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Angiostrongylus cantonensis

Angiostrongylus cantonensis, commonly known as the rat lungworm, is a metastrongylid parasite in the family Angiostrongylidae that primarily infects rats as definitive hosts but causes eosinophilic meningitis in humans and other incidental hosts. This zoonotic pathogen measures 16–26 mm in length for adult females and 13–20 mm for males, with larvae developing through multiple stages in intermediate hosts. Native to , it has spread globally, posing significant public health risks in tropical and subtropical regions. The life cycle of A. cantonensis begins when adult worms reside in the pulmonary arteries and right ventricle of rats, where females produce eggs that hatch into first-stage larvae (L1) in the lungs; these are then coughed up, swallowed, and excreted in feces. Gastropod mollusks, such as snails and slugs, ingest the L1 larvae from contaminated rat feces, in which the larvae molt to infectious third-stage larvae (L3) over 2–3 weeks. Rats complete the cycle by consuming infected mollusks, allowing L3 larvae to migrate to the brain and spinal cord before maturing in the lungs; paratenic hosts like freshwater prawns, crabs, or amphibians can also harbor L3 larvae. Humans acquire the infection accidentally by ingesting raw or undercooked intermediate hosts or contaminated produce, leading to larval migration to the central nervous system without completing the reproductive cycle. Epidemiologically, A. cantonensis is endemic in (e.g., , ), the Pacific Islands (e.g., ), and parts of the and , with more than 7,000 human cases reported globally as of 2025 and increasing outbreaks due to and invasive species. In humans, infection manifests as neuroangiostrongyliasis, with symptoms appearing 1–3 weeks post-exposure, including severe , , paresthesias, , , and low-grade fever; severe cases involve cranial nerve palsies, , or rarely death from increased intracranial pressure. relies on clinical history, cerebrospinal fluid analysis showing (>10% ), and supportive or , as larvae are rarely visualized. Treatment is primarily supportive, involving analgesics for pain, corticosteroids (e.g., ) to reduce inflammation, and sometimes repeated lumbar punctures to alleviate pressure; anthelmintics like are avoided or used cautiously due to potential worsening of symptoms from dying larvae. Prevention focuses on avoiding raw mollusks and washing produce thoroughly, alongside rat control and public education in endemic areas. Ongoing surveillance is crucial as the parasite expands into new regions like (e.g., first continental records in 2023) and mainland (e.g., in 2025).

History and Discovery

Initial Identification

The nematode parasite now known as Angiostrongylus cantonensis was first discovered in 1935 by , who identified it in the pulmonary arteries and hearts of domestic rats (Rattus norvegicus and Rattus rattus) collected in (formerly ), . described the as Pulmonema cantonensis, establishing it as a new and within the family Metastrongylidae based on its morphological features and location in the host. In the following years, additional reports emerged from researchers investigating similar parasites in s. During the , Nomura and colleagues documented A. cantonensis (then under its original ) in rat lungs across regions of and occupied territories, contributing early insights into its distribution in and referring to it as the "rat ." These findings built on Chen's description but did not yet connect the parasite to risks. The Pulmonema was later synonymized with Angiostrongylus by Dougherty in , reclassifying the as Angiostrongylus cantonensis to reflect its phylogenetic affinities within the Strongylida order. The first potential infection was recognized in 1945 in , where Nomura and Lin identified nematode larvae in the of a exhibiting eosinophilic meningitis, suspecting a link to rat lungworms but without definitive confirmation at the time. This case marked an early suspicion of zoonotic potential, though the etiological role of A. cantonensis in was not fully established until 1961, when experimental and epidemiological evidence solidified the connection.

Key Research Milestones and Outbreaks

In 1961, researchers led by Lyle Rosen confirmed the role of Angiostrongylus cantonensis as the causative agent of eosinophilic meningitis in humans through the recovery of the parasite from the of a deceased patient in and subsequent experimental infections in animal models, establishing a direct link between the rat lungworm and the disease. This built on earlier suspicions from outbreaks in the Pacific and provided the first definitive evidence in the , prompting intensified global surveillance for the parasite. During the 1960s and 1970s, significant outbreaks of eosinophilic meningitis linked to A. cantonensis occurred across Pacific Islands and , highlighting the parasite's zoonotic potential. In , , a major epidemic from 1958 to 1961 affected hundreds of individuals, primarily through consumption of raw snails, marking one of the earliest documented mass occurrences. Similar incidents in during this period involved hundreds of cases, often associated with eating raw or undercooked freshwater snails like Pila ampullacea, leading to widespread recognition of dietary risks in endemic areas. Research in the and expanded understanding of the parasite's geographical spread beyond and the Pacific, with studies documenting its presence in and the . In , A. cantonensis was first detected in rat populations along the eastern in the 1950s, followed by the first human case in 1971 near that underscored the role of invasive snails in transmission. studies during this era identified the parasite in wildlife and mollusks, setting the stage for later human infections and emphasizing vector dispersal via . Key diagnostic advancements in the 1970s included the development of serological tests, such as , which enabled reliable detection of anti-A. cantonensis antibodies in and , improving case confirmation and epidemiological tracking. By the 2000s, the recognized A. cantonensis as an emerging , integrating it into global reports on and advocating for enhanced control measures. Notable outbreaks in 2004–2005 further illustrated the parasite's expanding threat: in , outbreaks such as the one in in 2004 affected dozens due to contaminated snails. Concurrently, in , the first confirmed autochthonous human cases were reported in 2007 in the southeastern region, signaling the parasite's establishment in . In the 2010s and , the parasite continued to emerge in new regions, with the first human case reported in (Spain) in 2019 and detections in the mainland (e.g., ) by 2021, highlighting ongoing global spread facilitated by trade and climate factors.

Taxonomy and Morphology

Classification

Angiostrongylus cantonensis is classified within the kingdom Animalia, phylum Nematoda, class , order , superfamily Metastrongyloidea, family Angiostrongylidae, genus Angiostrongylus, and species A. cantonensis. This placement positions it among the metastrongyloid nematodes, a group characterized by their parasitic lifestyle in the lungs and vasculature of mammalian hosts. The family Angiostrongylidae encompasses several species that infect the cardiovascular and respiratory systems of vertebrates, with A. cantonensis distinguished by its specific adaptation to rodent definitive hosts. The species was first described in 1935 as Pulmonema cantonensis by from rats in (now ), , and independently as Hemostrongylus ratti by Yokogawa in 1937 from rats in . These names were later synonymized, and the current designation Angiostrongylus cantonensis was established in the following taxonomic revisions that recognized the Angiostrongylus. An additional , Parastrongylus cantonensis, has been used but is now generally accepted under the Angiostrongylus. A. cantonensis is differentiated from congeners like A. costaricensis, which causes abdominal by migrating to the mesenteric arteries of in the , and A. vasorum, the heartworm that primarily inhabits the pulmonary arteries and right ventricle of dogs and wild canids in and . These distinctions are based on host specificity, anatomical in the , and geographical distribution, with A. cantonensis uniquely associated with eosinophilic meningitis in accidental hosts. Since the 1990s, the 2 (ITS-2) region of has served as a key for differentiation, enabling precise identification through and restriction fragment length polymorphism (RFLP) patterns that distinguish A. cantonensis from A. costaricensis and other close relatives.

Physical Description

Angiostrongylus cantonensis is a slender, thread-like nematode characterized by its cylindrical body covered in a tough cuticle exhibiting transverse striations. Adult females typically measure 18–33 mm in length and 0.28–0.5 mm in width, while adult males are smaller, ranging from 15.5–23 mm in length and 0.2–0.35 mm in width; both sexes have a transparent body with a smoothly rounded anterior end. The mouth is simple, lacking a buccal capsule or lips, and features two or three small teeth arranged in a transverse row. Males possess a well-developed bursa supported by rays and long spicules for copulation, contributing to their distinctive morphology. The eggs of A. cantonensis are thin-shelled, oval-shaped structures measuring approximately 60–80 µm in length, containing developing embryos that hatch into first-stage larvae within the host's lungs. First-stage larvae (L1) are µm long and about 15 µm wide, with a bent and small tooth. Third-stage larvae (L3), the infective form to definitive hosts, are larger at 425–550 µm in length, featuring a notched with a pointed terminal projection and often encased in sheathed from previous molts.

Life Cycle

Developmental Stages

Adult female Angiostrongylus cantonensis deposit eggs in the small branches of the pulmonary arteries within the lungs of the definitive host, where they hatch into first-stage larvae (L1). These L1 larvae break into the alveolar spaces, ascend the bronchi and trachea to the , are swallowed into the digestive tract, and subsequently excreted in the feces. Upon ingestion by intermediate hosts such as mollusks, the L1 larvae penetrate the intestinal wall and migrate into the tissues, where they undergo two molts to develop into second-stage larvae () and then third-stage larvae (L3), the infective stage. This progression from L1 to L3 typically requires 2-3 weeks. In the definitive host, ingested L3 larvae excyst in the intestine, penetrate the gut wall, and migrate via the bloodstream to the ( and ), where they develop into young adults over about 4-6 weeks. The young adults then migrate through the venous system to the pulmonary arteries and right ventricle, where they fully mature into dioecious adults and reproduce. The prepatent period, from ingestion of L3 larvae to the appearance of L1 larvae in the feces, ranges from 37 to 45 days in experimentally infected rats, while the patent period during which L1 larvae are shed typically lasts 18-50 days. Larval development occurs with full progression to L3 between 20°C and 31°C; development ceases below approximately 15°C.

Transmission Dynamics

The transmission of Angiostrongylus cantonensis follows a fecal-oral route, wherein first-stage larvae (L1) are excreted in the feces of infected rats, leading to environmental contamination that exposes intermediate hosts to . These L1 larvae are ingested by mollusks, the primary intermediate hosts, where they molt and develop into the infective third-stage larvae (L3) over approximately 2–3 weeks, depending on and host species. Humans acquire the infection accidentally through ingestion of L3 larvae, most commonly via consumption of raw or undercooked mollusks such as snails and slugs, or through contaminated fresh produce like unwashed salads and vegetables that have contacted infected mollusks or their mucus. For instance, slime trails from infected gastropods can deposit L3 larvae on leafy greens, posing a risk during food preparation in endemic areas. Paratenic hosts play a key role in amplifying by harboring non-developing L3 larvae, which remain viable and infective; examples include freshwater prawns, crabs, frogs, and certain that inadvertently transport the larvae into the without supporting further parasite maturation. This mechanism extends the parasite's reach beyond direct consumption, increasing exposure opportunities in aquatic and terrestrial ecosystems. Direct human-to-human transmission does not occur, as humans function as dead-end hosts where the larvae cannot reproduce or produce eggs capable of perpetuating the cycle. L1 larvae exhibit limited environmental persistence, surviving up to 1–2 weeks in moist conditions such as water or damp soil, which is critical for their availability to intermediate hosts but declines rapidly under dry or high-temperature exposures.

Hosts and Ecology

Definitive Hosts

The definitive hosts of Angiostrongylus cantonensis are primarily species within the genus Rattus, including the Norway rat (Rattus norvegicus) and the black rat (Rattus rattus), with the Polynesian rat (Rattus exulans) also serving as a competent host in certain regions. In these rats, adult worms reside in the pulmonary arteries and right ventricle of the heart, where they mate and produce eggs that hatch into first-stage larvae (L1); these larvae migrate to the lungs, are coughed up, swallowed, and subsequently excreted in the feces to continue the life cycle. Prevalence of in endemic rat populations can be notably high, reaching up to 93.9% in wild spp. on eastern Hawai'i Island as detected by , with 72.7% harboring adult worms. In and Pacific regions, such as in , overall prevalence in rats is around 63.8%, with higher rates in R. exulans (77.4%) compared to R. rattus (47.6%). intensity typically ranges from a few to dozens of adult worms per infected rat, with examples including an average of 26.6 nematodes (range 1–100) in urban Rattus spp. and up to 62 worms in individual cases from the . In definitive hosts, A. cantonensis generally causes minimal pathology, allowing rats to remain or exhibit only mild respiratory or behavioral changes despite heavy burdens, which contributes to efficient parasite transmission. The parasite shows geographic adaptation, with higher prevalence and intensity observed in tropical and subtropical urban rat populations, where environmental conditions favor the .

Intermediate and Paratenic Hosts

The intermediate hosts of Angiostrongylus cantonensis are exclusively gastropod mollusks, including terrestrial snails and slugs as well as some aquatic species, which support the development of first-stage larvae (L1) into infective third-stage larvae (L3). Prominent examples include the giant African snail (Achatina fulica) and the golden apple snail (Pomacea canaliculata), both of which are facilitating the parasite's spread in non-native regions. In endemic areas, infection rates in these hosts can reach up to 45% for A. fulica and lower but significant levels for P. canaliculata (around 2%), highlighting their role in maintaining high larval burdens within snail populations. Within intermediate hosts, ingested L1 larvae undergo two molts to reach the infective L3 stage, a process that typically takes 13 to 21 days under optimal conditions, with L3 larvae remaining viable in the for up to a year. A single infected can produce thousands of L3 larvae, with reports documenting up to 20,000 per individual in some cases, enabling substantial parasite amplification during this developmental phase. Paratenic hosts, which do not support further larval development but serve as transport vectors, include a range of freshwater and terrestrial and vertebrates such as prawns, crabs, planarians, and frogs. In these , L3 larvae encyst in tissues like muscles or organs without molting, remaining infective until the host is consumed by a definitive host. These paratenic hosts contribute to amplification by accumulating larvae through predation on multiple infected hosts, thereby increasing the infective dose available to rats in food chains and enhancing overall parasite dissemination.

Epidemiology

Global Distribution and Emergence

Angiostrongylus cantonensis, the causative agent of rat lungworm disease, originated in and southern , where it was first identified in rats in in 1935. The parasite's global dissemination has been facilitated primarily by the movement of infected definitive hosts, such as Rattus rats, via international shipping routes. By the mid-20th century, it had spread to the Pacific region, with establishment in documented in 1961 through infections in rats and subsequent human cases. Similarly, the first reports in the emerged in the , including in around 1966, marking the beginning of its expansion into tropical and subtropical areas of . In the , introductions were noted by the late 1980s, likely through similar pathways involving trade and travel. Today, A. cantonensis is endemic in more than 30 countries, spanning , the Pacific Islands, parts of North and , and increasingly in and . Recent records include the first detection in in 2024 and 29% prevalence in urban rats in , , in 2024. Recent emergences highlight its ongoing expansion: in , 2024 surveys detected the parasite in both definitive rat hosts and intermediate hosts, confirming a new African focus. In the United States, a 2024 investigation in , , revealed a 20% prevalence of A. cantonensis in black rats (Rattus rattus) from a facility, suggesting local transmission cycles in environments. , previously considered free of the parasite, has seen initial detections, including fatal infections in non-human primates at a Spanish from 2020 to 2022 and in rats and gastropods in in 2024. Climate change is driving further emergence by altering the distribution of intermediate gastropod hosts, as warmer temperatures and shifting precipitation patterns expand suitable habitats for moisture-dependent snails. Modeling studies indicate that these environmental changes could facilitate a northward shift in the parasite's range by the 2050s, particularly in regions experiencing increased rainfall and milder winters, potentially introducing risks to temperate zones. The primary for with Angiostrongylus cantonensis is the ingestion of raw or undercooked intermediate hosts, particularly and slugs containing third-stage larvae. Infections can also result from consuming undercooked paratenic hosts such as prawns, crabs, frogs, or , or from larvae-contaminated and greens washed in unclean . In , where raw consumption is a in some regions, this accounts for a substantial portion of cases, with approximately 180 infections reported annually, predominantly in the northeast. Certain populations face elevated risks due to behavioral or environmental exposures. Children are particularly vulnerable owing to habits like , which increases accidental ingestion of larvae-laden , while travelers to endemic areas, such as the Pacific Islands or , represent a growing group through inadvertent consumption during . Immunocompromised individuals may experience more severe outcomes from even low-level exposures. Case incidence often peaks during rainy seasons, when increased moisture boosts populations and facilitates larval shedding onto produce. Globally, over 7,000 human cases of have been documented, though underreporting is widespread due to diagnostic challenges and non-notifiable status in many regions, suggesting true annual incidence may range from thousands to tens of thousands. In , trends show sustained endemicity; for instance, 125 cases (92 confirmed, 33 suspected) were reported in China's Dali Prefecture from 2007 to 2021, with peaks linked to seasonal snail festivals. , where the first human case was identified in 1945, has recorded hundreds of infections historically, though recent comprehensive counts remain limited. Incidence is rising in the , driven by the parasite's spread via invasive rats and mollusks. , detections have expanded to southern states like in 2024, with climate factors such as warmer temperatures and heavier rainfall promoting intermediate host proliferation. Animal infections, including in zoo-held like lemurs, have also surged in the , with multiple fatal cases reported in U.S. and facilities, highlighting zoonotic spillover risks and a 20% in rats near a zoo in 2024.

Human Angiostrongyliasis

Pathogenesis

Following of third-stage larvae (L3) of Angiostrongylus cantonensis, typically through contaminated food or hosts, the larvae are released in the human small intestine and rapidly penetrate the intestinal mucosa to enter the bloodstream. From there, they migrate via the to the (CNS), including the and , typically arriving within several days to a week. Within the CNS, the L3 larvae molt and develop into fourth-stage larvae and then immature adults, causing direct mechanical damage through their movement and burrowing into neural parenchyma. This triggers a robust inflammatory response, characterized by the recruitment of and formation of granulomatous lesions around the parasites. The immature adults typically survive for 2 to 8 weeks before dying, unable to reproduce or produce eggs in humans, as the host environment does not support full maturation or oviposition. Unlike in definitive hosts, where larvae migrate from the CNS to the lungs for maturation in pulmonary arteries, humans lack this compatible vascular site, resulting in the parasites becoming trapped and degenerating within the brain tissue. The host exacerbates CNS damage, with a predominant type 2 (Th2) profile driving activation and infiltration. Key mediators include interleukin-5 (IL-5), which promotes survival, recruitment, and degranulation, leading to heightened inflammation and tissue injury. Eosinophil-derived proteins, such as major basic protein, further contribute to neuronal damage and blood-brain barrier disruption. Disease severity is dose-dependent, with infections involving more than 10 larvae associated with more intense responses and worse outcomes, though human (CSF) typically lacks eggs or first-stage larvae due to the absence of .

Clinical Manifestations

Human infection with Angiostrongylus cantonensis typically manifests as eosinophilic meningitis, with an of 1 to 3 weeks following ingestion of infective larvae. During the acute phase, severe is the most common symptom, affecting 94% to 97% of patients, often accompanied by in approximately 50% of cases and in 50% to 70% of individuals. These sensory disturbances arise as larvae migrate through neural tissues, irritating the and causing . In severe cases, patients may experience (affecting about 60%), low-grade fever, and cranial nerve palsies, such as facial weakness or oculomotor dysfunction, occurring in up to 30% of cases. Rare complications include with altered mental status or seizures, particularly in heavy infections. Ocular angiostrongyliasis represents a distinct variant, where larvae invade the eye, leading to , , and potential permanent vision loss due to retinal damage from larval tracks. Most cases resolve spontaneously within 2 to 8 weeks, with symptoms gradually improving as the clears the non-reproductive larvae. However, chronic sequelae occur in approximately 10% of patients, manifesting as persistent , headache, or neuropathy lasting months. The fatality rate is low, less than 1%, though it is higher in young children and the elderly due to increased risk of severe .

Diagnosis, Treatment, and Prevention

Diagnostic Techniques

Diagnosis of Angiostrongylus cantonensis infection, also known as , relies on a combination of clinical evaluation, laboratory tests, and imaging, as no single test exists. The hallmark clinical finding is () eosinophilia, defined as more than 10% or an absolute count exceeding 10 per microliter, which occurs in over 95% of cases and strongly suggests the infection when accompanied by symptoms mimicking bacterial . This eosinophilic pleocytosis in is a key diagnostic indicator, often exceeding 20-70% in confirmed cases, and supports presumptive in endemic areas with relevant exposure history. Imaging techniques, particularly (MRI), aid in visualizing involvement. MRI commonly reveals leptomeningeal enhancement, hyperintense signals in the subcortical , and occasionally linear tracks suggestive of larval migration in the brain parenchyma. These findings, observed in a majority of patients with eosinophilic meningitis due to A. cantonensis, help differentiate from other causes but are not specific. Serological assays detect antibodies against A. cantonensis antigens, with enzyme-linked immunosorbent assay (ELISA) and Western blot targeting IgG being widely used. The 31-kDa antigen-based IgG ELISA demonstrates high sensitivity, often reported at 100% in experimental and clinical validations, while Western blot confirms specificity by identifying immunoreactive bands. These tests on serum or CSF achieve sensitivities of 80-100%, though cross-reactivity with other helminths can occur. Molecular methods, such as real-time polymerase chain reaction (RT-PCR) targeting A. cantonensis DNA, provide confirmatory evidence with detection in CSF samples, showing positivity in up to 67% of eosinophilic meningitis cases attributable to this parasite. PCR on blood is less sensitive but feasible for early detection in some hosts. Recent advances include environmental diagnostics via larval recovery from snail hosts. A 2024 technique involves extracting and examining the buccal cavity of intermediate snail species, such as Pomacea canaliculata, to recover A. cantonensis larvae, enabling rapid field identification of infection foci. Challenges in diagnosis stem from the absence of a definitive test, requiring integration of epidemiological exposure (e.g., consumption of raw mollusks), clinical features, and laboratory results. Differential diagnosis often includes gnathostomiasis, which presents with migratory subcutaneous swellings and radiculomyelitis rather than predominant meningitis, though both cause eosinophilia. This overlap necessitates serological or molecular confirmation to avoid misattribution.

Treatment Options

Treatment of human angiostrongyliasis primarily involves supportive care to manage symptoms such as and neck stiffness associated with eosinophilic meningitis, as there is no specific cure for this dead-end infection in humans. Analgesics, including nonsteroidal anti-inflammatory drugs or opioids as needed, are used to alleviate pain, while adequate hydration helps prevent complications from dehydration. Corticosteroids form the cornerstone of therapy to reduce inflammation caused by larval migration in the ; a typical regimen is at 1 mg/kg daily for 2 weeks, followed by a slow taper over an additional 2 weeks. Antiparasitic agents like (15 mg/kg/day divided into two doses for 14 days, not exceeding 800 mg/day) or are sometimes administered to target the larvae, but their use is controversial and must be cautious due to the risk of paradoxical worsening of from dying parasites releasing antigens. These drugs are typically combined with corticosteroids to mitigate this risk, with studies showing improved outcomes in moderate to severe cases when co-administered. , while effective in paralyzing larvae , is less commonly used in humans for this indication compared to . Most patients recover fully with supportive care and corticosteroids alone, as the larvae eventually die without completing their in humans. In mild cases, are often contraindicated to avoid unnecessary , with treatment limited to symptom relief. Recent clinical analyses, including a 2022 review, confirm that albendazole-corticosteroid combinations are effective in over 97% of treated human cases, reducing symptom duration and sequelae without significant adverse events.

Preventive Measures

Preventing infection with Angiostrongylus cantonensis, the causative agent of , primarily involves interrupting the parasite's through targeted practices, pest management, and community-level interventions. Food measures are essential to avoid accidental of infective third-stage larvae (L3), which reside in intermediate hosts such as snails and slugs or contaminate via their . Individuals in endemic areas should avoid eating raw or undercooked snails, slugs, freshwater prawns, land crabs, frogs, or other potential hosts, as these can harbor viable larvae. Thoroughly washing fruits and vegetables under running water removes adhering mollusks or contaminated mucus, while cooking potentially infected items like snails or slugs to an internal temperature of at least 74°C (165°F) kills the larvae. Hands and utensils should be washed after handling raw mollusks to prevent cross-contamination. Controlling populations, the definitive hosts where adult reside in the lungs, is critical to reducing environmental with L1 larvae shed in feces. Urban deratting programs, including trapping and rodenticides, combined with proper to eliminate sources and harborage sites, effectively break the transmission cycle in residential and agricultural settings. In , integrated rodent control has been emphasized as part of broader efforts to limit parasite reservoirs near human habitats. Public education campaigns in endemic regions promote awareness and behavioral changes to minimize exposure. In , a $1 million state initiative launched in 2017 included media broadcasts, school garden programs, and professional development for educators to teach avoidance of raw mollusks and promotion of garden hygiene, resulting in increased community vigilance. Similar efforts focus on messaging like thorough produce washing and prompt removal of snails from gardens. Surveillance systems aid early detection and response by intermediate host populations and human cases. Regular sampling of snails for L3 larvae , coupled with mandatory of suspected , enables targeted interventions in outbreak hotspots. in , such as hedgehogs or , has proven effective for tracking emergence in new areas. Vector management in high-risk agricultural zones employs molluscicides to suppress populations that amplify . Niclosamide and metaldehyde-based products, applied judiciously in farms and gardens, reduce intermediate host density without excessive environmental impact when integrated with cultural practices like habitat modification. In , such measures are recommended for commercial produce operations to prevent larval contamination. As expands suitable habitats for snails and rats into temperate regions, adaptive prevention includes heightened surveillance in vulnerable areas and tailored guidelines for emerging hotspots, emphasizing proactive mollusk control amid shifting seasonal patterns.

Zoonotic and Veterinary Impact

Infections in Animals

Angiostrongylus cantonensis infections in wildlife primarily affect rats as definitive hosts, where the parasite completes its with minimal clinical signs, often remaining even at high worm burdens. In contrast, serve as incidental hosts and experience severe neural angiostrongyliasis, manifesting as , central nervous system involvement with signs like , , and , frequently resulting in fatal outcomes due to larval migration-induced . Captive animals, especially in zoological settings, face significant risks from A. cantonensis. Between December 2020 and March 2022, three fatal cases of eosinophilic meningoencephalitis occurred in two red-fronted brown lemurs (Eulemur rufus) and one (Lemur catta) at Bioparc in , representing the first documented instances in . Similar outbreaks have been reported in zoos across the , involving species such as red ruffed lemurs (Varecia rubra) in and black-and-white ruffed lemurs (Varecia variegata) in , with affected animals exhibiting , neurological deficits, and high mortality rates. In other species, infections lead to notable neurological impairments. Horses develop motor weakness, , lameness, and lumbar paralysis from larval invasion of the . , such as the white-eared opossum (Didelphis albiventris), present with circling, depression, and other nervous signs culminating in eosinophilic meningoencephalitis. Amphibians like frogs act as paratenic dead-end hosts, harboring infective larvae without supporting further development or reproduction of the parasite. The pathology in non-human animals involves infective third-stage larvae penetrating the intestinal wall, migrating hematogenously to the , and eliciting severe , hemorrhage, and malacia along their tracks. In dogs, larval development arrests in the and without completing the reproductive cycle, leading to persistent neurological damage. Recent trends indicate rising infections in non-endemic environments, driven by global in and horticultural products that facilitate the introduction of infected rats and intermediate hosts. For instance, a 20% prevalence of A. cantonensis was detected in black rats at a , underscoring the zoonotic and veterinary risks in such facilities.

Public Health and Conservation Concerns

Angiostrongylus cantonensis poses a significant zoonotic threat as an emerging in non-tropical regions, with detections reported in the and in 2025. In August 2025, a 20% prevalence of the parasite was identified in black rats at a facility in , , , highlighting risks to both wildlife and humans in subtropical urban environments. Similarly, in southern Italy's region, the parasite was detected in rats and gastropods during the same period, marking its expansion into Mediterranean . In , infections were confirmed in from the protected of s'Albufera on in early 2025, and fatal cases occurred in non-human at a . Underreporting remains a critical barrier to control efforts, as the parasite is classified as a neglected due to low public awareness and diagnostic challenges, leading to incomplete surveillance in affected areas. Conservation concerns arise from the parasite's role in exacerbating the impacts of on ecosystems. Invasive rats, primary definitive hosts, facilitate the parasite's spread to remote s, where it infects native and endemic wildlife, potentially disrupting food webs and contributing to . hosts, such as invasive snails (e.g., the ), serve as vectors that amplify transmission while competing with native gastropods, further threatening fragile biota. In protected areas like Mallorca's wetlands, high prevalence in underscores risks to , including captive animals in zoos, where infections have caused mortality in non-human . Ecosystem-level effects, including altered parasite-host dynamics, highlight the need for integrated of invasive vectors to preserve . Economic burdens in Pacific regions, particularly , stem from outbreaks affecting and . Since becoming reportable in 2007, has confirmed over 80 cases of human angiostrongyliasis through 2017, with ongoing incidents in 2025, including three statewide, one on , incurring substantial healthcare and surveillance costs. State initiatives, such as a $1 million launched in 2017, illustrate the financial strain on resources for , testing, and , while infections linked to contaminated produce impact and deter in endemic areas. Future risks are amplified by , with models projecting substantial range expansion for A. cantonensis by 2100. In , simulations under increased temperature and precipitation scenarios forecast heightened habitat suitability at higher elevations, potentially extending the parasite's reach into previously unsuitable temperate zones globally. This expansion, driven by warmer conditions favoring vectors and populations, necessitates approaches that integrate human, animal, and environmental surveillance. Sentinel monitoring of wildlife, such as hedgehogs in , combined with systematic and gastropod sampling, enables early detection and coordinated interventions across sectors.

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