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Distribution Status of Hybrid Types in Large Liver Flukes, Fasciola Species (Digenea: Fasciolidae), from Ruminants and Humans in Vietnam
research-article
Author(s):
Thi Bich Nga Nguyen
1 ,
Nguyen Van De
2 ,
Thi Kim Lan Nguyen
3 ,
Huynh Hong Quang
4 ,
Huong Thi Thanh Doan
1 ,
Takeshi Agatsuma
5 ,
Thanh Hoa Le
1
,
*
Publication date (Electronic):
31 October 2018
Journal:
The Korean Journal of Parasitology
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Abstract
The aim of this study is to delineate ‘admixed hybrid’ and ‘introgressive’ Fasciola genotypes present in the Fasciola population in Vietnam. Adult liver flukes collected from ruminants in 18 Provinces were morphologically sorted out by naked eyes for small (S), medium (M) and large (L) body shapes; and human samples (n=14) from patients. Nuclear ribosomal (rDNA) ITS1 and ITS2, and mitochondrial (mtDNA) nad1 markers were used for determination of their genetic status. Total 4,725 worm samples of ruminants were tentatively classified by their size: 6% (n=284) small (S)-, 13% (n=614) medium (M)-, and 81% (n=3,827) large (L)-forms. All the representative (n=120, as 40 each group) and 14 human specimens, possessed maternal mtDNA of only F. gigantica and none of F. hepatica. Paternally, all (100%) of the L-(n=40) and 77.5% (n=31) of the M-flukes had single F. gigantica rDNA indicating ‘pure’ F. gigantica. A majority (90%, n=36) of the S- and 15% (n=6) of the M-worms had single F. hepatica rDNA, indicating their introgressive; the rest (10%, n=4) of the S- and 7.5% (n=3) of the M-flukes had mixture of both F. gigantica and F. hepatica rDNAs, confirming their admixed hybrid genetic status. Fourteen human samples revealed 9 (64%) of pure F. gigantica, 3 (22%) of introgressive and 2 (14%) of admixed hybrid Fasciola spp. By the present study, it was confirmed that the small worms, which are morphologically identical with F. hepatica, are admixed and/or introgressive hybrids of Fasciola spp., and able to be the pathogens of human fascioliasis.
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Most cited references37
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Chapter 2. Fasciola, lymnaeids and human fascioliasis, with a global overview on disease transmission, epidemiology, evolutionary genetics, molecular epidemiology and control.
Fascioliasis, caused by liver fluke species of the genus Fasciola, has always been well recognized because of its high veterinary impact but it has been among the most neglected diseases for decades with regard to human infection. However, the increasing importance of human fascioliasis worldwide has re-launched interest in fascioliasis. From the 1990s, many new concepts have been developed regarding human fascioliasis and these have furnished a new baseline for the human disease that is very different to a simple extrapolation from fascioliasis in livestock. Studies have shown that human fascioliasis presents marked heterogeneity, including different epidemiological situations and transmission patterns in different endemic areas. This heterogeneity, added to the present emergence/re-emergence of the disease both in humans and animals in many regions, confirms a worrying global scenario. The huge negative impact of fascioliasis on human communities demands rapid action. When analyzing how better to define control measures for endemic areas differing at such a level, it would be useful to have genetic markers that could distinguish each type of transmission pattern and epidemiological situation. Accordingly, this chapter covers aspects of aetiology, geographical distribution, epidemiology, transmission and control in order to obtain a solid baseline for the interpretation of future results. The origins and geographical spread of F. hepatica and F. gigantica in both the ruminant pre-domestication times and the livestock post-domestication period are analyzed. Paleontological, archaeological and historical records, as well as genetic data on recent dispersal of livestock species, are taken into account to establish an evolutionary framework for the two fasciolids across all continents. Emphasis is given to the distributional overlap of both species and the roles of transportation, transhumance and trade in the different overlap situations. Areas with only one Fasciola spp. are distinguished from local and zonal overlaps in areas where both fasciolids co-exist. Genetic techniques applied to liver flukes in recent years that are useful to elucidate the genetic characteristics of the two fasciolids are reviewed. The intra-specific and inter-specific variabilities of 'pure'F. hepatica and 'pure'F. gigantica were ascertained by means of complete sequences of ribosomal deoxyribonucleic acid (rDNA) internal transcribed spacer (ITS)-2 and ITS-1 and mitochondrial deoxyribonucleic acid (mtDNA) cox1 and nad1 from areas with only one fasciolid species. Fasciolid sequences of the same markers scattered in the literature are reviewed. The definitive haplotypes established appear to fit the proposed global evolutionary scenario. Problems posed by fasciolid cross-breeding, introgression and hybridization in overlap areas are analyzed. Nuclear rDNA appears to correlate with adult fluke characteristics and fasciolid/lymnaeid specificity, whereas mtDNA does not. However, flukes sometimes appear so intermediate that they cannot be ascribed to either F. hepatica-like or F. gigantica-like forms and snail specificity may be opposite to the one deduced from the adult morphotype. The phenotypic characteristics of adults and eggs of 'pure'F. hepatica and F. gigantica, as well as of intermediate forms in overlap areas, are compared, with emphasis on the definitive host influence on egg size in humans. Knowledge is sufficient to support F. hepatica and F. gigantica as two valid species, which recently diverged by adaptation to different pecoran and lymnaeid hosts in areas with differing environmental characteristics. Their phenotypic differences and ancient pre-domestication origins involve a broad geographical area that largely exceeds the typical, more local scenarios known for sub-species units. Phenomena such as abnormal ploidy and aspermic parthenogenesis in hybrids suggest that their separate evolution in pre-domestication times allowed them to achieve almost total genetic isolation. Recent sequencing results suggest that present assumptions on fasciolid-lymnaeid specificity might be wrong. The crucial role of lymnaeids in fascioliasis transmission, epidemiology and control was the reason for launching a worldwide lymnaeid molecular characterization initiative. This initiative has already furnished useful results on several continents. A standardized methodology for fasciolids and lymnaeids is proposed herein in order that future work is undertaken on a comparable basis. A complete understanding of molecular epidemiology is expected to help greatly in designing global actions and local interventions for control of fascioliasis.
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Hybridization in Parasites: Consequences for Adaptive Evolution, Pathogenesis, and Public Health in a Changing World
Kayla C. King, Rike Stelkens, Joanne P Webster … (2015)
Hybridization of parasites is an emerging public health concern at the interface of infectious disease biology and evolution. Increasing economic development, human migration, global trade, and climate change are all shifting the geographic distribution of existing human, livestock, companion animal, and wildlife parasites [1–9]. As a result, human populations encounter new infections more frequently, and coinfection by multiple parasites from different lineages or species within individual hosts occurs. Coinfection may have a large impact on the hosts and parasites involved, often as a result of synergistic or antagonistic interactions between parasites [10]. Indeed, mixed-species coinfections have been found to influence parasite establishment, growth, maturation, reproductive success, and/or drug efficacy [11–13]. However, coinfections can allow for heterospecific (between-species or between-lineage) mate pairings, resulting in parthenogenesis (asexual reproduction in which eggs occur without fertilization), introgression (the introduction of single genes or chromosomal regions from one species into that of another through repeated backcrossing), and whole-genome admixture through hybridization [14]. Recent molecular developments have revealed instances of fertile hybridization and introgression in plants [15], animals [16,17], and humans [18]. However, modern genetics and genomics have also uncovered the first confirmed cases of introgression within eukaryotic parasites [14,19]. Examples for such successful reticulate evolution in parasites include, but are not exclusive to, causative agents of important diseases initiated by fungi (Cryptococcus [20]), helminthic worms (Schistosoma, Fasciola, Ascaris, and Trichinella [21,22–24]), and protozoa (Plasmodium, Leishmania, Toxoplasma, and Trypanosoma [25,26–31]), as well as their vectors. These cases involve introgression between members of the neglected tropical diseases (NTDs) and/or neglected zoonotic diseases (NZDs)—highly debilitating diseases infecting more than a sixth of the world’s human population (and their livestock), with devastating consequences for individuals and communities. Such diseases are predominantly diseases of the world’s poorest communities, afflicting those people who are most at risk of contracting mixed parasitic infections (and hence also at risk for potential novel introgressed parasite infections) and at the same time least likely to get proper medical care once infected [32]. Evidence gathered to date, mainly from studies on nonparasitic animals and plants, suggests that hybridization can have a major evolutionary impact [33]. While hybridization can result in lower average fitness due to F1 sterility and inviability, caused by negative epistatic interactions [34–36] and the disruption of beneficial gene complexes [37,38], hybridization is at the same time a rich source of new genetic variation [39]. This can provide the raw material for natural selection to shape the evolution of ecologically relevant traits [33,40,41]. Thus, while a hybrid offspring, under certain conditions, may be less fit than its purebred offspring counterparts from either parental line, hybridization broadens the “working surface” for selection by producing a whole range of potentially adaptive phenotypes, ranging from one parent to the other and beyond. In nonparasitic taxa, hybridization has already been shown to promote geographic range expansions of populations (for example, in spiders [42]) as well as adaptation to new environments (Darwin finches [43]). There is also increasing evidence that hybridization can lead to the functional diversification of a group, as shown in Helianthus sunflowers [44], and even to speciation (reviewed in [40,45,46]). One key example of this is the case of “transgressive hybrids,” i.e., hybrids expressing extreme phenotypes that do not reside in either of the parental populations. These are “hopeful monsters” with respect to their evolutionary potential because they can diverge from their parents ecologically and may quickly become reproductively isolated from them [47–49]. In addition to broadening the selection surface, hybridization can also speed up the process of adaptation. After hybridization events, new alleles or allelic combinations that happen to be beneficial in the new environment are available immediately. This is in contrast to nonhybrid populations in which adaptation relies on alleles brought in via immigration or de novo mutation, both processes that require relatively longer periods of time [50,51]. As a consequence, populations with a hybrid origin may survive rapid environmental change better than their nonhybrid parents, as recently shown in yeast [52]. We predict that parasites are one of the major groups of organisms in which hybridization can have major impacts on the evolution and diversification of a group [14,19] and can lead to speciation [53], affecting key pathogenic traits and transmission. Hybridization in parasites may thus pose a serious challenge for the prevention, effective control, and therapy of disease [19]. While it has been suggested that hybridization and introgression between parasites can potentially drive the emergence and rapid evolution of novel zoonotic diseases [14], most studies to date are descriptive and do not consider the evolutionary consequences. Here, we review some of the most recent advances in the detection of hybridization in eukaryotic parasites (and their vectors) and discuss the significance of parasite hybridization for adaptive evolution and public health supported by relevant case studies in Schistosoma spp. (Box 1), Leishmania and Trypanosoma (Box 2), and the malaria vector Anopheles (Box 3). Given the role of infectious agents in our changing world, particularly in terms of emerging parasitic disease in response to anthropogenic change [32], it is time for a new and integrative perspective. Here, we argue for the integration of parasitology, disease biology, and evolutionary biology to understand the consequences of parasite hybridization to aid in the management and prevention of disease. Box 1. Case Example—Introgression in Helminths: Schistosomiasis Schistosoma spp. are the causative agents of schistosomiasis, a prevalent, chronic, and debilitating helminthic disease of humans and animals that occurs across much of the developing world. As early as 1948, there have been phenotypic reports of eggs indicative of potential Schistosoma haematobium–S. mattheei hybrids in Rhodesia/Zimbabwe [75], S. bovis–S. curassoni hybrids in West African ruminants, S. haematobium–S. mattheei hybrids in Southern African ruminants, and S. haematobium–S. bovis hybrids in humans from West Africa [76–78]. More recently, ITS1+2 and cox1 barcoding studies of viable schistosome miracidial larvae hatched from the stool and urine of Senegalese school children confirmed bidirectional hybridization between human S. haematocium and livestock S. bovis [67], as well as for S. haematobium and S. curassoni [79]. Studies from infected snails in Kenya have observed hybrid cercariae between S. mansoni from humans and its sister species, S. rodhaini, from rodents [80]. These authors, using microsatellite markers (ribosomal DNA [rDNA] and mitochondrial DNA [mtDNA]), demonstrated that these hybrids produce viable offspring through first or successive generation backcrosses with S. mansoni. Unlike the S. haematobium and S. bovis or S. currassoni hybrids described above, the direction of introgression appeared highly asymmetric, causing unidirectional gene flow from the rodent S. rodhaini to the human S. mansoni [80]. Recent evidence from infected humans in Senegal has also revealed the potential for introgressions between the more phylogenetically distant pairings of the two major human schistosome species in Africa, S. haematobium and S. mansoni, a pairing previously thought to result in unviable eggs exclusively through parthogenesis [81]. These studies combined provide convincing evidence that schistosome species readily hybridize in nature, which may have major implications in light of the current global push for human disease control programmes to shift from controlling morbidity to halting transmission [32]. How such introgression may alter host range is perhaps the most pressing area for future research. Many schistosome species infecting livestock have a broader geographical range beyond Asia and Africa, with compatible snail intermediate hosts present. Novel zoonotic hybrids may therefore have the potential to be a global disease, particularly in our current climate of global warming and increased human and animal movement and transportation. This may be highlighted most clearly where novel introgressed hybrids between human S. haematobium and livestock S. bovis have recently been identified, with substantial ongoing transmission amongst both local residents and tourists, within Europe [82–84]. Box 2. Case Example—Introgression in Protozoans: Leishmaniosis and Trypanosomiasis Introgressions can occur within the causative agents of protozoal diseases leishmaniasis and trypanosomiasis (Kinetoplastida: Trypanosomatidae) [85–88]. Approximately 30,000 people in 36 countries of sub-Saharan Africa suffer from human African trypanosomiasis (HAT), and Chagas disease has been classed as the most important vector-borne infection in Latin America, affecting an estimated 7–8 million humans, with around 21,000 deaths per year [89]. Leishmania parasites are another of the most important vector-borne pathogens in the developing world. Both Leishmania and Trypanosoma are also parasites with major zoonotic reservoirs. Two of the major lineages of Trypanosoma cruzi (discrete typing units [DTUs] III and IV) are now thought to have arisen by intraspecific hybridisation [87], despite their predominant mode of asexual reproduction, and introgression between subspecies has been associated with virulence [88]. Similarly, whilst asexual reproduction through clonal propagation has been proposed to be the major reproductive mechanism across the genus Leishmania, a hybridizing sexual cycle has been detected within its sand fly vector from across a range of geographical locations [90,91]. Whole-genome sequencing of Leishmania parasites isolated from sand flies from a Turkish endemic area indicated that variation in these parasites arose following a single cross between two phylogenetically distinct strains. Furthermore, whilst it appears that these populations do reproduce primarily clonally following this original hybridization event, subsequent recombination between the progeny does also occur [92]. The potentially large epidemiological consequences of such recombination events may be demonstrated by the observation that Leishmania infantum/L. major hybrids possess an enhanced host range, as hybrid offspring, and, unlike their parental single species, they are able to infect another vector, Phlebotomus papatasi [93]. Box 3. Case Example—Introgression in the Parasite Vector Anopheles: Malaria Anopheles has become a model organism at the interface of speciation genomics and epidemiology [94], showcasing the potential perils of hybridization for public health but also the possible benefits of using controlled and induced hybridization as a means for disease control. Anopheles mosquitoes are vectors for malaria, which is caused by parasitic protozoans belonging to the genus Plasmodium. Malaria affects 200 million people a year worldwide, with an estimated 0.5–1 million deaths per year, mostly among young children in sub-Saharan Africa, where 90% of the world’s malaria deaths occur [95]. There are approximately 60 different species of Anopheles found worldwide [96], and genomic sequences of 16 Anopheles species (including vector and nonvector species) have recently become available [94,97]. These sequences have revealed fast and flexible evolutionary rates with respect to traits affecting their transmission potential, shown extensive introgression between Anopheles species, and suggested that enhanced vectorial capacity and adaptation to humans as primary hosts can result from interspecific genetic exchange. A multilocus single nucleotide polymorphism (SNP) genotyping panel is also at hand to detect F1 hybrids and backcrosses between the main vectors of malaria, Anopheles gambiae sensu stricto (S form) and A. coluzzii (M form) [98]. Control of Anopheles through insecticides, such as dichlorodiphenyltrichloroethane (DDT) and pyrethroids, has contributed to the prevention of malaria, but resistance to insecticides has recently emerged in Anopheles populations [99,100]. Recent studies have demonstrated rapid adaptive introgression of the insecticide resistance mutation Vgsc-L1014F from A. gambiae to A. coluzzii, in response to strong anthropogenic selection from increased insecticide use [101,102]. Others have found gene flow occurring at rates “far from inconsequential” between other species of Anopheles (e.g., between A. gambiae and A. arabiensis in Uganda [99,103] and A. sinensis and A. kleini in Korea [104]). Experimental interpopulation crosses of A. gambiae, monitored for traits determining their malaria transmission potential, scored higher for fecundity, body size, adult longevity, and average blood meal size, compared to both parental strains [105]. It is thus conceivable that the fitness-enhancing potential of hybridization may also apply to closely related interspecific hybrid crosses. Hybridization between Anopheles species may have beneficial effects for disease control. Asymmetric introgression has recently been shown to transfer adaptive immunity and increased refractoriness to the Plasmodium pathogen from A. coluzzii to A. gambiae in Guinea [106]. Another opportunity for disease control is to modify the host preference of A. gambiae from humans to cattle by hybridizing it with A. quadriannulatus, a more zoophilic nonvector species, as a strategy to decrease its competence as malaria vector [107]. Consequences of Hybridization in Parasites Since multidrug resistance became a worldwide problem in pathogenic bacteria in the 1950s [54], we know that the exchange of genetic material via horizontal gene transfer among bacterial taxa has contributed to their evolution and pathogenesis [55,56]. Horizontal gene transfer can be advantageous and confer higher fitness, for instance, through the acquisition of antibiotic drug resistance [57] or through the spread of virulence factors; a well-studied example is the Shiga toxin genes exchanged between Escherichia coli and Shigella bacterial pathogens [58]. There are also several examples of recombinant human viruses that have exchanged genes with other strains with detrimental effects (Spanish flu, human rotavirus, and dengue fever; [59,60,61]). Conversely, despite their equally negative impact on host populations, not much is known about the hybridization of eukaryotic parasites, their frequency in the wild, or how hybridization may affect their spread and pathogenicity. Modern molecular techniques, however, can expose the signature of hybridization in the genome more rapidly and accurately, thereby increasing the number of recent reports of parasite hybridization. We outline what we believe will be the most important and/or potentially dangerous effects of hybridization in eukaryotic parasites: (1) the generation of novel and extreme infection phenotypes, (2) an increase in host range, being just one component of (3) an increase in transmission potential, (4) an increase in parasite evolutionary potential with consequences for host–parasite coevolution, (5) the breakdown of host-specific adaptations, and also (6) an altered response to drug therapy (Fig 1). 10.1371/journal.ppat.1005098.g001 Fig 1 Schematic of the drivers and consequences of parasite hybridization. As a result of new allelic combinations produced by hybridization, hybrid parasites may show enhanced phenotypic characteristics compared to the parents. Hybrids may be better at host exploitation, such that they may be more efficient at obtaining nutrition from the host, leading to higher fecundity or faster maturation time. Also, certain new hybrid parasite genotypes have been shown to be better at avoiding recognition and resistance from the host’s adaptive immune system, potentially leading to higher infectivity and unusual pathologies [29,62]. We thus predict that hybrid parasites are able to exploit novel resources and sites of infection within the host, which parental genotypes cannot utilize. Hybrid parasites may be able to infect a greater range of host species [14,19,63]. While parental parasites are often restricted to one host species, hybrid parasites may be able to exploit both. Interspecific Schistosoma spp. hybrids, for instance, are able to infect both parental intermediate snail hosts (Box 1) [21]. In addition, just as some hybrids of nonparasitic taxa adapt to new ecological conditions and colonize novel environments that neither of the parents can survive [44,49], we would predict that hybrid parasites may be able to infect entirely new host species. As an indication that this indeed occurs in the wild, two plant pathogenic fungi (Phytophthora spp. infecting alder trees [64] and Zymoseptoria pseudotritici infecting a range of grasses [53]) and one amphibian fungal pathogen (a new lineage of Batrachochytrium dendrobatidis causing dramatic outbreaks of chytridiomycosis [65 ]), which all emerged via hybridization, have been found to live on host species neither of their parents are found on. With increasing land use and current rates of anthropogenic change across both the environment and agricultural/livestock practices, we predict that recombinant parasite genotypes will be generated at an increasing rate. Encounters between previously isolated parasite species become more frequent when geographic and ecological barriers that previously existed between parasite species are lost. Taking together the potential impact of hybrid superiority and host range expansions (described in 2) and an increase in anthropogenically mediated parasite dispersal, the transmission of disease may become considerably facilitated [66,67]. This may lead to epidemics, threaten global food security, and endanger natural animal and plant populations. For instance, the increasing creation and alteration of water bodies for agriculture can lead to areas of overlap and co-occurrence of the different intermediate snail host species of Schistosoma parasites [66,68]. This generates ample opportunity for coinfections of the definitive host by different Schistosoma species, which may then hybridize. In addition, humans and livestock are drawn to the same water resources, where they can both release parasites and become infected, thus creating a “hotbed” for disease transmission between human and livestock. Evolutionary theory predicts that elevated virulence and genetic diversity, both potential outcomes of parasite hybridization, can increase the evolutionary potential of parasites and alter the host–parasite coevolutionary process [69]. For instance, for Phytophthora, hybridization has led to a range of new species with particularly aggressive pathogenicity [64], and hybrid lineages of the amphibian zoosporic fungus Batrachochytrium, which cause dramatic outbreaks of chytridiomycosis, have been found to be hypervirulent to many hosts [65]. In the context of coevolutionary races, higher virulence of hybrid parasites may impose stronger selection for host resistance. Hybridization in parasites could, however, also be maladaptive for the parasites because of fitness-reducing genetic incompatibilities (negative epistasis) and the breakdown of host-specific adaptations, potentially leading to reduced infectivity/virulence. While such outbreeding depression is well known from free-living organisms, studies on the fitness of hybrid parasites are scarce. Outbreeding depression has been reported in a snail–trematode host–parasite system (Potamopyrgus antipodarum–Microphallus sp.), in which hybrid parasites suffer from reduced infectivity in both parental host populations [70,71]. In such cases, we predict that hybrid parasites may be less likely to evade host immunity or they may fail to effectively colonize the correct organ or body site. Through recombination and segregation, hybrids may also lose beneficial alleles that the parents had acquired previously, such as those conferring drug resistance (see below). Hybrid parasite inferiority can also lead to unusual pathogensis, which may hamper diagnosis, particularly when two very different disease phenotype parasites are introgressed (Box 1). As such, hybridization between divergent parasite populations may both promote and alter pathogenesis, which has important implications on disease prevalence, pathology, and treatment. Hybridization may have a wide range of effects on drug efficacy in parasites. On the one hand, zoonotic hybrids may exhibit enhanced susceptibility to drugs if resistance alleles circulating in the human host parasite population are swamped by introgression of drug-susceptible alleles from the animal host parasite population. Furthermore, if hybridization between human and animal parasites increases the host range from human host specificity to that of a large animal host range reservoir, this could act against the establishment and spread of drug resistance [32]. Alternatively, hybridization could potentiate adaptive evolution within certain parasites in response to drug treatment (Box 1). One example for this is Cryptococcus serotype hybrids that are resistant to an antifungal drug usually used to treat infections with the individual parental serotypes [20]. More evidence for the adaptive introgression of drug resistance genes from nonsusceptible strains or species comes from Haemonchus nematodes that gained resistance against the broad-spectrum drug ivermectin through hybridization [72,73] and the introgression of anticoagulant rodent poison resistance by hybridization between Old World mice [74]. Conclusions Understanding and monitoring hybridization in animal and human parasites will be essential for optimizing and evaluating control strategies across potential hybrid zones. Relatively simple diagnostic procedures currently exist for detecting hybrids in some parasite groups (e.g., using a multilocus approach with mitochondrial cytochrome c oxidase subunit 1 (COX-1)/internal transcribed spacer (ITS) barcoding; [67]). However, the advancement of state-of-the-art genomic technologies will be helpful for more fine-scale detection of hybridization in parasites, to determine their evolutionary rates, and to identify patterns of cross transmission between host species (i.e., sources of transmission of zoonotic parasites to humans). Since hybrid parasites appear to be a particular problem in NTDs, there is a need to develop cheap, robust diagnostics appropriate to use in the field. The circumstances producing increased opportunity for hybridization are the same ones that cause increased rates for disease distribution and transmission. Thus, the likelihood of parasite hybridization is increasing with the intensification of world trade of plants and animals, human migration, land use, and drug administration (Fig 1). Interspecific hybridization and introgression appear to be viable strategies for many parasites to maintain transmission, with potentially major impacts on the evolution of virulence, infection persistence, drug resistance, and host range, as well as on the clinical outcomes of disease. The combined effects of anthropogenic distribution and increased hybridization opportunities could have hazardous and catalytic effects on epidemiology, imposing further challenges and constraints for their effective control. More empirical work on the differential transmission, infectivity, drug efficacy, pathogenesis, and evolution of hybrid parasite populations is therefore urgently required to guide policies on their monitoring and management.
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A prospective view of animal and human Fasciolosis
K Cwiklinski, S O'Neill, S E Donnelly … (2016)
Summary Fasciolosis, a food‐borne trematodiasis, results following infection with the parasites, Fasciola hepatica and Fasciola gigantica. These trematodes greatly affect the global agricultural community, infecting millions of ruminants worldwide and causing annual economic losses in excess of US $3 billion. Fasciolosis, an important zoonosis, is classified by WHO as a neglected tropical disease with an estimated 17 million people infected and a further 180 million people at risk of infection. The significant impact on agriculture and human health together with the increasing demand for animal‐derived food products to support global population growth demonstrate that fasciolosis is a major One Health problem. This review details the problematic issues surrounding fasciolosis control, including drug resistance, lack of diagnosis and the threat that hybridization of the Fasciola species poses to future animal and human health. We discuss how these parasites may mediate their long‐term survival through regulation and modulation of the host immune system, by altering the host immune homeostasis and/or by influencing the intestinal microbiome particularly in respect to concurrent infections with other pathogens. Large genome, transcriptome and proteomic data sets are now available to support an integrated One Health approach to develop novel diagnostic and control strategies for both animal and human disease.
Author and article information
Journal
Journal ID (nlm-ta): Korean J Parasitol
Journal ID (iso-abbrev): Korean J. Parasitol
Title:
The Korean Journal of Parasitology
Publisher:
The Korean Society for Parasitology and Tropical Medicine
ISSN
(Print):
0023-4001
ISSN
(Electronic):
1738-0006
Publication date
(Print):
October
2018
Publication date
(Electronic):
31
October
2018
Volume: 56
Issue: 5
Pages: 453-461
Affiliations
[1
]Institute of Biotechnology (IBT), Vietnam Academy of Science and Technology (VAST)
18. Hoang Quoc Viet Rd, Cau Giay, Hanoi, Vietnam
Author notes
Article
Publisher ID: kjp-56-5-453DOI: 10.3347/kjp.2018.56.5.453
PMC ID: 6243193
PubMed ID: 30419731
SO-VID: 313fac14-d847-4d8a-aedd-8e8084ffd05b
Copyright © Copyright © 2018 by The Korean Society for Parasitology and Tropical Medicine
License:
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
History
Date
received
: 2
September
2018
Date
revision received
: 16
October
2018
Date
accepted
: 17
October
2018
Categories
Subject:
Original Article
ScienceOpen disciplines: Parasitology
Data availability:
ScienceOpen disciplines: Parasitology