Meningitis In Humans Research Articles

Genetic Variation in Neisseria meningitidis Does Not Influence Disease Severity in Meningococcal Meningitis.

Neisseria meningitidis causes sepsis and meningitis in humans. It has been suggested that pathogen genetic variation determines variance in disease severity. Here we report results of a genome-wide association study of 486 N. meningitidis genomes from meningococcal meningitis patients and their association with disease severity. Of 369 meningococcal meningitis patients for whom clinical data was available, 44 (12%) had unfavorable outcome and 24 (7%) died. To increase power, thrombocyte count was used as proxy marker for disease severity. Bacterial genetic variants were called as k-mers, SNPs, insertions and deletions and clusters of orthologous genes (COGs). Population-level meningococcal genetic variation did not explain variance in disease severity (unfavorable outcome or thrombocyte count) in this cohort (h2 = 0.0%; 95% confidence interval: 0.0–0.9). Genetic variants in the bacterial uppS gene represented the top signal associated with thrombocyte count (p-value = 9.96e-07) but this did not reach statistical significance. We did not find an association between previously published variants in lpxL1, fHbp, and tps genes and unfavorable outcome or thrombocyte count. A power analysis based on simulated phenotypes based on real genetic data from 880 N. meningitidis genomes showed that we would be able to detect a continuous phenotype with h2 > = 0.5 with the population size available in this study. This rules out a major contribution of pathogen genetic variation to disease severity in meningococcal meningitis, and shows that much larger sample sizes are required to find specific low-effect genetic variants modulating disease outcome in meningococcal meningitis.

Streptococcus suis Meningitis in Humans: the Cause of Emerging Bacterial Infectious Diseases in Brazil? Case Report

Over the past few years, the number of reported human infections caused by ingestion of contaminated food has increased. S. suis infections caused by porcine products in humans present a wide variety of clinical manifestations after they invade the host, such as arthritis, septic shock, polyserositis, meningitis, and endocarditis. This article presents a rare case of meningitis in a Brazilian elderly male after consumption of porcine meat. Bacterial identification was performed with MALDI-TOF, a quick and accurate technique to identify this agent. The minimal inhibitory concentration of ceftriaxone was < 0.12 μg/ml, and the patient underwent a satisfactory course of treatment with ceftriaxone for 14 days. This case shows the importance of adopting sanitary inspection measures in order to avoid potentially lethal events associated with it, during handling, transportation and consumption of porcine meat in a developing country.

Records request response rate and vaccination status of first-time college students at a mid-sized Midwestern university

Objective: The purpose of this study was to establish the response rate of first-time college students to a vaccination records request, and to obtain student vaccination rates for selected vaccines. Participants: Student health records for the fall 2018 cohort of first-time college students were reviewed. Methods: Vaccination and response rates were compared based on sex, race/ethnicity, and home state. Results: There was a 66% response rate to the vaccination records request with no difference in response rate based on student demographics. Students exceeded most of the Healthy Campus 2020 vaccination targets. The human papillomavirus (HPV) and meningitis ACWY vaccines had the greatest room for improvement. Female students were significantly more likely to have a completed HPV vaccine series. Conclusions: Records response rates may be improved by students accessing and reporting state vaccination information during a required orientation. Following (CDC) guidelines for vaccination success may improve vaccination rates for HPV and menACWY.

First record of natural infection by Angiostrongylus cantonensis (Nematoda: Metastrongyloidea) in Belocaulus willibaldoi and Rattus norvegicus in an urban area of São Paulo city, SP, Brazil

Angiostrongylus cantonensis, a rat lungworm, is one of the leading causes of eosinophilic meningitis in humans. Infection in humans occurs by the ingestion of intermediate hosts, undercooked paratenic hosts or contaminated vegetables and fruits by mucus from infected molluscs. This zoonosis is widespread in tropical and subtropical areas of Southeast Asia, it has also been reported in the Pacific Islands as well as in other regions of Americas. In Brazil, human cases of angiostrongyliasis have been reported since 2007 in Southeast, Northeast, and South regions. In January 2011, we collected a batch of 30 Belocaulus willibaldoi slides in a neighborhood of São Paulo city (Parque Fernanda). Six of them were used for identifying species, and the others (24) were used in parasitological tests through digestion in peptic solution and then larvae isolation by the Rugai method. A total of 250 larvae were obtained and they had morphological traits of Angiostrongylus spp. Later, four Golden hamsters (Mesocricetus auratus) were infected with 38 larvae that allowed the recovery of young worms from the brain and lungs of rodents on the 21st and 30th day of infection. In this same neighborhood we captured rodents (Rattus norvegicus) that, after necropsy led us to recovery of 22 adult worms in the pulmonary arteries (14 males and 8 females) in May 2011. The larvae and worms obtained from natural infection were evaluated by morphological and morphometric parameters, as well as biological behavior patterns and molecular profile. All methodologies identified the parasite as Angiostrongylus cantonensis. In this way, we report for the first time, the natural infection by A. cantonensis in intermediate (B. willibaldoi) and definitive (R. norvegicus) hosts in a new urban region of Brazil.

Proteomic analysis of bEnd.3 cells infected with wild-type and stk-deficient strains of Streptococcus suis serotype 2 reveals protein and pathway regulation

Streptococcus suis serotype 2 (SS2) is a zoonotic pathogen causing meningitis in humans and pigs. However, information on the comparative protein expression of the blood-brain barrier (BBB) following SS2 infection is limited. Deletion of the serine/threonine kinase (stk) gene can decrease the ability of SS2 to invade the BBB. In the present study, bEnd.3 cells were used as the BBB model, and a SILAC comparative quantitative proteomic study of bEnd.3 cells infected with the SS2 ZY05719 or Δstk strain was performed to determine the differences between these strains infections. Compared with ZY05719-infected cells, 241 proteins were highly upregulated, and 81 were significantly downregulated in Δstk-infected cells. The obtained data revealed major changes in the proteins involved in RNA process, host cytoskeleton, tight junction disruption and immune response. Some differentially expressed proteins were screened by quantitative real-time PCR to examine their regulation at the transcriptional level, and western blot analysis was used to validate the changes of some selected proteins at the translational level. The results obtained in this study may be useful to understand the host response to SS2 infection and provide crucial clues to decipher how STK expression in SS2 helps the bacteria penetrate the BBB. SignificanceA SILAC comparative quantitative proteomic assay was performed in bEnd.3 cells infected with the SS2 ZY05719 or Δstk strain. 241 upregulated and 81 downregulated differentially expressed proteins (DEPs) were identified. DEPs are involved in RNA process, host cytoskeleton, tight junction disruption and immune response. Some DEPs were examined by qPCR and western blot assays, which were similar to those of their corresponding proteins in the quantitative proteomics analysis.

Structures of Echovirus 30 in complex with its receptors inform a rational prediction for enterovirus receptor usage

Receptor usage that determines cell tropism and drives viral classification closely correlates with the virus structure. Enterovirus B (EV-B) consists of several subgroups according to receptor usage, among which echovirus 30 (E30), a leading causative agent for human aseptic meningitis, utilizes FcRn as an uncoating receptor. However, receptors for many EVs remain unknown. Here we analyzed the atomic structures of E30 mature virion, empty- and A-particles, which reveals serotype-specific epitopes and striking conformational differences between the subgroups within EV-Bs. Of these, the VP1 BC loop markedly distinguishes E30 from other EV-Bs, indicative of a role as a structural marker for EV-B. By obtaining cryo-electron microscopy structures of E30 in complex with its receptor FcRn and CD55 and comparing its homologs, we deciphered the underlying molecular basis for receptor recognition. Together with experimentally derived viral receptor identifications, we developed a structure-based in silico algorithm to inform a rational prediction for EV receptor usage.

Role of Bacterial and Host DNases on Host-Pathogen Interaction during Streptococcus suis Meningitis.

Streptococcus suis is a zoonotic agent causing meningitis in pigs and humans. Neutrophils, as the first line of defense against S. suis infections, release neutrophil extracellular traps (NETs) to entrap pathogens. In this study, we investigated the role of the secreted nuclease A of S. suis (SsnA) as a NET-evasion factor in vivo and in vitro. Piglets were intranasally infected with S. suis strain 10 or an isogenic ssnA mutant. DNase and NET-formation were analyzed in cerebrospinal fluid (CSF) and brain tissue. Animals infected with S. suis strain 10 or S. suis 10ΔssnA showed the presence of NETs in CSF and developed similar clinical signs. Therefore, SsnA does not seem to be a crucial virulence factor that contributes to the development of meningitis in pigs. Importantly, DNase activity was detectable in the CSF of both infection groups, indicating that host nucleases, in contrast to bacterial nuclease SsnA, may play a major role during the onset of meningitis. The effect of DNase 1 on neutrophil functions was further analyzed in a 3D-cell culture model of the porcine blood–CSF barrier. We found that DNase 1 partially contributes to enhanced killing of S. suis by neutrophils, especially when plasma is present. In summary, host nucleases may partially contribute to efficient innate immune response in the CSF.

INVESTIGATING THE RAPID METHOD OF DIAGNOSING MENINGITIS IN HUMANS

Meningitis is a disease that can be caused by a variety of factors such as bacteria, viruses, or funguses. Occasionally, in the dangerous type of meningitis caused by bacteria, meningitis passes through the mucous membrane, enters the bloodstream, and causes various severe clinical syndromes, the most common of which is acute meningitis. Complications include hearing loss, vision loss, and memory impairments or even death. Despite bacterial treatment, at least 10% of patients, most of whom are young children, die within 1 or 2 days of onset, and 10 -20% of survivors face significant neurological consequences. Patients with meningitis should be identified immediately and the cause of the disease should be correctly identified. Various methods are used, including biochemical blood tests and spinal cord fluid analysis. This review article will first examine the bacteria that cause meningitis in humans and then samples of cerebrospinal fluid and detection will be discussed.

Inhibitory Effect of the Traditional Chinese Medicine Ephedra sinica granules on Streptococcus pneumoniae Pneumolysin.

Streptococcus pneumoniae (S. pneumoniae) is an opportunistic pathogen that causes pneumonia, meningitis and bacteremia in humans and animals. Pneumolysin (PLY), a major pore-forming toxin that is important for S. pneumoniae pathogenicity, is a promising target for the development of anti-infective agents. Ephedra sinica granules (ESG) is one of the oldest medical preparation with multiple biological activities (such as a divergent wind and cold effect); however, the detailed mechanism remains unknown. In this study, we found that ESG treatment significantly inhibited the oligomerization of PLY and then reduced the activity of PLY without affecting S. pneumoniae growth and PLY production. In a PLY and A549 cell co-incubation system, the addition of ESG resulted in significant protection against PLY-mediated cell injury. Furthermore, S. pneumoniae-infected mice showed decreased mortality, and alleviated tissue damage and inflammatory reactions following treatment with ESG. Our results indicate that ESG is a potential candidate treatment for S. pneumoniae infection that targets PLY. This finding partially elucidates the mechanism of the Chinese herbal formula ESG in the treatment of pneumococcal disease.

The excretory/secretory products of fifth-stage larvalAngiostrongylus cantonensis induces autophagy via the Sonic hedgehog pathway in mouse brain astrocytes.

Angiostrongyliasis is induced by the nematode Angiostrongylus cantonensis and leads to eosinophilic meningitis and meningoencephalitis in humans. Excretory-secretory products (ESPs) are important investigation targets for studying the relationship between hosts and nematodes. These products assist worms in penetrating the blood-brain barrier and avoiding the host immune response. Autophagy is a catabolic process that is responsible for digesting cytoplasmic organelles, proteins, and lipids and removing them through lysosomes. This process is essential to cell survival and homeostasis during nutritional deficiency, cell injury and stress. In this study, we investigated autophagy induction upon treatment with the ESPs of the fifth-stage larvae (L5) of A. cantonensis and observed the relationship between autophagy and the Shh pathway. First, the results showed that A. cantonensis infection induced blood-brain barrier dysfunction and pathological changes in the brain. Moreover, A. cantonensis L5 ESPs stimulated autophagosome formation and the expression of autophagy molecules, such as LC3B, Beclin, and p62. The data showed that upon ESPs treatment, rapamycin elevated cell viability through the activation of the autophagy mechanism in astrocytes. Finally, we found that ESPs induced the activation of the Sonic hedgehog (Shh) signaling pathway and that the expression of autophagy molecules was increased through the Shh signaling pathway. Collectively, these results suggest that A. cantonensis L5 ESPs stimulate autophagy through the Shh signaling pathway and that autophagy has a protective effect in astrocytes.

Identification of conditionally essential genes for Streptococcus suis infection in pigs

ABSTRACT Streptococcus suis is a Gram-positive bacterium and zoonotic pathogen that causes meningitis and sepsis in pigs and humans. The aim of this study was to identify genes required for S. suis infection. We created Tn-Seq libraries in a virulent S. suis strain 10, which was used to inoculate pigs in an intrathecal experimental infection. Comparative analysis of the relative abundance of mutants recovered from different sites of infection (blood, cerebrospinal fluid, and meninges of the brain) identified 361 conditionally essential genes, i.e. required for infection, which is about 18% of the genome. The conditionally essential genes were primarily involved in metabolic and transport processes, regulation, ribosomal structure and biogenesis, transcription, and cell wall membrane and envelope biogenesis, stress defenses, and immune evasion. Directed mutants were created in a set of 10 genes of different genetic ontologies and their role was determined in ex vivo models. Mutants showed different levels of sensitivity to survival in whole blood, serum, cerebrospinal fluid, thermic shock, and stress conditions, as compared to the wild type. Additionally, the role of three selected mutants was validated in co-infection experiments in which pigs were infected with both wild type and isogenic mutant strains. The genetic determinants of infection identified in this work contribute to novel insights in S. suis pathogenesis and could serve as targets for novel vaccines or antimicrobial drugs.

Morin inhibits Listeria monocytogenes virulence in vivo and in vitro by targeting listeriolysin O and inflammation

BackgroundListeria monocytogenes (L. monocytogenes) is a global opportunistic intracellular pathogen that can cause many infections, including meningitis and abortion in humans and animals; thus, L. monocytogenes poses a great threat to public safety and the development of the aquaculture industry. The isolation rate of Listeria monocytogenes in fishery products has always been high. And the pore-forming toxin listeriolysin O (LLO) is one of the most important virulence factors of L. monocytogenes. LLO can promote cytosolic bacterial proliferation and help the pathogen evade attacks from the host immune system. In addition, L. monocytogenes infection can trigger a series of severe inflammatory reactions.ResultsHere, we further confirmed that morin lacking anti-Listeria activity could inhibit LLO oligomerization. We also found that morin can effectively alleviate the inflammation induced by Listeria in vivo and in vitro and exerted an obvious protective effect on infected cells and mice.ConclusionsMorin does not possess anti-Listeria activity, neither does it interfere with secretion of LLO. However, morin inhibits oligomerisation of LLO and morin does reduce the inflammation caused during Listeria infection.

Experimental Infection of Dogs with Toscana Virus and Sandfly Fever Sicilian Virus to Determine Their Potential as Possible Vertebrate Hosts.

The sandfly-borne Toscana phlebovirus (TOSV), a close relative of the sandfly fever Sicilian phlebovirus (SFSV), is one of the most common causes of acute meningitis or meningoencephalitis in humans in the Mediterranean Basin. However, most of human phlebovirus infections in endemic areas either are asymptomatic or cause mild influenza-like illness. To date, a vertebrate reservoir for sandfly-borne phleboviruses has not been identified. Dogs are a prime target for blood-feeding phlebotomines and are the primary reservoir of human sandfly-borne Leishmania infantum. However, there are no definitive studies to assess whether dogs play a significant role as a reservoir host for human phlebovirus survival in the environment. Here, we have evaluated the susceptibility of domestic dogs to infection by TOSV and SFSV following the direct inoculation of the infectious virus. After experimental infection, the presence of viral RNA was investigated in plasma, urine, saliva, conjunctiva, faeces, semen, and bone marrow samples from 0 to 91 days postinoculation (dpi), as well as in plasma, saliva, and tears samples at 760 dpi. None of the challenged dogs developed clinical signs of infection with either TOSV or SFSV. SFSV RNA was never detected. TOSV RNA was not in any of the specimen types, except for plasma samples that showed low viral loads, although irregularly. None of the dogs developed detectable neutralizing antibodies after a single challenge dose of either TOSV or SFSV. However, a second challenge dose of virus given 56 days later elicited neutralizing antibodies, implying that the first inoculation of virus primed the animals for an anamnestic response following the second challenge. These results demonstrated that healthy domestic dogs are not highly susceptible to infection by TOSV or SFSV and do not develop significant viremia or excrete virus following infection. Consequently, dogs are unlikely natural reservoir hosts of infection and do not appear to play a significant role in phlebovirus transmission cycles.

TRIM32 Drives Pathogenesis in Streptococcal Toxic Shock-Like Syndrome and Streptococcus suis Meningitis by Regulating Innate Immune Responses.

Streptococcus suis is an emerging zoonotic agent that causes streptococcal toxic shock-like syndrome (STSLS) and meningitis in humans, with high mortality and morbidity. The pathogenesis of both STSLS and central nervous system (CNS) infections caused by S. suis is not well understood. TRIM32, a member of the tripartite motif (TRIM) protein family, has been reported to regulate host inflammatory responses. In this study, we showed that TRIM32 deficiency significantly reduced the level of bacteremia and the production of proinflammatory cytokines following severe S. suis infection, protecting infected mice from STSLS. The influence of TRIM32 gene deletion on a range of processes known to be involved in S. suis meningitis was also examined. Both levels of bacterial loads and indications of brain hemorrhage were reduced in infected Trim32-/- mice compared with infected wild-type (WT) controls. We also found that TRIM32 deficiency increased the permeability of the blood-brain barrier (BBB) and the recruitment of inflammatory monocytes during the early course of S. suis infection, potentially limiting the development of S. suis meningitis. Our results suggest that TRIM32 sensitizes S. suis-induced infection via innate immune response regulation.

Molecular Analysis of an IncF ColV-Like Plasmid Lineage That Carries a Complex Resistance Locus with a Trackable Genetic Signature.

IncF ColV plasmids are important plasmid incompatibility group that are currently restricted to the Enterobacteriaceae. These plasmids carry an important repertoire of virulence-associated genes (VAGs) that contribute to the ability of avian pathogenic Escherichia coli to cause disease in poultry. VAGs found on ColV plasmids have also been linked to urosepsis and meningitis in humans but the mechanisms that elicit these disease conditions are not well understood. Recently we described the sequence of a ColV plasmid pSDJ2009-52F that carried the typical repertoire of VAGs and a complex resistance gene locus flanked by IS26, an insertion element that plays an important role in mobilizing antibiotic resistance genes on plasmids and genomic islands. We recovered complete ColV-like plasmid sequences from public databases that shared >80% sequence identity with pSDJ2009-52F in geographically diverse regions of the world over a 20-year timeframe. Previously we noted that pSDJ2009-52F carries a unique genetic signature in the class 1 integron within the complex resistance locus that was presumably created by the action of IS26. Here we show that most ColV-like plasmids that are closely related to pSDJ2009-52F also carry the same signature. Our studies provide insight into how these signature-bearing plasmids and the mobile genetic elements they carry traffic between E. coli sequence types over large geographic distances.

Five Complete Genome Sequences Spanning the Dutch Streptococcus suis Serotype 2 and Serotype 9 Populations.

The zoonotic pathogen Streptococcus suis can cause septicemia and meningitis in humans. We report five complete genomes of Streptococcus suis serotype 2 and serotype 9, covering the complete phylogeny of serotype 9 Dutch porcine isolates and zoonotic isolates. The isolates include the model strain S10 and the Dutch emerging zoonotic lineage.

A mathematical model for co-dynamics of listeriosis and bacterial meningitis diseases

The co-infection of Listeriosis and Meningitis in humans is a public health burden globally with its endemicity mostly felt in the tropical and sub-tropical countries. In this study, we develop a novel deterministic model describing the Listeriosis-Meningitis co-infection dynamics. Two sub-models, namely the Listeriosis-only and Meningitis-only sub-models are presented and analysed. Mathematical analysis of each sub-model is carried out, as well as that of the co-infection model. We use Latin-hypercube sampling to determine the parameters affecting the severity of the infection co-dynamics. Results from the numerical simulations suggest that reduction in the Listeria pathogens in the environment and an increase in the Meningitis recovery rate decreases the rate of Listeriosis-Meningitis co-infections.

Diagnostic Value of Clinical and Laboratory Findings in Childhood Meningitis

Abstract Objective Acute meningitis in childhood is a serious infectious disease that requires immediate medical assessment to ensure appropriate treatment and healthy outcomes. The aim of this retrospective study was to evaluate clinical and laboratory findings in the diagnosis of acute meningitis in children. Materials and Methods Between February 2011 and March 2013, 258 children aged between 1 month and 18 years who were admitted to Konya Training and Research Hospital, Turkey, with clinically suspected meningitis and undergoing lumbar puncture were enrolled in the study. Patient charts were reviewed using a standardized data collection tool. Fifty-nine patients were excluded because of incomplete data or because they did not meet the enrollment criteria. Further statistical analysis was conducted on the remaining 199 patients. The diagnostic values of clinical and laboratory findings for acute meningitis were investigated. IBM SPSS 21.0 for Windows was used for the statistical analysis. Results Of the 199 patients (61.3% male; median age: 24 months), 101 (50.8%) were diagnosed with meningitis. A definitive diagnosis of bacterial meningitis was made in 16 patients, while 5 patients had probable bacterial meningitis. In addition, 80 patients diagnosed as aseptic meningitis and 47 of these patients had human enterovirus meningitis. Headache was more common in patients with meningitis. In patients without meningitis, the most common complaints were seizures or seizures accompanied by fever. Erythrocyte sedimentation rates (ESR), levels of cerebrospinal fluid protein, and cell counts in cerebrospinal fluid examinations were higher in the meningitis group. C-reactive protein, ESR, and procalcitonin higher than 22.55 mg/L, 36.5 mm/hour, and 6.795 mg/mL, respectively, indicated bacterial meningitis. Conclusion Our results showed that a combination of clinical and laboratory markers could facilitate recognition of bacterial meningitis in children.

Regulatory Mechanism of the Atypical AP-1-Like Transcription Factor Yap1 in Cryptococcus neoformans.

AP-1-like transcription factors play evolutionarily conserved roles as redox sensors in eukaryotic oxidative stress responses. In this study, we aimed to elucidate the regulatory mechanism of an atypical yeast AP-1-like protein, Yap1, in the stress response and virulence of Cryptococcus neoformansYAP1 expression was induced and involved not only by oxidative stresses, such as H2O2 and diamide, but also by other environmental stresses, such as osmotic and membrane-destabilizing stresses. Yap1 was distributed throughout both the cytoplasm and the nucleus under basal conditions and more enriched within the nucleus in response to diamide but not to other stresses. Deletion of the C-terminal cysteine-rich domain (c-CRD), where the nuclear export signal resides, increased nuclear enrichment of Yap1 under basal conditions and altered resistance to oxidative stresses but did not affect the role of Yap1 in other stress responses and cellular functions. As a potential upstream regulator of Yap1, we discovered that Mpk1 is positively involved, but Hog1 is mostly dispensable. Pleiotropic roles for Yap1 in diverse biological processes were supported by transcriptome data showing that 162 genes are differentially regulated by Yap1, with further analysis revealing that Yap1 promotes cellular resistance to toxic cellular metabolites produced during glycolysis, such as methylglyoxal. Finally, we demonstrated that Yap1 plays a minor role in the survival of C. neoformans within hosts.IMPORTANCE The human meningitis fungal pathogen, Cryptococcus neoformans, contains the atypical yeast AP-1-like protein Yap1. Yap1 lacks an N-terminal cysteine-rich domain (n-CRD), which is present in other fungal Yap1 orthologs, but has a C-terminal cysteine-rich domain (c-CRD). However, the role of c-CRD and its regulatory mechanism remain unknown. Here, we report that Yap1 is transcriptionally regulated in response to oxidative, osmotic, and membrane-destabilizing stresses partly in an Mpk1-dependent manner, supporting its role in stress resistance. The c-CRD domain contributed to the role of Yap1 only in resistance to certain oxidative stresses and azole drugs but not in other cellular functions. Yap1 has a minor role in the survival of C. neoformans in a murine model of systemic cryptococcosis.

Development of an immunochromatographic device to detect antibodies for rapid diagnosis of human angiostrongyliasis.

Cerebral angiostrongyliasis is a central nervous system disease caused by Angiostrongylus cantonensis and can produce eosinophilic meningitis or meningoencephalitis in humans. Sero-immunological techniques, such as the enzyme-linked immunosorbent assay (ELISA) and immunoblotting, are most commonly used for the diagnosis of human angiostrongyliasis. However, diagnosis in remote areas remains problematic because sophisticated equipment and specialized skills are required. To overcome, we have developed the immunochromatographic test (ICT) kit for rapid serological diagnosis of angiostrongyliasis through the detection of anti-A. cantonensis-specific antibodies in human serum. A recombinant A. cantonensis galectin-2 (rAcGal2) from young adult female worms was used as an antigen for the ICT kit development. Diagnostic values were evaluated and compared using the ELISA. The sensitivity, specificity and positive and negative predictive values of the ICT kit were 87.0, 96.5, 94.6 and 91.4%, respectively, and those of the ELISA were 91.0, 97.2, 95.8 and 94.0%, respectively. The concordance of the ICT kit was 93.9%. We, thus, determined that the ICT kit is sensitive and specific and provides reliable diagnostic results. It is rapid and simple to perform and can be utilized for both point-of-care diagnosis in the bedside laboratory and epidemiological surveys in endemic regions where access to diagnostic equipment is limited.