Pinta

1. Disease Information

2026-04-04
Falcon MONDO:0000979 Model: Edison Scientific Literature 25 citations

1. Disease Information

1.1 Definition and overview (current understanding)

Pinta is a neglected chronic skin disease and the most benign of the endemic treponematoses, in that it is classically described as involving only the skin (without the destructive bone/cartilage manifestations typical of late yaws). It has been described historically in Latin America for centuries and is also referred to as “mal del pinto” and “carate.” (stamm2015pintalatinamericas pages 1-3, rosa2021maldepinta pages 1-2)

1.2 Key identifiers (OMIM, Orphanet, ICD-10/ICD-11, MeSH, MONDO)

Within the retrieved full-text evidence set, explicit ontology/coding identifiers (MONDO, MeSH descriptor IDs, ICD-10/ICD-11 codes, Orphanet, OMIM) were not directly stated, and therefore cannot be asserted here with citations. The most authoritative retrieved recent resource is the CDC’s 2024 laboratory recommendations, which provide organism-level taxonomy and a brief epidemiologic locator but do not provide ICD/MeSH/MONDO mappings. (papp2024cdclaboratoryrecommendations pages 3-4, papp2024cdclaboratoryrecommendations pages 25-26)

1.3 Synonyms / alternative names

Common synonyms reported in peer-reviewed literature include “mal del pinto” and “carate.” (stamm2015pintalatinamericas pages 1-3, rosa2021maldepinta pages 1-2)

1.4 Evidence source type

Most of the disease-level information for pinta in the retrieved set is aggregated from reviews/perspectives and clinical microbiology/dermatology references, with limited modern case-based literature (e.g., a 2021 case report). (stamm2015pintalatinamericas pages 1-3, rosa2021maldepinta pages 1-2)


2. Etiology

2.1 Disease causal factors

Primary cause: infection with the spirochete Treponema carateum. (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3, papp2024cdclaboratoryrecommendations pages 3-4)

Taxonomic framing (current debate): Recent immunology review articles emphasize that the treponemal diseases are genetically and antigenically highly similar and historically were considered related; one 2023 review explicitly states that pinta is caused by “a different species … namely Treponema carateum.” (avilanieto2023syphilisvaccinechallenges pages 1-2)

2.2 Risk factors (human clinical/epidemiologic)

Transmission route: nonvenereal direct skin-to-skin contact with infectious lesions. (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3, papp2024cdclaboratoryrecommendations pages 3-4)

Sociodemographic/environmental context: classically described in poor rural tropical communities, often acquired in childhood or adolescence. (stamm2015pintalatinamericas pages 1-3, rosa2021maldepinta pages 1-2)

Geography as a risk determinant: tropical Latin America/Central and South America (including persistence in remote settings). CDC 2024 states: “Treponema carateum infection results in pinta which, although rare, is found in tropical areas of Latin America.” (papp2024cdclaboratoryrecommendations pages 3-4)

2.3 Protective factors

No pinta-specific protective genetic variants, host factors, or environmental protective factors were identified in the retrieved evidence set.

2.4 Gene–environment interactions

No host gene–environment interaction evidence was identified in the retrieved evidence set.


3. Phenotypes

3.1 Clinical spectrum and staging

Pinta is commonly described as a staged cutaneous illness: - Primary stage: papules/erythematous scaly plaques at the inoculation site appearing after infection (classically around weeks). (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3) - Secondary stage: disseminated lesions (“pintids”) with pigmentary changes developing months after infection; lesions may persist and remain infectious for years. (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3) - Late/tertiary stage: dyschromia/achromia and cutaneous atrophy occurring years after infection (e.g., 2–5 years in one classic description). (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 3-5)

A 2021 dermatology case report similarly emphasizes a three-stage evolution with early localized lesions, later generalized rash with hyper-/hypopigmented lesions, and late pigmentary change that can resemble vitiligo. (rosa2021maldepinta pages 1-2)

3.2 Differential diagnosis

Because late pinta can manifest as dyschromic patches, key differentials include tinea versicolor, vitiligo, melasma, leprosy, and other dermatoses. (mitja2013advancesinthe pages 2-3)

3.3 Histopathology (biopsy phenotypes)

Mitjà et al. summarize stage-linked pathology, including early “loss of melanin in basal cells and liquefaction degeneration” and late “epidermal atrophy and the presence of many melanophages in the dermis.” (mitja2013advancesinthe pages 3-5)

3.4 Suggested HPO terms

A staged phenotype-to-HPO mapping based on the retrieved literature is provided below.

Table (click to expand)
Stage/phenotype Description Timing Suggested HPO terms Evidence (citation IDs) URL Publication date
Primary lesion Initial pruritic, erythematous, scaly papule or plaque at inoculation site; enlarges and typically does not ulcerate ~3 weeks after infection; alternatively reported as 1–8 weeks after infection Pruritus (HP:0000989); Erythema (HP:0010783); Papule (HP:0200034); Plaque of skin (HP:0032316); Scaly skin (HP:0000958) (stamm2015pintalatinamericas pages 1-3, rosa2021maldepinta pages 1-2, mitja2013advancesinthe pages 2-3, mitja2013advancesinthe pages 3-5) https://doi.org/10.4269/ajtmh.15-0329; https://doi.org/10.1111/ijd.15264; https://doi.org/10.1371/journal.pntd.0002283 2015-11; 2021-11; 2013-10
Secondary disseminated lesions (“pintids”) Months to years after primary lesion, disseminated skin lesions develop with generalized rash and pigmentary change; lesions may remain active/infectious for years Months after infection in classic staging; generalized rash reported over 2–4 years Rash (HP:0000988); Abnormal skin pigmentation (HP:0000953); Hyperpigmentation of the skin (HP:0000952); Hypopigmentation of the skin (HP:0001010); Acral dyschromia (suggested, mapped broadly to abnormal skin pigmentation) (stamm2015pintalatinamericas pages 1-3, rosa2021maldepinta pages 1-2, mitja2013advancesinthe pages 2-3) https://doi.org/10.4269/ajtmh.15-0329; https://doi.org/10.1111/ijd.15264; https://doi.org/10.1371/journal.pntd.0002283 2015-11; 2021-11; 2013-10
Late pigmentary disease Late/tertiary pinta characterized by dyschromia, achromic or hypochromic lesions, and persistent depigmentation; cosmetic disfigurement may remain despite cure Usually 2–5 years after infection; other reports describe 3–10 years for late changes Dyschromia (suggested, mapped to Abnormal skin pigmentation HP:0000953); Achromia/Hypopigmentation of the skin (HP:0001010); Hyperpigmentation of the skin (HP:0000952); Vitiligo-like depigmentation (suggested, mapped to HP:0001010) (stamm2015pintalatinamericas pages 1-3, rosa2021maldepinta pages 1-2, mitja2013advancesinthe pages 2-3) https://doi.org/10.4269/ajtmh.15-0329; https://doi.org/10.1111/ijd.15264; https://doi.org/10.1371/journal.pntd.0002283 2015-11; 2021-11; 2013-10
Skin atrophy Chronic late lesions may show cutaneous thinning/atrophy accompanying pigment loss Late stage, usually years after untreated infection Skin atrophy (HP:0000962) (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 3-5) https://doi.org/10.4269/ajtmh.15-0329; https://doi.org/10.1371/journal.pntd.0002283 2015-11; 2013-10
Histopathologic early lesion correlate Early lesions show loss of melanin in basal cells and liquefaction degeneration Early/primary stage biopsy finding Decreased skin pigmentation (suggested, mapped to Hypopigmentation of the skin HP:0001010) (mitja2013advancesinthe pages 3-5) https://doi.org/10.1371/journal.pntd.0002283 2013-10
Histopathologic late lesion correlate Late lesions show epidermal atrophy and numerous dermal melanophages Late stage biopsy finding Skin atrophy (HP:0000962); Abnormality of skin pigmentation (HP:0000953) (mitja2013advancesinthe pages 3-5) https://doi.org/10.1371/journal.pntd.0002283 2013-10
Disease distribution/severity pattern Pinta is generally the most benign endemic treponematosis and is limited to the skin, without the ulcerative or destructive bone disease typical of some other treponematoses Chronic, slowly progressive if untreated Cutaneous abnormality (HP:0011121) (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3, mitja2013advancesinthe pages 3-5) https://doi.org/10.4269/ajtmh.15-0329; https://doi.org/10.1371/journal.pntd.0002283 2015-11; 2013-10
Prognostic note on treatment response Early lesions heal over months after treatment, but late pigmentary changes may be irreversible or only partially reversible After therapy; chronic untreated disease worsens cosmetically over years Abnormal skin pigmentation (HP:0000953) (rosa2021maldepinta pages 1-2, stamm2015pintalatinamericas pages 3-5) https://doi.org/10.1111/ijd.15264; https://doi.org/10.4269/ajtmh.15-0329 2021-11; 2015-11

Table: This table summarizes the main clinical stages and phenotypes of pinta, with suggested HPO mappings, timing, and severity/progression notes. It is useful for phenotype annotation and natural-history curation in a disease knowledge base.

3.5 Quality of life impact

The retrieved evidence emphasizes disfigurement/cosmetic persistence of late pigmentary changes even after cure, implying psychosocial and quality-of-life impact; however, no quantitative QoL instruments (e.g., SF-36, EQ-5D) were identified for pinta in the retrieved set. (rosa2021maldepinta pages 1-2, stamm2015pintalatinamericas pages 3-5)


4. Genetic / Molecular Information

4.1 Human causal genes and pathogenic variants

Not applicable as a primary genetic disorder. No host genetic susceptibility loci were identified in the retrieved evidence set.

4.2 Pathogen molecular data and taxonomy (what is known; key gaps)

  • Not-yet-cultivable / no extant isolates in common use: The 2015 pinta perspective notes that T. carateum is “not-yet-cultivable” and that isolates are not available for study, limiting experimentation and genomic characterization. (stamm2015pintalatinamericas pages 1-3, stamm2015pintalatinamericas pages 3-5)
  • Serologic and morphologic indistinguishability: T. carateum is described as morphologically and serologically indistinguishable from T. pallidum subspecies agents of syphilis/yaws/bejel, which contributes to diagnostic ambiguity. (stamm2015pintalatinamericas pages 1-3)
  • Insufficient genomic knowledge for confident subspecies placement: Both Mitjà et al. and Stamm emphasize that molecular knowledge is insufficient to confidently classify T. carateum as a T. pallidum subspecies, and that genomic differentiation methods used for T. pallidum subspecies have not been applied due to lack of isolates/genomic data. (mitja2013advancesinthe pages 3-5, stamm2015pintalatinamericas pages 1-3)

4.3 Suggested ontology terms (molecular/cellular)

Because pinta is a skin-limited treponemal infection with pigmentary pathology: - GO (Biological Process) suggestions (inferred from histology/clinical pathology): inflammatory response; immune response; melanin biosynthetic process (as a downstream phenotype driver); response to bacterium. (mitja2013advancesinthe pages 3-5) - CL (Cell Ontology) suggestions: melanocyte; macrophage (consistent with dermal melanophages); plasma cell (reported in biopsy infiltrates in a 2021 case). (rosa2021maldepinta pages 1-2, mitja2013advancesinthe pages 3-5)


5. Environmental Information

5.1 Non-genetic contributing factors

The evidence emphasizes exposure in tropical rural environments and direct skin contact transmission, rather than toxins/radiation/pollution. (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3)

5.2 Infectious agents

Primary agent: Treponema carateum. (stamm2015pintalatinamericas pages 1-3, papp2024cdclaboratoryrecommendations pages 3-4)


6. Mechanism / Pathophysiology

6.1 Causal chain (clinical mechanism summary)

1) Initial infection via direct skin-to-skin contact introduces T. carateum into skin. (stamm2015pintalatinamericas pages 1-3, papp2024cdclaboratoryrecommendations pages 3-4) 2) Primary localized lesion develops (scaly papule/plaque) without typical ulceration. (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3, mitja2013advancesinthe pages 3-5) 3) Dissemination within skin produces secondary lesions (“pintids”) and pigmentary change. (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3) 4) Chronic inflammatory and pigmentary remodeling results in long-lasting dyschromia/achromia and possible skin atrophy, with histology including melanophages in dermis and epidermal atrophy in late lesions. (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 3-5)

6.2 Upstream vs downstream mechanisms

6.3 Molecular profiling / omics

No pinta-specific transcriptomic/proteomic/metabolomic datasets were identified in the retrieved evidence set.


7. Anatomical Structures Affected

7.1 Organ/system level

Primary affected organ: skin (cutaneous-only disease emphasized in multiple sources). (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3)

7.2 Tissue/cell level

Affected tissues/cell processes include epidermis/dermis with pigmentary abnormalities; histology in late lesions includes melanophages. (mitja2013advancesinthe pages 3-5)

7.3 Suggested UBERON / GO CC

  • UBERON: skin of body.
  • GO Cellular Component suggestions: epidermis; dermis; melanosome (as a pigment-related cellular component inference). (mitja2013advancesinthe pages 3-5)

8. Temporal Development (Natural History)

8.1 Onset and course

8.2 Remission patterns


9. Inheritance and Population

9.1 Epidemiology (best-available quantitative data)

Modern surveillance data are limited; however, the retrieved literature provides several quantitative historical/field observations: - Historical burden: an estimated ~1 million cases occurred in Mexico, Central America, and northern South America in the 1950s (historical estimate cited in a 2015 perspective). (stamm2015pintalatinamericas pages 1-3) - Field prevalence example: a Panama village survey (1982–83) reported ~20% of the population with clinical evidence of pinta (active/inactive), cited in both a 2015 perspective and the 2013 PLoS NTD review. (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3) - Current burden: the 2015 perspective emphasizes that the “current prevalence … is unknown due to the lack of surveillance data.” (stamm2015pintalatinamericas pages 1-3)

9.2 Demographics

A 2013 review reports peak incidence in adults (15–50 years), while other sources emphasize acquisition in children/adolescents; these differences may reflect heterogeneous data sources and limited modern surveillance. (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 2-3)

9.3 Geographic distribution

Pinta is primarily associated with tropical areas of Latin America/Central and South America; CDC 2024 characterizes it as rare in tropical Latin America. (mitja2013advancesinthe pages 2-3, papp2024cdclaboratoryrecommendations pages 3-4)


10. Diagnostics

10.1 Clinical diagnosis

Diagnosis relies on compatible clinical lesions (scaly plaques progressing to dyschromic patches) plus epidemiologic context (residence/travel in historically endemic regions) and exclusion of mimics such as tinea versicolor or vitiligo. (mitja2013advancesinthe pages 2-3)

10.2 Serologic testing (standard approach; key limitation)

Across endemic treponematoses, diagnostics generally follow syphilis paradigms using both nontreponemal and treponemal tests: - Nontreponemal tests: RPR, VDRL. - Treponemal tests: TPHA/TPPA, FTA-Abs, ELISA. A core limitation is repeatedly emphasized: serology cannot distinguish pinta from other endemic treponematoses or venereal syphilis. (mitja2013advancesinthe pages 3-5, stamm2015pintalatinamericas pages 1-3)

A 2021 pinta case report illustrates this diagnostic approach with very high VDRL titer and positive FTA-Abs IgM/IgG in a compatible clinical context. (rosa2021maldepinta pages 1-2)

10.3 Direct detection / microscopy / molecular methods

Mitjà et al. emphasize that direct methods are constrained by inability to culture treponemes and the impracticality/low sensitivity of some direct tests in field settings; they note increasing use of PCR and genomic fingerprinting for endemic treponematoses in general, but definitive molecular diagnosis remains limited by availability. (mitja2013advancesinthe pages 1-2, mitja2013advancesinthe pages 3-5)

Recent (2024) authoritative diagnostic context: The CDC laboratory recommendations (2024) describe that direct detection is evolving toward molecular methods while serology remains central; the report also notes there are no FDA-cleared molecular tests marketed in the U.S. for T. pallidum (which has implications for distinguishing among treponematoses when patients have relevant travel histories). (papp2024cdclaboratoryrecommendations pages 25-26)

10.4 Differential diagnosis

Important differentials include tinea versicolor, vitiligo, melasma, leprosy, and other dermatoses causing pigmentary change. (mitja2013advancesinthe pages 2-3)


11. Outcome / Prognosis

11.1 Mortality/survival

No mortality or survival statistics specific to pinta were identified in the retrieved evidence set; pinta is generally characterized as skin-limited and “benign” relative to other treponematoses. (stamm2015pintalatinamericas pages 1-3)

11.2 Morbidity and complications

The main long-term morbidity described is chronic pigmentary change (dyschromia/achromia) and possible skin atrophy, which may be persistent despite cure. (stamm2015pintalatinamericas pages 3-5, rosa2021maldepinta pages 1-2)


12. Treatment

12.1 First-line therapy (real-world standard)

Long-acting intramuscular benzathine penicillin is widely described as curative across stages: - A 2015 perspective reports that a single intramuscular dose can render lesions noninfectious in <24 hours and provides dosing guidance (adults 1.2 million units; children 0.6 million units). (stamm2015pintalatinamericas pages 3-5) - A 2021 case report describes treatment with benzathine penicillin 2.4 million units IM and similarly notes rapid loss of infectiousness (within ~24 hours). (rosa2021maldepinta pages 1-2)

12.2 Alternatives / mass drug administration implications

A key implementation-relevant point is that mass azithromycin campaigns for yaws eradication could also affect pinta if T. carateum is azithromycin-sensitive (not directly proven in the retrieved evidence, but proposed as plausible). (stamm2015pintalatinamericas pages 3-5)

12.3 Treatment outcomes

Early lesions may heal over months after treatment; late pigmentary changes may persist. (stamm2015pintalatinamericas pages 3-5, rosa2021maldepinta pages 1-2)

12.4 Suggested MAXO terms (treatment actions)

  • Intramuscular benzathine penicillin therapy.
  • Antibiotic therapy (systemic).
  • Public health mass drug administration (azithromycin-based), as a plausible co-benefit when targeting yaws in co-endemic settings. (stamm2015pintalatinamericas pages 3-5)

12.5 Clinical trials

No pinta-specific interventional clinical trials were identified in the retrieved evidence set.


13. Prevention

13.1 Primary prevention

No vaccine exists for pinta. Prevention is primarily via reducing skin-to-skin exposure to infectious lesions and through community-level detection and treatment strategies. (stamm2015pintalatinamericas pages 1-3, papp2024cdclaboratoryrecommendations pages 3-4)

13.2 Public health control (historical and current implementation)

  • Historical implementation: mass penicillin campaigns in the 1950s–1960s markedly reduced endemic treponematoses and nearly eradicated them in many regions, but resurgence occurred where political commitment/resources waned. (mitja2013advancesinthe pages 1-2, stamm2015pintalatinamericas pages 3-5)
  • Modern implementation opportunity (indirect): yaws eradication strategies using azithromycin may have spillover benefits for pinta where co-endemic, contingent on antimicrobial susceptibility. (stamm2015pintalatinamericas pages 3-5)

14. Other Species / Natural Disease

No evidence for a non-human animal reservoir or naturally occurring pinta in other species was identified in the retrieved evidence set. (Note: other treponematoses have been discussed in non-human primates in general literature, but pinta-specific evidence was not retrieved here.)


15. Model Organisms

Pinta-specific experimental models are extremely limited in contemporary literature because T. carateum is not available as an isolate and is not cultivable in standard systems; this limits the feasibility of modern animal models, in vitro systems, and functional genomics. (stamm2015pintalatinamericas pages 3-5, stamm2015pintalatinamericas pages 1-3)


Recent developments and latest research (prioritizing 2023–2024)

1) Updated authoritative guidance acknowledging pinta in laboratory diagnostic context (2024): The CDC’s 2024 syphilis laboratory recommendations explicitly remind laboratorians and clinicians that nonvenereal treponematoses exist, and state: “Treponema carateum infection results in pinta which, although rare, is found in tropical areas of Latin America,” emphasizing travel/endemic-area context when interpreting serology and treponemal testing. URL: https://doi.org/10.15585/mmwr.rr7301a1 (Published Feb 2024). (papp2024cdclaboratoryrecommendations pages 3-4, papp2024cdclaboratoryrecommendations pages 1-3)

2) Modern immunology framing of treponemal disease relatedness (2023): A 2023 Frontiers in Immunology review on syphilis vaccines explicitly distinguishes pinta’s etiologic agent at the species level (“Treponema carateum”) while emphasizing the broader high similarity of pathogenic treponemes, reinforcing why serology alone cannot reliably separate treponemal syndromes and why genomic methods are central to treponemal taxonomy. URL: https://doi.org/10.3389/fimmu.2023.1126170 (Published Apr 2023). (avilanieto2023syphilisvaccinechallenges pages 1-2)

3) Genomics advances inform the broader treponemal complex but not pinta directly (2024 evidence set): Recent paleogenomic work on T. pallidum subspecies emphasizes very high sequence identity among syphilis/yaws/bejel genomes and the importance of ancient DNA to resolve evolutionary history; pinta is generally referenced as part of the treponemal disease complex, but the retrieved 2024 ancient-genome evidence does not provide pinta-specific genomes, highlighting the ongoing gap in T. carateum genomic characterization. (barquera2024ancientgenomesrevealb pages 1-4)


Expert interpretation and analysis (authoritative sources)

  • Diagnostic ambiguity is intrinsic to biology, not just test choice: Multiple sources converge that T. carateum infection produces serologic patterns indistinguishable from syphilis and other endemic treponematoses, so clinical epidemiology and careful differential diagnosis are essential to avoid misclassification (e.g., labeling pinta as sexually transmitted syphilis). (stamm2015pintalatinamericas pages 1-3, mitja2013advancesinthe pages 3-5)

  • The major bottleneck for “modernizing” pinta knowledge is lack of isolates/genomes: Reviews repeatedly emphasize that absence of T. carateum isolates and genomic data limits taxonomic certainty, molecular diagnostics, antimicrobial resistance surveillance, and vaccine-relevant antigen discovery, in contrast to accelerating genomics in syphilis/yaws/bejel research. (stamm2015pintalatinamericas pages 3-5, stamm2015pintalatinamericas pages 1-3)


Key abstract quotes (for evidence anchoring)

  • From Mitjà et al. (PLoS Negl Trop Dis, 2013) abstract on endemic treponematoses diagnosis: “Traditionally, the human treponematoses have been differentiated based upon their clinical manifestations and epidemiologic characteristics because the etiologic agents are indistinguishable in the laboratory.” URL: https://doi.org/10.1371/journal.pntd.0002283 (Published Oct 2013). (mitja2013advancesinthe pages 1-2)

Limitations of this report (evidence gaps)

  • Explicit MONDO/MeSH/ICD identifiers for pinta were not found in the retrieved full-text evidence set and therefore are not provided with citations.
  • Pinta-specific modern surveillance estimates (incidence/prevalence post-2000), antimicrobial susceptibility data (e.g., azithromycin MICs), and pathogen genome sequences were not identified in the retrieved evidence set.
  • No pinta-specific clinical trials were identified.

These gaps likely reflect the rarity of modern cases and limited laboratory material availability for T. carateum. (stamm2015pintalatinamericas pages 1-3, papp2024cdclaboratoryrecommendations pages 25-26)

References

  1. (stamm2015pintalatinamericas pages 1-3): Lola V. Stamm. Pinta: latin america's forgotten disease? The American journal of tropical medicine and hygiene, 93 5:901-3, Nov 2015. URL: https://doi.org/10.4269/ajtmh.15-0329, doi:10.4269/ajtmh.15-0329. This article has 20 citations.

  2. (stamm2015pintalatinamericas pages 3-5): Lola V. Stamm. Pinta: latin america's forgotten disease? The American journal of tropical medicine and hygiene, 93 5:901-3, Nov 2015. URL: https://doi.org/10.4269/ajtmh.15-0329, doi:10.4269/ajtmh.15-0329. This article has 20 citations.

  3. (papp2024cdclaboratoryrecommendations pages 3-4): John R. Papp, Ina U. Park, Yetunde Fakile, Lara Pereira, Allan Pillay, and Gail A. Bolan. Cdc laboratory recommendations for syphilis testing, united states, 2024. MMWR Recommendations and Reports, 73:1-32, Feb 2024. URL: https://doi.org/10.15585/mmwr.rr7301a1, doi:10.15585/mmwr.rr7301a1. This article has 199 citations.

  4. (rosa2021maldepinta pages 1-2): Ralph Vighi da Rosa, Daniele Damares Rodrigues de Souza, André Cartell, and Paulo Ricardo Martins Souza. Mal de pinta, first autochthonous case from south of brazil. International Journal of Dermatology, Nov 2021. URL: https://doi.org/10.1111/ijd.15264, doi:10.1111/ijd.15264. This article has 1 citations and is from a peer-reviewed journal.

  5. (mitja2013advancesinthe pages 2-3): Oriol Mitjà, David Šmajs, and Quique Bassat. Advances in the diagnosis of endemic treponematoses: yaws, bejel, and pinta. PLoS Neglected Tropical Diseases, 7:e2283, Oct 2013. URL: https://doi.org/10.1371/journal.pntd.0002283, doi:10.1371/journal.pntd.0002283. This article has 88 citations and is from a domain leading peer-reviewed journal.

  6. (avilanieto2023syphilisvaccinechallenges pages 1-2): Carlos Ávila-Nieto, Núria Pedreño-López, Oriol Mitjà, Bonaventura Clotet, Julià Blanco, and Jorge Carrillo. Syphilis vaccine: challenges, controversies and opportunities. Frontiers in Immunology, Apr 2023. URL: https://doi.org/10.3389/fimmu.2023.1126170, doi:10.3389/fimmu.2023.1126170. This article has 54 citations and is from a peer-reviewed journal.

  7. (mitja2013advancesinthe pages 3-5): Oriol Mitjà, David Šmajs, and Quique Bassat. Advances in the diagnosis of endemic treponematoses: yaws, bejel, and pinta. PLoS Neglected Tropical Diseases, 7:e2283, Oct 2013. URL: https://doi.org/10.1371/journal.pntd.0002283, doi:10.1371/journal.pntd.0002283. This article has 88 citations and is from a domain leading peer-reviewed journal.

  8. (papp2024cdclaboratoryrecommendations pages 25-26): John R. Papp, Ina U. Park, Yetunde Fakile, Lara Pereira, Allan Pillay, and Gail A. Bolan. Cdc laboratory recommendations for syphilis testing, united states, 2024. MMWR Recommendations and Reports, 73:1-32, Feb 2024. URL: https://doi.org/10.15585/mmwr.rr7301a1, doi:10.15585/mmwr.rr7301a1. This article has 199 citations.

  9. (mitja2013advancesinthe pages 1-2): Oriol Mitjà, David Šmajs, and Quique Bassat. Advances in the diagnosis of endemic treponematoses: yaws, bejel, and pinta. PLoS Neglected Tropical Diseases, 7:e2283, Oct 2013. URL: https://doi.org/10.1371/journal.pntd.0002283, doi:10.1371/journal.pntd.0002283. This article has 88 citations and is from a domain leading peer-reviewed journal.

  10. (papp2024cdclaboratoryrecommendations pages 1-3): John R. Papp, Ina U. Park, Yetunde Fakile, Lara Pereira, Allan Pillay, and Gail A. Bolan. Cdc laboratory recommendations for syphilis testing, united states, 2024. MMWR Recommendations and Reports, 73:1-32, Feb 2024. URL: https://doi.org/10.15585/mmwr.rr7301a1, doi:10.15585/mmwr.rr7301a1. This article has 199 citations.

  11. (barquera2024ancientgenomesrevealb pages 1-4): R Barquera, TL Sitter, CL Kirkpatrick, and DA Ramirez. Ancient genomes reveal a deep history of treponemal disease in the americas. Unknown journal, 2024.