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Whipple Disease

1. Disease Information

2026-04-04
Falcon MONDO:0005116 Model: Edison Scientific Literature 45 citations

1. Disease Information

1.1 Definition / overview

WD is a rare systemic infectious disorder caused by TW with protean gastrointestinal, rheumatologic, neurologic, and other systemic manifestations. (ahmad2022whipple’sdiseasereview pages 1-2, melas2021whipplesdiseasethe pages 1-2)

1.2 Key identifiers (from retrieved sources)

  • ICD-10-CM: K90.81 (used for case ascertainment in a US National Inpatient Sample analysis). Publication date: Dec 2022. URL: https://doi.org/10.1097/MD.0000000000032231 (ahmad2022whipple’sdiseasereview pages 1-2)

1.3 Other identifiers requested but not recoverable from the available full-text evidence in this run

  • MONDO ID: not available from retrieved evidence.
  • Orphanet (ORPHA) ID: not available from retrieved evidence.
  • MeSH descriptor: not available from retrieved evidence.
  • ICD-11 code: not available from retrieved evidence.

Note: The retrieved ICD-11/Orphanet mapping papers were methodological and did not provide the WD-specific mappings in the accessible text chunks returned here. (ahmad2022whipple’sdiseasereview pages 1-2)

1.4 Synonyms and alternative names (from retrieved sources)

1.5 Evidence sources (individual vs aggregated)

  • Aggregated disease-level resources: national inpatient database analysis (NIS) and national EHR aggregation (Explorys) for epidemiology and demographics. (ahmad2022whipple’sdiseasereview pages 2-2, elchert2019epidemiologyofwhipple’s pages 1-3)
  • Aggregated clinical cohorts: multicenter rheumatology cohort; single-center CNS cohort. (tison2021rheumatologicalfeaturesof pages 3-4, mecklenburg2023thespectrumof pages 1-1)
  • Individual patient reports: used mainly to illustrate atypical presentations and prolonged therapy. (ye2023whipple’sdiseasepresenting pages 2-5)

2. Etiology

2.1 Disease causal factors

2.2 Risk factors

Host susceptibility / immune context - WD occurs in a small fraction of exposed/carrier individuals, supporting a major role for host susceptibility. In a US inpatient study, TW carriage in stool is reported at ~1–11% in healthy individuals while progression to WD is <0.01%. (ahmad2022whipple’sdiseasereview pages 1-2) - Immunosuppression can worsen or unmask disease, including poor response/worsening under TNF inhibitors in a multicenter cohort. (tison2021rheumatologicalfeaturesof pages 1-2, dolmans2017clinicalmanifestationstreatment pages 18-20)

Occupational/environmental exposure - In a multicenter cohort/review, TW detection in stool was higher in sewage plant workers (12–26%) vs healthy controls, supporting exposure/carriage risk in certain occupations. (tison2021rheumatologicalfeaturesof pages 1-2)

Genetic susceptibility (risk alleles/polymorphisms) - HLA associations have been reported, including HLA-DRB1*13 and HLA-DQB1*06, and cytokine-related polymorphisms such as IL16, proposed to impair antigen presentation and predispose to chronic relapsing disease. (marth2016tropherymawhippleiinfection pages 2-3, dolmans2017clinicalmanifestationstreatment pages 5-7)

2.3 Protective factors

No protective genetic variants or environmental protective factors were identified in the retrieved evidence.

2.4 Gene–environment interactions

A plausible interaction model is supported: environmental/occupational exposure leading to carriage interacts with host immune-genetic susceptibility (HLA/cytokine regulation) to permit intracellular persistence and dissemination. Direct quantitative GxE effect sizes were not identified in the retrieved evidence. (tison2021rheumatologicalfeaturesof pages 1-2, marth2016tropherymawhippleiinfection pages 2-3)

3. Phenotypes

3.1 Core clinical phenotypes and characteristics

Gastrointestinal (classic WD) - Typical manifestations include chronic diarrhea, abdominal pain, weight loss, and malabsorption (classic intestinal involvement), with PAS-positive foamy macrophages in small-bowel lamina propria. (melas2021whipplesdiseasethe pages 1-2, song2023currentknowledgeof pages 1-2)

Rheumatologic - Arthritis/arthralgia often precedes GI symptoms; in a diagnostic overview case series, the classic course included a prodromal stage where arthritis is the first and most common manifestation (~75%). (melas2021whipplesdiseasethe pages 1-2)

Neurologic/CNS - Neurologic involvement is common and prognostically important; a 2023 CNS cohort reported neurologic involvement in 63.9% (23/36). (mecklenburg2023thespectrumof pages 1-1) - Frequent neurologic domains included cognitive, motor (pyramidal), and oculomotor dysfunction; specific signs such as oculomasticatory myorhythmia and supranuclear vertical gaze palsy are emphasized as WD-specific clues in CNS disease. (mecklenburg2023thespectrumof pages 1-1, mecklenburg2023thespectrumof pages 1-2)

Other organ involvement - Cardiovascular manifestations include culture-negative endocarditis (discussed as part of systemic spectrum in reviews/cohorts). (tison2021rheumatologicalfeaturesof pages 1-2, dolmans2017clinicalmanifestationstreatment pages 10-12) - Lymphadenopathy, fever, pleural/pericardial involvement, and uveitis are reported extraintestinal manifestations. (tison2021rheumatologicalfeaturesof pages 1-2)

3.2 Frequency data (available from retrieved sources)

3.3 Suggested HPO terms (non-exhaustive, to support KB population)

(Ontology IDs are provided conceptually; exact HP identifiers should be confirmed against the HPO browser during KB ingestion.) - Chronic diarrhea; abdominal pain; weight loss; malabsorption; lymphadenopathy. (melas2021whipplesdiseasethe pages 1-2, song2023currentknowledgeof pages 1-2) - Arthralgia/arthritis (migratory/seronegative); fever. (tison2021rheumatologicalfeaturesof pages 1-2, melas2021whipplesdiseasethe pages 1-2) - Cognitive impairment/dementia; supranuclear gaze palsy; myorhythmia; seizures (less common); stroke/ischemic cerebrovascular event. (mecklenburg2023thespectrumof pages 1-1, mecklenburg2023thespectrumof pages 1-2)

3.4 Quality of life impact

QoL instruments (SF-36/EQ-5D/PROMIS) and quantitative QoL estimates were not identified in the retrieved evidence. However, the long diagnostic delay and multisystem disability burden (arthritis, GI symptoms, cognitive impairment, stroke) imply substantial functional impact. (melas2021whipplesdiseasethe pages 1-2, mecklenburg2023thespectrumof pages 1-1)

4. Genetic/Molecular Information

4.1 Causal genes

WD is not a monogenic disorder in the retrieved evidence; instead, susceptibility is associated with immune-related polymorphisms and HLA alleles. (marth2016tropherymawhippleiinfection pages 2-3, dolmans2017clinicalmanifestationstreatment pages 5-7)

4.2 Reported susceptibility loci / variants (from retrieved sources)

Variant-level details (HGVS nomenclature), population allele frequencies (gnomAD), and ClinVar classifications were not available in the retrieved evidence.

4.3 Epigenetics, chromosomal abnormalities, modifier genes

Not identified in the retrieved evidence.

5. Environmental Information

5.1 Environmental/lifestyle factors

  • Occupational exposure context is supported by higher carriage among sewage workers. (tison2021rheumatologicalfeaturesof pages 1-2)
  • Specific lifestyle modifiers (diet, smoking, alcohol) were not identified in the retrieved evidence.

5.2 Infectious agent details

TW is an intracellular bacterium that can be difficult to culture and often requires molecular methods for detection; after entry, it survives within macrophages and can disseminate systemically. (dolmans2017clinicalmanifestationstreatment pages 1-3, dolmans2017clinicalmanifestationstreatment pages 7-8)

6. Mechanism / Pathophysiology

6.1 Causal chain (integrated model)

  1. Exposure and carriage: TW carriage in stool/saliva is relatively common in populations, including occupational groups. (tison2021rheumatologicalfeaturesof pages 1-2)
  2. Susceptible host immune state: predisposition associated with HLA alleles and immune-regulatory polymorphisms plus immune skewing (e.g., increased IL-10/IL-16 and reduced IL-12/IFN-γ). (marth2016tropherymawhippleiinfection pages 2-3)
  3. Failure of macrophage killing: TW is phagocytosed but persists intracellularly; impaired phagosome maturation and other macrophage defects enable replication and survival. (dolmans2017clinicalmanifestationstreatment pages 7-8)
  4. Dissemination: infected macrophages/lymphatic-blood dissemination leads to multisystem involvement (GI, joints, CNS, heart, etc.). (dolmans2017clinicalmanifestationstreatment pages 7-8, dolmans2017clinicalmanifestationstreatment pages 10-12)

6.2 Key immune mechanisms (host)

6.3 Suggested GO terms (biological processes; conceptual mapping)

6.4 Suggested CL (cell types; conceptual mapping)

6.5 Molecular profiling / omics

No transcriptomic/proteomic/metabolomic datasets were captured in the retrieved evidence, though intestinal infiltrating cells were described as showing an alternatively activated macrophage transcriptional pattern in the IRIS review. (song2023currentknowledgeof pages 7-9)

7. Anatomical Structures Affected

7.1 Organ-level involvement

7.2 Tissue/cell-level

7.3 Suggested UBERON terms (conceptual mapping)

8. Temporal Development

8.1 Onset

  • Often adult onset; national inpatient data show mean age ~60 among hospitalized cases. (ahmad2022whipple’sdiseasereview pages 2-2)
  • The course can include a prolonged prodrome (e.g., years of arthritis before GI disease), contributing to major diagnostic delays. (melas2021whipplesdiseasethe pages 1-2)

8.2 Progression / course patterns

9. Inheritance and Population

9.1 Epidemiology

9.2 Population demographics

  • NIS (2016–2018): male predominance (~67%), older age distribution (mean ~60), and higher risk in the US Midwest. (ahmad2022whipple’sdiseasereview pages 2-2)
  • Explorys (2012–2017): similar prevalence in men and women, higher prevalence in Caucasians vs African Americans, and higher prevalence in non-Hispanics; prevalence increases markedly with age, peaking at ages 80–84 (39.2/million). (elchert2019epidemiologyofwhipple’s pages 5-6)

9.3 Inheritance pattern

Not Mendelian; evidence supports complex susceptibility (HLA/cytokine polymorphisms) rather than single-gene inheritance. (marth2016tropherymawhippleiinfection pages 2-3)

10. Diagnostics

10.1 Histopathology

Direct abstract quote (diagnostic histology): - “typical foamy macrophages with granular diastase-resistant inclusions presenting a strong positive PAS reaction.” (Cureus case report/review; Jan 2023; https://doi.org/10.7759/cureus.34029) (viegas2023whyiswhipples pages 7-7)

10.2 PCR diagnostics (specimen-specific performance)

A large multicenter cohort reported the following sensitivities (classic WD vs non-classic WD): - Stool PCR: 100% vs 75% - Saliva PCR: 100% vs 75% - Small-bowel biopsy PCR: 89% vs 60% - Blood PCR: 50% vs 23% - Urine PCR: 33% vs 13% (tison2021rheumatologicalfeaturesof pages 3-4, tison2021rheumatologicalfeaturesof pages 1-2)

A case review additionally reported performance estimates and interpretive thresholds, including stool specificity ~97.6% and improved PPV when stool+saliva are both positive or fecal load exceeds >32,200 copies/mL. (viegas2023whyiswhipples pages 7-7)

10.3 CNS diagnostics (CSF and neuroimaging)

  • In a 2023 CNS cohort, TW DNA was detected in CSF more often in neurologically symptomatic patients (59.1%) than asymptomatic (30.8%), but PCR positivity did not perfectly match clinical syndromes. (mecklenburg2023thespectrumof pages 1-1)
  • Neuroimaging often implicated deep midline structures (e.g., hypothalamus, thalamus, periaqueductal region); aqueductal stenosis/hydrocephalus can occur and may require shunting. (mecklenburg2023thespectrumof pages 8-9)

10.4 Differential diagnosis (examples supported by evidence)

10.5 Advanced molecular diagnostics (recent developments)

  • Targeted/metagenomic sequencing approaches (e.g., NGS from bronchoalveolar lavage) are increasingly used to detect TW in respiratory specimens, though colonization vs causation remains a concern in some pneumonia presentations. (ye2023whipple’sdiseasepresenting pages 2-5)

11. Outcome / Prognosis

11.1 Mortality

11.2 Morbidity and complications

11.3 Relapse

12. Treatment

12.1 Standard antimicrobial therapy (current practice patterns)

Important expert analysis (antibiotic resistance/choice): - A major microbiology review notes genomic/in vitro evidence consistent with TMP-SMX failure (intrinsic trimethoprim resistance mechanisms) and reports a series in which “all 14 patients who were first treated with co-trimoxazole failed treatment,” supporting doxycycline+hydroxychloroquine as an alternative bactericidal regimen. (dolmans2017clinicalmanifestationstreatment pages 18-20)

12.2 Management of WD-associated IRIS

  • IRIS occurs in ~10% of classic cases after antibiotic therapy; first-line therapy is oral corticosteroids, and thalidomide is an option for steroid-resistant cases. (dolmans2017clinicalmanifestationstreatment pages 18-20)
  • Mechanistic framing: Th1 reconstitution and inflammatory cytokines can drive barrier dysfunction and systemic inflammation; PCR may be negative and antibiotics ineffective during IRIS, emphasizing immune modulation rather than escalation of antimicrobials. (song2023currentknowledgeof pages 1-2)

12.3 Real-world implementation examples (recent)

  • A 2023 case report (China) used ceftriaxone induction followed by prolonged doxycycline+hydroxychloroquine with radiologic lymph node regression over 44 months, illustrating long durations sometimes used in practice and the need for monitoring for inflammatory flares (suspected IRIS). Publication date: May 2023. URL: https://doi.org/10.1186/s12879-023-08276-y (ye2023whipple’sdiseasepresenting pages 2-5)

12.4 Suggested MAXO terms (conceptual mapping)

12.5 Clinical trials

No WD-specific interventional clinical trials were retrieved in this run.

13. Prevention

  • No vaccine or established primary prevention strategy was identified in the retrieved evidence.
  • Practical prevention in susceptible contexts is mainly secondary/tertiary: early recognition in patients with chronic seronegative arthritis plus GI/systemic features; avoidance/caution with immunosuppressive therapy (especially TNF inhibitors) until WD is excluded in suspicious cases; and long-term follow-up for relapse/late CNS disease. (tison2021rheumatologicalfeaturesof pages 1-2, dolmans2017clinicalmanifestationstreatment pages 18-20)

14. Other Species / Natural Disease

No natural disease in non-human species, zoonotic transmission, or animal reservoirs were identified in the retrieved evidence.

15. Model Organisms

No in vivo animal models were identified in the retrieved evidence. Mechanistic work emphasized human mucosal immunology and macrophage biology and historical advances in TW culture, implying in vitro macrophage infection systems as a key experimental platform. (dolmans2017clinicalmanifestationstreatment pages 1-3, dolmans2017clinicalmanifestationstreatment pages 7-8)

Recent developments (prioritizing 2023–2024)

  1. CNS spectrum refined with cohort-level CSF + imaging analysis (2023): A 36-patient series reported neurologic involvement in 63.9% and highlighted underrecognized ischemic stroke (27.7%) and imperfect correlation between CSF PCR positivity and neurologic symptoms, emphasizing the need for integrated clinical–CSF–imaging diagnosis and careful interpretation of PCR timing relative to antibiotics. Publication date: Aug 2023. URL: https://doi.org/10.1111/ene.15511 (mecklenburg2023thespectrumof pages 1-1)
  2. IRIS conceptual updates (2023): A dedicated review summarized IRIS pathophysiology, highlighting immune-driven inflammation with potential negative PCR and limited antibiotic responsiveness, and discussed corticosteroids and thalidomide for management. Publication date: Oct 2023. URL: https://doi.org/10.3389/fimmu.2023.1265414 (song2023currentknowledgeof pages 1-2)
  3. Expanded molecular diagnostics and atypical presentations (2023): A case report highlighted atypical symptoms and very prolonged antibiotic courses with imaging follow-up, and cautioned that TW detection by sequencing alone (especially in pneumonia) may represent colonization rather than disease. Publication date: May 2023. URL: https://doi.org/10.1186/s12879-023-08276-y (ye2023whipple’sdiseasepresenting pages 2-5)

Limitations of this report (evidence gaps due to tool-retrieved sources)

  • Specific MONDO, Orphanet, MeSH, and ICD-11 identifiers could not be extracted from the retrieved full texts; only ICD-10 K90.81 was explicitly available. (ahmad2022whipple’sdiseasereview pages 1-2)
  • Variant-level genetic details (HGVS, allele frequencies), formal QoL statistics, and robust prevention studies were not present in the retrieved evidence set.

References (retrieved within this run; URLs and dates)

Key 2023–2024 sources highlighted above: - Song X et al. Front Immunol. Oct 2023. “Current knowledge of the immune reconstitution inflammatory syndrome in Whipple disease: a review.” https://doi.org/10.3389/fimmu.2023.1265414 (song2023currentknowledgeof pages 1-2) - Mecklenburg J et al. Eur J Neurol. Aug 2023. “The spectrum of central nervous system involvement in Whipple's disease.” https://doi.org/10.1111/ene.15511 (mecklenburg2023thespectrumof pages 1-1) - Ye H et al. BMC Infect Dis. May 2023. “Whipple’s disease presenting as weight gain and constipation in a Chinese woman.” https://doi.org/10.1186/s12879-023-08276-y (ye2023whipple’sdiseasepresenting pages 2-5)

High-authority background reviews used for mechanisms/diagnostics/treatment: - Dolmans RAV et al. Clin Microbiol Rev. Apr 2017. https://doi.org/10.1128/CMR.00033-16 (dolmans2017clinicalmanifestationstreatment pages 13-17, dolmans2017clinicalmanifestationstreatment pages 18-20, dolmans2017clinicalmanifestationstreatment pages 7-8) - Marth T et al. Lancet Infect Dis. Mar 2016. https://doi.org/10.1016/S1473-3099(15)00537-X (marth2016tropherymawhippleiinfection pages 6-7, marth2016tropherymawhippleiinfection pages 2-3)

Epidemiology: - Ahmad AI et al. Medicine. Dec 2022. https://doi.org/10.1097/MD.0000000000032231 (ahmad2022whipple’sdiseasereview pages 2-2) - Elchert JA et al. Dig Dis Sci. Nov 2019. https://doi.org/10.1007/s10620-018-5393-9 (elchert2019epidemiologyofwhipple’s pages 1-3)

References

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  2. (song2023currentknowledgeof pages 1-2): Xiangyi Song, Ruifeng Duan, Liwei Duan, and Lijuan Wei. Current knowledge of the immune reconstitution inflammatory syndrome in whipple disease: a review. Frontiers in Immunology, Oct 2023. URL: https://doi.org/10.3389/fimmu.2023.1265414, doi:10.3389/fimmu.2023.1265414. This article has 10 citations and is from a peer-reviewed journal.

  3. (mecklenburg2023thespectrumof pages 1-2): Jasper Mecklenburg, Verena Moos, Annette Moter, Eberhard Siebert, Alexander Heinrich Nave, Thomas Schneider, Klemens Ruprecht, and Philipp Euskirchen. The spectrum of central nervous system involvement in whipple's disease. European Journal of Neurology, 30:3417-3429, Aug 2023. URL: https://doi.org/10.1111/ene.15511, doi:10.1111/ene.15511. This article has 11 citations and is from a domain leading peer-reviewed journal.

  4. (ahmad2022whipple’sdiseasereview pages 1-2): Akram I. Ahmad, Colin Wikholm, Ioannis Pothoulakis, Claire Caplan, Arielle Lee, Faith Buchanan, and Won Kyoo Cho. Whipple’s disease review, prevalence, mortality, and characteristics in the united states: a cross-sectional national inpatient study. Medicine, 101:e32231, Dec 2022. URL: https://doi.org/10.1097/md.0000000000032231, doi:10.1097/md.0000000000032231. This article has 18 citations and is from a peer-reviewed journal.

  5. (ahmad2022whipple’sdiseasereview pages 2-3): Akram I. Ahmad, Colin Wikholm, Ioannis Pothoulakis, Claire Caplan, Arielle Lee, Faith Buchanan, and Won Kyoo Cho. Whipple’s disease review, prevalence, mortality, and characteristics in the united states: a cross-sectional national inpatient study. Medicine, 101:e32231, Dec 2022. URL: https://doi.org/10.1097/md.0000000000032231, doi:10.1097/md.0000000000032231. This article has 18 citations and is from a peer-reviewed journal.

  6. (ahmad2022whipple’sdiseasereview pages 2-2): Akram I. Ahmad, Colin Wikholm, Ioannis Pothoulakis, Claire Caplan, Arielle Lee, Faith Buchanan, and Won Kyoo Cho. Whipple’s disease review, prevalence, mortality, and characteristics in the united states: a cross-sectional national inpatient study. Medicine, 101:e32231, Dec 2022. URL: https://doi.org/10.1097/md.0000000000032231, doi:10.1097/md.0000000000032231. This article has 18 citations and is from a peer-reviewed journal.

  7. (elchert2019epidemiologyofwhipple’s pages 5-6): Jamie Ann Elchert, Emad Mansoor, Mohannad Abou-Saleh, and Gregory S. Cooper. Epidemiology of whipple’s disease in the usa between 2012 and 2017: a population-based national study. Digestive Diseases and Sciences, 64:1305-1311, Nov 2019. URL: https://doi.org/10.1007/s10620-018-5393-9, doi:10.1007/s10620-018-5393-9. This article has 73 citations and is from a peer-reviewed journal.

  8. (elchert2019epidemiologyofwhipple’s pages 1-3): Jamie Ann Elchert, Emad Mansoor, Mohannad Abou-Saleh, and Gregory S. Cooper. Epidemiology of whipple’s disease in the usa between 2012 and 2017: a population-based national study. Digestive Diseases and Sciences, 64:1305-1311, Nov 2019. URL: https://doi.org/10.1007/s10620-018-5393-9, doi:10.1007/s10620-018-5393-9. This article has 73 citations and is from a peer-reviewed journal.

  9. (tison2021rheumatologicalfeaturesof pages 1-2): Alice Tison, Pauline Preuss, Clémentine Leleu, François Robin, Adrien Le Pluart, Justine Vix, Guillaume Le Mélédo, Philippe Goupille, Elisabeth Gervais, Grégoire Cormier, Jean-David Albert, Aleth Perdriger, Béatrice Bouvard, Jean-Marie Berthelot, Nathan Foulquier, and Alain Saraux. Rheumatological features of whipple disease. Scientific Reports, Jun 2021. URL: https://doi.org/10.1038/s41598-021-91671-9, doi:10.1038/s41598-021-91671-9. This article has 39 citations and is from a peer-reviewed journal.

  10. (mecklenburg2023thespectrumof pages 1-1): Jasper Mecklenburg, Verena Moos, Annette Moter, Eberhard Siebert, Alexander Heinrich Nave, Thomas Schneider, Klemens Ruprecht, and Philipp Euskirchen. The spectrum of central nervous system involvement in whipple's disease. European Journal of Neurology, 30:3417-3429, Aug 2023. URL: https://doi.org/10.1111/ene.15511, doi:10.1111/ene.15511. This article has 11 citations and is from a domain leading peer-reviewed journal.

  11. (vargasrodriguez2023whipplesdiseasea pages 3-5): LJ Vargas-Rodríguez and JL Ruiz-Muñoz. Whipple's disease: a systematic review of the literature. Unknown journal, 2023.

  12. (mecklenburg2023thespectrumof pages 4-5): Jasper Mecklenburg, Verena Moos, Annette Moter, Eberhard Siebert, Alexander Heinrich Nave, Thomas Schneider, Klemens Ruprecht, and Philipp Euskirchen. The spectrum of central nervous system involvement in whipple's disease. European Journal of Neurology, 30:3417-3429, Aug 2023. URL: https://doi.org/10.1111/ene.15511, doi:10.1111/ene.15511. This article has 11 citations and is from a domain leading peer-reviewed journal.

  13. (tison2021rheumatologicalfeaturesof pages 3-4): Alice Tison, Pauline Preuss, Clémentine Leleu, François Robin, Adrien Le Pluart, Justine Vix, Guillaume Le Mélédo, Philippe Goupille, Elisabeth Gervais, Grégoire Cormier, Jean-David Albert, Aleth Perdriger, Béatrice Bouvard, Jean-Marie Berthelot, Nathan Foulquier, and Alain Saraux. Rheumatological features of whipple disease. Scientific Reports, Jun 2021. URL: https://doi.org/10.1038/s41598-021-91671-9, doi:10.1038/s41598-021-91671-9. This article has 39 citations and is from a peer-reviewed journal.

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  16. (schiepatti2020longtermmorbidityand pages 6-7): Annalisa Schiepatti, Maria Luisa Nicolardi, Piero Marone, and Federico Biagi. Long-term morbidity and mortality in whipple's disease: a single-center experience over 20 years. Future microbiology, 15:847-854, Jul 2020. URL: https://doi.org/10.2217/fmb-2019-0315, doi:10.2217/fmb-2019-0315. This article has 12 citations and is from a peer-reviewed journal.

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  19. (dolmans2017clinicalmanifestationstreatment pages 1-3): Ruben A. V. Dolmans, C. H. Edwin Boel, Miangela M. Lacle, and Johannes G. Kusters. Clinical manifestations, treatment, and diagnosis of tropheryma whipplei infections. Clinical Microbiology Reviews, 30:529-555, Apr 2017. URL: https://doi.org/10.1128/cmr.00033-16, doi:10.1128/cmr.00033-16. This article has 245 citations and is from a highest quality peer-reviewed journal.

  20. (dolmans2017clinicalmanifestationstreatment pages 7-8): Ruben A. V. Dolmans, C. H. Edwin Boel, Miangela M. Lacle, and Johannes G. Kusters. Clinical manifestations, treatment, and diagnosis of tropheryma whipplei infections. Clinical Microbiology Reviews, 30:529-555, Apr 2017. URL: https://doi.org/10.1128/cmr.00033-16, doi:10.1128/cmr.00033-16. This article has 245 citations and is from a highest quality peer-reviewed journal.

  21. (marth2016tropherymawhippleiinfection pages 2-3): Thomas Marth, Verena Moos, Christian Müller, Federico Biagi, and Thomas Schneider. Tropheryma whipplei infection and whipple's disease. The Lancet. Infectious diseases, 16 3:e13-22, Mar 2016. URL: https://doi.org/10.1016/s1473-3099(15)00537-x, doi:10.1016/s1473-3099(15)00537-x. This article has 251 citations.

  22. (dolmans2017clinicalmanifestationstreatment pages 5-7): Ruben A. V. Dolmans, C. H. Edwin Boel, Miangela M. Lacle, and Johannes G. Kusters. Clinical manifestations, treatment, and diagnosis of tropheryma whipplei infections. Clinical Microbiology Reviews, 30:529-555, Apr 2017. URL: https://doi.org/10.1128/cmr.00033-16, doi:10.1128/cmr.00033-16. This article has 245 citations and is from a highest quality peer-reviewed journal.

  23. (dolmans2017clinicalmanifestationstreatment pages 10-12): Ruben A. V. Dolmans, C. H. Edwin Boel, Miangela M. Lacle, and Johannes G. Kusters. Clinical manifestations, treatment, and diagnosis of tropheryma whipplei infections. Clinical Microbiology Reviews, 30:529-555, Apr 2017. URL: https://doi.org/10.1128/cmr.00033-16, doi:10.1128/cmr.00033-16. This article has 245 citations and is from a highest quality peer-reviewed journal.

  24. (song2023currentknowledgeof pages 7-9): Xiangyi Song, Ruifeng Duan, Liwei Duan, and Lijuan Wei. Current knowledge of the immune reconstitution inflammatory syndrome in whipple disease: a review. Frontiers in Immunology, Oct 2023. URL: https://doi.org/10.3389/fimmu.2023.1265414, doi:10.3389/fimmu.2023.1265414. This article has 10 citations and is from a peer-reviewed journal.

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