animal pathogen
METPO:1004002 · CLASS · REVIEWED
A pathogen that infects organisms in the kingdom Metazoa.
Animal-pathogen metazoan host adaptation
Edge evidence
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metazoan-adapted virulence factors
enables
animal tissue colonization
RO:0002327Metazoan-adapted virulence factors enable adhesion and invasion of animal tissues.
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DOI:10.1146/annurev.micro.62.081307.162938virulence factors
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immune evasion
enables
animal tissue colonization
RO:0002327Immune evasion supports sustained colonization despite host defenses.
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DOI:10.1038/nrmicro1592secretion systems
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animal tissue colonization
causes
animal disease
biolink:causesEstablished colonization in animal tissues causes disease.
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DOI:10.1146/annurev.micro.62.081307.162938virulence factors
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animal disease
manifests as
animal pathogen
METPO:2007400Animal disease manifests the animal-pathogen trait.
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DOI:10.1146/annurev.micro.62.081307.162938virulence factors
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bacterial adhesins
enables
attachment to host cells and mucosa
RO:0002327Bacterial adhesins enable attachment to host cells, extracellular matrix, and mucosa.
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DOI:10.1093/femsre/fuae019
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attachment to host cells and mucosa
enables
animal tissue colonization
RO:0002327Attachment to host surfaces initiates colonization of metazoan barrier sites.
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DOI:10.1093/femsre/fuae019
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complement-regulator-binding surface proteins
mediates
complement evasion
Surface proteins binding host complement regulators (factor H, C4BP) mediate complement evasion.
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DOI:10.1093/femsre/fuae019
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complement evasion
enables
immune evasion
RO:0002327Complement evasion contributes to overall evasion of host immunity.
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DOI:10.1093/femsre/fuae019
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type III secretion system
enables
effector delivery into host-cell cytoplasm
RO:0002327T3SS injectisomes deliver effector proteins directly into the host-cell cytoplasm.
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DOI:10.1128/spectrum.02224-23
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effector delivery into host-cell cytoplasm
enables
immune evasion
RO:0002327T3SS effector delivery modulates host cells and supports immune evasion.
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DOI:10.1128/spectrum.02224-23
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type IV secretion system
enables
effector/toxin translocation into target cells
RO:0002327T4SS nanomachines translocate protein effectors or toxins into target cells.
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DOI:10.1038/s41579-023-00974-3
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effector/toxin translocation into target cells
enables
animal tissue colonization
RO:0002327T4SS effector/toxin translocation supports host-pathogen interactions and colonization.
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DOI:10.1038/s41579-023-00974-3
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low-iron host environment
enables
siderophore biosynthesis gene expression
RO:0002327Low iron derepresses Fur, enabling siderophore biosynthesis gene expression.
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DOI:10.1039/d4cb00175c
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TonB-dependent transporters
enables
siderophore-Fe3+ complex import
RO:0002327TonB-dependent transporters import siderophore-Fe3+ complexes into the periplasm.
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DOI:10.1039/d4cb00175c
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siderophore-Fe3+ complex import
enables
animal tissue colonization
RO:0002327Iron acquisition via siderophore uptake supports growth in iron-restricted host tissues.
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DOI:10.1039/d4cb00175c
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Provenance
- Source
- METPO (2025-11-25)
- Definition source
- DOI:10.1146/annurev.micro.62.081307.162938
Parent traits (1)
kg-microbe context
Matched 1 kg-microbe node via direct_metpo.
METPO:1004002[-1.564, -64.092, -0.620, -28.964, …]
Nearest neighbors in embedding space
- ecology human pathogen 0.775
- ecology pathogenic to host 0.487
- ecology opportunistic pathogen 0.487
- environment mesophilic 0.330
- morphology sporulation 0.320
- morphology motility 0.290
- environment microaerophilic 0.272
- morphology cell length 0.272
Deep research
# Curation report: **animal pathogen** (METPO:1004002) ## Executive curation recommendation The trait should represent the **realized, strain-level capacity of a microorganism to establish infection in a host belonging to Metazoa**, rather than the mere presence of a virulence-associated gene. A defensible general graph should center on five recurring functions: **host attachment/colonization, acquisition of host-limited nutrients, resistance or manipulation of host defenses, host damage, and persistence/dissemination**. Individual adhesins, secretion systems, toxins, capsules, and metabolic pathways should normally be modeled as taxon- or niche-specific implementations of those functions. A 2024 authoritative review frames bacterial host adaptation around colonization, nutrient acquisition, and immune evasion and emphasizes that host range varies from single-host restriction to infection of diverse vertebrates and invertebrates. It also notes that successful establishment requires adaptation to host-specific anatomy, physiology, immunity, and nutrient availability (published 13 July 2024; https://doi.org/10.1093/femsre/fuae019). (barber2024mechanismsofhost pages 1-2) | module | recommended graph status | representative nodes | strongest evidence type | principal caveat | |---|---|---|---|---| | Adhesion / host attachment | core | adhesin; fimbriae/pili; host receptor (E-cadherin, CEACAM, fibrinogen); biofilm-associated protein BAP | Broad review plus experimental host-specific binding examples across pathogens (barber2024mechanismsofhost pages 3-5, barber2024mechanismsofhost pages 5-6, lucidi2024pathogenicityandvirulence pages 4-5) | Exact adhesin-receptor pairs are often host- and taxon-specific, so curate generic adhesion as core and specific receptors as context/taxon-specific. | | Secretion systems / effector export | taxon-specific | type III secretion system; type I secretion system; type II secretion system; secreted effector; RTX toxin; LipA lipase | Strong mechanistic evidence in specific Gram-negative pathogens, including in vivo mutant phenotypes in *A. baumannii* (barber2024mechanismsofhost pages 7-8, lucidi2024pathogenicityandvirulence pages 5-7) | No single secretion system is universal across animal pathogens; avoid generalizing one apparatus to the whole trait. | | Toxins / host damage | core | toxin; pore-forming toxin; leukocidin; superantigen; urease; exotoxin A | Broad cross-pathogen review plus animal infection data and host-specific toxin tropism (barber2024mechanismsofhost pages 10-11, eidaroos2024theimpactof pages 1-2, yang2024unveilingthehidden pages 2-4) | Toxin classes are widespread but highly heterogeneous; individual toxins should usually be taxon-specific nodes. | | Capsule / complement evasion / anti-phagocytosis | core | capsule/capsular polysaccharide; factor H-binding protein; C4BP-binding protein; SCIN; CHIPS; C3b masking | Broad mechanistic review with direct complement-evasion and capsule-function evidence (barber2024mechanismsofhost pages 8-10, gao2024bacterialcapsulesoccurrence pages 5-7, gao2024bacterialcapsulesoccurrence pages 3-5) | Capsules can also reduce adhesion or vary by serotype; effects are sometimes conditional rather than uniformly positive for pathogenesis. | | Iron acquisition / nutritional immunity escape | core | siderophore; TonB-dependent receptor; transferrin-binding protein A (TbpA); hemoglobin receptor IsdB; calprotectin-binding receptor TdfH; heme uptake | Strong broad evidence from host-pathogen iron reviews and host-specific receptor examples (barber2024mechanismsofhost pages 5-6, ullah2023keyplayersin pages 1-2, stelitano2023ironacquisitionand pages 2-4) | Iron acquisition is broadly important, but named receptors are often host-restricted or lineage-specific; curate generic module as core, named proteins as context/taxon-specific. | | Quorum sensing / biofilm persistence | context | quorum sensing; autoinducer; LuxI/LuxR-like system; Agr; biofilm; extracellular matrix/EPS | Reviews and animal/clinical isolate studies linking QS to virulence/biofilm and biofilm to antimicrobial tolerance (juszczukkubiak2024molecularaspectsof pages 2-3, juszczukkubiak2024molecularaspectsof pages 5-7, eidaroos2024theimpactof pages 1-2) | Important for persistence and regulation, but not required for all animal pathogens or all infection stages; better as context unless trait graph models chronicity/persistence. | | Metabolic host adaptation / host nutrient use | context | lactose utilization; carbohydrate transporter; phenylacetic acid metabolism; hydrogenase/FHL; nickel-dependent urease maturation | Good recent evidence for host-specific nutrient adaptation in selected pathogens (barber2024mechanismsofhost pages 6-7, yang2024unveilingthehidden pages 2-4, lucidi2024pathogenicityandvirulence pages 4-5) | Often reflects niche-specific adaptation (mastitis, urinary tract, chronic infection) rather than a universal determinant of animal pathogenicity. | | Environmental cues / host microenvironment sensing | context | urea; anaerobiosis; stationary phase; osmotic stress; elevated glucose; folate stress / antibiotic exposure | Specific mechanistic studies showing cue-dependent induction of virulence modules (barber2024mechanismsofhost pages 6-7, yang2024unveilingthehidden pages 2-4, lucidi2024pathogenicityandvirulence pages 4-5) | Cue-response relationships are highly condition-, tissue-, and taxon-specific; curate only when linked to a defined infection niche. | *Table: This table prioritizes mechanistic modules for curation of the microbial trait animal pathogen, distinguishing broadly curatable core processes from context-dependent or taxon-specific mechanisms. It is useful for deciding which nodes and edges should enter a general TraitMech graph versus remain lineage- or niche-restricted.* ## 1. Trait scope and boundaries ### In scope * **Phenotype:** reproducible ability of a microbial strain to colonize or invade a Metazoan host and produce an infection phenotype under natural or experimentally justified conditions. * **Host range:** humans, livestock, companion animals, wildlife, fish, and invertebrate animals all qualify. “Animal pathogen” does not imply zoonosis or broad host range. * **Mechanistic realization:** attachment to host tissue, invasion or extracellular persistence, acquisition of limiting nutrients, evasion or manipulation of immunity, host-cell/tissue damage, and dissemination. * **Evidence standard:** infection of a relevant animal or validated host-cell/tissue model, preferably supported by genetic perturbation, complementation, biochemical interaction, or epidemiological attribution. ### Important distinctions 1. **Pathogenicity versus virulence.** Pathogenicity is the ability to cause infection/disease; virulence is its degree or severity. A low-virulence pathogen still belongs in the class. 2. **Colonizer/commensal versus pathogen.** Colonization may precede infection but is not sufficient by itself. Staphylococci illustrate this boundary: all are members of mammalian epithelial microbiota, yet only some species or lineages commonly cause disease, and colonization is a frequent source of infection (published 26 September 2023; https://doi.org/10.3390/ijms241914587). (cheung2023virulencemechanismsof pages 1-2) 3. **Opportunistic pathogen.** Opportunism is compatible with the trait, but host compromise, barrier disruption, device implantation, or dysbiosis should be represented as contextual enabling factors—not as microbial mechanisms. 4. **Zoonotic/vector-borne/reservoir status.** These are transmission/ecological traits. A strain can be an animal pathogen without transmission between animal species. 5. **Toxigenic but non-invasive microbes.** Intoxication from a preformed toxin does not automatically demonstrate infection; distinguish toxin producer, foodborne intoxication, and pathogen. 6. **Plant pathogens and environmental survival.** These do not satisfy METPO:1004002 unless the same strain has evidence of infection in a Metazoan host. 7. **Virulence-gene detection alone.** PCR detection, genome annotation, or in-vitro cytotoxicity is supporting evidence but not sufficient to assert the class. Host specificity is often quantitative rather than absolute. For example, *S. pseudintermedius* is a major canine pathogen but occurs at lower rates in other hosts; cats reportedly have an approximately 6.5-fold lower colonization rate than dogs. Therefore, host-specificity assertions should be attached to strain/lineage and host nodes rather than inferred from the species name alone. (cheung2023virulencemechanismsof pages 9-10) ## 2. Candidate nodes grouped by type Only high-confidence identifiers are supplied below. Label-only nodes are intentional where a universal identifier would be misleading or requires database verification. ### Trait, host, and environmental nodes | Candidate node | Type | Suggested grounding | Curation note | |---|---|---|---| | animal pathogen | microbial trait | **METPO:1004002** | Target node. | | Metazoa | host taxon | **NCBITaxon:33208** | Use a more specific host taxon whenever evidence permits. | | host epithelial surface | anatomical/environmental context | label-only | Includes skin and gastrointestinal, respiratory, and urogenital mucosa. | | bloodstream | host compartment | label-only | Iron-rich but complement-exposed systemic niche. | | intracellular pathogen-containing compartment | localization | label-only | Relevant to *Salmonella*, *Legionella*, *Chlamydia*, and mycobacteria. | | low iron / nutritional immunity | host environmental factor | label-only | Host sequestration of Fe and other metals. | | urea-rich urinary tract | host environmental factor | label-only | Relevant to urease-positive urinary pathogens. | | anaerobiosis | environmental factor | **ENVO term to verify** | Induces formate-hydrogenlyase-associated genes in *Proteus*. | | elevated host glucose | environmental factor | label-only | Contextual risk factor; affects both host immunity and pathogen physiology. |
Discussions and Knowledge Gaps
This record routes two independent paths to immune evasion -- complement-regulator binding by surface proteins, and effector delivery through the T3SS. In a given host, is either route sufficient on its own, or does established infection require both?
The graph draws both arrows into the same node without saying whether they are alternatives or partners. If either is sufficient, single-target antivirulence strategies are viable; if evasion needs both, only combination approaches will work, and the two edges should carry that dependency rather than reading as parallel routes.
Proposed experiments
- Isogenic single- and double-mutant serum and phagocyte survival isogenic mutant panel with ex vivo killing assays
Provenance
Curation history
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SEEDED_FROM_METPO · seed_from_metpo
imported from data/raw/metpo.owl (CLASS)
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CURATED_CAUSAL_GRAPH · claude
Added DOI-backed causal graph linking metazoan-adapted virulence factors, immune evasion, animal tissue colonization, and disease to the animal-pathogen trait.
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GROUND_CAUSAL_PREDICATES · claude
Grounded 1 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (RO:0002327×1).
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GROUND_CAUSAL_PREDICATES · claude
Grounded 1 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (biolink:causes×1).
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GROUND_CAUSAL_PREDICATES · claude
Grounded 1 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (METPO:2007400×1).
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RENAME_PREDICATE_LABELS · claude
Renamed 1 causal-edge predicate label(s) to align with existing groundings: supports → enables ×1.
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GROUND_CAUSAL_PREDICATES · claude
Grounded 1 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (RO:0002327×1).
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REMOVE_REDUNDANT_SYNONYM · claude
Removed 1 synonym(s) whose text duplicated the label (seeder redundancy; no information lost).
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ENRICH_CAUSAL_GRAPH · claude
Added 11 evidence-backed generic edges (12 new nodes) from the deep-research report.
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GROUND_CAUSAL_PREDICATES · claude
Grounded 10 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (RO:0002327×10).
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GROUND_CAUSAL_NODES · claude
Grounded 1 causal-node grounding field(s) via mappings/node_grounding.tsv (GO:0043684×1).
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CURATE_KNOWLEDGE_GAPS · claude
Replaced the scan's off-topic scraped sentence with a research question authored from this record's causal graph, anchored it via attaches_to, and sketched an experiment with a decision criterion. The scan's sentence and PMIDs are preserved in the discussion's notes.