iGeneTech Bioscience Co., Ltd.
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Fully Automatic & More Precise | iGeneTech Launches Integrated Solution for Syndrome Pathogen Detection

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    Foreword

    iGeneTech launches four syndrome pathogen identification panels covering 184 common pathogens. Paired with the IGT-AS01 automated workstation, the solution supports both manual and automated workflows, is compatible with diverse sample types, and requires no pre-cultivation or host depletion. It enables accurate pathogen identification and delivers an end-to-end solution for public health prevention, control, and research surveillance.

    Background

    Global public health prevention and control have drawn intense attention recently: Ethiopia has confirmed cases of Marburg virus disease, and Nipah virus outbreaks in Indonesia have triggered upgraded prevention measures in multiple countries. Meanwhile, the transition from winter to spring is a peak period for respiratory and gastrointestinal infectious diseases. Precise prevention and control of four major syndromes—fever with bleeding, respiratory, gastrointestinal, and encephalitis meningitis—have become key priorities in public health. Most of these syndromes are caused by various pathogens; some are highly pathogenic, lethal, and transmissible between humans. Rapid and accurate pathogen identification is critical for early detection and response in epidemic control.

    The four major syndromes differ in clinical features, pathogenesis, and causative pathogens, yet all spread rapidly and carry risks of cluster infections or severe cases, posing challenges to public health and population health.

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    Respiratory Syndrome[1-4]:

    Peak in autumn and winter, with common symptoms including fever, cough, nasal congestion, and sore throat, presenting as upper or lower respiratory tract infections. Major pathogens include influenza A virus, SARS-CoV-2, and Streptococcus pneumoniae. Transmission occurs mainly via droplets. High-risk groups include immunocompromised individuals and those with allergic constitutions, with frequent cluster infections in crowded settings.

    Gastrointestinal Syndrome[5]:

    A priority syndrome during winter–spring prevention and control, characterized by gastrointestinal disturbances such as nausea, vomiting, abdominal pain, and diarrhea. Common pathogens include norovirus, rotavirus, and Salmonella. Infections often result from contaminated food or environmental exposure. Mixed infections and emerging pathogens complicate clinical diagnosis and may lead to outbreaks.

    Fever with Bleeding Syndrome[6-7]:

    Defined by fever and systemic or localized bleeding. Typical pathogens include Crimean-Congo hemorrhagic fever virus, severe fever with thrombocytopenia syndrome virus (SFTSV), and dengue virus. After invasion, pathogens trigger a pathological cycle of inflammation activation, endothelial injury, and coagulation abnormalities. The syndrome is highly pathogenic and carries potential human-to-human transmission risk.

    Encephalitis Meningitis Syndrome[8-9]:

    A life-threatening syndrome caused by pathogens including Nipah virus, Japanese encephalitis virus, and Neisseria meningitidis. Pathogens cross the blood–brain barrier to invade the central nervous system, with typical symptoms of fever, headache, and altered consciousness. It progresses rapidly and has a high fatality rate.

     

    Covered Species in the Identification Panels

    Respiratory Syndrome PathogensGastrointestinal Syndrome PathogensEncephalitis Meningitis Syndrome PathogensFever with Bleeding Syndrome Pathogens
    Influenza A virusNorovirus GI/GIIJapanese encephalitis virusDengue virus
    Influenza B virusSapovirusWest Nile virusChikungunya virus
    Influenza C virusRotavirus A/B/CDengue virusZika virus
    Influenza D virusAstrovirusZika virusEbola virus
    Human parainfluenza virus 1Enteric adenovirusChikungunya virusMarburg virus
    Human parainfluenza virus 2Aichi virusNipah virusCrimean-Congo hemorrhagic fever virus
    Human parainfluenza virus 3CoxsackievirusEnterovirus 71Rift Valley fever virus
    Human parainfluenza virus 4EchovirusEnterovirusLassa virus
    Human respiratory syncytial virus AEnterovirus 71EchovirusHantavirus
    Human respiratory syncytial virus BHepatitis A virusCoxsackievirusSFTS virus
    Human metapneumovirusHepatitis E virusVaricella-zoster virusYellow fever virus
    Human coronavirus 229ESalmonella spp.CytomegalovirusKyasanur Forest disease virus
    Human coronavirus OC43Shigella spp.Epstein-Barr virusOmsk hemorrhagic fever virus
    Human coronavirus NL63Pathogenic Escherichia coliHuman herpesvirus 6Leptospira interrogans
    Human coronavirus HKU1Campylobacter jejuniMumps virusRickettsia rickettsii
    SARS-CoVYersinia enterocoliticaMeasles virusOrientia tsutsugamushi
    SARS-CoV-2Vibrio choleraeRubella virusPlasmodium falciparum
    MERS-CoVVibrio parahaemolyticusRabies virusPlasmodium vivax
    Human adenovirusClostridium perfringensLymphocytic choriomeningitis virusPlasmodium malariae
    Human bocavirusClostridium difficileStreptococcus pneumoniaePlasmodium ovale
    Rhinovirus A/B/CBacillus cereusNeisseria meningitidis
    EnterovirusListeria monocytogenesHaemophilus influenzae
    Epstein-Barr virusStaphylococcus aureusListeria monocytogenes
    CytomegalovirusGiardia lambliaEscherichia coli K1
    Human herpesvirus 6Cryptosporidium spp.Staphylococcus aureus
    Human herpesvirus 7Cyclospora cayetanensisMycobacterium tuberculosis
    Varicella-zoster virusEntamoeba histolyticaCryptococcus neoformans
    Streptococcus pneumoniae
    Cryptococcus gattii
    Staphylococcus aureus
    Aspergillus spp.
    Haemophilus influenzae
    Toxoplasma gondii
    Legionella pneumophila
    Naegleria fowleri
    Mycoplasma pneumoniae
    Acanthamoeba spp.
    Chlamydia pneumoniae


    Bordetella pertussis


    Pseudomonas aeruginosa


    Klebsiella pneumoniae


    Acinetobacter baumannii


    Moraxella catarrhalis


    Pneumocystis jirovecii


    Aspergillus fumigatus


    Candida albicans


     

     

    Using multiple strain sequences from the NCBI database as references, iGeneTech designed pathogen identification panels with differentiated probe strategies: conserved within species, specific between species for bacteria, fungi, and parasites; full-genome coverage for viruses. This design ensures comprehensive, zero-miss detection of pathogens.

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    Paired with iGeneTech’s proprietary automated workstation reagent strip system, the workflow supports fast, independent processing of single samples and flexible throughput scaling via multi-unit arrays, greatly reducing manual handling. Only nucleic acid extracted from samples, capture probes, and index sequences need to be added to the reagent strips to start fully automated processing with no extra manual intervention, fully meeting laboratory demands for operational flexibility and minimal turnaround time.

    Based on iGeneTech’s proprietary analytical pipeline for pathogen identification, raw sequencing data undergo quality control and host filtering; remaining reads are aligned against the pathogen reference database, and valid supporting read counts per species are tabulated and reported.

    Key Advantages

    Broad-spectrum and high-sensitivity, accurate and reliable

    Covers diverse pathogens including viruses, bacteria, and fungi. Optimized probes stably capture trace pathogen nucleic acids. Combined with efficient hybridization and enrichment, the system delivers unbiased, precise genomic identification.

    Simplified workflow, efficient and convenient

    Supports diverse samples (wastewater, human, environmental, etc.). No pre-cultivation or host depletion required. Paired with 0.5–1 hour rapid hybridization and automated processing, it drastically simplifies pre-treatment and shortens detection time.

    Fully integrated, walkaway detection

    All-in-one reagent strips integrate library preparation and capture. Single-sample independent operation enables samplein–libraryout processing. Multi-instrument matrix expansion supports flexible throughput.

    Physical isolation to prevent contamination, compact for strict environments

    Independent reaction units eliminate cross-contamination. The compact footprint (only 0.1 m²) fits directly into biological safety cabinets, meeting high-level containment requirements.

    End-to-End Detection Coverage

    The four syndrome identification probe kits, combined with magnetic bead–based extraction kits, RNA pathogen library construction & capture kits, and DNA pathogen library construction & capture kits, provide a seamless sample-to-data workflow. They support batch processing with automated liquid handling workstations and are compatible with multiple high-throughput sequencing platforms to suit diverse scenarios.

     

    Related Product Matrix: End-to-End Support from Extraction to Detection

    Product Name

    Specification

    Cat. No.

    Encephalitis Meningitis Syndrome Panel

    16 / 96 rxn

    PH2014841 / PH2014842

    Respiratory Syndrome Identification Panel

    16 / 96 rxn

    PH2014801 / PH2014802

    Gastrointestinal Syndrome Identification Panel

    16 / 96 rxn

    PH2014811 / PH2014812

    Fever with Bleeding Syndrome Panel

    16 / 96 rxn

    PH2014821 / PH2014822

    Magnetic Beads Based Pathogen DNA/RNA Co-Extraction Kit

    50 rxn

    E10021

    Magnetic Beads Based Pathogen DNA/RNA Co-Extraction Kit (Host Depletion)

    50 rxn

    E20011

    IGT® DNA Pathogen Microbial Library Prep & Capture KitIllumina

    16 rxn

    C11361 / C11431

    IGT® RNA Pathogen Microbial Library Prep & Capture KitIllumina

    16 rxn

    C11371 / C11441

    IGT-AS12 Automated Liquid Handling Workstation (Configuration 3)

    Configuration 3

    Q91013

     

    References

    [1] Gambotto A, Barratt-Boyes SM, de Jong MD, Neumann G, Kawaoka Y. 2008. Human infection with highly pathogenic H5N1 influenza virus. Lancet 371:1464–1475.[2] Gupta A, Madhavan MV, Sehgal K, Nair N, Mahajan S, et al. 2020. Extrapulmonary manifestations of COVID-19. Nat. Med. 26:1017–1032.[3] Andre G, Converso TR, Politano WR, Ferraz LF, Ribeiro ML, Leite LC, Darrieux M. 2017. Role of Streptococcus pneumoniae proteins in evasion of complement-mediated immunity. Front Microbiol 8:224.[4] Kim TS, Braciale TJ. 2009. Respiratory dendritic cell subsets differ in their capacity to support the induction of virus-specific cytotoxic CD8+ T cell responses. PLOS ONE 4:e4204.[5] Pathan N, Woolfall K, Popa M, et al. Selective digestive tract decontamination to prevent Healthcare associated infections in critically ill children: the PICNIC Multicentre randomised pilot clinical trial. Sci Rep 2023;13:21668. doi:10.1038/s41598-023-46232-7.[6] Zhang, W. K., Yan, J. M., Chu, M., Li, B., Gu, X. L., Jiang, Z. Z., … Yu, X. J. (2025). Bunyavirus SFTSV nucleoprotein exploits TUFM-mediated mitophagy to impair antiviral innate immunity. Autophagy, 21(1), 102–119. https://doi.org/10.1080/15548627.2024.2393067.[7] Wang, P., Liu, L., Liu, A., et al. Structure of severe fever with thrombocytopenia syndrome virus L protein elucidates the mechanisms of viral transcription initiation. Nat Microbiol 5, 864–871 (2020). https://doi.org/10.1038/s41564-020-0712-2.[8] Linder KA, Malani PN. Meningococcal Meningitis. JAMA. 2019;321(10):1014. doi:10.1001/jama.2019.0772.[9] Sala, F.A., Ditter, K., Dybkov, O., et al. Structural basis of Nipah virus RNA synthesis. Nat Commun 16, 2261 (2025). https://doi.org/10.1038/s41467-025-57219-5.

     


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