Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Characteristics Research Template

Target Disease

• Disease Name: Postinfectious Vasculitis
• MONDO ID: (if available)
• Category: Complex

Research Objectives

Please provide a comprehensive research report on Postinfectious Vasculitis covering all of the disease characteristics listed below. This report will be used to populate a disease knowledge base entry. Be thorough and cite primary literature (PMID preferred) for all claims.

For each section, suggested databases/resources are listed. These are the first places you should search for information on each topic.

1. Disease Information

Search first: OMIM, Orphanet, ICD-10/ICD-11, MeSH, PubMed

• What is the disease? Provide a concise overview.
• What are the key identifiers? (OMIM, Orphanet, ICD-10/ICD-11, MeSH, Mondo)
• What are the common synonyms and alternative names?
• Is the information derived from individual patients (e.g., EHR) or aggregated disease-level resources?

2. Etiology

• Disease Causal Factors: What are the primary causes? (genetic, environmental, infectious, mechanistic)
• Risk Factors:

  Search first: PubMed, Cochrane Library, UpToDate, clinical guidelines, ClinVar, ClinGen, GWAS Catalog, PheGenI, CTD, CDC, WHO, epidemiological databases

• Genetic risk factors (causal variants, susceptibility loci, modifier genes)
• Environmental risk factors (toxins, lifestyle, occupational exposures, age, sex, family history)
• Protective Factors:

  Search first: PubMed, Cochrane Library, clinical trial databases, GWAS Catalog, gnomAD, WHO, CDC, nutrition databases

• Genetic protective factors (protective variants, modifier alleles)
• Environmental protective factors (diet, lifestyle, exposures that reduce risk)
• Gene-Environment Interactions: How do genetic and environmental factors interact to influence disease?

  Search first: CTD, PubMed, PheGenI, GxE databases

3. Phenotypes

Search first: HPO (Human Phenotype Ontology), OMIM, Orphanet, PubMed, clinicaltrials.gov, MedDRA, SNOMED CT, DECIPHER, LOINC

For each phenotype, provide: - Phenotype type: symptoms, clinical signs, physical manifestations, behavioral changes, or laboratory abnormalities

For symptoms/signs: HPO, OMIM, Orphanet, PubMed For behavioral changes: HPO, DSM, RDoC (Research Domain Criteria), PubMed For laboratory abnormalities: LOINC, SNOMED CT, LabTests Online, PubMed - Phenotype characteristics: Search first: OMIM, Orphanet, HPO, PubMed - Age of symptom onset (neonatal, childhood, adult-onset, late-onset) - Symptom severity (mild, moderate, severe, variable) - Symptom progression (stable, progressive, episodic, fluctuating) - Frequency among affected individuals (percentage or qualitative) - Quality of life impact: Effects on daily functioning and well-being (per-phenotype when possible) Search first: EQ-5D database, SF-36, WHO QOL databases, PubMed - Suggest HPO (Human Phenotype Ontology) terms for each phenotype

4. Genetic/Molecular Information

• Causal Genes: Gene mutations or chromosomal abnormalities responsible for disease (gene symbols, OMIM IDs)

  Search first: OMIM, ClinVar, HGMD, Ensembl, NCBI Gene

• Pathogenic Variants:
• Affected genes (gene symbols, HGNC IDs) > Search first: OMIM, NCBI Gene, Ensembl, HGNC, UniProt, GeneCards
• Variant classification (pathogenic, likely pathogenic, VUS per ACMG/AMP guidelines) > Search first: ClinVar, ClinGen, ACMG/AMP guidelines, VarSome
• Variant type/class (missense, frameshift, nonsense, splice-site, structural)
• Allele frequency in population databases > Search first: gnomAD, 1000 Genomes, ExAC, TOPMed, dbSNP
• Somatic vs germline origin > Search first: COSMIC (somatic), ClinVar, ICGC, TCGA
• Functional consequences (loss of function, gain of function, dominant negative)
• Modifier Genes: Genes that modify disease severity or expression
• Epigenetic Information: DNA methylation, histone modifications, chromatin changes affecting disease

  Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

• Chromosomal Abnormalities: Large-scale genetic changes (aneuploidy, translocations, inversions)

  Search first: DECIPHER, ClinVar, ECARUCA, UCSC Genome Browser

5. Environmental Information

• Environmental Factors: Non-genetic contributing factors (toxins, radiation, pollution, occupational exposure)

  Search first: CTD (Comparative Toxicogenomics Database), TOXNET, PubMed, EPA databases

• Lifestyle Factors: Behavioral factors (smoking, diet, exercise, alcohol consumption)

  Search first: CDC databases, WHO, PubMed, NHANES

• Infectious Agents: If applicable, pathogens causing or triggering disease (bacteria, viruses, fungi, parasites)

  Search first: NCBI Taxonomy, ViPR, BV-BRC, MicrobeDB, GIDEON

6. Mechanism / Pathophysiology

• Molecular Pathways: Specific signaling cascades or biochemical pathways involved (Wnt, MAPK, mTOR, PI3K-AKT, etc.)

  Search first: KEGG, Reactome, WikiPathways, PathBank, BioCyc

• Cellular Processes: Cell-level mechanisms (apoptosis, autophagy, cell cycle dysregulation, inflammation, etc.)

  Search first: Gene Ontology (GO), Reactome, KEGG, PubMed

• Protein Dysfunction: How protein structure or function is altered (misfolding, aggregation, loss of function, gain of function)

  Search first: UniProt, PDB (Protein Data Bank), InterPro, Pfam, AlphaFold

• Metabolic Changes: Alterations in metabolic processes (energy metabolism, lipid metabolism, amino acid metabolism)

  Search first: KEGG, BioCyc, HMDB (Human Metabolome Database), BRENDA

• Immune System Involvement: Role of immune response (autoimmunity, immunodeficiency, chronic inflammation)

  Search first: ImmPort, Immunome Database, IEDB, Gene Ontology

• Tissue Damage Mechanisms: How tissues/ are injured (oxidative stress, ischemia, fibrosis, necrosis)

  Search first: PubMed, Gene Ontology, Reactome

• Biochemical Abnormalities: Specific molecular defects (enzyme deficiencies, receptor dysfunction, ion channel defects)

  Search first: BRENDA, UniProt, KEGG, OMIM, PubMed

• Epigenetic Changes: DNA methylation, histone modifications affecting gene expression in disease

  Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

• Molecular Profiling (if available):
• Transcriptomics/gene expression changes > Search first: GEO (Gene Expression Omnibus), ArrayExpress, GTEx, Human Cell Atlas, SRA
• Proteomics findings > Search first: PRIDE, ProteomeXchange, Human Protein Atlas, STRING, BioGRID
• Metabolomics signatures > Search first: MetaboLights, Metabolomics Workbench, HMDB, METLIN
• Lipidomics alterations > Search first: LIPID MAPS, SwissLipids, LipidHome, Metabolomics Workbench
• Genomic structural features > Search first: UCSC Genome Browser, Ensembl, NCBI, dbVar, DGV
• Advanced Technologies (if applicable):
• Single-cell analysis findings (cell-type specific mechanisms, cellular heterogeneity) > Search first: Human Cell Atlas, Single Cell Portal, GEO, CELLxGENE
• Spatial transcriptomics findings > Search first: GEO, Spatial Research, Vizgen, 10x Genomics data
• Multi-omics integration results > Search first: TCGA, ICGC, cBioPortal, LinkedOmics, PubMed
• Functional genomics screens (CRISPR, RNAi) > Search first: DepMap, GenomeRNAi, PubMed, BioGRID ORCS

For each mechanism, describe: - The causal chain from initial trigger to clinical manifestation - Which mechanisms are upstream vs downstream - What cell types and biological processes are involved - Suggest GO terms for biological processes and CL terms for cell types

7. Anatomical Structures Affected

• Organ Level:
• Primary organs directly affected
• Secondary organ involvement (complications, secondary effects)
• Body systems involved (cardiovascular, nervous, digestive, respiratory, endocrine, etc.)

  Search first: Uberon, FMA (Foundational Model of Anatomy), OMIM, HPO, ICD-11, MeSH, SNOMED CT

• Tissue and Cell Level:
• Specific tissue types affected (epithelial, connective, muscle, nervous)
• Specific cell populations targeted (with Cell Ontology terms)

  Search first: Uberon, Human Protein Atlas, Cell Ontology, Human Cell Atlas, CellMarker, PanglaoDB

• Subcellular Level:
• Cellular compartments involved (mitochondria, nucleus, ER, lysosomes) (with GO Cellular Component terms)

  Search first: Gene Ontology (Cellular Component), UniProt, Human Protein Atlas

• Localization:
• Specific anatomical sites (with UBERON terms) > Search first: FMA, Uberon, NeuroNames (for brain), SNOMED CT
• Lateralization (unilateral, bilateral, asymmetric) > Search first: HPO, clinical literature, imaging databases

8. Temporal Development

• Onset:
• Typical age of onset (congenital, pediatric, adult, geriatric)
• Onset pattern (acute, subacute, chronic, insidious)

  Search first: OMIM, Orphanet, HPO, PubMed

• Progression:
• Disease stages (early, intermediate, advanced, end-stage) > Search first: Cancer Staging Manual (AJCC), WHO classifications, PubMed
• Progression rate (rapid, slow, variable)
• Disease course pattern (episodic, relapsing-remitting, progressive, stable)
• Disease duration (self-limited, chronic lifelong)

  Search first: Disease registries, longitudinal cohort databases, natural history studies, PubMed, Orphanet, OMIM

• Patterns:
• Remission patterns (spontaneous, treatment-induced) > Search first: Clinical trial databases, disease registries, PubMed
• Critical periods (time windows of vulnerability or opportunity for intervention) > Search first: PubMed, developmental biology databases, clinical guidelines

9. Inheritance and Population

• Epidemiology:
• Prevalence (cases per 100,000 at given time)
• Incidence (new cases per 100,000 per year)

  Search first: Orphanet, CDC, WHO, GBD (Global Burden of Disease), national registries, SEER, disease registries

• For Genetic Etiology:
• Inheritance pattern (AD, AR, X-linked, mitochondrial, multifactorial, polygenic) > Search first: OMIM, Orphanet, ClinVar, GTR (Genetic Testing Registry)
• Penetrance (complete, incomplete, age-dependent) > Search first: ClinVar, OMIM, PubMed, ClinGen
• Expressivity (variable, consistent) > Search first: OMIM, ClinVar, PubMed
• Genetic anticipation (increasing severity in successive generations) > Search first: OMIM, PubMed (especially for repeat expansion disorders)
• Germline mosaicism > Search first: ClinVar, OMIM, genetic counseling literature, PubMed
• Founder effects (population-specific mutations) > Search first: gnomAD, population genetics databases, PubMed
• Consanguinity role > Search first: OMIM, population studies, genetic counseling resources
• Carrier frequency > Search first: gnomAD, carrier screening databases, GeneReviews, GTR
• Population Demographics:
• Affected populations (ethnic or demographic groups with higher prevalence) > Search first: gnomAD, 1000 Genomes, PAGE Study, PubMed, population registries
• Geographic distribution (endemic areas, regional variation) > Search first: WHO, CDC, GBD, Orphanet, geographic epidemiology databases
• Geographic distribution of specific variants
• Sex ratio (male:female) > Search first: Disease registries, OMIM, PubMed, epidemiological databases
• Age distribution of affected individuals > Search first: CDC, disease registries, SEER, Orphanet

10. Diagnostics

• Clinical Tests:
• Laboratory tests (blood, urine, tissue chemistry, specific enzyme assays) > Search first: LOINC, LabTests Online, PubMed
• Biomarkers (proteins, metabolites, genetic markers, circulating biomarkers) > Search first: FDA Biomarker List, BEST (Biomarkers, EndpointS, and other Tools), PubMed
• Imaging studies (X-ray, CT, MRI, PET, ultrasound) > Search first: RadLex, DICOM, Radiopaedia, imaging databases
• Functional tests (pulmonary function, cardiac stress tests) > Search first: LOINC, clinical guidelines, PubMed
• Electrophysiology (EEG, EMG, ECG, nerve conduction studies) > Search first: LOINC, clinical neurophysiology databases, PubMed
• Biopsy findings (histopathology, immunohistochemistry) > Search first: SNOMED CT, College of American Pathologists resources, PubMed
• Pathology findings (microscopic examination) > Search first: SNOMED CT, Digital Pathology databases, PubMed
• Genetic Testing:

  Search first: GTR (Genetic Testing Registry), GeneReviews, ClinGen

• Overview of recommended genetic testing approach
• Whole genome sequencing (WGS) utility > Search first: GTR, ClinVar, GEL (Genomics England), gnomAD
• Whole exome sequencing (WES) utility > Search first: GTR, ClinVar, OMIM, GeneMatcher
• Gene panels (which panels, which genes) > Search first: GTR, ClinVar, laboratory-specific databases
• Single gene testing > Search first: GTR, ClinVar, OMIM, GeneReviews
• Chromosomal microarray (CMA) > Search first: DECIPHER, ClinVar, dbVar, ECARUCA
• Karyotyping > Search first: Chromosome Abnormality Database, ClinVar, cytogenetics resources
• FISH > Search first: ClinVar, cytogenetics databases, PubMed
• Mitochondrial DNA testing > Search first: MITOMAP, MSeqDR, ClinVar, GTR
• Repeat expansion testing > Search first: GTR, ClinVar, repeat expansion databases, PubMed
• Omics-Based Diagnostics (if applicable):
• RNA sequencing / transcriptomics > Search first: GEO, ArrayExpress, GTEx, RNA-seq databases
• Proteomics > Search first: PRIDE, ProteomeXchange, FDA Biomarker database
• Metabolomics > Search first: MetaboLights, Metabolomics Workbench, HMDB
• Epigenomics > Search first: GEO, ENCODE, Roadmap Epigenomics, MethBase
• Liquid biopsy > Search first: COSMIC, ClinVar, liquid biopsy databases, PubMed
• Clinical Criteria:
• Standardized diagnostic criteria (DSM, ICD, society guidelines) > Search first: DSM-5, ICD-11, clinical society guidelines, UpToDate
• Differential diagnosis (other conditions to rule out, with distinguishing features) > Search first: DynaMed, UpToDate, clinical decision support systems
• Screening:
• Screening methods for asymptomatic individuals (newborn screening, carrier screening, cascade screening) > Search first: ACMG recommendations, CDC newborn screening, GTR

11. Outcome/Prognosis

• Survival and Mortality:
• Survival rate (5-year, 10-year, overall) > Search first: SEER, cancer registries, disease-specific registries, PubMed
• Life expectancy (with and without treatment if applicable) > Search first: Orphanet, disease registries, actuarial databases, PubMed
• Mortality rate > Search first: CDC, WHO, GBD, national mortality databases
• Disease-specific mortality (deaths directly attributable to disease) > Search first: Disease registries, CDC Wonder, GBD, PubMed
• Morbidity and Function:
• Morbidity (disease-related disability and health impacts) > Search first: GBD, WHO, disability databases, PubMed
• Disability outcomes (long-term functional impairments) > Search first: ICF (International Classification of Functioning), disability registries
• Quality of life measures (EQ-5D, SF-36, PROMIS, disease-specific tools) > Search first: EQ-5D database, SF-36, PROMIS, PubMed
• Disease Course:
• Complications (secondary problems: infections, organ failure, etc.) > Search first: ICD codes, disease registries, clinical databases, PubMed
• Recovery potential (likelihood and extent of recovery, with vs without treatment) > Search first: Natural history studies, rehabilitation databases, PubMed
• Prediction:
• Prognostic factors (age, disease severity, biomarkers, treatment response) > Search first: Prognostic models databases, clinical calculators, PubMed
• Prognostic biomarkers (molecular markers predicting disease course) > Search first: FDA Biomarker database, PubMed, cancer prognostic databases

12. Treatment

• Pharmacotherapy:
• Pharmacological treatments (drug names, drug classes, mechanisms of action) > Search first: DrugBank, RxNorm, ATC classification, DailyMed, FDA databases
• Pharmacogenomics (how genetic variants affect drug metabolism, efficacy, toxicity) > Search first: PharmGKB, CPIC (Clinical Pharmacogenetics), FDA Table of PGx Biomarkers
• Advanced Therapeutics:
• Gene therapy (viral vectors, CRISPR, gene replacement, gene editing) > Search first: ClinicalTrials.gov, FDA gene therapy database, ASGCT resources
• Cell therapy (stem cell transplant, CAR-T, cellular therapeutics) > Search first: ClinicalTrials.gov, FDA cell therapy database, FACT standards
• RNA-based therapies (ASOs, siRNA, mRNA therapies) > Search first: ClinicalTrials.gov, FDA approvals, PubMed
• Targeted therapies (treatments directed at specific molecular targets) > Search first: My Cancer Genome, OncoKB, ClinicalTrials.gov, FDA approvals
• Immunotherapies (checkpoint inhibitors, monoclonal antibodies) > Search first: Cancer Immunotherapy Database, FDA approvals, ClinicalTrials.gov
• Surgical and Interventional:
• Surgical interventions (types of surgery, timing, outcomes) > Search first: CPT codes, surgical registries, clinical guidelines, PubMed
• Supportive and Rehabilitative:
• Supportive care (symptom management, pain control, nutrition) > Search first: Clinical guidelines, Cochrane Library, PubMed
• Rehabilitation (physical therapy, occupational therapy, speech therapy) > Search first: Rehabilitation medicine databases, clinical guidelines, PubMed
• Experimental:
• Experimental treatments in clinical trials (with NCT identifiers if available) > Search first: ClinicalTrials.gov, EU Clinical Trials Register, WHO ICTRP
• Treatment Outcomes:
• Treatment response rates > Search first: Clinical trial databases, FDA reviews, systematic reviews, PubMed
• Side effects and adverse events > Search first: FDA Adverse Event Reporting System (FAERS), MedWatch, PubMed
• Treatment Strategy:
• Treatment algorithms (clinical pathways, decision trees) > Search first: Clinical practice guidelines, NCCN Guidelines, UpToDate
• Combination therapies > Search first: ClinicalTrials.gov, treatment guidelines, PubMed
• Personalized medicine approaches (genotype-guided treatment) > Search first: My Cancer Genome, CIViC, PharmGKB, precision medicine databases

For each treatment, suggest MAXO (Medical Action Ontology) terms where applicable.

13. Prevention

• Prevention Levels:
• Primary prevention (preventing disease occurrence: vaccination, risk factor modification) > Search first: CDC, WHO, USPSTF recommendations, Cochrane Library
• Secondary prevention (early detection and treatment: screening programs, early intervention) > Search first: USPSTF, CDC screening guidelines, WHO
• Tertiary prevention (preventing complications in those with disease) > Search first: Clinical guidelines, disease management protocols, PubMed
• Immunization: Vaccine strategies (if applicable)

  Search first: CDC vaccine schedules, WHO immunization, FDA vaccine database

• Screening and Early Detection:
• Screening programs (population-based: newborn screening, cancer screening) > Search first: CDC screening programs, USPSTF, cancer screening databases
• Genetic screening (carrier screening, preimplantation genetic diagnosis, prenatal testing) > Search first: ACMG recommendations, ACOG guidelines, GTR
• Risk stratification (identifying high-risk individuals for targeted prevention) > Search first: Risk prediction models, clinical calculators, PubMed
• Behavioral Interventions: Lifestyle modifications to reduce risk

  Search first: CDC, WHO, behavioral intervention databases, Cochrane Library

• Counseling: Genetic counseling (risk assessment, family planning guidance)

  Search first: NSGC resources, ACMG guidelines, GeneReviews

• Public Health:
• Public health interventions (sanitation, vector control, health education) > Search first: CDC, WHO, public health databases, PubMed
• Environmental interventions (reducing environmental risk factors) > Search first: EPA databases, WHO environmental health, PubMed
• Prophylaxis: Preventive medications or procedures

  Search first: Clinical guidelines, FDA approvals, PubMed

14. Other Species / Natural Disease

• Taxonomy: Species affected (with NCBI Taxon identifiers)

  Search first: NCBI Taxonomy

• Breed: Specific breeds affected (with VBO identifiers if applicable)

  Search first: VBO (Vertebrate Breed Ontology)

• Gene: Orthologous genes in other species (with NCBI Gene IDs)

  Search first: NCBI Gene

• Natural Disease:
• Naturally occurring disease in other species (companion animals, wildlife) > Search first: OMIA (Online Mendelian Inheritance in Animals), VetCompass, PubMed
• Veterinary relevance and importance in animal health > Search first: OMIA, veterinary databases, PubMed
• Comparative Biology:
• Comparative pathology (similarities and differences across species) > Search first: OMIA, comparative pathology databases, PubMed
• Evolutionary conservation of disease mechanisms > Search first: HomoloGene, OrthoMCL, Alliance of Genome Resources
• Transmission (if applicable):
• Zoonotic potential > Search first: CDC zoonotic diseases, WHO zoonoses, GIDEON
• Cross-species susceptibility > Search first: NCBI Taxonomy, veterinary databases, PubMed

15. Model Organisms

• Model Types:
• Model organism type (mammalian, invertebrate, cellular, in vitro) > Search first: Alliance of Genome Resources, model organism databases
• Specific model systems (mouse, rat, zebrafish, Drosophila, C. elegans, yeast, cell lines, organoids, iPSCs) > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, SGD, ATCC, Cellosaurus
• Induced models (drug treatment, surgical intervention, environmental manipulation) > Search first: MGI, model organism databases, PubMed
• Genetic Models:
• Types available (knockout, knock-in, transgenic, conditional, humanized) > Search first: MGI, IMPC, KOMP, EuMMCR, IMSR
• Model Characteristics:
• Phenotype recapitulation (how well model reproduces human disease features) > Search first: Model organism databases, comparative studies, PubMed
• Model limitations (aspects of human disease not captured) > Search first: Model organism databases, PubMed, review articles
• Applications:
• Research applications (what aspects of disease can be studied) > Search first: Model organism databases, PubMed
• Resources:
• Model databases > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, IMSR, EMMA, MMRRC

Citation Requirements

• Cite primary literature (PMID preferred) for all mechanistic and clinical claims
• Prioritize recent reviews and landmark papers
• Include direct quotes from abstracts where possible to support key statements
• Distinguish evidence source types: human clinical, model organism, in vitro, computational

Output Format

Structure your response as a comprehensive narrative organized by the sections above. For each section, provide: - Factual content with specific details (numbers, percentages, gene names, variant nomenclature) - Ontology term suggestions (HPO, GO, CL, UBERON, CHEBI, MAXO, MONDO) where applicable - Evidence citations with PMIDs - Direct quotes from abstracts to support key claims - Clear indication when information is not available or not applicable for this disease

This report will be used to populate a disease knowledge base entry with: - Pathophysiology descriptions with causal chains - Gene/protein annotations (HGNC, GO terms) - Phenotype associations (HP terms) with frequencies - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Treatment annotations (MAXO terms) - Evidence items with PMIDs and exact abstract quotes - Epidemiology, prognosis, diagnostic, and prevention information - Animal model descriptions with phenotype recapitulation details

Postinfectious Vasculitis — Comprehensive Disease Characteristics Report (2023–2024 prioritized)

Target disease

Disease name: Postinfectious vasculitis (a.k.a. infection-triggered/secondary vasculitis)

High-level framing: “Postinfectious vasculitis” is not a single clinicopathologic disease entity in most modern classifications; rather, it is a secondary vasculitis syndrome in which vascular inflammation is temporally and mechanistically linked to a preceding or ongoing infection (and sometimes to an infection-induced immune response after pathogen clearance). The best-supported, common contemporary examples include IgA vasculitis (Henoch–Schönlein purpura) after upper respiratory infection, cutaneous small-vessel (leukocytoclastic) vasculitis after infections, and infectious/secondary CNS vasculitis/vasculopathy after neurotropic viruses or bacterial meningitis. (nikolaishvili2023viralinfectionsmay pages 1-2, hoshina2024vasculitisinthe pages 1-2, benadji2023cerebrovascularcomplicationsin pages 1-2)

MONDO ID: Not identified in the retrieved sources for a standalone “postinfectious vasculitis” entity; in practice it is commonly represented via subtype entities (e.g., IgA vasculitis) and/or “secondary vasculitis” groupings. (No MONDO-specific evidence retrieved)

1. Disease information

1.1 Concise overview

Postinfectious vasculitis refers to vascular inflammation occurring as a complication of infection, mediated either by: 1) immune-complex deposition (type III hypersensitivity mechanisms), 2) postinfectious autoimmunity (e.g., ANCA or other autoantibodies), and/or 3) direct pathogen–endothelium interactions (endothelial invasion and endotheliitis in some infections). These processes can affect small, medium, or large vessels and can be organ-limited (skin-only) or systemic (skin + kidneys, GI tract, joints; or CNS arteriopathy with stroke). (frasier2023secondaryvasculitisattributable pages 1-2, hu2024immunoglobulinavasculitis pages 4-4, benadji2023cerebrovascularcomplicationsin pages 1-2, hoshina2024vasculitisinthe pages 2-3)

1.2 Key synonyms / alternative names

Because this is a syndrome descriptor, synonym usage is phenotype-dependent: - Secondary vasculitis in the context of infection (post-COVID secondary vasculitis; infectious CNS vasculitis). (frasier2023secondaryvasculitisattributable pages 1-2, hoshina2024vasculitisinthe pages 1-2) - Infection-associated vasculitis / infectious vasculopathy (especially in CNS contexts). (hoshina2024vasculitisinthe pages 2-3, benadji2023cerebrovascularcomplicationsin pages 1-2) - Specific postinfectious vasculitides: IgA vasculitis/Henoch–Schönlein purpura, cutaneous small-vessel vasculitis/leukocytoclastic vasculitis, post-varicella arteriopathy (not fully extracted here), etc. (nikolaishvili2023viralinfectionsmay pages 1-2, frasier2023secondaryvasculitisattributable pages 1-2, hoshina2024vasculitisinthe pages 2-3)

1.3 Key identifiers (ICD/MeSH/OMIM/Orphanet/MONDO)

• No single ICD/MeSH/OMIM identifier for the umbrella term “postinfectious vasculitis” was established from the retrieved evidence.
• A practical KB approach is to represent secondary vasculitis and link it to infection triggers, and/or map to subtype diagnoses (e.g., IgA vasculitis; infectious CNS vasculitis/vasculopathy) as separate entries. (hoshina2024vasculitisinthe pages 1-2, hu2024immunoglobulinavasculitis pages 1-2)

1.4 Evidence provenance

The evidence base in the retrieved corpus is largely: - Aggregated: reviews (IgA vasculitis pathophysiology; viral triggers; post-COVID secondary vasculitis) and cohorts (COMBAT meningitis cohort; CNS vasculitis cohort). (hu2024immunoglobulinavasculitis pages 1-2, nikolaishvili2023viralinfectionsmay pages 1-2, frasier2023secondaryvasculitisattributable pages 1-2, benadji2023cerebrovascularcomplicationsin pages 1-2, hoshina2024vasculitisinthe pages 1-2) - Case-based: COVID-associated vasculitis reports summarized in review form; infection-triggered CNS vasculitis cases within cohorts. (frasier2023secondaryvasculitisattributable pages 1-2, hoshina2024vasculitisinthe pages 1-2)

2. Etiology

2.1 Primary causes and causal factors

Postinfectious vasculitis is acquired, driven by infections that trigger immune dysregulation and vascular injury.

Major etiologic mechanisms (current understanding)

• Immune complex disease / type III hypersensitivity: In COVID-19-associated vasculitis, a proposed “escalation from type 2 T-helper immune response (humoral immunity) to type 3 hypersensitivity (immune complex disease)” is described, with immune complex deposition in vessel walls driving inflammation. (frasier2023secondaryvasculitisattributable pages 1-2)
• IgA vasculitis (immune complex small-vessel vasculitis): IgA vasculitis is described as “a small-vessel leukocytoclastic vasculitis caused by immune complex deposition.” (nikolaishvili2023viralinfectionsmay pages 1-2)
• Localized cerebral vasculitis after bacterial meningitis: For cerebrovascular complications (CVC) in bacterial meningitis, the “predominant pathophysiological mechanism… is localized cerebral vasculitis,” promoting thrombosis/infarction/hemorrhage via coagulation activation and inhibited fibrinolysis. (benadji2023cerebrovascularcomplicationsin pages 1-2)

2.2 Infectious triggers (pathogens)

2.2.1 IgA vasculitis triggers (2024 synthesis)

A 2024 IgA vasculitis review lists broad infection triggers including (non-exhaustive): - Bacteria: Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, Haemophilus parainfluenzae, Mycoplasma pneumoniae. (hu2024immunoglobulinavasculitis pages 4-4) - Viruses: parainfluenza, influenza, rhinovirus, rotavirus, EBV, hepatitis A/B/C, SARS-CoV-2, CMV. (hu2024immunoglobulinavasculitis pages 4-4)

2.2.2 Viral triggers and vaccines in IgA vasculitis (2023)

A 2023 review emphasizes that “the majority of cases are preceded by upper respiratory tract infections,” historically linked to “group A β-hemolytic streptococcus and common respiratory tract viruses,” and that “during the current coronavirus pandemic, SARS-CoV-2 infection was identified as a main trigger factor,” with additional reports following COVID-19 immunization. (nikolaishvili2023viralinfectionsmay pages 1-2)

2.2.3 CNS infectious vasculitis triggers (2024 cohort)

In a 44-patient CNS vasculitis cohort, infection-related etiologies included varicella zoster virus, HSV-1, and bacterial meningitis. (hoshina2024vasculitisinthe pages 2-3)

2.2.4 Post-COVID secondary vasculitis

A 2023 review reports growing recognition of vasculitis after COVID-19 and notes that vasculitis “may develop less than two weeks after COVID-19 or during a later onset of the disease.” (frasier2023secondaryvasculitisattributable pages 1-2)

2.3 Risk factors

2.3.1 Host susceptibility (genetic predisposition)

• The IgA vasculitis review states that HSP/IgA vasculitis may be induced by immune reactions “in genetically predisposed subjects,” and reports “a strong association with HLA class II alleles, specifically HLA-DRB1 alleles.” (nikolaishvili2023viralinfectionsmay pages 1-2)

2.3.2 Clinical predictors in infection-related CNS vascular complications

• In bacterial meningitis, CVC risk was independently associated with advanced age, altered mental status, and seizures within 48 hours (multivariable ORs below). (benadji2023cerebrovascularcomplicationsin pages 1-2)

2.4 Protective factors

Direct protective factors for “postinfectious vasculitis” as a unified entity were not established from the retrieved evidence. However, for infection-associated stroke/vasculopathy, vaccination is discussed as associated with lower stroke rates (see Prevention). (clarke2024viralinfectionand pages 1-2)

2.5 Gene–environment interactions

Evidence is indirect in the retrieved corpus: genetic susceptibility (HLA-DRB1) is posited to interact with infection-triggered immune activation to produce immune complexes and vessel injury in IgA vasculitis. (nikolaishvili2023viralinfectionsmay pages 1-2)

3. Phenotypes (clinical spectrum)

3.1 Common phenotypes and suggested HPO terms

Below are core postinfectious vasculitis phenotypes represented in the retrieved evidence.

A) IgA vasculitis (Henoch–Schönlein purpura)

• Key clinical features: “Palpable purpura, gastrointestinal symptoms, joint involvement, and renal disease characterize immunoglobulin A vasculitis (IgAV).” (hu2024immunoglobulinavasculitis pages 1-2)
• Suggested HPO:
  • Palpable purpura / purpura: HP:0000979 (Purpura)
  • Abdominal pain: HP:0002027
  • Arthralgia: HP:0002829
  • Hematuria: HP:0000790
  • Proteinuria: HP:0000093
  • Nephritis: HP:0000123
• Onset: Predominantly pediatric; most cases age 2–8 years, but can occur in adults. (nikolaishvili2023viralinfectionsmay pages 1-2)
• Disease course: Often self-limited; “a small proportion… develop chronic kidney failure or end-stage renal disease.” (hu2024immunoglobulinavasculitis pages 1-2)

B) Cutaneous small-vessel vasculitis / leukocytoclastic vasculitis (LCV)

• In post-COVID vasculitis review context, “the most common vasculitis associated with COVID-19 patients is leucocytoclastic (LCV), immunoglobulin A (IgA), and Kawasaki disease.” (frasier2023secondaryvasculitisattributable pages 1-2)
• Suggested HPO:
  • Skin rash: HP:0000988
  • Purpura: HP:0000979
  • Skin ulcer (if present): HP:0001059

C) CNS postinfectious/secondary vasculitis or vasculopathy

• Presentation: The CNS vasculitis cohort highlights stroke-predominant presentations; infectious cases had acute/subacute stroke and frequent large–middle vessel involvement. (hoshina2024vasculitisinthe pages 2-3)
• Suggested HPO:
  • Ischemic stroke: HP:0002140
  • Seizures: HP:0001250
  • Headache: HP:0002315
  • Altered mental status: HP:0000716 (or HP:0004372 Confusion)

3.2 Frequency / proportions (recent numeric data)

• COVID-related vasculitis cohort summarized in a 2024 IgA vasculitis review: among 41 patients with COVID-related vasculitis, 30 had IgA vasculitis; among those IgA vasculitis cases, 30% had fever and 43.3% had renal involvement. (hu2024immunoglobulinavasculitis pages 5-5)

4. Genetic / molecular information

4.1 Causal genes

No monogenic “causal gene” for the umbrella concept of postinfectious vasculitis is supported in the retrieved evidence.

4.2 Susceptibility loci / immunogenetics

• HLA class II (HLA-DRB1) association is cited for IgA vasculitis susceptibility. (nikolaishvili2023viralinfectionsmay pages 1-2)

4.3 Molecular effectors implicated (mechanistic candidates)

• Immune complexes: IgA-containing immune complexes are a defining pathogenic feature for IgA vasculitis. (nikolaishvili2023viralinfectionsmay pages 1-2)
• Aberrant IgA glycosylation: IgAV mechanisms include “aberrantly glycosylated IgA.” (hu2024immunoglobulinavasculitis pages 1-2)
• Anti-endothelial cell antibodies (AECA): Included among “main pathogenic mechanisms” and described as drivers of endothelial injury (via ADCC/CDC) and neutrophil recruitment. (hu2024immunoglobulinavasculitis pages 1-2, hu2024immunoglobulinavasculitis pages 4-4)
• Neutrophils and NETs: A 2023 Immunological Reviews article highlights immune-complex–driven NET formation via Fcγ receptors and Mac-1, linking immune complexes to neutrophil-mediated vascular injury. (aymonnier2023theneutrophila pages 22-22)

Suggested GO/CL annotations (mechanism-linked)

• GO biological processes (suggested):
• GO:0006954 inflammatory response
• GO:0006956 complement activation
• GO:0030449 regulation of complement activation
• GO:0034097 response to cytokine
• GO:0030198 extracellular matrix organization (downstream vessel wall remodeling; conceptual)
• GO:0042119 neutrophil activation
• GO:0038063 neutrophil extracellular trap formation (NETosis; term may vary by ontology version)
• CL cell types (suggested):
• CL:0000775 neutrophil
• CL:0000540 macrophage
• CL:0000548 endothelial cell

5. Environmental information

5.1 Infectious environmental exposures

Infections are the central environmental exposure class for this syndrome, with prominent triggers including URT infections, streptococcal infections, SARS-CoV-2 infection, and neurotropic viral infections (VZV/HSV) in CNS vasculitis contexts. (nikolaishvili2023viralinfectionsmay pages 1-2, frasier2023secondaryvasculitisattributable pages 1-2, hoshina2024vasculitisinthe pages 2-3)

5.2 Lifestyle factors

Not established in the retrieved evidence for postinfectious vasculitis specifically.

6. Mechanism / pathophysiology

6.1 Mechanistic causal chains (upstream → downstream)

A) Immune-complex small-vessel vasculitis (IgA vasculitis paradigm)

1) Infection trigger (often URT infection; multiple viruses/bacteria reported) (nikolaishvili2023viralinfectionsmay pages 1-2, hu2024immunoglobulinavasculitis pages 4-4) 2) Aberrant IgA biology: abnormally/aberrantly glycosylated IgA1; immune response generates antigen–antibody complexes (nikolaishvili2023viralinfectionsmay pages 1-2, hu2024immunoglobulinavasculitis pages 1-2) 3) Large immune complexes deposit in small vessels of skin/kidney/gut/joints (defining feature) (nikolaishvili2023viralinfectionsmay pages 1-2) 4) Complement activation and leukocyte recruitment → endothelial injury, leukocytoclastic vasculitis, organ manifestations (concept supported by immune-complex deposition and complement pathway activation language) (nikolaishvili2023viralinfectionsmay pages 1-2)

B) Immune-complex/Th2-to-type III escalation model (COVID-associated vasculitis)

A 2023 review proposes that COVID-19 vasculitis can involve an “escalation from type 2 T-helper immune response… to type 3 hypersensitivity (immune complex disease)” with immune complex deposition in vessel walls and cytokine release (including IL-6). (frasier2023secondaryvasculitisattributable pages 1-2)

C) Infection-related CNS vasculitis/vasculopathy leading to stroke

• In a CNS vasculitis cohort, infection-related cases (VZV/HSV/bacterial meningitis) commonly presented with acute/subacute stroke and large–middle vessel involvement on imaging. (hoshina2024vasculitisinthe pages 2-3)

D) Bacterial meningitis → localized cerebral vasculitis → cerebrovascular complications

• Mechanism explicitly described: localized cerebral vasculitis activates coagulation and inhibits fibrinolysis, causing thrombosis, infarction, and/or hemorrhage. (benadji2023cerebrovascularcomplicationsin pages 1-2)

6.2 Key pathways (high-level)

• Complement pathway (alternative complement activation noted in IgA vasculitis pathogenesis discussion). (nikolaishvili2023viralinfectionsmay pages 1-2)
• Fc receptor signaling / immune complex–neutrophil axis (FcγRIIA/FcγRIIIB, Mac-1) promoting NETs. (aymonnier2023theneutrophila pages 22-22)

7. Anatomical structures affected

7.1 Organ-level involvement (common)

• Skin (cutaneous vasculitis; palpable purpura). (hu2024immunoglobulinavasculitis pages 1-2, frasier2023secondaryvasculitisattributable pages 1-2)
• Kidney (IgA vasculitis nephritis; proteinuria/nephritic syndrome). (hu2024immunoglobulinavasculitis pages 1-2)
• GI tract and joints (IgA vasculitis). (hu2024immunoglobulinavasculitis pages 1-2)
• Central nervous system (secondary/infectious CNS vasculitis causing stroke). (hoshina2024vasculitisinthe pages 2-3)
• Large vessels (aorta) in post-COVID aortitis cases. (frasier2023secondaryvasculitisattributable pages 3-4)

Suggested UBERON terms (examples)

• Skin: UBERON:0002097
• Kidney: UBERON:0002113
• Small blood vessel: UBERON:0001638
• Aorta: UBERON:0000947
• Brain: UBERON:0000955

8. Temporal development (onset, progression)

• IgA vasculitis: Most common in children (2–8 years), often after URT infection, frequently self-limited, but renal involvement can be refractory and progress to CKD/ESRD in a minority. (nikolaishvili2023viralinfectionsmay pages 1-2, hu2024immunoglobulinavasculitis pages 1-2)
• Post-COVID vasculitis: Can occur “less than two weeks after COVID-19 or during a later onset of the disease.” (frasier2023secondaryvasculitisattributable pages 1-2)
• Secondary CNS vasculitis: In a cohort, secondary CNS vasculitis had shorter median time to diagnosis (15 days) vs primary (30 days). (hoshina2024vasculitisinthe pages 2-3)

9. Inheritance and population

9.1 Epidemiology (available recent statistics)

Because “postinfectious vasculitis” is a syndrome label, epidemiology is best represented by its major phenotypes.

IgA vasculitis incidence

• The 2024 IgA vasculitis review reports global pediatric predominance and provides annual incidence ranges: 6.79–55.9 per 100,000 children/adolescents (<17 years) across countries; adult incidence 0.1–0.8 per 100,000 in some population studies. (hu2024immunoglobulinavasculitis pages 1-2)
• A 2023 review cites an incidence of 20.4 per 100,000 population (in children, in the cited reference context) and that males are affected “twice as frequently as females.” (nikolaishvili2023viralinfectionsmay pages 1-2)

Community-acquired bacterial meningitis (as a postinfectious vasculitis context for CVC)

• Annual incidence: “around 2/100,000 inhabitants.” (benadji2023cerebrovascularcomplicationsin pages 1-2)

Primary CNS vasculitis (useful differential benchmark)

• Estimated incidence: 2.4 per 1 million person-years; mortality 8–23%; ~40% unfavorable outcomes (not postinfectious but central for differential). (salvarani2024primarycentralnervous pages 1-2)

9.2 Population demographics

• CNS vasculitis cohort: median age 54 years; 25% men. (hoshina2024vasculitisinthe pages 1-2)

10. Diagnostics

10.1 Core diagnostic principles (real-world implementation)

Postinfectious vasculitis diagnosis generally requires: 1) Demonstration of vasculitis/vasculopathy in an organ system, 2) Exclusion of primary vasculitis mimics, 3) Evidence of temporal/causal linkage to infection (microbiology, serology, clinical syndrome), and 4) In some phenotypes, biopsy confirmation (e.g., CNS; skin; kidney).

A) IgA vasculitis

• Recognize classic clinical tetrad and monitor renal disease to prevent long-term complications. (hu2024immunoglobulinavasculitis pages 1-2)

B) CNS vasculitis: differentiating primary vs infectious/secondary

A 2024 cohort provides practical discriminators: - Secondary CNS vasculitis had higher fever incidence, more frequent low CSF glucose, and unique CSF oligoclonal bands (especially in infectious and CTD-associated vasculitis). (hoshina2024vasculitisinthe pages 1-2) - Vessel-wall MRI enhancement was frequent, particularly in secondary cases (data summarized in extracted evidence). (hoshina2024vasculitisinthe pages 3-5)

C) Bacterial meningitis with cerebrovascular complications (CVC)

• CVC defined by focal clinical deficits and/or CT/MRI evidence of ischemic/hemorrhagic lesions, sometimes “associated… with vasculitis and/or thrombophlebitis.” (benadji2023cerebrovascularcomplicationsin pages 1-2)

10.2 Differential diagnosis

• For suspected CNS vasculitis, a NEJM review emphasizes that differential includes secondary cerebral vasculitis and infections, and that angiography specificity is low; biopsy can be definitive. (salvarani2024primarycentralnervous pages 1-2)

11. Outcomes / prognosis

11.1 CNS infectious/secondary vasculitis outcomes

• In the CNS vasculitis cohort (mixed etiologies), mortality was 20.5% overall, higher in secondary (26.3%) than primary (16.0%). (hoshina2024vasculitisinthe pages 1-2)

11.2 Bacterial meningitis CVC burden

• CVC occurred in 25.3% (128/506) of bacterial meningitis cases in the COMBAT cohort and are described as influencing morbidity/mortality in the broader literature background. (benadji2023cerebrovascularcomplicationsin pages 1-2)

11.3 IgA vasculitis renal prognosis

• Renal involvement ranges “from mild proteinuria to severe nephritic or nephrotic syndrome,” motivating monitoring to prevent long-term complications. (hu2024immunoglobulinavasculitis pages 1-2)

12. Treatment

12.1 Treatment principles

Treat postinfectious vasculitis by jointly addressing: - The trigger infection (antimicrobials/antivirals when active or suspected), and - The immune-mediated vascular injury (corticosteroids, IVIG, and immunosuppressants in selected contexts).

12.2 Phenotype-specific evidence (2023–2024)

A) Post-COVID secondary vasculitis (aortitis; Kawasaki-like)

A 2023 review summarizes reported regimens and outcomes: - Aortitis: corticosteroids such as prednisolone 40 mg (symptoms alleviated within ~2 weeks) and prednisone 60 mg (symptom resolution) are reported in case-based evidence. (frasier2023secondaryvasculitisattributable pages 3-4) - Kawasaki-like disease: IVIG plus aspirin (infant) and IVIG + corticosteroids (adult), with early treatment (<4 days) associated with reduced coronary aneurysm development and improved LV function (summary statement). (frasier2023secondaryvasculitisattributable pages 3-4)

B) Infectious/secondary CNS vasculitis (cohort evidence)

In a 2024 single-center cohort: - 80% of infectious vasculitis patients received antimicrobial therapy. - Some VZV vasculitis cases received IV methylprednisolone (IVMP). - Time to treatment was faster in secondary vs primary CNS vasculitis (median 1.0 vs 6.0 days). (hoshina2024vasculitisinthe pages 3-5)

C) Bacterial meningitis CVC

• Adjunctive dexamethasone was not statistically different between those with/without CVC in COMBAT (p=0.84), though background notes RCT/meta-analyses show benefit for pneumococcal meningitis outcomes. (benadji2023cerebrovascularcomplicationsin pages 1-2)

Suggested MAXO terms (examples)

• Systemic glucocorticoid therapy: MAXO:0000648 (glucocorticoid therapy; exact MAXO ID may vary)
• Intravenous immunoglobulin therapy: MAXO:0000743 (IVIG therapy; verify exact MAXO)
• Antimicrobial therapy: MAXO:0000747 (antibiotic therapy)
• Antiviral therapy: MAXO:0000748

(MAXO identifiers should be verified against the current MAXO release; included here as suggested mappings.)

13. Prevention

13.1 Infection prevention as vasculitis prevention

Because infection is upstream, prevention emphasizes infection prevention (e.g., vaccination) and rapid infection treatment.

13.2 Vaccination and reduced infection-associated stroke risk (proxy prevention for infectious vasculopathy)

A 2024 review on viral infection and stroke reports that a large Canadian analysis of >4 million residents found lower stroke rates associated with vaccination status, and a French study found an increasing reduction in stroke risk with more regular vaccination over 5 years; it also emphasizes herpetic infections (chickenpox/shingles) as causes of cerebral vasculopathies. (clarke2024viralinfectionand pages 1-2)

14. Other species / natural disease

No animal natural disease evidence for “postinfectious vasculitis” was retrieved in the provided corpus.

15. Model organisms

No dedicated model organism evidence for “postinfectious vasculitis” as a unified entity was retrieved in the provided corpus. Mechanistic inference in the retrieved evidence focuses on human immunopathology (immune complexes, complement, neutrophils/NETs). (aymonnier2023theneutrophila pages 22-22, nikolaishvili2023viralinfectionsmay pages 1-2)

Recent developments (2023–2024 highlights)

1) Post-COVID secondary vasculitis: Increasing recognition that vasculitis may appear early or later after SARS-CoV-2 infection, with mechanistic emphasis on immune-complex disease and endothelial involvement, and with case-based evidence for steroid/IVIG benefit in selected phenotypes (aortitis, Kawasaki-like disease). (frasier2023secondaryvasculitisattributable pages 1-2, frasier2023secondaryvasculitisattributable pages 3-4) 2) IgA vasculitis mechanistic refinement (2024): Integration of aberrant IgA glycosylation, anti-endothelial antibodies, complement-dependent injury, and neutrophil effector pathways in infection-triggered IgAV. (hu2024immunoglobulinavasculitis pages 1-2, hu2024immunoglobulinavasculitis pages 4-4) 3) CNS postinfectious vasculitis cohort-level characterization (2024): Distinguishing CSF features (low glucose, oligoclonal bands), fever, imaging patterns, and real-world immunosuppressive/antimicrobial treatment patterns in infectious CNS vasculitis. (hoshina2024vasculitisinthe pages 1-2, hoshina2024vasculitisinthe pages 3-5) 4) Bacterial meningitis vascular complications quantified (2023): Prospective cohort quantifies cerebrovascular complications at ~25%, consistent with vasculitis-mediated injury mechanisms. (benadji2023cerebrovascularcomplicationsin pages 1-2)

Evidence map artifact

The following table provides a compact mapping from triggers → mechanisms → diagnostics → treatments with recent numeric data.

Table: This table summarizes representative recent evidence for major postinfectious/secondary vasculitis phenotypes, mechanisms, diagnostics, treatments, and available quantitative findings. It is useful as a compact evidence map for disease-knowledge-base curation.

Key statistics (quick reference)

• IgA vasculitis pediatric incidence: 6.79–55.9 per 100,000/year (<17y); adult incidence 0.1–0.8 per 100,000/year in some studies. (hu2024immunoglobulinavasculitis pages 1-2)
• COMBAT bacterial meningitis cohort CVC prevalence: 25.3% (128/506); pneumococcal 29.4%, meningococcal 15.3%. (benadji2023cerebrovascularcomplicationsin pages 1-2)
• CNS vasculitis cohort: 43.2% secondary, 22.7% infectious; mortality 20.5% overall. (hoshina2024vasculitisinthe pages 1-2)

Limitations and gaps

• Ontology identifiers (MONDO/MeSH/ICD) for “postinfectious vasculitis” as a single entity were not available in the retrieved evidence; mapping should be performed via subtype diagnoses and/or “secondary vasculitis” parent classes.
• PMIDs were not present in the retrieved full-text snippets; the report therefore cites DOI URLs and journal metadata from the retrieved documents.
• Many postinfectious vasculitis claims remain case-report dominated (especially COVID-associated vasculitis), and population-level incidence for the umbrella syndrome is not established in the retrieved evidence.

References

1. (nikolaishvili2023viralinfectionsmay pages 1-2): Mariam Nikolaishvili, Ani Pazhava, and Vito Di Lernia. Viral infections may be associated with henoch–schönlein purpura. Journal of Clinical Medicine, 12:697, Jan 2023. URL: https://doi.org/10.3390/jcm12020697, doi:10.3390/jcm12020697. This article has 48 citations.

2. (hoshina2024vasculitisinthe pages 1-2): Yoji Hoshina, Alen Delic, Ka-Ho Wong, Stephanie Lyden, Robert Kadish, Tammy L. Smith, Melissa A. Wright, Daisuke Shimura, and Stacey L. Clardy. Vasculitis in the central nervous system: etiology, characteristics, and outcomes in a large single-center cohort. The Neurohospitalist, 14:129-139, Dec 2024. URL: https://doi.org/10.1177/19418744231223283, doi:10.1177/19418744231223283. This article has 6 citations.

3. (benadji2023cerebrovascularcomplicationsin pages 1-2): Amine Benadji, Thomas Debroucker, Guillaume Martin-Blondel, Laurent Argaud, Virginie Vitrat, Charlotte Biron, Michel Wolff, Bruno Hoen, Xavier Duval, and Sarah Tubiana. Cerebrovascular complications in patients with community-acquired bacterial meningitis: occurrence and associated factors in the combat multicenter prospective cohort. BMC Infectious Diseases, Jun 2023. URL: https://doi.org/10.1186/s12879-023-08320-x, doi:10.1186/s12879-023-08320-x. This article has 12 citations and is from a peer-reviewed journal.

4. (frasier2023secondaryvasculitisattributable pages 1-2): Kelly M Frasier, Caroline Gallagher-Poehls, Mikayla Cochrane, and Debosree Roy. Secondary vasculitis attributable to post-covid syndrome. Cureus, Aug 2023. URL: https://doi.org/10.7759/cureus.44119, doi:10.7759/cureus.44119. This article has 16 citations.

5. (hu2024immunoglobulinavasculitis pages 4-4): Ya‐Chiao Hu, Yao‐Hsu Yang, and Bor‐Luen Chiang. Immunoglobulin a vasculitis: the clinical features and pathophysiology. The Kaohsiung Journal of Medical Sciences, 40:612-620, Jun 2024. URL: https://doi.org/10.1002/kjm2.12852, doi:10.1002/kjm2.12852. This article has 12 citations.

6. (hoshina2024vasculitisinthe pages 2-3): Yoji Hoshina, Alen Delic, Ka-Ho Wong, Stephanie Lyden, Robert Kadish, Tammy L. Smith, Melissa A. Wright, Daisuke Shimura, and Stacey L. Clardy. Vasculitis in the central nervous system: etiology, characteristics, and outcomes in a large single-center cohort. The Neurohospitalist, 14:129-139, Dec 2024. URL: https://doi.org/10.1177/19418744231223283, doi:10.1177/19418744231223283. This article has 6 citations.

7. (hu2024immunoglobulinavasculitis pages 1-2): Ya‐Chiao Hu, Yao‐Hsu Yang, and Bor‐Luen Chiang. Immunoglobulin a vasculitis: the clinical features and pathophysiology. The Kaohsiung Journal of Medical Sciences, 40:612-620, Jun 2024. URL: https://doi.org/10.1002/kjm2.12852, doi:10.1002/kjm2.12852. This article has 12 citations.

8. (clarke2024viralinfectionand pages 1-2): Michael Clarke, Sarina Falcione, Roobina Boghozian, Raluca Todoran, Yiran Zhang, Maria Guadalupe C. Real, Alexis StPierre, Twinkle Joy, and Glen C. Jickling. Viral infection and ischemic stroke: emerging trends and mechanistic insights. Journal of the American Heart Association, Sep 2024. URL: https://doi.org/10.1161/jaha.124.035892, doi:10.1161/jaha.124.035892. This article has 23 citations.

9. (hu2024immunoglobulinavasculitis pages 5-5): Ya‐Chiao Hu, Yao‐Hsu Yang, and Bor‐Luen Chiang. Immunoglobulin a vasculitis: the clinical features and pathophysiology. The Kaohsiung Journal of Medical Sciences, 40:612-620, Jun 2024. URL: https://doi.org/10.1002/kjm2.12852, doi:10.1002/kjm2.12852. This article has 12 citations.

10. (aymonnier2023theneutrophila pages 22-22): Karen Aymonnier, Jennifer Amsler, Peter Lamprecht, Alan Salama, and Véronique Witko‐Sarsat. The neutrophil: a key resourceful agent in immune‐mediated vasculitis. Immunological Reviews, 314:326-356, Nov 2023. URL: https://doi.org/10.1111/imr.13170, doi:10.1111/imr.13170. This article has 41 citations and is from a domain leading peer-reviewed journal.

11. (frasier2023secondaryvasculitisattributable pages 3-4): Kelly M Frasier, Caroline Gallagher-Poehls, Mikayla Cochrane, and Debosree Roy. Secondary vasculitis attributable to post-covid syndrome. Cureus, Aug 2023. URL: https://doi.org/10.7759/cureus.44119, doi:10.7759/cureus.44119. This article has 16 citations.

12. (salvarani2024primarycentralnervous pages 1-2): Carlo Salvarani, Gene G. Hunder, and Robert D. Brown. Primary central nervous system vasculitis. The New England journal of medicine, 391 11:1028-1037, Sep 2024. URL: https://doi.org/10.1056/nejmra2314942, doi:10.1056/nejmra2314942. This article has 42 citations and is from a highest quality peer-reviewed journal.

13. (hoshina2024vasculitisinthe pages 3-5): Yoji Hoshina, Alen Delic, Ka-Ho Wong, Stephanie Lyden, Robert Kadish, Tammy L. Smith, Melissa A. Wright, Daisuke Shimura, and Stacey L. Clardy. Vasculitis in the central nervous system: etiology, characteristics, and outcomes in a large single-center cohort. The Neurohospitalist, 14:129-139, Dec 2024. URL: https://doi.org/10.1177/19418744231223283, doi:10.1177/19418744231223283. This article has 6 citations.

14. (nikolaishvili2023viralinfectionsmay pages 11-13): Mariam Nikolaishvili, Ani Pazhava, and Vito Di Lernia. Viral infections may be associated with henoch–schönlein purpura. Journal of Clinical Medicine, 12:697, Jan 2023. URL: https://doi.org/10.3390/jcm12020697, doi:10.3390/jcm12020697. This article has 48 citations.