Bejel (endemic syphilis) is a chronic non-venereal treponematosis caused by Treponema pallidum subsp. endemicum (TEN), classically acquired in childhood in hot, arid regions through direct skin/mucosal contact and shared contaminated utensils rather than by sexual transmission.
UNANIMOUS
INTEGRATED
pathophysiologyepidemiology
| Provider | Stance | Score | Evidence |
| falcon |
CONCORDANT |
85% |
Classical onset typically in childhood (2–15 years) in endemic settings
Falcon frames bejel as a classically childhood, arid-region, nonvenereal treponematosis caused by TEN and spread through mucosal/skin contact.
|
| openscientist |
CONCORDANT |
95% |
Unlike venereal syphilis, bejel is not primarily sexually transmitted but spreads through direct contact with infectious lesions or contaminated fomites (e.g., shared drinking vessels) in communities with poor hygiene and overcrowding. The disease predominantly affects children in arid tropical and subtropical environments.
OpenScientist states the non-venereal fomite/contact route, the childhood predominance, and the arid endemic geography directly.
PMID:24396138
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Bejel progresses through a staged course analogous to syphilis: a primary (often subclinical) oral mucosal lesion, a secondary mucocutaneous stage with osteoperiostitis, and, if untreated, a tertiary stage of destructive gummatous lesions of skin, bone, and the nasopharynx (gangosa).
UNANIMOUS
INTEGRATED
phenotype
| Provider | Stance | Score | Evidence |
| falcon |
CONCORDANT |
80% |
Bejel classically targets oral/nasal mucosa and bone, with destructive osteitis in late disease
Falcon describes the same staged progression with oral/nasal mucosal and bone involvement and late destructive (gummatous/gangosa) disease.
|
| openscientist |
CONCORDANT |
95% |
The disease progresses through primary (often subclinical oral mucous patches), secondary (mucocutaneous and osteoperiosteal lesions), and tertiary stages (destructive gummatous lesions of skin, bone, and nasopharynx)
OpenScientist gives the explicit primary/secondary/tertiary staging with the same organ involvement.
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Overview
Both providers characterize bejel (endemic syphilis) as a chronic non-venereal treponematosis caused by Treponema pallidum subsp. endemicum (TEN), one of the three endemic treponematoses, classically acquired in childhood in hot arid regions and treated with benzathine penicillin G. Both foreground the modern paradigm shift: molecularly confirmed, sexually transmitted TEN in MSM that is clinically indistinguishable from venereal syphilis and invisible to standard serology.
Agreement
The reports converge on the causative agent and non-venereal childhood epidemiology; the near-identity (>99%) of the ~1.14 Mbp TEN genome to the other pathogenic subspecies; the primary/secondary/tertiary staged clinical course with oral mucosal, osteoperiosteal, and destructive gummatous (gangosa) manifestations; the emergence of sexually transmitted TEN in MSM (both cite ~12% of typed MSM syphilis samples in Japan); the diagnostic limitation that serology cannot distinguish subspecies (requiring MLST of TP0136/TP0548/TP0705); TprK-mediated antigenic variation/immune evasion; benzathine penicillin G as first-line with no penicillin resistance; the A2058G macrolide-resistance threat; and a favorable prognosis with early treatment despite irreversible untreated tertiary destruction.
Divergence
OpenScientist is substantially more comprehensive (69 publications synthesized), supplying formal identifiers (MONDO:0001714, ICD-10 A65, ICD-11 1A62), a detailed molecular-immunology cascade (TprK → TLR2/JAK1/STAT1/IDO macrophage polarization; CD4/CD8 responses), experimental therapeutics (linezolid), an LSH-hamster congenital-transmission model, and non-human-primate (baboon) reservoir data. Falcon adds the Ghana lesion-differential study (serology-PCR discordance; H. ducreyi/HSV) and quantitative historical WHO burden/campaign figures. The one genuine scientific divergence is the nearest-relative framing of TEN: Falcon emphasizes ~99.7% identity to TPA, whereas OpenScientist places TEN phylogenetically closest to yaws-causing TPE — not a contradiction, since both agree the subspecies are near-identical. Quantitative differences (e.g., tertiary-disease fraction ~10% vs ~10-15%) are minor.
Integration
Promotable to kb/disorders/Bejel.yaml: the TEN etiology and non-venereal childhood epidemiology; the staged pathophysiology/phenotype nodes (primary mucosal, secondary mucocutaneous/osteoperiosteal, tertiary gummatous gangosa); the emerging sexually transmitted TEN/MSM epidemiology; the serology-cannot-distinguish-subspecies diagnostic limitation with MLST typing; TprK antigenic-variation immune evasion; benzathine penicillin G first-line with no penicillin resistance; the A2058G macrolide-resistance caveat; and the rarely-fatal-but-disfiguring prognosis.
Not integrated (leads)
Retained as leads pending source verification: the detailed TLR2/JAK1/STAT1/IDO immune cascade, experimental linezolid, the hamster congenital model and non-human-primate reservoir biology, pre-Columbian paleogenomics, and the Ghana lesion-differential statistics — richer than the core curated mechanism set and best confirmed against primary abstracts before promotion.
Cross-provider synthesis comparing the falcon (Edison Scientific Literature) and openscientist reports for Bejel. No CONTRADICTORY stances were assigned: the providers agree on all core claims, with divergence limited to coverage depth, recency, and the TPA-vs-TPE nearest-relative framing of the TEN genome. best_matching_text values are verbatim excerpts from the cited report files; literature evidence snippets were intentionally left unpopulated pending fetch-reference verification of the underlying PMIDs/DOIs.