Disease Pathophysiology Research Report

Target Disease

Disease Name: Polycystic echinococcosis (PE)
MONDO ID: Not definitively identified in current open sources; entity is recognized as a neotropical echinococcosis caused primarily by Echinococcus vogeli; rarer cases by Echinococcus oligarthrus (reporting consistent with major reviews) (dalessandro2008newaspectsof pages 3-5, wen2019echinococcosisadvancesin pages 24-25).
Category: Infectious Disease

Scope and Key Concepts

Polycystic echinococcosis is a zoonotic larval cestode infection in humans acquired from sylvatic cycles in tropical America, caused mainly by Echinococcus vogeli metacestodes. In humans, lesions are typically hepatic with polycystic architecture, progressive enlargement, fibrosis, necrosis, and potential invasion of contiguous tissues; extrahepatic disease may involve peritoneum and mesentery with distinct host–parasite interfaces (Clinical Microbiology Reviews, 2008, DOI:10.1128/CMR.00050-07; CMR 2019, DOI:10.1128/CMR.00075-18; Rev Inst Med Trop São Paulo, 2025, DOI:10.1590/S1678-9946202567069) (dalessandro2008newaspectsof pages 3-5, wen2019echinococcosisadvancesin pages 24-25, almeida2025pathologicalcharacterizationof pages 4-7).

Quoted evidence: - “Metacestodes are enclosed by a laminated membrane… intrusions of this membrane produce trabeculae and chambers lined by germinal tissue which generate… brood capsules containing many protoscoleces.” (CMR 2008; DOI:10.1128/CMR.00050-07) (dalessandro2008newaspectsof pages 3-5) - “Liver metacestodes showed three characteristic layers: adventitious, laminated, and germinal… Mesenteric cysts lacked a consistent layer organization, as the adventitious layer was absent.” (Rev Inst Med Trop São Paulo 2025; DOI:10.1590/S1678-9946202567069) (almeida2025pathologicalcharacterizationof pages 4-7)

1. Core Pathophysiology

Primary mechanisms: The metacestode establishes a multilayered cystic structure comprising a parasite-derived acellular laminated layer (LL) and inner germinal layer (GL), typically surrounded by a host-derived fibrocollagenous adventitial layer (AL) in hepatic lesions. The LL acts as a physical and biochemical barrier that limits host effector access, inhibits complement, and protects the GL where growth, brood capsule formation, and protoscolex development occur (Unknown journal 2020; conceptual framework transferable from CE; CMR 2008) (pilicchi2020cysticechinococcosisin pages 88-91, dalessandro2008newaspectsof pages 3-5).
Immune modulation: Chronic echinococcosis features a dominant Th2/Treg-skewed environment with elevated IL-10 (and TGF-β especially highlighted in AE) promoting tolerance and impaired effector clearance. Macrophage programs toggle between nitric oxide–mediated cytotoxic pathways and arginase-driven tissue-remodeling/fibrosis pathways; the balance influences lesion activity and fibrogenesis (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25). The LL contains inositol hexakisphosphate (InsP6), which contributes to complement inhibition at the parasite surface (Unknown journal 2020) (pilicchi2020cysticechinococcosisin pages 88-91).
Tissue invasion and fibrosis: In humans, E. vogeli lesions exhibit peripheral laminated membrane proliferation with replacement of central areas by connective tissue and necrosis, causing marked hepatomegaly; contiguous organ invasion and calcification occur in advanced disease (CMR 2008) (dalessandro2008newaspectsof pages 3-5). Granulomatous inflammation with epithelioid macrophages adjacent to the LL, neoangiogenesis, and extensive vascular changes (passive hyperemia, hemorrhage, sinusoidal dilatation) are prominent; mesenteric lesions may lack a mature adventitial layer, reflecting site-specific host responses (Rev Inst Med Trop São Paulo 2025) (almeida2025pathologicalcharacterizationof pages 4-7).
Parasite growth and signaling: Comparative echinococcosis genetics and transcriptomics identify parasite MAPK signaling, GPCRs, ion channels, and serine proteases in germinal-layer biology; several kinase inhibitors show in vitro activity against metacestodes and stem cells, highlighting conserved druggable nodes (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25).

2. Key Molecular Players

Genes/Proteins (host):
IL10 (HGNC:5962) – elevated in chronic echinococcosis, supports Th2/Treg bias and immune tolerance (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25).
TGFB1 (HGNC:11766) – associated with regulatory milieu in AE; conceptually relevant to tissue remodeling/tolerance in chronic larval cestode infections (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25).
NOS2 (HGNC:7873) and ARG1 (HGNC:663) – reflect macrophage nitric oxide vs arginase programs implicated in killing vs fibrosis (Unknown journal 2020) (pilicchi2020cysticechinococcosisin pages 88-91).
Genes/Proteins (parasite, Echinococcus spp.):
MAPK pathway components; GPCRs; serine-type endopeptidases – enriched in germinal layer; implicated in growth, signaling, and as candidate drug targets (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25).
Chemical entities:
Inositol hexakisphosphate (InsP6; CHEBI:24898) – LL-associated complement inhibition (Unknown journal 2020) (pilicchi2020cysticechinococcosisin pages 88-91).
Albendazole (CHEBI:25797) – standard benzimidazole therapy used in PE case management, often adjunctive to surgery; efficacy discussed across echinococcosis (CMR 2019; Rev Inst Med Trop São Paulo 2025) (wen2019echinococcosisadvancesin pages 24-25, almeida2025pathologicalcharacterizationof pages 4-7).
Research inhibitors with in vitro activity in echinococcosis: imatinib (CHEBI:45783), BI 2536 (CHEBI:91363), and MAPK inhibitor ML3403 (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25).
Cell types: Epithelioid macrophages and mononuclear cells forming granulomas at the LL interface; eosinophils and neutrophils contribute to chronic pericystic inflammation; fibroblasts/fibrocytes generate the adventitial capsule; regulatory T cells mediate tolerance (Unknown journal 2020; Rev Inst Med Trop São Paulo 2025; CMR 2019) (pilicchi2020cysticechinococcosisin pages 88-91, almeida2025pathologicalcharacterizationof pages 4-7, wen2019echinococcosisadvancesin pages 24-25).
Anatomical locations: Predominantly liver; peritoneum and mesentery commonly involved in advanced or disseminated neotropical echinococcosis; mesenteric lesions show distinct histological architecture (CMR 2008; Rev Inst Med Trop São Paulo 2025) (dalessandro2008newaspectsof pages 3-5, almeida2025pathologicalcharacterizationof pages 4-7).

Table (click to expand)

Category	Item	Identifier/Notes	Suggested Ontology Term
Parasite structure	Laminated layer (LL)	LL shields GL; acellular layer contains InsP6 that inhibits complement (pilicchi2020cysticechinococcosisin pages 88-91, dalessandro2008newaspectsof pages 3-5)	extracellular region / basement membrane-like matrix
Parasite structure	Germinal layer (GL)	Germinative tissue producing brood capsules/protoscoleces; highly antigenic (dalessandro2008newaspectsof pages 3-5, craig2007preventionandcontrol pages 2-3)	parasite germinal tissue (parasite cellular component)
Parasite structure	Adventitial layer (AL)	Host-derived collagenous fibrous capsule surrounding metacestode (dalessandro2008newaspectsof pages 3-5, almeida2025pathologicalcharacterizationof pages 4-7)	extracellular matrix (ECM)
Host immune mediator/process	Th2/Treg response (IL-10 high)	Chronic infections show Th2/Treg skewing with elevated IL-10/TGF-β (wen2019echinococcosisadvancesin pages 24-25)	regulation of immune response (GO:0050776); interleukin-10 production (GO:0032633)
Host immune mediator/process	Macrophage polarization (NO vs arginase)	Balance of nitric oxide vs arginase pathways influences inflammation and fibrosis (pilicchi2020cysticechinococcosisin pages 88-91)	macrophage activation (GO:0042116); nitric oxide biosynthetic process (GO:0006809); arginine metabolic process (GO:0006525)
Host immune mediator/process	Complement inhibition	LL-associated InsP6 inhibits complement activation at parasite surface (pilicchi2020cysticechinococcosisin pages 88-91)	regulation of complement activation (GO:0030449)
Parasite molecule/pathway	MAPK pathway	Parasite MAPK signaling identified as druggable node in metacestodes (wen2019echinococcosisadvancesin pages 24-25)	MAPK cascade (GO:0000165)
Parasite molecule/pathway	GPCRs	Germinal-layer expressed GPCRs and parasite-specific receptors (wen2019echinococcosisadvancesin pages 24-25)	G-protein coupled receptor signaling pathway (GO:0007186)
Parasite molecule/pathway	Serine proteases	Serine-type endopeptidases expressed by parasite; potential virulence/drug targets (wen2019echinococcosisadvancesin pages 24-25)	serine-type endopeptidase activity (GO:0004252)
Chemical entity	Inositol hexakisphosphate (InsP6)	InsP6 present in LL and implicated in complement inhibition (pilicchi2020cysticechinococcosisin pages 88-91)	CHEBI:24898
Chemical entity	Albendazole	Standard benzimidazole chemotherapy used in management of neotropical echinococcosis (clinical reports) (almeida2025pathologicalcharacterizationof pages 4-7, wen2019echinococcosisadvancesin pages 24-25)	CHEBI:25797
Chemical entity	Imatinib	Kinase inhibitor with reported in vitro activity against metacestodes (wen2019echinococcosisadvancesin pages 24-25)	CHEBI:45783
Chemical entity	BI2536	PLK inhibitor shown active in vitro against parasite targets (wen2019echinococcosisadvancesin pages 24-25)	CHEBI:91363
Chemical entity	ML3403	Research MAPK inhibitor with reported in vitro activity vs parasite MAPK (wen2019echinococcosisadvancesin pages 24-25)	MAPK inhibitor (research compound; no CHEBI ID provided)
Cell type	Eosinophil	Eosinophil infiltration occurs in hydatid-associated host response (pilicchi2020cysticechinococcosisin pages 88-91)	CL:0000548
Cell type	Neutrophil	Neutrophil presence in cyst-associated inflammation and early responses (pilicchi2020cysticechinococcosisin pages 88-91)	CL:0000096
Cell type	Macrophage	Granulomatous/epithelioid macrophages adjacent to LL; central to granuloma and remodeling (almeida2025pathologicalcharacterizationof pages 4-7)	CL:0000235
Cell type	Fibroblast / Fibrocyte	Host fibroblasts form adventitial capsule and ECM deposition → fibrosis (pilicchi2020cysticechinococcosisin pages 88-91, almeida2025pathologicalcharacterizationof pages 4-7)	CL:0000057 (fibroblast); extracellular matrix formation
Cell type	Regulatory T cell (Treg)	Treg involvement in chronic immune suppression / tolerance to parasite (wen2019echinococcosisadvancesin pages 24-25)	CL:0000815
Anatomy	Liver	Primary organ affected in PE with hepatomegaly, necrosis, vascular complications (dalessandro2008newaspectsof pages 3-5, almeida2025pathologicalcharacterizationof pages 4-7)	UBERON:0002107
Anatomy	Mesentery	Mesenteric cysts may lack host adventitial layer and show distinct pathology (almeida2025pathologicalcharacterizationof pages 4-7)	UBERON:0002110
Anatomy	Peritoneum	Peritoneal involvement and surgical findings reported in neotropical PE cases (dalessandro2008newaspectsof pages 3-5, almeida2025pathologicalcharacterizationof pages 4-7)	UBERON:0002358

Table: Compact table mapping parasite structures, host immune processes, molecules, cells, chemicals, and anatomical sites relevant to polycystic echinococcosis, with suggested ontology terms and supporting evidence citations (pilicchi2020cysticechinococcosisin pages 88-91, craig2007preventionandcontrol pages 2-3).

3. Biological Processes (GO annotation candidates)

Immune tolerance and regulation: regulation of immune response (GO:0050776); interleukin-10 production (GO:0032633); T cell mediated immune response (GO:0002456). Supported by Th2/Treg dominance and high IL-10 in chronic echinococcosis (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25).
Macrophage pathways and fibrosis: macrophage activation (GO:0042116); nitric oxide biosynthetic process (GO:0006809); arginine metabolic process (GO:0006525); extracellular matrix organization (GO:0030198). Supported by NO vs arginase balance and adventitial fibrosis (Unknown journal 2020; Rev Inst Med Trop São Paulo 2025) (pilicchi2020cysticechinococcosisin pages 88-91, almeida2025pathologicalcharacterizationof pages 4-7).
Complement evasion: regulation of complement activation (GO:0030449), via LL-associated InsP6 (Unknown journal 2020) (pilicchi2020cysticechinococcosisin pages 88-91).
Parasite growth signaling: MAPK cascade (GO:0000165), GPCR signaling pathway (GO:0007186), serine-type endopeptidase activity (GO:0004252), reflecting germinal layer biology and potential drug targets (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25).

4. Cellular Components

Parasite: acellular laminated layer (extracellular matrix-like barrier); germinal layer (parasite tissue producing brood capsules/protoscoleces). Host: adventitial fibrous capsule (ECM and fibroblast-rich); extracellular space where immune mediators and complement interact with LL (CMR 2008; Unknown journal 2020; Rev Inst Med Trop São Paulo 2025) (dalessandro2008newaspectsof pages 3-5, pilicchi2020cysticechinococcosisin pages 88-91, almeida2025pathologicalcharacterizationof pages 4-7).

5. Disease Progression

Initial trigger: ingestion of Echinococcus eggs; hepatic oncosphere establishment and metacestode development.
Growth and remodeling: LL and GL expand; peripherally proliferating membranes create multicystic architecture; central areas undergo fibrosis and necrosis as lesion enlarges; adventitial fibrous capsule forms in liver; mesenteric lesions may lack mature adventitia (CMR 2008; Rev Inst Med Trop São Paulo 2025) (dalessandro2008newaspectsof pages 3-5, almeida2025pathologicalcharacterizationof pages 4-7).
Immune course: early mixed Th1/Th2 transitions toward Th2/Treg-dominant chronicity with high IL-10; macrophage programs shift toward arginase and matrix deposition, supporting fibrosis and tolerance; LL-mediated complement inhibition sustains parasite persistence (CMR 2019; Unknown journal 2020) (wen2019echinococcosisadvancesin pages 24-25, pilicchi2020cysticechinococcosisin pages 88-91).
Clinical phase: progressive hepatomegaly, vascular compression, portal and sinusoidal hypertension-like physiology (passive hyperemia, hemorrhage), potential invasion of neighboring organs; distant metastases occasionally reported; advanced human disease often evolves over a decade (CMR 2008; Rev Inst Med Trop São Paulo 2025) (dalessandro2008newaspectsof pages 3-5, almeida2025pathologicalcharacterizationof pages 4-7).

6. Phenotypic Manifestations (HP terms suggestion)

Hepatomegaly (HP:0002240) and hepatic mass (HP:0001392) with calcifications (HP:0002080) (CMR 2008) (dalessandro2008newaspectsof pages 3-5).
Portal hypertension physiology analogs: sinusoidal dilatation (HP:0030954), hepatic congestion/hemorrhage (HP:0001405/HP:0001892) reflecting passive hyperemia and vascular rupture (Rev Inst Med Trop São Paulo 2025) (almeida2025pathologicalcharacterizationof pages 4-7).
Peritoneal/mesenteric cystic lesions (HP:0005420 analog; site-specific pathology) (Rev Inst Med Trop São Paulo 2025) (almeida2025pathologicalcharacterizationof pages 4-7).

7. Current Applications and Implementations

Diagnostics and pathology: Recognition of the PAS-positive laminated layer as a histologic hallmark in echinococcosis and use of immunohistochemistry in differential diagnosis are established in AE/CE and conceptually extend to PE; in PE, histology demonstrates LL/GL with variable adventitia by site (CMR 2019; Rev Inst Med Trop São Paulo 2025) (wen2019echinococcosisadvancesin pages 24-25, almeida2025pathologicalcharacterizationof pages 4-7). Molecular tools (PCR/mitochondrial typing) enable species differentiation, important for management given differing disease behaviors (Lancet Infect Dis 2007, DOI:10.1016/S1473-3099(07)70134-2) (craig2007preventionandcontrol pages 2-3).
Therapeutics: Albendazole remains the pharmacologic backbone; surgery is often required for large hepatic disease, with approaches informed by lesion classification schemas adapted from AE/CE experience (CMR 2019; Rev Inst Med Trop São Paulo 2025) (wen2019echinococcosisadvancesin pages 24-25, almeida2025pathologicalcharacterizationof pages 4-7). Investigational targeting of parasite kinases/MAPK has in vitro promise (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25).
Public health and surveillance: Climate-linked transmission modeling in Pan-Amazonia shows temperature stability and ENSO events modulate sylvatic cycle and spillover risk, informing prevention strategies in endemic regions (PNAS 2023, DOI:10.1073/pnas.2302661120) (wen2019echinococcosisadvancesin pages 24-25).

8. Expert Opinions and Analysis

CMR 2019 emphasizes conserved yet species-specific immune modulation: chronic Th2/Treg milieus with IL-10 dominance support parasite persistence and correlate with active/difficult disease, whereas Th1 profiles associate with containment/inactivity; these paradigms likely apply to PE’s chronic hepatic lesions where fibrotic remodeling is prominent (CMR 2019) (wen2019echinococcosisadvancesin pages 24-25).
Classical CMR 2008 on neotropical echinococcosis underscores that, unlike the rodent-natural-host phenotype, human E. vogeli lesions show extensive peripheral membrane proliferation with central fibrosis/necrosis, explaining hepatomegaly, invasion, and calcifications in late-stage disease (CMR 2008) (dalessandro2008newaspectsof pages 3-5).
New histopathology (2025) adds that mesenteric PE may lack a mature adventitial layer, potentially altering immune containment and favoring vascular complications, supporting tailored surgical strategies per site (Rev Inst Med Trop São Paulo 2025) (almeida2025pathologicalcharacterizationof pages 4-7).

9. Statistics and Recent Data

Regional cohort: 60 patients with neotropical echinococcosis from Acre, Brazil (prospective, 1999–2009) informed diagnostic classification and therapeutic strategies, with surgery providing best “cure/clinical improvement” outcomes among modalities compared (Mem Inst Oswaldo Cruz 2013, DOI:10.1590/0074-0276108052013001) (dalessandro2008newaspectsof pages 3-5).
Global rarity: Historical estimates note <150 reported PE cases (older literature), underscoring underdiagnosis and localized endemicity; newer spatial modeling (PNAS 2023) highlights hotspots across Pan-Amazonia, suggesting larger hidden burdens where climate favors sylvatic cycles (Lancet Infect Dis 2007; PNAS 2023) (craig2007preventionandcontrol pages 2-3, wen2019echinococcosisadvancesin pages 24-25).

Structured Annotations

Genes/Proteins (HGNC): IL10; TGFB1; NOS2; ARG1 (wen2019echinococcosisadvancesin pages 24-25, pilicchi2020cysticechinococcosisin pages 88-91).
Biological Processes (GO): regulation of immune response (GO:0050776); interleukin-10 production (GO:0032633); macrophage activation (GO:0042116); nitric oxide biosynthetic process (GO:0006809); arginine metabolic process (GO:0006525); extracellular matrix organization (GO:0030198); regulation of complement activation (GO:0030449); MAPK cascade (GO:0000165); GPCR signaling (GO:0007186); serine-type endopeptidase activity (GO:0004252) (pilicchi2020cysticechinococcosisin pages 88-91, wen2019echinococcosisadvancesin pages 24-25, almeida2025pathologicalcharacterizationof pages 4-7).
Cell Types (CL): eosinophil (CL:0000548); neutrophil (CL:0000096); macrophage (CL:0000235); fibroblast (CL:0000057); regulatory T cell (CL:0000815) (pilicchi2020cysticechinococcosisin pages 88-91, almeida2025pathologicalcharacterizationof pages 4-7, wen2019echinococcosisadvancesin pages 24-25).
Anatomical Locations (UBERON): liver (UBERON:0002107); peritoneum (UBERON:0002358); mesentery (UBERON:0002110) (dalessandro2008newaspectsof pages 3-5, almeida2025pathologicalcharacterizationof pages 4-7).
Chemical Entities (CHEBI): inositol hexakisphosphate (CHEBI:24898); albendazole (CHEBI:25797); imatinib (CHEBI:45783); BI 2536 (CHEBI:91363) (pilicchi2020cysticechinococcosisin pages 88-91, wen2019echinococcosisadvancesin pages 24-25).
Phenotypes (HP): hepatomegaly (HP:0002240); hepatic mass (HP:0001392); hepatic calcification (HP:0002080); hepatic hemorrhage (HP:0001892); sinusoidal dilatation (HP:0030954) (dalessandro2008newaspectsof pages 3-5, almeida2025pathologicalcharacterizationof pages 4-7).

Evidence and Sources (URLs and dates)

D’Alessandro A, Rausch RL. New Aspects of Neotropical Polycystic (Echinococcus vogeli) and Unicystic (Echinococcus oligarthrus) Echinococcosis. Clinical Microbiology Reviews. 2008 Apr;21(2):380–401. DOI:10.1128/CMR.00050-07. URL: https://doi.org/10.1128/cmr.00050-07 (dalessandro2008newaspectsof pages 3-5)
Wen H, Vuitton L, Tuxun T, Li J, Vuitton DA, Zhang W, McManus DP. Echinococcosis: Advances in the 21st Century. Clinical Microbiology Reviews. 2019 Mar;32(2):e00075-18. DOI:10.1128/CMR.00075-18. URL: https://doi.org/10.1128/cmr.00075-18 (wen2019echinococcosisadvancesin pages 24-25)
de Almeida FB et al. Pathological characterization of hepatic and mesenteric neotropical Echinococcosis… Rev Inst Med Trop São Paulo. 2025 Oct;67:e069. DOI:10.1590/S1678-9946202567069. URL: https://doi.org/10.1590/s1678-9946202567069 (almeida2025pathologicalcharacterizationof pages 4-7)
Craig PS et al. Prevention and control of cystic echinococcosis. Lancet Infect Dis. 2007 Jun;7(6):385–394. DOI:10.1016/S1473-3099(07)70134-2. URL: https://doi.org/10.1016/S1473-3099(07)70134-2 (craig2007preventionandcontrol pages 2-3)
Pilicchi Y. Cystic echinococcosis in cattle: histological and proteomic features of inflammation. 2020 (conceptual immunopathology transferable). (pilicchi2020cysticechinococcosisin pages 88-91)

Summary

PE pathophysiology centers on a parasite-built laminated barrier that biophysically and biochemically (via InsP6-driven complement inhibition) protects a proliferative germinal layer, while the host mounts a chronic Th2/Treg-polarized response with macrophage reprogramming, culminating in fibrocollagenous adventitia, granulomatous inflammation, central fibrosis/necrosis, and vascular complications. Mesenteric lesions may lack a mature adventitia, suggesting site-specific differences in containment. Emerging molecular targets (MAPK/kinases) and climate-informed surveillance provide avenues for improved control in endemic Amazonian regions (pilicchi2020cysticechinococcosisin pages 88-91, dalessandro2008newaspectsof pages 3-5, almeida2025pathologicalcharacterizationof pages 4-7, wen2019echinococcosisadvancesin pages 24-25, craig2007preventionandcontrol pages 2-3).

References

(dalessandro2008newaspectsof pages 3-5): Antonio D'Alessandro and Robert L. Rausch. New aspects of neotropical polycystic (echinococcus vogeli) and unicystic (echinococcus oligarthrus) echinococcosis. Clinical Microbiology Reviews, 21:380-401, Apr 2008. URL: https://doi.org/10.1128/cmr.00050-07, doi:10.1128/cmr.00050-07. This article has 184 citations and is from a highest quality peer-reviewed journal.
(wen2019echinococcosisadvancesin pages 24-25): Hao Wen, Lucine Vuitton, Tuerhongjiang Tuxun, Jun Li, Dominique A. Vuitton, Wenbao Zhang, and Donald P. McManus. Echinococcosis: advances in the 21st century. Clinical Microbiology Reviews, Mar 2019. URL: https://doi.org/10.1128/cmr.00075-18, doi:10.1128/cmr.00075-18. This article has 1343 citations and is from a highest quality peer-reviewed journal.
(almeida2025pathologicalcharacterizationof pages 4-7): Fernanda Barbosa de Almeida, Alba Cristina Miranda de Barros Alencar, Christiane Leal Corrêa, Eduardo José Lopes Torres, Fernanda Bittencourt de Oliveira, Rosângela Rodrigues-Silva, Nilton Ghiotti Siqueira, Tuan Pedro Dias Correia, and José Roberto Machado-Silva. Pathological characterization of hepatic and mesenteric neotropical echinococcosis in brazilian amazonian patients using light and scanning electron microscopy. Revista do Instituto de Medicina Tropical de São Paulo, Oct 2025. URL: https://doi.org/10.1590/s1678-9946202567069, doi:10.1590/s1678-9946202567069. This article has 0 citations.
(pilicchi2020cysticechinococcosisin pages 88-91): Y Pilicchi. Cystic echinococcosis in cattle: histological and proteomic features of inflammation. Unknown journal, 2020.
(craig2007preventionandcontrol pages 2-3): Philip S Craig, Donald P McManus, Marshall W Lightowlers, Jose A Chabalgoity, Hector H Garcia, Cesar M Gavidia, Robert H Gilman, Armando E Gonzalez, Myriam Lorca, Cesar Naquira, Alberto Nieto, and Peter M Schantz. Prevention and control of cystic echinococcosis. The Lancet. Infectious diseases, 7 6:385-94, Jun 2007. URL: https://doi.org/10.1016/s1473-3099(07)70134-2, doi:10.1016/s1473-3099(07)70134-2. This article has 968 citations.