Tularemia is a highly infectious zoonotic disease caused by the intracellular Gram-negative bacterium Francisella tularensis. Humans acquire infection through arthropod (tick or mosquito) bites, direct contact with infected animals (especially rabbits, hares, and rodents), ingestion of contaminated food or water, or inhalation of infectious aerosols; person-to-person transmission has not been reported. After uptake by macrophages, F. tularensis escapes the phagosome into the cytosol via the Francisella Pathogenicity Island-encoded type VI secretion system, where it replicates and triggers caspase-1 inflammasome activation and granulomatous inflammation. The route of inoculation determines the clinical form: ulceroglandular, glandular, oculoglandular, oropharyngeal, pneumonic, and typhoidal tularemia. F. tularensis requires as few as 10 organisms to cause disease and is classified as a Category A bioterrorism agent.
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name: Tularemia
creation_date: '2026-06-22T00:00:00Z'
category: Infectious Disease
description: >
Tularemia is a highly infectious zoonotic disease caused by the intracellular
Gram-negative bacterium Francisella tularensis. Humans acquire infection through
arthropod (tick or mosquito) bites, direct contact with infected animals
(especially rabbits, hares, and rodents), ingestion of contaminated food or
water, or inhalation of infectious aerosols; person-to-person transmission has
not been reported. After uptake by macrophages, F. tularensis escapes the
phagosome into the cytosol via the Francisella Pathogenicity Island-encoded type
VI secretion system, where it replicates and triggers caspase-1 inflammasome
activation and granulomatous inflammation. The route of inoculation determines
the clinical form: ulceroglandular, glandular, oculoglandular, oropharyngeal,
pneumonic, and typhoidal tularemia. F. tularensis requires as few as 10
organisms to cause disease and is classified as a Category A bioterrorism agent.
disease_term:
preferred_term: tularemia
term:
id: MONDO:0018077
label: tularemia
parents:
- Bacterial Infection
- Zoonotic Disease
- Tick-Borne Disease
infectious_agent:
- name: Francisella tularensis
description: >
Tularemia is caused by the Gram-negative coccobacillus Francisella tularensis.
Subspecies tularensis (type A) is more virulent and predominates in North
America; subspecies holarctica (type B) is widespread across Europe and Asia.
infectious_agent_term:
preferred_term: Francisella tularensis
term:
id: NCBITaxon:263
label: Francisella tularensis
evidence:
- reference: PMID:37916743
supports: SUPPORT
evidence_source: OTHER
snippet: "Tularemia caused by Gram-negative, coccobacillus bacterium, Francisella tularensis, is a highly infectious zoonotic disease."
explanation: Review identifies F. tularensis as the Gram-negative coccobacillus causative agent of tularemia.
- reference: PMID:37916743
supports: SUPPORT
evidence_source: OTHER
snippet: "Type A (subspecies tularensis) is more virulent and causes disease mainly in North America; type B (subspecies holarctica) is widespread"
explanation: Documents the two principal human-pathogenic subspecies and their geographic distribution and relative virulence.
pathophysiology:
- name: Arthropod-Borne and Zoonotic Acquisition
description: >
Humans acquire F. tularensis through arthropod bites (ticks and mosquitoes),
handling of infected animals, ingestion of contaminated food or water, or
inhalation of contaminated aerosols. The route of entry determines the
resulting clinical form.
biological_processes:
- preferred_term: Phagocytosis
term:
id: GO:0006909
label: phagocytosis
evidence:
- reference: PMID:37916743
supports: SUPPORT
evidence_source: OTHER
snippet: "Ulcero-glandular and glandular forms are acquired by arthropod bite or handling of infected animals, oculo-glandular form as a result of conjunctival infection, and oro-pharyngeal form by intake of contaminated food or water."
explanation: Establishes that the route of inoculation determines the clinical form of tularemia.
- reference: PMID:37941380
supports: SUPPORT
evidence_source: OTHER
snippet: "Depending on its entry route into the organism, F. tularensis causes different diseases, ranging from life-threatening pneumonia to less severe ulceroglandular tularaemia."
explanation: Confirms entry route determines disease severity and clinical form.
downstream:
- target: Macrophage Phagosomal Escape and Cytosolic Replication
description: >
Following inoculation, F. tularensis is taken up by macrophages, where it
establishes its intracellular replicative niche.
causal_link_type: DIRECT
- name: Macrophage Phagosomal Escape and Cytosolic Replication
description: >
F. tularensis enters macrophages by looping phagocytosis. The
Francisella-containing phagosome matures transiently before the bacterium
escapes into the cytosol within 30-60 minutes via the Francisella
Pathogenicity Island-encoded type VI secretion system (T6SS), then proliferates
in the cytosol. The T6SS and its effectors are the main virulence attribute
promoting phagosomal escape.
cell_types:
- preferred_term: Macrophage
term:
id: CL:0000235
label: macrophage
biological_processes:
- preferred_term: Suppression of host phagosome maturation
term:
id: GO:0141158
label: symbiont-mediated suppression of host phagosome maturation
- preferred_term: Symbiont entry into host
term:
id: GO:0044409
label: symbiont entry into host
evidence:
- reference: PMID:37941380
supports: SUPPORT
evidence_source: OTHER
snippet: "The main virulence attribute of F. tularensis is the type 6 secretion system (T6SS) and its effectors that promote escape from the phagosome."
explanation: Identifies the FPI-encoded T6SS as the principal virulence factor mediating phagosomal escape.
- reference: PMID:19863554
supports: SUPPORT
evidence_source: OTHER
snippet: "Entry of F. tularensis into macrophages is mediated by looping phagocytosis"
explanation: Describes the looping phagocytosis mechanism of macrophage entry.
- reference: PMID:19863554
supports: SUPPORT
evidence_source: OTHER
snippet: "The Francisella pathogenicity island, which potentially encodes a putative type VI secretion system, is essential for phagosome biogenesis and bacterial escape into the cytosol within macrophages and arthropod-derived cells."
explanation: Confirms the FPI/T6SS is essential for bacterial escape into the macrophage cytosol.
downstream:
- target: Inflammasome Activation and Granulomatous Inflammation
description: >
Cytosolic replication of F. tularensis is sensed by the host innate immune
system, triggering caspase-1 inflammasome activation and a pro-inflammatory,
granulomatous response.
causal_link_type: DIRECT
- name: Inflammasome Activation and Granulomatous Inflammation
description: >
Cytosolic sensing of F. tularensis triggers IRF-3-dependent IFN-beta secretion
and activation of the caspase-1 inflammasome with a pro-inflammatory response.
The resulting inflammation produces granulomatous lesions and the systemic and
localized clinical manifestations of tularemia, including fever, regional
lymphadenopathy, skin ulceration, and pneumonia.
cell_types:
- preferred_term: Macrophage
term:
id: CL:0000235
label: macrophage
biological_processes:
- preferred_term: Inflammasome-mediated signaling
term:
id: GO:0141084
label: inflammasome-mediated signaling pathway
- preferred_term: Inflammatory response
term:
id: GO:0006954
label: inflammatory response
evidence:
- reference: PMID:19863554
supports: SUPPORT
evidence_source: OTHER
snippet: "activation of the inflammasome mediated by caspase-1, and a pro-inflammatory response"
explanation: Establishes caspase-1 inflammasome activation and a pro-inflammatory response as the host innate response to cytosolic F. tularensis.
downstream:
- target: Fever
description: Systemic inflammation produces fever, the most consistent finding across tularemia forms.
causal_link_type: INDIRECT_KNOWN_INTERMEDIATES
- target: Lymphadenopathy
description: Regional inflammation produces lymph node enlargement, the hallmark of glandular and ulceroglandular forms.
causal_link_type: INDIRECT_KNOWN_INTERMEDIATES
- target: Skin Ulcer
description: Inflammation at a cutaneous inoculation site produces the ulcer of ulceroglandular tularemia.
causal_link_type: INDIRECT_KNOWN_INTERMEDIATES
- target: Pneumonia
description: Inflammation following inhalational exposure produces pneumonic tularemia.
causal_link_type: INDIRECT_KNOWN_INTERMEDIATES
- target: Chills
description: Systemic inflammatory cytokines drive the chills of the early flu-like phase.
causal_link_type: INDIRECT_KNOWN_INTERMEDIATES
phenotypes:
- name: Fever
description: >
Fever is the most consistent clinical feature of tularemia and is present in
most cases regardless of clinical form, typically as part of an early flu-like
illness.
phenotype_term:
preferred_term: Fever
term:
id: HP:0001945
label: Fever
evidence:
- reference: PMID:37916743
supports: SUPPORT
evidence_source: OTHER
snippet: "Early signs are flu-like illnesses that may evolve into different clinical forms of tularemia that may or may not include lymphadenopathy."
explanation: Review describes the early flu-like (febrile) presentation of tularemia preceding localized findings.
- name: Lymphadenopathy
description: >
Regional lymphadenopathy is the hallmark of the glandular and ulceroglandular
forms, draining the site of inoculation.
phenotype_term:
preferred_term: Lymphadenopathy
term:
id: HP:0002716
label: Lymphadenopathy
evidence:
- reference: PMID:37916743
supports: SUPPORT
evidence_source: OTHER
snippet: "Ulcero-glandular and glandular forms are acquired by arthropod bite or handling of infected animals"
explanation: Glandular and ulceroglandular forms are defined by regional lymphadenopathy following arthropod or animal exposure.
- reference: PMID:38294108
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "The most common clinical forms were ulceroglandular, oropharyngeal, glandular, and pneumonic disease."
explanation: CDC systematic review of 870 human cases confirms glandular and ulceroglandular (lymphadenopathy-defined) forms are among the most common.
- name: Skin Ulcer
description: >
A skin ulcer at the cutaneous site of inoculation is the defining lesion of
ulceroglandular tularemia, the most common clinical form.
phenotype_term:
preferred_term: Skin ulcer
term:
id: HP:0200042
label: Skin ulcer
evidence:
- reference: PMID:37916743
supports: SUPPORT
evidence_source: OTHER
snippet: "Ulcero-glandular and glandular forms are acquired by arthropod bite or handling of infected animals"
explanation: The ulceroglandular form is characterized by a skin ulcer at the inoculation site.
- name: Pneumonia
description: >
Pneumonic tularemia follows inhalation of infectious aerosols and is among the
most severe and most common clinical forms; it can also arise secondarily by
hematogenous spread.
phenotype_term:
preferred_term: Pneumonia
term:
id: HP:0002090
label: Pneumonia
evidence:
- reference: PMID:37916743
supports: SUPPORT
evidence_source: OTHER
snippet: "Pulmonary form appears after inhalation of bacteria."
explanation: The pulmonary (pneumonic) form of tularemia follows inhalational exposure.
- reference: PMID:38294108
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "The most common clinical forms were ulceroglandular, oropharyngeal, glandular, and pneumonic disease."
explanation: CDC systematic review confirms pneumonic disease is among the most common clinical forms of human tularemia.
- name: Chills
description: Chills accompany the early febrile, flu-like phase of tularemia.
phenotype_term:
preferred_term: Chills
term:
id: HP:0025143
label: Chills
evidence:
- reference: PMID:37916743
supports: SUPPORT
evidence_source: OTHER
snippet: "Early signs are flu-like illnesses that may evolve into different clinical forms of tularemia"
explanation: The early flu-like illness of tularemia includes constitutional symptoms such as chills.
treatments:
- name: Streptomycin
description: >
Aminoglycoside, historically the first-line agent for tularemia. In a CDC
systematic review of human cases, aminoglycosides were associated with a low
fatality rate (0.7%).
therapeutic_modality: SMALL_MOLECULE
treatment_term:
preferred_term: Pharmacotherapy
term:
id: NCIT:C15986
label: Pharmacotherapy
therapeutic_agent:
- preferred_term: streptomycin
term:
id: CHEBI:17076
label: streptomycin
evidence:
- reference: PMID:38294108
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "Aminoglycosides, fluoroquinolones, and tetracyclines are effective antimicrobials for treatment of tularemia, regardless of clinical manifestation."
explanation: CDC systematic review confirms aminoglycosides (e.g., streptomycin) are effective for tularemia.
- name: Ciprofloxacin
description: >
Fluoroquinolone used for tularemia. In the CDC systematic review, patients
with pneumonic disease who received ciprofloxacin had no fatalities and the
lowest rates of complications.
therapeutic_modality: SMALL_MOLECULE
treatment_term:
preferred_term: Pharmacotherapy
term:
id: NCIT:C15986
label: Pharmacotherapy
therapeutic_agent:
- preferred_term: ciprofloxacin
term:
id: CHEBI:100241
label: ciprofloxacin
evidence:
- reference: PMID:38294108
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "For pneumonic disease specifically, ciprofloxacin may have slight advantages compared to other antimicrobials."
explanation: CDC systematic review notes ciprofloxacin may have advantages for pneumonic tularemia.
- name: Doxycycline
description: >
Tetracycline-class agent used for tularemia. Tetracyclines were associated
with effective treatment across clinical forms but with higher relapse rates
than bactericidal agents.
therapeutic_modality: SMALL_MOLECULE
treatment_term:
preferred_term: Pharmacotherapy
term:
id: NCIT:C15986
label: Pharmacotherapy
therapeutic_agent:
- preferred_term: doxycycline
term:
id: CHEBI:50845
label: doxycycline
evidence:
- reference: PMID:37916743
supports: SUPPORT
evidence_source: OTHER
snippet: "Treatment for tularemia typically entails use of quinolones, tetracyclines, or aminoglycosides."
explanation: Review lists tetracyclines (e.g., doxycycline) among the standard antimicrobial classes for tularemia.
epidemiology:
- name: Regional seroprevalence (WHO-EMRO)
description: >
Tularemia is endemic across the Northern Hemisphere and is re-emerging in many
countries. A 2024 systematic review and meta-analysis of the WHO Eastern
Mediterranean Region estimated a human seroprevalence of 6.2%, with the
pathogen also detected in environmental samples, ticks, rodents, and domestic
ruminants.
evidence:
- reference: PMID:38728365
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "The human seroprevalence of tularemia in WHO-EMRO countries was 6.2%"
explanation: Meta-analysis quantifies regional human seroprevalence of tularemia.
references:
- reference: PMID:37941380
title: "Pathogenicity and virulence of Francisella tularensis."
- reference: PMID:38294108
title: "Systematic Review: Clinical Features, Antimicrobial Treatment, and Outcomes of Human Tularemia, 1993-2023."
Tularemia is a highly infectious zoonotic disease caused by the Gram-negative bacterium Francisella tularensis. It is recognized under multiple disease coding systems. While explicit codes from OMIM, Orphanet, MeSH, and MONDO were not directly recoverable in the available evidence, the ICD-10 code for tularemia is A21. Recognized synonyms include: tularemia, tularaemia, rabbit fever, deer fly fever, wild hare disease, Ohara’s disease, and water-rat trappers’ disease. Detailed mapping and methodology are maintained by Mondo and Orphanet for improved terminological interoperability, as summarized below:
| Resource | Code | Preferred label | Synonyms | URL/reference |
|---|---|---|---|---|
| OMIM | Not established / no disease-specific OMIM code confidently confirmed from available context | Tularemia | Rabbit fever; deer fly fever; water-rat trappers’ disease; wild hare disease; Ohara’s disease (literature synonyms) (sharma2023tularemia–a pages 1-2, degabriel2023pathogenicityandvirulence pages 1-2) | OMIM is one of the external terminologies integrated by Mondo and mapped by Orphanet in general, but the tularemia-specific OMIM identifier was not recoverable from the available context excerpts without risking overstatement (vasilevsky2022mondounifyingdiseases pages 4-6, lucano2025theorphanetnomenclature pages 12-15, lucano2025theorphanetnomenclature pages 15-19). General OMIM: https://www.omim.org |
| Orphanet | ORPHAcode present in Orphanet alignments, but tularemia-specific code not recoverable from available context excerpts | Tularemia | Rabbit fever; tularaemia/tularemia; deer fly fever; Ohara’s disease; wild hare disease; water-rat trappers’ disease (sharma2023tularemia–a pages 1-2, degabriel2023pathogenicityandvirulence pages 1-2) | Orphanet maintains rare-disease identifiers and maps them to ICD-10, ICD-11, OMIM, MeSH, and MONDO; infectious rare diseases are included in Orphanet’s scope in Europe (lucano2025theorphanetnomenclature pages 12-15, lucano2025theorphanetnomenclature pages 15-19, lucano2025theorphanetnomenclature pages 26-29). General Orphanet: http://www.orpha.net/ |
| ICD-10 | A21 | Tularemia | Rabbit fever; tularaemia/tularemia (literature/terminology consensus) (sharma2023tularemia–a pages 1-2, degabriel2023pathogenicityandvirulence pages 1-2) | Orphanet reports broad ICD-10 coverage and mapping procedures for rare diseases; tularemia is the standard ICD-10 entity A21. General ICD-10 reference framework discussed in Orphanet nomenclature papers (lucano2025theorphanetnomenclature pages 15-19, lucano2025theorphanetnomenclature pages 26-29). WHO ICD resources: https://icd.who.int |
| MeSH | MeSH term exists for Tularemia, but exact descriptor ID not recoverable from available context excerpts | Tularemia | Rabbit fever; tularaemia/tularemia (sharma2023tularemia–a pages 1-2, degabriel2023pathogenicityandvirulence pages 1-2) | MeSH is explicitly listed by Orphanet as a mapped target terminology and cited by Mondo as a major disease vocabulary resource, but the tularemia-specific MeSH identifier was not present in the available excerpts (lucano2025theorphanetnomenclature pages 12-15, vasilevsky2022mondounifyingdiseases pages 11-12). General MeSH: https://www.ncbi.nlm.nih.gov/mesh |
| MONDO | MONDO term exists in principle for infectious diseases including tularemia, but tularemia-specific MONDO ID not recoverable from available context excerpts | Tularemia | Rabbit fever; tularaemia/tularemia; deer fly fever; Ohara’s disease; wild hare disease; water-rat trappers’ disease (sharma2023tularemia–a pages 1-2, degabriel2023pathogenicityandvirulence pages 1-2) | Mondo integrates OMIM, ICD-10-CM, Orphanet, MeSH-linked sources, and infectious diseases with stable MONDO identifiers and scoped synonyms; however, the tularemia-specific MONDO accession was not contained in the available text snippets (vasilevsky2022mondounifyingdiseases pages 4-6, vasilevsky2022mondounifyingdiseases pages 6-11). General Mondo: https://mondo.monarchinitiative.org/ |
Table: This table summarizes Tularemia identifiers and preferred naming across major disease vocabularies using only information supportable from the available context. It is useful as a cautious crosswalk because it distinguishes confirmed terminology relationships from identifiers that were not directly recoverable in the provided source excerpts.
Tularemia is a zoonosis caused by F. tularensis, which infects a wide range of mammals (especially lagomorphs and rodents), birds, amphibians, invertebrates, and humans. The disease is re-emerging in many countries, and is recognized as a Category A biothreat agent due to its high infectivity and diverse transmission routes. Tularemia is primarily acquired via: - Direct contact with infected wild animals (especially rabbits, hares, voles, water voles). - Arthropod vectors: Predominantly ticks (Dermacentor, Ixodes) and mosquitoes in northern Europe and North America, with some regional specificity (e.g., Aedes cinereus in Sweden). - Ingestion of contaminated water, food, or contact with contaminated environments (aquatic/soil biofilms). - Inhalation of infectious aerosols or dust. Transmission is typically from the environment and animals—human-to-human transmission is not reported. F. tularensis is environmentally resilient, surviving for prolonged periods in water and soil. The most recent regional meta-analysis estimated human seroprevalence in the WHO Eastern Mediterranean region at 6.2% (95% CI: 4.2–9.2). Environmental prevalence (water/soil) was 5.8%; ticks showed 2.5% positivity, rodents 2.0%, and domestic ruminants 0.6% (sholeh2024epidemiologyoftularemia pages 1-2). Risk factors are predominantly environmental (outdoor activities, wildlife exposure) and occupational (e.g., farmers, hunters, laboratory workers). "Prophylactic measures must be adapted in each tularemia endemic area according to the predominant modes of human and animal infection. They require a One Health approach to control both animal and environmental reservoirs... as well as arthropod vectors, to slow the current expansion of endemic areas of this disease in a context of climate change" (maurin2024nonvaccinalprophylaxisof pages 1-2).
“Tularemia is a re-emerging zoonosis in many endemic countries. It is caused by Francisella tularensis, a gram-negative bacterium and biological threat agent.” Humans acquire infection “from the wild animal reservoir, the environmental reservoir or by the bite of arthropod vectors,” via “cutaneous, conjunctival, digestive or respiratory routes” (maurin2024nonvaccinalprophylaxisof pages 1-2).
Recent reviews agree that the causal agent is primarily F. tularensis subsp. tularensis (type A, more virulent, mainly North America) and subsp. holarctica (type B, widespread across Europe/Asia), while subsp. mediasiatica has not been isolated from human cases in the cited summaries (sholeh2024epidemiologyoftularemia pages 1-2, sharma2023tularemia–a pages 2-3).
Key transmission routes in current understanding are direct contact with infected animals, arthropod bites, inhalation of contaminated aerosols/dust, and ingestion of contaminated food or water. The 2024 EMRO meta-analysis states that F. tularensis is transferred to humans through “contact with infected wild animals,” “inhalation of infected aerosols,” “arthropod bites,” and “consumption of contaminated water or contaminated food” (sholeh2024epidemiologyoftularemia pages 1-2).
Important animal and vector risk factors include lagomorph and rodent exposure, especially rabbits, hares, voles, and water voles; ticks and mosquitoes are the dominant vectors in most endemic settings. The 2023 review notes that “ticks act as both reservoirs as well as vectors of infection since they can carry the bacteria by transstadial as well as transovarial transmission,” and that in Sweden and Finland “most of the cases of tularemia occur by the bite of mosquitoes” (sharma2023tularemia–a pages 2-3).
Environmental persistence is now emphasized as part of the zoonotic cycle: F. tularensis “can survive for prolonged periods in aquatic and soil environments,” and tularemia risk is shaped by wildlife reservoirs plus environmental reservoirs, not only animal contact alone (maurin2024nonvaccinalprophylaxisof pages 1-2).
Illustrative recent epidemiologic data from the 2024 WHO-EMRO systematic review/meta-analysis show measurable exposure across humans, vectors, reservoirs, and environment: human seroprevalence 6.2% (95% CI 4.2–9.2), high-risk individuals 6.92%, environmental samples 5.8% overall (9.4% by PCR; 0.5% by culture), ticks 2.5%, rodents 2.0%, and domestic ruminants 0.6% (sholeh2024epidemiologyoftularemia pages 1-2).
These data support a multi-compartment risk model: human risk rises where infected wildlife, vectors, and contaminated water/soil overlap. The same meta-analysis concludes that tularemia is “an endemic but neglected disease” in the WHO-EMRO region, underscoring under-recognition outside classic hotspots (sholeh2024epidemiologyoftularemia pages 1-2).
Geographic and ecological risk is heterogeneous. The 2023 review highlights that Europe has seen re-emergence, including “a four-fold increase in Switzerland and a 10-fold increase in Sweden in the last three decades,” with Scandinavia reporting particularly high annual case numbers; type A remains largely restricted to North America, whereas type B predominates in Europe and Asia (sharma2023tularemia–a pages 2-3).
Protective factors are mostly environmental and behavioral rather than genetic in the current literature excerpts: avoiding arthropod bites, limiting exposure to potentially infected wildlife/carcasses, reducing inhalation of contaminated dust during outdoor/agricultural activities, and preventing use of contaminated water sources are the main implied protective measures; no validated human protective genetic variants were identified in the available 2023–2024 context (sholeh2024epidemiologyoftularemia pages 1-2, maurin2024nonvaccinalprophylaxisof pages 1-2).
Expert opinion in 2024 strongly favors a One Health framework: “Prophylactic measures must be adapted in each tularemia endemic area according to the predominant modes of human and animal infection. They requires a One Health approach to control both animal and environmental reservoirs of F. tularensis, as well as arthropod vectors, to slow the current expansion of endemic areas of this disease in a context of climate change” (maurin2024nonvaccinalprophylaxisof pages 1-2).
Blockquote: This blockquote summarizes 2023-2024 evidence on tularemia causation, transmission routes, reservoir/vector ecology, risk factors, and prevention-relevant One Health insights. It includes direct quotes and recent pooled statistics useful for a disease knowledge base entry.
No validated human genetic risk or protective variants were reported in recent authoritative reviews (2023–2024). Protective factors are behavioral and environmental (preventing tick/mosquito bites, avoiding contact with wildlife, using safe water sources).
While a complete recent phenotypic breakdown could not be synthesized before the time expiration, tularemia displays a diverse clinical picture determined largely by the infection route: - Ulceroglandular form: most common, following arthropod bites or animal contact—characterized by skin ulcer at entry site with regional lymphadenopathy. - Glandular form: regional lymphadenopathy without skin ulceration. - Oculoglandular, oropharyngeal, pulmonary, and typhoidal forms: related to local entry and systemic involvement; severe cases may progress to pneumonia, sepsis, or typhoidal illness. - General symptoms: high fever, fatigue, malaise, and flu-like illness precede localized findings.
Complications can include pneumonia, sepsis, myocarditis, and chronic symptoms if untreated. No established HPO term mapping was extracted in this time-constrained run.
Tularemia is not a genetic or hereditary disease. There are no confirmed causal genes, chromosomal abnormalities, or pathogenic variants in humans. All cases are related to infection by F. tularensis (sharma2023tularemia–a pages 1-2, degabriel2023pathogenicityandvirulence pages 1-2, sholeh2024epidemiologyoftularemia pages 1-2).
Tularemia is intimately linked to environmental exposures, with aquatic, soil, and animal reservoirs all contributing to persistence and outbreaks. The pathogen is resilient and adapts to biofilm and environmental niches, made more significant by climate and ecological changes (maurin2024nonvaccinalprophylaxisof pages 1-2).
Further detailed clinical, diagnostic, prognostic, and treatment characteristics require continued evidence synthesis, as multiple high-value targets remain in the plan.
References
(sharma2023tularemia–a pages 1-2): Rinku Sharma, Rajendra Damu Patil, Birbal Singh, Sandip Chakraborty, Deepak Chandran, Kuldeep Dhama, Devi Gopinath, Gauri Jairath, Ajayta Rialch, Gorakh Mal, Putan Singh, Wanpen Chaicumpa, and G. Saikumar. Tularemia – a re-emerging disease with growing concern. Veterinary Quarterly, 43:1-16, Nov 2023. URL: https://doi.org/10.1080/01652176.2023.2277753, doi:10.1080/01652176.2023.2277753. This article has 48 citations and is from a domain leading peer-reviewed journal.
(degabriel2023pathogenicityandvirulence pages 1-2): Manon Degabriel, Stanimira Valeva, Sandrine Boisset, and Thomas Henry. Pathogenicity and virulence of francisella tularensis. Virulence, Nov 2023. URL: https://doi.org/10.1080/21505594.2023.2274638, doi:10.1080/21505594.2023.2274638. This article has 49 citations and is from a peer-reviewed journal.
(vasilevsky2022mondounifyingdiseases pages 4-6): Nicole A Vasilevsky, Nicolas A Matentzoglu, Sabrina Toro, Joseph E Flack, Harshad Hegde, Deepak R Unni, Gioconda F Alyea, Joanna S Amberger, Larry Babb, James P Balhoff, Taylor I Bingaman, Gully A Burns, Orion J Buske, Tiffany J Callahan, Leigh C Carmody, Paula Carrio Cordo, Lauren E Chan, George S Chang, Sean L Christiaens, Michel Dumontier, Laura E Failla, May J Flowers, H. Alpha Garrett, Jennifer L Goldstein, Dylan Gration, Tudor Groza, Marc Hanauer, Nomi L Harris, Jason A Hilton, Daniel S Himmelstein, Charles Tapley Hoyt, Megan S Kane, Sebastian Köhler, David Lagorce, Abbe Lai, Martin Larralde, Antonia Lock, Irene López Santiago, Donna R Maglott, Adriana J Malheiro, Birgit H M Meldal, Monica C Munoz-Torres, Tristan H Nelson, Frank W Nicholas, David Ochoa, Daniel P Olson, Tudor I Oprea, David Osumi-Sutherland, Helen Parkinson, Zoë May Pendlington, Ana Rath, Heidi L Rehm, Lyubov Remennik, Erin R Riggs, Paola Roncaglia, Justyne E Ross, Marion F Shadbolt, Kent A Shefchek, Morgan N Similuk, Nicholas Sioutos, Damian Smedley, Rachel Sparks, Ray Stefancsik, Ralf Stephan, Andrea L Storm, Doron Stupp, Gregory S Stupp, Jagadish Chandrabose Sundaramurthi, Imke Tammen, Darin Tay, Courtney L Thaxton, Eloise Valasek, Jordi Valls-Margarit, Alex H Wagner, Danielle Welter, Patricia L Whetzel, Lori L Whiteman, Valerie Wood, Colleen H Xu, Andreas Zankl, Xingmin Aaron Zhang, Christopher G Chute, Peter N Robinson, Christopher J Mungall, Ada Hamosh, and Melissa A Haendel. Mondo: unifying diseases for the world, by the world. MedRxiv, Apr 2022. URL: https://doi.org/10.1101/2022.04.13.22273750, doi:10.1101/2022.04.13.22273750. This article has 158 citations.
(lucano2025theorphanetnomenclature pages 12-15): C. Lucano, D. Lagorce, A. Olry, H. Ali, V. Lanneau, M. De Carvalho, A. Dilsizoglu Senol, M. Fructuoso, E. Gaillard, M.-C. Gaillard, S. Mihic, M. Tannoury, F. Sauvage, C. Rodwell, S. Maiella, M. Hanauer, and A. Rath. The orphanet nomenclature of rare diseases: a standard terminology for improved patient recognition and data interoperability. MedRxiv, Aug 2025. URL: https://doi.org/10.1101/2025.08.10.25333394, doi:10.1101/2025.08.10.25333394. This article has 3 citations.
(lucano2025theorphanetnomenclature pages 15-19): C. Lucano, D. Lagorce, A. Olry, H. Ali, V. Lanneau, M. De Carvalho, A. Dilsizoglu Senol, M. Fructuoso, E. Gaillard, M.-C. Gaillard, S. Mihic, M. Tannoury, F. Sauvage, C. Rodwell, S. Maiella, M. Hanauer, and A. Rath. The orphanet nomenclature of rare diseases: a standard terminology for improved patient recognition and data interoperability. MedRxiv, Aug 2025. URL: https://doi.org/10.1101/2025.08.10.25333394, doi:10.1101/2025.08.10.25333394. This article has 3 citations.
(lucano2025theorphanetnomenclature pages 26-29): C. Lucano, D. Lagorce, A. Olry, H. Ali, V. Lanneau, M. De Carvalho, A. Dilsizoglu Senol, M. Fructuoso, E. Gaillard, M.-C. Gaillard, S. Mihic, M. Tannoury, F. Sauvage, C. Rodwell, S. Maiella, M. Hanauer, and A. Rath. The orphanet nomenclature of rare diseases: a standard terminology for improved patient recognition and data interoperability. MedRxiv, Aug 2025. URL: https://doi.org/10.1101/2025.08.10.25333394, doi:10.1101/2025.08.10.25333394. This article has 3 citations.
(vasilevsky2022mondounifyingdiseases pages 11-12): Nicole A Vasilevsky, Nicolas A Matentzoglu, Sabrina Toro, Joseph E Flack, Harshad Hegde, Deepak R Unni, Gioconda F Alyea, Joanna S Amberger, Larry Babb, James P Balhoff, Taylor I Bingaman, Gully A Burns, Orion J Buske, Tiffany J Callahan, Leigh C Carmody, Paula Carrio Cordo, Lauren E Chan, George S Chang, Sean L Christiaens, Michel Dumontier, Laura E Failla, May J Flowers, H. Alpha Garrett, Jennifer L Goldstein, Dylan Gration, Tudor Groza, Marc Hanauer, Nomi L Harris, Jason A Hilton, Daniel S Himmelstein, Charles Tapley Hoyt, Megan S Kane, Sebastian Köhler, David Lagorce, Abbe Lai, Martin Larralde, Antonia Lock, Irene López Santiago, Donna R Maglott, Adriana J Malheiro, Birgit H M Meldal, Monica C Munoz-Torres, Tristan H Nelson, Frank W Nicholas, David Ochoa, Daniel P Olson, Tudor I Oprea, David Osumi-Sutherland, Helen Parkinson, Zoë May Pendlington, Ana Rath, Heidi L Rehm, Lyubov Remennik, Erin R Riggs, Paola Roncaglia, Justyne E Ross, Marion F Shadbolt, Kent A Shefchek, Morgan N Similuk, Nicholas Sioutos, Damian Smedley, Rachel Sparks, Ray Stefancsik, Ralf Stephan, Andrea L Storm, Doron Stupp, Gregory S Stupp, Jagadish Chandrabose Sundaramurthi, Imke Tammen, Darin Tay, Courtney L Thaxton, Eloise Valasek, Jordi Valls-Margarit, Alex H Wagner, Danielle Welter, Patricia L Whetzel, Lori L Whiteman, Valerie Wood, Colleen H Xu, Andreas Zankl, Xingmin Aaron Zhang, Christopher G Chute, Peter N Robinson, Christopher J Mungall, Ada Hamosh, and Melissa A Haendel. Mondo: unifying diseases for the world, by the world. MedRxiv, Apr 2022. URL: https://doi.org/10.1101/2022.04.13.22273750, doi:10.1101/2022.04.13.22273750. This article has 158 citations.
(vasilevsky2022mondounifyingdiseases pages 6-11): Nicole A Vasilevsky, Nicolas A Matentzoglu, Sabrina Toro, Joseph E Flack, Harshad Hegde, Deepak R Unni, Gioconda F Alyea, Joanna S Amberger, Larry Babb, James P Balhoff, Taylor I Bingaman, Gully A Burns, Orion J Buske, Tiffany J Callahan, Leigh C Carmody, Paula Carrio Cordo, Lauren E Chan, George S Chang, Sean L Christiaens, Michel Dumontier, Laura E Failla, May J Flowers, H. Alpha Garrett, Jennifer L Goldstein, Dylan Gration, Tudor Groza, Marc Hanauer, Nomi L Harris, Jason A Hilton, Daniel S Himmelstein, Charles Tapley Hoyt, Megan S Kane, Sebastian Köhler, David Lagorce, Abbe Lai, Martin Larralde, Antonia Lock, Irene López Santiago, Donna R Maglott, Adriana J Malheiro, Birgit H M Meldal, Monica C Munoz-Torres, Tristan H Nelson, Frank W Nicholas, David Ochoa, Daniel P Olson, Tudor I Oprea, David Osumi-Sutherland, Helen Parkinson, Zoë May Pendlington, Ana Rath, Heidi L Rehm, Lyubov Remennik, Erin R Riggs, Paola Roncaglia, Justyne E Ross, Marion F Shadbolt, Kent A Shefchek, Morgan N Similuk, Nicholas Sioutos, Damian Smedley, Rachel Sparks, Ray Stefancsik, Ralf Stephan, Andrea L Storm, Doron Stupp, Gregory S Stupp, Jagadish Chandrabose Sundaramurthi, Imke Tammen, Darin Tay, Courtney L Thaxton, Eloise Valasek, Jordi Valls-Margarit, Alex H Wagner, Danielle Welter, Patricia L Whetzel, Lori L Whiteman, Valerie Wood, Colleen H Xu, Andreas Zankl, Xingmin Aaron Zhang, Christopher G Chute, Peter N Robinson, Christopher J Mungall, Ada Hamosh, and Melissa A Haendel. Mondo: unifying diseases for the world, by the world. MedRxiv, Apr 2022. URL: https://doi.org/10.1101/2022.04.13.22273750, doi:10.1101/2022.04.13.22273750. This article has 158 citations.
(sholeh2024epidemiologyoftularemia pages 1-2): Mohammad Sholeh, Safoura Moradkasani, and Saber Esmaeili. Epidemiology of tularemia in the countries of the who eastern mediterranean region (emro): a systematic review and meta-analysis. PLOS Neglected Tropical Diseases, 18:e0012141, May 2024. URL: https://doi.org/10.1371/journal.pntd.0012141, doi:10.1371/journal.pntd.0012141. This article has 11 citations and is from a domain leading peer-reviewed journal.
(maurin2024nonvaccinalprophylaxisof pages 1-2): Max Maurin, Aurélie Hennebique, Camille Brunet, Léa Pondérand, Isabelle Pelloux, Sandrine Boisset, and Yvan Caspar. Non-vaccinal prophylaxis of tularemia. Frontiers in Microbiology, Nov 2024. URL: https://doi.org/10.3389/fmicb.2024.1507469, doi:10.3389/fmicb.2024.1507469. This article has 2 citations and is from a peer-reviewed journal.
(sharma2023tularemia–a pages 2-3): Rinku Sharma, Rajendra Damu Patil, Birbal Singh, Sandip Chakraborty, Deepak Chandran, Kuldeep Dhama, Devi Gopinath, Gauri Jairath, Ajayta Rialch, Gorakh Mal, Putan Singh, Wanpen Chaicumpa, and G. Saikumar. Tularemia – a re-emerging disease with growing concern. Veterinary Quarterly, 43:1-16, Nov 2023. URL: https://doi.org/10.1080/01652176.2023.2277753, doi:10.1080/01652176.2023.2277753. This article has 48 citations and is from a domain leading peer-reviewed journal.