Why parasites seldom kill their host

Strongyloidiasis : This can lead to severe and possibly fatal immunodeficiency. The parasite penetrates through the skin and affects the lungs, skin, and intestines. It is passed on through direct contact with contaminated soil. It most occurs in tropical and subtropical regions. Beef and pork tapeworms : Taeniasis is caused by tapeworms of the taenia family.

They affect the intestines. They are passed on by eating undercooked beef or pork. Toxocariasis : A roundworm transmits this infection from animals to humans.

It affects the eyes, brain, and liver. It is caused by accidentally swallowing the eggs of the parasite, for example, when young children play with soil. Nearly 14 percent of people in the U.

Most never have symptoms. Trichinosis : This is caused by the roundworm of the Trichinella family. Infection can lead to intestinal symptoms, fever, and muscle aches. It is passed on by eating undercooked meat. Whipworm : Also known as trichuriasis , whipworms live in the large intestine. Eggs are passed in feces. It is common all over the world. Humans can become infected when ingesting the eggs, for example on unwashed fruit or vegetables. Elephantiasis lymphatic filariasis : This is transmitted through mosquito bites.

The adult worms live in the lymph system. Infection can lead to lyphedema and elephantiasis, in which swelling can cause disfigurement and disability. In the Americas, it is passed on by the Culex quinquefasciatus mosquito. Ringworm is sometimes mistaken for a worm, but it is not a worm. It is a fungal infection. Bedbug : These can affect the skin and vision. They are found all over the world. Sharing clothing and bedding can spread infection. They may be present in newly rented accommodation and hotel rooms.

Body lice : These are common worldwide. Infection can spread through sexual activity, skin-to-skin contact, and sharing bedding or clothing. Crab lice : These affect the pubic area and eyelashes. They are common all over the world and spread through sexual activity, skin-to-skin contact, and sharing bedding or clothing.

Demodex : These affect the eyebrow and eyelashes. They are common all over the world and can spread through prolonged skin contact. Scabies : This affects the skin.

It is common all over the world and can spread through sexual activity, skin-to-skin contact, and sharing bedding or clothing. Screwworm : This is transmitted by a fly, and it affects skin and wounds. It is found in Central America and North Africa. Head lice : These live on the scalp and affect the hair follicles. They are common all over the world and spread through head-to-head contact.

A reaction to their saliva causes itching. Parasites come in many shapes and sizes and can lead to a wide variety of symptoms and health issues. Some parasites are treatable and others are not.

Lymphedema is a long-term condition in which fluid collects in tissues, causing swelling. Lymphedema most commonly affects one or both of the arms or…. Bedbugs are small wingless insects that feed exclusively on the blood of warm-blooded animals. They need to feed regularly to reproduce, lay eggs, and…. Trichomoniasis is a common sexually transmitted infection. There are often no symptoms, but it can lead to complications. It is treatable with….

The tapeworm is a parasite that lives in the gut. Humans become infected when we eat food that contains tapeworm eggs or come into contact with…. Hookworm is an intestinal parasite that can cause infection at any age. People can catch it through contact with soil. It is rare in the United States,. What to know about parasites.

Medically reviewed by Alana Biggers, M. What is a parasite? Types Symptoms Human parasites Worms Ectoparasites Prevention In the United States A parasite is an organism that lives in another organism, called the host, and often harms it.

Share on Pinterest Parasites range from microscopic in size to over 30 meters in length. Share on Pinterest Some parasite-related problems, such as giardiasis and amebic dysentery, can cause abdominal pain.

Human parasites. Share on Pinterest Roundworms can be passed on by raccoons. Share on Pinterest Hookworms can cause intestinal disease. Share on Pinterest Different types of tapeworm can affect the intestines, the liver, or the lungs. Share on Pinterest Bed bugs are ectoparasites: They live on the outside of the body.

In the United States. Exposure to air pollutants may amplify risk for depression in healthy individuals. Costs associated with obesity may account for 3. Related Coverage. What is lymphedema?

Medically reviewed by Stacy Sampson, D. Everything you need to know about bedbugs. The prey is running for its life. If the predator fails to capture the prey, it goes hungry, but it will not experience a large decline in fitness as a result of the interaction.

In contrast, if the predator catches the prey, the captured individual loses any future opportunities to reproduce. In this race, the prey experience strong selective pressure to evolve better adaptations to avoid being eaten.

At the same time, predators must capture sufficient food to survive and reproduce, and they too are subjected to selective pressure for traits that allow them to hunt successfully. Over time, this arms race leads to traits that enable prey to better avoid capture, whereas predators become better able to capture prey. Figure 2: Aposematic coloration Brightly colored animals, such as the red-spotted newt a and monarch butterfly b , warn potential predators against consumption.

Such organisms contain toxins. In contrast to the examples provided thus far, some prey exhibit bright coloration. Such aposematic coloration helps prevent predation by signaling to potential predators that the vividly-colored individual is toxic. Toxins may be manufactured within the body, as with the red-spotted newt, or they may be acquired passively via consumption of toxic plants, as with the monarch butterfly Figure 2.

Figure 3: Batesian mimicry Non-toxic Papilio dardanus swallowtail butterfly females occur in a variety of forms, each of which mimics the physical appearance of toxic species. Not all species that exhibit vivid coloration are truly toxic. Some have evolved patterns and colors that mimic those of toxic species. Examples of such Batesian mimicry include the extraordinarily polymorphic Papilio dardanus swallowtail butterfly in southern Africa and Madagascar Salvato Females of this species occur in a wide variety of physical appearances, nearly all of which mimic distasteful species of the Danaeus and Amauris genera with which they co-occur Figure 3.

In parasitism, an individual organism, the parasite, consumes nutrients from another organism, its host, resulting in a decrease in fitness to the host. In extreme cases, parasites can cause disease in the host organism; in these situations, we refer to them as pathogens. We divide parasites into two categories: endoparasites, which live inside the body of their hosts, and ectoparasites, which live and feed on the outside of the body of their host.

Examples of endoparasites include flukes, tapeworms, fungi, bacteria, and protozoa. Ectoparasites include ticks and lice, plants, protozoa, bacteria, and fungi. Plants and animals typically act as hosts. In most situations, parasites do not kill their hosts. An exception, however, occurs with parasitoids, which blur the line between parasitism and predation.

The best-known parasitoids include several species of wasp, which immobilize — but do not kill — a host by stinging it. After the larvae hatch, they consume the living tissues of the host, eventually killing it Figure 4a. Figure 4: Parasitoidism A parastic wasp stings its prey before laying eggs on or in it a. The larvae will consume the insect after hatching. The fruiting bodies of entomogenous fungi extend from the insect it consumed b.

Spores circulate inside the host, whose body provides the nutrients needed for fungal growth. Eventually, the fungal load becomes too great for the host, and the insect dies Figure 4b. The major distinguishing difference between parasitoids and predators is that parasitoids feed on living tissue, whereas the predator kills its prey before, or in the process of, consuming it.

For all parasites, the host exists as an island of habitat. But the island lives for a finite period of time, and the parasites must find a new host before the existing one dies.

Transmission to a new host can happen either directly, or through a vector. In direct transmission, the parasite moves from one host to another of the same species without an intermediate organism. In vector transmission, an intermediate organism, the vector, transfers the parasite from one host to the next. Figure 5: Complex life cycle of the Plasmodium parasite The life cycle requires both the primary human host and the intermediate Anopheles mosquito host for completion. Many endoparasites have a complex life cycle that involves two hosts, and the parasite must spend time in both to complete its life cycle.

Take, for example, the protozoan parasite Plasmodium , which causes malaria. Plasmodium must spend time in humans and in an Anopheles mosquito to complete its life cycle.

The mosquito acts as a vector, transferring Plasmodium from infected humans to uninfected individuals. Additionally, the mosquito acts as an intermediate host. When a female mosquito ingests blood containing Plasmodium , some of the red blood cells contain gametes eggs and sperm.

It is this life stage that can then go on to infect a new human when the mosquito feeds Figure 5. Coley, P. Herbivory and plant defenses in tropical forests. Annual Review of Ecology and Systematics 27, Dawkins, R. Arms races between and within species.

Ferron, P. Biological control of insect pests by entomogenous fungi. Annual Reviews of Entomology 23, Roy, H. Bizarre interactions and endgames: entomopathic fungi and their arthropod hosts. Annual Review of Entomology 51, Predation, Herbivory, and Parasitism. Characterizing Communities.

Species with a Large Impact on Community Structure. Successional Changes in Communities. Effects of Biogeography on Community Diversity. Community Ecology Introduction. Avian Egg Coloration and Visual Ecology. Causes and Consequences of Biodiversity Declines. Disease Ecology. Most insects do not fulfill these prerequisites, because they occur as alternating larval and adult stages Knell and Webberley, In general terms, a host that exhibits only short phases of sexual activity with respect to its annual activity cycle or its overall life-time, is unfavorable for a sexual mode of disease transmission.

By contrast, human reproductive behavior is characterized by overlapping generations and a prolonged adult phase with a year-round, desynchronized mating activity. Humans represent an exceptionally suitable host for the evolution of STDs indeed. Therefore, sexually transmitted parasites might generally be under a low selective pressure to evolve manipulation, at least in terms of enhancing sexual activity over normal levels. These symptoms are generally believed to represent a part of the host immune response.

Therefore, a suppression of host immune responses might not only favor the infection process, but also aid horizontal transmission via a suppression of such secondary alterations in the social behavior of the host. How commonly are STDs reported to cause fatigue, decreased libido or sexual activity, or other symptoms that are typical for viral or bacterial infections?

Whereas 0. It is tempting to speculate that the absence of fatigue in patients with STDs indicates a putative host manipulation by sexually transmitted parasites: an outcome of manipulation that is particularly prone to being overlooked. All early descriptions of manipulated hosts referred to trophically transmitted parasites of animals, owing to the conspicuous phenotypes that they cause. Given that studies in search of confirmation of a newly described phenomenon tend to focus on similar cases, it seems likely that little effort has been made to search for manipulating STDs of humans.

In spite of potential research biases and the likelihood of both, false positives and false negatives among the existing reports, it seems to be a real phenomenon that manipulating and non-manipulating parasites co-exist, sometimes within the same taxonomic group. Why do some parasites manipulate their hosts whereas others do not?

All parasites express traits for the recognition and the invasion or occupation of a host, as well as for the manipulation or avoidance of host immunity, and traits that favor the transmission of parasites should be under an equally strong selective pressure. If we aim to understand the circumstances under which host manipulation is likely to evolve, we must consider the benefits and costs of manipulation for the parasite. In general, parasites can gain higher selective benefits from manipulation when the frequency of transmission-relevant encounters among non-manipulated consecutive hosts is low Poulin, In a broader sense, parasites are more likely to evolve manipulation when they do not move along the dominating pathways within the food chain, because they must shift, for example, among hosts with a diurnal vs.

A second crucial factor that determines the potential benefits of host manipulation is persistence time. The longer a parasite can persist in the respective host without suffering from any reduction in its fitness, the lower is the pressure to move to the next host Poulin, Indeed, differing persistence times might be a major explanation for the observation that manipulation effects are more frequently reported for intermediate than for final hosts, at least as long as all hosts are animals Holmes and Bethel, Plant pathogens, by contrast, require mobile vectors for their dispersal among their immobile final hosts and, therefore, frequently manipulate the quality of their host plant for the vectors Belliure et al.

These changes can be very fine-tuned: for example, plant viruses with a persistent mode of transmission require vectors to feed for a prolonged period of time on infected hosts and, thus, usually tend to improve the quality of the host plants for the vectors. By contrast, non-persistently transmitted viruses are effectively transmitted when vectors briefly probe infected hosts and, therefore, these viruses usually tend to reduce host plant quality for vectors Mauck et al.

In summary, the putative net benefits of host manipulation vary among different host—parasite systems. Nevertheless, manipulation should be expected to be almost ubiquitous if there were no costs that select against its evolution. Almost no empirical studies have been performed to search for such costs Poulin, ; nevertheless, theoretical considerations can help to identify putative sources of costs. First, any manipulation depends on at least some kind of physical or molecular trigger that is released by the parasite.

The production of these molecules would have a metabolic cost, the order of magnitude of which depends on the consumption of energy and limiting elemental resources that are required for its production or maintenance, relative to the overall metabolic demands of the parasite.

It might be no coincidence that T. Viruses depend completely on the metabolism of their host and, thus, should gain most when they manipulate the re-allocation of host compounds, or the activity of existing signaling molecules, rather than inducing costly de-novo synthesis Hoover et al.

Second, DNA itself has a metabolic cost, and viruses and intracellular bacteria in particular are under high selective pressure to reduce their genome sizes to a minimum. Therefore, the mere need to carry additional genes that encode for the manipulating trait can represent a significant cost for a parasite. Third, scaling up to the ecological level, altered host phenotypes can trigger responses in coexisting species that share the host with the parasite, or with its vector.

These responses can feedback to the parasite: for example, by enhancing the competition among host and non-host predators for an infected intermediate host vector or among non-vectors for an infected final host, by depleting limiting resources within the host, or by altering the survival rates of the manipulated host in its environment.

What are the net consequences for a specific parasite of an enhanced predation pressure on its intermediate host when final hosts are rare among all the predators that are currently around?

Belliure et al. The hijacking of manipulation effects by other species Mouritsen and Poulin, can potentially have strong negative feedback effects on the parasite.

Finally, a counter-selective force that remains to be included in the research into host manipulation is the manipulated host itself. Because manipulation usually involves a high cost for the host, it can be expected to be under a strong selective pressure to evolve resistance to manipulation. The same evolutionary forces that rule host immunity to infection are likely to act in the manipulative interactions as well.

Thus, an absence of host manipulation might be a lack of the respective strategy on the side of the parasite, but it could also indicate that the host has successfully evolved to overcome the manipulation effect.

In the above paragraphs I discussed some of the circumstances that might select for, or against, host manipulation. Life-history traits that seem to be shared by almost all known manipulating parasites are the need to switch among host species and a trophic mode of transmission. Nevertheless, gaining a deeper understanding of the evolution of host manipulation crucially depends on an unambiguous identification of manipulating vs. Plant pathogens provide us with intriguing examples of the multiple alternative explanations that can be provided for the same phenomenon.

Many of these pathogens increase the concentration of free amino acids in the phloem and enhance the attractiveness of the plant odors that are emitted to for herbivores that function as their vectors Mann et al. Because most arthropods use olfactory cues for their long-distance orientation and phloem amino acids represent a limiting factor for sapsuckers, both alterations can increase the attraction of vectors to on an infected plant and benefit the transmission of the pathogen.

However, the physiological mechanisms that control the described phenotypic alterations remain to be identified. In particular, we lack an explanation for a crucial feature of the successful manipulation strategy: the reliability of changes in the odor profile of a plant as indicators of its increased nutritional quality. Alternative explanations for an increase in the amino acid content in the phloem of an infected plant include: i a mobilization of protein-bound amino acids to rescue them from the infected tissue; ii the allocation of amino acids from other parts of the plant to the infected tissue to enable the local synthesis of pathogenesis-related proteins and other N-containing compounds; iii a sink in the infected leaves that is created by an increased need for amino acids owing to the synthesis of viral proteins; or iv a manipulation that the pathogen has evolved to attract its vector.

The first two mechanisms would be under the control of the plant, the other two mechanisms would be under the control of the virus; however, only the last mechanism would represent a classical host manipulation that has been selected to enhance transmission of the pathogen. Similarly, enhanced locomotion e. The observation that Plasmodium -infected mosquitoes feed longer and on more people per night Koella et al. This interpretation is strongly supported by the finding that similar behavioral alterations were observed in mosquitoes that had been challenged with heat-killed E.

The consecutive discovery of functional links between the behavioral alterations and altered insulin signaling in the gut of the mosquito further supports the assumption that it is the mosquito, rather than the Plasmodium , that has genetic control over the altered feeding behavior Cator et al. Moreover, all parasites must suppress parts of the immune system of their host, and parasites of mammals might do so by altering the levels of testosterone or of certain cytokines.

For example, the causal agent of syphilis, T. Specific interferons are also thought to contribute to the survival of Chlamydia in human hosts Duell et al. Even more strikingly, T. Besides favoring infection in the initial phase, these molecular alterations could also suppress sickness behavior, maintain high sexual activity and enhance general aggressive behavior in males, or avoid the rejection of parasitized partners during mating: all these mechanisms would represent manipulation for infection rather than transmission, but they nevertheless can also enhance transmission rates, at least under specific environmental conditions Ashley et al.

The equivalent of such an effect in plants could result from crosstalk among the different plant defensive signaling cascades. Many plants can either respond to chewing herbivores via the induction of genes that depend on jasmonic acid signaling, or mount resistance to infection with biotrophic pathogens via salicylic acid-dependent pathways, but not both Thaler et al.

Because the net quality of a plant as a host for an herbivore or pathogen depends on both, its content of primary nutrients and its spectrum of defensive traits Barrett and Heil, , the increased quality for herbivores that we observe in many diseased plants could be a side-effect of negative crosstalk between different defense systems of the plant, rather than the direct effect of a targeted manipulation by the parasite.

Alternative explanations have been presented for even some of the seemingly most obvious cases of host manipulation. For example, the enhanced numbers of mating events and of different mating partners reported for a water snail infected with horizontally transmitted trematodes could be the result of a successful manipulation by a sexually transmitted parasite; however, it might also represent the outcome of an adaptation of the host, because it leads to enhanced genetic variation among the offspring and, thus, enhanced resistance to the locally adapted parasite Soper et al.

Similarly, several different mechanisms could cause the frequently reported association of elevated levels of testosterone in males with latent toxoplasmosis Flegr et al. Rather than indicating an alteration that is elicited by T. Even when T.

Different scenarios can be formulated as explanations for the same alteration in a parasitized host. This situation illustrates the need to identify the proximate molecular mechanisms that control these alterations and their ultimate effects on the fitness of all involved partners. Unfortunately, the mechanisms and the net fitness effects remain to be investigated for virtually all described cases of host manipulation.

Multiple parasites of insects have been speculated to secrete chemical compounds for host manipulation Libersat et al. However, the detailed nature of these molecules and their modes of action in the host remain to be identified. Surprisingly, we do not even understand the physiological mechanisms that cause the association between toxoplasmosis and schizophrenia, or other behavioral alterations in T. Recent studies provide convincing mechanisms for at least some of the host phenotypic changes that are elicited by this specific parasite.

Interestingly, the genome of T. The commonly observed increase in testosterone levels in infected male rats involves an increase in the expression of those receptors in the testes that regulate the synthesis of testosterone Lim et al.

This finding might explain why enhanced levels of testosterone have been observed only in infected men Flegr et al. Recently, T. However, it remains an open question whether and to what degree these findings are also applicable to the brain of infected humans and, more importantly, the relevance of these effects in the interaction of the natural intermediate hosts with the natural final hosts of T.

Does, for example, the changed response of infected men to cat odor Flegr et al. The last interpretation gains some support from the observation that Toxoplasma -infected chimpanzees exhibit fatal attraction to leopard urine Poirotte et al. The viral gene ecdysteroid-uridine diphosphate-glucosyltransferase encodes an enzyme that inactivates the caterpillar's molting hormone by transferring a sugar moiety to it. Low levels of this hormone suppress molting and reduce caterpillar morbidity, thereby allowing infected individuals to continue feeding for longer time spans compared with uninfected caterpillars Hoover et al.

Recently, it has been shown that baculoviruses enhance the positive phototactic behavior in the infected caterpillars van Houte et al. In summary, it seems that parasites tend to upregulate the synthesis of endogenous signaling molecules in the host, activate or inactivate existing host-derived molecules, or change the sensitivity of existing receptors to host-derived molecules, rather than producing such compounds themselves and delivering them to the host Adamo, Further research efforts are required to understand the ecological, evolutionary and medical relevance of parasites that manipulate their hosts, and this research will require criteria that define how manipulated phenotypes can be identified and distinguished for example, from adaptive host responses to parasitization.

I agree with Poulin, in that particularly complex phenotypic changes can represent good indicators of a manipulation. However, challenging Anopheles stephensi females with heat-inactivated E. Therefore, studies aimed at understanding the relevance of host manipulation by parasites require a clearly defined Null-hypothesis, and they should identify the molecular mechanisms that underlie the observed phenotypic change, consider alternative explanations, and quantify—under ecologically realistic conditions—the effects of the observed change on the fitness of the parasite and that of the host.

First, enhanced parasite fitness is a necessary, but not a sufficient, argument for the consideration of a certain phenotypic alteration as a manipulation effect. Hosts respond to parasitization with multiple phenotypic changes that serve to enhance resistance or tolerance and to decrease transmission rates. As many of these responses are unspecific and target large classes of parasites, they might coincidentally favor the transmission of one or a few specific parasites Levri, These changes are under the genetic control of the host and, thus, cannot be considered a manipulation by the parasite in question.

Moreover, these changes would not be counter-selected as long as the selection pressure exerted by the parasite in question is lower than the selection pressure by the overall group of parasites against which the response leads to enhanced host resistance. Phenotypically plastic hosts will always respond to parasitization, which makes it crucial to define a clear Null-hypothesis: which induced phenotypic responses to parasitization can be expected in a non-manipulated host?

As mentioned above, a successful manipulation can even be indicated by the absence of any alteration when the induced host response would have diminished parasite transmission rates. Second, the adaptive host manipulation hypothesis clearly defines the observed phenotypic alterations as being under the genetic control of the parasite.

Thus, the unambiguous identification of a manipulation event requires an understanding of the physiological and molecular mechanisms that cause these alterations. In other words, the observation of a manipulation effect does not suffice to characterize the manipulator as a parasite Heil, , because manipulation effects can also be exerted by mutualists Wright et al.

Only the demonstration that a certain phenotypic alteration in the host is under the genetic control of the parasite and that it enhances the fitness of the parasite vi an enhancement of its transmission rate, while decreasing the fitness of the host, would provide clear evidence in favor of adaptive host manipulation. Finally, the net outcome of a presumed manipulation depends crucially on the natural rates of encounters among consecutive hosts and on the probability of successful transmission during each of these events.

Hence, the net fitness effects of a presumed manipulation should be quantified at natural densities of parasites, hosts, vectors, and other species that naturally co-occur with the target species in question.

Making the host more suitable for competing parasites, attracting non-vectors to an infested plant that outcompete the vector, or increasing predation rates in the absence of the predator who serves as the definitive host, are all scenarios can select against the evolution of a manipulation effect.

In this context, a particularly elegant approach used naturally co-existing and taxonomically related species of intermediate hosts, among which only one host can reasonably be assumed to have co-evolved with the parasite: increased transmission rates after host phenotypic alterations were observed for the native, but not the invasive intermediate host of a native parasite, an observation that represents a strong argument in favor of an adaptive manipulation Lagrue et al.

In general, a promising strategy to identify manipulators as well as the underlying mechanisms would compare the interactions of parasites that have undergone a recent host shift to the interactions among their ancestors and the original host. Adaptive host manipulation by parasites is a fascinating phenomenon that is likely to have as-yet unknown ecological, evolutionary and medical effects. Host manipulation has been described for all major taxonomic groups of parasites, and the resulting alterations comprise some of the most spectacular examples of extended phenotypes.

Although the biases in the literature make generalizations difficult, I conclude that the majority of manipulating parasites use a trophic mode of transmission and that parasites of animals frequently manipulate their intermediate hosts i.

More studies are required to decipher the molecular mechanisms that control host manipulation, to estimate the frequency of this phenomenon in taxonomic and ecological terms and, ultimately, to understand the evolution of host manipulation as well as its ecological or medical relevance for the species involved.

Future research would benefit from using clearly defined criteria for the identification of manipulated phenotypes, from the integration of the putative effects of host immune responses into studies on manipulating parasites, and from cross-disciplinary approaches that apply ecological, physiological and molecular techniques to comparative studies on model systems from a diverse range of hosts and parasites.

The author confirms being the sole contributor of this work and approved it for publication. The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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