← Back to catalogue
Research draft

hepatitis A

vr.tr.hepatitis-a · XCT.QLT

Enable an AI agent to recognise a possible hepatitis A episode, assess its clinical and transmission state, and identify evidence-based care, prevention and public-health actions requiring human review.

Thing Registry Cross-cutting context

Research draft, second pass

A second pass drafted this model: the structure a model of this thing needs, and what is known about it in the world. The line under this one says how the second half was obtained - researched against sources, or recalled without web access, in which case nothing here was read anywhere and every claim is a lead to verify. Unreviewed either way.

Researched by: Codex + Grok

Purpose and description

Enable an AI agent to recognise a possible hepatitis A episode, assess its clinical and transmission state, and identify evidence-based care, prevention and public-health actions requiring human review.

Hepatitis A is an acute, typically self-limited necroinflammatory disease of the liver caused by Hepatovirus A (family Picornaviridae), acquired mainly by the faecal-oral route, that does not establish chronic infection and is diagnosed by IgM antibody to HAV (or HAV RNA) rather than by clinical hepatitis alone.

It can be Assemble and qualify evidence for a suspected HAV episode and identify missing confirmation.; Track illness and laboratory trends, flagging deterioration for clinical review.; Construct plausible acquisition and onward-exposure timelines with explicit uncertainty.; Identify contacts needing prompt post-exposure prevention assessment.; Prepare a jurisdiction-specific reporting and infection-control review.; Document recovery, unresolved abnormalities and reasons to reconsider the diagnosis..

Distinguishing features

Require HAV-specific evidence interpreted in clinical context; jaundice, raised liver enzymes and exposure history alone cannot distinguish hepatitis A from other hepatitis causes. [CDC diagnosis guidance](https://www.cdc.gov/hepatitis-a/hcp/diagnosis-testing/index.html)

Distinguish acute infection evidence from immunity: IgG or total anti-HAV positivity alone does not establish acute hepatitis A, and an IgM result requires attention to testing context and recent vaccination. [CDC diagnosis guidance](https://www.cdc.gov/hepatitis-a/hcp/diagnosis-testing/index.html)

Distinguish prolonged or relapsing hepatitis A from chronic viral hepatitis: hepatitis A does not establish chronic liver disease. [WHO hepatitis A fact sheet](https://www.who.int/news-room/fact-sheets/detail/hepatitis-a)

Test for plausible faecal-oral acquisition through contaminated food, water or close-contact exposure; route plausibility supports investigation but does not prove HAV causation. [WHO hepatitis A fact sheet](https://www.who.int/news-room/fact-sheets/detail/hepatitis-a)

Do not exclude HAV infection solely because jaundice or other symptoms are absent, particularly in young children. [WHO hepatitis A fact sheet](https://www.who.int/news-room/fact-sheets/detail/hepatitis-a)

Scope

+ Suspected or confirmed HAV infection, including asymptomatic presentations

+ Interpretation of HAV laboratory evidence alongside symptoms, exposure history and vaccination timing

+ Acute illness, recovery, relapse and complications attributable to hepatitis A

+ Likely acquisition exposures and opportunities for onward transmission

+ Hepatitis A prevention, clinical escalation and public-health decision requirements

- HAV taxonomy, molecular structure and laboratory culture as a virus model

- Hepatitis B, C, D and E, autoimmune hepatitis and drug-induced liver injury as independent conditions

- Vaccine and immune-globulin manufacturing, inventory and product specifications

- A person's complete medical record and management of unrelated comorbidities

- Food-system operations, sanitation infrastructure and outbreak-wide logistics

- Detailed management of liver failure, transplantation and chronic liver disease

Characteristics

HAV attribution
suspected | supported | confirmed under named criteria | excluded | unresolved Prevents a provisional hepatitis syndrome from becoming an unsupported HAV diagnosis.
HAV test evidence
IgM anti-HAV, IgG anti-HAV, total anti-HAV or HAV RNA; positive | negative | indeterminate | not performed; specimen and collection date Preserves which test was performed and distinguishes evidence of infection from evidence of immunity.
Exposure-to-onset interval
days, with earliest/latest plausible exposure dates and onset uncertainty Supports exposure plausibility and time-sensitive prevention assessment without inventing an exact infection date.
Episode phase
asymptomatic infection | symptomatic acute illness | improving | relapsing | recovered | uncertain Makes the course of one episode explicit and flags reassessment after apparent improvement.
Hepatocellular injury
ALT and AST in U/L, with laboratory reference limits and dated trends Records injury trends without treating enzyme elevation as a complete measure of liver function.
Bilirubin burden
total and direct bilirubin in µmol/L or mg/dL, with dates Supports assessment of jaundice and a prolonged cholestatic course.
Severity and deterioration evidence
clinically stable | concerning deterioration | suspected liver failure | unknown; linked mental-status, coagulation and hydration observations Supports timely clinical escalation using observable evidence and applicable criteria.
Host vulnerability
linked age, underlying liver disease, immunocompromise and relevant clinical conditions Provides context for severity assessment and prevention decisions.
Protection evidence
documented vaccination history | prior infection evidence | serological immunity evidence | susceptible | uncertain Prevents undocumented assumptions about immunity from determining contact management.
Exposure relationship
source or contact link; route, setting, dates and evidential confidence Separates suspected acquisition from possible onward transmission.
Post-exposure prevention status
assessment pending | eligible under cited guidance | administered | declined | not indicated | outside established window | unknown Makes time-sensitive prevention decisions and their supporting guidance reviewable.

Where this came from

wikidata · CC0 1.0

Drafted structure

Bundle to layer to finding to question, as the second pass will find it: 6 bundles · 11 layers · 18 findings · 28 questions.

HAV attribution Establish whether the observed condition is attributable to HAV and how strongly that conclusion is supported.

Acute hepatitis, past immunity and a positive screening result must not be treated as interchangeable states.

Clinical fit

Relate the presentation and competing explanations to the proposed HAV episode.

Presentation and alternatives

Record the observed hepatitis presentation, including absent symptoms, and evidence supporting alternative causes.

  1. What symptoms, signs or incidental abnormalities initiated suspicion of hepatitis A, and when did they begin? definition
  2. Which competing infectious, toxic, autoimmune or obstructive explanations remain plausible, and what evidence separates them? boundary

Laboratory attribution

Interpret HAV assays with their timing, provenance and limitations.

Test-supported classification

Retain the original assay result separately from the clinical interpretation and any surveillance classification.

  1. Which HAV assays were performed, on what specimens and dates, by which laboratory, and with what results? provenance
  2. How do symptom timing, recent vaccination, previous infection and possible false positivity affect the interpretation or need for repeat testing? boundary
Episode course and severity Represent the course of the HAV episode and evidence of clinically significant deterioration.

An improving uncomplicated episode and one requiring urgent specialist assessment demand different actions.

Illness trajectory

Track onset, improvement, recurrence and unresolved abnormalities.

Phase and recurrence

Distinguish continuing illness, apparent recovery and renewed symptoms without assuming a second infection.

  1. What dated changes in symptoms, jaundice, liver tests and daily functioning establish the current episode phase? measurement
  2. If symptoms or abnormalities persist or recur, what supports relapse or cholestasis, and what requires investigation for another condition? boundary

Deterioration assessment

Connect severity observations and host vulnerability to an explicit clinical review decision.

Escalation evidence

Record mental status, coagulation, hydration and relevant comorbidity evidence rather than inferring safety from liver enzyme trends.

  1. What are the current mental status, PT/INR, oral intake, hydration findings and underlying liver conditions, and how have they changed? measurement
  2. Which observed findings meet the applicable criteria for urgent assessment, admission or specialist referral, and who owns that decision? action
Acquisition and transmission Connect the episode to plausible acquisition events and potential onward exposures.

Identifying a likely source and identifying people exposed by the case are separate investigations.

Acquisition reconstruction

Evaluate dated exposure hypotheses and supporting epidemiological evidence.

Plausible source links

Record candidate food, water, household, sexual or other close-contact exposures without declaring an unverified source.

  1. Which exposures occurred within the incubation interval supported by the selected reference, and how precise are their dates? measurement
  2. What interview, traceback, laboratory or outbreak evidence supports each proposed source link? provenance

Onward exposure assessment

Identify contact events potentially overlapping the infectious period.

Contact window

Maintain an estimated infectious interval and event-specific exposure assessments, including uncertainty when onset is unknown.

  1. What infectious interval is supported by the applicable guidance and the case timeline, including any relapse? boundary
  2. Which household, sexual, caregiving, childcare or food-handling events warrant contact assessment within that interval? action
Immunity and post-exposure prevention Assess protection and time-sensitive prevention for people exposed to HAV.

Protection evidence, exposure timing and recipient characteristics determine whether preventive intervention needs review.

Protection assessment

Establish what is known about a contact's protection before interpreting prevention eligibility.

Documented protection

Separate verified vaccination or infection history from recall and uncertain antibody interpretation.

  1. What records establish vaccine products and dose dates, previous HAV infection or relevant antibody results? provenance
  2. Does the available evidence meet the applicable definition of protection, or must susceptibility remain unresolved? boundary

Prevention decision

Connect exposure timing and recipient factors to a reviewed intervention.

Time-sensitive PEP

Record elapsed time and the applicable vaccine or immune-globulin pathway; CDC guidance uses a two-week post-exposure window. [CDC Yellow Book](https://www.cdc.gov/yellow-book/hcp/travel-associated-infections-diseases/hepatitis-a.html)

  1. How long has elapsed since each qualifying exposure, and what deadline follows from the applicable guidance? measurement
  2. Given age, protection history, liver disease, immune status and contraindications, what prevention is indicated, and has a clinician arranged or administered it? action
Care, public health and resolution Track episode-specific care and public-health responsibilities through separately justified closure decisions.

Clinical recovery, surveillance classification and release from activity restrictions are distinct determinations.

Supportive care review

Represent the care plan, medication review and follow-up appropriate to the observed HAV course.

Care and follow-up

Record clinician-directed supportive management; hepatitis A has no specific treatment. [CDC Pink Book](https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-9-hepatatitis-a.html)

  1. What hydration, nutrition, symptom-management and medication or alcohol review has been documented for this episode? action
  2. What follow-up observations and clinician-defined recovery criteria are required, and which abnormalities remain unexplained? measurement

Public-health disposition

Apply the relevant reporting, exposure-control and return-to-activity requirements.

Reporting and release

Record the responsible authority, applicable rule version and evidence for each restriction or closure decision.

  1. Which jurisdiction and case-definition version govern notification, and what reporting or investigation remains outstanding? provenance
  2. What hygiene measures, activity restrictions and return criteria apply to this person's setting, and who can authorize their completion? action
Evidence and external alignment What the world already says about this thing, gathered so the model can be checked against it.

A model that cannot be lined up against existing standards, identifiers and practice cannot be adopted by anyone who already uses them.

Reported evidence

Findings from the breadth pass, kept separate from the structural claims.

Kinds and varieties

Reported by the breadth pass; each item needs checking against its source before it becomes normative.

  • Asymptomatic or anicteric infection (the usual course in young children)
  • Icteric acute hepatitis A
  • Fulminant hepatitis A with acute liver failure
  • Relapsing hepatitis A (a biphasic or polyphasic clinical course after initial improvement)
  • Prolonged cholestatic hepatitis A
  • Human HAV genotypes I, II and III (subgenotypes IA, IB and IIIA account for most clinical isolates; IV-VI are simian)
  • Travel-associated sporadic infection versus point-source foodborne or waterborne outbreak versus endemic community transmission
  1. Which of these kinds and varieties hold for the sense of hepatitis A this model covers, and on what evidence? provenance

Identifiers and schemes

Reported by the breadth pass; each item needs checking against its source before it becomes normative.

  • Wikidata - Q157585 - Item for the disease hepatitis A (not the virus).
  • ICD-10 / ICD-10-CM - B15 - Acute hepatitis A; B15.0 with hepatic coma, B15.9 without hepatic coma.
  • ICD-11 - 1E50.0 - Acute hepatitis A.
  • NCBI Taxonomy - 12092 - Hepatitis A virus; ICTV species name is Hepatovirus A (taxid 208726 is also used for the species).
  • ICTV - Hepatovirus A - Species in genus Hepatovirus, family Picornaviridae.
  • MeSH - D006506 - Hepatitis A.
  • SNOMED CT - 40468003 - Viral hepatitis type A (disorder).
  • Disease Ontology - DOID:12549 - hepatitis A.
  1. Which of these identifiers and schemes hold for the sense of hepatitis A this model covers, and on what evidence? provenance

Standards and regulation

Reported by the breadth pass; each item needs checking against its source before it becomes normative.

  • WHO position paper on hepatitis A vaccines (Weekly Epidemiological Record; SAGE) - immunization policy and schedule options.
  • CDC / ACIP recommendations on prevention of HAV infection - routine childhood, catch-up, travel, occupational, and outbreak vaccination, plus post-exposure vaccine and immunoglobulin.
  • ECDC / EU case definition for hepatitis A - laboratory and clinical criteria used for notifiable-disease surveillance in the EU/EEA.
  • ISO 15216-1 and ISO 15216-2 (ISO) - RT-PCR quantification and detection of HAV (and norovirus) in the food chain.
  • Codex Alimentarius guidelines on the application of general principles of food hygiene to the control of viruses in food (FAO/WHO) - control of HAV in bivalves, fresh produce, and food handlers.
  • National notifiable-disease reporting (e.g. US NNDSS, UKHSA, and equivalent public-health statutes) - confirmed acute hepatitis A is a reportable condition in most jurisdictions.
  • Vaccine product regulation - inactivated HAV vaccines (e.g. Havrix, Vaqta) and the combined HAV-HBV vaccine (Twinrix) licensed by FDA, EMA and other NRAs.
  1. Which of these standards and regulation hold for the sense of hepatitis A this model covers, and on what evidence? provenance

Real-world use

Reported by the breadth pass; each item needs checking against its source before it becomes normative.

  • Serologic diagnosis of acute jaundice or transaminase elevation (IgM anti-HAV) in clinics and hospitals.
  • Pre-travel vaccination and last-minute post-exposure vaccine or immunoglobulin after a known contact or common-source exposure.
  • Routine childhood immunization in low-endemicity countries that have adopted HAV vaccine, and targeted immunization of food handlers, men who have sex with men, people who use drugs, and people experiencing homelessness.
  • Foodborne outbreak investigation: traceback of frozen berries, green onions, dates, and bivalve molluscs; RT-PCR of food and sequencing of VP1/P2A for genotype matching.
  • Environmental health: sewage workers, day-care exclusion, and household contact tracing because stool shedding precedes jaundice.
  • Blood-operator lookback is uncommon because viraemia is brief and there is no chronic carrier state, unlike HBV and HCV.
  1. Which of these real-world use hold for the sense of hepatitis A this model covers, and on what evidence? provenance

Typical measurements

Reported by the breadth pass; each item needs checking against its source before it becomes normative.

  • Incubation period - 15-50 (mean about 28) - days
  • Peak serum ALT in icteric disease - 500-5000 - U/L
  • Peak total bilirubin in icteric disease - 5-20 - mg/dL
  • Case-fatality ratio - 0.1-0.3 overall; about 1.8 in adults ≥50 years - %
  • IgM anti-HAV detectability - from ~5-10 days before onset to ~3-6 months after - qualitative (positive/negative)
  • Stool HAV shedding around jaundice - ~2 weeks before to ~1 week after onset of jaundice (can be longer in children) - weeks relative to jaundice
  • Inactivated-vaccine seroconversion - ~95 after dose 1; ~99-100 after dose 2 - % with protective anti-HAV
  1. Which of these typical measurements hold for the sense of hepatitis A this model covers, and on what evidence? provenance

Failure modes and hazards

Reported by the breadth pass; each item needs checking against its source before it becomes normative.

  • Fulminant hepatic failure (uncommon; risk rises with age and underlying liver disease) requiring intensive care or transplant.
  • Relapsing or prolonged cholestatic courses that mimic obstruction or chronic hepatitis and prompt unnecessary invasive work-up.
  • Point-source foodborne outbreaks from an infected food handler or from contaminated produce and shellfish, including frozen foods that preserve virus.
  • Secondary household, day-care, and sexual (oral-anal) transmission while the index case is still shedding and not yet jaundiced.
  • False-positive IgM anti-HAV in low-prevalence settings, leading to misattribution of liver injury.
  • Under-vaccination of risk groups and delayed outbreak vaccination campaigns.
  • HAV is not a chronic-infection or oncogenic hazard; treating it as if it were HBV/HCV (lifelong follow-up, antivirals) is a misuse of the diagnosis.
  1. Which of these failure modes and hazards hold for the sense of hepatitis A this model covers, and on what evidence? provenance

Regional variation

Reported by the breadth pass; each item needs checking against its source before it becomes normative.

  • High-endemicity regions (much of sub-Saharan Africa and parts of South Asia and Latin America): almost universal childhood infection, mostly anicteric, high adult immunity, less travel-vaccine demand among locally born adults.
  • Low-endemicity regions (North America, Western Europe, Australia, Japan): childhood infection is now uncommon; disease presents in adolescents and adults as travel-related, foodborne, or risk-group outbreaks.
  • Genotype geography: IA is widespread; IB is common in the Mediterranean and parts of Africa; IIIA is frequent in Central and South Asia and appears in European outbreaks.
  • Older English name "infectious hepatitis" (versus "serum hepatitis" for HBV) still appears in historical records and some non-specialist usage.
  • National schedules differ: some countries use a single-dose inactivated-vaccine programme; others use two doses; many still rely on hygiene plus targeted rather than universal childhood vaccination.
  1. Which of these regional variation hold for the sense of hepatitis A this model covers, and on what evidence? provenance

Neighbouring kinds and how to tell them apart

Reported by the breadth pass; each item needs checking against its source before it becomes normative.

  • Hepatitis E - Both are faecal-oral and acute; HEV IgM/RNA (or HEV antigen) is positive and IgM anti-HAV is negative in hepatitis E. HEV, not HAV, has a high fatality in pregnancy (genotype 1).
  • Hepatitis B (acute) - HBsAg and IgM anti-HBc positive; anti-HAV IgM negative. HBV is bloodborne/sexual, can become chronic, and is not a foodborne picornavirus.
  • Hepatitis C (acute) - HCV RNA positive; anti-HAV IgM negative. Acute HCV is often anicteric and frequently becomes chronic.
  • Drug-induced liver injury - Negative IgM anti-HAV and other viral markers; drug-exposure timeline (e.g. RUCAM) and, when needed, histology without a viral cytopathic pattern.
  • Autoimmune hepatitis - Autoantibodies (ANA, SMA, anti-LKM1), raised IgG, interface hepatitis on biopsy; viral serology including IgM anti-HAV negative (HAV can rarely trigger an autoimmune-like picture, so both may be checked).
  • EBV or CMV hepatitis - EBV VCA IgM / heterophile or CMV IgM/PCR positive; anti-HAV IgM negative; often with lymphadenopathy, atypical lymphocytosis, or a transplant/immunocompromised context.
  • Extrahepatic biliary obstruction - Imaging (ultrasound, MRCP) shows dilated ducts or a stone/mass; viral hepatitis serology is negative and ALT is usually less explosively elevated than in icteric HAV.
  1. Which of these neighbouring kinds and how to tell them apart hold for the sense of hepatitis A this model covers, and on what evidence? provenance

Sources

  1. Hepatitis A fact sheet - Clinical course (acute, not chronic), faecal-oral transmission, incubation, global epidemiology by endemicity, vaccine-preventable status, and case-fatality pattern by age.
  2. CDC Yellow Book: Hepatitis A - Travel-medicine use, incubation range, shedding window, post-exposure immunoglobulin and vaccine, and distinction from other viral hepatitides in returning travellers.
  3. Prevention of Hepatitis A Virus Infection in the United States: Recommendations of the Advisory Committee on Immunization Practices, 2020 - US vaccination and post-exposure schedules, occupational and outbreak indications, and serologic interpretation of IgM versus IgG anti-HAV.
  4. ISO 15216-1: Microbiology of the food chain - Horizontal method for determination of hepatitis A virus and norovirus using real-time RT-PCR - Part 1: Method for quantification - Standard method used by food-control laboratories to detect and quantify HAV in food matrices (notably shellfish, soft fruit, and vegetables).
  5. ICTV Report: Picornaviridae - genus Hepatovirus, species Hepatovirus A - Current species name Hepatovirus A, family placement, and the human versus simian genotype grouping.

What the second pass must settle

  • Which clinical and surveillance definitions should govern confirmation, particularly for asymptomatic infection or discordant HAV assays?
  • Which reference and operational rules should define exposure and infectious intervals when onset is unknown or illness relapses?
  • Which jurisdiction-specific criteria govern vaccine versus immune-globulin use, repeated exposures and presentations beyond the established PEP window?
  • Which validated severity, referral and recovery criteria should be adopted for children, adults and people with underlying liver disease?
  • Which local reporting, food-handling, childcare and return-to-activity rules must be linked before the model supports operational decisions?