animal pathogen

METPO:1004002 · CLASS · REVIEWED

A pathogen that infects organisms in the kingdom Metazoa.

Animal-pathogen metazoan host adaptation

DOI-backed graph linking metazoan-adapted virulence factors, immune-evasion strategies, and animal-tissue colonization to the animal-pathogen phenotype.

Animal-pathogen metazoan host adaptation Interactive directed graph showing evidence-backed causal relationships for animal pathogen.

Edge evidence

  • metazoan-adapted virulence factors enables animal tissue colonization RO:0002327

    Metazoan-adapted virulence factors enable adhesion and invasion of animal tissues.

    • DOI:10.1146/annurev.micro.62.081307.162938 virulence factors Supports virulence factors as enablers of animal tissue colonization.
  • immune evasion enables animal tissue colonization RO:0002327

    Immune evasion supports sustained colonization despite host defenses.

    • DOI:10.1038/nrmicro1592 secretion systems Supports effector-delivery-based immune evasion in animal pathogens.
  • animal tissue colonization causes animal disease biolink:causes

    Established colonization in animal tissues causes disease.

    • DOI:10.1146/annurev.micro.62.081307.162938 virulence factors Supports colonization-to-disease progression in animal hosts.
  • animal disease manifests as animal pathogen METPO:2007400

    Animal disease manifests the animal-pathogen trait.

    • DOI:10.1146/annurev.micro.62.081307.162938 virulence factors Supports the trait endpoint.
  • bacterial adhesins enables attachment to host cells and mucosa RO:0002327

    Bacterial adhesins enable attachment to host cells, extracellular matrix, and mucosa.

    • DOI:10.1093/femsre/fuae019 Expression of bacterial surface adhesins is critical for adherence to host tissues; common colonization mechanism across body sites.
  • attachment to host cells and mucosa enables animal tissue colonization RO:0002327

    Attachment to host surfaces initiates colonization of metazoan barrier sites.

    • DOI:10.1093/femsre/fuae019 Colonization of metazoan barrier sites commonly begins with adhesion to host surfaces.
  • complement-regulator-binding surface proteins mediates complement evasion

    Surface proteins binding host complement regulators (factor H, C4BP) mediate complement evasion.

    • DOI:10.1093/femsre/fuae019 Surface proteins in diverse bacterial pathogens bind fH and C4BP to mediate evasion of complement proteins.
  • complement evasion enables immune evasion RO:0002327

    Complement evasion contributes to overall evasion of host immunity.

    • DOI:10.1093/femsre/fuae019 Complement evasion is a major determinant shaping immune resistance in animal pathogens.
  • type III secretion system enables effector delivery into host-cell cytoplasm RO:0002327

    T3SS injectisomes deliver effector proteins directly into the host-cell cytoplasm.

    • DOI:10.1128/spectrum.02224-23 T3SSs form syringe-like structures allowing effector proteins to be delivered from bacteria into the host-cell cytoplasm.
  • effector delivery into host-cell cytoplasm enables immune evasion RO:0002327

    T3SS effector delivery modulates host cells and supports immune evasion.

    • DOI:10.1128/spectrum.02224-23 Effector delivery into host cytoplasm is a canonical virulence mechanism subverting host defenses.
  • type IV secretion system enables effector/toxin translocation into target cells RO:0002327

    T4SS nanomachines translocate protein effectors or toxins into target cells.

    • DOI:10.1038/s41579-023-00974-3 Many T4SSs have acquired functionalities relating to translocation of effector proteins or toxins, supporting host-pathogen interactions.
  • effector/toxin translocation into target cells enables animal tissue colonization RO:0002327

    T4SS effector/toxin translocation supports host-pathogen interactions and colonization.

    • DOI:10.1038/s41579-023-00974-3 T4SSs are versatile nanomachines central to host-pathogen interactions.
  • low-iron host environment enables siderophore biosynthesis gene expression RO:0002327

    Low iron derepresses Fur, enabling siderophore biosynthesis gene expression.

    • DOI:10.1039/d4cb00175c When iron decreases, Fur releases Fe2+ allowing siderophore biosynthesis gene expression.
  • TonB-dependent transporters enables siderophore-Fe3+ complex import RO:0002327

    TonB-dependent transporters import siderophore-Fe3+ complexes into the periplasm.

    • DOI:10.1039/d4cb00175c Siderophore-Fe3+ complexes are imported via TonB-dependent transporters into the periplasm.
  • siderophore-Fe3+ complex import enables animal tissue colonization RO:0002327

    Iron acquisition via siderophore uptake supports growth in iron-restricted host tissues.

    • DOI:10.1039/d4cb00175c Iron scavenging uptake is central to nutrient acquisition in host environments.

Provenance

Source
METPO (2025-11-25)
Definition source
DOI:10.1146/annurev.micro.62.081307.162938

kg-microbe context

Matched 1 kg-microbe node via direct_metpo.

  • METPO:1004002 [-1.564, -64.092, -0.620, -28.964, …]

512-dim DeepWalkSkipGramEnsmallen embedding from kg-microbe (2026-04-25).

Nearest neighbors in embedding space

Top-8 cosine-similar METPO traits from the 2026-04-25 deepwalk (512-D).

Deep research

Generated by just research-trait; source: research/traits/ecology/animal_pathogen-deep-research-falcon.md

Unreviewed literature output — not curated TraitMech content Ontology identifiers suggested below have not been resolved against their ontologies, and some are known to be wrong. Check any CURIE against the source before using it.
# 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. |

Showing the first 60 of 253 lines of findings; the linked file also carries the run's front matter and the prompt it was given — read the full report.

Discussions and Knowledge Gaps (1)

Open questions attached to this trait. Seeded by just knowledge-gap-scan and curated; see the corpus-wide index.

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?

KNOWLEDGE GAP OPEN kgscan-30bcdf4a32b0 · raised by claude · 2026-08-17

Attached to causal_graphs#immune_evasion

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 Model systems: isolate of a T3SS-bearing animal pathogen, naive host serum, primary phagocytes from the same host species Perturbations: deletion of the complement-regulator binding protein, deletion of the T3SS structural apparatus, the double deletion Readouts: survival in non-heat-inactivated serum, intracellular survival after phagocyte challenge, surface-bound complement regulator by flow cytometry Decides it: whether either single mutant is attenuated to the same degree as the double mutant Supports if: single mutants retain near-wild-type survival and only the double is attenuated -- the routes are independently sufficient Refutes if: either single mutant is attenuated as severely as the double -- the routes are not redundant and evasion requires both
Provenance

Scan provenance (#409). The kg-microbe-kgscan pass raised this discussion with the prompt 'Knowledge gap for animal pathogen: Prokaryotes in such plastispheres are unknown to date.', whose sentence came from PMID:40891913. That sentence is about prokaryotes of marine plastispheres, not about this trait: the scan matched the hedging vocabulary of a gap statement without checking that the gap was about the trait it was filed under. The prompt above was authored instead from this record's own causal graph, and none of these references are carried as its evidence, because they support the scraped sentence rather than the question. The scan attached 3 further references whose snippets concern neither that sentence nor this trait; all 4 are reproduced here so nothing it produced is lost: PMID:40891913 'Prokaryotes in such plastispheres are unknown to date.'; PMID:42279816 'However, in South America, their use is still limited because of complicated regulations and inconsistent evidence requirements.'; PMID:41639266 'However, the interacting effects of climate factors and seasonal variations in nutritional components on PMCs remain poorly understood.'; PMID:42197358 'While plant growth-promoting bacteria (PGPB) are known to alleviate heavy metal toxicity, their role under MP-HM co-contamination and the differential responses of rhizosphere microbial communities remain unclear.'.

Curation history

  1. · SEEDED_FROM_METPO · seed_from_metpo

    imported from data/raw/metpo.owl (CLASS)

  2. · 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.

  3. · GROUND_CAUSAL_PREDICATES · claude

    Grounded 1 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (RO:0002327×1).

  4. · GROUND_CAUSAL_PREDICATES · claude

    Grounded 1 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (biolink:causes×1).

  5. · GROUND_CAUSAL_PREDICATES · claude

    Grounded 1 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (METPO:2007400×1).

  6. · RENAME_PREDICATE_LABELS · claude

    Renamed 1 causal-edge predicate label(s) to align with existing groundings: supports → enables ×1.

  7. · GROUND_CAUSAL_PREDICATES · claude

    Grounded 1 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (RO:0002327×1).

  8. · REMOVE_REDUNDANT_SYNONYM · claude

    Removed 1 synonym(s) whose text duplicated the label (seeder redundancy; no information lost).

  9. · ENRICH_CAUSAL_GRAPH · claude

    Added 11 evidence-backed generic edges (12 new nodes) from the deep-research report.

  10. · GROUND_CAUSAL_PREDICATES · claude

    Grounded 10 causal-edge predicate_id field(s) via mappings/predicate_grounding.tsv (RO:0002327×10).

  11. · GROUND_CAUSAL_NODES · claude

    Grounded 1 causal-node grounding field(s) via mappings/node_grounding.tsv (GO:0043684×1).

  12. · 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.