They can also destroy tissue, from the entire reproductive tissue of snails (Scott, 1988) to the tongues of fish (Zimmer, 2013) to cells destroyed by viruses as they reproduce. Parasites like tapeworms or ticks also redirect host resources for themselves, weakening their hosts. For this reason, parasites are regularly associated with lower survival, reproduction, and movement in their hosts (Scott, 1988).
Artificial manipulation gives us some of the most robust conclusions about the effects of parasites. A meta-analysis found that 62% of studies demonstrated that providing animals with antiparasitic drugs improved at least one of: survival, fecundity, or body condition or another physiological metric. (36% of studies observed no improvement, and one study noted a decline in host condition.) (Pedersen & Fenton, 2015)
Some examples of artificially treated animals:
- Grouse treated with antihelminthic drugs had more eggs than non-treated birds, implying that parasites had a reproductive cost (Newborn & Foster, 2002).
- Blue tits treated with antihelminthic drugs had better body condition (body weight and general appearance) and exhibited more parental care than control birds (Tomás et al., 2007).
- The delivery of an antihelminthic drug improved the survival of soay sheep, except in years where the population was experiencing a major crash (where it’s unclear if enough agent was given to meaningfully reduce the worm burden) (Coltman, Pilkington, Smith, & Pemberton, 1999). See the section “Starvation and disease cycles”.
- Providing finches with insecticide-soaked nesting materials resulted in more nestling birds surviving to adulthood (Lindström, Foufopoulos, Pärn, & Wikelski, 2004).
Animals artificially infected with parasites also often fare less well:
- Nematode-parasitized beetles are more likely to lose fights to other beetles. (Vasquez, Willoughby, & Davis, 2015)
- Monarch butterflies infected with high numbers of a protozoan blood parasite “experienced lower survival to adulthood, lower body mass upon eclosion, smaller forewings and had shorter adult lifespans” (low numbers are apparently fine). Flying ability, including endurance, is reduced and the famous yearly migration might take a week longer for infected butterflies than for uninfected ones (Bradley & Altizer, 2005).
- On the other hand, Soay sheep infected with a nematode didn’t show a substantial change in conditions (Gulland, 1992). That said, synergistic effects have been observed in mixed infections before, so possibly just adding one more species didn’t affect the overall parasite ecosystem (Petney & Andrews, 1998).
In another version of experimental manipulation, Pickering and Pottinger (1998) found that when a stress hormone was added to water, trout were more likely to die from bacterial or fungal disease (Pickering & Pottinger, 1989). Increased stress is known to lead to immune suppression, and this experiment suggests a direct link between the two.
Effects on mortality
In nature, parasitic diseases rarely kill animals directly, although this does happen. More commonly, they make hosts more vulnerable to death from other causes.
A meta-study found that mortality was 2.65 times higher among animals infected with parasites than among uninfected animals (Robar, Burness, & Murray, 2010). In mammals, death directly caused by disease appears to be rare. One meta-study found that only 3.2-3.8% of medium to large mammal deaths in North America were attributed to disease. However, disease also drastically increases the risk of natural predation, being hunted, starving, and possibly vehicle collision – all of which (except hunting) are much more frequent causes of death (Collins & Kays, 2011).
Overall impacts from parasitism vary based on geography, host clade, parasite clade, and many other factors. Parasite-associated mortality is higher among amphibians, fish, and molluscs than arthropods, birds, and mammals (Robar et al., 2010). A different review claims that mortality is especially high in invertebrate hosts of parasites (Roy M. Anderson & May, 1978). Mortality from parasites also varies dramatically by latitude, increasing at least 8.4-fold as one moves from polar areas toward the equator. Helminth parasites tend to have the highest effect on mortality (a 3.86-fold increase on chance of death), and microparasites have the lowest (an average 1.36-fold increase) (Robar et al., 2010).
Non-autochthonous species can be highly successful, and often have more biomass in areas they’re introduced to than either autochthonous competitors or populations of the same species in their own autochthonous ranges – despite large incumbency advantages for autochthonous populations (e.g. being better adapted to the terrain.) A proposed reason for this is that, as they move, non-autochthonous species lose some of their complement of potential parasites, and experience fewer parasite-related health problems (Torchin et al., 2003).
Some recently observed epizootics have wide ranges and affect many species. One is starfish wasting disease, which appears to be caused by densovirus. It recently killed millions of starfish along the North American west coast (Hill, 2016) and causes “fragmentation of the body and death” (“Sea Star Wasting Syndrome,” 2017) within a few days. Another is the amphibian fungal disease chytridiomycosis, which, beginning in the 1990s, emerged into populations worldwide and drove dozens of species to extinction (Borrell, 2009). In both cases, human activities have been implicated at least partially as a cause, but the exact causes are still somewhat mysterious. Their far-reaching effects on large numbers of animals are not. When a disease decimates a population, the effects can be additive: the ecological ramifications from one population declining due to infection can lead to the decline and even local extinction of other populations (Scott, 1988). Loss of population is an indicator for individual welfare and death, so this suggests that disease in one species can negatively affect the welfare of another via ecological disruption.
Quantitatively, in terms of larger-scale events, disease caused 54% of die-offs (>25% of a population dying in a short amount of time) in large carnivorous mammals, and 15% of die-offs in large herbivorous mammals (Young, 1994). Disease is also the most common cause of analyzed larger-scale die-offs, representing over 90% of a population, 700 million tons of dead biomass, or over one billion individuals. These are attributed to disease 26.3% of the time – the most common single cause (Fey et al., 2015).
Parasitoids necessarily kill their hosts
Species that use the parasitoid strategy– wasps, flies, beetles, nematodes, and other animals, as well as some fungi and microparasites (e.g. rabies virus in humans)– necessarily kill their hosts (“Midwest Biological Control News,” n.d.). The parasitoid wasp family in particular is worth noting. They usually use a sharp ovipositor to lay their eggs inside moth or butterfly larvae. The larval wasps feed on the flesh of the host and usually proceed to eat them from the inside out (Sekar, n.d.). This animal compelled Charles Darwin to write:
“There seems to me too much misery in the world. I cannot persuade myself that a beneficent & omnipotent God would have designedly created the Ichneumonidæ [a parasitoid wasp family] with the express intention of their feeding within the living bodies of caterpillars, or that a cat should play with mice.” (Darwin, 1860)
Parasitoid wasps are widespread and enormously successful. One family, Braconidae, is estimated to contain more individual species the entire phylum Vertebrata (Yates, n.d.). A study of samples from North and South America found between 6% and 27% of gathered caterpillars were infected with parasitoid wasp larvae (Stireman et al., 2005).
Parasitoids share some overlap with the behavior-altering parasites. Two other examples of this overlap are the cordyceps fungus that cause ants to “behave as zombies” (Hughes et al., 2011) and position themselves to best incubate the fungus, or the Nematomorpha worm, which causes its grasshopper hosts to drown themselves (Thomas et al., 2002). Other parasites with multi-stage life cycles can make their prey hosts much more susceptible to predation by a specific predator host, so that the parasite can continue its lifecycle (Robert Poulin, 2010). In such cases, it seems possible that the animal is no longer conscious or responding to damage – if they were, they might be more likely to flee or interrupt the process. In other cases, however, hosts are alive and active during the entire process (Sekar, n.d.).
Starvation and disease cycles
As mentioned above, the severity and frequency of disease in the wild are influenced by body condition and environmental factors. This results in a “vicious cycle” (Beldomenico & Begon, 2010) that fuels much disease, death, and suffering in the wild.
In this cycle, and variations thereupon, animals are stressed, perhaps from lower food abundance or increased predation pressure. As a result of this stress, animals are more likely to get parasite infections. These infections further decrease their ability to search for food or evade predators, leading to worsening conditions and more stress. Many parasites even cause immunosuppression, so that infection with one parasite increases the chance that a host will be infected with another (or a third, and so on).
The effect of parasites on population cycles has been especially well-characterized in the wild Soay sheep of the St. Kilda archipelago. Large numbers of internal nematode parasites cause anorexia and decreased digestion of protein, and infected sheep are immunosuppressed. This seems to be responsible for the population crashes seen every three or four years, in tandem with an increasing population and declining food resources. The Soay sheep have no predators in the study area, so food, parasites, and weather (“Population Ecology,” n.d.) seem to be the major factors on their population (“Vegetation,” n.d.).
Parasite-related die-offs have also been observed in Quebec ducks, bighorn sheep (Scott, 1988), mice (Pedersen & Greives, 2008), grouse (Hudson, Dobson, & Newborn, 1998), autumnal moths (Klemola, Tanhuanpää, Korpimäki, & Ruohomäki, 2002), and possibly larch bud moths (R. M. Anderson & May, 1980). Earlier, we discussed that 29% of large mammal die-offs (when over 25% of a population dies) are attributed to disease. More common is starvation from winter or drought, which causes 46% of die-offs (Young, 1994). It seems possible, however, based on the above numbers, that these are somewhat entwined.
Small experiments with deer (Maublanc et al., 2009), mice (Pedersen & Greives, 2008), and grouse (Hudson et al., 1998) have found that, in predator-free conditions, supplying food freely in a small environment leads to periodic population crashes, but that antihelminthic drugs stabilized the population and removed crashes. This suggests that parasites were a major causal factor in regular population crashes. Given our understanding of parasites on population crashes, it seems worth further study on the effects of feeding and antiparasitic drugs, and whether they reliably stabilize host populations in the absence of predators.
On the other hand, elk in Wyoming that are artificially fed have higher rates of parasites than unfed wild elk in the winter, but fewer in the spring. A possible explanation is that food supplementation increases ability to fight parasites in the spring, but in the winter, parasite infection increases (due to crowding at feeding sites and lower immune function from other causes, e.g., environmental stress) (Hines, Ezenwa, Cross, & Rogerson, 2007).
The sanitation effect
Packer et al. (2003) propose a model in which predators, by consuming the most diseased members of a population, actually act as a quarantine and reduce the effects of parasites on the rest of the population (Packer, Holt, Hudson, Lafferty, & Dobson, 2003). Predation generally reduces parasite load in prey populations. This is likely to be particularly true for macroparasites that increase morbidity rather than mortality. This explains a few unusual observations: for instance, that predator removal doesn’t always increase abundance of prey species. In interactions where more predators decrease density of prey, disease in prey is also possibly reduced due to fewer opportunities for spread (Sorensen et al., 2014).
Barber-Meyer et al. (2007) calls this the “sanitation effect” and found evidence that wolf predation did decrease the prevalence of some diseases among elk, but did not affect, or even increased, others. The effect is clearly not consistent – in this case, for instance, differences may have been caused by the degree to which diseases cause visible symptoms or increased crowding as a response to increased risk of wolf predation (Barber-Meyer et al., 2007).
Many costly evolutionary functions or trade-offs in animals are associated with resisting parasites. For this to have left such a strong mark on the evolution of their hosts, natural selection indicates that parasitism must be associated frequently with mortality (Sheldon & Verhulst, 1996). The abundance of antiparasitic strategies in wild animals, and the extreme fitness costs posed by some of them, suggests that parasites pose an even larger fitness cost.
Among vertebrates, a prime example of this type of feature is the adaptive immune system 3The part of the immune system that ‘learns’ from novel pathogens; also known as the acquired immune system. This is contrasted with the innate immune system, which protects the body from pathogens generically, and includes things like like inflammation responses and the skin as a physical barrier. itself. Minor immune system responses, such as to a vaccination, cause host metabolic rates to increase by 15-30%. More extensive immune responses, such as sepsis, cause the human metabolic rate to increase by 25-55% (Lochmiller & Deerenberg, 2000). This is an enormous energy expenditure and, when combined with the decreased appetite that accompanies illness in most animals, it can quickly lead to malnutrition.
Adaptive immune systems also create the risk of immune or autoimmune disease, in which the immune system inappropriately treats innocuous stimuli or even host tissue as foreign and launches immune attacks against the body. These can be incapacitating or fatal.
Another cost is migration: movements of animal populations, which are, at times, hugely energetically expensive. This massive energy expenditure has been used as a piece of evidence for the migratory escape hypothesis, which claims that migration has evolved to let animals escape from parasite-infected areas. The migratory culling hypothesis, relatedly, claims that the stress of migration winnows out parasite-infected animals and strengthens the population at the cost of these individuals (Altizer, Bartel, & Han, 2011). Animals like the aforementioned parasite-weakened monarch butterflies are less able to keep up and more likely to die along the migration route (Bartel, Oberhauser, De Roode, & Altizer, 2011). Of course, moving to new locations also involves encountering new potential pathogens,which increases the odds of a spillover event (Fritzsche McKay & Hoye, 2016).
In mammals, sleep has been implicated as a possible adaptation to fight parasitism. During sleep, more energy is available to supply the immune system. Mammals often sleep more when fighting infections and have worse outcomes from infection when forced to sleep less. Mammal species that sleep for longer tend to have more white blood cells and fewer infections (Preston, Capellini, McNamara, Barton, & Nunn, 2009). The fitness cost of spending hours of the day prone and unresponsive to the environment is clearly high, so the increased parasite load associated with less sleep would be even higher than the risks and opportunity costs from sleeping.
Reducing harms from parasitism
Reducing suffering from parasitism is probably tractable. Giving antiparasitic medicine to wild animals has already been studied in the interest of: reducing threats to humans and livestock (e.g (Rupprecht, Hanlon, & Slate, 2004)), preserving threatened populations (Wobeser, 2002), and, as previously discussed, studying the impacts of parasites. This indicates a possible common cause between reducing wild-animal suffering and those interested in conservation or in human or livestock health.
It seems like broad-spectrum treatment often results in an increase in animal welfare, even among animals that are not experiencing unusual levels of disease. The results would presumably be even more drastic for reducing a disease known to be causing obvious harm to infected individuals. Important considerations would be the effects of such a treatment on population size (e.g. whether population size would increase as a result and whether this would lead to a net increase in suffering, even though new animals would be less affected by parasites), the effectiveness of treatment and ability to deliver and maintain treatment over time, and the possibility of the evolution of treatment-resistant parasites.
A detailed analysis of the costs, benefits, and most effective interventions is beyond the scope of this paper, but is worth exploring.
It is difficult to determine how bad mortality from parasitism is when there is scarce data on how bad other causes of death in the wild are, like starvation or predation, or on how animals would die in the absence of parasitism. Parasites occasionally directly cause host death, but are more likely to increase host suffering and increase the odds of a host dying from starvation or predation, both of which seem like very painful means of dying. Disease also causes large-scale die-offs, including some rare events and some cyclical events. Parasitoids seem generally very painful if the host is conscious during the infection cycle.
Aside from increased mortality from causes that are possibly more painful, parasites largely decrease their hosts’ quality of life, from obvious and major tissue damage to minor malnutrition. Several metrics – especially experimental manipulations of parasite levels and the significant fitness cost of anti-parasite adaptations – suggest that animals are better off non-parasitized. They are also ubiquitous – most large wild animals have parasites at any given time. Because of this, while there is still much to learn about other experiences of wild animals, the scale and impact of parasitism suggests that it is a significant source of suffering in nature. Reducing suffering from parasitism and disease seems possibly tractable as a cause area in its own right and should also be considered when exploring other measures to reduce wild-animal suffering.
Appendix: Measuring parasite / disease load in wild animals
Why is measuring disease or parasite load difficult?
There are technical obstacles to assessing the true burden of parasites or disease on wild animals, which is a possible reason why this field is under-researched (Scott, 1988). These obstacles can loosely be grouped into:
- Properties of the host and its response to parasites and disease.
- Properties of the parasite.
- Statistical difficulties.
Looking for visual evidence of infection seems straightforward but isn’t a reliable clue that an animal is sick or not. For one thing, animals can conceal symptoms. Some social animals decrease sickness behavior when trying to mate, do parental care, or compete with conspecifics. The reduction in behavior doesn’t necessarily imply that the host has recovered. Since many disease symptoms are adaptive to reducing disease, e.g. fevers, this concealing behavior is costly and can increase the chance of being harmed by the parasite (Lopes, 2014).
Searching for sick or dead animals also isn’t reliable for accurate counts – many sick animals, especially fish, are more likely to be eaten before they die (except in rare cases, like mass die-offs) (Lester, 1984). They are also likely to be eaten by predators or scavengers shortly after they die. Other animals hide when sick. As such, it’s easy to misrepresent a parasite’s effect on mortality or morbidity.
Looking for external parasites usually involves killing or at least sedating an animal, and looking for internal parasites involves killing the animal. This makes it difficult and expensive to conduct accurate studies of parasite burden.
Many wild animals are infected with many of the wide variety of parasite species. Researchers will often examine just one parasite or group of parasites, rather than all parasites. This may be due to convenience, specific interest, or having tools that only make sense for analyzing a certain type of parasite. This makes it difficult to look at overall effects from parasite burdens.
Screening for viruses or bacteria is challenging, even once a sample is obtained. While it’s possible to do metagenomic analyses of an animal’s metabiome or virome, neither have indicators that mark them as a parasite of the host itself. Most viral DNA will belong to bacterial viruses. Although those can be excluded, it’s then hard to tell if the remaining eukaryotic viruses are in fact parasites of the host (unless the viruses are already well-characterized, which most are not) or associated with pathologies. With bacteria, the difference between commensals and parasites isn’t clear.
Perhaps the most crucial obstacle is that disease is both caused by and causes other factors: body mass, body condition, altered behavior, starvation or loss of appetite, difficulty finding food, and immunosuppression. Causation cannot be determined by comparing an animal’s parasite burden to another aspect of its condition – only correlation. As described below, there are studies in which parasite levels are directly manipulated, which better capture true causation.
Common methods of finding animals for research include traps, hunting, looking for corpses, or visual observation. Animals that are sick or dying tend be less active and will even hide, and thus are less likely than healthy animals to be found by all of these methods. Animals weakened by disease are also more likely to be eaten by predators before the disease can kill them.
In many cases, especially with macroparasites (Scott, 1988), a small number of individuals have many more parasites than average and have disproportionate effects on parasite transmission and burden in the population. In these cases, when surveying only a small number of wild animals, researchers are likely to miss the worst afflicted.
How do researchers study disease or parasite load?
These are some types of studies used:
- Screening for biomarkers for specific diseases – e.g. antibodies, DNA
- Looking for parasites on living or dead animals
- Looking for physical symptoms of disease – e.g., body condition, weight, fever
- Immunological investment – blood lymphocyte counts (immunological investment) or inflammatory response (neutrophil and monocyte counts) (Beldomenico et al., 2008) (for comparing between individuals)
- This method may not be good for directly comparing between species, since reliance on this strategy varies – species with less exposure to parasites have more intense changes in response (Lindström et al., 2004)
- Total death causes – putting tracking collars on animals and retrieving them later to see which animals died, and of what.
- Artificially treating animals (e.g. with antihelminthic drugs) and observing outcomes (Pedersen & Fenton, 2015)
- Artificially infecting animals (e.g. with a known quantity of parasite eggs) and observing outcomes.
- Cortisol levels, especially in fish (includes parasite as well as environmental stress) (Pickering & Pottinger, 1989)
- Autopsies on predators (looking for infected prey animals in the stomach)
- Lester (1984) describes some elegant statistical methods for determining rate of mortality from a parasite in the wild, given that it may have already altered the study population. (Lester, 1984)
Experimental manipulation is worth discussing in more detail, because it cleanly allows for determination of cause and effect. Researchers can artificially manipulate parasite levels in two ways:
- They can treat animals by giving them a dose of an antihelminthic agent, an antiviral agent, etc. This reduces the level of all of that class of parasite (helminth worm, virus, etc) present in the animal. In this type of study, the intensity of infection decreases 90% of the time, so this strategy effectively reduces parasite load (Pedersen & Fenton, 2015). (Notably, very few studies of this type examine microparasites – viruses, bacteria, protozoa, etc.)
- Researchers can also artificially infect the animal with a known quantity of a specific parasite, usually one known to be endemic in the population already. Unfortunately, this type of experiment is clearly likely to have deleterious effects on animal welfare.
After time passes, either the overall population plus a control group is studied, or the animals are caught again and studied after a specific amount of time. The results give strong evidence that observed changes are caused by parasite infection, rather than vice versa.
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References [ + ]
|1.||↑||Not originating in the place where found; non-native or introduced|
|2.||↑||Originating in the place where found; native or local.|
|3.||↑||The part of the immune system that ‘learns’ from novel pathogens; also known as the acquired immune system. This is contrasted with the innate immune system, which protects the body from pathogens generically, and includes things like like inflammation responses and the skin as a physical barrier.|