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Echinococcus

Echinococcus is a genus of small tapeworms (cestodes) in the family Taeniidae that parasitize the intestines of carnivorous definitive hosts, such as dogs and foxes, while their larval stages cause echinococcosis—a potentially life-threatening zoonotic disease—in intermediate hosts including livestock, wildlife, and humans.^[1]^[2] The genus comprises several species, with E. granulosus (responsible for cystic echinococcosis) and E. multilocularis (causing alveolar echinococcosis) being the most significant for human health, alongside rarer species like E. vogeli and E. oligarthrus that lead to neotropical forms of the disease.^[1]^[2] Transmission occurs primarily through the ingestion of infective eggs shed in the feces of definitive hosts, contaminating food, water, or environments in endemic areas.^[1]^[2] The life cycle of Echinococcus species is indirect and complex, involving definitive hosts where adult worms (2–7 mm long) mature and produce eggs containing oncospheres, which are released into the environment via feces.^[1] In intermediate hosts, ingested eggs hatch, and larvae migrate to organs—most commonly the liver and lungs—forming hydatid cysts that can grow slowly over years and contain protoscolices capable of developing into adults if ingested by a definitive host.^[1] Humans act as dead-end intermediate hosts, with cysts often remaining asymptomatic until complications arise, such as rupture leading to anaphylaxis or secondary infections.^[2] Cystic echinococcosis from E. granulosus produces unilocular, fluid-filled cysts with a thick laminated wall, whereas alveolar echinococcosis from E. multilocularis results in infiltrative, tumor-like multilocular lesions that mimic malignancy and have a high fatality rate (up to 90%) if untreated.^[1]^[2] According to the Global Burden of Disease Study 2021, echinococcosis had a global prevalence of approximately 633,000 cases in 2021, causing 1,364 deaths and 105,072 disability-adjusted life years, with incidence and prevalence increasing from 1990 to 2021 while deaths and DALYs declined; projections suggest rising cases through 2046.^[3] Earlier 2015 estimates indicated over 1 million cases annually, around 19,300 deaths, 871,000 DALYs, and economic losses exceeding US$3 billion due to impacts on livestock and healthcare.^[2] E. granulosus is distributed worldwide in rural pastoral communities, particularly in parts of Africa, Asia, South America, and the Mediterranean, while E. multilocularis is confined to the northern hemisphere, including Europe, northern Asia, and parts of North America.^[1]^[2] Prevention strategies emphasize a One Health approach, including regular deworming of dogs (at least four times per year), improved slaughterhouse hygiene, vaccination of livestock (e.g., EG95 vaccine for sheep against CE), and public health education to reduce contact with contaminated sources.^[2] Diagnosis typically involves imaging (ultrasound, CT) and serology, with treatment combining surgery, percutaneous aspiration, and antiparasitic drugs like albendazole.^[1]^[2]

Taxonomy and Classification

Etymology and History

The genus name Echinococcus is derived from the Greek words echinos, meaning "hedgehog" or "spiny," and kokkos, meaning "berry" or "seed," reflecting the small, berry-like size of the protoscolices and the spiny hooklets on the hexacanth embryo.^[4]^[5] The scientific recognition of Echinococcus began with early observations of hydatid cysts. In 1760, Peter Simon Pallas described hydatid cysts in various mammals, noting their similarities to those in humans and classifying them among the "bladder worms."^[6]^[7] By 1766, Pallas further hypothesized a connection between these cysts and tapeworm larvae, marking an initial step toward understanding the parasite's life cycle.^[6] In 1801, Karl Asmus Rudolphi formally described the adult worm as Taenia echinococcus and established the genus Echinococcus, distinguishing it from other taeniid tapeworms based on its minute size and morphology.^[5]^[8] A pivotal advancement occurred in the 1850s when Rudolf Virchow linked alveolar hydatid disease to Echinococcus species, identifying the larval stage as the causative agent through pathological examinations in humans.^[9] Early epidemiological reports of Echinococcus infections emerged primarily from Europe and Asia during the 19th century, with hydatid cysts noted in livestock and wildlife across regions like Germany, Switzerland, Russia, and the Alps.^[10] Human cases were documented by the 1860s, including fatal alveolar infections in southern Germany and cystic forms in Iceland, highlighting the zoonotic risks in pastoral communities.^[11]^[12]

Species Overview

The genus Echinococcus comprises nine recognized species of small tapeworms in the family Taeniidae, primarily distinguished by their adult morphology, larval cyst formation, and host preferences. These species, as per the 2020 international consensus, include E. granulosus sensu stricto, E. equinus, E. ortleppi, E. canadensis, E. felidis, E. multilocularis, E. shiquicus, E. vogeli, and E. oligarthrus. They vary in geographic distribution, with E. granulosus s.s. being the most widespread and zoonotically significant.^[13]^[14]^[15] Echinococcus granulosus sensu stricto (formerly sheep strain, G1-G3) features adults measuring 2-7 mm in length with 3-4 proglottids, including an immature, mature, and gravid segment. Larval stages form unilocular, fluid-filled hydatid cysts. Definitive hosts are primarily dogs and other wild canids, while intermediate hosts include domestic ungulates such as sheep, goats, and cattle. It is distributed worldwide in rural pastoral communities.^[1]^[15]^[13] E. equinus (formerly horse strain, G4) yields adults of 3-6 mm with 3-4 proglottids and unilocular cysts. It cycles between dogs as definitive hosts and equids (horses, donkeys) as intermediate hosts, mainly in Europe and Africa, and is considered non-zoonotic for humans.^[15]^[13] E. ortleppi (formerly cattle strain, G5) has adults of 3-5 mm with 3-4 proglottids and produces unilocular cysts primarily in cattle as intermediate hosts. Definitive hosts include dogs and wolves. It is reported in Africa (e.g., South Africa, Kenya), South America (e.g., Peru), Europe (e.g., Italy), and Asia (e.g., India, China), with rare human infections.^[13]^[16] E. canadensis (G6–G10, including camel, pig, and cervid strains) has adults 2-6 mm long with 3-4 proglottids and unilocular cysts. Definitive hosts are canids such as dogs, wolves, and coyotes; intermediate hosts vary by genotype, including camels (G6), pigs (G7, G9), and cervids like reindeer and moose (G8, G10). Distribution is global but genotype-specific: G6 in Asia and Africa, G7 and G9 in Europe, G8-G10 in North America and Eurasia. It is zoonotic but less common in humans than E. granulosus s.s.^[1]^[13]^[17] E. felidis (African lion strain) produces small adults (2.5-3.5 mm) with 3 proglottids and unilocular cysts. Definitive hosts are lions and spotted hyenas; intermediate hosts include antelopes and warthogs. It is endemic to sub-Saharan Africa, with no reported human infections.^[13]^[18] In contrast, E. multilocularis, known as the fox tapeworm, produces smaller adults of 1.2-4.5 mm with 3-5 proglottids. Its larval cysts are multilocular and invasive, forming alveolar-like masses rather than discrete fluid-filled structures. Definitive hosts are foxes, dogs, and other wild canids, with rodents serving as primary intermediate hosts.^[1]^[13]^[15] The Neotropical species E. vogeli features adults up to 5.6 mm long with up to 6 proglottids and develops polycystic larval stages that aggregate into multichambered cysts. It maintains a sylvatic cycle with bush dogs as definitive hosts and rodents like pacas as intermediate hosts, primarily in South America.^[1]^[13] Similarly, E. oligarthrus, rarer and also restricted to Central and South America, has adults up to 2.9 mm with up to 6 proglottids; its cysts are typically polycystic or unicystic. Definitive hosts are wild felids such as pumas, and intermediate hosts include rodents like agoutis and pacas.^[1]^[13] E. shiquicus is endemic to the Tibetan plateau, where adults are small (similar to other species at around 2-4 mm) and produce cysts of undetermined structure but likely unilocular. Definitive hosts are Tibetan foxes, and intermediate hosts are plateau pikas, with no reported human infections.^[15]^[13]

Phylogenetic Relationships

The genus Echinococcus is monophyletic within the family Taeniidae, diverging from the paraphyletic genus Taenia over 10 million years ago during the late Miocene, with the taeniid lineage beginning to diversify approximately 11.2 million years ago.^[19] The Echinococcus clade itself represents a relatively young group, originating around 5.8 million years ago at the end of the Miocene, likely in North America or Asia based on host-parasite co-evolutionary patterns involving canid or felid definitive hosts.^[19]^[20] This radiation is characterized by rapid speciation and global dispersal, facilitated by mammalian host migrations, such as the formation of the Panamanian land bridge around 3 million years ago, which enabled the southward movement of carnivore ancestors.^[19] Phylogenetic analyses, primarily derived from complete mitochondrial genomes and nuclear protein-coding genes, position the Neotropical species E. oligarthrus and E. vogeli as basal to the rest of the genus, reflecting their ancient divergence and endemicity to Central and South America.^[20]^[19] The former E. granulosus sensu lato complex forms a derived clade that has been split into distinct species: E. granulosus sensu stricto (G1–G3), E. equinus (G4), E. ortleppi (G5), and E. canadensis (G6–G10), which exhibit varying host specificities and geographic distributions.^[20] In contrast, E. multilocularis clusters closely with E. shiquicus as sister species, distinct from the E. granulosus s.l. complex, highlighting separate evolutionary trajectories within the alveolar echinococcosis-causing lineage. E. felidis forms a separate lineage associated with felid hosts in Africa.^[20] A 2020 international consensus by the World Association of Echinococcosis resolved longstanding nomenclature debates by formally recognizing nine species in the genus, elevating certain genotypes to species status—such as E. granulosus sensu stricto (encompassing G1–G3), E. equinus (G4), E. ortleppi (G5), and E. canadensis (G6–G10)—based on genomic, morphological, and epidemiological evidence, while standardizing terms to avoid ambiguity in research and clinical contexts.^[21] Genetic delineation across these taxa relies heavily on mitochondrial DNA markers, particularly the cytochrome c oxidase subunit 1 (cox1) gene, which provides high-resolution sequencing for identifying strains and detecting subtle variations.^[20] Evidence of infrequent hybridization, or introgressive events, has been observed between E. granulosus strains (e.g., G1 and G3), as indicated by shared polymorphisms in mitochondrial and nuclear loci, potentially contributing to genetic diversity and adaptive evolution in endemic regions.^[22]

Morphology and Biology

Adult Worm Characteristics

The adult worms of Echinococcus species are small, ribbon-like cestodes in the family Taeniidae, exhibiting a triploblastic, acoelomate body plan typical of flatworms, with no digestive, circulatory, or respiratory systems; instead, they absorb nutrients osmotically through their syncytial tegument from the host's small intestine.^[23]^[13] The body comprises three main regions: an anterior scolex for attachment, a short unsegmented neck, and a strobila consisting of 3 to 6 proglottids that develop sequentially from the neck.^[1]^[13] The scolex is subspherical and equipped with four circular suckers for adhesion to the host mucosa, along with a retractable rostellum bearing 25 to 50 chitinous hooklets arranged in one or two rows, which aid in grasping the intestinal wall.^[1]^[24] Overall worm length varies by species, typically ranging from 1.2 to 7 mm; for example, E. granulosus adults measure 2 to 7 mm, while E. multilocularis are smaller at 1.2 to 4.5 mm, reflecting adaptations to their definitive carnivore hosts.^[1]^[25] The proglottids progress from immature (lacking reproductive structures) to mature (with developing organs) and finally gravid (egg-filled), with the terminal gravid proglottid often longer than wide.^[1]^[13] As hermaphroditic organisms, each mature proglottid contains a single set of reproductive organs, including multiple testes, a cirrus sac with an eversible cirrus for insemination, ovaries, a vitellarium, and a branched uterus that expands in the gravid stage to store thousands of eggs.^[1]^[24] Self-fertilization or cross-fertilization between worms occurs via the lateral genital pore, leading to the production of fertile eggs within the uterus of the gravid proglottid, which are released into the host's feces upon proglottid detachment.^[13]^[25]

Egg and Oncosphere Stages

The eggs of Echinococcus species are ovoid to spherical in shape, measuring 30–40 μm in diameter, and are morphologically similar to those of other taeniid cestodes.^[26] They consist of a thick outer embryophore, which is a keratin-like layer providing structural protection and exhibiting a dark, striated appearance, surrounding the inner oncosphere.^[26] The oncosphere, or hexacanth embryo, is the infective larval stage within the egg, characterized by a syncytial tegument, penetration glands, and six hooklets arranged in a bilateral pattern that enable host tissue invasion.^[1] These eggs are fully embryonated upon release from the gravid proglottids of the adult worm in the definitive host's feces, rendering them immediately infectious to intermediate hosts without requiring further environmental maturation.^[27] In the external environment, Echinococcus eggs demonstrate notable resilience under favorable conditions but are vulnerable to physical stressors. They remain viable and infective for several months to up to one year in cool, moist settings at temperatures between 4°C and 15°C, facilitating environmental transmission.^[26] The eggs exhibit resistance to freezing temperatures, surviving prolonged exposure to subzero conditions, which contributes to their persistence in temperate climates.^[15] However, they are highly sensitive to desiccation, with viability lost within one day at 0% relative humidity or four days at 25% relative humidity, and to elevated temperatures, being inactivated at 60–80°C within minutes.^[26] Upon ingestion by an intermediate host, such as livestock or humans, the eggs are exposed to gastric and intestinal enzymes that disrupt the outer envelopes, releasing the oncosphere into the duodenal lumen.^[1] Activation of the oncosphere occurs in the presence of bile, prompting it to use its hooklets and glandular secretions to penetrate the intestinal mucosa and enter the bloodstream or lymphatic system for dissemination to target organs.^[26] This penetration mechanism underscores the egg's role as the primary vehicle for initiating larval development in intermediate hosts.^[28]

Larval Development

The larval stage of Echinococcus, known as the metacestode, develops in intermediate hosts following ingestion of eggs containing oncospheres, which hatch and migrate to target organs such as the liver or lungs. This stage is characterized by the formation of fluid-filled vesicles that enable asexual proliferation, contrasting with the adult worm's sexual reproduction in definitive hosts. The metacestode's morphology and growth vary by species, reflecting adaptations to different host environments and transmission dynamics.^[13] In E. granulosus, the metacestode forms a unilocular hydatid cyst, consisting of an outer acellular laminated layer, an inner germinal layer, and an enclosing host-derived fibrous capsule. Brood capsules bud endogenously from the germinal layer and develop protoscoleces through invagination, serving as infective units for definitive hosts; the cyst fluid often contains "hydatid sand," comprising free protoscoleces and cellular debris. Asexual reproduction occurs via endogenous budding (internal daughter cysts) or exogenous budding (on the cyst wall), allowing expansion without host immune clearance. Cysts grow slowly at 1-5 cm per year and can persist for 10-50 years, remaining viable in asymptomatic infections.^[13]^[29]^[28] For E. multilocularis, the metacestode develops as a multilocular alveolar cyst, exhibiting an infiltrative, tumor-like growth pattern with small vesicles interconnected by a spongy matrix. Protoscoleces form within vesicles via exogenous budding, where new vesicles proliferate externally from the germinal layer, enabling continuous invasion of host tissue. This form lacks the large unilocular structure of E. granulosus and instead mimics malignancy through its progressive, non-encapsulated expansion. Growth is insidious and persistent, often lasting decades if untreated, though specific rates are less defined than in cystic forms.^[13]^[29] The metacestodes of E. vogeli and E. oligarthrus produce polycystic forms, comprising multiple small, discrete or interconnected cysts primarily in abdominal organs or muscles. In E. vogeli, cysts feature a thick laminated layer and sparse protoscoleces, with asexual reproduction through budding that forms multilocular clusters; E. oligarthrus cysts are similarly polycystic but with a thinner laminated layer and abundant calcareous corpuscles in protoscoleces. These structures grow more slowly than alveolar forms and can persist long-term in intermediate hosts like rodents, though human data remain limited.^[30]^[29]

Life Cycle

Definitive and Intermediate Hosts

The life cycle of Echinococcus species relies on definitive hosts, which are carnivorous mammals harboring the sexually mature adult tapeworms in their small intestine, and intermediate hosts, which are typically herbivorous or omnivorous mammals supporting the asexual larval stages. Definitive hosts ingest protoscolices from hydatid cysts in the organs of infected intermediate hosts, allowing the worms to mature and produce eggs that are shed in feces. Intermediate hosts acquire infection by ingesting embryonated eggs contaminated in the environment, leading to the development of metacestode stages in their tissues, such as liver or lungs. Humans function as accidental intermediate hosts for multiple Echinococcus species but represent dead-end infections, as they rarely transmit larvae to definitive hosts.^[2]^[31] For E. granulosus (the causative agent of cystic echinococcosis), definitive hosts are primarily domestic dogs (Canis familiaris), with other wild and domestic canids including wolves (Canis lupus), foxes (Vulpes spp.), coyotes (Canis latrans), and jackals serving as suitable hosts where adult worms, typically 2–7 mm long, reside attached to the intestinal mucosa. The classic transmission cycle involves dogs as definitive hosts and sheep (Ovis aries) as primary intermediate hosts, in which unilocular hydatid cysts form in organs like the liver and lungs; additional intermediate hosts encompass cattle, goats, swine, camels, and yaks, among other ungulates. Pigs may occasionally function as paratenic hosts, ingesting eggs and transporting viable oncospheres without substantial larval maturation or cyst formation. This host specificity underpins pastoral cycles maintained through livestock farming practices.^[2]^[31]^[32]^[33] In the case of E. multilocularis (responsible for alveolar echinococcosis), definitive hosts center on wild canids such as red foxes (Vulpes vulpes) in sylvatic cycles, with wolves, coyotes, domestic dogs, and domestic cats also capable of supporting adult worms measuring 1–4 mm in the small intestine. Intermediate hosts are predominantly small rodents, including voles (Microtus spp.), deer mice (Peromyscus maniculatus), meadow voles (Microtus pennsylvanicus), and house mice (Mus musculus), where larvae develop into infiltrative, multilocular metacestodes that mimic malignant tumors. The fox-rodent cycle exemplifies high host specificity, sustaining the parasite in northern hemisphere wildlife reservoirs, though spillover to domestic cycles occurs via dogs.^[34]^[2]^[32] Other Echinococcus species exhibit similar but regionally distinct host associations; for instance, E. vogeli uses bush dogs (Speothos venaticus) as definitive hosts and rodents as intermediate hosts in neotropical polycystic cycles. Across species, paratenic hosts like certain rodents or wild boars can facilitate larval transport by predation without supporting reproduction, enhancing transmission opportunities in complex ecosystems.^[35]^[33]

Transmission Pathways

The primary transmission pathway for Echinococcus species is the fecal-oral route, in which eggs are shed in the feces of infected definitive hosts, such as dogs or foxes, and subsequently ingested by intermediate hosts, including livestock or humans, through contaminated food, water, soil, or vegetation.^[2]^[36] This route is facilitated by the robust nature of the eggs, which can survive in the environment for months, including under freezing conditions, allowing contamination of grazing areas or water sources in endemic regions.^[36] Direct contact with infected animals or their environments also contributes to transmission, particularly in humans, where handling contaminated dog fur, feces, or infected animal offal—such as during slaughter or farming activities—leads to inadvertent ingestion via poor hand hygiene.^[2]^[37] In endemic areas with close human-animal interactions, such as rural pastoral communities, this mechanism heightens risk for individuals like farmers, hunters, or veterinarians who may transfer eggs from contaminated hands to the mouth.^[37] Human infections are accidental, as people serve as dead-end intermediate hosts, with the vast majority occurring through ingestion of eggs rather than other routes.^[2] Rare cases have been documented via organ transplantation from infected donors carrying larval cysts.^[38]

Environmental Factors

The eggs of Echinococcus species, particularly E. granulosus and E. multilocularis, exhibit remarkable resilience to a wide range of temperatures, surviving from -50°C to over 65°C, though viability is optimal between 4°C and 25°C where they can remain infectious for extended periods. For instance, E. granulosus eggs have been shown to survive several months at 0–4°C, 32 weeks at 6°C, 4.5 weeks at 10–21°C, and just 3 weeks at 30°C.^[39] E. multilocularis eggs tolerate -18°C for up to 240 days and 4°C for 478 days.^[40] Moisture plays a critical role in this durability; eggs thrive in cool, humid environments, remaining viable for up to a year in such soils, but they are highly sensitive to desiccation, becoming inactivated within one day at 0% relative humidity. Extreme conditions further limit survival: eggs are killed by exposure to temperatures above 65°C for more than 2–3 hours, direct sunlight (which can inactivate 90% within hours through drying and UV effects), or repeated freezing-thawing cycles that disrupt their protective layers. Soil and water contamination represent primary environmental reservoirs for Echinococcus eggs, particularly in pastoral and agro-pastoral regions where livestock grazing and poor sanitation facilitate shedding from infected canids. Studies in endemic areas have detected eggs in 2.7–25% of soil samples from pastoral settings, such as 25% in Kenyan huts and 4.1% in Kazakhstani gardens, with survival lasting up to 41 months in arid Patagonian soils or 240 days in European winter soils for E. multilocularis.^[41]^[42]^[43] Water bodies, including irrigation channels and waterholes, amplify spread, showing contamination rates up to 60% in Kenyan pastoral water sources and facilitating egg dispersal onto vegetation; irrigation practices in agricultural zones further exacerbate this by contaminating crops like strawberries (up to 81.3% in Tunisia).^[41]^[44] In sylvatic cycles, wildlife activities contribute to persistent soil contamination in forested or rural habitats, underscoring the role of these media in non-host-to-host transmission. Climatic variations significantly influence Echinococcus transmission dynamics, with warmer, humid conditions in pastoral regions correlating with higher dog infection rates and egg survival, as evidenced by positive associations between humidity and cystic echinococcosis incidence (odds ratio 1.13).^[39] Global warming poses risks of range expansion, particularly for E. multilocularis, whose suitable habitats are projected to shift northward into previously unsuitable northern latitudes in Europe and North America by the mid-21st century under climate change scenarios, driven by milder winters that prolong egg viability.^[45] Anthropogenic environmental changes, including altered land use and increased humidity from irrigation, may further intensify these effects in endemic zones, potentially elevating human exposure through extended environmental persistence of eggs.

Echinococcosis

Cystic Form

Cystic echinococcosis, primarily caused by Echinococcus granulosus, results in the formation of unilocular hydatid cysts within intermediate hosts, including humans. Globally, cystic echinococcosis results in an estimated 200,000 new human cases per year (as of 2019 data).^[2] Following ingestion of eggs, oncospheres hatch in the intestine, penetrate the mucosa, and migrate via the bloodstream or lymphatics to lodge primarily in the liver (approximately 70% of cases) or lungs (about 20%), with less frequent involvement of organs such as the spleen, kidneys, brain, or bones.^[1]^[28] These cysts develop slowly over an incubation period ranging from 5 to 50 years, often remaining asymptomatic until they exceed 10 cm in diameter, at which point they exert a mass effect on surrounding tissues.^[1]^[28] The hydatid cysts consist of an inner germinal layer that produces protoscolices and an outer acellular laminated layer, encapsulated by a host-derived fibrous adventitia.^[28] Growth is gradual, typically at a rate of 1–5 cm per year, leading to progressive compression of adjacent structures; in hepatic cases, this can cause biliary obstruction, jaundice, or portal hypertension.^[46] Cysts are classified as fertile if they contain viable protoscolices capable of further development upon rupture, or sterile if devoid of them, which influences disease transmission potential and host immune responses.^[28] Complications arise mainly from cyst rupture or secondary events, with rupture triggering IgE-mediated anaphylaxis that manifests as urticaria, angioedema, or life-threatening shock due to antigen release.^[28]^[47] Spillage of contents can also lead to secondary echinococcosis through dissemination of protoscolices or bacterial superinfection, occurring in up to 7.3% of hepatic cases and causing suppuration or abscess formation.^[28]^[47]

Alveolar Form

Alveolar echinococcosis (AE) is caused by the larval stage of Echinococcus multilocularis, a tapeworm primarily maintained in a sylvatic life cycle involving foxes as definitive hosts and rodents, such as voles, as intermediate hosts. Humans become accidental intermediate hosts by ingesting eggs shed in fox feces, typically through contaminated food, water, or direct contact in endemic areas. Upon ingestion, eggs hatch in the small intestine, releasing oncospheres that penetrate the intestinal wall and migrate via the portal vein to the liver, where they develop into multilocular metacestode cysts.^[1]^[48] The pathogenesis of AE is characterized by the formation of multilocular cysts that exhibit continuous exogenous budding, lacking the discrete brood capsules seen in other forms, resulting in a sponge-like, infiltrative growth pattern. These cysts mimic malignancy due to their ability to invade surrounding tissues, particularly the liver parenchyma, and can metastasize to distant sites such as the lungs and brain through vascular dissemination. This tumor-like progression leads to progressive destruction of hepatic architecture, often remaining asymptomatic for years before causing significant organ dysfunction. Unlike the more contained cystic form, AE's invasive nature contributes to its higher lethality if not addressed early.^[48]^[1]^[49] Complications of AE arise from its destructive hepatic involvement, including secondary biliary cirrhosis due to chronic obstruction and inflammation, as well as portal hypertension from vascular compression and fibrosis. Advanced disease can lead to liver failure, cholangitis, and secondary infections, with untreated cases showing a 5-year survival rate below 50%, often approaching 10% in palliative or advanced scenarios without curative intervention. The overall fatality rate exceeds that of cystic echinococcosis, underscoring the need for aggressive management.^[50]^[48]^[49] AE is endemic in the northern hemisphere, particularly central Europe (e.g., France, Germany, Switzerland), parts of Asia (e.g., China, Japan), and North America (e.g., Alaska, northern Canada), where expanding fox populations and habitat overlap with human settlements facilitate the rodent-fox transmission cycle. Incidence is low globally but can reach 1-20 cases per 100,000 in high-risk areas, with climate and land-use changes potentially expanding its range.^[1]^[48]^[49]

Polycystic Form

Polycystic echinococcosis, also known as neotropical echinococcosis, is a rare zoonotic infection caused by the larval stages of Echinococcus vogeli and Echinococcus oligarthrus, primarily affecting humans in Central and South America. Unlike the more common cystic form caused by E. granulosus or the alveolar form by E. multilocularis, this variant involves the development of multiple discrete cysts rather than expansive or metastatic growth.^[1]^[51] In E. vogeli infections, oncospheres ingested from contaminated food or water hatch and migrate to the liver, where they form multichambered, fluid-filled cysts up to 4-6 cm in diameter, characterized by exogenous and endogenous budding that leads to proliferation and dissemination to the peritoneum, lungs, and other abdominal organs. These lesions often exhibit internal septa and a thick laminated layer, with protoscoleces present in the cysts, enabling further larval development.^[52]^[51] In contrast, E. oligarthrus typically produces unicystic or less subdivided polycystic structures with a thinner laminated layer, showing concentric expansion without significant proliferation; these cysts more frequently involve subcutaneous tissues, muscles, orbit, or heart rather than visceral organs.^[52]^[51] Clinically, E. vogeli manifests with multiple small cysts in the liver and peritoneum, leading to chronic abdominal pain, palpable masses, weight loss, and jaundice due to hepatic involvement or biliary obstruction; larger lesions with internal septa can mimic tumors and cause hepatic insufficiency in advanced cases. Complications include cyst rupture during surgery, resulting in secondary dissemination and a reported mortality rate of up to 22% in operative settings, though the form is less aggressive than alveolar echinococcosis with lower metastatic potential but high recurrence rates post-resection.^[52]^[1] For E. oligarthrus, presentations are rarer and often localized, such as orbital cysts causing exophthalmos and potential blindness or submandibular masses leading to pressure effects, with limited systemic complications reported.^[52]^[51] This form is exceedingly rare, accounting for less than 1% of global echinococcosis cases, with over 250 documented human infections by E. vogeli across neotropical countries, mainly in the Amazon basin of Brazil, Colombia, and Ecuador, sustained by a sylvatic cycle involving bush dogs as definitive hosts and rodents like pacas as intermediates. E. oligarthrus has only about 3-5 confirmed human cases worldwide, linked to wild felids in the same regions, underscoring its minimal public health impact compared to other species.^[52]^[1]^[51]^[53]

Epidemiology

Global Distribution

_Echinococcus species exhibit varied global distributions, with E. granulosus being the most widespread, affecting humans and livestock across multiple continents. Cystic echinococcosis caused by E. granulosus is cosmopolitan, present on every continent except Antarctica, and is classified by the World Health Organization as a neglected tropical disease.^[2] Globally, over 1 million people are affected by echinococcosis at any given time, predominantly cystic forms in endemic regions.^[2] E. granulosus is hyperendemic in pastoral communities of the Mediterranean basin, South America (such as Argentina and Peru), North and East Africa, western China, Russia, and Australia, where livestock prevalence can reach 20%–95% in slaughterhouses.^[2]^[28] In these areas, human incidence exceeds 50 cases per 100,000 person-years, with prevalence up to 5%–10%.^[2] The parasite's transmission involves domestic cycles with dogs as definitive hosts and herbivores like sheep and cattle as intermediates, sustaining high burdens in agricultural settings.^[28] In contrast, E. multilocularis, responsible for alveolar echinococcosis, is restricted to the Holarctic region of the northern hemisphere, including Europe, Asia (particularly China and the Russian Federation), and North America.^[2] In North America, it is endemic in the northern tundra zones of Alaska and Canada, as well as north-central regions like the Midwest United States, with evidence of southward expansion into areas such as southern Ontario and urban coyote populations in Alberta.^[34]^[54] Recent detections as of 2025 include Quebec, New York, and Washington state, indicating ongoing emergence.^[55]^[56]^[57] Sylvatic cycles predominate, involving foxes and small rodents, though domestic involvement is increasing.^[34] The neotropical species E. vogeli and E. oligarthrus are confined to Central and South America, where they maintain sylvatic cycles with bush dogs and rodents as hosts.^[1] These parasites cause polycystic and unicystic echinococcosis, respectively, with over 250 human cases reported across more than 12 countries in Central and South America.^[53] Their distribution remains focal and limited compared to E. granulosus, primarily in forested and rural ecosystems.^[1]

Incidence and Risk Factors

Echinococcosis, particularly the cystic form caused by Echinococcus granulosus, results in an estimated 200,000 to 1 million human cases worldwide, with approximately 200,000 new infections annually.^[2]^[58] This form accounts for about 90% of all human echinococcosis cases globally, predominantly in regions with livestock pastoralism.^[2] The mortality rate for untreated or complicated cystic echinococcosis stands at 2-4%, often due to cyst rupture or secondary infections.^[59] Incidence is markedly higher in pastoral communities, such as those in Peru's central highlands, where rates can exceed 27 cases per 100,000 population annually.^[60] Key risk factors include occupational exposure, such as working in slaughterhouses where contact with infected animal viscera is common, increasing infection likelihood through accidental ingestion of parasite eggs.^[61] Behavioral factors like owning dogs without regular deworming or consuming raw vegetables contaminated by dog feces also elevate transmission risks, as eggs can persist in soil and water.^[62]^[63] Immunosuppression, from conditions like HIV or immunosuppressive therapy, heightens disease severity and complicates diagnosis due to altered immune responses.^[64] Additionally, climate change may expand the geographic range of intermediate hosts and vectors by altering temperature and precipitation patterns, potentially increasing endemic areas.^[65] As a zoonosis, echinococcosis imposes a significant economic burden, with annual global losses to the livestock industry exceeding $3 billion due to organ condemnation, reduced productivity, and control measures.^[66] Humans serve as accidental dead-end hosts, unable to sustain the parasite's life cycle, which underscores the disease's reliance on animal reservoirs for persistence.^[2]

Diagnosis

Clinical Symptoms

Echinococcosis often remains asymptomatic for many years, as the slow-growing cysts or lesions typically do not cause noticeable effects until they reach significant size or lead to organ compression. In cystic echinococcosis, the majority of cases are discovered incidentally during imaging for unrelated issues, with symptoms emerging only when cysts enlarge to cause pressure on surrounding tissues.^[67]^[2] Hepatic involvement, the most common site in adults, manifests with right upper quadrant pain, hepatomegaly, nausea, vomiting, and occasionally jaundice due to biliary obstruction as cysts compress liver structures. Pulmonary cysts, more prevalent in children, produce symptoms such as chronic cough, chest pain, hemoptysis, and dyspnea, particularly when cysts grow large enough to impair lung function. In the alveolar form, primarily affecting the liver, patients experience insidious onset with weight loss, abdominal pain, general malaise, and signs of hepatic failure, often mimicking malignancy due to the infiltrative, tumor-like growth.^[67]^[2]^[68] Complications arise from cyst rupture, triggered by trauma or spontaneous pressure, leading to severe anaphylactic reactions including urticaria, hypotension, and shock from the release of antigenic cyst fluid; rupture into the biliary tree or peritoneum can also cause cholangitis or peritonitis. In children, pulmonary manifestations predominate over hepatic ones compared to adults, where liver cysts are far more frequent, reflecting differences in cyst localization and growth patterns.^[67]^[2]^[69]

Imaging Techniques

Ultrasound is the primary imaging modality for diagnosing cystic echinococcosis (CE), serving as the first-line technique due to its accessibility, cost-effectiveness, and ability to classify cysts according to the World Health Organization Informal Working Group on Echinococcosis (WHO-IWGE) system.^[2]^[70] This standardized classification divides CE into five stages—CE1 (active, unilocular anechoic cyst), CE2 (active, multivesicular with daughter cysts), CE3 (transitional, with detached endocyst membranes), CE4 (inactive, heterogeneous content), and CE5 (inactive, calcified wall)—guiding treatment decisions based on cyst viability and activity.^[71]^[2] Ultrasound can also detect characteristic features such as hydatid sand, which appears as mobile, low-level internal echoes within the cyst fluid, indicating viable protoscolices.^[72]^[70] For alveolar echinococcosis (AE) and polycystic echinococcosis (PE), computed tomography (CT) and magnetic resonance imaging (MRI) are essential for characterization, as these forms present with more complex, infiltrative lesions that ultrasound may not fully delineate.^[73]^[74] CT excels at identifying peripheral calcifications, irregular margins, and multilocular structures resembling a "honeycomb" or solid mass with necrosis, which help distinguish AE from malignancies like cholangiocarcinoma.^[75]^[76] MRI provides superior soft-tissue contrast, revealing hypointense walls on T2-weighted images, internal septations, and vascular involvement, aiding differentiation from tumors through assessment of lesion invasiveness and biliary tree compression.^[73]^[74] In PE, caused by Echinococcus vogeli or E. oligarthrus, CT and MRI typically show interconnected polycystic masses with thick septa and minimal calcification, often in the liver or peritoneum.^[77] Plain radiography, particularly chest X-ray, plays a limited role in detecting pulmonary involvement of CE, where intact cysts appear as well-defined, round or oval opacities, often in the lower lobes, without surrounding consolidation.^[78]^[79] However, X-ray has significant limitations in early detection, as small or uncomplicated cysts may be missed, and it cannot assess cyst integrity or complications like rupture, necessitating advanced imaging for confirmation.^[80]^[79] These imaging findings often correlate with clinical symptoms such as chest pain or cough in pulmonary cases.^[72]

Serological and Molecular Tests

Serological tests for echinococcosis primarily detect host antibodies against parasite antigens, aiding in the confirmation of infection when imaging is inconclusive. Enzyme-linked immunosorbent assay (ELISA) is the most commonly used method, targeting IgG antibodies to antigens such as hydatid fluid or antigen B from Echinococcus granulosus. For cystic echinococcosis (CE), commercial ELISAs exhibit sensitivities of 80-94% and specificities of 84-96%, depending on the antigen preparation and cyst stage.^[81]^[82] For alveolar echinococcosis (AE) caused by E. multilocularis, ELISAs using native antigens like Em2 (a glycoprotein fraction) achieve sensitivities of 80-96% and specificities of 88-99%.^[82] Western blot serves as a confirmatory test following positive ELISA results, offering higher specificity by identifying specific antibody bands to Echinococcus antigens. In CE, Western blot detects IgG to multiple bands from E. granulosus protoscolex antigens with sensitivities of 83% and specificities up to 99%. For AE, it confirms reactivity to Em2 and Em18 antigens, reducing cross-reactivity compared to ELISA alone.^[82] These assays are particularly useful in endemic areas for screening but require integration with clinical findings. Molecular tests provide direct detection of parasite DNA, enabling species identification and monitoring treatment efficacy. Polymerase chain reaction (PCR) targeting mitochondrial genes such as nad1 (NADH dehydrogenase subunit 1) is applied to cyst fluid, biopsy samples, or blood, confirming Echinococcus species with high specificity. In clinical samples from CE patients, nad1 PCR identifies strains like E. canadensis G7, with successful amplification in up to 64% of histologically confirmed cases. Post-treatment, PCR on cyst fluid assesses viability, detecting residual DNA in inactive lesions.^[83] Despite their utility, serological tests face limitations including cross-reactivity with other helminths such as Taenia species, cysticercosis, and fascioliasis, leading to false positives in up to 50% of cases with related infections. False negatives occur in 10-40% of CE patients, particularly with early-stage (CE1) or inactive (CE4-5) cysts, single small lesions, or extrahepatic locations, due to low antigen exposure or immune evasion. Molecular methods, while specific, may yield false negatives in degraded samples or low-parasite-load blood, necessitating sample optimization.^[84]

Treatment

Surgical Options

Surgical options for managing Echinococcus infections primarily involve procedures to remove or inactivate cysts, tailored to the form of the disease—cystic echinococcosis (CE) caused by Echinococcus granulosus or alveolar echinococcosis (AE) caused by E. multilocularis—and the cyst's location, size, and stage. For CE, the PAIR technique (puncture, aspiration, injection of a scolicidal agent like hypertonic saline or ethanol, and reaspiration) is recommended for accessible, uncomplicated hepatic cysts classified as CE1, CE2, or CE3a under WHO ultrasound staging, offering a minimally invasive alternative to open surgery with success rates exceeding 90% when performed under ultrasound guidance by experienced teams.^[85]^[86] Total pericystectomy, involving complete excision of the cyst and its surrounding fibrous pericyst, is a radical approach for CE to minimize recurrence, particularly for superficial or solitary liver cysts, though it carries risks of biliary injury in up to 10% of cases.^[87]^[88] In AE, which infiltrates liver tissue like a malignancy, radical surgery such as extended liver resection or total pericystectomy is the preferred curative option when feasible, aiming for complete (R0) resection margins to achieve 5-year survival rates of 80-90% in operable cases.^[89]^[90] Without adjunct antiparasitic therapy, recurrence rates after radical resection for AE range from 10% to 30%, often due to microscopic residual lesions, emphasizing the need for long-term follow-up with imaging.^[89] Laparoscopic approaches, including partial or total pericystectomy, are increasingly used for both CE and AE in selected patients with peripheral lesions, reducing postoperative pain and hospital stay compared to open surgery while maintaining comparable recurrence rates of 5-10%.^[91]^[92] Surgery is contraindicated for cysts in vital areas such as the brainstem or heart, multiple inaccessible cysts, or inactive asymptomatic lesions to avoid complications like anaphylaxis from rupture or unnecessary morbidity.^[93]^[94] In such cases, percutaneous or pharmacological management may be considered alongside supportive care.^[86]

Antiparasitic Drugs

The primary antiparasitic drugs for treating echinococcosis are benzimidazoles, including albendazole and mebendazole, which target the larval stages (cysts or metacestodes) of Echinococcus granulosus (cystic echinococcosis, CE) and E. multilocularis (alveolar echinococcosis, AE).^[95] These agents act by binding to β-tubulin in the parasite, inhibiting microtubule polymerization and disrupting essential cellular processes such as glucose uptake and mitosis, ultimately leading to the death of protoscoleces and degeneration of the germinal layer.^[96] Albendazole is the preferred first-line therapy due to its superior bioavailability compared to mebendazole.^[97] For CE, albendazole is administered at 10–15 mg/kg/day (maximum 800 mg/day) in two divided doses with meals, typically in cycles of 28 days on followed by 14 days off, for 3–6 months or longer depending on cyst response and location.^[95] In AE, treatment is long-term, often lifelong for inoperable cases, at the same daily dose without mandatory cycles to maintain suppression of parasite growth.^[98] Efficacy in CE varies by cyst stage and site but generally achieves cyst stabilization or resolution in 70–90% of cases with prolonged therapy, though relapse can occur in up to 20%.^[99] For inoperable AE, benzimidazoles improve 10-year survival rates to over 90% by controlling progression, though they are primarily parasitostatic rather than curative.^[100] Common side effects include reversible hepatotoxicity (elevated transaminases in 10–15% of patients) and myelosuppression such as neutropenia (less than 5%), necessitating regular monitoring of liver function and blood counts.^[101] Mebendazole serves as an alternative benzimidazole, dosed at 40–50 mg/kg/day in three divided doses, particularly when albendazole is contraindicated or unavailable, though its lower absorption limits efficacy.^[95] Praziquantel, at 40 mg/kg weekly, may be added as an adjunct to enhance protoscolicidal activity or target rare adult worm infections in humans, often in combination with benzimidazoles for improved outcomes in disseminated or recurrent cases.^[102] These drugs are frequently integrated with surgical interventions to reduce recurrence risk, but standalone medical therapy is standard for inoperable or high-risk lesions.^[95]

Supportive Care

Supportive care in echinococcosis focuses on alleviating symptoms, managing complications from cyst rupture or chronic disease progression, and enhancing patient well-being alongside primary interventions such as surgery or antiparasitic therapy. These measures are essential for patients with cystic or alveolar forms, particularly when cysts involve the liver or lungs, leading to potential organ dysfunction or allergic responses.^[95] Anaphylaxis is a life-threatening complication often triggered by cyst rupture, releasing hydatid fluid antigens that provoke severe allergic reactions including hypotension, urticaria, and bronchospasm. Immediate management follows standard anaphylaxis protocols, with intramuscular epinephrine (0.3–0.5 mg in adults) as the first-line agent to reverse hemodynamic instability, supplemented by intravenous fluids for volume resuscitation. Antihistamines such as diphenhydramine (25–50 mg IV) and corticosteroids like hydrocortisone (100–200 mg IV) are administered to mitigate inflammation and prevent biphasic reactions, with close monitoring in an intensive care setting.^[103]^[104]^[105] Patients with chronic liver involvement from alveolar echinococcosis often experience malnutrition due to consumptive effects, appetite loss, and associated conditions like hepatitis, affecting up to 30% of cases. Nutritional support entails screening tools such as the Nutritional Risk Screening 2002 (NRS 2002) or Mini Nutritional Assessment-Short Form (MNA-SF) to identify at-risk individuals, followed by tailored interventions including high-protein diets (1.2–1.5 g/kg/day) and enteral supplementation to maintain energy intake (30–35 kcal/kg/day) and prevent hepatic encephalopathy. Pain from cyst pressure or inflammation is managed with analgesics, typically non-opioid options like acetaminophen or NSAIDs for mild cases, escalating to opioids such as tramadol for severe discomfort, while avoiding hepatotoxic agents in liver-compromised patients.^[106]^[107]^[108] Secondary bacterial infections, such as abscesses or empyema from cyst leakage, occur in approximately 40% of complicated pulmonary cases and require vigilant monitoring through imaging and cultures, with broad-spectrum antibiotics (e.g., cephalosporins) initiated pre- and postoperatively to cover common pathogens like Staphylococcus or Streptococcus. Palliative measures for inoperable large cysts include percutaneous drainage techniques like tube thoracostomy or thoracentesis to relieve pressure, reduce pain, and prevent further complications in symptomatic patients. In long-term cases, particularly alveolar echinococcosis mimicking malignancy, psychological support is crucial to address the high burden of anxiety, depression, and reduced quality of life, involving multidisciplinary assessment for mental health disorders and counseling to foster resilience.^[109]^[110]

Prevention and Control

Veterinary Interventions

Veterinary interventions for Echinococcus primarily target the definitive hosts, such as dogs and foxes, and intermediate hosts like sheep, to disrupt the parasite's lifecycle and reduce transmission in animal populations. These strategies emphasize regular deworming, vaccination of livestock, and stringent controls at slaughter facilities, which have proven effective in endemic regions when implemented consistently. Deworming campaigns using praziquantel are a cornerstone of control efforts, administered to dogs at a dose of 5 mg/kg orally or subcutaneously every 4-6 weeks to eliminate adult Echinococcus worms from the intestines. This approach is particularly vital in endemic areas, where mass treatment programs target both owned and stray dogs to prevent environmental contamination with eggs, with studies showing significant reductions in transmission after sustained application over several years. For wildlife reservoirs like foxes, which serve as definitive hosts in sylvatic cycles, baiting with praziquantel-laced formulations distributed via ground or aerial methods has been employed to achieve broad coverage without direct handling, though logistical challenges persist in remote habitats. Emerging tools like smart deworming collars, which automatically deliver praziquantel every 1-2 months, have shown promise in field trials for improving treatment compliance and reducing infection rates in dogs.^[25]^[111]^[112]^[113]^[114] Vaccination focuses on protecting intermediate hosts, with the recombinant EG95 vaccine administered to sheep demonstrating high efficacy of approximately 90-99% against infection with Echinococcus granulosus, significantly lowering cyst development upon challenge. Developed from an oncosphere antigen, EG95 is typically given as two doses to lambs, providing long-term immunity that can last up to four years or more with booster vaccinations, and field trials in regions like Argentina and China have confirmed its role in reducing overall prevalence in livestock populations. However, no comparable vaccine exists for wildlife definitive hosts, limiting options for sylvatic cycle interruption and necessitating integrated approaches with deworming.^[115]^[116]^[117] Slaughterhouse controls are essential for preventing access by dogs to infected offal, which serves as a key transmission route. Routine inspection of livestock viscera during slaughter identifies hydatid cysts, allowing for condemnation and safe disposal of infected organs through incineration or burial to avoid scavenging, with regulatory frameworks in endemic countries mandating such practices to break the cycle. These measures, combined with improved hygiene standards at abattoirs, have contributed to measurable declines in Echinococcus prevalence in monitored livestock, though enforcement varies by region.^[118]^[119]^[120]

Human Health Measures

Human health measures for preventing Echinococcosis focus on reducing exposure to the parasite's eggs through personal hygiene, community education, and targeted screening in vulnerable populations. These actions are particularly crucial in endemic regions where close human-animal interactions increase transmission risks.^[2] Hygiene practices play a central role in minimizing ingestion of Echinococcus eggs, which are primarily shed in the feces of infected dogs and can contaminate soil, water, food, and hands. Individuals should wash hands thoroughly with soap and warm water after contact with dogs, gardening, or handling soil, and before preparing or eating food, as this reduces the hand-to-mouth transfer of eggs. Washing fruits and vegetables under running water is essential to remove potential contamination from dog feces, especially in areas where animals roam freely. Cooking meat, particularly offal from livestock, to an internal temperature of at least 71°C (160°F) kills any viable protoscolices that might be present, further preventing accidental ingestion during consumption.^[121]^[122]^[15] Education efforts aim to build awareness and promote behavioral changes in communities to curb transmission. Public campaigns, often delivered through schools and local health programs, emphasize avoiding close contact with stray dogs in endemic zones, as these animals are common reservoirs for the parasite. School-based initiatives targeting children, who are at higher risk due to playful interactions with dogs, teach the importance of handwashing and not feeding dogs raw meat scraps that could perpetuate the cycle. Community workshops in high-prevalence areas, such as pastoral regions, have demonstrated reduced infection rates by fostering knowledge of transmission routes and hygiene norms.^[2]^[123]^[124] Screening programs using abdominal ultrasound are recommended for early detection in high-risk human populations, enabling timely intervention before cysts grow large or cause complications. In endemic areas, periodic ultrasound surveys target groups like pastoralists and school-aged children, who face elevated exposure from livestock handling or environmental contamination. For instance, mass screening using abdominal ultrasound in 13 rural localities of Turkey identified a prevalence of 1.6% (95% CI 1.1–2.2%) among screened individuals, highlighting the tool's value in resource-limited settings where ultrasonography is non-invasive and cost-effective. These efforts complement broader integrated strategies but prioritize human-focused monitoring.^[2]^[125]^[126]

One Health Approaches

The One Health approach to Echinococcus control integrates human, animal, and environmental health sectors to address the zoonotic nature of the parasite, emphasizing multisectoral collaboration to break transmission cycles. The World Health Organization (WHO) and Food and Agriculture Organization (FAO) have spearheaded joint initiatives, such as the One Health Joint Plan of Action (2022–2026), which promotes coordinated efforts among health, veterinary, and environmental authorities to tackle neglected zoonoses like echinococcosis.^[127] Surveillance networks play a critical role in this framework; for instance, the European Echinococcosis Registry (EurEchinoReg) facilitates data sharing on human alveolar echinococcosis cases across Europe, enabling early detection and cross-border monitoring.^[128] Additionally, climate modeling predicts shifts in Echinococcus distribution due to environmental changes, with studies projecting expanded suitable habitats for E. multilocularis in northern latitudes and Alpine regions under future warming scenarios, informing proactive control strategies.^[129] Success stories demonstrate the efficacy of integrated One Health programs. In New Zealand, a comprehensive campaign from the 1950s to the early 2000s, involving regular dog dosing with praziquantel, restrictions on raw offal feeding, and livestock monitoring, led to provisional freedom from E. granulosus transmission by 2002, drastically reducing human incidence from over 10 cases per 100,000 in the 1960s to near zero.^[130] Similarly, Tasmania's control program, initiated in 1962 and combining dog treatment, offal disposal regulations, and community education, achieved eradication of hydatid disease by the 1990s, with ongoing surveillance to maintain this status and prevent reintroduction.^[131] Despite these advances, One Health approaches face significant challenges, particularly from wildlife reservoirs that sustain transmission cycles beyond human or livestock interventions. Species like foxes and wild canids serve as difficult-to-control definitive hosts for E. multilocularis, complicating eradication in endemic regions such as northern Europe and circumpolar areas.^[132] As a neglected tropical disease, echinococcosis also suffers from insufficient global funding; recent cuts in official development assistance have strained programs, with the U.S. withdrawal from NTD initiatives in 2025 threatening progress in endemic countries despite the disease's substantial economic burden, estimated at millions in annual healthcare and livestock losses.^[133]^[134]

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Aug 5, 2020 · A diagnostic sensitivity of 91 % and specificity of 82 % of the hydatid fluid antigen in the commercial ELISA Echinococcus granulosus test ( ...
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Native antigens and three commercial tests showed high diagnostic sensitivities (Se: 86–96%) and specificities (Sp: 96–99%) for the diagnosis of AE and CE in ...
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Three therapeutic modalities exist to treat hepatic cystic echinococcosis: chemotherapy, surgery, and percutaneous drainage.
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Sep 17, 2020 · Albendazole (ABZ), a broad-spectrum benzimidazole drug widely used to treat parasitic infections, is the drug of choice for the management of CE ...
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Fluid replacement should be assured by crystalloids. For vasopressor, epinephrine is the first-line treatment in most guidelines on perioperative management of ...
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Additionally, perforated pulmonary hydatid cyst patients require preoperative antibiotic and supportive treatment. These are the main reasons why perforated ...
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Jan 7, 2019 · Our results show how important it is that AE patients are thoroughly assessed with regard to psychological symptoms and mental disorders ...
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supervision, and this should improve the safe disposal of offal to interrupt the disease cycle. Slaughterhouses provide opportunities for surveillance of.
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Jun 8, 2021 · The study suggests that education program for echinococcosis control should be initiated in school children because most infections acquire ...
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Jul 29, 2019 · Using abdominal ultrasound, we examined 24,687 people from rural areas of Romania, Bulgaria and Turkey, estimating that 151,000 people may have ...
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The One Health Joint Plan of Action (2022–2026) (OH JPA) set out in this document is guided by the areas of One Health collaboration set out in the strategic ...
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Apr 23, 2025 · Footnotes. [1] (external link) The Ministry for Primary Industries declared New Zealand provisionally free of hydatids in 2002.
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Apr 9, 2024 · The Tasmanian program was based on treating infected dogs and denying dogs access to the offal of sheep, cattle, goats and pigs. Hydatid disease ...
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Ten genotypes are recognised and the group is roughly divided into Echinococcus granulosus sensu stricto (ss. G1–G3) and sensu lato (sl. G1–G10). The current ...
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Neglected tropical diseases further neglected due to ODA cuts
Jun 4, 2025 · The recent withdrawal of funding by the United States from NTD projects jeopardizes the success of 19 years of investment in the global effort ...
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The economic evaluation of Cystic echinococcosis control strategies ...
Jul 7, 2022 · Cystic echinococcosis (CE) is a zoonotic neglected tropical disease (zNTD) which imposes considerable financial burden to endemic countries.