◆

Subtypes

3

Infection-triggered IgA vasculitis

IgA vasculitis is a common postinfectious small-vessel vasculitis pattern, often following upper respiratory or viral infection triggers.

Infection-associated cutaneous small-vessel vasculitis

Cutaneous leukocytoclastic vasculitis can occur after infectious triggers and may be organ-limited.

Infectious or secondary CNS vasculitis

CNS vasculitis can occur secondary to infections, including viral and bacterial meningitic or encephalitic contexts.

⚙

Pathophysiology

7

Direct or contiguous vessel-wall infection

Some infection-associated vasculitides arise when pathogens directly or contiguously inflame the vascular wall.

endothelial cell link

inflammatory response link ↑ INCREASED

Downstream

Leukocyte-mediated vessel-wall injury Direct vascular infection or contiguous spread can initiate local vessel-wall inflammation.

Show evidence (1 reference)

PMID:26362741 SUPPORT Human Clinical

"Vasculitis due to infection may occur as a consequence of the inflammation of vessel walls due to direct or contiguous infection, type II or immune complex-mediated reaction, cell-mediated hypersensitivity, or inflammation due to immune dysregulation triggered by bacterial toxin and/or..."

This review explicitly identifies direct or contiguous infection as one mechanism of infection-related vasculitis.

Immune-complex vascular deposition after infection

Infectious antigens can promote type II or immune-complex mediated vascular reactions; in IgA vasculitis, aberrantly glycosylated IgA1-containing immune complexes deposit in small vessels of the skin, kidney, gut, and joints.

endothelial cell link

immune response link ⚠ ABNORMAL complement activation link ↑ INCREASED

Downstream

Leukocyte-mediated vessel-wall injury Immune-complex deposition promotes complement and leukocyte effector injury in affected small vessels.

Show evidence (2 references)

PMID:26362741 SUPPORT Human Clinical

"Vasculitis due to infection may occur as a consequence of the inflammation of vessel walls due to direct or contiguous infection, type II or immune complex-mediated reaction, cell-mediated hypersensitivity, or inflammation due to immune dysregulation triggered by bacterial toxin and/or..."

This review explicitly includes immune-complex mediated reactions among infection-related vasculitis mechanisms.

DOI:10.3390/jcm12020697 SUPPORT Human Clinical

"Serum aberrant IgA1 may form large antigen–antibody complexes which, due to a defective clearance, are able to deposit in the small vessels of the skin, kidney, gut, and joints."

This IgA vasculitis review supports infection-triggered immune-complex deposition in classic target tissues.

Infection-triggered IgA endothelial and neutrophil injury

IgA vasculitis mechanisms include aberrantly glycosylated IgA, anti-endothelial cell antibodies, and neutrophil effector activity after infection triggers.

endothelial cell link neutrophil link

leukocyte migration link ↑ INCREASED

Downstream

Leukocyte-mediated vessel-wall injury Neutrophil and endothelial antibody mechanisms contribute to small-vessel inflammation after infection triggers.

Show evidence (1 reference)

DOI:10.1002/kjm2.12852 SUPPORT Human Clinical

"Disease mechanisms involve various factors, including the interplay of aberrantly glycosylated IgA, anti-endothelial cell antibodies, and neutrophils following infection triggers, which are the main pathogenic mechanisms of IgAV."

This directly supports IgA, anti-endothelial antibody, and neutrophil mechanisms after infection triggers.

Microbial toxin or superantigen immune dysregulation

Bacterial toxins or superantigens can trigger immune dysregulation that promotes vascular inflammation after infection.

immune response link ⚠ ABNORMAL

Downstream

Leukocyte-mediated vessel-wall injury Dysregulated immune activation can feed into inflammatory vessel-wall damage.

Show evidence (1 reference)

PMID:26362741 SUPPORT Human Clinical

"Vasculitis due to infection may occur as a consequence of the inflammation of vessel walls due to direct or contiguous infection, type II or immune complex-mediated reaction, cell-mediated hypersensitivity, or inflammation due to immune dysregulation triggered by bacterial toxin and/or..."

This review explicitly supports toxin or superantigen-triggered immune dysregulation.

T- and B-cell activation after infection

T- and B-cell activation is a proposed mechanism in infection-associated vasculitis, including postinfectious settings in which the pathogen has triggered ongoing immune inflammation.

adaptive immune response link ⚠ ABNORMAL

Downstream

Leukocyte-mediated vessel-wall injury Adaptive immune activation can sustain vascular inflammation after infection.

Show evidence (1 reference)

PMID:40089428 SUPPORT Human Clinical

"The exact pathogenesis of infection associated vasculitis is not clear although direct spread, immune complex deposition and T/B cell activation are proposed."

This supports T/B cell activation as a proposed infection-associated vasculitis mechanism while preserving uncertainty.

Molecular mimicry and infection-induced autoantibodies

Some infections can generate autoantibodies such as ANCA through molecular mimicry, confounding distinction between primary systemic vasculitis and infection-associated vasculitis.

adaptive immune response link ⚠ ABNORMAL

Downstream

Leukocyte-mediated vessel-wall injury Infection-associated autoantibody production can amplify inflammatory vascular injury or mimic primary vasculitis.

Show evidence (1 reference)

PMID:40089428 SUPPORT Human Clinical

"Infections can produce autoantibodies such as Anti-neutrophil cytoplasmic antibody through molecular mimicry and could confound clinical judgement."

This supports molecular mimicry and autoantibody production as infection-associated vasculitis mechanisms.

Leukocyte-mediated vessel-wall injury

Immune activation after infection can damage the vascular wall and produce postinfectious vasculitic syndromes in skin, kidney, gut, joints, CNS, or other affected tissues.

neutrophil link

leukocyte migration link ↑ INCREASED

Show evidence (1 reference)

DOI:10.1002/kjm2.12852 SUPPORT Human Clinical

"Disease mechanisms involve various factors, including the interplay of aberrantly glycosylated IgA, anti-endothelial cell antibodies, and neutrophils following infection triggers, which are the main pathogenic mechanisms of IgAV."

This supports neutrophil participation in infection-triggered IgA vasculitis mechanisms.

⬡

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.

●

Phenotypes

11

Cardiovascular 3

Infection-associated vasculitis Vasculitis (HP:0002633)

Show evidence (1 reference)

PMID:26362741 SUPPORT Human Clinical

"As immunosuppressive therapy administered in the absence of antimicrobial therapy may increase morbidity and fail to effect the resolution of infection-associated vascular inflammation, it is important to consider infectious entities as potential inciting factors in vasculitis syndromes."

This supports infection-associated vascular inflammation as the diagnostic context.

Vessel-size variable vasculitis mimicry Vasculitis (HP:0002633)

Show evidence (1 reference)

PMID:40089428 SUPPORT Human Clinical

"Infections can mimic small, medium or large vessel vasculitis."

This supports variable vessel-size mimicry in infection-associated clinical presentations.

Ischemic stroke Ischemic stroke (HP:0002140)

The Falcon report summarizes Hoshina et al. 2024 full-text results as acute/subacute stroke in infectious CNS vasculitis patients; the local DOI/PMID caches expose only the abstract, so no direct evidence snippet is attached here.

Digestive 1

Gastrointestinal symptoms Abnormality of the digestive system (HP:0025031)

Show evidence (1 reference)

DOI:10.1002/kjm2.12852 SUPPORT Human Clinical

"Palpable purpura, gastrointestinal symptoms, joint involvement, and renal disease characterize immunoglobulin A vasculitis (IgAV)."

This supports gastrointestinal symptoms in IgA vasculitis.

Genitourinary 2

Proteinuria Proteinuria (HP:0000093)

Show evidence (1 reference)

DOI:10.1002/kjm2.12852 SUPPORT Human Clinical

"Renal involvement ranging from mild proteinuria to severe nephritic or nephrotic syndrome highlights the importance of monitoring kidney function in patients with IgAV."

This supports proteinuria as part of IgA vasculitis renal involvement.

Hematuria Hematuria (HP:0000790)

Show evidence (1 reference)

DOI:10.1002/kjm2.12852 PARTIAL Human Clinical

"Renal involvement ranging from mild proteinuria to severe nephritic or nephrotic syndrome highlights the importance of monitoring kidney function in patients with IgAV."

This supports nephritic renal involvement in IgA vasculitis; hematuria is represented as the HPO-bound nephritic urinary manifestation.

Metabolism 1

Fever Fever (HP:0001945)

Show evidence (1 reference)

DOI:10.1177/19418744231223283 SUPPORT Human Clinical

"Compared to primary CNS vasculitis, secondary CNS vasculitis exhibits higher fever incidence (observed in infectious and connective tissue disorder [CTD]-associated vasculitis), low glucose levels (mostly in infectious vasculitis) and unique cerebrospinal fluid oligoclonal bands (observed in..."

This supports fever in infectious/secondary CNS vasculitis.

Constitutional 2

Abdominal pain Abdominal pain (HP:0002027)

Show evidence (1 reference)

PMID:32631771 SUPPORT Human Clinical

"Here, we report the case of a 36-year-old woman who presented to the emergency department hypotensive and tachycardic after 1 week of fevers, abdominal pain, vomiting and diarrhea, and was found to have the classic phenotype of complete Kawasaki's Disease including nonexudative conjunctivitis,..."

This supports abdominal pain in a postinfectious Kawasaki-like vasculitis presentation.

Joint involvement Arthralgia (HP:0002829)

Show evidence (1 reference)

DOI:10.1002/kjm2.12852 SUPPORT Human Clinical

"Palpable purpura, gastrointestinal symptoms, joint involvement, and renal disease characterize immunoglobulin A vasculitis (IgAV)."

This supports joint involvement in IgA vasculitis.

Other 2

Anti-neutrophil cytoplasmic antibody positivity

Show evidence (1 reference)

PMID:40089428 SUPPORT Human Clinical

"Infections can produce autoantibodies such as Anti-neutrophil cytoplasmic antibody through molecular mimicry and could confound clinical judgement."

This supports ANCA positivity or related autoantibody findings in infection-associated contexts.

Palpable purpura Palpable purpura (HP:0031363)

Show evidence (1 reference)

DOI:10.1002/kjm2.12852 SUPPORT Human Clinical

"Palpable purpura, gastrointestinal symptoms, joint involvement, and renal disease characterize immunoglobulin A vasculitis (IgAV)."

This supports palpable purpura as a key IgA vasculitis phenotype in postinfectious contexts.

💊

Treatments

4

Antimicrobial therapy for active infection-associated vasculitis

Action: Pharmacotherapy NCIT:C15986

Management should identify and treat the infectious inciting factor when active, because immunosuppression without antimicrobial therapy can worsen outcomes or fail to resolve vascular inflammation.

Show evidence (1 reference)

PMID:26362741 SUPPORT Human Clinical

"As immunosuppressive therapy administered in the absence of antimicrobial therapy may increase morbidity and fail to effect the resolution of infection-associated vascular inflammation, it is important to consider infectious entities as potential inciting factors in vasculitis syndromes."

This supports treating or excluding active infection before immunosuppression.

Carefully selected anti-inflammatory or immunosuppressive therapy

Action: Pharmacotherapy NCIT:C15986

Anti-inflammatory or immunosuppressive therapy may be considered only after accounting for the infectious trigger, disease mechanism, and risk of worsening uncontrolled infection.

Show evidence (1 reference)

PMID:40089428 PARTIAL Human Clinical

"It is very important for the clinician to be aware of the various infections which mimic vasculitis, since inadvertent immunosuppression in these patients can be fatal."

This supports caution with immunosuppression in infection-associated vasculitis or mimics.

Intravenous methylprednisolone-based induction for CNS vasculitis

Action: Pharmacotherapy NCIT:C15986

Agent: corticosteroid ↗

Secondary or infectious CNS vasculitis may require corticosteroid induction, often with adjunctive immunosuppressive therapy after infectious causes are treated or accounted for.

Show evidence (1 reference)

DOI:10.1177/19418744231223283 SUPPORT Human Clinical

"Intravenous methylprednisolone was the predominant induction therapy (63.6%), and cyclophosphamide was the most used adjunctive therapy."

This cohort supports corticosteroid induction and cyclophosphamide adjunctive therapy in CNS vasculitis management.

IVIG, aspirin, and corticosteroids for Kawasaki-like postinfectious inflammation

Action: Pharmacotherapy NCIT:C15986

Agent: corticosteroid ↗ acetylsalicylic acid ↗ human immunoglobulin G ↗

Kawasaki-like inflammatory disease after COVID-19 can respond rapidly to IVIG, aspirin, and corticosteroid therapy in reported cases.

Show evidence (1 reference)

PMID:32631771 SUPPORT Human Clinical

"She was treated for Kawasaki Disease Shock Syndrome (KDSS) with pulse dose solumedrol, IVIG, and aspirin with near resolution of symptoms and normalization of vital signs within 1 day and subsequent improvement in her laboratory abnormalities."

This case report supports IVIG, aspirin, and corticosteroids in a postinfectious Kawasaki-like vasculitis presentation.

{ }

Source YAML

click to show

name: Postinfectious Vasculitis
creation_date: "2026-05-05T11:41:54Z"
updated_date: "2026-05-05T12:37:52Z"
description: >-
  Postinfectious vasculitis is secondary vasculitis that follows or accompanies
  an infectious trigger. Infection-associated vascular inflammation can affect
  small, medium, or large vessels and may arise through direct or contiguous
  infection of vessel walls, immune-complex reactions, cell-mediated
  hypersensitivity, molecular mimicry, autoantibody production, or immune
  dysregulation triggered by microbial products.
category: Complex
disease_term:
  preferred_term: postinfectious vasculitis
  term:
    id: MONDO:0018837
    label: postinfectious vasculitis
parents:
- Vascular disorder
synonyms:
- Post-infectious vasculitis
- Infection-associated vasculitis
has_subtypes:
- name: Infection-triggered IgA vasculitis
  display_name: Infection-triggered IgA vasculitis
  description: >-
    IgA vasculitis is a common postinfectious small-vessel vasculitis pattern,
    often following upper respiratory or viral infection triggers.
- name: Infection-associated cutaneous small-vessel vasculitis
  display_name: Infection-associated cutaneous small-vessel vasculitis
  description: >-
    Cutaneous leukocytoclastic vasculitis can occur after infectious triggers
    and may be organ-limited.
- name: Infectious or secondary CNS vasculitis
  display_name: Infectious or secondary CNS vasculitis
  description: >-
    CNS vasculitis can occur secondary to infections, including viral and
    bacterial meningitic or encephalitic contexts.
pathophysiology:
- name: Direct or contiguous vessel-wall infection
  description: >-
    Some infection-associated vasculitides arise when pathogens directly or
    contiguously inflame the vascular wall.
  cell_types:
  - preferred_term: endothelial cell
    term:
      id: CL:0000115
      label: endothelial cell
  biological_processes:
  - preferred_term: inflammatory response
    modifier: INCREASED
    term:
      id: GO:0006954
      label: inflammatory response
  downstream:
  - target: Leukocyte-mediated vessel-wall injury
    description: Direct vascular infection or contiguous spread can initiate local vessel-wall inflammation.
  evidence:
  - reference: PMID:26362741
    reference_title: Vasculitis related to viral and other microbial agents.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Vasculitis due to infection may occur as a consequence of the inflammation of vessel walls due to direct or contiguous infection, type II or immune complex-mediated reaction, cell-mediated hypersensitivity, or inflammation due to immune dysregulation triggered by bacterial toxin and/or superantigen production.
    explanation: This review explicitly identifies direct or contiguous infection as one mechanism of infection-related vasculitis.
- name: Immune-complex vascular deposition after infection
  description: >-
    Infectious antigens can promote type II or immune-complex mediated vascular
    reactions; in IgA vasculitis, aberrantly glycosylated IgA1-containing
    immune complexes deposit in small vessels of the skin, kidney, gut, and
    joints.
  cell_types:
  - preferred_term: endothelial cell
    term:
      id: CL:0000115
      label: endothelial cell
  biological_processes:
  - preferred_term: immune response
    modifier: ABNORMAL
    term:
      id: GO:0006955
      label: immune response
  - preferred_term: complement activation
    modifier: INCREASED
    term:
      id: GO:0006956
      label: complement activation
  downstream:
  - target: Leukocyte-mediated vessel-wall injury
    description: Immune-complex deposition promotes complement and leukocyte effector injury in affected small vessels.
  evidence:
  - reference: PMID:26362741
    reference_title: Vasculitis related to viral and other microbial agents.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Vasculitis due to infection may occur as a consequence of the inflammation of vessel walls due to direct or contiguous infection, type II or immune complex-mediated reaction, cell-mediated hypersensitivity, or inflammation due to immune dysregulation triggered by bacterial toxin and/or superantigen production.
    explanation: This review explicitly includes immune-complex mediated reactions among infection-related vasculitis mechanisms.
  - reference: DOI:10.3390/jcm12020697
    reference_title: Viral Infections May Be Associated with Henoch–Schönlein Purpura
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Serum aberrant IgA1 may form large antigen–antibody complexes which, due to a defective clearance, are able to deposit in the small vessels of the skin, kidney, gut, and joints.
    explanation: This IgA vasculitis review supports infection-triggered immune-complex deposition in classic target tissues.
- name: Infection-triggered IgA endothelial and neutrophil injury
  description: >-
    IgA vasculitis mechanisms include aberrantly glycosylated IgA,
    anti-endothelial cell antibodies, and neutrophil effector activity after
    infection triggers.
  cell_types:
  - preferred_term: endothelial cell
    term:
      id: CL:0000115
      label: endothelial cell
  - preferred_term: neutrophil
    term:
      id: CL:0000775
      label: neutrophil
  biological_processes:
  - preferred_term: leukocyte migration
    modifier: INCREASED
    term:
      id: GO:0050900
      label: leukocyte migration
  downstream:
  - target: Leukocyte-mediated vessel-wall injury
    description: Neutrophil and endothelial antibody mechanisms contribute to small-vessel inflammation after infection triggers.
  evidence:
  - reference: DOI:10.1002/kjm2.12852
    reference_title: "Immunoglobulin A vasculitis: The clinical features and pathophysiology"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Disease mechanisms involve various factors, including the interplay of aberrantly glycosylated IgA, anti-endothelial cell antibodies, and neutrophils following infection triggers, which are the main pathogenic mechanisms of IgAV.
    explanation: This directly supports IgA, anti-endothelial antibody, and neutrophil mechanisms after infection triggers.
- name: Microbial toxin or superantigen immune dysregulation
  description: >-
    Bacterial toxins or superantigens can trigger immune dysregulation that
    promotes vascular inflammation after infection.
  biological_processes:
  - preferred_term: immune response
    modifier: ABNORMAL
    term:
      id: GO:0006955
      label: immune response
  downstream:
  - target: Leukocyte-mediated vessel-wall injury
    description: Dysregulated immune activation can feed into inflammatory vessel-wall damage.
  evidence:
  - reference: PMID:26362741
    reference_title: Vasculitis related to viral and other microbial agents.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Vasculitis due to infection may occur as a consequence of the inflammation of vessel walls due to direct or contiguous infection, type II or immune complex-mediated reaction, cell-mediated hypersensitivity, or inflammation due to immune dysregulation triggered by bacterial toxin and/or superantigen production.
    explanation: This review explicitly supports toxin or superantigen-triggered immune dysregulation.
- name: T- and B-cell activation after infection
  description: >-
    T- and B-cell activation is a proposed mechanism in infection-associated
    vasculitis, including postinfectious settings in which the pathogen has
    triggered ongoing immune inflammation.
  biological_processes:
  - preferred_term: adaptive immune response
    modifier: ABNORMAL
    term:
      id: GO:0002250
      label: adaptive immune response
  downstream:
  - target: Leukocyte-mediated vessel-wall injury
    description: Adaptive immune activation can sustain vascular inflammation after infection.
  evidence:
  - reference: PMID:40089428
    reference_title: Infection associated Vasculitides.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The exact pathogenesis of infection associated vasculitis is not clear although direct spread, immune complex deposition and T/B cell activation are proposed.
    explanation: This supports T/B cell activation as a proposed infection-associated vasculitis mechanism while preserving uncertainty.
- name: Molecular mimicry and infection-induced autoantibodies
  description: >-
    Some infections can generate autoantibodies such as ANCA through molecular
    mimicry, confounding distinction between primary systemic vasculitis and
    infection-associated vasculitis.
  biological_processes:
  - preferred_term: adaptive immune response
    modifier: ABNORMAL
    term:
      id: GO:0002250
      label: adaptive immune response
  downstream:
  - target: Leukocyte-mediated vessel-wall injury
    description: Infection-associated autoantibody production can amplify inflammatory vascular injury or mimic primary vasculitis.
  evidence:
  - reference: PMID:40089428
    reference_title: Infection associated Vasculitides.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Infections can produce autoantibodies such as Anti-neutrophil cytoplasmic antibody through molecular mimicry and could confound clinical judgement.
    explanation: This supports molecular mimicry and autoantibody production as infection-associated vasculitis mechanisms.
- name: Leukocyte-mediated vessel-wall injury
  description: >-
    Immune activation after infection can damage the vascular wall and produce
    postinfectious vasculitic syndromes in skin, kidney, gut, joints, CNS, or
    other affected tissues.
  cell_types:
  - preferred_term: neutrophil
    term:
      id: CL:0000775
      label: neutrophil
  biological_processes:
  - preferred_term: leukocyte migration
    modifier: INCREASED
    term:
      id: GO:0050900
      label: leukocyte migration
  evidence:
  - reference: DOI:10.1002/kjm2.12852
    reference_title: "Immunoglobulin A vasculitis: The clinical features and pathophysiology"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Disease mechanisms involve various factors, including the interplay of aberrantly glycosylated IgA, anti-endothelial cell antibodies, and neutrophils following infection triggers, which are the main pathogenic mechanisms of IgAV.
    explanation: This supports neutrophil participation in infection-triggered IgA vasculitis mechanisms.
phenotypes:
- category: Cardiovascular
  name: Infection-associated vasculitis
  diagnostic: true
  description: Vessel-wall inflammation temporally and etiologically linked to infection defines postinfectious vasculitis.
  phenotype_term:
    preferred_term: Vasculitis
    term:
      id: HP:0002633
      label: Vasculitis
  evidence:
  - reference: PMID:26362741
    reference_title: Vasculitis related to viral and other microbial agents.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      As immunosuppressive therapy administered in the absence of antimicrobial therapy may increase morbidity and fail to effect the resolution of infection-associated vascular inflammation, it is important to consider infectious entities as potential inciting factors in vasculitis syndromes.
    explanation: This supports infection-associated vascular inflammation as the diagnostic context.
- category: Cardiovascular
  name: Vessel-size variable vasculitis mimicry
  description: Infections can mimic small-, medium-, or large-vessel vasculitis, complicating diagnosis.
  phenotype_term:
    preferred_term: Vasculitis
    term:
      id: HP:0002633
      label: Vasculitis
  evidence:
  - reference: PMID:40089428
    reference_title: Infection associated Vasculitides.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Infections can mimic small, medium or large vessel vasculitis.
    explanation: This supports variable vessel-size mimicry in infection-associated clinical presentations.
- category: Immunologic
  name: Anti-neutrophil cytoplasmic antibody positivity
  description: Infection-associated molecular mimicry can produce ANCA and complicate clinical classification.
  phenotype_term:
    preferred_term: Anti-neutrophil cytoplasmic antibody positivity
  review_notes: >-
    The reviewer-suggested HP:0410009 resolves locally to abnormality of the
    somatic nervous system, so this remains preferred-term-only.
  evidence:
  - reference: PMID:40089428
    reference_title: Infection associated Vasculitides.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Infections can produce autoantibodies such as Anti-neutrophil cytoplasmic antibody through molecular mimicry and could confound clinical judgement.
    explanation: This supports ANCA positivity or related autoantibody findings in infection-associated contexts.
- category: Dermatologic
  name: Palpable purpura
  diagnostic: true
  description: Palpable purpura is a defining manifestation of IgA vasculitis, a common infection-triggered small-vessel vasculitis.
  phenotype_term:
    preferred_term: Palpable purpura
    term:
      id: HP:0031363
      label: Palpable purpura
  evidence:
  - reference: DOI:10.1002/kjm2.12852
    reference_title: "Immunoglobulin A vasculitis: The clinical features and pathophysiology"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Palpable purpura, gastrointestinal symptoms, joint involvement, and renal disease characterize immunoglobulin A vasculitis (IgAV).
    explanation: This supports palpable purpura as a key IgA vasculitis phenotype in postinfectious contexts.
- category: Gastrointestinal
  name: Gastrointestinal symptoms
  description: Gastrointestinal symptoms characterize IgA vasculitis.
  phenotype_term:
    preferred_term: Gastrointestinal symptoms
    term:
      id: HP:0025031
      label: Abnormality of the digestive system
  evidence:
  - reference: DOI:10.1002/kjm2.12852
    reference_title: "Immunoglobulin A vasculitis: The clinical features and pathophysiology"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Palpable purpura, gastrointestinal symptoms, joint involvement, and renal disease characterize immunoglobulin A vasculitis (IgAV).
    explanation: This supports gastrointestinal symptoms in IgA vasculitis.
- category: Gastrointestinal
  name: Abdominal pain
  description: Abdominal pain can occur in COVID-associated Kawasaki-like postinfectious inflammatory disease.
  phenotype_term:
    preferred_term: Abdominal pain
    term:
      id: HP:0002027
      label: Abdominal pain
  evidence:
  - reference: PMID:32631771
    reference_title: COVID-19 associated Kawasaki-like multisystem inflammatory disease in an adult.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Here, we report the case of a 36-year-old woman who presented to the emergency department hypotensive and tachycardic after 1 week of fevers, abdominal pain, vomiting and diarrhea, and was found to have the classic phenotype of complete Kawasaki's Disease including nonexudative conjunctivitis, cracked lips, edema of the hands and feet, palmar erythema, a diffuse maculopapular rash, and cervical lymphadenopathy.
    explanation: This supports abdominal pain in a postinfectious Kawasaki-like vasculitis presentation.
- category: Renal
  name: Proteinuria
  description: Renal involvement in IgA vasculitis ranges from proteinuria to severe nephritic or nephrotic syndrome.
  phenotype_term:
    preferred_term: Proteinuria
    term:
      id: HP:0000093
      label: Proteinuria
  evidence:
  - reference: DOI:10.1002/kjm2.12852
    reference_title: "Immunoglobulin A vasculitis: The clinical features and pathophysiology"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Renal involvement ranging from mild proteinuria to severe nephritic or nephrotic syndrome highlights the importance of monitoring kidney function in patients with IgAV.
    explanation: This supports proteinuria as part of IgA vasculitis renal involvement.
- category: Renal
  name: Hematuria
  description: >-
    Nephritic renal involvement in IgA vasculitis can include hematuria.
  phenotype_term:
    preferred_term: Hematuria
    term:
      id: HP:0000790
      label: Hematuria
  evidence:
  - reference: DOI:10.1002/kjm2.12852
    reference_title: "Immunoglobulin A vasculitis: The clinical features and pathophysiology"
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Renal involvement ranging from mild proteinuria to severe nephritic or nephrotic syndrome highlights the importance of monitoring kidney function in patients with IgAV.
    explanation: >-
      This supports nephritic renal involvement in IgA vasculitis; hematuria is
      represented as the HPO-bound nephritic urinary manifestation.
- category: Musculoskeletal
  name: Joint involvement
  description: Joint involvement is part of the IgA vasculitis phenotype.
  phenotype_term:
    preferred_term: Joint involvement
    term:
      id: HP:0002829
      label: Arthralgia
  evidence:
  - reference: DOI:10.1002/kjm2.12852
    reference_title: "Immunoglobulin A vasculitis: The clinical features and pathophysiology"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Palpable purpura, gastrointestinal symptoms, joint involvement, and renal disease characterize immunoglobulin A vasculitis (IgAV).
    explanation: This supports joint involvement in IgA vasculitis.
- category: Constitutional
  name: Fever
  description: Fever is enriched in secondary CNS vasculitis, especially infectious vasculitis.
  phenotype_term:
    preferred_term: Fever
    term:
      id: HP:0001945
      label: Fever
  evidence:
  - reference: DOI:10.1177/19418744231223283
    reference_title: "Vasculitis in the Central Nervous System: Etiology, Characteristics, and Outcomes in a Large Single-Center Cohort"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Compared to primary CNS vasculitis, secondary CNS vasculitis exhibits higher fever incidence (observed in infectious and connective tissue disorder [CTD]-associated vasculitis), low glucose levels (mostly in infectious vasculitis) and unique cerebrospinal fluid oligoclonal bands (observed in infectious and CTD-associated vasculitis).
    explanation: This supports fever in infectious/secondary CNS vasculitis.
- category: Neurological
  name: Ischemic stroke
  subtype: Infectious or secondary CNS vasculitis
  description: >-
    Infectious or secondary CNS vasculitis can present with ischemic stroke.
  phenotype_term:
    preferred_term: Ischemic stroke
    term:
      id: HP:0002140
      label: Ischemic stroke
  notes: >-
    The Falcon report summarizes Hoshina et al. 2024 full-text results as
    acute/subacute stroke in infectious CNS vasculitis patients; the local
    DOI/PMID caches expose only the abstract, so no direct evidence snippet is
    attached here.
treatments:
- name: Antimicrobial therapy for active infection-associated vasculitis
  description: >-
    Management should identify and treat the infectious inciting factor when
    active, because immunosuppression without antimicrobial therapy can worsen
    outcomes or fail to resolve vascular inflammation.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
  evidence:
  - reference: PMID:26362741
    reference_title: Vasculitis related to viral and other microbial agents.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      As immunosuppressive therapy administered in the absence of antimicrobial therapy may increase morbidity and fail to effect the resolution of infection-associated vascular inflammation, it is important to consider infectious entities as potential inciting factors in vasculitis syndromes.
    explanation: This supports treating or excluding active infection before immunosuppression.
- name: Carefully selected anti-inflammatory or immunosuppressive therapy
  description: >-
    Anti-inflammatory or immunosuppressive therapy may be considered only after
    accounting for the infectious trigger, disease mechanism, and risk of
    worsening uncontrolled infection.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
  evidence:
  - reference: PMID:40089428
    reference_title: Infection associated Vasculitides.
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      It is very important for the clinician to be aware of the various infections which mimic vasculitis, since inadvertent immunosuppression in these patients can be fatal.
    explanation: This supports caution with immunosuppression in infection-associated vasculitis or mimics.
- name: Intravenous methylprednisolone-based induction for CNS vasculitis
  description: >-
    Secondary or infectious CNS vasculitis may require corticosteroid induction,
    often with adjunctive immunosuppressive therapy after infectious causes are
    treated or accounted for.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: corticosteroid
      term:
        id: CHEBI:50858
        label: corticosteroid
  evidence:
  - reference: DOI:10.1177/19418744231223283
    reference_title: "Vasculitis in the Central Nervous System: Etiology, Characteristics, and Outcomes in a Large Single-Center Cohort"
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Intravenous methylprednisolone was the predominant induction therapy (63.6%), and cyclophosphamide was the most used adjunctive therapy.
    explanation: This cohort supports corticosteroid induction and cyclophosphamide adjunctive therapy in CNS vasculitis management.
- name: IVIG, aspirin, and corticosteroids for Kawasaki-like postinfectious inflammation
  description: >-
    Kawasaki-like inflammatory disease after COVID-19 can respond rapidly to
    IVIG, aspirin, and corticosteroid therapy in reported cases.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: corticosteroid
      term:
        id: CHEBI:50858
        label: corticosteroid
    - preferred_term: acetylsalicylic acid
      term:
        id: CHEBI:15365
        label: acetylsalicylic acid
    - preferred_term: human immunoglobulin G
      term:
        id: NCIT:C80829
        label: Human Immunoglobulin G
  evidence:
  - reference: PMID:32631771
    reference_title: COVID-19 associated Kawasaki-like multisystem inflammatory disease in an adult.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      She was treated for Kawasaki Disease Shock Syndrome (KDSS) with pulse dose solumedrol, IVIG, and aspirin with near resolution of symptoms and normalization of vital signs within 1 day and subsequent improvement in her laboratory abnormalities.
    explanation: This case report supports IVIG, aspirin, and corticosteroids in a postinfectious Kawasaki-like vasculitis presentation.

📚

References & Deep Research

Deep Research

1

Falcon ▸

Disease Characteristics Research Template

Edison Scientific Literature 27 citations 2026-05-05T07:58:03.102553

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.

Phenotype/entity	Typical infectious triggers	Key mechanism(s)	Diagnostic features/tests	Treatment approaches reported	Recent numeric data/statistics	Key cited source (with URL, year/month)
COVID-19–associated secondary vasculitis (cutaneous LCV/IgA, aortitis, Kawasaki-like)	SARS-CoV-2 infection; vasculitis may develop in <2 weeks or later during/after infection (frasier2023secondaryvasculitisattributable pages 1-2, frasier2023secondaryvasculitisattributable pages 3-4)	Proposed immune-mediated pathways include Th2/humoral escalation to type III hypersensitivity with immune-complex deposition, cytokine release including IL-6, and direct endothelial/vascular invasion via ACE2; Kawasaki-like presentations also linked to immune hyperresponse/STING signaling (frasier2023secondaryvasculitisattributable pages 1-2, frasier2023secondaryvasculitisattributable pages 3-4)	CT and FDG-PET for aortitis; inflammatory markers ESR, CRP, IL-6 elevated; phenotypes include cutaneous small-vessel vasculitis/LCV, IgA vasculitis, aortitis, giant cell/ophthalmic arteritis, Kawasaki-like disease (frasier2023secondaryvasculitisattributable pages 1-2, frasier2023secondaryvasculitisattributable pages 3-4)	Prednisolone/prednisone 40–60 mg reported for aortitis; IVIG plus aspirin for Kawasaki-like disease (frasier2023secondaryvasculitisattributable pages 3-4)	Review discussed 65 articles; reported labs in representative cases included ESR 57 and 109 mm/hr, CRP 8.7 and 10.73 mg/dL, IL-6 54.44 pg/mL, hemoglobin 10.4 g/dL (frasier2023secondaryvasculitisattributable pages 1-2, frasier2023secondaryvasculitisattributable pages 3-4)	Frasier et al., Secondary Vasculitis Attributable to Post-COVID Syndrome, Cureus, 2023 Aug. URL: https://doi.org/10.7759/cureus.44119 (frasier2023secondaryvasculitisattributable pages 1-2, frasier2023secondaryvasculitisattributable pages 3-4)
IgA vasculitis as postinfectious small-vessel vasculitis	Bacterial triggers reported include Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, Haemophilus parainfluenzae, Mycoplasma pneumoniae; viral triggers include parainfluenza, influenza, rhinovirus, rotavirus, EBV, hepatitis A/B/C, SARS-CoV-2, CMV; also parasites/yeast and post-vaccination triggers listed (hu2024immunoglobulinavasculitis pages 4-4)	Multi-hit model involving galactose-deficient IgA1, IgA/IgG immune complexes, anti-endothelial cell antibodies, complement-dependent cytotoxicity, ADCC, neutrophil recruitment via IL-8 and leukotriene B4, and NET/ROS-mediated injury (hu2024immunoglobulinavasculitis pages 4-4, hu2024immunoglobulinavasculitis pages 5-5)	Suggested/mechanistic diagnostics include measurement of serum IgA immune complexes and demonstration of IgA binding to PMNs; clinical spectrum includes palpable purpura with GI/joint/renal disease (hu2024immunoglobulinavasculitis pages 5-5, nikolaishvili2023viralinfectionsmay pages 11-13)	No treatment details provided in the cited mechanistic snippets; review context notes consensus guidance exists but specifics are not in the extracted evidence (nikolaishvili2023viralinfectionsmay pages 11-13, hu2024immunoglobulinavasculitis pages 5-5)	In a COVID-related vasculitis cohort, 30 of 41 patients had IgA vasculitis; among these, 30% had fever and 43.3% had renal involvement (hu2024immunoglobulinavasculitis pages 5-5)	Hu et al., Immunoglobulin A vasculitis: The clinical features and pathophysiology, Kaohsiung J Med Sci, 2024 Jun. URL: https://doi.org/10.1002/kjm2.12852 (hu2024immunoglobulinavasculitis pages 4-4, hu2024immunoglobulinavasculitis pages 5-5)
Infectious/secondary CNS vasculitis cohort findings	Infectious causes in cohort included varicella zoster virus (4/44, 9.1%), HSV-1 (1/44, 2.3%), and bacterial meningitis (2/44, 4.5%) (hoshina2024vasculitisinthe pages 2-3)	Secondary/infectious CNS vasculitis associated with stroke-predominant presentation; imaging often showed large–middle vessel disease; diagnostic distinctions included inflammatory CSF abnormalities rather than a single unique mechanism in the snippet (hoshina2024vasculitisinthe pages 2-3, hoshina2024vasculitisinthe pages 3-5)	Features favoring secondary/infectious disease: fever, low CSF glucose, unique CSF oligoclonal bands, and vessel-wall MRI enhancement; vasculitic changes seen on blood-vessel imaging in many cases (hoshina2024vasculitisinthe pages 2-3, hoshina2024vasculitisinthe pages 1-2, hoshina2024vasculitisinthe pages 3-5)	IV methylprednisolone was predominant induction therapy; cyclophosphamide common adjunctive/maintenance agent; 80% of infectious vasculitis patients received antimicrobials; some VZV cases also received IV methylprednisolone/high-dose prednisone (hoshina2024vasculitisinthe pages 1-2, hoshina2024vasculitisinthe pages 3-5)	Among 44 patients, 19 (43.2%) had secondary CNS vasculitis and 10 (22.7%) were infection-related; all infectious vasculitis patients had acute/subacute stroke; 7/10 (70%) had large–middle vessel involvement; low CSF glucose in 41.2% vs 8.7% primary; unique OCB in 63.6% vs 0 primary; mortality 20.5% overall, 26.3% secondary; time to diagnosis 15 vs 30 days (hoshina2024vasculitisinthe pages 2-3, hoshina2024vasculitisinthe pages 1-2, hoshina2024vasculitisinthe pages 3-5)	Hoshina et al., Vasculitis in the Central Nervous System: Etiology, Characteristics, and Outcomes in a Large Single-Center Cohort, The Neurohospitalist, 2024 Dec. URL: https://doi.org/10.1177/19418744231223283 (hoshina2024vasculitisinthe pages 2-3, hoshina2024vasculitisinthe pages 1-2, hoshina2024vasculitisinthe pages 3-5)
Cerebrovascular complications in bacterial meningitis attributed to localized cerebral vasculitis	Community-acquired bacterial meningitis, especially pneumococcal and meningococcal disease; these account for ~85% of adult cases (benadji2023cerebrovascularcomplicationsin pages 1-2)	Predominant mechanism described as localized cerebral vasculitis leading to coagulation activation, inhibited fibrinolysis, thrombosis, infarction, and hemorrhage; less common mechanisms include vasospasm, DIC, and septic emboli (benadji2023cerebrovascularcomplicationsin pages 1-2)	CVC defined by focal clinical signs and/or CT/MRI lesions; focal signs include motor, cerebellar, visual, sensory deficits, aphasia, and pyramidal syndromes (benadji2023cerebrovascularcomplicationsin pages 1-2)	Adjunctive dexamethasone was not associated with CVC in this cohort (p=0.84), although prior trials cited in the excerpt showed benefit on death/neurologic sequelae in pneumococcal meningitis (benadji2023cerebrovascularcomplicationsin pages 1-2)	Bacterial meningitis annual incidence about 2/100,000; published CVC rates 10–29%; in COMBAT, 128/506 (25.3%) had CVC, including 78/265 (29.4%) pneumococcal, 17/111 (15.3%) meningococcal, 29/117 (24.8%) other bacteria; independent associations: age OR 1.01, altered mental status OR 2.23, seizures within 48 h OR 1.90 (benadji2023cerebrovascularcomplicationsin pages 1-2)	Benadji et al., Cerebrovascular complications in patients with community-acquired bacterial meningitis, BMC Infect Dis, 2023 Jun. URL: https://doi.org/10.1186/s12879-023-08320-x (benadji2023cerebrovascularcomplicationsin pages 1-2)
Neutrophil/NET mechanisms linking immune complexes to vasculitis	Infection-triggered immune-complex vasculitis context; infections are implied upstream triggers in immune-complex disease and IgA vasculitis (aymonnier2023theneutrophila pages 22-22, hu2024immunoglobulinavasculitis pages 5-5)	Soluble and immobilized immune complexes drive NET formation through FcγRIIA/FcγRIIIB and Mac-1, linking immune-complex deposition to neutrophil-driven endothelial injury; neutrophils also implicated in crescentic glomerulonephritis (aymonnier2023theneutrophila pages 22-22)	Mechanistic evidence includes NET induction by immune complexes and patient serum IgA causing significant DNA release from PMNs; during acute IgA vasculitis, IgA binds peripheral PMNs (aymonnier2023theneutrophila pages 22-22, hu2024immunoglobulinavasculitis pages 5-5)	No disease-specific treatment protocol in the snippet; neutrophils are described as proposed therapeutic targets (aymonnier2023theneutrophila pages 22-22)	Review cites a 417-patient single-center IgA vasculitis cohort as epidemiologic context for neutrophil involvement (aymonnier2023theneutrophila pages 22-22)	Aymonnier et al., The neutrophil: A key resourceful agent in immune-mediated vasculitis, Immunological Reviews, 2023 Nov. URL: https://doi.org/10.1111/imr.13170 (aymonnier2023theneutrophila pages 22-22)

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

(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.
(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.
(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.
(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.
(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.
(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.
(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.
(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.
(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.
(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.
(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.
(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.
(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.
(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.

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Subtypes

Pathophysiology

Pathograph

Phenotypes

Treatments

Source YAML

References & Deep Research

Deep Research

Disease Characteristics Research Template

Target Disease

Research Objectives

1. Disease Information

2. Etiology

3. Phenotypes

4. Genetic/Molecular Information

5. Environmental Information

6. Mechanism / Pathophysiology

7. Anatomical Structures Affected

8. Temporal Development

9. Inheritance and Population

10. Diagnostics

11. Outcome/Prognosis

12. Treatment

13. Prevention

14. Other Species / Natural Disease

15. Model Organisms

Citation Requirements

Output Format

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

Target disease

1. Disease information

1.1 Concise overview

1.2 Key synonyms / alternative names

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

1.4 Evidence provenance

2. Etiology

2.1 Primary causes and causal factors

Major etiologic mechanisms (current understanding)

2.2 Infectious triggers (pathogens)

2.2.1 IgA vasculitis triggers (2024 synthesis)

2.2.2 Viral triggers and vaccines in IgA vasculitis (2023)

2.2.3 CNS infectious vasculitis triggers (2024 cohort)

2.2.4 Post-COVID secondary vasculitis

2.3 Risk factors

2.3.1 Host susceptibility (genetic predisposition)

2.3.2 Clinical predictors in infection-related CNS vascular complications

2.4 Protective factors

2.5 Gene–environment interactions

3. Phenotypes (clinical spectrum)

3.1 Common phenotypes and suggested HPO terms

A) IgA vasculitis (Henoch–Schönlein purpura)

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

C) CNS postinfectious/secondary vasculitis or vasculopathy

3.2 Frequency / proportions (recent numeric data)

4. Genetic / molecular information

4.1 Causal genes

4.2 Susceptibility loci / immunogenetics

4.3 Molecular effectors implicated (mechanistic candidates)

Suggested GO/CL annotations (mechanism-linked)

5. Environmental information

5.1 Infectious environmental exposures

5.2 Lifestyle factors

6. Mechanism / pathophysiology

6.1 Mechanistic causal chains (upstream → downstream)

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

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

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

D) Bacterial meningitis → localized cerebral vasculitis → cerebrovascular complications

6.2 Key pathways (high-level)

7. Anatomical structures affected

7.1 Organ-level involvement (common)

Suggested UBERON terms (examples)

8. Temporal development (onset, progression)

9. Inheritance and population

9.1 Epidemiology (available recent statistics)

IgA vasculitis incidence

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

Primary CNS vasculitis (useful differential benchmark)