Glanders is a highly contagious zoonotic bacterial infection caused by Burkholderia mallei. It primarily affects equids but can infect humans, and disease is marked by pulmonary nodular lesions and ulcerative skin or mucous membrane involvement.
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name: Glanders
creation_date: "2026-05-09T13:55:08Z"
updated_date: "2026-05-09T13:55:08Z"
category: Infectious
description: >-
Glanders is a highly contagious zoonotic bacterial infection caused by
Burkholderia mallei. It primarily affects equids but can infect humans, and
disease is marked by pulmonary nodular lesions and ulcerative skin or mucous
membrane involvement.
references:
- reference: PMID:40498787
title: "Glanders: An ancient and emergent disease with no vaccine or treatment on site"
found_in:
- Glanders-deep-research-falcon.md
findings:
- statement: Glanders is a potentially fatal zoonosis that affects equids and humans.
supporting_text: "Glanders is a highly contagious and potentially fatal zoonotic disease that primarily affects equines but can also infect humans."
- reference: PMID:19884331
title: "Burkholderia mallei cluster 1 type VI secretion mutants exhibit growth and actin polymerization defects in RAW 264.7 murine macrophages"
found_in:
- Glanders-deep-research-falcon.md
findings:
- statement: T6SS-1 supports intracellular growth and actin-based motility in macrophage infection models.
supporting_text: "T6SS-1 plays a critical role in growth and actin-based motility following uptake"
- reference: PMID:38125681
title: Influence of genomic variations on glanders serodiagnostic antigens using integrative genomic and transcriptomic approaches
found_in:
- Glanders-deep-research-falcon.md
findings:
- statement: B. mallei genomic variation complicates glanders serodiagnosis.
supporting_text: "This variability can make the serodiagnosis of glanders challenging."
- reference: PMID:37887766
title: "Glanders Diagnosis in an Asymptomatic Mare from Brazil: Insights from Serology, Microbiological Culture, Mass Spectrometry, and Genome Sequencing"
found_in:
- Glanders-deep-research-falcon.md
findings:
- statement: Integrated culture, MALDI-TOF, PCR, and WGS can confirm B. mallei in asymptomatic infected equids.
supporting_text: "The diagnosis was established through a multi-pronged approach encompassing microbiological culture, mass spectrometry, and genome sequencing."
- reference: PMID:36060742
title: Evaluation of two different vaccine platforms for immunization against melioidosis and glanders
found_in:
- Glanders-deep-research-falcon.md
findings:
- statement: Mouse aerosol challenge models have been used for B. mallei vaccine evaluation.
supporting_text: "Studies were conducted in the C57BL/6 mouse model to evaluate the humoral and cell-mediated immune response and protective efficacy"
disease_term:
preferred_term: glanders
term:
id: MONDO:0005774
label: glanders
classifications:
harrisons_chapter:
- classification_value: infectious disease
evidence:
- reference: PMID:40498787
supports: SUPPORT
evidence_source: OTHER
snippet: "Glanders is a highly contagious and potentially fatal zoonotic disease that primarily affects equines but can also infect humans."
explanation: The review classifies glanders as a zoonotic infectious disease affecting equids and humans.
- classification_value: bacterial infectious disease
evidence:
- reference: PMID:40498787
supports: SUPPORT
evidence_source: OTHER
snippet: "Caused by the bacterium Burkholderia mallei, the disease is characterized by nodular lesions in the lungs and ulcerations of the skin and mucous membranes."
explanation: The review identifies B. mallei as the bacterial cause of glanders.
definitions:
- name: Zoonotic Burkholderia mallei infection
definition_type: CASE_DEFINITION
description: >-
Glanders is a zoonotic infection caused by B. mallei that mainly affects
equids but can infect humans and cause pulmonary nodules plus ulcerative
skin or mucosal lesions.
scope: Human and equid glanders
evidence:
- reference: PMID:40498787
supports: SUPPORT
evidence_source: OTHER
snippet: "Glanders is a highly contagious and potentially fatal zoonotic disease that primarily affects equines but can also infect humans."
explanation: Defines glanders as a potentially fatal zoonosis involving equids and humans.
- reference: PMID:40498787
supports: SUPPORT
evidence_source: OTHER
snippet: "Caused by the bacterium Burkholderia mallei, the disease is characterized by nodular lesions in the lungs and ulcerations of the skin and mucous membranes."
explanation: Defines the etiologic agent and major lesion pattern.
parents:
- primary bacterial infectious disease
- burkholderia infectious disease
synonyms:
- Burkholderia mallei infection
- farcy
- infection due to Pseudomonas mallei
infectious_agent:
- name: Burkholderia mallei
infectious_agent_term:
preferred_term: Burkholderia mallei
term:
id: NCBITaxon:13373
label: Burkholderia mallei
description: >-
Gram-negative bacterial pathogen that causes glanders in animals and humans.
evidence:
- reference: PMID:40498787
supports: SUPPORT
evidence_source: OTHER
snippet: "Caused by the bacterium Burkholderia mallei, the disease is characterized by nodular lesions in the lungs and ulcerations of the skin and mucous membranes."
explanation: Identifies B. mallei as the causal bacterium.
- reference: PMID:37887766
supports: SUPPORT
evidence_source: MODEL_ORGANISM
snippet: "The strain was identified as B. mallei using PCR and confirmed by MALDI-TOF mass spectrometry."
explanation: Veterinary diagnostic study confirms B. mallei identification from an infected equid.
transmission:
- name: Equid-associated zoonotic exposure
description: >-
Equids are the primary affected hosts, and humans are accidental hosts after
zoonotic exposure to infected animals or contaminated materials.
evidence:
- reference: PMID:40498787
supports: SUPPORT
evidence_source: OTHER
snippet: "Glanders is a highly contagious and potentially fatal zoonotic disease that primarily affects equines but can also infect humans."
explanation: Supports zoonotic transmission from the primary equid host context to humans.
progression:
- phase: Pulmonary and mucocutaneous lesion phase
notes: >-
Clinically recognized glanders includes pulmonary nodular lesions and
ulcerations of skin or mucous membranes.
evidence:
- reference: PMID:40498787
supports: SUPPORT
evidence_source: OTHER
snippet: "Caused by the bacterium Burkholderia mallei, the disease is characterized by nodular lesions in the lungs and ulcerations of the skin and mucous membranes."
explanation: Supports the major pulmonary and ulcerative lesion pattern.
- phase: Severe or chronic disease course
notes: >-
Disease severity ranges from rapidly fatal infection to protracted or
chronic disease, especially in endemic or untreated contexts.
evidence:
- reference: PMID:36060742
supports: SUPPORT
evidence_source: OTHER
snippet: "produce similar multifaceted diseases which range from rapidly fatal to protracted and chronic"
explanation: Supports a spectrum from rapidly fatal to chronic disease.
pathophysiology:
- name: Intracellular macrophage survival and T6SS-1 actin-based spread
description: >-
B. mallei is a facultative intracellular pathogen. T6SS-1 supports
intracellular growth and actin-based motility after uptake by macrophages,
promoting cell-to-cell spread and multinucleated giant cell formation.
cell_types:
- preferred_term: macrophage
term:
id: CL:0000235
label: macrophage
biological_processes:
- preferred_term: defense response to Gram-negative bacterium
modifier: DYSREGULATED
term:
id: GO:0050829
label: defense response to Gram-negative bacterium
- preferred_term: symbiont-mediated actin polymerization-dependent cell-to-cell migration in host
modifier: ABNORMAL
term:
id: GO:0070360
label: symbiont-mediated actin polymerization-dependent cell-to-cell migration in host
evidence:
- reference: PMID:19884331
supports: SUPPORT
evidence_source: IN_VITRO
snippet: "facultative intracellular pathogen that causes severe disease in animals and humans."
explanation: Identifies B. mallei as an intracellular pathogen in the glanders mechanism literature.
- reference: PMID:19884331
supports: SUPPORT
evidence_source: IN_VITRO
snippet: "significant growth defects were observed in comparison to controls."
explanation: T6SS-1 mutant macrophage assays support a role in intracellular growth.
- reference: PMID:19884331
supports: SUPPORT
evidence_source: IN_VITRO
snippet: "the mutants exhibited actin polymerization defects resulting in inefficient intra- and intercellular spread characteristics."
explanation: Supports actin-polymerization-dependent intracellular and intercellular spread.
downstream:
- target: Multinucleated giant cell formation
description: >-
B. mallei T6SS-1 activity contributes to multinucleated giant cell
formation in infected macrophage monolayers.
evidence:
- reference: PMID:19884331
supports: SUPPORT
evidence_source: IN_VITRO
snippet: "mutants lacked the ability to induce multinucleated giant cell formation."
explanation: T6SS-1 mutant loss of giant-cell formation supports this downstream phenotype.
- name: Serodiagnostic antigen variation
description: >-
B. mallei genome plasticity alters gene content and expression, including
genes encoding serodiagnostic antigens, which can reduce robustness of
serologic diagnosis across strains.
biological_processes:
- preferred_term: immune response
modifier: DYSREGULATED
term:
id: GO:0006955
label: immune response
evidence:
- reference: PMID:38125681
supports: SUPPORT
evidence_source: COMPUTATIONAL
snippet: "This variability can make the serodiagnosis of glanders challenging."
explanation: Genomic variability is linked to serodiagnostic difficulty.
- reference: PMID:38125681
supports: SUPPORT
evidence_source: COMPUTATIONAL
snippet: "differences in gene content ranging from 31 to 715 genes with an average of 334 gene presence-absence variations"
explanation: Quantifies gene-content variation across B. mallei genomes.
- reference: PMID:38125681
supports: SUPPORT
evidence_source: COMPUTATIONAL
snippet: "The affected genes included some encoded proteins used as serodiagnostic antigens, which were lost due mainly to structural variations."
explanation: Directly links genome structural variation to loss of serodiagnostic antigen genes.
phenotypes:
- name: Pulmonary nodular lesions
description: Pulmonary glanders is characterized by nodular lesions in the lungs.
phenotype_term:
preferred_term: Pneumonia
term:
id: HP:0002090
label: Pneumonia
evidence:
- reference: PMID:40498787
supports: SUPPORT
evidence_source: OTHER
snippet: "the disease is characterized by nodular lesions in the lungs"
explanation: Supports pulmonary involvement; Pneumonia is the closest verified HPO respiratory infection phenotype.
- name: Ulcerations of skin and mucous membranes
description: Glanders can cause ulcerative lesions involving skin and mucous membranes.
phenotype_term:
preferred_term: Skin ulcer
term:
id: HP:0200042
label: Skin ulcer
evidence:
- reference: PMID:40498787
supports: SUPPORT
evidence_source: OTHER
snippet: "ulcerations of the skin and mucous membranes."
explanation: Supports ulcerative cutaneous and mucosal involvement.
diagnosis:
- name: Serological testing with genomic-antigen limitations
description: >-
Serological testing is central to glanders diagnosis, but B. mallei genome
variation can alter serodiagnostic antigen presence and expression.
diagnosis_term:
preferred_term: diagnostic procedure
term:
id: MAXO:0000003
label: diagnostic procedure
evidence:
- reference: PMID:38125681
supports: SUPPORT
evidence_source: COMPUTATIONAL
snippet: "Currently, the diagnosis of glanders is heavily reliant on serological tests."
explanation: Supports serology as a major diagnostic approach.
- reference: PMID:38125681
supports: SUPPORT
evidence_source: COMPUTATIONAL
snippet: "This variability can make the serodiagnosis of glanders challenging."
explanation: Supports genomic variation as a diagnostic limitation.
- name: Integrated culture, MALDI-TOF, PCR, and WGS confirmation
description: >-
Confirmation can combine microbiological culture, mass spectrometry, PCR,
and whole-genome sequencing for B. mallei identification and strain context.
diagnosis_term:
preferred_term: diagnostic procedure
term:
id: MAXO:0000003
label: diagnostic procedure
evidence:
- reference: PMID:37887766
supports: SUPPORT
evidence_source: MODEL_ORGANISM
snippet: "The diagnosis was established through a multi-pronged approach encompassing microbiological culture, mass spectrometry, and genome sequencing."
explanation: Supports integrated confirmation using culture, mass spectrometry, and genome sequencing.
- reference: PMID:37887766
supports: SUPPORT
evidence_source: MODEL_ORGANISM
snippet: "The strain was identified as B. mallei using PCR and confirmed by MALDI-TOF mass spectrometry."
explanation: Supports PCR and MALDI-TOF as confirmatory components.
treatments:
- name: Prolonged antimicrobial therapy
description: >-
Human glanders treatment relies on prolonged antimicrobial therapy, with
duration and regimen guided by severity, susceptibility, and melioidosis
treatment experience.
treatment_term:
preferred_term: pharmacotherapy
term:
id: MAXO:0000058
label: pharmacotherapy
evidence:
- reference: PMID:36060742
supports: SUPPORT
evidence_source: OTHER
snippet: "Antibiotic treatment is prolonged with variable results, hence effective vaccines are urgently needed."
explanation: Supports prolonged antibiotic treatment as a central management issue.
- name: Experimental vaccine platforms
description: >-
Vaccine candidates, including capsule conjugate plus Hcp1 subunit platforms,
have shown preclinical protection in mouse aerosol challenge models but are
not established clinical therapy.
treatment_term:
preferred_term: vaccination
term:
id: MAXO:0001017
label: vaccination
evidence:
- reference: PMID:36060742
supports: PARTIAL
evidence_source: MODEL_ORGANISM
snippet: "Studies were conducted in the C57BL/6 mouse model to evaluate the humoral and cell-mediated immune response and protective efficacy"
explanation: Supports preclinical vaccine evaluation, not licensed human or veterinary use.
animal_models:
- species: Mouse
genotype: C57BL/6 aerosol challenge model
description: >-
C57BL/6 mouse model used to test immune responses and protective efficacy
of Burkholderia vaccine candidates against lethal aerosol challenge,
including B. mallei FMH.
associated_phenotypes:
- Lethal aerosol challenge infection
- Pulmonary cytokine response
evidence:
- reference: PMID:36060742
supports: SUPPORT
evidence_source: MODEL_ORGANISM
snippet: "Studies were conducted in the C57BL/6 mouse model to evaluate the humoral and cell-mediated immune response and protective efficacy"
explanation: Supports the use of C57BL/6 mice for glanders vaccine efficacy modeling.
datasets: []
Question: You are an expert researcher providing comprehensive, well-cited information.
Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies
Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.
Please provide a comprehensive research report on Glanders covering all of the disease characteristics listed below. This report will be used to populate a disease knowledge base entry. Be thorough and cite primary literature (PMID preferred) for all claims.
For each section, suggested databases/resources are listed. These are the first places you should search for information on each topic.
Search first: OMIM, Orphanet, ICD-10/ICD-11, MeSH, PubMed
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For each phenotype, provide: - Phenotype type: symptoms, clinical signs, physical manifestations, behavioral changes, or laboratory abnormalities
For symptoms/signs: HPO, OMIM, Orphanet, PubMed For behavioral changes: HPO, DSM, RDoC (Research Domain Criteria), PubMed For laboratory abnormalities: LOINC, SNOMED CT, LabTests Online, PubMed - Phenotype characteristics: Search first: OMIM, Orphanet, HPO, PubMed - Age of symptom onset (neonatal, childhood, adult-onset, late-onset) - Symptom severity (mild, moderate, severe, variable) - Symptom progression (stable, progressive, episodic, fluctuating) - Frequency among affected individuals (percentage or qualitative) - Quality of life impact: Effects on daily functioning and well-being (per-phenotype when possible) Search first: EQ-5D database, SF-36, WHO QOL databases, PubMed - Suggest HPO (Human Phenotype Ontology) terms for each phenotype
Search first: OMIM, ClinVar, HGMD, Ensembl, NCBI Gene
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For each mechanism, describe: - The causal chain from initial trigger to clinical manifestation - Which mechanisms are upstream vs downstream - What cell types and biological processes are involved - Suggest GO terms for biological processes and CL terms for cell types
Search first: Uberon, FMA (Foundational Model of Anatomy), OMIM, HPO, ICD-11, MeSH, SNOMED CT
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Search first: Orphanet, CDC, WHO, GBD (Global Burden of Disease), national registries, SEER, disease registries
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For each treatment, suggest MAXO (Medical Action Ontology) terms where applicable.
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Structure your response as a comprehensive narrative organized by the sections above. For each section, provide: - Factual content with specific details (numbers, percentages, gene names, variant nomenclature) - Ontology term suggestions (HPO, GO, CL, UBERON, CHEBI, MAXO, MONDO) where applicable - Evidence citations with PMIDs - Direct quotes from abstracts to support key claims - Clear indication when information is not available or not applicable for this disease
This report will be used to populate a disease knowledge base entry with: - Pathophysiology descriptions with causal chains - Gene/protein annotations (HGNC, GO terms) - Phenotype associations (HP terms) with frequencies - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Treatment annotations (MAXO terms) - Evidence items with PMIDs and exact abstract quotes - Epidemiology, prognosis, diagnostic, and prevention information - Animal model descriptions with phenotype recapitulation details
Glanders is a highly contagious zoonotic disease caused by the Gram-negative, facultative intracellular bacterium Burkholderia mallei that primarily affects equids (horses, donkeys, mules) and only rarely infects humans, typically via occupational exposure. Clinically, equine disease classically presents as nasal, pulmonary, and cutaneous/lymphatic forms; the cutaneous form is often called farcy. Contemporary control relies on surveillance and early diagnosis (serology plus confirmatory testing) and, in many jurisdictions, euthanasia of infected animals rather than treatment; in humans, aggressive prolonged antibiotic therapy is recommended. Recent (2023–2024) research emphasizes diagnostic challenges from strain genomic variability and demonstrates field-realistic molecular methods (e.g., LAMP) and integrated workflows (culture/PCR/MALDI-TOF/WGS) for confirmation and epidemiologic tracing. (moriya2025detectionofburkholderia pages 1-2, torres2025glandersanancient pages 7-9, charron2023influenceofgenomic pages 1-2, suniga2023glandersdiagnosisin pages 1-2, torres2025glandersanancient pages 9-10)
| Category | Key facts | Citations |
|---|---|---|
| Disease / agent | Glanders is a highly contagious zoonotic disease caused by Burkholderia mallei, a nonmotile, facultative intracellular Gram-negative bacterium; cutaneous/lymphatic disease is often termed farcy. | (moriya2025detectionofburkholderia pages 1-2, torres2025glandersanancient pages 3-5, burtnick2010burkholderiamalleicluster pages 1-2) |
| Primary hosts / reservoirs | Natural reservoir hosts are mainly equids: horses, donkeys, and mules. Donkeys and mules more often develop acute disease; horses more often have chronic or subclinical infection and may remain occult shedders. Humans are accidental hosts. | (moriya2025detectionofburkholderia pages 1-2, prince2023glandersatreatable pages 1-3, nielsen2022assessmentofthe pages 7-8) |
| Transmission | Spread occurs by direct contact with infected animals/secretions, inoculation through broken skin or harness trauma, inhalation of aerosols/dust, ingestion of contaminated feed/water, and mucosal exposure; human infection is usually occupational and human-to-human transmission is uncommon. | (moriya2025detectionofburkholderia pages 1-2, prince2023glandersatreatable pages 1-3, torres2025glandersanancient pages 7-9) |
| Clinical forms in equids | Main equine presentations: nasal, pulmonary, and cutaneous/farcy forms; acute disease is more common in donkeys/mules and may be rapidly fatal, while horses often show chronic disease with nodules, ulcers, lymphangitis, cough, dyspnea, fever, and weight loss. | (moriya2025detectionofburkholderia pages 1-2, siddique2023burkholderia(malleiand pages 4-7, prince2023glandersatreatable pages 3-5) |
| Clinical forms in humans | Human disease includes cutaneous/localized, pulmonary, chronic/disseminated, and septicemic forms; organ abscesses can involve liver, spleen, and kidneys, and untreated pneumonic disease may be fatal within 10–30 days. | (siddique2023burkholderia(malleiand pages 1-4, siddique2023burkholderia(malleiand pages 4-7, torres2025glandersanancient pages 7-9) |
| Key diagnostics | Standard veterinary diagnosis relies on serology, especially complement fixation test (CFT); confirmatory/adjunct methods include mallein testing, ELISA, western blot, culture, PCR, MALDI-TOF, and WGS. Culture is definitive but often insensitive in field samples. | (tikmehdash2024isolationserologicaland pages 1-2, suniga2023glandersdiagnosisin pages 1-2, torres2025glandersanancient pages 7-9) |
| Recent diagnostic development: antigen variation | Integrative genomics/transcriptomics showed major strain-to-strain variability affecting serodiagnostic antigens: 31–715 gene presence/absence differences (mean 334) and 388 differentially expressed genes between two reference strains, explaining variable serologic performance across lineages. | (charron2023influenceofgenomic pages 1-2) |
| Recent diagnostic development: Iran field screening | In East Azerbaijan, Iran, 350 horses were screened: 11 CFT-positive, of which 6 were confirmed by malleination and 5 were false positives; 1 CFT-negative horse was positive by mallein/ELISA/PCR, for 7 total diagnosed cases. Authors recommend ELISA as a complement to CFT. | (tikmehdash2024isolationserologicaland pages 1-2) |
| Recent diagnostic development: Brazil genomic case confirmation | An asymptomatic Brazilian mare was diagnosed by serology, culture, PCR, MALDI-TOF, and WGS; the isolate belonged to lineage 3, sublineage 2, with a 5.51 Mb genome, 65.8% GC, 5871 genes, and 5583 CDSs. | (suniga2023glandersdiagnosisin pages 1-2, suniga2023glandersdiagnosisin pages 5-7) |
| Recent diagnostic development: LAMP / molecular testing | A dried-format LAMP assay targeting the ITS region detected 10 genomic copies of B. mallei DNA and showed 87.5% agreement with real-time PCR on positive equine swabs and 100% agreement on negatives, offering a simpler field-deployable alternative where PCR resources are limited. | (nakase2025anovelreadytouse pages 1-2) |
| Quantitative epidemiology | Brazil reported 3385 glanders cases (1999–2022), including 715 cases in the most recent 3 years; a Pará study estimated 1.68% prevalence of infected properties. In one Brazilian outbreak series, 37.5% of infected horses were asymptomatic and culture yielded only 8.2% positivity despite PCR confirmation in all tested animals. | (suniga2023glandersdiagnosisin pages 1-2, torres2025glandersanancient pages 5-7) |
| Geographic distribution | Current endemic/re-emerging areas include Brazil, India, Iran, Iraq, Pakistan, Mongolia, parts of the Middle East, Northern Africa, and South/Central America; many formerly affected regions eradicated glanders during the 20th century. | (torres2025glandersanancient pages 1-3, torres2025glandersanancient pages 5-7, nielsen2022assessmentofthe pages 7-8) |
| Pathophysiology / virulence | Important mechanisms include intracellular survival, vacuolar escape, actin-based motility, multinucleated giant-cell formation, serum resistance, capsule/LPS-mediated immune evasion, and virulence functions mediated by T3SS, T6SS-1, VirAG, Hcp1, and BimA. | (burtnick2010burkholderiamalleicluster pages 1-2, burtnick2010burkholderiamalleicluster pages 6-7, burtnick2010burkholderiamalleicluster pages 2-3, siddique2023burkholderia(malleiand pages 1-4) |
| Treatment | For animals, treatment is generally discouraged because eradication is unreliable and zoonotic risk persists; policy usually favors euthanasia. For humans, expert reviews support an intensive IV phase (ceftazidime, imipenem, or meropenem for 10–14 days) followed by an eradication phase (doxycycline or trimethoprim–sulfamethoxazole for 3–6 months). | (torres2025glandersanancient pages 9-10, torres2025glandersanancient pages 7-9, prince2023glandersatreatable pages 5-7) |
| Prevention / control | No licensed vaccine exists for humans or animals. Control depends on surveillance, quarantine, testing of exposed equids, euthanasia of infected animals, carcass/material decontamination, and biosecurity. B. mallei is susceptible to common disinfectants, heat, and UV. | (prince2023glandersatreatable pages 7-10, torres2025glandersanancient pages 9-10, torres2025glandersanancient pages 1-3) |
| Vaccine research / notable antigen | Hcp1 is a leading antigen in diagnostics and vaccine development; experimental platforms include CPS-CRM197 + Hcp1, Hcp1-LPS glycoconjugates, live-attenuated mutants (e.g., ΔtonB, CLH001), and gold nanoparticle vaccines. Protection in animals is promising but partial/variable, and no candidate is licensed. | (badten2024burkholderiapseudomalleicomplex pages 13-14, torres2025glandersanancient pages 9-10, biryukov2022evaluationoftwo pages 1-2, torres2025glandersanancient pages 7-9) |
Table: This table condenses disease-definition, clinical, epidemiologic, diagnostic, mechanistic, and intervention facts about glanders into a knowledge-base-ready format. It emphasizes recent quantitative findings and links each row to supporting context IDs for traceability.
Glanders is an infectious zoonosis caused by B. mallei; it is historically important (including biothreat concerns) and remains re-emerging/endemic in parts of Asia, the Middle East, Africa, and South America. (torres2025glandersanancient pages 3-5, torres2025glandersanancient pages 1-3)
Key clinical concept: equine glanders is commonly described in nasal, pulmonary, and cutaneous forms; the cutaneous/lymphatic form is termed farcy. (moriya2025detectionofburkholderia pages 1-2, torres2025glandersanancient pages 7-9)
This tool-assisted literature retrieval did not return authoritative ontology mappings (MONDO ID, MeSH ID, Orphanet, ICD-10/ICD-11 codes) within the retrieved full-text evidence. Consequently, this report cannot cite those identifiers from primary sources in-context and flags them as not available in the current evidence set.
Most mechanistic assertions here derive from controlled in vitro or animal-model studies (e.g., macrophage infection models) and expert reviews synthesizing multiple sources, while clinical/epidemiologic data include outbreak/case reports and regional surveillance screening studies. (suniga2023glandersdiagnosisin pages 1-2, torres2025glandersanancient pages 9-10, burtnick2010burkholderiamalleicluster pages 1-2)
Glanders is caused by Burkholderia mallei, a nonmotile, facultative intracellular Gram-negative bacillus. (burtnick2010burkholderiamalleicluster pages 1-2)
Equids (primary reservoir): transmission occurs through direct contact with infected animals/secretions, inhalation of aerosols/dust, ingestion of contaminated feed/water, and inoculation via skin trauma (e.g., harness-related). Asymptomatic carriers can intermittently shed bacteria. (moriya2025detectionofburkholderia pages 1-2, prince2023glandersatreatable pages 3-5)
Humans (accidental host): exposure is usually occupational (animal handlers, veterinarians, laboratory exposure) via broken skin, inhalation, or mucosal contact; human-to-human transmission is described as uncommon/rare. (prince2023glandersatreatable pages 1-3, torres2025glandersanancient pages 7-9)
No specific host genetic protective variants or validated environmental protective factors were identified in the retrieved evidence corpus.
Not applicable in the classic human genetics sense; disease is primarily infectious. However, exposure context (animal husbandry, animal movement/importation, and biosecurity) strongly modifies risk. (prince2023glandersatreatable pages 7-10)
Nasal glanders: pustules/ulcers of nasal mucosa (conchae/septum), sticky/yellow discharge, and regional lymphadenopathy. (moriya2025detectionofburkholderia pages 1-2)
Pulmonary glanders: nodular abscesses in lungs with cough, dyspnea, systemic illness/fever; can progress to pneumonia. (moriya2025detectionofburkholderia pages 1-2)
Cutaneous/lymphatic glanders (farcy): nodular lymphangitis with abscess “buds” (~0.5–2.5 cm) that ulcerate and discharge; enlarged lymphatics. (moriya2025detectionofburkholderia pages 1-2, torres2025glandersanancient pages 7-9)
Course differences by species: donkeys/mules more often show acute disease that can be rapidly fatal; horses often develop chronic disease and may survive for years, including occult carriage. (moriya2025detectionofburkholderia pages 1-2, torres2025glandersanancient pages 3-5)
Asymptomatic infection: an important transmission-relevant state; review evidence reports 37.5% asymptomatic among infected horses in a Brazilian outbreak series. (torres2025glandersanancient pages 5-7)
Suggested HPO terms (examples): - Fever (HP:0001945) - Cough (HP:0012735) - Dyspnea (HP:0002094) - Nasal discharge (HP:0001738) - Nasal ulceration (HP:0032474) / mucosal ulceration (HP:0001074) - Pneumonia (HP:0002090) - Skin ulcer (HP:0001059) - Lymphangitis (HP:0001045) - Lymphadenopathy (HP:0002716)
Human presentations include cutaneous/local disease (papular lesions that ulcerate), pulmonary disease (can progress to pneumonia/abscess), disseminated/chronic disease, and septicemic disease with internal organ abscesses (e.g., liver, spleen, kidneys). (siddique2023burkholderia(malleiand pages 4-7, torres2025glandersanancient pages 7-9)
Temporal note: incubation is variable; acute cases may occur within 1–14 days and chronic disease can develop over weeks; untreated pneumonic cases may be fatal within 10–30 days. (torres2025glandersanancient pages 7-9)
Suggested HPO terms (examples): - Skin papule (HP:0010011) - Sepsis (HP:0100806) - Liver abscess (HP:0031151) - Splenic abscess (no direct HPO term commonly used; can map to Splenomegaly HP:0001744 and “abscess” phenotypes as appropriate)
The retrieved evidence set did not include standardized QoL instrument data (e.g., EQ-5D/SF-36) for glanders.
Not applicable: glanders is not a monogenic or polygenic inherited disorder.
Whole-genome sequencing of a Brazilian outbreak isolate (BAC 86/19) yielded a genome size ~5.51 Mb and enabled assignment to lineage 3, sublineage 2. (suniga2023glandersdiagnosisin pages 1-2, suniga2023glandersdiagnosisin pages 5-7)
Diagnostic relevance of pathogen genome plasticity: a 2023 integrative genomics/transcriptomics study reported large gene content differences across B. mallei isolates and showed that some serodiagnostic antigens may be lost due to structural variation, complicating serologic diagnosis. (charron2023influenceofgenomic pages 1-2)
Abstract-anchored quote supporting this point: Charron et al. reported “differences in gene content ranging from 31 to 715 genes with an average of 334 gene presence-absence variations,” and that affected genes “included some encoded proteins used as serodiagnostic antigens.” (charron2023influenceofgenomic pages 1-2)
Not applicable to host genetics in this evidence set; no pathogen epigenetic mechanisms were retrieved.
Environmental risk factors in the retrieved evidence are primarily exposure-related (contact with infected equids or contaminated materials) rather than environmental reservoirs (unlike B. pseudomallei). Transmission is supported by inhalation/ingestion/mucosal routes, and control emphasizes disinfection and biosecurity. (moriya2025detectionofburkholderia pages 1-2, prince2023glandersatreatable pages 7-10)
Exposure → entry (mucosa, inhalation, broken skin) → intracellular infection → dissemination and suppurative lesions → clinical disease.
Mechanistic evidence supports that B. mallei is facultative intracellular, escapes endocytic vacuoles, enters host cytoplasm, and uses actin-based motility for intra-/intercellular spread—processes that link early infection to tissue lesions and dissemination. (burtnick2010burkholderiamalleicluster pages 1-2)
Key virulence determinants include: - Type III secretion system (T3SS): essential for early vacuolar escape and access to intracellular actin pools, supporting actin-based motility and multinucleated giant cell formation. (burtnick2010burkholderiamalleicluster pages 1-2) - Type VI secretion system cluster 1 (T6SS-1): required for virulence; mutants (e.g., tssE) show intracellular growth defects, impaired actin polymerization, and failure to induce multinucleated giant cell formation in macrophages. (burtnick2010burkholderiamalleicluster pages 1-2, burtnick2010burkholderiamalleicluster pages 6-7) - Capsule / LPS-associated immune evasion: capsule described as preventing immune killing; LPS-associated serum resistance is implicated by survival in normal human serum and loss of LPS in serum-sensitive strains. (siddique2023burkholderia(malleiand pages 1-4)
A 2025 expert review summarizes immunologic observations in naturally infected equids, reporting strong IgG responses and elevated cytokines including IL-1β, MCP-1, IL-17, IL-6, IFN-γ, and TNF-α, and highlights Hcp1 as a prominent antigenic target. (torres2025glandersanancient pages 7-9, torres2025glandersanancient media 41fd19e0)
GO Biological Process (examples): - GO:0052040 “negative regulation by symbiont of host immune response” (conceptual fit for immune evasion) - GO:0030260 “bacterial-type flagellum-dependent cell motility” is not appropriate for B. mallei (non-motile); instead consider actin-based intracellular movement processes (host actin polymerization) - GO:0075525 “interleukin-17 production” (host response; aligns with reported IL-17 elevation)
Cell Ontology (CL) cell types (examples): - CL:0000236 macrophage (supported by macrophage infection model data) (burtnick2010burkholderiamalleicluster pages 1-2)
Primary (equids): - Respiratory system: lung (UBERON:0002048), nasal mucosa (UBERON:0001825) - Integumentary/lymphatic: skin (UBERON:0002097), lymphatic vessel (UBERON:0001986), lymph node (UBERON:0000029) (conceptually consistent with lymphangitis/lymphadenopathy) (moriya2025detectionofburkholderia pages 1-2, torres2025glandersanancient pages 7-9)
Humans: pulmonary involvement and systemic organ abscesses (liver, spleen, kidneys). (torres2025glandersanancient pages 7-9)
Not applicable (infectious disease). Epidemiology is driven by animal movement, biosecurity, and regional endemicity. (torres2025glandersanancient pages 5-7)
Diagnosis in animals is “heavily reliant on serological tests” in many settings, and culture can be hazardous and insensitive in field samples. (suniga2023glandersdiagnosisin pages 1-2, tikmehdash2024isolationserologicaland pages 1-2)
1) Integrated confirmation + genomic epidemiology (Brazil; published Oct 2023) - Multi-pronged diagnosis (serology, culture, PCR, MALDI-TOF, WGS) confirmed B. mallei from an asymptomatic mare in a 2019 outbreak; WGS provided lineage assignment and genomic parameters. (suniga2023glandersdiagnosisin pages 1-2, suniga2023glandersdiagnosisin pages 5-7) - Abstract quote: “The diagnosis was established through a multi-pronged approach encompassing microbiological culture, mass spectrometry, and genome sequencing.” (suniga2023glandersdiagnosisin pages 1-2)
2) Strain variation undermining serodiagnosis (Frontiers in Veterinary Science; Dec 2023) - Gene presence/absence variation and differential expression affect antigens used for serology; this is directly relevant to test robustness across endemic regions. (charron2023influenceofgenomic pages 1-2)
3) Field screening performance and false positives (Iran; May 2024) - Screening of 350 horses: 11 CFT-positive, 6 confirmed by mallein, 5 false positives; 1 CFT-negative but positive on mallein/ELISA/PCR; total 7 diagnosed. (tikmehdash2024isolationserologicaland pages 1-2)
4) Operational molecular diagnostics for resource-limited settings (LAMP; Jan 2025; included due to strong “implementation” relevance) - Dried-format LAMP targeting ITS detected 10 genomic copies and matched real-time PCR with 87.5% agreement for positives and 100% for negatives on equine swabs, supporting deployment where PCR is constrained. (nakase2025anovelreadytouse pages 1-2)
The retrieved evidence set did not provide a systematic differential diagnosis list; in practice, differentials include other causes of equine respiratory disease, ulcerative nasal disease, and nodular cutaneous/lymphangitic syndromes.
The evidence set did not provide modern survival curves or population-level case-fatality rates for 2023–2024.
A 2025 expert review recommends prolonged, aggressive antimicrobial therapy guided by susceptibility testing and experience from melioidosis: an intensive IV phase (10–14 days; ceftazidime, imipenem, or meropenem), followed by a prolonged eradication phase (3–6 months; doxycycline or trimethoprim–sulfamethoxazole). (torres2025glandersanancient pages 9-10)
Suggested MAXO terms (examples): - MAXO:0000746 antibiotic therapy - MAXO:0000058 intravenous drug administration
International veterinary policy generally discourages treating infected equids (due to relapse and zoonotic risk) and favors euthanasia plus quarantine/testing for contacts. (torres2025glandersanancient pages 9-10, torres2025glandersanancient pages 7-9)
Nevertheless, a field treatment example cited in a 2023 review describes 23 horses treated over 84 days with oral doxycycline, IV enrofloxacin, and trimethoprim+sulphadiazine, with no relapses reported at end of therapy and negative follow-up indicators (e.g., sentinel horses/foals). (prince2023glandersatreatable pages 5-7)
Suggested MAXO terms (examples): - MAXO:0001084 euthanasia - MAXO:0000746 antibiotic therapy - MAXO:0000915 quarantine
No licensed vaccine exists for humans or animals. (torres2025glandersanancient pages 9-10)
Control measures include surveillance and testing, strict quarantine of exposed animals, euthanasia of confirmed cases, and thorough disinfection and disposal of contaminated materials. (prince2023glandersatreatable pages 7-10, torres2025glandersanancient pages 7-9)
A 2024 review of Burkholderia pseudomallei complex vaccines highlights Hcp1 (a T6SS component) as an important immunogenic target in natural infection and summarizes mouse data where intranasal Hcp1 with adjuvants produced substantial protection; glycoconjugate approaches (e.g., Hcp1-LPS constructs on gold nanoparticles) can enhance LPS-specific antibody responses and protection. (badten2024burkholderiapseudomalleicomplex pages 13-14)
Expert limitations highlighted across reviews include: safety concerns for live-attenuated vaccines (reversion/persistence), incomplete protection against chronic disease or high-dose exposures, and dependence on immunization route/adjuvant. (torres2025glandersanancient pages 9-10, biryukov2022evaluationoftwo pages 1-2)
Beyond equids and humans, occasional infections have been reported in other mammals (e.g., felids, camels, dogs), while cattle and pigs are described as resistant in an expert review. (torres2025glandersanancient pages 3-5)
Zoonotic acquisition can occur via direct contact and, in carnivores, by consumption of infected meat. (torres2025glandersanancient pages 3-5, prince2023glandersatreatable pages 1-3)
1) Genomics informing surveillance and diagnostics: WGS-confirmed Brazilian outbreak isolate lineage assignment (lineage 3, sublineage 2) illustrates how genomics supports tracing and diagnostic development. (Published Oct 2023; https://doi.org/10.3390/pathogens12101250) (suniga2023glandersdiagnosisin pages 1-2)
2) Evidence-based critique of serodiagnostic robustness: 2023 genomics/transcriptomics study demonstrates that antigen loss/differential expression can undermine serology across B. mallei diversity—an actionable warning for national screening programs. (Published Dec 2023; https://doi.org/10.3389/fvets.2023.1217135) (charron2023influenceofgenomic pages 1-2)
3) Screening data demonstrating CFT false positives in practice: Iran screening study highlights how combining CFT with mallein, ELISA, and PCR improves classification (e.g., 5/11 CFT positives were false positives). (Published May 2024; https://doi.org/10.30466/vrf.2024.2010651.4002) (tikmehdash2024isolationserologicaland pages 1-2)
The following extracted regions from a 2025 expert review capture compact statements about (i) clinical forms and (ii) immune response markers (Hcp1 and cytokines) and (iii) diagnostic modalities and transmission routes, supporting key summary claims. (torres2025glandersanancient media e5c7470e, torres2025glandersanancient media 41fd19e0, torres2025glandersanancient media 90115587, torres2025glandersanancient media c5f72073)
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